Abstract As the largest human microecosystem, intestinal microorganisms participate in human material and energy metabolisms and pose a significant impact on human health. Diabetes mellitus is likely to cause imbalance of abundance and component alterations in intestinal microorganisms, and reduce the diversity and balance, leading to intestinal microflora dysregulation. It has been shown that intestinal microflora dysregulation may promote diabetes development and progression through the reduction of intestinal microbial metabolites, inflammatory reaction and insulin resistance. This review summarizes the involvement of intestinal microorganisms in the pathogenesis of diabetes through metabolites including short-chain fatty acid, bile acid and lipopolysaccharide, and describes the current status of intestinal microorganisms-mediated treatments for diabetes, so as to provide the theoretical basis for the researches on diabetes and intestinal microorganisms.

Silent mating type information regulation 2 homolog-1 ( SIRT1 ) is a nicotinamide adenine dinucleotide ( NAD)-dependent deacetylase, which can deacetylate histone and non-histone proteins and is involved in many life proces-ses, such as energy metabolism, cell senescence and apoptosis.SIRT1 can enhance the cellular energy supply, inhibit cell apoptosis, alleviate inflammation, enhance the resistance of oxidative stress and improve the function of endothelial cells by deacetylating relevant factors in many vascular-related diseases.This article summarizes the current research progress in the function and signal pathway of SIRT1 in ischemic stroke, atherosclerosis and tumors.

Objective This study was provided the evidence of infection respiratory tract clinical treatment through examining 695 cases of pathogen .Methods Using indirect immunofluorescence(IFA) IgM antibody with 9 respiratory pathogen in serum of 695 patients from August 2015 to March 2016 with respiratory tract infection from espiratory ,pediatrician ,thoracic surgery clinics were detected in this paper in order to provide the basis for clinical treatment .Results The results showed that single pathogen de‐tection positive rate was 33 .9% in 695 cases ,The top three of positive rate were MP(14 .1% ) ,IFB(9 .6% ) ,RSV(4 .8% );the posi‐tive rate of two mixed infection was 7 .79% ;The postive rate of MP ,IFB have obvious difference in seasons ,but which of Coxiella burneti was no obvious seasonal difference;there was an obvious difference between the sex ratio .Conclusion MP ,IFB ,RSV infec‐tion were given priority to detection rate in our region .

BACKGROUND:At present, there are few reports about construction of the model of acute high altitude stress-induced gastrointestinal injury. Construction of a stable high altitude stress-induced gastrointestinal injury model has become a premise of the current studies on acute stress-induced gastrointestinal injury and related diseases. OBJECTIVE: To establish rat models of acute high altitude stress-induced gastrointestinal ischemia/reperfusion injury. METHODS:Twenty-four male Wistar rats were randomly divided into normal control (lower limit of high altitude) , sham (high altitude) and ischemia/reperfusion (high altitude) groups (n=8 rats/group). Rats from al groups underwent a rush for high altitude region. The root of the superior mesenteric artery of rats in the ischemia/reperfusion group was clamped by a vascular clip to completely block blood flow for 60 minutes, and then intestinal blood flow was recovered for reperfusion for 60 minutes. The rats in the sham group were only 

ObjectiveTo investigate the effect of mesenchymal stem cells (MSCs) transfected with hepatic growth factor (HGF) gene on the survival volume of free grain fat grafts.Methods MSCs of male Wistar rats were transfected with Ad-GFP or Ad-HGF.The transfection infectivity of Ad-GFP to MSCs,the expression of HGF were measured using ELISA assay.150 rats were randomly divided into 5 groups:control group (group A),MSCs group (group B),Ad HGF group (group C),MSCs transplanted with Ad-GFP group (group D),and MSCs transplanted with Ad-HGF (MSCsHGF) group (group E).Then,the same volume of frain fat graft,mixed with DMEM LG andMSCs,Ad HGF,MSCs-GFP,MSCs HGF respectively,were transplanted to rats back,but control group were only mixed with DMEM-LG.Fat graft was obtained on days 3,5,7,14,28,and 60 after implantation.The volume of fat graft was measured by messcylinder,and the expression of HGF and CD34 in transplanted fat tissue were detected by immunohistochemistry.ResultsThe transfection infectivity of Ad-GFP to MSCs was 89.6 ％ at 100 MOI,the expression of HGF in MSCs culture medium reached to the level after being transfected with Ad-HGF for 48 h.Compared with other 4 groups,at days 3,5,7,and 14 post-transplantation,the expression of HGF in E group transplanted fat of group E had statistics significance (P＜0.05).The persentage of survival volume of fat graft in group E was significantly higher than that of other group ( P＜0.05) at days 28,and 60 post transplantation.ConclusionsMSCs transplanted with Ad-HGF could secrete HGF and increase the survival volume of fat grafts.

