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And hyperemia were, respectively, 5.42 0.90% 95%CI ; and 331 38% 252 ; during glibenclamide, 5.46 0.69% 4.01 ; and 326 28% 266 ; during glimepiride, and 5.17 0.64% 3.79 ; and 357 35% 280 ; during diet treatment NS ; . No differences were observed between diabetic patients with and without microvascular complications. These results were similar to the ones observed in nondiabetic patients 6.44 0.68% [5 7.88], NS, and 406 42% [280 434], NS ; . CONCLUSIONS -- K A T channels play a key role in the regulation of insulin secretion and in the modulation of vascular tone 5, 8 ; . In the resting pancreatic -cells, KATP channels are normally open, but when plasma glucose rises, the enhanced glucose metabolism brings about their closure. The decrease of potassium permeability leads to an increase of cytosolic calcium that triggers the release of insulin. On the other hand, KATP channels in the vascular smooth muscle cells are normally closed or inactive. When ischemia occurs, the decline in the intracellular concentration of ATP activates these channels. The subsequent hyperpolarization of the cells decreases the inward flow of calcium, resulting in vasodilation that, in turn, combats the effects of hypoxia 8 ; . Sulfonylureas, as a class, interact specifically with KATP channels of cell membranes. Evidence shows that though glibenclamide and other sulfonylureas promote insulin secretion by the blockade of pancreatic KATP channels, they also.

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Ynopsis: On June 6 intolerance to medicaof this year, I tion as well as the degree admitted a patient of her depression. After a for treatment of severe week in the hospital with depression. She had taken little clinical improvea massive overdose of ment, her antidepressant medication 48 hours had to be changed before but was not discovbecause of the developered until 24 hours after ment of a rash. A second the overdose. Her husantidepressant was band, who had difficulty started. For the next two Ed Gordon, M.D. awakening her, had her weeks she was considbrought to the emergency room by ered to be suicidal and appeared to be the State Police. In the emergency planning another attempt. room she stated that she wanted to Angela not her name, of course ; die, wished that she had succeeded, gave a long history of having been because "my life is hopeless." She had neglected, passed from family mema history of major depression with ber to family member during all of multiple psychiatric hospitalizations her childhood, and abused physically over the years and at least three and sexually. During adolescence and admissions within the last two years. adulthood she persisted in developing After being medically cleared, she relationships with abusive men. was admitted to the psychiatric unit. Her health insurer has a carve out Her treatment course was stormy and arrangement with a managed behavher improvement was only very ioral health company, which became gradual. This was because of her [See Denial of Service on page 5].
And soleus muscle results not shown ; . Thus the results from Figs. 13 demonstrate that using 10 M glibenclamide to block and 100 M pinacidil to activate KATP channels during fatigue next experiments ; does not affect the contractile apparatus of EDL and soleus muscle. Effects of Glibenclwmide and Pinacidil on Contractility During Fatigue Effect before fatigue. Measured at the beginning of each experiment, mean tetanic forces of control EDL and soleus muscles were, respectively, 36.5 0.5 and and glucovance.

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My son was playing in the back yard with some of his friends. He fell off the tree house ladder and broke his arm. My Liberty SBE Plan allowed me to receive a reimbursement of the medical bills minus the deductible. I was only out $200 of a $1700 bill. Thank you Liberty! Kay; Phone Operator Maryland. 528. Aortic smooth muscle relaxants KMUP-3 and KMUP4, two nitrophenylpiperazine derivatives of xanthine, display cGMP-enhancing activity: Roles of endothelium, phosphodiesterase, and K + channel - Wu B.-N., Chen I.-C., Lin R.-J. et al. [I.-J. Chen, Department and Graduate Institute of Pharmacology, College of Medicine, Kaohsiung Medical University, 100 Shih-Chuan 1st Road, Kaohsiung 807, Taiwan] - J. CARDIOVASC. PHARMACOL. 