0.05),but the positive degrees were distinctly different(P0.05). Conclusion:The status of p53 may be related with multidrug resistance and the p53 positive tumors possibly show low sensitivity to chemotherapy.

Humans ; Multiple Myeloma ; drug therapy

Objective To evaluate the efficacy and security of combined recombinant human endostatin with GP chemotherapy for the treatment of advanced non-small-cell lung cancer (NSCLC).Methods Non- randomized concurrent control was used.32 patients were treated by recombinant human endostatin combined with chemotherapy as test group,40 patients of control group only received chemotherapy.The response rate (RR),the clinical benefit rate (CBR) and the time to progression (TTP) were observed.Results The total RR in two groups were 40.6 ％ and 20.0 ％ (x2 =3.66,P =0.07).The total CBR were 68.8 ％ and 42.5 ％ (x2 =4.93,P =0.034).The total time to progression were 5.2 months and 3.9 months (P =0.042).Incidence of adverse reactions of experimental group and control group was no significant difference.Conclusion Combined recombinant human endostatin and chemotherapy can improve the curative effect (RR,CBR and TTP) of advanced NSCLC.

Adult ; Cardiac Catheterization ; adverse effects ; Female ; Heart Septal Defects, Atrial ; therapy ; Hemolysis ; Humans

Aim Tostudytheinfluencesofsulfated polysaccharides ( SPPM60-D) on the regulation of free calcium concentration ( [ Ca2+] i ) of T lymphocytes of mice in vitro and explore the mechanisms involved. Methods Polysaccharides(PPM60)wereextracted from masson pine pollen with hot water and 60% etha-nol. PPM60-D was separated and purified from PPM60 with Sephacryl S-400HR. Sulfated polysaccharides ( SPPM60-D ) were derivated by chlorosulfonic acid-pyridine method and the [ Ca2+] i of T lymphocytes were measured by fluorescence spectrophotometer. IL-2 and IL-4 were measured by ELISA kits. Results ConAandSPPM60-Dcouldincrease[Ca2+]iinT lymphocytes by 211. 5% and 201. 8% respectively ( P<0. 01). 2-APB, LY294002, U73122 and verapamil rather than TAK-242 could significantly inhibit the in-crease of [ Ca2+] i induced by SPPM60-D. SPPM60-D could significantly increase the level of IL-2 and IL-4 in supernatant ( P <0. 01 ) . 2-APB rather than TAK-242 could significantly inhibit the increase of cyto-kines.Conclusion ItisspeculatedthatSPPM60-D could increase [ Ca2+ ] i via TCR/CD3-PI3K-PLC-IP3 R-Ca2+ signal pathway through TCD/CD3 receptor in T lymphocytes so that it could improve the level of IL-2 and IL-4 in supernatant in T lymphocytes.

Adolescent ; Adult ; Aged ; Cholesteatoma, Middle Ear ; congenital ; pathology ; Female ; Humans ; Male ; Melanocytes ; Middle Aged ; Young Adult

A? plays a crucial role in Alzheimer's Disease and the soluble A? oligomers have been recognized as the emerging neurotoxins,which ultimately cause memory impairment and neuronal loss through different mechanisms.The development of novel drugs targeting A? oligomers indicates new and promising therapy approaches for AD.The pathological roles as the proximal toxins in AD and the compounds,targeting soluble A? oligomers,which are currently in preclinical and early clinical development,are reviewed.

Objective To investigate the risk factors related to mortality of children with deep fungal infection in pediatric intensive care unit(PICU).Methods A retrospective case-control study was applied.Ninty-six patients admitted to PICU with clinical or definite diagnosis of deep fungal infection from Nov 2005 to Mar 2009 were included.The risk factors related to mortality wereanalyzed with the logistic regression analysis.The research factors included:sex,age,primary diseases,complications,invasive operations and therapeutic measures etc.Results Of all 96 children,28 died (28.2％).According to the analytical results of multivariate logistic regression,the variables significantly associated with mortality were immunosuppressive (OR =185.770,95 ％ CI 11.467 ～ 3 009.507),mechanical ventilation (OR =11.555,95 ％ CI 2.780 ～ 48.039),hypoproteinemia (OR =1.246,95％ CI 1.133 ～ 1.369) and low pediatric critical illness score (OR =1.086,95 ％ CI 1.008 ～ 1.169).Conclusion The risk factors related to mortality of children with deep fungal infection in PICU were immunosuppressive,mechanical ventilation,hypoproteinemia and low pediatric critical illness score.

Adrenocorticotropic Hormone ; blood ; Animals ; Female ; Hypoxia ; metabolism ; Male ; Rats ; Rats, Wistar

Objective To evaluate the anti-tumor effects of chemotherapeutic drugs on human gastric cancer cells. Methods From April 2006 to February 2007, 84 patients with gastric cancer underwent surgical resection at General Hospital of Jinan Military Command. The single-cell suspension of these gastric tumors was prepared. The gastric cancer cells were cultured with hydroxycamptothecin, cisplatin, adriamycin, 5-fluorouracil and mitomycin for 48 hours, and changes in activity of the gastric cancer cells were studied via MTT assay. The expression of survivin and PTEN was detected by immunohistochemistry. Data were analyzed by chi-square test, rank sum test and Fisher exact test. Results The anti-tumor effects of different chemotherapeutic drugs were different, and the poorly-differentiated gastric cancer cells were more sensitive to the cytotoxic effects of chemotherapeutic drugs than the well-differentiated gastric cancer cells. The expression levels of survivin in the signet ring cell carcinoma, mucinous adenocarcinoma and other poorly-differentiated adenocarcinoma were significantly higher than those in papillary carcinoma and tubular carcinoma (χ~2 = 10.625, P <0.05), while the expression of PTEN was inverse to that of survivin (χ~2 = 6.060, P < 0.05). The expression of survivin was related to the resistance of the gastric cancer cells to 5-fluorouracil and adriamycin (χ~2 = 6.609, 6.350, P < 0.05). Conclusions In vitro chemosensitivity assay is helpful in selecting the chemotherapeutic regimen for specific types of gastric cancer. Survivin may contribute to the chemotherapy-resistance of certain types of gastric cancer cells, and its expression is related to that of PTEN.