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Gene almost recovers to its baseline after a period of time in response to chronic MPL infusion despite continuous presence of the drug 12 ; . In various earlier reports we presented data demonstrating that the glucocorticoid receptor GR ; is strongly down-regulated in response to MPL 12, 13, 15, ; . Since GR mediates the effect of the drug, the large reduction in this effector molecule should greatly reduce the driving force for changes in gene expression, thus reducing the effect of the drug. The second gene, Figure 5 right ; showing enhanced expression is tryptophan 2, 3-dioxygenase Tdo2 ; , the first enzyme in the kynurenine pathway 20 ; . For this gene, the enhanced expression in response to the single bolus dose is more sustained than Odc1. However, the chronic time profile shows a second and higher period of enhanced expression that continues throughout the entire 168 hour infusion period. These data illustrate that enhanced expression to corticosteroids probably involves multiple mechanisms, and that our initial classification of enhanced regulation is too simplistic. Of the 358 genes, the profiles of 104 showed down-regulation following both dosing regimens. As with enhanced regulation, this classification is inadequate to capture the multiple.
Aminimanizani A, Beringer PM, Kang J, et al. Distribution and elimination of tobramycin administered in single or multiple daily doses in adult patients with cystic fibrosis. Journal of Antimicrobial Chemotherapy 2002; 50: 553-559. Barclay ML, Begg EJ, Duffull SB, et al. Experience of once-daily aminoglycoside dosing using a target area under the concentration-time curve. Aust NZ J Med 1995; 25: 230-235. Begg EJ, Barclay ML, Duffull SB. A suggested approach to once-daily aminoglycoside dosing. Br J clin Pharmac 1995; 39: 605-609. Contopoulos-Ioannidis DG, Giotis ND, Baliatsa DV, et al. Extended-Interval Aminoglycoside Administration for Children: A Meta-analysis. Pediatrics 2004; 114 1 ; : e111-e118. Master V, Roberts GW, Coulthard KP, et al. Efficacy of Once-Daily Tobramycin Monotherapy for Acute Pulmonary Exacerbations of Cystic Fibrosis: A Preliminary Study. Pediatric Pulmonology 2001; 31: 367-376. Rybak MJ, Abate BJ, Kang SL, et al. Prospective Evaluation of the Effect of an Aminoglycoside Dosing Regimen on Rates of Observed Nephrotoxicity and Ototoxicity. Antimicrobial Agents and Chemotherapy 1999; 43 7 ; : 1549-1555. Smyth A, Tan KH-V, Hyman-Taylor P, Mulheran M, et al. Once versus three-times daily regimens of tobramycin treatment for pulmonary exacerbations of cystic fibrosis-the TOPIC study: a randomized controlled trial. Lancet 2005; 365: 573-578. Vic P, Ategbo S, Turck D, O Husson M, et al. Efficacy, tolerance, and pharmacokinetics of once daily tobramycin for pseudomonas exacerbations in cystic fibrosis. Arch Dis Child 1998; 78: 536-539. Vic P, Ategbo S, Turck D, et al. Tolerance, pharmacokinetics and efficacy of once daily amikacin for treatment of Pseudomonas aeruginosa pulmonary exacerbations in cystic fibrosis patients. Eur J Pediatr 1996; 155: 948-953, for example, propranolol erowid.
Lori A, Flores 9302 Antwerp Cove Houston, TX 77070 713 ; 294-6985 Mike Frontz Bexar County Forensic Sciences Center 73337 Louis Pasteur Dr. San Antonio, TX 78229 210 ; 335-4031 Michael Carlo, Ph.D. 124 Kilt Road San Angelo, TX 76901-9512 915 ; 942-0263 Kathy Erwin Texas Department of Public Safety P.O. Box 4143, MSC0460 Austin, TX 78765 512 ; 424-2105 Robert G. Schoenfeld, Ph.D. 7204 Aztec Road, N.E. Albuquerque NM 87110 505 ; 884-4997 Chris Heartsill Institute of Forensic Sciences 5230 Medical Center Dr. Dallas, TX 75235 214 ; 920-5966 Phil Kemp, Ph. D. Office of the Chief Medical Examiner 901 N. Stonewall Oklahoma City, OK 73117 405 ; 239-7141.
