Objective To explore the relationship between vitamin D receptor(VDR)gene polymorphisms and genetic susceptibility in gestational diabetes mellitus(GDM).Methods A total of 240 patients with GDM who were hospitalized in the Obstetrics and Gynecology Department of Wuhan Yaxin General Hospital were enrolled in this study from January 2019 to January 2022(GDM group),and another 240 healthy pregnant women matched were selected as normal control(NC)group during the same period.The general information,FPG,HbA1c,2 hour postprandial blood glucose(2 hPG),insulin resistance index(HOMA-IR),serum 25 hydroxyvitamin D[25(OH)D]level,and VDR gene polymorphisms were compared between the two groups.The correlation between HOMA-IR and 25(OH)D levels was evaluated by Pearson analysis.The influencing factors for GDM genetic susceptibility were analyzed by logistic regression model.The pregnancy outcomes of GDM patients were analyzed by follow-up to the end of pregnancy.Results The prevalence of DM family history,FPG,2 hPG,HbA1c and HOMA-IR were higher(P<0.05),whilethe serum 25(OH)D was lower in GDM group than in NC group(P<0.05).There was significant difference in the distribution of genotype and allele frequency of FokI locus of VDR gene between the two groups(P<0.05).Pearson correlation analysis showed that serum 25(OH)D was negatively correlated with FPG,2 hPG,HbA1c and HOMA-IR(P<0.05).Logistic regression analysis showed that DM family history,VDR gene FokI genotype GA and AA were the influencing factors for GDM genetic susceptibility.The incidence of adverse pregnancy outcome was higher in patients with FokI AA genotype than in patients with GA and GG genotypes(P<0.05).The incidence of adverse pregnancy outcome was higher in patients with GA genotype than in patients with GG genotype(P<0.05).Conclusions The VDR gene FokI locus gene polymorphism is associated with the genetic susceptibility to GDM,and its GA and AA genotypes both increase the risk of GDM susceptibility and the incidence of adverse pregnancy outcomes.

Humans ; Gastrointestinal Microbiome ; Constipation/therapy* ; Probiotics/therapeutic use* ; Patients

Acute pancreatitis (AP) is a severe disease with an increasing incidence rate in clinical practice. Although most patients have mild pancreatitis, the fatality rate of severe pancreatitis remains at a relatively high level, and therefore, early-stage, simple, and accurate clinical scoring systems are urgently needed to determine the severity of AP, so as to facilitate effective disease management and symptomatic treatment and reduce the fatality rate of patients. At present, a large number of studies have demonstrated that the scoring systems such as Ranson score, APACHE Ⅱ score, BISAP score, CTSI score, and some serological markers have been used to evaluate the severity and prognosis of AP, but all of them have certain limitations. This article reviews the research advances in the existing scoring systems, single serological markers, and related modified scoring systems in recent years. Through a literature review, it is concluded that there is no a single scoring system or a single indicator that can cover the whole process of AP diagnosis and treatment and accurately judge the severity of AP, and therefore, it is necessary to develop a new scoring system or combine various indicators for comprehensive evaluation.

[Abstract] Objective: To investigate the effect of sphingosine kinase 1 (SphK1) knockdown on the proliferation and migration of colon cancer RKO cells induced by mesenchymal stem cells (MSCs). Methods: RKO cells were treated with MSCs conditioned medium (MSC-CM) or control medium (Control-CM), respectively. Cell proliferation was detected by CCK-8 assay. Cell migration ability was tested by Transwell chamber assay. The proteins expression of Ki-67, MMP-2/9, CD44 and CD133 was detected by Western blotting. Then, the expression of SphK1 in RKO cells was suppressed by targeted gene lentivirus shRNA vector transfection. The effects of SphK1 knockdown on the proliferation, migration and protein expressions of Ki-67, MMP-2/9, CD44 and CD133 of RKO cells induced by MSC-CM were observed. Results: The RKO cells proliferation was promoted by MSC-CM in a time-dependent manner; moreover (P<0.05), the migration ability of cells was significantly enhanced after being treated with MSC-CM(P<0.01). In addition, MSC-CM significantly increased the protein expressions of Ki-67, MMP-2/9, CD44 and CD133(all P<0.05 or P<0.01). Lentiviral ShRNA vector transfection could significantly inhibit the expression of SphK1. Down-regulation of SphK1 significantly inhibited the proliferation, migration and protein expressions of Ki-67, MMP-2/9, CD44 and CD133 of RKO cells induced by MSC-CM(all P<0.05 or P<0.01). Conclusion: MSC-CM promotes the proliferation and migration of colon cancer RKO cells. Down-regulation of SphK1 reverses the cell proliferation and migration induced by MSC-CM via inhibiting the expression of MMP-2/9, CD44 and CD133.

