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Atrial natriuretic peptide (ANP) is a member of the natriuretic peptide family that exerts various biological effects via acting on the receptor-guanylyl cyclase system, increasing the content of intracellular cyclic guanosine monophosphate (cGMP).

ANP has a variety of cardioprotective effects and is considered to be a very promising adjunct drug for the reperfusion therapy in patients with AMI.

[MeSH-major] Atrial Natriuretic Factor / administration & dosage. Myocardial Infarction / therapy. Ventricular Remodeling / drug effects

[MeSH-minor] Angioplasty, Balloon, Coronary / adverse effects. Animals. Disease Models, Animal. Dogs. Humans. Myocardial Reperfusion Injury / prevention & control. Rabbits. Rats. Renin-Angiotensin System / drug effects. Sympathetic Nervous System / drug effects

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(PMID = 18490430.001).

[ISSN] 1522-9645

[Journal-full-title] European heart journal

[ISO-abbreviation] Eur. Heart J.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 85637-73-6 / Atrial Natriuretic Factor

[Number-of-references] 85

   

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[Title] Effect of combined treatment with melatonin and methylprednisolone on neurological recovery after experimental spinal cord injury.

Secondary injury following the primary impact includes a number of biochemical and cellular alterations leading to tissue necrosis and cell death.

Methylprednisolone (MP), by reducing edema and protecting the cell membrane against peroxidation, is the only pharmacological agent with a proven clinically beneficial effect on SCI.

The purpose of this study was to examine the effect of MP and melatonin on neurological, ultrastructural, and electrophysiological recovery.

Weight-drop trauma was performed for each group and a 30-mg/kg single dose of MP for rats in group 1, a 10-mg/kg single dose of melatonin for rats in group 2, and MP and melatonin in the same doses for rats in group 3 were administered immediately after trauma.

The motor and somatosensory evoked potentials were recorded at the 4th hour, the 24th hour, and on the 10th day of the study for six rats in each group.

Electron microscopic studies were performed to determine the effects of melatonin, MP, and the combined treatment with MP and melatonin on axons, neurons, myelin, nucleus, and intracytoplasmic edema.

The groups treated with MP, melatonin, and a combination of both had significantly enhanced electrophysiological, biochemical, and neurological recovery and also showed better ultrastructural findings than the trauma and vehicle groups.

Although combined treatment was significantly more effective on lipid peroxidation than melatonin or MP treatments alone, at the 10th day, neurobehavioral, electrophysiological, and ultrastructural recovery were at the same level.

In conclusion, MP, melatonin, and MP and melatonin combined treatment modalities improved functional recovery at the same level.

Future studies involving different doses of melatonin and different dose combinations with MP could promise better results since each drug has a different anti-oxidative mechanism of action.

[MeSH-major] Melatonin / pharmacology. Methylprednisolone / pharmacology. Recovery of Function / drug effects. Spinal Cord / drug effects. Spinal Cord Injuries / drug therapy

[MeSH-minor] Animals. Axons / drug effects. Axons / pathology. Axons / ultrastructure. Disease Models, Animal. Drug Therapy, Combination. Edema / drug therapy. Edema / physiopathology. Edema / prevention & control. Evoked Potentials, Motor / drug effects. Evoked Potentials, Motor / physiology. Evoked Potentials, Somatosensory / drug effects. Evoked Potentials, Somatosensory / physiology. Female. Free Radical Scavengers / pharmacology. Free Radical Scavengers / therapeutic use. Lipid Peroxidation / drug effects. Lipid Peroxidation / physiology. Microscopy, Electron, Transmission. Myelin Sheath / drug effects. Myelin Sheath / pathology. Myelin Sheath / ultrastructure. Nerve Degeneration / drug therapy. Nerve Degeneration / physiopathology. Nerve Degeneration / prevention & control. Neural Pathways / drug effects. Neural Pathways / pathology. Neural Pathways / physiopathology. Neuroprotective Agents / pharmacology. Neuroprotective Agents / therapeutic use. Oxidative Stress / drug effects. Oxidative Stress / physiology. Rats. Treatment Outcome

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(PMID = 15232723.001).

[ISSN] 0940-6719

[Journal-full-title] European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society

[ISO-abbreviation] Eur Spine J

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Free Radical Scavengers; 0 / Neuroprotective Agents; JL5DK93RCL / Melatonin; X4W7ZR7023 / Methylprednisolone

[Other-IDs] NLM/ PMC3454055

   

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[Title] Management of disease- and treatment-related complications in patients with multiple myeloma.

Treatment of myeloma has dramatically changed after introduction of novel agents, such as thalidomide, lenalidomide and bortezomib, with a significant improvement in response rate and survival of patients with myeloma.

For newly diagnosed patients not eligible for transplant, the standards of care are now considered melphalan and prednisone (MP) plus thalidomide and MP plus bortezomib.

Ongoing randomized trials are evaluating lenalidomide plus MP and lenalidomide plus dexamethasone.

For newly diagnosed patients eligible for transplant, new induction regimens included the combination of high-dose dexamethasone plus thalidomide, high-dose dexamethasone plus lenalidomide (RD) and high-dose dexamethasone plus bortezomib (VD).

The combinations RD, VD and bortezomib plus pegylated-liposomal-doxorubicin have received the US Food and Drug Administration approval for the treatment of relapsed myeloma.

Disease control leads to improvement of all myeloma-related complications (anemia, bone disease, immune dysfunction and renal impairment), but physicians should take into account the choice of the therapeutic strategy, the expected toxicity profile of each of these regimens, together with the patient's biologic age and comorbidities.

Supportive care is an essential part of myeloma therapy, both for the treatment of myeloma-related complications, together with anti-myeloma treatment, and for the management of treatment-emergent adverse events.

This chapter will provide an overview of frequency and management of main complications related to the disease itself and to the use of new drugs in newly diagnosed and relapsed patients with myeloma.

[MeSH-major] Antineoplastic Combined Chemotherapy Protocols / adverse effects. Multiple Myeloma / complications

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(PMID = 20467920.001).

[ISSN] 1559-131X

[Journal-full-title] Medical oncology (Northwood, London, England)

[ISO-abbreviation] Med. Oncol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

   

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2. Troglitazone significantly increased peak isovolumic left ventricular pressure (LVP(max)), peak rate of rise of LVP (dP/dt(max)), peak rate of fall of LVP (dP/dt(min)) in isolated rat hearts perfused at a constant coronary flow and heart rate.

This inotropic effect of troglitazone was not inhibited by pretreatment with carbachol (muscarine receptor agonist), H89 (protein kinase A inhibitor), U73122 (phospholipase C inhibitor), H7 (protein kinase C inhibitor), verapamil (L-type Ca2+ channel antagonist), thapsigargin (Ca(2+)-adenosine triphosphatase inhibitor) or ryanodine (ryanodine receptor opener).

3. Radioimmunoassay showed that the cyclic adenosine monophosphate concentration in the left ventricle was not increased by troglitazone.

[MeSH-major] Calcium / pharmacology. Cardiotonic Agents / pharmacology. Chromans / pharmacology. Thiazoles / pharmacology. Thiazolidinediones. Ventricular Pressure / drug effects

[MeSH-minor] Animals. Calcium Channels, L-Type / metabolism. Cyclic AMP / metabolism. Cyclic AMP-Dependent Protein Kinases / metabolism. Dose-Response Relationship, Drug. Heart Ventricles / drug effects. Heart Ventricles / metabolism. Isoproterenol / pharmacology. Male. Patch-Clamp Techniques. Rats. Rats, Wistar. Ryanodine / pharmacology. Sarcoplasmic Reticulum / metabolism. Thapsigargin / pharmacology

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(PMID = 11498516.001).

[ISSN] 0007-1188

[Journal-full-title] British journal of pharmacology

[ISO-abbreviation] Br. J. Pharmacol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Calcium Channels, L-Type; 0 / Cardiotonic Agents; 0 / Chromans; 0 / Thiazoles; 0 / Thiazolidinediones; 15662-33-6 / Ryanodine; 67526-95-8 / Thapsigargin; E0399OZS9N / Cyclic AMP; EC 2.7.11.11 / Cyclic AMP-Dependent Protein Kinases; I66ZZ0ZN0E / troglitazone; L628TT009W / Isoproterenol; SY7Q814VUP / Calcium

[Other-IDs] NLM/ PMC1621161

   

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For a long time heartburn was not considered a symptom for serious illness.

There is strong evidence for a protective effect of Hp-infection in the development of GERD.

In pangastritis, caused by Hp-infection, gastric acid production is inhibited resulting in a reduction of stomach-acid-concentration.

This may be caused by either the chronic infection itself and the resulting atrophy of the stomach-mucosa, by the ammonia-producing HP-bacteria, or an increase in acid re-absorbtion of gastric epithelium.

Today, PPI are the medication of choice in both acute and long-term (prophylactic) therapy of GERD.

The so called "step-up-strategy" of medication is no longer recommended.

Only in the case of persisting symptoms medication was further increased to high-dose PPI therapy.

In the past this increase in medication lead to a prolonged healing process and consequently to higher medication costs.

Studies have shown that a "step-down"-therapy, beginning with high dose PPI, is highly preferable, since it is much more effective.

Depending on the degree of the symptoms, however, medication may also be applied "on-demand".

The BfArM has approved this kind of medication application only for Esomeprazol (Nexium mups 20 mg).

[MeSH-minor] Anti-Ulcer Agents / administration & dosage. Cross-Sectional Studies. Humans. Incidence. Laryngitis / drug therapy. Laryngitis / epidemiology. Laryngitis / etiology. Proton Pump Inhibitors

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(PMID = 12624841.001).

[ISSN] 0935-8943

[Journal-full-title] Laryngo- rhino- otologie

[ISO-abbreviation] Laryngorhinootologie

[Language] ger

[Publication-type] English Abstract; Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Anti-Ulcer Agents; 0 / Proton Pump Inhibitors

   

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Stimulation of several G-protein-coupled receptors (GPCRs) promotes intracellular production of cyclic adenosine 3',5'-monophosphate (cAMP) and subsequently activates protein kinase A (PKA).

Molecular organisation of PKA-effector association occurs by A kinase anchoring proteins (AKAPs), which target kinase action to specific intracellular sites.

Some AKAPs interact directly with specific cAMP-hydrolysing phosphodiesterase (PDE) isoforms allowing for the assembly of multi-protein complexes that create focal points of intracellular cAMP signalling.

Pharmacological PDE inhibition increases intracellular cAMP concentrations and augments excitation-contraction coupling in heart failure.

However, chronic PDE inhibitor treatment causes severe cardiac side effects and increases mortality.

Moreover, cAMP hydrolysing PDE activity was found decreased in heart failure which may contribute to disease progression via chronic PKA-dependent dysregulation of Ca2+ transport proteins.

