воскресенье, 29 июня 2008 г.

The effect of omeprazole on ultrastructural changes in gastric parietal cells

You have forgotten your username or password, we can .My Menu Saved Items дё­ж–‡(з®ЂдЅ") дё­ж–‡(з№Ѓй«") English Deutsch н•њкµ­м–ґ ж—Ґжњ¬иЄћ Franais Espaol Ш§Щ„Ш№Ш±ШЁЩЉШ© Р СѓСЃСЃРєРёР№ Journal Article THE EFFECT OF OMEPRAZOLE ON ULTRASTRUCTURAL CHANGES IN GASTRIC PARIETAL CELLS Journal Publisher Springer Japan ISSN 0944-1174 (Print) 1435-5922 (Online) Issue Category Original Article DOI 10.Pages 1-8 Subject Collection SpringerLink Date Thursday, June 26, 2008 ORIGINAL ARTICLE The effect of omeprazole on ultrastructural changes in gastric parietal cells Hiroyuki Karasawa1 , Norio Tani1 and Takeshi Miwa1 (1) Department of Internal Medicine, Tokai University School of Medicine, Bohseidai, Isehara, 259-11 Isehara, Japan RECEIVED: 17 July 1987 ACCEPTED: 8 August 1987 Summary This study was designed topare the effects of omeprazole and cimetidine on ultrastructural changes in parietal cells of guinea pigs during histamine stimulation.And cimetidine remarkably inhibited acid secretion induced by histamine stimulation.However, failed to prevent the morphological transition of parietal cells to an active stage during histamine stimulation, in contrast to cimetidine which inhibited the morphological transition.Addition, it was noticed that administration of omeprazole caused vacuolation in approximately 27% of all parietal cells.Phenomenon was not seen in control animals with histamine stimulation alone and only very rarely in cimetidine treated animals.Findings suggested that vacuoles originated in secretory canaliculi of parietal cells.Results may be the key to explain the difference of the inhibitory mechanism between omeprazole which acts on the final step of the intracellular process (so-called proton pump) and cimetidine which acts on the H2-receptor site of plasma membrane.Key Words Cimetidine - H+/K+ATPase - Omeprazole - Parietal cell - Vacuolation References secured to subscribers.Find Query Builder Close Clear Within all content Within this journal Within this issue Export this article Export this article as RIS Text В© Springer.
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суббота, 28 июня 2008 г.

Data show significantly more patients were pain-free with treximet (sumatriptan and naproxen sodium) tablets in the acute treatment of probable migraine without aura in adults

According to new data, Treximet is the first migraine-specific medication to demonstrate pain-free results in patients with probable migraine without aura.Data were presented today at the 50th Annual Scientific Meeting of the American Headache Society in Boston.Typically, this migraine sub-population experiences pain symptoms which may include pain on one side of the head, moderate to severe pain, throbbing pain or worse pain when moving or bending, but do not present with an associated symptom, such as nausea or vomiting or sensitivity to light and sound."The study findings are promising, as helping patients with this condition find adequate pain relief is often challenging," stated Stephen Silberstein, MD, professor of neurology and director of the Jefferson Headache Center at , and a lead author of the study.Superior to placebo in producing pain-freedom at two hours and sustained pain-freedom from two through 24 hours.Recently approved for the acute treatment of migraine attacks with or without aura in adults, Treximet is the first and only migraine product designed to target multiple mechanisms of migraine bybining a triptan and an anti-inflammatory pain reliever in a single tablet.Rmended dosage for patients prescribed Treximet is one tablet and should only be used where a clear diagnosis of migraine has been established.Is not indicated for the treatment of probable migraine.About the Study The randomized, placebo-controlled, parallel group, single attack, multi-center study evaluated 679 men and women who have a history of probable migraine of at least six months and moderate to severe pain lasting at least four to 72 hours.Were randomized to Treximet or placebo, and were allowed to take a second dose of Treximet or their usual medication at two hours following initial treatment.Endpoints were pain-free at two hours and sustained pain-free from two through 24 hours.Treximet was superior to placebo in producing pain-freedom at two hours post-dose and sustained pain-free results from two through 24 hours: Nearly one-third of subjects (29 percent) who took Treximet were pain-free at two hourspared to 11 percent of subjects who took placebo, Nearly one-quarter of subjects (24 percent) who took Treximet achieved sustained pain-free results from two through 24 hourspared to 9 percent of subjects who took placebo.Secondary endpoints were: pain-freedom at 30 minutes, one hour and four hours; sustained pain-relief from two through 24 hours; pain relief at 30 minutes, one hour, two hours and four hours; use of rescue medication within 24 hours post-dose; intermediate sustained pain-relief at one to two hours and two to four hours; intermediate sustained pain-freedom at one to two hours and two to four hours; and incidence of neck and sinus pain, photophobia, phonophobia and nausea at two and four hours.Was superior to placebo in producing pain-freedom and pain-relief at four hours post-dose, sustained pain-relief from two through 24 hours, as well as producing intermediate sustained pain-relief and pain-freedom at two through four hours (and one to two hours for intermediate pain-freedom).Addition, significantly fewer subjects taking Treximet required the use of rescue medicationpared to those taking placebo.Other secondary endpoints were not statistically significant.Treximet was generally well-tolerated, with no new or unexpected adverse events, reported as 11 percent of subjects taking Treximetpared to 7 percent of subjects taking placebo.Mostmon drug-related adverse events (greater than or equal to 2 percent and greater than placebo) reported in this study were dizziness and dry mouth.This study was funded by GlaxoSmithKline.GlaxoSmithKline GlaxoSmithKline one of the world's leading research-based pharmaceutical and healthcarepanies ismitted to improving the quality of human life by enabling people to do more, feel better and live longer.Detailedpany information, see GlaxoSmithKline's website: www.Important Safety Information About Treximet Prescription Treximet is indicated for the acute treatment of migraine attacks, with or without aura, in adults.Should only be used where a clear diagnosis of migraine headache has been established.Treximet may cause an increased risk of serious cardiovascular thrombotic events, myocardial infarction, and stroke, which can be fatal.Risk may increase with duration of use.With cardiovascular disease or risk factors for cardiovascular disease may be at greater risk.Contains a non-steroidal anti-inflammatory drug (NSAID).Products cause an increased risk of serious gastrointestinal adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal.Events can occur at any time during use and without warning symptoms.Patients are at greater risk for serious gastrointestinal events.Treximet is contraindicated in patients with history, symptoms, or signs of ischemic cardiac, cerebrovascular, or peripheral vascular syndromes and in patients with other significant underlying cardiovascular diseases.Should not be given to patients in whom unrecognized coronary artery disease is predicted by the presence of risk factors without a prior cardiovascular evaluation.Should not be given to patients with uncontrolled hypertension because theponents have been shown to increase blood pressure.Concurrent administration of MAO-A inhibitors or use of Treximet within two weeks of discontinuation of MAO-A inhibitor therapy is contraindicated.Any ergotamine-containing or ergot-type medication (like dihydroergotamine and methysergide) should not be used within 24 hours of each other.Treximet contains sumatriptan, it should not be administered with another 5-HT1 agonist.Contraindicated in patients with hepatic impairment.Contraindicated in patients who have had allergic reactions to products containing naproxen.Is also contraindicated in patients in whom aspirin or other NSAIDs/analgesic drugs induce the syndrome of asthma, rhinitis, and nasal polyps.Of reactions have the potential of being fatal.Is contraindicated in patients with hypersensitivity to sumatriptan, naproxen, or any otherponent of the product.Cerebrovascular events have been reported in patients treated with sumatriptan.A number of cases, it appears possible that the cerebrovascular events were primary.Is important to advise patients not to administer Treximet if a headache being experienced is atypical.The development of a potentially life-threatening serotonin syndrome may occur with triptans, including treatment with Treximet, particularly duringbined use with selective serotonin reuptake inhibitors (SSRIs) or selective norepinephrine reuptake inhibitors (SNRIs).Products, including Treximet, should be prescribed with extreme caution in those with a prior history of ulcer disease or gastrointestinal bleeding.Should not be used in late pregnancy because NSAID-containing products have been shown to cause premature closure of the ductus arteriosus.Should not be used during early pregnancy unless the potential benefit justifies the potential risk to the fetus.Prescribing Information for Treximet please visit .Enquiries: US Media enquiries: Nancy Pekarek (215) 751 7709 Sarah Alspach (215) 751 7709 Mary Anne Rhyne (919) 483 2839 Robin Gaitens (919) 483 2839 US Analyst/Investor enquiries: Frank Murdolo (215) 751 7002 Tom Curry (215) 751 5419 CONTACT: US Media enquiries: Nancy Pekarek, +1-215-751-7709, or SarahAlspach, +1-215-751-7709, or Mary Anne Rhyne, +1-919-483-2839, or RobinGaitens, +1-919-483-2839; or US Analyst, Investor enquiries: Frank Murdolo,+1-215-751-7002, or Tom Curry, +1-215-751-5419, all of GlaxoSmithKline Web site: http://www.Symbol: (NYSE:GSK) Terms and conditions of use apply Copyright 2008 PR Newswire Association LLC.Rights reserved.United Business Mediapany CLINICAL TRIAL RESULTS ARCHIVE 2008: 2007: 2006: MORE NEWS RESOURCES Services Recent Searches Recently Approved What's New Keep track of all your medications.Assembles all relevant medical information in a simple, easy to read format.In-depth consumer information, FDA alerts, drugparisons and interactions.Top 10 Searches In The Pipeline - - - - - - - - - - - The drugs drug database is powered by MicromedexTM, Facts &parisonsTM and MultumTM.Last updated 30 April 2008.
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пятница, 27 июня 2008 г.

