Biopsy ; Child, Preschool ; Female ; Humans ; Infant ; Lung ; pathology ; Lung Diseases, Interstitial ; diagnosis ; pathology ; Male

Adenocarcinoma ; pathology ; Carcinoma, Small Cell ; pathology ; Carcinoma, Squamous Cell ; pathology ; Cytodiagnosis ; methods ; Humans ; Lung Neoplasms ; pathology ; Sensitivity and Specificity ; Specimen Handling ; methods ; Sputum

With computer and manual search of literatures on the comparison of concurrent with sequential adjuvant radio-chemotherapy after mastectomy for breast cancer, 4 eligible randomized controlled trials were found; the RevMan 5.0 software was used for Meta-analysis. The results showed that concurrent radio-chemotherapy reduced local recurrence more prominently than sequential radio-chemotherapy in patients with positive axillary lymph nodes( P = 0. 003 ). However, differences in 5-year overall survival,5-year disease-free survival and metastasis-free survival between two groups were not significant (P =0. 670,P =0. 200, P =0. 350).

Cell Proliferation ; Colony-Forming Units Assay ; Glioma ; pathology ; Hematopoietic Stem Cells ; pathology ; Humans ; Stem Cells ; cytology ; metabolism

Objective To explore the risk factors in elderly type 2 diabetes mellitus with cerebral infarction. Methods Retrospective investigarion was performed on 148 elderly hospitalized patients with type 2 diabetes.The patients were classified based on the presence or absence of cerebral infarction and compared with 60 controls.Logis- tic regression analysis was used to reveal the risk factors for cerebral infarction.Results The levels of systolic blood pressure(SBP),body mass index (BMI),fasting blood glucose (FBG),total cholesterol (TC),triglyceride (TG) and plasma fibrinogen(Fg) were higher in the patients with cerebral infarction[141.15?17.46)mmHg,(23.81?3.53)kg/m~2,(8.82?2.81)mmol/L,(5.69?1.15)mmol/L,(2.08?0.75)mmol/L and (4.08?0.65)g/L] than those without cerebral infarction[(129.78?14.65) mmHg,(22.18?3.22)kg/m~2,(7.06?1.72 )mmol/L,(5.09?1.12)mmol/L,(1.62?0.43)mmol/L and (3.48?0.58)g/L].The logistic analysis showed COUR,SBP,FBG, TC,TG and Fg were the independent risk factors for cerebral infarction.Conclusion Early intervention of the inde- pendent risk factors including SBP,FBG,TC,TG and Fg in elderly patients with type 2 diabetes was important for reduction and postponement of cerebral infarction.

