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1. Machet L, De Muret A, Wiezberka E, Bernez A, Abdallah-Lotf M, Linassier C, Petrella T: [Agranular CD4+ CD56+ CD123+ hematodermic neoplasm (blastic NK-cell lymphoma) revealed by cutaneous localization: 2 cases]. Ann Dermatol Venereol; 2004 Nov;131(11):969-73
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  • [Title] [Agranular CD4+ CD56+ CD123+ hematodermic neoplasm (blastic NK-cell lymphoma) revealed by cutaneous localization: 2 cases].
  • BACKGROUND: Agranular CD4+ CD56+ hematodermic neoplasm (blastic NK-cell lymphoma) has been recently described.
  • Preliminary histological examination of cutaneous biopsy taken in both patients showed a malignant proliferation suggesting a cutaneous lymphoma, and the patients were referred.
  • Histological examination of new biopsies showed a very similar proliferation in the 2 cases of monotonous medium-sized mononuclear cells without expression of the common antigens CD3 and CD20 and the expression of CD4, CD56, and CD123.
  • No rearrangement of the T-cell receptor gene or the immunoglobulin heavy chain gene were evidenced.
  • Thrombocytopenia associated with the abnormal presence of 15 p. 100 of circulating CD4+ CD56+ cells was initially found in the second patient.
  • The first patient was treated with chemotherapy, with complete remission.
  • The patient died one year after the diagnosis of the disease, in spite of intensification of the treatment.
  • Treatment is still ongoing in the second patient.
  • COMMENTS: The histological presentation of these two patients was very similar with an unusual phenotype of tumor cells expressing CD4, CD56, CD123, but not expressing CD3 and CD20.
  • Some cases have been published under the "term of blastic NK lymphoma" which is the actual term for the disease in the WHO classification.
  • However, the tumor cells derive from the dendritic plasmacytoid cells, also called type 2 dendritic cells, and perhaps from a common precursor to lymphocyte T and dendritic plasmacytoid cells.
  • [MeSH-major] Antigens, CD4 / analysis. Antigens, CD56 / analysis. Killer Cells, Natural. Lymphoma, Non-Hodgkin / immunology. Lymphoma, Non-Hodgkin / pathology. Receptors, Interleukin-3 / analysis. Skin Neoplasms / immunology. Skin Neoplasms / pathology
  • [MeSH-minor] Aged. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Fatal Outcome. Humans. Interleukin-3 Receptor alpha Subunit. Male. Phenotype

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  • (PMID = 15602384.001).
  • [ISSN] 0151-9638
  • [Journal-full-title] Annales de dermatologie et de vénéréologie
  • [ISO-abbreviation] Ann Dermatol Venereol
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antigens, CD4; 0 / Antigens, CD56; 0 / IL3RA protein, human; 0 / Interleukin-3 Receptor alpha Subunit; 0 / Receptors, Interleukin-3
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2. Landolsi A, Chabchoub I, Limem S, Gharbi O, Chaafai R, Hochlef M, Fatma LB, Trimech M, Krifa A, Ajmi S, Mokni M, Hadj Hmida MB, Ahmed SB: [Primary digestive tract lymphoma in central region of Tunisia: anatomoclinical study and therapeutic results about 153 cases]. Bull Cancer; 2010 Apr;97(4):435-43
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  • [Title] [Primary digestive tract lymphoma in central region of Tunisia: anatomoclinical study and therapeutic results about 153 cases].
  • [Transliterated title] Les lymphomes primitifs du tube digestif (LPTD) dans le centre tunisien: étude anatomoclinique et résultats thérapeutiques à propos de 153 cas.
  • Primary gastro-intestinal lymphoma (PGIL) is the most common type of extra-nodal non Hodgkin's lymphoma.
  • Their clinical and histological presentations are heterogeneous depending on the site of the lesion.
  • There is no consensus regarding the role of surgery and chemotherapy in the therapeutic approach.
  • In our country epidemiology of the disease is unknown with IPSID being the most frequent type.
  • We report anatomo-clinical features and prognostic factors of PGIL and compare intestinal to gastric forms in our region.
  • The median age was 52 years and the sex-ratio 2.1.
  • Tumor sites were gastric (67%), intestinal (26%) and gastrointestinal (7%).
  • Abdominal pain (87%) followed by vomiting and diarrhoea (37 and 15%) were the most common symptoms.
  • Performance status (PS) < 2 was seen in 80% of patients, high grade lymphoma in 70.5% of cases and B phenotype was noted in 85%.
  • MALT lymphoma accounts for 50% of cases, and IPSID for only 5% of PGIL.
  • About 47.5% of cases were stage IE, 138 patients had chemotherapy with an objective response rate of 77%.
  • Only 46% of patients had surgery (14 for surgical complication, 6 for residual tumor after chemotherapy and 22 to have histological diagnosis).
  • In high grade lymphoma patients favorable prognostic factors for OS included young age < or = 60 years, PS < 2, normal serum LDH, hemoglobin > 12 g/dL, B phenotype, localised stage (IE-IIE1), anthracycline-based chemotherapy regimen, achieving complete or partial response to induction chemotherapy and no relapse.
  • In low-grade lymphoma patients, none of these factors had a significant correlation with OS: age < or = 60 years, PS < 2, stage (IE-IIE1), response to induction chemotherapy, relapse.
  • Compared to gastric lymphomas, intestinal cases occurred at a younger age, frequently with diarrhoea, weight loss, and occlusion.
  • They are more often high-grade, T phenotype and have locally advanced stage (IIE); surgery is more common in this group.
  • We conclude that stomach is the main site of PGIL in our region, intestinal lymphoma is less frequent and IPSID has become rare.
  • Recent progress in chemotherapy has allowed good therapeutic results with a conservative approach.
  • Surgery may be performed in case of emergency or for residual lesions after medical treatment.
  • [MeSH-major] Gastrointestinal Neoplasms. Lymphoma, Non-Hodgkin
  • [MeSH-minor] Abdominal Pain / etiology. Adolescent. Adult. Aged. Aged, 80 and over. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Diarrhea / etiology. Female. Humans. Male. Middle Aged. Prognosis. Retrospective Studies. Tunisia. Vomiting / etiology. Young Adult

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  • (PMID = 20395189.001).
  • [ISSN] 1769-6917
  • [Journal-full-title] Bulletin du cancer
  • [ISO-abbreviation] Bull Cancer
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
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3. Dutta U, Udawat H, Noor MT, Sidhu GS, Kochhar R, Vaiphei K, Singh K: Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori. J Gastrointest Cancer; 2010 Sep;41(3):212-5
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  • [Title] Regression of immunoproliferative small intestinal disease after eradication of Helicobacter pylori.
  • A 20-year-old male presented with low-grade fever, abdominal pain, anorexia, and weight loss of 4-month duration.
  • Contrast-enhanced computed tomography of the abdomen revealed extensive proximal small-bowel thickening with mesenteric lymphadenopathy.
  • Upper gastrointestinal endoscopy and enteroscopy revealed thickening of folds with multiple small superficial ulceration involving antrum, duodenum, and jejunum.
  • The duodenal and jejunal biopsy was suggestive of immunoproliferative small intestinal disease, stage 0 (Salem) or stage A (Galian).
  • He underwent H. pylori eradication following which he had significant clinical improvement; repeat evaluation at 6 months showed dramatic improvement in his clinical, radiological, and histological parameters.
  • [MeSH-major] Anti-Bacterial Agents / therapeutic use. Helicobacter Infections / complications. Immunoproliferative Small Intestinal Disease / drug therapy. Immunoproliferative Small Intestinal Disease / microbiology
  • [MeSH-minor] 2-Pyridinylmethylsulfinylbenzimidazoles / therapeutic use. Amoxicillin / therapeutic use. Clarithromycin / therapeutic use. Doxycycline / therapeutic use. Drug Therapy, Combination. Helicobacter pylori. Humans. Lansoprazole. Male. Omeprazole / therapeutic use. Organometallic Compounds / therapeutic use. Tinidazole / therapeutic use. Young Adult

