995 resultados para 37.01


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Revista elaborada pela Assessoria de Comunicação e Imprensa da Reitoria da UNESP

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The Janie Rice Papers consists of correspondence, newspaper clippings, letters of appreciation, and certificates of awards concerning her career as a teacher at the Winthrop Training School, her work with the Baptist Church in Chester, SC and her establishment of a Janie Carroll Rice scholarship at Winthrop.

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AIMS Primary percutaneous coronary intervention (PPCI) is the preferred reperfusion therapy in ST-elevation myocardial infarction (STEMI). We conducted this study to evaluate the contemporary status on the use and type of reperfusion therapy in patients admitted with STEMI in the European Society of Cardiology (ESC) member countries. METHODS AND RESULTS A cross-sectional descriptive study based on aggregated country-level data on the use of reperfusion therapy in patients admitted with STEMI during 2010 or 2011. Thirty-seven ESC countries were able to provide data from existing national or regional registries. In countries where no such registries exist, data were based on best expert estimates. Data were collected on the use of STEMI reperfusion treatment and mortality, the numbers of cardiologists, and the availability of PPCI facilities in each country. Our survey provides a brief data summary of the degree of variation in reperfusion therapy across Europe. The number of PPCI procedures varied between countries, ranging from 23 to 884 per million inhabitants. Primary percutaneous coronary intervention and thrombolysis were the dominant reperfusion strategy in 33 and 4 countries, respectively. The mean population served by a single PPCI centre with a 24-h service 7 days a week ranged from 31 300 inhabitants per centre to 6 533 000 inhabitants per centre. Twenty-seven of the total 37 countries participated in a former survey from 2007, and major increases in PPCI utilization were observed in 13 of these countries. CONCLUSION Large variations in reperfusion treatment are still present across Europe. Countries in Eastern and Southern Europe reported that a substantial number of STEMI patients are not receiving any reperfusion therapy. Implementation of the best reperfusion therapy as recommended in the guidelines should be encouraged.

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A 23-month-old tomcat was referred to our clinic because of male behavioral problems, cryptorchidism, and an undefined intra-abdominal organ resembling a uterus. Ultrasonography and computed tomography showed 2 fluid-filled tubular structures dorsolaterally to the bladder and connected to the pelvic urethra. The cat was castrated, and the tubular structures were surgically removed. Histology identified them as Müllerian duct remnants. The testes were hypoplastic, the epididymes and deferent ducts were normal. Cytogenetic analyses revealed the presence of a mosaic 37,X/38,XY karyotype which explains the clinical findings.

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OBJECTIVE To assess whether palliative primary tumor resection in colorectal cancer patients with incurable stage IV disease is associated with improved survival. BACKGROUND There is a heated debate regarding whether or not an asymptomatic primary tumor should be removed in patients with incurable stage IV colorectal disease. METHODS Stage IV colorectal cancer patients were identified in the Surveillance, Epidemiology, and End Results database between 1998 and 2009. Patients undergoing surgery to metastatic sites were excluded. Overall survival and cancer-specific survival were compared between patients with and without palliative primary tumor resection using risk-adjusted Cox proportional hazard regression models and stratified propensity score methods. RESULTS Overall, 37,793 stage IV colorectal cancer patients were identified. Of those, 23,004 (60.9%) underwent palliative primary tumor resection. The rate of patients undergoing palliative primary cancer resection decreased from 68.4% in 1998 to 50.7% in 2009 (P < 0.001). In Cox regression analysis after propensity score matching primary cancer resection was associated with a significantly improved overall survival [hazard ratio (HR) of death = 0.40, 95% confidence interval (CI) = 0.39-0.42, P < 0.001] and cancer-specific survival (HR of death = 0.39, 95% CI = 0.38-0.40, P < 0.001). The benefit of palliative primary cancer resection persisted during the time period 1998 to 2009 with HRs equal to or less than 0.47 for both overall and cancer-specific survival. CONCLUSIONS On the basis of this population-based cohort of stage IV colorectal cancer patients, palliative primary tumor resection was associated with improved overall and cancer-specific survival. Therefore, the dogma that an asymptomatic primary tumor never should be resected in patients with unresectable colorectal cancer metastases must be questioned.

