Objective To investigate the association between expression of the epithelial?to?mesenchymal transition(EMT)biomarkers and the malignant progression of gastric cancer in primary tumors and metastases and their possible correlation with progression of gastric cancer(GC). Methods The EMT biomarkers including E?cadherin,β?catenin,N?cadherin,Snail and TGF?β1 were detected by immunohistochemical method for 145 cases of gastric cancer(GC),25 cases of abnormal hyperplasia,13 cases of intestinal metaplasia,42 cases of lymph node metastasis and 40 cases of normal gastric mucosa tissues. Results Positive rates of TGF?β1,Snail,E?cadherin,β?catenin and N?cadherin were 73.5%,65.5%, 14.5%,53.1%and 35.9%,respectively,in gastric cancer tissues and 100%,100%,0%,27.5%and 2.5%,respectively,in normal gastric tissues, with a significant difference between the two groups(P<0.05). The decreased expression of E?cadherin andβ?catenin and the increased expression of TGF?β1 were related to the depth of invasion of gastric cancer(P<0.05). The expression of E?cadherin was correlated positively with the expres?sion ofβ?catenin,but negatively with the expression of TGF?β1. Whereas,the expression of N?cadherin was correlated positively with the expression of TGF?β1(P<0.05). The expression of E?cadherin andβ?catenin in lymph node metastasis was significantly higher than that in gastric cancer tis?sues,while the expression of TGF?β1 was lower than in gastric cancer tissues(P<0.05). Conclusion The increased expression of TGF?β1 and Snail and the decreased expression of E?cadherin,β?catenin,and N?cadherin are involved in the processes of invasion and metastasis of GC. The transformation of E?cadherin to N?cadherin and the expression of TGF?β1 may play an important role in the development of GC. In lymph node me?tastasis,the phenomenon of mesenchymal?to?epithelial transition(MET)occurs.

Objective:To explore the predictive value of pre-treatment platelet-to-albumin ratio (PAR) in short-term prognosis of endoscopic treatment for cirrhosis with esophageal and gastric variceal bleeding(EGVB).Methods:By retrospective analysis method, the clinical data of 195 cirrhotic patients with EVGB from January 2019 to April 2022 treatment at Bengbu First People′s Hospital were collected and analyzed. The PAR was calculated according to platelet count and albumin. The independent risk factors that affecting 6-week rebleeding and death were analyzed by univariate and multivariate Cox regression, the receiver operating characteristic (ROC) curve was drawn to evaluate the predictive value of PAR for rebleeding and death, and Kaplan-Meier survival analysis was used to evaluate the rebleeding rate and survival rate of patients with different PAR ratios.Results:Among 195 patients, 36 patients were rebleeding and 159 patients were non-rebleeding within 6 weeks; while 15 cases died and 180 cases survived. The platelet count, PAR in the rebleeding group were lower than those in the non-rebleeding group, the direct bilirubin, triglyceride, alanine transaminase, prothrombin time and mortality in the rebleeding group were higher than those in the non-rebleeding group: 74.0(66.5, 88.8) × 10 9/L vs. 98.0(85.0, 111.0)×10 9/L, 2.48(2.18, 2.78) vs. 3.35(2.81, 4.04), 18.5(14.0, 23.8) μmol/L vs. 16.0(11.0, 20.0) μmol/L, (4.73 ± 2.52) mmol/L vs. (3.94 ± 1.65) mmol/L, 36.0(27.0, 46.0)U/L vs. 21.0(13.3, 33.0)U/L, (14.78 ± 1.63) s vs. (13.47 ± 0.87) s, 36.11%(13/36) vs. 1.26%(2/159), there were statistical differences ( P<0.05). Cox multivariate regression showed that PAR, alanine transaminase were the independent risk factors for the rebleeding ( P<0.05), PAR was the independent risk factor for the death within 6 weeks ( P<0.05). The area under the curve (AUC) of PAR for predicting 6-week rebleeding and death was 0.876, 0.776, the cut-off was 2.94, 2.71, the specificity was 69.8%, 72.2%, the sensitivity was 94.4%, 73.3%, respectively. According to the cut-off of PAR to predict rebleeding, the 6-week rebleeding rate in the PAR≤2.94 group was higher than that in the PAR>2.94 group ( χ2 = 36.88, P<0.01). According to the cut-off of PAR to predict death, the 6-week mortality rate in the PAR≤2.71 group was higher than in the PAR>2.71 group ( χ2 = 16.44, P<0.01). Conclusions:PAR can be used as a predictor for rebleeding and death within 6 weeks of EGVB in cirrhotic patients.

OBJECTIVETo study biological effect of recombinant human erythropoietin (RhEPO) on the expression of oligodendrocyte in the neuron glia antigen 2(NG2), Nogo receptor-interacting protein 1(LINGO-1), myelin basic protein (MBP) and myelin associated glycoprotein (MAG), and to explore the protective mechanism of RhEPO for oligodendrocyte after cerebral infarction.

METHODSExperimental rats were randomly divided into the treatment group (RhEPO at a dose of 3 000 U/kg) or saline control group. Both groups received intraperitoneal injection of RhEPO after cerebral ischemia in 30 min, 3 h, 6 h, 12 h and 24 h, which was administered daily for 7 days. The modified neurological severity score (mNSS) and histology were analyzed, and immunohistochemistry was used to detect the protein expression of NG2, MAG, MBP and LINGO-1.

RESULTSThe overall mNSS of RhEPO treatment group significantly decreased compared with the saline control group on the seventh day after cerebral infarction (P<0.05). Such treatment effect was more obvious in the treatment group at 30 min and 3 h (P<0.01). Compared with the saline control group, the numbers of NG2 positive cells increased in RhEPO treatment group. In contrast, the expression of LINGO-1 protein significantly decreased (P<0.05), with a dramatic decrease observed at 30 min and 3 h (P<0.01). However, the expression of MBP protein decreased more significantly in saline control group, while the level of the MAG protein expression increased. The differences were statistically significant (P<0.05), especially at 30 min (P<0.01).

CONCLUSIONSAfter cerebral ischemia, RhEPO promotes the proliferation of NG2 positive cells, and inhibits the expression of LINGO-1 and MAG proteins. RhEPO improves the proliferation and differentiation of oligodendrocyte precursor cells, which in turn protects neuronal function, particularly at the early phase of ischemia.