The paper reported a case of brachial artery ligation treatment of arteriovenous graft infection with arteriovenous graft exposure and bleeding. Based on the experience of vascular access center and the review of relevant literature, the causes and treatment options of this complication were analyzed, and the feasibility and safety of brachial artery ligation were elaborated for the treatment of this complication, to provide references for clinical diagnosis and treatment.

Objective:To investigate the protective effect of overexpressed tripartite motif containing (TRIM27) on severe acute pancreatitis (SAP) in mice and its possible mechanism.Methods:Twenty-four mice were randomly divided into the sham operation + control virus group (AAV-GFP group), sham operation + overexpression of TRIM27 group (AAV-TRIM27 group), SAP + control virus group (SAP+AAV-GFP group), SAP + overexpression of TRIM27 group (SAP + AAV-TRIM27 group), with 6 mice in each group. SAP model of mice was established by intraperitoneal injection of L-arginine (4 mg/kg). The sham operation group was injected with equal volume of normal saline, and the virus group was injected with control or TRIM27 overexpression adeno-associated virus (2×10 11 μg/ per mice). The serum and pancreatic tissue samples were collected 72 h after modeling. The levels of serum amylase, lipase, tumor necrosis factor α (TNF-α), interleukin-1b (IL-1b), IL-6, macrophage chemoattractant protein-1 (MCP-1) and the expression of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) in pancreatic tissue were detected by enzyme-linked immunosorbent assay. Hematoxylin eosin staining was used to observe the pathological damage of pancreatic tissue. The expressions of myeloperoxidase (MPO) and Ly6g positive inflammatory cells in mouse pancreas were observed by immunohistochemistry. The expression of p-p65, p65, p-ASK1, ASK1, p-JNK, JNK, p-p38 and p38 in pancreatic tissue were detected by Western blot. Results:The expression of TRIM27 in pancreatic of mice was significantly down regulated after SAP ( P<0.05); after overexpression of TRIM27 by adeno-associated virus, the expression of TRIM27 in mouse pancreas was significantly up-regulated ( P<0.05). There was no significant difference in the indexes of mice between the AAV-GFP group and AAV-TRIM27 group ( P>0.05). Compared with the SAP + AAV-GFP group, the levels of serum amylase, lipase, TNF-α, IL-1b, IL-6 and MCP-1 in mice of the SAP + AAV-TRIM27 group were significantly decreased, MDA in pancreatic tissue was decreased, SOD and GSH were increased, MPO and Ly6g inflammatory cells were significantly decreased, and p-p65, p-ASK1, p-JNK, and p-p38 protein expression were down regulated. Conclusions:Overexpression of TRIM27 alleviates SAP in mice by inhibiting inflammatory response and oxidative stress, and its mechanism may be through inhibiting NFκB/MAPK signaling pathway.

Objective:To provide evidence for optimizing the screening strategy for gastric cancer (GC), we evaluated the risk of incident GC for individuals with different precancerous gastric lesions in a prospective cohort study.Methods:Based on the National Upper Gastrointestinal Cancer Early Detection Program launched in Linqu, Shandong, a high-risk area of gastric cancer in China, we included a total of 14 087 subjects diagnosed with different gastric lesions stages by endoscopic screening from 2012 to 2018. Study subjects were prospectively followed up until December 31, 2019. The incidence of GC during the follow-up was ascertained by repeated endoscopic examinations, cancer, death registry reports, and active follow-up of study subjects and was confirmed by reviewing medical records extracted from the hospital information management system. The Poisson regression model was applied to calculate the relative risk ( RR) and 95% CI for GC occurrence among subjects with different gastric lesions. Results:Among 14 087 subjects with different gastric lesions as determined by their first endoscopic examination in 2012-2018, 7 608 (54.00%) had a global diagnosis of superficial gastritis (SG), 2 848 (20.22%) had chronic atrophic gastritis (CAG), 3 103 (22.03%) had intestinal metaplasia (IM), and 520 (3.69%) had low-grade intestinal neoplasia (LGIN). During the follow-up, 109 subjects were diagnosed with GC, including 63 with high-grade intestinal neoplasia (HGIN) and 46 with invasive GC. Compared to subjects having normal gastric mucosa or SG, those with CAG ( RR=3.85, 95% CI: 2.04-7.28), IM ( RR=5.18, 95% CI: 2.79-9.60), and LGIN ( RR=19.08, 95% CI: 9.97-36.53) had significantly increased risk of progression to GC. Individuals with these gastric lesions had an elevated risk of developing HGIN and invasive GC. For subjects with LGIN, the RR was 22.96 (95% CI: 9.71-54.27) for developing HGIN and 14.64 (95% CI: 5.37-39.93) for developing invasive GC. Subgroup analyses found that all age group subjects with LGIN diagnosed during the initial endoscopic examination had a significantly increased risk of developing the GC. Conclusions:Our large-scale prospective study on a high-risk area of GC showed that most residents aged 40-69 years had gastric lesions of different stages. Subjects with more advanced gastric lesions had a significantly increased risk of progression to GC.

