Routine nasogastric suction may be unnecessary after a pancreatic resection

AbstractBackgroundMost surgeons routinely place a nasogastric tube at the time of a pancreatic resection. The goal of the present study was to evaluate the outcome when a pancreatic resection is performed without routine post-operative nasogastric suction.MethodsOne hundred consecutive patients underwent a pancreatic resection (64a pancreaticoduodenectomy, 98% pylorus sparing and 36a distal pancreatectomy). In the first cohort (50 patients), a nasogastric tube was routinely placed at the time of surgery and in the second cohort (50 patients) the nasogastric was removed in the operating room. Outcomes for these two cohorts were recorded in a prospective database and compared using the χ2 or Fisher's exact test and Wilcoxon's rank-sum test.ResultsDemographical, surgical and pathological details were similar between the two cohorts. A post-operative complication occurred in 22 (44%) in each group (P= 1.000). There were no statistically significant differences in the frequency or severity of complications, or length of stay between groups. The spectrum of complications experienced by the two cohorts was similar including complications that could potentially be related to the use of nasogastric suction such as delayed gastric emptying, anastomotic leak, wound dehiscence and pneumonia. There was no difference between the two groups in the number of patients who required post-operative nasogastric tube placement (or replacement) [2 (4%) vs. 4 (8%), P= 0.678].ConclusionIt may be safe to place a nasogastric tube post-operatively in a minority of patients after a pancreatic resection and spare the majority the discomfort associated with routine post-operative nasogastric suction

Down-regulation of pancreatic and duodenal homeobox-1 by somatostatin receptor subtype 5: a novel mechanism for inhibition of cellular proliferation and insulin secretion by somatostatin

Somatostatin (SST) is a regulatory peptide and acts as an endogenous inhibitory regulator of the secretory and proliferative responses of target cells. SST's actions are mediated by a family of seven transmembrane domain G protein-coupled receptors that comprise five distinct subtypes (SSTR1-5). SSTR5 is one of the major SSTRs in the islets of Langerhans. Homeodomain-containing transcription factor pancreatic and duodenal homeobox-1 (PDX-1) is essential for pancreatic development, β cell differentiation, maintenance of normal β cell functions in adults and tumorigenesis. Recent studies show that SSTR5 acts as a negative regulator for PDX-1 expression and that SSTR5 mediates somatostatin's inhibitory effect on cell proliferation and insulin expression/excretion through down-regulating PDX-1 expression. SSTR5 exerts its inhibitory effect on PDX-1 expression at both the transcriptional level by down-regulating PDX-1 mRNA and the post-translational level by enhancing PDX-1 ubiquitination. Identification of PDX-1 as a transcriptional target for SSTR5 may help in guiding the choice of therapeutic cancer treatments

Interleukin 10-Mediated Response and Correlated Anemia in a Patient with Advanced Non-Small Cell Lung Carcinoma

Anemia in cancer patients is associated with poor quality of life, reduced response to therapy, and decreased overall survival. We describe a case of a 56-year old woman with advanced metastatic non-small cell lung carcinoma who demonstrated marked response to a novel combinational immunotherapy approach involving a long-acting PEGylated construct of recombinant human Interleukin-10 with Nivolumab, an anti-PD-L1 checkpoint inhibitor. While on treatment, the patient developed severe anemia and hyper-ferritinemia requiring RBC transfusion support. Here we discuss a possible novel immune mechanism of IL10-mediated anemia in correlation with tumor response

Somatostatin Receptor 1 and 5 Double Knockout Mice Mimic Neurochemical Changes of Huntington's Disease Transgenic Mice

Selective degeneration of medium spiny neurons and preservation of medium sized aspiny interneurons in striatum has been implicated in excitotoxicity and pathophysiology of Huntington's disease (HD). However, the molecular mechanism for the selective sparing of medium sized aspiny neurons and vulnerability of projection neurons is still elusive. The pathological characteristic of HD is an extensive reduction of the striatal mass, affecting caudate putamen. Somatostatin (SST) positive neurons are selectively spared in HD and Quinolinic acid/N-methyl-D-aspartic acid induced excitotoxicity, mimic the model of HD. SST plays neuroprotective role in excitotoxicity and the biological effects of SST are mediated by five somatostatin receptor subtypes (SSTR1-5). and R6/2 mice. Conversely, the expression of somatostatin receptor subtypes, enkephalin and phosphatidylinositol 3-kinases were strain specific. SSTR1/5 appears to be important in regulating NMDARs, DARPP-32 and signaling molecules in similar fashion as seen in HD transgenic mice.This is the first comprehensive description of disease related changes upon ablation of G- protein coupled receptor gene. Our results indicate that SST and SSTRs might play an important role in regulation of neurodegeneration and targeting this pathway can provide a novel insight in understanding the pathophysiology of Huntington's disease

MANUAL OF SURGERY

xxiii,1320 hlm; 12,5 x 21 c

Schwartz's principles of surgery

New Yorkxxi, 1866 p.: illus.; 28 c

MANUAL OF SURGERY

xxiii,1320 hlm; 12 x 21 c

MANUAL OF SURGERY

xxiii, 1320 hlm. ; 12 x 21 c