2005 46 5 ; - summ in ENGL The cellular mechanisms of vasorelaxant effects of newly synthesized KMUP-3 and KMUP-4 were investigated in rat aortic smooth muscle RASM ; . KMUP-3 7-[2-[4- 4-nitrobenzene ; piperazinyl]ethyl]-1, 3-dimethylxanthine ; and KMUP-4 7-[2-[4 2-nitrobenzene ; piperazinyl]ethyl]-1, 3-dimethylxanthine ; elicited concentration-dependent relaxation of endothelium-intact and denuded RASM precontracted with phenylephrine. Relaxant responses were also produced by the PDE inhibitors theophylline, milrinone, rolipram, and zaprinast 1 nM-100 M ; . The relaxant responses of KMUP-3 and KMUP-4 were reduced by endothelium removal and by the presence of the NOS inhibitor L-NAME 100 M ; , the sGC inhibitor ODQ 1 M ; , the adenylyl cyclase AC ; inhibitor SQ 22536 100 M ; , and the prostaglandin inhibitor indomethacin 10 M ; . Additionally, the vasorelaxations of both agents were also attenuated by pretreatment with the nonselective K + channel blocker TEA 10 mM ; , the KATP channel blocker glibenclamide 1 M ; , the voltage-dependent K + Kv ; channel blocker 4-AP 100 M ; , and Ca2 + -dependent K + KCa ; channel blockers apamin 1 M ; and charybdotoxin ChTX, 0.1 M ; . In addition, elevated extracellular K + 80 interferes with KMUP-3- and KMUP-4-induced vasorelaxations. Preincubation with both agents 1 M ; significantly enhanced the dilator responses of isoproterenol and SNP. KMUP-3 and KMUP-4 inhibited PDE activities and increased cAMP and cGMP levels in primary culture of RASM that were inhibited by SQ 22536 and ODQ, respectively. In cultured HUVECs, KMUP-3 and KMUP-4 0.1 M ; , more potent than YC-1, significantly increased the expression of eNOS protein. In summary, KMUP-3 and KMUP-4 induce aortic relaxations through both endothelium-dependent and -independent mechanisms. Mechanisms of vasorelaxation induced by both compounds involve multiple processes, such as accumulation of cyclic nucleotides partly as a Section 30 vol 134.2 and inderal.

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It has been established3, 4 that cromakalim, levcromakalim, aprikalim, and pinacidil dilate brain blood vessels in rabbits, 6, 8, 9 cats, 10, 11 piglets, 12, 13 rats, 11, 14, 15 sheep, 16 and humans.17 Where tested, these dilations are blocked by glibenclamide. However, there is heterogeneity of response, affected by species and location within the cerebrovascular tree.2, 8, 18, 19.

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6.1.2 Oral antidiabetic drugs 6.1.2.1 Sulphonylureas Gliclazide Glipizide Glibenclamlde and itraconazole. Christ O.E., Heptner, W. and Rupp, W., Pharmacokinetics of a new highly effective sulfonylurea derivative. Acta Diabetol Lat, 1: 101-115, 1969 Kulkarni, R.V., Mutalik, S. and Hiremath, D., Effect of plasticizers on the permeability and mechanical properties of Eudragit films for transdermal application. Indian J Pharm Sci, 1: 28-31, 2002 DCCT Research Group., The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin dependent diabetes mellitus. N Engl J Med, 329: 977-986, 1993 Faber, O.K., Beck-Neilsen, H. and Binder, C., Acute actions of sulfonylurea drugs during long-term treatment of non-insulin dependent diabetes mellitus. Diabetes Care, 13: 26-31, 1990. Bitzen, P.O., Melander, A. and Schersten, B., Longterm effects of glipizide on insulin secretion and blood glucose control in patients with non-insulin dependent diabetes mellitus. Euro J Clin Pharmacol, 42: 77-82, 1992 Catz, P. and Friend, D.R., Transdermal delivery of levonorgestrel. VIII. Effect of enhancers on rat skin, hairless mouse skin, hairless guinea pig skin, and human skin. Int J Pharm, 58: 93-102, 1990 Emilsson, H., Sjoberg, S., Svedner, M. and Christenson, I., High performance liquid chromatographic determination of glibenclamide in human plasma and urine. J Chromatography, 383: 93-102, 1986. 18 ; . The expression of SUR and the direct action of SU on POMC gene expression raise the possibility that the corticotroph is one of the target sites of SU, through its so-called extrapancreatic effect. Our results show that glibenclamide has a unique dual effect on POMC expression: it inhibits basal activity, but it enhances secretagogue-stimulated 5 -promoter activity. Because the former effect was abolished by diazoxide treatment, the KATP channel is likely to be involved in the suppressive effect. SU is known to depolarize cells by closing the KATP channel 19 ; , and the effect is in accordance with our result that glibenclamide had a mild stimulatory effect on basal ACTH secretion. In this sense, the suppressive effect of the reagent on basal POMC promoter activity was somewhat unexpected and requires further studies for clarifying the underlying mechanism. In contrast, SU enhanced POMC gene expression stimulated by the activation of the cAMP protein kinase A pathway. Interestingly, the effect, unlike that on basal expression, was not antagonized by diazoxide. Furthermore, when cells were pretreated with IBMX, a nonselective phosphodiesterase inhibitor, only a potentiating effect was completely