Sarcopaenia, obesity, sarcopaenic obesity and outcomes following hepatic resection for colorectal liver metastases: a systematic review and meta-analysis.

Background: Obesity is a risk factor for the development of colorectal cancer. Limited evidence exists about outcomes for obese patients undergoing hepatic resection for colorectal liver metastases (CRLM). Sarcopaenia is characterised by a decline in muscle function and muscle mass.

Cancer of the uncinate process of the pancreas: surgical anatomy and clinicopathological features.

Background: The clinicopathological features of uncinate process pancreatic cancer (UPPC) are poorly described. Furthermore the anatomy of the uncinate process and its division during surgery are central to pancreaticoduodenectomy for UPPC. We set out to describe the embryology and anatomy of the uncinate process and the clinicopathological features of UPPC.

p38 MAP kinase inhibition promotes primary tumour growth via VEGF independent mechanism.

Background: The surgical insult induces an inflammatory response that activates P38 MAP kinases and solid tumours can also release cytokines. Therfore inhibition of these pathways may reduce tumour growth We set out to examine the effects of P38-MAPK inhibition on apoptosis, proliferation, VEGF release and cell cycle effects in-vitro and on primary tumour growth in-vivo.

Methods: 4T-1 cells (2 x 105 cells/well) were incubated, in 24 well plates with control, 25, 50 or 100 ng/ml of SB-202190 for 24 hours.

Managing arterial collaterals due to coeliac axis stenosis during pancreaticoduodenectomy.

Context: Coeliac artery stenosis is a condition affecting a minority of patients undergoing pancreaticoduodenectomy. In such cases, the development of collateral pathways through the blood supply of the pancreatic head provides challenges for surgical management.

Case Report: We report a case of coeliac artery stenosis in a patient undergoing pancreaticoduodenectomy.

NF-kappaB and p38 MAPK inhibition improve survival in endotoxin shock and in a cecal ligation and puncture model of sepsis in combination with antibiotic therapy.

Background: Nuclear factor-kappa B (NF-kappaB) and p38 mitogen-activated protein kinase (MAPK) are critical intracellular signal transduction pathways that mediate the systemic inflammatory response syndrome. Antibiotics induce bacterial lysis, which also contributes to cytokine production and the inflammatory response by activating NF-kappaB and p38 kinase. In this study, we set out to examine the effects of inhibition of p38 MAPK and NF-kappaB translation in in vivo models of sepsis.

The role of P38 MAPK and PKC in BLP induced TNF-alpha release, apoptosis, and NFkappaB activation in THP-1 monocyte cells.

Background: P38 mitogen activated protein kinase (p38 MAPK) is a critical mediator of the inflammatory response, which makes it a suitable candidate as a novel therapeutic strategy for inflammatory conditions. In this study, we set out to examine the precise role of both protein kinase C (PKC) and P38 MAPK signaling kinases in bacterial lipoprotein (BLP) induced nuclear factor-kappa B (NFkappaB) activation and tumor necrosis factor-alpha (TNFalpha) release in THP-1 monocytic cell line.

Materials And Methods: THP-1 cells were incubated with BLP(0-1000 ng/mL), phorbol myristate acetate (PMA; 0-100 microg/mL) or a combination of both for 6 and 24 h, with or without pretreatment with SB202190, a specific inhibitor of p38 MAPK and bisindolylmaleimide I, a specific inhibitor of PKC (0-200 microm).

Hypertonic saline enhances host response to bacterial challenge by augmenting receptor-independent neutrophil intracellular superoxide formation.

Objective: This study sought to determine whether hypertonic saline (HTS) infusion modulates the host response to bacterial challenge.

Methods: Sepsis was induced in 30 Balb-C mice by intraperitoneal injection of Escherichia coli (5 x 107 organisms per animal). In 10 mice, resuscitation was performed at 0 and 24 hours with a 4 mL/kg bolus of HTS (7.