Objective:To investigate the predictive value of dynamic platelet and hemagglutination-related parameters in patients with acute pancreatitis (AP).Methods:The patients admitted to the Department of Emergency Surgery in the First Affiliated Hospital of Zhengzhou University from January 2020 to December 2020 were analyzed. According to the inclusion criteria and exclusion criteria, patients with AP were retrospectively enrolled. According to the Chinese Guidelines for the Diagnosis and Treatment of Acute Pancreatitis (Shenyang, 2019), the patients were divided into two groups: severe acute pancreatitis (SAP group) and non-severe acute pancreatitis (non-SAP group) [including mild acute pancreatitis (MAP) and moderate severe acute pancreatitis (MSAP)]. A normal distribution of the maximum and mean aggregation rates of dynamic platelets (arachiidonic acid), plateletcrit (PCT) and bedside index for severity in acute pancreatitis (BISAP) scores and other measurement data were tested by t test, while measurement data of prothrombin time (PT), fibrinogen (FIB) and D-dimer that did not conform to normal distribution were tested by Mann-Whitney U test. χ 2 test was used for the counting data such as sex, age and etiology of patients in the two groups. The prognostic value of statistically significant indicators for non-SAP group and SAP group was further analyzed by receiver operating characteristic (ROC) curve. Results:A total of 146 patients with AP were enrolled, including 50 patients in SAP group and 96 in non-SAP group. The maximum and average aggregation rates of dynamic platelet (aracidonic acid) in the SAP group were (71.76±17.62) % and (67.91±18.10) %, PT (12.02±1.33) s, FIB (4.76±2.08) g/L, D-dimer (3.75±6.04) μg/L, PCT (0.23±0.08) %, and BISAP scores (1.42±1.18), which were all significantly higher than those in the non-SAP group [the maximum and average aggregation rates of dynamic platelet (arachiidonic acid) (46.65±20.11) % and (42.50±20.71) %, PT (11.50±1.51) s and FIB (3.91±1.48) g/L, D-dimer (1.00±1.37) μg/L, PCT (0.19±0.06) %, BISAP scores (0.45±0.66)] (all P<0.05). According to area under the ROC curve, the maximum and average aggregation rates of dynamic platelets (arachiidonic acid) in serum of patients with SAP were 0.83 and 0.82, respectively, and the sensitivities were 0.56 and 0.68, respectively. The specificity was 0.99 and 0.81, respectively, which was better than PT, FIB, D-dimer, PCT and BISAP scores in predicting the severity of AP. Conclusions:The maximum and average aggregation rates of dynamic platelets (arachidonic acid), PT, FIB, D-dimer, PCT and BISAP scores can be used as predictors of the severity of acute pancreatitis. The maximum and average aggregation rates of dynamic platelets (arachiidonic acid) were the best in predicting the severity of AP.

Objective To investigate the growth inhibition of human osteosareoma cell line(MG-63) intervened by Hydralazine and 5'-aza-2'-deoxycytidine (5-Aza-CdR),and the effect on the mRNA expression of gene WW domain-containing oxidoreductase (WWOX).Methods Certain volume of 5 × 104/ml of human osteosarcoma cell line MG-63 in logarithmic growth phase were added into 96-well plate.There were Hydralazine group (drug concentration,0.1,1.0,10 μmol/L),5-Aza-CdR group (drug concentration,5,10,20 μmol/L),Hydralazine combined with 5-Aza-CdR group (drug concentration,0.1 μmo/L + 5 μmol/L,1.0 μmol/L + 10 μmol/L,10 μmol/L + 20 μmol/L) and control group (culture medium).Methyl thiazol tetrazolium(MTT) colorimetric methods were used to test the growth inhibition of MG-63 cells intervened by different concentrations of Hydralazine and 5'-aza -2'-deoxycytidine (5-Aza-CdR).Flow cytometry AnnexinV-FITC/PI methods were used to assay the effects of Hydralazine and 5-Aza-CdR inducing apoptosis in osteosarcoma cells in vitro.Real-time polymerase chain reaction (Real-Time PCR)methods were used to detect amplification of WWOX mRNA induced by Hydralazine combined with 5-Aza-CdR or alone.Western-blotting methods were used to examine the expression of WWOX in MG-63 cells.Results Hydralazine and 5-Aza-CdR effectively inhibited the growth of MG-63 cells in a concentration and time-dependent manner.Combined effect was more obvious.Further more the expression levels of WWOX mRNA and protein were increased significantly in combined groups as compared with other groups.Conclusion Hydralazine and 5-Aza-CdR could effectively inhibit the proliferation of MG-63 cells and induce apoptosis which is concurrent with the promotion of the expression of WWOX.The mechanism may be that Hydralazine/5-Aza-CdR effectively cause the demethylated of WWOX gene CpG-rich promoter regions,leading to the high expression of WWOX and inhibit the growth of MG-63 cells.The use of hydralazine in the treatment of osteosarcoma is worthy of further investigation.

