Background and purpose: Chemokines play an important role in cancer occurrence and development. However, little about the function of CCL26 in esophageal squamous cell carcinoma (ESCC) is reported. This study was designed to observe and study the expression of chemokine CCL26 in ESCC tissues and to analyze their association with pathological features of ESCC. Methods: Expressions of chemokine CCL26 in 197 ESCC tissues and their corresponding paraneoplastic normal esophageal tissues were determined by tissue array and immunohistochemistry (IHC) technique, and its correlations to age, gender, lymph nodes metastasis, TNM stage, general classification and 5-year survival rate of ESCC patients were further analyzed. Results: ①CCL26 was expressed in both ESCC and paraneoplastic normal esophageal tissues. The expression of CCL26 in ESCC tissues was signiifcantly higher than that in paraneoplastic normal esophageal tissues (61.8%vs 20.6%, P<0.05).②The expression of CCL26 was correlated with lymph node metastasis, but not correlated with age, gender, tumor cell differentiation, and general classiifcation (P>0.05).③Survival analysis showed that the abnormal expression of CCL26 was associated with 5-year survival rate of patients with ESCC. The 5-year survival rate of ESCC patients with CCL26 positive expression was obviously lower than that of ESCC patients with CCL26 negative expression. Conclusion: CCL26 upexpression might play an important role in the progression and development of ESCC patients. The high level of CCL26 expression is correlated with lymph node metastasis and poor survival. Detection of CCL26 expression may have important prognostic values in ESCC patients.

Objective To evaluate the efficacy and safety of sorafenib in the treatment of advanced renal cell carcinoma.Methods The clinical date of 33 patients with advanced renal cell carcinoma from September 2007 to April 2012 was reviewed retrospectively.26 were males and 7 were females,with an average age of 69 years.Pathological diagnosis showed 30 clear cell RCCs,2 papillary RCCs,and 1 unclassified RCC.These patients were treated by sorafenib 400 mg twice a day until intolerable toxicity or disease progression.The primary end points were objective response rate,clinical benefit rate,median survival time,median progression-free survival and the incidence of adverse reaction.Results All patients were evaluable for response and toxicity,with 8 patients (24％) of partial remission,19 cases (58％) of stable disease,and 6 cases (18％) of disease progression.The disease control rate was 82％,the median progression-free survival was 10.2 months,while the median survival time was 16.5 months.The common adverse reactions included hand-foot skin reaction (61％),diarrhea (46％),hypertension (21％).Most adverse reactions occurred around the second week after drug therapy,with the duration unequal.The majority of adverse reactions could be released by symptomatic treatment,which did not affect the medication.Conclusion Sorafenib has good short term efficacy for patients with advanced renal cell carcinoma,and most adverse reactions were tolerable.

Objective:To optimize the macroporous resin separation process for total flavonoids in papaya. Methods:The content of total flavonoids in papaya was selected as the index, and the resin model, sample solution concentration, ratio of diameter and height, the flow rate of adsorption, type and volume of eluent, type and volume of impurity removing solvent, elution velocity and the other parameters were investigated. Results:The optimal purification process was as follows: the macroporous resin type was D-140, the sample solution concentration was 0. 1 g·ml-1 , the sample volume was 2BV, the ratio of diameter and height was 1∶9, washing the impurities with 3BV water, eluting with 3BV 10% ethanol first followed by 3BV 50% ethanol with 2BV·h-1 , and collecting 50%ethanol elution. The total flavonoids content was 52%. Conclusion:The optimized process can separate and purify the total flavonoids in papaya effectively.

Objective To explore the effect of oxaliplatin ( OXA) on enhancing radiosensitivity in human hepatocellular carcinoma cell line HepG2 . Methods 50% inhibition concentration ( IC50 ) of HepG2 cells treated with OXA was measured by using MTT method at 6, 12, 24, 48 hours. Then clone formation assay was applied to obtain sensitizing enhancement ratio ( SER) of OXA combing IR, according to the survival fraction of three groups 10?14 days after treatments:placebo?treated group ( C) ,radiation group ( IR, single dose of 1 Gy,2 Gy,4 Gy,6 Gy,8 Gy,10 Gy) and IR synchronizing OXA group ( IR+3 mg/L OXA) . The proportions of cell apoptosis were analyzed using flow cytometry at 24 hours after treatment. At last, we semi?quantitative tested the expression of extracellular regulated protein kinase 1/2 ( ERK 1/2 ) and DNA damage repair protein Ku?70 of the C,IR and IR+OXA groups. Statistical analysis was performed by T test. Results The IC50 of OXA on HepG2 cells is 54?4 mg/L at 6 hours,29?1 mg/L at 12 hours,17?8 mg/L at 24 hours and 10?5 mg/L at 48 hours.3 mg/L was selected in clone formation assay at which 80?90% HepG2 cells survived at 24 hours. The SER ( SF2 ) is calculated as 1?59. Flow cytometry showed the proportion of survival cells in IR+OXA group is significantly lower than those of IR group ( P=0?005) ,OXA group ( P=0?008) and C group ( P=0?001) . The expressions of ERK 1/2 were inhibited in IR and IR+OXA groups compared by that of control group. But the expression of ERK 1/2 in IR group showed increasing after 48 hours which was higher than that of IR+OXA group. For Ku?70,the changes of expression were similar with that of ERK 1/2. Conclusion Oxaliplatin presented enhancing radiosensitivity in human hepatocellular carcinoma cell line HepG2 in vitro.

