Objective To investigate the effects of dexamethasone(DEX)on the secretion of interleukin (IL)-17 and interferon(IFN)-γ and the proportion of Th17,Tc17,Th1 ,Tc1 cells in peripheral blood mononuclear cells(PBMCs)of patients with systemic lupus erythematosus(SLE). Methods Thirty hospitalized SLE patients were recruited and twenty-two healthy volunteers were recruited as healthy controls. PBMCs were separated from SLE patients and healthy controls and then was cultured in vitro by medium or PMA/Ionomycin or PMA/Ionomycin +dexamethasone for six hours. Four- color immunofluorescent staining and flow cytometric assay were used to analyze the percentage of Th17,Tc17,Th1,Tc1 cells in PBMCs. Concentrations of IL-17 and IFN-γ in plasma and the supernatants of PBMCs which were cultured for 24 hours were measured by enzyme linked immunosorbent assay (ELISA). Results The plasma concentrations of IL-17 and IFN-γwere elevated in SLE patients as compared to the controls(P ＜ 0.05). No significant differences were observed between patients and controls for the spontaneous production of IL-17 and IFN-γ or percentage of T subsets expressed by PBMCs. After the stimulation of PMA,compared with the controls,the level of IL-17 was significantly elevated in the supematants of PBMCs and the percentages of Th17 and Tc1 in SLE patients increased significantly(P ＜ 0. 05). However,there showed no significant differences between SLE patients and the controls for the percentages of Th1 and Tc17 cells. DEX could significantly decrease the production of IL-17(P ＜ 0. 01)and the percentages of Th17,Tc1 cells by the active PBMCs(P ＜ 0. 05). Conclusions There is abnormal expression of T subset cells and their cytokines in vivo of SLE patients. DEX can interfere with immunological pathological process in the cytokine network imbalance of SLE patients and shows powerful inhibition of IL - 17. Our results may provide some laboratory evidence for the clinical application of corticosteroids.

Brain ; pathology ; Humans ; Infant, Newborn ; Lung ; pathology ; Male ; Seizures ; etiology ; pathology ; Tomography, X-Ray Computed ; Tuberous Sclerosis ; complications ; pathology

Animals ; Cardiovascular Diseases ; etiology ; metabolism ; Humans ; Inflammation ; metabolism ; Periodontitis ; complications ; metabolism ; microbiology ; Platelet Aggregation ; physiology ; Porphyromonas gingivalis ; pathogenicity ; RNA, Messenger ; metabolism ; Receptor, PAR-1 ; metabolism ; Receptor, PAR-2 ; genetics ; metabolism ; Receptors, Proteinase-Activated ; metabolism ; Receptors, Thrombin ; metabolism

Apgar Score ; Autopsy ; Fatal Outcome ; Heart Neoplasms ; diagnosis ; diagnostic imaging ; pathology ; Heart Ventricles ; diagnostic imaging ; Humans ; Infant, Newborn ; Male ; Myxoma ; complications ; diagnosis ; diagnostic imaging ; pathology ; Rare Diseases ; Ultrasonography

The origin and development of umbilical therapy in traditional Chinese medicine is explored from related literature in the history. As a result, the Shang period is regarded as initial period of umbilical therapy, while periods from Han Dynasty, Jin Dynasty and Southern-Northern Dynasties to Sui Dynasty and Tang Dynasty could be taken as stage of primary development. Time from Song Dynasty, Jin Dynasty and Yuan Dynasty to Ming and Qing Dynasties is believed as mature stage. Also the manipulation, application principle, indications and contraindications of umbilical therapy are explained. A brief overview of modern development of umbilical therapy is also described.
China ; History, 15th Century ; History, 16th Century ; History, 17th Century ; History, 18th Century ; History, 19th Century ; History, 20th Century ; History, Ancient ; History, Medieval ; Humans ; Medicine in Literature ; Medicine, Chinese Traditional ; history ; methods ; Umbilicus ; physiology

Burns, Inhalation ; complications ; Humans ; Male ; Middle Aged ; Nitric Acid ; adverse effects ; Pulmonary Edema ; chemically induced ; therapy

Adolescent ; Adult ; Busulfan ; therapeutic use ; Female ; Hematopoietic Stem Cell Transplantation ; methods ; Humans ; Male ; Middle Aged ; Transplantation Conditioning ; methods ; Young Adult

Glucagon-like peptide 1(GLP-1) is an important member of incretin.Takingitoralymay stimulate the terminal ileum and colon L cel s to secrete GLP-1. After GLP-1 biding specific receptor GLP-1 receptor ( GLP-1R), it exerts the roles of promoting glucose-dependent insulin secretion, inhibiting glucagon secretion, and decreasing plasma glucagon level. The molecular mass of GLP-1 is relatively smal er and can directly cross the blood-brain barrier, and both central and peripheral nervous systems have the GLP-1R expression. GLP-1 significantly improves neurological deficits and reduces infarct volume. It may exert neuroprotective effect through the mechanisms of inhibiting the inflammatory response, oxidative stress, and cel apoptosis. This article review s the discovery of GLP-1, its biological characteristics and neuroprotective effect in cerebral ischemia.

OBJECTIVE:To optimize the extraction technology for Huangshen electuary.METHODS:In this experiment the optimum extraction technology for Huangshen electuary was investigated by the L9(34) orthogonal test with the content of Astragaloside Ⅳ as technology index.The effects of three factors including the extraction times,time length of extraction and solvent ratio were investigated.RESULTS:The best extraction technology for Huangshen electuary was as follows:the solid-liquid ratio was 1∶10 and the decoction was carried out for 3 times(2 hours/time).CONCLUSION:The optimum extraction technology for Huangshen electuary is stable and feasible.

AIM: To investigate the anti-proliferative and apoptosis-inducing effect of honokiol on U937 cell line in vitro. METHODS: Proliferation of U937 cells and PBMCs were analyzed by MTT assay. Flow Cytometry and cell morphological observation were performed to find out whether honokiol could affect cell cycle and induce apoptosis of U937 as well as PBMCs in vitro. RT-PCR and Western blotting techniques were used to detect the changes in mRNA expression and protein production of bcl-2 and bax in U937 cells after treated with honokiol. RESULTS: Honokiol could significantly inhibit the proliferation of U937 cells at IC_ 50 concentration of 11.8 ?g/mL, but slightly inhibit the proliferation of PBMCs, at IC_ 50 concentration of 40.3 ?g/mL, respectively. Most honokiol-treated cells were arrested at G_0/G_1 phase. CONCLUSION: Honokiol could inhibit the proliferation and induce apoptosis of U937 cells, while has little effect on the proliferation and survival of PBMCs. Bax might be involved in the gene regulation related to honokiol-induced apoptosis.