Objective: To investigate the prevalence of nutritional risk,malnutrition and application of nutritional support in department of digestive trad in our hospital in Ningbo.Methods: The information of 205 patients were collected in our hospital.Nutrition status was assessed according to Nutrition Risk Screening(NRS) published by ESPEN in 2002.Results: A total of 205 patients were enrolled,and 189 patients(92.2%)underwent NRS 2002.Prevalence of malnutrition was 20.0% and nutritional risk was 32.7%.Totally 18 patients(8.8%) receiving nutritional support had a NRS2002≥3.The PN∶EN ratio was 2.6 ∶1. Conclusion: A large proportion of inpatients were at nutritional risk or malnutrition in our hospital.The application of PN and EN is inappropriate in inpatients.Evidence-based guidelines are required to improve this situation.

Objective To explore the feasibility of mechanical chest compression to establish a rat model of car?diopulmonary resuscitation ( CPR) . Methods 4?month old healthy male Sprague Dawley rats were randomly divided into control group ( n=6 ) and model group ( n=10 ) . After induction of anaesthesia with 10% chloraldurate ( 3 ml/kg, i. p. ) , tracheal intubation and left femoral artery cannulation were performed. Under electrocardiographic and artery blood pressure monitoring, tracheal obstruction ( TO) was performed to rats in model group. At 2 min after the cardiac arrest ( CA) occurred, CPRs were administered to the rats using a self?made animal chest compressor, which provided chest?com?pression at a rate of 200 bpm. Results Shortly after TO, rats in the model group had respiratory arrest, cyanosis and ar?rhythmia. Electrocardiography indicated that CA occurred within 4-5 min, with a decreased artery systolic blood pressure ( <40 mmHg) and a zero pulse pressure. Return of spontaneous circulation ( ROSC) after the CPR was successfully a?chieved in 8 rats (80%), with a transient reperfusion arrhythmia. Finally, 60% of the rats (n=6) recovered to con?sciousness and survived for 24 hrs. The serum biochemical analysis indicated that there were electrolyte disturbances, aci?dosis, impaired renal functions and increased myocardial enzyme spectrum. Pathological examination revealed cardiac rhab? domyolysis, no?reflow phenomenon in renal glomeruli, decrease of neurons and pulmonary congestion in the model group rats. Conclusions Mechanical chest compression can provide minimal cardiac output for the requirement of CPR incardiac arrestin rats. It is feasible to establish rat CPR model with the mechanical chest compression.

Objective To analyze the impact of hepatitis B virus (HBV) replication and its coded X gene (HBx) expression on cell gene expression profile,especially the immune related gene expression level changes.Methods Overexpressed HBx gene was transiently transfected through lenti-virus and pcDNA3,the RNA-Seq and RT-qPCR methods were used to detect the expression levels of immune related genes,which were verified in HBV replication cell line.Results This study found that the HBV replication and HBx expression suppressed the expression of immune checkpoint PD-1 ligand gene (PD-L1/CD274) in a dose-dependent manner,while the expression of H-box mutant in HBx gene lost this inhibition effect.Conclusion HBV/HBx possesses the ability for inhibiting PD-L1/CD274 ligand gene expression,may relieve the checkpoint of antigen-specific T cell activation in viral infection acute stage,activates cytotoxic T cells,which may cause that T cell attack and clear highly replicated cells,helps virus to enter the lower replication status,and reaches the balance status between virus-host and lays a basis of HBV chronic infection.