BACKGROUND:Nowadays, growth factors are commonly used to induce bone marrow mesenchymal stem cells. However, this is a high-cost method with a great amount of growth factors. In addition, the chondrogenic potential of bone marrow mesenchymal stem cells wil decrease significantly with increasing times of culture. OBJECTIVE:To observe the directed differentiation of bone marrow mesenchymal stem cells co-cultured with human synovial fluid. METHODS:Human bone marrow mesenchymal stem cells were isolated and cultured by adherence screening method. The synovial fluid of the knee was aspirated from healthy volunteers by aseptic operation. Passage 3 human bone marrow mesenchymal stem cells were co-cultured with the fol owing media:synovial fluid+complete medium;synovial fluid+bone marrow mesenchymal stem cells+complete medium;bone marrow mesenchymal stem cells+complete medium. The morphology and growth of the cells were observed under an inverted microscope every day. At days 7, 14 and 21 of induction, toluidine blue staining and immunocytochemical staining were performed.
RESULTS AND CONCLUSION:After co-culture with human synovial fluid, human bone marrow mesenchymal stem cells proliferated slowly, and varied from fusiform to oval or polygonal;toluidine blue and col agen II staining were positive. These findings indicate that the synovial fluid has a positive role in the chondrogenic differentiation of bone marrow mesenchymal stem cells. The synovial fluid may contain substances that promote the chondrogenic differentiation of bone marrow mesenchymal stem cells.

Aim To investigate apoptosis induced by 3,3'-diethyl-9-methylthia-carbocyanine iodide(DMTCCI) , an inhibitor of DNA primase found in our previous study, and the mechanism of DMTCCI in human myelogenous leukemia HL-60 cells. Methods HL-60 cells were cultured in RPMI-1640 medium and treated with different concentrations of DMTCCI. MTT assay was used to detect growth inhibition.Flow cytometry and DNA ladders were used to detect apoptosis. Western blotting was used to observe the expression of survivin, Bcl-xL, Bad, Bax, Bcl-2, caspase-9, caspase-3, caspase-6, PARP, DFF45 and lamin B protein. Caspase-3 activity was measured by ApoAlert Caspase-3 Assay Kit. Results DMTCCI inhibited proliferation of human leukemia HL-60 cells with IC50 value of 0. 24 μmol · L-1. The results of flow cytometry and DNA ladders showed that DMTCCI could induce apoptosis of HL-60 cells. The expression levels of protein survivin and Bcl-xL were down-regulated, Bad and Bax were up-regulated,while Bcl-2 protein had no change in response to DMTCCI treatment in HL-60 cells. Treatment of HL-60cells with DMTCCI induced the proteolytic cleavage of caspase-9, caspase-3, caspase-6, PARP, DFF45and lamin B protein. Caspase-3 activity apparently increased at 3 h and reached a peak at 12 h after exposure to 1 μmol · L-1 of DMTCCI in HL-60 cells. Conclusion DMTCCI inhibited proliferation and induced apoptosis of human leukemia HL-60 cells. Bcl-2 family proteins, survivin and caspases family proteins might playa role in the apoptosis process induced by DMTCCI.

Aim The aim of this study is to determine effect of ST2325 on HER2/neu tyrosine kinase signal pathway and cell cycle in breast cancer BT474 cells. Methods Protein expression was detected with immunoblot analysis. Cell cycle distribution was examined using flow cytometry.Results ST2325 inhibited tyrosine phosphorylation of HER-2/neu in a dose-dependent manner with half maximal inhibition occurring at a concentration of 8.7 ?mol?L -1 without reduced HER-2/neu receptor protein expression. Activation of MAPK and AKT, downstream molecules of HER-2/neu-mediated signal transduction pathway was inhibited following exposure to ST2325. After BT474 cells were treated with different concentrations of ST2325 for 24 h, the results of flow cytometry analysis showed cell cycle arrest in G 1 phase. Western blot assay showed up-regulation of p27 protein expression and decrease of hyperphosphorylated Rb and cyclin D1 protein expression.Conclusions ST2325 inhibits HER2 tyrosine kinase phosphorylation and induces G 1 arrest in BT474 cells. Cell cycle arrest in G 1 is associated with p27 up-regulation, decrease of cyclin D1 protein and hyperphosphorylated Rb.

Cyclins, CDKs and CKIs in cell cycle play important roles in maintaining cell cycle and regulation of the process cell cycle. Many endogenous and extraneous inhibitors have effects on cell cycle by modulating functions of cyclins, CDKs and CKIs. Several highlighted points in the researches of cell cycle and related proteins, inhibitors were reviewed, including the latest advances on their applications in cancer therapy.