University of Wisconsin-Madison

About: University of Wisconsin-Madison is a education organization based out in Madison, Wisconsin, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 108707 authors who have published 237594 publications receiving 11883575 citations.

Work system design for patient safety: the SEIPS model

Abstract: Models and methods of work system design need to be developed and implemented to advance research in and design for patient safety. In this paper we describe how the Systems Engineering Initiative for Patient Safety (SEIPS) model of work system and patient safety, which provides a framework for understanding the structures, processes and outcomes in health care and their relationships, can be used toward these ends. An application of the SEIPS model in one particular care setting (outpatient surgery) is presented and other practical and research applications of the model are described.

Do Non-Audit Services Compromise Auditor Independence? Further Evidence

Abstract: This paper challenges the findings of Frankel, Johnson and Nelson (FJN) (2002). The results of our discretionary accruals tests differ from FJN's when we adjust discretionary current accruals for firm performance. In our earnings benchmark tests, in contrast to FJN we find no statistically significant association between firms meeting analyst forecasts and auditor fees. Our market reaction tests also provide different results than those reported by FJN. Overall, our study indicates that FJN's results are sensitive to research design choices, and we find no systematic evidence supporting their claim that auditors violate their independence as a result of clients purchasing relatively more nonaudit services.

Principles of solid-organ preservation by cold storage.

Abstract: Presentation d'une nouvelle solution de conservation convenant aussi bien pour le refroidissement de l'organe in situ dans l'organisme du donneur que pour la conservation in vitro sous hypothermie. Integration des principes de base de l'ischemie hypothermique anaerobie et du metabolisme specifique de l'organe. La methode est appliquable non seulement au rein mais aussi au foie, au pancreas et probablement a d'autres organes

Disruption of the clock components CLOCK and BMAL1 leads to hypoinsulinaemia and diabetes

Abstract: During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis — a rhythmic process that is disturbed in people with diabetes. Experiments in mice now show that the pancreatic islets contain their own biological clock, which orchestrates insulin secretion during the sleep–wake cycle. The transcription factors CLOCK and BMAL1 are vital for this process, and mice with defective copies of the genes Clock and Bmal1 develop hypoinsulinaemia and diabetes. By demonstrating that a local tissue clock integrates circadian and metabolic signals in pancreatic β-cells, this work suggests that circadian analyses are crucial for deeper understanding of metabolic phenotypes, as well as for the treatment of metabolic diseases such as type 2 diabetes. Circadian rhythms control many physiological functions. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis — a rhythmic process that is disturbed in people with diabetes. These authors show that pancreatic islets contain their own clock: they have self-sustained circadian oscillations of CLOCK and BMAL1 genes and proteins, which are vital for the regulation of circadian rhythms. Without this clock, a cascade of cellular failure and pathology initiates the onset of diabetes mellitus. The molecular clock maintains energy constancy by producing circadian oscillations of rate-limiting enzymes involved in tissue metabolism across the day and night1,2,3. During periods of feeding, pancreatic islets secrete insulin to maintain glucose homeostasis, and although rhythmic control of insulin release is recognized to be dysregulated in humans with diabetes4, it is not known how the circadian clock may affect this process. Here we show that pancreatic islets possess self-sustained circadian gene and protein oscillations of the transcription factors CLOCK and BMAL1. The phase of oscillation of islet genes involved in growth, glucose metabolism and insulin signalling is delayed in circadian mutant mice, and both Clock5,6 and Bmal17 (also called Arntl) mutants show impaired glucose tolerance, reduced insulin secretion and defects in size and proliferation of pancreatic islets that worsen with age. Clock disruption leads to transcriptome-wide alterations in the expression of islet genes involved in growth, survival and synaptic vesicle assembly. Notably, conditional ablation of the pancreatic clock causes diabetes mellitus due to defective β-cell function at the very latest stage of stimulus–secretion coupling. These results demonstrate a role for the β-cell clock in coordinating insulin secretion with the sleep–wake cycle, and reveal that ablation of the pancreatic clock can trigger the onset of diabetes mellitus.