Cell Line, Tumor ; Chromosome Aberrations ; Comparative Genomic Hybridization ; methods ; Gene Amplification ; Gene Dosage ; Gene Expression ; Humans ; Receptor, Fibroblast Growth Factor, Type 1 ; genetics ; metabolism ; Rhabdomyosarcoma ; genetics ; metabolism ; pathology ; Rhabdomyosarcoma, Alveolar ; genetics ; metabolism ; pathology ; Rhabdomyosarcoma, Embryonal ; genetics ; metabolism ; pathology

OBJECTIVETo study the efficacy of Xiaoyao Powder (XYP) combined with interferon alpha (IFN-alpha) in treating HBeAg positive chronic hepatitis B (CHB) patients and the effect on their quality of life (QOL).

METHODSTotally 193 patients with HBeAg-positive CHB confirmed by liver biopsy were randomly assigned to 2 groups, Group A (94 cases) and Group B (99 cases). IFN-alpha1b was subcutaneously injected to patients in Group A at the dose of 50 microg, thrice per week. Those in Group B additionally took XYP. The therapeutic course for all was 24 weeks. Clinical efficacy was observed by assessing ALT restoration rate, HBeAg negative rate, HBeAg conversion rate, HBV DNA negative rate, complete response rate, partial response rate, and symptoms integral. The evaluation of QOL was performed by using chronic liver disease questionnaire (CLDQ) score. Adverse reaction occurrence rate was observed in the two groups.

RESULTSBetter effects were obtained in Group A on ALT restoration rate, HBeAg negative rate, HBV DNA negative rate, complete response rate, partial response rate, TCM symptoms integral, the total effective rate of TCM sysmptoms, CLDQ score, and adverse reaction rates, showing statistical difference when compared with Group B (P < 0.05, P < 0.01).

CONCLUSIONXYP could elevate the efficacy of TCM symptoms of HBeAg-positive CHB patients and anti-viral effect, improve their QOL, and reduce adverse reaction of IFN-alpha.

Adult ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Hepatitis B e Antigens ; Hepatitis B, Chronic ; drug therapy ; Humans ; Interferon-alpha ; therapeutic use ; Male ; Quality of Life ; Treatment Outcome

Animals ; Cell Hypoxia ; Glucose ; metabolism ; Mifepristone ; pharmacology ; Oxidative Stress ; PC12 Cells ; Progesterone ; pharmacology ; Rats

AIM: To investigate the effect of advanced glycosylation end products on the expression of receptor for advanced glycosylation end products in human monocyte-derived dendritic cells. METHODS: Monocytes were purified (over 98%) using anti-CD14+ microbeads. After 8 d culture in RPMI-1640 medium containing rhGM-CSF (100 ?g/L) and rhIL-4 (50 ?g/L), immature MDCs were derived, then exposed to AGE-BSA (0 or 200 mg/L) for 24 h. Expression of RAGE was semi-quantified by RT-PCR and Western blotting. At the same time, supernatants were collected. IFN-? and IL-12 were analyzed by ELISA. RESULTS: mRNA and protein of RAGE incubated by 200 mg/L AGE-BSA was higher than that in control at 24 h. Treatment of DCs with AGE-BSA resulted in about two-fold increase in the expression of RAGE (P

AIM: The purpose of this study is to investigate the mechanisms related to oxidized low-density lipoprotein(ox-LDL) and dendritic cells(DCs) in the process of atherosclerosis.METHODS: Human DCs were prepared from human CD14~+ peripheral blood monocytes using rhGM-CSF((100 ?g/L)) and rhIL-4(40 ?g/L).Cells were incubated with(100 mg/L) native or oxidized LDL for 72 h.The formation of foam cells was investigated by electron microscopy and oil red O staining.Phenotypic and immune functional assays were used with FACS,FITC-dextran phagocytosis,allogeneic mixed T lymphocytes reaction and secretion of Th1/Th2(IL-12/IL-2) cytokines were also conduced.RESULTS: DCs treated with ox-LDL,but not native LDL were induced into foam cells after cultured for 72 h.Compared with native LDL,ox-LDL-treated DCs were less potent in FITC-dextran phagocytosis.ox-LDL promoted allogeneic T cells proliferation.Moreover,ox-LDL upregulated CD80(72.4? 9.6 vs 89.5?10.1,P

Objective To observe the protective effect of progesterone on brain edema in newborn rats with hypoxic-ischemic encephalopathy(HIE).Methods Fifty-two 7-day-old neonatal rats were randomly divided into 5 groups:normol control group(group A),hypoxic-ischemic group (group B) and pretreatment groups(group C,D and E).Rats were subjected to left common carotid artery ligation,then were exposed to 8% oxygen and 92% nitrogen for 2.5 hours to establish HIE model.Progesterone was injected intraperitoneally into the groups C,D and E rats respectively at 30 minutes before hypoxia.All rats were killed at the 24 hours after operations,then the contents of water,sodium,potassium were mensurated. Results The contentation of water in group B was higher than that in group A,the contentation of water,sodium in groups C,D and E were significantly lower compared with group B, but the contents potassium were no difference between group C,E and B. Conclusion Progesterone exerts a prominent preventive and protetive effects on the hypoxic ischemic brain edema in newborn rats.

