Objective To find the reasonable treatment strategy by analyzing the failure pattern and survival rates of radical resection of gastric cancer.Methods Data were collected from 110 patients with radical resection and adjuvant treatment of gastric cancer,counted up the number of cases that failure in different ways.The survival rate after operation was calculated by Kaplan-Meier.The chi-square test was used to find the differences in survival rates between different differentiation,location and gender.Results 1,3,5-year survival rates of 110 cases were 83.64％ (92/110),46.36％ (51/110),35.45％ (39/110),respectively.Malignant ascites was the main failure type for postoperative of gastric cancer,approximately accounting for 41.51％ (22/53),abdominal lymph node metastasis accounting for 30.19％ (16/53),anastomotic recurrence accounting for 13.21％ (7/53),abdominal implantation and mesenteric metastasis accounting for 9.43％ (5/53),organ metastasis accounting for 5.66％ (3/53).The 5-year local failure rate of concurrent chemoradiotherapy group was a little lower than that in adjuvant chemotherapy alone group (15.00％ ∶22.22％).The 1-year survival rates of adjuvant chemotherapy alone and concurrent chemoradiotherapy group were 84.44％ and 80.00％ respectively,with no significant difference (x2 =0.236,P =0.627).However,the 3,5-year survival rates of the two groups were 66.67％ vs 40.00％ and 53.33％ vs 20.00％ respectively,with statistically significant differences (x2 =4.930,P =0.026 ; x2 =7.294,P =0.007).Conclusion Peritoneal metastasis is the most common failure pattern for the patients with gastric cancer who received radical operation and adjuvant treatment.The relapse rate of concurrent chemoradiotherapy group is lower than that in adjuvant chemotherapy alone group,but the overall survival rate is similar.

Objective To explore the related factors influencing the prognosis of children with Tourette syndrome ( TS) . Methods We collected 420 outpatient cases of TS children in the department of pediatrics of Guangdong Provincial Hospital of Traditional Chinese Medicine from January of 2007 to October of 2010 as the research objects. Using the unified survey questionnaire, we observed the influencing factors of TS prognosis such as sex, onset age, mother’s pregnancy situation, the perinatal period, partiality for food intake, family relationship, the first symptom, the severity of disease, underlying diseases, comorbidities ( such as attention deficit hyperactivity disorder, anxiety disorder, and obsessive-compulsive disorder) , family history of psychiatric or neurological diseases, trace elements levels, electroencephalogram (EEG), antistreptolycin O (ASO), course of disease, and maintenance treatment. The related factors of prognosis was analyzed with single factor and multiple factors Logistic regression analysis. Results Among the 420 cases of TS children, 396 cases were included into the final analysis, 24 were lost and the follow-up lost rate was 5.7%. The remission rate of TS was 78.3%, and the uncured rate was 21.7%. The results of preliminary screening of the influencing factors by single factor Logistic analysis showed that the related influencing factors for TS prognosis were 12, and they were course of diseases, abnormal birth history, father’s education level, mother’s education level, upbringing methods, family history of psychiatric or neurological diseases, underlying disease history, comorbidities history, abnormal ASO, the severity of disease, the frequency of disease relapse, and the medication history of western medicine (P<0.05) . And then the obtained 12 factors were analyzed by the multiple fac tors Lo gistic regression analysis, the results showed that upbringing methods, comorbidities history, the severity of disease, and the frequency of disease relapse were correlated with TS prognosis ( P < 0.05) . Conclusion TS children will have poor prognosis when their parents spoil, indiscipline, beat and scold, and dictate them, or when the children have severe illness state, frequent recurrence of the disease, and the history of comorbidities ( atten tion deficit hyperactivity disorder, anxiety disorder, obsessive-compulsive disorder, etc.) .

Objective To detect NRAS gene mutations in patients with acral melanoma, and to analyze their relationship with the prognosis of acral melanoma. Methods Clinical and pathological data were collected from 55 patients with pathologically diagnosed acral melanoma. DNA was extracted from paraffin?embedded specimens from lesions of the 55 patients and 15 patients with nevus. PCR and direct DNA sequencing were performed to detect NRAS gene mutations. Univariate and multivariate analyses were performed using the Cox′s proportional hazards regression model. Results Of the 55 patients, 6(10.9%)carried the Q61R mutation in codon 61 of the NRAS gene. No mutations were found in exon 1 or 2 of the NRAS gene in any of these paraffin?embedded specimens, and none of the pigmented nevus specimens harbored NRAS gene mutations. Of the 6 patients carrying NRAS gene mutations, 4 had lymph node metastasis. Multivariate Cox regression analysis showed that independent factors of poor prognosis included advanced clinical stage(RR = 2.54, 95% CI: 1.062- 6.066, P < 0.05), not receiving surgical resection(RR = 2.98, 95% CI:1.316- 3.525, P < 0.05), and carrying NRAS gene mutations (RR = 2.73, 95% CI: 0.932- 3.257, P < 0.05). Conclusions NRAS gene mutations may be associated with lymph node metastasis in patients with acral melanoma. The prognosis of acral melanoma may be associated with clinical staging, treatment strategies and NRAS gene mutations. Additionally, NRAS gene mutations may serve as a new index for predicting prognosis of acral melanoma.