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  • (PMID = 20300878.001).
  • [ISSN] 1941-6636
  • [Journal-full-title] Journal of gastrointestinal cancer
  • [ISO-abbreviation] J Gastrointest Cancer
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / 2-Pyridinylmethylsulfinylbenzimidazoles; 0 / Anti-Bacterial Agents; 0 / Organometallic Compounds; 033KF7V46H / Tinidazole; 0K5C5T2QPG / Lansoprazole; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; HS813P8QPX / bismuth tripotassium dicitrate; KG60484QX9 / Omeprazole; N12000U13O / Doxycycline
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4. Iemitsu M, Shimojo N, Maeda S, Irukayama-Tomobe Y, Sakai S, Ohkubo T, Tanaka Y, Miyauchi T: The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations. Am J Physiol Heart Circ Physiol; 2008 Jul;295(1):H136-44
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  • [Title] The benefit of medium-chain triglyceride therapy on the cardiac function of SHRs is associated with a reversal of metabolic and signaling alterations.
  • The spontaneously hypertensive rat (SHR) is a model of cardiomyopathy that displays a genetic defect in cardiac fatty acid (FA) translocase/CD36, a plasma membrane long-chain FA transporter.
  • Therapy with medium-chain FAs, which do not require CD36-facilitated transport, has been shown to improve cardiac function and hypertrophy in SHRs despite persistent hypertension.
  • However, little is known about the underlying molecular mechanisms.
  • The aim of this study was to document the impact of medium-chain triglyceride (MCT) therapy in SHRs on the expression level and activity of metabolic enzymes and signaling pathways.
  • Four-week-old male SHRs were administered MCT (SHR-MCT) or long-chain triglyceride (SHR-LCT) for 16 wk.
  • The SHR-MCT group displayed improved cardiac dysfunction [as assessed by left ventricular (LV) end-diastolic pressure and the positive and negative first derivatives of LV pressure/P value], a shift in the beta-myosin heavy chain (MHC)-to-alpha-MHC ratio, and cardiac hypertrophy compared with the SHR-LCT group without an effect on blood pressure.
  • Administration of MCT of SHRs reversed the LCT-induced reduction in the cardiac FA metabolic enzymatic activities of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD) and medium-chain acyl-CoA dehydrogenase (MCAD).
  • In the SHR-MCT group, the protein expression and transcriptional regulation of myocardial peroxisome proliferator-activated receptor-alpha, which regulates the transcription of LCHAD and MCAD genes, corresponded to the changes seen in those enzymatic activities.
  • Collectively, the observed changes in the myocardial activity of metabolic enzymes and signaling pathways may contribute to the improved cardiac dysfunction and hypertrophy in SHRs following MCT therapy.
  • [MeSH-major] Cardiomegaly / prevention & control. Energy Metabolism / drug effects. Hypertension / drug therapy. Myocardium / metabolism. Signal Transduction / drug effects. Triglycerides / pharmacology. Ventricular Dysfunction, Left / prevention & control
  • [MeSH-minor] 3-Hydroxyacyl CoA Dehydrogenases / metabolism. Acyl-CoA Dehydrogenase / metabolism. Animals. Antigens, CD36 / metabolism. Blood Pressure / drug effects. Disease Models, Animal. JNK Mitogen-Activated Protein Kinases / antagonists & inhibitors. JNK Mitogen-Activated Protein Kinases / metabolism. Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase. Male. Myosin Heavy Chains / metabolism. PPAR alpha / metabolism. Phosphorylation. RNA, Messenger / metabolism. Rats. Rats, Inbred SHR. Rats, Inbred WKY. Time Factors. Transcription, Genetic. Ventricular Myosins / metabolism. Ventricular Pressure / drug effects

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  • (PMID = 18456726.001).
  • [ISSN] 0363-6135
  • [Journal-full-title] American journal of physiology. Heart and circulatory physiology
  • [ISO-abbreviation] Am. J. Physiol. Heart Circ. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antigens, CD36; 0 / Bmyo protein, rat; 0 / Cd36 protein, rat; 0 / PPAR alpha; 0 / RNA, Messenger; 0 / Triglycerides; EC 1.1.1.- / 3-Hydroxyacyl CoA Dehydrogenases; EC 1.1.1.211 / Long-Chain-3-Hydroxyacyl-CoA Dehydrogenase; EC 1.3.8.7 / Acyl-CoA Dehydrogenase; EC 2.7.11.24 / JNK Mitogen-Activated Protein Kinases; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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5. Tanaka M, Nakae S, Terry RD, Mokhtari GK, Gunawan F, Balsam LB, Kaneda H, Kofidis T, Tsao PS, Robbins RC: Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease. Blood; 2004 Dec 1;104(12):3789-96
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  • [Title] Cardiomyocyte-specific Bcl-2 overexpression attenuates ischemia-reperfusion injury, immune response during acute rejection, and graft coronary artery disease.
  • This damage ultimately leads to the development of graft coronary artery disease (GCAD), which limits long-term graft survival.
  • To assess the role of the antiapoptotic factor Bcl-2 in the process of GCAD, we transplanted hearts from FVB transgenic mice overexpressing human Bcl-2 under the control of alpha-myosin heavy chain promoter into allogenic C57BL/6 mice.
  • Bcl-2 overexpression led to reduced cytochrome c-mediated caspase-9-dependent cardiomyocyte apoptosis and local inflammation (neutrophil infiltration and proinflammatory cytokine production) in cardiac allografts during ischemia-reperfusion injury and also led to reduced immune responses (inflammatory cell infiltration, production of T(H)1 cytokines and chemokines, and expression of adhesion molecules) during acute and chronic rejection without affecting host CD4(+) and CD8(+) cell responses in the spleen.
  • In conclusion, our findings suggest that the modulation of Bcl-2 expression by pharmacologic up-regulation or gene transfer may be of clinical benefit in the short- and long-term function of cardiac allografts.
  • [MeSH-major] Graft Rejection / prevention & control. Heart Transplantation / adverse effects. Myocytes, Cardiac / metabolism. Proto-Oncogene Proteins c-bcl-2 / pharmacology. Reperfusion Injury / therapy
  • [MeSH-minor] Animals. Apoptosis / drug effects. Coronary Artery Disease / etiology. Coronary Artery Disease / prevention & control. Coronary Artery Disease / therapy. Genetic Vectors. Humans. Immunity / drug effects. Inflammation / drug therapy. Male. Mice. Mice, Transgenic


6. Li B, Liao YH, Cheng X, Ge H, Guo H, Wang M: Effects of carvedilol on cardiac cytokines expression and remodeling in rat with acute myocardial infarction. Int J Cardiol; 2006 Aug 10;111(2):247-55
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  • METHODS: Rats with AMI induced by left anterior descending branch ligation were randomized to carvedilol and control group which were further compared to sham-operated group.
  • We studied the effects of 4-weeks therapy with carvedilol starting 24 h after infarction on 1) hemodynamics, 2) tissue weights, 3) myocardial cytokines (TNF-alpha, IL-1beta, IL-6, IL-10 and TGF-beta1) expression by semi-quantitative RT-PCR and immunoblotting, 4) matrix metalloproteinases activity by gelatin zymography, 5) collagen expression by immunohistochemistry, 6) myocardium fetal gene (alpha and beta myosin heavy chain) expression.
  • RESULTS: Treatment with carvedilol 1) reduced the pro-inflammatory cytokines and fibrogenic cytokine TGF-beta1 levels in myocardium and was associated with the amelioration of the elevated left ventricular diastolic pressure.
  • 2) increased anti-inflammatory cytokine, IL-10 protein expression.
  • 3) reduced matrix metalloproteinases-2 and matrix metalloproteinases-9 activity 4) reduced myocardial collagens 5) did not modify fetal gene re-expression.
  • One mechanism underlying the beneficial effects of carvedilol on post-infarction myocardial remodeling may be modulation of the balance between pro- and anti-inflammatory cytokines as well as fibrogenic cytokines and extracellular matrix (ECM) remodeling.
  • [MeSH-major] Carbazoles / pharmacology. Cytokines / blood. Myocardial Infarction / blood. Propanolamines / pharmacology. Vasodilator Agents / pharmacology
  • [MeSH-minor] Animals. Disease Models, Animal. Heart / drug effects. Heart / physiopathology. Interleukin-10 / blood. Interleukin-1beta / blood. Interleukin-6 / blood. Male. Rats. Rats, Wistar. Transforming Growth Factor beta / blood. Tumor Necrosis Factor-alpha / blood

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  • (PMID = 16310260.001).
  • [ISSN] 0167-5273
  • [Journal-full-title] International journal of cardiology
  • [ISO-abbreviation] Int. J. Cardiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Ireland
  • [Chemical-registry-number] 0 / Carbazoles; 0 / Cytokines; 0 / Interleukin-1beta; 0 / Interleukin-6; 0 / Propanolamines; 0 / Transforming Growth Factor beta; 0 / Tumor Necrosis Factor-alpha; 0 / Vasodilator Agents; 0K47UL67F2 / carvedilol; 130068-27-8 / Interleukin-10
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7. Hainsey T, Csiszar A, Sun S, Edwards JG: Cyclosporin A does not block exercise-induced cardiac hypertrophy. Med Sci Sports Exerc; 2002 Aug;34(8):1249-54
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Cyclosporin A does not block exercise-induced cardiac hypertrophy.
  • It is unclear what impact CsA may have on the myocardial response to exercise, a physiological model of overload.
  • PURPOSE: The purpose of the study was to determine whether CsA would alter exercise-induced cardiac hypertrophy.
  • METHODS: Thirty male rats were assigned to vehicle or CsA injection (15 mg.kg.d(-1)) and then assigned to sedentary or exercise training.
  • Animals were swum for 60 min.d(-1) for 1 wk.
  • RESULTS: One week of swim training significantly increased plantaris cytochrome oxidase activity, as well as significantly increasing left ventricular (LV) weight and the left ventricular:body weight (LV/BW) ratio.
  • Exercise did not alter right ventricular (RV) weight or the RV/BW ratio.
  • RNA analysis found that exercise significantly increased atrial natriuretic factor (ANF)-mRNA levels but did not influence alpha-myosin heavy chain (MHC) expression.
  • CsA treatment, but not exercise, was associated with a significant increase in betaMHC expression.
  • Western blot analysis determined that betaMHC protein was also significantly increased in the CsA-treated animals.
  • CONCLUSION: CsA did not block exercise-induced cardiac hypertrophy but did significantly influence the myocardial phenotype.
  • The CsA-sensitive calcium dependent pathways, important for pathological forms of overload-induced hypertrophy, were not essential to the early adaptations to exercise and that a different mechanism or signal transduction pathway was engaged.
  • The data also indicate that CsA alone may induce a shift in the MHC isoform expression toward that associated with a pathological phenotype.
  • Whether this phenotype shift contributes to the lowered exercise capacity found in transplant patients remains to be determined.