Stability-indicating simultaneous hptlc method for olanzapine and fluoxetine in combined tablet dosage form

College of Pharmaceutical Education and Research, College Campus, Modasa-383 315, India 2 L.College of Pharmacy, Navrangpura, Ahmedabad-380 009, India Date of Submission 21-Jul-2006 Date of Decision 25-Oct-2007 Date of Acceptance 21-Apr-2008 CORRESPONDENCE ADDRESS: C R Shah Department of Quality Assurance, Shri B.Shah College of Pharmaceutical Education and Research, College Campus, Modasa-383 315 India SOURCE OF SUPPORT: None, CONFLICT OF INTEREST: None Abstract A rapid, selective and stability-indicating high performance thin layer chromatographic method was developed and validated for the simultaneous estimation of olanzapine and fluoxetine inbined tablet dosage form.And fluoxetine were chromatographed on silica gel 60 F 254 TLC plate using methanol:toluene (4:2 v/v) as the mobile phase and spectrodensitometric scanning-integration was performed at a wavelength of 233 nm using a Camag TLC Scanner III.System was found to givepact spots for both olanzapine (R f value of 0.And fluoxetine (R f value of 0.The polynomial regression data for the calibration plots showed good linear relationship with r 2 =0.The concentration range of 100-800 ng/spot for olanzapine and 1000-8000 ng/spot for fluoxetine with r 2 =0.The method was validated in terms of linearity, accuracy, precision, recovery and specificity.Limit of detection and the limit of quantification for the olanzapine were found to be 30 and 100 ng/spot, respectively and for fluoxetine 300 and 1000 ng/spot, respectively.And fluoxetine were degraded under acidic, basic and oxidation degradation conditions which showed all the peaks of degraded product were well resolved from the active pharmaceutical ingredient.Drugs were not further degraded after thermal and photochemical degradation.Method was found to be reproducible and selective for the simultaneous estimation of olanzapine and fluoxetine.The method could effectively separate the drugs from their degradation products, it can be employed as a stability-indicating method.KEYWORDS: Stability indicating method, forced degradation, olanzapine, fluoxetine, HPTLC, simultaneous estimation HOW TO CITE THIS ARTICLE: Shah CR, Suhagia BN, Shah NJ, Patel DR, Patel NM.HPTLC method for olanzapine and fluoxetine inbined tablet dosage form.J Pharm Sci 2008;70:251-5 HOW TO CITE THIS URL: Shah CR, Suhagia BN, Shah NJ, Patel DR, Patel NM.HPTLC method for olanzapine and fluoxetine inbined tablet dosage form.J Pharm Sci ;70:251-5.Olanzapine is an antipsychotic agent, chemically a thienobenzodiazepine described as a 2-methyl-4-(4-methyl-1-piperazinyl)-10H-thieno ,3-b] ,benzodiazepine and fluoxetine is an antidepressant agent, selective serotonin reuptake inhibitor (SSRI), chemically described as a (±)-N-methyl-3-phenyl-3-propylamine .Inbination with fluoxetine is used in treatment-resistant depression (TRD).A slightly smaller increase of serotonin than fluoxetine alone .Survey reveals that few spectrophotometric, GC and HPLC methods are reported for the estimation of olanzapine and fluoxetine alone in formulations and biological samples such as urine and plasma ,,, .Or stress studies of drug substance and products play an integral role in the development of pharmaceuticals .Results of degradation studies facilitate the stability indicating method (SIM) development.Survey indicates that, stability indicating HPTLC method has not been developed for quantitative determination of olanzapine and fluoxetine inbined dosage form.Current ICH guidelines requires that the analysis of stability samples should be done by using stability indicating assay methods developed and validated after stress testing on drug under variety of conditions, including hydrolysis (at various pH's), oxidation, photolysis and thermal degradation .Ideal SIM is one that quantifies the drug and also resolves its degradation product.Very viable alternative for stability indicating analysis of olanzapine and fluoxetine inbined dosage form is HPTLC.Advantages of HPTLC is that several samples can be run simultaneously by using a small quantity of mobile phase unlike HPLC, thus lowering analysis time and cost per analysis , .Present investigation an attempt has been made to develop accurate and precise stability indicating HPTLC method for the simultaneous estimation of olanzapine and fluoxetine inbined dosage forms .Standard were procured as a gift sample from Sun Pharmaceuticals Ltd.Silica gel 60F 254 TLC plates (10Ч10 cm, layer thickness 0.E.Mumbai) were used as a stationary phase.Chemicals and reagents used were of analytical grade.5 mg of olanzapine and 20 mg of fluoxetine (Olanex-F) were procured from a local pharmacy.Camag HPTLC systemprising of Camag Linnomate V automatic sample applicator, Hamilton syringe (100 µl), Camag TLC Scanner 3, Camag WinCATS software, Camag Twin-trough chamber (10Ч10 cm) and ultrasonicator were used during study.Fluoxetine (25 mg) each were weighed accurately, dissolved and diluted with methanol to obtain the final concentration of 100 µg/ml and 1000 µg/ml, respectively.Tablets were weighed accurately and ground to fine powder.Equivalent to 25 mg of olanzapine and fluoxetine were transferred to conical flask and mixed with methanol.Solution was sonicated for 15 min.Extracts were filtered through Whatmann filter paper No.And residue was washed thoroughly with methanol.And washing were pooled and transferred to a 25 ml volumetric flask and volume was made up to 25 ml with methanol.Dilutions were made to get 100 µg/ml of olanzapine and 1000 µg/ml of fluoxetine.Were prewashed with methanol.Of plates was done in an oven at 50 o for 5 min.Chromatographic conditions maintained were precoated silica gel 60F 254 aluminum sheets (10x10 cm) as stationary phase, methanol: toluene (4:2 v/v) as mobile phase, chamber and plate saturation time of 30 min, migration distance allowed was 72 mm, wavelength scanning was done at 233 nm keeping the slit dimension at 5Ч0.A deuterium lamp provided the source of radiation.µl standard solutions of olanzapine and fluoxetine were spotted and developed.Measurements were performed at 233 nm in reflectance mode with Camag TLC scanner 3 using Win CATS software.1-8 µl of standard solution of olanzapine (100 µg/ml) and 1-8 µl of fluoxetine (1000 µg/ml) were applied on the TLC plate.Plate was dried, developed and analyzed photometrically as described earlier.Standard calibration curve was generated using regression analysis with Microsoft excel.The developed method was validated in terms of linearity, accuracy, limit of detection, limit of quantification, intra-day and inter-day precision and repeatability of measurement as well as repeatability of sample application .Of sample solutions of the marketed formulation was spotted on to the same plate followed by development scanning.Was repeated in triplicate.Content of the drug was calculated from the peak areas recorded.Accurately weighed olanzapine (50 mg) and fluoxetine (500 mg) was transferred in 50 ml of volumetric flask and dissolved in methanol (25 ml).Hydroxide, hydrochloric acid solution (25 ml, 1 N) and hydrogen peroxide (25 ml, 3 % v/v) were added.Final solution was transferred in 100 ml of round bottom flask and refluxed at 90±2 o for 6 h.Time intervals of 0, 30, 60, 90, 120, 180 and 360 minutes, 2.The solution was transferred in series of 25 ml of volumetric flasks and diluted to the mark with mobile phase to stop further degradation.Sample (400 ng/spot) was analyzed employing HPTLC method.Thermal stress, the drug substance in solid state was subjected to dry heat at 60 o for 10 days and for photo degradation, the drug substance in solid state was exposed to UV at 254 nm for 10 days.A solvent system that would give dense andpact spots with significant R f values was desired for quantification of olanzapine and fluoxetine in pharmaceutical formulations.Mobile phase consisting of methanol: toluene (4:2 v/v) gave R f values of 0.And 0.For olanzapine and fluoxetine, respectively .The linear regression data (n=5) showed a good linear relationship over a concentration range of 100-800 ng/spot and 1000-8000 ng/spot for olanzapine and fluoxetine, respectively.Signal-to-noise ratios of 3 and 10 were considered as LOD and LOQ, respectively.LOD and LOQ for olanzapine was found to be 30 and 100 ng/spot and for fluoxetine, 300 and 1000 ng/spot respectively.Intra-day precision was determined by analyzing standard solutions in the concentration range of 200 ng/spot to 500 ng/spot for olanzapine and 2000 ng/spot to 5000 ng/spot for fluoxetine for three times on the same day while inter-day precision was determined by analyzing corresponding standards daily for five day over a period of one week.Intra-day and inter-day coefficients of variation for both drugs were found to be in the range of 0.% and 0.%, respectively.Values indicate that the method is precise.Of sample application was assessed by spotting 3 µl of drug solution seven times on a TLC plate followed by development of plate and recording the peak area for 5 spots.% RSD for peak area values of olanzapine and fluoxetine were found to be 0.0.Repeatability of measurement of peak area was determined by spotting 3 µl of olanzapine and fluoxetine solution on a TLC plate and developing the plate.Separated spot was scanned seven times without changing the position of the plate and % RSD for measurement of peak area of olanzapine and fluoxetine were found to be 0.0.To confirm the specificity of the proposed method, the solution of the formulation was spotted on the TLC plate, which was than developed and scanned.Was observed that the excipients present in the formulation did not interfere with the peaks of olanzapine and fluoxetine.Studies of the drugs were carried out for the accuracy parameter.Studies were carried out at three levels i.Level recovery studies.Stock solutions from tablet formulation of 100 µg/ml for olanzapine and 1000 µg/ml for fluoxetine were prepared.Were made and recovery studies were performed.Recovery value of olanzapine and fluoxetine were found to be 99.% and 101.Respectively while assay value of olanzapine and fluoxetine were found to be 101.% and 101.%, respectively.Low RSD value indicated the suitability of the method for routine analysis of olanzapine and fluoxetine in pharmaceutical dosage forms.Degradation studies (for 0-360 min) indicate that olanzapine and fluoxetine showed good degradation in acidic and basic condition, which started to degrade after 30 min and continued up to 180 min.Showed good degradation in oxidation condition, started to degrade after 30 min and continued to degrade up to 360 min, while olanzapine did not show any degradation up to 360 min.Fluoxetine did not show any degradation in UV light at 254 nm as well as in thermal stress at 60 o up to 10 days .Developed stability indicating HPTLC technique for the simultaneous estimation is simple, precise, specific, accurate and the statistical analysis proved that method is reproducible and selective for the analysis of olanzapine and fluoxetine in bulk drug and tablet formulations.Acknowledgements The authors are thankful to Sun Pharmaceuticals Ltd.For the gift sample of olanzapine and fluoxetine.Are thankful to Principal and management for providing necessary facilities and encouragement.References Manickam A, Donna A, William CW, Stephen RM.By high performance liquid chromatography with electrochemical detection.Drug Monit 1997;19:307-13.Labat L, Deveaux M, Dallet P, Dubost JP.Of new antidepressants and their metabolites by micellar electrokinetic capillary chromatography.Chromatogr B Biomed Sci Appl 2002;773:17-23.Zhang W, Kenneth WP, David TW, Potts BD, Bao J, Tollefson GD, et al.Of olanzapine and other antipsychotic agents inbination with fluoxetine on norepinephrine and dopamine release in rat prefrontal cortex.2000;23:250-62.Raggi MA, Casamenti G, Mandrioli R, Lzzo G, Kenndler E.Olanzapine in tablets by HPLC, CZE, derivative spectrometry and linear voltammetry.Pharm Biomed Anal 2000;23:973-81.Bugamelli F, Volterra V, Raggi MA, Casamenti G, Mandrioli R.Fluoxetine and norfluoxetine in human plasma by high-pressure liquid chromatography with fluorescence detection.Biomed Anal 1998;18:193-9.Bao J, Potts BD.Of olanzapine in rat brain tissue by high-performance liquid chromatography with electrochemical detection.Chromatogr B Biomed Sci Appl 2001;752 : 61-7.Dasoondi B, Shah P, Gandhi C, Bhat KM.Of HPLC assays method for the estimation of olanzapine in human plasma and its application to pharmacokinetics.J Pharm Sci 2003;40:350-4.Khan GJ, Trivedi C, Soni K, Khan IJ, Saraf MN.Method development, validation andparative bioavailability studies of fluoxetine extended release tablets in healthy human volunteers.2005;42:580-4.Reynolds DW, Facchine KL, Mullaney FJ, Alsante KM, Hatajik TD, Michel MG.Guidance and best practices for conducting forced degradation studies.2002;15:48-56.ICH.Stability testing of new drug substances and products.On Harmonization, Geneva: 1993 October.Sethi PD.Performance thin layer chromatography: Quantitative analysis of pharmaceutical formulation.Ed.Delhi: CBS Publishers; 1996.3-62.Fried B, Sharma J.Layer chromatography: Techniques and application.Ed.York: Marcel Dekker; 1994.11-22.ICH.
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четверг, 26 июня 2008 г.

