Sharma H, Aqil M, Imam F, Alam MS, Kapur P, Pillai KK. A pharmacovigilance study in the department of medicine of a university teaching hospital. Pharmacy Practice 2007; 5 1 ; : 46-49.
We are happy to present dr. Hajo Grundmann as the new projectleader of EARSS. He is a senior medical microbiologist and Master of Science in Communicable Diseases Epidemiology from the London School of Hygiene and he`s an active member in a number of ESCMID study groups. At the moment he has a position as special senior lecturer in medical microbiology & infectious diseases at the Faculty of Medicine, University of Nottingham and he works as Project Director Ifakara Health Research and Development Centre, Tanzania Swiss Tropical Institute, Basel. We look forward to cooperate with him. He will start working at EARSS RIVM at the 1st of March 2003. New countries delivering data in 2002: Three new countries started reporting data to EARSS in 2002; Estonia, Romania and Slovakia, which brings the total number of reporting countries to 28, for instance, alpha lipoic acid dmae.
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Common side effects include the following: fatigue anemia irritability itching skin rash sinus congestion and cough 1 2 3 « previous page glossary next page » next: surgery printer-friendly format email to a friend last editorial review: 10 21 2005 emedicinehealth is a first aid and consumer health information site written by physicians for patients and consumers.
CHIEF COMPLAINT: Leg weakness HISTORY OF PRESENT ILLNESS: A 20-year-old Laotian man with no significant medical history presented after awaking in the middle of the night with profound weakness of his lower extremities. He was unable to bear weight and also noted a milder degree of upper extremity weakness. He had no back pain or sensory changes, nor had he noted any change in bowel or bladder function. On the night prior to admission he reported having a mild frontal headache and an episode of vomiting. He had played soccer the day prior to admission without any difficulty. On further review of his history, the patient recalled a similar episode that occurred approximately one month prior, during which he experienced similar transient lower extremity weakness that resolved spontaneously after 12 hours. He and amantadine.
To promote effective use and management of antivirals and vaccine, Ontario will develop the following tools: Fact sheets on antivirals i.e., who will receive them, where to access them, how to take them ; Antiviral comparison chart An algorithm for antiviral treatment Guidelines for handling and managing antivirals including dispensing procedures and how to limit wastage Clinical guidelines for antiviral use and patient care in health care settings Fact sheets on immunization i.e., benefits, location of immunization clinics.
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Tial screening test for Wilson's disease is measurement of serum ceruloplasmin Table 2 ; . The levels will be reduced in approximately 85 percent of affected patients. Patients should also be examined by an ophthalmologist for KayserFleischer rings. If the ceruloplasmin level is normal and Kayser Fleischer rings are absent, but the physician still suspects that Wilson's disease may be present, the next test is a 24-hour urine collection for a quantitative assessment of copper excretion. Excretion of more than 100 g of copper per day is suggestive of Wilson's disease. The diagnosis is usually confirmed by liver biopsy to measure hepatic copper levels. Patients with Wilson's disease have hepatic copper levels of more than 250 g per gram of liver, dry weight. Although the gene responsible for Wilson's disease has been identified, the number of disease-specific mutations is so great that molecular diagnosis is not yet feasible.
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Non-fatal myocardial infarction, unstable angina or sudden cardiac death in AFCAPS TexCAPS. In each trial, a clear and consistently significant reduction in risk of the primary endpoint was found in patients on active treatment compared with placebo.[5-9] As summarised in table II, statistically significant, or strong trends toward significant, risk re Adis International Limited. All rights reserved.
