Biometry ; Clinical Protocols ; Cryoultramicrotomy ; methods ; Diagnostic Techniques and Procedures ; Frozen Sections ; utilization ; Humans ; Orthopedics ; methods

Antigens, Surface ; blood ; Diagnosis, Differential ; Glutamate Carboxypeptidase II ; blood ; Humans ; Male ; Neoplasm Staging ; Prostate-Specific Antigen ; blood ; Prostatic Hyperplasia ; pathology ; Prostatic Neoplasms ; etiology ; metabolism ; pathology ; Racemases and Epimerases ; analysis

Objective To analyze the risk factors for postoperative stricture after endoscopic submucosal dissection (ESD) for early stage esophageal cancer.Methods The data of 362 patients with early esophageal cancer treated by ESD from January 2007 to February 2012 were reviewed to investigate the risk factors of postoperative stricture.Results Esophageal stricture after ESD occurred in 42 patients (11.6％)with a mean time from ESD to stricture of (58.5 ± 12.3) days.The rates of mild,median and severe stricture were 16.7％ (7/42),38.1％ (16/42) and 45.2％ (19/42),respectively.Multivariate analysis revealed that lesion range ＞ 3/4 esophageal circumference (odds ration [OR]:44.2 ; 95％ confidence interval [CI]:4.4-443.6) and tumor invasion beyond m2 (OR:14.2; 95 ％ CI:2.7-74.2) were independent risk factors.Stricture level was related to lesion's circumferential extension (relational coefficient (φ) =0.47,P ＜ 0.05) and tumor invasion depth (relational coefficient (φ) =0.647,P ＜ 0.05).Conclusion Circumferential extension and invasion depth of early esophageal cancer were independent risk factors for post-ESD esophageal stricture and related with the degree of stricture.

Objective To explore the reason of misdiagnosis and discuss the reoperation in thyroid carcinoma.Methods The data of 77 patients that had reoperation because of misdiagnosis were analyzed.Results The daignosis of all 77 cases were only based on pre-operative physical and uhrasound examination.The post-reoperative follow up (3～41 monthes):no case was found local recurrence.Conclusions The preoperative frozen section may avoid misdaignosis and the effect of reoperation for misdaignosed cases are satisfactory.

OBJECTIVETo investigate the effect of HER2/neu overexpression on the wild p53 gene expression, cell proliferation and sensitivity to gamma-irradiation via phosphatidylinositol 3-kinase (PI3K) pathway in human breast cancer cell MCF7.

METHODSLipofectin-mediated gene transfection method was used to transfer HER2/neu into MCF7 cells. Expression of HER2/neu, p53, Akt and p-Akt protein after PI3K pathway inhibitor LY294002 treatment was determined by Western blot. Cell proliferation and cell surviving fraction after gamma-irradiation treatment were assayed by MTT.

RESULTSEighteen of HER2/neu stably transfected MCF7 cell clones were established, one of them was HER2/neu overexpressing. HER2/neu overexpressing MCF7 cells showed higher p-Akt expression and lower p53 expression than those of parental MCF7 cells, which could be abrogated by LY294002. HER2/neu overexpressing MCF7 cells had higher proliferation rate and lower sensitivity to gamma-irradiation than those of parental MCF7 cells, which could be opposed by LY294002.

CONCLUSIONOverexpression of HER2/neu induces reduced expression of wild-type p53 protein, relatively high cell proliferation and low sensitivity to gamma-irradiation in breast cancer cell MCF7 by activating PI3K/Akt pathway, which may contribute to therapeutic resistance in some breast cancer patients with wild-type p53 gene status.

Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Cesium Radioisotopes ; Chromones ; pharmacology ; Female ; Gene Expression Regulation, Neoplastic ; Genes, erbB-2 ; Humans ; Morpholines ; pharmacology ; Phosphatidylinositol 3-Kinases ; antagonists & inhibitors ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Radiation Tolerance ; Receptor, ErbB-2 ; biosynthesis ; genetics ; Signal Transduction ; Transfection ; Tumor Suppressor Protein p53 ; metabolism

OBJECTIVETo identify the differentially expressed microRNAs (miRNAs) between esophageal squamous carcinoma (ESC) and adjacent non-tumorous tissue (NT).

METHODSThe expression levels of the miRNAs were detected in 3 fresh ESC and NT samples by hybridization with miRNAs microarray chip. Real-time quantitative RT-PCR was performed to confirm the results of the microarray analysis. The expressions of hsa-miR-126 and hsa-miR-518b in ESC were validated by real-time quantitative RT-PCR in another independent 15 matched samples.

RESULTSA total of 11 miRNAs exhibited differential expressions in ESC samples as compared to their expressions in the NT samples, including a 1 up-regulated miRNA and 10 down-regulated miRNAs. Compared with normal esophageal samples, the ESC tissues showed up-regulated hsa-miR-126 and down-regulated hsa-miR-518b expression.

CONCLUSIONhsa-miR-126 and hsa-miR-518b are differentially expressed in ESC, and they might play important roles in the carcinogenesis and progression of ESC.