Objective The purpose of this study was to examine effects of Isopsoralen on the osteoblast proliferation and differentiation and find its possible molecular mechanisms for anti-osteoporosis.Methods OCT-1 cells were cultured with common methods.While growing well,cells were cultured with 3 doses(10 μg·mL-1,30u μg·mL-1 and 60 μg·mL-1)of Isopsoralen for 48 h,or with purified bone morphogenetic protein 2(BMP2)protein(50 ng·mL-1).We first determined the effect of Isopsoralen on cell proliferation by MTT assay.The real time RT-PCR was also used to quantify changes in the mRNA levels of several genes,such as BMP2,Runt-related transcription factor 2(Runx2),and Osterix(Osx).We also used the Western blot analysis to evaluate the expression of Runx2 and Osx proteins.At last we used the BMP2loxp/loxp mice to isolate the primary calvaria osteoblasts,cultured with Isopsoralen of the best dose for 48 h after the in vitro conditional gene knockout technology,and tested the gene expressions of Runx2 and Osx.And the alkaline Phosphatase(ALP)staining was also performed.Result Isopsoralen(10 μg·mL-1)can promote osteoblast proliferation obviously.From the real time RT-PCR analysis,Isopsoralen can enhance the BMP2 mRNA levels,the effect of 10 μg·mL-1 was the best,and 30 μg·mL-1 followed.In addition,we found that Isopsoralen(10 μg·mL-1)can enhance the Runx2 mRNA levels significantly.We also found that lower doses of Isopsoralen can enhance the Osx mRNA levels,the effect of 30 μg·mL-1 was the best,and 10 μg·mL-1 followed.From the Western blot analysis,low doses of Isopsoralen(10 μg·mL-1 and 30 μg·mL-1)can stimulate the expression of Runx2 protein.Besides,three doses of Isopsoralen can stimulate the expression of Osx protein,and the effect of 10 μg·mL-1 and 30 μg·mL-1 are better.Finally,the results of in vitro conditional gene knockout experiment showed that the overexpression of Runx2 and Osx genes in osteoblasts,as well as ALP staining,induced by Isopsoralen are BMP2 dependent.Conclusions In this study,we firstly demonstrate that Isopsoralen can stimulate osteoblast proliferation and differentiation by mediating BMP2/Runx2/Osx signaling pathway.

Objective: To investigate the effects of ginsenoside Rg3 on the formation of vasculogenic mimicry (VM) in gastric cancer cell line SGC7901 and its molecular mechanism. Methods: MTT assay was used to detect the effect of different concentrations of Rg3 on the proliferation of SGC7901 cells. SGC7901 cells were grouped as follows: BML-284 group, XAV-939 group, Rg3 group, Rg3+ BML-284 group and blank group. Transwell chamber assay was used to detect cell invasion and migration; the formation of VM was observed by tube formation assay; the secretion of MMP-9 and MMP2 was detected by ELISA; the mRNA expressions of GSK-3β and Wnt2B were detected by qPCR; the expression of β-Catenin protein in cells was analyzed by WB; and nuclear entry of β-Catenin was examined by Immunofluorescence. Results: Ginsenoside Rg3 inhibited the proliferation of SGC7901 cells in a time- and concentrationdependent manner; compared with the blank group, 40 mg/L Rg3 significantly inhibited the invasion and migration of SGC7901 cells (both P<0.05) and VM formation (P<0.05); in the meanwhile, the expressions of intracellular GSK-3β, Wnt2B mRNA and β-catenin protein, as well as the nuclear entry of β-catenin were significantly inhibited (all P<0.05). The invasion, migration and VM formation of SGC7901 cells in Rg3+BML-284 group were not significantly different from those in the blank group (all P>0.05). Conclusion: Rg3 can inhibit cell invasion, migration and VM formation in SGC7901 cells by inhibiting the activation of Wnt/β-Catenin pathway.

DNA damage response (DDR) is a highly conserved genome surveillance mechanism that preserves cell viability in the presence of chemotherapeutic drugs. Hence, small molecules that inhibit DDR are expected to enhance the anti-cancer effect of chemotherapy. Through a recent chemical library screen, we identified shikonin as an inhibitor that strongly suppressed DDR activated by various chemotherapeutic drugs in cancer cell lines derived from different origins. Mechanistically, shikonin inhibited the activation of ataxia telangiectasia mutated (ATM), and to a lesser degree ATM and RAD3-related (ATR), two master upstream regulators of the DDR signal, through inducing degradation of ATM and ATR-interacting protein (ATRIP), an obligate associating protein of ATR, respectively. As a result of DDR inhibition, shikonin enhanced the anti-cancer effect of chemotherapeutic drugs in both cell cultures and in mouse models. While degradation of ATRIP is proteasome dependent, that of ATM depends on caspase- and lysosome-, but not proteasome. Overexpression of ATM significantly mitigated DDR inhibition and cell death induced by shikonin and chemotherapeutic drugs. These novel findings reveal shikonin as a pan DDR inhibitor and identify ATM as a primary factor in determining the chemo sensitizing effect of shikonin. Our data may facilitate the development of shikonin and its derivatives as potential chemotherapy sensitizers through inducing ATM degradation.