[MeSH-minor] Animals. Cyclic Nucleotide Phosphodiesterases, Type 4. Heart Diseases / drug therapy. Heart Diseases / enzymology. Humans. Phosphodiesterase Inhibitors / administration & dosage

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(PMID = 16981825.001).

[ISSN] 1744-7631

[Journal-full-title] Expert opinion on therapeutic targets

[ISO-abbreviation] Expert Opin. Ther. Targets

[Language] eng

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] England

[Chemical-registry-number] 0 / Phosphodiesterase Inhibitors; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4

[Number-of-references] 104

   

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[Title] In vitro activity of cycloSal-nucleoside monophosphates and polyhydroxycarboxylates against orthopoxviruses.

Because variola virus might be used as a pathogen in biological attacks, there is an urgent need to provide effective antiviral drugs for the treatment of orthopoxvirus infections.

Thus, the aim of the present study was to test the antiviral activity of 3 pro-nucleotides of the acyclic nucleoside analogues aciclovir (ACV), 3 of penciclovir (PCV) and 38 of the cyclic nucleoside analogue brivudin (BVDU), on the basis of cycloSaligenyl-nucleoside monophosphate approach against vaccinia virus and cowpox virus in vitro.

As result, three cycloSal-monophosphate derivatives of ACV proved to be potent inhibitors of both vaccinia virus and cowpox virus replication in vitro.

Among the tested monophosphate derivatives of cycloSal-PCV and cycloSal-BVDU, selected substances showed a promising antiviral activity against vaccinia virus and cowpox virus.

In conclusion, by the delivery of nucleoside monophosphates from neutral, membrane-permeable prodrugs on the basis of the cycloSaligenyl-nucleotide concept, different ACV, PCV and BVDU derivatives can act as potent and selective inhibitors of orthopoxvirus replication.

However, most of the cycloSal-monophosphate derivatives of BVDU had a higher cytotoxicity than their parent nucleosides.

[MeSH-major] Acyclovir / analogs & derivatives. Antiviral Agents / pharmacology. Bromodeoxyuridine / analogs & derivatives. Organophosphates / pharmacology. Orthopoxvirus / drug effects

[MeSH-minor] Animals. Cercopithecus aethiops. Cowpox virus / drug effects. Microbial Sensitivity Tests. Tetrazolium Salts / metabolism. Vaccinia virus / drug effects. Vero Cells. Viral Plaque Assay. Virus Replication / drug effects

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(PMID = 16076502.001).

[ISSN] 0166-3542

[Journal-full-title] Antiviral research

[ISO-abbreviation] Antiviral Res.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antiviral Agents; 0 / Organophosphates; 0 / Tetrazolium Salts; 117038-70-7 / 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-((phenylamino)carbonyl)-2H-tetrazolium hydroxide; G34N38R2N1 / Bromodeoxyuridine; X4HES1O11F / Acyclovir

   

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FdUMP[10], a 10mer of 5-fluoro-2'-deoxyuridine 5'-monophosphate (FdUMP), the thymidylate synthase inhibitory metabolite of 5-fluorouracil (FU), is most closely correlated with the DNA topoisomerase I (Top1) inhibitor camptothecin in the National Cancer Institute COMPARE analysis, but not with FU.

[MeSH-major] Antineoplastic Agents / pharmacology. DNA Topoisomerases, Type I / metabolism. DNA, Neoplasm / metabolism. Fluorodeoxyuridylate / analogs & derivatives. Fluorodeoxyuridylate / pharmacology

[MeSH-minor] Animals. Camptothecin / analogs & derivatives. Camptothecin / pharmacology. Cell Death / drug effects. DNA Damage. DNA, Single-Stranded / metabolism. Drug Screening Assays, Antitumor. Fluorouracil / metabolism. Fluorouracil / pharmacology. Leukemia P388 / drug therapy. Leukemia P388 / enzymology. Mice. Quinazolines / pharmacology. Thiophenes / pharmacology. Thymidine / deficiency. Thymidine / metabolism. Thymidylate Synthase / antagonists & inhibitors. Thymidylate Synthase / metabolism. Topoisomerase I Inhibitors

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(PMID = 15930305.001).

[ISSN] 0008-5472

[Journal-full-title] Cancer research

[ISO-abbreviation] Cancer Res.

[Language] eng

[Grant] United States / NCI NIH HHS / CA / U01 CA102532

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / DNA, Neoplasm; 0 / DNA, Single-Stranded; 0 / FdUMP(10); 0 / Quinazolines; 0 / Thiophenes; 0 / Topoisomerase I Inhibitors; 134-46-3 / Fluorodeoxyuridylate; EC 2.1.1.45 / Thymidylate Synthase; EC 5.99.1.2 / DNA Topoisomerases, Type I; FCB9EGG971 / raltitrexed; U3P01618RT / Fluorouracil; VC2W18DGKR / Thymidine; XT3Z54Z28A / Camptothecin

   

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The gold standard of therapy at MS relapse are iv glucocorticoids (GC).

The aim of the study was to assess the changes on the different subsets of circulating CD8+ T-lymphocytes at relapse and after iv GC therapy.

PATIENTS AND METHODS: We consecutively studied 20 patients at MS relapse before and at day 5 after initiation of i.v. methyl-prednisolone (MP) therapy (1 g/day for 3-5 days).

RESULTS: Treatment with i.v.

MP suppressed activated (CD8+CD38+HLA-DR+, p=0.05) and effector memory (CD8+CD27-CD45RO+) T-lymphocytes (p=0.07).

After i.v. MP treatment, positive correlation between regulatory CD4+CD25+high T-lymphocytes and CD8+CD25+ T-lymphocytes was observed (r=0.74; p<0.0001).

MP may contribute to changes observed on the differentiation of CD8+ T-lymphocytes, namely blocking their complete maturation, and expansion of regulatory CD8+ T-lymphocytes.

MP in inhibiting axonal damage which may add a neuroprotective effect on MS relapse.

[MeSH-major] CD8-Positive T-Lymphocytes / drug effects. Glucocorticoids / therapeutic use. Methylprednisolone / therapeutic use. Multiple Sclerosis, Chronic Progressive / drug therapy. Multiple Sclerosis, Chronic Progressive / immunology

[MeSH-minor] Adult. CD4-Positive T-Lymphocytes / drug effects. CD4-Positive T-Lymphocytes / immunology. Female. Flow Cytometry. Humans. Interleukin-2 Receptor alpha Subunit / immunology. Interleukin-2 Receptor alpha Subunit / metabolism. Linear Models. Male. Middle Aged. T-Lymphocytes, Regulatory / drug effects. T-Lymphocytes, Regulatory / immunology. Young Adult

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(PMID = 18835045.001).

[ISSN] 0165-5728

[Journal-full-title] Journal of neuroimmunology

[ISO-abbreviation] J. Neuroimmunol.

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Glucocorticoids; 0 / Interleukin-2 Receptor alpha Subunit; X4W7ZR7023 / Methylprednisolone

   

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[Title] HP(2-9)-magainin 2(1-12), a synthetic hybrid peptide, exerts its antifungal effect on Candida albicans by damaging the plasma membrane.

In our previous study, HP(2-9)-MA(1-12), HP-MA for short, a hybrid peptide incorporating residues 2-9 of Helicobacter pylori ribosomal protein L1 (HP) and residues 1-12 of magainin 2 (MA) was shown to have strong antibacterial activity.

In this study the antifungal activity of HP-MA was evaluated using various fungi, and it was shown that the activity was increased when compared with the parent peptides.

In order to investigate the fungicidal mechanism(s) of HP-MA its action against fungal cell membranes was examined by the potassium-release test, which showed that HP-MA caused an increase in the amount of K+ released from the cells.

Furthermore, HP-MA induced significant morphological changes.

These facts suggested that the fungicidal effect of HP-MA involves damaging the fungal cell membranes.

[MeSH-major] Antifungal Agents / pharmacology. Candida albicans / drug effects. Peptide Fragments / pharmacology

[MeSH-minor] Antimicrobial Cationic Peptides / chemistry. Candidiasis / drug therapy. Circular Dichroism. Magainins. Potassium / metabolism. Ribosomal Proteins / chemistry. Xenopus Proteins / chemistry

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(PMID = 15119592.001).

[ISSN] 1075-2617

[Journal-full-title] Journal of peptide science : an official publication of the European Peptide Society

[ISO-abbreviation] J. Pept. Sci.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Antifungal Agents; 0 / Antimicrobial Cationic Peptides; 0 / Magainins; 0 / Peptide Fragments; 0 / Ribosomal Proteins; 0 / Xenopus Proteins; 0 / ribosomal protein L1; 108433-95-0 / magainin 2 peptide, Xenopus; RWP5GA015D / Potassium

   

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[Title] Reduction of C-reactive protein and the use of anti-hypertensives.

Inflammatory markers such as C-reactive protein are increased in the blood of patients with hypertension and predict the development of cardiovascular disease.

Moreover, C-reactive protein may be a pro-inflammatory molecule under certain circumstances.

C-reactive protein and high blood pressure in combination have additional predictive value for cardiovascular outcomes, as they contribute as independent determinants of cardiovascular risk.

Therapeutic intervention aimed to reduce vascular inflammation in hypertensive patients has been proposed.

Recent lines of evidence suggest that lifestyle modification and pharmacological approaches may reduce blood pressure and inflammation in patients with hypertension.

[MeSH-major] Antihypertensive Agents / therapeutic use. C-Reactive Protein / analysis. Inflammation / drug therapy

[MeSH-minor] Angiotensin II Type 1 Receptor Blockers / pharmacology. Biomarkers / analysis. Humans. Hypertension / drug therapy. Hypertension / physiopathology. Renin-Angiotensin System / drug effects. Renin-Angiotensin System / physiology

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(PMID = 18200816.001).

[ISSN] 1176-6344

[Journal-full-title] Vascular health and risk management

[ISO-abbreviation] Vasc Health Risk Manag

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Review

[Publication-country] New Zealand

[Chemical-registry-number] 0 / Angiotensin II Type 1 Receptor Blockers; 0 / Antihypertensive Agents; 0 / Biomarkers; 9007-41-4 / C-Reactive Protein

[Number-of-references] 93

[Other-IDs] NLM/ PMC2350124

   

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Evidence exists that nitric oxide (NO) may mediate both protective and pathological responses during brain hypoxia (HP).

Reactive oxygen species have also been implicated in the pathophysiological response of the brain tissues to HP.

Therefore, this study investigated whether a NO precursor, l-arginine (l-arg), a free radical scavenger, idebenone (ID), and their combination would reduce neurological injury resulting from hemic hypoxia (HP) in rats.

Moreover, brain lipid peroxides were significantly enhanced, while reduced glutathione, l-ascorbic acids, adenosine triphosphate (ATP) contents, and the activities of catalase and superoxide dismutase, were significantly reduced in the brain tissue.