[N. Sitachitta, Department of Chemistry, University of Hawaii at Manoa, Honolulu, HI 96822, United States] - J. NAT. PROD. 2005 68 9 ; - summ in ENGL A collection of an undescribed marine sponge of the genus Plakortis yielded four new "polyketide-derived" metabolites, lehualides A-D 1-4 ; . The structures of compounds 1-4 were elucidated by interpretation of spectral data. Compound 2 demonstrated cytotoxicity against an ovarian cancer cell line, while compound 4 was active against both ovarian cancer and leukemia cell lines. 2005 American Chemical Society and American Society of Pharmacognosy. 611. Versatile acenaphtho[1, 2-b]pyrrol-carbonitriles as a new family of heterocycles: Diverse SN ArH reactions, cytotoxicity and spectral behavior - Liu F., Xiao Y., Qian X. et al. [X. Qian, State Key Laboratory of Fine Chemicals, Dalian University of Technology, Zhongshan Road 158, Dalian 116012, China] - TETRAHEDRON 2005 61 47 ; - summ in ENGL The diverse reactivity of highly electron-deficient 8-oxo-8Hacenaphtho[1, 2-b]pyrrol-9-carbonitrile 1 is attractive for the preparation of derivatives bearing different substituents via SN ArH reaction with N, O, S nucleophiles. These derivatives were versatile, possessing potential antitumor activities and displaying tunable fluorescence spectral behavior. 612. Proteasome inhibitors can alter the signaling pathways and attenuate the P-glycoprotein-mediated multidrug resistance Fujita T., Washio K., Takabatake D. et al. [H. Doihara, 2-5-1, Shitaka-cho, Okayama-city, Okayama 700-8558, Japan] - INT. J. CANCER 2005 117 4 ; - summ in ENGL Numerous signaling pathways were reported to be involved in the resistance for conventional cytotoxic drugs, although one of the main reasons is the overexpression of P-glycoprotein P-gp ; in multidrug resistant cancer cells. The overexpression of P-gp has been associated with the resistance to a wide range of anticancer drugs. Doxorubicin and paclitaxel are substrates of this transporter system and have an important role for the various human malignancies. In the present study, drug-sensitive MCF7 and multidrug resistant MCF7 ADR characterized by overexpression of P-gp ; human breast cancer cell lines were used as an experimental model. We have found that PS341 and MG132, proteasome inhibitors, reduced the degree of the multidrug resistance MDR ; in MCF7 ADR cells. This phenomenon was accompanied by a decrease in the IC50 value of doxorubicin and paclitaxel from 55.9 3.46 to 0.60 0.08 M, and from 17.61 1.77 to 0.59 0.12 M, respectively. The IC50 values of sensitive cells for doxorubicin and paclitaxel were about 0.42 and 0.83 M, respectively. The effect of PS341 and MG132 on MCF7 ADR cells was associated with a significant decrease in both protein and gene levels of P-gp expression. Moreover, with regard to the expression of possible signal transduction pathways of mitogen-activated protein kinase MAPK ; related to the activation of mdr1, proteasome inhibitors did significantly influence the activation of these proteins. Western blot analysis revealed that 24 hr exposure of multidrug resistant MCF7 ADR cells with proteasome inhibitors did change the levels of DNA binding activity of nuclear factor-kappaB NF-kappaB ; , pERK1 2, c-Jun, and p-cJun. In conclusion, we could remark that proteasome inhibitors especially PS341 ; attenuate the resistance of MCF7 ADR cells for P-gp substrate drugs of doxorubicin and paclitaxel. Several proteins are supposed to be associated with the resensitization of the cells to conventional cytotoxic drugs, although decreased activity of P-gp is at least involved in the proteasome inhibitor-related resensitization. And influence with MAPK pathways, which have been reported to be associated with the regulation of P-gp, might be contributed to the resensitization brought by proteasome inhibitors. 2005 Wiley-Liss, Inc. 613. Inter-alu PCR detects high frequency of genetic alterations in glioma cells exposed to sub-lethal cisplatin - Srivastava T., Seth A., Datta K. et al. [S. Sinha, Department of Biochemistry, All India Institute of Medical Sciences, New Delhi-110029, India] - INT. J. CANCER 2005 117 4 ; - summ in ENGL Increased genomic instability contributes to higher frequency of secondary drug resistance and neoplastic progression in tumors as 121 and cordarone.
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Although the use of subjective terms is sometimes unavoidable in the context of risk assessment e.g., to evaluate sufficiency of evidence ; , the decision whether or not it evidence is "convincing" should be left to the reader. Furthermore, what constitutes consistent evidence or the lack of it is unclear when the scope is as broad as the authors implied in their reference to a "causal relation between RF exposure and any adverse health effect." This review of epidemiologic evidence addressed the issue of causation without any consideration of the concept of causation in epidemiology, and it failed in its essential task to assess the possible association between exposure to RF and health. Concerning cancer, Moolgavkar and Luebeck 2003 ; have shown that agents that increase the growth rate of preneoplastic cells may have a distinctly greater impact on cancer incidence than agents that induce malignant transformation. However, this holds only for agents that act for prolonged periods of time. Regarding the natural history of cancer, a noticeable effect at the population level will only occur many years and possibly decades ; after first contact with the promoting agent. Although Ahlbom et al. 2004 ; pointed to the insufficient latencies in epidemiologic studies, they did not draw the straightforward conclusion--to assess the relationship between the latencies covered in the studies and their outcome. Although there is agreement between Ahlbom et al. 2004 ; and us Kundi 2004 and elavil.
