Use of pre-, pro- and synbiotics in patients with acute pancreatitis:A meta-analysis

AIM: To assess the clinical outcomes of pre-, pro-and synbiotics therapy in patients with acute pancreatitis. METHODS: The databases including Medline, Embase, the Cochrane Library, Web of Science and Chinese Biomedicine Database were searched for all relevant randomized controlled trials that studied the effects of pre-, pro- or synbiotics in patients with acute pancreatitis. Main outcome measures were postoperative infections, pancreatic infections, multiple organ failure (MOF), systemic inflammatory response syndrome (SIRS), length of hospital stay, antibiotic therapy and mortality. RESULTS: Seven randomized studies with 559 acute pancreatic patients were included. Pre-, pro-or synbiot-ics treatment showed no influence on the incidence of postoperative infections [odds ratios (OR) 0.30, 95% conf idence interval (CI): 0.09-1.02, P = 0.05], pancre- atic infection (OR 0.50, 95% CI: 0.12-2.17, P = 0.36), MOF (OR 0.88, 95% CI: 0.35-2.21, P = 0.79) and SIRS (OR 0.78, 95% CI: 0.20-2.98, P = 0.71). There were also no signif icant differences in the length of antibiotic therapy (OR 0.75, 95% CI: 0.50-1.14, P = 0.18) and the mortality (OR 0.75, 95% CI: 0.25-2.24, P = 0.61). However, Pre-, pro-or synbiotics treatment was associ- ated with a reduced length of hospital stay (OR -3.87, 95% CI: -6.20 to -1.54, P = 0.001). When stratifying for the severity of acute pancreatitis, the main results were similar. CONCLUSION: Pre-, pro-or synbiotics treatment shows no significant influence on patients with acute pancreatitis. There is a lack of evidence to support the use of probiotics/synbiotics in this area.

Treatment of chronic proliferative cholangitis with c-myc shRNA

AIM： To investigate the feasibility and effectiveness of c-myc shRNA in inhibiting the hyperplastic behavior and lithogenic potentiality of chronic proliferative cholangitis （CPC）, in order to prevent stone recurrence and biliary restenosis. METHODS： An animal model of CPC was established by giving intralumenally 0.5 mL of c-myc shRNA. Then, the effects of c-myc shRNA on hyperplastic behavior and lithogenic potentiality of CPC were evaluated by histological observation, immunohistochemistry, real- time PCR and Western blotting for c-myc, proliferating cell nuclear antigen （PCNA）, procollagen m, mucin 5AC, enzymatic histochemistry for 13-glucuronidase, and biochemistry for hydroxyproline in the diseased bile duct. RESULTS： Treatment with c-myc shRNA efficiently suppressed the hyperplasia of biliary epithelium, submucosal gland, and collagen fiber by inhibiting mRNA and protein expression of c-myc. More importantly, it decreased the lithogenic potentiality of CPC by inhibiting the expression of mucin 5AC and the secretion of endogenous 13-glucuronidase. Further investigation indicated that c-myc shRNA-3 had a better inhibitory effect on CPC. CONCLUSION： Treatment with c-myc shRNA-3 can control CPC and reduce the lithogenic potentiality of CPC.

Monitoring of clinical islet transplantation

Islet transplantation has recently emerged as one of the most promising therapeutic approaches to improving glycometabolic control in diabetic patients. The Edmonton trials demonstrated a marked improvement in the short-term rate of success of islet transplantation, with an 80% rate of insulin-independence being at 1 year after transplantation, as reported by several institutions worldwide. Unfortunately, this rate consistently decreases to 10% by 5 years post-transplantation.

Neuroprotective effect of exogenous vascular endothelial growth factor on rat spinal cord neurons in vitro hypoxia

Background Vascular endothelial growth factor （VEGF） is well known as a hypoxia-induced protein. That it markedly increased expression of VEGF and improvement of rat motor function after spinal cord injury suggested that VEGF could play a neuroprotective role in ischaemic tolerance. This study investigated whether vascular endothelial growth factor has direct neuroprotective effects on rat spinal cord neurons. Methods We employed primary cultures of embryonic rat spinal cord neurons, then administrated different concentrations of VEGF164 in the culture medium before hypoxia when the number of neurons was counted and the cell viability was detected by MTT. The neuronal apoptosis and expression of VEGF and its receptor genes were evaluated by terminal deoxynucleotidyl transferase mediated dUTP nick-end labelling （TUNEL） and immunohistochemistry. The VEGFR2/FLK-1 inhibitor, SU1498, was used to confirm whether the neuroprotective effect of VEGF was mediated through VEGFR2/Flk-1 receptors. Result In hypoxic conditions,the number and viability of neurons decreased progressively, while the number of TUNEL-positive cells increased along with the prolongation of hypoxic exposure. When the concentration of VEGF in cell culture medium reached 25 ng/ml, the cell viability increased 11% and neuronal apoptosis reduced to half, this effect was dose dependent and led to an approximately 25% increase in cell viability and about threefold decrease in TUNEL-positive cells at a maximally effective concentration of 100 ng/ml. In normal conditions, VEGF/Flk-1 but not VEGF/Flt-1 gene expressed at a low level： after hypoxia, the expression of VEGF/Flk-1, but not VEGF/Flt-1 was significantly increased. The protective effect of VEGF was blocked by the VEGFR2/Flk-1 receptor tyrosine kinase inhibitor, SU1498. Conclusions VEGF has direct neuroprotective effects on rat spinal cord neurons, which may be mediated in vitro through VEGFR2/Flk-1 receptors.