Insulin resistance (IR) is a complex metabolic disorder related to several diseases including type 2 diabetes (T2DM), hypertension and dyslipidemia. These diseases are all independent risk factors for cardiovascular disease. Lipid metabolism disorder has toxic effects on cells and may cause or aggravate IR in performance of elevated plasma levels of triglyceride (TG) and free fatty acids (FFA), the last one is an independent risk factor for IR. It has been clear that FFA may induce IR by endoplasmic reticulum (ER) stress, oxidative stress, apoptosis and inflammation, although the specific mechanisms remained unknown. The present paper summarizes the related molecules involved in the pathogenic process of IR and its mechanism, might provide a theoretical basis for the molecular mechanism of IR caused by FFA, and therapeutic reference for clinical treatment of IR and prevention of T2DM.

Objective:To explore the status of volume management behavior in patients with peritoneal dialysis, and to explore the relationship between health belief and volume management behavior.Methods:Convenient sampling was used to select 129 patients who underwent regular dialysis in the peritoneal dialysis center of the General Hospital of Ningxia Medical University from January to December 2019. The general condition questionnaire, Health Belief Scale, and Capacity Management Behavior Scale for patients with peritoneal dialysis were used.Results:The total score of the Capacity Management Behavior Scale of peritoneal dialysis patients was 20.23±3.54. Among all the entries: "Weigh and record the infusion volume and drainage volume" and "Regular monitoring of renal function and electrolytes and other related examinations as directed by the doctor" scored higher; while the item "Eat less high-salt and high-sodium food and adjust fluid intake according to the amount of ultrafiltration, edema and urine output" item scored lower; single factor analysis found that different educational levels, different employment conditions, whether had diabetes mellius and different over hydration had statistical significance ( F value was 3.911, t values were 2.409, 4.990, 6.070, P<0.05). The dimension of the perception maintenance capacity balance disorder was negatively correlated with the total score and each dimension of the capacity management behavior( r values were -0.243, -0.260, -0.299, P<0.05) , and the liquid intake self-efficacy dimension is positively correlated with the total score and each dimension of the capacity management behavior ( r values were 0.329, 0.397, 0.393, P<0.05). Conclusions:The level of capacity management behavior of peritoneal dialysis patients needs to be improved; employment status, and whether he has diabetes or not are the influencing factors of the patients' capacity management behavior; in health beliefs, perception of maintenance of volume balance disorders and self-efficacy and peritoneal dialysis are correlated with patients' capacity management behaviors.

OBJECTIVETo evaluate the effects of hepatocyte growth factor (HGF) on the prevention of scar formation and the promotion of wound healing by gene transfer.

METHODSA total of 12 female New Zealand rabbits were used in this study. Rabbits were anesthetized with an intravenous injection of sodium pentobarbital, and identical wounds were made over the ventral surface of each ear. Five circular wounds, 7 mm in diameter, were created in each ear by excision through the skin to the underlying cartilage using sterile technique. After the surgical procedures, 10 of the rabbits were randomly allocated to five groups, with 2 rabbits in each group: Ad-HGF group 1, Ad-HGF group 2, Ad-HGF group 3, Ad-GFP (a reporter gene) group and the solvent group. Immediately after surgery, 6 x 10(7) pfu Ad-HGF, 6 x 10(8) pfu Ad-HGF, 6 x 10(9) pfu of Ad-HGF, 6 x 10(9) pfu of Ad-GFP, or same volume of solvent (PBS, pH 7.2) was applied once to each wound in groups 1 to 5, respectively. One additional rabbit was used to evaluate the transfer efficiency of the adenovirus vector by transferring Ad-GFP (6 x 10(9) pfu) into its wounds. Ice slides of wounds from this animal were observed under fluorescence microscopy. Another additional rabbit was used to evaluate the expression of HGF and TGFbeta1 after transferring Ad-HGF (6 x 10(9) pfu) into each of its wound. Immunohistochemistry was used for detection.