PRONESTYL-SR, 29 pro-otic, 44 propafenone hcl, 29 propantheline bromide [CARE], 50 proparacaine, hcl, -fluorescein, 76 PROPINE [G], 73 propofol [INJ], 2 propoxyphene hcl, w apap [CARE], 22 propoxyphene napsylate w apap [CARE], 22 propranolol hcl, 29, 33 propranolol hcl w hctz, 33 propylthiouracil, 45 PROQUAD [INJ], 54 PROQUIN XR, 11 PROSCAR [G], 88 PROSED DS [CARE], 88 proset d, 84 PROSOL [INJ], 62 PROSTIGMIN, 26 PROSTIN E2 VAGINAL SUPPOSITORY, 66 PROSTIN VR PEDIATRIC [G][INJ], 34 PROTAMINE SULFATE, 63 pro-tannate [CARE], 79 PROTID [CARE], 80 PROTONIX, 53 PROTONIX IV [INJ], 53 PROTOPAM CHLORIDE [INJ], 43 PROTOPIC, 41 PROVENTIL HFA, 85 PROVENTIL inh, 85 PROVERA [G], 72 PROVIGIL, 23 PROVISC [INJ], 76 PROZAC, WEEKLY [G], 27 PRUDOXIN [CARE], 41 pse 120 msc 2.5, 86 pse 15 cpm 2, cpm, 80 pse bpm, 80 pseubrom, -pd, 80 pseudo cm [CARE], 80 pseudo gg tr, max, 84 pseudoephedrine gg, w guaifenesin, 84 pseudoephedrine hcl, 86 pseudoephedrine w chlorphenir [CARE], 80 pseudovent, 400, ped, 84 PSORCON E, 40 PSORIATEC, 37.
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CONTROL ID: 142762 TITLE: Distribution of transgenic mRNA in the hearts of transgenic mice expressing GFP-tagged Kir6.2 and Kir2.1 K + channel subunits CATEGORY: Ion Channels SUB-CATEGORY: Heart &Cardiac Muscle AUTHORS ALL ; : Dobrzynski, Halina 1; Greener, Ian G.2; Flagg, Thomas P.3; Tellez, James O.1; Chandler, Natalie J.2; Lopatin, Anatoli N.4; Nichols, Colin G.3; Boyett, Mark R.1; Billeter, Rudolf 2. AUTHORS INSTITUTIONS: H. Dobrzynski, J.O. Tellez, M.R. Boyett, Division of Cardiovascular &Endocrine Sciences, Manchester University, Manchester, UNITED KINGDOMI.G. Greener, N.J. Chandler, R. Billeter University of Leeds, Leeds, UNITED KINGDOMT.P. Flagg, C.G. Nichols Washington University, St Louis, MOA.N. Lopatin University of Michigan, Ann Arbor, MI ABSTRACT BODY: In heart, Kir6.2 is responsible for the ATP-sensitive K + current IKATP ; and Kir2.1 is in part responsible for the background inward rectifier K + current IK1 ; . In this study, transgenic mice expressing either GFP-tagged Kir6.2 or Kir2.1 K + channel subunits under the control of the cardiac -myosin heavy chain -MHC ; promoter were generated. We have investigated the distribution of Kir6.2-GFP and Kir2.1-GFP mRNA in the sinoatrial node SAN ; , compact atrioventricular node AVN ; , His bundle, and working myocardium from these transgenic mice. Digoxigenin labelled sense and anti-sense riboprobes were made specific for GFP, and in situ hybridisation was carried out on 10 m tissue sections mounted on glass slides. We observed that Kir6.2-GFP mRNA was expressed in the SAN n 3 ; , atrium n 3 ; and ventricle n 3 ; of transgenic hearts, but was absent in the compact AVN n 3 ; and His bundle n 3 ; . Kir2.1-GFP mRNA was expressed in the atrium n 3 ; and ventricle n 3 ; , but was absent in the SAN n 3 ; , compact AVN n 3 ; and His bundle n 3 ; . Kir6.2-GFP and Kir6.2-GFP mRNA was observed in tissue sections from non-transgenic mice from the same litter. The presence or absence of Kir6.2-GFP and Kir2.1-GFP mRNA in the SAN, AVN, His bundle, atrium and ventricle faithfully follows the presence or absence of Kir6.2-GFP and Kir2.1-GFP proteins in these heart tissues Dobrzynski et al., in preparation ; . These patterns do not correspond to the expected distribution of -MHC mRNA, whose core promoter was used in the construct. They do, however, largely correspond to the expected distribution of Kir6.2 and Kir2.1 mRNA and protein in the SAN, AVN and His bundle. This suggests transcriptional regulation of the genes, i.e. control at the level of the transcript, leading to directed exclusion of both transcript and protein from the specific conducting tissues. This may be an important mechanism controlling the expression of the wild-type Kir6.2 and Kir2.1 genes. Ethical Requirements: Where applicable, the experiments described here conform with Physiological Society ethical requirements. No Image Selected ; No Table Selected ; CONTACT E-MAIL ONLY ; : bmshd leeds.ac.