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Vitamin D has immunomodulatory properties in the defence against pathogens. Its insufficiency is a widespread feature of cystic fibrosis (CF) patients, which are repeatedly suffering from rhinovirus (RV)-induced pulmonary exacerbations.To investigate whether vitamin D has antiviral activity, primary bronchial epithelial cells from CF children were pre-treated with vitamin D and infected with RV16. Antiviral and anti-inflammatory activity of vitamin D was assessed. RV and LL-37 levels were measured in bronchoalveolar lavage (BAL) of CF children infected with RV.Vitamin D reduced RV16 load in a dose-dependent manner in CF cells (10(-7 )M, p<0.01). The antiviral response mediated by interferons remained unchanged by vitamin D in CF cells. Vitamin D did not exert anti-inflammatory properties in RV-infected CF cells. Vitamin D increased the expression of the antimicrobial peptide LL-37 up to 17.4-fold (p<0.05). Addition of exogenous LL-37 decreased viral replication by 4.4-fold in CF cells (p<0.05). An inverse correlation between viral load and LL-37 levels in CF BAL (r=-0.48, p<0.05) was observed.RV replication in primary CF bronchial cells was reduced by vitamin D through the induction of LL-37. Clinical studies are needed to determine the importance of an adequate control of vitamin D for prevention of virus-induced pulmonary CF exacerbations.

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1 Brief von Margot von Mendelssohn an Max Horkheimer, 20.05.1948; 6 Briefe zwsichen Charles E. Merriam und Max Horkheimer, 1940-1941; 4 Briefe zwischen Josef Messinger und Max Horkheimer, 1940; 1 Curriculum Vitae von Alfred Meusel an Max Horkheimer; 1 Brief von Max Horkheimer an Gerhard Meyer, 17.10.1938; 3 Briefe zwischen Hans A. Meyer und Max Horkheimer´09.10.1939, 1947; 2 Briefe zwischen Julie Meyer und Max Horkheimer, 12.04.1941, 15.04.1941; 43 Briefe zwischen Hermann Meyer-Lindenberg, Oscar Meyer und Max Horkheimer sowie Briefwechsel mit Hadley Cantril; 2 Briefe zwischen Hadley Cantril und Theodor W. Adorno, 22.05.1941, 28.05.1941; 1 Brief von Jerome Michael an Margot von Mendelssohn, 10.01.1941; 2 Briefe und 2 Beilagen zwischen Joseph Mire und Max Horkheimer, 16.03.1941, 28.03.1941; 6 Briefe zwischen Mitchell, Silberberg & Knupp, Los Angeles und Max Horkheimer, 1942, 1943; 1 Brief von Friedrich Pollock an Wesley C. Mitchell, 06.08.1940; 3 Briefe zwischen Hans Mohr und Max Horkheimer, 29.03.1946, 1946; 1 Brief von Herbert Moeller Morton an Max Horkheimer, 25.02.1940; 1 Brief von Max Horkheimer an den Chairman of the Committee on General Scholarships, Cambridge Massachusetts, 01.03.1940; 2 Briefe von David H. Moses an Max Horkheimer, 1939; 1 Brief von Franz Neumann an Philip Mosley, 28.04.1941; 49 Briefe zwischen Dorthy I. Mulgrave und Max Horkheimer, 1936-1940; 1 Brief von Max Horkheimer an das Municipal Court, San Francisco, 24.12.1948;

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1 Telegramm von Leo Löwenthal an Frederick Pollock, 12.10.1953; 2 Briefe von Frederick Pollock an Frederick J. Hacker (Arzt), Oktober 1953; 1 Brief von Frederick J. Hacker (Arzt), an Theodor W. Adorno, 06.12.1950; 1 Brief von Frederick Pollock an Frederick Wild, 28.09.1953; 1 Brief von Frederick Wild an Max Horkheimer, 15.08.1953; 1 Brief von der Frankfurter Bücherstube an Frederick Pollock, 08.04.1953; 1 Brief von der Frankfurter Bücherstube an den Kurator W. Rau, 08.04.1953; 1 Brief von Frederick Pollock an die Guaranty Trust Company, 20.03.1953; 1 Brief von Germaine Krull-Ivens an Frederick Pollock, 14.01.1953;