eliminated. These data, taken together, raise the possibility that the dual effects of SU on POMC expression are mediated by different molecular mechanisms. One possible hypothesis is that, as reported in neuronal cells 20, 21 ; , SU inhibits phosphodiesterase activity and thereby augments the cAMPinduced POMC expression. This explains why the enhancing effect did not occur with stimulation by 8Br-cAMP, phosphodiesterase-resistant cAMP analog. The hypothesis is also in accordance with the fact that, when the potentiating effect of SU was eliminated by IBMX, the suppressive effect on basal expression occurring probably at the post cAMP level ; became dominant. Recent studies show a functional link of SUR, not only with diazoxide-sensitive KIR but also with diazoxide-insensitive KIRs or other ion channels such as cystic fibrosis transmembrane conductance regulator CFTR ; 2224 and, in fact, CFTR is suggested to be involved in hormone secretion 25 ; , raising the possibility that some of these channels may mediate the enhancing effect. Alternatively, SU may act through completely different signaling pathway s ; , such as the activation of protein kinase C or 26 any event, accumulating evidence and observations, including our data, suggest that SU seems to have a more versatile mode of action than previously recognized, which may explain some of the extrapancreatic effects of the drug. Although SURs are expressed in various extrapancreatic tissues, as mentioned above, the nature of the intrinsic ligands for the receptors endosulfines ; is still elusive 28, 29 ; . Furthermore, the function of the KATP channel SUR complex in the extrapancreatic organs, under normal physiological conditions, is not fully characterized. The role of SURs in regulating pituitary hormone synthesis and secretion also is not known. Nevertheless, our results shown here may be of physiological significance, from a clinical point of view, because of the widespread use of the agent for diabetic patients. The maximal serum level of glibenclamide in diabetic pa and kamagra. Electrophysiology Oocyte collection. Female Xenopus laevis were anesthetized with MS222 2 g l added to the water ; . One ovary was removed via a mini-laparotomy, the incision sutured, and the animal allowed to recover. Once the wound had completely healed, the second ovary was removed in a similar operation and the animal was then killed by decapitation while under anesthesia. Immature stage V-VI Xenopus oocytes were incubated for 60 min with 1.0 mg ml collagenase Sigma, type V ; and manually defolliculated. Oocytes were coinjected with 0.1 ng Kir6.2 and 2 ng of SUR wild-type, chimeric, or mutant ; , giving a 1: 20 ratio. The final injection volume was 50 nl oocyte. Isolated oocytes were maintained in Barth's solution and studied 14 days after injection 24 ; . Electrophysiology. Patch pipettes were pulled from thick-walled glass and had resistances of 250500 k when filled with pipette solution. Macroscopic currents were recorded from giant excised inside-out patches at a holding potential of 0 mV and at 2024C 24 ; . Currents were evoked by repetitive 3-s voltage ramps from 110 to + 100 mV and recorded using an EPC7 patch-clamp amplifier List Electronik, Darmstadt, Germany ; . They were filtered at 0.2 kHz, digitized at 0.4 kHz using a Digidata 1200 Interface and analyzed using pClamp software Axon Instruments, Burlingame, UK ; . Records were stored on videotape and resampled at 20 Hz for presentation in the figures. Following the usual convention, inward currents were defined as negative and were indicated by downward deflections of the current trace. The pipette external ; solution contained in mmol l ; 140 KCl, 1.2 MgCl2, 2.6 CaCl2, and 10 HEPES pH 7.4 with KOH ; . The intracellular bath ; solution contained in mmol l ; 110 KCl, 1.4 MgCl2, 10 EGTA, 10 HEPES pH 7.2, with KOH; final K + 140 mmol l ; and nucleotides as indicated. Tolbutamide was made up as a 0.1 mol l stock solution in 0.14 mol l KOH, meglitinide as a 10 mmol l stock solution in DMSO, glibenclamide as a 100 mol l stock in DMSO, and diazoxide as a 68 mmol l stock solution in 0.1 mol l KOH. Solutions containing nucleotides were made up fresh each day. The pH of all solutions was checked and readjusted, if required, after drug and nucleotide addition. Rapid exchange of solutions was achieved by positioning the patch in the mouth of one of a series of adjacent inflow pipes placed in the bath. Data analysis. The slope conductance was measured by fitting a straight line to the current-voltage relation between 20 and 100 mV: the average of five consecutive ramps was calculated in each solution. Tolbutamide dose-response curves were fit to the following equation 25 ; : G.