Diabetes in children

Many children are admitted to hospital withplications of diabetes, such as diabetic ketoacidosis (DKA).THE SIGNS OF DIABETES?Know what signs to look for in your child?May not know the symptoms of diabetes.You know what to look for in your child?Of diabetes are: feeling very tired, feeling very thirsty most or all of the time, even though you're drinking lots of water, going to the toilet a lot (passing large amounts of urine), and losing weight suddenly, or not growing normally.SYMPTOMS AFFECT CHILDREN?When there's too much sugar () in your that your body can't cope with.Produces a hormone called , which helps change sugar into energy.Your body doesn't make enough , or can't use the properly, too much sugar remains in your .Three types of diabetes: TYPE 1 DIABETES - where your body produces no at all.Usually develop before the age of 40.Often develop in teenagers.All people with diabetes, only 5-15% have type 1.2 DIABETES - when your body produces too little , or when your body doesn't react properly to .Can develop in children as young as seven, although they moremonly affect adults over 40.2 is much moremon - about 95% of people with diabetes have type 2.INSIPIDUS is a rare condition where your body cannot retain enough water.Usually affects adults.Of type 1 and type 2 are the same, although they can develop in different ways.Symptoms of diabetes insipidus are similar.'further information' section to read more about these types of diabetes, including their symptoms and treatment.IF DIABETES SYMPTOMS AREN'T TREATED?Important to recognise diabetes symptoms early Symptoms of diabetes can be treated, to control how much sugar is in your .Example: Some people can control their condition by eating a healthy diet and taking regular exercise.Others need daily injections of .It's really important to recognise diabetes symptoms early and seek advice about treatment.Symptoms aren't controlled, this can lead to: TOO LITTLE SUGAR IN YOUR - this can cause a 'hypo' (hypoglycaemia), and TOO MUCH SUGAR IN YOUR (hyperglycaemia) - this can lead to diabetic ketoacidosis (DKA).ARE THE SIGNS OF A HYPO?A hypo can include: feeling shaky and irritable, sweating, tingling lips, feeling weak, hunger, and feeling sick.Severe hypo, you can be drowsy and confused, and you may lose consciousness.THE SIGNS OF DKA?Urgent medical treatment Diabetic ketoacidosis (DKA) is a build-up of acids in your , caused by your body breaking down fats instead of sugar.Can develop in diabetic people if their symptoms are not controlled or treated.DKA can include: , feeling or being sick, a high temperature, , and a fruity smell on your breath, which may smell like pear drops or nail varnish.Eventually cause unconsciousness and even death.If your child has symptoms of DKA or a severe hypo, they need emergency medical treatment - dial 999 for an ambulance.Think your child has early symptoms of diabetes, speak with your GP.Important to start treatment as soon as possible.Some pharmacies may offer free diabetes tests - you can ask at your local pharmacy for more information.Link below to find your nearest pharmacy, or you can call NHS Direct on 0845 4647.(Diabetes UK) (Diabetes UK) (Diabetes UK) Last updated on 24 June 2008 Missed a pill?
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среда, 25 июня 2008 г.

Abbott and Partnership for a Drug-Free America Launch 'Not In My House'

PUBLISHED NEWS OUR RSS NEWS CHANNELS SPONSORED ADS Abbott and Partnership for a Drug-Free America Launch 'Not In My House' Wednesday, 25 June 2008 A house is the one place where a family should feel safe and secure, yet it is here that teens are prone to get prescription drugs to misuse and abuse.Help prevent teen prescription drug misuse and abuse, the Partnership for a Drug-Free America(R) and Abbott today launched "Not In My House", a national education initiative that provides parents with useful information and tips to help them limit teen access to medicines.2007 national survey of teens (1000, ages 13 to 18) and their parents (600) conducted by the Partnership with support from Abbott, uncovered startling information about the attitudes and behaviors that can contribute to teen prescription drug abuse: More than half of teens who reported abusing prescription medications said they got the medications in their own home (15 percent) or from a parent or relative (11 percent) or friend (24 percent).More than half of the teens who tried medication without a prescription believe it is safer than street drugs and there is nothing wrong with taking them once in a while.Partying, experimenting and relaxing are the top three reasons teens give for trying prescription drugs that aren't theirs.Include dealing with physical pain or anxiety, trying to stay awake and getting more school work done.Top three reasons 27 percent of parents believe it is okay to give a teen a prescription drug that was not prescribed for that teen: getting hurt, bad menstrual cramps or problems sleeping."With one in five teenagers reporting abuse of a prescription medication to get high, parents must open their eyes to the dangers of this new tier of teen substance abuse," said Steve Pasierb, CEO, the Partnership for a Drug-Free America.And their parents have a false sense of security, mistakenly believing it's somehow safer to abuse prescription medication than street drugs.Issue demands the immediate action of parents, both by learning the facts and safeguarding medications at home as well as talking with teens about this very real threat to their health.The website, , offers insight on talking about the dangers of prescription drug misuse and abuse with teens, helps explain how the teen brain may make them more vulnerable to addiction, details the teen drug culture and lingo and gives three simple steps parents can take to help secure their homes: Monitor: An inventory of prescription medications in the home can help parents know what they have and what they do not need anymore.Count the pills left in the bottle or package after each dose.Supply should be checked regularly for missing pills.Secure: Prescription drugs should not be readily accessible to everyone in the house.Should treat prescription medicines the same way they treat other valuables in their homes.Should be stored in a safe and secure place for those who need them.Dispose: Leftover or expired prescription medications should be disposed of properly.Should be placed in a non-see-through container with something unpleasant mixed in, like old coffee grounds or kitty litter.Container should be sealed and put in the trash."Prescription medicines have an important role in health care, but they have significant risks when they are misused and abused," says Jeff Haas, general manager, Pain Care, Abbott.The Partnership have developed the 'Not in My House' education initiative to help teach parents the importance of securing medications in their homes to help protect their children.THE "NOT IN MY HOUSE" EXPERTS and ADVOCATES Gary and Jordan Neal, father and sister of Harrison who died at 17 years of age afterbining prescription and over-the-counter medicines Steve Pasierb, CEO of the Partnership for a Drug Free America Dr.Wolf, noted teen psychologist and author of numerous books on parenting teens and children Dr.Brady, nationally-renowned addiction medicine specialist ABOUT THE PARTNERSHIP FOR A DRUG-FREE AMERICA The Partnership for a Drug-Free America is a nonprofit organization that unites parents, renowned scientists andmunications professionals to help families raise healthy children.Known for its research-based national public education programs, the Partnership motivates and equips parents to prevent their children from using drugs and alcohol, and to find help and treatment for family and friends in trouble.Of this effort is an online resource center at drugfree.Interactive tools that translate the latest science and research on teen behavior, addiction and treatment into easy to understand tips and tools.ABOUT ABBOTT Abbott is a global, broad-based health carepany devoted to the discovery, development, manufacture and marketing of pharmaceuticals and medical products, including nutritionals, devices and diagnostics.More than 68,000 people and markets its products in more than 130 countries.
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вторник, 24 июня 2008 г.

An alternative topical treatment of osteoarthritis of the knee with cutaneous diclofenac solution

Pages 1805-1816 (doi:10.1805) An alternative topical treatment of osteoarthritis of the knee with cutaneous diclofenac solutionIik zgneyUniversity of Ege, Department of Pharmaceutical Technology, Faculty of Pharmacy, 35100 Bornova, Izmir, Turkey +90 232 343 4000/5132; +90 232 388 5258; _Background_: Osteoarthritis (OA) is the mostmon chronic degenerative disease, which is characterised by the destruction of the articular cartilage and subchondral bone.Treatment of OA is based primarily on the use of nonsteroidal anti-inflammatory drugs (NSAIDs) and analgesics.Are disadvantages to routinely using NSAIDs in OA.NSAIDs represent a potentially important advance in this regard as they may be significantly safer than oral NSAIDs.Solution (Pennsaid(R)) was developed for the treatment of symptomatic OA of the knee and contains diclofenac sodium as an active ingredient and dimethyl sulfoxide (DMSO), a penetration enhancer.To review: i) dermal drug application; ii) the treatment of OA with systemic and topical NSAID therapies; and iii) the clinical efficiency of Pennsaid on the topical treatment of OA of the knee.A literature search was carried out on skin, topical drug delivery, treatment of OA and assessment of published clinical studies with Pennsaid.
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понедельник, 23 июня 2008 г.

