Objective To study the effects of glutamine (Gln) combined with growth hormone (GH) on the levels of cytokine (TNF-?, IL-1, IL-6), coritsol and amino acid metabolism in septic rats. Methods Ten out of 79 SD rats were randomly collected as the control group. Thirty of 69 septic SD rats, which were made by cecal ligation and perforation (CLP) method and were given parenteral nutrition (PN) lived to day 6. They were also randomly divided into three groups as follows: septic group (n=10), parenteral supplemented glutamine group (Gln group, n=10), and Gln combined with GH (Gln+GH group, n=10). On the 6th day, blood drew from portal veins of the dead rats was used to detect the levels of TNF-?, IL-1, IL-6 and cortisol by ELISA. The plasma concentrations of free amino acids were determined by amino acid auto-analyzer. The muscle tissue of extensor digitorum longus was used to determine 3-methyl-histidine (3-MH) by high performance liquid chromatographic (HPLC). Results Except for the control group, most rats developed celiac abscess, hepatic abscess and pulmonary infection. The serum levels of TNF-?, IL-1, IL-6 and cortisol were significantly higher in the septic group than those of the other three groups, and they were significantly lower in the Gln+GH group than those of the Gln group, P

Objective: To investigate the influences of IGF-1 on the stress hormone,GLUT-4 and its mRNA expression.Methods: The SD rats with abdominal infection established by cecal ligation and perforation method were randomly divided into three groups: pyaemic group(n=10),parenteral nutrition group(PN group,n=10) and IGF-1 Group(n=10).10 healthy rats was used as the normal group(n=10).On the sixth day,blood was sampled to determine the level of glucose,insulin,glucagon and IGF-1.The expressions of GLUT-4 and its mRNA in muscle were detected by immuno-histochemistry and Real-Time PCR methods.Results: The plasma levels of glucose,insulin and glucagon in the IGF-1 group were significantly lower than those in the pyaemic group and PN group(P

Objective:To investigate the influences of IGF-1 on the stress homone,InsR?、? gene expression and protein content in pyaemia rats.Methods:SD rats with abdominal infection models established by cecal ligation and perforation method were randomly divided into three groups: pyaemic group(n=10),parenteral nutrition group(PN group,n=10) and IGF-1 Group (n=10),and 10 SD rats were used as normal group(n=10).On the sixth day,Vena Cava blood was sampled to determine the level of glucose,insulin,glucagon,and IGF-1.In addition,the expression of the InsR?、? in liver and muscle were detected by immunohistochemistry and Real-Time PCR methods.Results:The plasma glucose,insulin,glucagon in the IGF-1 group were significantly lower than that of the pyaemic group and PN group(P

Objective To study the clinicopathologic characteristics and the prognostic factors of gastric stump cancer (GSC). Methods A total of forty-seven patients with GSC from Jan 2000 to Dec 2006 were enrolled in this study for retrospective analysis. Initial surgery was performed for gastric benign disease in 39 patients and for malignant disease in 8 patients, which were divided into 2 groups for analysis. The prognosis of all 47 patients were analyzed. Results The mean interval between previous gastrectomy and diagnosis of GSC was 24.4 years. Tumor developed mostly in the patients with Billroth- Ⅱ reconstruction, and male more than female. Tumor located at anastomotic site mostly, at stump stomach and cardia secondly. The mean interval for patients who had undergone their first gastrectomy for malignant disease was shorter than that with benign disease(P＜0.05). Histology, therapy and prognosis showed no significant differences between two groups (P＞0.05). Disease TNM stage and total radical gastrectomy were shown to be significant predictor for the outcome of patients with GSC (P ＜0.01). Conclusion Now the GSC patients with initial surgery performed for malignant disease are increased, which are no siginificant different to patients with benign disease. Early diagnosis and an aggressive surgical approach are crucial to achieve better outcomes for patients with GSC.

Objective To study the molecular pathway of osteoblastic differentiation induced by substance P (SP), a neurotransmitter. Methods Mesenchymal stem cells were isolated and cultured, and treated with SP or its receptor (NK1) antagonist to induce osteoblastic cell differentiation, respectively. Alkaline phosphatase activity was determined; Osterix gene expression was detected by RT-PCR after 1-2 weeks for three times. The data of each culture condition were analyzed using SPSS12.0 statistical software to determine whether the differences between conditions were significant. Results After 4-5 days' culture, bone marrow stromal cells became spindle-shaped, triangular or polygonic. They covered the plate surface, formed extensive cell sheets in each group after 11-12 days of culture, and then induced differentiation to osteoblast. SP up-regulated the important transcription factor Osterix gene expression significantly (P<0.05). Conclusion The up-regulation of Osterix gene expression by SP may stimulate osteoblastic cell differentiation. SP's regulation depends on its receptor NK1.