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Alpha-lipoic acid neuropathy
Hideyuki Ishida, Naoko Higashijima, Hiroe Nakazawa Department of Physiology, School of Medicine Tokai University, Isehara, Japan Mitochondrial Ca2 + [Ca2 + ]m ; overload is major trigger of the mitochondrial permeability transition pore PTP ; opening which may be a central coordinating event of apoptotic and necrotic cell death. We have recently reported that the mitochondrial ATPsensitive K mitoKATP ; channel opener diazoxide and nicorandil can prevent [Ca2 + ]m overload with accompanying depolarization of the mitochondrial membrane. However, the effects of mitoKATP channel opener on the mitochondrial PTP opening remain elusive. We therefore examined whether mitoKATP channel opener inhibits the PTP opening. Exposure of myocytes to 0.1 mM ouabain for 60 min eventually resulted in hypercontracture 551% ; . This ouabain-induced hypercontracture was blunted by application of 0.1 mM diazoxide and 0.1 mM nicorandil 284% and 372%, P 0.001 vs ouabain ; . This hypercontracture was attenuated by application of 10 M Ru360, inhibitor of the mitochondrial Ca2 + uniporter, and 0.1 mM Tiron, radical scavenger, and 0.4 M cyclosporine A CsA ; inhibitor of PTP opening 382%, 293%, 292%, P 0.001 vs ouabain, Figure A ; . On the other hand, 5 M phenylarsine oxide PAO ; , a potent opener of PTP, evoked the hypercontracture 442% ; . Although CsA blunted PAO-induced hypercontracture 203%, P 0.001 vs PAO ; , diazoxide, nicorandil, Ru360 and Tiron could not attenuate Figure B ; . These results suggest that mitoKATP channels can not directly affect the PTP. However, the activation of mitoKATP channels attenuates the mitochondrial Ca2 + overload and thereby prevents the following PTP opening, for instance, alpha lipoic acid.
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EXERCISE TRAINING, ANTIOXIDANTS, AND INSULIN ACTION and type 2 diabetes. In: Antioxidants in Diabetes Management, edited by Packer L, Rosen P, Tritschler HJ, King GL, and Azzi A. New York: Dekker, 2000, p. 303318. Henriksen EJ and Halseth AE. Early alterations in soleus GLUT-4, glucose transport, and glycogen in voluntary running rats. J Appl Physiol 76: 18621867, 1994. Henriksen EJ, Jacob S, Streeper RS, Fogt DL, Hokama JY, and Tritschler HJ. Stimulation by alha-lipoic acid of glucose transport activity in skeletal muscle of lean and obese Zucker rats. Life Sci 61: 805812, 1997. Holloszy JO and Hansen PA. Regulation of glucose transport into skeletal muscle. Rev Physiol Biochem Pharmacol 128: 99 193, Ivy JL, Zderic TW, and Fogt DL. Prevention and treatment of noninsulin-dependent diabetes mellitus. Exerc Sport Sci Rev 27: 135, 1999. Jacob S, Henriksen EJ, Tritschler HJ, Augustin HJ, and Dietze GJ. Improvement of insulin-stimulated glucose disposal in type 2 diabetes after repeated parenteral administration of thioctic acid. Exp Clin Endocrinol Diabetes 104: 284288, 1996. Jacob S, Ruus P, Hermann R, Tritschler HJ, Maerker E, Renn W, Augustin HJ, Dietze GJ, and Rett K. Oral administration of rac lipoic acid modulates insulin sensitivity in patients with type 2 diabetes mellitus--a placebo controlled pilot trial. Free Radic Biol Med 27: 309314, 1999. Jacob S, Streeper RS, Fogt DL, Hokama JY, Tritschler HJ, Dietze GJ, and Henriksen EJ. The antioxidant alpha-lipioc acid enhances insulin-stimulated glucose metabolism in insulinresistant rat skeletal muscle. Diabetes 45: 10241029, 1996. James DE, Burleigh KM, Kraegen EW, and