Antibodies with beta-adrenergic activity from chronic chagasic patients modulate the qt interval and m cell action potential duration

EUROPACE ADVANCE ACCESS ORIGINALLY PUBLISHED ONLINE ON MAY 30, 2008 Europace 2008 10(7):868-876; doi:10.This Article All Versions of this Article: 10/7/868 _most recent_ Services Google Scholar PubMed Social Bookmarking Repolarization ANTIBODIES WITH BETA-ADRENERGIC ACTIVITY FROM CHRONIC CHAGASIC PATIENTS MODULATE THE QT INTERVAL AND M CELL ACTION POTENTIAL DURATION EMILIANO HORACIO MEDEI1,, JOS H.ROBERTO C.LUCIANE BARCELLOS1, MASAKO O.SERGE SICOURI4, MARCELO V.ANTONIO C.DE CARVALHO1 _ 1 Instituto de Biofsica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Bloco GCCS, Cidade Universitria, Ilha do Fundo, Rio de Janeiro, RJ 21949-900, Brasil; 2 Hospital Universitrio Clementino Fraga Filho, Universidade do Brasil, Rio de Janeiro, Brasil; 3 Fundao CECIERJ, Rio de Janeiro, Brasil; 4 Masonic Medical Research Laboratory, Utica, NY, USA; 5 Hospital Ramos Mejia, Cardiac Division, Buenos Aires, Argentina _ Aims: The aim of this study was to investigate whether the sera from chronic chagasic patients (CChPs) with beta-1 adrenergic activity (Ab-) can modulate ventricular repolarization.Activity has been described in CChP.The L-type calcium current and heart rate in isolated hearts, but its effects on ventricular repolarization has not been described.Methods and results: In isolated rabbit hearts, under pacing condition, QT interval was measured under Ab- perfusion.Was also tested in guinea pig ventricular M cells.The immunoglobulin fraction (IgG-) of the Ab- was tested on Ito, ICa, and Iks currents in rat, rabbit, and guinea pig myocytes, respectively.Activity shortened the QT interval.Effect was abolished in the presence of propranolol.Sera from CChP without beta-adrenergic activity (Ab-) did not modulate QT interval.M cell action potential duration (APD) was reversibly shortened by Ab-.Inhibited this effect of Ab-, and Ab- did not modulate the AP of M cells.Was not modulated by isoproterenol nor by IgG-.IgG- increased ICa and IKs.The shortening of the QT interval and APD in M cells and the increase of IKs and ICa induced by IgG- contribute to repolarization changes that may trigger malignant ventricular arrhythmias observed in patients with chronic chagasic or idiopathic cardiomyopathy.KEY WORDS: Antibodies, Chagas' disease, Electrophysiology, M cells, QT interval Corresponding author.+55 21 25626558; fax: +55 21 22808193.Br/emedei70{at}hotmail Manuscript submitted 4 March 2008.After revision 6 May 2008.
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воскресенье, 22 июня 2008 г.

Lack of chfr gene expression sets stage for breast cancer

ARBOR, Mich.A University of Michigan study reveals in detail how breast cells produce new cells that are predisposed to be cancerous, unless they receive the protective action of the CHFR gene.CHFR expression is missing in more than a third of breast cancers.This gene is also a hot area of interest among researchers trying to explain colorectal, stomach, lung and other forms of cancer.The new study reveals how and why new "daughter" cells, produced as cells in body tissues renew themselves, receive too few or too many chromosomes if expression of the CHFR gene is missing or low.Loss of CHFR can lead to the survival of genetically unstable cells loaded with too many chromosomes, which can lead to cancer."Our findings show that loss of CHFR disrupts normal chromosome segregation in breast cells during cell division and creates genomic instability, which can drive genetic mechanisms that accelerate the development of cancer," says Elizabeth Petty, M.A U-M professor in the departments of human genetics and internal medicine and the senior author of the study.Appears online ahead of print in the journal _Neoplasia_.The new knowledge eventually could provide the scientific basis for diagnostic markers and identify which patients can benefit from specific types of cancer drugs."Our previous findings, and the work of others, have shown that cancer cells cultured in the lab that have low or absent CHFR expression are more susceptible to treatment with a class of drugs called taxanes, such as paclitaxel (Taxol) and docetaxel, that attack the dividing cells when they are trying to separate their chromosomes," says Lisa Privette, Ph.The study's first author, a recent U-M Medical School graduate and now a researcher at Cincinnati Children's Hospital."These drugs are frequently used to treat breast cancer and other types of cancer and they work by targeting the structure used to separate chromosomes.Provides further evidence for this correlation and begins to explain how the expression of CHFR alters the cell's response to these kinds of drugs.Why do some women lack CHFR function or have low function in the first place?Says that there's no evidence that women inherit mutations that lead to low or absent CHFR protein."It's likely that some other mechanism is shutting down CHFR," she says.We are actively looking at ways in which CHFR may be turned off in normal cells, in hopes that we can find a molecular switch to keep it turned on and decrease the risk of cancer development.Context: The study adds important insights in the continuing search for the roles different genes play in breast cancer.Cell culture studies, Petty's research team previously showed that loss of CHFR was associated with increased tumor size, and that normal breast epithelial cells would develop traits of cancer cells if CHFR was blocked.The new study, the researchers report what happens inside a dividing cell nucleus when CHFR is missing.One prime moment in which cancer can begin is when alterations in certain biochemical signals disturb the process by which one cell divides into two.Normal cell division, chromosomes inside the nucleus copy themselves, then line up in the middle of a structure, the mitotic spindle, which forms to aid cell division.Two copies then neatly separate and move to the ends of the spindle, where they be two bundles of identical genetic material.Be the cell's operating instructions for two new daughter cells.If the spindle doesn't form correctly, genetic material bes unstable and doesn't divide properly, resulting in cancer-prone cells containing too many chromosomes.That the spindle is affected is important, because some cancer drugs interact with the mitotic spindle as a way to curb cell division.Research details: Petty and her team studied normal and cancerous human breast tissue samples in cell culture to find out how CHFR affects certain proteins.Focused on proteins that regulate how spindles form and how chromosomes divide and form along the spindle.Found that CHFR interacts with alpha tubulin, a protein important in forming mitotic spindles, and with a key mitotic spindle checkpoint regulator, MAD2, previously implicated in breast cancer.That when CHFR is absent, MAD2 does not do its job.Without CHFR not only have problems creating the structure or apparatus necessary to separate the chromosomes between the two daughter cells during cell division.Also have an impaired ability to detect and correct the problem before the chromosomes separate," says Privette."Prior to our findings, we knew that breast cancer cells often had the wrong number of chromosomes, but no one had identified any gene, or group of genes, that could account for the high frequency of this problem," says Privette.The new study, she says, "provides one reason why the majority of breast cancer cells have too many chromosomes, which is a major hallmark of malignant cancers.A lot of work remains, and other genes are likely involved, our work on the role of CHFR in breast cancer development is an interesting and important piece of a very large puzzle.### Funding for the study came from the National Institutes of Health (National Cancer Institute) and the U.Department of Defense Breast Cancer Research Fund.Citation: Neoplasia, Vol.
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Get more How should a patient taking lithium for bipolar disorder with serum creatinine levels outside the normal range and a gradually decreasing egfr be managed?

суббота, 21 июня 2008 г.

Cymbalta approved for fibromyalgia

SLIDESHOWS : Know What to Look For : Keep Your Feet Healthy From Problems : The 9 Best Diet Tips Ever : Surprising Ways to Reduce Them New & Updated On MedicineNet : Are You Protecting Yourself?: Tim Russert and Kelsey Grammer : When is This Type of Biopsy Rmended?: How to Manage Symptoms What Are the Different Types of Biopsy?: The Little Blue Pill That Could : Would You Be Able to Recognize the Symptoms?: Is There a Connection?Patient Discussions: Viewers share theirments on questions asked by our Doctors.OTHER STORIES : Get Prevention Tips : Learn About Bike Safety : For a Breast Biopsy : Can You Prevent This Potentially Fatal Disease?TERMS 1 2 3 4 5 TOP VIEWED ARTICLES 1 2 3 4 5 MOSTMON SYMPTOMS & SIGNS TIP: To get started, click on the or button, or make a selection from the .Health categories: Popular health centers: Publications: MedicineNet: Weply with the worthy information: .1996-2008 MedicineNet, Inc.
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пятница, 20 июня 2008 г.

HIV Tests Cost-Effective for Some Seniors (HealthDay)