Objective To detect the expression of human telomerase reverse transcriptase (hTERT) mRNA in the melanoma, and to analyze the relationship between the expression and subtypes and clinicopathological features of melanoma. Methods Expression of hTERT mRNA was detected by real-time quantitative PCR in 64 cases of melanoma and 30 cases of nevus. SPSS 17.0 software was used to analyze the relationship between hTERT mRNA expression and clinical pathological features of melanoma. Results The relative expression of hTERT mRNA in melanoma tissues was higher than that in nevus tissues [(52.43±5.42) vs (21.38±3.73), t= 4.72, P= 0.000]. The expression of hTERT mRNA in melanoma had no significant correlation with age, gender, ethnicity (all P> 0.05), but had relationship with subtypes, lymph node metastasis, Clark classification (all P< 0.05). The expression of hTERT mRNA in mucosal melanoma was significantly higher than that of acral and non-acral melanoma (t= 7.71, P= 0.001), while the expression of acral and non-acral melanoma had no difference (P> 0.05). Conclusions The expression of hTERT mRNA in melanoma is high, especially in mucosal melanoma. hTERT may play an important role in the occurrence and development of melanoma.

OBJECTIVEImmortal cell line of human embryonic esophageal epithelium (SHEE) was induced by E6E7 genes of human papillomavirus (HPV) type 18 in our laboratory. To identify the fully malignant transformation at its 85th passage (SHEE85), the malignant phenotype, tumorigenesis and invasive potency were studied.

METHODThe cultured SHEE85 cells were observed under the light and the electron microscope (EM) for cell morphology, analyzed by flow cytometry for cell cycle. The tumorigenesis was assayed by plating cells in soft-agar and transplanting cells into the nude mice and SCID mice. To detect invasive potency, cells were cultured on amniotic membrane in vitro and transplanted into peritoneal cavity of mice in vivo.

RESULTSSHEE85 cells were crowded in cultivation with different sizes and shapes under light microscope, and displayed proliferative morphology under EM. Proliferative index was 47% with 12% hyperploidy cells in determination of DNA histogram. Many large colonies grew in soft-agar (4%) and the transplanted tumors were found in all 4 nude and 4 SCID mice, with strong invasive potency demonstrated in vitro and in vivo.

CONCLUSIONThe immortal esophageal epithelial cell line induced by HPV18 E6 E7 is derived from a fully malignant transformation with a strong invasive potency at the 85th passage. It is also a reliable model for studying the cellular and molecular mechanisms of carcinogenesis of the esophageal carcinoma.

Animals ; Cell Division ; genetics ; Cell Transformation, Neoplastic ; Cell Transformation, Viral ; genetics ; Cells, Cultured ; Epithelial Cells ; cytology ; ultrastructure ; virology ; Esophagus ; cytology ; Humans ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Mice, SCID ; Microscopy, Electron ; Neoplasm Transplantation ; Neoplasms, Experimental ; pathology ; Oncogene Proteins, Viral ; genetics ; Papillomaviridae ; genetics ; Ploidies ; Transplantation, Heterologous

OBJECTIVEStudy on the promoter effects of sodium butyrate in high or low dosages on carcinogenesis process, based on the immortalization of human fetal esophageal epithelium induced by human papillomavirus (HPV) 18E(6)E(7) genes.

METHODSThe immortalized esophageal epithelium SHEE was treated with high concentration of the sodium butyrate (80 mmol/L) and then with low concentration (5 mmol/L) for 8 weeks respectively. The cells were cultured continuously without sodium butyrate for 14 weeks. The morphology, proliferation and apoptosis of the cells were studied by phase contrast microscopy, immunohistochemistry and flow cytometry. The dead and the viable cells were assayed by fluorescent microscopy with Hoechst 33342 and Propidium iodide staining. Tumorigenesis of the cells was assessed by soft agar colony formation and by transplantation of cells into nude mice and SCID mice.

RESULTSWhen cells were exposed to high concentration of sodium butyrate, cell death was increased leaving few live cells. When cells were cultured in the medium with low concentration of sodium butyrate, the first proliferative stage appeared. Removal of the butyrate caused the cell to enter a crisis stage with a long doubling time resembling senescent cells. After the crisis stage, the cells progressed to the second proliferation stage with continuous replication and atypical hyperplasia. At the end of the second proliferative stage, carcinogenesis of the cells appeared with large colonies in soft-agar and tumor formation in transplanted SCID mice and nude mice.

