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1. Steiner T, Pilz J, Schellinger P, Wirtz R, Friederichs V, Aschoff A, Hacke W: Multimodal online monitoring in middle cerebral artery territory stroke. Stroke; 2001 Nov;32(11):2500-6
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  • BACKGROUND AND PURPOSE: Patients with large middle cerebral artery infarction and elevated intracranial pressure (ICP) who are undergoing invasive intensive care therapy require technical monitoring.
  • Furthermore, the effects of what is considered to be standard antiedema medical treatment are not fully understood.
  • METHODS: ICP, cerebral perfusion pressure (CPP), and partial brain tissue oxygen pressure (PbrO(2)) were continuously measured within the white matter of the frontal lobe unilaterally or bilaterally.
  • We analyzed the effects of antiedema drugs and looked for pattern changes in the PbrO(2) before transtentorial herniation in patients in whom this could not be prevented.
  • A total of 297 antiedema drug administrations were analyzed in 11 patients.
  • Hyper-HAES and mannitol were most often associated with an increase in CPP and PbrO(2), whereas the use of thiopental and tromethamine led to negative or contrary effects, although ICP was decreased in every case.
  • CONCLUSIONS: Multimodal monitoring can be used to monitor antiedema drug effects.
  • Furthermore, this method might help to optimize the timing of invasive therapy in space-occupying infarction.
  • [MeSH-major] Infarction, Middle Cerebral Artery / drug therapy. Monitoring, Physiologic / methods. Online Systems
  • [MeSH-minor] Brain Edema / drug therapy. Feasibility Studies. Frontal Lobe / chemistry. Frontal Lobe / physiopathology. Humans. Intracranial Hypertension. Intracranial Pressure / drug effects. Oxygen / analysis. Partial Pressure

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  • (PMID = 11692007.001).
  • [ISSN] 1524-4628
  • [Journal-full-title] Stroke; a journal of cerebral circulation
  • [ISO-abbreviation] Stroke
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] S88TT14065 / Oxygen
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2. Le Foll B, Sokoloff P, Stark H, Goldberg SR: Dopamine D3 receptor ligands block nicotine-induced conditioned place preferences through a mechanism that does not involve discriminative-stimulus or antidepressant-like effects. Neuropsychopharmacology; 2005 Apr;30(4):720-30
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  • Environmental stimuli previously paired with drug taking appear to play a critical role in nicotine dependence.
  • Converging anatomical, pharmacological, and behavioral evidence implicates dopamine D3 receptors (D3Rs) in the mechanisms underlying stimulus-controlled drug-seeking behavior.
  • This study assessed the effects of BP 897, a D3R partial agonist and ST 198, a D3R antagonist, on nicotine-induced conditioned place preferences (CPPs), used as a measure of drug-seeking behavior, on food-maintained responding and on discrimination performance under a two-lever-choice nicotine discrimination procedure.
  • BP 897 and ST 198 both blocked the expression of nicotine-induced CPP at doses selective for D3R.
  • They had no effect on locomotor activity in the CPP apparatus and no significant effect on nicotine discrimination performance or food-maintained responding under the discrimination procedure.
  • Involvement of antidepressant actions in the effects of BP 897 and ST 198 on CPP is unlikely, since we found no effect of D3R blockade with BP 897 or genetic depletion of D3Rs in a forced swimming test, used as a behavioral test for antidepressant activity.
  • This suggests that D3R ligands reduce the motivational effects of nicotine by a mechanism distinct from those of nicotine replacement therapy and bupropion, the two currently used aids for smoking cessation in humans.
  • [MeSH-major] Dopamine Agents / pharmacology. Nicotine / antagonists & inhibitors. Receptors, Dopamine D2 / agonists. Spatial Behavior / drug effects. Tobacco Use Disorder / drug therapy
  • [MeSH-minor] Acrylamides / pharmacology. Animals. Antidepressive Agents / pharmacology. Conditioning (Psychology) / drug effects. Conditioning (Psychology) / physiology. Discrimination (Psychology) / drug effects. Discrimination (Psychology) / physiology. Disease Models, Animal. Dopamine Agonists / pharmacology. Dopamine Antagonists / pharmacology. Drug Interactions / physiology. Female. Isoquinolines / pharmacology. Ligands. Limbic System / drug effects. Limbic System / metabolism. Limbic System / physiopathology. Male. Mice. Mice, Knockout. Piperazines / pharmacology. Rats. Rats, Sprague-Dawley. Receptors, Dopamine D3

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  • (PMID = 15562293.001).
  • [ISSN] 0893-133X
  • [Journal-full-title] Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
  • [ISO-abbreviation] Neuropsychopharmacology
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ((E)-N-4-(1,2,3,4-tetrahydroisoquinolin-2-yl)butyl)-3-phenylacrylamide; 0 / Acrylamides; 0 / Antidepressive Agents; 0 / BP 897; 0 / Dopamine Agents; 0 / Dopamine Agonists; 0 / Dopamine Antagonists; 0 / Drd3 protein, mouse; 0 / Drd3 protein, rat; 0 / Isoquinolines; 0 / Ligands; 0 / Piperazines; 0 / Receptors, Dopamine D2; 0 / Receptors, Dopamine D3; 6M3C89ZY6R / Nicotine
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3. Antoniazzi F, Zamboni G, Bertoldo F, Lauriola S, Tatò L: Bone development during GH and GnRH analog treatment. Eur J Endocrinol; 2004 Aug;151 Suppl 1:S47-54
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  • [Title] Bone development during GH and GnRH analog treatment.
  • Treatment of precocious puberty with GnRH analogs (GnRHa), by reducing sex steroid levels, leads to a situation of hypoestrogenism that may theoretically have a detrimental effect on bone mass during pubertal development.
  • A reduction in bone mineral density (BMD) during GnRHa treatment has been demonstrated, but GnRHa treatment in patients with central precocious puberty (CPP) does not seem to impair the achievement of normal peak bone mass (PBM) at final height.
  • In children and adolescents with GH deficiency (GHD), BMD assessed by dual-energy X-ray absorptiometry (DEXA) and bone turnover are significantly reduced, but they are stimulated by GH treatment.
  • GH treatment leads to improved bone density, function of the dose and duration of treatment, and patients may require prolonged GH treatment beyond the time of growth to improve PBM.
  • After the discontinuation of GH therapy, the more active population had higher bone mineral content (BMC) levels than patients with low physical activity.
  • In our experience, the therapeutic association of GH and calcium also represents a valuable tool in pursuing a proper BMC in GHD patients.

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  • (PMID = 15339244.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 12629-01-5 / Human Growth Hormone; 33515-09-2 / Gonadotropin-Releasing Hormone; 79561-22-1 / LHRH, Ala(6)-Gly(10)-ethylamide-; 9002-72-6 / Growth Hormone
  • [Number-of-references] 69
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4. Municchi G, Marconcini S, D'Ambrosio A, Berardi R, Acquaviva A: Central precocious puberty in multisystem Langerhans cell histiocytosis: a case report. Pediatr Hematol Oncol; 2002 Jun;19(4):273-8
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  • The authors describe a girl with multisystem Langerhans cell histiocytosis (LCH) who developed central precocious puberty (CPP).
  • She subsequently developed diabetes insipidus with a documented lesion of the pituitary stalk; she received chemotherapy and began therapy with l-desamino-8-D-argininevasopressin.
  • Growth hormone deficiency was diagnosed at the age of 4.4 years and GH replacement therapy started.
  • The patient has been off therapy for LCH since the age of 6.
  • Signs of pubertal development appeared at 7.5 years (bone age 8 years) and gonadotropin-releasing hormone analog (GnRHa) treatment was started.
  • During the observation period she developed central hypothyroidism.
  • Development of CPP during LCH is extremely rare; to the authors 'knowledge, no patient has been described so far.
  • The authors believe that CPP was secondary to LCH and did not represent a casual finding, even in the absence of hypothalamic-pituitary axis involvement.
  • The possibility of CPP development should be considered during the follow-up of these patients.


5. Nomura Y, Yasumoto S, Yanai F, Akiyoshi H, Inoue T, Nibu K, Tsugu H, Fukushima T, Hirose S: Survival and late effects on development of patients with infantile brain tumor. Pediatr Int; 2009 Jun;51(3):337-41
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  • [Title] Survival and late effects on development of patients with infantile brain tumor.
  • BACKGROUND: Most infants with brain tumor may have a poor prognosis.
  • The aim of the present study was to retrospectively analyze the survival and outcome with regard to mental and physical development in 11 subjects with brain tumor; these tumors were diagnosed when the patients were under 1 year of age.
  • METHODS: The histological diagnoses of these tumors were astrocytoma, n = 3; pineocytoma, n = 2; teratoma, n = 1; ependymoma, n = 1; atypical teratoid/rhabdoid tumor, n = 1; glioblastoma, n = 1; medulloblastoma, n = 1; and choroid plexus papilloma, n = 1.
  • Surgical resection was performed in eight patients, and adjuvant chemotherapy was administered to all except one patient with choroid plexus papilloma.
  • Radiotherapy was additionally performed for four of the 10 chemotherapy patients.
  • Among the surviving patients, five were under no treatment for 50-167 months after the diagnosis (median duration, 89 months), while one received chemotherapy for 20 months.
  • Five patients exhibited mental retardation, and one patient experienced normal development after surgical removal of his choroid plexus papilloma.
  • Diencephalic syndrome developed in one patient with pilomyxoid astrocytoma that necessitated hormone replacement therapy, and bodyweight over +2 SD was observed in two patients.
  • The remaining five patients died 11-111 months after diagnosis (median duration, 24 months).
  • CONCLUSION: The prognosis of infantile brain tumor with regard to mortality and developmental outcome remains poor.
  • [MeSH-major] Astrocytoma / mortality. Brain Neoplasms / mortality. Child Development. Pinealoma / mortality
  • [MeSH-minor] Chemotherapy, Adjuvant. Female. Humans. Infant. Infant, Newborn. Magnetic Resonance Imaging. Male. Prognosis. Quality of Life. Radiotherapy, Adjuvant


6. Lu L, Zeng S, Liu D, Ceng X: Inhibition of the amygdala and hippocampal calcium/calmodulin-dependent protein kinase II attenuates the dependence and relapse to morphine differently in rats. Neurosci Lett; 2000 Sep 22;291(3):191-5
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  • Based on the recent finding that calcium/calmodulin protein kinase II (CaMKII) is essential in learning and memory processes, the present study was performed to examine whether inhibition of hippocampal and amygdala CaMKII prevents the dependence and relapse to morphine.
  • Microinjection of KN-62 into both hippocampus and amygdala suppressed the development of formation and reactivation of morphine conditioned place preference (CPP).
  • However, inhibition of CaMKII in amygdala, but not in hippocampus, could attenuate the maintenance of morphine CPP.
  • Inhibition of this kinase may have some therapeutic benefit in the treatment of opiate dependence and relapse.
  • [MeSH-minor] Animals. Behavior, Animal / drug effects. Calcium-Calmodulin-Dependent Protein Kinase Type 2. Conditioning (Psychology) / drug effects. Enzyme Inhibitors / administration & dosage. Male. Microinjections. Morphine / pharmacology. Naloxone / pharmacology. Rats. Rats, Sprague-Dawley. Substance Withdrawal Syndrome / drug therapy. Substance Withdrawal Syndrome / enzymology

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  • (PMID = 10984639.001).
  • [ISSN] 0304-3940
  • [Journal-full-title] Neuroscience letters
  • [ISO-abbreviation] Neurosci. Lett.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] IRELAND
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 127191-97-3 / KN 62; 36B82AMQ7N / Naloxone; 76I7G6D29C / Morphine; 84477-87-2 / 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinases
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7. Kumar B, Saraswat A, Kaur I: Rediscovering hydroxyurea: its role in recalcitrant psoriasis. Int J Dermatol; 2001 Aug;40(8):530-4
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • BACKGROUND: There is an acute paucity of second-line systemic agents for the treatment of extensive chronic plaque psoriasis (CPP).
  • Recent studies using hydroxyurea in patients with HIV infection and sickle cell anemia have rekindled interest in this old drug and have provided more data regarding safety and dosage.
  • OBJECTIVE: We wanted to test the efficacy and tolerability of hydroxyurea in patients with extensive CPP who had to discontinue first-line oral agents for any reason.
  • Thirty-one patients, including 26 with prior history of systemic antipsoriatic therapy were given hydroxyurea 1-1.5 g per day for a median duration of 36 weeks.
  • They were followed up for a mean period of 36.1 +/- 13.8 weeks.
  • All adverse effects were mild and reversible and none of the patients required cessation of therapy.
  • CONCLUSION: Hydroxyurea is an effective, very safe but relatively slower acting alternative for patients with extensive CPP over the short-to-medium term.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Hydroxyurea / therapeutic use. Psoriasis / drug therapy
  • [MeSH-minor] Adult. Female. Humans. Male. Middle Aged. Prospective Studies. Skin Pigmentation / drug effects

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  • (PMID = 11703528.001).
  • [ISSN] 0011-9059
  • [Journal-full-title] International journal of dermatology
  • [ISO-abbreviation] Int. J. Dermatol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; X6Q56QN5QC / Hydroxyurea
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8. Llena C, Forner L, Baca P: Anticariogenicity of casein phosphopeptide-amorphous calcium phosphate: a review of the literature. J Contemp Dent Pract; 2009;10(3):1-9
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • AIM: This review of the literature examines the role of the natural components of saliva in maintaining tooth mineralization and the role of different casein phosphopeptide amorphous calcium phosphate-based (CPP-ACP) compounds in controlling demineralization/remineralization and their clinical applications.
  • BACKGROUND: A group of peptides, known as CPP, have been shown to stabilize calcium and phosphate preserving them in an amorphous or soluble form known as amorphous calcium phosphate (ACP).
  • Calcium and phosphate are essential components of enamel and dentine and form highly insoluble complexes, but in the presence of CPP they remain soluble and biologically available.
  • This CPP-ACP complex applied to teeth by means of chewing-gum, toothpaste, lozenges, mouth rinses, or sprays is able to adhere to the dental biofilm and enamel hydroxyapatite providing bioavailable calcium and phosphate ions.
  • REVIEW RESULTS: Significantly high levels of calcium and phosphate have been found in both biofilm and subsurface incipient caries lesions and in lower level demineralization of enamel or dentine surfaces previously treated with CPP-ACP based compounds.
  • When placed on the surface of a tooth with early carious lesions, pastes with CPP-ACP complexes can prevent tooth demineralization and improve enamel remineralization and enhance fluoride activity.
  • CLINICAL SIGNIFICANCE: Use of CPP-ACP based compounds offers a potential for use in the prevention of dental caries.
  • [MeSH-major] Cariostatic Agents / therapeutic use. Caseins / therapeutic use. Dental Caries / prevention & control
  • [MeSH-minor] Biofilms. Calcium / pharmacokinetics. Dental Enamel / metabolism. Dental Plaque / chemistry. Dentin / metabolism. Humans. Phosphates / pharmacokinetics. Saliva / physiology. Tooth Erosion / prevention & control. Tooth Remineralization / methods. Xerostomia / drug therapy

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  • (PMID = 19430620.001).
  • [ISSN] 1526-3711
  • [Journal-full-title] The journal of contemporary dental practice
  • [ISO-abbreviation] J Contemp Dent Pract
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cariostatic Agents; 0 / Caseins; 0 / Phosphates; 0 / casein phosphopeptide-amorphous calcium phosphate nanocomplex; SY7Q814VUP / Calcium
  • [Number-of-references] 31
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9. Lang EW, Chesnut RM: A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients. Br J Neurosurg; 2000 Apr;14(2):117-26
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  • [Title] A bedside method for investigating the integrity and critical thresholds of cerebral pressure autoregulation in severe traumatic brain injury patients.
  • To avoid ischaemic secondary insults after severe head injury (SHI) it would be helpful to know the relationship between cerebral perfusion pressure (CPP) and intracranial pressure (ICP).
  • Mean arterial pressure (MAP) was varied to detect changes in intracranial pressure (ICP) indicative of intact AR.
  • Three types of responses were observed:.
  • (3) MAP elevation lowers ICP; Changes between types 1/2 and type 3 suggests AR breakpoints.
  • Varying response types and breakpoints were observed between and within patients.
  • Lower AR breakpoints were seen from 60 to 80 mmHg CPP, upper breakpoints were as high as 112.
  • CPP monitoring achieves a twofold utility in targeted therapy:.
  • Although the precise relationship between pAR breakpoints and the adequacy of cerebral perfusion to meet metabolic needs remains unclear, a technique such as described here is simple and has much to offer in targeting therapy toward specific pathophysiological processes in traumatic brain injury.
  • [MeSH-major] Brain Injuries / physiopathology. Homeostasis / physiology. Intracranial Pressure / physiology. Point-of-Care Systems
  • [MeSH-minor] Adolescent. Adult. Blood Pressure / drug effects. Blood Pressure / physiology. Cerebrovascular Circulation / drug effects. Cerebrovascular Circulation / physiology. Glasgow Coma Scale. Humans. Male. Middle Aged. Phenylephrine / pharmacology. Vasoconstrictor Agents / pharmacology

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  • (PMID = 10889883.001).
  • [ISSN] 0268-8697
  • [Journal-full-title] British journal of neurosurgery
  • [ISO-abbreviation] Br J Neurosurg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Vasoconstrictor Agents; 1WS297W6MV / Phenylephrine
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10. Chiu WT, Lin TJ, Lin JW, Huang SJ, Chang CK, Chen HY: Multicenter evaluation of propofol for head-injured patients in Taiwan. Surg Neurol; 2006;66 Suppl 2:S37-42
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  • BACKGROUND: The present study was a multicenter, retrospective study which aimed to evaluate the efficacy of propofol, a new choice of pharmacotherapy in head-injured patients.
  • Data on patients' demographics, laboratory data, GCS score, ICP, CPP, concurrent medications, and therapeutic outcomes were collected.
  • Mean CPP for the first 5 days in the ICU was 71.10 +/- 15.32 mm Hg in the propofol group and 43.20 +/- 29.92 mm Hg in the nonpropofol group (P<.001).
  • [MeSH-major] Brain Injuries / drug therapy. Brain Injuries / mortality. Hypnotics and Sedatives / therapeutic use. Propofol / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Child. Female. Glasgow Coma Scale. Humans. Male. Middle Aged. Retrospective Studies. Survival Rate. Taiwan / epidemiology. Treatment Outcome

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  • (PMID = 17071254.001).
  • [ISSN] 0090-3019
  • [Journal-full-title] Surgical neurology
  • [ISO-abbreviation] Surg Neurol
  • [Language] eng
  • [Publication-type] Controlled Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hypnotics and Sedatives; YI7VU623SF / Propofol
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11. Yang H, Liu S, Cai H, Wan L, Li S, Li Y, Cheng J, Lu X: Chondroitin sulfate as a molecular portal that preferentially mediates the apoptotic killing of tumor cells by penetratin-directed mitochondria-disrupting peptides. J Biol Chem; 2010 Aug 13;285(33):25666-76
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  • [Title] Chondroitin sulfate as a molecular portal that preferentially mediates the apoptotic killing of tumor cells by penetratin-directed mitochondria-disrupting peptides.
  • The use of cell-penetrating peptides (CPPs) as drug carriers for targeted therapy is limited by the unrestricted cellular translocation of CPPs.
  • The preferential induction of tumor cell death by penetratin (Antp)-directed peptides (PNC27 and PNC28), however, suggests that the CPP Antp may contribute to the preferential cytotoxicity of these peptides.
  • The IC(50) values of PNC27 in tumor cells were 2-3 times lower than in normal cells.
  • However, all three engineered peptides demonstrated similar cytotoxic effects in tumor and normal cells.
  • Another three chimeric peptides containing the leader peptide Antp with different mitochondria-disrupting peptides (KLA-Antp (KGA), B27-Antp (BA27), and B28-Antp (BA28)), preferentially induced apoptosis in tumor cells.
  • The IC(50) values of these peptides (3-10 microM) were 3-6 times lower in tumor cells than in normal cells.
  • In contrast, TAT-directed peptides (TAT-KLA (TK), TAT-B27 (TB27), and TAT-B28 (TB28)), were cytotoxic to both tumor and normal cells.
  • Furthermore, Antp-directed peptides bind chondroitin sulfate (CS), and the removal of endogenous CS reduces the cytotoxic effects of Antp-directed peptides in tumor cells.
  • The overexpression of CS in tumor cells is positively correlated to the cell entry and cytotoxicity of Antp- directed peptides.
  • These results suggest that CS overexpression in tumor cells is an important molecular portal that mediates the preferential cytotoxicity of Antp-directed peptides.
  • [MeSH-major] Apoptosis / drug effects. Carrier Proteins / pharmacology. Chondroitin Sulfates / pharmacology. Mitochondria / drug effects. Mitochondria / metabolism. Peptides / pharmacology
  • [MeSH-minor] Animals. Biological Transport / drug effects. Cell Line. Cell Line, Tumor. Cell Survival / drug effects. Female. Glycosaminoglycans / metabolism. Glycosaminoglycans / pharmacology. HeLa Cells. Humans. Mice. Mice, Inbred BALB C. Mice, Nude. Tumor Suppressor Protein p53 / pharmacology. Tumor Suppressor Protein p53 / therapeutic use. Xenograft Model Antitumor Assays

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  • [Cites] Cancer Res. 2006 Nov 1;66(21):10233-7 [17079438.001]
  • [Cites] AAPS J. 2006;8(3):E532-51 [17025272.001]
  • [Cites] Eur J Cancer. 2007 Jun;43(9):1460-6 [17446061.001]
  • [Cites] Cancer Res. 2007 Jul 1;67(13):6368-75 [17616696.001]
  • [Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):788-93 [17635149.001]
  • [Cites] J Pharm Sci. 2008 Jan;97(1):144-62 [17763452.001]
  • [Cites] Acc Chem Res. 2008 Jan;41(1):98-107 [17705444.001]
  • [Cites] Bioconjug Chem. 2008 Jan;19(1):70-5 [18001077.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Mar 1;60(4-5):580-97 [18045730.001]
  • [Cites] Org Biomol Chem. 2008 Jul 7;6(13):2242-55 [18563254.001]
  • [Cites] In Vivo. 2008 May-Jun;22(3):385-9 [18610752.001]
  • [Cites] J Biol Chem. 2008 Aug 29;283(35):24274-84 [18603532.001]
  • [Cites] Biochim Biophys Acta. 2008 Dec;1786(2):126-38 [18440319.001]
  • [Cites] Ann Surg Oncol. 2008 Dec;15(12):3588-600 [18931881.001]
  • [Cites] Curr Drug Discov Technol. 2008 Dec;5(4):289-301 [19075609.001]
  • [Cites] Bioconjug Chem. 2008 Dec;19(12):2363-74 [19053306.001]
  • [Cites] Cancer Metastasis Rev. 2009 Jun;28(1-2):233-45 [19160015.001]
  • [Cites] J Biol Chem. 1999 Dec 3;274(49):34924-31 [10574967.001]
  • [Cites] Curr Opin Cell Biol. 2000 Aug;12(4):400-6 [10873818.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Oct 23;98(22):12438-43 [11606716.001]
  • [Cites] Mol Cell Biol. 2002 Mar;22(6):1926-35 [11865069.001]
  • [Cites] Cancer Res. 2002 Aug 1;62(15):4282-8 [12154030.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Nov 1;298(3):439-49 [12413961.001]
  • [Cites] Oncogene. 2003 Mar 13;22(10):1431-44 [12629507.001]
  • [Cites] Blood. 2003 Aug 15;102(4):1307-15 [12738679.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35109-14 [12837762.001]
  • [Cites] Cell Mol Life Sci. 2004 Jul;61(14):1785-94 [15241554.001]
  • [Cites] J Biol Chem. 1996 Nov 8;271(45):28375-81 [8910461.001]
  • [Cites] Cell. 1997 Feb 7;88(3):323-31 [9039259.001]
  • [Cites] Biochemistry. 1997 Feb 25;36(8):2104-11 [9047309.001]
  • [Cites] Proc Natl Acad Sci U S A. 1998 May 26;95(11):6079-84 [9600920.001]
  • [Cites] Nat Med. 1999 Sep;5(9):1032-8 [10470080.001]
  • [Cites] Int J Cancer. 2005 May 20;115(1):55-64 [15645452.001]
  • [Cites] Biochem J. 2005 Sep 1;390(Pt 2):407-18 [15859953.001]
  • [Cites] Cancer Res. 2005 Sep 1;65(17):7840-6 [16140953.001]
  • [Cites] Cancer Res. 2005 Dec 1;65(23):10646-50 [16322205.001]
  • [Cites] Mol Cancer Ther. 2006 Jan;5(1):20-8 [16432159.001]
  • [Cites] Cancer Res. 2006 Apr 1;66(7):3764-72 [16585203.001]
  • [Cites] Int J Cancer. 2006 Oct 1;119(7):1577-85 [16688716.001]
  • [Cites] Mol Cancer Ther. 2006 Aug;5(8):1944-9 [16928814.001]
  • [Cites] J Am Chem Soc. 2007 Apr 25;129(16):4961-72 [17397150.001]
  • (PMID = 20484051.001).
  • [ISSN] 1083-351X
  • [Journal-full-title] The Journal of biological chemistry
  • [ISO-abbreviation] J. Biol. Chem.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Carrier Proteins; 0 / Glycosaminoglycans; 0 / PNC-27; 0 / Peptides; 0 / Tumor Suppressor Protein p53; 0 / penetratin; 9007-28-7 / Chondroitin Sulfates
  • [Other-IDs] NLM/ PMC2919130
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12. Nishiyama T, Yokoyama T, Matsukawa T, Hanaoka K: Continuous nicardipine infusion to control blood pressure after evacuation of acute cerebral hemorrhage. Can J Anaesth; 2000 Dec;47(12):1196-201
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  • PURPOSE: To explore the long-term effects of the calcium antagonist, nicardipine, on cerebral hemodynamics in patients with acute cerebral hemorrhage, we investigated the effects of nicardipine infusion on intracranial pressure (ICP), middle cerebral arterial blood flow velocity (Vmca) , and computed tomographical (CT) findings of bleeding and edema.
  • Blood pressure, heart rate, conscious level, Vmca, pulsatility index (PI, using transcranial Doppler), ICP, cerebral perfusion pressure (CPP) and platelet counts were monitored.
  • CT examination was also performed to detect the changes of bleeding (hematoma) and/or brain edema.
  • The CPP decreased at 24 hr (75 +/- 14 mmHg, P = 0.026) and 72 hr (73 +/- 15 mmHg, P = 0.024) from the baseline (99 +/- 17 mmHg).
  • CONCLUSION: In patients with acute cerebral hemorrhage, nicardipine infusion to decrease blood pressure by 20 to 30% had no effect on Vmca, ICP, cerebral bleeding and edema, but decreased CPP.
  • [MeSH-major] Blood Pressure / drug effects. Calcium Channel Blockers / therapeutic use. Cerebral Hemorrhage / physiopathology. Nicardipine / therapeutic use
  • [MeSH-minor] Aged. Brain Edema / drug therapy. Brain Edema / physiopathology. Cerebrovascular Circulation / drug effects. Female. Heart Rate / drug effects. Humans. Intracranial Pressure / drug effects. Male. Middle Aged. Middle Cerebral Artery / physiology. Platelet Count. Tomography, X-Ray Computed

  • NCI CPTAC Assay Portal. NCI CPTAC Assay Portal .
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  • (PMID = 11132741.001).
  • [ISSN] 0832-610X
  • [Journal-full-title] Canadian journal of anaesthesia = Journal canadien d'anesthésie
  • [ISO-abbreviation] Can J Anaesth
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; CZ5312222S / Nicardipine
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13. Udy A, Boots R, Senthuran S, Stuart J, Deans R, Lassig-Smith M, Lipman J: Augmented creatinine clearance in traumatic brain injury. Anesth Analg; 2010 Dec;111(6):1505-10
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  • [Title] Augmented creatinine clearance in traumatic brain injury.
  • BACKGROUND: Hypertonic saline and/or norepinephrine infusion are routinely used to achieve a desired cerebral perfusion pressure (CPP) in the management of traumatic brain injury (TBI).
  • METHODS: This was an observational cohort study in TBI patients older than 16 years with normal serum creatinine concentrations, requiring maintenance of CPP.
  • Demographic data, use of vasoactive medications, fluid balance, feeding regimen, and hemodynamic variables were recorded throughout the study period.
  • The mean maximum CrCl was 179 mL/min/1.73 m(2) while receiving CPP therapy (95% confidence interval [CI], 159-198), returning to a mean of 111 mL/min/1.73 m(2) (95% CI, 91-131; P < 0.001) when measured after discharge from the intensive care unit.
  • The mean CrCl in the intensive care unit while not receiving CPP therapy was 150 mL/min/1.73 m(2) (95% CI, 134-167; P = 0.03).
  • The mean time to reach peak CrCl while receiving active treatment was 4.7 days (95% CI, 3.0-6.4).
  • CONCLUSIONS: Augmented CrCls are common in TBI patients receiving active management of CPP and persist even after discontinuation of such therapy.
  • Further work is needed to clarify the impact of such clearances on renally excreted drugs in this setting.
  • [MeSH-major] Adrenergic alpha-Agonists / administration & dosage. Brain Injuries / therapy. Creatinine / urine. Fluid Therapy. Norepinephrine / administration & dosage
  • [MeSH-minor] Adult. Biomarkers / urine. Female. Humans. Intensive Care Units. Intracranial Pressure / drug effects. Male. Queensland. Time Factors. Treatment Outcome. Up-Regulation. Young Adult

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  • (PMID = 21048095.001).
  • [ISSN] 1526-7598
  • [Journal-full-title] Anesthesia and analgesia
  • [ISO-abbreviation] Anesth. Analg.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenergic alpha-Agonists; 0 / Biomarkers; AYI8EX34EU / Creatinine; X4W3ENH1CV / Norepinephrine
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14. Baviera M, Invernizzi RW, Carli M: Haloperidol and clozapine have dissociable effects in a model of attentional performance deficits induced by blockade of NMDA receptors in the mPFC. Psychopharmacology (Berl); 2008 Feb;196(2):269-80
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  • OBJECTIVE: The aim of this study was to compare the effects of conventional and atypical antipsychotics in a model of attentional performance deficit of schizophrenia induced by blockade of N-methyl-D: -aspartate (NMDA) receptors in the medial prefrontal cortex.
  • MATERIALS AND METHODS: Attentional performance was assessed using the five-choice serial reaction time task.
  • The task provides indices of attentional functioning (% correct responses), executive control (measured by anticipatory and perseverative responding), decision time (measured by correct response latency), and omissions.
  • Haloperidol and clozapine were given intraperitoneally (IP) to animals that had received vehicle or a competitive NMDA receptor antagonist, 3-(R)-2-carboxypiperazin-4-propyl-1-phosphonic acid (CPP), directly into the medial prefrontal cortex.
  • RESULTS: Fifty nanograms/side of CPP reduced accuracy (% correct responses) and increased anticipatory and perseverative responding.
  • Haloperidol (0.03 mg/kg IP) reduced the CPP-induced anticipatory and perseverative overresponding but not the impairment in accuracy.
  • CPP increased decision time and omissions, but these effects were not affected by either haloperidol or clozapine.
  • [MeSH-major] Attention / drug effects. Clozapine / pharmacology. Haloperidol / pharmacology. Prefrontal Cortex / drug effects. Schizophrenia / physiopathology
  • [MeSH-minor] Analysis of Variance. Animals. Antipsychotic Agents / administration & dosage. Antipsychotic Agents / pharmacology. Behavior, Animal / drug effects. Dopamine Antagonists / administration & dosage. Dopamine Antagonists / pharmacology. Dose-Response Relationship, Drug. Injections, Intraperitoneal. Male. Microinjections. Piperazines / administration & dosage. Piperazines / toxicity. Rats. Reaction Time / drug effects. Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors. Serial Learning / drug effects. Serotonin Antagonists / administration & dosage. Serotonin Antagonists / pharmacology

