Esophageal cancer is a unique malignant disease in China. A fundamental difference exists between the Chinese population and the western population on esophageal cancer in terms of epidemiology, histogenesis, and carcinogenic risk factors. Therefore, ap-plying the western academic achievements to Chinese is difficult. Thus, Chinese scientists have the responsibility to conquer esopha-geal cancer in China. This article reviews the progress of esophageal cancer focused on the molecular mechanism for interactions of ge-netic and environmental risk factors and human esophageal multistage carcinogenesis.

Objective To investigate the effect of a selective cyclooxygenase-2 inhibitor on tumor metastasis,tumor angiogenesis,and vascular endothelial growth factor(VEGF)of orthotopic implanted human gastric carcinoma in non.obesity diabetes(NOD)severe combined immune deficiency(SCID)mice.Methods Human gastric cancer SGC-7901 tissues were orthotopically implanted into the stomach of the NOD SCID mice.Forty mice were randomly divided into two groups which received either intravenous injections of 0.9% Nacl solution (0.9% NaCL solution group)or 50mg/kg.d Nimesulide(Nimesulide group)twice weekly for two weeks.Mice were sacrificed in the 5th week after implantation.Tissues from stomach and other organs were obtained for histopathologieal evaluation.The intratumoral microvessel density(MVD)and VEGF protein expression in tumor were evaluated by immunochemical method.Results The tumor metastasis rates were 18/20 in 0.9% Nacl solution group and 5/20 in Nimesulide group(P＜0.05).MVD was 9.5±2.9 in 0.9% NaCl solution group and 3.9±2.1 in Nimesulide group(P＜0.01).VEGF protein expression was 90% in 0.9%NaCl solution group and 25% in Nimesulide group(P＜0.01).Conclusions Nimesulide can inhibit the metastasis or gastric cancer through inhibiting tumor VEGF expression and tumor angiogenesis with no obvious anticoagulant activity.

AIM:To examine the expression profiles of both genes and proteins in hippocampus of rats with temporal lobe epilepsy(TLE)for revealing the molecular mechanisms of TLE and looking for the candidate targets and new therapeutic approaches in clinical practice.METHODS:Rat temporal lobe epilepsy was induced by administration of lithium chloride and pilocarpine(LiCl-PILO).The expression spectra of genes and proteins were constructed through the techniques of cDNA microarray,two-dimensional(2D)electrophoresis and Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry(MALDI-TOF MS).Subsequently,the differentially expressed genes and proteins were identified and analyzed.RESULTS:There were 192 genes of differential expression observed in hippocampal tissues of LiCl-PILO-induced temporal lobe epilepsy,and 159 genes have been registered in Genbank database,in which 84 genes were up-regulated while 75 genes were down-regulated.78 protein spots of differential display were screened out,in which 31 proteins were detected to be down-regulated and 47 were up-regulated.Finally,5 proteins were identified.CONCLUSION:These genes and proteins found in our study may play pivotal roles in the pathogenic mechanisms of epilepsy and may promise new therapeutic targets for refractory epilepsy in the future.

Objective To use thrombelastography (TEG) and conventional coagulation tests (CCTs) to diagnose disseminated intravascular coagulation (DIC) and find a better diagnostic method.Methods Patients with potential DIC factors,DIC clinical manifestation or DIC patients suspected by laboratory tests were included after their admission into our hospital.TEGs and CCTs were detected,respectively.DIC score was evaluated.The single factor logistic regression was used to evaluate the correlation between TEG and CCTs as well as the diagnostic accuracy.Results The international normalized ratio (INR) in CCTs of the DIC patients were significantly higher,the reaction rime (R),clot formation time (K),angle rate of clot formation (α),maximum amplitude (MA),and composite index (CI) figures in TEG were significantly increased (P ＜ 0.05).The sensitivity and specificity of TEG were 82.4％,and 62.2％,which were significantly higher than 21.6％ and 47.2％ in CCTs (P ＜ 0.05).Single factor logistic regression results show that odd ratio (OR) in prothrombin time (PT) and INR of CCTs was 1.23 and 1.27,respectively.The OR in R,K,α,MA,and CI of TEG was 5.13,6.14,1.37,1.25,and 3.02,respectively.Conclusions Compared to CCTs,TEG is more indicative of the conditions of DIC patients and it might be a better way to predict the DIC risks,which is of greater value in clinical diagnosis.

Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00%(6/30), 24.24%(8/33), and 21.05%(16/76), respectively;χ2=0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells. Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

Objective To investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC). Methods The expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting. Results All the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00%(6/30), 24.24%(8/33), and 21.05%(16/76), respectively;χ2=0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells. Conclusion Aberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

OBJECTIVETo investigate the role of triggering receptors expressed on myeloid cells-1 (TREM-1) in the oncogenesis and progression of hepatocellular carcinoma (HCC).

METHODSThe expression and localization of TREM-1 were detected by immunohistochemistry in 76 specimens of HCC, 33 specimens of liver cirrhosis, 30 specimens of hepatitis and 20 normal liver tissues. The association between TREM-1 expression and the clinicopathologic parameters of HCC was analyzed. Human normal hepatic cell line LO2 and HCC cell line SMMC-7721 were examined for TREM-1 expression pattern using RT-PCR and Western blotting.

