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2. Olpe, H. P.; Demikeville, H.; Baltzer, W. L.; Koella, W. P.; Wolf, P.; Haas, H. L. Eur. J. Pharmacol. 1978, 52, 133 Chang, M. Y.; Sun, P. P.; Chen, S. T.; Chang, N. C. Tetrahedron Lett. 2003, 44, 52715273, and Ref. 11 cited therein. 4. Abbedante, G.; Hughes, R.; Prager, R. H. Aust. J. Chem. 1994, 47, 14411452. Camps, P.; Mu~oz-Torrero, D.; Snchez, L. Tetrahedron: n a Asymmetry 2004, 15, 311321, and Refs. 1421 cited therein. 6. Kamlet, M. J. J. Am. Chem. Soc. 1955, 77, 48964898. For related reaction conditions, see: Corey, E. J.; Zhang, F.-Y. Org. Lett. 2000, 2, 42574259.
RELATIONSHIP BETWEEN TISSUE LIPID PEROXIDATION AND TISSUE CONCENTRATION OF COPPER, CADMIUM, MERCURY AND LEAD IN SHEEP D. Sopkov Institute of Physiology, University of Veterinary Medicine, Kosice, the Slovak Republic Heavy metals have been reported to affect health status both in human and animals. Long-term occupational exposure to mercury is one of the risk factors for increased lipid peroxidation in miners 1 ; . Peroral administration of mercuric chloride increases lipid peroxidation in the liver and kidney tissue of Japanese quails 2 ; . Chronic exposure to heavy metals alters the ruminal enzyme activity of sheep 3, 4 ; . The aim of the study was to determine the effect of heavy metal intake by diet on the malondialdehyde MDA ; level in the tissue of gastrointestinal tract, kidney and liver of sheep. The experiment was carried out on twelve female sheep of mixed breed, weighing from 30 to 35 kg. Six sheep in the first group were from a laboratory farm and were fed with hay ad libitum and 300g of barley for one day. The second group was grazed on natural pasture in a territory near a copper production works. Mercury, copper, cadmium and lead concentrations were determined by atomic absorption spectrophotometry. The second group of sheep had significantly higher concentration of copper and cadmium in the tissue of rumen wall, duodenum, colon wall, liver and kidney. Lead concentration was significantly higher in the rumen wall, colon, liver and kidney, but not differences were found in duodenum. Mercury concentration was significantly higher only in kidney tissue. Malondialdehyde concentration was significantly higher in reticulum epithelium, omasum, duodenum, colon, colon wall and kidney medulla. The highest concentration of MDA was found in liver. Our results show that the lipid peroxidation is one of the molecular mechanisms of cell injury in chronic heavy metal poisoning. 1. Kobal AB et al.: J. Trace Elem. Med. Biol. 17: 261-274, 2004. Faix S et al.: Acta Vet. Brno, 72: 23-26, 2003. Faixov Z, Faix S: Acta Vet. Brno, 71: 451-455, 2002. Faixova Z et al.: Acta Vet. Beograd, 56: 17-23, 2006. Supported by grant VEGA No. 1 2443 05. ARE THERE ANY DIFFERENCES IN THE EXPRESSION OF MYOSIN HEAVY CHAIN ISOFORMS BETWEEN SLOW AND FAST RAT SKELETAL MUSCLES? T. Soukup Institute of Physiology, Academy of Science Prague, Czech Republic Skeletal muscles of small rodents contain four main fiber types, namely type 1, 2A, 2X D and 2B fibers containing myosin heavy chain MyHC ; 1, 2a, 2x d and 2b isoforms. Each of these MyHC isoforms is the product of a distinct gene and their expression is believed to be primarily transcriptionally controlled. In most rat muscles, messenger RNA mRNA ; transcripts for MyHC1, 2a, 2x d and 2b and their corresponding protein products were found with the exception of the slow antigravity soleus SOL ; muscle, where typically only MyHC1 and 2a transcripts and protein isoforms were demonstrated under normal conditions. We have shown that both fast extensor digitorum longus EDL ; muscle and slow SOL muscle express all four MyHC1, 2a, 2x d and 2b mRNA transcripts under normal conditions in euthyroid, as well as in experimental hypothyroid and hyperthyroid i.e. after chronic treatment with methimazole and T3, respectively ; 2- to 7-month-old female inbred Lewis rats 1-4 ; . In the SOL muscle, this is not matched, however, by the expression of corresponding four isoforms, as we have found that 2x d and 2b protein isoforms are not normally present at levels detectable by SDS-PAGE. We have also shown that the chronic hypothyroid and hyperthyroid status affects the expression of MyHC isoforms both at the mRNA and protein levels. From our results we can conclude that alteration of the thyroid status leads to typical changes in the expression of MyHC mRNA transcripts and MyHC protein isoforms in the EDL and SOL muscles, due to the different fiber type composition based on different physiological demands of either muscle. These changes correspond to those described after shorter periods of altered thyroid status. The characteristic phenotype differences between EDL and SOL muscles remain thus preserved even after 7 months of thyroid hormone status alteration. 1 2 3, for example, hyzaar.