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The award is named in memory of the nationally regarded physician from Evanston Northwestern HealthcareHighland Park Hospital who was the founding director of the Highland Park Hospital Breast Center. Dr. Arthur G. Michel has left an enormous legacy of hope, compassion and dignity. Dr. Gabram is director of the Breast Clinic Program for Loyola University Medical Center and Program Director for the General Surgery Residency program. Her far-reaching initiatives have ranged from research in sentinel node and bone marrow micrometastases to integrating her medical school breast disease curriculum. In addition, Dr. Gabram serves as co-chair of the Y-ME Illinois Medical Advisory Committee where she is committed to spreading the word about Y-ME to physicians throughout Illinois, and to assisting Y-ME with identifying resources for uninsured and underinsured women throughout the state.
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339. San L, Cam J, Peri J, Mata R, Porta M. Efficacy of clonidine, guanfacine and methadone in the rapid detoxification of heroin addicts: a controlled clinical trial. British Journal of Addiction 1990; 85 1 ; : 1417. [1] [3] 340. San L, Fernndez T, Cam J, Gossop M. Efficacy of methadone versus methadone and guanfacine in the detoxification of heroin-addicted patients. Journal of Substance Abuse Treatment 1994; 11 5 ; : 4639. [1] [3] 341. San L, Pomarol G, Peri JM, Olle JM, Cami J. Follow-up after a six-month maintenance period on naltrexone versus placebo in heroin addicts. British Journal of Addiction 1991; 86 8 ; : 983-90. [8] [14] 342. Santo Domingo Carrasco J, Bravo Ortiz MF, Barroso Canizares A, Caballero Martin L. [Double-blind study of the efficacy of tetrabamate and tiapride in the treatment of alcohol deprivation syndrome]. Medicina Clinica Barcelona ; 1985; 85 13 ; : 533-6. [19] 343. Savage C, Karp EG, Curran SF, Hanlon TE, McCabe OL. Methadone LAAM maintenance: a comparison study. Comprehensive Psychiatry 1976; 17 3 ; : 415-24. [12] 344. Scaggs LS. A substance abuse awareness prevention program: knowledge, attitudes and behaviours. Unpublished Ph.D. Dissertation, Ohio State University 1985. [17] 345. Schinke SP, Tepavac L, Cole KC. Preventing Substance Use Among Native American Youth: ThreeYear Results. Addictive Behaviours 2000; 25 3 ; : 387-97. [17] [29] 346. Schneider U, Paetzold W, Eronat V, Huber TJ, Seifert J, Wiese B et al. Buprenorphine and carbamazepine as a treatment for detoxification of opiate addicts with multiple drug misuse: a pilot study. Addiction Biology 2000; 5: 65-9. [2] 347. Schottenfeld R, Pakes J, Oliveto A, Ziedonis D, Kosten T. Buprenorphine versus methadone maintenance treatment for concurrent opioid dependence and cocaine abuse. Archives of General Psychiatry 1997; 54 8 ; : 713-20. [9] [11] 348. Sees KL, Delucchi KL, Masson C, Rosen A, Clark HW, Robillard H et al. Methadone maintenance versus 180-day psychosocially enriched detoxification for treatment of opioid dependence: a randomized controlled trial. JAMA 2000; 283 10 ; : 1303-10 [10] 349. Seifert J, Metzner C, Paetzold W, Borsutzky M, Passle T, Rollnik J et al. Detoxification of opiate addicts with multiple drug abuse: a comparison of buprenorphine versus methadone. Pharmacopsychiatry 2002; 35: 159-64. [1] [2] 350. Seifert J, Peters E, Jahn K, Metzner C, Ohlmeier M, te Wildt B et al. Treatment of alcohol withdrawal: chlormethiazole versus. carbamazepine and the effect on memory performancea pilot study. Addiction Biology 2004; 9 1 ; : 43-51. [19] 351. Sellers EM, Naranjo CA, Harrison M, Devenyi P, Roach C, Sykora K. Diazepam loading: simplified treatment of alcohol withdrawal. Clinical Pharmacology and Therapeutics 1983; 34 6 ; : 822-6. [20] 352. Sellers EM, Zilm DH, Degani NC. Comparative efficacy of propranolol and chlordiazepoxide in alcohol withdrawal. Journal of Studies on Alcohol 1977; 38 11 ; : 2096-108. [20] 353. Senay E, Jaffe J, diMenza S, Renault P. A 48-week study of methadone, methadyl acetate, and minimal services. In: Opiate Addiction: Origins and Treatment. New York: W.H. Winston and Sons, 1974. [12] and ramipril.