Histopathological examination of the brain tissue supported these biochemical findings.

This study showed that ID and l-arg were capable of reducing neurological injury following HP in rat, and support the idea of the usefulness of l-arg and ID as prophylaxis from hypoxic brain injury.

[MeSH-major] Antioxidants / therapeutic use. Arginine / therapeutic use. Hypoxia, Brain / prevention & control. Nitrates / adverse effects. Nitric Oxide / metabolism. Ubiquinone / analogs & derivatives

[MeSH-minor] Adenosine Triphosphate / metabolism. Animals. Brain / pathology. Catalase / metabolism. Creatine Kinase / blood. Disease Models, Animal. Drug Administration Schedule. Drug Combinations. Gliosis / etiology. Hemoglobins / metabolism. L-Lactate Dehydrogenase / blood. Male. Nervous System Diseases / drug therapy. Nervous System Diseases / etiology. Neurons / drug effects. Neurons / pathology. Random Allocation. Rats. Rats, Wistar. Superoxide Dismutase / metabolism. Time Factors

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[Copyright] 2010 Elsevier Inc. All rights reserved.

(PMID = 20637840.001).

[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 / Antioxidants; 0 / Drug Combinations; 0 / Hemoglobins; 0 / Nitrates; 1339-63-5 / Ubiquinone; 31C4KY9ESH / Nitric Oxide; 8L70Q75FXE / Adenosine Triphosphate; 8M4L3H2ZVZ / sodium nitrate; 94ZLA3W45F / Arginine; EC 1.1.1.27 / L-Lactate Dehydrogenase; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 2.7.3.2 / Creatine Kinase; HB6PN45W4J / idebenone

   

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[Title] Early metabolic reactivation versus antioxidant therapy after a traumatic spinal cord injury in adult rats.

In order to prove if early metabolic reactivation is a better therapeutic option than antioxidant therapy in the acute phase of TSCI, spinal cord contusions were performed in adult rats using a well-characterized weight drop technique at thoracic 9 level.

After TSCI, pyrophosphate of thiamine or non-degradable cocarboxylase (NDC) enzyme was used to maintain energy levels, antioxidants such as superoxide dismutase and catalase (ANT) were used to decrease oxidative damage and methylprednisolone (MP), which has both therapeutic properties, was used as a control.

Rats were divided into one sham group and six with TSCI; one of them received no treatment, and the rest were treated with NDC, MP, NDC + MP, NDC + ANT or ANT.

The ANT group decreased lactate and creatine phosphokinase levels and increased the amount of preserved tissue (morphometric analysis) as well as functional recovery (Basso, Beattie and Bresnahan or BBB motor scale).

In contrast, NDC treatment increased lipid peroxidation, measured through thiobarbituric acid reactive substances (TBARS) levels, as well as spinal cord tissue destruction and functional deficit.

While increased antioxidant defence after a TSCI may currently be an ideal therapeutic strategy, the usefulness of metabolic reactivation should be tested in the sub-acute or chronic phases of TSCI and new strategies must continue to be tested for the early ones.

[MeSH-major] Antioxidants / therapeutic use. Spinal Cord Injuries / drug therapy. Thiamine Pyrophosphate / therapeutic use. Vitamin B Complex / therapeutic use

[MeSH-minor] Acute Disease. Aging. Animals. Catalase / therapeutic use. Creatine Kinase / metabolism. Female. Lactic Acid / metabolism. Lipid Peroxidation / drug effects. Male. Random Allocation. Rats. Rats, Long-Evans. Recovery of Function. Spinal Cord / drug effects. Spinal Cord / metabolism. Spinal Cord / pathology. Superoxide Dismutase / therapeutic use. Thiobarbituric Acid Reactive Substances / metabolism. Treatment Outcome

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(PMID = 19563509.001).

[ISSN] 1440-1789

[Journal-full-title] Neuropathology : official journal of the Japanese Society of Neuropathology

[ISO-abbreviation] Neuropathology

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Australia

[Chemical-registry-number] 0 / Antioxidants; 0 / Thiobarbituric Acid Reactive Substances; 12001-76-2 / Vitamin B Complex; 33X04XA5AT / Lactic Acid; EC 1.11.1.6 / Catalase; EC 1.15.1.1 / Superoxide Dismutase; EC 2.7.3.2 / Creatine Kinase; Q57971654Y / Thiamine Pyrophosphate

   

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OBJECTIVE: To assess antibacterial activity of levofloxacin to Helicobacter pylori (Hp) strains In Vitro and In Vivo.

To examine the effects of pH variation on the susceptibility of Hp to levofloxacin, Mueller-Hinton agar with 7% defibrinated sheep blood was adjusted to a pH range of 4.0, 5.0, 7.0 by adding hydrochloric acid.

85 Hp-positive Patients with chronic active gastritis or active peptic ulcer disease were consecutively recruited in a prospective, open-label study.

Their Hp status was assessed by (13)C-urea breath test and/or endoscopy 4 - 6 weeks after the end of treatment.

A dual-resistance to amoxicillin and clarithromycin was demonstrated in five Hp strains (9.6%), which were all susceptible to levofloxacin.

76 patients (PP and ITT analysis, 91.7%; 90.6%) become Hp-negative.

CONCLUSION: In the present study, we report a high rate of resistance to amoxicillin and clarithromycin in this region.

Omeprazole/levofloxacin-based triple therapy, including amoxicillin, is attractive because they combine a high eradication efficacy with an excellent tolerability and safety profile.

[MeSH-major] Helicobacter Infections / drug therapy. Helicobacter pylori / drug effects. Levofloxacin. Ofloxacin / therapeutic use

[MeSH-minor] Adolescent. Adult. Aged. Drug Resistance, Bacterial. Female. Humans. Male. Microbial Sensitivity Tests. Middle Aged

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(PMID = 14642083.001).

[ISSN] 0376-2491

[Journal-full-title] Zhonghua yi xue za zhi

[ISO-abbreviation] Zhonghua Yi Xue Za Zhi

[Language] chi

[Publication-type] Clinical Trial; English Abstract; Journal Article; Randomized Controlled Trial

[Publication-country] China

[Chemical-registry-number] 6GNT3Y5LMF / Levofloxacin; A4P49JAZ9H / Ofloxacin

   

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In the present study, the potential role of IL-12 was analyzed in an experimental colitis model in scid mice reconstituted with syngeneic CD45RBhighCD4+ T cells.

Real-time reverse transcription-PCR studies demonstrated that IL-12 p40 mRNA in inflamed colon is induced shortly after T cell transfer and maintained at a stable level after week 4, at the time when wasting disease starts.

Administration of anti-IL-12 on days 0,14, and 28 (early treatment) or on days 28, 42, and 56 (delayed treatment) after T cell transfer, effectively prevented or, respectively cured wasting disease and colitis in scid recipients.

Anti-IL-12 treatment abrogated mucosal inflammation with significantly diminished leukocyte infiltration (CD4 cells, macrophages) and CD54 expression, and down-regulated proinflammatory cytokines IFN-gamma and IL-2.

[MeSH-minor] Animals. Antibodies / immunology. Antibodies / pharmacology. Antibodies / therapeutic use. Cells, Cultured. Chemotaxis, Leukocyte / drug effects. Chronic Disease. Colon / drug effects. Colon / immunology. Colon / metabolism. Colon / pathology. Disease Models, Animal. Female. Immunohistochemistry. Inflammation / drug therapy. Inflammation / immunology. Inflammation / metabolism. Inflammation / pathology. Intercellular Adhesion Molecule-1 / metabolism. Interferon-gamma / metabolism. Kinetics. Mice. Mice, Inbred BALB C. Mice, SCID. RNA, Messenger / genetics. RNA, Messenger / metabolism. Recurrence. Spleen / immunology

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(PMID = 11465113.001).

[ISSN] 0014-2980

[Journal-full-title] European journal of immunology

[ISO-abbreviation] Eur. J. Immunol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Germany

[Chemical-registry-number] 0 / Antibodies; 0 / RNA, Messenger; 126547-89-5 / Intercellular Adhesion Molecule-1; 187348-17-0 / Interleukin-12; 82115-62-6 / Interferon-gamma

   

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Murine Trypanosoma brucei brucei infection leads to elevated plasma endotoxin-like activity levels not related to parasitaemia levels accompanied by the development of acute-phase response and increased plasma levels of serum amyloid P (SAP) and haptoglobin (Hp).

Plasma endotoxin-like activity levels, irrespective of treatment, were elevated three- to fourfold, beginning 7 days after infection.

Plasma protein concentrations increased markedly following infection from 7 days after infection (DAI).

Peak Hp and SAP concentrations in ciprofloxacin-treated and -untreated infected mice were attained 7 and 14 DAI, respectively.

Thereafter, both protein levels gradually declined until the end of the experiment, but Hp levels for non-treated mice declined up to 21 DAI and thereafter significantly increased on 28 and 35 DAI.

[MeSH-minor] Animals. Anti-Bacterial Agents / therapeutic use. Bacterial Infections / drug therapy. Ciprofloxacin / therapeutic use. Female. Haptoglobins / analysis. Mice. Serum Amyloid P-Component / analysis

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(PMID = 19527451.001).

[ISSN] 1365-3024

[Journal-full-title] Parasite immunology

[ISO-abbreviation] Parasite Immunol.

[Language] eng

[Grant] United Kingdom / Wellcome Trust / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Bacterial Agents; 0 / Endotoxins; 0 / Haptoglobins; 0 / Serum Amyloid P-Component; 5E8K9I0O4U / Ciprofloxacin

   

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Ten genes, involved in cell cycle control, nucleic acid binding, and protein phosphorylation, among other functions, underwent more than 5-fold change.

Of the downregulated genes we chose Inosine monophosphate dehydrogenase 2 (IMPDH2) for further validation by quantitative RT-PCR.

In vitro and in vivo drug sensitivity analyses revealed that inhibition of ZNRD1 and IMPDH2 activity sensitized SGC7901/VCR cells to methotrexate.

Taken together, the findings suggest that ZNRD1 could act as a modulator of methotrexate chemotherapy in gastric cancer cells through the regulation of IMPDH2 and Bcl-2.

[MeSH-major] DNA-Binding Proteins / genetics. DNA-Binding Proteins / metabolism. Genes, bcl-2. IMP Dehydrogenase / antagonists & inhibitors. Methotrexate / pharmacology. Stomach Neoplasms / drug therapy. Stomach Neoplasms / genetics

[MeSH-minor] Antimetabolites, Antineoplastic / pharmacology. Apoptosis / drug effects. Base Sequence. Cell Line, Tumor. DNA, Neoplasm / genetics. Drug Resistance, Multiple / genetics. Drug Resistance, Multiple / physiology. Drug Resistance, Neoplasm / genetics. Drug Resistance, Neoplasm / physiology. Gene Expression Regulation, Neoplastic / drug effects. Glutathione / metabolism. Glutathione Transferase / metabolism. Humans. Oligonucleotide Array Sequence Analysis. Proto-Oncogene Proteins c-bcl-2 / metabolism. RNA, Messenger / genetics. RNA, Messenger / metabolism. RNA, Neoplasm / genetics. RNA, Neoplasm / metabolism. RNA, Small Interfering / genetics

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(PMID = 16609701.001).