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  • (PMID = 12165678.001).
  • [ISSN] 0195-9131
  • [Journal-full-title] Medicine and science in sports and exercise
  • [ISO-abbreviation] Med Sci Sports Exerc
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R29 HL059417; United States / NHLBI NIH HHS / HL / P01 HL 43023; United States / NHLBI NIH HHS / HL / R29 HL 59417
  • [Publication-type] Comparative Study; Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 83HN0GTJ6D / Cyclosporine; EC 1.9.3.1 / Electron Transport Complex IV
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8. Lombardi R, Rodriguez G, Chen SN, Ripplinger CM, Li W, Chen J, Willerson JT, Betocchi S, Wickline SA, Efimov IR, Marian AJ: Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms. Circulation; 2009 Mar 17;119(10):1398-407
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  • [Title] Resolution of established cardiac hypertrophy and fibrosis and prevention of systolic dysfunction in a transgenic rabbit model of human cardiomyopathy through thiol-sensitive mechanisms.
  • BACKGROUND: Cardiac hypertrophy, the clinical hallmark of hypertrophic cardiomyopathy (HCM), is a major determinant of morbidity and mortality not only in HCM but also in a number of cardiovascular diseases.
  • There is no effective therapy for HCM and generally for cardiac hypertrophy.
  • We posit that treatment with N-acetylcysteine, a precursor of glutathione, the largest intracellular thiol pool against oxidative stress, could reverse cardiac hypertrophy and fibrosis in HCM.
  • METHODS AND RESULTS: We treated 2-year-old beta-myosin heavy-chain Q403 transgenic rabbits with established cardiac hypertrophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per group).
  • Transgenic rabbits in the placebo group had cardiac hypertrophy, fibrosis, systolic dysfunction, increased oxidized to total glutathione ratio, higher levels of activated thiol-sensitive active protein kinase G, dephosphorylated nuclear factor of activated T cells (NFATc1) and phospho-p38, and reduced levels of glutathiolated cardiac alpha-actin.
  • Treatment with N-acetylcysteine restored oxidized to total glutathione ratio, normalized levels of glutathiolated cardiac alpha-actin, reversed cardiac and myocyte hypertrophy and interstitial fibrosis, reduced the propensity for ventricular arrhythmias, prevented cardiac dysfunction, restored myocardial levels of active protein kinase G, and dephosphorylated NFATc1 and phospho-p38.
  • CONCLUSIONS: Treatment with N-acetylcysteine, a safe prodrug against oxidation, reversed established cardiac phenotype in a transgenic rabbit model of human HCM.
  • Because there is no effective pharmacological therapy for HCM and given that hypertrophy, fibrosis, and cardiac dysfunction are common and major predictors of clinical outcomes, the findings could have implications in various cardiovascular disorders.

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  • (PMID = 19255346.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] ENG
  • [Grant] None / None / / R01 HL068884-04; None / None / / P50 HL054313-090012; United States / NHLBI NIH HHS / HL / P50 HL054313; United States / NHLBI NIH HHS / HL / R01 HL068884-02; None / None / / P50 HL054313-060012; United States / NHLBI NIH HHS / HL / R01 HL068884-04; United States / NIAMS NIH HHS / AR / R01 AR056223; United States / NHLBI NIH HHS / HL / R01 HL068884-01; United States / NHLBI NIH HHS / HL / P50 HL054313-080012; None / None / / R01 HL068884-03; United States / NHLBI NIH HHS / HL / R01-HL68884; United States / NHLBI NIH HHS / HL / R01 HL068884-03; United States / NHLBI NIH HHS / HL / R01 HL068884; United States / NHLBI NIH HHS / HL / P50 HL054313-070012; None / None / / P50 HL054313-100012; None / None / / P50 HL054313-08S10012; None / None / / P50 HL054313-080012; United States / NHLBI NIH HHS / HL / P50 HL054313-08S10012; United States / NHLBI NIH HHS / HL / R01 HL068884-05; United States / NHLBI NIH HHS / HL / P50 HL054313-090012; None / None / / R01 HL068884-05; None / None / / P50 HL054313-070012; None / None / / R01 HL068884-02; United States / NHLBI NIH HHS / HL / R01-HL67322; United States / NHLBI NIH HHS / HL / P50 HL054313-100012; United States / NHLBI NIH HHS / HL / R01 HL067322; United States / NHLBI NIH HHS / HL / P50 HL054313-060012; None / None / / R01 HL068884-01
  • [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 / Actins; 0 / Antioxidants; 0 / NFATC Transcription Factors; 0 / Sulfhydryl Compounds; EC 2.7.11.24 / p38 Mitogen-Activated Protein Kinases; EC 3.6.4.1 / Myosin Heavy Chains; GAN16C9B8O / Glutathione; WYQ7N0BPYC / Acetylcysteine
  • [Other-IDs] NLM/ NIHMS113912; NLM/ PMC2773801
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9. Henderson KK, Danzi S, Paul JT, Leya G, Klein I, Samarel AM: Physiological replacement of T3 improves left ventricular function in an animal model of myocardial infarction-induced congestive heart failure. Circ Heart Fail; 2009 May;2(3):243-52
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  • [Title] Physiological replacement of T3 improves left ventricular function in an animal model of myocardial infarction-induced congestive heart failure.
  • In a rodent model of myocardial infarction-induced CHF and low serum T(3), we hypothesized that replacing T(3) to euthyroid levels would improve left ventricular function without producing untoward signs of thyrotoxicosis.
  • METHODS AND RESULTS: Adult male Sprague-Dawley rats were subjected to left anterior descending coronary artery ligation (myocardial infarction).
  • One week post-myocardial infarction, left ventricular fractional shortening was significantly reduced to 22+/-1% in CHF animals versus 38+/-1% for sham-operated controls (P<0.001).
  • At 9 weeks post-myocardial infarction, systolic function (+dP/dt max) was significantly attenuated in CHF animals (4773+/-259 versus 6310+/-267 mmHg/s; P<0.001) as well as diastolic function measured by half time to relaxation (15.9+/-1.2 versus 11.1+/-0.3 ms; P<0.001).
  • alpha-myosin heavy chain expression was also significantly reduced by 77% (P<0.001), and beta-myosin heavy chain expression was increased by 21%.
  • Continuous T(3) replacement was initiated 1 week post-myocardial infarction with osmotic mini-pumps (6 microg/kg/d), which returned serum T(3) concentrations to levels similar to Sham controls while resting conscious heart rate, arterial blood pressure and the incidence of arrhythmias were not different.
  • At 9 weeks, systolic function was significantly improved by T(3) replacement (6279+/-347 mmHg/s; P<0.05) and a trend toward improved diastolic function (12.3+/-0.6 ms) was noted.
  • T(3) replacement in CHF animals also significantly increased alpha- and reduced beta-MHC expression, (P<0.05).
  • CONCLUSIONS: These data indicate that T(3) replacement to euthyroid levels improves systolic function and tends to improve diastolic function, potentially through changes in myocardial gene expression.
  • [MeSH-major] Heart Failure / therapy. Hormone Replacement Therapy. Myocardial Contraction. Myocardial Infarction / complications. Triiodothyronine / administration & dosage. Ventricular Dysfunction, Left / therapy
  • [MeSH-minor] Animals. Blood Pressure. Diastole. Disease Models, Animal. Gene Expression Regulation. Heart Rate. Hypertrophy, Left Ventricular / etiology. Hypertrophy, Left Ventricular / physiopathology. Hypertrophy, Left Ventricular / therapy. Infusion Pumps, Implantable. Male. Myosin Heavy Chains / genetics. RNA, Messenger / metabolism. Rats. Rats, Sprague-Dawley. Recovery of Function. Systole. Time Factors. Ventricular Myosins / genetics

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  • (PMID = 19808346.001).
  • [ISSN] 1941-3297
  • [Journal-full-title] Circulation. Heart failure
  • [ISO-abbreviation] Circ Heart Fail
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / RNA, Messenger; 06LU7C9H1V / Triiodothyronine; EC 3.6.1.- / Ventricular Myosins; EC 3.6.4.1 / Myosin Heavy Chains
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10. Ghoshal UC, Chetri K, Banerjee PK, Choudhuri G, Pal BB, Dabadghao S, Dhar K, Naik S, Naik SR: Is immunoproliferative small intestinal disease uncommon in India? Trop Gastroenterol; 2001 Jan-Mar;22(1):14-7
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  • [Title] Is immunoproliferative small intestinal disease uncommon in India?
  • Till date only three series of immunoproliferative small intestinal disease (IPSID) describing 22 patients have been reported from India.
  • Seven patients with IPSID in two tertiary referral centers in India are included in the study.
  • Diagnosis was based on typical clinical features [diarrhoea (7/7), weight loss (7/7), clubbing (6/7), fever (3/7), abdominal pain and lump (3/7)], biochemical evidence of malabsorption and duodenal biopsy findings.
  • All patients were young males (mean age 29.8 +/- 11.8 years, range 17-53).
  • Atypical features included gastric involvement (1/7), colonic involvement (1/7) and appearance of pigmented nails following anti-cancer chemotherapy (1/7) which disappeared six months after omitting doxorubin from chemotherapy regimen.
  • In the latter patient S. stercoralis became disseminated after anti-malignant chemotherapy.
  • One patient had gastric H. pylori infection.
  • This raises doubt on efficacy of tetracycline alone in treatment of IPSID.
  • One other patient was misdiagnosed and treated as intestinal tuberculosis.
  • Early diagnosis and administration of chemotherapy may improve survival in this disease.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / epidemiology
  • [MeSH-minor] Adolescent. Adult. Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / therapeutic use. Doxorubicin / therapeutic use. Humans. India / epidemiology. Middle Aged. Prednisolone / therapeutic use. Prognosis. Tetracycline / therapeutic use. Vincristine / therapeutic use

