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Tight glycemic control using an artificial endocrine pancreas may play an important role in preventing infection after pancreatic resection 被引量:2
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作者 Kazuhiro Hanazaki 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第29期3787-3789,共3页
It is well known that perioperative hyperglycemia is the main cause of infectious complications after surgery.To improve perioperative glycemic control,we wish to highlight and comment on an interesting paper publishe... It is well known that perioperative hyperglycemia is the main cause of infectious complications after surgery.To improve perioperative glycemic control,we wish to highlight and comment on an interesting paper published recently by the Annals of Surgery entitled:"Early postoperative hyperglycemia is associated with postoperative complications after pancreatoduodenectomy(PD)" by Eshuis et al.The authors concluded that early postoperative glucose levels more than 140 mg/dL was significantly associated with complications after PD.Since we recommend that perioperative tight glycemic control(TGC) is an effective method to prevent postoperative complications including surgical site infection after distal,proximal,and total pancreatic resection,we support strongly this conclusion drawn in this article.However,if early postoperative glucose control in patients undergoing PD was administrated by conventional method such as sliding scale approach as described in this article,it is difficult to maintain TGC.Therefore,we introduce a novel perioperative glycemic control using an artificial endocrine pancreas against pancreatogenic diabetes after pancreatic resection including PD. 展开更多
关键词 Tight glycemic control Pancreatic resection Surgical site infection Artificial endocrine pancreas
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Metabolic rewiring of stem cells and differentiated cells in cancer: the hypothetical consequences of a GABA deficiency in endocrine pancreas
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作者 Maurice Israёl 《Journal of Cancer Metastasis and Treatment》 2019年第2期65-76,共12页
The carcinogenic mechanism proposed considers that stem cells committed to repair tissues and differentiated cells, acquire different metabolic properties, if there is an associated GABA deficiency suppressing a contr... The carcinogenic mechanism proposed considers that stem cells committed to repair tissues and differentiated cells, acquire different metabolic properties, if there is an associated GABA deficiency suppressing a control system of the endocrine pancreas. This control system mediated by GABA, released with insulin, normally turns off glucagon and somatostatin release when insulin is released. A consequence of the GABA deficiency in pancreas and adrenals is a hybrid insulin-glucagon-somatostatin message, received by new mitotic stem cells displaying then a hybrid metabolic rewiring. This gives them a selective metabolic advantage over differentiated cells that become insulin resistant and only receive the glucagon- somatostatin part of the hormonal message. Indeed, their insulin receptors are desensitized by the persistent leakage of insulin resulting from the GABA deficiency that fails to close the insulin release mechanism. Thus differentiated cells are simply rewired to be plundered by stem cells. The metabolic advantage gained by stem cells blocks their own differentiation and maintains their mitotic capacity. Inevitable mutations of mitotic cells follow, the immune system is unable to eliminate a geometrically increasing number of altered stem cells, a selection of the most aggressive but metabolically successful population takes place when cancer is declared. 展开更多
关键词 Cancer metabolism endocrine pancreas ADRENALS GABA stem cells differentiated cells
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Regeneration of β cells from cell phenotype conversion among the pancreatic endocrine cells
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作者 Tianjiao Wei Rui Wei Tianpei Hong 《Chronic Diseases and Translational Medicine》 CSCD 2022年第1期1-4,共4页
The prevalence of diabetes has increased dramatically, with over 537 million adults affected worldwide.1 In both type 1 and type 2 diabetes, pancreatic islet β cell dysfunction is common pathogenesis.
关键词 cell trans-differentiation endocrine pancreas βcell dedifferentiation βcell regeneration
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