Objective To evaluate the effects of active cycle of breathing techniques (ACBT) on respiratory complications of postoperative lung cancer patients. Methods One hundred non-small-cell lung cancer patients who underwent pulmonary lobectomy or segmentectomy in thoracic surgery department from April 2012 to January 2014 were assigned into the control group , while the experiment group were paired patients from February 2014 to December 2014. We applied ACBT to the experiment group for 5 days after surgical resection and afterward compared the two groups in view of incidence of respiratory complications . Result The incidences of pulmonary infection, atelectasis and hypoxemia in the experiment group were all significantly lower than those in control group (P<0.05). Conclusion ACBT strengthens endurance and force of patients′respiratory muscle group, and therefore reduces postoperative pulmonary complications.

[ ABSTRACT] AIM:To observe the influences of different concentrations of MG132 on apoptosis and beta-amyloid protein ( Aβ) generation in SH-SY5Y cells, and to explore the underlying mechanism.METHODS:SHSY-5Y cells were incubated with MG132 for 24 h.The final concentrations of MG132 were 2.5, 5 and 10μmol/L.The cell viability was de-termined by MTT assay.The cell apoptosis was assessed by flow cytometry.The levels of Aβwere measured by ELISA. The relative protein levels were detected by Western blot.RESULTS:In the SH-SY5Y cells, MG132 reduced the cell via-bility, induced the cell apoptosis, increased the level of Aβ, and increased the expression of the related proteins for Aβgeneration in a concentration-dependent manner.CONCLUSION: MG132 induces apoptosis and increases the levels of Aβ1-42 and Aβ1-40 by regulating the proteins related to Aβgeneration in the SH-SY5Y cells.

Objective To construct a Nomogram model that can accurately predict early death of metastatic colon cancer (mCC). Methods A total of 6 669 patients from the SEER database were identified using inclusion and exclusion criteria. Multivariate logistic regression was used to identify risk factors for early mortality and to construct a Nomogram. The predictive performance of the Nomogram was evaluated by C-index, calibration curve, and decision curve analysis (DCA). Results Primary tumor location, differentiation grade, T stage, M stage, bone metastases, brain metastases, CEA, tumor size, age and marital status were independent factors for early death in patients with mCC. A Nomogram was constructed based on these variables. The C-index and the calibration curve of the Nomogram showed the good predictive ability of the nomogram. DCA showed that the Nomogram had a superior clinical net benefit in predicting early death compared with TNM stage. Conclusion The developed Nomogram has good predictive ability and can help guide clinicians to identify patients with high-risk mCC for individualized diagnosis and treatment.

OBJECTIVETo investigate the roll of bone sialoprotein (BSP), a secreted glycoprotein, found in mineralized tissues in the development and progression of human esophageal squamous cell carcimoma (ESCC), and explore its association with clinicopathological characteristics and five-year survival of the patients.

METHODSThe expression of BSP was determined in 211 primary ESCC tumors and their paired nontumorous tissues using tissue-array, RT-PCR and immunohistochemistry.

RESULTSPrimary ESCC tissues showed a significantly higher expression rate of BSP mRNA than their paired nontumorous tissues (93.8% vs. 16.6%, P < 0.001), the same with BSP protein (56.9% vs. 31.3%, P < 0.001). The expression rate of BSP protein was correlated to lymph node metastasis and TNM stage (P < 0.05). The 5-year survival rate of BSP protein-positive ESCC patients was significantly lower than that of BSP protein-negative ESCC patients (P < 0.05). Multivariate analysis showed that tumor differentiation, TNM staging and BSP protein expression were independent factors affecting the prognosis of ESCC patients (P < 0.05).

