OBJECTIVE: To study the preventing effects of p-coumaric acid(p-CA) on acute hypoxia-induced pulmonary edema by mice experiments. METHODS: Acute-hypoxia model was established using a normobaric hypoxia chamber in vivo. Salidroside was set as a positive control drug. And the test period was 7 d using a method of intragastric administration. The measurements including pulmonary water content, HE staining, inflammatory factors, anti-oxidative indexes and Na+, K+-ATPase were performed to determine the efficacies and mechanisms of p-CA on preventive against acute hypoxia-induced pulmonary edema. RESULTS: As compared with the normal group, pulmonary water contents increased significantly by 3.56% in the mice treated with acute hypoxia (9.5% O2) for 6 h (control group) (P<0.01), and administration with p-CA (25, 100 mg•kg-1•d-1) for 7 d could significantly reduce this index (P<0.05), which was as effective as the positive group. The action mechanisms of p-CA could be due to its abilities of improving the activity of Na+, K+-ATPase, enhancing antioxidant capacity (SOD↑, CAT↑ and MDA↓) and inhibiting inflammatory factors (IL-1β and IL-6). CONCLUSION: p-CA has greater preventive effects on acute hypoxia-induced pulmonary edema in mice.

Purpose To detect the expression and the function of MCP-1 and its receptor CCR2 in wet agerelated macular degenerative (wAMD) model mouse retina. Methods C57BL/6J mouse were enrolled into the study. Model mouse of wAMD was induced with laser. Frozen sections were prepared for histopathological tests. Immunofluorescence study for MCP-1 and CCR2 was carried out. Co-expression study for CCR2/ CDllb or CCR2/CD68 was carried out. Total protein and total mRNA from the eyes of both wAMD and wild type mouse were extracted. The expression of mRNA and protein of MCP-1 and CCR2 in the eyes were determined by reverse transcription-poly-merase chain reaction (RT-PCR) and Western blots test, respectively. Results In wild type mouse, both MCP-1 and its receptor CCR2 were not detected in the retina. However in wAMD mouse, an obvious up-regulated MCP-1 and CCR2 expression was seen in the retinal pigment epithelium (RPE) cells accompanied with the increased expression of their mRNA and protein. The co-expression study showed that CCR2 co-ex-pressed with CDllb, but not with CD68. Conclusion MCP-1 and its receptor CCR2 may play a role in the wAMD through stimulation of microglia.

Objective To determine whether different antihypertensive drugs may have different effects on the hematoma and prognosis of intracerebral hemorrhage (ICH) patients to provide reference for drug choices in the clinical blood pressure control of patients with ICH.Methods Ninety three ICH patients,admitted to our hospital from January 2010 to January 2012,were chosen in our study and divided into nimodipine treatment group,urapidil treatment group and control group.Hematoma volumes of the patients were recorded at admission,24 and 72 hours after admission,respectively.The neurological disability grades of the patients were also recorded at discharge.Results The hematoma expanded in all of the three groups at 24 and 72 hours of admission,but not enjoying difference as compared with that before admission (P＞0.05); the hematoma expansion in the nimodipine group was obviously restricted as compared with that in the urapidil group and control group at 24 and 72 hours of admission (P=0.026,P=0.019; P=0.016,P=0.022).Significant differences on the prognosis in the three groups were noted (P＜0.05); the function recovery in the nimodipine group was significantly better as compared with that in the urapidil group and control group (P＜0.05).Conclusion Nimodipine have better effect on the early hematoma expansion and function recovery of ICH patients as compared with urapidil; nimodipine should be first chosen in clinic.

BACKGROUNDThe Notch-regulated ankyrin repeat protein (NRARP) is recently found to promote proliferation of breast cancer cells. The role of NRARP in carcinogenesis deserves extensive investigations. This study attempted to investigate the expression of NRARP in thyroid cancer tissues and assess the influence of NRARP on cell proliferation, apoptosis, cell cycle, and invasion in thyroid cancer.

METHODSThirty-four cases with thyroid cancer were collected from the Department of General Surgery, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine between 2011 and 2012. Immunohistochemistry was used to detect the level of NRARP in cancer tissues. Lentivirus carrying NRARP-shRNA (Lenti-NRARP-shRNA) was applied to down-regulate NRARP expression. Cell viability was tested after treatment with Lenti-NRARP-shRNA using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptosis and cell cycle distribution were determined by flow cytometry. Cell invasion was tested using Transwell invasion assay. In addition, expressions of several cell cycle-associated and apoptosis-associated proteins were examined using Western blotting after transfection. Student's t-test, one-way analysis of variance (ANOVA), or Kaplan-Meier were used to analyze the differences between two group or three groups.

RESULTSNRARP was highly expressed in thyroid cancer tissues. Lenti-NRARP-shRNA showed significantly inhibitory activities against cell growth at a multiplicity of infection of 10 or higher (P < 0.05). Lenti-NRARP-shRNA-induced G1 arrest (BHT101: 72.57% ± 5.32%; 8305C: 75.45% ± 5.26%) by promoting p21 expression, induced apoptosis by promoting bax expression and suppressing bcl-2 expression, and inhibited cell invasion by suppressing matrix metalloproteinase-9 expression.

CONCLUSIONDownregulation of NRARP expression exerts significant antitumor activities against cell growth and invasion of thyroid cancer, that suggests a potential role of NRARP in thyroid cancer targeted therapy.

Adult ; Aged ; Animals ; Apoptosis ; genetics ; physiology ; Cell Cycle ; genetics ; physiology ; Cell Line, Tumor ; Cell Proliferation ; genetics ; physiology ; Cell Survival ; genetics ; physiology ; Female ; Humans ; In Vitro Techniques ; Kaplan-Meier Estimate ; Male ; Mice ; Mice, Nude ; Middle Aged ; Neoplasm Proteins ; genetics ; metabolism ; Proteins ; genetics ; metabolism ; RNA, Small Interfering ; genetics ; Thyroid Neoplasms ; genetics ; metabolism ; mortality ; pathology