ObjectiveTo explore the cause and treatment of multi-drug resistant pulmonary tuberculosis (MDR-TB) in patients with human immunodeficiency virus (HIV) infection. Methods24 cases with HIV and MDR-TB who were found in some AIDS-high areas in Henan were analyzed.ResultsAll cases were later-required drug-resistant ones. The main reasons were unreasonable plan for chemotherathy,improper management to the patients, side-effect of drugs,immunosuppression and low drug-tolerance. After anti-virus and 9～12 months long anti-tuberculosis chemotherathy,7 cases died and other 17 survival patients improved in clinical symptoms and signs, including no tubercle bacillus were found in sputum of 15 cases,the focal of infection were absorbed in 16 cases,the pulmonary cavity closure rate was 66.7%(4/6)and the count of CD4+ lymphocyte was higher than before.ConclusionThe patients with HIV and MDR-TB are difficult to cure and the mortality rate is high;the short-term effect of the anti-virus and multi-drug antituberculosis chemotherathy is better.

Objective To study the relationship between cardiovascular diseases (CVD)and 24-h peritoneal protein losses (PPL) in continuous ambulatory peritoneal dialysis (CAPD)patients. Methods One hundred and seventy-eight CAPD patients in our department were enrolled in this study. Their 24-h PPL was measured and other clinical data were recorded at the beginning. Meanwhile, Doppler ultrasound examination was performed. They were then followed-up prospectively for the development of CVD. Results The average of 24-h PPL was (5.0±1.8) g.Patients with diabetic status or preexisting CVD or carotid arteries arteriosclerosis had higher 24-h PPL than those without (t=2.082, P=0.039; t=2.601, P=0.010; t=2.217, P=0.029). 24-h PPL was positively correlated with left ventricular end-diastolic diameter (LVDd), interventricular septal thickness (IVSTd), posterior wall diameter of left ventricle at end-diastolic (LVPWd) and left ventricular mass index (LVMI) (r=0.222, P=0.040; r=0.217, P=0.043; r=0.339, P=0.002; r=0.305, P=0.007). It was negatively correlated with ejection fraction of left ventricle (r=0.221, P=0.040). One hundred and fourteen CAPD patients were prospectively followed-up for at least twelve months. Patients developing CVD were 40.4% and 19.3% for high and low PPL groups respectively (x2=6.035, P=0.014). In the multivariable logistic regression analysis, the 24-h PPL was one of the independent factors for developing CVD. Conclusions There is a significant and independent relationship between 24-h PPL and new cardiovascular events. 24-h PPL may be an important predictor of cardiovascular disease.

OBJECTIVETo study the inhibitory effect of Acanthopanax giraldii Harms Var. Hispidus Hoo polysaccharides (AGP) on SGC-7901 gastric cancer cells and its possible mechanism.

METHODSCell doubling time analysis, colony forming assay and MTT assay were adopted to study the inhibitory effect and its characteristics. We also analyzed the amount of protein expressed by oncogenes, antioncogenes and cell factors using flow cytometric analysis.

RESULTSAGP inhibited the proliferation of SGC-7901 cells and cell colony forming ability. AGP did not inhibit the viability and function of lymphocytes of peripheral blood in healthy subjects and human embryonic tenocytes, except for the highest dosage of AGP (P < 0.05), which slightly inhibited the viability and function of the two types of normal cells. AGP inhibited the viability and function of SGC-7901 cells, except for the lowest dosages of AGP I and AGP III. There was a dose-effect relationship between the dosage of the AGP and SGC-7901 cells. The effect of the AGP at the molecular level was associated with the low protein expression of the c-myc and bcl-2 genes and the high protein expression of the p53, bax, fas and fas-L genes, as well as the cell factor TGF beta(1). The inhibitory effect of AGP was weaker than that of CDDP, but was stronger than that of Vitamin C.

CONCLUSIONSAcanthopanax giraldii Harms Var. Hispidus Hoo polysaccharides selectively inhibited the proliferation, the colony forming ability, and the viability and function of human gastric cancer cells through the low protein expression of c-myc, bcl-2 and the high protein expression of p53, fas, fas-L and the cell factor TGF beta(1). The different inhibitory characteristics on the normal cells and cancer cells are possibly caused by gene and the cell factor expressions.

Cell Division ; drug effects ; Dose-Response Relationship, Drug ; Drugs, Chinese Herbal ; chemistry ; pharmacology ; Humans ; Neoplastic Stem Cells ; drug effects ; Polysaccharides ; pharmacology ; Stomach Neoplasms ; drug therapy ; pathology ; Tumor Cells, Cultured ; drug effects