Objective To explore the causes and management of postoperative complications of laparoscopic Roux-en-Y gastric bypass (LRYGB).Methods The retrospective cross-sectional study was conducted.The clinical data of 450 patients with metabolic diseases who underwent LRYGB between June 2004 and November 2016 were collected,including 283 (58 in hospital consultation) in the First Affiliated Hospital of Jinan University,140 in the Jihua Hospital Affiliated to Jinan University and 27 in the Zhengzhou Hospital of Jinan University.Observation indicators:situations of surgical completion,follow-up situations,occurrence,treatment and prognosis of complications.Follow-up using outpatient examination and telephone interview was performed to detect postoperative complications once at month 1,3,6 and 12 within 1 year postoperatively and once every year after 1 year postoperatively up to March 2017.Measurement data with skewed distribution were described as M (range).Count data were evaluated by the ratio,and comparison between groups was analyzed using the chi-square test.Results All the 450 patients with metabolic diseases underwent successful LRYGB,including 50 receiving LRYGB during surgical internship period and 400 receiving LRYGB after surgical internship period,without conversion to open surgery.All the 450 patients were followed up for 70 months (range,1-153 months).Twenty-seven patients had postoperative complications,with an incidence of 6.00％ (27/450).The incidence of postoperative complications was 20.00％(10/50) in 50 patients receiving LRYGB during surgical internship period and 4.25％ (17/400) in 400 patients receiving LRYGB after surgical internship period,with a statistically significant difference (x2 =16.86,P＜ 0.05).Of 27 patients with postoperative complications,1 was complicated with fulminant acute pancreatitis and died from multiple organ failure at day 15 postoperatively,5 with intra-abdominal bleeding,2 with anastomotic leakage,3 with gastrojejunal anastomosis stenosis,2 with gastrojejunal anastomosis ulcer,1 with improper anastomosis,1 with respiratory failure,1 with umbilicus infection,3 with internal hernia,2 with dumping syndrome,6 with weight-loss failure (1 refused to undergo revision surgery),and patients with postoperative complications were improved or cured by surgery or conservative treatment except one death.Conclusions The incidence of complications in patients receiving LRYGB after surgical internship period is significantly reduced,and complications needs to make the individualized treatment plan.

BACKGROUND: The proliferation of peripheral blood stem cells among peripheral blood mononuclear cells (PBMCs) invitro remains unclear. There is no optimal marker for tracing PBMCs transplanted in vivo.OBJECTIVE: To observe the degree of PBMC proliferation in stem cell medium by EdU labeling and to explore thefeasibility of EdU-labeled peripheral blood stem cells.METHODS: New Zealand rabbit PBMCs were isolated and cultured for 1 to 5 days in stem cell medium supplementedwith EdU. The cells were observed and counted at 0, 1, 2, 3, 4 and 5 days in culture. The cells were harvested at eachtime point and stained with EdU fluorescent reagents. Then, confocal microscopy and flow cytometry were used to detectEdU-labeled cells.RESULTS AND CONCLUSION: (1) Freshly isolated rabbit PBMCs were rounded and showed clear outline. After 1 dayculture, most of the cells were suspended in the medium, spherical or round. There were also a few cell clusters andadherent cells scattered in a triangle or polygon shape; after 2 days culture, more cell debris were observed, and mostcells were round; when cultured for 3-5 days, increased cell debris, smaller cell mass and decreased cell densitysignificantly were observed. (2) With the prolongation of culture time, the cell count decreased gradually. (3) Whencultured for 1 day, EdU labeled cells in red were scattered. The number of cells marked with EdU red label increasedsignificantly at day 2 and remained unchanged after 3 days of culture. At 5 days of culture, the number of red cellsmarkedly decreased; the highest positive rate of EdU-labeled cells was (2.38±0.10)% at 2 days after culture. To conclude,these results showed that the proportion of proliferating cells in rabbit PBMCs was very low. EdU is capable of labelingproliferative cells among PBMCs.

Exosomes (EXOs) are formed by intracellular multivesicular bodies and carry a variety of biomacromolecules such as lipids, proteins, encoding and non-coding RNAs, and mitochondrial DNA. EXOs can be released in vivo by different cell types, including hepatocytes, hepatic stellate cells, and immune cells and play the role of intercellular communication. More and more studies have shown that EXOs are involved in the development, progression, and prognosis of chronic hepatitis B (CHB) and hepatocellular carcinoma (HCC) caused by hepatitis B virus (HBV) infection and are expected to become potential biomarkers for the early diagnosis and prognostic evaluation of HBV-related HCC. This article reviews the role of EXOs in the host infection process of HBV and the importance of EXOs in the development, progression, and prognosis of CHB and HCC, in order to provide new ideas for the basic and clinical research in this field.

Interleukin-27 (IL-27), a heterodimeric cytokine, plays a protective role in diabetes. Ghrelin, a gastric hormone, provides a hunger signal to the central nervous system to stimulate food intake. The relationship between IL-27 and ghrelin is still unexplored. Here we investigated that signal transducer and activator of transcription 3 (STAT3)-mechanistic target of rapamycin (mTOR) signaling mediates the suppression of ghrelin induced by IL-27. Co-localization of interleukin 27 receptor subunit alpha (WSX-1) and ghrelin was observed in mouse and human gastric mucosa. Intracerebroventricular injection of IL-27 markedly suppressed ghrelin synthesis and secretion while stimulating STAT3-mTOR signaling in both C57BL/6J mice and high-fat diet-induced-obese mice. IL-27 inhibited the production of ghrelin in mHypoE-N42 cells. Inhibition of mTOR activity induced by siRNA or rapamycin blocked the suppression of ghrelin production induced by IL-27 in mHypoE-N42 cells. siRNA also abolished the inhibitory effect of IL-27 on ghrelin. IL-27 increased the interaction between STAT3 and mTOR in mHypoE-N42 cells. In conclusion, IL-27 suppresses ghrelin production through the STAT3-mTOR dependent mechanism.