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  • (PMID = 11398237.001).
  • [ISSN] 0250-636X
  • [Journal-full-title] Tropical gastroenterology : official journal of the Digestive Diseases Foundation
  • [ISO-abbreviation] Trop Gastroenterol
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] India
  • [Chemical-registry-number] 5J49Q6B70F / Vincristine; 80168379AG / Doxorubicin; 8N3DW7272P / Cyclophosphamide; 9PHQ9Y1OLM / Prednisolone; F8VB5M810T / Tetracycline; VAP-cyclo protocol
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11. Magdelaine-Beuzelin C, Vermeire S, Goodall M, Baert F, Noman M, Assche GV, Ohresser M, Degenne D, Dugoujon JM, Jefferis R, Rutgeerts P, Lefranc MP, Watier H: IgG1 heavy chain-coding gene polymorphism (G1m allotypes) and development of antibodies-to-infliximab. Pharmacogenet Genomics; 2009 May;19(5):383-7
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] IgG1 heavy chain-coding gene polymorphism (G1m allotypes) and development of antibodies-to-infliximab.
  • OBJECTIVE: The chimeric anti-tumor necrosis factor-alpha antibody infliximab is known to induce antibodies-to-infliximab (ATI) in some treated patients.
  • Immunogenicity in murine variable domains is expected; however, constant domains of its human heavy gamma1 chain may also be implicated as it expresses G1m1 and G1m17 allotypes.
  • This allelic form may be immunogenic in patients that are homozygous for the G1m3 allotype commonly expressed in Caucasoid populations.
  • METHODS: As G1m allotypic divergence may explain the presence of ATI or may influence their concentration, a genotyping method was developed and validated to determine antithetical (i.e. mutually exclusive) G1m3 and G1m17 allotypes (amino acid 120 of CH1 according to the international ImMunoGeneTics information system unique numbering) at the IGHG1 gene level (CH1 359g/a nucleotide polymorphism).
  • Two hundred forty-five blood donors and 118 previously described patients suffering from Crohn's disease, treated with infliximab, and having developed ATI in 73 of them, were genotyped.
  • RESULTS: The IGHG1 CH1 359g/a polymorphism does not depart from the Hardy-Weinberg equilibrium in the control population, and allele frequencies were similar in controls and patients.
  • No association was found between the patient G1m allotypes and the presence of ATI or their concentration.
  • It remains possible that anti-Gm1 antibodies are not well detected by the enzyme-linked immunosorbent assays used for ATI detection and/or that the G1m allotypes are minor antigens on IgG1.
  • CONCLUSION: The IGHG1 polymorphism does not seem to play a major role in the induction of ATI.
  • Further analyses will be required to determine whether it is also the case for humanized or fully human antibodies bearing the same G1m allotypes.
  • [MeSH-major] Antibodies, Monoclonal / immunology. Antibody Formation / genetics. Immunoglobulin G / genetics. Immunoglobulin Heavy Chains / genetics
  • [MeSH-minor] Anti-Inflammatory Agents / immunology. Anti-Inflammatory Agents / therapeutic use. Case-Control Studies. Cohort Studies. Crohn Disease / blood. Crohn Disease / drug therapy. Crohn Disease / genetics. Crohn Disease / immunology. Gene Frequency. Genotype. Humans. Immunoglobulin Allotypes / genetics. Infliximab. Models, Molecular

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  • (PMID = 19319024.001).
  • [ISSN] 1744-6872
  • [Journal-full-title] Pharmacogenetics and genomics
  • [ISO-abbreviation] Pharmacogenet. Genomics
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents; 0 / Antibodies, Monoclonal; 0 / Immunoglobulin Allotypes; 0 / Immunoglobulin G; 0 / Immunoglobulin Heavy Chains; B72HH48FLU / Infliximab
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12. Fernández-Ruiz E, Cabrerizo M, Ortega M, Blas C, Llamas P, Santos-Roncero M, Nieto S, Acevedo A, Pérez G, Nicolás C, Fernández-Rañada JM, Arranz R: High molecular response rate and clinical correlation in patients with follicular lymphoma treated with cyclophosphamide-vincristine-prednisone plus interferon alpha 2b. Clin Cancer Res; 2003 Jul;9(7):2497-503
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  • [Title] High molecular response rate and clinical correlation in patients with follicular lymphoma treated with cyclophosphamide-vincristine-prednisone plus interferon alpha 2b.
  • PURPOSE: The role of molecular monitoring of minimal residual disease (MRD) in low-grade non-Hodgkin's lymphoma is controversial.
  • We have performed a prospective study of the molecular behavior of 35 patients with follicular non-Hodgkin's lymphoma who received cyclophosphamide-vincristine-prednisone chemotherapy in conjunction with IFN-alpha 2b.
  • EXPERIMENTAL DESIGN: Bcl-2 and clonal immunoglobulin heavy chain (IgH) gene rearrangements were assayed at diagnosis by PCR in lymph node and bone marrow (BM) and sequentially after treatment.
  • RESULTS: Molecular markers were detected in BM of 29 (83%) patients at diagnosis: Bcl-2 rearrangement in 20 patients (90% major breakpoint and 10% minor cluster) and clonal IgH rearrangement in 9 of 15 patients negative for Bcl-2.
  • Molecular and clinical response was noted in 25 (86%) patients after induction treatment.
  • A correlation between clinical and molecular response was found in 24 patients with molecular markers in BM at diagnosis and >2 years of follow-up: 94% of patients with undetectable MRD showed continuous clinical remission, whereas 50% of patients who reverted back to positive molecular markers relapsed (P < 0.05).
  • CONCLUSIONS: The rate of molecular response is high in patients treated with cyclophosphamide-vincristine-prednisone and IFN and MRD sequential analysis is useful for disease surveillance.
  • [MeSH-major] Antineoplastic Combined Chemotherapy Protocols / therapeutic use. Cyclophosphamide / administration & dosage. Interferon-alpha / therapeutic use. Lymphoma, Follicular / drug therapy. Prednisone / administration & dosage. Vincristine / administration & dosage
  • [MeSH-minor] Adult. Aged. Bone Marrow / metabolism. Disease-Free Survival. Female. Follow-Up Studies. Genetic Markers. Humans. Immunoglobulin Heavy Chains / immunology. Lymphatic Metastasis. Male. Middle Aged. Polymerase Chain Reaction. Prospective Studies. Proto-Oncogene Proteins c-bcl-2 / metabolism. Recombinant Proteins. Time Factors. Treatment Outcome

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  • (PMID = 12855623.001).
  • [ISSN] 1078-0432
  • [Journal-full-title] Clinical cancer research : an official journal of the American Association for Cancer Research
  • [ISO-abbreviation] Clin. Cancer Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Genetic Markers; 0 / Immunoglobulin Heavy Chains; 0 / Interferon-alpha; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / Recombinant Proteins; 5J49Q6B70F / Vincristine; 8N3DW7272P / Cyclophosphamide; 99210-65-8 / interferon alfa-2b; VB0R961HZT / Prednisone
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13. Schmidt-Schweda S, Holubarsch C: First clinical trial with etomoxir in patients with chronic congestive heart failure. Clin Sci (Lond); 2000 Jul;99(1):27-35
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  • [Title] First clinical trial with etomoxir in patients with chronic congestive heart failure.
  • In the failing human myocardium, both impaired calcium homoeostasis and alterations in the levels of contractile proteins have been observed, which may be responsible for reduced contractility as well as diastolic dysfunction.
  • In addition, levels of a key protein in calcium cycling, i.e. the sarcoplasmic reticulum Ca(2+)-ATPase, and of the alpha-myosin heavy chain have been shown to be enhanced by treatment with etomoxir, a carnitine palmitoyltransferase inhibitor, in normal and pressure-overloaded rat myocardium.
  • We therefore studied, for the first time, the influence of long-term oral application of etomoxir on cardiac function in patients with chronic heart failure.
  • A dose of 80 mg of etomoxir was given once daily to 10 patients suffering from heart failure (NYHA functional class II-III; mean age 55+/-4 years; one patient with ischaemic heart disease and nine patients with dilated idiopathic cardiomyopathy; all male), in addition to standard therapy.
  • The left ventricular ejection fraction was measured echocardiographically before and after a 3-month period of treatment.
  • Central haemodynamics at rest and exercise (supine position bicycle) were defined by means of a pulmonary artery catheter and thermodilution.
  • All 10 patients improved clinically; no patient had to stop taking the study medication because of side effects; and no patient died during the 3-month period.
  • Maximum cardiac output during exercise increased from 9.72+/-1.25 l/min before to 13.44+/-1.50 l/min after treatment (P<0.01); this increase was mainly due to an increased stroke volume [84+/-7 ml before and 109+/-9 ml after treatment (P<0.01)].
  • Resting heart rate was slightly reduced (not statistically significant).
  • During exercise, for any given heart rate, stroke volume was significantly enhanced (P<0.05).
  • The left ventricular ejection fraction increased significantly from 21.5+/-2.6% to 27.0+/-2.3% (P<0.01).
  • Thus, although the results of this small pilot study are not placebo-controlled, all patients seem to have benefitted from etomoxir treatment.
  • Etomoxir, which has no acute inotropic or vasodilatory properties and is thought to increase gene expression of the sarcoplasmic reticulum Ca(2+)-ATPase and the alpha-myosin heavy chain, improved clinical status, central haemodynamics at rest and during exercise, and left ventricular ejection fraction.
  • [MeSH-major] Enzyme Inhibitors / therapeutic use. Epoxy Compounds / therapeutic use. Heart Failure / drug therapy
  • [MeSH-minor] Adult. Aged. Exercise Test / drug effects. Heart Rate / drug effects. Hemodynamics / drug effects. Humans. Male. Middle Aged. Stroke Volume / drug effects. Thermodilution

