Vorschläge zur Verbesserung des israelitischen Gottesdienstes : nebst e. Predigt über die Sidra Reeh 5 B. M. XI. 26 - XVI. 18. als Probe aus e. größeren Samml.

seinen Glaubensgenossen vorgelegt von A. Bock

Von Willebrand Factor Improves Risk Prediction in Addition to N-Terminal Pro-B-type Natriuretic Peptide in Patients Referred to Coronary Angiography and Signs and Symptoms of Heart Failure and Preserved Ejection Fraction.

BACKGROUND Heart failure with preserved ejection fraction (HFpEF) represents a growing health burden associated with substantial mortality and morbidity. Consequently, risk prediction is of highest importance. Endothelial dysfunction has been recently shown to play an important role in the complex pathophysiology of HFpEF. We therefore aimed to assess von Willebrand factor (vWF), a marker of endothelial damage, as potential biomarker for risk assessment in patients with HFpEF. METHODS AND RESULTS Concentrations of vWF were assessed in 457 patients with HFpEF enrolled as part of the LUdwigshafen Risk and Cardiovascular Health (LURIC) study. All-cause mortality was observed in 40% of patients during a median follow-up time of 9.7 years. vWF significantly predicted mortality with a hazard ratio (HR) per increase of 1 SD of 1.45 (95% confidence interval, 1.26-1.68; P<0.001) and remained a significant predictor after adjustment for age, sex, body mass index, N-terminal pro-B-type natriuretic peptide (NT-proBNP), renal function, and frequent HFpEF-related comorbidities (adjusted HR per 1 SD, 1.22; 95% confidence interval, 1.05-1.42; P=0.001). Most notably, vWF showed additional prognostic value beyond that achievable with NT-proBNP indicated by improvements in C-Statistic (vWF×NT-proBNP: 0.65 versus NT-proBNP: 0.63; P for comparison, 0.004) and category-free net reclassification index (37.6%; P<0.001). CONCLUSIONS vWF is an independent predictor of long-term outcome in patients with HFpEF, which is in line with endothelial dysfunction as potential mediator in the pathophysiology of HFpEF. In particular, combined assessment of vWF and NT-proBNP improved risk prediction in this vulnerable group of patients.

Ms. Ff. Mus. 1119 - Am XI post Trinit. : Herr! sey mir gnädig, denn mir ist angst pp. ; C. A. T. B., 2 violini, 2 oboe se piace, 1 viola, violoncello et organo

von Telemann. [Textdichter: Gottfried Simonis]

Ms. hebr. oct. 156 - Šeʾēlōt u-tešūbōt ṣemaḥ ṣedeq

Vorbesitzer: Abraham Merzbacher;

[Sefer Yetsirah] id est Liber Iezirah, qui Abrahamo patriarchæ adscribitur : unà cum commentario rabi Abraham f. D super 32 Semitis Sapientiæ, à quibus liber Iezirah incipit

translatus & notis illustratus à Joanne Stephano Rittanglio

The molecular basis for beta-lactamase gene expression in B. anthracis, B. cereus and B. thuringiensis