And Development 151 ; , VA Medical Center, 2002 Blvd., Houston, Texas 77030. for publication August 31, 1992; accepted for publication 18, 1992.
Paul D. Thompson, et al, JAMA 2003; 289: 1681-1690 Corsini A. Cardiovasc Drugs Ther 2003; 17: 257277 and atacand.
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18. Kagami S, Border WA, Miller DE, and Noble NA. Angiotensin II stimulates extracellular matrix protein synthesis through induction of transforming growth factor- expression in rat glomerular mesangial cells. J Clin Invest 93: 24312437, 1994. Kagami S, Kuhara T, Okada K, Kuroda Y, Border WA, and Noble NA. Dual effects of angiotensin II on the plasminogen plasmin system in rat mesangial cells. Kidney Int 51: 664671, 1997. Kerins DM, Hao Q, and Vaughan DE. Angiotensin induction of PAI-1 expression in endothelial cells is mediated by the hexapeptide angiotensin IV. J Clin Invest 96: 25152520, 1995. Kim S, Ohta K, Hamaguchi A, Omura T, Yukimura T, Miura K, Inada Y, Ishimura Y, Chatani F, and Iwao H. Angiotensin II type I receptor antagonist inhibits the gene expression of transforming growth factor- 1 and extracellular matrix in cardiac and vascular tissues of hypertensive rats. J Pharmacol Exp Ther 273: 509515, 1995. Nakamura T, Obata J, Onizuka M, Kimura H, Ohno S, Yoshida Y, Kawachi H, and Shimizu F. Candesartan prevents the progression of mesangioproliferative nephritis in rats. Kidney Int 63: S226S228, 1997. 23. Negoescu A, Lafeuillade B, Pellerin S, Chambaz EM, and Feige JJ. Transforming growth factors beta stimulate both thrombospondin-1 and CISP thrombospondin-2 synthesis by bovine adrenocortical cells. Exp Cell Res 217: 404409, 1995. Noda M, Matsuo T, Fukuda R, Ohta M, Nagano H, Shibouta Y, Naka T, Nishikawa K, and Imura Y. Effect of candesartan cilexetil TCV-116 ; in rats with chronic renal failure. Kidney Int 56: 898909, 1999. Obata J, Nakamura T, Kuroyanagi R, Yoshida Y, Guo DF, and Inagami T. Candesartan prevents the progression of glomerulosclerosis in genetic hypertensive rats. Kidney Int 63: S229S231, 1997. 26. Olson BA, Day JR, and Laping NJ. Age-related expression of renal thrombospondin 1 mRNA in F344 rats: Resemblance to diabetes-induced expression in obese Zucker rats. Pharmacology 58: 200208, 1999. Otsuka F, Yamauchi T, Kataoka H, Mimura Y, Ogura T, and Makino H. Effects of chronic inhibition of ACE and AT1 receptors on glomerular injury in Dahl salt-sensitive rats. J Physiol Regulatory Integrative Comp Physiol 274: R1797R1806, 1998. 28. Ribeiro SMF, Poczatek M, Schultz-Cherry S, Villain M, and Murphy-Ullrich JE. The activation sequence of thrombospondin-1 interacts with the latency-associated peptide to.
Summarized in Table 1. The patient remained stable until September 2001, when and serophene.
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In addition, low reimbursement rates were also a factor affecting the supply of adolescent primary care providers in the three states in which plans paid Medicaid or comparable rates -- Connecticut, Maryland, and Missouri. Primary care providers in these plans perceived that rates did not compensate them fairly for the added time needed to treat adolescents. Compared with commercial rates, rates paid for S-CHIP enrollees in these states were substantially lower.24 Rates in Missouri were lowest: one plan paid just over half of the commercial rate for preventive visits; the other paid less than a quarter, as shown in Table II. By contrast, rates paid by the plans we interviewed in California and Utah were either equal to or higher than commercial rates. Hospital-based adolescent clinics in California and Connecticut faced additional reimbursement problems in that and clomiphene.