Only News Photos Video/Audio HIV TESTS COST-EFFECTIVE FOR SOME SENIORS BY RANDY DOTINGA _HealthDay Reporter_ _Wed Jun 18, 11:47 PM ET_ WEDNESDAY, June 18 (HealthDay News) While older adults may seem the least likely group of Americans to be infected with HIV, a new study suggests it would be cost-effective for doctors to routinely give AIDS tests to some sexually active people in their 60s and 70s.Fact, an HIV diagnosis and subsequent treatment could potentially add an average of six to nine months to an older persons life, said study co-author Dr.K. "Just because you have someone whos older doesnt mean you shouldnt think about HIV and HIV screening," said Owens, a senior investigator at the VA Palo Alto Health Care System in California and professor of medicine at Stanford University.Older Americans have been largely overlooked throughout the years of the AIDS epidemic, although they are hardly immune.Government only rmends routine HIV testing up until the age of 64.Still, an estimated 20 percent of HIV patients are older than 50, Owens said.Research with older veterans has suggested that as many as one in 200 is infected with the virus that causes AIDS, he said.AIDS threat facing older Americans is often ignored, because "people find it difficult to imagine their parents and grandparents being sexually active," said Rowena Johnston, vice president of research with the Foundation for AIDS Research.For the new study, published in the June 17 issue of the _Annals of Internal Medicine_, Owens and his colleagues created a mathematical formula to determine the costs and benefits of routinely testing people aged 55 to 75.The researchers found that its cost-effective to test people in that age group if the prevalence of undiagnosed HIV infection is greater than 1 in 1,000 and those being tested have sexual partners at risk of infection.They reported it may cost $30,000 in tests to lengthen a sexually active 65-year-old persons life by something known as a "quality-adjusted life year," aplicated measurement that takes into account the difficulty of life during illness.Average, diagnosing a 65-year-old with HIV instead of allowing him to remain untreated could lengthen his life by six to nine months, Owens said."Thats actually a lot.A pretty big change," he said.Of the interventions we do change life expectancy by a week, a few weeks, maybe a month.AIDS tests typically cost from $10 to $70, Owens said.Johnston said doctors with older patients "should to be aware they may be carrying their own biases.Worth taking into account the persons sexual history and whether they have risk factors.Still, some observers may question the studys assumption that more than one in 1,000 older adults have HIV and are undiagnosed, said Frank Myers, director of clinical epidemiology and safety systems at Scripps Mercy Hospital in San Diego."This study, with its assumptions of HIV prevalence, will not be enough to change HIV screening rmendations by itself," Myers said.Added, he hopes the research will motivate health-care providers to ask patients about HIV risk factors and target them with messages about prevention.MORE INFORMATION For more about older adults and AIDS, visit the .Yahoo!RMEND THIS STORY Rmend It: Not at All Somewhat Moderately Highly Very Highly Average (Not Rated) _AP_ _AP_ _AP_ _AP_ _AP_ _AP_ _AP_ _Reuters_ _Reuters_ _AP_ _ ABC News - Wed Jun 18, 9:02 PM ET_ _ KDKA Pittsburgh - Wed Jun 18, 5:13 PM ET_ _ ABC News - Wed Jun 18, 11:01 AM ET_ _ FOX News - Wed Jun 18, 3:03 PM ET_ Health Video News Search Search Related Searches: Yahoo!Topic Pages In-depth coverage on topics such as and .Elsewhere On The Web ABC NEWS: ABC NEWS: TIME: YAHOO!How to give and get perfectly good stuff for free, reducing waste.From Y!Find answers on Yahoo!Add Headlines To Your Personalized My Yahoo!Health - HealthDay AIDS/HIV Seniors/Aging News NEWS ALERTS __ Get an alert when there are new stories about: Annals of Internal Medicine HIV risk factors AIDS epidemic change life expectancy Scripps Mercy Hospital - - SEARCH: All News Yahoo!Only News Photos Video/Audio PRIMARY NAVIGATION Copyright 2008 HealthDay.Rights reserved.Contained above is intended for general reference purposes only.Is not a substitute for professional medical advice or a medical exam.Seek the advice of your physician or other qualified health professional before starting any new treatment.
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[cellular genetics] regulation of neurogenesis and epidermal growth factor receptor signaling by the insulin receptor/target of rapamycin pathway in drosophila

Vol.843-853, June 2008, Copyright 2008 doi:10.Article All Versions of this Article: 179/2/843 _most recent_ Services Google Scholar PubMed REGULATION OF NEUROGENESIS AND EPIDERMAL GROWTH FACTOR RECEPTOR SIGNALING BY THE INSULIN RECEPTOR/TARGET OF RAPAMYCIN PATHWAY IN DROSOPHILA HELEN MCNEILL, GAVIN M.AND JOSEPH M._ Samuel Lunenfeld Research Institute, Toronto, Ontario M5G 1X5, Canada and The Wolfson Centre For Age-Related Diseases, King's College, London SE1 1UL, United Kingdom _ 1 _Corresponding author:_ The Wolfson Centre For Age-Related Disease, King's College London, Guy's Campus, London, SE1 1UL, United Kingdom.Joseph_matthew. Determining how growth and differentiation are coordinated is key to understanding normal development, as well as disease states such as cancer, where that control is lost.Have previously shown that growth and neuronal differentiation are coordinated by the insulin receptor/target of rapamycin (TOR) kinase (InR/TOR) pathway.We show that the control of growth and differentiation diverge downstream of TOR.Regulates growth by controlling the activity of S6 kinase (S6K) and eIF4E.Of _s6k_ delays differentiation, and is epistatic to the loss of _tsc2_, indicating that S6K acts downstream or in parallel to TOR in differentiation as in growth.Loss of _eIF4E_ inhibits growth but does not affect the timing of differentiation.Also show, for the first time in Drosophila, that there is crosstalk between the InR/TOR pathway and epidermal growth factor receptor (EGFR) signaling.Signaling regulates the expression of several EGFR pathwayponents including _pointedP2_ (_pntP2_).Addition, reduction of EGFR signaling levels phenocopies inhibition of the InR/TOR pathway in the regulation of differentiation.
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четверг, 19 июня 2008 г.

Suprapharmacologic doses of intravenous dexamethasone followed by cyclosporine in the treatment of toxic epidermal necrolysis

Doses of intravenous dexamethasone followed by cyclosporine in the treatment of toxic epidermal necrolysis.J Dermatol Venereol Leprol 2008;74:265-7 HOW TO CITE THIS URL: Rai R, Srinivas CR.Doses of intravenous dexamethasone followed by cyclosporine in the treatment of toxic epidermal necrolysis.J Dermatol Venereol Leprol ;74:265-7.Sir, Toxic epidermal necrolysis (TEN) is a widespread, life-threatening, mucocutaneous disease usually due to drugs, but vaccinations, malignancy, and graft versus host disease (GVHD) have also been implicated.It may also be idiopathic in which it is not possible to identify any cause.Represents epidermal detachment involving more than 30%.Pathogenesis involves cytotoxic-mediated immune reaction targeted at the destruction of keratinocytes expressing foreign antigens.It has been shown that in the fluid contained in the bullae of patients with TEN, T-lymphocytes predominate in the initial phases, while subsequently the cells of the monocyte-macrophagic line prevail and probably contribute to the progression of the necrosis through TNF production.Epidermal keratinocytes express large amounts of Fas ligand (CD95L), and interaction between these and Fas (CD95) on the effector cells are directly in epidermal necrolysis.The role of genetic factors in the pathogenesis of TEN remains to be clarified.Of TEN usually occurs 7-21 days after the beginning of medical treatment, and the rare cases of relapse initiate within 48 hrs of taking the drug, thus suggesting the existence of an immunological memory.Various modalities of treatment include steroids, cyclosporine, intravenous immunoglobulin, thalidomide, cyclophosphamide, pentoxifylline, N acetyl cysteine, and plasmapherisis.The use of corticosteroids is a much-debated question.Have described a dramatic improvement in patients with TEN treated with corticosteroids.Steroids can be given intravenously or as suprapharmacologic doses intravenously.Of suprapharmacologic intravenous doses of dexamethasone, at an early stage of the disease, may contribute to a reduced mortality rate in SJS/TEN without increasing the healing time.Use of steroids modifies the cell-mediated immune response in the pathogenesis of TEN.The principal cellular populations involved in the pathogenesis of TEN (activated T-lymphocytes, macrophages, keratinocytes), interferes with the metabolism of TNF, and possesses an anti-apoptosis property that causes the death of keratinocytes in TEN.We report three patients of TEN who were treated with suprapharmacologic doses of intravenous dexamethasone followed by cyclosporine.A 40-year-old male presented with TEN after therapy with phenytoin for epilepsy since 1 month.Diagnosis was confirmed by histopathology with frozen sections and H and E-stained sections.Nursed in isolation and was administered intravenous with 100mg of dexamethasone in 5% glucose for 4 days till no new lesions appeared.Started on day 5 at the dose of 2 mg/kg weight till the patient's general condition improved, and then tapered at the dose of 50mg every 3 rd day, and stopped after 2 weeks when the patient hadplete remission and re-epithelization of skin lesions.A 55-year-old female presented with TEN after carbamazepine.The diagnosis by frozen section, she was administered 100mg of dexamethasone in 5% glucose for 2 days, when no new lesions appeared.Was administered on day 3 in the same regime as in Case 1.A 22-year-old female presented with TEN after ciprofloxacin.The diagnosis on frozen sections and H and E-stained sections of skin biopsy, she was administered suprapharmacologic doses of intravenous dexamethasone in the form of 100mg of dexamethasone in 5% glucose for 2 days, when no new lesions appeared.Was administered on day 3 in the same regime as in Case 1.Patients were taken in succession and treated in isolation in a tertiary care hospital, where the clinical diagnosis of TEN was confirmed by frozen and H and E sections of skin biopsy.Diagnosis of TEN was confirmed by frozen sections, treatment was started on the same day, even when new lesions were appearing.All patients, electrolytes and input-output chart were monitored.Supportive treatment like antibiotics, fluid replacement, daily dressing, and nutritional support was given.Of TEN in a burn unit or in isolation has considerably improved patients' prognosis and survival.Care and nursing, such as protection of the cutaneous and mucosal surfaces involved, monitoring of the electrolytic balance, fluid replacement, nutritional support, and the prevention and treatment of infection, are the mainstays of treatment.Help to arrest the disease progress by modifying the cell-mediated immune response and preventing the progression of the disease when given within 72 hours.By administering steroids early and for a short duration, the side-effects like gastrointestinal bleeding, delayed wound healing, and increased risk of infection can be prevented.Cyclosporine has anti-apoptosis property and decreases the time taken forplete re-epithelization, it helps arrest further progression of the disease.Although steroids could have been continued till the person recovered, the risk of septicemia and other associatedplications due to steroids is reported to increase mortality.The role of steroids is in the early phase and does not have any effect after 72 hrs, the steroids given early and for a short duration may help improve the prognosis.Cyclosporine is reported to be effective in TEN by interrupting the disease progression and decreasing the time taken forplete re-epithelization, we feel that thebination of initial high dose of steroid and subsequent cyclosporine will be a safe alternative to treat this condition associated with high mortality.Reduce mortality in toxic epidermal necrolysis, suprapharmacologic doses of intravenous corticosteriods at an early stage of the disease, followed by cyclosporine, appear to be a rational option to influence the immune system, which leads to apoptosis and necrolysis, and results in early recovery.Of intravenous dexamethasone, given at an early stage of the disease, contribute to a reduced mortality rate and modify the cell-mediated immune response in the pathogenesis of TEN.An anti-apoptosis property that causes the death of keratinocytes in TEN.Using abination of both, the immune response is modified and the side-effects of steroids are minimized, and the disease progression is interrupted by cyclosporine.Be a safe alternative in the management of TEN.References Wolkenstein PE, Roujeau JC, Revuz J.Induced toxic epidermal necrolysis.Dermatol 1998;16:399-409.Revuz JE, Roujen JC.Epidermal necrolysis.Medicine of Surgery.Saunders Press; 1995.704-11.Paquet P, Pierard GE.Fraction of tumour necrosis factor-a, interleukin-6 and their receptors in toxic epidermal necrolysis.Dermatol 1998;130:605-8.Viard I, Wehrli, Bullani R, Salomon D, Saurat JH, French LE.Toxic epidermal necrolysis by blockage of CD95 with human intravenous immunoglobulin.1998;282:490-3.Sharma VK.For Stevens-Johnson syndrome and toxic epidermal necrolysis and psoriasis.Guidelinesmittee Indian Association of Dermatologists Venereologists and Leprologists.2007.7-19.JD.Of acquired bullous skin diseases.Eng J Med 1995;333:1475-84.Cheriyan S, Patterson R, Greenberger PA.Oue of Stevens-Johnson syndrome treated with corticosteroids.Proc 1995;16:151-5.Kardaun SH, Jonkman MF.Pulse therapy for Stevens-Johnson syndrome/toxic epidermal necrolysis.Derma Venereol 2007;87:144-8.Paquet P, Pierard GE.Cyclosporin A be beneficial to mitigate drug-induced toxic epidermal necrolysis?1999;198:198-202.Toxic epidermal necrolysis: A retrospective study.J Dermatol 1997;36:923-5.Arevalo JM, Lorente JA, Herrada G, Jimenez-Reys J.
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An open-label pilot study to evaluate the efficacy of sildenafil citrate in middle-aged men with late-onset dysthymia.

