999 resultados para Rubens, Peter Paul, 1577-1640.


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Back row against wall, left to right: Josef Molling, Margaret Molling nee Benjamin, Werner Wolff, Miss Hermann (called "Ferna", Peter Molling's governess), " Selma" (partially hidden, Anna Marianne/Berthold Nathan's cook), "Lisbeth" (Anna Marianne/Berthold's maid), Ilse Joachim, Ernst Joachim, Annemarie Nathan (3rd wife of Julius Nathan), Julius Nathan (brother of Berthold Nathan), Ernst Kallmes (son of Ceilchen nee Wolff, Helene's sister). Very tall against the wall: Max Benjamin (son of Helene). Third row, left to right: Mathilde Kaufmann nee Benjamin, Adolf Molling, Paul Nathan (son of Anna Marianne/Berthold), Marianne Rasmussen (daughter of Waldemar), Hildegard Weinberger (friend of bride), Herta Albrecht (friend of bride), Dr. Franz Gruenberg (friend of groom), Leonie Wolff nee Simon (wife of Werner Wolff), Lina Molling nee Marx (wife of Richard), Waldemar Benjamin-Rasmussen (son of Helene/David), Luzi's Husband, Minka Bernard nee Nathan (sister of Berthold Nathan), Richard Molling (brother of Claerchen), Albert Wolff (brothter of Moritz Wolff). Second row, seated, left to right: Helene Benjamin nee Wolff, Berthold Nathan, Anna Marianne Nathan nee Benjamin, bride Eva Wolff nee Nathan, groom Adolf Wolff, Claerchen Wolff nee Molling, Moritz Wolff, standing Luzi Rasmussen nee Gruen (wife of Waldemar). Front row, children on floor, left to right: Peter Molling, Elizabeth Benjamin-Rasmussen mar. Engel, Louis Peter Wolff, Helmut Benjamin Rasmussen (became Henry)

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Left to right: Margot Molling, Ilse Molling, Adolf Molling, Paul Goldschmidt (husband of Ilse Molling)

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left to right: Margot Molling, Ilse Molling, Adolf Molling, Paul Goldschmidt (husband of Ilse Molling)

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Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10−8). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms.

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Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10−8), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ~2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

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Paul was the son from a previous marriage of Hermann's first wife Olga Judey nee Fischmann

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Paul was the son from a previous marriage of Hermann Judey's first wife Olga Judey nee Fischmann

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Paul was the son from a previous marriage of Hermann Judey's first wife Olga Judey nee Fischmann

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Background An Advanced Pharmacy Practice Framework for Australia (the ‘APPF’) was published in October 2012. Further to the release of the APPF, the Advanced Pharmacy Practice Framework Steering Committee planned to develop an advanced practice recognition model for Australian pharmacists. Aim To gauge the perspectives of the pharmacy profession relating to advanced practice, via an online survey, in order to inform the design of the model. Method A survey was developed and administered to Australian pharmacists through SurveyMonkey . The survey content was based on findings from a review of national and international initiatives for recognition of advanced practice in pharmacy and other health disciplines, including medicine and nursing. Results The results of the survey showed that a high proportion of respondents considered they were already working at, or working towards achieving, an advanced level of practice. The responses relating to the assessment methods showed a clear preference for ‘submission of a professional portfolio’. A ‘written examination’ had a low level of support and in relation to an ‘oral examination by a panel’ there was a marked preference for a panel of multidisciplinary health professionals over a panel of pharmacists. Conclusion The survey outcomes will inform the development of an advanced pharmacy practice recognition model for Australian pharmacists, particularly in relation to the assessment methods. Survey outcomes also demonstrated that there is scope to further enhance the application of the APPF in the development and recognition of advanced practitioners, and to build greater awareness of the breadth of competencies encompassed by ‘advanced practice’.

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There is evidence across several species for genetic control of phenotypic variation of complex traits1, 2, 3, 4, such that the variance among phenotypes is genotype dependent. Understanding genetic control of variability is important in evolutionary biology, agricultural selection programmes and human medicine, yet for complex traits, no individual genetic variants associated with variance, as opposed to the mean, have been identified. Here we perform a meta-analysis of genome-wide association studies of phenotypic variation using ~170,000 samples on height and body mass index (BMI) in human populations. We report evidence that the single nucleotide polymorphism (SNP) rs7202116 at the FTO gene locus, which is known to be associated with obesity (as measured by mean BMI for each rs7202116 genotype)5, 6, 7, is also associated with phenotypic variability. We show that the results are not due to scale effects or other artefacts, and find no other experiment-wise significant evidence for effects on variability, either at loci other than FTO for BMI or at any locus for height. The difference in variance for BMI among individuals with opposite homozygous genotypes at the FTO locus is approximately 7%, corresponding to a difference of ~0.5 kilograms in the standard deviation of weight. Our results indicate that genetic variants can be discovered that are associated with variability, and that between-person variability in obesity can partly be explained by the genotype at the FTO locus. The results are consistent with reported FTO by environment interactions for BMI8, possibly mediated by DNA methylation9, 10. Our BMI results for other SNPs and our height results for all SNPs suggest that most genetic variants, including those that influence mean height or mean BMI, are not associated with phenotypic variance, or that their effects on variability are too small to detect even with samples sizes greater than 100,000.

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Dedication to Paul by Eugen Ernst