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  • [Cites] Neuron. 2006 Feb 16;49(4):603-15 [16476668.001]
  • [Cites] Neuropharmacology. 1999 Aug;38(8):1185-94 [10462131.001]
  • [Cites] Behav Neurosci. 2001 Aug;115(4):812-25 [11508720.001]
  • [Cites] J Neurosci. 1997 Dec 1;17(23):9285-97 [9364074.001]
  • [Cites] Psychopharmacology (Berl). 2006 Jul;187(1):73-85 [16767417.001]
  • [Cites] Synapse. 2005 Apr;56(1):12-20 [15700289.001]
  • [Cites] Schizophr Bull. 1999;25(2):201-22 [10416727.001]
  • [Cites] Neuropsychopharmacology. 2001 Oct;25(4):476-88 [11557161.001]
  • [Cites] Behav Brain Res. 1999 Apr;100(1-2):99-112 [10212057.001]
  • [Cites] Eur J Pharmacol. 2005 Sep 5;519(1-2):114-7 [16099452.001]
  • [Cites] Behav Neurosci. 2001 Aug;115(4):799-811 [11508719.001]
  • [Cites] Psychopharmacology (Berl). 1998 May;137(1):33-42 [9631954.001]
  • [Cites] Psychopharmacology (Berl). 2002 Oct;163(3-4):362-80 [12373437.001]
  • [Cites] Behav Brain Res. 1983 Sep;9(3):361-80 [6639741.001]
  • [Cites] Psychopharmacology (Berl). 1999 Oct;146(4):348-61 [10550486.001]
  • [Cites] J Pharmacol Exp Ther. 1997 Nov;283(2):666-74 [9353384.001]
  • [Cites] Psychopharmacology (Berl). 1992;106(2):228-34 [1532259.001]
  • [Cites] Psychopharmacology (Berl). 2003 May;167(3):304-14 [12677356.001]
  • [Cites] Neuropsychopharmacology. 2006 Sep;31(9):1854-63 [16319908.001]
  • [Cites] Neuron. 2004 May 27;42(4):653-63 [15157425.001]
  • [Cites] Neuropsychopharmacology. 2002 Jun;26(6):716-28 [12007742.001]
  • [Cites] Am J Psychiatry. 1996 Mar;153(3):321-30 [8610818.001]
  • [Cites] J Pharmacol Exp Ther. 1998 Dec;287(3):839-46 [9864262.001]
  • [Cites] Neuroscience. 1993 Feb;52(3):595-604 [8450961.001]
  • [Cites] Behav Brain Res. 1997 Dec;89(1-2):135-49 [9475622.001]
  • [Cites] Brain Res. 1995 Jan 23;670(1):165-8 [7719718.001]
  • [Cites] J Pharmacol Exp Ther. 1997 Oct;283(1):226-34 [9336328.001]
  • [Cites] J Pharmacol Exp Ther. 1993 Sep;266(3):1374-84 [8103793.001]
  • [Cites] Neuropsychopharmacology. 2006 Sep;31(9):1900-9 [16421514.001]
  • [Cites] Psychopharmacology (Berl). 1987;91(4):458-66 [3108926.001]
  • [Cites] J Neurosci. 2000 Feb 1;20(3):1208-15 [10648725.001]
  • [Cites] Neuropsychopharmacology. 1998 Feb;18(2):63-101 [9430133.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2003 Oct;27(7):1159-72 [14642974.001]
  • [Cites] Psychopharmacology (Berl). 1999 Jul;145(2):193-204 [10463321.001]
  • [Cites] Am J Psychiatry. 2004 Jun;161(6):985-95 [15169686.001]
  • [Cites] J Neurosci. 1999 Jun 1;19(11):4585-94 [10341256.001]
  • [Cites] Psychopharmacology (Berl). 1998 Jan;135(2):194-200 [9497025.001]
  • [Cites] Neuropsychopharmacology. 2006 Apr;31(4):757-67 [16192987.001]
  • [Cites] Cereb Cortex. 1996 May-Jun;6(3):470-81 [8670672.001]
  • [Cites] J Clin Psychiatry. 1994 Sep;55 Suppl B:8-14 [7961581.001]
  • [Cites] J Comp Neurol. 2002 Jan 21;442(4):392-404 [11793342.001]
  • [Cites] Behav Brain Res. 2003 Jan 6;138(1):59-69 [12493630.001]
  • [Cites] J Neural Transm Gen Sect. 1995;101(1-3):127-48 [8695043.001]
  • [Cites] J Neurochem. 2001 Mar;76(5):1521-31 [11238736.001]
  • [Cites] Psychopharmacology (Berl). 1993;111(3):339-44 [7870972.001]
  • [Cites] Psychopharmacology (Berl). 2003 Nov;170(3):309-19 [12904968.001]
  • [Cites] Psychopharmacology (Berl). 2004 Nov;176(3-4):376-85 [15232674.001]
  • [Cites] J Pharmacol Exp Ther. 1994 Nov;271(2):787-94 [7965797.001]
  • [Cites] Neuropsychopharmacology. 2007 Feb;32(2):273-83 [16641946.001]
  • [Cites] Eur Neuropsychopharmacol. 1996 Nov;6(4):305-10 [8985714.001]
  • [Cites] J Neurosci. 1996 Jan;16(1):373-9 [8613804.001]
  • [Cites] Am J Psychiatry. 1991 Oct;148(10):1301-8 [1654746.001]
  • [Cites] Neuropsychopharmacology. 2004 Sep;29(9):1637-47 [15127084.001]
  • [Cites] Neuropsychopharmacology. 1996 Feb;14 (2):87-96 [8822531.001]
  • [Cites] Schizophr Bull. 1999;25(2):233-55 [10416729.001]
  • [Cites] Brain Res. 2002 Aug 30;947(2):157-65 [12176156.001]
  • [Cites] Br J Psychiatry. 1993 Oct;163:451-5 [7902766.001]
  • [Cites] Biol Psychiatry. 2001 Nov 15;50(10 ):750-7 [11720693.001]
  • [Cites] Neuroscience. 1998 Mar;83(2):489-99 [9460757.001]
  • [Cites] Neuropsychopharmacology. 1995 Feb;12(1):57-64 [7766287.001]
  • [Cites] Psychopharmacology (Berl). 2005 Apr;179(1):99-107 [15678364.001]
  • [Cites] Neuropsychopharmacology. 1994 Nov;11(3):167-77 [7865098.001]
  • [Cites] Neurosci Lett. 1993 Apr 2;152(1-2):61-4 [8100055.001]
  • [Cites] Cereb Cortex. 2003 Apr;13(4):400-8 [12631569.001]
  • [Cites] Eur J Pharmacol. 1996 Aug 1;309(1):1-11 [8864686.001]
  • [Cites] Am J Psychiatry. 2001 Feb;158(2):176-84 [11156796.001]
  • [Cites] Psychopharmacology (Berl). 2003 Sep;169(3-4):404-11 [12590356.001]
  • [Cites] Biol Psychiatry. 2002 Jun 15;51(12):972-8 [12062881.001]
  • [Cites] J Neurophysiol. 2001 Feb;85(2):659-70 [11160501.001]
  • [Cites] Schizophr Bull. 2000;26(1):119-36 [10755673.001]
  • [Cites] J Neurosci. 2004 Jan 28;24(4):773-80 [14749421.001]
  • [Cites] Arch Gen Psychiatry. 2000 Mar;57(3):249-58 [10711911.001]
  • [Cites] Brain. 1993 Oct;116 ( Pt 5):1159-75 [8221053.001]
  • (PMID = 17940750.001).
  • [ISSN] 0033-3158
  • [Journal-full-title] Psychopharmacology
  • [ISO-abbreviation] Psychopharmacology (Berl.)
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Dopamine Antagonists; 0 / Piperazines; 0 / Receptors, N-Methyl-D-Aspartate; 0 / Serotonin Antagonists; 98Y1I8ZD4M / 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; J60AR2IKIC / Clozapine; J6292F8L3D / Haloperidol
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15. Pak AC, Ashby CR Jr, Heidbreder CA, Pilla M, Gilbert J, Xi ZX, Gardner EL: The selective dopamine D3 receptor antagonist SB-277011A reduces nicotine-enhanced brain reward and nicotine-paired environmental cue functions. Int J Neuropsychopharmacol; 2006 Oct;9(5):585-602
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  • [Title] The selective dopamine D3 receptor antagonist SB-277011A reduces nicotine-enhanced brain reward and nicotine-paired environmental cue functions.
  • Increasing evidence suggests that enhanced dopamine (DA) neurotransmission in the nucleus accumbens (NAc) may play a role in mediating the reward and reinforcement produced by addictive drugs and in the attentional processing of drug-associated environmental cues.
  • The meso-accumbens DA system is selectively enriched with DA D3 receptors, a DA receptor subtype increasingly implicated in reward-related brain and behavioural processes.
  • From a variety of evidence, it has been suggested that selective DA D3 receptor antagonism may be a useful pharmacotherapeutic approach for treating addiction.
  • The present experiments tested the efficacy of SB-277011A, a selective DA D3 receptor antagonist, in rat models of nicotine-enhanced electrical brain-stimulation reward (BSR), nicotine-induced conditioned locomotor activity (LMA), and nicotine-induced conditioned place preference (CPP).
  • SB-277011A, given intraperitoneally within the dose range of 1-12 mg/kg, dose-dependently reduced nicotine-enhanced BSR, nicotine-induced conditioned LMA, and nicotine-induced CPP.
  • The results suggest that selective D3 receptor antagonism constitutes a new and promising pharmacotherapeutic approach to the treatment of nicotine dependence.
  • [MeSH-major] Brain / drug effects. Conditioning, Operant / drug effects. Dopamine Antagonists / pharmacology. Nicotine / pharmacology. Nicotinic Agonists / pharmacology. Nitriles / pharmacology. Reward. Tetrahydroisoquinolines / pharmacology
  • [MeSH-minor] Analysis of Variance. Animals. Area Under Curve. Association Learning / drug effects. Behavior, Animal / drug effects. Cues. Dose-Response Relationship, Drug. Drug Interactions. Male. Motor Activity / drug effects. Rats. Rats, Long-Evans

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  • [Cites] J Pharmacol Exp Ther. 2000 Sep;294(3):1154-65 [10945872.001]
  • [Cites] Synapse. 1998 May;29(1):72-9 [9552176.001]
  • [Cites] Neuropsychopharmacology. 2003 Feb;28(2):329-38 [12589386.001]
  • [Cites] Behav Brain Res. 1998 Nov;96(1-2):185-8 [9821554.001]
  • [Cites] Annu Rev Psychol. 1989;40:191-225 [2648975.001]
  • [Cites] Pharmacol Biochem Behav. 1993 Oct;46(2):453-7 [8265701.001]
  • [Cites] Psychopharmacology (Berl). 2003 Dec;170(4):409-22 [12955296.001]
  • [Cites] Neuropsychopharmacology. 2003 Jun;28(6):1150-9 [12700684.001]
  • [Cites] Behav Neurosci. 1987 Apr;101(2):209-14 [3580122.001]
  • [Cites] Prog Neurobiol. 1998 Dec;56(6):613-72 [9871940.001]
  • [Cites] Eur J Pharmacol. 2001 Aug 24;426(1-2):R1-2 [11525784.001]
  • [Cites] Life Sci. 1996;58(25):PL365-72 [8649214.001]
  • [Cites] Psychopharmacology (Berl). 1995 Jul;120(1):10-20 [7480530.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 1989 Jan-Feb;339(1-2):208-13 [2725697.001]
  • [Cites] Nature. 1996 Jul 18;382(6588):255-7 [8717040.001]
  • [Cites] Science. 1975 Feb 14;187(4176):547-9 [1114313.001]
  • [Cites] Synapse. 1995 Oct;21(2):140-8 [8584975.001]
  • [Cites] Behav Pharmacol. 1995 Jun;6(4):333-347 [11224342.001]
  • [Cites] Behav Brain Res. 2000 Aug;113(1-2):97-103 [10942036.001]
  • [Cites] Ciba Found Symp. 1990;152:153-62; discussion 162-8 [2209252.001]
  • [Cites] Exp Clin Psychopharmacol. 1999 Feb;7(1):72-8 [10036612.001]
  • [Cites] Neuropharmacology. 2004;47 Suppl 1:190-201 [15464137.001]
  • [Cites] Synapse. 2003 Mar;47(3):176-83 [12494400.001]
  • [Cites] Neuroreport. 2003 Jan 20;14(1):93-8 [12544838.001]
  • [Cites] Synapse. 2002 May;44(2):61-3 [11891877.001]
  • [Cites] Eur J Pharmacol. 2000 Oct 27;407(1-2):47-51 [11050289.001]
  • [Cites] Eur J Pharmacol. 1988 Jul 7;151(2):233-42 [2844553.001]
  • [Cites] Respiration. 2002;69(5):381-4 [12232442.001]
  • [Cites] Pharmacol Rev. 1997 Sep;49(3):231-52 [9311022.001]
  • [Cites] Eur J Pharmacol. 2000 Mar 30;393(1-3):295-314 [10771025.001]
  • [Cites] Brain Res Brain Res Rev. 2005 Jul;49(1):77-105 [15960988.001]
  • [Cites] Eur J Pharmacol. 1987 Sep 23;141(3):395-9 [3666033.001]
  • [Cites] J Med Chem. 2000 May 4;43(9):1878-85 [10794704.001]
  • [Cites] Psychopharmacology (Berl). 1996 Feb;123(3):280-8 [8833421.001]
  • [Cites] Psychiatr Med. 1985;3(4):445-60 [2893431.001]
  • [Cites] Recent Adv Biol Psychiatry. 1961;4:288-309 [13916635.001]
  • [Cites] Synapse. 2000 Feb;35(2):160-2 [10611642.001]
  • [Cites] Neuropsychopharmacology. 2003 May;28(5):839-49 [12637956.001]
  • [Cites] J Neurosci. 2002 Nov 1;22(21):9595-603 [12417684.001]
  • [Cites] Behav Brain Res. 2003 Jul 14;143(1):65-74 [12842297.001]
  • [Cites] Neurosci Biobehav Rev. 1989 Summer-Fall;13(2-3):123-8 [2530477.001]
  • [Cites] Synapse. 2003 Jun 1;48(3):154-6 [12645041.001]
  • [Cites] Neuropharmacology. 2005 Sep;49(4):525-41 [15963538.001]
  • [Cites] Am J Addict. 2000 Fall;9(4):285-313 [11155784.001]
  • [Cites] Nicotine Tob Res. 2002 Aug;4(3):259-66 [12215234.001]
  • [Cites] Behav Brain Res. 1987 Oct;26(1):57-62 [3675835.001]
  • [Cites] NIDA Res Monogr. 1994;145:191-206 [8742814.001]
  • [Cites] Neuropsychopharmacology. 2003 Jul;28(7):1272-80 [12700694.001]
  • [Cites] Neuropsychobiology. 2002;45(2):87-94 [11893865.001]
  • [Cites] Synapse. 1997 May;26(1):93-4 [9097409.001]
  • [Cites] Pharmacol Biochem Behav. 1999 Apr;62(4):659-72 [10208371.001]
  • [Cites] Pharmacol Biochem Behav. 2005 May;81(1):190-7 [15894078.001]
  • [Cites] Psychopharmacology (Berl). 1976 Aug 17;48(3):311-8 [823588.001]
  • [Cites] Mol Psychiatry. 2003 Feb;8(2):225-30 [12610655.001]
  • [Cites] Physiol Behav. 1985 Sep;35(3):395-403 [3840902.001]
  • [Cites] Ann N Y Acad Sci. 1992 Jun 28;654:192-8 [1632583.001]
  • [Cites] J Neurosci. 1997 Nov 1;17(21):8580-7 [9334429.001]
  • [Cites] Synapse. 1998 Oct;30(2):181-93 [9723788.001]
  • [Cites] Drug Discov Today. 2005 Jul 1;10(13):917-25 [15993811.001]
  • [Cites] Br J Pharmacol. 1989 Sep;98(1):135-40 [2804543.001]
  • [Cites] Synapse. 1999 Jan;31(1):76-86 [10025686.001]
  • [Cites] Synapse. 2005 Jul;57(1):17-28 [15858839.001]
  • [Cites] Psychopharmacology (Berl). 2002 Feb;160(1):56-66 [11862374.001]
  • [Cites] Science. 1993 Jun 18;260(5115):1814-6 [8099761.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Feb 13;98(4):1976-81 [11172061.001]
  • [Cites] Curr Opin Pharmacol. 2005 Feb;5(1):107-18 [15661634.001]
  • [Cites] Behav Pharmacol. 2003 May;14(3):191-8 [12799520.001]
  • [Cites] J Neurosci. 2001 Aug 1;21(15):5841-6 [11466456.001]
  • [Cites] Pharmacol Biochem Behav. 1991 Jun;39(2):465-8 [1682950.001]
  • [Cites] Eur J Neurosci. 2005 Jun;21(12):3427-38 [16026480.001]
  • [Cites] Psychopharmacologia. 1960 Feb 12;1:251-6 [13834123.001]
  • [Cites] Eur J Pharmacol. 2001 Jul 20;424(2):85-90 [11476753.001]
  • [Cites] Psychopharmacology (Berl). 2000 May;149(4):388-96 [10867966.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Apr 11;97(8):4321-6 [10760299.001]
  • [Cites] Eur J Pharmacol. 1986 Dec 16;132(2-3):337-8 [3816984.001]
  • [Cites] Drugs Today (Barc). 2004 Apr;40(4):355-65 [15190388.001]
  • [Cites] Psychopharmacology (Berl). 1982;78(3):204-9 [6296898.001]
  • [Cites] Pharmacol Biochem Behav. 2001 Jan;68(1):135-45 [11274718.001]
  • [Cites] Pharmacol Biochem Behav. 1992 Apr;41(4):755-9 [1594644.001]
  • [Cites] Nature. 1999 Jul 22;400(6742):371-5 [10432116.001]
  • [Cites] Addiction. 2000 Aug;95(8):1173-83 [11092065.001]
  • [Cites] J Med Chem. 2005 Jun 2;48(11):3663-79 [15916415.001]
  • [Cites] Pharmacol Biochem Behav. 1994 Aug;48(4):853-62 [7972288.001]
  • [Cites] Pharmacol Biochem Behav. 1997 Aug;57(4):915-21 [9259024.001]
  • [Cites] Neuropsychopharmacology. 2003 Nov;28(11):1903-15 [12915863.001]
  • [Cites] Nat Med. 2003 Jun;9(6):762-7 [12740572.001]
  • [Cites] Psychopharmacology (Berl). 2005 May;179(3):567-75 [15619116.001]
  • [Cites] Behav Neurosci. 1993 Feb;107(1):161-5 [8095392.001]
  • [Cites] Psychopharmacology (Berl). 2005 Apr;178(4):481-92 [15765262.001]
  • [Cites] Psychopharmacology (Berl). 2004 Oct;176(1):57-65 [15083257.001]
  • [Cites] Brain Res. 1994 Aug 8;653(1-2):278-84 [7982062.001]
  • [Cites] Neuroreport. 1997 Jul 7;8(9-10):2373-7 [9243643.001]
  • [Cites] Neuropsychopharmacology. 2005 Apr;30(4):720-30 [15562293.001]
  • [Cites] Psychopharmacology (Berl). 1992;107(2-3):285-9 [1615127.001]
  • [Cites] Trends Pharmacol Sci. 1991 Dec;12(12):467-73 [1792691.001]
  • [Cites] Psychopharmacology (Berl). 1997 Nov;134(2):187-92 [9399383.001]
  • [Cites] J Pharmacol Exp Ther. 1994 Oct;271(1):294-301 [7965727.001]
  • [Cites] Can J Psychol. 1977 Dec;31(4):195-203 [608135.001]
  • (PMID = 16942635.001).
  • [ISSN] 1461-1457
  • [Journal-full-title] The international journal of neuropsychopharmacology
  • [ISO-abbreviation] Int. J. Neuropsychopharmacol.
  • [Language] eng
  • [Grant] United States / Intramural NIH HHS / / Z99 DA999999
  • [Publication-type] Comparative Study; Journal Article; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Dopamine Antagonists; 0 / Nicotinic Agonists; 0 / Nitriles; 0 / SB 277011; 0 / Tetrahydroisoquinolines; 6M3C89ZY6R / Nicotine
  • [Other-IDs] NLM/ NIHMS493706; NLM/ PMC3732043
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16. Concolino D, Muzzi G, Pisaturo L, Piccirillo A, Di Natale P, Strisciuglio P: Precocious puberty in Sanfilippo IIIA disease: diagnosis and follow-up of two new cases. Eur J Med Genet; 2008 Sep-Oct;51(5):466-71
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  • [Title] Precocious puberty in Sanfilippo IIIA disease: diagnosis and follow-up of two new cases.
  • We observed two children affected by MPS IIIA with central precocious puberty (CPP) both treated with GnRH agonists.
  • The occurrence of CPP in both patients with MPS IIIA suggests that it is necessary to look for an association between the two conditions.
  • The follow-up of our two patients leads us to believe also that GnRH agonist treatment can have a beneficial effect on final height and probably on the improvement of behavioural problems.
  • [MeSH-major] Mucopolysaccharidosis III / complications. Mucopolysaccharidosis III / diagnosis. Mutation. Puberty, Precocious / complications
  • [MeSH-minor] Adolescent. Body Height / drug effects. Brain / pathology. Child. Child Behavior Disorders / complications. Child Behavior Disorders / drug therapy. DNA Mutational Analysis. Gonadotropin-Releasing Hormone / agonists. Humans. Luteolytic Agents / therapeutic use. Magnetic Resonance Imaging / methods. Male. Triptorelin Pamoate / therapeutic use

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  • (PMID = 18586597.001).
  • [ISSN] 1769-7212
  • [Journal-full-title] European journal of medical genetics
  • [ISO-abbreviation] Eur J Med Genet
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Luteolytic Agents; 33515-09-2 / Gonadotropin-Releasing Hormone; 57773-63-4 / Triptorelin Pamoate
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17. Maffeis C, Franceschi R, Moghetti P, Camilot M, Lauriola S, Tatò L: Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog. Eur J Endocrinol; 2007 Jan;156(1):99-103
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  • [Title] Circulating ghrelin levels in girls with central precocious puberty are reduced during treatment with LHRH analog.
  • No data are available for girls with central precocious puberty (CPP).
  • AIMS: To explore ghrelin changes before, during, and after GnRH analog treatment in girls with CPP.
  • SUBJECTS AND METHODS: A sample of 20 Caucasian girls (8.08 +/- 0.65 years of age) with CPP was recruited.
  • Height and weight, bone age, LH, FSH, 17beta estradiol (E(2)), and ghrelin were measured before starting treatment with GnRH analog, 18 months after therapy began and again 6 months after therapy discontinuation.
  • RESULTS: LH and E(2) serum levels decreased significantly during treatment (2.45 +/- 2.03 vs 0.67 +/- 0.49 UI/l, P < 0.01 and 28.17 +/- 9.7 vs 15 pmol/l, P < 0.01 respectively), returning to baseline levels after the discontinuation of therapy (4.75 +/- 1.66 UI/l and 29.23 +/- 6.99 pmol/l respectively).
  • LH peaked following LHRH stimulation significantly (P < 0.01) decreased during treatment (24.45 +/- 14.17 vs 1.3 +/- 0.18 UI/l) and then increased after therapy discontinuation (12.58 +/- 6.09, P < 0.01).
  • Ghrelin decreased significantly (P < 0.05) during treatment (1849 +/- 322 vs 1207 +/- 637 pg/ml), and increased, though not significantly (P = 0.09) after therapy withdrawal (1567 +/- 629 pg/ml).
  • CONCLUSIONS: Contrary to what is expected in physiologic puberty, where ghrelin is progressively reduced, the prepubertal hormone milieau induced by GnRHa treatment in patients suffering from central precocious puberty (CPP) did not promote an increase in ghrelin circulating levels.
  • Therefore, in CPP, ghrelin secretion seems to be independent from pubertal development per se.
  • Concomitant estrogen suppression during treatment may play a potential role in the regulation of ghrelin secretion in these girls.

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  • (PMID = 17218731.001).
  • [ISSN] 0804-4643
  • [Journal-full-title] European journal of endocrinology
  • [ISO-abbreviation] Eur. J. Endocrinol.
  • [Language] ENG
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Ghrelin; 0 / Gonadal Steroid Hormones; 0 / Peptide Hormones; 33515-09-2 / Gonadotropin-Releasing Hormone; 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone
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18. Martínez-León MI, Weil-Lara B, Herrero-Hernández A: [Papilloma and carcinoma of the choroid plexus in pediatric patients]. Radiologia; 2007 Jul-Aug;49(4):279-86
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  • [Title] [Papilloma and carcinoma of the choroid plexus in pediatric patients].
  • [Transliterated title] Papiloma y carcinoma de plexos coroideos en la edad pediátrica.
  • Papillomas of the choroid plexus are rare tumors of neuroectodermal origin; they represent less than 5% of all central nervous system (CNS) tumors in pediatric patients.
  • Choroid plexus carcinomas are even rarer.
  • We reviewed the incidence of these neoplasms at our reference hospital and found six tumors of the choroid plexus (five papillomas and one carcinoma) in five patients.
  • All five patients underwent computed tomography (CT) examination.
  • All patients had tumors located in the lateral ventricles, and one patient had a second tumor located in the third ventricle.
  • All patients underwent surgery; total resection was achieved in the five papillomas, whereas the carcinoma was partially resected and the patient is currently undergoing chemotherapy.
  • The three patients with a single papilloma are disease free at follow-up (range 7 months to 11 years).
  • The patient with two papillomas shows good recovery at follow-up, whereas the patient with carcinoma of the choroid plexus has a poor prognosis.
  • [MeSH-major] Carcinoma. Choroid Plexus Neoplasms. Papilloma
  • [MeSH-minor] Female. Humans. Infant. Infant, Newborn. Male. Prenatal Diagnosis


19. Fishbain DA, Lewis JE, Cole B, Cutler B, Rosomoff HL, Rosomoff RS: Lidocaine 5% patch: an open-label naturalistic chronic pain treatment trial and prediction of response. Pain Med; 2006 Mar-Apr;7(2):135-42
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  • [Title] Lidocaine 5% patch: an open-label naturalistic chronic pain treatment trial and prediction of response.
  • OBJECTIVE: There have been a few open-label nonplacebo reports on the successful use of lidocaine 5% patch (L5P) for other types of pain besides postherpetic neuralgia, such as chronic low back pain.
  • The purpose of this report was to describe the results of a retrospective review of this open-label naturalistic L5P chronic pain treatment trial and to attempt to delineate predictors of perceived clinical response.
  • DESIGN: Consecutive CPPs were selected for this clinical trial according to the following inclusion criteria: the CPPs with pain greater than 6-month duration and either a hyperalgesic pain area or trigger point, which could be covered by one L5P, were offered a 3-day L5P naturalistic treatment trial.
  • The senior author also completed a baseline information tool on each CPP entering this naturalistic trial.
  • The apparent CPP perceived clinical improvement was not associated with any particular useful clinical indicator.
  • As such, at present, no variable can be recommended for use in selecting CPPs for such a naturalistic L5P clinical treatment trial.
  • [MeSH-major] Lidocaine / administration & dosage. Pain, Intractable / drug therapy
  • [MeSH-minor] Administration, Cutaneous. Adult. Aged. Aged, 80 and over. Anesthetics, Local / administration & dosage. Chronic Disease / drug therapy. Female. Humans. Logistic Models. Male. Middle Aged. Pain Clinics. Pain Measurement. Pain Threshold / drug effects. Pain Threshold / physiology. Predictive Value of Tests. Retrospective Studies. Treatment Outcome

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  • (PMID = 16634726.001).
  • [ISSN] 1526-2375
  • [Journal-full-title] Pain medicine (Malden, Mass.)
  • [ISO-abbreviation] Pain Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anesthetics, Local; 98PI200987 / Lidocaine
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20. Hu L, Chu NN, Sun LL, Zhang R, Han JS, Cui CL: Electroacupuncture treatment reverses morphine-induced physiological changes in dopaminergic neurons within the ventral tegmental area. Addict Biol; 2009 Sep;14(4):431-7
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  • [Title] Electroacupuncture treatment reverses morphine-induced physiological changes in dopaminergic neurons within the ventral tegmental area.
  • These transient morphological changes are accompanied by a reduced sensitivity of morphine-induced conditioned place preference (CPP) after chronic exposure to the drug.
  • In this study we examined alterations in the firing rate of DAergic neurons by means of extracellular recording following chronic morphine exposure and applied 100 Hz electroacupuncture (EA) treatment to reverse the reduced firing rate of these neurons.
  • In the first set of experiments we show that in rats, which received chronic morphine treatment for 14 days, a small dose of morphine was not able to induce a CPP response anymore.
  • However, the sensitivity to morphine was reinstated by consecutive EA treatment for 10 days.
  • Our findings suggest that 100 Hz EA is a potential therapy for the treatment of opiate addiction by normalizing the activity of VTA DA neurons.
  • [MeSH-major] Analgesics, Opioid / pharmacology. Dopamine / metabolism. Electroacupuncture / methods. Morphine / pharmacology. Neurons / drug effects. Neurons / metabolism. Ventral Tegmental Area / drug effects. Ventral Tegmental Area / metabolism
  • [MeSH-minor] Animals. Choice Behavior. Drug Administration Schedule. Male. Rats. Rats, Sprague-Dawley. Substantia Nigra / drug effects. Substantia Nigra / metabolism

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  • (PMID = 19489751.001).
  • [ISSN] 1369-1600
  • [Journal-full-title] Addiction biology
  • [ISO-abbreviation] Addict Biol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 76I7G6D29C / Morphine; VTD58H1Z2X / Dopamine
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21. Nanobashvili A, Woldbye DP, Husum H, Bolwig TG, Kokaia M: Neuropeptide Y Y5 receptors suppress in vitro spontaneous epileptiform bursting in the rat hippocampus. Neuroreport; 2004 Feb 9;15(2):339-43
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  • In the present study, using the new highly selective Y5 receptor antagonist, CGP71683A, and agonist, [cPP]hPP, we show that the Y5 receptor subtype is centrally involved in NPY-induced suppression of spontaneous epileptiform (interictaform) bursting in the CA3 area of rat hippocampal slices.
  • This novel finding underscores the importance of Y5 receptors as a potential target for future antiepileptic therapy, particularly, for interictal components of temporal lobe epilepsy.
  • [MeSH-minor] Action Potentials / drug effects. Action Potentials / physiology. Animals. Anticonvulsants / pharmacology. Female. In Vitro Techniques. Magnesium Deficiency / metabolism. Male. Naphthalenes / pharmacology. Neurons / drug effects. Neurons / metabolism. Pyrimidines / pharmacology. Rats. Rats, Wistar

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  • (PMID = 15076765.001).
  • [ISSN] 0959-4965
  • [Journal-full-title] Neuroreport
  • [ISO-abbreviation] Neuroreport
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / CGP 71683 A; 0 / Naphthalenes; 0 / Neuropeptide Y; 0 / Pyrimidines; 0 / Receptors, Neuropeptide Y; 0 / neuropeptide Y5 receptor
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22. Abekawa T, Ito K, Koyama T: Role of the simultaneous enhancement of NMDA and dopamine D1 receptor-mediated neurotransmission in the effects of clozapine on phencyclidine-induced acute increases in glutamate levels in the rat medial prefrontal cortex. Naunyn Schmiedebergs Arch Pharmacol; 2006 Dec;374(3):177-93
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  • Clozapine (CLZ) can improve both the positive and negative symptoms of treatment-resistant schizophrenia (TRS), which does not respond to typical antipsychotics.
  • This suggests that elucidation of the pharmacological mechanism for CLZ could lead to further clarification of the pathophysiology of TRS.
  • This study examined the effects of CLZ on phencyclidine (PCP)-induced hyperlocomotion and on the acute increases in glutamate levels that occur in the medial prefrontal cortex (mPFC) in order to test the hypothesis that CLZ effect is associated with the simultaneous enhancement of N-methyl-D: -aspartate (NMDA) and dopamine D(1) receptor-mediated neurotransmission.
  • CLZ also blocked, in a dose-related manner, acute increases in glutamate levels in the mPFC that were induced by local perfusion with a competitive NMDA receptor antagonist, CPP, in this region.
  • Although an enhanced blocking effect of the sub-threshold concentration of NMDA perfusion on PCP-induced acute increases in glutamate levels in the mPFC was noted after co-perfusion with a dopamine D(1) receptor agonist, SKF-38393, perfusion with SKF-38393 did not reverse the CLZ blocking of PCP-induced increases in glutamate levels.
  • [MeSH-major] Antipsychotic Agents / pharmacology. Behavior, Animal / drug effects. Clozapine / pharmacology. Glutamic Acid / metabolism. Receptors, Dopamine D1 / drug effects. Receptors, N-Methyl-D-Aspartate / drug effects
  • [MeSH-minor] Analysis of Variance. Animals. Dose-Response Relationship, Drug. Drug Resistance. Haloperidol / pharmacology. Humans. Male. Microdialysis. Motor Activity / drug effects. Phencyclidine. Prefrontal Cortex / metabolism. Rats. Rats, Sprague-Dawley. Schizophrenia / drug therapy. Schizophrenia / physiopathology