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  • (PMID = 10887055.001).
  • [ISSN] 0143-5221
  • [Journal-full-title] Clinical science (London, England : 1979)
  • [ISO-abbreviation] Clin. Sci.
  • [Language] eng
  • [Publication-type] Clinical Trial; Clinical Trial, Phase I; Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Enzyme Inhibitors; 0 / Epoxy Compounds; MSB3DD2XP6 / etomoxir
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14. Nakai K, Takenobu Y, Takimizu H, Akimaru S, Ito H, Maegawa H, Marsala M, Katsube N: Effects of orally administered OP-1206 alpha-CD with loxoprofen-Na on walking dysfunction in the rat neuropathic intermittent claudication model. Prostaglandins Leukot Essent Fatty Acids; 2003 Oct;69(4):269-73
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  • [Title] Effects of orally administered OP-1206 alpha-CD with loxoprofen-Na on walking dysfunction in the rat neuropathic intermittent claudication model.
  • An orally active prostaglandin E1 analogue, OP-1206 alpha-CD improves walking dysfunction in the rat spinal stenosis model.
  • Loxoprofen-Na, a non-steroidal anti-inflammatory drug, is used to relieve chronic pain in patients with lumbar spinal canal stenosis.
  • To determine whether the OP-1206 alpha-CD in combination with loxoprofen-Na could induce a greater therapeutical effect on walking dysfunction and spinal cord blood flow (SCBF) than OP-1206 alpha-CD treatment alone after chronic spinal stenosis in the rat.
  • After surgery, walking function was measured using a treadmill apparatus and SCBF was measured using a laser-Doppler flow meter.
  • Drugs were administered orally twice a day for 11 days from the day 3 post-surgery.
  • OP-1206 alpha-CD elicited a significant improvement of walking dysfunction on days 7 and 14 post-surgery and significantly increased spinal cord blood flow on day 15, whereas walking dysfunction and SCBF of rats treated with loxoprofen-Na alone remained unchanged.
  • Combined treatment of OP-1206 alpha-CD with loxoprofen-Na did not provide additive therapeutical effect.
  • These results suggest that a significant improvement seen after OP-1206 alpha-CD treatment is primarily mediated by improvement of the local spinal cord blood flow.
  • This effect is not ameliorated or potentiated by a combined treatment with loxoprofen-Na.
  • [MeSH-major] Alprostadil / analogs & derivatives. Alprostadil / pharmacology. Intermittent Claudication / drug therapy. Phenylpropionates / pharmacology. Walking. alpha-Cyclodextrins
  • [MeSH-minor] Administration, Oral. Animals. Cyclodextrins. Disease Models, Animal. Drug Therapy, Combination. Male. Prostaglandins E, Synthetic / administration & dosage. Prostaglandins E, Synthetic / pharmacology. Rats. Rats, Wistar. Regional Blood Flow / drug effects. Spinal Cord / blood supply. Spinal Stenosis / drug therapy. Spinal Stenosis / physiopathology

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  • (PMID = 12907137.001).
  • [ISSN] 0952-3278
  • [Journal-full-title] Prostaglandins, leukotrienes, and essential fatty acids
  • [ISO-abbreviation] Prostaglandins Leukot. Essent. Fatty Acids
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Phenylpropionates; 0 / Prostaglandins E, Synthetic; 0 / alpha-Cyclodextrins; 3583H0GZAP / loxoprofen; 74397-12-9 / ONO 1206; F5TD010360 / Alprostadil; Z1LH97KTRM / alpha-cyclodextrin
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15. Flagg TP, Cazorla O, Remedi MS, Haim TE, Tones MA, Bahinski A, Numann RE, Kovacs A, Schaffer JE, Nichols CG, Nerbonne JM: Ca2+-independent alterations in diastolic sarcomere length and relaxation kinetics in a mouse model of lipotoxic diabetic cardiomyopathy. Circ Res; 2009 Jan 2;104(1):95-103
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  • [Title] Ca2+-independent alterations in diastolic sarcomere length and relaxation kinetics in a mouse model of lipotoxic diabetic cardiomyopathy.
  • Previous studies demonstrated increased fatty acid uptake and metabolism in MHC-FATP transgenic mice that overexpress fatty acid transport protein (FATP)1 in the heart under the control of the alpha-myosin heavy chain (alpha-MHC) promoter.
  • Doppler tissue imaging and hemodynamic measurements revealed diastolic dysfunction, in the absence of changes in systolic function.
  • The experiments here directly test the hypothesis that the diastolic dysfunction in MHC-FATP mice reflects impaired ventricular myocyte contractile function.
  • In vitro imaging of isolated adult MHC-FATP ventricular myocytes revealed that mean diastolic sarcomere length is significantly (P<0.01) shorter than in wild-type (WT) cells (1.79+/-0.01 versus 1.84+/-0.01 microm).
  • In addition, the relaxation rate (dL/dt) is significantly (P<0.05) slower in MHC-FATP than WT myocytes (1.58+/-0.09 versus 1.92+/-0.13 microm/s), whereas both fractional shortening and contraction rates are not different.
  • Application of 40 mmol/L 2,3-butadionemonoxime (a nonspecific ATPase inhibitor that relaxes actin-myosin interactions) increased diastolic sarcomere length in both WT and MHC-FATP myocytes to the same length, suggesting that MHC-FATP myocytes are partially activated at rest.
  • Direct measurements of intracellular Ca(2+) revealed that diastolic [Ca(2+)](i) is unchanged in MHC-FATP myocytes and the rate of calcium removal is unexpectedly faster in MHC-FATP than WT myocytes.
  • Moreover, diastolic sarcomere length in MHC-FATP and WT myocytes was unaffected by removal of extracellular Ca(2+) or by buffering of intracellular Ca(2+) with the Ca(2+) chelator BAPTA (100 micromol/L), indicating that elevated intracellular Ca(2+) does not underlie impaired diastolic function in MHC-FATP ventricular myocytes.
  • Functional assessment of skinned myocytes, however, revealed that myofilament Ca(2+) sensitivity is markedly increased in MHC-FATP, compared with WT, ventricular cells.
  • Collectively, these data demonstrate that derangements in lipid metabolism in MHC-FATP ventricles, which are similar to those observed in the diabetic heart, result in impaired diastolic function that primarily reflects changes in myofilament function, rather than altered Ca(2+) cycling.
  • [MeSH-major] Diabetes Complications / physiopathology. Fatty Acid Transport Proteins / physiology. Fatty Acids / metabolism. Heart Failure, Diastolic / physiopathology. Myocytes, Cardiac / physiology. Sarcomeres / ultrastructure
  • [MeSH-minor] Animals. Calcium / physiology. Chelating Agents / pharmacology. Diacetyl / analogs & derivatives. Diacetyl / pharmacology. Diastole. Disease Models, Animal. Egtazic Acid / analogs & derivatives. Egtazic Acid / pharmacology. Heart Ventricles / pathology. Isometric Contraction. Mice. Mice, Transgenic. Myocardial Contraction. Myocardium / metabolism. Myosin Heavy Chains / biosynthesis. Myosin Heavy Chains / genetics. Recombinant Fusion Proteins / physiology

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  • (PMID = 19023131.001).
  • [ISSN] 1524-4571
  • [Journal-full-title] Circulation research
  • [ISO-abbreviation] Circ. Res.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Chelating Agents; 0 / Fatty Acid Transport Proteins; 0 / Fatty Acids; 0 / Recombinant Fusion Proteins; 0 / Slc27a1 protein, mouse; 19SQ93LM6H / diacetylmonoxime; 526U7A2651 / Egtazic Acid; EC 3.6.4.1 / Myosin Heavy Chains; K22DDW77C0 / 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid; K324J5K4HM / Diacetyl; SY7Q814VUP / Calcium
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16. Lecuit M, Abachin E, Martin A, Poyart C, Pochart P, Suarez F, Bengoufa D, Feuillard J, Lavergne A, Gordon JI, Berche P, Guillevin L, Lortholary O: Immunoproliferative small intestinal disease associated with Campylobacter jejuni. N Engl J Med; 2004 Jan 15;350(3):239-48
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  • [Title] Immunoproliferative small intestinal disease associated with Campylobacter jejuni.
  • BACKGROUND: Immunoproliferative small intestinal disease (also known as alpha chain disease) is a form of lymphoma that arises in small intestinal mucosa-associated lymphoid tissue (MALT) and is associated with the expression of a monotypic truncated immunoglobulin alpha heavy chain without an associated light chain.
  • Early-stage disease responds to antibiotics, suggesting a bacterial origin.
  • METHODS: We performed polymerase chain reaction (PCR), DNA sequencing, fluorescence in situ hybridization, and immunohistochemical studies on intestinal-biopsy specimens from a series of patients with immunoproliferative small intestinal disease.
  • RESULTS: Analysis of frozen intestinal tissue obtained from an index patient with immunoproliferative small intestinal disease who had a dramatic response to antibiotics revealed the presence of Campylobacter jejuni.
  • A follow-up retrospective analysis of archival intestinal-biopsy specimens disclosed campylobacter species in four of six additional patients with immunoproliferative small intestinal disease.
  • CONCLUSIONS: These results indicate that campylobacter and immunoproliferative small intestinal disease are associated and that C. jejuni should be added to the growing list of human pathogens responsible for immunoproliferative states.
  • [MeSH-major] Campylobacter jejuni / isolation & purification. Immunoproliferative Small Intestinal Disease / microbiology
  • [MeSH-minor] Anti-Bacterial Agents. Anti-Ulcer Agents / therapeutic use. Campylobacter Infections. DNA, Bacterial / analysis. Drug Therapy, Combination / therapeutic use. Female. Genes, Immunoglobulin. Humans. Immunoglobulin A / blood. Immunoglobulin Fragments / analysis. Immunoglobulin Fragments / genetics. Immunohistochemistry. In Situ Hybridization, Fluorescence. Intestine, Small / immunology. Intestine, Small / microbiology. Intestine, Small / pathology. Middle Aged. Omeprazole / therapeutic use. Polymerase Chain Reaction. Sequence Analysis, DNA