ARTICLE LINKS: AN OPEN-LABEL PILOT STUDY TO EVALUATE THE EFFICACY OF SILDENAFIL CITRATE IN MIDDLE-AGED MEN WITH LATE-ONSET DYSTHYMIA.BRIEF REPORT Journal of Nervous Seidman, Stuart N.++ _ ABSTRACT: Late onset dysthymic disorder (DD) in middle-aged and elderly men responds poorly to established antidepressants.Studies noted an improvement in mood apanying sildenafil citrate treatment for erectile dysfunction.Sought to evaluate whether sildenafil's mood effects were independent of the effect on erectile function.6-week open label study was conducted with 20 male participants, aged 41-60 who were diagnosed with DD and who had normal erectile function.With sildenafil citrate 25 mg per day for 6 weeks.Primary oue measure was the 21-item Hamilton Depression Rating Scale.And sexual symptoms were also evaluated using self-report questionnaires.With sildenafil resulted in a significant reduction in Hamilton Depression Rating Scale mean scores: from 14.3.Baseline to 6.
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среда, 18 июня 2008 г.

Ibd and ibd mimicking enterocolitis in children younger than 2 years of age

You have forgotten your username or password, we can .My Menu Saved Items дё­ж–‡(з®ЂдЅ") дё­ж–‡(з№Ѓй«") English Deutsch н•њкµ­м–ґ ж—Ґжњ¬иЄћ Franais Espaol Ш§Щ„Ш№Ш±ШЁЩЉШ© Р СѓСЃСЃРєРёР№ Journal Article IBD AND IBD MIMICKING ENTEROCOLITIS IN CHILDREN YOUNGER THAN 2В YEARS OF AGE Journal Publisher Springer Berlin / Heidelberg ISSN 0340-6199 (Print) 1432-1076 (Online) Category Original Paper DOI 10.Subject Collection SpringerLink Date Wednesday, June 11, 2008 ORIGINAL PAPER IBD and IBD mimicking enterocolitis in children younger than 2 years of age Z.I.S.I.N., S.A.2 (1) Department of Reproduction and Development Sciences, University of TriesteIRCCS Burlo Garofolo, Trieste, Italy (2) Clinica Pediatrica, UniversitГ  di TriesteIRCCS Burlo Garofolo, Via dell'Istria 65/1, 34134 Trieste, Italy RECEIVED: 28 October 2007 REVISED: 10 March 2008 ACCEPTED: 17 March 2008 PUBLISHED ONLINE: 11 June 2008 Abstract Inflammatory bowel disease (IBD) is umon in children younger than 2 years of age.Criteria for differentiating IBD from other diseases with similar clinical presentation is unclear.Describe 16 patients who, between 1984 and 2004, received a histological diagnosis of IBD during the first two years of life.Presented with histological Crohn's disease, eight with ulcerative colitis and two with indeterminate colitis.Median age at diagnosis was 125 days (range 1 day to 18 months) and the medium follow up was 89 months (range 65 days to 20 years).Disease appeared to be very severe: four children (25%) underwent total parenteral nutrition (TPN), two received colectomy (12.Three patients died.Of the patients required an aggressive, multidrug, immunosuppressive approach (azathioprine , Infliximab, thalidomide, cyclosporine A).Child presented with a hypogammaglobulinaemia without any specific immunodeficiency, while in the other patients, Wiskott-Aldrich syndrome (WAS) (4 cases) and chronic granulomatous disease (CGD) (2 cases) were identified.6/16 cases, allergic colitis was first considered; these cases initially underwent cow's milk protein-free diet as the only therapy before IBD was finally diagnosed.Conclusion, early IBD has a severe prognosis and often needs an aggressive therapeutic approach.An improper diagnosis of allergic colitis might cause an important diagnostic delay.Severe immunodeficiencies, such as WAS and CGD, may represent a problem in terms of differential diagnosis and might be wrongly diagnosed as very early onset IBD.Keywords IBD - Enterocolitis - Immunodeficiency N.EMAIL: References secured to subscribers.Find Query Builder Close Clear Within all content Within this journal Export this article Export this article as RIS Text В© Springer.
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[protein structure and folding] determinants of cytochrome p450 2c8 substrate binding: structures of complexes with montelukast, troglitazone, felodipine, and 9-cis-retinoic acid

Chem.283, Issue 25, 17227-17237, June 20, 2008 This Article All Versions of this Article: 283/25/17227 _most recent_ Services Google Scholar PubMed Related Collections Social Bookmarking DETERMINANTS OF CYTOCHROME P450 2C8 SUBSTRATE BINDING STRUCTURES OFPLEXES WITH MONTELUKAST, TROGLITAZONE, FELODIPINE, AND 9-CIS-RETINOIC ACID GUILLAUME A.JASON K.STEFAAN SANSEN, PATRICK M.DAVID STOUT, AND ERIC F.From the Departments of Molecular and Experimental Medicine and Molecular Biology, The Scripps Research Institute, La Jolla, California 92037 and the Laboratoire de Chimie et Biochimie Pharmacologiques et Toxicologiques, CNRS UMR 8601, Universit Paris Descartes, 45 Rue des Saints Pres, 75270 Paris Cedex 06, France Although a crystal structure and a pharmacophore model are available for cytochrome P450 2C8, the role of protein flexibility and specific ligand-protein interactions that govern substrate binding are poorly understood.Crystal structures of P450 2C8 This work was supported, in whole or in part, by National Institutes of Health Grant GM031001 (to E.J.This work was also supported by Pfizer Global Research and Development and the Sam and Rose Stein Charitable Trust.Of this work were carried out at the Stanford Synchrotron Radiation Laboratory, a national user facility operated by Stanford University on behalf of the United States Department of Energy, Office of Basic Energy Sciences.Synchrotron Radiation Laboratory Structural Molecular Biology Program is supported by the United States Department of Energy, Office of Biological and Environmental Research, by the National Center for Research Resources Biomedical Technology Program, and by NIGMS, National Institutes of Health.Costs of publication of this article were defrayed in part by the payment of page charges.Article must therefore be hereby marked "_advertisement_" in accordance with 18 U.Section 1734 solely to indicate this fact.The on-line version of this article (available at ) contains supplemental material.This article was selected as a Paper of the Week.1 Present address: F.Roche Ltd.Discovery Research Basel, CH-4070 Basel, Switzerland.2 Present address: Dept.Structural Biology, Takeda San Diego, San Diego, CA 92121.3 To whom correspondence should be addressed: Dept.Molecular and Experimental Medicine, The Scripps Research Inst.N.Pines Rd.La Jolla, CA 92037.
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вторник, 17 июня 2008 г.

Effect of switching drug formulations from immediate-release to extended-release oros methylphenidate: a chart review of spanish adults with attention-deficit hyperactivity disorder.

ARTICLE LINKS: EFFECT OF SWITCHING DRUG FORMULATIONS FROM IMMEDIATE-RELEASE TO EXTENDED-RELEASE OROS METHYLPHENIDATE: A CHART REVIEW OF SPANISH ADULTS WITH ATTENTION-DEFICIT HYPERACTIVITY DISORDER.ORIGINAL RESEARCH ARTICLE CNS Drugs.2008.Josep Antoni 1 2; Bosch, Rosa 1; Castells, Xavier 1 3; Valero, Sergi 1; Nogueira, Mariana 1; Gomez, Nuria 1; Yelmo, Silvia 1; Ferrer, Marc 1 2; Martinez, Yolanda 1; Casas, Miguel 1 2 _ ABSTRACT: Background: The potential advantages of osmotic-release oral system (OROS) methylphenidate (Concerta(R)) over immediate-release (IR) methylphenidate (Rubifen(R)) in adults with attention-deficit hyperactivity disorder (ADHD), with respect to medication adherence, effectiveness and tolerability, are yet to be determined.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Methylphenidate was more effective than IR methylphenidate (p = 0.Reducing symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Stopped treatment with methylphenidate because of adverse events.The adherence, effectiveness and tolerability of OROS methylphenidate versus IR methylphenidate in adults with ADHD.Was hypothesized (after data collection) that adherence and effectiveness would be higher with OROS methylphenidate than with the IR formulation.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Methylphenidate was more effective than IR methylphenidate (p = 0.Reducing symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Mostmon adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Patients stopped treatment with methylphenidate because of adverse events.A chart review was carried out from April 2004 until April 2005.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Was more effective than IR methylphenidate (p = 0.Symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Mostmon adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Patients stopped treatment with methylphenidate because of adverse events.ADHD outpatient program in a general hospital in Spain.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Methylphenidate was more effective than IR methylphenidate (p = 0.Reducing symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Stopped treatment with methylphenidate because of adverse events.Adults with ADHD who met DSM-IV-TR criteria and who did not have any other current major psychiatric disorder.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Methylphenidate was more effective than IR methylphenidate (p = 0.Reducing symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Stopped treatment with methylphenidate because of adverse events.Were treated with IR methylphenidate three times daily for 3 months and then switched to OROS methylphenidate once daily.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Methylphenidate was more effective than IR methylphenidate (p = 0.Reducing symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Mostmon adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Patients stopped treatment with methylphenidate because of adverse events.Measure: Effectiveness was assessed by means of the ADHD rating scale-IV (ADHD-RS-IV) and the Clinical Global Impression-Improvement (CGI-I) scale at 3 months (coinciding with treatment switch) and at 6 months.Simplified Medication Adherence Questionnaire (SMAQ) was used to assess treatment adherence, and was administered at both 3 and 6 months.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Was more effective than IR methylphenidate (p = 0.Symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Mostmon adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Patients stopped treatment with methylphenidate because of adverse events.Adult ADHD patients (mean age +/- SD: 30 +/- 9.= 48 men ) were included in this study.Mean baseline ADHD-RS-IV score was 34.= 10.The mean daily dose of IR methylphenidate was 52.(SD = 13.As three divided doses.The treatment switch, the mean OROS methylphenidate daily dose was 57.(SD = 16.Once daily.From IR methylphenidate to OROS methylphenidate was associated with a statistically significant improvement in all items of the SMAQ questionnaire.Was more effective than IR methylphenidate (p = 0.Symptoms of ADHD.Percentage of responders was 28.IR methylphenidate and 91.OROS formulation (p = 0.OROS methylphenidate was preferred by 97% of patients.Mostmon adverse events for each formulation were dry mouth (30% IR methylphenidate) and mood instability (31% OROS methylphenidate).Patients stopped treatment with methylphenidate because of adverse events.Switch from IR to OROS methylphenidate was associated with an improvement in both adherence and effectiveness.
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Vkorc1 and cyp2c9 polymorphisms are associated with warfarin dose requirements in turkish patients