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CONSISTENCY WITH WHATCOM TRANSPORTATION PLAN The projects contained in the 2007-2009 years of the TIP are consistent with the goals of the Whatcom Transportation Plan WTP ; . WCOG prepares the TIP based on local agency TIPs, and all projects are considered for their consistency with the WTP. FINANCIAL PLAN This TIP is based on, and therefore consistent with, the region's Whatcom Transportation Plan WTP ; required under Title 23 CFR Part 450. Financial feasibility for the region is well-stated in that plan. Any questions regarding feasibility of any TIP project may be answered by referring to the WTP required by state law. Financial sections in the plan detail financial feasibility thoroughly at the project level. FUNDING PROGRAMS Bridge Replacement and Rehabilitation Program BR ; The Bridge Replacement and Rehabilitation Program is used to fund improvements to bridges determined to be deficient because of structural problems, physical deterioration, or functional obsolescence. The program assists local governments replace or rehabilitate roadway bridges over waterways, topographical barriers, other roadways, railroads, canals, ferry landings, etc. Typical projects may be total bridge replacement at or near its existing location, total replacement of a bridge in the general corridor, removal of a deficient structure and provision of alternative access, and rehabilitation or replacement of major structural members that increases the structural integrity and life of the bridge. Funding of projects in this program is on a competitive basis. All jurisdictions must inventory their bridges according to state procedures. A statewide priority listing is established based in the inventory. Bridge projects are evaluated and selected on a priority basis by a committee comprised of city, county and WSDOT representatives.
Research Institute of Medicinal Plants, Pozna, Poland * e-mail: Przemyslaw M. Mrozikiewicz pmm post The use of plants in pharmacotherapy dates back several centuries. Herbal medicine usually relied on tradition and generally is only weakly supported by empirical data. The belief of herbal drugs being much safer than synthetic drugs has gained popularity in recent years and led to remarkable growth on phytopharmaceutical market. In order to be valuable herbal medicinal products are currently expected to gather comparable standards concerning the assessment of efficacy, safety, biopharmaceutical quality, and understanding mechanism of action similarly, to synthetic drugs. Nevertheless, these requirements are rarely fulfilled. Opposite to synthetic drugs herbal medicines were long time weakly investigated and considered as traditional healing methods not necessary to serious investigation. Moreover, it is necessary to note that herbal medicines, because of complex content, are more difficult to investigate that chemical substances. The advances in analytical technology have led to discovery of many new active constituents and an ever-increasing list of putatively active constituents. We observe currently growing tendency to investigate pharmacokinetics parameter of herbal substances. Establishing the pharmacological basis for efficacy of herbs is a constant challenge. Of particular interest is the question of bioavailability to assess to what degree and how fast compounds are absorbed after administration of herbs. Moreover, we are observing growing tendency to elucidate the molecular mechanism of action if herbal medicines. Modern biotechnology is nowadays often applied to search for pharmacological points of action oh herbals directly in the cells. A better understanding of the pharmacokinetics, bioavailability, and molecular mechanisms of action of phytopharmaceuticals can help in designing rational dosage regimens and also reasonable prediction of possible interactions between herbal and synthetic medicines and mebeverine and cilexetil, for example, irbesartan.
1. De Gasparo M, Catt KJ, Inagami T, Wright JW, Unger Th. International union of pharmacology. XXIII. The angiotensin II receptors. Pharmacol Rev 2000; 52: 41572. Johnston CI. Angiotensin II type 1 receptor blockade: a novel therapeutic concept. Blood Pressure 2000; 1 Suppl ; : 913. 3. Unger T. Pharmacology of AT1 -receptor blockers. Blood Pressure 2001; 10 Suppl 3 ; : 510. 