[ISSN] 0829-8211

[Journal-full-title] Biochemistry and cell biology = Biochimie et biologie cellulaire

[ISO-abbreviation] Biochem. Cell Biol.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Canada

[Chemical-registry-number] 0 / Antimetabolites, Antineoplastic; 0 / DNA, Neoplasm; 0 / DNA-Binding Proteins; 0 / Proto-Oncogene Proteins c-bcl-2; 0 / RNA, Messenger; 0 / RNA, Neoplasm; 0 / RNA, Small Interfering; 0 / ZNRD1 protein, human; EC 1.1.1.205 / IMP Dehydrogenase; EC 1.1.1.205 / IMPDH2 protein, human; EC 2.5.1.18 / Glutathione Transferase; GAN16C9B8O / Glutathione; YL5FZ2Y5U1 / Methotrexate

   

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BACKGROUND: This study was conducted to elucidate the prevalence of Helicobacter pylori in patients with a perforated duodenal ulcer and to determine whether eradication of H. pylori prevent ulcer recurrence following simple repair of the perforation.

Antral mucosal biopsies (to determine the status of HP by rapid urease test, culture and histological examination/staining) were obtained during laparotomy by passing a biopsy forceps through the perforation site. H. pylori positive patients who had undergone patch repair were randomized into the eradication group who received amoxicillin, metranidazole plus omperazole and the control group was given omeprazole alone.

These patients were randomly divided into the triple therapy group (34 patients) and the control group (31 patients).

Eradication of H. pylori was significantly higher in the triple therapy group than the control group and initial ulcer healing was significantly better in the eradication group.

CONCLUSION: H. pylori was present in a high proportion of patients with duodenal ulcer perforation.

[MeSH-major] Anti-Infective Agents / therapeutic use. Anti-Ulcer Agents / therapeutic use. Duodenal Ulcer / surgery. Helicobacter Infections / drug therapy. Helicobacter pylori. Peptic Ulcer Perforation / surgery

[MeSH-minor] Adult. Amoxicillin / therapeutic use. Drug Therapy, Combination. Female. Humans. Male. Metronidazole / therapeutic use. Middle Aged. Omeprazole / therapeutic use. Prevalence. Secondary Prevention

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(PMID = 19138577.001).

[ISSN] 1743-9159

[Journal-full-title] International journal of surgery (London, England)

[ISO-abbreviation] Int J Surg

[Language] eng

[Publication-type] Journal Article; Randomized Controlled Trial

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Infective Agents; 0 / Anti-Ulcer Agents; 140QMO216E / Metronidazole; 804826J2HU / Amoxicillin; KG60484QX9 / Omeprazole

   

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[Title] Magnetic quantitative reverse transcription PCR: a high-throughput method for mRNA extraction and quantitative reverse transcription PCR.

Over the past few years high-throughput platforms for real-time quantitative PCR have become widely available.

One method that stands out with respect to free up- or downscaling of sample size and reliability is the isolation of mRNA using oligodeoxythymidylate [oligo(dT)25]-coated magnetic particles.

In combining this magnetic separation of mRNA with real-time reverse transcription PCR (RT-PCR), we have achieved a highly reproducible, economic, and fast way of analyzing large sample numbers.

We present a solution to this problem that enables excellent adjustment of cDNA amounts prior to the real-time PCR.

Furthermore, as the mRNA is rapidly isolated from crude plant extracts, our method is widely applicable to herbaceous plant species and various tissue types without cumbersome adjustments.

Lastly, due to its flexibility, the method presented here can easily be adapted to specific requirements of various users and has great potential for further automation.

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(PMID = 17824388.001).

[ISSN] 0736-6205

[Journal-full-title] BioTechniques

[ISO-abbreviation] BioTechniques

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't; Technical Report

[Publication-country] England

[Chemical-registry-number] 0 / RNA, Messenger; 0 / RNA, Plant

   

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[Title] [Assessment on intermittent intravenous cyclophosphamide pulse therapy in diffuse proliferative lupus nephritis].

OBJECTIVE: To determine whether intravenous cyclophosphamide pulse therapy (IVCY) is effective for treating patients with diffuse proliferative lupus nephritis (DPLN) who were 1) refractory to methylprednisolone pulse therapy (MP) or 2) could not be treated with MP because of severe diabetes or steroid induced psychosis.

Five of them received IVCY after a failure to achieve renal remission with at least 2 cycles of MP therapy.

Bolus therapy with cyclophosphamide (0.5 g/m2 body surface area) was given once a month for 6 consecutive months and then once every 3 months for a total treatment period of 1 year.

Adverse events were mild and did not require any treatment, with 2 cases of leukocytopenia without fever or major infection.

CONCLUSIONS: IVCY was 1) effective in the treatment of DPLN which was refractory to MP and 2) relatively safe with minimal side effects.

[MeSH-major] Cyclophosphamide / administration & dosage. Lupus Nephritis / drug therapy

[MeSH-minor] Adult. Female. Humans. Injections, Intravenous. Middle Aged. Pulse Therapy, Drug. Treatment Outcome

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(PMID = 10920685.001).

[ISSN] 0300-9157

[Journal-full-title] Ryūmachi. [Rheumatism]

[ISO-abbreviation] Ryumachi

[Language] jpn

[Publication-type] Clinical Trial; English Abstract; Journal Article

[Publication-country] JAPAN

[Chemical-registry-number] 8N3DW7272P / Cyclophosphamide

   

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[Title] Viability and safety of combination drug therapies for erectile dysfunction.

PURPOSE: In some patients with erectile dysfunction (ED) oral, topical or intracavernous drug therapy fails.

However, several classes of drugs demonstrate efficacy for ED, creating the potential for pharmacological combinations preferable to implantation of a penile prosthesis.

MATERIALS AND METHODS: Preliminary reports suggest that combining oral, topical or intracavernous drugs may salvage patients in whom monotherapy fails.

RESULTS: Agents that lead to activation or increases in cyclic nucleotides (cyclic adenosine monophosphate and guanosine monophosphate) with or without nitric oxide donors or nitrates, or alpha-adrenergic antagonists have been used to treat ED.

Combination strategies may allow lower drug doses and reduced adverse effects.

CONCLUSIONS: The encouraging preliminary observations combined with the potential for adverse events provide a scientific rationale for prospective, randomized clinical trials with adequate numbers of subjects.

[MeSH-major] Alprostadil / administration & dosage. Erectile Dysfunction / drug therapy. Phosphodiesterase Inhibitors / administration & dosage. Piperazines / administration & dosage. Vasodilator Agents / administration & dosage

[MeSH-minor] Apomorphine / administration & dosage. Dopamine Agonists. Drug Therapy, Combination. Humans. Male. Purines. Sildenafil Citrate. Sulfones

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(PMID = 12853768.001).

[ISSN] 0022-5347

[Journal-full-title] The Journal of urology

[ISO-abbreviation] J. Urol.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Dopamine Agonists; 0 / Phosphodiesterase Inhibitors; 0 / Piperazines; 0 / Purines; 0 / Sulfones; 0 / Vasodilator Agents; BW9B0ZE037 / Sildenafil Citrate; F5TD010360 / Alprostadil; N21FAR7B4S / Apomorphine

[Number-of-references] 20

   

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[Title] Pharmacokinetic, pharmacodynamic, and outcome investigations as the basis for mycophenolic acid therapeutic drug monitoring in renal and heart transplant patients.

The following are important experimentally-based reasons for recommending the incorporation of target therapeutic concentration monitoring of mycophenolic acid:.

(1) the MPA dose-interval area-under-the-concentration-time curve, and less precisely, MPA predose concentrations predict the risk for development of acute rejection;.

(3) the greater than 10-fold interindividual variation of MPA area under the concentration time curve values in heart and renal transplant patients receiving a fixed dose of the parent drug;.

(4) drug-drug interactions involving other immunosuppressives are such that when switching from one to another (eg, from cyclosporine to tacrolimus or vice-versa) substantial changes in MPA concentrations can occur in patients receiving a fixed dose of the parent drug;.

(5) significant effects of liver and kidney diseases on the steady-state total and free mycophenolic acid area under the concentration time curve values;.

Current investigations are focused on determination of the most optimal sampling time and for mycophenolic acid target therapeutic concentration monitoring.

Further investigations are needed to evaluate the pharmacologic activity of the newly described acyl glucuronide metabolite of mycophenolic acid which has been shown to inhibit, in vitro, inosine monophosphate dehydrogenase.

[MeSH-major] Heart Transplantation / methods. Kidney Transplantation / methods. Mycophenolic Acid / pharmacokinetics. Mycophenolic Acid / therapeutic use

[MeSH-minor] Area Under Curve. Graft Rejection / drug therapy. Humans. Immunosuppressive Agents / pharmacokinetics. Immunosuppressive Agents / pharmacology. Immunosuppressive Agents / therapeutic use. Time Factors. Treatment Outcome

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(PMID = 11239510.001).

[ISSN] 0009-9120

[Journal-full-title] Clinical biochemistry

[ISO-abbreviation] Clin. Biochem.

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Immunosuppressive Agents; HU9DX48N0T / Mycophenolic Acid

[Number-of-references] 37

   

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[Title] [Indication of H. pylori eradication therapy].

In the guideline, for H. pylori the Japanese Society of Helicobacter published diagnosis and treatment in July 2000.

Only peptic ulcers and low grade MALT lymphomas are recommended as an indication of H. pylori eradication and other diseases such as atrophic gastritis, post EMR state for early gastric cancer and post-operated stomach due to gastric cancer, hyperplastic polyps and non-ulcer dyspepsia, were not included.

In addition, Japanese social security foundation approves only peptic ulcers for indication of H. pylori eradication treatment.

However, eradication therapy for atrophic gastritis should be considered in aspect of decreasing gastric cancer risk.

Since accumulated epidemiological, experimental and clinical data strongly support its positive correlation with cancer risk, patients in high risk group for gastric cancer should be included for a target eradication therapy.

Indication of the treatment should be expanded to histological gastritis caused by H. pylori in our country, where prevalence of gastric cancer is very high.

[MeSH-major] Helicobacter Infections / drug therapy. Helicobacter pylori

[MeSH-minor] Humans. Peptic Ulcer / drug therapy. Practice Guidelines as Topic. Stomach Neoplasms / prevention & control

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(PMID = 12607324.001).