Continue in the present 180-day reform--or form, excuse me. We need to examine further if identical rewards should be granted for successful invalidity and non-infringement claims. At present, I with the mind to preserve at least some sort of financial incentive to encourage vigorous patent challenges by generic drug firms. While I think changes to the current system may be in order, I opposed to the McCain-Schumer rolling exclusivity. Now with regard to the 30-month stay, my preliminary review at this point is that the provisions of the McCain-Schumer bill related to the 30-month stay may be--or may overcorrect the problem, but may in fact be somewhat understated in the first place. We just need to find out more about the facts and we should wait until these facts are brought forward, because they are being--they are under study and they are going to be brought forward. As I understand SA12, the current statutory 30-month stay would be eliminated in favor of a system of case-by-case application for injunctive relief. Now, I hope that this hearing and the forthcoming FTC study shed some light on the facts of the matter concerning improper and consecutive 30-month stays. I also want to see what the FDA concludes with respect to the scope of the alleged consecutive stay problem, and what its recommendations are to address this situation. What is often left unsaid by advocates of changing the law is that the Hatch-Waxman bill created a unique provision in the Patent Code that essentially allowed generic drug firms to infringe pioneer firm patents. This was a huge change. I don't think people realize who aren't familiar with this bill and with this area what a huge change that was in the law. A change that no other--no other--excuse me--I got my--industries enjoy. There is a point--that's a point I cannot overemphasize. As a general rule, Title 35 provides that no one can make, use or sell a product while it is under patent. There is one exception to this general rule against patent infringement. This provision, the so-called Bolar Amendment of the Hatch-Waxman bill is codified at 35 U.S.C. 271 e ; . Here's what it says. Now, do we have the chart there? Okay. "It shall not be an act of infringement to make or use a patented invention solely for uses reasonably related to the development and submission of information under a federal law which regulates the manufacture, use or sale of drugs or veterinary biological products." What this means--that means drugs. What this means is the generic drug firms and only generic drug firms among all other generic product industries gets statutory protection from activities that would otherwise constitute blatant acts of patent infringement. This is the only case that Hatch-Waxman gave that right. Anyone involved in the negotiations will tell you that the Bolar provision was significant in striking the final balance that led to the passage of Hatch-Waxman. In my mind, the Bolar amendment is directly related to the 30-month stay, which allowed what was thought of as a reasonable time for courts to act responsibly on patent changes initiated by generics. The reason why no one would simply buy the argument that the changes in the 30-month stay proposed--or 30-month rule proposed by SA12 only.