You have forgotten your username or password, we can .My Menu Saved Items дё­ж–‡(з®ЂдЅ") дё­ж–‡(з№Ѓй«") English Deutsch н•њкµ­м–ґ ж—Ґжњ¬иЄћ Franais Espaol Ш§Щ„Ш№Ш±ШЁЩЉШ© Р СѓСЃСЃРєРёР№ Journal Article _VKORC1_ AND _CYP2C9_ POLYMORPHISMS ARE ASSOCIATED WITH WARFARIN DOSE REQUIREMENTS IN TURKISH PATIENTS Journal Publisher Springer Berlin / Heidelberg ISSN 0031-6970 (Print) 1432-1041 (Online) Category Pharmacogenetics DOI 10.Subject Collection SpringerLink Date Tuesday, June 10, 2008 PHARMACOGENETICS _VKORC1_ and _CYP2C9_ polymorphisms are associated with warfarin dose requirements in Turkish patients G.T.Langaee2, H.N.T.A.Hatemi1, A.S.And J.Johnson2, 3 (1) University of Istanbul, Istanbul, Turkey (2) Department of Pharmacy Practice and Center for Pharmacogenomics, University of Florida College of Pharmacy, Gainesville, FL, USA (3) Department of Pharmacy Practice, University of Florida College of Pharmacy, P.Box 100486, Gainesville, FL 32610, USA RECEIVED: 18 January 2008 ACCEPTED: 12 May 2008 PUBLISHED ONLINE: 10 June 2008 Abstract Objectives The objective of this study was to determine the quantitative influence of vitamin K epoxide reductaseplex subunit 1 (_VKORC1_) and cytochrome P450 2C9 (_CYP_ _2C9_) polymorphisms on warfarin dose requirements in Turkish patients.Methods A total of 205 patients taking warfarin for >2 months were enrolled in the study.Acid (DNA) samples from these patients were genotyped for polymorphisms in _VKORC1_ and _CYP2C9_ genes.Linear regression analysis was used to determine the independent effects of genetic and non-genetic factors on mean warfarin dose requirements.Results The _VKORC1_ promoter polymorphism (3673 G>A) was associated with differences in weekly mean varfarin dose: for GG genotype the dose was 43.For GA genotype 33.And for AA genoype 25.(_P_ Within all content Within this journal Export this article Export this article as RIS Text В© Springer.
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понедельник, 16 июня 2008 г.

Demonstration of an anti-oxidative stress mechanism of quetiapine. implications for the treatment of alzheimer’s disease

He, Xiaokun Li, Jiming Kong, Xin-Min Li (2008) Demonstration of an anti-oxidative stress mechanism of quetiapine.The treatment of Alzheimer's disease doi:10.06519.Abstract DEMONSTRATION OF AN ANTI-OXIDATIVE STRESS MECHANISM OF QUETIAPINE Implications For The Treatment Of Alzheimer's Disease Haiyun Xu, Haitao Wang, Lixia Zhuang, Bin Yan, Yingxin Yu, Zelan Wei, Yanbo Zhang, Lillian E.Steven J.Jue He, Xiaokun Li, Jiming Kong and Xin-Min Li 1 Department of Anatomy, Southern Illinois University at Carbondale, IL, USA 2 Laboratory of Neuropharmacology, Wenzhou Medical College, Zhenjiang, China 3 Neuropsychiatry Research Unit, University of Saskatchewan, Saskatoon, Canada 4 School of Life Science and Technology, Beijing Institute of Technology, China 5 Department of Pharmacology, University of Saskatchewan, Saskatoon, Canada 6 Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada 7 Department of Psychiatry, University of Manitoba, Winnipeg, Canada X.Li, Department of Psychiatry, Faculty of Medicine, University of Manitoba, PZ432-771 Bannatyne Avenue, Winnipeg, Manitoba, Canada Fax: +1 204 789 3929 Tel: +1 204 787 7432 E-mail: X.Laboratory of Neuropharmacology, School of Pharmaceutical Science, Wenzhou Medical College, Zhenjiang, China Fax: +86 577 86689983 Tel: +86 577 8669350 E-mail: These authors contributed equally to this workAD, Alzheimer's disease; APD, antipsychotic drug; APP, amyloid precursor protein; A, amyloid ; EPR, electron paramagnetic resonance; HBSS, Hanks' balanced salt solution; PD, Parkinson's disease; PS-1, presenilin-1; ROS, reactive oxygen species; ThT, thioflavin T.Shown that quetiapine, a new antipsychotic drug, protects cultured cells against oxidative stress-related cytotoxicities induced by amyloid (A)25-35, and that quetiapine prevents memory impairment and decreases A plaques in the brains of amyloid precursor protein (APP)/presenilin-1 (PS-1) double-mutant mice.Aim of this study was to understand why quetiapine has these protective effects.The cytotoxicity of both A(25-35) and A(1-40) requires fibril formation, our first experiments determined the effect of quetiapine on A(25-35) aggregation.Inhibited A(25-35) aggregation in cell-free aqueous solutions and blocked the fibrillar aggregation of A(25-35), as observed under an electron microscope.Then investigated why quetiapine inhibits A(25-35) aggregation.The aggregation of A(25-35), a hydroxyl radical (OH) was released, which in turn amplified A(25-35) aggregation.Blocked OH-induced A(25-35) aggregation and scavenged the OH produced in the Fenton system and in the A(25-35) solution, as analyzed using electron paramagnetic resonance spectroscopy.Newpounds formed by quetiapine and OH were observed in MS analysis.We applied A(25-35) to PC12 cells to observe the effect of quetiapine on living cells.Increased levels of intracellular reactive oxygen species and calcium in PC12 cells and caused cell death, but these toxic effects were prevented by quetiapine.Results demonstrate an anti-oxidative stress mechanism of quetiapine, which contributes to its protective effects observed in our previous studies and explains the effectiveness of this drug for Alzheimer's disease patients with psychiatric and behavioralplications.THIS ARTICLE SEARCH InSynergyPubMed (MEDLINE)CrossRefBy keywordsAlzheimer's diseaseanti-oxidantbeta-peptideoxidative stressquetiapineBy authorHaiyun XuHaitao WangLixia ZhuangBin YanYingxin YuZelan WeiYanbo ZhangLillian E.
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Tailored enoxaparin reduces bleeding, bruising risk

Usually given at a dose of 1 mg/kg twice a day or 1.With a smaller dose of 1.Daily given to patients with a creatine clearance rate below 30 ml/minute, B Green (University of Queensland, Brisbane, Queensland, Australia) and co-workers explain.Results have suggested that anti-Xa levels could be optimized by adjusting enoxaparin doses for obesity and giving greater consideration to the extent of renal impairment.Further, the team randomly assigned 122 patients with pulmonary embolism, deep vein thrombosis, acute coronary syndromes, or atrial fibrillation to receive standard enoxaparin therapy or individualized enoxaparin treatment.Individualized doses, those weighing less than 100 kg based on their ideal (lean) body weight were given enoxaparin 1 mg/kg twice daily, while those weighing more than 100 kg were given enoxaparin 1.Twice daily.Renal impairment, defined as creatine clearance of less than 50 ml/minute, in the individualized treatment group were given standard treatment for the first 48 hours, followed by a fraction of the usual enoxaparin doses depending on creatine clearance.Ranged from 0.Dose in patients with a clearance of 10-19 ml/minute to 0.Dose for those with a rate of 40-49 ml/minute.That patients in the standard and individualized treatment groups did not significantly differ with regard to total body weight (74.Vs 76.Length of hospital stay (3.3.Per day (128 mg vs 137 mg), or average total dose (499 mg vs 464 mg).Events occurred in nine (15%) patients given standard enoxaparin therapypared with just one (2%) patient whose treatment was tailored (relative risk=0.Furthermore, while standard treatment was associated with three episodes of hematuria, three injection/venupuncture site bleeds, two hematemesis episodes, and one episode of epistaxis, just one case of hematemesis was reported among the individualized treatment patients.
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воскресенье, 15 июня 2008 г.