CONCLUSIONSThe malignant change of the immortalized epithelium by the effects of sodium butyrate is the consequence of a two-stage mortality mechanism: cells death by butyrate cytotoxicity and cell crisis by abrogation of sodium butyrate. These data reveal that in high dosage, sodium butyrate induces cell death and in low dosage, it induces cell proliferation, which emphasizes the importance of butyrate as a promotor of carcinogenesis.

Animals ; Butyrates ; toxicity ; Carcinogens ; toxicity ; Cell Death ; drug effects ; Cell Division ; drug effects ; Cell Line, Transformed ; Cell Transformation, Neoplastic ; chemically induced ; Esophageal Neoplasms ; etiology ; Esophagus ; pathology ; Humans ; Mice ; Mice, Inbred BALB C ; Papillomaviridae ; pathogenicity

Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.

OBJECTIVE: To investigate the degeneration mechanics of outer hair cells in guinea pig. METHOD: The mechanics of outer hair cells isolated by enzyme were observed under inverted microscope for 6-8 h continuously. RESULT: Over half of living outer hair cells could keep good conditions in 6 hours. During the degeneration there was always a longitudinal fold line from tip to base. Presence or absence of calcium, as well as lossing of stereociliary bundle, couldn't change the conditions of out hair cells. CONCLUSION Neither calcium nor stereociliary bundle is the decisive cause in keeping outer hair cells alive, and its degeneration may be basically related with something surrounding the cell.
Animals ; Calcium ; Cells, Cultured ; Cochlea ; cytology ; pathology ; Culture Media ; Guinea Pigs ; Hair Cells, Auditory ; cytology

OBJECTIVE: In order to meet the needs of electrophysiology outer hair cells, we investigate a method to separate outer hair cells simply and effectively. METHOD: The basal membrane was dissected combined with spiral ligament and axis of cochlea, then incubated with enzyme, and then mechanically triturated by micropipette. RESULT: A large number of living outer hair cells were obtained. Of 80% cells could keep good condition in 6 hours. CONCLUSION If increasing the enzyme concentration slightly and the large part of cochlea without outer bone was enzymes, we can get living outer hair cells easily.
Animals ; Cell Separation ; methods ; Cochlea ; cytology ; Guinea Pigs ; Hair Cells, Auditory ; cytology

Objective:To explore the population who benefit from primary tumor resection (PTR) of asymptomatic metastatic colorectal cancer (mCRC) .Methods:The clinicopathological data of 121 patients with asymptomatic mCRC with unresectable liver metastases treated in the First Affiliated Hospital of Yangtze University from January 2014 to January 2019 were retrospectively analyzed. Kaplan-Meier method was used to draw the survival curve accompanied with log-rank test. Cox regression model was used to analyze the prognostic factors.Results:The median overall survival (OS) of 121 mCRC patients was 20 months, and the 3- and 5-year survival rates were 34.71% and 10.74%. The median OS of PTR and non-PTR patients were 21 months and 18 months respectively, with no statistically significant difference ( χ2=0.79, P=0.375) . In 65 mCRC patients received targeted therapy, the median OS of PTR and non-PTR patients were 25 months and 28 months respectively, with no statistically significant difference ( χ2=1.65, P=0.199) . In 84 patients with mCRC of the left colon and rectum, the median OS of PTR and non-PTR patients were 24 months and 18 months respectively, with a statistically significant difference ( χ2=4.25, P=0.039) . In 37 patients with mCRC of the right colon, the median OS of PTR and non-PTR patients were 19 months and 17 months respectively, with no statistically significant difference ( χ2=0.18, P=0.675) . In 64 mCRC patients who received liver local treatment, the median OS of PTR and non-PTR patients were 36 months and 17 months respectively, with a statistically significant difference ( χ2=12.60, P<0.001) . In 57 mCRC patients who did not receive liver local treatment, the median OS of PTR and non-PTR patients were 15 months and 17 months respectively, with no significant difference ( χ2=0.58, P=0.445) . Univariate analysis showed that the location of the primary tumor ( HR=0.51, 95% CI: 0.25-0.76, P=0.025) , the degree of differentiation ( HR=1.46, 95% CI: 1.13-9.45, P=0.004) , the maximum diameter of the liver metastases ( HR=1.86, 95% CI: 1.35-4.60, P=0.012) , the level of serum carcinoembryonic antigen ( HR=3.55, 95% CI: 2.55-8.45, P<0.001) , local treatment of liver metastases ( HR=0.35, 95% CI: 0.19-0.93, P<0.001) were influencing factors for OS of asymptomatic mCRC patients with unresectable liver metastases. Multivariate analysis showed that the primary sites of the left colon and rectum ( HR=0.43, 95% CI: 0.25-0.93, P=0.039) , local treatment of liver metastases ( HR=0.78, 95% CI: 0.27-0.86, P<0.001) were independent influencing factors for OS of asymptomatic mCRC patients with unresectable liver metastases. Conclusion:Asymptomatic mCRC patients with unresectable liver metastases with primary sites of the left colon and rectum and local treatment of liver metastases can benefit from PTR.