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Note ; 1. The number of claims shown in this table indicates one case per payment type, which does not correspond to those in Table 1. 2. Because the figures of the benefit amounts are rounded to the nearest thousand, the sum of the benefit amounts in each fiscal year is not always identical to the total, for example, p4opranolol and weight gain.
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Please forward your ideas, articles and pictures to the Editorial committee member in your area, editor, or associate editor. While every effort is made to include late submissions, articles received after the submission deadline may not be published due to production time-lines. For additional copies of the Palliser Expedition please contact Central Stores: Derrin Thibault: dthibault palliserhealth.
Varying in size from 5 mm to 100 mm. The larger nodules are usually found to be cavitating. CECT scan of the thorax can undoubtedly pick up nodular and cavitating lesions which are not obvious on chest radiography4. In a radiological review of 91 cases with pulmonary manifestations of Wegener's granulomatosis, solitary or multiple pulmonary nodule 62% ; was the most common finding and cavitation in the nodules were present in 38 per cent 5. Limited Wegener's granulomatosis, in which there is only pulmonary involvement with no evidence of extra pulmonary involvement has been described and pulmonary lesions in both forms of disease are same1, 6. The differential diagnosis of pulmonary involvement in Wegener's granulomatosis often includes infections, neoplasms, connective tissue diseases and granulomatous diseases. Early diagnosis and institution of treatment is crucial in this life threatening disorder and as the drugs used to treat Wegener's granulomatosis are potentially toxic and could worsen some of these conditions, a definitive diagnosis is essential. The diagnosis of Wegener 's granulomatosis is usually made by the histological demonstration of vasculitis, granulomatous inflammation and necrosis. Since these histological features are often patchy in distribution with the likelihood of obtaining a positive biopsy result being influenced by the organ site and, particularly the amount of tissue obtained7, 8. Antineutrophilic cytoplasmic antibodies ANCA ; have a high degree of association with Wegener's granulomatosis. Since their description, two main immunofluorescent patterns of ANCA have been described; a cytoplasmic pattern c-ANCA and a perinuclear pattern pANCA, positivity of both have broadly different disease association. The c-ANCA is positive in more than 90% of patients with active Wegener's granulomatosis 4, 9 . In `limited' Wegener's granulomatosis, that is, without active glomerulonephritis, the sensitivity of cANCA is 65 to per cent.9 None of the studies of c-ANCA in normal individuals showed positive result4, 10 and sertraline.