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  • [Cites] J Neurosci. 1998 Jul 15;18(14):5545-54 [9651235.001]
  • [Cites] Arch Gen Psychiatry. 1988 Sep;45(9):789-96 [3046553.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2004 Jan;28(1):173-80 [14687871.001]
  • [Cites] Psychopharmacology (Berl). 2003 Sep;169(3-4):215-33 [12955285.001]
  • [Cites] Science. 1998 Aug 28;281(5381):1349-52 [9721099.001]
  • [Cites] J Neurosci. 2003 Feb 1;23(3):867-75 [12574415.001]
  • [Cites] J Neurochem. 1998 Jan;70(1):198-209 [9422363.001]
  • [Cites] Neuropsychopharmacology. 1996 May;14(5):301-7 [8703299.001]
  • [Cites] Brain Res Bull. 2002 Mar 15;57(5):623-30 [11927365.001]
  • [Cites] Pharmacol Toxicol. 1999 May;84(5):193-6 [10361974.001]
  • [Cites] Eur J Pharmacol. 1979 Nov 16;59(3-4):169-79 [575093.001]
  • [Cites] J Comp Neurol. 1992 Feb 15;316(3):314-47 [1577988.001]
  • [Cites] NIDA Res Monogr. 1978 Aug;(21):241-53 [101872.001]
  • [Cites] Brain Res. 2000 Jun 9;867(1-2):250-4 [10837822.001]
  • [Cites] Arch Gen Psychiatry. 1994 Mar;51(3):199-214 [8122957.001]
  • [Cites] Eur J Pharmacol. 1976 Nov;40(1):45-56 [1033072.001]
  • [Cites] J Pharmacol Exp Ther. 1997 Oct;283(1):226-34 [9336328.001]
  • [Cites] Eur J Neurosci. 2003 Mar;17(6):1306-12 [12670320.001]
  • [Cites] J Neurophysiol. 2002 May;87(5):2324-36 [11976371.001]
  • [Cites] J Pharmacol Exp Ther. 2005 May;313(2):594-603 [15659539.001]
  • [Cites] Synapse. 1997 Nov;27(3):242-61 [9329159.001]
  • [Cites] J Pharmacol Exp Ther. 2000 Feb;292(2):731-6 [10640312.001]
  • [Cites] J Clin Psychiatry. 1994 Sep;55 Suppl B:8-14 [7961581.001]
  • [Cites] Am J Psychiatry. 2002 Feb;159(2):255-62 [11823268.001]
  • [Cites] Br J Pharmacol. 1998 May;124(2):377-85 [9641556.001]
  • [Cites] Psychopharmacology (Berl). 1998 Jul;138(1):89-95 [9694531.001]
  • [Cites] Neuropsychopharmacology. 1998 Mar;18(3):197-209 [9471117.001]
  • [Cites] Biol Psychiatry. 1997 Oct 15;42(8):664-8 [9325559.001]
  • [Cites] Am J Psychiatry. 1991 Oct;148(10):1301-8 [1654746.001]
  • [Cites] Psychopharmacology (Berl). 2003 Sep;169(3-4):247-56 [12898123.001]
  • [Cites] J Neurochem. 2004 Oct;91(1):189-99 [15379899.001]
  • [Cites] Biol Psychiatry. 2001 Nov 15;50(10 ):750-7 [11720693.001]
  • [Cites] Cereb Cortex. 2001 May;11(5):452-62 [11313297.001]
  • [Cites] J Neurosci Methods. 1995 Mar;57(1):93-9 [7791370.001]
  • [Cites] Neuroscience. 1981;6(5):863-73 [6113562.001]
  • [Cites] J Pharmacol Exp Ther. 1993 May;265(2):498-508 [7684443.001]
  • [Cites] Neuropsychopharmacology. 1995 Aug;13(1):9-19 [8526975.001]
  • [Cites] Synapse. 2003 May;48(2):66-79 [12619040.001]
  • [Cites] Eur J Pharmacol. 1998 Jan 2;341(1):45-56 [9489855.001]
  • (PMID = 17103144.001).
  • [ISSN] 0028-1298
  • [Journal-full-title] Naunyn-Schmiedeberg's archives of pharmacology
  • [ISO-abbreviation] Naunyn Schmiedebergs Arch. Pharmacol.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Antipsychotic Agents; 0 / Receptors, Dopamine D1; 0 / Receptors, N-Methyl-D-Aspartate; 3KX376GY7L / Glutamic Acid; J1DOI7UV76 / Phencyclidine; J60AR2IKIC / Clozapine; J6292F8L3D / Haloperidol
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23. Turk DC, Swanson KS, Gatchel RJ: Predicting opioid misuse by chronic pain patients: a systematic review and literature synthesis. Clin J Pain; 2008 Jul-Aug;24(6):497-508
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  • However, a minority may develop aberrant drug behaviors.
  • OBJECTIVE: To synthesize the evidence of published strategies for identifying at-risk patients to guide clinicians' decisions and practices for prescribing opioid treatment for chronic pain patients (CPP).
  • Studies were limited to human studies in the English language related to screening for predictors of aberrant drug behaviors in CPP who were prescribed long-term opioids.
  • We included studies reviewing, developing measures, or investigating outcomes related to screening for aberrant opioid behaviors in CPP.
  • RESULTS: We identified 6 published articles addressing clinician-based predictors of substance misuse of opioids and 9 published studies evaluating the predictive ability of clinical interviews and self-report measures for aberrant opioid behaviors in CPP.
  • CONCLUSION: Review of the published studies reveals that no one procedure or set of predictor variables is sufficient to identify CPP at-risk for opioid misuse or abuse.
  • Strong predictors include a personal history of illicit drug and alcohol abuse.
  • Prospective studies, especially ones with CPP who have not already been started on chronic opioid therapy, are needed.
  • [MeSH-major] Analgesics, Opioid / adverse effects. Opioid-Related Disorders / etiology. Pain / drug therapy
  • [MeSH-minor] Chronic Disease. Humans. MEDLINE / statistics & numerical data. Predictive Value of Tests

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  • (PMID = 18574359.001).
  • [ISSN] 1536-5409
  • [Journal-full-title] The Clinical journal of pain
  • [ISO-abbreviation] Clin J Pain
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / 5K23GM071400-03
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Opioid
  • [Number-of-references] 64
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24. Belfort MA: Is high cerebral perfusion pressure and cerebral flow predictive of impending seizures in preeclampsia? A case report. Hypertens Pregnancy; 2005;24(1):59-63
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  • Transcranial Doppler ultrasound was used to demonstrate elevated estimated cerebral perfusion pressure (CPP) and cerebral flow index (CFI) in a preeclamptic patient.
  • She subsequently developed eclampsia.
  • After magnesium sulfate therapy her CPP and CFI were within the normal range and she did not experience further seizures.
  • This finding suggests that cerebral overperfusion may be at least one of the etiologies involved in the pathogenesis of eclampsia.
  • [MeSH-major] Intracranial Hypertension / ultrasonography. Pre-Eclampsia / ultrasonography. Pregnancy Outcome. Seizures / diagnosis. Ultrasonography, Doppler, Transcranial
  • [MeSH-minor] Adult. Blood Flow Velocity. Cerebrovascular Circulation / physiology. Eclampsia / diagnosis. Eclampsia / drug therapy. Female. Humans. Magnesium Sulfate / therapeutic use. Parity. Predictive Value of Tests. Pregnancy. Pregnancy Trimester, Third. Risk Assessment


25. Crookes BA, Cohn SM, Bonet H, Burton EA, Nelson J, Majetschak M, Varon AJ, Linden JM, Proctor KG: Building a better fluid for emergency resuscitation of traumatic brain injury. J Trauma; 2004 Sep;57(3):547-54
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  • [Title] Building a better fluid for emergency resuscitation of traumatic brain injury.
  • Three series of experiments were designed to evaluate the therapeutic potential of HEX+/-ATL-146e for emergency resuscitation from traumatic brain injury (TBI) + hemorrhagic hypotension.
  • In Series 1, resuscitation consisted of unlimited crystalloid (n = 8) or HEX (n = 8) to correct systolic arterial pressure >100 mm Hg and heart rate <100 bpm for the first 60 minutes ("emergency phase"), and then maintain cerebral perfusion pressure (CPP) > 70 mm Hg for 60-240 minutes.
  • In Series 2 (n = 31), resuscitation consisted of a 1 L bolus of HEX + ATL-146e (10 ng/kg/min, n = 10) or HEX +placebo (n = 10) followed by crystalloid to the same endpoints.
  • Upon resuscitation, these values corrected but intracranial pressure progressively rose from <5 mm Hg to 15-20 mm Hg.
  • Series 1: With HEX (n = 8) versus crystalloid (n = 8), CPP was less labile, acid/base was maintained, and the fluid requirement was reduced by 60% (all p < 0.05) Series 2: With ATL-146e (n = 10) versus placebo (n = 10), stroke volume and cardiac output were improved by 40-60%, and the fluid requirement was reduced by 30% (all p < 0.05).
  • An adenosine A2A agonist combined with 1 L of HEX safely and effectively counteracted a decrease in cardiac performance noted after TBI+hemorrhage without causing hypotension or bradycardia.
  • [MeSH-major] Brain Injuries / therapy. Cyclohexanecarboxylic Acids / therapeutic use. Hydroxyethyl Starch Derivatives / therapeutic use. Plasma Substitutes / therapeutic use. Purines / therapeutic use. Resuscitation / methods
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Cardiac Output / drug effects. Female. Male. Shock, Hemorrhagic / therapy. Stroke Volume / drug effects. Swine

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  • (PMID = 15454801.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / ATL 146e; 0 / Cyclohexanecarboxylic Acids; 0 / Hydroxyethyl Starch Derivatives; 0 / Plasma Substitutes; 0 / Purines
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26. Said Hassane F, Saleh AF, Abes R, Gait MJ, Lebleu B: Cell penetrating peptides: overview and applications to the delivery of oligonucleotides. Cell Mol Life Sci; 2010 Mar;67(5):715-26
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  • Cell penetrating peptides (CPP), also named protein transduction domains, comprise short and usually basic amino acids-rich peptides originating from proteins able to cross biological barriers, such as the viral Tat protein, or are rationally designed.
  • They have emerged as a new class of non-viral vectors allowing the delivery of various biomolecules across biological barriers from low molecular weight drugs to nanosized particles.
  • Encouraging data with CPP-conjugated oligonucleotides have been obtained both in vitro and in vivo in animal models of diseases such as Duchenne muscular dystrophy.
  • Whether CPP-cargo conjugates enter cells by direct translocation across the plasma membrane or by endocytosis remains controversial.
  • [MeSH-major] Cells / metabolism. Drug Delivery Systems. Oligonucleotides / administration & dosage. Peptides / pharmacokinetics
  • [MeSH-minor] Animals. Cell Membrane Permeability / drug effects. Gene Transfer Techniques. Humans. Muscular Dystrophy, Duchenne / therapy

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  • [Cites] Curr Protein Pept Sci. 2003 Apr;4(2):133-40 [12678852.001]
  • [Cites] FEBS Lett. 2007 Feb 20;581(4):702-6 [17274989.001]
  • [Cites] Proc Natl Acad Sci U S A. 2004 Dec 21;101(51):17867-72 [15601762.001]
  • [Cites] J Biol Chem. 2003 Sep 5;278(36):34141-9 [12773529.001]
  • [Cites] Cardiovasc Res. 2007 Mar 1;73(4):699-709 [17234167.001]
  • [Cites] Org Lett. 2003 Sep 18;5(19):3459-62 [12967299.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Mar 1;60(4-5):452-72 [18164781.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Mar 1;60(4-5):499-516 [18093693.001]
  • [Cites] Biochemistry. 1998 May 5;37(18):6235-9 [9572837.001]
  • [Cites] Biochim Biophys Acta. 2004 Oct 11;1665(1-2):48-56 [15471570.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):14814-9 [18806224.001]
  • [Cites] J Biol Chem. 1994 Apr 8;269(14):10444-50 [8144628.001]
  • [Cites] Eur J Biochem. 2001 Mar;268(5):1304-14 [11231282.001]
  • [Cites] J Control Release. 2005 Jan 20;102(1):247-53 [15653149.001]
  • [Cites] J Biol Chem. 2005 Apr 15;280(15):15300-6 [15687490.001]
  • [Cites] Bioconjug Chem. 2000 May-Jun;11(3):301-5 [10821645.001]
  • [Cites] Bioconjug Chem. 1999 Mar-Apr;10(2):186-91 [10077466.001]
  • [Cites] Biochem Soc Trans. 2007 Aug;35(Pt 4):821-5 [17635156.001]
  • [Cites] FASEB J. 1998 Jan;12(1):67-77 [9438412.001]
  • [Cites] J Biol Chem. 2001 Jul 13;276(28):26204-10 [11346640.001]
  • [Cites] Biochim Biophys Acta. 2001 Dec 1;1515(2):101-9 [11718666.001]
  • [Cites] Hum Mol Genet. 2009 Nov 15;18(22):4405-14 [19692354.001]
  • [Cites] Nucleic Acids Res. 2001 Oct 1;29(19):3965-74 [11574678.001]
  • [Cites] J Pharm Sci. 2008 Jan;97(1):144-62 [17763452.001]
  • [Cites] J Control Release. 2008 Nov 24;132(1):21-5 [18727945.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jan 2;98(1):42-7 [11120883.001]
  • [Cites] Biochem J. 2002 Nov 1;367(Pt 3):761-9 [12137567.001]
  • [Cites] J Biol Chem. 2003 Dec 12;278(50):50188-94 [14517218.001]
  • [Cites] Nucleic Acids Res. 1997 Jul 15;25(14):2730-6 [9207018.001]
  • [Cites] J Virol. 2007 Jun;81(11):5637-48 [17344287.001]
  • [Cites] Nat Med. 2004 Mar;10(3):310-5 [14770178.001]
  • [Cites] Lancet Neurol. 2009 Oct;8(10):918-28 [19713152.001]
  • [Cites] Curr Opin Mol Ther. 2001 Apr;3(2):147-52 [11338927.001]
  • [Cites] Nucleic Acids Res. 2008 Nov;36(20):6343-54 [18796528.001]
  • [Cites] J Biol Chem. 2003 Sep 12;278(37):35109-14 [12837762.001]
  • [Cites] Proc Natl Acad Sci U S A. 1994 Jan 18;91(2):664-8 [8290579.001]
  • [Cites] Oligonucleotides. 2006 Summer;16(2):145-57 [16764538.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Mar 1;60(4-5):608-13 [18037528.001]
  • [Cites] J Biol Chem. 1997 Jun 20;272(25):16010-7 [9188504.001]
  • [Cites] Trends Neurosci. 2007 Jun;30(6):260-7 [17418905.001]
  • [Cites] Science. 1999 Sep 3;285(5433):1569-72 [10477521.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Aug 17;60(11):1241-51 [18508157.001]
  • [Cites] Nat Med. 2006 Feb;12(2):175-7 [16444267.001]
  • [Cites] Nat Biotechnol. 2009 Jun;27(6):567-71 [19448630.001]
  • [Cites] Bioconjug Chem. 2000 Nov-Dec;11(6):762-71 [11087323.001]
  • [Cites] J Control Release. 2009 Mar 19;134(3):221-7 [19105971.001]
  • [Cites] Adv Drug Deliv Rev. 2005 Feb 28;57(4):579-96 [15722165.001]
  • [Cites] Nucleic Acids Res. 2007;35(13):4495-502 [17584792.001]
  • [Cites] Biochem Biophys Res Commun. 2002 Feb 22;291(2):367-71 [11846414.001]
  • [Cites] J Pept Res. 2000 Nov;56(5):318-25 [11095185.001]
  • [Cites] Mol Biol Cell. 2004 May;15(5):2347-60 [15020715.001]
  • [Cites] Traffic. 2007 Jul;8(7):848-66 [17587406.001]
  • [Cites] Proc Natl Acad Sci U S A. 2008 Aug 26;105(34):12128-33 [18713866.001]
  • [Cites] Nat Biotechnol. 1998 Sep;16(9):857-61 [9743120.001]
  • [Cites] Proc Natl Acad Sci U S A. 2001 Jul 17;98(15):8786-91 [11438707.001]
  • [Cites] J Biol Chem. 2009 Feb 6;284(6):3370-8 [19047062.001]
  • [Cites] Biol Cell. 2008 Apr;100(4):201-17 [18341479.001]
  • [Cites] Mol Pharmacol. 2002 Oct;62(4):864-72 [12237333.001]
  • [Cites] Mol Pharm. 2009 May-Jun;6(3):686-95 [19397332.001]
  • [Cites] N Engl J Med. 2007 Dec 27;357(26):2677-86 [18160687.001]
  • [Cites] J Control Release. 2006 Feb 21;110(3):595-604 [16377019.001]
  • [Cites] Hum Mol Genet. 2008 Dec 15;17(24):3909-18 [18784278.001]
  • [Cites] Mol Ther. 2007 Sep;15(9):1587-92 [17579573.001]
  • [Cites] Nucleic Acids Res. 2005 Nov 30;33(21):6837-49 [16321967.001]
  • [Cites] Int J Mol Sci. 2008 Jun;9(7):1276-320 [19325804.001]
  • [Cites] Eur J Cardiothorac Surg. 2005 Jan;27(1):117-21 [15621482.001]
  • [Cites] Chembiochem. 2006 Oct;7(10):1497-515 [16972294.001]
  • [Cites] RNA. 2007 Oct;13(10):1609-24 [17684229.001]
  • [Cites] Nucleic Acids Res. 2008 Nov;36(20):6418-28 [18842625.001]
  • [Cites] FEBS Lett. 2006 Feb 20;580(5):1451-6 [16460737.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431.001]
  • [Cites] New Biol. 1991 Nov;3(11):1121-34 [1777485.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Mar 1;60(4-5):517-29 [18037527.001]
  • [Cites] J Neurosci. 2004 Aug 4;24(31):6880-8 [15295022.001]
  • [Cites] J Control Release. 2006 Dec 1;116(3):304-13 [17097177.001]
  • [Cites] Nucleic Acids Res. 2009 Aug;37(14):4559-69 [19483097.001]
  • [Cites] Biochemistry. 2001 Feb 13;40(6):1824-34 [11327845.001]
  • [Cites] Adv Drug Deliv Rev. 2008 Mar 1;60(4-5):548-58 [18053612.001]
  • [Cites] Curr Pharm Des. 2008;14(24):2415-47 [18781991.001]
  • [Cites] J Med Chem. 2002 Aug 15;45(17):3612-8 [12166934.001]
  • [Cites] J Pept Sci. 2008 Apr;14(4):455-60 [18236382.001]
  • [Cites] Bioconjug Chem. 2005 Sep-Oct;16(5):1176-80 [16173795.001]
  • [Cites] Hum Mol Genet. 1998 Jul;7(7):1083-90 [9618164.001]
  • [Cites] Curr Pharm Des. 2008;14(34):3628-36 [19075739.001]
  • [Cites] J Gene Med. 2006 Feb;8(2):207-16 [16285002.001]
  • [Cites] Cancer Res. 2001 Mar 1;61(5):1768-75 [11280720.001]
  • [Cites] Cell. 1988 Dec 23;55(6):1189-93 [2849510.001]
  • [Cites] Mol Ther. 2008 Sep;16(9):1624-9 [18545222.001]
  • [Cites] Biochim Biophys Acta. 1998 Nov 11;1414(1-2):127-39 [9804921.001]
  • [Cites] Expert Opin Drug Deliv. 2006 Nov;3(6):739-46 [17076596.001]
  • [Cites] Nat Med. 2000 Nov;6(11):1253-7 [11062537.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Jan 4;102(1):198-203 [15608067.001]
  • [Cites] J Control Release. 2007 Apr 2;118(2):216-24 [17239466.001]
  • [Cites] Chem Biol. 2005 Aug;12(8):923-9 [16125104.001]
  • [Cites] Biopolymers. 2008;90(5):604-10 [18381624.001]
  • [Cites] J Biol Chem. 2001 Feb 23;276(8):5836-40 [11084031.001]
  • [Cites] Pharm Res. 2004 Sep;21(9):1662-9 [15497694.001]
  • (PMID = 19898741.001).
  • [ISSN] 1420-9071
  • [Journal-full-title] Cellular and molecular life sciences : CMLS
  • [ISO-abbreviation] Cell. Mol. Life Sci.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / MC/ U105178803
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] Switzerland
  • [Chemical-registry-number] 0 / Oligonucleotides; 0 / Peptides
  • [Number-of-references] 99
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27. Zhang H, Zhao Q, Bhattacharya S, Waheed AA, Tong X, Hong A, Heck S, Curreli F, Goger M, Cowburn D, Freed EO, Debnath AK: A cell-penetrating helical peptide as a potential HIV-1 inhibitor. J Mol Biol; 2008 May 2;378(3):565-80
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  • The capsid domain of the human immunodeficiency virus type 1 (HIV-1) Gag polyprotein is a critical determinant of virus assembly, and is therefore a potential target for developing drugs for AIDS therapy.
  • Using this structural information, we have utilized a structure-based rational design approach to stabilize the alpha-helical structure of CAI and convert it to a cell-penetrating peptide (CPP).
  • This proof-of-concept cell-penetrating peptide may aid validation of capsid as an anti-HIV-1 drug target and may help in designing peptidomimetics and small molecule drugs targeted to this protein.

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  • [Cites] Nature. 2000 Sep 21;407(6802):409-13 [11014200.001]
  • [Cites] Biophys J. 2001 Jul;81(1):586-94 [11423440.001]
  • [Cites] AIDS. 2001;15 Suppl 5:S13-20 [11816161.001]
  • [Cites] J Virol. 2002 Mar;76(6):2641-7 [11861830.001]
  • [Cites] J Virol. 2002 Jul;76(14):6900-8 [12072491.001]
  • [Cites] Virology. 2006 Apr 25;348(1):84-95 [16442581.001]
  • [Cites] J Virol. 2006 Jun;80(12):5716-22 [16731910.001]
  • [Cites] J Virol. 2006 Aug;80(16):7939-51 [16873251.001]
  • [Cites] PLoS Biol. 2006 Dec;4(12):e435 [17147474.001]
  • [Cites] J Virol. 2007 Jul;81(14):7476-90 [17507489.001]
  • [Cites] Antimicrob Agents Chemother. 2002 Nov;46(11):3597-605 [12384371.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431.001]
  • [Cites] J Mol Biol. 2003 Jan 24;325(4):759-72 [12507478.001]
  • [Cites] J Mol Biol. 2003 Apr 11;327(5):1013-20 [12662926.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11273-8 [13679575.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Nov 11;100(23):13555-60 [14573704.001]
  • [Cites] Angew Chem Int Ed Engl. 2005 Oct 14;44(40):6525-9 [16172999.001]
  • [Cites] J Virol. 2004 Jan;78(2):922-9 [14694123.001]
  • [Cites] J Virol. 2004 Feb;78(3):1375-83 [14722292.001]
  • [Cites] J Virol. 2004 Mar;78(5):2545-52 [14963157.001]
  • [Cites] Bioorg Med Chem Lett. 2004 Mar 22;14(6):1403-6 [15006371.001]
  • [Cites] J Virol. 2004 Jun;78(11):5670-8 [15140964.001]
  • [Cites] Protein Sci. 2004 Jun;13(6):1512-23 [15152086.001]
  • [Cites] Biochemistry. 2004 Aug 17;43(32):10435-41 [15301542.001]
  • [Cites] Science. 2004 Sep 3;305(5689):1466-70 [15353804.001]
  • [Cites] J Gen Virol. 2004 Oct;85(Pt 10):2903-13 [15448352.001]
  • [Cites] Antimicrob Agents Chemother. 2004 Nov;48(11):4349-59 [15504864.001]
  • [Cites] J Virol. 1986 Aug;59(2):284-91 [3016298.001]
  • [Cites] J Exp Med. 1991 Dec 1;174(6):1557-63 [1836013.001]
  • [Cites] J Gen Virol. 1994 Jun;75 ( Pt 6):1469-74 [8207412.001]
  • [Cites] J Virol. 1996 Aug;70(8):5106-14 [8764018.001]
  • [Cites] Science. 1997 Oct 31;278(5339):849-53 [9346481.001]
  • [Cites] Eur J Biochem. 1997 Oct 15;249(2):592-600 [9370371.001]
  • [Cites] Virology. 1998 Nov 10;251(1):1-15 [9813197.001]
  • [Cites] Biochemistry. 2004 Nov 9;43(44):13926-31 [15518540.001]
  • [Cites] J Biol Chem. 2005 May 6;280(18):17664-70 [15734744.001]
  • [Cites] Nat Struct Mol Biol. 2005 Aug;12(8):678-82 [16041386.001]
  • [Cites] Nat Struct Mol Biol. 2005 Aug;12(8):671-7 [16041387.001]
  • [Cites] Biochemistry. 2000 Sep 26;39(38):11657-66 [10995233.001]
  • [Cites] Proc Natl Acad Sci U S A. 2000 Mar 28;97(7):3503-8 [10725407.001]
  • [Cites] J Virol. 2000 Apr;74(8):3859-70 [10729160.001]
  • [Cites] J Virol. 2004 Jan;78(2):724-32 [14694104.001]
  • (PMID = 18374356.001).
  • [ISSN] 1089-8638
  • [Journal-full-title] Journal of molecular biology
  • [ISO-abbreviation] J. Mol. Biol.
  • [Language] ENG
  • [Grant] United States / Intramural NIH HHS / / Z01 BC010778-01; United States / NIGMS NIH HHS / GM / P41 GM066354-05; United States / NIGMS NIH HHS / GM / GM-66354; United States / NIGMS NIH HHS / GM / P41 GM066354; United States / NIGMS NIH HHS / GM / P41 GM066354-01; United States / NIGMS NIH HHS / GM / GM066354-01
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, N.I.H., Intramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-HIV Agents; 0 / Gene Products, gag; 0 / NYAD-1 peptide; 0 / Peptides; 0 / Peptides, Cyclic
  • [Other-IDs] NLM/ NIHMS76587; NLM/ PMC2695608
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28. Ward C, Phipps K, de Sousa C, Butler S, Gumley D: Treatment factors associated with outcomes in children less than 3 years of age with CNS tumours. Childs Nerv Syst; 2009 Jun;25(6):663-8
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  • [Title] Treatment factors associated with outcomes in children less than 3 years of age with CNS tumours.
  • INTRODUCTION: This study aimed to document cognitive outcomes in children treated for brain tumours with surgery and/or chemotherapy before the age of 3 years and to investigate the relationship between treatment factors and cognitive outcome.
  • MATERIALS AND METHODS: Participants were 31 children aged 7-14 years who had been diagnosed and treated for brain tumours under the age of 3 years.
  • Lower socio-economic status, younger age at treatment, having undergone more than one surgical intervention, motor problems and speech and language difficulties were found to be related to cognitive functioning.
  • [MeSH-major] Brain Neoplasms / drug therapy. Brain Neoplasms / surgery. Cognition
  • [MeSH-minor] Age Factors. Astrocytoma / complications. Astrocytoma / drug therapy. Astrocytoma / surgery. Child, Preschool. Combined Modality Therapy. Disabled Children. Ependymoma / complications. Ependymoma / drug therapy. Ependymoma / surgery. Female. Humans. Infant. Intelligence. Intelligence Tests. Language Disorders / complications. Male. Memory. Movement Disorders / complications. Neuropsychological Tests. Papilloma, Choroid Plexus / complications. Papilloma, Choroid Plexus / drug therapy. Papilloma, Choroid Plexus / surgery. Socioeconomic Factors. Treatment Outcome. Vision Disorders / complications

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  • [Cites] J Neurophysiol. 2005 Dec;94(6):4108-20 [16033937.001]
  • [Cites] Psychooncology. 2002 Jan-Feb;11(1):74-9 [11835594.001]
  • [Cites] Pediatr Rehabil. 2004 Jan-Mar;7(1):1-14; discussion 15-6 [14744668.001]
  • [Cites] J Clin Oncol. 2005 Aug 1;23(22):5198-204 [16051961.001]
  • [Cites] Neurology. 2004 Apr 27;62(8):1311-6 [15111667.001]
  • [Cites] Lancet Oncol. 2004 Jul;5(7):399-408 [15231246.001]
  • [Cites] Dev Neuropsychol. 2000;18(2):237-72 [11280966.001]
  • [Cites] Ann Neurol. 1999 Dec;46(6):834-41 [10589535.001]
  • [Cites] Childs Nerv Syst. 1998 Apr-May;14(4-5):179-84 [9660119.001]
  • [Cites] J Speech Hear Res. 1984 Jun;27(2):232-44 [6738035.001]
  • [Cites] J Pediatr. 2007 Sep;151(3):284-8, 288.e1 [17719939.001]
  • [Cites] J Neurosci Nurs. 1990 Aug;22(4):220-6 [2144556.001]
  • [Cites] J Child Neurol. 1992 Jul;7(3):281-90 [1634751.001]
  • [Cites] Pediatr Neurol. 2000 Feb;22(2):106-12 [10738915.001]
  • [Cites] Early Hum Dev. 2008 Nov;84(11):769-76 [18639396.001]
  • [Cites] Pediatr Neurosurg. 2005 Jan-Feb;41(1):15-21 [15886508.001]
  • [Cites] Brain. 2003 Sep;126(Pt 9):1998-2008 [12876140.001]
  • (PMID = 19247674.001).
  • [ISSN] 1433-0350
  • [Journal-full-title] Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery
  • [ISO-abbreviation] Childs Nerv Syst
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Germany
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29. Hobbs A, Foster P, Prescott C, Scotland R, Ahluwalia A: Natriuretic peptide receptor-C regulates coronary blood flow and prevents myocardial ischemia/reperfusion injury: novel cardioprotective role for endothelium-derived C-type natriuretic peptide. Circulation; 2004 Sep 7;110(10):1231-5
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  • [Title] Natriuretic peptide receptor-C regulates coronary blood flow and prevents myocardial ischemia/reperfusion injury: novel cardioprotective role for endothelium-derived C-type natriuretic peptide.
  • BACKGROUND: Ischemia/reperfusion (I/R) injury complicates myocardial infarction and stroke by exacerbating tissue damage and increasing risk of mortality.
  • We have recently identified C-type natriuretic peptide (CNP) as an endothelium-derived hyperpolarizing factor in the mesenteric resistance vasculature and described a novel signaling pathway involving activation of natriuretic peptide receptor C (NPR-C), which plays a pivotal role in the regulation of local blood flow.
  • METHODS AND RESULTS: CNP and (Cys18)-atrial natriuretic factor (4-23) amide (cANF(4-23)) elicited dose-dependent decreases in coronary perfusion pressure (CPP) that were blocked by Ba(2+) and ouabain in the isolated Langendorff rat heart.
  • CNP and cANF(4-23) reduced infarct size after 25 minutes of global ischemia and 120 minutes of reperfusion, maintaining CPP and left ventricular pressure at preischemic values.
  • Moreover, this newly defined pathway represents a protective mechanism against I/R injury and a novel target for therapeutic intervention in ischemic cardiovascular disorders.
  • [MeSH-major] Coronary Circulation / drug effects. Natriuretic Peptide, C-Type / physiology. Receptors, Atrial Natriuretic Factor / physiology
  • [MeSH-minor] Acetylcholine / pharmacology. Animals. Atrial Natriuretic Factor / pharmacology. Atrial Natriuretic Factor / therapeutic use. Barium / pharmacology. Drug Evaluation, Preclinical. Endothelium, Vascular / drug effects. Endothelium, Vascular / secretion. Male. Myocardial Infarction / drug therapy. Myocardial Infarction / pathology. Myocardial Reperfusion Injury / prevention & control. NG-Nitroarginine Methyl Ester / pharmacology. Nitric Oxide / physiology. Ouabain / pharmacology. Peptide Fragments / pharmacology. Peptide Fragments / therapeutic use. Rats. Rats, Wistar. Signal Transduction. Vasodilation / drug effects. Vasodilator Agents / pharmacology. Vasodilator Agents / therapeutic use


30. Ciccocioppo R, Economidou D, Fedeli A, Massi M: The nociceptin/orphanin FQ/NOP receptor system as a target for treatment of alcohol abuse: a review of recent work in alcohol-preferring rats. Physiol Behav; 2003 Jun;79(1):121-8
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  • [Title] The nociceptin/orphanin FQ/NOP receptor system as a target for treatment of alcohol abuse: a review of recent work in alcohol-preferring rats.
  • Studies aimed at the pharmacological characterization of the receptor, which mediates the effect, have shown that the C-terminal 13 amino acid sequence is crucial for activity and that the selective NOP receptor antagonist [Nphe(1)]N/OFQ(1-13)NH(2) blocks the effect of N/OFQ on ethanol drinking.
  • In place conditioning studies, N/OFQ abolishes the conditioned place preference (CPP) induced by ethanol in msP rats, or by morphine in nonselected Wistar rats; these findings suggest that N/OFQ is able to abolish the rewarding properties of ethanol and morphine.
  • Together, these findings suggest that N/OFQ and its receptor may represent an interesting target for pharmacological treatment of alcohol abuse.
  • [MeSH-minor] Animals. Association Learning / drug effects. Association Learning / physiology. Conditioning, Classical / drug effects. Conditioning, Classical / physiology. Ethanol / pharmacology. Humans. Injections, Intraventricular. Mice. Morphine / pharmacology. Morphine Dependence / physiopathology. Motivation. Rats. Social Environment. Stress, Psychological / complications. Ventral Tegmental Area / drug effects. Ventral Tegmental Area / physiopathology

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  • (PMID = 12818717.001).
  • [ISSN] 0031-9384
  • [Journal-full-title] Physiology & behavior
  • [ISO-abbreviation] Physiol. Behav.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Alcohol Deterrents; 0 / Opioid Peptides; 0 / Peptide Fragments; 0 / Receptors, Opioid; 0 / nociceptin orphanin FQ(1-17)OH; 0 / nociceptin receptor; 3K9958V90M / Ethanol; 76I7G6D29C / Morphine
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31. El-Andaloussi S, Johansson HJ, Holm T, Langel U: A novel cell-penetrating peptide, M918, for efficient delivery of proteins and peptide nucleic acids. Mol Ther; 2007 Oct;15(10):1820-6
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  • We present a novel CPP, M918, that efficiently translocates various cells in a non-toxic fashion.
  • Our data demonstrate that M918 is a novel CPP that can be used to translocate different cargoes inside various cells efficiently.
  • [MeSH-minor] Amino Acid Sequence. Endocytosis. Glycosaminoglycans / metabolism. HeLa Cells. Humans. Molecular Sequence Data. RNA Splicing / drug effects

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  • (PMID = 17622242.001).
  • [ISSN] 1525-0016
  • [Journal-full-title] Molecular therapy : the journal of the American Society of Gene Therapy
  • [ISO-abbreviation] Mol. Ther.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glycosaminoglycans; 0 / Peptide Nucleic Acids; 0 / Proteins
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32. Han Y, Li CS: [Effects of hypertension state induced by norepinephrine on liver in a swine model of cardiopulmonary resuscitation]. Zhongguo Wei Zhong Bing Ji Jiu Yi Xue; 2010 Feb;22(2):89-92
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  • At the same time, the animals of two groups received normal saline at the speed of 10 ml * kg(-1) * h(-1).
  • RESULTS: The heart rate (HR), MAP, cardiac output (CO) and coronary perfusion pressure (CPP) were obviously higher, while the oxygen extraction ratio was lower in the HT group than in the NP group.
  • [MeSH-major] Heart Arrest / therapy. Hypertension / chemically induced. Liver / drug effects. Norepinephrine / pharmacology
  • [MeSH-minor] Animals. Cardiopulmonary Resuscitation. Disease Models, Animal. Female. Hemodynamics / drug effects. Male. Swine. Ventricular Fibrillation / pathology. Ventricular Fibrillation / physiopathology. Ventricular Fibrillation / therapy