Objective To investigate the role of microRNA-21 (miRNA-21) in promoting proliferation of Kazakh's esophageal squamous cell carcinoma (ESCC) cell line Eca109 and Kazakh's ESCC tissues, and its effects on the expression of programmed cell death 4(PDCD4)gene.Methods TheEca109cellsweredividedintomiRNA-21Mimicsgroup(transfersequence:5′-UCAACAUCAGUCUGAUAAGCUA-3′),miRNA-21inhibitorgroup(transfersequence:5′-UAGCUUAUCAGACUGAUGUUGA-3′), negative control group (the transfer random sequence)and normal control group (no transfection).The cells were seeded at 4.5 × 105/well in 6-well cell culture plates. According to RNA interference technology,thecells were transfected with LipofectamineTM 2000. After transfection, the cell proliferation was determined by cell number counting.The expression of miRNA-21 was detected by real-time quantitative polymerase chain reaction (qRT-PCR), and the expression of PDCD4 protein was measured by Western blot.Meanwhile, the expression of miRNA-21 and PDCD4 protein were performed in 18 pairs of Kazakh's ESCC and corresponding adjacent normal esophageal mucosa.ResultsAt 48 hour after transfection,compared with normal control group, the cell number increased 36％ (P=0.002) in miRNA-21 Mimics group, decreased 28％ (P=0.002) in miRNA-21 inhibitor group, and did not change significantly in negative control group (P=0.515). At 48 hour after transfection, the relative expression of miRNA-21 in miRNA-21 Mimics group, miRNA-21 inhibitor group, negative control group and normal controlgroup was 0.37±0.10, 9.17± 1.08, 0.74±0.23 and 1.04±0.34,respectively, and the relative protein expression of PDCD4 was 1.47 ± 0.11, 0.61±0.09, 0.89 ±0.12 and 0.79±0.02 accordingly.Compared with normal control group, the relative expression of miRNA-21 decreased (P=0.031) and the relative protein expression of PDCD4 up regulated (P=0.001) in miRNA-21 inhibitor group, the relative expression of miRNA-21 increased (P=0.001) and the relative protein expression of PDCD4 down regulated (P=0.030) in miRNA-21 Mimics group,and there was no significant difference in negative control group (P=0.272 and 0.541).In 16 pairs of Kazakh's ESCC tissues, the expression of miRNA-21 was significantly higher in tumor tissues (0.11 ±0.09) than that of corresponding adjacent esophageal normal tissues (0.03 ± 0.03, P=0.001), while the relative protein expression of PDCD4 was significantly lower (0.92 ± 0.39) than that of corresponding adjacent normal esophageal tissues (1.57 ± 0.80, P=0.004). And the higher expression of miRNA-21, the lower relative protein expression of PDCD4 (r=-0.538, P=0.046).ConclusionmiRNA-21 may promoted the cell proliferation through inhibiting PDCD4 expression,which involved in the pathogenesis of Kazakh's ESCC.

Objective To investigate the effects of monocytes on phenotypic changes of human proximal tubular HK-2 cells and the mechanism.Methods Monocytes were co-cultured with HK-2 cells.Morphological changes of HK-2 cells were detected by inverted phase contrast microscope.Expressions of E-cadherin,α-SMA and fibronectin were assessed by RT-PCR,Western blotting and immunocytochemical staining.Flow cytometry techniques was applied to evaluate intercellular cell adhesion molecule-1 (ICAM-1) expression on HK-2 cells.The intracellular signal was investigated by gene microarr ay.Results The typical epithelial cell morphology of HK-2 cells disappeared after co-culture with monocytes,accompanied by decreased E-cadherin expression and increased α-SMA and fibronectin expression (all P＜0.05).The expression of ICAM-1 on HK-2 cells was increased by monocytes stimulation.Interestingly,administration of CD18 antibody directly inhibited the phenotypic change of HK-2 cells.Furthermore,NF-κB signaling might be critical in mediating this process,and blockade of this signaling pathway could inhibit 1CAM-1 expression and epithelial mesenchymal transition (EMT) formation.Conclusion Monocytes can directly induce EMT of HK-2 cells via up-regulating ICAM-1 through NF-κB signaling pathway.

Objective To investigate the effects of ischemic preconditioning on pneumocyte apoptosis and the expression of HSFT0 after lung isehemia-reperfusion(I/R) in rats and discuss its possible mechanism of extenu-ating ischemia-repedusion injury. Method Thirtysix male Sprague-Dawley rats were randomly divided into three groups [ sham operation(SO ) group, ischemia-teperfusion(L/R) group, and ischemic preconditioning(IP) group],twelve in each group. Lung croas-clamping was used to build the L/R model. In IP group, three cycles of 5-minute-ischemia + 5-minute-reperfusion were given to the pulmonary artery before the procedure. Sham operation rats had a thoracotomy only. Two hours(or five hours) reperfusion was given to both L/R and IP group. Tenninal-deoxynucleotidyl Transferase Mediated d-UTP Nick End Labeiing(TUNEL) was used to evaluate apoptosis. Expression of HSP/0 in lung was observed by immunohistochemical stain and image analysis. Index of quantitative assessment of histologic lung injury(IQA), wet to dry weight ratio(W/D) were measured. The pathological change of lung tissue was observed under both hght and electron microscopy. Statistical analysis was carried out by One-way Anova. Scheffe test was used for intragroup comparison. Results The apoptosis index and expression of HSP70、W/D,IQA of hng tissue in I/R group were higher than those in the sham operation group (P<0.01). Compared with the L/R group, the apoptosis index and expression of HSP70, W/D, IQA of lung tissue significantly decreased (P<0.01), the levels of expression of HSPTO increased significantly in IP group ( P<0.01 ). The pathological and ultrastructure change of lung tissue was better in IP group than those in I/R group. Condusions Ischemic preconditioning can extenuate lung I/R injury by the possible mechanism of increasing the expression of HSPT0 which inhibits the apoptosis during lung I/R injury.