Objective To investigate the effect of enteral and parenteral nutrition on gut microecology in rats with abdominal infection. Methods Fourteen Sprague-Dawley (SD) model rats of abdominal infection, which had survived for more than 6 days were divided into two groups: PN group ( n =7) and PN+EN group ( n =7) via jejunostomy and jugular vein respectively for another 5 days. The nutrition support in the two groups was isonitrogen and isocaloric. At sacrifice on the sixth day, occludin and IgA level in plasma cells of intestine epithelium of the gut were measured by immunohistochemistry. Vena cava blood and homogenated tissue of liver, lung and mesenteric lymph nodes were cultured to determine bacterial translocations, and portal vein blood was tested for endotoxin. Results The expression of occludin and IgA in the small and large intestine in PN+EN group were stronger than PN group ( P

AIM:To investigate the protective effects of astrocyte protein phosphatase 2A (PP2A) up-regula-tion on APP/PS1 double transgenic mice.METHODS:An eGFP-wtPP2A lentivirus with glial fiber acidic protein promoter was constructed to specifically increase PP2A expression in the astrocytes.The mice were divided into wild -type mice +vector virus group (Con), APP/PS1 transgenic mice +vector virus group (APP/PS1) and APP/PS1 transgenic mice +eGFP-wtPP2A lentivirus group (PP2A) by lateral ventricular injection of the lentivirus.Four weeks after injection of the vi-rus, the immunofluorescence of brain slices were used to detect the level of β-amyloid protein ( Aβ) .Golgi staining was used to detect the changes of dendritic spine density and morphology.Electron microscopy was applied to detect the thickness of postsynaptic density (PSD).The Morris water maze test was applied to examine the learning and memory abilities of the mice.RESULTS: Up-regulation of PP2A in the astrocytes attenuated Aβlevel increasing in APP/PS1 group.Up-regulation of PP2A in the astrocytes significantly attenuated both decreases in the dendritic spine density and the percentage of mushroom-like dendritic spines in the hippocampal CA3 region of APP/PS1 mice.Up-regulation of PP2A in the astrocytes significantly attenuated the reduced thickness of PSD in APP/PS1 group.Up-regulation of PP2A in the astro-cytes attenuated the escape latency extending in APP/PS1 group .CONCLUSION: Up-regulation of PP2A in the astro-cytes reduces AD-like pathological changes, and attenuates synaptic impairment, synaptic plasticity deficits and cognitive impairment in the APP/PS1 double transgenic mice.

Intrathecal (I. T.)administration of K opioid dynorphin A (1-17) is used as a model of neurological dysfunction which lnvolved in spinal cord injury and secondary affection according to several previous reports. 5-amlno-2-phosphoveroleric acid (APV ), an NMDA receptor antagonist, can significantlly prevent the hindlimb paralysis in rats produced by I. T. dynorPhin A (1-17). To further investigate the mechanisms, we establis11 a nlodel of [3H]L,-Glu release in rats spinal slices influenced by dynorphin A (dynA ) (1-17). [3H]L-Glu release evoked by high [K+] (5Ommol/L,)is a Ca2+-dependent process. DynA (1-17) slgnificantly inhibited [3H]L,-Glu release at 1O-8mol/L,, but very significantly enhanced [3H]L-Glu release at 10-6 mol /L. The synthetic k agonist U50, 488H, which has no neurotoxic effect, inhibited [3H]L-Glu release at both high and low concentrations and did not have any enhancing effect. The results suggest that the analgesic effect of dynA (1-17) at physiological dosage may be rnediated by presynaptic K opioid receptor through the inhibition of Ca2+ influx and L-Glu release;but dynA (1-l7)enhanced L-Glu release through a non-opioid pathway and induced hindlimb paralysis at high neurotoxic dosage.

This study is to investigate the anti-angiogenetic effect of arenobufagin in vitro and in vivo. The anti-proliferation effect of arenobufagin on CNE-2, Hep2, SH-SY5Y, LOVO, PC-3 and DU145 cells as well as human umbilical vein endothelial cells (HUVECs) was determined by MTT assay. Cell morphological changes of LOVO and HUVECs after arenobufagin treatment were observed by microscopy. Arenobufagin inhibited the proliferation of CNE-2, Hep2, SH-SY5Y, LOVO, PC-3, DU145 and HUVECs in a dose-dependent manner. Furthermore, it was obviously observed that the subcytotoxic concentration of arenobufagin in human carcinoma cells induced a marked decrease in the viability of HUVECs. Chick embryo chorioallantoic membrane (CAM) model was used to detect the anti-angiogenetic effect of arenobufagin in vivo. Arenobufagin significantly suppressed the angiogenesis of CAM. Cell cycle analysis demonstrated that G2/M phase was arrested and the sub-G1 peak appeared with the increase of arenobufagin concentration. PI/Annexin V double staining assay further demonstrated that arenobufagin could induce apoptosis in a dose- and time-dependent manner. Mitochondrial potential collapse detected by flow cytometric analysis was increased after arenobufagin treatment. It also observed that PARP was cleaved to p85 active form by Western blotting. Taken together, arenobufagin has significant anti-angiogenetic effect in vitro and in vivo, and the action mechanisms behind its anti-angiogenesis may be associated with cell cycle arrest and apoptosis of vein endothelial cells.

Objective:This study aimed to establish a mouse model of breast cancer by inoculating human breast cancer cells into mice with normal immune function. Methods:Forty female BALB/C mice were randomized into four groups, with 10 mice in each group. The four groups were established according to the dosage of cyclophosphamide and prednisone, namely, the control group, low dose group, medium dose group, and high dose group. The mouse models of breast cancer were established by injecting human breast cancer cells into the fat pad of the right second breast of mice in the groups. Mice in the four groups were observed based on the time of tumorigenesis, rate of tumor formation, tumor imaging and pathological features, and metastasis of vital internal organs. Results:In the high dose group, the time of tumor formation was lower than that of the other groups, but the rate of tumor formation was high. Some visceral metastases occurred in the mice. By contrast, the medium dose group revealed completely opposite results. No death and tumor formation in both the control and low dose groups were reported. Conclusion:A human breast carcinoma model in mice was successfully established. Using this model, the onset and development of breast cancer could be much better imitated in the normal immune system of mice.