Objective To explore the expressions of superoxide dismutase(SOD)and matrix metalloproteinase-3(MMP-3) in the brain tissues of newborn rat after hypoxic-ischemic(HI) and the effects of progesterone(PROG) on SOD and MMP-3 expression.Methods Seventy-two neonatal SD rats were randomly divided into 4 groups:normal control group(normal group),sham-operated group,HI group and PROG group.The model of neonatal rat with hypoxic-ischemic brain damage(HIBD) was made.The permeability of the blood-brain barrier was observed by using transmission electron microscopy,the level of SOD in the brain was assessed by hydroxylammoniumchloride autoxidation,MMP-3 protein expression in cerebral cortex part of the brain was detected by immunohistochemical.SPSS 12.0 software was used to analyze the data.Results In normal group and sham-operated group,capillary vessel′s morphology of blood brain barrier of neonatal rats were integrity and smooth,and structure were clarity.The permeability of blood-brain barrier in HI group was obviously enhanced and had slight changes in PROG group.Compared with the sham-operated group,the level of SOD in HI group significantly decreased(P

Objective To observe the effects of recruitment maneuver (RM) and tidal volume with different amount of gas after RM ventilation on lung diastole function in rats with acute lung injury (ALI). Method ALI rat models were induced by intravenous infusion of lipopolysaccharide (LPS) in dose of 6 mg/kg. Twenty-five rats were randomly(random number) divided into control group ( n = 5), ALI group ( n = 5), low tidal volume group (LV group,VT= 6 mL/kg, n = 5), sustained inflation (SI) with low tidal volume (SI+ LV group, VT=6 mL/kg, n = 5), and SI with moderate tidal volume group (SI+ MV group, VT= 12 mL/kg, n = 5). The RM carried out by using SI with airway pressure 30 cmH-2O for 30 seconds, and the positive end-expiratory pressure (PEEP)was set at 5 cmH2O. Lung tissue was taken after mechanical ventilation for 5 hours. The mean arterial pressure (MAP) was monitored throughout the entire course of experiment. Endothelin-1 ( ET-1 ), endothelial nitricoxide synthase (eNOS), and acetylcholine-(Ach-) induced endothelium-dependent relaxation response of isolated pulmonary artery rings were investigated after mechanical ventilation for 5 hours. Results The LPS increased the ET-1 level in lung tissue, decreased the level of eNOS in lung tissue, and impaired the Ach-induced endothelium-dependent relaxation response in pulmonary vassals, without obvious influence on systemic hemodynamics. SI + LV significantly reduced LPS-induced elevation of ET-1 level, and increased the level of eNOS, and significantly lessened endothelial dysfunction and ameliorated dysfunction od endothelium-dependent relaxation in pulmonary vas sals. Conclusions RM with high tidal volume or lowtidal volume ventilation could improve the lung vascular endothelial function of rats with acute lung injury, and RM with low tidal volume ventilation could lessen more the injury of lung vascular endothelial diastole function in rats with acute lung injury.

Recombinant human BMP-2 was compounded with chitosan/gelatin/hydroxyapatite(HCG) scaffold and the complex was sterilized by 60Co radiating. Osteoblast isolated from cranial bones of newborn rat was primary cultured and seeded onto the complexes. 3 days after culturing, scanning electron microscope(SEM) was applied to detect the compatibility of the cell with the complex. SEM showed osteoblast attached closely with the complex and grew well in its pores. Then the complexes with osteoblast modification were implanted into athymic nude mice subcutaneously. 8 weeks after implantation, X-ray photograph and histological observation were applied to detect the bone formation of the complexes. Under X-ray a high-density areas consistent with the shape of the implanted complex could be seen. Histological observation also proved there was bone formation in the interspace of the complex. A conclusion was drawn that rhBMP-2 compounded HCG scaffold had good osteogenesis ability in vivo.

The exploration of drug toxicity and mechanisms is a vital component in ensuring the safe use of drugs in clinical practice, as this topic has attracted widespread concern. The intestinal flora holds great significance for drug metabolism, efficacy and mechanism, and is an instrumental metabolic organ that facilitates material information transfer and biotransformation. However, an increasing number of studies have shown that intestinal bacteria are closely related to the toxicity of specific drugs. On the one hand, drugs are transformed into toxic metabolites under the influence of intestinal bacteria, thus inducing direct drug toxicity. On the other hand, the composition and function of the intestinal flora are altered under drug influence, resulting in disruption of endogenous metabolic pathways. Consequently, this disruption compromises the intestinal barrier and affects other organs, leading to indirect drug toxicity. This review meticulously compiles recent examples of drug toxicity attributed to intestinal bacteria, explores in depth the contention that metabolic enzymes of gut microbiota may be of great influence on oral drug toxicity, and outlines prospective avenues for future research on gut microbiota and drug toxicity and mechanisms. This not only provides novel perspectives for the judicious clinical utilization of drugs but also offers insights for the safety assessment of innovative pharmaceuticals.