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Poster #1018 Marrow Derived Muscle Colonies Arise from Single Cells Mehrdad Abedi, MD, Roger Williams Medical Center, Providence, RI, USA; Bethany Foster, Roger Williams Medical Center, Providence, RI, USA; Gerald Colvin, DO, Roger Williams Medical Center, Providence, RI, USA; Peter Quesenberry, MD, Roger Williams Medical Center, Providence, RI, USA We have previously established a model of plasticity of marrow to skeletal muscle that is based on transplantation of GFP positive marrow and cardiotoxin injury to the tibialis muscle. In these experiments, we have observed colonies of GFP positive muscle fibers, defined as 3 or more myocytes. We noted that individual GFP positive fibers showed marked heterogeneity of fluorescence. In sharp contrast, colonies of GFP + cells, showed homogeneous fluorescence. This was confirmed by using confocal microscopy and by measuring the mean fluorescent intensity of the individual cells in the colonies. When the intensity of the green fluorescence in individual fibers was graded, 95% of the colonies counted, showed homogenous intensity of green fluorescence. Therefore the probability of 95% of colonies to have a minimum of 3 homogenous fibers by random association is less than 0.0001. The incidence of muscle colonies remained the same between the experiments that received marrow cells directly into muscle or the one that received intravenous infusion of marrow cells followed by mobilization of their stem cells that suggest colonies are not the result of injection of clump of cells into the muscle. The incidence increased in experiments with multiple cycles of mobilization and injury and also in mdx mouse that has spontaneous ongoing regeneration of its muscles. Cotransplantation of marrow cells from yellow fluorescent protein YFP ; and cyan fluorescent protein CFP ; transgenics into C57BL 6 mice followed by cardiotoxin injury showed colonies that were either from YFP or CFP cells. No mixed colonies were found. Transplantation of YFP marrow cells before injury followed by CFP cells after injury and vice versa showed colonies only from cells that were infused at the time of transplantation. Colonies were seen only in samples that received CD45, C-Kit and or Sca positive marrow cells and not in those negative populations. Evaluation of marrow cells homed into uninjured muscle revealed a GFP + CD45 negative population 4 weeks after transplantation that produced Myf5 + and MyoD + myoblasts three days after injury. Immunohistochemistry of cardiotoxin injured samples post transplant also revealed marrow derived GFP positive and Myf5 positive cells. These data suggests that marrow derived muscle colonies are a clonal phenomenon arising from a hematopoietic marrow stem cell population. Poster #1019 Identification of Key Biological Modules in a Murine Model of Hypoxic Pulmonary Hypertension Sina A. Gharib, MD, University of Washington, Seattle, WA, USA; David Madtes, MD, Fred Hutchinson Cancer Research Center, Seattle , WA, USA; Daniel Luchtel, MD, University of Washington, Seattle, WA, USA Rationale: The genetic aspects of pulmonary vascular remodeling due to chronic pulmonary hypertension are still largely unknown. Global expression profiling allows simultaneous and unbiased investigation of many candidate genes involved in this process. Methods: Ninety male, inbred, Balb C mice were randomly assigned to hypoxia PiO2 75 torr ; or control PiO2 150 torr ; . The hypoxic group was returned to normoxia after 3 weeks exposure and kept at sea level for an additional 2 weeks. Temporal profiles of 15, 389 genes during progression and subsequent regression of pulmonary hypertension were obtained using cDNA microarrays. Rigorous statistical methods were utilized to identify significant gene expression and to cluster genes with similar temporal patterns. Real-time PCR was used to confirm the expression of several candidate genes. Results: Cluster analysis classified candidate genes into groups and sildenafil and propranolol, for instance, propranolol stress.
REGULATION OF PROTEIN-TYROSINE-PHOSPHATASE-MEG2 BY PHOSPHATI-DYLINOSITOL3, 4, 5-PHOSPHATE MODULATES SMALL GTPASE RAB28 IN PHAGOCYTOSIS V Kwok * , E Vachon * , V Cherepanov * , X Wang * , M Glogauer, CW Chow * , GP Downey * * Division of Respirology, Faculty of Medicine, University of Toronto; CIHR Group in Matrix Dynamics, Faculty of Dentistry, University of Toronto Introduction: PTP-MEG2 is a cytosolic protein-tyrosine-phosphatase PTP ; containing a Sec14 homology lipid binding domain, which was found to be associated with phosphatidylinositol-4, 5-bisphosphates PIP2 ; and phosphatidylinositol-3, 4, 5-triphosphate PIP3 ; in vitro. Rab family GTPases are often implicated in membrane and intracellular vesicle transport and Rab28 GTPase was demonstrated to be a binding partner of PTP-MEG2. PTPMEG2 was previously shown to localize in granules, secretory vesicle membranes and associated with nascent phagosomes. However, little is known about the molecular basis of these functions including its substrates and regulation of its subcellular distribution. Hypothesis: PTP-MEG2 activity-regulated by PIP3 modulates Rab28 function during phagosome maturation. Objectives: - To demonstrate that PTP-MEG2 binds specifically to and is activated by PIP3 of nascent phagosomes. - To study how PTP-MEG2 and Rab28 GTPase are recruited to developing phagosomes. - To analyse the functional significance of PIP3 and Rab28 GTPase in regulating signaling events associated with phagosome maturation. Methods and Results: 1. Transfected PTP-MEG2 and Rab28 have cytosolic distributions. They colocalize and both have granular expressions. Murine RAW264.7 macrophages and COS-2A cells were used for transfection, immunofluorescence.