[ISSN] 0047-1852

[Journal-full-title] Nihon rinsho. Japanese journal of clinical medicine

[ISO-abbreviation] Nippon Rinsho

[Language] jpn

[Publication-type] English Abstract; Journal Article

[Publication-country] Japan

   

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[Title] Single and short-term dosing effects of levocetirizine on adenosine monophosphate bronchoprovocation in atopic asthma.

AIMS: Adenosine monophosphate (AMP) acts indirectly via primed airway mast cells to induce bronchial hyper-responsiveness, which in turn correlates with eosinophilic asthmatic inflammation and atopic disease expression.

There was a 1-week washout period prior to each randomized treatment.

The provocative concentration of AMP producing a 20% fall in FEV1 (PC20) was measured after each washout at baseline and at 4-6 h following the first and last doses of each randomized treatment.

RESULTS: Baseline mean +/- SEM values after washout prior to each randomized treatment comparing levocetirizine vs placebo were not significantly different for prechallenge FEV1 (% predicted) 83 +/- 4 vs 82 +/- 4, or AMP PC20 (mg ml(-1)) 45 +/- 24 vs 45 +/- 22, respectively.

[MeSH-major] Asthma / drug therapy. Cetirizine / administration & dosage. Histamine H1 Antagonists, Non-Sedating / administration & dosage

[MeSH-minor] Adenosine Monophosphate. Adult. Aged. Bronchial Hyperreactivity / drug therapy. Bronchial Provocation Tests. Cross-Over Studies. Double-Blind Method. Female. Forced Expiratory Volume / drug effects. Humans. Male. Middle Aged

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[Cites] Am J Respir Crit Care Med. 2001 Jun;163(7):1546-50 [11401871.001]

[Cites] Am J Respir Crit Care Med. 2001 Oct 1;164(7):1127-32 [11673197.001]

[Cites] J Allergy Clin Immunol. 2001 Nov;108(5 Suppl):S147-334 [11707753.001]

[Cites] Am J Respir Crit Care Med. 2002 Feb 1;165(3):327-31 [11818315.001]

[Cites] Eur Respir J. 1997 Oct;10(10):2216-24 [9387943.001]

[Cites] Clin Exp Allergy. 2003 Mar;33(3):287-94 [12614440.001]

[Cites] Am J Respir Crit Care Med. 2003 May 1;167(9):1232-8 [12456382.001]

[Cites] Br J Clin Pharmacol. 2003 Jul;56(1):104-11 [12848782.001]

[Cites] Am J Respir Crit Care Med. 1995 Sep;152(3):1107-36 [7663792.001]

[Cites] J Allergy Clin Immunol. 2003 Feb;111(2):337-41 [12589354.001]

(PMID = 15206990.001).

[ISSN] 0306-5251

[Journal-full-title] British journal of clinical pharmacology

[ISO-abbreviation] Br J Clin Pharmacol

[Language] eng

[Publication-type] Clinical Trial; Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Histamine H1 Antagonists, Non-Sedating; 415SHH325A / Adenosine Monophosphate; YO7261ME24 / Cetirizine

[Other-IDs] NLM/ PMC1884543

   

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The incidences of dose-limiting toxicity, principally neutropenia and thrombocytopenia, were unacceptably high at ILX-295501 doses exceeding 1000 mg/m(2), which was determined to be the MTD for both minimally pretreated and heavily pretreated (HP) patients.

One HP patient with non-small cell lung carcinoma experienced a partial response.

The initial drug distribution phase was rapid [harmonic mean half-life (t(1/2alpha)), 2.1 +/- 7.0 min], whereas the terminal elimination phase was slow (harmonic mean t(1/2beta,) 150.6 +/- 80.2 h).

CONCLUSIONS: The recommended dose for Phase II studies of the oral DSU ILX-295501 administered weekly for 3 weeks every 4 weeks is 1000 mg/m(2)/day for both minimally pretreated and HP patients.

[MeSH-major] Antineoplastic Agents / pharmacokinetics. Antineoplastic Agents / toxicity. Neoplasms / drug therapy. Sulfonylurea Compounds / pharmacokinetics. Sulfonylurea Compounds / toxicity

[MeSH-minor] Administration, Oral. Adult. Aged. Aged, 80 and over. Benzofurans. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Male. Metabolic Clearance Rate. Middle Aged. Phenylurea Compounds. Tablets

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(PMID = 14654534.001).

[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] Clinical Trial; Clinical Trial, Phase I; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Benzofurans; 0 / Phenylurea Compounds; 0 / Sulfonylurea Compounds; 0 / Tablets; 150869-74-2 / N-(5-(2,3-dihydrobenzofuryl)sulfonyl)-N'-(3,4-dichlorophenyl)urea

   

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[Title] Sildenafil and vardenafil, types 5 and 6 phosphodiesterase inhibitors, induce caspase-dependent apoptosis of B-chronic lymphocytic leukemia cells.

Type 4 phosphodiesterase (PDE4) inhibitors reportedly induce apoptosis in chronic lymphocytic leukemia (CLL) cells.

Following clinical improvement of one previously untreated CLL patient with sildenafil therapy, we evaluated the in vitro induction of apoptosis in CLL cells by 4 PDE5/6 inhibitors, including sildenafil, vardenafil, zaprinast, and methoxyquinazoline (MQZ).

Vardenafil was 3 and 30 times more potent an inducer of apoptosis than sildenafil and MQZ, respectively.

Both vardenafil and sildenafil failed to elevate adenosine 3'5' cyclic monophosphate (cAMP) levels, largely excluding an inhibitory effect on cAMP-PDE3, -PDE4, and -PDE7.

Drug-induced apoptosis was inhibited by the caspase inhibitor z-VAD.fmk, prevented by interleukin-4 (IL-4), and significantly reduced by stromal-derived factor1-alpha (SDF-1alpha).

We conclude that vardenafil and sildenafil induce caspase-dependent apoptosis of B-CLL cells in vitro and thus might be considered in the treatment of CLL patients.

[MeSH-major] Apoptosis / drug effects. Imidazoles / pharmacology. Leukemia, Lymphocytic, Chronic, B-Cell / pathology. Phosphodiesterase Inhibitors / pharmacology. Piperazines / pharmacology

[MeSH-minor] 3',5'-Cyclic-GMP Phosphodiesterases. Case-Control Studies. Caspases / physiology. Cell Culture Techniques. Chemokine CXCL12. Chemokines, CXC / metabolism. Cyclic AMP / metabolism. Cyclic Nucleotide Phosphodiesterases, Type 5. Cyclic Nucleotide Phosphodiesterases, Type 6. Humans. Leukocytes, Mononuclear. Male. Middle Aged. Phosphoric Diester Hydrolases / chemistry. Purines. Sildenafil Citrate. Sulfones. Triazines. Vardenafil Dihydrochloride

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(PMID = 12393651.001).

[ISSN] 0006-4971

[Journal-full-title] Blood

[ISO-abbreviation] Blood

[Language] eng

[Publication-type] Case Reports; Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / CXCL12 protein, human; 0 / Chemokine CXCL12; 0 / Chemokines, CXC; 0 / Imidazoles; 0 / Phosphodiesterase Inhibitors; 0 / Piperazines; 0 / Purines; 0 / Sulfones; 0 / Triazines; 5O8R96XMH7 / Vardenafil Dihydrochloride; BW9B0ZE037 / Sildenafil Citrate; E0399OZS9N / Cyclic AMP; EC 3.1.4.- / Phosphoric Diester Hydrolases; EC 3.1.4.35 / 3',5'-Cyclic-GMP Phosphodiesterases; EC 3.1.4.35 / Cyclic Nucleotide Phosphodiesterases, Type 5; EC 3.1.4.35 / Cyclic Nucleotide Phosphodiesterases, Type 6; EC 3.1.4.35 / PDE5A protein, human; EC 3.1.4.35 / PDE6B protein, human; EC 3.4.22.- / Caspases

   

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(1) faster HIV disease progression in thalassemia major patients receiving inadequate doses of iron-chelating drug;.

(3) higher iron stores and mortality among patients with haptoglobin Hp 2-2 phenotype; and (4) shorter survival among patients with high bone marrow iron deposition.

These studies largely involved men in developed countries.

Among HIV-infected pregnant women in Africa with a high prevalence of iron deficiency, no relationship was found between indicators of iron status and HIV disease severity.

The available data do not contraindicate the current practice of iron supplementation in developing countries where there is a high prevalence of both HIV infection and iron deficiency.

[MeSH-minor] Anemia, Iron-Deficiency / complications. Anemia, Iron-Deficiency / drug therapy. Anemia, Iron-Deficiency / epidemiology. Female. Humans. Infant. Pregnancy. Prevalence

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[Copyright] Copyright 2001 Harcourt Publishers Ltd.

(PMID = 11601873.001).

[ISSN] 0306-9877

[Journal-full-title] Medical hypotheses

[ISO-abbreviation] Med. Hypotheses

[Language] eng

[Grant] United States / NIAID NIH HHS / AI / AI41956; United States / NICHD NIH HHS / HD / HD30042; United States / NICHD NIH HHS / HD / HD32247

[Publication-type] Journal Article; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.

[Publication-country] Scotland

[Chemical-registry-number] E1UOL152H7 / Iron

   

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[Title] Natriuretic peptides, their receptors, and cyclic guanosine monophosphate-dependent signaling functions.

The mammalian members are atrial natriuretic peptide, B-type natriuretic peptide, C-type natriuretic peptide, and possibly osteocrin/musclin.

Single allele-inactivating mutations in the promoter of human NPR-A are associated with hypertension and heart failure, whereas homozygous inactivating mutations in human NPR-B cause a form of short-limbed dwarfism known as acromesomelic dysplasia type Maroteaux.

The physiological effects of natriuretic peptides are elicited through three classes of cGMP binding proteins: cGMP-dependent protein kinases, cGMP-regulated phosphodiesterases, and cyclic nucleotide-gated ion channels.

In this comprehensive review, the structure, function, regulation, and biological consequences of natriuretic peptides and their associated signaling proteins are described.

[MeSH-minor] Animals. Growth Disorders / drug therapy. Heart Diseases / drug therapy. Humans. Hypertension / drug therapy. Obesity / drug therapy. Protein Structure, Tertiary / physiology. Receptor Cross-Talk / physiology

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(PMID = 16291870.001).

[ISSN] 0163-769X

[Journal-full-title] Endocrine reviews

[ISO-abbreviation] Endocr. Rev.

[Language] eng

[Grant] United States / NHLBI NIH HHS / HL / R01HL66397

[Publication-type] Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review

[Publication-country] United States

[Chemical-registry-number] 0 / Natriuretic Peptides; 0 / Receptors, Peptide; H2D2X058MU / Cyclic GMP

[Number-of-references] 344

   

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The concept that the consumption of a diet rich in flavonoids can be associated with a reduced risk for cardiovascular disease is becoming increasingly accepted.