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  • (PMID = 20170612.001).
  • [ISSN] 1003-0603
  • [Journal-full-title] Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue
  • [ISO-abbreviation] Zhongguo Wei Zhong Bing Ji Jiu Yi Xue
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] X4W3ENH1CV / Norepinephrine
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33. Baudy RB, Fletcher H 3rd, Yardley JP, Zaleska MM, Bramlett DR, Tasse RP, Kowal DM, Katz AH, Moyer JA, Abou-Gharbia M: Design, synthesis, SAR, and biological evaluation of highly potent benzimidazole-spaced phosphono-alpha-amino acid competitive NMDA antagonists of the AP-6 type. J Med Chem; 2001 May 10;44(10):1516-29
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  • [Title] Design, synthesis, SAR, and biological evaluation of highly potent benzimidazole-spaced phosphono-alpha-amino acid competitive NMDA antagonists of the AP-6 type.
  • A series of 2-amino-(phosphonoalkyl)-1H-benzimidazole-2-alkanoic acids was synthesized and evaluated for NMDA receptor affinity using a [3H]CPP binding assay.
  • Several compounds of the AP-6 type demonstrated potent and selective NMDA antagonistic activity both in vitro and in vivo.
  • In particular, [R(-)]-2-amino-3-(5-chloro-1-phosphonomethyl-1H-benzoimidazol-2-yl)-propionic acid (1) displayed an IC(50) value of 7.1 nM in the [3H]CPP binding assay and an ED(50) value of 0.13 mg/kg (ip) in the NMDA lethality model.
  • Compound 1, when administered intravenously as a single bolus dose of 3 mg/kg following permanent occlusion of the middle cerebral artery in the rat, reduced the volume of infarcted brain tissue by 45%.
  • These results support a promising therapeutic potential for compound 1 as a neuroprotective agent.
  • [MeSH-minor] Animals. Arterial Occlusive Diseases / complications. Binding, Competitive. Brain / metabolism. Brain / pathology. Carotid Artery Diseases / complications. Drug Evaluation, Preclinical. In Vitro Techniques. Infarction, Middle Cerebral Artery / drug therapy. Infarction, Middle Cerebral Artery / etiology. Infarction, Middle Cerebral Artery / pathology. Male. Mice. Models, Molecular. Organophosphonates. Radioligand Assay. Rats. Rats, Inbred F344. Stereoisomerism

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  • (PMID = 11334562.001).
  • [ISSN] 0022-2623
  • [Journal-full-title] Journal of medicinal chemistry
  • [ISO-abbreviation] J. Med. Chem.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-amino-3-(5-chloro-1-phosphonomethyl-1H-benzoimidazol-2-yl)propionic acid; 0 / Benzimidazoles; 0 / Excitatory Amino Acid Antagonists; 0 / Neuroprotective Agents; 0 / Organophosphonates; 0 / Propionates; 0 / Receptors, N-Methyl-D-Aspartate
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34. Soustiel JF, Mahamid E, Chistyakov A, Shik V, Benenson R, Zaaroor M: Comparison of moderate hyperventilation and mannitol for control of intracranial pressure control in patients with severe traumatic brain injury--a study of cerebral blood flow and metabolism. Acta Neurochir (Wien); 2006 Aug;148(8):845-51; discussion 851
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  • [Title] Comparison of moderate hyperventilation and mannitol for control of intracranial pressure control in patients with severe traumatic brain injury--a study of cerebral blood flow and metabolism.
  • OBJECTIVE: To compare the respective effects of established measures used for management of traumatic brain injury (TBI) patients on cerebral blood flow (CBF) and cerebral metabolic rates of oxygen (CMRO2), glucose (CMRGlc) and lactate (CMRLct).
  • METHODS: Thirty-six patients suffering from severe traumatic brain injury (TBI) were prospectively evaluated.
  • Intracranial and cerebral perfusion pressure (ICP, CPP), CBF and arterial jugular differences in oxygen, glucose and lactate contents were measured for calculation of CMRO2, CMRGlc and CMRLct.
  • [MeSH-major] Brain Edema / therapy. Brain Injuries / complications. Cerebrovascular Circulation / drug effects. Hyperventilation / metabolism. Intracranial Hypertension / therapy. Mannitol / therapeutic use
  • [MeSH-minor] Adolescent. Adult. Aged. Brain Ischemia / etiology. Brain Ischemia / physiopathology. Brain Ischemia / therapy. Cerebral Cortex / drug effects. Cerebral Cortex / metabolism. Cerebral Cortex / physiopathology. Diuretics, Osmotic / therapeutic use. Female. Glucose / metabolism. Glycolysis / drug effects. Glycolysis / physiology. Humans. Lactic Acid / metabolism. Male. Middle Aged. Oxygen Consumption / drug effects. Prospective Studies. Respiration, Artificial / adverse effects. Respiration, Artificial / standards. Treatment Outcome

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  • (PMID = 16763735.001).
  • [ISSN] 0001-6268
  • [Journal-full-title] Acta neurochirurgica
  • [ISO-abbreviation] Acta Neurochir (Wien)
  • [Language] eng
  • [Publication-type] Clinical Trial; Comparative Study; Journal Article
  • [Publication-country] Austria
  • [Chemical-registry-number] 0 / Diuretics, Osmotic; 33X04XA5AT / Lactic Acid; 3OWL53L36A / Mannitol; IY9XDZ35W2 / Glucose
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35. Wang YQ, Zhou W, Liu YY, Liu YH, Peng T, Wang ZR: [The role of circadian gene period1 in morphine reward in mice]. Space Med Med Eng (Beijing); 2004 Oct;17(5):383-5
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  • OBJECTIVE: To investigate the role of circadian gene Period1 on drug dependence.
  • Conditional place preference (CPP) paradigm used to investigate the effect of intracerebroventricular (ICV) injection of pcDNA 3.1-per1RZ on drug reward in BALB/C mice.
  • CPP test displayed the block of drug reward in pcDNA 3.1-per1RZ ICV injection group.
  • Period1 expression in brain was attenuated of pcDNA 3.1-per1RZ ICV injection group demonstrated by western blot.
  • CONCLUSION: Interfere the Period1 expression in brain could attenuate the psychological dependence of drug in mammals.
  • [MeSH-major] Circadian Rhythm / genetics. Morphine / pharmacology. Morphine Dependence / drug therapy. Nuclear Proteins / pharmacology. Substance-Related Disorders / drug therapy
  • [MeSH-minor] Animals. Behavior, Animal / drug effects. Behavior, Animal / physiology. Cell Cycle Proteins. Disease Models, Animal. Genetic Therapy. Mice. Mice, Inbred BALB C. Period Circadian Proteins. RNA, Messenger / metabolism

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  • (PMID = 15926241.001).
  • [ISSN] 1002-0837
  • [Journal-full-title] Hang tian yi xue yu yi xue gong cheng = Space medicine & medical engineering
  • [ISO-abbreviation] Space Med Med Eng (Beijing)
  • [Language] chi
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Nuclear Proteins; 0 / Per1 protein, mouse; 0 / Period Circadian Proteins; 0 / RNA, Messenger; 76I7G6D29C / Morphine
  • [Other-IDs] NASA/ 00031288
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36. Takamatsu Y, Yamanishi Y, Hagino Y, Yamamoto H, Ikeda K: Differential effects of donepezil on methamphetamine and cocaine dependencies. Ann N Y Acad Sci; 2006 Aug;1074:418-26
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  • Donepezil, a choline esterase inhibitor, has been widely used as a medicine for Alzheimer's disease.
  • Recently, a study showed that donepezil inhibited addictive behaviors induced by cocaine, including cocaine-conditioned place preference (CPP) and locomotor sensitization to cocaine.
  • In counterbalanced CPP tests, the intraperitoneal (i.p.) administration of 3 mg/kg donepezil prior to 2 mg/kg METH i.p. failed to inhibit METH CPP, whereas pretreatment with 3 mg/kg donepezil abolished the CPP for cocaine (10 mg/kg, i.p.).
  • [MeSH-minor] Amphetamine-Related Disorders / drug therapy. Animals. Behavior, Animal / drug effects. Cocaine-Related Disorders / drug therapy. Conditioning (Psychology). Male. Mice. Mice, Inbred C57BL. Motor Activity / drug effects

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  • (PMID = 17105940.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Indans; 0 / Piperidines; 8SSC91326P / donepezil
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37. Stocchetti N, Rossi S, Zanier ER, Colombo A, Beretta L, Citerio G: Pyrexia in head-injured patients admitted to intensive care. Intensive Care Med; 2002 Nov;28(11):1555-62
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  • (b) to elucidate the relationships between pyrexia and neurological severity, length of stay in the ICU, intracranial hypertension, and cerebral perfusion pressure (CPP); and (c) to describe the effects of antipyretic therapy on temperature, intracranial pressure (ICP) and CPP.
  • PATIENTS: 110 patients with traumatic brain injury.
  • Various antipyretic therapies were used in 66 patients.
  • Pharmacological treatment was slightly effective (mean temperature reduction 0.58+/-0.7 degrees C) but caused a significant drop in CPP (6.5+/-12.5 mmHg).
  • Its incidence is higher in more severe cases and is correlated with a longer ICU stay.
  • It may affect ICP, but its contribution is difficult to assess when other major causes of increased intracranial volume are present.
  • Antipyretic therapy is poorly effective for controlling body temperature and may be deleterious for CPP.
  • [MeSH-major] Analgesics, Non-Narcotic / therapeutic use. Craniocerebral Trauma / complications. Fever / drug therapy. Fever / etiology
  • [MeSH-minor] Adolescent. Adult. Aged. Aged, 80 and over. Chi-Square Distribution. Female. Humans. Intensive Care Units / statistics & numerical data. Intracranial Pressure. Length of Stay / statistics & numerical data. Logistic Models. Male. Middle Aged. Retrospective Studies. Risk Factors. Statistics, Nonparametric

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  • (PMID = 12415441.001).
  • [ISSN] 0342-4642
  • [Journal-full-title] Intensive care medicine
  • [ISO-abbreviation] Intensive Care Med
  • [Language] eng
  • [Publication-type] Journal Article; Multicenter Study
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Analgesics, Non-Narcotic
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38. Bortolato M, Campolongo P, Mangieri RA, Scattoni ML, Frau R, Trezza V, La Rana G, Russo R, Calignano A, Gessa GL, Cuomo V, Piomelli D: Anxiolytic-like properties of the anandamide transport inhibitor AM404. Neuropsychopharmacology; 2006 Dec;31(12):2652-9
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  • We also evaluated whether AM404 might influence motivation (in the conditioned place preference (CPP) test), sensory reactivity (acoustic startle reflex) and sensorimotor gating (prepulse inhibition (PPI) of the startle reflex).
  • In the CPP test, AM404 (1.25-10 mg kg(-1), i.p.) elicited rewarding effects in rats housed under enriched conditions, but not in rats kept in standard cages.
  • These results support a role of anandamide in the regulation of emotion and point to the anandamide transport system as a potential target for anxiolytic drugs.
  • [MeSH-major] Anxiety Disorders / drug therapy. Arachidonic Acids / metabolism. Arachidonic Acids / pharmacology. Brain / drug effects. Cannabinoid Receptor Modulators / metabolism. Carrier Proteins / drug effects. Polyunsaturated Alkamides / metabolism
  • [MeSH-minor] Animals. Animals, Newborn. Anti-Anxiety Agents / pharmacology. Anxiety, Separation / drug therapy. Anxiety, Separation / metabolism. Anxiety, Separation / physiopathology. Behavior, Animal / drug effects. Behavior, Animal / physiology. Disease Models, Animal. Endocannabinoids. Male. Maze Learning / drug effects. Maze Learning / physiology. Neural Inhibition / drug effects. Neural Inhibition / physiology. Piperidines / pharmacology. Pyrazoles / pharmacology. Rats. Rats, Sprague-Dawley. Rats, Wistar. Receptor, Cannabinoid, CB1 / agonists. Receptor, Cannabinoid, CB1 / antagonists & inhibitors. Receptor, Cannabinoid, CB1 / metabolism. Reflex, Startle / drug effects. Reflex, Startle / physiology

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  • (PMID = 16541083.001).
  • [ISSN] 0893-133X
  • [Journal-full-title] Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
  • [ISO-abbreviation] Neuropsychopharmacology
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA-12447; United States / NIDA NIH HHS / DA / DA-3412
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Anxiety Agents; 0 / Arachidonic Acids; 0 / Cannabinoid Receptor Modulators; 0 / Carrier Proteins; 0 / Endocannabinoids; 0 / N-(4-hydroxyphenyl)arachidonylamide; 0 / Piperidines; 0 / Polyunsaturated Alkamides; 0 / Pyrazoles; 0 / Receptor, Cannabinoid, CB1; 158681-13-1 / rimonabant; 94421-68-8 / anandamide
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39. Fabi A, Salesi N, Di Cocco B, Vidiri A, Visca P, Pace A, Carapella C, De Paula U, Mirri A, Cognetti F: Choroid plexus carcinoma in the adult: is there a role for chemotherapy? J Exp Clin Cancer Res; 2005 Sep;24(3):493-6
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  • [Title] Choroid plexus carcinoma in the adult: is there a role for chemotherapy?
  • Choroid plexus carcinoma is a rare primary brain neoplasm arising from epithelial differentiated tissue, originating from the choroids plexus of the ventricles and, in 90% of the cases, in the lateral and fourth ventricles.
  • This neoplasm is seen mainly in children and reported infrequently in adults.
  • The treatment of choroid plexus carcinoma is based on scarce evidence in literature.
  • We report a rare case of an adult woman affected by a choroid plexus tumour and a discussion on the therapeutic management of this uncommon adult malignancy.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Choroid Plexus Neoplasms / drug therapy. Papilloma / drug therapy

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  • (PMID = 16270538.001).
  • [ISSN] 0392-9078
  • [Journal-full-title] Journal of experimental & clinical cancer research : CR
  • [ISO-abbreviation] J. Exp. Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Italy
  • [Chemical-registry-number] 0 / Contrast Media; BG3F62OND5 / Carboplatin; K2I13DR72L / Gadolinium DTPA; Q20Q21Q62J / Cisplatin
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40. Himmelseher S, Pfenninger E: [Neuroprotection in neuroanesthesia: current practices in Germany]. Anaesthesist; 2000 May;49(5):412-9
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  • Since the questions concerning "neuroprotective therapy" were linked to a general survey on clinical neuroanesthesia performed by the scientific neuroanesthesia working group of the DGAI, the only departments that were assessed were those which had participated in an earlier study on neuroanesthesia in 1991.
  • Therapy varied considerably between departments.
  • Following head trauma 69% of injured patients were managed with enhanced cerebral perfusion pressure (CPP) within the range of 70-90 mmHg.
  • If necessary, CPP increase was induced by vasopressors (exogenous supply of catecholamines in 100% of instances) and the administration of fluids (97% of instances).
  • The most commonly used therapeutic approaches to treat intracranial hypertension were mannitol (95% of instances), hyperventilation (91% of instances), cerebrospinal fluid drainage (89% of instances), and barbiturates (86% of instances).
  • Tris (hydroxymethyl)-aminomethane was administered in almost 49%, mild hypothermia in 37%, and hypertonic-hyperoncotic solutions in 28% of patients treated for an increase in intracranial pressure.
  • Following intracranial aneurysm surgery "triple-H" therapy was used in 74% of patients, applied as hemodilution in 94% and as hypervolemia and hypertension in 87% of instances.
  • It was used in 83% of patients during perioperative care and in 52% of patients during intensive care therapy.
  • Specific neuroprotective drugs were applied in 68% of departments, with barbiturates (38% of instances), nimodipine (23% of instances), and corticosteroids (10% of instances) as the main agents named.
  • These brain-protective medications were administered especially in intracranial hypertension in 30%, in intracranial aneurysms in 21%, and in subarachnoid hemorrhages subsequent to head trauma in 18% of instances described.
  • CONCLUSION: These findings demonstrate that the neuroprotective therapy administered in anesthesiological departments in Germany is not yet standardized, i.e., there is a wide variation.
  • [MeSH-minor] Blood Pressure / physiology. Cerebrovascular Circulation / drug effects. Cerebrovascular Circulation / physiology. Craniocerebral Trauma / surgery. Data Collection. Germany. Humans. Hypothermia, Induced. Intracranial Aneurysm / surgery. Intracranial Hypertension / prevention & control. Intracranial Hypertension / therapy. Neuroprotective Agents / therapeutic use. Respiration, Artificial. Surveys and Questionnaires

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  • (PMID = 10883355.001).
  • [ISSN] 0003-2417
  • [Journal-full-title] Der Anaesthesist
  • [ISO-abbreviation] Anaesthesist
  • [Language] ger
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] GERMANY
  • [Chemical-registry-number] 0 / Neuroprotective Agents
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41. Tseng MY, Al-Rawi PG, Czosnyka M, Hutchinson PJ, Richards H, Pickard JD, Kirkpatrick PJ: Enhancement of cerebral blood flow using systemic hypertonic saline therapy improves outcome in patients with poor-grade spontaneous subarachnoid hemorrhage. J Neurosurg; 2007 Aug;107(2):274-82
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  • [Title] Enhancement of cerebral blood flow using systemic hypertonic saline therapy improves outcome in patients with poor-grade spontaneous subarachnoid hemorrhage.
  • METHODS: Thirty-five patients with poor-grade spontaneous SAH received 2 ml/kg 23.5% hypertonic saline intravenously, and they underwent bedside transcranial Doppler (TCD) ultrasonography and intracranial pressure (ICP) monitoring.
  • Seventeen of them underwent Xe-enhanced computed tomography (CT) scanning for measuring CBF.
  • RESULTS: The authors observed a maximum increase in blood pressure by 10.3% (p < 0.05) and cerebral perfusion pressure (CPP) by 21.2% (p < 0.01) at 30 minutes, followed by a maximum decrease in ICP by 93.1% (p < 0.01) at 60 minutes.
  • Changes in ICP and CPP persisted for longer than 180 and 90 minutes, respectively.
  • A dose-dependent effect of CBF increments on favorable outcome was seen on Xe-CT scans (mRS Score 1-3, odds ratio 1.27 per 1 ml/100 g tissue x min, p = 0.045).
  • CONCLUSIONS: Bolus systemic hypertonic saline therapy may be used for reversal of cerebral ischemia to normal perfusion in patients with poor-grade SAH.
  • [MeSH-major] Cerebrovascular Circulation / drug effects. Homeostasis / drug effects. Saline Solution, Hypertonic / administration & dosage. Subarachnoid Hemorrhage / physiopathology. Subarachnoid Hemorrhage / therapy
  • [MeSH-minor] Adult. Aged. Blood Flow Velocity / drug effects. Blood Pressure / drug effects. Female. Follow-Up Studies. Humans. Injections, Intravenous. Intracranial Pressure / drug effects. Male. Middle Aged. Treatment Outcome

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  • [CommentIn] J Neurosurg. 2008 Mar;108(3):632; author reply 632-3 [18312116.001]
  • (PMID = 17695380.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Grant] United Kingdom / Medical Research Council / / G0001237; United Kingdom / Medical Research Council / / G0600986; United Kingdom / Medical Research Council / / G9439390
  • [Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Saline Solution, Hypertonic
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42. da Silva JC, de Lima Fde M, Valença MM, de Azevedo Filho HR: Hypertonic saline more efficacious than mannitol in lethal intracranial hypertension model. Neurol Res; 2010 Mar;32(2):139-43
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  • [Title] Hypertonic saline more efficacious than mannitol in lethal intracranial hypertension model.
  • BACKGROUND: Medical management of brain edema and elevated intracranial pressure (ICP) is a crucial challenge in neurosurgical practice.
  • Depending on the cause, the treatments for brain edema fall into three categories: stabilization of the blood-brain barrier, depletion of brain water and surgical decompression.
  • Although mannitol is the mainstay of hyperosmolar therapy, hypertonic saline (HS) is emerging as an effective alternative to traditional osmotic agents.
  • METHODS: Experimental elevated ICP (50 mmHg) was induced in rabbits using an intracranial balloon.
  • During 90 minutes, continuous recording of ICP, mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) was realized.
  • There was statistical difference between mannitol and HS; the 10% NaCl group had lower values of ICP (p=0.0116) and higher values of MAP (p<0.0001) and CPP (p<0.0001).
  • CONCLUSION: The findings demonstrate higher efficacy of the 10% NaCl treatment in this comparison with 20% mannitol.
  • Further efforts should be directed toward development of clinical studies using iso-osmotic doses of mannitol and HS in specific etiologies of intracranial hypertension.
  • [MeSH-major] Disease Models, Animal. Intracranial Hypertension / drug therapy. Mannitol / therapeutic use. Saline Solution, Hypertonic / therapeutic use
  • [MeSH-minor] Animals. Intracranial Pressure / drug effects. Intracranial Pressure / physiology. Male. Rabbits. Treatment Outcome

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  • (PMID = 19309542.001).
  • [ISSN] 1743-1328
  • [Journal-full-title] Neurological research
  • [ISO-abbreviation] Neurol. Res.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Saline Solution, Hypertonic; 3OWL53L36A / Mannitol
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43. Dhanikula AB, Lamontagne D, Leroux JC: Rescue of amitriptyline-intoxicated hearts with nanosized vesicles. Cardiovasc Res; 2007 Jun 1;74(3):480-6
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  • OBJECTIVE: Amitriptyline, one of the most prescribed antidepressants, is reported to claim a large number of human lives due to drug overdose related cardiac arrest.
  • Vesicles bearing an internal pH of 3.0 or 7.4 were then infused into amitriptyline pre-intoxicated isolated rat hearts, and changes in coronary perfusion pressure (CPP), the first derivative of left ventricular pressure (dP/dt max) and heart rate were monitored.
  • RESULTS: Based on the recoveries in CPP observed, the efficacies of the formulations were ranked as follows: control=pH 7.4-spherulites<pH 3.0-spherulites; whereas the ranking for the recoveries in heart rate was: control<pH 7.4-spherulites<pH 3.0-spherulites.
  • The significantly faster and higher recoveries in pH 3.0- vs. 7.4-spherulite-treated hearts demonstrated the importance of pH-gradient formulation for efficient extraction of tissue-bound amitriptyline.
  • CONCLUSION: These data suggest that spherulites have a protective effect against acute cardiovascular failure following intoxication with amitriptyline and possibly other cardiotoxic drugs.
  • [MeSH-major] Amitriptyline / toxicity. Antidepressive Agents, Tricyclic / toxicity. Heart Arrest / chemically induced. Heart Arrest / therapy. Lipids / administration & dosage
  • [MeSH-minor] Animals. Heart / drug effects. Lipid Metabolism. Male. Nanoparticles. Perfusion. Rats. Rats, Sprague-Dawley

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  • (PMID = 17359955.001).
  • [ISSN] 0008-6363
  • [Journal-full-title] Cardiovascular research
  • [ISO-abbreviation] Cardiovasc. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antidepressive Agents, Tricyclic; 0 / Lipids; 1806D8D52K / Amitriptyline
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44. Pillai A, Rajeev K, Chandi S, Unnikrishnan M: Intrinsic brainstem choroid plexus papilloma. Case report. J Neurosurg; 2004 Jun;100(6):1076-8
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  • [Title] Intrinsic brainstem choroid plexus papilloma. Case report.
  • The authors report an intrinsic brainstem lesion that was diagnosed initially as a pontine cavernoma, which finally proved to be a choroid plexus papilloma.
  • Choroid plexus papillomas are rare tumors of the central nervous system and are usually intraventricular in location.
  • The occurrence of this tumor in an intraparenchymal location is extremely rare, and its occurrence within the brainstem is previously unreported.
  • The authors also report a trial of chemotherapy with lomustine in the management of the residual tumor.
  • [MeSH-major] Brain Stem Neoplasms / pathology. Choroid Plexus Neoplasms / pathology. Glioma / pathology
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Female. Humans. Lomustine / therapeutic use. Middle Aged

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  • (PMID = 15200124.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 7BRF0Z81KG / Lomustine
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45. Velázquez-Sánchez C, Ferragud A, Hernández-Rabaza V, Nácher A, Merino V, Cardá M, Murga J, Canales JJ: The dopamine uptake inhibitor 3 alpha-[bis(4'-fluorophenyl)metoxy]-tropane reduces cocaine-induced early-gene expression, locomotor activity, and conditioned reward. Neuropsychopharmacology; 2009 Nov;34(12):2497-507
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  • Benztropine (BZT) analogs, a family of high-affinity dopamine transporter ligands, are molecules that exhibit pharmacological and behavioral characteristics predictive of significant therapeutic potential in cocaine addiction.
  • Here, we examined in mice the effects of 3 alpha-[bis(4'-fluorophenyl)metoxy]-tropane (AHN-1055) on motor activity, conditioned place preference (CPP) and c-Fos expression in the striatum.
  • Interaction assays showed that cocaine's ability to stimulate locomotor activity was decreased by AHN-1055 treatment, but not by treatment with D-amphetamine.
  • Remarkably, the BZT analog dose-dependently blocked cocaine-induced CPP without producing CPP when given alone, and blocked in conditioned mice cocaine-stimulated early-gene activation in the nucleus accumbens and dorsomedial striatum.
  • These observations provide evidence that AHN-1055 does not behave as a classical psychomotor stimulant and that some of its properties, including attenuation of cocaine-induced striatal c-Fos expression, locomotor stimulation, and CPP, support its candidacy, and that of structurally related molecules, as possible pharmacotherapies in cocaine addiction.
  • [MeSH-major] Benztropine / analogs & derivatives. Cocaine-Related Disorders / drug therapy. Conditioning, Classical / drug effects. Dopamine Uptake Inhibitors / pharmacology. Gene Expression / drug effects. Motor Activity / drug effects
  • [MeSH-minor] Animals. Brain / drug effects. Brain / metabolism. Cocaine / pharmacology. Dose-Response Relationship, Drug. Male. Mice. Nomifensine / pharmacology. Proto-Oncogene Proteins c-fos / metabolism. Reward. Space Perception / drug effects. Stereotyped Behavior / drug effects

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  • (PMID = 19606084.001).
  • [ISSN] 1740-634X
  • [Journal-full-title] Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
  • [ISO-abbreviation] Neuropsychopharmacology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Uptake Inhibitors; 0 / N-methyl-3-(bis(4'-fluorophenyl)methoxy)tropane; 0 / Proto-Oncogene Proteins c-fos; 1LGS5JRP31 / Nomifensine; 1NHL2J4X8K / Benztropine; I5Y540LHVR / Cocaine
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46. Braun K, Ehemann V, Wiessler M, Pipkorn R, Didinger B, Mueller G, Waldeck W: High-resolution flow cytometry: a suitable tool for monitoring aneuploid prostate cancer cells after TMZ and TMZ-BioShuttle treatment. Int J Med Sci; 2009;6(6):338-47
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  • [Title] High-resolution flow cytometry: a suitable tool for monitoring aneuploid prostate cancer cells after TMZ and TMZ-BioShuttle treatment.
  • If metastatic prostate cancer gets resistant to antiandrogen therapy, there are few treatment options, because prostate cancer is not very sensitive to cytostatic agents.
  • Temozolomide (TMZ) as an orally applicable chemotherapeutic substance has been proven to be effective and well tolerated with occasional moderate toxicity especially for brain tumors and an application to prostate cancer cells seemed to be promising.
  • Unfortunately, TMZ was inefficient in the treatment of symptomatic progressive hormone-refractory prostate cancer (HRPC).
  • The reasons could be a low sensitivity against TMZ the short plasma half-life of TMZ, non-adapted application regimens and additionally, the aneuploid DNA content of prostate cancer cells suggesting different sensitivity against therapeutical interventions e.g. radiation therapy or chemotherapy.
  • The modular-composed carrier consists of a transmembrane transporter (CPP), connected to a nuclear localization sequence (NLS) cleavably-bound, which in turn was coupled with TMZ.
  • The NLS-sequence allows an active delivery of the TMZ into the cell nucleus after transmembrane passage of the TMZ-BioShuttle and intra-cytoplasm enzymatic cleavage and separation from the CPP.
  • This TMZ-BioShuttle could contribute to improve therapeutic options exemplified by the hormone refractory prostate cancer.
  • The high-resolution flow cytometric analysis showed to be an appropriate system for a better detection and distinction of several cell populations dependent on their different DNA-indices as well as changes in proliferation of cell populations after chemotherapeutical treatment.
  • [MeSH-major] Aneuploidy. Antineoplastic Agents, Alkylating / administration & dosage. Dacarbazine / analogs & derivatives. Drug Monitoring / methods. Drug Resistance, Neoplasm. Flow Cytometry / methods. Prostatic Neoplasms / drug therapy
  • [MeSH-minor] Cell Line, Tumor. DNA, Neoplasm / analysis. Drug Delivery Systems. Humans. Male

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  • [Cites] Cancer Chemother Pharmacol. 2000;45(6):509-12 [10854140.001]
  • [Cites] Med Res Rev. 2010 Jan;30(1):23-66 [19536866.001]
  • [Cites] Nature. 2001 May 17;411(6835):366-74 [11357144.001]
  • [Cites] J Mol Biol. 2002 Apr 26;318(2):237-43 [12051833.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2002 Oct 1;54(2):427-35 [12243818.001]
  • [Cites] Biochem Soc Trans. 2002 Nov;30(Pt 6):952-8 [12440953.001]
  • [Cites] Anticancer Res. 2002 Nov-Dec;22(6C):4147-50 [12553046.001]
  • [Cites] Urol Int. 2003;70(1):1-14 [12566808.001]
  • [Cites] Cancer Lett. 2003 May 8;194(1):125-31 [12706866.001]
  • [Cites] Cell Cycle. 2004 Jan;3(1):46-50 [14657665.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 2004 Jul 15;59(4):928-42 [15234026.001]
  • [Cites] Chembiochem. 2004 Oct 4;5(10):1432-47 [15457527.001]
  • [Cites] Int J Cancer. 1978 Mar 15;21(3):274-81 [631930.001]
  • [Cites] Biochem Pharmacol. 1987 Feb 15;36(4):457-62 [3470008.001]
  • [Cites] Adv Cancer Res. 1991;57:1-46 [1950701.001]
  • [Cites] Biochem Int. 1992 Aug;27(4):567-77 [1417893.001]
  • [Cites] J Histochem Cytochem. 1994 Jun;42(6):697-704 [8189032.001]
  • [Cites] Curr Opin Immunol. 1994 Apr;6(2):279-89 [8011211.001]
  • [Cites] J Urol. 1994 Nov;152(5 Pt 2):1816 [7933240.001]
  • [Cites] J Urol. 1994 Nov;152(5 Pt 2):1837-42 [7523731.001]
  • [Cites] Cancer Res. 1995 Jul 15;55(14):2959-62 [7606709.001]
  • [Cites] Antimicrob Agents Chemother. 1995 Dec;39(12):2620-4 [8592990.001]
  • [Cites] J Clin Oncol. 1996 May;14(5):1617-25 [8622080.001]
  • [Cites] Cancer Res. 1997 Feb 1;57(3):524-31 [9012485.001]
  • [Cites] Int J Cancer. 1997 May 16;71(4):698-704 [9178829.001]
  • [Cites] J Clin Oncol. 1998 Jun;16(6):2272-9 [9626231.001]
  • [Cites] Int J Radiat Oncol Biol Phys. 1998 Jun 1;41(3):491-500 [9635694.001]
  • [Cites] Semin Nephrol. 1998 Sep;18(5):505-18 [9754603.001]
  • [Cites] Oncogene. 1998 Dec 24;17(25):3225-36 [9916985.001]
  • [Cites] Cancer Lett. 1999 Apr 26;138(1-2):101-6 [10378780.001]
  • [Cites] J Natl Cancer Inst. 1999 Sep 15;91(18):1574-80 [10491435.001]
  • [Cites] Ann Oncol. 2004 Nov;15(11):1613-21 [15520061.001]
  • [Cites] Radiother Oncol. 2004 Dec;73 Suppl 2:S119-22 [15971325.001]
  • [Cites] JAMA. 2005 Jul 13;294(2):238-44 [16014598.001]
  • [Cites] In Vivo. 2006 Jan-Feb;20(1):17-23 [16433023.001]
  • [Cites] Ann Oncol. 2006 Jun;17(6):952-6 [16565212.001]
  • [Cites] Hinyokika Kiyo. 2006 Jul;52(7):515-21 [16910582.001]
  • [Cites] Cochrane Database Syst Rev. 2006;(4):CD005247 [17054249.001]
  • [Cites] J Mol Histol. 2006 Sep;37(5-7):253-60 [16841236.001]
  • [Cites] CA Cancer J Clin. 2007 Jan-Feb;57(1):43-66 [17237035.001]
  • [Cites] Urology. 2007 Feb;69(2):347-51 [17320676.001]
  • [Cites] BJU Int. 2007 Mar;99(3):497-501 [17092283.001]
  • [Cites] Amino Acids. 2007;32(3):373-9 [17077962.001]
  • [Cites] Drug Resist Updat. 2007 Feb-Apr;10(1-2):51-8 [17387035.001]
  • [Cites] Clin Genitourin Cancer. 2007 Mar;5(4):278-83 [17553208.001]
  • [Cites] Pathol Oncol Res. 2007;13(2):84-90 [17607368.001]
  • [Cites] J Clin Oncol. 2007 Sep 1;25(25):3965-70 [17761981.001]
  • [Cites] Cancer Treat Rev. 2007 Oct;33(6):521-7 [17658220.001]
  • [Cites] Hepatology. 2007 Sep;46(3):759-68 [17663418.001]
  • [Cites] Int J Oncol. 2008 Feb;32(2):341-7 [18202756.001]
  • [Cites] Biochim Biophys Acta. 2008 Jan;1779(1):3-16 [18078840.001]
  • [Cites] Biostatistics. 2008 Apr;9(2):333-54 [17873151.001]
  • [Cites] Int J Med Sci. 2008;5(5):273-84 [18797509.001]
  • [Cites] J Pept Sci. 2009 Mar;15(3):235-41 [19177421.001]
  • [Cites] Br J Cancer. 2008 Sep 16;99(6):900-10 [19238631.001]
  • [Cites] Biomaterials. 2009 Jul;30(20):3466-75 [19304320.001]
  • [Cites] Oncol Rep. 2009 Aug;22(2):345-8 [19578775.001]
  • [Cites] BMC Cancer. 2009;9:210 [19563641.001]
  • [Cites] DNA Repair (Amst). 2009 Sep 2;8(9):1153-65 [19501553.001]
  • [Cites] Int J Cancer. 2009 Dec 15;125(12):2978-90 [19422046.001]
  • [Cites] Nature. 2001 May 17;411(6835):342-8 [11357141.001]
  • (PMID = 19946604.001).
  • [ISSN] 1449-1907
  • [Journal-full-title] International journal of medical sciences
  • [ISO-abbreviation] Int J Med Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / DNA, Neoplasm; 7GR28W0FJI / Dacarbazine; 85622-93-1 / temozolomide
  • [Other-IDs] NLM/ PMC2781174
  • [Keywords] NOTNLM ; Flow Cytometry / Prostate Cancer Cells / TMZ-BioShuttle
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47. Català-Temprano A, Claret Teruel G, Cambra Lasaosa FJ, Pons Odena M, Noguera Julián A, Palomeque Rico A: Intracranial pressure and cerebral perfusion pressure as risk factors in children with traumatic brain injuries. J Neurosurg; 2007 Jun;106(6 Suppl):463-6
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  • [Title] Intracranial pressure and cerebral perfusion pressure as risk factors in children with traumatic brain injuries.
  • OBJECT: The authors evaluated the initial intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as prognostic factors in severe head injury in children and tried to determine the optimal CPP range.
  • METHODS: The authors performed a 9-year retrospective review of all patients with severe traumatic brain injuries (TBIs) who required invasive ICP monitoring and were admitted to the pediatric intensive care unit at their institution between January 1995 and December 2003.
  • An unfavorable outcome was observed in more than 60% of patients with an initial CPP lower than 40 mm Hg.
  • CONCLUSIONS: Initial ICP and CPP measurements were useful as prognostic factors in pediatric patients with severe TBIs: patients with initial CPPs between 40 and 70 mm Hg were found to have a better neurological prognosis than those with CPPs either higher or lower than that range.
  • [MeSH-major] Blood Pressure. Brain Injuries / physiopathology. Cerebrovascular Circulation. Intracranial Pressure
  • [MeSH-minor] Adolescent. Child. Child, Preschool. Glasgow Coma Scale. Glasgow Outcome Scale. Humans. Infant. Intracranial Hypertension / drug therapy. Intracranial Hypertension / etiology. Prognosis. Retrospective Studies. Risk Factors. Trauma Severity Indices. Treatment Outcome