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  • [Copyright] Copyright 2004 Massachusetts Medical Society
  • [CommentIn] Rev Gastroenterol Disord. 2005 Summer;5(3):181-2 [16156008.001]
  • [CommentIn] N Engl J Med. 2004 Apr 15;350(16):1685-6; author reply 1685-6 [15084705.001]
  • [CommentIn] N Engl J Med. 2004 Jan 15;350(3):213-5 [14724298.001]
  • (PMID = 14724303.001).
  • [ISSN] 1533-4406
  • [Journal-full-title] The New England journal of medicine
  • [ISO-abbreviation] N. Engl. J. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Anti-Ulcer Agents; 0 / DNA, Bacterial; 0 / Immunoglobulin A; 0 / Immunoglobulin Fragments; KG60484QX9 / Omeprazole
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17. Lieber CS: New concepts of the pathogenesis of alcoholic liver disease lead to novel treatments. Curr Gastroenterol Rep; 2004 Feb;6(1):60-5
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] New concepts of the pathogenesis of alcoholic liver disease lead to novel treatments.
  • Activation of methionine to S-adenosylmethionine is depressed in alcoholics.
  • CYP2E1 is also induced in Kupffer cells, promoting their activation and release of inflammatory cytokines, including tumor necrosis factor (TNF)-alpha.
  • The TNF-alpha inhibitor pentoxifylline decreased mortality from alcoholic hepatitis.
  • PPC was beneficial in patients with alcoholic hepatitis, and it opposed fibrosis in heavy drinkers and decreased aminotransferases in patients with hepatitis C.
  • The antioxidant silymarin also successfully opposed alcoholic cirrhosis in baboons and in some but not all clinical trials; this effect also pertains to a-tocopherol.
  • Finally, replacing long-chain with medium-chain triglycerides opposed the fatty liver experimentally and clinically.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Antioxidants / therapeutic use. Cytokines / metabolism. Liver Diseases, Alcoholic / drug therapy. Liver Diseases, Alcoholic / physiopathology
  • [MeSH-minor] Alcoholism / complications. Colchicine / therapeutic use. Drug Therapy, Combination. Female. Humans. Lipid Peroxidation. Liver Function Tests. Male. Prognosis. Randomized Controlled Trials as Topic. Risk Assessment. S-Adenosylmethionine / therapeutic use. Severity of Illness Index. Treatment Outcome

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  • (PMID = 14720455.001).
  • [ISSN] 1522-8037
  • [Journal-full-title] Current gastroenterology reports
  • [ISO-abbreviation] Curr Gastroenterol Rep
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Review
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Antioxidants; 0 / Cytokines; 7LP2MPO46S / S-Adenosylmethionine; SML2Y3J35T / Colchicine
  • [Number-of-references] 55
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18. Wolf CM, Arad M, Ahmad F, Sanbe A, Bernstein SA, Toka O, Konno T, Morley G, Robbins J, Seidman JG, Seidman CE, Berul CI: Reversibility of PRKAG2 glycogen-storage cardiomyopathy and electrophysiological manifestations. Circulation; 2008 Jan 15;117(2):144-54
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  • A genetic approach that utilizes a binary inducible transgenic system was used to investigate the disease mechanism and to assess preventability and reversibility of disease features in a mouse model of glycogen-storage cardiomyopathy.
  • METHODS AND RESULTS: Transgenic (Tg) mice expressing a human N488I PRKAG2 cDNA under control of the tetracycline-repressible alpha-myosin heavy chain promoter underwent echocardiography, ECG, and in vivo electrophysiology studies.
  • Transgene suppression by tetracycline administration caused a reduction in cardiac glycogen content and was initiated either prenatally (Tg(OFF(E-8 weeks))) or at different time points during life (Tg(OFF(4-16 weeks)), Tg(OFF(8-20 weeks)), and Tg(OFF(>20 weeks))).
  • One group never received tetracycline, expressing transgene throughout life (Tg(ON)).
  • Tg(ON) mice developed cardiac hypertrophy followed by dilatation, ventricular preexcitation involving multiple accessory pathways, and conduction system disease, including sinus and atrioventricular node dysfunction.
  • CONCLUSIONS: Using an externally modifiable transgenic system, cardiomyopathy, cardiac dysfunction, and electrophysiological disorders were demonstrated to be reversible processes in PRKAG2 disease.
  • Transgene suppression during early postnatal development prevented the development of accessory electrical pathways but not cardiomyopathy or conduction system degeneration.
  • Taken together, these data provide insight into mechanisms of cardiac PRKAG2 disease and suggest that glycogen-storage cardiomyopathy can be modulated by lowering glycogen content in the heart.

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  • (PMID = 18158359.001).
  • [ISSN] 1524-4539
  • [Journal-full-title] Circulation
  • [ISO-abbreviation] Circulation
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / HL076751-02; United States / NHLBI NIH HHS / HL / R01 HL076751-02; United States / NHLBI NIH HHS / HL / R01 HL076751-03; United States / NHLBI NIH HHS / HL / R01 HL076751; United States / NHLBI NIH HHS / HL / HL076751-03; United States / NHLBI NIH HHS / HL / R01 HL076751-04; United States / NHLBI NIH HHS / HL / R01 HL076751-01A1; United States / NHLBI NIH HHS / HL / HL076751-01A1; United States / NHLBI NIH HHS / HL / HL076751-04
  • [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 / Multienzyme Complexes; 9005-79-2 / Glycogen; EC 2.7.11.1 / AMP-Activated Protein Kinases; EC 2.7.11.1 / Protein-Serine-Threonine Kinases; F8VB5M810T / Tetracycline
  • [Other-IDs] NLM/ NIHMS238048; NLM/ PMC2957811
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19. Sanganalmath SK, Babick AP, Barta J, Kumamoto H, Takeda N, Dhalla NS: Antiplatelet therapy attenuates subcellular remodelling in congestive heart failure. J Cell Mol Med; 2008 Sep-Oct;12(5A):1728-38
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  • [Title] Antiplatelet therapy attenuates subcellular remodelling in congestive heart failure.
  • Antiplatelet agents, sarpogrelate (SAR), a 5-HT(2A) receptor antagonist, and cilostazol (CIL), a phosphodiesterase III (PDE-III) inhibitor, are used for the treatment of peripheral vascular disease.
  • At end of the treatment period, haemodynamic measurements were performed and the left ventricle was processed for the determination of sarcoplasmic reticulum (SR) Ca(2+)-uptake and -release activities, and expression of SR Ca(2+)-pump, phospholamban and ryanodine receptors, as well as myofibrillar ATPase activities, expression of alpha- and beta-myosin heavy chain (MHC) isoforms, and phosphorylation of phospholamban and cardiac troponin-I (c Tn-I).
  • Marked haemodynamic changes in the MI-induced CHF were associated with depressions in SR Ca (+)-uptake and -release activities as well as in protein content and gene expression for SR proteins.
  • Furthermore, myofibrillar Ca(2+)-stimulated ATPase activity, as well as protein content and gene expression for alpha-MHC were decreased whereas those for beta-MHC were increased in the failing heart.
  • The MI-associated changes in cardiac function, SR and myofibillar activities, as well as SR and myofibrillar protein and gene expression were attenuated by treatment with SAR or CIL.
  • The results suggest that SAR and CIL improve cardiac function by ameliorating subcellular remodelling in the failing heart and indicate the potential therapy of CHF with antiplatelet agents.
  • [MeSH-major] Blood Platelets. Heart Failure / therapy
  • [MeSH-minor] Adenosine Triphosphatases / metabolism. Animals. Calcium / metabolism. Gene Expression Regulation. Hemodynamics. Male. Myosin Heavy Chains / metabolism. Protein Isoforms / metabolism. Proteins / genetics. Proteins / metabolism. RNA, Messenger / genetics. Rats. Rats, Sprague-Dawley. Sarcoplasmic Reticulum / metabolism. Subcellular Fractions / metabolism

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  • (PMID = 18088389.001).
  • [ISSN] 1582-1838
  • [Journal-full-title] Journal of cellular and molecular medicine
  • [ISO-abbreviation] J. Cell. Mol. Med.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Romania
  • [Chemical-registry-number] 0 / Protein Isoforms; 0 / Proteins; 0 / RNA, Messenger; EC 3.6.1.- / Adenosine Triphosphatases; EC 3.6.4.1 / Myosin Heavy Chains; SY7Q814VUP / Calcium
  • [Other-IDs] NLM/ PMC3918089
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20. Ommen HB, Schnittger S, Jovanovic JV, Ommen IB, Hasle H, Østergaard M, Grimwade D, Hokland P: Strikingly different molecular relapse kinetics in NPM1c, PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11 acute myeloid leukemias. Blood; 2010 Jan 14;115(2):198-205
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  • [Title] Strikingly different molecular relapse kinetics in NPM1c, PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11 acute myeloid leukemias.
  • Early relapse detection in acute myeloid leukemia is possible using standardized real-time quantitative polymerase chain reaction (RQ-PCR) protocols.
  • However, optimal sampling intervals have not been defined and are likely to vary according to the underlying molecular lesion.
  • In 74 patients experiencing hematologic relapse and harboring aberrations amenable to RQ-PCR (mutated NPM1 [designated NPM1c], PML-RARA, RUNX1-RUNX1T1, and CBFB-MYH11), we observed strikingly different relapse kinetics.
  • The median doubling time of the CBFB-MYH11 leukemic clone was significantly longer (36 days) than that of clones harboring other markers (RUNX1-RUNX1T1, 14 days; PML-RARA, 12 days; and NPM1c, 11 days; P < .001).
  • Furthermore, we used a mathematical model to determine frequency of relapse detection and median time from detection of minimal residual disease to hematologic relapse as a function of sampling interval length.
  • For example, to obtain a relapse detection fraction of 90% and a median time of 60 days, blood sampling every sixth month should be performed for CBFB-MYH11 leukemias.
  • By contrast, in NPM1c(+)/FLT3-ITD(-), NPM1c(+)/FLT3-ITD(+), RUNX1-RUNX1T1, and PML-RARA leukemias, bone marrow sampling is necessary every sixth, fourth, and fourth and second month, respectively.
  • These data carry important implications for the development of optimal RQ-PCR monitoring schedules suitable for evaluation of minimal residual disease-directed therapies in future clinical trials.
  • [MeSH-major] Biomarkers, Tumor / biosynthesis. Core Binding Factor Alpha 2 Subunit / biosynthesis. Core Binding Factor beta Subunit / biosynthesis. Gene Expression Regulation, Leukemic. Leukemia, Myeloid, Acute / metabolism. Myosin Heavy Chains / biosynthesis. Nuclear Proteins / biosynthesis. Oncogene Proteins, Fusion / biosynthesis
  • [MeSH-minor] Bone Marrow / metabolism. Female. Humans. Kinetics. Male. Monitoring, Physiologic / methods. Neoplasm, Residual. Recurrence. Retrospective Studies. Time Factors

