ObjectiveTo study the situation of neural invasion in pancreatic cancer and investigate its related clinical factors. Methods The neural invasion in 73 cases of pancreatic cancer patients was retrospective analysed. The correlation between neural invasion and clinicopathological parameters,and survival rate was investigated.Results In 73 cases of pancreatic cancer,neural invasion occurred in 38(52.1％) patients,among whom intra-pancreatic neural invasion rate was 15.8％ (n =6) ; and both intrapancreatic and external pancreatic plexus invasion rate was 84.2％ ( n =32).Neural invasion was not related with gender,age,and pathological type,degree of differentiation,tumor size and lymph node metastasis (P ＞ 0.05 ).But the presence of abdominal pain,vascular invasion,the expression of EGFR and VEGF in tumor tissue was significantly related with neural invasion (P ＜0.01 ).The median survival of patients in neural invasion group was 8 months,which were significantly shorter than that of in patients without neural invasion (13 months,x2 =4.69,P =0.030).Conclusions Neural invasion has a high incidence in pancreatic cancer,and it can cause obvious abdominal pain.And it is related with vascular invasion and the expression of EGFR and VEGF in tumor tissue.Neural invasion is one of the factors affecting the survival rate.

Objective: To observe the effect of ω-3 fish oil emulsion on the experimental severe acute pancreatitis(SAP)through the morphologic alteration of pancreas,the level of serum amylase(AMS)and the functions of liver and kidney,and explore its possible mechanism. Methods: Rat model of SAP was produced by injecting 5% Sodium Cholate(1 ml/kg)into the biliopancreatic duct.Male Sprague-Dawley rats were randomly divided into 4 groups: normal group(n=6),fish oil emulsion treatment group(FOG,n=18),soybean oil emulsion treatment group(SOG,n=18) and normal sodium treatment group(NSG,n=18).Then fish oil emulsion(FO,10 ml/kg);soybean oil emulsion(SO,10 ml/kg)and normal sodium(NS,10 ml/kg)were intravenously injected respectively 120 minutes.The pancreatitis were confirmed by levels of serum AMS and histopathologic score.ALT,AST,BUN and Cr were tested 24 hours after the treatments.Expressions of IL-1β and IL-10 were tested by ELISA.The activated NF-kappa B was examined in the pancreases. Results: Lower level of serum AMS(P<0.05)and lower histopathology score(P<0.05) appeared in FOG.Compared with NS,FO decreased the levels of serum ALT and BUN significantly (P<0.05).FO significantly attenuated the expression of IL-1β (P<0.05).FO downregulated the activity of NF-kappa B efficiently.Conclusions: By down-regulating the levels of IL-1β together with up-regulating the level of IL-10,FO reduces inflammatory damage at the beginning of AP.

ObjectiveTo evaluate the safety, feasibility and efficacy of transplantation of purified peripheral blood CD34+ cells in treatment of critical ischemia of the lower extremities.MethodsFrom May 2009 to March 2010, seven cases of critical ischemia of the lower extremities received purified peripheral blood CD34+ cells transplantation, among those 6 were caused by thromboangiitis obliterans and 1 by thrombosis coexistent with nodular erythema. Mean age was ( 39 ± 11 ) years ( range 23 - 54 ), and all patients were not suitable for surgical or endovascular revascularization. G-CSF was subcutaneously injected for 5 days before apheresis for peripheral blood mononuclear cells. Then CliniMACS system was used to isolate the CD34+ cells. If the number of CD34+ cells was between 105/kg and 106/kg , they were all intramuscular injected into patients' calf and foot. ResultsTechnical success and limb salvage were achieved in all cases. The mean number of transplanted cells was (7. 1 ±2.3) × 105/kg [ range(4.6 ×105 -1 × 106 )/kg]. All cases were followed-up, ranging from 6 - 14 months (mean 8 ± 3 months). One month after transplantation, the rest pain was obviously relieved in all cases, and the Wong-Baker FACES pain rating scale score significantly decreased from 7. 1 ±2. 0(4 - 10)to 1. 1 ± 1.1 (0 -2) ,P =0. 0000. The pain-free walking distance was significantly improved from (4 ± 4) min (range 1 -10 min)to (12 ± 7 ) min (range 5 - 21min , P =0.04) at 3 months and(20.4 ± 12.5) min(range 6 -40 min, P = 0.02) at 6 months, respectively. The ankle-brachial index increased from 0. 54 ± 0. 18 ( range 0. 41 - 0. 87 ) to 0.66 ±0. 13(range 0. 52-0. 86 , P=0. 17)at 3 months and 0.72 ±0. 13(range 0.56 -0.91, P=0. 07)at 6 months, respectively. Of 6 cases with the toe ulcer, the ulcer was healed in 3 and apparently shrank in 3. Transcutaneous partial oxygen pressure rose from (29 ± 14)mm Hg(range 10 -52 mm Hg)to 46 ±14 mm Hg ( range 27 - 63 mm Hg, P = 0. 04) at 3 months and (57 ± 10) mm Hg( range 41 - 66 mm Hg, P =0.001) at 6 months,respectively.No serious complications were found either perioperatively or postoperatively.ConclusionsTransplantation of purified peripheral blood CD34+ cells is safe, feasible and effective in the treatment of critical ischemia of the lower extremities.

Free fatty acids (FFAs) are important substrates for mitochondrial oxidative metabolism and ATP synthesis but also cause serious stress to various tissues, contributing to the development of metabolic diseases. CD36 is a major mediator of cellular FFA uptake. Inside the cell, saturated FFAs are able to induce the production of cytosolic and mitochondrial reactive oxygen species (ROS), which can be prevented by co-exposure to unsaturated FFAs. There are close connections between oxidative stress and organellar Ca²⁺ homeostasis. Highly oxidative conditions induced by palmitate trigger aberrant endoplasmic reticulum (ER) Ca²⁺ release and thereby deplete ER Ca²⁺ stores. The resulting ER Ca²⁺ deficiency impairs chaperones of the protein folding machinery, leading to the accumulation of misfolded proteins. This ER stress may further aggravate oxidative stress by augmenting ER ROS production. Secondary to ER Ca²⁺ release, cytosolic and mitochondrial matrix Ca²⁺ concentrations can also be altered. In addition, plasmalemmal ion channels operated by ER Ca²⁺ depletion mediate persistent Ca²⁺ influx, further impairing cytosolic and mitochondrial Ca²⁺ homeostasis. Mitochondrial Ca²⁺ overload causes superoxide production and functional impairment, culminating in apoptosis. This vicious cycle of lipotoxicity occurs in multiple tissues, resulting in β-cell failure and insulin resistance in target tissues, and further aggravates diabetic complications.
Adenosine Triphosphate ; Apoptosis ; Calcium* ; Cytosol ; Diabetes Complications ; Endoplasmic Reticulum ; Fatty Acids, Nonesterified ; Homeostasis ; Insulin Resistance ; Ion Channels ; Metabolic Diseases ; Metabolism ; Oxidative Stress* ; Protein Folding ; Reactive Oxygen Species ; Superoxides