The mechanism of islet regeneration remains poorly understood, bu

The mechanism of islet regeneration remains poorly understood, but the identification of islet progenitor sources is critical for understanding beta-cell regeneration. One potential source is the islet proper, via the dedifferentiation, proliferation, and redifferentiation of facultative progenitors residing within the islet. Neogenesis, or that the new pancreatic

islets can derive from progenitor cells present within the ducts has been reported, but the existence and identity of the progenitor cells have been debated.\n\nIn this review, we focus on pancreatic ductal cells, which are islet progenitors capable of differentiating into islet beta-cells. Islet neogenesis, https://www.selleckchem.com/products/kpt-8602.html seen as budding of hormone-positive cells from the ductal epithelium, is considered to be one mechanism for normal islet growth after birth and in regeneration, and has suggested the presence of pancreatic stem cells. Numerous results support the neogenesis hypothesis, the evidence for the hypothesis in the adult comes primarily from morphological

studies that have in common the production of damage to all or part of the pancreas, with consequent inflammation and repair. Ro-3306 nmr Although numerous studies support a ductal origin for new islets after birth, lineage-tracing experiments are considered the “gold standard” of proof. Lineage-tracing experiments show that pancreatic duct cells act as progenitors, giving rise to new islets U0126 ic50 after birth and after injury. The identification of differentiated pancreatic ductal cells as an in vivo progenitor for pancreatic beta-cells has implications for a potentially important, expandable source of new islets for diabetic replenishment therapy. (C) 2009 Elsevier Inc. All rights reserved.”
“Background: Little is known about psychological risk factors in cerebrovascular disease. We examined the association between psychological distress and risk of death due to cerebrovascular disease.\n\nMethods:

We obtained data from 68 652 adult participants of the Health Survey for England (mean age 54.9 [standard deviation 13.9) yr, 45.0% male sex) with no known history of cardiovascular diseases at baseline. We used the 12-item General Health Questionnaire (GHQ-12) to assess the presence of psychological distress. We followed participants for eight years for cause-specific death using linkage to national registers.\n\nResults: There were 2367 deaths due to cardiovascular disease during follow-up. Relative to participants with no symptoms of psychological distress (GHQ-12 score 0) at baseline, people with psychological distress (GHQ-12 score 4, 14.7% of participants) had an increased risk of death from cerebrovascular disease (adjusted hazard ratio [HR] 1.66, 95% confidence interval [CI] 1.32-2.08) and ischemic heart disease (adjusted HR 1.59, 95% CI 1.34-1.88). There was also evidence of a dose response effect with increasing GHQ-12 score (p for trend < 0.001 in all analyses).

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