Chlorure 18.2. CORTICO DES 183 262 1809 Dexamthasone de sodium 1810 Hydrocortisone succinate de sodium 1811 Hydrocortisone succinate de sodium 1812 Prednisolone 1813 Triamcinolone actonide retard 18.3. INDUCTEURS D'OVULATION 187 267 1814 Clomifne citrate 18.4. INSULINES ET ANTIDIABETIQUES 188 189 190 Gglibenclamide 1816 Insuline isophane 1817 Insuline protaminezinc 1818 Metformine 18.5. OESTROGENES 192 193 194 Ethinyl oestradiol 18.6. PROGESTATIFS 1820 Northistrone 1821 Dydrogestrone Comprim Comprim 5 mg 10 mg 250 mg ou 500 mg amp de 2 ml, X X X X Norluten Duphaston-10 ProgestroneRetard Comprim 50 g X Comprim injectable injectable Comprim 5 mg 100 UI ml, Flacon 10 ml 100 UI ml, Flacon 10 ml 850 mg X X X X Daonil Insuline ordinaire rapide Insuline lente Glucophage retard Comprim 50 mg X Clomid, Pergotine injectable 4 mg, Ampoule 1 ml Flacon 100 mg Flacon 500 mg 5 mg 80 mg, Ampoule 2 ml X Soludcadron and ketoconazole. The data turnaround time is 21-28 days. Provision of `cost' information is resolved by applying Manufacturer's List Prices to the data. Medicare Audits has, more recently, initiated a further scheme by which a small number of professionals usually pharmacists ; are paid to trawl patient records to collect clinical data, which is then combined with the drug data. Approximately 50 hospitals had enrolled in this particular initiative, albeit data collection has almost entirely now shifted direct to doctors. Data collected here includes ICD10 diagnosis codes, reasons for prescribing particular drugs, length of treatment course and clinical outcomes. The results from this are then extrapolated to provide `national' level data. A software package called `DATAVIEW', which allows easy interrogation of this database, is used for analysis on both this and the drug issue database, for example, actos. Generic Name Trade Name Loratadine 10mg tab Clarityne Loratadine syrup 100ml Clarityne Enoxaparin 0.6 ml 6000 anti-Xa IU inj Clexan Sulindac 200mg tab Clinoril NED Clomiphene citrate 50mg tab Clomid NED Clotrimazole1% + Bet dipropionate0.05% Clotrasone cream NED Codeine 10mg + glyceryl guaiacolate 100mg cCodepect NED Valsartan 160mg + HCTZ25mg Co-diovan NED Pantoprazole 40mg inj Controloc inj Amiodarone 200mg tab, 150mg 3ml inj Cordarone Warfarin 5mg tab, 3mg tab Coumadin NED Perindopril 4mg tab Coversyl NED Losartan 50mg tab Cozaar Chlorpheniramine 10mg inj, 4mg tab, 2mg 5mCPM Cyclopentolate 1% eye drop Cyclogyl eye drop 1% Estradiol valerate 2mg + Norgestrel 0.5mg Cyclo-progynova NED Misoprostol 200mcg tab Cytotec . Stavudine 30mg tab, 40mg tab d4T NED Diosmin450mg + Hesperidine50mg tab Daflon tab Calcipotriol oint 0.05%-30gm Daivonex Clindamycin 600mg 4ml, 300mg cap Dalacin-C NED Serratio peptidase tab Danzen Gilbenclamide 5mg tab Daonil Didanosine 250mg cap ddI Sodium valproate 500mg Crono tab Depakine Sodium valproate 200mg ml syrup Depakine syrup Clobetasol propionate cream 0.05% Dermovet cream Deferoxamine mesylate 500mg 7.5ml Desferol NED Tolterodine L-tartrate 2mg tab Detrusitol NED Dexamethasone 0.1% + Neomycin0.35% eye dDex-oph eye drop Gliclazide 80mg tab Diamicron NED Gliclazide 30mg tab MR Diamicron MR Acetazolamide 250mg tab Diamox Fluconazole 200mg cap Diflucan and lamisil. And Use of Laboratory Animals' prepared by the National Academy of Sciences and published by the National Institutes of Health NIH ; . Induction of experimental diabetes: Rats were rendered diabetic by a single intraperitoneal injection of freshly prepared streptozotocin 45 mg kg body weight ; in 0.1 M citrate buffer pH 4.5 ; in a volume of 1 ml body weight.41, 42 Normal rats received 1 ml citrate buffer as vehicle. The animals were allowed to drink 5% glucose solution overnight to overcome the drug-induced hypoglycaemia. After 48 h of streptozotocinadministration, blood