Beyond insulin replacement: addressing the additional needs of the diabetes patient

00847.Abstract REVIEW ARTICLE BEYOND INSULIN REPLACEMENT: ADDRESSING THE ADDITIONAL NEEDS OF THE DIABETES PATIENT G.Of Diabetes and Endocrinology, Scripps Clinic Torrey Pines, San Diego, CA, USAGeorge Dailey, Department of Diabetes and Endocrinology, Scripps Clinic Torrey Pines, 10666 North Torrey Pines Road, La Jolla, CA 92037, USA.1Department of Diabetes and Endocrinology, Scripps Clinic Torrey Pines, San Diego, CA, USA George Dailey, Department of Diabetes and Endocrinology, Scripps Clinic Torrey Pines, 10666 North Torrey Pines Road, La Jolla, CA 92037, USA.INTEREST: G.Has served as an investigator, speaker and occasional consultant for sanofi-aventis as well as Eli Lilly andpany, Novo Nordisk, Amylin and Merck (USA).Of type 2 diabetes mellitus (T2DM) typically focuses on correcting dysglycaemia to reduce risk for microvascular and macrovascularplications, possibly by reducing glucose-mediated oxidative stress.Other cardiometabolic risk factors, including abdominal obesity and dyslipidaemia are often overlooked in the quest for perfect glucose control.Currently used antidiabetic agents, including insulin, metformin, sulphonylureas and thiazolidinediones, have limited efficacy on these risk factors.Number of new therapeutic agents are undergoing clinical development, including glucagon-like peptide 1 mimetics (exenatide and liraglutide) and dipeptidyl peptidase 4 inhibitors (sitagliptin and vildagliptin), which target the incretin system, and the cannabinoid-1 receptor antagonists (rimonabant), which target the endocannabinoid system, may hold some promise for meeting these unmet needs.This review, the clinical properties of these agents and potential treatment pathways to best use these agents are discussed for improving the management of T2DM and cardiovascular risk.
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Impact of energy intake and expenditure on neuronal plasticity

You have forgotten your username or password, we can .My Menu Saved Items дё­ж–‡(з®ЂдЅ") дё­ж–‡(з№Ѓй«") English Deutsch н•њкµ­м–ґ ж—Ґжњ¬иЄћ Franais Espaol Ш§Щ„Ш№Ш±ШЁЩЉШ© Р СѓСЃСЃРєРёР№ Journal Article IMPACT OF ENERGY INTAKE AND EXPENDITURE ON NEURONAL PLASTICITY Journal Publisher Humana Press Inc.ISSN 1535-1084 (Print) 1559-1174 (Online) Category Original Paper DOI 10.Subject Collection SpringerLink Date Tuesday, June 10, 2008 ORIGINAL PAPER Impact of Energy Intake and Expenditure on Neuronal Plasticity Alexis M.And Mark P.(1) Cellular and Molecular Neuroscience Section, Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Balitmore, MD, USA RECEIVED: 11 March 2008 ACCEPTED: 6 May 2008 PUBLISHED ONLINE: 10 June 2008 Abstract The Roman poet Horace was among the first to recognize that when "clogged with yesterday's excess, the body drags the mind down with it.Considerable attention has been paid in neuroscience to the enhancement of neuronal function by wheel running and caloric restriction, far less is known about the other side of this issue.Are the consequences of unhealthy habits to central nervous system function?Exposure to excessive caloric intake impairs neuronal function and also contributes to obesity and other risk factors for diabetes.A disease characterized by reduced sensitivity to glucose and insulin, is also associated with deficits in brain structure and function.Enhancement of somatic metabolism by wheel running or caloric restriction improves central neuroplasticity.Studies reveals a relationship between global metabolic efficiency and neuroplasticity in the hippocampus, a brain region that is essential for learning and memory.Specific principles upheld by these findings are suggestive of a continuum, with global metabolic alterations fluctuating in concert with neuroplasticity in the hippocampus.Keywords Diet - Hippocampus - Caloric restriction - Exercise MARK P.EMAIL: References secured to subscribers.Find Query Builder Close Clear Within all content Within this journal Export this article Export this article as RIS Text В© Springer.
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A drug for longer lashes?

About Us RSC Publishing Members Education Policy Library Chemsoc Conferences News Chemistry World A DRUG FOR LONGER LASHES?2008 US drugmaker Allergan, the California-basedpany that makes antiwrinkle treatment Botox, has developed a new cosmetic drug that makes eyelashes grow longer, thicker and darker.June thepany announced it would file for US Food and Drug Administration approval for the drug before the end of September - confirming speculation it would make an eyelash-boosting drug based on bimatoprost, the active ingredient its glaa drug Lumigan.Growth is one of themonest side-effects of Lumigan, which in 2001 was approved in the US as a glaa treatment to reduce pressure inside the eye in the US.Cosmetic effects were discovered in a similar way, when doctors giving the injection to relieve muscle spasms and treat crossed eyes noticed that wrinkles around the eyes were also reduced.Now reformulated bimatoprost to be applied directly to the base of the eyelashes - and recentlypleted clinical trials have confirmed produces significant eyelash growth, Allergan says.Taken as a glaa formulation, the drugs side effects include eye redness and darkening of the eyelid and eye colour due to increased pigmentation.Darkened eye colour is likely to be permanent.Toment on the incidence of side effects triggered by the eyelash formulation during clinical trials.It has been in discussions with the FDA over the drug throughout its development, and expects the regulator's decision on the drug's approval in 2009.Says it is also assessing demand for the product outside the US, and plans to seek approvals accordingly.A synthetic member of the prostaglandin family, a group of signalling molecules produced naturally by the body and all based on a five-membered ring bearing two side chains.Claims it holds patents in the US and abroad that give it exclusive rights to make prostaglandin-based eyelash treatments, and in November 2007 sued severalpanies it claimed were infringing its patent.That month, the FDA sent US marshals to seize 12,862 tubes of Age Intervention Eyelash, a product sold by California-based Jan Marini Skin Research that was found to contain bimatoprost.It will make about $1.(Ј0.From sales of Botox during 2008, and predicts sales of its eyelash drug could exceed $500 million in annual sales, based on the estimate that the global mascara market is worth $3.Each year.Allergan announcement, New York-based Goldman Sachs analyst James Kelly concluded that FDA approval was likely for the drug even though it will be marketed as a cosmetic.Are less concerned about FDA conservatism, given the history of the product in the eye,' he said.Forecast the product would launch in 2009, with sales peaking at $500 million.
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суббота, 14 июня 2008 г.

A drug for longer lashes?

About Us RSC Publishing Members Education Policy Library Chemsoc Conferences News Chemistry World A DRUG FOR LONGER LASHES?2008 US drugmaker Allergan, the California-basedpany that makes antiwrinkle treatment Botox, has developed a new cosmetic drug that makes eyelashes grow longer, thicker and darker.June thepany announced it would file for US Food and Drug Administration approval for the drug before the end of September - confirming speculation it would make an eyelash-boosting drug based on bimatoprost, the active ingredient its glaa drug Lumigan.Growth is one of themonest side-effects of Lumigan, which in 2001 was approved in the US as a glaa treatment to reduce pressure inside the eye in the US.Cosmetic effects were discovered in a similar way, when doctors giving the injection to relieve muscle spasms and treat crossed eyes noticed that wrinkles around the eyes were also reduced.Now reformulated bimatoprost to be applied directly to the base of the eyelashes - and recentlypleted clinical trials have confirmed produces significant eyelash growth, Allergan says.Taken as a glaa formulation, the drugs side effects include eye redness and darkening of the eyelid and eye colour due to increased pigmentation.Darkened eye colour is likely to be permanent.Toment on the incidence of side effects triggered by the eyelash formulation during clinical trials.It has been in discussions with the FDA over the drug throughout its development, and expects the regulator's decision on the drug's approval in 2009.Says it is also assessing demand for the product outside the US, and plans to seek approvals accordingly.A synthetic member of the prostaglandin family, a group of signalling molecules produced naturally by the body and all based on a five-membered ring bearing two side chains.Claims it holds patents in the US and abroad that give it exclusive rights to make prostaglandin-based eyelash treatments, and in November 2007 sued severalpanies it claimed were infringing its patent.That month, the FDA sent US marshals to seize 12,862 tubes of Age Intervention Eyelash, a product sold by California-based Jan Marini Skin Research that was found to contain bimatoprost.It will make about $1.(Ј0.From sales of Botox during 2008, and predicts sales of its eyelash drug could exceed $500 million in annual sales, based on the estimate that the global mascara market is worth $3.Each year.Allergan announcement, New York-based Goldman Sachs analyst James Kelly concluded that FDA approval was likely for the drug even though it will be marketed as a cosmetic.Are less concerned about FDA conservatism, given the history of the product in the eye,' he said.Forecast the product would launch in 2009, with sales peaking at $500 million.
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пятница, 13 июня 2008 г.

Can you tell me whether there is any interaction between orlistat and oral contraceptives?

Pilot service has been created to help members of the primary care teams of England get answers to their clinical questions.This is the first visit to the site we rmend you read "".IMPORTANT ANNOUNCEMENT: As of June 27th the NLH Q" name="updateContentForm"> Can you tell me whether there is any interaction between orlistat and oral contraceptives?10/Jun/08 ANSWER: In October 2007 the Faculty of Sexual and Reproductive Healthcare answered the question 'For women using oral contraceptives is it safe to use Orlistat?They gave the following answer: _"Orlistat (marketed under the trade name Xenical) also known as tetrahydrolipstatin, is a drug designed to treat obesity.Is the saturated derivative of lipstatin—a potent natural inhibitor of pancreatic lipases isolated from the bacterium Streptomyces toxytricini.Primary function is preventing the absorption of fats from the human diet, thereby reducing caloric intake.To the summary of product characteristics for Orlistat (Xenical), no interactions with oral contraceptives have been observed.Does not suggest any interaction between hormonal contraceptives and Orlistat.Could not find any evidence of adverse reactions or loss of efficiency of oral contraceptives due to the drug interactions with Orlistat.The CEU suggests that it is safe to use Orlistat while using oral contraceptives.The CKS guideline on contraception reports: _"Orlistat:_ - Although no interactions between COCs and orlistat have been demonstrated in specific studies, orlistat may indirectly reduce the availability of COCs and lead to unexpected pregnancies in some cases .An additional contraceptive method is rmended if the woman has severe diarrhoea whilst taking orlistat.The CKS guideline on obesity uses slightly different wording: _"No direct interaction between oral contraceptives and orlistat has been demonstrated in specific drug-drug interaction studies.May indirectly reduce the availability of oral contraceptives through its action on the gastrointestinal tract.A woman experiences severe diarrhoea whilst taking orlistat an additional contraceptive method is rmended .REFERENCES 1) 2) 3) The NLH Question Answering Service aims to answer questions quickly, it is not a systematic review.You have any doubt as to the implications of this contact the Q&A Service Provider for further information.
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