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  • (PMID = 17566403.001).
  • [ISSN] 0022-3085
  • [Journal-full-title] Journal of neurosurgery
  • [ISO-abbreviation] J. Neurosurg.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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48. Celik T, Kayir H, Ceyhan M, Demirtaş S, Coşar A, Uzbay IT: CPP and amlodipine alter the decrease in basal acetylcholine and choline release by audiogenic stimulus in hippocampus of ethanol-withdrawn rats in vivo. Brain Res Bull; 2004 Sep 30;64(3):243-9
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  • [Title] CPP and amlodipine alter the decrease in basal acetylcholine and choline release by audiogenic stimulus in hippocampus of ethanol-withdrawn rats in vivo.
  • Effects of N-methyl-D-aspartate (NMDA) receptor and Ca2+ channel antagonists on extracellular acetylcholine and choline release in the hippocampus of ethanol-withdrawn rats were investigated by in vivo microdialysis.
  • Either an NMDA receptor antagonist (+/-)-3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) or a calcium channel antagonist amlodipine was administered, and 15 min later, an audiogenic stimulus (100 dB, 1 min) was applied to rats.
  • CPP (15 mg/kg) and amlodipine (20 mg/kg) reversed the decrement in acetylcholine and increment in choline release in EW rats.
  • [MeSH-major] Acetylcholine / metabolism. Amlodipine / pharmacology. Ethanol / adverse effects. Hippocampus / drug effects. Piperazines / pharmacology. Substance Withdrawal Syndrome / metabolism
  • [MeSH-minor] Acoustic Stimulation / adverse effects. Alcohol-Induced Disorders, Nervous System / drug therapy. Alcohol-Induced Disorders, Nervous System / metabolism. Alcohol-Induced Disorders, Nervous System / physiopathology. Animals. Body Weight / drug effects. Calcium Channel Blockers / pharmacology. Choline / metabolism. Disease Models, Animal. Down-Regulation / drug effects. Down-Regulation / physiology. Drug Interactions / physiology. Epilepsy, Reflex / chemically induced. Epilepsy, Reflex / drug therapy. Epilepsy, Reflex / physiopathology. Excitatory Amino Acid Agonists / pharmacology. Glutamic Acid / metabolism. Male. Microdialysis. Neural Pathways / drug effects. Neural Pathways / metabolism. Neural Pathways / physiopathology. Rats. Rats, Wistar. Seizures / chemically induced. Seizures / drug therapy. Seizures / physiopathology. Synaptic Transmission / drug effects. Synaptic Transmission / physiology

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  • (PMID = 15464861.001).
  • [ISSN] 0361-9230
  • [Journal-full-title] Brain research bulletin
  • [ISO-abbreviation] Brain Res. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / Excitatory Amino Acid Agonists; 0 / Piperazines; 100828-16-8 / 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; 1J444QC288 / Amlodipine; 3K9958V90M / Ethanol; 3KX376GY7L / Glutamic Acid; N91BDP6H0X / Choline; N9YNS0M02X / Acetylcholine
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49. Tatò L, Savage MO, Antoniazzi F, Buzi F, Di Maio S, Oostdijk W, Pasquino AM, Raiola G, Saenger P, Tonini G, Voorhoeve PG, International Workshop on Management of Puberty for Optimum Auxological Results: Optimal therapy of pubertal disorders in precocious/early puberty. J Pediatr Endocrinol Metab; 2001 Jul;14 Suppl 2:985-95
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  • [Title] Optimal therapy of pubertal disorders in precocious/early puberty.
  • GnRHa have been used in the treatment of central precocious puberty (CPP) for a decade and some final results of this therapy are now available.
  • Treatment preserves height potential in younger patients and a complete recovery of the hypothalamic-pituitary-gonadal axis occurs at the end of treatment.
  • However, some aspects of the management of CPP are still debated.
  • The possibility of progression of premature thelarche into precocious puberty, the pathogenesis of organic and idiopathic precocious puberty, the criteria for decision to treat and to stop treatment and the utility of an association with GH treatment will be better understood in the future.
  • Follow-up of patients after stopping therapy includes frequency and characteristics of menses, the possible higher incidence of polycystic ovary-like syndrome and the correct achievement of a normal peak bone mass and body composition.
  • [MeSH-major] Puberty, Precocious / therapy
  • [MeSH-minor] Adolescent. Body Height / drug effects. Child. Female. Growth Hormone / adverse effects. Growth Hormone / therapeutic use. Humans. Male

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  • (PMID = 11529405.001).
  • [ISSN] 0334-018X
  • [Journal-full-title] Journal of pediatric endocrinology & metabolism : JPEM
  • [ISO-abbreviation] J. Pediatr. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Guideline; Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 9002-72-6 / Growth Hormone
  • [Number-of-references] 76
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50. Patel MB, Feinstein AJ, Saenz AD, Majetschak M, Proctor KG: Prehospital HBOC-201 after traumatic brain injury and hemorrhagic shock in swine. J Trauma; 2006 Jul;61(1):46-56
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  • [Title] Prehospital HBOC-201 after traumatic brain injury and hemorrhagic shock in swine.
  • BACKGROUND: Data are limited on the actions of hemoglobin based oxygen carriers (HBOCs) after traumatic brain injury (TBI).
  • Supplemental NS was administered to both groups to maintain mean arterial pressure (MAP) >60 mm Hg until 60 minutes, and to maintain cerebral perfusion pressure (CPP) >70 mm Hg from 60 to 300 minutes.
  • The control group received mannitol (1 g/kg) and blood (10 mL/kg) at 90 minutes and half (n = 5) received CPP directed phenylephrine (PE) therapy after 120 minutes.
  • RESULTS: With HBOC administration, MAP, CPP, and brain tissue PO2 were restored within 30 minutes and maintained until 300 minutes.
  • In contrast, with control, MAP and brain tissue PO2 did not correct until 120 minutes, after mannitol, transfusion and 40% more crystalloid.
  • Furthermore, without PE, CPP did not reach target and 0/5 could be extubated.
  • CONCLUSIONS: After TBI, a single HBOC-201 bolus with minimal supplements provided rapid resuscitation, while maintaining CPP and improving brain oxygenation, without causing cardiac dysfunction, coagulopathy, cytokine release, or brain structural changes.
  • [MeSH-major] Blood Substitutes / toxicity. Brain Injuries / therapy. Fluid Therapy / methods. Hemoglobins / toxicity. Shock, Hemorrhagic / therapy
  • [MeSH-minor] Analysis of Variance. Animals. Blood Coagulation / drug effects. Brain / drug effects. Brain / pathology. Cerebrovascular Circulation / drug effects. Cytokines / blood. Drug-Related Side Effects and Adverse Reactions. Female. Hemodynamics / drug effects. Male. Swine

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  • (PMID = 16832248.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Grant] United States / NIGMS NIH HHS / GM / T32 GM08749-01
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Blood Substitutes; 0 / Cytokines; 0 / HBOC 201; 0 / Hemoglobins
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51. Esmaeili B, Basseda Z, Dehpour AR: Antagonism of muscarinic M1 receptors by dicyclomine inhibits the consolidation of morphine-associated contextual memory. Brain Res Bull; 2008 Jul 1;76(4):380-7
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  • M1 muscarinic receptor has been shown to be involved in cognitive functions of the brain.
  • Conditioned place preference (CPP) paradigm involves memory for the association between environmental stimuli and the rewarding properties produced by a treatment.
  • Using a balanced CPP design, we studied the possible involvement of M1 muscarinic receptors on the acquisition, expression and consolidation of morphine place conditioning in male mice.
  • Subcutaneous administration of morphine sulphate-induced CPP in a dose-dependent manner.
  • Using a 6-day schedule of conditioning, it was found that dicyclomine, an M1 muscarinic antagonist, significantly reduced the time spent by mice in the morphine compartment when given immediately, but not 6h, after each conditioning session (consolidation).
  • It had no effect when administered 30 min before each conditioning session during CPP training period (acquisition) or 30 min before testing for place preference in the absence of morphine (expression).
  • It is concluded that M1 muscarinic receptors may play a time-dependent role in the consolidation of reward-related memory of morphine.
  • [MeSH-major] Dicyclomine / pharmacology. Learning / drug effects. Memory / drug effects. Morphine / pharmacology. Receptor, Muscarinic M1 / antagonists & inhibitors
  • [MeSH-minor] Animals. Brain / drug effects. Brain / metabolism. Conditioning (Psychology) / drug effects. Conditioning (Psychology) / physiology. Dose-Response Relationship, Drug. Drug Interactions / physiology. Male. Mice. Morphine Dependence / drug therapy. Morphine Dependence / metabolism. Muscarinic Antagonists / pharmacology. Narcotics / pharmacology. Reward. Time Factors

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  • (PMID = 18502314.001).
  • [ISSN] 1873-2747
  • [Journal-full-title] Brain research bulletin
  • [ISO-abbreviation] Brain Res. Bull.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Muscarinic Antagonists; 0 / Narcotics; 0 / Receptor, Muscarinic M1; 4KV4X8IF6V / Dicyclomine; 76I7G6D29C / Morphine
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52. Wang B, Luo F, Xia YQ, Han JS: Peripheral electric stimulation inhibits morphine-induced place preference in rats. Neuroreport; 2000 Apr 7;11(5):1017-20
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  • Conditioned place preference (CPP) is a commonly used model to detect rewarding effect of drugs.
  • To observe the effect of peripheral electric stimulation (PES) on morphine-induced CPP, we trained the rats with morphine in a CPP paradigm.
  • PES of 2 and 2/100 Hz significantly decreased CPP in morphine-trained animals in a naloxone reversible manner, while PES of 100 Hz, foot shock, needle insertion, or plain restraining, showed no effect.
  • Thus, PES with a low-frequency component (2 Hz) could specifically inhibit the expression of morphine-induced CPP, presumably via activation of opioid receptors.
  • [MeSH-major] Acupuncture Therapy / methods. Analgesics, Opioid / pharmacology. Conditioning (Psychology) / drug effects. Morphine / pharmacology. Morphine Dependence / therapy. Peripheral Nerves / physiology
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Male. Rats. Rats, Sprague-Dawley. Time Factors. Transcutaneous Electric Nerve Stimulation

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  • (PMID = 10790875.001).
  • [ISSN] 0959-4965
  • [Journal-full-title] Neuroreport
  • [ISO-abbreviation] Neuroreport
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] ENGLAND
  • [Chemical-registry-number] 0 / Analgesics, Opioid; 76I7G6D29C / Morphine
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53. Eun JS, Bae K, Yun YP, Hong JT, Kwon HN, Oh KW: Inhibitory effects of paeonol on morphine-induced locomotor sensitization and conditioned place preference in mice. Arch Pharm Res; 2006 Oct;29(10):904-10
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  • The inhibitory effects of paeonol, a major compound of Paeoniae radix, on the development of locomotor sensitization, conditioned place preference (CPP) and dopamine receptor supersensitivity induced by the repeated administration of morphine were investigated through behavioral experiments.
  • Repeated administration of morphine develops sensitization (reverse tolerance), a progressive enhancement of locomotion, which is used as a model for studying the drug-induced drug-seeking behaviors, and CPP, which is used as a model for studying drug reinforcement.
  • Paeonol inhibited morphine-induced hyperlocomotion, sensitization and CPP.
  • In addition, paeonol inhibited the development of postsynaptic dopamine receptors supersensitivity, which may be an underlying common mechanism that mediates the morphine-induced dopaminergic behaviors such as sensitization and CPP.
  • These results provide evidence that paeonol exerts anti-dopaminergic activity, and it is suggested that paeonol may be useful for the prevention and therapy of these adverse actions of morphine.
  • [MeSH-major] Acetophenones / pharmacology. Conditioning (Psychology) / drug effects. Morphine / antagonists & inhibitors. Motor Activity / drug effects. Spatial Behavior / drug effects
  • [MeSH-minor] Administration, Oral. Animals. Behavior, Animal / drug effects. Dopamine Antagonists / administration & dosage. Dopamine Antagonists / pharmacology. Dose-Response Relationship, Drug. Injections, Subcutaneous. Male. Mice. Mice, Inbred ICR. Paeonia / chemistry. Plant Roots / chemistry. Receptors, Dopamine / physiology

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  • (PMID = 17121187.001).
  • [ISSN] 0253-6269
  • [Journal-full-title] Archives of pharmacal research
  • [ISO-abbreviation] Arch. Pharm. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Acetophenones; 0 / Dopamine Antagonists; 0 / Receptors, Dopamine; 3R834EPI82 / paeonol; 76I7G6D29C / Morphine
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54. Yu LL, Wang XY, Zhao M, Liu Y, Li YQ, Li FQ, Wang X, Xue YX, Lu L: Effects of cannabinoid CB1 receptor antagonist rimonabant in consolidation and reconsolidation of methamphetamine reward memory in mice. Psychopharmacology (Berl); 2009 Jun;204(2):203-11
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  • OBJECTIVES: The purpose of this study was to examine whether rimonabant, a cannabinoid CB1 receptor antagonist, would disrupt the consolidation and reconsolidation of methamphetamine-related reward memory, using conditioned place preference paradigm (CPP).
  • MATERIALS AND METHODS: Separate groups of male Kunming mice were trained to acquire methamphetamine CPP.
  • Vehicle or rimonabant (1 mg/kg or 3 mg/kg, i.p.) was given at different time points: immediately after each CPP training session (consolidation), 30 min before the reactivation of CPP (retrieval), or immediately after the reactivation of CPP (reconsolidation).
  • Methamphetamine CPP was retested 24 h and 1 and 2 weeks after rimonabant administration.
  • RESULTS: Rimonabant at doses of 1 and 3 mg/kg significantly inhibited the consolidation of methamphetamine CPP.
  • Only high-dose rimonabant (3 mg/kg) disrupted the retrieval and reconsolidation of methamphetamine CPP.
  • Rimonabant had no effect on methamphetamine CPP in the absence of methamphetamine CPP reactivation.
  • CONCLUSIONS: Our findings suggest that cannabinoid CB1 receptors play a major role in methamphetamine reward memory, and cannabinoid CB1 receptor antagonists may be a potential pharmacotherapy to manage relapse associated with drug-reward-related memory.
  • [MeSH-major] Central Nervous System Stimulants / pharmacology. Memory / drug effects. Methamphetamine / pharmacology. Piperidines / pharmacology. Pyrazoles / pharmacology. Receptor, Cannabinoid, CB1 / antagonists & inhibitors
  • [MeSH-minor] Animals. Dose-Response Relationship, Drug. Male. Mice. Reward

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  • [Cites] Neurobiol Learn Mem. 2008 Jul;90(1):1-9 [18342551.001]
  • [Cites] Drug Alcohol Rev. 2008 May;27(3):236-42 [18368604.001]
  • [Cites] Addiction. 1996 Jul;91(7):921-49; discussion 951-65 [8688822.001]
  • [Cites] Learn Mem. 2006 May-Jun;13(3):316-21 [16705137.001]
  • [Cites] Eur J Neurosci. 2007 Apr;25(7):2191-200 [17419755.001]
  • [Cites] Annu Rev Neurosci. 2007;30:123-52 [17417939.001]
  • [Cites] Neuropharmacology. 2002 Oct;43(5):857-67 [12384171.001]
  • [Cites] Eur J Neurosci. 2004 Oct;20(7):1849-57 [15380006.001]
  • [Cites] Acta Pharmacol Sin. 2007 Oct;28(10):1505-18 [17883935.001]
  • [Cites] Nat Med. 2001 Oct;7(10 ):1151-4 [11590440.001]
  • [Cites] J Neurosci. 2008 May 21;28(21):5602-10 [18495894.001]
  • [Cites] Nature. 1993 Sep 2;365(6441):61-5 [7689702.001]
  • [Cites] Drug Alcohol Rev. 2008 May;27(3):253-62 [18368606.001]
  • [Cites] Neuroscience. 1998 Mar;83(2):393-411 [9460749.001]
  • [Cites] Psychopharmacology (Berl). 2006 Mar;185(1):19-28 [16374599.001]
  • [Cites] Dialogues Clin Neurosci. 2007;9(4):389-97 [18286799.001]
  • [Cites] Science. 2002 Apr 26;296(5568):678-82 [11976437.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Feb 21;103(8):2932-7 [16473939.001]
  • [Cites] Am J Addict. 2001 Summer;10(3):201-17 [11579619.001]
  • [Cites] J Neurosci. 2008 Dec 3;28(49):13248-57 [19052216.001]
  • [Cites] Brain Res. 2006 Feb 23;1075(1):60-7 [16464439.001]
  • [Cites] Trends Neurosci. 2003 Feb;26(2):65-72 [12536129.001]
  • [Cites] Ann N Y Acad Sci. 2004 Oct;1025:515-27 [15542757.001]
  • [Cites] Neurosci Lett. 2005 Jun 3;380(3):270-5 [15862900.001]
  • [Cites] J Psychopharmacol. 2002 Jun;16(2):139-43 [12095072.001]
  • [Cites] Drug Alcohol Rev. 2008 May;27(3):243-52 [18368605.001]
  • [Cites] Neuropsychopharmacology. 2004 Aug;29(8):1470-8 [15085091.001]
  • [Cites] Behav Brain Res. 2007 Mar 12;178(1):146-53 [17239969.001]
  • [Cites] Neurobiol Learn Mem. 2007 Jan;87(1):93-100 [16905344.001]
  • [Cites] Learn Mem. 2008 May 05;15(5):304-14 [18463174.001]
  • [Cites] J Neurochem. 2007 Dec;103(6):2505-17 [17953657.001]
  • [Cites] Nature. 2005 Sep 22;437(7058):556-9 [16100511.001]
  • [Cites] Drug Alcohol Rev. 2008 May;27(3):229-35 [18368603.001]
  • [Cites] Psychopharmacology (Berl). 2007 Apr;191(2):223-31 [17211653.001]
  • [Cites] Neuroreport. 2007 Jul 16;18(11):1153-6 [17589317.001]
  • [Cites] Hippocampus. 2001;11(1):8-17 [11261775.001]
  • [Cites] Learn Mem. 2006 Jul-Aug;13(4):426-30 [16882859.001]
  • [Cites] Eur J Pharmacol. 2008 Jul 28;589(1-3):122-6 [18534572.001]
  • [Cites] Alcohol Clin Exp Res. 2007 Dec;31(12):2001-5 [17949470.001]
  • [Cites] Am J Psychiatry. 2005 Aug;162(8):1414-22 [16055762.001]
  • [Cites] Drug Alcohol Rev. 2008 Mar;27(2):185-9 [18264880.001]
  • [Cites] Behav Pharmacol. 2005 Sep;16(5-6):395-404 [16148444.001]
  • [Cites] Eur J Pharmacol. 2003 Sep 23;477(3):213-7 [14522359.001]
  • [Cites] J Neurosci. 2001 Dec 1;21(23 ):9506-18 [11717385.001]
  • [Cites] Prog Neurobiol. 1999 Jul;58(4):315-48 [10368032.001]
  • [Cites] Neurobiol Learn Mem. 2005 Mar;83(2):119-24 [15721795.001]
  • [Cites] Pharmacol Biochem Behav. 2005 Jun;81(2):396-406 [15925401.001]
  • [Cites] J Pharmacol Exp Ther. 2005 Mar;312(3):875-83 [15525797.001]
  • [Cites] Alcohol Alcohol. 2005 Jan-Feb;40(1):46-53 [15582988.001]
  • [Cites] Neurosci Biobehav Rev. 2004 Jan;27(8):827-39 [15019432.001]
  • [Cites] Trends Pharmacol Sci. 1994 Oct;15(10):374-9 [7809953.001]
  • [Cites] Trends Pharmacol Sci. 2005 Aug;26(8):420-6 [15992935.001]
  • [Cites] Jpn J Pharmacol. 2000 Nov;84(3):229-36 [11138722.001]
  • [Cites] Neuron. 2005 Sep 15;47(6):873-84 [16157281.001]
  • [Cites] Nat Rev Neurosci. 2008 Mar;9(3):182-94 [18270514.001]
  • [Cites] J Neurosci. 1995 Mar;15(3 Pt 2):2301-11 [7891168.001]
  • [Cites] J Physiol Biochem. 2000 Mar;56(1):17-24 [10879677.001]
  • [Cites] Neuroreport. 2006 Sep 18;17(13):1443-7 [16932155.001]
  • [Cites] Nature. 1990 Aug 9;346(6284):561-4 [2165569.001]
  • [Cites] J Neurosci. 2006 Aug 16;26(33):8531-6 [16914679.001]
  • [Cites] Eur J Neurosci. 2007 Jun;25(11):3417-21 [17553010.001]
  • [Cites] Acta Pharmacol Sin. 2006 Feb;27(2):140-4 [16412261.001]
  • [Cites] Proc Natl Acad Sci U S A. 2007 Jul 10;104(28):11580-4 [17592122.001]
  • [Cites] Eur J Pharmacol. 2004 Sep 13;498(1-3):119-23 [15363985.001]
  • [Cites] Psychopharmacology (Berl). 2007 Dec;195(2):193-201 [17661018.001]
  • [Cites] Pharmacol Biochem Behav. 2005 Jun;81(2):387-95 [15935455.001]
  • [Cites] Neuropharmacology. 2004;47 Suppl 1:33-46 [15464124.001]
  • [Cites] Annu Rev Neurosci. 2006;29:565-98 [16776597.001]
  • [Cites] Neurocase. 2001;7(5):357-82 [11744778.001]
  • [Cites] Proc Natl Acad Sci U S A. 2003 Feb 4;100(3):1393-8 [12538878.001]
  • [Cites] Neurobiol Learn Mem. 2008 Sep;90(2):374-81 [18524639.001]
  • [Cites] Trends Neurosci. 2006 Dec;29(12):695-703 [17084911.001]
  • [Cites] Trends Neurosci. 1990 Oct;13(10):420-3 [1700516.001]
  • [Cites] Pharmacol Biochem Behav. 2005 Jun;81(2):263-84 [15936806.001]
  • (PMID = 19148622.001).
  • [ISSN] 1432-2072
  • [Journal-full-title] Psychopharmacology
  • [ISO-abbreviation] Psychopharmacology (Berl.)
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 0 / Piperidines; 0 / Pyrazoles; 0 / Receptor, Cannabinoid, CB1; 44RAL3456C / Methamphetamine; RML78EN3XE / rimonabant
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55. Levy ML, Goldfarb A, Hyder DJ, Gonzales-Gomez I, Nelson M, Gilles FH, McComb JG: Choroid plexus tumors in children: significance of stromal invasion. Neurosurgery; 2001 Feb;48(2):303-9
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  • [Title] Choroid plexus tumors in children: significance of stromal invasion.
  • OBJECTIVE: A group of choroid plexus tumors fit the cellular criteria for choroid plexus papilloma (CPP) except for invasion into the adjacent parenchyma, with associated loss of the normal villus architecture at the site of invasion.
  • These tumors retain a benign cellular appearance.
  • In the existing literature, it is unclear whether these tumors are classified as choroid plexus carcinomas or as CPPs.
  • In our experience, although evidence of invasion is present, these tumors tend to exhibit benign behavior.
  • We suggest that stromal invasion of this type remains consistent with a benign clinical course, although surgical results may demonstrate higher morbidity rates, given the invasive nature of the tumors.
  • After gross total tumor removal, none of the eight children with CPPs received adjuvant therapy at our institution; all are alive without evidence of tumor recurrence after surgical excision (mean, 108 mo).
  • The one patient who underwent subtotal resection received chemotherapy at another facility.
  • CONCLUSION: It is recommended that CPPs with a benign cellular appearance but with evidence of local parenchymal invasion and loss of the normal villus architecture at the site of invasion be classified as CPPs.
  • Patients with these tumors respond to surgical therapy alone, without the need for adjuvant treatment.
  • [MeSH-major] Choroid Plexus Neoplasms / pathology. Choroid Plexus Neoplasms / surgery. Papilloma / pathology. Papilloma / surgery
  • [MeSH-minor] Child. Child, Preschool. Humans. Infant. Neoplasm Invasiveness. Retrospective Studies. Treatment Outcome

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  • (PMID = 11220372.001).
  • [ISSN] 0148-396X
  • [Journal-full-title] Neurosurgery
  • [ISO-abbreviation] Neurosurgery
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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56. Koos B, Paulsson J, Jarvius M, Sanchez BC, Wrede B, Mertsch S, Jeibmann A, Kruse A, Peters O, Wolff JE, Galla HJ, Söderberg O, Paulus W, Ostman A, Hasselblatt M: Platelet-derived growth factor receptor expression and activation in choroid plexus tumors. Am J Pathol; 2009 Oct;175(4):1631-7
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  • [Title] Platelet-derived growth factor receptor expression and activation in choroid plexus tumors.
  • Choroid plexus tumors are intraventricular neoplasms predominantly affecting young children.
  • In contrast to choroid plexus papillomas, choroid plexus carcinomas progress frequently, necessitating the development of adjuvant treatment concepts.
  • The finding of PDGF receptor expression in choroid plexus tumors prompted us to elucidate PDGF receptor activation state using a novel method, in situ proximity ligation assay, on formalin-fixed, paraffin-embedded, archival samples of 19 choroid plexus tumors.
  • As assessed by in situ proximity ligation assay, the proportion of phosphorylated PDGF receptor alpha was low in choroid plexus papillomas and choroid plexus carcinomas, whereas phosphorylated PDGF receptor beta was found to be significantly higher in choroid plexus carcinomas.
  • In the immortalized choroid plexus epithelial cell line Z310 expressing PDGF receptor beta, PDGF-BB exhibited a time- and dose-dependent proliferative response, which was significantly attenuated by imatinib (gleevec).
  • In conclusion, our findings suggest that PDGF receptor beta is functionally involved in the biology of choroid plexus tumors and may represent a molecular target for therapy.
  • In addition, this study demonstrates the feasibility and usefulness of in situ proximity ligation assay for monitoring receptor tyrosine kinase activation in formalin-fixed, paraffin-embedded, archival tissues.
  • [MeSH-major] Choroid Plexus Neoplasms / metabolism. Receptor, Platelet-Derived Growth Factor alpha / metabolism. Receptor, Platelet-Derived Growth Factor beta / metabolism
  • [MeSH-minor] Animals. Cell Line. Cell Line, Transformed. Cell Proliferation / drug effects. Epithelial Cells / drug effects. Epithelial Cells / metabolism. Epithelial Cells / pathology. Female. Humans. Immunohistochemistry. Infant. Male. Papilloma / metabolism. Papilloma / pathology. Phosphorylation / drug effects. Platelet-Derived Growth Factor / pharmacology. Rats

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  • [Cites] Nat Genet. 2001 Oct;29(2):143-52 [11544480.001]
  • [Cites] Comput Methods Programs Biomed. 2009 Apr;94(1):58-65 [18950895.001]
  • [Cites] Brain Res. 2002 Dec 27;958(2):371-80 [12470873.001]
  • [Cites] Cytokine Growth Factor Rev. 2004 Aug;15(4):197-204 [15207811.001]
  • [Cites] Mol Cancer. 2003 Jan 3;2:1 [12537587.001]
  • [Cites] Blood. 2004 Nov 1;104(9):2655-60 [15231574.001]
  • [Cites] EMBO J. 1992 Feb;11(2):543-50 [1311251.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 May;64(5):391-7 [15892296.001]
  • [Cites] Am J Surg Pathol. 2006 Jan;30(1):66-74 [16330944.001]
  • [Cites] J Neurooncol. 2006 Jan;76(2):105-9 [16205964.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Nov;65(11):1069-73 [17086103.001]
  • [Cites] Adv Cancer Res. 2007;97:247-74 [17419949.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] Mol Cell Proteomics. 2007 Sep;6(9):1500-9 [17565975.001]
  • [Cites] Mod Pathol. 2008 Mar;21(3):265-70 [18157090.001]
  • [Cites] Genes Dev. 2008 May 15;22(10):1276-312 [18483217.001]
  • [Cites] Nat Rev Drug Discov. 2002 Jul;1(7):493-502 [12120256.001]
  • (PMID = 19717644.001).
  • [ISSN] 1525-2191
  • [Journal-full-title] The American journal of pathology
  • [ISO-abbreviation] Am. J. Pathol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Platelet-Derived Growth Factor; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor alpha; EC 2.7.10.1 / Receptor, Platelet-Derived Growth Factor beta
  • [Other-IDs] NLM/ PMC2751559
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57. Follis F, Blisard K, Varvitsiotis PS, Pett SB Jr, Temes T, Wernly JA: Competitive NMDA receptor antagonists and spinal-cord ischemia. J Invest Surg; 2000 Mar-Apr;13(2):117-21; discussion 123-4
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  • Accordingly, we investigated the protective effect during spinal cord ischemia of two competitive antagonists, 4-(3-phosphonopropyl)-2-piperazine-carboxylic acid (CPP) and cis-4-(phosphonomethyl)-2-piperidine-carboxylic acid (CGS).
  • Male Sprague-Dawley rats underwent intrathecal administration of 10 microL saline, CGS, and CPP 10 mM solutions, in a randomized blinded fashion, and were subjected to balloon occlusion of the thoracic aorta.
  • In the acute protocol, 21 rats divided in 3 groups of 7 (saline, CPP, and CGS) were used to calculate the aortic occlusion time (AOT) resulting in paraplegia in 50% of animals (P50).
  • In the chronic study, 24 rats divided in 4 groups of 6 (saline, CPP, CGS, sham) underwent 12-min occlusion.
  • In the acute study, the P50 of CGS (10 min 48 s) and CPP (11 min 11 s) was longer than saline (10 min 27 s).
  • In the chronic groups, analysis of variance of neurologic (p = .66) and histologic (p = .66) scores did not disclose differences between CGS, CPP, and saline.
  • In conclusion, blockade of NMDA receptors with CPP or CGS may afford some protection for durations of occlusion around the P50, but it is not beneficial when ischemic injury is more protracted.
  • [MeSH-major] Excitatory Amino Acid Antagonists / pharmacology. Pipecolic Acids / pharmacology. Piperazines / pharmacology. Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors. Spinal Cord Ischemia / drug therapy
  • [MeSH-minor] Acute Disease. Animals. Arterial Occlusive Diseases / drug therapy. Chronic Disease. Disease Models, Animal. Male. Paraplegia / drug therapy. Rats. Rats, Sprague-Dawley. Spinal Cord / blood supply. Spinal Cord / chemistry

