Autoimmune Diseases ; Hereditary Autoinflammatory Diseases ; Humans

Child ; Humans ; Immune System Diseases ; genetics ; Immunogenetics ; Pediatrics

Epstein-Barr Virus Infections ; Humans ; Lymphoproliferative Disorders ; diagnosis ; genetics

Blood Flow Velocity ; Child ; Coronary Aneurysm ; diagnostic imaging ; Humans ; Mucocutaneous Lymph Node Syndrome ; diagnostic imaging ; Ultrasonography, Doppler

Animals ; Colonic Neoplasms ; metabolism ; pathology ; Female ; Humans ; Liver Neoplasms ; metabolism ; secondary ; Lymphatic Metastasis ; Neoplasm Proteins ; metabolism ; Ovarian Neoplasms ; metabolism ; pathology ; Protein Tyrosine Phosphatases ; metabolism ; Stomach Neoplasms ; metabolism ; pathology

Acute Disease ; Child ; Cytidine Deaminase ; genetics ; Humans ; Leukemia ; genetics ; Polymorphism, Single Nucleotide ; genetics

Objective: To observe the effect of cilostazol on the ion channel of right ventricular cells in experimental rats, and to explore the ion channel mechanism of ciolstazol for preventing the ventricular arrhythmia in Brugada syndrome.
Methods: Our research was composed of 2 groups: ①Perfusion group, the cells were treated in 4 sub-groups by cilostazole at 1, 2, 5, 50μmol/L respectively, and there were 9, 5, 3, 7 cells were recorded at each sub-group to observe the differences of current density Ito at before and after treatment. ②Oral group, which included 4 sub-groups:Control 1 with 7 rats, Experiment 1 with 5 rats, and Control 2 with 8 rats, Experiment 2 with 6 rats respectively. The differences of current density Ito and ICa,L were studied between each Control and Experiment sub-groups.
Results: In Perfusion group,①with cilostazole 1, 2, 5, 50μmol/L treatment, the current density Ito decreased in all sub-groups, when the self-command voltage at+60mV, the Ito was signiifcantly different in each sub-group at before and after treatment, all P<0.05.②When each command voltage decreasing, the reduction rates of Ito were similar among 4 sub-groups, all P>0.05. In Oral group,①When the self-command voltage from-50mV reached the maximum of+60mV, the Ito was similar between Control 1 and Experiment 1 sub-groups, P>0.05.②When the self-command voltage at+10mV, the current density of ICa,L was slightly higher in Control 2 sub-group than that in Experiment 2 sub-group, P>0.05.
Conclusion: Direct perfusion of cilostazole in right ventricular cells may inhibit Ito in experimental rats, such effect was similar with cilostazole treatment at (1-50)μmol/L. Cilostazole might prevent the ventricular arrhythmia in Brugada syndrome in experimental rats.

Aim To study the immunomodulatory activity of total flavonoids of Litsea Coreana Leveille (LCTF) on cyclophosphamide(CY)-induced immunosuppressive mice. Methods CY (50 mg?kg-1) was administered by intraperitoneal(ip)injection for 2 consecutive days to induce immunosuppressive model. Carbon clearance, quantitative hemolysis and DNFB-induced delayed-type hypersensitivity(DTH) were applied to assay effects of LCTF on nonspecific immunity, humoral immunity and cellular immunity. Results In carbon clearance test, the clearance index (K) and values of phagocytic index (?) were elevated by LCTF (200 and 400 mg?kg-1), indicating the phagocytosis of macrophages was enhanced in immunosuppressive mice.In quantitative hemolysis, productions of IgM and IgG in serum and hemolysin in splenocytes were enhanced in immunosuppressive mice by LCTF (100 and 200 mg?kg-1). LCTF (200 and 400 mg?kg-1) obviously increased DTH reactivity in immunosuppressive mice. LCTF not only increased percentages of T cells expressing CD4+ and CD8+,but also enhanced the ratio of the two subset of T lymphocyte,and LCTF (200 and 400 mg?kg-1) could also improve IL-2 production of spleen lymphocytes. Conclusion LCTF showed significant immunomodulatory property on immunosuppressive mice through specific and nonspecific immunity.

Aim To investigate the effects of baicalin on cognitive function in global cerebral ischemia reper-fusion rats, and the probable mechanism involved. Methods Sixty male Sprague-Dawley(SD) rats were randomly divided into Sham operation group ( S group) , global cerebral ischemia reperfusion group ( I/R group) , global cerebral ischemia reperfusion + ba-icalin treatment group ( I/RB group) , twenty in each. Model was induced via the bilateral occlusion of the
common carotid arteries plus hemorrhagic hypotension. 12 h after reperfusion, rats in I/RB group were given baicalin (100 mg·kg-1 ) saline solution by intragas-tric administration twice per day for 7 days. Rats in S group and I/R group were given the corresponding dose of saline infusion at the same time. Morris water maze test was employed to detect spatial learning and memo-ry. BrdU immunohistochemistry was used to detect the proliferation of neural precursor cells ( NPCs ) in the
brain. Expression of COX-2 in the brain tissue was measured by Western blot. Results Compared to I/R group, baicalin improved spatial learning and memory damage ( P <0. 05 ) , increased the number of BrdU-positive cells in the DG and SVZ ( P<0. 01 ) , and re-duced the expression of COX-2 in the brain ( P <0. 01 ) . Conclusions Baicalin could ameliorate cog-
nitive function in the rats with global cerebral ischemia reperfusion, which might be associated with its inhibi-tory effects on the expression of COX-2 , thereby in-creasing the proliferation of NPCs in the brain.

AIM: To investigate the potential role of 14-3-3 tau in trophoblast cells on invasiveness. METHODS: 14-3-3 tau expression was detected in first-trimester villi, deciduas and human trophoblastic cell line (BeWo) by immunohistochemistry. Small interference RNA (siRNA) targeting 14-3-3 tau was transfected into BeWo cells. The effects of down-regulated 14-3-3 tau on invasion of human trophoblasts cell line BeWo were examined by matrigel invasion assay, and the transcription, translation of E-cadherin and snail were estimated by RT-PCR or Western blotting. U0126 was used to detect the extracellular-signal related kinase 1/2 (ERK1/2) function on down-regulation of 14-3-3 tau induced cell invasion. RESULTS: 14-3-3 tau was detected in the invasive trophoblastic cells in the first trimester villi and that invaded to the deciduas. BeWo cells also expressed 14-3-3 tau. Down-regulation of 14-3-3 tau increased the invasive cell-number of BeWo, as well as the expression of snail, and inhibited E-cadherin. U0126 inhibited the enhanced invasiveness in these cells induced by the down-regulation of 14-3-3 tau. CONCLUSION: 14-3-3 tau may regulate the invasiveness of human trophoblastic cells through ERK1/2 signaling pathway.