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The internal medicine physician discharged the patient with the following instructions: follow up with the endocrinologist in one month for a thyroid scan; see the nephrologist within two weeks; and call the internal medicine physician's office to schedule an appointment immediately after arriving home. The patient was discharged on a high-potassium, low-sodium diet and was given information on this diet. The nephrologist prescribed the beta-blocker Propranllol for treatment of the thyrotoxicosis. It was later discovered that this prescription was filled, but not taken by the patient. Three days after his discharge, the patient was brought back to the ED by ambulance. Seven hours before becoming ill, he had eaten a large, carbohydrate-rich meal. His potassium level on admission was 1.3 mEq L. While in the ED, the patient suffered cardiac arrhythmias. Resuscitative efforts lasted more than one hour, but were unsuccessful. An autopsy was performed and the pathologist concluded the patient died as a result of TPP, precipitated by a high-carbohydrate meal. one that many physicians may never see. According to nephrology and endocrinology experts, the patient did not need long-term potassium supplementation once he left the hospital because his potassium level stabilized following replacement therapy. Propranalol, which blocks the peripheral action of excess thyroid hormone and reduces the frequency and severity of TPP attacks, was prescribed appropriately. All the experts reviewing this case, including the plaintiff's experts, agreed that if the patient had taken Propranalol as prescribed, he would not have suffered a fatal attack of TPP. The main allegations against the physicians involved the discharge instructions and the failure to instruct the patient to follow a low-carbohydrate diet. The patient's wife claimed the Pdopranolol was not taken because there was confusion over the reason for its prescription and that they had not been given a doctor's number to call with any questions. The nephrologist's discharge summary clearly indicated that the patient understood why Propganolol was being prescribed. The discharge instruction sheet, signed by the patient, listed phone numbers for all three physicians, but none of the physicians were ever contacted. The patient also failed to make the follow-up appointments as instructed at discharge. During the investigation of this claim, it was also discovered that the plaintiff did not follow the low-sodium diet. The patient's wife testified that he consumed 12 soft drinks daily after leaving the hospital. The meal the patient consumed before his death consisted of a fast-food hamburger and French fries. Regarding the failure to counsel the patient about a low-carbohydrate diet, the plaintiff's internal medicine expert claimed that any physician treating a patient for TPP must advise the patient to reduce carbohydrate intake. Further, the standard of care would require a physician to tell the patient that a high carbohydrate load could increase continued on page 14.
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Voltage sensitive dye requires the removal of the dura, thus exposing the cortex. For two major reasons, it was not possible, till recently, to maintain an animal in this state while recording optically for a period longer than a few weeks: 1 ; Deterioration of the physiological condition mainly due to high susceptibility of the exposed tissue for re-occurrence of infection. 2 ; Deterioration of the cortical opacity due to leptomeningeal arachnoid-pia membranes ; reactive proliferation that starts immediately following cortical exposure. Without an appropriate treatment, the cortical tissue becomes opaque rather quickly to a degree in which the OI technique becomes impossible. The ability to record simultaneously from many cortical sites chronically in awake behaving animals has important applications in neuroscience research Kruger and Bach, 1981; Legendy et al., 1984; Deadwyler and Hampson, 1997; Nicolelis et al., 1997, 1998; Rousche and Normann, 1998; Laubach et al., 2000; Wessberg et al., 2000 ; . Thus, the need for an effective dural substitute that would have optimal application features suitable to the requirements of the OI technique, as well as, for the conventional single unit recording needs, had become evident. Recently, we have developed methods which.
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