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  • (PMID = 10801049.001).
  • [ISSN] 0894-1939
  • [Journal-full-title] Journal of investigative surgery : the official journal of the Academy of Surgical Research
  • [ISO-abbreviation] J Invest Surg
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] UNITED STATES
  • [Chemical-registry-number] 0 / Excitatory Amino Acid Antagonists; 0 / Pipecolic Acids; 0 / Piperazines; 0 / Receptors, N-Methyl-D-Aspartate; 100828-16-8 / 3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid; 4VGJ4A41L2 / selfotel
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58. Barton VN, Donson AM, Kleinschmidt-DeMasters BK, Gore L, Liu AK, Foreman NK: PARP1 expression in pediatric central nervous system tumors. Pediatr Blood Cancer; 2009 Dec 15;53(7):1227-30
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  • BACKGROUND: Despite advances in therapy, outcome in many high-grade pediatric central nervous system (CNS) tumors remains poor.
  • The focus of neuro-oncology research has thus turned towards identifying novel therapeutic targets.
  • Poly(ADP-ribose) polymerase-1 (PARP1) is a DNA repair protein that has been studied in a variety of malignancies and may interfere with therapy-induced DNA damage, however expression in pediatric CNS tumors is unknown.
  • PROCEDURE: We evaluated PARP1 mRNA expression in 81 pediatric CNS tumors using microarray technology.
  • CONCLUSION: These findings indicate that PARP1 is expressed in high-grade pediatric CNS tumors, implicating PARP1 inhibition as a potential therapeutic target.
  • [MeSH-major] Central Nervous System Neoplasms / metabolism. Gene Expression Profiling. Glioma / metabolism. Neoplasm Proteins / biosynthesis. Poly(ADP-ribose) Polymerases / biosynthesis
  • [MeSH-minor] Child. Choroid Plexus Neoplasms / genetics. Choroid Plexus Neoplasms / metabolism. Choroid Plexus Neoplasms / pathology. DNA Damage. DNA Repair. Drug Delivery Systems. Humans. Neuroectodermal Tumors, Primitive / genetics. Neuroectodermal Tumors, Primitive / metabolism. Neuroectodermal Tumors, Primitive / pathology. Oligonucleotide Array Sequence Analysis. Papilloma / genetics. Papilloma / metabolism. Papilloma / pathology. RNA, Messenger / biosynthesis. RNA, Neoplasm / biosynthesis. Single-Blind Method

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  • [Copyright] (c) 2009 Wiley-Liss, Inc.
  • (PMID = 19533660.001).
  • [ISSN] 1545-5017
  • [Journal-full-title] Pediatric blood & cancer
  • [ISO-abbreviation] Pediatr Blood Cancer
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Neoplasm Proteins; 0 / RNA, Messenger; 0 / RNA, Neoplasm; EC 2.4.2.30 / PARP1 protein, human; EC 2.4.2.30 / Poly(ADP-ribose) Polymerases
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59. Russo SJ, Festa ED, Fabian SJ, Gazi FM, Kraish M, Jenab S, Quiñones-Jenab V: Gonadal hormones differentially modulate cocaine-induced conditioned place preference in male and female rats. Neuroscience; 2003;120(2):523-33
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  • In the present study, conditioned place preference (CPP), a measure of non-contingent reward, was used to determine the effects of endogenous gonadal hormones and of estrogen and progesterone replacement on cocaine reward.
  • Although both intact and gonadectomized male and female rats showed a significant CPP for cocaine, ovariectomy attenuated the magnitude of CPP.
  • These alterations coincided with a decrease in serum levels of corticosterone.
  • In ovariectomized rats, pretreatment with progesterone inhibited cocaine CPP while estrogen plus progesterone potentiated the magnitude of CPP.
  • [MeSH-major] Cocaine / pharmacology. Conditioning (Psychology) / drug effects. Estrogens / pharmacology. Progesterone / pharmacology. Sex Characteristics
  • [MeSH-minor] Analysis of Variance. Anesthetics, Local / pharmacology. Animals. Behavior, Animal. Biogenic Monoamines / metabolism. Cesarean Section / methods. Chromatography, High Pressure Liquid / instrumentation. Chromatography, High Pressure Liquid / methods. Corticosterone / blood. Drug Interactions. Exploratory Behavior / drug effects. Exploratory Behavior / physiology. Female. Hormone Replacement Therapy / methods. Male. Motor Activity / drug effects. Motor Activity / physiology. Nucleus Accumbens / drug effects. Nucleus Accumbens / metabolism. Radioimmunoassay / methods. Rats. Rats, Inbred F344. Reaction Time. Reward. Time Factors. Ventral Tegmental Area / drug effects. Ventral Tegmental Area / metabolism

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  • (PMID = 12890521.001).
  • [ISSN] 0306-4522
  • [Journal-full-title] Neuroscience
  • [ISO-abbreviation] Neuroscience
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / DA12136; United States / NIGMS NIH HHS / GM / GM60654; United States / NINDS NIH HHS / NS / NS-41073; United States / NCRR NIH HHS / RR / RR-03037
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anesthetics, Local; 0 / Biogenic Monoamines; 0 / Estrogens; 4G7DS2Q64Y / Progesterone; I5Y540LHVR / Cocaine; W980KJ009P / Corticosterone
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60. Gupta B, Torchilin VP: Transactivating transcriptional activator-mediated drug delivery. Expert Opin Drug Deliv; 2006 Mar;3(2):177-90
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  • [Title] Transactivating transcriptional activator-mediated drug delivery.
  • However, the TATp remains the most popular CPP used for a variety of purposes.
  • This review article attempts to bring together the available data on TAT-mediated intracellular uptake of a broad range of molecules and nanoparticles.
  • [MeSH-major] Drug Carriers. Gene Products, tat / administration & dosage
  • [MeSH-minor] Animals. Antibodies. Arginine / chemistry. Cell Membrane / metabolism. Genetic Therapy. Humans. Nanostructures. Peptides / administration & dosage. Peptides / chemistry. Protein Transport

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  • (PMID = 16506946.001).
  • [ISSN] 1742-5247
  • [Journal-full-title] Expert opinion on drug delivery
  • [ISO-abbreviation] Expert Opin Drug Deliv
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antibodies; 0 / Drug Carriers; 0 / Gene Products, tat; 0 / Peptides; 94ZLA3W45F / Arginine
  • [Number-of-references] 120
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61. Jackson KJ, Walters CL, Miles MF, Martin BR, Damaj MI: Characterization of pharmacological and behavioral differences to nicotine in C57Bl/6 and DBA/2 mice. Neuropharmacology; 2009 Sep;57(4):347-55
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  • [Title] Characterization of pharmacological and behavioral differences to nicotine in C57Bl/6 and DBA/2 mice.
  • Approximately 50-70% of the risk for developing nicotine dependence is attributed to genetics; therefore, it is of great significance to characterize the genetic mechanisms involved in nicotine reinforcement and dependence in hopes of generating better smoking cessation therapies.
  • The overall goal of these studies was to characterize behavioral and pharmacological responses to nicotine in C57Bl/6 (B6) and DBA/2 (D2) mice, two inbred strains commonly used for genetic studies on behavioral traits.
  • B6 and D2 mice where subjected to a battery of behavioral tests to measure nicotine's acute effects, calcium-mediated antinociceptive responses, tolerance to chronic treatment with osmotic mini pumps, and following three days of nicotine withdrawal.
  • B6, but not D2 mice, developed tolerance to nicotine and nicotine conditioned place preference (CPP).
  • These results provide a thorough, simultaneous evaluation of the pharmacological and behavioral differences to experimenter-administered nicotine as measured in several behavioral tests of aspects that contribute to smoking behavior.

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  • [Cites] Psychopharmacology (Berl). 2007 Feb;190(3):269-319 [16896961.001]
  • [Cites] Psychopharmacology (Berl). 2006 Mar;184(3-4):456-63 [16463055.001]
  • [Cites] Eur J Pharmacol. 2005 May 23;516(1):40-5 [15922326.001]
  • [Cites] Pharmacol Biochem Behav. 1999 Oct;64(2):221-8 [10515295.001]
  • [Cites] Addiction. 1997 Oct;92(10):1277-87 [9489045.001]
  • [Cites] J Pharmacol Exp Ther. 1991 Oct;259(1):392-402 [1920127.001]
  • [Cites] Pharmacol Biochem Behav. 1989 Jul;33(3):667-78 [2587608.001]
  • [Cites] Pharmacol Biochem Behav. 1988 May;30(1):269-78 [3174752.001]
  • [Cites] Pharmacol Biochem Behav. 1985 Aug;23(2):325-30 [4059317.001]
  • [Cites] Pharmacol Biochem Behav. 1977 Jan;6(1):25-30 [850690.001]
  • [Cites] Mol Pharmacol. 2002 Aug;62(2):334-42 [12130686.001]
  • [Cites] Eur J Pharmacol. 2000 Sep 15;404(1-2):103-10 [10980268.001]
  • [Cites] Neuropsychopharmacology. 2000 May;22(5):451-65 [10731620.001]
  • [Cites] J Pharmacol Exp Ther. 1983 Jul;226(1):291-302 [6864548.001]
  • [Cites] J Pharmacol Exp Ther. 2008 Apr;325(1):302-12 [18184829.001]
  • [Cites] J Pharmacol Exp Ther. 2007 Jul;322(1):399-407 [17446302.001]
  • [Cites] Mol Pharmacol. 2007 Mar;71(3):826-34 [17158199.001]
  • [Cites] Eur J Pharmacol. 1980 Oct 17;67(2-3):313-6 [6893963.001]
  • (PMID = 19619563.001).
  • [ISSN] 1873-7064
  • [Journal-full-title] Neuropharmacology
  • [ISO-abbreviation] Neuropharmacology
  • [Language] ENG
  • [Grant] United States / NIDA NIH HHS / DA / DA012610-02; United States / NIAAA NIH HHS / AA / U01 AA016662; United States / NIDA NIH HHS / DA / R01 DA012610; United States / NIAAA NIH HHS / AA / R01 AA013678; United States / NIAAA NIH HHS / AA / U01 AA016667; United States / NIDA NIH HHS / DA / #DA/ 12610; United States / NIDA NIH HHS / DA / R01 DA012610-02
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Nicotinic Agonists; 6M3C89ZY6R / Nicotine; EC 2.7.11.17 / Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • [Other-IDs] NLM/ NIHMS133451; NLM/ PMC2753410
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62. Bidwell GL 3rd, Raucher D: Cell penetrating elastin-like polypeptides for therapeutic peptide delivery. Adv Drug Deliv Rev; 2010 Dec 30;62(15):1486-96
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  • [Title] Cell penetrating elastin-like polypeptides for therapeutic peptide delivery.
  • Current treatment of solid tumors is limited by side effects that result from the non-specific delivery of drugs to the tumor site.
  • Alternative targeted therapeutic approaches for localized tumors would significantly reduce systemic toxicity.
  • Peptide therapeutics are a promising new strategy for targeted cancer therapy because of the ease of peptide design and the specificity of peptides for their intracellular molecular targets.
  • However, the utility of peptides is limited by their poor pharmacokinetic parameters and poor tissue and cellular membrane permeability in vivo.
  • This review article summarizes the development of elastin-like polypeptide (ELP) as a potential carrier for thermally targeted delivery of therapeutic peptides (TP), and the use of cell penetrating peptides (CPP) to enhance the intracellular delivery of the ELP-fused TPs.
  • CPP-fused ELPs have been used to deliver a peptide inhibitor of c-Myc function and a peptide mimetic of p21 in several cancer models in vitro, and both polypeptides are currently yielding promising results in in vivo models of breast and brain cancer.

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  • [Copyright] Copyright © 2010 Elsevier B.V. All rights reserved.
  • [Cites] Cancer Res. 1987 Dec 15;47(24 Pt 1):6437-43 [2824033.001]
  • [Cites] Cancer Metastasis Rev. 1987;6(4):559-93 [3327633.001]
  • [Cites] J Cell Biol. 1989 Feb;108(2):389-400 [2563728.001]
  • [Cites] J Natl Cancer Inst. 1989 Apr 19;81(8):570-6 [2649688.001]
  • [Cites] Prog Biophys Mol Biol. 1992;57(1):23-57 [1549698.001]
  • [Cites] J Biol Chem. 1994 Jan 21;269(3):1785-93 [8294427.001]
  • [Cites] J Biol Chem. 1994 Apr 8;269(14):10444-50 [8144628.001]
  • [Cites] Recent Results Cancer Res. 1995;138:81-90 [7899701.001]
  • [Cites] Curr Biol. 1995 Mar 1;5(3):275-82 [7780738.001]
  • [Cites] Molecules. 2009;14(6):1999-2015 [19513001.001]
  • [Cites] Crit Rev Ther Drug Carrier Syst. 2009;26(2):119-55 [19673689.001]
  • [Cites] Expert Opin Drug Deliv. 2009 Oct;6(10):1033-47 [19637980.001]
  • [Cites] Expert Opin Drug Deliv. 2009 Oct;6(10):1079-90 [19645633.001]
  • [Cites] Expert Opin Drug Deliv. 2009 Oct;6(10):1049-64 [19743895.001]
  • [Cites] Nat Mater. 2009 Dec;8(12):993-9 [19898461.001]
  • [Cites] Int J Cancer. 2010 Jan 15;126(2):533-44 [19588502.001]
  • [Cites] Adv Drug Deliv Rev. 2010 Feb 17;62(2):231-9 [20004693.001]
  • [Cites] Biochem Pharmacol. 2007 Mar 1;73(5):620-31 [17161827.001]
  • [Cites] Cancer Res. 2007 May 1;67(9):4418-24 [17483356.001]
  • [Cites] Invest New Drugs. 2007 Aug;25(4):313-26 [17483874.001]
  • [Cites] J Drug Target. 2007 Aug-Sep;15(7-8):457-64 [17671892.001]
  • [Cites] Mol Pharmacol. 2000 Apr;57(4):679-86 [10727512.001]
  • [Cites] Eur J Pharm Biopharm. 2000 Jul;50(1):147-60 [10840198.001]
  • [Cites] FASEB J. 2001 Jan;15(1):31-33 [11099487.001]
  • [Cites] Int J Hyperthermia. 2001 Jan-Feb;17(1):1-18 [11212876.001]
  • [Cites] Cancer Res. 2001 Feb 15;61(4):1548-54 [11245464.001]
  • [Cites] Exp Cell Res. 2001 May 1;265(2):234-41 [11302688.001]
  • [Cites] Annu Rev Biomed Eng. 1999;1:241-63 [11701489.001]
  • [Cites] J Histochem Cytochem. 2002 Feb;50(2):185-95 [11799137.001]
  • [Cites] Surgery. 2002 Jan;131(1 Suppl):S78-84 [11821791.001]
  • [Cites] Biomacromolecules. 2002 Mar-Apr;3(2):357-67 [11888323.001]
  • [Cites] J Urol. 2002 Oct;168(4 Pt 1):1597-602 [12352464.001]
  • [Cites] Nat Rev Cancer. 2002 Oct;2(10):764-76 [12360279.001]
  • [Cites] Biochemistry. 2002 Dec 3;41(48):14150-7 [12450378.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431.001]
  • [Cites] AAPS PharmSci. 2002;4(4):E26 [12645998.001]
  • [Cites] Curr Protein Pept Sci. 2003 Apr;4(2):125-32 [12678851.001]
  • [Cites] Curr Protein Pept Sci. 2003 Apr;4(2):133-40 [12678852.001]
  • [Cites] J Control Release. 2003 Aug 28;91(1-2):31-43 [12932635.001]
  • [Cites] Pharm Res. 2004 Mar;21(3):389-93 [15070086.001]
  • [Cites] Science. 1983 Jul 22;221(4608):368-70 [6408733.001]
  • [Cites] Biopolymers. 1985 Dec;24(12):2345-56 [4092092.001]
  • [Cites] Proc Natl Acad Sci U S A. 1986 Aug;83(16):5948-52 [3461466.001]
  • [Cites] J Biol Chem. 1995 Jun 16;270(24):14255-8 [7782278.001]
  • [Cites] J Biol Chem. 1995 Sep 15;270(37):22008-16 [7665622.001]
  • [Cites] Oncogene. 1996 Feb 1;12(3):595-607 [8637717.001]
  • [Cites] Curr Biol. 1997 Jan 1;7(1):71-80 [8999999.001]
  • [Cites] Br J Cancer. 1997;75(7):1028-34 [9083339.001]
  • [Cites] J Biol Chem. 1997 Jun 20;272(25):16010-7 [9188504.001]
  • [Cites] Anticancer Res. 1997 Jul-Aug;17(4B):2895-7 [9329557.001]
  • [Cites] J Control Release. 1996 May;39(2-3):121-9 [11539926.001]
  • [Cites] Semin Oncol. 1997 Dec;24(6):616-25 [9422258.001]
  • [Cites] Oncogene. 1998 Jan 22;16(3):311-20 [9467956.001]
  • [Cites] Trends Cell Biol. 1998 Feb;8(2):84-7 [9695814.001]
  • [Cites] Cancer Res. 1998 Aug 15;58(16):3654-9 [9721875.001]
  • [Cites] Cancer Res. 1999 Jul 15;59(14):3480-8 [10416614.001]
  • [Cites] Science. 1999 Sep 3;285(5433):1569-72 [10477521.001]
  • [Cites] Drug Discov Today. 2004 Dec 1;9(23):1012-9 [15574317.001]
  • [Cites] Adv Drug Deliv Rev. 2005 Feb 28;57(4):609-36 [15722167.001]
  • [Cites] Adv Drug Deliv Rev. 2005 Feb 28;57(4):637-51 [15722168.001]
  • [Cites] Mol Cancer Ther. 2005 Jul;4(7):1076-85 [16020665.001]
  • [Cites] J Control Release. 2005 Nov 28;108(2-3):396-408 [16157413.001]
  • [Cites] Biochem Pharmacol. 2006 Jan 12;71(3):248-56 [16316634.001]
  • [Cites] Trends Biotechnol. 2006 Jan;24(1):39-47 [16307811.001]
  • [Cites] Drug Discov Today. 2006 Sep;11(17-18):812-8 [16935749.001]
  • [Cites] J Control Release. 2006 Nov 28;116(2):170-8 [16919353.001]
  • [Cites] Chemotherapy. 2007;53(1):73-6 [17202815.001]
  • [Cites] Pharm Res. 2008 Mar;25(3):683-91 [17762916.001]
  • [Cites] Adv Drug Deliv Rev. 2008 May 22;60(8):899-914 [18406004.001]
  • [Cites] Curr Opin Oncol. 2008 Jul;20(4):438-43 [18525341.001]
  • [Cites] J Control Release. 2008 Aug 7;129(3):179-86 [18547669.001]
  • [Cites] Biochim Biophys Acta. 2008 Dec;1786(2):126-38 [18440319.001]
  • [Cites] Curr Pharm Des. 2008;14(34):3628-36 [19075739.001]
  • [Cites] Eur J Pharm Biopharm. 2009 Mar;71(3):409-19 [19070661.001]
  • [Cites] J Control Release. 2009 Apr 2;135(1):2-10 [19095020.001]
  • [Cites] Br J Pharmacol. 2009 May;157(2):195-206 [19309362.001]
  • (PMID = 20478348.001).
  • [ISSN] 1872-8294
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / R21 CA113813; United States / NCI NIH HHS / CA / R43 CA135799; United States / NCI NIH HHS / CA / R43 CA135799-01A2; United States / NCI NIH HHS / CA / R21 CA113813-01A2
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Cell-Penetrating Peptides; 0 / Peptides; 9007-58-3 / Elastin
  • [Other-IDs] NLM/ NIHMS206184; NLM/ PMC2964383
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63. Bitler BG, Schroeder JA: Anti-cancer therapies that utilize cell penetrating peptides. Recent Pat Anticancer Drug Discov; 2010 Jun;5(2):99-108
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Anti-cancer therapies that utilize cell penetrating peptides.
  • Importantly, they can be linked to a variety of cargo, including anti-cancer therapeutics, making CPPs an efficient, effective and non-toxic mechanism for drug delivery.
  • In this review, we discuss a number of CPP conjugated therapies (CTTs) that are either patented are in the progress of patenting, and show strong promise for clinical efficacy.
  • In addition, many of these CTTs also increase sensitivity to current anti-cancer therapy modalities, including radiation and other DNA damaging chemotherapies, thereby decreasing the toxic dosage required for effective treatment.
  • Mechanistically, these CTTs function in a dominant-negative manner by blocking tumor-specific protein-protein interactions with the CPP-conjugated peptide or protein.
  • The treatment of both cell lines and mouse models demonstrates that this method of molecular targeting results in equal if not greater efficacy than current standards of care, including DNA damaging agents and topoisomerase inhibitors.
  • For the treatment of invasive carcinoma, these CTTs have significant clinical potential to deliver highly targeted therapies without sacrificing the patient's quality of life.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Cells / metabolism. Drug Delivery Systems / methods. Peptide Fragments / administration & dosage. Peptide Fragments / pharmacokinetics
  • [MeSH-minor] Amino Acid Sequence. Animals. Gene Expression Regulation, Neoplastic / drug effects. Humans. Mice. Models, Biological

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  • (PMID = 19961434.001).
  • [ISSN] 2212-3970
  • [Journal-full-title] Recent patents on anti-cancer drug discovery
  • [ISO-abbreviation] Recent Pat Anticancer Drug Discov
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review
  • [Publication-country] United Arab Emirates
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Peptide Fragments
  • [Number-of-references] 85
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64. Szendei G, Hernádi Z, Dévényi N, Csapó Z: Is there any correlation between stages of endometriosis and severity of chronic pelvic pain? Possibilities of treatment. Gynecol Endocrinol; 2005 Aug;21(2):93-100
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  • [Title] Is there any correlation between stages of endometriosis and severity of chronic pelvic pain? Possibilities of treatment.
  • We report herein findings on 181 patients, suffering from pelvic endometriosis confirmed by histology, whose main symptom was chronic pelvic pain (CPP).
  • The short form of the McGill pain questionnaire was used for the evaluation of CPP.
  • After the first operative intervention, therapy with a gonadotropin-releasing hormone (GnRH) analog was given for 6 months.
  • Second-look laparoscopy was performed 8-10 weeks after the end of GnRH-analog treatment, which was followed by a non-conventionally administered, monophasic oral contraceptive (OC) treatment.
  • In the long term, 118 patients received the non-conventionally administered, monophasic OC treatment, which contained a third-generation progestogen, to be taken continuously for at least 6 months.
  • The other 63 patients who did not receive OC treatment for one reason or another were evaluated as a control group.
  • We analyzed data on CPP before the first surgical intervention, then following therapy with the GnRH analog at the second-look operation, and then after 6, 12, 18 and 24 months.
  • We also reviewed potential causes of CPP, especially focused on endometriosis.
  • No correlation was found between the stage of endometriosis according to R-AFS score and the severity of CPP.
  • At the 24-month follow-up after second-look laparoscopy, the non-conventionally administered monophasic OC treatment was found not only to significantly reduce pain scores, but also the required radical operative solution (hysterectomy plus bilateral adnexectomy) for CPP by OC users.
  • [MeSH-major] Contraceptives, Oral, Combined / therapeutic use. Endometriosis / drug therapy. Gonadotropin-Releasing Hormone / therapeutic use. Pelvic Pain / prevention & control
  • [MeSH-minor] Combined Modality Therapy. Drug Administration Schedule. Dysmenorrhea / drug therapy. Dyspareunia / drug therapy. Female. Humans. Laparoscopy. Pain Measurement. Secondary Prevention

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  • (PMID = 16109595.001).
  • [ISSN] 0951-3590
  • [Journal-full-title] Gynecological endocrinology : the official journal of the International Society of Gynecological Endocrinology
  • [ISO-abbreviation] Gynecol. Endocrinol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Contraceptives, Oral, Combined; 33515-09-2 / Gonadotropin-Releasing Hormone
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65. Stoilova TB, Kovalchuk SI, Egorova NS, Surovoy AY, Ivanov VT: Gramicidin A-based peptide vector for intracellular protein delivery. Biochim Biophys Acta; 2008 Oct;1778(10):2026-31
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  • The development of the peptide-based vectors for the intracellular delivery of biologically active macromolecules has opened new prospects of their application in research and therapy.
  • Earlier the amphipathic cell-penetrating peptide (CPP) Pep-1 was reported to mediate cellular uptake of proteins without covalent binding to them.
  • In this work we studied the ability of a series of membrane-active amphipathic peptides, based on the gramicidin A sequence, to transport a model protein across the eukaryotic cell membrane.
  • In addition, a series of new gramicidin analogues were prepared and the effect of N-terminus modification of gramicidin on the protein transduction efficiency was studied.
  • [MeSH-major] Anti-Bacterial Agents / metabolism. Cell Membrane Permeability. Drug Delivery Systems. Genetic Vectors / metabolism. Gramicidin / metabolism. Peptides / metabolism

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  • (PMID = 18339303.001).
  • [ISSN] 0006-3002
  • [Journal-full-title] Biochimica et biophysica acta
  • [ISO-abbreviation] Biochim. Biophys. Acta
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Peptides; 1405-97-6 / Gramicidin; EC 3.2.1.23 / beta-Galactosidase
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66. Li SX, Wang ZR, Li J, Peng ZG, Zhou W, Zhou M, Lu L: Inhibition of Period1 gene attenuates the morphine-induced ERK-CREB activation in frontal cortex, hippocampus, and striatum in mice. Am J Drug Alcohol Abuse; 2008;34(6):673-82
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  • OBJECTIVE: Recent studies demonstrated that the Period1 gene (Per1) is involved in behavioral alterations induced by addictive drugs.
  • We explored the effects of inhibiting expression in brain of Per1 on morphine conditioned place preference (CPP) and morphine-induced phosphorylation of extracellular signal-regulated kinase (ERK) and cAMP-response element binding protein (CREB) in mice.
  • After testing CPP, mice were sacrificed and phosphorylated ERK and CREB in the frontal cortex, hippocampus, and striatum were examined by immunohistochemistry.
  • RESULTS: Mice pretreated with DRz164 did not acquire morphine CPP.
  • We suggested that per1 gene may be a potential treatment target for drug addition.
  • [MeSH-major] Cell Cycle Proteins / drug effects. Cyclic AMP Response Element-Binding Protein / drug effects. Extracellular Signal-Regulated MAP Kinases / drug effects. Morphine / pharmacology. Nuclear Proteins / drug effects
  • [MeSH-minor] Animals. Conditioning, Operant / drug effects. Corpus Striatum / metabolism. DNA, Catalytic / pharmacology. Drug Delivery Systems. Frontal Lobe / metabolism. Gene Expression Regulation / drug effects. Hippocampus / metabolism. Male. Mice. Mice, Inbred BALB C. Morphine Dependence / drug therapy. Morphine Dependence / physiopathology. Period Circadian Proteins. Phosphorylation / drug effects. RNA, Messenger / drug effects. RNA, Messenger / metabolism. Reward

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  • (PMID = 18850497.001).
  • [ISSN] 1097-9891
  • [Journal-full-title] The American journal of drug and alcohol abuse
  • [ISO-abbreviation] Am J Drug Alcohol Abuse
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Cyclic AMP Response Element-Binding Protein; 0 / DNA, Catalytic; 0 / Nuclear Proteins; 0 / Per1 protein, mouse; 0 / Period Circadian Proteins; 0 / RNA, Messenger; 76I7G6D29C / Morphine; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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67. Langford CF, Udvari Nagy S, Ghoniem GM: Levator ani trigger point injections: An underutilized treatment for chronic pelvic pain. Neurourol Urodyn; 2007;26(1):59-62
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Levator ani trigger point injections: An underutilized treatment for chronic pelvic pain.
  • AIMS: We conducted this study to examine the role of trigger point injections in females with chronic pelvic pain (CPP) of at least 6 months duration and specific levator ani trigger points.
  • METHODS: This prospective study included 18 consecutive female patients with CPP and specific palpable levator ani trigger points.
  • CONCLUSION: In the management of CPP, a non-surgical office-based therapy such as trigger point injections can be effective in selected patients.
  • [MeSH-major] Anesthetics, Local / administration & dosage. Anus Diseases / complications. Bupivacaine / administration & dosage. Myofascial Pain Syndromes / drug therapy. Pelvic Pain / drug therapy
  • [MeSH-minor] Adult. Aged. Anti-Inflammatory Agents / administration & dosage. Chronic Disease. Drug Therapy, Combination. Female. Humans. Injections, Intramuscular. Lidocaine / administration & dosage. Middle Aged. Pain Measurement. Palpation. Prospective Studies. Spasm / diagnosis. Spasm / drug therapy. Spasm / etiology. Treatment Outcome. Triamcinolone / administration & dosage. Vagina

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  • [Copyright] Copyright 2006 Wiley-Liss, Inc.
  • (PMID = 17195176.001).
  • [ISSN] 0733-2467
  • [Journal-full-title] Neurourology and urodynamics
  • [ISO-abbreviation] Neurourol. Urodyn.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anesthetics, Local; 0 / Anti-Inflammatory Agents; 1ZK20VI6TY / Triamcinolone; 98PI200987 / Lidocaine; Y8335394RO / Bupivacaine
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68. Lee PA, Houk CP: Gonadotropin-releasing hormone analog therapy for central precocious puberty and other childhood disorders affecting growth and puberty. Treat Endocrinol; 2006;5(5):287-96
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  • [Title] Gonadotropin-releasing hormone analog therapy for central precocious puberty and other childhood disorders affecting growth and puberty.
  • Gonadotropin-releasing hormone (GnRH) analog therapy relies primarily on the ability of these compounds to bind to and modulate GnRH-receptor activity.
  • GnRH analogs have been used in pediatric patients where endogenous gonadotropin release is undesirable or potentially harmful, such as in: (i) patients with central precocious puberty (CPP);.
  • (ii) healthy short children where pubertal delay would provide an opportunity to supplement pre-pubertal linear growth; and (iii) children with malignancies and other disorders where treatment requires the use of gonadotoxic compounds.
  • In the first two groups of patients, GnRH agonists may be used alone or in conjunction with somatropin (growth hormone [GH]) to prevent early skeletal maturation and increase the subsequent adult height, while in the latter case, GnRH agonists are used alone or in conjunction with GnRH antagonists in an attempt to preserve gonadal function.In children and adolescents with CPP, timely use of GnRH agonists alone can result in an adult height within the genetic potential of the individual (target height); however, minimal height is gained when GnRH agonist therapy is commenced after a marked advancement of skeletal age.
  • This provides the rationale for combined therapy with GnRH agonists and somatropin in such patients, and studies have shown improved growth with this approach compared with GnRH agonists alone.
  • Combination therapy with GnRH agonists and somatropin has also been shown to increase adult heights to a greater extent than GnRH agonists alone in pediatric patients with concomitant CPP and GH deficiency, those with idiopathic short stature, and those born small for gestational age; however, such combination therapy has shown no increased benefit over somatropin alone in pediatric patients with GH deficiency.
  • Limited results in children and adolescents with congenital adrenal hyperplasia and chronic primary hypothyroidism have also shown increased growth rates, while no growth benefit was seen in pediatric renal transplant recipients.GnRH analogs also have potential as gonadoprotective agents; studies of GnRH agonists used alone and in combination with GnRH antagonists in women undergoing cytotoxic therapy have shown increased preservation of reproductive potential in patients who were receiving GnRH analog therapy versus those who were not.The adverse effects of GnRH analogs mainly consist of menopausal-like complaints.
  • Increases in bodyweight and body mass index in children receiving GnRH agonist therapy have been shown; however, these increases do not persist after discontinuation of therapy.
  • Adult bone mineral density and fertility are also not adversely affected by childhood GnRH agonist therapy.GnRH analog therapy appears to be both well tolerated and effective in pediatric patients, as it allows the preservation or improvement of adult height, and shows no longstanding negative effects on body composition, bone density, reproductive function, or endocrine physiology.
  • These agents may also be useful for preservation of gonadal function in children and adolescents undergoing cytotoxic therapy.
  • [MeSH-minor] Body Height / drug effects. Drug Therapy, Combination. Humans. Puberty. Sexual Maturation

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  • (PMID = 17002488.001).
  • [ISSN] 1175-6349
  • [Journal-full-title] Treatments in endocrinology
  • [ISO-abbreviation] Treat Endocrinol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] New Zealand
  • [Chemical-registry-number] 33515-09-2 / Gonadotropin-Releasing Hormone
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69. Biala G, Staniak N, Budzynska B: Effects of varenicline and mecamylamine on the acquisition, expression, and reinstatement of nicotine-conditioned place preference by drug priming in rats. Naunyn Schmiedebergs Arch Pharmacol; 2010 Apr;381(4):361-70
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  • [Title] Effects of varenicline and mecamylamine on the acquisition, expression, and reinstatement of nicotine-conditioned place preference by drug priming in rats.
  • In the present study, we used the conditioned place preference (CPP) paradigm to investigate the establishment, extinction, reinstatement, and cross-reinstatement of nicotine-induced place conditioning in rats.
  • Once established, nicotine CPP was extinguished by repeated testing.
  • These priming injections of both drugs induced a marked preference for the compartment previously paired with nicotine.
  • Furthermore, given the important role of alpha4beta2 (a4b2) nicotinic receptor subtype in the acquisition and maintenance of nicotine dependence, we evaluated and compared the efficacy of varenicline, a partial a4b2 nicotinic receptor agonist (0.5, 1, and 2 mg/kg, subcutaneously (s.c.
  • ), a non-selective nicotinic receptor antagonist, in blocking nicotine-induced CPP as well as reinstatement of nicotine CPP provoked by nicotine and morphine.
  • It was shown that both nicotinic receptor ligands attenuated the acquisition and expression of nicotine CPP as well as the expression of reinstatement of nicotine CPP provoked by both drugs.
  • Our results indicate similar cholinergic mechanisms, probably through the a4b2 receptors involved in the rewarding effects of nicotine and morphine in rats and may suggest that nicotinic receptors could be a potential target for developing pharmacotherapeutic strategies to treat and prevent nicotine and/or opioid addiction and relapse.
  • [MeSH-major] Nicotine / administration & dosage. Nicotinic Agonists / pharmacology. Nicotinic Antagonists / pharmacology. Receptors, Nicotinic / drug effects
  • [MeSH-minor] Animals. Benzazepines / administration & dosage. Benzazepines / pharmacology. Conditioning, Classical / drug effects. Dose-Response Relationship, Drug. Male. Mecamylamine / administration & dosage. Mecamylamine / pharmacology. Morphine / administration & dosage. Morphine / pharmacology. Quinoxalines / administration & dosage. Quinoxalines / pharmacology. Rats. Rats, Wistar. Reward. Tobacco Use Disorder / physiopathology. Varenicline