In the present study we investigated the effects of the following four diets on blood pressure and cholesterol ester levels in hypercholesterolemic Golden Syrian hamsters: a high-fat, high-cholesterol diet (HFHC); a HFHC with 2% cranberry concentrate powder (HFHC+CE); a HFHC with 0.1% rutin (HFHC+Rutin); and a HFHC with 30 mg/kg vitamin E (HFHC+Vit.E).

Ratios of plasma high-density lipoprotein cholesterol (HDL-C) to very-low-density lipoprotein cholesterol and of plasma HDL-C to low-density lipoprotein cholesterol were significantly higher in animals consuming HFHC+Vit.E than in animals fed the other three diets.

[MeSH-major] Antioxidants / therapeutic use. Cardiovascular Diseases / prevention & control. Diet. Flavonols / therapeutic use. Hypercholesterolemia / drug therapy. Plant Preparations / therapeutic use. Vitamin E / therapeutic use

[MeSH-minor] Abdominal Fat / drug effects. Animals. Blood Glucose / metabolism. Blood Pressure / drug effects. Cholesterol / blood. Cholesterol, Dietary / administration & dosage. Cricetinae. Dietary Fats / administration & dosage. Disease Models, Animal. Drug Therapy, Combination. Heart Rate / drug effects. Mesocricetus. Phytotherapy. Powders. Rutin / pharmacology. Rutin / therapeutic use. Vaccinium macrocarpon / chemistry

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(PMID = 20136443.001).

[ISSN] 1557-7600

[Journal-full-title] Journal of medicinal food

[ISO-abbreviation] J Med Food

[Language] eng

[Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Antioxidants; 0 / Blood Glucose; 0 / Cholesterol, Dietary; 0 / Dietary Fats; 0 / Flavonols; 0 / Plant Preparations; 0 / Powders; 1406-18-4 / Vitamin E; 5G06TVY3R7 / Rutin; 97C5T2UQ7J / Cholesterol

   

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BACKGROUND: Ecto-5'-nucleotidase (NT5E, also known as CD73) hydrolyzes extracellular adenosine 5'-monophosphate (AMP) to adenosine in nociceptive circuits.

Recombinant mNT5E hydrolyzed AMP in biochemical assays and was inhibited by alpha,beta-methylene-adenosine 5'-diphosphate (alpha,beta-me-ADP; IC50 = 0.43 microM), a selective inhibitor of NT5E. mNT5E exhibited a dose-dependent thermal antinociceptive effect that lasted for two days when injected intrathecally in wild-type mice.

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(PMID = 20398264.001).

[ISSN] 1744-8069

[Journal-full-title] Molecular pain

[ISO-abbreviation] Mol Pain

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / NS067688-02; United States / NINDS NIH HHS / NS / NS060725-04; United States / NINDS NIH HHS / NS / R01 NS060725; United States / NINDS NIH HHS / NS / R01 NS067688-01; United States / NINDS NIH HHS / NS / NS060725-03; United States / NINDS NIH HHS / NS / R01 NS060725-04; United States / NINDS NIH HHS / NS / NS060725-02; United States / NIGMS NIH HHS / GM / T32GM008719; United States / NINDS NIH HHS / NS / R01 NS060725-03; United States / NINDS NIH HHS / NS / NS067688-01; United States / NINDS NIH HHS / NS / R01 NS067688-02; United States / NINDS NIH HHS / NS / R01NS067688; United States / NINDS NIH HHS / NS / R01 NS060725-02; United States / NINDS NIH HHS / NS / F30NS063507; United States / NINDS NIH HHS / NS / NS060725-01; United States / NINDS NIH HHS / NS / R01 NS060725-01; United States / NINDS NIH HHS / NS / R01 NS067688; United States / NINDS NIH HHS / NS / R01NS060725

[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 / Analgesics; 0 / Receptor, Adenosine A1; 0 / Recombinant Proteins; 415SHH325A / Adenosine Monophosphate; EC 3.1.3.5 / 5'-Nucleotidase

[Other-IDs] NLM/ PMC2874211

   

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DIC was diagnosed in 52 patients (32%); 28 patients at diagnosis and 24 soon after the initiation of induction chemotherapy.

Leukocyte counts, C-reactive protein, and lactate dehydrogenase were significantly higher in the DIC+ group.

On multivariate logistic-regression analysis, variables that were independently associated with the development of DIC were high C-reactive protein, high leukocyte count, negative expressions of CD13 and HLA-DR, and cytogenetics with a normal karyotype or 11q23 abnormality.

[MeSH-minor] Acute Disease. Aged. Antigens, CD13 / analysis. C-Reactive Protein / analysis. Chromosomes, Human, Pair 11. Cytogenetics. Female. HLA-DR Antigens / analysis. Humans. Leukocyte Count. Male. Multivariate Analysis. Prevalence. Retrospective Studies. Treatment Outcome

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(PMID = 17875527.001).

[ISSN] 0925-5710

[Journal-full-title] International journal of hematology

[ISO-abbreviation] Int. J. Hematol.

[Language] eng

[Publication-type] Journal Article

[Publication-country] Japan

[Chemical-registry-number] 0 / HLA-DR Antigens; 9007-41-4 / C-Reactive Protein; EC 3.4.11.2 / Antigens, CD13

   

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[Title] Phosphodiesterase-4 inhibitors in the treatment of inflammatory lung disease.

Phosphodiesterases (PDE) belong to an important family of proteins that regulate the intracellular levels of cyclic nucleotide second messengers.

Targeting PDE with selective inhibitors may offer novel therapeutic strategies in the treatment of various conditions, and in the context of respiratory disease these include asthma and chronic obstructive pulmonary disease (COPD).

The rationale for such an approach stems, in part, from the clinical efficacy of theophylline, an orally active drug that is purportedly a nonselective PDE inhibitor.

In addition, intracellular cyclic adenosine monophosphate (cAMP) levels regulate the function of many of the cells thought to contribute to the pathogenesis of respiratory diseases such as asthma and COPD, and these cells also selectively express PDE4.

This has offered pharmaceutical companies the opportunity to selectively targeting these enzymes for the treatment of these diseases.

Finally, the success of targeting PDE5 in the treatment of erectile dysfunction provides clinical proof of concept for the targeting of PDE in disease.

Whether a 'Viagra' of the airways can be found for the treatment of asthma and COPD remains to be seen, but positive results from recent clinical studies examining the efficacy of selective PDE4 inhibitors such as cilomilast and roflumilast offer some optimism.

However, one of the major issues to be resolved is the tolerability profile associated with this drug class that is a consequence of PDE4 inhibition.

While cilomilast and roflumilast have low emetic potential they are not free from emesis and various strategies are being investigated in the hope of developing a PDE4 inhibitor without this adverse effect.

[MeSH-major] 3',5'-Cyclic-AMP Phosphodiesterases / antagonists & inhibitors. Lung Diseases / drug therapy. Phosphodiesterase Inhibitors / pharmacology

[MeSH-minor] Animals. Asthma / drug therapy. Asthma / enzymology. Clinical Trials as Topic. Cyclic AMP / metabolism. Cyclic Nucleotide Phosphodiesterases, Type 4. Humans. Pulmonary Disease, Chronic Obstructive / drug therapy. Pulmonary Disease, Chronic Obstructive / enzymology

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(PMID = 14636078.001).

[ISSN] 0012-6667

[Journal-full-title] Drugs

[ISO-abbreviation] Drugs

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] New Zealand

[Chemical-registry-number] 0 / Phosphodiesterase Inhibitors; E0399OZS9N / Cyclic AMP; EC 3.1.4.17 / 3',5'-Cyclic-AMP Phosphodiesterases; EC 3.1.4.17 / Cyclic Nucleotide Phosphodiesterases, Type 4

[Number-of-references] 176

   

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In this study, mice were treated with oral or i.v. dFdC at a single dose (1qdx1d) or at multiple doses once daily for 7 days (1qdx7d) or seven times daily (7qdx1d).

Blood, liver, kidneys, and lungs were collected at several time points.

The nucleosides dFdC and dFdU as well as the nucleotides gemcitabine monophosphate (dFdC-MP), diphosphate, and triphosphate (dFdC-TP) and dFdU monophosphate, diphosphate (dFdU-DP), and triphosphate (dFdU-TP) were simultaneously quantified by high-performance liquid chromatography with ultraviolet and radioisotope detection.

We demonstrate that phosphorylated metabolites of both dFdC and dFdU are formed in mice, primarily consisting of dFdC-MP, dFdC-TP, and dFdU-TP.

The presence of dFdC-MP, dFdC-TP, and dFdU-TP in plasma and urine suggests efflux of these potentially toxic metabolites.

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(PMID = 18490432.001).

[ISSN] 1521-009X

[Journal-full-title] Drug metabolism and disposition: the biological fate of chemicals

[ISO-abbreviation] Drug Metab. Dispos.

[Language] eng

[Publication-type] Journal Article

[Publication-country] United States

[Chemical-registry-number] 0 / Antineoplastic Agents; 0W860991D6 / Deoxycytidine; B76N6SBZ8R / gemcitabine

   

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[Title] Pharmacological basis for cladribine resistance.

Cladribine, unlike many other drugs, is toxic to both dividing and indolent lymphoid malignancies.

Cladribine is a prodrug and must be phosphorylated intracellularly to cladribine-monophosphate (MP) by the nuclear/cystosol enzyme deoxycytidine kinase (dCK) and the mitochondrial enzyme deoxyguanosine kinase.

The cytotoxicity mainly depends on the accumulation of cladribine-triphosphates (TP) after phosphorylation of cladribine-MP by nucleoside monophosphate kinase and nucleoside diphosphate kinase.

5'-Nucleotidase (5'-NT) dephosphorylates cladribine-MP and the accumulation of cladribine-TP depends on the ratio of dCK and 5'-NT in the cells.

The mechanisms underlying cladribine resistance are multifactorial, e.g. decreased nucleoside transport, decreased activity or deficiency of dCK, altered intracellular pools of competing nucleotides, altered regulation of ribonucleotide reductase and increased drug inactivation by 5'-NT.

[MeSH-major] Adenosine Triphosphate / analogs & derivatives. Antineoplastic Agents / pharmacology. Cladribine / analogs & derivatives. Cladribine / pharmacology. Drug Resistance, Neoplasm / physiology. Ribonucleotide Reductases / metabolism

[MeSH-minor] 5'-Nucleotidase / antagonists & inhibitors. 5'-Nucleotidase / metabolism. Biological Transport. Deoxycytidine Kinase / metabolism. Hematologic Neoplasms / drug therapy. Humans

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(PMID = 14692522.001).

