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Evolving Process (evolving + process)

Distribution by Scientific Domains

Medical Sciences	75%

Selected Abstracts

Vanishing Trials: The Bankruptcy Experience

JOURNAL OF EMPIRICAL LEGAL STUDIES, Issue 3 2004
Elizabeth Warren
The federal bankruptcy system provides two critical points of comparison with data about the overall trends of federal lawsuits and trials. The first is the rising number of bankruptcy filings, which indicates that a growing number of collection actions and debtor-creditor disputes are funneled into the bankruptcy system for relatively quick, cheap resolution. The second point of comparison focuses on adversary proceedings, the lawsuit-like subset of disputes that sometimes are resolved within a bankruptcy. The trend lines here suggest that the number of adversary proceedings filed is climbing, while the number of such disputes that are actually resolved by trial is declining. Like the data about the federal court system generally, these data suggest that the trial is quietly vanishing from the bankruptcy system. Data about the number of judges and about business and nonbusiness bankruptcy cases make it possible to explore two competing hypotheses,a Judicial Workload Hypothesis and a Cost Hypothesis,to explain the overall findings. The data are not conclusive, but they are consistent with the view that judicial workloads explain less of the decline in the number of trials than an increase in litigants' costs of resolving disputes in bankruptcy. The data are also consistent with a vision of bankruptcy as an evolving process that is increasingly standardized (and cheaper) for nonbusiness debtors, while it is highly individualized (and more costly) for business cases. If that vision is right, it has implications both for understanding the changing role of the trial and for considering various statutory proposals to differentiate further the treatment of large business, small business, and nonbusiness cases. [source]

Proliferative drive and liver carcinogenesis: Too much of a good thing?

JOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 12 2009
Narci C Teoh
Abstract There have been innumerable studies published in the attempt to identify gene expression signatures in hepatocellular carcinoma (HCC). When all the regulators and targets of the differentially expressed genes are analyzed from larger studies, the most striking theme is upregulation of mitosis-promoting and cell proliferation genes in HCC compared with ,liver-specific gene clusters' in non-tumorous tissue. A major limitation of expression profiling is that it only provides a ,snapshot' of what is an evolving process and thus cannot distinguish the differences in gene expression that are primary effectors of dysregulated growth from those that represent downstream consequences. The development of HCC in a chronically diseased liver, often referred to as hepatocarcinogenesis, is a multistep process characterized by the progressive accumulation and interplay of genetic alterations causing aberrant growth, malignant transformation of liver parenchymal cells, followed by vascular invasion and metastasis. This review will discuss HCC precursor lesions, draw on the ,proliferation cluster' genes highlighted from HCC expression profiling studies, relate them to a selection of regulatory networks important in liver regeneration, cell cycle control and their potential significance in the pathogenesis of HCC or primary liver cancer. [source]

Progressive Renal Vascular Proliferation and Injury in Obese Zucker Rats

MICROCIRCULATION, Issue 4 2010
RADU ILIESCU
Microcirculation (2010) 17, 250,258. doi: 10.1111/j.1549-8719.2010.00020.x Abstract Objective:, Obesity, an independent risk factor for chronic kidney disease, may induce renal injury by promoting inflammation. Inflammatory cytokines can induce neovascularization in different organs, including the kidneys. However, whether obesity triggers renal neovascularization and, if so, its effect on renal function has never been investigated. Methods:, Blood pressure, proteinuria, and glomerular filtration rate (GFR) were measured in vivo. Renal microvascular (MV) architecture was studied by 3D micro-CT in lean and obese Zucker rats (LZR and OZR, n = 7/group) at 12, 22, and 32 weeks of age. Renal inflammation was assessed by quantifying interleukin (IL)-6, tumor necrosis factor (TNF)-alpha, and ED-1 expression, as renal fibrosis in trichrome-stained cross-sections. Results:, Mild inflammation and lower GFR was only observed in younger OZR, without renal fibrosis or changes in MV density. Interestingly, renal MV density increased in OZR at 32 weeks of age, accompanied by pronounced increase in renal IL-6 and TNF-alpha, ED-1+ cells, proteinuria, decreased GFR, and fibrosis. Conclusions:, This study shows increased renal cortical vascularization in experimental obesity, suggesting neovascularization as an evolving process as obesity progresses. Increased renal vascularization, possibly triggered by inflammation, may reflect an initially compensatory mechanism in obesity. However, increased inflammation and inflammatory-induced neovascularization may further promote renal injury as obesity advances. [source]

Allgrove syndrome with features of familial dysautonomia: A novel mutation in the AAAS gene

ACTA PAEDIATRICA, Issue 9 2006
Essam A. Ismail
Abstract Allgrove syndrome (or triple-A syndrome) is a rare autosomal recessive disorder characterized by alacrima, achalasia, adrenal insufficiency (glucocorticoid in the majority of cases) and autonomic/neurological abnormalities. This disease is now known to be caused by mutation in the AAAS gene located on chromosome 12q13. Diagnosis should be readily available when the full-blown features are there, but it becomes less apparent when presentation is atypical or in the evolving process. We present a brother and sister (12 and 19 y old, respectively) born to consanguineous parents of Palestinian origin with Allgrove syndrome. The index patient was erroneously diagnosed to be a case of familial dysautonomia before the diagnosis of adrenal insufficiency was made at the age of 7.5 y, while his elder sister had only alacrima from birth and developed achalasia at the age of 15 y. She started to develop early evidence of adrenal disease at the age of 19 y. Both of them had neuroautonomic dysfunction. The diagnosis of Allgrove syndrome was confirmed in these two patients by studying the gene mutation in the family. The sequencing of the AAAS gene in the two patients identified a novel homozygous mutation within intron 5 (IVS5+1(G),A). Both parents as well as all three other children were heterozygous for the same mutation. Conclusion: These two cases illustrate the heterogenous nature and the intrafamilial phenotypic variability of Allgrove syndrome. [source]