Objective To establish an animal model by placing one end of PICC in the hepatic portal vein of a beagle dog and leaving the other end out of its body.Methods Six Beagle dogs were given respiration anesthesia through orotracheal intubation.An incision was made through the right rectus abdominalis to locate the superior mesenteric vein (SMA) and the main hepatic portal vein.The left branch of SMA was separated and cut to put PICC into the main hepatic portal vein before being ligated and fixed.The other end of PICC was elicited through the right abdominal wall and passed beneath the skin to the back neck and fastened in case of movement.Results The anesthetic effect was good and all the operations were successful.The mean operation time was about an hour and the mean blood loss was about 15 ml.The incision healed 5-7 d after operation.Conclusion The establishment of the model can improve the effects of liver-targeting drugs,which can cut down the dosage,lower the cost of treatment and experiment and reduce the adverse effect of medicines.Through PICC,we can directly draw blood from the hepatic portal vein to measure the blood concentration before the first pass elimination.Then according to the concentration,we can calculate the absorption rate in the gastrointestinal tract,which can facilitate related experimental studies.

Liver transplantation is a mature treatment for children with end-stage liver disease. With the development of surgical techniques, immunosuppressive therapy, and infection monitoring in recent years, there have been significant increases in the survival rates of patients and liver transplants, helping children to achieve long-term survival. Meanwhile, several issues have emerged, such as viral infection, complications, new-onset tumors, quality of life, and self-management. Therefore, this article reviews related issues in long-term survival in children after liver transplantation from the two aspects of medical treatment and nursing and provides several regimens for reference, so as to provide a basis for long-term high-quality survival in children after liver transplantation. Here, these issues are reviewed.

Objective Given that psychosocial stress can contribute to a series of diseases,such as inflammatory bowel disease and irritable bowel syndrome,we aimed to establish an experimental chronic restraint mouse intestinal stress injury model as a basis for exploring the pathogenic mechanism of chronic restraint stress-induced gastrointestinal diseases,and for developing preventive and curative measures.Methods Eighteen male SPF-grade BALB/c mice were acclimatized for 7 days and then divided into a control group and a chronic restraint stress group according to body weight,using a randomized numerical table method.The mice were subjected to restraint stress for 3 hours per day for 14 days to establish an intestinal injury model.The model was evaluated by observing body weight,pathological changes in intestinal histomorphology,expression of tight junction proteins,apoptosis of intestinal epithelial cells,and mRNA expression levels of inflammatory cytokines.Results After 14 days of chronic restraint stress,model mice showed weight loss,shortened duodenal villus height,abnormal crypt structure,a decreased villus/crypt ratio,colonic mucosal inflammatory cell infiltration,and irregular crypt structure.Protein immunoblotting,immunohistochemistry,and immunofluorescence staining showed that the expression levels of the duodenal and colonic tight junction proteins Occludin and Claudin-1 were significantly decreased in mice after chronic restraint stress(P＜0.05),while expression levels of the apoptotic protein cleaved-caspase-3 in intestinal epithelial cells were significantly increased(P＜0.05).Regarding the mRNA expression levels of intestinal inflammatory factors and chemokines,chronic restraint stress for 14 days significantly increased the gene expression levels of interleukin(IL)-1β,IL-6,monocyte chemoattractant protein-1(MCP-1),tumor necrosis factor-α,and IL-10 in the duodenum of mice(P＜0.05),and significantly increased the gene expression levels ofIL-1β,IL-6,and MCP-1 in the colon(P＜0.001).Conclusions The use of a behavioral restriction device to restrain mice continuously for 14 days led to abnormal intestinal tissue structure,intestinal barrier dysfunction,and intestinal epithelial cell apoptosis,and triggered an intestinal inflammatory response in the stressed mice,indicating successful establishment of a mouse model of intestinal injury by chronic restraint stress.