4. Pfeffer MA, Swedberg K, Granger CB, et al. Effects of candesartan on mortality and morbidity in patients with chronic heart failure: the CHARM-Overall programme. Lancet 2003; 362: 75966. Noda M, Shibouta Y, Inada Y, et al. Inhibition of rabbit aortic angiotensin II AII ; receptor by CV-11974, a new nonpeptide AII antagonist. Biochem Pharmacol 1993; 46: 3118. Fabiani ME, Dinh DT, Nassis L, et al. In vivo inhibition of angiotensin receptors in the rat kidney by candesartan cilexetil: a comparison with losartan. J Hypertens 2000; 13: 100513. Timmermans PBMWM. Pharmacological properties of angiotensin II receptor antagonists. Can J Cardiol 1999; 15 Suppl F ; : 26F28F. 8. Morsing P, Adler G, Brandt-Eliasson U, et al. Mechanistic differences of various AT1 -receptor blockers in isolated vessels of different origin. Hypertension 1999; 33: 140613. Ojima M, Inada Y, Shibouta Y, et al. Candesartan CV-11974 ; dissociates slowly from the angiotensin AT1 receptor. Eur J Pharmacol 1997; 319: 13746. Vanderheyden PML, Fierens FLP, de Backer J-P, et al. Reversible and syntopic interaction between angiotensin receptor antagonists on Chinese hamster ovary cells expressing human angiotensin II type 1 receptors. Biochem Pharmacol 2000; 59: 92735. Vanderheyden PML, Fierens FLP, Vauquelin G. Angiotensin II type 1 receptor antagonists. Why do some of them produce insurmountable inhibition? Biochem Pharmacol 2000; 60: 155763. Vauquelin G, Fierens FLP, Vanderheyden PML. Distinction between surmountable and insurmountable angiotensin II AT1 receptor antagonists. In: Epstein M, Brunner HR Eds ; . Angiotensin II receptor antagonists. Philadelphia, PA: Hanley & Belful, 2000: 10518. 13. Vanderheyden PML, Fierens FLP, De Backer JP, et al. Distinction between surmountable and insurmountable selective AT1 receptor antagonists by use of CHO-K1 cells expressing human angiotensin II AT1 receptors. Br J Pharmacol 1999; 126: 105765. Elmfeldt D, Olofsson B, Meredith P. The relationships between dose and antihypertensive effect of four AT1 receptor blockers. Differences in potency and efficacy. Blood Pressure 2002; 11: 293301. Lacourci`re Y, Asmar R. A comparison of the efficacy and duration e of action of candesartan cilexetil and losartan as assessed by clinic and ambulatory blood pressure after a missed dose, in truly hypertensive patients. A placebo-controlled, forced titration study. J Hypertens 1999; 12: 11817. Meredith PA. Clinical comparative trials of angiotensin II type 1 AT1 ; receptor blockers. Blood Pressure 2001; 10 Suppl 3 ; : 1117. 17. Gradman AH. AT1 -receptor blockers: differences that matter. J Hum Hypertens 2002; 16 Suppl 3 ; : S916. 18. Inada Y, Wada T, Ojima M, et al. Protective effects of candesartan cilexetil TCV-116 ; against stroke, kidney dysfunction and cardiac hypertrophy in stroke-prone spontaneously hypertensive rats. Clin Exp Hypertens 1997; 19: 107999. Garcia JH, Wagner S, Liu KF, et al. Neurological deficit and extent of neuronal necrosis attributable to middle cerebral artery occlusion in rats. Statistical validation. Stroke 1995; 26: 62735. Groth W, Blume A, Gohlke P, et al. Chronic pre-treatment with candesartan improves recovery from focal cerebral ischaemia in rats. J Hypertens 2003; 21: 217582. Gohlke P, von Kgelgen S, Jrgensen T, et al. Effects of orally u u applied candesartan cilexetil on central responses to angiotensin II in conscious rats. J Hypertens 2002; 20: 90918. Culman J, Blume A, Gohlke P, et al. The reninangiotensin system in the brain: possible therapeutic implications for AT1 -receptor blockers. J Hum Hypertens 2002; 16: S6470. 23. Dirnagl U, Iadecola C, Moskowitz MA. Pathobiology of ischaemic stroke: an integrated review. Trends Neurosci 1999; 22: 3917.
`Respiration' brings together the results of both clinical and experimental investigations on all aspects of the respiratory system in health and disease. Clinical improvements in the diagnosis and treatment of chest and lung diseases are covered, as are the latest findings in physiology, biochemistry, pathology, immunology and pharmacology. The journal includes classic features such as editorials that accompany original articles in clinical and basic science research, case reports and letters to the editor. Some of the recently included sections are: rapid communications, technical notes, `the eye catcher', `what's your diagnosis', `the opinion corner' and discussions of clinico-pathological conferences. This modern mix of different features and a stringent peer-review process by a dedicated editorial board make `Respiration' a complete guide to progress in thoracic medicine and combivir.
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One patient was not taking any antipsychotic medication at the time of the audit and the medication details of one further patient could not be obtained. Table 20: Rochdale baseline audit: antipsychotic drugs prescribed to sample.
Acknowledgment. The authors wish to thank Dr. K. Matsuno Santen Pharmaceutical Co., Japan ; for generous gift of SA4503.
After single and repeated administration, the pharmacokinetics of candesartan are linear for oral doses up to 32 mg of candesartan cilexetil.
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