RESULTSThe effect of HGF on reducing excessive dermal scarring was observed by adenovirus-mediated gene transfer. Transfection of the human HGF cDNA into skin wounds through an adenoviral vector suppressed the over-expression of TGFbeta1, which plays an essential role in the progression of dermal fibrogenesis. Application of HGF to the wounds significantly enhanced wound healing and inhibited over scarring.

CONCLUSIONHGF gene therapy could be a new approach for preventing excessive dermal scarring in wound healing.

Animals ; Cicatrix ; prevention & control ; Female ; Gene Transfer Techniques ; Hepatocyte Growth Factor ; pharmacology ; Rabbits ; Random Allocation ; Wound Healing ; drug effects ; physiology

OBJECTIVETo construct a recombinant adenovirus (pAdxsi-GFP-HIF) encoding human hypoxia inducible factor 1 α gene (HIF-1 α) and to express it in endothelial cells.

METHODSHIF-1 α gene was obtained from human lung cancer cell line A549, which was cultured in hypoxia condition, by RT-PCR. The HIF-1 α gene was subcloned into shuttle vector p Shuttle-CMV-EGFP at KpnI and BamHI sites. After identified with restriction enzymes, plasmid p Shuttle-GFP-HIF was linearized by digestion with restriction endonuclease I-CeuI and I-SceI, and subsequently cotransformed into E.coli DH5a with adenoviral backbone plasmid pAdxsi to make homologous recombination. After linearized by PacI, the homologous recombinant adenovirus plasmid was transfected into 293 cells to package and amplify. The recombinant adenovirus was infected with human umbilical vein endothelial cells (ECV304), and the expression level of HIF-1 α protein was evaluated by ELISA.

RESULTSThe recombinant adenovirus vector containing HIF-1 α gene (pAdxsi-GFP-HIF) was successfully constructed and amplified with titer of 3.38 X 10(10) pfu/mL. The green fluorescence protein was detected under fluorescent microscope in ECV304 at 24h after transfection and with a stronger degree after 48h. The concentration of HIF-1 protein was (48.93 ±3.86)ng/mL in supernatant at 48 h after transfection.

CONCLUSIONA recombinant adenovirus vector pAdxsi-GFP-HIF, encoding human hypoxia inducible factor 1 α gene, has been constructed in vitro and expressed successfully in ECV304 cells.

Adenoviridae ; genetics ; Cells, Cultured ; Genetic Vectors ; Human Umbilical Vein Endothelial Cells ; metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; Plasmids ; genetics

The present study developed an oral hepatocyte growth factor (HGF) gene therapy strategy for gastric ulcers treatment. An attenuated Salmonella typhimurium that stably expressed high HGF (named as TPH) was constructed, and the antiulcerogenic effect of TPH was evaluated in a rat model of gastric ulcers that created by acetic acid subserosal injection. From day 5 after injection, TPH (1 × 10⁹ cfu), vehicle (TP, 1 × 10⁹ cfu), or sodium bicarbonate (model control) was administered orally every alternate day for three times. Then ulcer size was measured at day 21 after ulcer induction. The ulcer area in TPH-treated group was 10.56 ± 3.30 mm², which was smaller when compared with those in the TP-treated and model control groups (43.47 ± 4.18 and 56.25 ± 6.38 mm², respectively). A higher level of reepithelialization was found in TPH-treated group and the crawling length of gastric epithelial cells was significantly longer than in the other two groups (P < 0.05). The microvessel density in the ulcer granulation tissues of the TPH-treated rats was 39.9 vessels/mm², which was greater than in the TP-treated and model control rats, with a significant statistical difference. These results suggest that TPH treatment significantly accelerates the healing of gastric ulcers via stimulating proliferation of gastric epithelial cells and enhancing angiogenesis on gastric ulcer site.
Acetic Acid ; Animals ; Epithelial Cells ; Genetic Therapy ; Granulation Tissue ; Hepatocyte Growth Factor* ; Hepatocytes* ; Microvessels ; Models, Animal ; Rats* ; Salmonella typhimurium ; Salmonella* ; Sodium Bicarbonate ; Stomach Ulcer* ; Ulcer