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  • (PMID = 19901261.001).
  • [ISSN] 1528-0020
  • [Journal-full-title] Blood
  • [ISO-abbreviation] Blood
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / AML1-ETO fusion protein, human; 0 / Biomarkers, Tumor; 0 / CBFB protein, human; 0 / Core Binding Factor Alpha 2 Subunit; 0 / Core Binding Factor beta Subunit; 0 / MYH11 protein, human; 0 / Nuclear Proteins; 0 / Oncogene Proteins, Fusion; 0 / promyelocytic leukemia-retinoic acid receptor alpha fusion oncoprotein; 117896-08-9 / nucleophosmin; EC 3.6.4.1 / Myosin Heavy Chains
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21. Berentsen S, Beiske K, Tjønnfjord GE: Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy. Hematology; 2007 Oct;12(5):361-70
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  • [Title] Primary chronic cold agglutinin disease: an update on pathogenesis, clinical features and therapy.
  • Chronic cold agglutinin disease (CAD) is a subgroup of autoimmune hemolytic anemia.
  • Primary CAD has traditionally been defined by the absence of any underlying or associated disease.
  • The results of therapy with corticosteroids, alkylating agents and interferon-alpha have been poor.
  • Cold reactive immunoglobulins against erythrocyte surface antigens are essential to pathogenesis of CAD.
  • These cold agglutinins are monoclonal, usually IgMkappa autoantibodies with heavy chain variable regions encoded by the V(H)4-34 gene segment.
  • By flowcytometric and immunohistochemical assessments, a monoclonal CD20+kappa+B-lymphocyte population has been demonstrated in the bone marrow of 90% of the patients, and lymphoplasmacytic lymphoma is a frequent finding.
  • Novel attempts at treatment for primary CAD have mostly been directed against the clonal B-lymphocytes.
  • Phase 2 studies have shown that therapy with the chimeric anti-CD20 antibody rituximab produced partial response rates of more than 50% and occasional complete responses.
  • In this review, we discuss the clinical and pathogenetic features of primary CAD, emphasizing the more recent data on its close association with clonal lymphoproliferative bone marrow disorders and implications for therapy.
  • We also review the management and outline some perspectives on new therapy modalities.
  • [MeSH-minor] Adrenal Cortex Hormones / therapeutic use. Alkylating Agents / therapeutic use. Antibodies, Monoclonal / therapeutic use. Antibodies, Monoclonal, Murine-Derived. B-Lymphocytes / pathology. Bone Marrow / pathology. Clone Cells / pathology. Cryoglobulins / analysis. Cryoglobulins / immunology. Humans. Immunotherapy. Interferon-alpha / therapeutic use. Lymphoproliferative Disorders / complications. Lymphoproliferative Disorders / drug therapy. Lymphoproliferative Disorders / pathology. Rituximab

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  • (PMID = 17891600.001).
  • [ISSN] 1607-8454
  • [Journal-full-title] Hematology (Amsterdam, Netherlands)
  • [ISO-abbreviation] Hematology
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Alkylating Agents; 0 / Antibodies, Monoclonal; 0 / Antibodies, Monoclonal, Murine-Derived; 0 / Cryoglobulins; 0 / Interferon-alpha; 0 / cold agglutinins; 4F4X42SYQ6 / Rituximab
  • [Number-of-references] 88
  • [Other-IDs] NLM/ PMC2409172
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22. Hara T, Tsurumi H, Kato T, Imao Y, Kojima Y, Kojima K, Kitagawa J, Katsumura N, Araki H, Takami T, Moriwaki H: Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression. Intern Med; 2008;47(4):299-303
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  • [Title] Immunoproliferative small intestinal disease with protein loss complicated with duodenal T cell lymphoma during progression.
  • A 52-year-old man was admitted to our hospital in October 2001 with abdominal pain.
  • Abdominal X-ray indicated a diagnosis of ileus.
  • Histopathological and immunological examination resulted in a diagnosis of immunoproliferative small intestinal disease (IPSID).
  • He was treated with THP-COP therapy (pirarubicin, cyclophosphamide, vincristine, and prednisolone), which resulted in complete remission.
  • Outpatient follow-up revealed hypoalbuminemia in May 2003 and upper gastrointestinal endoscopy showed duodenal mucosal nodularity.
  • He was diagnosed with relapsed IPSID and salvage chemotherapy was started.
  • Follow-up endoscopy confirmed that the therapy was effective, but uncovered another duodenal mucosal nodularity.
  • Immunohistochemical staining revealed T-cell lymphoma.
  • Chemotherapy was discontinued and the patient died in December 2004.
  • [MeSH-major] Duodenal Neoplasms / etiology. Immunoproliferative Small Intestinal Disease / complications. Lymphoma, T-Cell / etiology
  • [MeSH-minor] Disease Progression. Fatal Outcome. Humans. Male. Middle Aged. Proteins / metabolism

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  • (PMID = 18277034.001).
  • [ISSN] 1349-7235
  • [Journal-full-title] Internal medicine (Tokyo, Japan)
  • [ISO-abbreviation] Intern. Med.
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] Japan
  • [Chemical-registry-number] 0 / Proteins
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23. Lee CJ, Yang J: alpha-Cyclodextrin-modified infrared sensing system for rapidly determining the enantiomeric composition of chiral compounds. Talanta; 2008 Feb 15;74(5):1104-12
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  • [Title] alpha-Cyclodextrin-modified infrared sensing system for rapidly determining the enantiomeric composition of chiral compounds.
  • This paper describes a new infrared (IR) sensing method for rapidly determining the enantiomeric compositions of chiral compounds through the use of a chirality-selective compound immobilized on the surface of the evanescent-wave sensing elements. alpha-Cyclodextrin (alpha-CD) was selected as this agent and it was immobilized on a zinc selenide sensing element to allow different analytical signals to be generated for each compound of a pair of enantiomers.
  • Theoretical working equations were developed to monitor the response of the ATR-IR spectroscopic sensor during this process.
  • The difference between the formation constants of enantiomers was crucial to the sensitivity when determining the enantiomeric compositions.
  • A linear relationship between the analytical signals and the mole fraction of the enantiomers was obtained under conditions in which the concentration of the chiral compound was sufficiently low.
  • Based on the detected time profiles, this sensing method had a fast response: the detection time could be <10min.
  • With a flow-cell configuration, the time to finish one determination can be shorter than 10min with similar sensitivity and accuracy as in static sensing system.
  • [MeSH-major] Spectroscopy, Fourier Transform Infrared / instrumentation. Spectroscopy, Fourier Transform Infrared / methods. Stereoisomerism. alpha-Cyclodextrins / analysis
  • [MeSH-minor] Equipment Design. Flow Injection Analysis. Hydrogen-Ion Concentration. Organic Chemicals / analysis. Time

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  • (PMID = 18371757.001).
  • [ISSN] 1873-3573
  • [Journal-full-title] Talanta
  • [ISO-abbreviation] Talanta
  • [Language] eng
  • [Publication-type] Evaluation Studies; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Organic Chemicals; 0 / alpha-Cyclodextrins; Z1LH97KTRM / alpha-cyclodextrin
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24. Li L, Takemura G, Li Y, Miyata S, Esaki M, Okada H, Kanamori H, Ogino A, Maruyama R, Nakagawa M, Minatoguchi S, Fujiwara T, Fujiwara H: Granulocyte colony-stimulating factor improves left ventricular function of doxorubicin-induced cardiomyopathy. Lab Invest; 2007 May;87(5):440-55
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  • [Title] Granulocyte colony-stimulating factor improves left ventricular function of doxorubicin-induced cardiomyopathy.
  • It is not well-known yet how granulocyte colony-stimulating factor (G-CSF) affects nonischemic cardiomyopathy, though its beneficial effects on acute myocardial infarction are well-established.
  • Here, we show that a single injection of doxorubicin (DOX, 15 mg/kg) induced left ventricular dilatation and dysfunction in mice within 2 weeks, and that these effects were significantly attenuated by human recombinant G-CSF (100 microg/kg/day for 5 days).
  • G-CSF also protected hearts against DOX-induced cardiomyocyte atrophy/degeneration, fibrosis, inflammatory cell infiltration and down regulation of GATA-4 and sarcomeric proteins, myosin heavy chain, troponin I and desmin, both in vivo and in vitro.
  • No DOX-induced apoptotic effects were seen, nor were there any changes in tumor necrosis factor-alpha or transforming growth factor-beta1 levels.
  • Inhibition of ERK activation, but not cyclooxygenase-2 inhibition, completely abolished beneficial effect of G-CSF on cardiac function.
  • G-CSF did not promote differentiation of bone marrow cells into cardiomyocytes according to the experiment using green fluorescent protein-chimeric mice, and inhibition of CXCR4+ cell homing using AMD3100 did not diminish the effect of G-CSF.
  • In conclusion, these findings imply the therapeutic usefulness of G-CSF mainly through restoring ERK activation against DOX-induced nonischemic cardiomyopathy.
  • [MeSH-major] Cardiomyopathy, Dilated / prevention & control. Cardiotonic Agents / therapeutic use. Granulocyte Colony-Stimulating Factor / therapeutic use. Ventricular Dysfunction, Left / prevention & control
  • [MeSH-minor] Animals. Animals, Newborn. Antibiotics, Antineoplastic / toxicity. Apoptosis / drug effects. Cell Survival / drug effects. Cells, Cultured. Disease Models, Animal. Dose-Response Relationship, Drug. Doxorubicin / toxicity. Drug Combinations. Drug Therapy, Combination. Enzyme Activation / drug effects. Extracellular Signal-Regulated MAP Kinases / metabolism. Male. Mice. Mice, Inbred C57BL. Myocytes, Cardiac / drug effects. Myocytes, Cardiac / ultrastructure. Recombinant Proteins