The susceptibility of most Bacillus anthracis strains to β-lactam antibiotics is intriguing considering that the B. anthracis genome harbors two β-lactamase genes, bla1 and bla2, and closely-related species, Bacillus cereus and Bacillus thuringiensis, typically produce β-lactamases. This work demonstrates that B. anthracis bla expression is affected by two genes, sigP and rsp, predicted to encode an extracytoplasmic function sigma factor and an antisigma factor, respectively. Deletion of the sigP/rsp locus abolished bla expression in a penicillin-resistant clinical isolate and had no effect on bla expression in a prototypical penicillin-susceptible strain. Complementation with sigP/rsp from the penicillin-resistant strain, but not the penicillin-susceptible strain, conferred β-lactamase activity upon both mutants. These results are attributed to a nucleotide deletion near the 5' end of rsp in the penicillin-resistant strain that is predicted to result in a nonfunctional protein. B. cereus and B. thuringiensis sigP and rsp homologues are required for inducible penicillin resistance in those species. Expression of the B. cereus or B. thuringiensis sigP and rsp genes in a B. anthracis sigP/rsp-null mutant confers resistance to β-lactam antibiotics, suggesting that while B. anthracis contains the genes necessary for sensing β-lactam antibiotics, the B. anthracis sigP/rsp gene products are insufficient for bla induction. ^ Because alternative sigma factors recognize unique promoter sequence, direct targets can be elucidated by comparing transcriptional profiling results with an in silico search using the sigma factor binding sequence. Potential σP -10 and -35 promoter elements were identified upstream from bla1 bla2 and sigP. Results obtained from searching the B. anthracis genome with the conserved sequences were evaluated against transcriptional profiling results comparing B. anthracis 32 and an isogenic sigP/rsp -null strain. Results from these analyses indicate that while the absence of the sigP gene significantly affects the transcript levels of 16 genes, only bla1, bla2 and sigP are directly regulated by σP. The genomes of B. cereus and B. thuringiensis strains were also analyzed for the potential σP binding elements. The sequence was located upstream from the sigP and bla genes, and previously unidentified genes predicted to encode a penicillin-binding protein (PBP) and a D-alanyl-D-alanine carboxypeptidase, indicating that the σ P regulon in these species responds to cell-wall stress caused by β-lactam antibiotics. ^ β-lactam antibiotics prevent attachment of new peptidoglycan to the cell wall by blocking the active site of PBPs. A B. cereus and B. thuringiensis pbp-encoding gene located near bla1 contains a potential σP recognition sequence upstream from the annotated translational start. Deletion of this gene abolished β-lactam resistance in both strains. Mutations in the active site of the PBP were detrimental to β-lactam resistance in B. cereus, but not B. thuringiensis, indicating that the transpeptidase activity is only important in B. cereus. I also found that transcript levels of the PBP-encoding gene are not significantly affected by the presence of β-lactam antibiotic. Based on these data I hypothesize that the gene product acts a sensor of β-lactam antibiotic. ^

Physical oceanography and current velocity during Nathaniel B. Palmer cruise NBP97-05

An extensive set of conductivity-temperature-depth (CTD)/lowered acoustic Doppler current profiler (LADCP) data obtained within the northwestern Weddell Sea in August 1997 characterizes the dense water outflow from the Weddell Sea and overflow into the Scotia Sea. Along the outer rim of the Weddell Gyre, there is a stream of relatively low salinity, high oxygen Weddell Sea Deep Water (defined as water between 0° and ?0.7°C), constituting a more ventilated form of this water mass than that found farther within the gyre. Its enhanced ventilation is due to injection of relatively low salinity shelf water found near the northern extreme of Antarctic Peninsula's Weddell Sea shelf, shelf water too buoyant to descend to the deep-sea floor. The more ventilated form of Weddell Sea Deep Water flows northward along the eastern side of the South Orkney Plateau, passing into the Scotia Sea rather than continuing along an eastward path in the northern Weddell Sea. Weddell Sea Bottom Water also exhibits two forms: a low-salinity, better oxygenated component confined to the outer rim of the Weddell Gyre, and a more saline, less oxygenated component observed farther into the gyre. The more saline Weddell Sea Bottom Water is derived from the southwestern Weddell Sea, where high-salinity shelf water is abundant. The less saline Weddell Sea Bottom Water, like the more ventilated Weddell Sea Deep Water, is derived from lower-salinity shelf water at a point farther north along the Antarctic Peninsula. Transports of Weddell Sea Deep and Bottom Water masses crossing 44°W estimated from one LADCP survey are 25 ? 10**6 and 5 ? 10**6 m**3/s, respectively. The low-salinity, better ventilated forms of Weddell Sea Deep and Bottom Water flowing along the outer rim of the Weddell Gyre have the position and depth range that would lead to overflow of the topographic confines of the Weddell Basin, whereas the more saline forms may be forced to recirculate within the Weddell Gyre.