The intestine is the largest immune and metabolic site in the body and is thus important for animal health.The integrity of the mucosal barrier and function are fundamental factors protecting the health of the intestine.Stress has been reported to have profound effects on the gastrointestinal tract,including altering gut permeability,the intestinal barrier,and homeostasis.Tryptophan is a functional essential amino acid that alters the gut microbiota and regulates intestine structural and functional change,thus contributing to host physiology and metabolism.Changes in tryptophan metabolism and its metabolites in brain and intestinal tissues during stress suggest that tryptophan may play an important role in the stress response.We therefore review the literature on the mechanisms underlying stress-related diseases and the role of tryptophan metabolism in the regulation of gut homeostasis,with particular focus on functional bowel disorders and their relationship to stress,to provide a theoretical foundation for targeting tryptophan in stress-related intestine diseases.

OBJECTIVE: To investigate the status of anxiety and depression in field training military officers and soldiers and analyze the impact of coping styles and personality traits.METHODS: Self-rating Anxiety Scale, Self-Rating Depression scale, Simple Coping Style Questionnaire and Eysenck Personality Questionnaire were used to evaluate 494 field training military officers and soldiers by judgment sampling method. RESULTS: The rates of anxiety and depression symptoms of the officers and soldiers in field training were 13.0% and 23.1%, respectively. The results of multivariate logistic regression analysis showed that the higher the negative coping style, mental quality and neurotic scores of the officers and soldiers in the field, the lower the scores of internal and external, the worse the interpersonal relationship and family relationship, the higher the risk of anxiety(P<0.05). The higher the mental quality and neurotic scores of the officers and soldiers in the field, the lower of the position, the lower the scores of positive coping style and internal and external, the worse the interpersonal relationship and family relationship, the higher the risk of depression(P<0.05). CONCLUSION: Anxiety and depression are the main negative emotions in the field training officers and soldiers. Negative coping style, pathological personality tendency and interpersonal relationship are the main influencing factors of negative emotion.

Objective To construct recombinant human butyrylcholinesterase(rhBChE)knock-in goat fetal fibroblast cell lines(GFFs)by using clustered regularly interspaced short palindromic repeats(CRISPR)/CRISPR-associated protein 9(Cas9)-mediated homology-directed repair mechanism for subsequent production of goat expressing rhBChE.Methods The efficient sgRNA sites targeting goat[3-casein(CSN2)gene were designed and screened,and the targeting efficiency of the sgRNA in goat mammary epithelial cells(GMECs)was confirmed by electro-transfection,flow sorting,and sequencing of PCR products.The red fluorescent reporter gene homology repair vector(P2A-mCherry)targeting the sgRNA was constructed,and then the integration and expression efficiency was detected by flow cytometry.The rhBChE homology repair vector(P2A-rhBChE)targeting the sgRNA of CSN2 gene was constructed in GFFs,the rhBChE positive cell clones were obtained via electro-transfection and flow sorting,and the rhBChE knock-in cell lines was identified by sequencing of PCR products.Results The sgRNA4 was identified as an efficient target of goat CSN2 gene,which could be also used for targeted integration of other genes.Three rhBChE knock-in cell lines were successfully constructed.Conclusion The rhBChE knock-in GFFs targeting goat CSN2 gene lays the foundation for the production of mammary bioreactors expressing rhBChE.

Objective To explore the experience of infantile liver transplantation ,reconstructing portal vein (PV) and avoid the higher incidence of portal vein low flow and complications .Methods The clinical data were reviewed for 152 infantile liver transplantations performed by a single surgery group .And 114 cases with PV risk factors underwent customized PV reconstructions .All of them were diagnosed as cholestatic liver diseases and 106 (93％ ) belonged to biliary atresia .Forty-two cases (36％ ) had 2 or more risk factors .Results Most cases (n= 106 ,93％ ) underwent living donor transplantations using lateral left graft while another 8 cases had deceased donor transplantations . Four types of PV reconstructions were adopted based upon individual conditions :left/right branch of PV trunk (n= 103) ,autogenous patch PV venoplastic reconstruction (n= 3) ,duct-to-duct of PV trunk (n= 5) and donor PV duct-to-recipient confluence of SMV/CV and SV (n= 3) .Graft size reduction was performed when GRWR > 4 .5％ (n= 16) .During a median follow-up period of 6 .5 (1 .5-13) months ,there were 3 LPVF (2 .6％ ) ,2PVS (1 .7％ ) and 1 PVT (0 .8％ ) .Three LPVF cases was corrected by PV stenting ,two cases of PVS were stable after anticoagulation therapy while one PVT case undergoing thromboectomy plus PV stenting resumed a normal PV flow .Conclusions PV reconstruction of high-risk infants require comprehensive risk evaluations ,precise surgical skills and customized strategies .For PV complications ,stenting is both safe and feasible .

