998 resultados para 186-2


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Print No: 186

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Venoms from Bothrops jararacussu, Bothrops asper, Bothrops atrox, Bothrops pirajai, Bothrops moojeni, Bothrops alternatus and Bothrops (Bothriopsis) bilineata were fractionated using a simplified procedure based on ion-exchange chromatography on CM-Sepharose at pH 8.0 or reverse phase HPLC. The resulting elution profiles showed important differences in the myotoxin content of these venoms. The venoms from B. alternatus, B. atrox and Bothriopsis bilineata did not contain the major myotoxin found in the other venoms. The amino acid sequence of the first 50 residues of the N-terminal region of the PLA(2)-like myotoxins showed a homology of 90-96% with other bothropic myotoxins. All of the myotoxins isolated induced rat paw edema, increased the level of plasma creatine kinase and produced myonecrosis together with polymorphonuclear cell infiltration.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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Background Calstabins 1 and 2 bind to Ryanodine receptors regulating muscle excitation-contraction coupling. Mutations in Ryanodine receptors affecting their interaction with calstabins lead to different cardiac pathologies. Animal studies suggest the involvement of calstabins with dilated cardiomyopathy. Results We tested the hypothesis that calstabins mutations may cause dilated cardiomyopathy in humans screening 186 patients with idiopathic dilated cardiomyopathy for genetic alterations in calstabins 1 and 2 genes (FKBP12 and FKBP12.6). No missense variant was found. Five no-coding variations were found but not related to the disease. Conclusions These data corroborate other studies suggesting that mutations in FKBP12 and FKBP12.6 genes are not commonly related to cardiac diseases.

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We evaluated the association of QT interval corrected for heart rate (QT(c)) and resting heart rate (rHR) with mortality (all-causes, cardiovascular, cardiac, and ischaemic heart disease) in subjects with type 1 and type 2 diabetes.

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REASON FOR PERFORMING STUDY: The development of clinical illness in foals is usually predetermined by perinatal history, management or stressful environmental conditions. OBJECTIVES: To determine potential risk factors for an increased incidence of infectious diseases during the first 30 days post partum. METHODS: The population consisted of Thoroughbred foals born on stud farms in the Newmarket (UK) area in 2005 (n = 1031). They were followed for their first 30 days. Factors suspected to influence the incidence of infectious neonatal diseases were examined in a logistic regression approach for each of the 3 outcomes (total infectious diseases, systemic disease with diarrhoea and total infectious diseases excluding diarrhoea). All 28 factors were either foal or mare or stud farm related. RESULTS: Several significant risk factors for a higher disease incidence, such as birth complications, colostrum intake by stomach tube and leucocytosis 12-48 h post partum were identified. The factor 'boarding stud' seemed to be protective against disease. CONCLUSION: Some factors, such as the mare's time at stud before foaling, the mare's rotavirus vaccination schedule and fibrinogen-values that empirically had been linked to the outcome previously were not confirmed as relevant. This included the reported useful prophylactic treatment with antimicrobial drugs. POTENTIAL RELEVANCE: Factors to be considered when evaluating newborn foals include: stud management, the birth process, route of colostrum intake, white and red blood cells, and the date of birth. These may help to detect foals at risk to develop an infection so that targeted prophylactic measures can be initiated.

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Toll-like receptor-2 (TLR2) mediates host responses to gram-positive bacterial wall components. TLR2 function was investigated in a murine Streptococcus pneumoniae meningitis model in wild-type (wt) and TLR2-deficient (TLR2(-/-)) mice. TLR2(-/-) mice showed earlier time of death than wt mice (P<.02). Plasma interleukin-6 levels and bacterial numbers in blood and peripheral organs were similar for both strains. With ceftriaxone therapy, none of the wt but 27% of the TLR2(-/-) mice died (P<.04). Beyond 3 hours after infection, TLR2(-/-) mice had higher bacterial loads in brain than did wt mice, as assessed with luciferase-tagged S. pneumoniae by means of a Xenogen-CCD (charge-coupled device) camera. After 24 h, tumor necrosis factor activity was higher in cerebrospinal fluid of TLR2(-/-) than wt mice (P<.05) and was related to increased blood-brain barrier permeability (Evans blue staining, P<.02). In conclusion, the lack of TLR2 was associated with earlier death from meningitis, which was not due to sepsis but to reduced brain bacterial clearing, followed by increased intrathecal inflammation.

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Vorbesitzer: Eljāqīm Carmoly

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5 Briefe zwischen Konrad Wittwer und Max Horkheimer, 1936, 1938, 1939; 1 Brief von Max Horkheimer an Joseph Wohl, 18.08.1934; 1 Brief von Max Horkheimer an Hedwig Wollenberger, 25.02.1941; 2 Briefe zwischen Richard Wolf und Max Horkheimer, 22.10.1938, 07.11.1938; 2 Briefe zwischen Martha Wolfenstein und Max Horkheimer, 11.10.1937, 19.10.1937; 1 Brief von Clemy Wolff an Leo Löwenthal, 05.03.1941; 2 Briefe zwischen Ilse Wolff und Max Horkheimer, 29.08.1937, 03.09.1937; 1 Brief von Max Horkheimer an Howard Woolston, 25.03.1941; 1 Einladung von der Women's Conference, 1935; 1 Brief von Max Horkheimer an die Women's Conference, 15.03.1935; 1 Brief von der World Foundation an Max Horkheimer, 26.11.1937; 2 Briefe vom World Jewish Congress an Max Horkheimer, 1942, 1945; 1 Brief von Max Horkheimer an Francis Henry Russel, 28.09.1942; 1 Brief von Max Horkheimer an Dr. Opie, 28.09.1942; 1 Brief der Württembergische Hypothekenbank an Max Horkheimer, 24.12.1930; 12 Briefe zwischen Rösle Wuestholz und Max Horkheimer, 1935-1937, 1939; 1 Brief von Max Horkheimer an Frida Wunderlich, 22.11.1937; 1 Brief von Max Horkheimer an die Yale University Library, 22.12.1938; 2 Briefe zwischen Owen D. Young und Max Horkheimer, 22.04.1940, April 1940; 3 Briefe zwischen Hans Zeisel und Max Horkheimer, 21.07.1941, 1941, 1944; 2 Briefe zwischen der Zentrale Hilfsstelle für deutsche Flüchtlingskinder Prag und Max Horkheimer, 01.03.1938, 25.04.1938; 6 Briefe zwischen Gregory Zilboorg und Max Horkheimer, 1939; 16 Briefe und Beilage an Max Horkheimer und F. Pollock von Edgar Zilsel, 1939-1942; 1 Brief vom Social Science Research Counsil an Edgar Zilsel, 01.04.1940; 1 Brief von The Rockefeller Foundation an Edgar Zilsel, 20.06.1939; 9 Briefe und Beilage von Max Horkheimer und F. Pollock an Edgar Zilsel, 1939-1942 sowie Briefwechsel mit Betty Drury; 10 Briefe zwischen The Rockefeller Foundation und Max Horkheimer, 1939-1940; 1 Brief von Max Horkheimer an Edgar Zilsel, 20.06.1939; 12 Briefe zwischen Betty Drury und F. Pollock, 1939-1940; 7 Briefe zwischen Alexander Zinnemann und Max Horkheimer, 1936;

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Vorbesitzer: Dominikanerkloster Frankfurt am Main