AIM: To study the effect of vascular endothelial growth factor(VEGF) on hematopoietic differentiation from mouse embryonic stem cells(ESC) in vitro.METHODS: ES-D3 was allowed to grow on mouse fetal fibroblast feeder layer,and then was developed into embryoid bodies(EB).EB cells were transferred into medium supplemented with different concentration of VEGF and VEGF+SCF for 1 week.Six groups,including.VEGF 5 ?g/L,VEGF 10 ?g/L,VEGF 20 ?g/L, VEGF 5 ?g/L+SCF,VEGF 10 ?g/L+SCF and VEGF 20 ?g/L+SCF,were designed.The group of spontaneous differentiation without cytokine(s) was used as control.Hematopoietic transcription factor GATA-2 and early hematopoietic differentiation genes(c-kit and ?-H1) were detected by RT-PCR.The content of CD34~+ cells in each group were measured by flow cytometry.The cells derived from ESC were incubated in semisolid methycellulose cultures.The numbers of total colony-forming units in culture(CFU-C) were counted by reverse microscope.RESULTS: ES-D3 grew and formed EB at day 4.VEGF had a stimulatory effect as a single factor on the expression of genes associated with early hematopoietic differentiation(GATA-2,c-kit and ?-H1),the generation of CD34~+ cells and CFU-C in EB.The effects of VEGF+SCF were the most potent in the experimental groups according to the percent of CD34~+ cells and the numbers of hematopoietic colonies.The most highest inducing efficacy was achieved in VEGF 20 ?g/L or VEGF 10 ?g/L combined with SCF.CONCLUSION: VEGF promotes the differentiation of ESC into hematopoietic cells in vitro.The strongest effect was achieved when VEGF was combined with SCF.

Objective To develop a model of type 2 diabetes with early renal injury on spontaneously hypertensive rats (SHR). Methods The 6-week old SHR were fed with the diets enriched with sucrose (20%, W/W), lard (10%, W/W), cholesterol (2.5%, W/W) and chleolate (1%, W/W) to induce insulin resistance. Hyperglycemia was developed by intraperitoneal injection of streptozotocin (STZ, 35 mg/kg). Wistar-Kyoto rats (WKY) were used as normal controls. Rats with plasma glucose (PGL) ≥ 16.7 mmol/L were diagnosed as diabetes. Eight weeks after the induction of diabetes, plasma triglyceride (TG), cholesterol (CHO), glucose, systolic pressure(SP), 24-h urine protein excretion (Upro) were examined in all the rats, and the homeostasis model assessment of insulin resistance (HOMA-IR) was analyzed. Renal pathological changes were studied by immunohistochemical staining and electron microscope. Results After 2 weeks on the high sucrose and fat diets, the model rats exhibited significant increase in basal PGL, TG and CHO levels as compared to control rats (P<0.05, respectively). The insulin resistance was developed in model rats demonstrated by the higher HOMA-IR (5.03±0.38 vs 2.61±0.34, P<0.05). At the end of the experiment, model rats were associated with hypertension. Upro level was significantly increased in model rats compared with that in controls [(57.58±16.54) mg/24 h vs (5.35±1.90) mg/24 h, P<0.01]. The kidney hypertrophy index (KWI) was significantly increased in the model rats compared to controls (P <0.05). Moreover, the diabetic model rats showed glomerular hypertrophy, foot process effacement, micro villous transformation, glomerular basement membrane (GBM) thickening. Conclusion A rat model is successfully established, which presents typical features of human type 2 diabetes and can be served as an ideal model to study the diabetic nephropathy.