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  • (PMID = 17334414.001).
  • [ISSN] 0023-6837
  • [Journal-full-title] Laboratory investigation; a journal of technical methods and pathology
  • [ISO-abbreviation] Lab. Invest.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Antibiotics, Antineoplastic; 0 / Cardiotonic Agents; 0 / Drug Combinations; 0 / Recombinant Proteins; 143011-72-7 / Granulocyte Colony-Stimulating Factor; 80168379AG / Doxorubicin; EC 2.7.11.24 / Extracellular Signal-Regulated MAP Kinases
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25. Zhu W, Li Y, Liu L, Chen Y, Wang C, Xi F: Supramolecular hydrogels from cisplatin-loaded block copolymer nanoparticles and α-cyclodextrins with a stepwise delivery property. Biomacromolecules; 2010 Nov 8;11(11):3086-92
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  • [Title] Supramolecular hydrogels from cisplatin-loaded block copolymer nanoparticles and α-cyclodextrins with a stepwise delivery property.
  • A stepwise anticancer drug delivery system based on an injectable supramolecular hydrogel was presented.
  • In this system, poly(ethylene glycol)-b-poly(acrylic acid) (PEG-b-PAA) block copolymer nanoparticles containing cisplatin were released by erosion of the hydrogels and then the cisplatin was released from the nanoparticles by exchanging with chloride ions.
  • By mixing α-cyclodextrins (α-CDs) and the PEG-b-PAA micelles with their PAA cores loaded with the cisplatin in water, the novel supramolecular hydrogels were generated by threading α-CDs onto the PEG segments and forming physical cross-links of molecular necklaces.
  • Structures and properties of the supramolecular hydrogels containing cisplatin were studied by wide-angle X-ray diffraction (XRD) and rheology measurements, respectively.
  • In vitro cytotoxicity studies showed that the cisplatin-loaded hydrogels inhibited the growth of human bladder carcinoma EJ cells with a similar potency as that of the free cisplatin, whereas the hydrogels without cisplatin showed no cytotoxicity.
  • These results suggested that the cisplatin-coordinated PEG-b-PAA/α-CD supramolecular hydrogels hold great potential as an injectable system for sustained delivery of cisplatin in cancer therapy.
  • [MeSH-major] Acrylic Resins / chemistry. Antineoplastic Agents / pharmacology. Cisplatin / pharmacology. Drug Delivery Systems. Hydrogels / chemistry. Polyethylene Glycols / chemistry. alpha-Cyclodextrins / chemistry
  • [MeSH-minor] Cell Line, Tumor. Cell Proliferation / drug effects. Cell Survival / drug effects. Dose-Response Relationship, Drug. Drug Screening Assays, Antitumor. Humans. Macromolecular Substances / chemical synthesis. Macromolecular Substances / chemistry. Macromolecular Substances / pharmacology. Micelles. Particle Size. Structure-Activity Relationship. Surface Properties

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  • (PMID = 20958000.001).
  • [ISSN] 1526-4602
  • [Journal-full-title] Biomacromolecules
  • [ISO-abbreviation] Biomacromolecules
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Acrylic Resins; 0 / Antineoplastic Agents; 0 / Hydrogels; 0 / Macromolecular Substances; 0 / Micelles; 0 / alpha-Cyclodextrins; 30IQX730WE / Polyethylene Glycols; 9003-01-4 / carbopol 940; Q20Q21Q62J / Cisplatin
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26. Huf M, Kolárová H, Bajgar R, Macecek J, Tomecka M, Nevrelová P, Mosinger J, Tomek P, Strnad M: Spectral characteristics of the supramolecular complexes of polypyrrolic sensitizers and cyclodextrin carriers: usage in photodynamic therapy of tumors. Acta Medica (Hradec Kralove); 2004;47(4):309-11
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  • [Title] Spectral characteristics of the supramolecular complexes of polypyrrolic sensitizers and cyclodextrin carriers: usage in photodynamic therapy of tumors.
  • The objective of our work was to describe the photophysical properties (absorption and fluorescence) of the sensitizers TPPS4, ZnTPPS4 a PdTPPS4 and above all the complexes of these sensitizers with cyclodextrin carriers HP-alpha-CD, HP-beta-CD and HP-gamma-CD (2-hydroxypropyl-alpha, beta, gamma-cyclodextrin) in a suitable environment for the cultivation of cancerous cell lines, and to determine the optimal radioactive conditions for maximizing photodynamic effects in cancerous cells.

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  • (PMID = 15841917.001).
  • [ISSN] 1211-4286
  • [Journal-full-title] Acta medica (Hradec Kralove)
  • [ISO-abbreviation] Acta Medica (Hradec Kralove)
  • [Language] ENG
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Czech Republic
  • [Chemical-registry-number] 0 / Cyclodextrins; 0 / Drug Carriers; 0 / Polymers; 0 / Porphyrins; 0 / Pyrroles; 0 / Radiation-Sensitizing Agents; 30604-81-0 / polypyrrole
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27. Ramadeen A, Laurent G, dos Santos CC, Hu X, Connelly KA, Holub BJ, Mangat I, Dorian P: n-3 Polyunsaturated fatty acids alter expression of fibrotic and hypertrophic genes in a dog model of atrial cardiomyopathy. Heart Rhythm; 2010 Apr;7(4):520-8
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  • [Title] n-3 Polyunsaturated fatty acids alter expression of fibrotic and hypertrophic genes in a dog model of atrial cardiomyopathy.
  • BACKGROUND: We previously showed that omega-3 polyunsaturated fatty acids (PUFAs) reduce vulnerability to atrial fibrillation (AF).
  • OBJECTIVE: The purpose of this study was to use a genome-wide approach to identify gene expression profiles involved in a new model of AF vulnerability and to determine whether they were altered by PUFA therapy.
  • Two groups were paced using simultaneous atrioventricular pacing (SAVP) at 220 bpm for 14 days to induce atrial enlargement, fibrosis, and susceptibility to AF.
  • One group was supplemented with oral PUFAs (850 mg/day) for 21 days, commencing 7 days before the start of pacing (SAVP-PUFAs).
  • The second group received no PUFAs (SAVP-No PUFAs).
  • Atrial tissue was sampled at the end of the protocol.
  • Gene expression was analyzed in four dogs randomly selected from each group (n = 12) via microarray.
  • Results were confirmed with quantitative real-time polymerase chain reaction (RT-PCR) and histology on all 36 dogs.
  • RESULTS: Microarray or quantitative RT-PCR results showed that SAVP-No PUFAs dogs had significantly increased mRNA levels of protein kinase B (Akt), epidermal growth factor (EGF), JAM3, myosin heavy chain alpha (MHCalpha), and CD99 and significantly decreased levels of Smad6 compared with CTRL dogs.
  • Quantitative RT-PCR showed that PUFA supplementation was associated with significant down-regulation of Akt, EGF, JAM3, MHCalpha, and CD99 levels compared with SAVP-No PUFAs dogs.
  • CONCLUSION: The effect of PUFAs on these fibrosis, hypertrophy, and inflammation related genes suggests that, in this model, PUFA-mediated prevention of AF may be due to attenuation of adverse remodeling at the genetic level in response to mechanical stress.
  • [MeSH-major] Atrial Fibrillation / prevention & control. Atrial Function / drug effects. Cardiomyopathies / genetics. Cardiovascular Agents / pharmacology. Fatty Acids, Omega-3 / pharmacology. Heart Atria / drug effects
  • [MeSH-minor] Animals. Disease Models, Animal. Dogs. Fibrosis / genetics. Gene Expression / drug effects. Hypertrophy / genetics. Stress, Mechanical


28. Ben Ammar A, Cheikh I, Jouini M, Belkahla N, Fadhel SF, Hager O, Maamouri N, Chaabouni H, Ben Safta Z, Haouet S: [Alpha heavy chain disease. A Tunisian case]. Tunis Med; 2006 Sep;84(9):581-4
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  • [Title] [Alpha heavy chain disease. A Tunisian case].
  • [Transliterated title] Maladie des chaines lourdes alpha. A propos d'un cas tunisien.
  • Alpha heavy chain disease is a rare affection in the West and reported mainly in developing countries with the improvement of hygienic conditions, the disease become rare in Tunisia, the last case was reported in 1991.
  • The aim of the study is to report a new Tunisian case and to describe clinical, endoscopical and histological characteristics of the disease.
  • The patient in a 37 years old male, presented with chronic diarrhoea associated with malabsorption syndrome.
  • The diagnosis of alpha heavy chain disease was confirmed by histological examination of the resected intestine after surgery for intestinal obstruction.
  • The patient received chemotherapy.
  • [MeSH-major] Immunoproliferative Small Intestinal Disease / diagnosis
  • [MeSH-minor] Adult. Humans. Intestinal Obstruction / etiology. Intestinal Obstruction / surgery. Male

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  • (PMID = 17263208.001).
  • [ISSN] 0041-4131
  • [Journal-full-title] La Tunisie médicale
  • [ISO-abbreviation] Tunis Med
  • [Language] fre
  • [Publication-type] Case Reports; English Abstract; Journal Article
  • [Publication-country] Tunisia
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