[ ABSTRACT] AIM:To investigate the effects of sphingosine kinase l ( SphK1) and focal adhesion kinase ( FAK) on the epithelial-mesenchymal transition ( EMT) of human colon cancer HCT 116 cells.METHODS:Human colon cancer HCT116 cells were divided into 3 groups.N, N-dimethylsphingosine (DMS) was used to suppress the activity of SphK1. PF573228 was used to suppress the activation of FAK .The cells treated with equal volume of culture medium severed as control group.The cell viability was measured by MTT assay .The protein expression of SphK1, FAK and the EMT relative protein E-cadherin, N-cadherin, vimentin and matrix metalloproteinase (MMP) 2 was analyzed by Western blot.The mR-NA expression of SphK1, sphingosine-1-phosphate (S1P), FAK, E-cadherin and vimentin was detected by real-time PCR. The ability of tumor cell migration was measured by wound-healing assay.RESULTS:The cell viability of HCT116 cells was suppressed by DMS and PF 573228 in dose and time dependent manners .DMS significantly suppressed the expression of SphK1, FAK, N-cadherin, vimentin and MMP2, meanwhile enhanced the expression of E-cadherin.PF573228 reduced the expression of FAK , SphK1, N-cadherin, vimentin and MMP2, meanwhile increased the expression of E-cadherin (P<0.01).In addition, the migration ability of HCT116 cells was significantly decreased by treating with DMS and PF573228 (P<0.01).Compared with control group , the mRNA expression of FAK, SphK1, S1P and vimentin was de-creased, while the expression of E-cadherin was increased significantly in PF573228 group and DMS group (P<0.05). CONCLUSION:SphK1 and FAK signaling pathways may play an important role in the occurrence of EMT in the colon cancer HCT116 cells.

Laparoscopic vagal-sparing esophagogastrectomy for the treatment of early esophageal cancer has the advantages of minimal invasion,functional sparing and better quality of life,and it can radically resect the tumor.The clinical data of 3 patients in the Daping Hospital of Third Military Medical University and 9 patients in the Xijing Hospital of Digestive Diseases who received laparoscopic vagal-sparing esophagogastrectomy from September 2009 to August 2013 were retrospectively analyzed.All the 12 patients were followed up for 1-24 months.One patient was complicated with transit hoarseness and 1 with cervical anastomotic fistular,and they were cured by conservative treatment; 1 patient was complicated with cervical anastomotic stricture,and was cured by dilatation for 3 times; no dysphagia and recurrence was observed in the other 9 patients during the follow-up.Laparoscopic vagal-sparing esophagogastrectomy is a good option for early esophageal cancer and benign esophageal diseases.

In order to clone and express alcohol dehydrogenase II (ADH2) gene from Saccharomyces cerevisiae in E. coli BL21 (DE3) efficiently, we extracted the total RNA as template and obtained ADH2 gene by RT-PCR and connected ADH2 gene to pTAT plasmids to gain recombinant expression plasmid pTAT-ADH2, then transformed this recombinant expression plasmid pTAT-ADH2 into E. coli BL21 (DE3). The recombinant was induced by IPTG to express ADH2. After purification, ADH2 activity was tested in vitro and toxicologic test was done in mouse. Sequence test showed that the acquired fragments exhibited 90% homology to ADH2 gene sequence from GenBank report. The target gene expressed efficiently and took up to approximant 50% of total protein by SDS-PAGE and band scanning analysis. The purified protein exhibited the identified activity through biochemical test and mouse toxicological test. As a result, the acquired ADH2 gene was highly homology to the published sequence and expressed at a high level in E. coli BL21 (DE3), more importantly, ADH2 proved to have ethanol dehydrogenase activity.
Alcohol Dehydrogenase ; genetics ; isolation & purification ; Animals ; Cloning, Molecular ; Escherichia coli ; genetics ; metabolism ; Genetic Vectors ; Mice ; Random Allocation ; Recombinant Proteins ; biosynthesis ; genetics ; isolation & purification ; Saccharomyces cerevisiae ; enzymology ; genetics ; Saccharomyces cerevisiae Proteins ; genetics ; isolation & purification

ObjectiveTo study the injuries of liver after ischemia-reperfusion of small intestine of the rat.MethodsModels of ischemia-reperfusion of small intestine was made with rats. At 0 min, 30 min, 1h, 2h, 1d, 3d,7d after reperfusion, the concentration of nitric oxide(NO), superoxide dismutase (SOD) in the serum was examed and the expression of Bax, Bcl-2 and p53 in the liver was observed by the immunohistochemical SP method.ResultsThe concentration of NO increased apparently 0 min after reperfusion, but decreased 2 h after, then increased gradually to a peak at 7th day. But for SOD, the concentration decreased 0 min after reperfusion, increased 2 h after,and decreased to the lowest level at 7th day. The immunohistochemical SP positive cells were observed in sinus endothelial cells and hepatocytes. The ratio of positive cells of Bax,p53 and Bcl-2 began to increase 0 minute after reperfusion and increased continuously 30 min after, while that of Bcl-2 was higher than that of Bax(P<0.01). It decreased apparently 2h after, and then increased till 7d after reperfusion,while the ratio of Bax positive cells was higher than that of Bcl-2(P<0.01).ConclusionThe change of concentration of NO, SOD and the expression of positive cells of Bax, Bcl-2 and p53 might play a important role in apoptosis and injuries of the liver after ischemia-reperfusion of small intestine of rat.

Objective　To introduce the management experience in the first cause of living-related small bowel transplantation in China. Methods　An 18-year-old male patient with short gut syndrome received a living-related small bowel transplantation with the graft taken from his father(44-year-old). A segment of 150?!cm distal ileum was resected from the donor. Treatment of immunosuppression, antibiotics, antithrombosis and nutrition support were given posttransplantatively. Results　Recently the recipient has a good life quality for 19 months. Conclusions　Living-related small bowel trnasplantation can be effectively used to treat short gut syndrome, and the posttransplantative management is the key to the successful transplantation.