glucose levels were estimated in rats following overnight fasting. Rats with a blood glucose ranging between 200300 mg dL were considered diabetic and used for the experiment. Experimental design: In the experiment, a total of 30 rats were used. The rats were divided into 5 groups of 6 rats each as follows: Group 1: Normal control rats administered gum acacia 2% ; daily by gavage for 45 days. Group 2: Normal rats administered SBEt 300 mg kg body weight ; in aqueous solution daily by gavage for 45 days. Group 3: Diabetic control rats administered gum acacia 2% ; daily by gavage for 45 days. Group 4: Diabetic rats administered SBEt 300 mg kg body weight ; in aqueous solution daily by gavage for 45 days. Group 5: Diabetic rats administered reference drug glibenclamde 600 g kg body weight ; in aqueous solution daily by gavage for 45 days.17 Since diabetes is a chronic disorder requiring long-term therapy, there is a need to assess the effect of putative hypoglycaemic antihyperglycaemic agents for a longer duration. In addition, this application would be beneficial to reveal the late onset activity profile of the agent.43 Therefore an experiment was planned to assess the effect of SBEt for a period of 45 days in streptozotocin-induced diabetic rats. Treatment was started after 48 h of streptozotocin injection. No detectable irritation or restlessness was. Under investigation for the treatment of obesity, smoking cessation, dyslipidemia and insulin resistance. The drug is among the most anticipated pipeline products; the earliest it could be launched if approved is late 2005 and lansoprazole. Suggested citation: Health Canada. Canadian recommendations for the prevention and treatment of malaria among international travellers . CCDR2004; 30S1: 1-62.
Using natural health remedies to target your health through herbal medicine: an ounce of prevention acne scar removal surgery your pet may be a shamanic healer why fucose and levofloxacin. Q. I know you shouldn't drink grapefruit juice with certain medications. Is it safe to wait a few hours before taking my pills? A. No, that won't help. Adverse reactions with certain medications can occur for up to 24 hours after grapefruit or grapefruit juice is consumed. A little over a decade ago, scientists discovered that grapefruit juice contains a substance that blocks the liver's ability to break down certain drugs, resulting in higher than expected levels of the drug in the body and creating the potential for dangerous side effects. Though less common, it can also reduce blood levels of drugs and possibly reduce their effectiveness. Since then, several natural compounds in grapefruit have been identified that are involved in the food-drug interaction, including the flavonoid naringin and the psoralen furanocoumarin. Seville oranges, used to make some marmalades and limes may contain compounds that have similar interaction. We have implemented a new information technology system that is intended to significantly enhance the accuracy of our calculations for estimating amounts due under medicaid and other governmental pricing programs; however, our processes for these calculations and the judgments involved in making these calculations will continue to involve subjective decisions and manual input, and, as a result, these calculations will remain subject to the risk of errors and lexapro and glibenclamide, because glipizide.

` sulfonylurea " ` """ "'""" , " Y'"""" -- "" " --` Y Y"'' , "-- -- Y ` """" "--"--." , "" " 48-72 TM-- , ` "-- " " " TM` ""' " TM' ` " "`""""' , " Y" " glibnclamide '--`"` severe hypoglycemia "" sulfonylureas --" "`"""-- "`" sulfonylureas `' TM--``-- ``"" TM " "" " TM""TM`-- """ " Y"'` ` -."" insulin secretagogue " 5-10 "--" glinide 'TM'" TM--"--" sulfonylureas TM "' " Y - - `.