CONCLUSIONSThe abnormal expression of BSP may play a significant role in the malignant progression and prognosis of ESCC, and BSP might be a marker reflecting the biologial behavior of ESCC.

Blotting, Western ; Carcinoma, Squamous Cell ; diagnosis ; metabolism ; Esophageal Neoplasms ; diagnosis ; metabolism ; Humans ; Immunohistochemistry ; Integrin-Binding Sialoprotein ; genetics ; metabolism ; Lymphatic Metastasis ; Neoplasm Staging ; Prognosis ; RNA, Messenger ; Survival Rate

Objective: To investigate the expression of ALC1 protein during esophageal squamous cell carcinoma (ESCC) development and progression, so as to explore its association with clinicopathological characteristics and overall survival of ESCC patients, and the effect of ALC1 overexpression on malignant biological behavior of esophageal squamous cells. Methods: Immunohistochemistry (IHC) was used to detect ALC1 protein expression in 245 primary ESCC tissues and their paired normal esophageal mucous membranes, and to determine its correlation to gender, age, tumor cell differentiation, invasion, TNM stage, lymph nodes metastasis, and overall surviv-al rate of ESCC patients. MTT assay, colony formation assay, transwell invasion, and wound healing assay were used to observe the ef-fect of ALC1 on ESCC cell proliferation, invasion, and migration. Results: The expression ratio of ALC1 in esophageal squamous cell car-cinoma was higher compared with that in their paired normal esophageal mucous membranes (41.6% vs . 21.2% , P<0.05). Upregula-tion of ALC1 was associated with ESCC invasion, TNM stage, and lymph node metastasis (P<0.05). The overall survival of ESCC patients with ALC1 overexpression was significantly lower than that in patients with downregulated ALC1 expression (P=0.002). Therefore, ALC1 may promote the proliferation, invasion, and migration of ESCC cells. Conclusions: ALC1 upregulation may play an important role in the progression and development of ESCC. Upregulation of ALC1 leads to poorer disease prognosis, and could promote the prolifera-tion, invasion, and migration of the KYSE30 ESCC cells. Therefore, ALC1 may have potential prognostic value for ESCC patients.

Objective To investigate the role of cell adhesion molecule L1 like (CALL) in the genesis and development of esophageal squamous cell carcinoma (ESCC).Methods From July 2007 to December 2010,a total of 100 patients with ESCC who received radical resection of esophageal cancer were enrolled.The ESCC tissues and corresponding tumor-adjacent normal tissues were obtained.The expression of CALl was determined by tissue microarray technology and immunohistochemical staining.The CALL over-expressed esophageal cancer cell line was established.The effects of CALL on cell migration and invasion were detected by wound-healing assay and Transwell assay,respectively.The effects of CALL on actin microfilament was analyzed by filamentous actin (F-actin) staining.Chi square test,Fisher's exact test,multivariate analysis and t test were performed for statistical analysis.Results The positive expression rate of CALL in ESCC tissues was 56 ％ (56/100),which was lower than that of tumor-adjacent normal tissues (95％,95/100),and the difference was statistically significant (x2=41.114,P＜0.01).There were statistically significant differences in CALL expression at protein level among patients with ESCC of different differentiation degree,different pathological T stage,lymph node metastasis and different TNM stage (x2=13.702,5.317,21.453,Fisher's exact test;all P＜ 0.05).The five year disease related survival rate of ESCC patients with down-regulated expression of CALL was 0(0/49),which was lower than those with normal CALL expression (25.5％,13/51),and the difference was statistically significant (x2 =43.338,P＜0.01).The median survival time of CALL expression down-regulated group was 17 months,and that of normal expressed group was 38 months.CALL expression was an independent risk factor of disease special survival rate (hazard ratio (HR) 0.353,95％ confidence interval (CI) 0.188 to 0.666,P=0.001).The results of wound-healing assay showed that the migration ability of CALL overexpressed CALL-k30 cells was lower than that of Vec-k30 cells in control group on 24 hours after wound.The results of Transwell invasion test showed the number of migrating cells penetrating CALL k30 cells attached to the inferior surface of the membrane was 44.000±13.748,which was less than that of the Vec k30 cells (154.333±25.007),and the difference was statistically significant (t=5.136,P=0.036).The results of F-actin staining demonstrated that actin filaments of CALL-k30 cells was 234.667 ± 65.118,which was lower than that of Vec-k30 cells (597.000± 119.929),and the difference was statistically significant (t=4.707,P=0.042).Conclusions CALL lowers the migration and invasion abilities of esophageal cancer cells by inhibiting F-actin microfilaments.Its abnormal expression may play an important role in the genesis,development and prognosis of ESCC.