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  • [Cites] Addiction. 2008 Jan;103(1):146-54 [18028247.001]
  • [Cites] Neuropharmacology. 2007 Mar;52(3):985-94 [17157884.001]
  • [Cites] Prog Neurobiol. 1998 Dec;56(6):613-72 [9871940.001]
  • [Cites] Prog Neurobiol. 2004 Dec;74(6):363-96 [15649582.001]
  • [Cites] Naunyn Schmiedebergs Arch Pharmacol. 1993 Jan;347(1):9-13 [8095326.001]
  • [Cites] Brain Res. 2001 Jun 8;903(1-2):62-5 [11382388.001]
  • [Cites] Nicotine Tob Res. 2007 Mar;9(3):315-27 [17365764.001]
  • [Cites] Neuron. 2002 Mar 14;33(6):905-19 [11906697.001]
  • [Cites] J Med Chem. 2005 May 19;48(10):3474-7 [15887955.001]
  • [Cites] J Neurosci. 2002 Dec 15;22(24):10935-40 [12486188.001]
  • [Cites] J Neurosci. 2003 Apr 15;23(8):3176-85 [12716925.001]
  • [Cites] Neuropharmacology. 2007 Mar;52(3):755-63 [17097117.001]
  • [Cites] Behav Neurosci. 1993 Dec;107(6):1077-87 [8136061.001]
  • [Cites] Curr Drug Targets CNS Neurol Disord. 2002 Aug;1(4):413-21 [12769613.001]
  • [Cites] J Pharmacol Exp Ther. 2009 Apr;329(1):225-30 [19126781.001]
  • [Cites] Psychopharmacology (Berl). 2006 Mar;184(3-4):619-27 [16308727.001]
  • [Cites] Trends Neurosci. 1997 Feb;20(2):92-8 [9023878.001]
  • [Cites] J Neurosci. 1992 Jul;12(7):2765-84 [1613557.001]
  • [Cites] Neuroscience. 2005;136(2):531-8 [16216430.001]
  • [Cites] Eur Neuropsychopharmacol. 1999 Mar;9(3):227-33 [10208292.001]
  • [Cites] Psychopharmacology (Berl). 1999 Nov;147(2):135-42 [10591880.001]
  • [Cites] Neuropharmacology. 2000 Oct;39(13):2740-55 [11044744.001]
  • [Cites] Trends Pharmacol Sci. 2007 Jul;28(7):316-25 [17573127.001]
  • [Cites] Eur J Pharmacol. 2007 May 7;562(1-2):92-102 [17336285.001]
  • [Cites] Nature. 2005 Jul 7;436(7047):103-7 [16001069.001]
  • [Cites] Pharmacol Rep. 2005 Nov-Dec;57(6):755-60 [16382193.001]
  • [Cites] Psychopharmacology (Berl). 1999 Feb;142(1):85-94 [10102787.001]
  • [Cites] JAMA. 2006 Jul 5;296(1):64-71 [16820548.001]
  • [Cites] JAMA. 1994 Feb 23;271(8):589-94 [8301790.001]
  • [Cites] J Pharmacol Exp Ther. 2003 Jul;306(1):407-20 [12682217.001]
  • [Cites] Eur J Pharmacol. 2006 May 10;537(1-3):85-93 [16616917.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 2006 Jan;30(1):15-21 [16202496.001]
  • [Cites] Psychopharmacology (Berl). 2006 Nov;189(1):27-36 [17019569.001]
  • [Cites] Nat Med. 2002 May;8(5):447-9 [11984581.001]
  • [Cites] Nature. 1998 Jan 8;391(6663):173-7 [9428762.001]
  • [Cites] Synapse. 2000 Feb;35(2):129-36 [10611638.001]
  • [Cites] Am J Health Syst Pharm. 2007 Jul 1;64(13):1381-4 [17592002.001]
  • [Cites] Prog Neuropsychopharmacol Biol Psychiatry. 1994 Sep;18(5):925-33 [7972862.001]
  • [Cites] Pharmacol Biochem Behav. 1997 Aug;57(4):915-21 [9259024.001]
  • [Cites] Pharmacol Biochem Behav. 2008 Mar;89(1):116-25 [18178244.001]
  • [Cites] Neuron. 2001 Aug 16;31(3):349-52 [11516393.001]
  • [Cites] Eur J Neurosci. 2003 Apr;17 (7):1329-37 [12713636.001]
  • [Cites] Psychopharmacology (Berl). 2000 Jan;147(4):347-55 [10672627.001]
  • [Cites] Psychopharmacology (Berl). 1992;107(2-3):285-9 [1615127.001]
  • [Cites] Pol J Pharmacol. 2003 May-Jun;55(3):327-35 [14506311.001]
  • [Cites] Curr Opin Pharmacol. 2005 Feb;5(1):53-9 [15661626.001]
  • [Cites] Pharmacol Biochem Behav. 1999 Apr;62(4):743-51 [10208381.001]
  • (PMID = 20217050.001).
  • [ISSN] 1432-1912
  • [Journal-full-title] Naunyn-Schmiedeberg's archives of pharmacology
  • [ISO-abbreviation] Naunyn Schmiedebergs Arch. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Germany
  • [Chemical-registry-number] 0 / Benzazepines; 0 / Nicotinic Agonists; 0 / Nicotinic Antagonists; 0 / Quinoxalines; 0 / Receptors, Nicotinic; 0 / nicotinic receptor alpha4beta2; 6EE945D3OK / Mecamylamine; 6M3C89ZY6R / Nicotine; 76I7G6D29C / Morphine; W6HS99O8ZO / Varenicline
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70. Stubbe HD, Greiner C, Westphal M, Rickert CH, Aken HV, Eichel V, Wassmann H, Daudel F, Hinder F: Cerebral response to norepinephrine compared with fluid resuscitation in ovine traumatic brain injury and systemic inflammation. Crit Care Med; 2006 Oct;34(10):2651-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cerebral response to norepinephrine compared with fluid resuscitation in ovine traumatic brain injury and systemic inflammation.
  • OBJECTIVE: Traumatic brain injury is frequently accompanied by a systemic inflammatory response.
  • The present study investigated the cerebral effects of cerebral perfusion pressure (CPP) management performed by either fluid resuscitation or vasopressor treatment of low CPP induced by systemic inflammation.
  • At hour 10, one group (n = 6) was infused with hydroxyethyl starch until CPP reached 60-70 mm Hg.
  • A second group (n = 6) received norepinephrine for CPP elevation.
  • Head trauma increased intracranial pressure and decreased brain tissue oxygen tension.
  • Endotoxemia induced a hyperdynamic cardiovascular response with increased internal carotid blood flow in the presence of systemic hypotension and decreased CPP.
  • Hydroxyethyl starch infusion further increased internal carotid blood flow from (mean +/- sd) 247 +/- 26 (hour 10) to 342 +/- 42 mL/min (hour 13) and intracranial pressure from 20 +/- 4 (hour 10) to a maximum of 25 +/- 3 mm Hg (hour 12) but did not significantly affect brain tissue oxygen tension, sinus venous oxygen saturation and oxygen extraction fraction.
  • Norepinephrine increased internal carotid blood flow from 268 +/- 19 to 342 +/- 58 mL/min and intracranial pressure from 22 +/- 11 to 24 +/- 11 mm Hg (hour 10 vs. hour 13) but significantly increased sinus venous oxygen saturation from 49 +/- 4 (hour 10) to a maximum of 59 +/- 6 mm Hg (hour 12) and decreased oxygen extraction fraction.
  • The increase in brain tissue oxygen tension during norepinephrine treatment was not significant.
  • CONCLUSION: We conclude that despite identical carotid blood flows, only CPP management with norepinephrine reduced the cerebral oxygen deficit in this model.
  • [MeSH-major] Brain Injuries / therapy. Cerebrovascular Circulation. Fluid Therapy. Norepinephrine / therapeutic use. Systemic Inflammatory Response Syndrome / therapy. Vasoconstrictor Agents / therapeutic use
  • [MeSH-minor] Animals. Hemodynamics / drug effects. Intracranial Pressure / drug effects. Sheep

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  • [CommentIn] Crit Care Med. 2006 Oct;34(10):2697-8 [16983278.001]
  • (PMID = 16932232.001).
  • [ISSN] 0090-3493
  • [Journal-full-title] Critical care medicine
  • [ISO-abbreviation] Crit. Care Med.
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Vasoconstrictor Agents; X4W3ENH1CV / Norepinephrine
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71. Takahashi M, Yamamoto J, Aoyama Y, Soejima Y, Akiba D, Nishizawa S: Efficacy of multi-staged surgery and adjuvant chemotherapy for successful treatment of atypical choroid plexus papilloma in an infant: case report. Neurol Med Chir (Tokyo); 2009 Oct;49(10):484-7
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  • [Title] Efficacy of multi-staged surgery and adjuvant chemotherapy for successful treatment of atypical choroid plexus papilloma in an infant: case report.
  • A 12-month-old girl presented with a rare atypical choroid plexus papilloma manifesting as conscious disturbance and vomiting.
  • Only partial removal of the tumor was performed because of excessive intraoperative hemorrhage at the first surgery.
  • The histological diagnosis was atypical choroid plexus papilloma.
  • To control the intraoperative hemorrhage, embolization of the feeding artery was performed before the second surgery, and the tumor was macroscopically totally removed.
  • MR imaging disclosed a small residual tumor which showed relatively rapid growth.
  • Two months later, MR imaging showed a cystic lesion with a small nodule adjacent to the midbrain, indicating dissemination of the tumor.
  • The lesion was successfully treated with chemotherapy.
  • Atypical choroid plexus papilloma was recently defined in the classification of the World Health Organization, so clinical data based on these criteria are lacking to establish the therapeutic strategy.
  • Total resection of atypical choroid plexus papilloma is the most reliable treatment at present.
  • However, postoperative chemotherapy should be considered for recurrence or dissemination.
  • [MeSH-major] Brain / surgery. Lateral Ventricles / surgery. Papilloma, Choroid Plexus / drug therapy. Papilloma, Choroid Plexus / surgery
  • [MeSH-minor] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cerebral Arteries / pathology. Cerebral Arteries / physiopathology. Craniotomy. Embolization, Therapeutic. Female. Humans. Infant. Intraoperative Complications / etiology. Intraoperative Complications / physiopathology. Intraoperative Complications / therapy. Lethargy / etiology. Magnetic Resonance Imaging. Neoplasm Metastasis / drug therapy. Neoplasm Metastasis / pathology. Neurosurgical Procedures. Postoperative Hemorrhage / etiology. Postoperative Hemorrhage / physiopathology. Postoperative Hemorrhage / therapy. Reoperation. Tomography, X-Ray Computed. Treatment Outcome. Ventriculostomy. Vomiting / etiology

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  • (PMID = 19855149.001).
  • [ISSN] 1349-8029
  • [Journal-full-title] Neurologia medico-chirurgica
  • [ISO-abbreviation] Neurol. Med. Chir. (Tokyo)
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
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72. Klouche K, Weil MH, Sun S, Tang W, Zhao DH: A comparison of alpha-methylnorepinephrine, vasopressin and epinephrine for cardiac resuscitation. Resuscitation; 2003 Apr;57(1):93-100
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  • We had previously observed significantly better outcomes with a selective alpha(2)-adrenergic agonist when compared with epinephrine.
  • The present study was, therefore, undertaken to compare a selective alpha(2)-adrenergic vasopressor drug with vasopressin, epinephrine, and saline placebo.
  • Left ventricular pressure, dP/dt(40), -dP/dt, and cardiac index were measured for an interval of 240 min after resuscitation.
  • Except for saline controls, comparable increases in coronary perfusion pressure (CPP) were observed after each drug intervention.
  • [MeSH-major] Cardiopulmonary Resuscitation / methods. Nordefrin / pharmacology. Vasoconstrictor Agents / pharmacology. Vasopressins / pharmacology. Ventricular Fibrillation / therapy
  • [MeSH-minor] Analysis of Variance. Animals. Cardiac Output / physiology. Disease Models, Animal. Dose-Response Relationship, Drug. Drug Administration Schedule. Electrocardiography. Hemodynamics / physiology. Male. Probability. Rats. Rats, Sprague-Dawley. Sensitivity and Specificity. Survival Rate

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  • (PMID = 12668305.001).
  • [ISSN] 0300-9572
  • [Journal-full-title] Resuscitation
  • [ISO-abbreviation] Resuscitation
  • [Language] eng
  • [Grant] United States / NHLBI NIH HHS / HL / HL-54322
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Vasoconstrictor Agents; 11000-17-2 / Vasopressins; R81X549E70 / Nordefrin
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73. Lewis HD, Husain A, Donnelly RJ, Barlos D, Riaz S, Ginjupalli K, Shodeinde A, Barton BE: Creation of a novel peptide with enhanced nuclear localization in prostate and pancreatic cancer cell lines. BMC Biotechnol; 2010 Oct 28;10:79
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  • [Title] Creation of a novel peptide with enhanced nuclear localization in prostate and pancreatic cancer cell lines.
  • BACKGROUND: For improved uptake of oligonucleotide-based therapy, the oligonucleotides often are coupled to peptides that facilitate entry into cells.
  • To this end, novel cell-penetrating peptides (CPPs) were designed for mediating intracellular uptake of oligonucleotide-based therapeutics.
  • The novel peptides were based on taking advantage of the nuclear localization properties of transcription factors in combination with a peptide that would bind putatively to cell surfaces.
  • It was observed that adding a glutamate peptide to the N-terminus of the nuclear localization signal (NLS) of the Oct6 transcription factor resulted in a novel CPP with better uptake and better nuclear colocalization than any other peptide tested.
  • RESULTS: Uptake of the novel peptide Glu-Oct6 by cancer cell lines was rapid (in less than 1 hr, more than 60% of DU-145 cells were positive for FITC), complete (by 4 hr, 99% of cells were positive for FITC), concentration-dependent, temperature-dependent, and inhibited by sodium azide (NaN3).
  • Substitution of Phe, Tyr, or Asn moieties for the glutamate portion of the novel peptide resulted in abrogation of novel CPP uptake; however none of the substituted peptides inhibited uptake of the novel CPP when coincubated with cells.
  • Live-cell imaging and analysis by imaging flow cytometry revealed that the novel CPP accumulated in nuclei.
  • Finally, the novel CPP was coupled to a carboxyfluorescein-labeled synthetic oligonucleotide, to see if the peptide could ferry a therapeutic payload into cells.
  • CONCLUSIONS: These studies document the creation of a novel CPP consisting of a glutamate peptide coupled to the N-terminus of the Oct6 NLS; the novel CPP exhibited nuclear colocalization as well as uptake by prostate and pancreatic cancer cell lines.

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  • [Cites] Curr Pharm Des. 2001 Nov;7(17):1839-62 [11562312.001]
  • [Cites] Cell Mol Life Sci. 2010 Mar;67(5):715-26 [19898741.001]
  • [Cites] Chem Biol. 2002 Aug;9(8):943-8 [12204694.001]
  • [Cites] Cancer Res. 2002 Oct 1;62(19):5470-5 [12359755.001]
  • [Cites] J Biol Chem. 2003 Jan 3;278(1):585-90 [12411431.001]
  • [Cites] Adv Drug Deliv Rev. 2003 Feb 10;55(2):267-80 [12564980.001]
  • [Cites] Biochem Biophys Res Commun. 2003 Jul 18;307(1):100-7 [12849987.001]
  • [Cites] Cancer Res. 2003 Aug 15;63(16):4766-72 [12941791.001]
  • [Cites] J Cell Biochem. 2004 Feb 15;91(3):528-39 [14755683.001]
  • [Cites] Cancer Biol Ther. 2004 Jun;3(6):551-8 [15044850.001]
  • [Cites] Cancer Biol Ther. 2004 Jun;3(6):559-60 [15153802.001]
  • [Cites] Mol Cancer Ther. 2004 Oct;3(10):1183-91 [15486184.001]
  • [Cites] EMBO J. 1991 Jul;10(7):1733-9 [2050110.001]
  • [Cites] J Biol Chem. 1992 Nov 25;267(33):23484-8 [1429691.001]
  • [Cites] Biochem Pharmacol. 1994 Sep 15;48(6):1310-3 [7945427.001]
  • [Cites] J Biol Chem. 1996 May 31;271(22):13228-33 [8662737.001]
  • [Cites] J Biol Chem. 1996 Jul 19;271(29):17512-8 [8663425.001]
  • [Cites] Front Biosci. 2005;10:1302-12 [15769626.001]
  • [Cites] Clin Cancer Res. 2005 May 1;11(9):3288-95 [15867225.001]
  • [Cites] J Control Release. 2005 Dec 10;110(1):189-201 [16253378.001]
  • [Cites] Ann N Y Acad Sci. 2005 Nov;1059:106-44 [16382049.001]
  • [Cites] Bioconjug Chem. 2006 May-Jun;17(3):750-8 [16704214.001]
  • [Cites] Proc Natl Acad Sci U S A. 2006 Aug 15;103(33):12505-10 [16895983.001]
  • [Cites] Cancer Res. 2006 Sep 15;66(18):9171-7 [16982760.001]
  • [Cites] Biochem J. 2007 Apr 15;403(2):335-42 [17217340.001]
  • [Cites] Virology. 2007 Jun 20;363(1):91-103 [17320140.001]
  • [Cites] Biochemistry. 2007 Jun 26;46(25):7581-9 [17536840.001]
  • [Cites] Mol Cancer Ther. 2008 Jun;7(6):1543-50 [18566225.001]
  • [Cites] J Immunol Methods. 2008 Jul 31;336(2):91-7 [18539294.001]
  • [Cites] Neuropharmacology. 2008 Sep;55(4):396-402 [18554669.001]
  • [Cites] Cancer Gene Ther. 2009 Oct;16(10):786-93 [19363465.001]
  • [Cites] Clin Cancer Res. 2002 Apr;8(4):1271-6 [11948142.001]
  • (PMID = 21029412.001).
  • [ISSN] 1472-6750
  • [Journal-full-title] BMC biotechnology
  • [ISO-abbreviation] BMC Biotechnol.
  • [Language] ENG
  • [Grant] United States / NCI NIH HHS / CA / CA 121782
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Cell-Penetrating Peptides; 0 / Nuclear Localization Signals; 0 / Organic Cation Transport Proteins; 0 / Peptide Nucleic Acids; 0 / SLC22A16 protein, human; 3KX376GY7L / Glutamic Acid
  • [Other-IDs] NLM/ PMC2987774
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74. Takamatsu Y, Yamamoto H, Ogai Y, Hagino Y, Markou A, Ikeda K: Fluoxetine as a potential pharmacotherapy for methamphetamine dependence: studies in mice. Ann N Y Acad Sci; 2006 Aug;1074:295-302
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  • [Title] Fluoxetine as a potential pharmacotherapy for methamphetamine dependence: studies in mice.
  • The monoamine transporters are the main targets of psychostimulant drugs, including methamphetamine (METH) and cocaine.
  • Interestingly, the rewarding effects of cocaine are retained in dopamine transporter (DAT) knockout (KO) mice, while serotonin transporter (SERT) and DAT double KO mice do not exhibit conditioned place preference (CPP) to cocaine.
  • ) CPP and locomotor sensitization to 1 mg/kg METH (i.p.) in C57BL/6J mice.
  • Fluoxetine treatment before both the conditioning and preference tests abolished METH CPP.
  • A two-way analysis of variance (ANOVA) revealed that METH CPP tended to be lower in mice pretreated with fluoxetine before the preference test than in control mice pretreated with saline before the preference test.
  • These results suggest that fluoxetine, a widely used medication for depression, may be also a useful tool for treating METH dependence.
  • [MeSH-major] Amphetamine-Related Disorders / drug therapy. Dopamine Agents / toxicity. Fluoxetine / therapeutic use. Methamphetamine / toxicity. Motor Activity / drug effects. Serotonin Uptake Inhibitors / therapeutic use

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  • (PMID = 17105925.001).
  • [ISSN] 0077-8923
  • [Journal-full-title] Annals of the New York Academy of Sciences
  • [ISO-abbreviation] Ann. N. Y. Acad. Sci.
  • [Language] eng
  • [Grant] United States / NIDA NIH HHS / DA / R01 DA11946
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Dopamine Agents; 0 / Serotonin Uptake Inhibitors; 01K63SUP8D / Fluoxetine; 44RAL3456C / Methamphetamine
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75. Narotam PK, Puri V, Roberts JM, Taylon C, Vora Y, Nathoo N: Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects of intravenous nicardipine on cerebral oxygenation. J Neurosurg; 2008 Dec;109(6):1065-74
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  • [Title] Management of hypertensive emergencies in acute brain disease: evaluation of the treatment effects of intravenous nicardipine on cerebral oxygenation.
  • This study explores the effect of nicardipine on regional brain tissue O(2) (PbtO(2)) during treatment of acute hypertensive emergencies.
  • All patients had a parenchymal PbtO(2) and intracranial pressure bolt inserted following resuscitation.
  • Intravenous nicardipine (5-15 mg/hour) was titrated to systolic BP < 160 mm Hg, diastolic BP < 90 mm Hg, mean arterial BP (MABP) 90-110 mm Hg, and PbtO(2) > 20 mm Hg.
  • Physiological parameters-intracranial pressure, PbtO(2), central venous pressure, systolic BP, diastolic BP, MABP, fraction of inspired O(2), and cerebral perfusion pressure (CPP)-were compared before infusion, at 4 hours, and at 8 hours using a t-test.
  • RESULTS: Sixty episodes of hypertension were reported in 30 patients (traumatic brain injury in 13 patients; aneurysmal subarachnoid hemorrhage in 11; intracerebral and intraventricular hemorrhage in 3 and 1, respectively; arteriovenous malformation in 1; and hypoxic brain injury in 1).
  • Nicardipine was effective in 87% of the patients (with intravenous beta blockers in 4 patients), with a 19.7% reduction in mean 4-hour MABP (115.3 +/- 13.1 mm Hg preinfusion vs 92.9 +/- 11.40 mm Hg after 4 hours of therapy, p < 0.001).
  • No deleterious effect on mean PbtO(2) was recorded (26.74 +/- 15.42 mm Hg preinfusion vs 27.68 +/- 12.51 mm Hg after 4 hours of therapy, p = 0.883) despite significant reduction in CPP.
  • Less dependence on normobaric hyperoxia was achieved at 8 hours (0.72 +/- 0.289 mm Hg preinfusion vs 0.626 +/- 0.286 mm Hg after 8 hours of therapy, p < 0.01).
  • Subgroup analysis revealed that 12 patients had low pretreatment PbtO(2) (10.30 +/- 6.49 mm Hg), with higher CPP (p < 0.001) requiring hyperoxia (p = 0.02).
  • In this group, intravenous nicardipine resulted in an 83% improvement in 4- and 8-hour PbtO(2) levels (18.1 +/- 11.33 and 19.59 +/- 23.68 mm Hg, respectively; p < 0.01) despite significant reductions in both mean MABP (120.6 +/- 16.65 vs 95.8 +/- 8.3 mm Hg, p < 0.001) and CPP (105.00 +/- 20.7 vs 81.2 +/- 15.4 mm Hg, p < 0.001).
  • CONCLUSIONS: Intravenous nicardipine is effective for the treatment of hypertensive neurological emergencies and has no adverse effect on PbtO(2).
  • [MeSH-major] Antihypertensive Agents / therapeutic use. Brain Injuries / physiopathology. Cerebral Hemorrhage / physiopathology. Hypertension / drug therapy. Intracranial Arteriovenous Malformations / physiopathology. Nicardipine / therapeutic use. Subarachnoid Hemorrhage / physiopathology
  • [MeSH-minor] Acute Disease. Adult. Aged. Blood Pressure / drug effects. Blood Pressure / physiology. Brain / metabolism. Female. Humans. Hypoxia, Brain / physiopathology. Infusions, Intravenous. Male. Middle Aged. Oxygen / metabolism. Prospective Studies


76. Endoh T, Ohtsuki T: Cellular siRNA delivery using cell-penetrating peptides modified for endosomal escape. Adv Drug Deliv Rev; 2009 Jul 25;61(9):704-9
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  • RNAi-mediated silencing of specific genes is a promising strategy for gene therapy.
  • To utilize RNAi for therapy, an efficient and safe method for delivery of RNA into the cell cytosol is necessary.
  • This review focuses on CPP-based RNA delivery strategies.
  • In using CPP-based RNA delivery, most of the RNA internalized by the cell is entrapped in endosomes.
  • [MeSH-minor] Amino Acid Sequence. Animals. Drug Carriers. Fluorescent Dyes. Gene Silencing. Genetic Therapy. Humans. Molecular Sequence Data. Photosensitizing Agents / pharmacology. RNA Interference. RNA-Binding Proteins / chemistry. RNA-Binding Proteins / metabolism

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  • (PMID = 19383521.001).
  • [ISSN] 1872-8294
  • [Journal-full-title] Advanced drug delivery reviews
  • [ISO-abbreviation] Adv. Drug Deliv. Rev.
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Drug Carriers; 0 / Fluorescent Dyes; 0 / Peptides; 0 / Photosensitizing Agents; 0 / RNA, Small Interfering; 0 / RNA-Binding Proteins
  • [Number-of-references] 74
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77. Sadler R, Herzig V, Schmidt WJ: Repeated treatment with the NMDA antagonist MK-801 disrupts reconsolidation of memory for amphetamine-conditioned place preference. Behav Pharmacol; 2007 Nov;18(7):699-703
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  • [Title] Repeated treatment with the NMDA antagonist MK-801 disrupts reconsolidation of memory for amphetamine-conditioned place preference.
  • Long-lasting drug-associated memories can contribute to relapse; therefore these memories must be inactivated to enable sustainable success in addiction therapy.
  • As drug associations are usually acquired over several conditioning events, we assume that an effective treatment should be repeatedly applied to achieve persistent effects.
  • In this study, we examine whether 10 repeated memory reactivation tests followed by systemic N-methyl-D-aspartate receptor antagonist MK-801 (0.1 mg/kg) administrations can disrupt memory reconsolidation in rats, leading to a reduction of well-established amphetamine-conditioned place preference (CPP).
  • We found that immediate (but not 60-min delayed) administration of MK-801 after the tests reduced amphetamine-CPP expression after at least four treatments.
  • These effects were specific to CPP expression as no MK-801-induced change in locomotion was observed during all tests.
  • We discuss these results as being caused by MK-801 disrupting memory reconsolidation and we propose the applied repeated-treatment regimen as a new therapeutic research strategy to persistently disrupt drug-associated memories.
  • [MeSH-major] Amphetamine / pharmacology. Central Nervous System Stimulants / pharmacology. Conditioning, Operant / drug effects. Dizocilpine Maleate / pharmacology. Memory / drug effects. Receptors, N-Methyl-D-Aspartate / antagonists & inhibitors
  • [MeSH-minor] Animals. Behavior, Animal / drug effects. Male. Motor Activity / drug effects. Rats. Rats, Sprague-Dawley

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  • (PMID = 17912055.001).
  • [ISSN] 0955-8810
  • [Journal-full-title] Behavioural pharmacology
  • [ISO-abbreviation] Behav Pharmacol
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Central Nervous System Stimulants; 0 / Receptors, N-Methyl-D-Aspartate; 6LR8C1B66Q / Dizocilpine Maleate; CK833KGX7E / Amphetamine
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78. Eugster EA, Clarke W, Kletter GB, Lee PA, Neely EK, Reiter EO, Saenger P, Shulman D, Silverman L, Flood L, Gray W, Tierney D: Efficacy and safety of histrelin subdermal implant in children with central precocious puberty: a multicenter trial. J Clin Endocrinol Metab; 2007 May;92(5):1697-704
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  • CONTEXT: GnRH analog (GnRHa) therapy for central precocious puberty (CPP) typically involves im injections.
  • The histrelin implant is a new treatment that provides a continuous slow release of the GnRHa histrelin.
  • OBJECTIVE: The objective of the study was to investigate the safety and efficacy of the subdermal histrelin implant for the treatment of CPP in treatment naive and previously treated children.
  • PATIENTS: Girls ages 2-8 yr (naive) or 2-10 yr (previously treated) and boys 2-9 yr (naive) or 2-11 yr (previously treated) with clinical evidence of CPP and a pretreatment pubertal response to leuprolide stimulation were eligible.
  • CONCLUSIONS: The subdermal histrelin implant achieves and maintains excellent suppression of peak LH and sex steroid levels for 1 yr in children with CPP.
  • The treatment is well tolerated.
  • [MeSH-major] Gonadotropin-Releasing Hormone / analogs & derivatives. Puberty, Precocious / drug therapy
  • [MeSH-minor] Age Determination by Skeleton. Body Mass Index. Bone and Bones / radiography. Breast / growth & development. Child. Child, Preschool. Drug Implants. Estradiol / blood. Female. Follicle Stimulating Hormone / blood. Growth / drug effects. Humans. Luteinizing Hormone / blood. Male. Prospective Studies. Testosterone / blood

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  • (PMID = 17327379.001).
  • [ISSN] 0021-972X
  • [Journal-full-title] The Journal of clinical endocrinology and metabolism
  • [ISO-abbreviation] J. Clin. Endocrinol. Metab.
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Multicenter Study; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Drug Implants; 33515-09-2 / Gonadotropin-Releasing Hormone; 3XMK78S47O / Testosterone; 4TI98Z838E / Estradiol; 9002-67-9 / Luteinizing Hormone; 9002-68-0 / Follicle Stimulating Hormone; H50H3S3W74 / histrelin
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79. Hasselblatt M, Mühlisch J, Wrede B, Kallinger B, Jeibmann A, Peters O, Kutluk T, Wolff JE, Paulus W, Frühwald MC: Aberrant MGMT (O6-methylguanine-DNA methyltransferase) promoter methylation in choroid plexus tumors. J Neurooncol; 2009 Jan;91(2):151-5
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  • [Title] Aberrant MGMT (O6-methylguanine-DNA methyltransferase) promoter methylation in choroid plexus tumors.
  • Aberrant methylation of the MGMT (O6-methylguanine-DNA methyltransferase) DNA-repair gene is a predictive marker for the response to chemotherapy with alkylating agents (e.g., temozolomide) in malignant gliomas.
  • Since temozolomide is considered for the treatment of choroid plexus tumors, MGMT promoter methylation status was retrospectively assessed in 36 choroid plexus tumors using methylation specific PCR, combined bisulfite restriction analysis (COBRA), and clone sequencing.
  • In conclusion, MGMT promoter methylation is frequent in choroid plexus tumors and can be quantified using COBRA.
  • Determination of MGMT promoter methylation status might be useful for the stratification of patients for alkylator-based treatments in future clinical trials.
  • [MeSH-major] Choroid Plexus Neoplasms / genetics. DNA Methylation / genetics. O(6)-Methylguanine-DNA Methyltransferase / genetics. Promoter Regions, Genetic / genetics
  • [MeSH-minor] Antineoplastic Agents, Alkylating / therapeutic use. Carcinoma / genetics. Child, Preschool. CpG Islands. Female. Humans. Infant. Male. Papilloma / genetics. Retrospective Studies. Sequence Analysis, DNA. Sulfites / pharmacology

