25-Hydroxyvitamin D deficiency is prevailing in patients with chronic kidney disease,Vitamin D in addition to influence the metabolism of calcium and phosphorus,also participates in regulation of renal anemia.This paper will be reported 25-Hydroxyvitamin D regulates renal anemia from three aspects of the relationship of vitamin D and iron metabolism,erythropoietin (EPO) and micro inflammation.

Asthma ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Medicine, Chinese Traditional ; Phytotherapy

[Objective] To observe the cure effect of combination of TCM and WM on osteoporosis.[Method] Randomly divide the patients into 3 groups,group A takes trout calcitonin,B is added with self-made Zhuanggu Bushen Decoction,C is added with acupuncture on the basis above.Meanwhile all take calcium and active vitamin D for assistance,compare the results after 2 courses.[Result] In group A,3 were cured,3 had marked effect,4 effective,total effective rate 40%;in B,they were 6,6,4 and 64% respectively;in C,they were 8,10,5 and 92% respectively.In comparison,B was better than A,C better than B.[Conclusion] Combination of TCM and WM has marked cure effect on osteoporosis.

Candidiasis ; drug therapy ; immunology ; metabolism ; Diabetes Mellitus, Type 1 ; complications ; drug therapy ; immunology ; therapy ; Humans ; Lupus Erythematosus, Systemic ; drug therapy ; immunology ; metabolism ; Mycoses ; complications ; immunology ; therapy ; Paraneoplastic Syndromes ; drug therapy ; immunology ; metabolism ; Pemphigus ; drug therapy ; immunology ; metabolism

The mechanism of the development of sporadic renal cell carcinomas is complicated,which is different from that of hereditary renal-cell carcinoma.Genetics abnormality such as loss of 3p,VHLgene mutations may help differentiate pathological subtype of renal cell carcinoma and some gene markers may be useful predictors for prognosis.The current status of genetic study in renal cell carcinomas is reviewed in this article.

Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; CD3 Complex ; metabolism ; Chromosomes, Human, Pair 3 ; Chromosomes, Human, Pair 5 ; Cyclophosphamide ; therapeutic use ; Doxorubicin ; therapeutic use ; Gene Rearrangement, T-Lymphocyte ; Humans ; L-Lactate Dehydrogenase ; metabolism ; Lymphoma, T-Cell, Peripheral ; drug therapy ; genetics ; metabolism ; pathology ; Mutation ; Neoplasm Staging ; Prednisone ; therapeutic use ; Vincristine ; therapeutic use

Anti-Asthmatic Agents ; therapeutic use ; Asthma ; epidemiology ; etiology ; therapy ; Body Mass Index ; Child ; Child, Preschool ; Chronic Disease ; Humans ; Obesity ; complications ; epidemiology ; prevention & control ; Risk Factors

Objective: To evaluate the effect of alendronate on osteoprotegerin (OPG) and receptor of activator of nuclear factor κB-ligand (RANKL) expression in human marrow stroma cells (hMSCs) in vitro. Methods: hMSCs were isolated from human marrow, cultured in vitro, and randomly divided into two groups: alendronate group, hMSCs culture fluid containing 1 × 10-7 mol/ L alendronate; control group, no special treatment but culturing hMSCs in DMEM. Two weeks after treatment, the expressions of OPG and RANKL were evaluated by RT-PCR and Western blot. Results: hMSCs became uniform spindle-shaped fibroblasts. As cells proliferated, they formed colonies and showed whirlpool arrangement. After one week's treatment, hMSCs in alendronate group had reduced processes and gradually showed disc shape, which did not happen in control group but kept fibroblast shape and just increased in density. In RT-PCR, the ratio of OPG/RANKL in alendronate group and control group was 8.77±1.16 and 4.58±1.27, respectively. In Western blot, the ratio of OPG/RANKL in alendronate group and control group was 2.58±0.47 and 1.52±0.32, respectively. The ratio of OPG/RANKL was higher in alendronate group than in control group (P<0.01). Conclusion: Alendronate enhances OPG expression and inhibits RANKL expression of hMSCs in vitro.

Objective: To evaluate the effect of alendronate on osteoprotegerin (OPG) and receptor of activator of nuclear factor κB-ligand (RANKL) expression in human marrow stroma cells (hMSCs) in vitro. Methods: hMSCs were isolated from human marrow, cultured in vitro, and randomly divided into two groups: alendronate group, hMSCs culture fluid containing 1 × 10-7 mol/ L alendronate; control group, no special treatment but culturing hMSCs in DMEM. Two weeks after treatment, the expressions of OPG and RANKL were evaluated by RT-PCR and Western blot. Results: hMSCs became uniform spindle-shaped fibroblasts. As cells proliferated, they formed colonies and showed whirlpool arrangement. After one week's treatment, hMSCs in alendronate group had reduced processes and gradually showed disc shape, which did not happen in control group but kept fibroblast shape and just increased in density. In RT-PCR, the ratio of OPG/RANKL in alendronate group and control group was 8.77±1.16 and 4.58±1.27, respectively. In Western blot, the ratio of OPG/RANKL in alendronate group and control group was 2.58±0.47 and 1.52±0.32, respectively. The ratio of OPG/RANKL was higher in alendronate group than in control group (P<0.01). Conclusion: Alendronate enhances OPG expression and inhibits RANKL expression of hMSCs in vitro.

OBJECTIVE: To study the growth inhibitory and apoptosis-inducing effect of wogonin on hepatocarcinoma cell line HepG2. METHODS: HepG2 cell line was treated with various concentrations of wogonin. Proliferation was determined by MTT test and morphology observation. Flow cytometry was applied to detect the wogonin-induced apoptosis and to analyse the cell cycle. Western blot was used to detect HDAC1 and HDAC2 expression. RESULTS: Wogonin had a growth inhibitory and apoptosis-inducing effect on HepG2 cell. The cell showed G2/M arrest by cell cycle analysis. A characteristic apoptosis change including nuclear disintergration and chromatin agglomerate was displayed. Western blot results show increase of cleave PARP, but not change in HDAC1, HDAC2 expression. CONCLUSION: Wogonin has a growth inhibitory and apoptosis-inducing effect on hepatocarcinoma cell line HepG2.