Chisholm DJ. Effect of acute exercise and prolonged training on insulin response to intravenous glucose in vivo in rat. J Appl Physiol 55: 16601664, 1983. James DE, Kraegen EW, and Chisholm DJ. Effect of exercise training on whole-body insulin sensitivity and responsiveness. J Appl Physiol 56: 12171222, 1984. James DE, Kraegen EW, and Chisholm DJ. Effects of exercise training on in vivo insulin action in individual tissues of the rat. J Clin Invest 76: 657666, 1985. Konrad T, Vincini P, Kusterer K, Hoflich A, Assadkhani A, Bohles HJ, Sewell A, Tritschler HJ, Cobelli C, and Usadel KH. Alpah-lipoic acid treatment decreases serum lactate and pyruvate concentrations and improves glucose effectiveness in lean and obese patients with type 2 diabetes. Diabetes Care 22: 280286, 1999. Maddux BA, See W, Lawrence JC Jr, Goldfine AL, Goldfine ID, and Evans JL. Protection against oxidative stressinduced insulin resistance in rat L6 muscle cells by micromolar concentrations of -lipoic acid. Diabetes 50: 404410, 2001. Neufer PD, Shinebarger MH, and Dohm GL. Effect of training and detraining on skeletal muscle glucose transporter GLUT4 ; content in rats. Can J Physiol Pharmacol 70: 1286 1290, Packer L, Witt EH, and Tritschler HJ. Slpha-lipoic acid as a biological antioxidant. Free Radic Biol Med 19: 227250, 1995. Peth JA, Kinnick TR, Youngblood EB, Tritschler HJ, and Henriksen EJ. Effects of a unique conjugate of alpha-lipoic acid and gamma-linolenic acid on insulin action in the obese Zucker rat. J Physiol Regulatory Integrative Comp Physiol 278: R453R459, 2000. 28. Reznick AZ and Packer L. Oxidative damage to proteins: spectrophotometric method for carbonyl assay. Methods Enzymol 233: 357363, 1994. Rodnick KJ, Henriksen EJ, James DE, and Holloszy JO. Exercise training, glucose transporters, and glucose transport in rat skeletal muscles. J Physiol Cell Physiol 262: C9C14, 1992. 30. Rodnick KJ, Holloszy JO, Mondon CE, and James DE. Effects of exercise training on insulin-regulatable glucose-transporter protein levels in rat skeletal muscle. Diabetes 39: 1425 1429, Saengsirisuwan V, Kinnick TR, Schmit MB, and Henriksen EJ. Interactions of exercise training and alpha-lipoic acid on glucose transport in obese Zucker rat. J Appl Physiol 91: 145 153, Schepkin V, Kawabata T, and Packer L. NMR study of lipoic acid binding to bovine serum albumin. Biochem Mol Biol Int 33: 879886, 1994. Singh HPP and Bowman RH. Effect of D, L-alpha lipoic acid on the citrate concentration and phosphofructokinase activity of perfused hearts from normal and diabetic rats. Biochem Biophys Res Commun 41: 555561, 1970. Slentz CA, Gulve EA, Rodnick KJ, Henriksen EJ, Youn JH, and Holloszy JO. Glucose transporters and maximal transport are increased in endurance-trained rat soleus. J Appl Physiol 73: 486492, 1992. Srere PA. Citrate synthase. Methods Enzymol 13: 310, 1969. Streeper RS, Henriksen EJ, Jacob S, Hokama JY, Fogt DL, and Tritschler HJ. Differential effects of lipoic acid stereoisomers on glucose metabolism in insulin-resistant skeletal muscle. J Physiol Endocrinol Metab 273: E185E191, 1997. 37. Strodter D, Lehmann E, Lehmann U, Tritschler HJ, Bret zel RG, and Federlin K. The influence of thioctic acid on metabolism and function of the diabetic heart. Diabetes Res Clin Pract 29: 1926, 1995. Uyeda K and Racker E. Regulatory mechanisms in carbohydrate metabolism. VII. Hexokinase and phosphofructokinase. J Biol Chem 240: 46824688, 1965.
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