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  • [Cites] Cell Mol Neurobiol. 2005 Sep;25(6):1067-71 [16392037.001]
  • [Cites] Mol Carcinog. 1999 Feb;24(2):85-9 [10078935.001]
  • [Cites] J Neurooncol. 2007 Dec;85(3):345-51 [17576522.001]
  • [Cites] Oncogene. 2001 Aug 16;20(36):5033-42 [11526488.001]
  • [Cites] Surg Neurol. 2006 Jul;66(1):62-7; discussion 67-8 [16793445.001]
  • [Cites] Proc Natl Acad Sci U S A. 1996 Sep 3;93(18):9821-6 [8790415.001]
  • [Cites] Lancet. 1999 Jun 19;353(9170):2126 [10382700.001]
  • [Cites] Proc Natl Acad Sci U S A. 2005 Nov 1;102(44):15785-90 [16243968.001]
  • [Cites] Brain Pathol. 2008 Oct;18(4):520-32 [18400046.001]
  • [Cites] Clin Cancer Res. 2007 Nov 15;13(22 Pt 1):6712-8 [18006772.001]
  • [Cites] Cancer Genet Cytogenet. 2006 Apr 1;166(1):74-81 [16616114.001]
  • [Cites] J Clin Oncol. 2002 Dec 15;20(24):4684-91 [12488414.001]
  • [Cites] Lab Invest. 2007 Oct;87(10 ):1055-65 [17700563.001]
  • [Cites] Acta Neuropathol. 2007 Aug;114(2):97-109 [17618441.001]
  • [Cites] J Neurooncol. 2007 May;83(1):17-29 [17206475.001]
  • [Cites] Microsc Res Tech. 2001 Jan 1;52(1):104-11 [11135453.001]
  • [Cites] Oncogene. 2006 Feb 16;25(7):1111-7 [16186793.001]
  • [Cites] Pediatr Blood Cancer. 2007 Nov;49(6):808-11 [17588234.001]
  • [Cites] J Neuropathol Exp Neurol. 2006 Nov;65(11):1069-73 [17086103.001]
  • [Cites] Nucleic Acids Res. 1994 Nov 11;22(22):4614-9 [7984409.001]
  • [Cites] Cancer Res. 1997 Sep 1;57(17):3672-7 [9288770.001]
  • [Cites] N Engl J Med. 2005 Mar 10;352(10 ):997-1003 [15758010.001]
  • [Cites] Pediatr Blood Cancer. 2007 Apr;48(4):403-7 [16609952.001]
  • [Cites] J Neurooncol. 2004 Mar-Apr;67(1-2):159-65 [15072463.001]
  • [Cites] Am J Surg Pathol. 2006 Jan;30(1):66-74 [16330944.001]
  • [Cites] J Neuropathol Exp Neurol. 2005 May;64(5):391-7 [15892296.001]
  • (PMID = 18795231.001).
  • [ISSN] 0167-594X
  • [Journal-full-title] Journal of neuro-oncology
  • [ISO-abbreviation] J. Neurooncol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antineoplastic Agents, Alkylating; 0 / Sulfites; EC 2.1.1.63 / O(6)-Methylguanine-DNA Methyltransferase; OJ9787WBLU / hydrogen sulfite
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80. Anpalagan A, Condous G: Is there a role for use of levonorgestrel intrauterine system in women with chronic pelvic pain? J Minim Invasive Gynecol; 2008 Nov-Dec;15(6):663-6
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  • This review focuses on the available evidence for the use of levonorgestrel (LNG) intrauterine system (IUS) in women with chronic pelvic pain (CPP).
  • Laparoscopic surgery was shown to be useful in clarifying the underlying cause in women with CPP, with 70% having abnormal findings at laparoscopy.
  • Up to 36% need repeated surgery during a 5-year period after the primary procedure.
  • The absolute reduction in recurrence of dysmenorrhea in women who also had the LNG IUS inserted at the time of surgery was 35% (95% CI 9%-61%).
  • Insertion of the LNG IUS at the time of primary laparoscopic surgery in women with CPP caused by endometriosis has the potential to reduce postoperative pain scores.
  • This nonsurgical option could potentially reduce the rate of repeated laparoscopies in women with CPP and, in turn, reduce overall intervention rates.
  • [MeSH-major] Contraceptive Agents, Female / therapeutic use. Levonorgestrel / therapeutic use. Pelvic Pain / drug therapy
  • [MeSH-minor] Clinical Trials as Topic. Dysmenorrhea / drug therapy. Female. Humans. Menstruation Disturbances / complications. Menstruation Disturbances / diagnosis

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  • (PMID = 18774757.001).
  • [ISSN] 1553-4650
  • [Journal-full-title] Journal of minimally invasive gynecology
  • [ISO-abbreviation] J Minim Invasive Gynecol
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Contraceptive Agents, Female; 5W7SIA7YZW / Levonorgestrel
  • [Number-of-references] 21
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81. Stoner J, Martin G, O'Mara K, Ehlers J, Tomlanovich M: Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model. Acad Emerg Med; 2003 Mar;10(3):187-91
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  • [Title] Amiodarone and bretylium in the treatment of hypothermic ventricular fibrillation in a canine model.
  • Despite mixed experimental data, some authors view bretylium as the drug of choice in hypothermic VF.
  • OBJECTIVES: To compare defibrillation rates from hypothermic VF after drug therapy with amiodarone, bretylium, and placebo.
  • Thirty anesthetized dogs were mechanically ventilated and instrumented to monitor coronary perfusion pressure (CPP), rectal core temperature, and electrocardiogram (ECG).
  • Ventricular fibrillation was induced as needed with a transthoracic AC current.
  • Return of spontaneous circulation (ROSC) was defined as a sustainable ECG rhythm generating a corresponding arterial pressure tracing lasting a minimum of 15 minutes.
  • RESULTS: CPR was adequate based on CPP > 15 mm Hg in all animals.
  • Mean (+/-SD) CPP was 35.3 +/- 18.8 mm Hg with an overall lower trend in the amiodarone group (p = 0.06).
  • [MeSH-major] Amiodarone / therapeutic use. Anti-Arrhythmia Agents / therapeutic use. Bretylium Compounds / therapeutic use. Ventricular Fibrillation / drug therapy
  • [MeSH-minor] Animals. Disease Models, Animal. Dogs. Hypothermia, Induced. Random Allocation

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  • (PMID = 12615580.001).
  • [ISSN] 1069-6563
  • [Journal-full-title] Academic emergency medicine : official journal of the Society for Academic Emergency Medicine
  • [ISO-abbreviation] Acad Emerg Med
  • [Language] eng
  • [Publication-type] Comparative Study; Evaluation Studies; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Arrhythmia Agents; 0 / Bretylium Compounds; N3RQ532IUT / Amiodarone; RZR75EQ2KJ / bretylium
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82. Cavus E, Meybohm P, Doerges V, Hugo HH, Steinfath M, Nordstroem J, Scholz J, Bein B: Cerebral effects of three resuscitation protocols in uncontrolled haemorrhagic shock: a randomised controlled experimental study. Resuscitation; 2009 May;80(5):567-72
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  • BACKGROUND: To compare haemodynamic and cerebral variables during aggressive fluid resuscitation vs. administration of a hypertonic starch solution (HS) combined with either noradrenaline [norepinephrine] or arginine vasopressin in an animal model of uncontrolled haemorrhagic shock.
  • Thirty minutes after drug administration, bleeding was controlled manually.
  • RESULTS: Mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), and brain tissue oxygen pressure (P(bt)O(2)) decreased significantly with haemorrhage in all groups (p<0.05).
  • AVP/HS resulted in a faster and higher increase of MAP and CPP compared to both NA/HS and FR (p<0.001 vs. FR; p<0.01 vs. NA/HS).
  • Compared to FR, P(bt)O(2) increased faster with AVP/HS and NA/HS (p<0.05) after therapy, and ICP was lower at the end of the study period (p<0.05).
  • CONCLUSIONS: Following uncontrolled haemorrhagic shock in this animal model, combination of HS with arginine vasopressin increased CPP and cerebral oxygenation faster than aggressive fluid resuscitation, without re-increasing ICP.
  • [MeSH-major] Clinical Protocols. Resuscitation / methods. Shock, Hemorrhagic / therapy
  • [MeSH-minor] Animals. Arginine Vasopressin / administration & dosage. Brain / blood supply. Brain / drug effects. Brain / physiopathology. Cerebrovascular Circulation / drug effects. Combined Modality Therapy / methods. Disease Models, Animal. Female. Fluid Therapy / methods. Hydroxyethyl Starch Derivatives / administration & dosage. Hypertonic Solutions / administration & dosage. Male. Norepinephrine / administration & dosage. Oxygen Consumption / drug effects. Plasma Substitutes / administration & dosage. Prospective Studies. Random Allocation. Swine. Treatment Outcome. Vasoconstrictor Agents / administration & dosage

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  • (PMID = 19217706.001).
  • [ISSN] 0300-9572
  • [Journal-full-title] Resuscitation
  • [ISO-abbreviation] Resuscitation
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Hydroxyethyl Starch Derivatives; 0 / Hypertonic Solutions; 0 / Plasma Substitutes; 0 / Vasoconstrictor Agents; 113-79-1 / Arginine Vasopressin; X4W3ENH1CV / Norepinephrine
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83. Iwasaki K, Mishima K, Egashira N, Al-Khatib IH, Ishibashi D, Irie K, Kobayashi H, Egawa T, Fujiwara M: Effect of nilvadipine on the cerebral ischemia-induced impairment of spatial memory and hippocampal apoptosis in rats. J Pharmacol Sci; 2003 Oct;93(2):188-96
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  • However, mRNA expression of the apoptosis-related early oncogene bax and CPP 32 (caspase-3) was observed after 24 h.
  • In these rats, nilvadipine, but not amlodipine, significantly improved memory, concomitantly decreased hippocampal apoptosis, and suppressed both bax and CPP 32 expression.
  • These results suggest that nilvadipine improved the memory impairment in repeated ischemia by reducing bax and CPP 32 expression and suppressing the induction of apoptosis in the hippocampus.
  • Nilvadipine may have a neuroprotective effect and could be a useful pharmacotherapeutic agent for cerebrovascular dementia.
  • [MeSH-major] Brain Ischemia / psychology. Calcium Channel Blockers / pharmacology. Hippocampus / cytology. Memory Disorders / drug therapy. Memory Disorders / psychology. Nifedipine / pharmacology. Space Perception / drug effects
  • [MeSH-minor] Animals. Apoptosis / drug effects. Calibration. Genes, bcl-2 / genetics. Glyceraldehyde-3-Phosphate Dehydrogenases / genetics. Male. Maze Learning / drug effects. RNA, Messenger / biosynthesis. Rats. Rats, Wistar. Reverse Transcriptase Polymerase Chain Reaction

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  • (PMID = 14578587.001).
  • [ISSN] 1347-8613
  • [Journal-full-title] Journal of pharmacological sciences
  • [ISO-abbreviation] J. Pharmacol. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Calcium Channel Blockers; 0 / RNA, Messenger; 0214FUT37J / nilvadipine; EC 1.2.1.- / Glyceraldehyde-3-Phosphate Dehydrogenases; I9ZF7L6G2L / Nifedipine
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84. Biala G, Budzynska B, Staniak N: Effects of rimonabant on the reinstatement of nicotine-conditioned place preference by drug priming in rats. Behav Brain Res; 2009 Sep 14;202(2):260-5
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  • [Title] Effects of rimonabant on the reinstatement of nicotine-conditioned place preference by drug priming in rats.
  • Drug addiction is a chronic disorder characterized by a relatively high rate of relapse even after long period of abstinence.
  • In the present study, we used the conditioned place preference (CPP) paradigm to investigate the establishment, extinction, reinstatement and cross-reinstatement of nicotine-induced place conditioning in rats.
  • Nicotine produced a place preference to the initially less-preferred compartment paired with its injections during conditioning (0.5mg/kg, i.p., three drug sessions).
  • Once established, nicotine CPP was extinguished by repeated testing.
  • Following this extinction phase, the reinstatement of CPP was investigated.
  • These priming injections of both drugs induced a marked preference for the compartment previously paired with nicotine.
  • Furthermore, the objective of the present study was to evaluate the efficacy of CB1 cannabinoid receptor antagonist rimonabant (0.5, 1 and 2mg/kg, i.p.) in blocking the reinstatement of nicotine-induced CPP provoked by nicotine and morphine.
  • It was shown that rimonabant attenuated the reinstatement of nicotine-conditioned response induced by both drugs.
  • The outcome of our studies may suggest that CB1 receptor antagonists may become a promising target for effective pharmacotherapy of tobacco addiction and polydrug abuse.
  • [MeSH-major] Central Nervous System Agents / administration & dosage. Conditioning, Classical / drug effects. Morphine / administration & dosage. Nicotine / administration & dosage. Nicotinic Agonists / administration & dosage. Piperidines / administration & dosage. Pyrazoles / administration & dosage
  • [MeSH-minor] Analysis of Variance. Animals. Extinction, Psychological. Male. Random Allocation. Rats. Rats, Wistar. Receptor, Cannabinoid, CB1 / antagonists & inhibitors. Spatial Behavior / drug effects

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  • (PMID = 19463710.001).
  • [ISSN] 1872-7549
  • [Journal-full-title] Behavioural brain research
  • [ISO-abbreviation] Behav. Brain Res.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Central Nervous System Agents; 0 / Nicotinic Agonists; 0 / Piperidines; 0 / Pyrazoles; 0 / Receptor, Cannabinoid, CB1; 158681-13-1 / rimonabant; 6M3C89ZY6R / Nicotine; 76I7G6D29C / Morphine
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85. Bordman R, Jackson B: Below the belt: approach to chronic pelvic pain. Can Fam Physician; 2006 Dec;52(12):1556-62
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  • OBJECTIVE: To present a practical approach to the symptom complex called chronic pelvic pain (CPP).
  • Chronic pelvic pain is defined as nonmenstrual pain lasting 6 months or more that is severe enough to cause functional disability or require medical or surgical treatment.
  • MAIN MESSAGE: While the source of pain in CPP can be gynecologic, urologic, gastrointestinal, musculoskeletal, or psychoneurologic, 4 conditions account for most CPP: endometriosis, adhesions, interstitial cystitis, and irritable bowel syndrome.
  • Nonnarcotic analgesics are first-line therapy for pain relief; hormonal therapies are beneficial if the pain has a cyclical component.
  • CONCLUSION: Although caring for patients with CPP can be challenging and frustrating, family physicians are in an ideal position to manage and coordinate their care.
  • [MeSH-major] Pelvic Pain / diagnosis. Pelvic Pain / therapy
  • [MeSH-minor] Abdominal Pain / etiology. Adult. Chronic Disease. Cystitis, Interstitial / complications. Cystitis, Interstitial / diagnosis. Cystitis, Interstitial / drug therapy. Endometriosis / complications. Endometriosis / diagnosis. Endometriosis / drug therapy. Female. Humans. Irritable Bowel Syndrome / complications. Irritable Bowel Syndrome / diagnosis. Irritable Bowel Syndrome / therapy. Physical Examination

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  • [Cites] Br Med Bull. 2004;72:15-29 [15767561.001]
  • [Cites] Clin Obstet Gynecol. 1998 Jun;41(2):422-35 [9646974.001]
  • [Cites] Am Fam Physician. 1999 Oct 15;60(6):1753-62, 1767-8 [10537390.001]
  • [Cites] Baillieres Best Pract Res Clin Obstet Gynaecol. 2000 Jun;14(3):467-94 [10962637.001]
  • [Cites] Cochrane Database Syst Rev. 2000;(4):CD000387 [11034686.001]
  • [Cites] J Am Board Fam Pract. 2001 Mar-Apr;14(2):95-106 [11314930.001]
  • [Cites] Int J Gynaecol Obstet. 2001 Sep;74 Suppl 1:S15-20 [11549395.001]
  • [Cites] Obstet Gynecol Surv. 2001 Dec;56(12):757-64 [11753178.001]
  • [Cites] J Obstet Gynaecol Can. 2002 Jan;24(1):37-61; quiz 74-6 [12196887.001]
  • [Cites] Fertil Steril. 2002 Nov;78(5):961-72 [12413979.001]
  • [Cites] Obstet Gynecol. 2003 Mar;101(3):594-611 [12636968.001]
  • [Cites] Obstet Gynecol Clin North Am. 2003 Mar;30(1):133-50 [12699262.001]
  • [Cites] J Urol. 2003 Sep;170(3):807-9 [12913704.001]
  • [Cites] Obstet Gynecol Surv. 2003 Sep;58(9):615-23 [12972837.001]
  • [Cites] J Fam Pract. 2003 Dec;52(12):942-50 [14653980.001]
  • [Cites] Obstet Gynecol. 2004 Mar;103(3):589-605 [14990428.001]
  • [Cites] J Reprod Med. 2004 Mar;49(3 Suppl):230-4 [15088861.001]
  • [Cites] Obstet Gynecol. 1991 May;77(5):740-4 [1826544.001]
  • [Cites] Br J Obstet Gynaecol. 1992 Jan;99(1):59-62 [1547175.001]
  • [Cites] Urology. 1997 May;49(5A Suppl):58-63 [9146003.001]
  • [Cites] J Gen Intern Med. 1997 Jul;12(7):439-45 [9229283.001]
  • [Cites] Clin Obstet Gynecol. 1997 Sep;40(3):554-63 [9328736.001]
  • [Cites] Obstet Gynecol. 2003 Aug;102(2):397-408 [12907119.001]
  • (PMID = 17279236.001).
  • [ISSN] 1715-5258
  • [Journal-full-title] Canadian family physician Médecin de famille canadien
  • [ISO-abbreviation] Can Fam Physician
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Canada
  • [Other-IDs] NLM/ PMC1783755
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86. Bourré L, Giuntini F, Eggleston IM, Mosse CA, Macrobert AJ, Wilson M: Effective photoinactivation of Gram-positive and Gram-negative bacterial strains using an HIV-1 Tat peptide-porphyrin conjugate. Photochem Photobiol Sci; 2010 Dec;9(12):1613-20
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  • Given that cell-penetrating peptides (CPP) are cationic and often amphipathic, similar to membrane-active antimicrobial peptides, it may be possible to use CPP conjugation to improve the delivery of photosensitisers for antimicrobial photodynamic therapy (antimicrobial PDT).
  • Using the highest light dose, treatment with the Tat-porphyrin achieved reductions of 6.6 log(10) and 6.37 log(10) in the viable counts of Staphylococcus aureus and Streptococcus pyogenes, and reductions of 5.74 log(10) and 6.6 log(10) in the viable counts of Pseudomonas aeruginosa and Escherichia coli.
  • These findings demonstrate that the use of CPP to deliver a photosensitiser is an effective way of improving the uptake and the treatment efficacy of antimicrobial PDT.
  • [MeSH-major] Gram-Negative Bacteria / drug effects. Gram-Positive Bacteria / drug effects. Peptides / chemistry. Photosensitizing Agents / chemistry. Porphyrins / chemistry. tat Gene Products, Human Immunodeficiency Virus / chemistry
  • [MeSH-minor] Amino Acid Sequence. Antimicrobial Cationic Peptides / pharmacology. Escherichia coli / drug effects. Pseudomonas aeruginosa / drug effects. Spectrometry, Fluorescence. Staphylococcus aureus / drug effects. Streptococcus pyogenes / drug effects

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  • (PMID = 20931134.001).
  • [ISSN] 1474-9092
  • [Journal-full-title] Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology
  • [ISO-abbreviation] Photochem. Photobiol. Sci.
  • [Language] eng
  • [Grant] United Kingdom / Biotechnology and Biological Sciences Research Council / / BB/D011329/1; United Kingdom / Biotechnology and Biological Sciences Research Council / / BBD0113291; United Kingdom / Biotechnology and Biological Sciences Research Council / / BBD0127831
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Antimicrobial Cationic Peptides; 0 / Peptides; 0 / Photosensitizing Agents; 0 / Porphyrins; 0 / tat Gene Products, Human Immunodeficiency Virus
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87. Johnston AJ, Steiner LA, O'Connell M, Chatfield DA, Gupta AK, Menon DK: Pharmacokinetics and pharmacodynamics of dopamine and norepinephrine in critically ill head-injured patients. Intensive Care Med; 2004 Jan;30(1):45-50
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  • PATIENTS: Eight patients with a head injury, requiring dopamine or norepinephrine infusions to support cerebral perfusion pressure (CPP).
  • INTERVENTION: Patients received in randomised order, either dopamine or norepinephrine to achieve and maintain a CPP of 70 mmHg, and then, following a 30-min period of stable haemodynamics, a CPP of 90 mmHg.
  • However, there was a significant quadratic relationship between the infusion rate of dopamine and cardiac index (r2=0.431), and systemic vascular resistance index (r2=0.605), with a breakpoint (at which cardiac index reduced and SVRI increased) at a dopamine plasma level of approximately 50 nM/l (corresponding to an infusion rate of approximately 15 microg.kg(-1).min(-1)).
  • [MeSH-major] Craniocerebral Trauma / drug therapy. Dopamine. Norepinephrine. Vasoconstrictor Agents
  • [MeSH-minor] Adult. Cardiotonic Agents / metabolism. Cardiotonic Agents / pharmacokinetics. Cardiotonic Agents / pharmacology. Catecholamines / blood. Critical Illness / therapy. Cross-Over Studies. Dose-Response Relationship, Drug. Drug Monitoring. Female. Heart Rate / drug effects. Humans. Infusions, Intravenous. Intracranial Pressure / drug effects. Linear Models. Male. Metabolic Clearance Rate. Middle Aged. Prospective Studies. Vascular Resistance / drug effects

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  • [Cites] Eur J Clin Pharmacol. 1984;26(2):163-9 [6723754.001]
  • [Cites] Am J Med Genet. 2001 Jul 8;105(5):464-70 [11449400.001]
  • [Cites] Clin Exp Pharmacol Physiol. 1990 May;17(5):361-9 [2354553.001]
  • [Cites] Am J Hum Genet. 2001 Feb;68(2):515-22 [11170900.001]
  • [Cites] Crit Care Med. 2000 May;28(5):1353-62 [10834678.001]
  • [Cites] Hum Genet. 2002 Dec;111(6):521-37 [12436243.001]
  • [Cites] Intensive Care Med. 1998 Jun;24(6):564-8 [9681777.001]
  • [Cites] Br J Pharmacol. 1991 Apr;102(4):831-6 [1713108.001]
  • [Cites] Crit Care Med. 2001 Jul;29(7 Suppl):S117-20 [11445745.001]
  • [Cites] Crit Care Med. 1993 Nov;21(11):1652-7 [8222680.001]
  • [Cites] Intensive Care Med. 1997 Jan;23(1):31-7 [9037637.001]
  • [Cites] Am J Med Genet. 1997 Jul 25;74(4):439-42 [9259381.001]
  • [Cites] Anesthesiology. 2000 Feb;92(2):338-46 [10691218.001]
  • [Cites] Eur J Pharmacol. 2000 Feb 11;389(1):1-12 [10686290.001]
  • [Cites] J Chromatogr. 1982 Aug 13;231(1):25-39 [7119063.001]
  • [Cites] Crit Care Med. 1988 Mar;16(3):217-20 [3342635.001]
  • [Cites] J Pharmacol Exp Ther. 1989 Apr;249(1):131-3 [2709327.001]
  • [Cites] Intensive Care Med. 1998 Nov;24(11):1217-20 [9876986.001]
  • [Cites] Int J Clin Monit Comput. 1994 Nov;11(4):223-32 [7738416.001]
  • [Cites] Intensive Care Med. 2002 May;28(5):547-53 [12029400.001]
  • [Cites] Am J Med Genet. 2002 Jul 8;114(5):491-6 [12116182.001]
  • [Cites] J Pediatr. 1990 Sep;117(3):472-6 [2391608.001]
  • [Cites] Crit Care Med. 1984 Jan;12(1):22-5 [6690200.001]
  • [Cites] Crit Care Med. 1991 Aug;19(8):1008-11 [1860323.001]
  • [Cites] Acta Anaesthesiol Scand. 1981 Aug;25(4):328-31 [7315181.001]
  • [Cites] Crit Care Med. 2001 Aug;29(8):1526-31 [11505120.001]
  • [Cites] Hum Genet. 1998 Sep;103(3):273-9 [9799080.001]
  • [Cites] Am J Med Genet. 2002 Mar 8;114(2):154-8 [11857576.001]
  • [Cites] Crit Care Med. 1989 Nov;17(11):1166-9 [2791595.001]
  • [Cites] Br J Anaesth. 1995 Apr;74(4):419-23 [7734262.001]
  • (PMID = 14586494.001).
  • [ISSN] 0342-4642
  • [Journal-full-title] Intensive care medicine
  • [ISO-abbreviation] Intensive Care Med
  • [Language] eng
  • [Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Cardiotonic Agents; 0 / Catecholamines; 0 / Vasoconstrictor Agents; VTD58H1Z2X / Dopamine; X4W3ENH1CV / Norepinephrine
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88. Schulz D, Buddenberg T, Huston JP: Extinction-induced "despair" in the water maze, exploratory behavior and fear: effects of chronic antidepressant treatment. Neurobiol Learn Mem; 2007 May;87(4):624-34
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Extinction-induced "despair" in the water maze, exploratory behavior and fear: effects of chronic antidepressant treatment.
  • Specifically, the removal of a hidden platform in the water maze induced extinction of previously reinforced escape behavior and behavioral immobility, indicative of "despair", which also correlated with indices of fear.
  • Here, we tested the effects of antidepressants on extinction in the water maze, and expected that such drugs would attenuate the rate of extinction of a conditioned place preference (CPP) and also any emotionally relevant behavior that is induced by the loss of reinforcement, such as immobility.
  • Daily treatment with desipramine hydrochloride (DMI, 10mg/kg) or fluoxetine (FLX, 10 mg/kg) commenced 1 day before the first of 11 extinction trials without the platform, administered 48 h apart, and continued thereafter, as the rats were tested in an open field and elevated-plus maze.
  • As compared to controls, DMI increased the resistance-to-extinction of CPP, attenuated immobility, and increased wall climbing behavior.
  • [MeSH-major] Antidepressive Agents / pharmacology. Exploratory Behavior / drug effects. Extinction, Psychological / physiology. Fear / drug effects. Maze Learning / drug effects
  • [MeSH-minor] Affect. Animals. Conditioning, Classical / drug effects. Conditioning, Classical / physiology. Depressive Disorder / drug therapy. Desipramine / pharmacology. Disease Models, Animal. Drug Administration Schedule. Escape Reaction. Fluoxetine / pharmacology. Immobility Response, Tonic / drug effects. Immobility Response, Tonic / physiology. Male. Rats. Rats, Wistar. Statistics, Nonparametric

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  • (PMID = 17223365.001).
  • [ISSN] 1074-7427
  • [Journal-full-title] Neurobiology of learning and memory
  • [ISO-abbreviation] Neurobiol Learn Mem
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Validation Studies
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antidepressive Agents; 01K63SUP8D / Fluoxetine; TG537D343B / Desipramine
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89. Jacka MJ, Zygun D: Survey of management of severe head injury in Canada. Can J Neurol Sci; 2007 Aug;34(3):307-12
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: To determine: 1. the degrees of consensus and disagreement among Canadian critical care clinicians regarding the appropriateness (benefit exceeding risk) of common therapeutic manoeuvres in patients with severe closed head injury (CHI), and 2. the frequency with which clinicians employed these manoeuvres.
  • In a scenario of diffuse axonal injury (DAI), clinicians agreed strongly that fever reduction, early enteral feeding, intensive glucose control, and cerebral perfusion pressure (CPP)-directed management were appropriate.
  • The appropriateness ratings of the interventions considered in the scenario of an intracranial contusion mirrored the DAI scenario.
  • The correlation between CPP-guided therapy and the use of the EVD was weak.
  • CONCLUSIONS: This survey has described current practice with regard to treatment of patients with severe CHI.
  • Suggested priorities for evaluation include the use of osmotic diuretics, anticonvulsants, and intracranial manometry.
  • [MeSH-major] Brain Injuries / therapy. Critical Care / methods. Head Injuries, Closed / therapy. Health Care Surveys. Neurology / methods. Neurosurgery / methods. Practice Patterns, Physicians' / statistics & numerical data
  • [MeSH-minor] Adult. Anticonvulsants / therapeutic use. Canada / epidemiology. Diffuse Axonal Injury / drug therapy. Diffuse Axonal Injury / physiopathology. Diuretics, Osmotic / therapeutic use. Female. Hematoma, Epidural, Cranial / drug therapy. Hematoma, Epidural, Cranial / physiopathology. Hematoma, Epidural, Cranial / surgery. Humans. Hypothermia, Induced / utilization. Intensive Care Units. Intracranial Hypertension / diagnosis. Intracranial Hypertension / prevention & control. Intracranial Hypertension / therapy. Male. Malnutrition / prevention & control. Malnutrition / therapy. Middle Aged. Risk Assessment

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  • (PMID = 17803027.001).
  • [ISSN] 0317-1671
  • [Journal-full-title] The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques
  • [ISO-abbreviation] Can J Neurol Sci
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Canada
  • [Chemical-registry-number] 0 / Anticonvulsants; 0 / Diuretics, Osmotic
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90. Lamvu G, Williams R, Zolnoun D, Wechter ME, Shortliffe A, Fulton G, Steege JF: Long-term outcomes after surgical and nonsurgical management of chronic pelvic pain: one year after evaluation in a pelvic pain specialty clinic. Am J Obstet Gynecol; 2006 Aug;195(2):591-8; discussion 598-600
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • OBJECTIVE: The purpose of this study was to describe long-term outcomes for women with chronic pelvic pain (CPP) after evaluation in a CPP specialty clinic.
  • STUDY DESIGN: This was a prospective observational cohort study of women treated for CPP at the UNC Pelvic Pain clinic between 1993 and 2000.
  • The primary outcome was improvement in pain and the main exposure was treatment group: primarily medical (pharmacotherapy, psychotherapy, physical therapy, or combinations of the 3) or surgical (hysterectomy, resection or ablative procedures, oophrectomy, diagnostic surgery, pain mapping, vulvar or vestibular repair).
  • Univariate, bivariate, and multivariable analyses were performed to look for relationships between background characteristics, treatment group, and improvement in pain.
  • RESULTS: Of 370 participants; 189 had surgical treatment and 181 had medical treatment.
  • Improvement in pain was similar in both treatment groups and odds of improvement were equal even after adjusting for background characteristics, psychosocial comorbidity, and previous treatments.
  • CONCLUSION: One year after evaluation in a CPP specialty clinic, women experienced modest improvements in pain and depression after recommended surgical or nonsurgical treatment.
  • [MeSH-minor] Adolescent. Adult. Aged. Chronic Disease. Comorbidity. Depression / etiology. Female. Follow-Up Studies. Humans. Logistic Models. Middle Aged. Multivariate Analysis. Pain Measurement. Prospective Studies. Sex Offenses. Treatment Outcome

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  • (PMID = 16729951.001).
  • [ISSN] 1097-6868
  • [Journal-full-title] American journal of obstetrics and gynecology
  • [ISO-abbreviation] Am. J. Obstet. Gynecol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
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91. Meybohm P, Cavus E, Bein B, Steinfath M, Weber B, Hamann C, Scholz J, Dörges V: Small volume resuscitation: a randomized controlled trial with either norepinephrine or vasopressin during severe hemorrhage. J Trauma; 2007 Mar;62(3):640-6
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  • BACKGROUND: The present study was designed to evaluate the effects of hypertonic-hyperoncotic hydroxyethyl starch solution (HHS) combined with either norepinephrine (NE) or arginine vasopressin (AVP) on cerebral perfusion pressure (CPP) and brain metabolism after hemorrhagic shock.
  • After 30 minutes of therapy, bleeding was controlled by manual compression and all surviving animals were observed for 1 hour.
  • RESULTS: After hemodynamic decompensation, AVP resulted in a significantly higher increase of CPP (mean +/- SD; 47 +/- 19 versus 28 +/- 9 mm Hg; p < 0.01) and cerebral venous partial pressure of oxygen (66 +/- 8 versus 49 +/- 9 mm Hg; p < 0.05) compared with NE after 10 minutes of therapy.
  • Brain metabolism was found comparable in both groups at any time.
  • CONCLUSIONS: AVP was comparable to NE with respect to hemodynamics and blood gases, as well as brain metabolism in surviving animals throughout the study period.
  • [MeSH-major] Hydroxyethyl Starch Derivatives / therapeutic use. Norepinephrine / therapeutic use. Plasma Substitutes / therapeutic use. Resuscitation / methods. Shock, Hemorrhagic / therapy. Vasoconstrictor Agents / therapeutic use. Vasopressins / therapeutic use
  • [MeSH-minor] Animals. Blood Pressure / drug effects. Brain / metabolism. Cardiac Output / drug effects. Cerebrovascular Circulation / drug effects. Microdialysis. Oxygen / blood. Sus scrofa

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  • Hazardous Substances Data Bank. VASOPRESSIN .
  • Hazardous Substances Data Bank. Norepinephrine .
  • Hazardous Substances Data Bank. OXYGEN .
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  • (PMID = 17414341.001).
  • [ISSN] 0022-5282
  • [Journal-full-title] The Journal of trauma
  • [ISO-abbreviation] J Trauma
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Hydroxyethyl Starch Derivatives; 0 / Plasma Substitutes; 0 / Vasoconstrictor Agents; 11000-17-2 / Vasopressins; S88TT14065 / Oxygen; X4W3ENH1CV / Norepinephrine
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92. Krstevska-Konstantinova M, Jancevska A, Gucev Z: Autoimmune thyroiditis and diabetes mellitus type 1 after long-term gonadotropin-releasing hormone agonist treatment for central precocious puberty: evolution or coincidence? J Pediatr Endocrinol Metab; 2010 Apr;23(4):403-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Autoimmune thyroiditis and diabetes mellitus type 1 after long-term gonadotropin-releasing hormone agonist treatment for central precocious puberty: evolution or coincidence?
  • Very few abnormalities in endocrine function have been reported during long term gonadotropin-releasing hormone agonist (GnRHa) treatment in girls.
  • Most authors agree that this therapy is safe and effective.
  • We present an unusual outcome of long term GnRHa therapy in two girls with central precocious puberty(CPP) of idiopathic or organic origin.
  • They have received monthly depot injections of triptorelin acetate for a time period of 8 years.
  • Another girl with a hypothalamic hamartoma developed diabetes mellitus at the age of 9 years.
  • Both of these girls were early diagnosed for CPP, at 6 months and 8 months respectively, and given GnRHa treatment.
  • So far, it is not known whether these autoimmune diseases are related to the GnRHa treatment or are simply a coincidence.
  • However, we suggest a closer monitoring of girls with CPP who have had a long period of treatment.
  • [MeSH-major] Diabetes Mellitus, Type 1 / etiology. Puberty, Precocious / drug therapy. Thyroiditis, Autoimmune / etiology. Triptorelin Pamoate / therapeutic use
  • [MeSH-minor] Child. Female. Hamartoma / complications. Hamartoma / drug therapy. Humans. Luteolytic Agents / therapeutic use. Pituitary Diseases / complications. Pituitary Diseases / drug therapy