Objective: We observed the effect of the opening and closing pressure sensors on the pediatric liver transplantation. Methods: The 100 cases of pediatric patients who suffered biliary atresia were chose to this study from July 1^st 2018 to Dec 31^st 2018. They received the living donor liver transplantation. The samples were divided into control group and test group according to the random number table. We observed the volume of blood lost during the process of blood sample collecting. The hemoglobin (HB) and infection rate of catheter were also recorded. Results: The test group didn′t lose blood when collecting the sample, and the time of collecting the blood sample in the test group was (22.0 ± 4.2) s, which was shorter than that of in the control group (47.0 ± 7.8) s, the difference was significant, t=9.321, P<0.05. The difference of HB and infection rate of catheter after 24 hours between two groups was not significant, P>0.05. Conclusion The closing pressure sensor may be more advanced when used to avoid the loss of blood and prevent the infection.

Objective By simulating acute hypoxic conditions, an experimental model of intestinal stress injury in plateau mice was established to explore the pathogenic mechanism of acute gastrointestinal diseases in plateau, and to lay foundation for preventive and therapeutic measures.MethodsThirty-six SPF-grade adult male BALB/c mice were randomly divided into four groups: normoxic 24 h, normoxic 72 h, hypoxic 24 h, and hypoxic 72 h, based on body weight using a randomized numerical table method, with nine mice in each group. Mice in the normoxic group were kept in a conventional barrier environment, while those in the hypoxic group were placed in a hypoxic chamber within the barrier environment with oxygen concentration set at 10% to simulate plateau conditions. They were subjected to stress for 24 h and 72 h, respectively, in order to establish a model of intestinal injury induced by acute hypoxia. After modeling, the mice were weighed, anesthetized with 1% pentobarbital sodium, and then euthanized by cervical dislocation. Duodenal and colonic tissues were collected. Histopathological morphology of intestinal tissues was observed after HE staining. Western blotting and immunohistochemistry were used to detect the expression levels of tight junction-related proteins in intestinal tissues. Real-time fluorescence quantitative PCR was performed to measure the expression levels of inflammatory cytokines and chemokines. TUNEL staining was used to assess apoptotic activity of intestinal epithelial cells, thus evaluating intestinal injury-related phenotypes in this model.Results Compared with the normoxic groups, mice in the 24 h and 72 h hypoxia groups showed weight loss, shortened duodenal villi, abnormal crypt structure, and decreased villus/crypt ratio. The colonic mucosa was infiltrated with inflammatory cells and irregular crypt structure. Expression levels of Occludin and zonula occludens-1 (ZO-1) were significantly decreased in duodenal and colonic tissues of mice in the 24 h and 72 h hypoxia groups (P<0.05). The expression of pro-apoptotic protein Bax was significantly up-regulated while expression of anti-apoptotic protein Bcl-2 was significantly down-regulated in duodenal tissues (P<0.05). Apoptotic activity of intestinal epithelial cells was significantly enhanced (P<0.05). In addition, interleukin (IL)-1β, IL-6, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor-α (TNF-α) mRNA levels were significantly increased in duodenal tissues after 24 and 72 h of hypoxic stress(P<0.05). After 24 h of hypoxic stress, there was no significant change in the expression levels of inflammatory cytokines in colon tissues (P>0.05), but after 72 h, the expression levels of pro-inflammatory factors IL-1β, TNF-α, IL-6, MCP-1, and anti-inflammatory factor IL-10 mRNAs significantly increased in colon tissues of mice (P<0.05).Conclusion The usage of a hypoxia chamber to simulate an acute hypoxic environment in plateau can lead to abnormal intestinal tissue structure, intestinal barrier dysfunction, and induce intestinal epithelial cell apoptosis, triggering an intestinal inflammatory response in stress mice. These findings indicate the successful construction of a mouse model for an acute hypoxic stress-induced intestinal injury.