[ISSN] 1042-8194

[Journal-full-title] Leukemia & lymphoma

[ISO-abbreviation] Leuk. Lymphoma

[Language] eng

[Publication-type] Journal Article; Review

[Publication-country] England

[Chemical-registry-number] 0 / Antineoplastic Agents; 0 / cladribine triphosphate; 47M74X9YT5 / Cladribine; 8L70Q75FXE / Adenosine Triphosphate; EC 1.17.4.- / Ribonucleotide Reductases; EC 2.7.1.74 / Deoxycytidine Kinase; EC 3.1.3.5 / 5'-Nucleotidase

[Number-of-references] 101

   

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[Title] Combination of thymidine phosphorylase gene transfer and deoxyinosine treatment greatly enhances 5-fluorouracil antitumor activity in vitro and in vivo.

Cancer, 80: 1726-1733, 1999) or associating FUra with 2'-deoxyinosine (d-Ino), a modulator providing the tumors with TP cofactor deoxyribose 1-phosphate (J.

Results showed a near 4000 times increase of cell sensitivity in vitro after double (genetic + biochemical) modulation.

This potentiation of tumor response was accompanied by a total change in the FUra anabolic pathway with a 5000% increase of cytosolic fluorodeoxyuridine monophosphate, a stronger and longer inhibition of thymidylate synthase, and 300% augmentation of DNA damage.

Besides, whereas thymidine failed to inhibit FUra cytotoxicity in LS174T wild-type cells, the potentiation of the antitumor activity observed in the modulating regimen was partly reversed by thymidine, indicative of thymidylate synthase as the main drug target.

Results showed that whereas FUra alone was completely ineffective on wild-type tumor growth, the size of TP-transfected tumors in animals treated with the FUra/d-Ino combination was reduced by 80% (P < 0.05).

Our results suggest that FUra exhibits stronger antiproliferative activity when activated via TP through the DNA pathway and that high tumoral TP activity therefore leads to enhanced sensitivity to fluoropyrimidines.

[MeSH-major] Colorectal Neoplasms / therapy. Fluorouracil / therapeutic use. Genetic Therapy. Inosine / analogs & derivatives. Inosine / therapeutic use. Thymidine Phosphorylase / genetics

[MeSH-minor] Animals. Apoptosis / drug effects. Cell Division / drug effects. Combined Modality Therapy. Drug Synergism. Gene Transfer Techniques. Humans. In Vitro Techniques. Mice. Mice, Nude. Thymidylate Synthase / antagonists & inhibitors. Thymidylate Synthase / metabolism. Thymine Nucleotides / metabolism. Tritium. Tumor Cells, Cultured / drug effects. Tumor Cells, Cultured / metabolism

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(PMID = 12467230.001).

[ISSN] 1535-7163

[Journal-full-title] Molecular cancer therapeutics

[ISO-abbreviation] Mol. Cancer Ther.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Thymine Nucleotides; 10028-17-8 / Tritium; 5A614L51CT / Inosine; EC 2.1.1.45 / Thymidylate Synthase; EC 2.4.2.4 / Thymidine Phosphorylase; HN0RQ6SBWQ / deoxyinosine; U3P01618RT / Fluorouracil

   

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However, the potential toxicity of SOSs on eukaryotic cells has not been documented in vitro.

For this purpose, hydrogen peroxide (HP) was used as a positive control of oxidative damage.

When these solutions were used at concentrations indicated for wound care (i.e. undiluted MCN or 880 mM HP), HP was significantly more toxic than MCN.

After 5 and 30 minutes of exposure, cell viability was 38% and 5%, respectively, in 880 mM HP-treated cells versus 75% and 70% in MCN-treated populations, respectively.

HP induced both apoptosis and necrosis, whereas MCN induced only necrosis.

Genotoxic and ageing studies were then conducted at sublethal HP concentrations as previously reported in the literature.

Cellular DNA and RNA were partially degraded only in HDFs exposed to 500 microM HP for 30 minutes but not in those exposed to undiluted MCN.

At this same concentration, HP induced the formation of 8-hydroxy-2'deoxyguanosine adducts in HDFs but this effect was neither observed in control- nor observed in MCN-treated cells.

HDFs were further exposed to 5 microM HP or 10% MCN for 1 month.

The expression of senescence-associated-beta-galactosidase was only significantly elevated in cells chronically exposed to 5 microM HP.

Altogether, these results show that MCN is significantly less cytotoxic than antiseptic HP concentrations (i.e.

[MeSH-major] Disinfectants / pharmacology. Fibroblasts / drug effects. Fibroblasts / pathology. Hydrogen Peroxide / pharmacology. Skin / cytology

[MeSH-minor] Anti-Infective Agents, Local / pharmacology. Apoptosis / drug effects. Cell Survival / drug effects. Cells, Cultured. DNA Adducts / drug effects. DNA Damage / drug effects. Deoxyguanosine / analogs & derivatives. Deoxyguanosine / metabolism. Humans. Hydrogen-Ion Concentration. Necrosis / chemically induced. Oxidative Stress / drug effects. RNA Stability / drug effects. beta-Galactosidase / metabolism

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(PMID = 17924880.001).

[ISSN] 1742-4801

[Journal-full-title] International wound journal

[ISO-abbreviation] Int Wound J

[Language] eng

[Publication-type] Journal Article

[Publication-country] England

[Chemical-registry-number] 0 / Anti-Infective Agents, Local; 0 / DNA Adducts; 0 / Disinfectants; 0 / superoxidized water; 88847-89-6 / 8-oxo-7-hydrodeoxyguanosine; BBX060AN9V / Hydrogen Peroxide; EC 3.2.1.23 / beta-Galactosidase; G9481N71RO / Deoxyguanosine

   

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[Title] [Long-term therapeutic effect of triple therapy consisted of omeperazole, clarithromycin and amoxycillin in children with Helicobacter pylori infection and approach to re-treatment after failure of the treatment].

OBJECTIVE: Helicobacter pylori (Hp) infection presents high prevalence in the world, but there are few pediatric assays evaluating antimicrobial treatment using a short regimen of triple therapy.

To evaluate the eradication rate and long term therapeutic effect of a triple therapy consisted of omeperazole, clarithromycin (CLA) and amoxycillin (AMO) on Hp infection, the authors explored the alternative therapeutic programs and their effects after first therapeutic failure.

METHODS: A total of 192 children with Hp infection were divided into two groups: 157 children were given the triple therapy for one week (CLA group); 35 children were given another triple therapy composed of omeperazole, metronidazole (MET) and AMO for two weeks (MET group).

All of the children were followed up for 1 - 36 months after the therapies ended.

Twenty-two children in whom Hp was eradicated with CLA triple therapy were followed up for 3 years.

The children of the two groups who had therapeutic failure were given re-treatment as follows.

CLA triple therapy was given for one week to the children who had failure after MET triple therapy; increased doses of CLA with longer treatment course was given to the children who had failure after CLA triple therapy.

A tetra therapy consisted of omeperazole, colloidal bismuth subcitrate (CBS), furazolidone (FUR) and AMO was given to the children in whom the re-treatment failed.

RESULTS: The Hp eradication and ulcer recovery rate of CLA group was 90.4% (142/157) and 96.9% (32/33), respectively; the Hp eradication rate of MET group was 77% (27/35).

The recurrence rate of 22 Hp eradicated children treated with CLA triple therapy was 4.5% (1/22) during the 3-year follow-up.

The eradication rate of the three re-treatment programs for 29 children was 75% (6/8), 77% (11/15) and 100% (6/6), respectively. CONCLUSION:.

(1) Omeperazole, CLA and AMO triple therapy for one week was the best to eradicate Hp infection with high eradication rate, few side effects, short period of treatment, good compliance and low recurrence rate. (2) Proper increase of CLA dose and longer therapeutic course may increase the eradication rate.

Omeperazole, CBA, FUR and AMO tetra therapeutic program may be used as an alternative treatment in patients who develop resistance to CLA triple therapy.

[MeSH-major] Amoxicillin / therapeutic use. Clarithromycin / therapeutic use. Drug Therapy, Combination / therapeutic use. Helicobacter Infections / drug therapy. Omeprazole / therapeutic use

[MeSH-minor] Adolescent. Anti-Ulcer Agents / administration & dosage. Anti-Ulcer Agents / therapeutic use. Child. Child, Preschool. Female. Follow-Up Studies. Helicobacter pylori / drug effects. Humans. Male. Metronidazole / administration & dosage. Metronidazole / therapeutic use. Recurrence. Time Factors. Treatment Outcome

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(PMID = 15265423.001).

[ISSN] 0578-1310

[Journal-full-title] Zhonghua er ke za zhi = Chinese journal of pediatrics

[ISO-abbreviation] Zhonghua Er Ke Za Zhi

[Language] chi

[Publication-type] Clinical Trial; Comparative Study; Controlled Clinical Trial; English Abstract; Journal Article

[Publication-country] China

[Chemical-registry-number] 0 / Anti-Ulcer Agents; 140QMO216E / Metronidazole; 804826J2HU / Amoxicillin; H1250JIK0A / Clarithromycin; KG60484QX9 / Omeprazole

   

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[Title] Triazole inhibitors of Cryptosporidium parvum inosine 5'-monophosphate dehydrogenase.

Cryptosporidium parvum is an important human pathogen and potential bioterrorism agent.

This protozoan parasite cannot salvage guanine or guanosine and therefore relies on inosine 5'-monophosphate dehydrogenase (IMPDH) for biosynthesis of guanine nucleotides and hence for survival.

The 1,2,3-triazole CpIMPDH inhibitors provide new tools for elucidating the role of IMPDH in C. parvum and may serve as potential therapeutics for treating cryptosporidiosis.

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(PMID = 19624136.001).

[ISSN] 1520-4804

[Journal-full-title] Journal of medicinal chemistry

[ISO-abbreviation] J. Med. Chem.

[Language] ENG

[Grant] United States / NINDS NIH HHS / NS / R21 NS067497; United States / NIAID NIH HHS / AI / U01AI075466; United States / NIAID NIH HHS / AI / U01 AI075466; United States / NIAID NIH HHS / AI / U01 AI075466-01; United States / NIAID NIH HHS / AI / AI075466-01

[Publication-type] 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.

[Publication-country] United States

[Chemical-registry-number] 0 / Antiprotozoal Agents; 0 / Enzyme Inhibitors; 0 / Triazoles; EC 1.1.1.205 / IMP Dehydrogenase

[Other-IDs] NLM/ NIHMS167141; NLM/ PMC2810100

   

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[Title] Long-term therapy with inhaled iloprost in patients with pulmonary hypertension.

Iloprost was inhaled 6-9 times daily with a night pause employing a jet nebulizer delivering an inhaled single dose of 4microg at the mouthpiece.

Thirty-six patients completed at least 630 days of therapy (25 IPAH, 11 PHother), 19 patients dropped out prematurely and 8 patients died (3 IPAH, 5 PHother).

There were no drug-induced toxicities and only mild to moderate side effects.