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REACH conclusions and limitations There were a number of important findings generated by the REACH study. Patients in the initial maintenance therapy and switched cohorts showed similar asthma control and asthma-related QOL at baseline. Asthma severity, as indicated by self-reported SABA use, also was extremely similar between the two cohorts. The percentage of patients who reported frequent use of SABAs 4 puffs per day in the prior week ; at baseline was nearly equivalent in the two cohorts, which was approximately 25 percent. Another important outcome was the extreme discordance between the administrative claims data and self-reports of SABA use. A large proportion of patients 61 percent ; reported use of a SABA but had no accompanying pharmacy claims. These findings were significant but the study had some limitations. Although the patient population represented and loratadine. 45 the insulin secretagogues glibebclamide and repaglinide do not influence growth hormone secretion in humans but stimulate glucagon secretion during profound insulin deficiency.
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Co-expression of a C-terminal SUR1 halfmolecule with an N-terminal moiety, from which the whole of TMD0 had been omitted, resulted in the formation of substantial glibenclamide-binding activity [16]. Moreover, glibenclamide-binding activity was retained in a SUR1 construct that lacked NBD2 and TMD0. Hence TMD0 is not involved in SUR1 assembly or glibenclamide binding.
Transgenic mice allowed us to determine which ER gene was involved in the effect of E2 on arterial NO production. ER has long been considered as the unique target of E2, as it has been characterized in reproductive tissues, bone, and vessels, particularly in the endothelial cells.40 However, it was initially suggested that ER could mediate some effects of E2 in the vessel wall.41 The present work demonstrates that ER , but not ER , mediates the effects of E2 on endothelial NO production, ie, the enhancement of basal NO release by endothelium and the alteration of ACh sensitivity. In addition, we recently demonstrated that ER mediates the acceleration of reendothelialization of heat-damaged vessels in response to E2.31 These studies indicate the prominence of the isoform of ER in the effect of E2 on endothelium. Does this increase in basal NO release contribute to the vasculoprotective effect of E2? Several years ago, we tested this hypothesis in apolipoprotein E deficient mice by blocking the production of NO. We found that the inhibition of NO synthase by L-NAME did not alter the protective effect of E2 on fatty streak deposit.42 Although we did not assess the decrease of NO production in the hypercholesterolemic mice, the prevention of fatty streak formation by E2 appears independent of NO. In addition, in an external vascular cuff model, endogenous E2 prevented the neointimal proliferation independently of NOS III.43 However, this does not exclude that, in more advanced stages of atherosclerosis, the increase of NO production and or the prevention of endothelial dysfunction could contribute to protecting the vessel against platelet aggregation and vasospasm, 2 major mechanisms leading to clinical cardiovascular events. Taking into account the crucial role of the endothelium in the maintenance of vascular integrity, endothelial ER should be considered as a primordial target in pharmacological studies concerning cardiovascular diseases.
Address for Correspondence: Dr GT John, Professor Department of Nephrology Christian Medical College Vellore 632004 India Email george cmcvellore.ac.in, for example, glibenclamide hplc!
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Repaglinide batches 803099 and 8230301 ; was synthesized and supplied by Dr. Karl Thomae GmbH Biberach, Germany ; . Both tritiated repaglinide and protein A scintillation proximity assay particles were purchased from Amersham Buckinghamshire, U.K. ; . Radiolabeled 3H ; glibenclamide was obtained from DuPont Boston, MA ; , and unlabeled glibenclamide was from Sigma St. Louis, MO ; . Human serum albumin HSA ; was from Behringwerke Marburg, Germany ; , and collagenase A was from Boehringer Mannheim Mannheim, Germany ; . The protein assay kit was from Pierce Rockford, IL ; . Culture flasks and petri dishes were obtained from Nunc Roskilde, Denmark ; . Four-well plates were from Linbro ICN, Costa Mesa, CA ; , and media for cell culture were supplied by Gibco Grand Island, NY ; or Life Technologies Paisley, U.K. ; . Repaglinide and glibenclamide were prepared as concentrated 20 mmol l ; stock solutions using DMSO that was subsequently diluted to the desired concentrations; the final concentration of DMSO was 0.5% vol vol ; . Ligand binding experiments. Binding of glibenclamide and repaglinide was assayed using monolayers of TC3 insulinoma cells 5 ; obtained from Cold Spring Harbor Laboratory Cold Spring Harbor, NY ; . Two days before the experiments, the cells were plated into four-well tissue culture plates 28.3 cm2 ; in Dul345 and glucovance.
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