RESULTSAll the normal liver samples showed negative expression of TREM-1 protein, which was significantly up-regulated in the other 3 tissues. The positivity rates of TREM-1 expression were not significantly different between hepatitis, cirrhosis and HCC tissues [20.00% (6/30), 24.24% (8/33), and 21.05% (16/76), respectively; Χ² =0.195, P=0.907]. Different from chronic hepatitis and liver cirrhosis tissues where TREM-1 expression was located mainly in the nucleus and occasionally in the cytoplasm of the hepatocytes, HCC tissues showed a cellular localization of TREM-1 protein almost exclusively in the cytoplasm. In HCC, TREM-1 expression was negatively correlated with the histological grade of the tumor (r=-0.261, P=0.023) but not related with the patients' age, gender, tumor size, clinical stage, pre-existing hepatitis and cirrhosis, lymph node metastasis, or intrahepatic vascular embolism (all P>0.05). In the in vitro experiments, low levels of TREM-1 mRNA and protein expressions were detected in LO2 cells line, but their expressions were markedly up-regulated in SMMC-7721 cells.

CONCLUSIONAberrant enhancement of the expression and cytoplasmic accumulation of TREM-1 may correlate closely with the oncogenesis and progression of HCC.

Carcinogenesis ; Carcinoma, Hepatocellular ; metabolism ; Cell Line ; Cell Line, Tumor ; Cell Nucleus ; Cytoplasm ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Hepatocytes ; metabolism ; Humans ; Immunohistochemistry ; Liver Cirrhosis ; Liver Neoplasms ; metabolism ; Membrane Glycoproteins ; metabolism ; Receptors, Immunologic ; metabolism ; Triggering Receptor Expressed on Myeloid Cells-1 ; Up-Regulation

Objective:To explore the differences in bacterial community structure between proximal colon cancer (PC), distal colon cancer (DC), and rectal cancer (RC), and the values of featured microbiota in differentiating PC with tumor markers.Methods:This case-control study enrolled 85 newly diagnosed colorectal cancer patients, including 22 PC, 15 DC and 48 RC patients, and 8 colorectal adenoma patients from May 2019 to July 2022 at the Department of General Surgery, Anyang Oncology Hospital. The blood and fecal samples were collected before surgery and then subjected to biochemical tests for tumor markers and 16S rDNA tests, respectively. SPSS (27.0.1) was applied to perform the t-test, one-way ANOVA, Mann-Whitney U test, Kruskal-Wallis H test, and Chi-Squared Test. Also, the receiver operating characteristic curve (ROC) was plotted on tumor markers and/or f_Bacteroidaceae with SPSS software .Results:All groups had significant differences in the CA125 ( F=3.543, P<0.05), CA72-4 ( F=3.596, P<0.05), and serum tumor-associated materials (TAM) levels ( F=5.787, P<0.01). In PC group, the levels of CA125 [PC vs RC, (36.84±6.30) kU/L vs (12.73±4.21) kU/L, P<0.01] and CA72-4 [PC vs RC, (45.56±10.86) kU/L vs (3.30±7.63) kU/L, P<0.01] were significantly higher than that of the RC group, while the level of TAM was remarkably elevated in PC group than in RC group [PC vs RC, (124.84±5.19) U/ml vs (102.44±3.63) U/ml, P<0.001] and CRA group [PC vs CRA, (124.84±5.19) U/ml vs (95.39±8.42) U/ml, P<0.01]. The LEfSe analysis showed that the featured microbiota in the PC group included f_Bacteroidaceae, f_Neisseriaceae, f_Clostridiaceae_1, f_Spirochaetaceae, and so on. The largest area under the ROC belonged to the combination of TAM and f_Bacteroidaceae, which reached 0.845 (95% CI 0.747-0.944), with sensitivity being 0.857 and specificity being 0.815. Conclusions:There is heterogeneity in gut microbiota composition among PC, DC, RC, and CRA. The combination of gut microbiota and tumor biomarkers demonstrated good differentiating effects in proximal colon cancers.

Chiari malformation type 1 (CM1) is a rare condition where agreed classification and treatment are still missing. In 2019, 34 international experts from Europe achieved a consensus on the definition, diagnosis, and treatment of CM1 in children, aiming to guide the clinical diagnosis and treatment of CM1 in children. Now the consensus is interpreted based on recent international research achievements, aiming to provide references for accurate clinical assessment and individualized treatment of CM1 in children.

Chiari malformation (CM) is the most common cause of syringomyelia, where agreed criterions on classification and treatment are still missing. In 2019, 29 international experts from Europe achieved a consensus on the definition, classification, diagnosis and treatment of CM and syringomyelia in adults, aiming to guide the clinical diagnosis and treatment of these diseases. Now the consensus is interpreted based on recently published literature at home and abroad, aiming to provide references for standardized diagnosis and treatment of CM and syringomyelia in adults.