Biomarkers, Tumor ; metabolism ; Carcinoma, Squamous Cell ; genetics ; pathology ; Esophageal Neoplasms ; genetics ; pathology ; Gene Expression Profiling ; methods ; Gene Expression Regulation, Neoplastic ; Humans ; MicroRNAs ; genetics ; Tumor Cells, Cultured

Ventral tegmental area (VTA) is an important relay station of signal transmission in the reward system. The plasticity of VTA dopaminergic neurons directly influences actions of other regions of the reward system. Studies concerning the plasticity of VTA dopaminergic neurons focus mainly on synaptic plasticity, while much less attention has been given to the plasticity of intrinsic excitability of the neurons. The aim of the present study was to investigate the effect of high-frequency stimulation (HFS) on the plasticity of excitability of VTA neuron. Whole-cell patch-clamping was performed on VTA dopaminergic neurons in midbrain slices bathed with PTX, AP-5 and CNQX, and HFS was introduced to cell soma. The result showed that, after HFS induction the pharmacologically isolated neurons showed increased input resistance and firing frequency, as well as decreased rheobase. Meanwhile, the steady-state whole-cell current decreased, and the hyperpolarization-activated current (I(h)) decreased. These results suggest that HFS on soma induces a long-term potentiation of excitability in VTA dopaminergic neurons, and the underlying mechanism involves the changes of membrane current.
Animals ; Dopaminergic Neurons ; cytology ; Long-Term Potentiation ; Patch-Clamp Techniques ; Ventral Tegmental Area ; physiology

OBJECTIVETo investigate the pollution of hexavalent chromium in the electroplating workplace and screen the biomarkers of chromium exposure.

MATERIALField occupational health investigation was conducted in 25 electroplating workplaces. 157 electroplating workers and 93 healthy unexposed controls were recruited. The epidemiological information was collected with face to face interview. Chromium in erythrocytes was determined by graphite furnace atomic absorption spectrophotometer.

RESULTSThe median of short-term exposure concentration of chromium in the air at electroplating workplace was 0.06 mg/m(3) (median) and ranging from 0.01 (detect limit) to 0.53 mg/m(3)). The median concentration of Cr (VI) in erythrocytes in electroplating workers was 4.41 (2.50 ∼ 5.29) µg/L, which was significantly higher than that in control subjects [1.54 (0.61 ∼ 2.98) µg/L, P < 0.01]. After stratified by potential confounding factors such as gender, age, smoking status and alcohol consumption, significant differences still existed between electroplating workers and control subjects, except for the subjects of age less than 30 years old (P = 0.11).

CONCLUSIONThere was hexavalent chromium pollution in electroplating workplace. Occupational hazards prevention measures should be taken to control the chromium pollution hazards.

Adult ; Air Pollutants, Occupational ; analysis ; Chromium ; blood ; Electroplating ; Environmental Monitoring ; Erythrocytes ; chemistry ; Female ; Humans ; Male ; Middle Aged ; Occupational Exposure ; analysis ; Workplace ; Young Adult

OBJECTIVETo investigate the role of the PI3K/Akt signaling pathway in hydrogen sulfide-induced alterations in expression of collagen I and collagen III in hepatic stellate cells.

METHODSIn vitro cultured rat hepatic stellate cells (HSC-T6) were treated with hydrogen sulfide, or left untreated for use as controls, and divided into groups for treatment with different inhibitors for the various factors involved in the PI3K/Akt signaling pathway. Reverse transcription-PCR was used to measure Collagen I and collagen III mRNA expression. Western blotting was used to detect the protein expression of PI3K and p-Akt, which are upstream proteins of the PI3K/Akt pathway.

RESULTSCompared with the untreated control cells, the hydrogen sulfide treated cells showed elevated expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F =14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt (F =23.522, P less than 0.05). Compared to the cells treated with hydrogen sulfide alone, the cells treated with the various inhibitors showed lower expression of collagen I mRNA (F =14.635, P less than 0.05), collagen III mRNA (F=14.620, P less than 0.05), PI3K protein (F =26.672, P less than 0.05), and p-Akt protein (F =23.522, P less than 0.05).

CONCLUSIONHydrogen sulfide can activate the PI3K/Akt pathway and elevate the expression of collagen I and collagen III in rat hepatic stellate cells.

Animals ; Cells, Cultured ; Collagen Type I ; metabolism ; Collagen Type III ; metabolism ; Hepatic Stellate Cells ; drug effects ; metabolism ; Hydrogen Sulfide ; pharmacology ; Phosphatidylinositol 3-Kinases ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; RNA, Messenger ; genetics ; Rats ; Signal Transduction

Objective To observe the protective effects of a mixture for protecting liver and supplementing stomach (保肝益胃合剂) on rat acute liver damage induced by carbon tetrachloride (CCl_4). Methods The model of rat acute liver damage was established by injection of CCl_4 2 ml/kg into the abdominal cavity.The rat models were treated respectively by the mixture for protecting liver and supplementing stomach 30 g?kg~(-1)?d~(-1),the polyene phosphatide acid radical choline capsule [Yi Shanfu (易善复), 180 mg?kg~(-1)?d~(-1)],the glycyrrhizic acid diaminogen capsule [Gan Lixin (甘利欣),30 mg?kg~(-1)?d~(-1)] infused into the stomach.The activities of serum alanine transaminase (ALT) and aspartate transaminase (AST) were detected.In the mean time,the liver pathological changes were observed,the degree of liver cell necrosis was evaluated,and the rat mortality was noted in various groups of treatment.Results The values of ALT,AST and the score of liver cell necrosis in the group treated with the mixture for protecting liver and supplementing stomach [(1.168?1.066) kU/L,(1.845?2.212) kU/L,(0.56?0.53) score] were significantly lower than those in the model group [(4.982?3.502) kU/L,(7.030?3.616) kU/L, (1.38?0.92) scores],and all the differences being statistically significant (all P