CONCLUSION: Inhaled iloprost is well tolerated as long-term therapy and no substantial dose increase is required.

Although uncontrolled, the data suggest a long-term clinical benefit from continued therapy with inhaled iloprost.

[MeSH-minor] Administration, Inhalation. Adolescent. Adult. Aged. Dose-Response Relationship, Drug. Drug Administration Schedule. Female. Humans. Male. Middle Aged. Prospective Studies. Time Factors. Treatment Outcome. Young Adult

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(PMID = 20153158.001).

[ISSN] 1532-3064

[Journal-full-title] Respiratory medicine

[ISO-abbreviation] Respir Med

[Language] eng

[Databank-accession-numbers] ClinicalTrials.gov/ NCT00414687

[Publication-type] Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't

[Publication-country] England

[Chemical-registry-number] 0 / Vasodilator Agents; JED5K35YGL / Iloprost

   

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[Title] Characterization of reactions of antimoniate and meglumine antimoniate with a guanine ribonucleoside at different pH.

It has been shown previously that Sb(V) forms mono- and bis-adducts with adenine and guanine ribonucleosides, suggesting that ribonucleosides may be a target for pentavalent antimonial drugs in the treatment of leishmaniasis.

In the present work, the reactions of antimoniate (KSb(OH)(6)) and meglumine antimoniate (MA) with guanosine 5'-monophosphate (GMP) have been characterized at 37 degrees C in aqueous solution and two different pH (5 and 6.5), using ESI(-)-MS and (1)H NMR.

The (1)H NMR anomeric region was explored for determining the concentrations of mono- and bis-adducts.

When MA was used, instead of antimoniate, formation of 1:1 Sb-GMP complex occurred, but with a slower rate constant.

Thermodynamic and kinetic data are consistent with the formation of 1:1 Sb-ribonucleoside complexes in vertebrate hosts, following treatment with pentavalent antimonial drugs.

[MeSH-major] Antimony / metabolism. Antiprotozoal Agents / metabolism. Guanosine Monophosphate / metabolism. Hydrogen-Ion Concentration. Meglumine / metabolism. Organometallic Compounds / metabolism

[MeSH-minor] Animals. Leishmaniasis / drug therapy. Nuclear Magnetic Resonance, Biomolecular. Spectrometry, Mass, Electrospray Ionization. Thermodynamics

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(PMID = 16937264.001).

[ISSN] 0966-0844

[Journal-full-title] Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine

[ISO-abbreviation] Biometals

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Netherlands

[Chemical-registry-number] 0 / Antiprotozoal Agents; 0 / Organometallic Compounds; 6HG8UB2MUY / Meglumine; 75G4TW236W / meglumine antimoniate; 85-32-5 / Guanosine Monophosphate; 9IT35J3UV3 / Antimony

   

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BACKGROUND: A critical role of soluble guanylate cyclase and nitric oxide-dependent cyclic 3',5'-guanosine monophosphate (cGMP) production for glomerular matrix expansion has recently been documented in a rat model of acute anti-thy1 glomerulonephritis.

In week 16, analysis included effects on systolic blood pressure, proteinuria, kidney function, glomerular and tubulointerstitial matrix protein accumulation, expression of transforming growth factor-beta1 (TGF-beta1), fibronectin and plasminogen activator inhibitor type 1 (PAI-1), macrophage infiltration, cell proliferation, basal and nitric oxide-stimulated cGMP production as well as tubulointerstitial mRNA expression of alpha 1 and beta 1 soluble guanylate cyclase.

RESULTS: The moderately elevated systolic blood pressure seen in the chronic glomerulosclerosis group was comparably decreased by both treatments.

Bay 41-2272 treatment enhanced glomerular and tubulointerstitial nitric oxide-cGMP signaling significantly.

In contrast, hydralazine therapy did not significantly affect renal nitric oxide-cGMP signaling, macrophage number, cell proliferation, matrix protein expression and accumulation.

[MeSH-major] Glomerulosclerosis, Focal Segmental / drug therapy. Glomerulosclerosis, Focal Segmental / metabolism. Isoantibodies / pharmacology. Pyrazoles / pharmacology. Pyridines / pharmacology. Receptors, Cytoplasmic and Nuclear / metabolism

[MeSH-minor] Animals. Biomarkers. Blood Pressure / drug effects. Body Weight. Chronic Disease. Disease Progression. Eating. Enzyme Activation / drug effects. Fibrosis. Gene Expression. Guanylate Cyclase. Hydralazine / pharmacology. Kidney Glomerulus / enzymology. Kidney Glomerulus / pathology. Kidney Glomerulus / physiology. Male. Nitric Oxide / metabolism. Proteinuria / drug therapy. Proteinuria / immunology. Proteinuria / metabolism. Rats. Rats, Wistar. Signal Transduction / physiology. Vasodilator Agents / pharmacology

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(PMID = 15954895.001).

[ISSN] 0085-2538

[Journal-full-title] Kidney international

[ISO-abbreviation] Kidney Int.

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / 3-(4-Amino-5-cyclopropylpyrimidine-2-yl)-1-(2-fluorobenzyl)-1H-pyrazolo(3,4-b)pyridine; 0 / Biomarkers; 0 / Isoantibodies; 0 / Pyrazoles; 0 / Pyridines; 0 / Receptors, Cytoplasmic and Nuclear; 0 / Vasodilator Agents; 0 / anti-Thy antibody; 26NAK24LS8 / Hydralazine; 31C4KY9ESH / Nitric Oxide; EC 4.6.1.2 / Guanylate Cyclase; EC 4.6.1.2 / soluble guanylyl cyclase

   

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This paper presents a method exploiting the high efficiency of capillary electrophoresis and the complexing properties of cyclodextrins to achieve the separation of the four stereoisomers of this weakly basic compound (pKa = 7.4).

For this purpose, the combination of a neutral cyclodextrin, hydroxypropyl-gamma-cyclodextrin (HP-gamma-CD), and an anionic cyclodextrin, carboxymethyl-beta-cyclodextrin (CM-beta-CD), was added to the separation buffer running in an uncoated silica capillary.

After selection of the suitable cyclodextrin system, satisfactorily separation conditions were as follows: 30 mM phosphate buffer (pH 6.4) containing 10 mM of HP-gamma-CD and 10 mM of CM-beta-CD, running voltage +30 kV.

The resulting run time and resolutions were respectively about 17 min and between 1.95 and 2.84.

[MeSH-minor] Angina Pectoris / drug therapy. Humans. Molecular Structure. Reproducibility of Results. Stereoisomerism

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(PMID = 15881082.001).

[ISSN] 1615-9306

[Journal-full-title] Journal of separation science

[ISO-abbreviation] J Sep Sci

[Language] eng

[Publication-type] Journal Article

[Publication-country] Germany

[Chemical-registry-number] 0 / Cardiovascular Agents; 0 / beta-Cyclodextrins; 0 / carboxymethyl-beta-cyclodextrin; 0 / gamma-Cyclodextrins; 0 / hydroxypropyl-gamma-cyclodextrin

   

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[Title] Heme arginate therapy enhanced adiponectin and atrial natriuretic peptide, but abated endothelin-1 with attenuation of kidney histopathological lesions in mineralocorticoid-induced hypertension.

Correspondingly, HO activity, adiponectin, adenosine monophosphate-activated protein kinase (AMPK), ANP, cGMP, antioxidants such as bilirubin, ferritin, superoxide dismutase, and catalase, and total antioxidant capacity were increased, whereas ET-1, transforming growth factor beta (TGF-beta), fibronectin, and 8-isoprostane were abated.

Because 8-isoprostane stimulates ET-1 to potentiate oxidative stress and fibrosis, up-regulating HO-1 enhanced tissue antioxidant status alongside cellular targets such as adiponectin, AMPK, ANP, and cGMP to suppress ET-1, TGF-beta, and fibronectin with a corresponding decline of renal lesions, proteinuria/albuminuria, and thus improved renal function.

[MeSH-major] Adiponectin / metabolism. Arginine / therapeutic use. Atrial Natriuretic Factor / metabolism. Endothelin-1 / metabolism. Heme / therapeutic use. Hypertension / drug therapy. Kidney / drug effects. Kidney Diseases / prevention & control

[MeSH-minor] Animals. Blood Pressure / drug effects. Blotting, Western. Desoxycorticosterone / analogs & derivatives. Disease Models, Animal. Heme Oxygenase (Decyclizing) / metabolism. Male. Mineralocorticoids. Rats. Rats, Sprague-Dawley

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(PMID = 20392817.001).

[ISSN] 1521-0103

[Journal-full-title] The Journal of pharmacology and experimental therapeutics

[ISO-abbreviation] J. Pharmacol. Exp. Ther.

[Language] eng

[Grant] Canada / Canadian Institutes of Health Research / /

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] United States

[Chemical-registry-number] 0 / Adiponectin; 0 / Endothelin-1; 0 / Mineralocorticoids; 0 / atrial natriuretic peptide, rat; 40GP35YQ49 / Desoxycorticosterone; 42VZT0U6YR / Heme; 85637-73-6 / Atrial Natriuretic Factor; 94ZLA3W45F / Arginine; EC 1.14.99.3 / Heme Oxygenase (Decyclizing); R1B526117P / heme arginate

   

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PURPOSE: Colforsin, a water-soluble forskolin derivative, directly activates adenylate cyclase and thereby increases the 3',5'-cyclic adenosine monophosphate (cAMP) level in vascular smooth muscle cells.

The results suggest that colforsin could be effective in the treatment of PH.

[MeSH-major] Colforsin / analogs & derivatives. Hypertension, Pulmonary / drug therapy. Vasodilator Agents / therapeutic use

[MeSH-minor] 8-Bromo Cyclic Adenosine Monophosphate / pharmacology. Animals. Chronic Disease. Dinoprost / pharmacology. Drug Synergism. Fluorescent Dyes. Fura-2. Hypertrophy, Right Ventricular / drug therapy. Hypertrophy, Right Ventricular / physiopathology. Hypoxia / drug therapy. In Vitro Techniques. Isometric Contraction / drug effects. Male. Muscle Contraction / drug effects. Potassium Chloride / pharmacology. Pulmonary Artery / drug effects. Rats. Rats, Wistar. Vasodilation / drug effects

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(PMID = 20300779.001).

[ISSN] 1438-8359

[Journal-full-title] Journal of anesthesia

[ISO-abbreviation] J Anesth

[Language] eng

[Publication-type] Journal Article; Research Support, Non-U.S. Gov't

[Publication-country] Japan

[Chemical-registry-number] 0 / Fluorescent Dyes; 0 / Vasodilator Agents; 1F7A44V6OU / Colforsin; 23583-48-4 / 8-Bromo Cyclic Adenosine Monophosphate; 660YQ98I10 / Potassium Chloride; B7IN85G1HY / Dinoprost; TSN3DL106G / Fura-2