Objective To explore the value of chemosensitivity assay in vitro on breast cancer.MethodsIn vitro chemosensitivity of 6 species of chemotherapeutic agents applied to 38 cases of breast cancer patients were detected by tissue culture-end point staining-computer image analysis(TECIA).ResultsThe sensitivity to chemotherapeutic agents commonly used in the breast cancer level from high to low was as follow:Doxorubicin(ADM),Paclitaxel(TAX),Vinorelbine(NVB),Cyclophosphamide(CTX),Cisplatin(DDP)and Fluorouracil(FU).ConclusionDrugs sensitivity experiment of cancer in vitro by TECIA has an important value to instruct clinical medication and individual chemotherapy for breast cancer.

Objective:Calcium/calmodulin-dependent kinase kinase (CAMKK2) is activated in prostate cancer (PCa). The aim of our study is to identify the effects of preadipocyte and CAMKK2 on the PCa cell invasion.Methods:The coculture system between PCa cells and preadipocyte cells (3T3L1) was established and then Transwell assay was used to determine the invasive effect after coculture. Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to investigate the CAMKK2 expression in the coculture system.Results:The 3T3L1 cells promoted the invasion of PCa cells (DU145 and 22RV1; P<0.01). Meanwhile, the 3T3L1 cells can increased expression of CAMKK2 in PCa cells ( P<0.01). CAMKK2 reversed the invasive effects of preadipocyte cells on the PCa cells. Conclusions:Our study demonstrates that the preadipocyte may promote the PCa cell invasion possibly by mediating the CAMKK2 expression.

ObjectiveTo investigate the effect of curcumin on the cycle arrest of human colon cancer HCT116 cells and decipher the possible molecular mechanism. MethodThe methyl thiazolyl tetrazolium （MTT） method was employed to examine the effects of curcumin （0， 12.5， 25， 50， 75， 100 μmol·L^-1） and 5-fluorouracil （5-FU， 600 μmol·L^-1） on the proliferation of HCT116 cells at different time points （24， 48， 72 h）. Flow cytometry was employed to examine the cycle of HCT116 cells treated with curcumin （0， 25， 50， 75 μmol·L^-1） and 5-FU. Western blot was employed to determine the expression of proteins in the Janus kinase 1 （JAK1）/signal transducer and activator of transcription 1 （STAT1） /cyclin-dependent kinase inhibitor 1A （p21） pathway in HCT116 cells. The binding of STAT1 to p21 promoter region was detected by chromatin immunoprecipitation （ChIP）. Small interfering RNA （siRNA） was employed to measure the role of STAT1 in regulating the expression of p21 and that of JAK1 in regulating the activation of STAT1 by Western blot and cellular immunofluorescence， respectively. ResultCompared with the blank group， the HCT-116 cells treated with curcumin and 5-FU showed decreased viability （P<0.05）， increased proportions of cells in the G₀/G₁ phase （P<0.05）， decreased proportions of cells in the S phase and G₂/M phase （P<0.05）， down-regulated protein level of phosphorylated p21 （P<0.05）， and up-regulated protein level of p21 （P<0.05）. Compared with the curcumin group， the p21 siRNA+ curcumin group presented decreased proportion of cells in G₀/G₁ phase （P<0.05）. Compared with the blank group， curcumin elevated the level of phosphorylated STAT1 （p-STAT1） （P<0.05）. Compared with the curcumin group， the curcumin + STAT1 siRNA group showcased up-regulated protein level of p21 in HCT116 cells （P<0.05）. The mechanism study showed that curcumin treatment enhanced the enrichment of STAT1 in the p21 promoter region （P<0.05） compared with the blank group. Compared with the blank group， curcumin up-regulated the level of phosphorylated JAK1 （p-JAK1） （P <0.05）. Compared with the curcumin group， the curcumin + STAT1 siRNA group demonstrated up-regulated protein levels of p-STAT1 and p21 in HCT116 cells （P<0.05）. ConclusionCurcumin may induce the cycle arrest of human colon cancer HCT116 cells by activating the JAK1/STAT1/p21 signaling pathway.

Pediatric acute respiratory distress syndrome(PARDS)is a pulmonary inflammation syndrome caused by a variety of proinflammatory factors induced by many causes, which is mainly characterized by noncardiogenic pulmonary edema.The main pathophysiological feature is the destruction of the integrity of the alveolar capillary membrane, and the loss of the alveolar epithelial-endothelial barrier function.In the PARDS′s clinical practice, the mainstay of the treatment is supportive.Although there is still no clear definition and general consensus or guidelines, appropriate liquid therapy is an important part of non-ventilatory treatment measures.Proper fluid management strategy is helpful to improve pulmonary edema, maintain normal circulatory perfusion, prevent functional failure of important organs and improve the prognosis of patients.According to volume status, implementing the goal-oriented and phased differentiated fluid management strategy is significant for the therapy of PARDS patients.However, the effects of fluid strategy management according to PARDS phenotypes remain to be evaluated.

Background: Abnormal glucose metabolism is one of the malignant characteristics of tumors. LncRNA plays an important role in the process of aerobic glycolysis of tumors. Aims: To investigate the expression of LncRNA MEG3 in gastric cancer and its correlation with glycolysis. Methods: RT-qPCR was used to detect the mRNA expression of MEG3 in gastric cancer and paracancerous tissue. Immunohistochemical EnVision method was used to detect the protein expressions of PKM2, LDHA, mTOR, HIF-1α in gastric cancer and paracancerous tissue. Relationship between expressions of above-mentioned indices and clinicopathological features of gastric cancer were analyzed. The correlation between MEG3 and glycolysis level of gastric cancer was analyzed by Spearman correlation analysis, and its possible mechanism was explored. Results: The expression of MEG3 in gastric cancer tissue was significantly lower than that in paracancerous tissue (P< 0.05), and was correlated with lymph node metastasis (P<0.05). The positivity rates of expression of PKM2, LDHA, mTOR and HIF-1α in gastric cancer tissue were significantly higher than those in paracancerous tissue, and were correlated with the depth of tumor invasion, lymph node metastasis and pTNM stage (P<0.05). Spearman correlation analysis showed that the expression of MEG3 was negatively correlated with the expressions of PKM2, LDHA, mTOR and HIF-1α (r=-0.346，r= -0.306，r=-0.389, r=-0.338; P<0.05). The expression of MEG3 in HIF-1α