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2 Briefe von Frederick Pollock an Theodor W. Adorno, Juni 1954; 1 Brief von Frederick Pollock an Rosenberg, 27.10.1954; 1 Brief von Lotte Steinberger an Frederick Pollock, 23.05.1954; 1 Brief von dem British Consulate General (Los Angeles) an Frederick Pollock, 27.03.1954; 1 Brief von Max Horkheimer an das British Consulate General (Los Angeles), 26.01.1954;

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The hypermodified, hydrophobic 2-methylthio-N$\sp6$-(dimethylallyl)-adenosine (ms${2{\cdot}6}\atop1$A) residue occurs $3\sp\prime$ to the anticodon in tRNA species that read codons beginning with U. The first step (i$\sp6$A37 formation) of this modification is catalyzed by dimethylallyl diphosphate:tRNA dimethyallyltransferase (EC 2.5.1.8), which is the product of the miaA gene. Subsequent steps were proposed to be catalyzed by MiaB and MiaC enzymes to complete the ms${2{\cdot}6}\atop1$A37 modification. The study of functions of the ms${2{\cdot}6}\atop1$A37 is very important because this modified base is one of the best candidates for a role in global control in response to environmental stress. This dissertation describes the further delineation of functions of the ms${2{\cdot}6}\atop1$A37 modification in E. coli K-12 cells. This work provides significant information on functions of tRNA modifications in E. coli cells to adapt to stressful environmental conditions. Three hypotheses were tested in this work.^ The first hypothesis tested was that non-optimal translation processes cause increased spontaneous mutagenesis by the induction of SOS response in starving cells. To test this hypothesis, I measured spontaneous mutation rates of wild type cells and various mutant strains which are defective in tRNA modification, SOS response, or oxidative damage repair. I found that the miaA mutation acts as a mutator that increased Lac$\sp+$ reversion rates and Trp$\sp+$ reversion frequencies of the wild-type cells in starving conditions. However, the lexA3(Ind)(which abolishes the induction of SOS response) mutation abolished the mutator phenotype of the miaA mutant. The recA430 mutation, not other identified SOS genes, decreased the Lac$\sp+$ reversion to a less extent than that of the lexA3(Ind) mutation. These results suggest that RecA together with another unidentified SOS gene product are responsible for the process.^ The second hypothesis tested was that MiaA protein binds to full-length tRNA$\sp{\rm Phe}$ molecules in form of a protein dimer. To test this hypothesis, three versions of the MiaA protein and seven species of tRNA substrates were purified. Binding studies by gel mobility shift assays, filter binding assays and gel filtration shift assays support the hypothesis that MiaA protein binds to full-length tRNA$\sp{\rm Phe}$ as a protein dimer but as a monomer to the anticodon stem-and-loop. These results were further supported by using steady state enzyme kinetic studies.^ The third hypothesis tested in this work was that the miaB gene in E. coli exists and is clonable. The miaB::Tn10dCm insertion mutation of Salmonella typhimurium was transduced to E. coli K-12 cells by using P$\sb1$ and P$\sb{22}$ bacteriophages. The insertion was confirmed by HPLC analyses of nucleotide profiles of miaB mutants of E. coli. The insertion mutation was cloned and DNA sequences adjacent to the transposon were sequenced. These DNA sequences were 86% identical to the f474 gene at 14.97 min chromosome of E. coli. The f474 gene was then cloned by PCR from the wild-type chromosome of E. coli. The recombinant plasmid complemented the mutant phenotype of the miaB mutant of E. coli. These results support the hypothesis that the miaB gene of E. coli exists and is clonable. In summary, functions of the ms${2{\cdot}6}\atop1$A37 modification in E. coli cells are further delineated in this work in perspectives of adaptation to stressful environmental conditions and protein:tRNA interaction. (Abstract shortened by UMI.) ^