Objective:To study inhibited tecomerase activity of HL-60 cells in human cancer cell by Icarrin(ICA) and its mechanism.Methods:MTT assay,NBT assay, TRAP-PCR,RT-PCR assay,Flow Cytometry.Results:ICA inhibited telomerase activity in HL-60 cells significantly.It was negative correlation between telomerase activity and the expression ratio of CD11b antigen in HL-60 cells.It can induced HL-60 cells to differentiate into mature granulocytes.It can changed cell cycle distribution of HL-60 cells,which was reflected by the accumulation of the vast majority of cells in the G0/G1phase and the loss of cells in the S phase. It can downregulated cell proliferation related gene c-myc;upregulated p21 gene protein and mRNA expression.Conclusion:This study proved mechanism of ICA on inhibited telomerase activity from gene-protein-effect of cell level in HL-60 cells.

We innovated video assessment integrated teaching method on the basis of clinical case discussion,teaching rounds,problem-based learning,case method and micro teaching.According to this video feedback teaching,students became teaching subject and teacher acted as guide.In order to realize the purposes of early contact with clinical practice,more clinical practice and repeated clinical practice teaching,we implemented student-centered small class teaching,which was heuristic,inquisitive,interactive and was discussion-based.At the same time with the help of medical simulation equipment and video feedback teaching,this method developed students' life-long learning ability and work competence and combined theory with practice,demonstration with imitation as well as standards with innovation.This method was not only suitable for theoretical study but also for skills training,especially for standardization training.

AIM Mechanism of icariin (ICA) and pseudomonas jinanensis agent (PJA) on anti-metasta-sis of a highly metastatic human lung tumor cell line (PG) and the effect type of the combination of ICA,PJA were studied. METHODS PG cells were treated with ICA、PJA, or the combination of both in vitro. Adhesion assay, invasion assay, migration assay, flow cytometry (FCM) and immunohistochemical straining were used. The effects of ICA and PJA combination were evaluated with Q method of Jin Zheng-Jun. RESULTS ICA、PJA could decrease PG cells adhesive ratio to laminin substrate in a time-dependent manner ( P

Objective To study the effect on Henoch-Schnlein purpura nephritis with cyclophosphamide (CTX) intravenous pulse therapy.Methods Fourty cases of Henoch-Schonlein purpura nephritis were divided into observation group and control group.The observation group:8～10 mg/(kg?time) of CTX was added into 100 mL of saline which was dropped intravenously,2 days was a period of treatment, intermission of 30 d, and the total duration was 4-6 months. The control group only applied prednisone and dipyridamole.Results After CTX pulse therapy 24 h proteinuria determination and hematuria decreased obviously. The effect before and after therapy had significant difference (P

Objective To study the effect of glucocorticoid receptor(GCR) on the treatment of patients with nephrotic syndrome(NS) and to observe the accommodation effect of herbal gynostemmae,acanthopanax senticosus harns on GCR levels.Methods The patients were divided into 3 groups: the healthy control group,treatment group Ⅰ(GC only) and treatment group Ⅱ(combination with herbal gynostemmae,acanthopanax senticosus harns and GC),radioligand binding assay was used to measure the GCR levels of each group.At the same time,the urine protein ratio within 24 hours was observed in each group.Results Compared with healthy control group,the GCR levels of treatment group Ⅰ and Ⅱ were both reduced,but after 4 weeks of treatment in the treatment group Ⅱ,not only GCR level recovered but also the urine protein were decreased faster than treatment group Ⅰ.Conclusions Herbal gynostemmae,acanthopanax senticosus harns can accommodate the GCR levels of children with NS.They can also eliminate urine protein and cure NS ideally.

Objective: To investigate the influence of Icarrin(ICA) on transforming growth factor ?2(TGF?2) expression by PG cells and the mechanisms of reversion of TGF?2 mediated immunosuppression by ICA.Methods: Cell proliferation and cytotoxici- ty were assayed by MTT assay. mRNA level of TGF?2 and perforin was detected by RT-PCR assay. assay.Expression of TGF?2 and IL- 2R? was analysed by folw cytometry assay. Results: ICA could inhibit the protein and mRNA expression of TGF?2 in PG cells. It could also reverse the supressed cytotoxicity of LAK, CD3AK cells by TGF?2. The IL-2R? expression on LAK and perforin gene transcription and proliferation of CD3AK inhibited by TGF?2 were also partly recovered. Conclusion: The anti-anti-tumor activity of ICA is at least partly due to its capability of inhibiting TGF?2 expression in tumor cells and restoring the cytotoxicity of immunocompetent cells inhibited by TGF?2.

Human CD3AK cells were prepared from peripheral blood mononuclear cells by culturing with recombinant IL-2 and antiCD3AK McAb. The mechanism and regulation of CD3AK cytotoxic activity with cytokines (rhIFN-?, rhIFN-?, TNF) and chernotherapeutic agents (CDDP or ADM) were observed by LDH-release assay, ABC-CELISA and the flow cytometric assay. The results showed: (1) Adhesion molecules ICAM-l/LFA-1 participated in CD3AK-mediated killing of tumor cells, hrlFN-? and TNF enhanced cytotoxicity of CD3AK through this pathway. (2) CD3AK could indirectly kill tumor cells by releasing soluable cytotoxic factors. (3) The membrane-associated TNF may be involved in CD3AK-mediated cytotoxicity. (4) CD3AK cells could induce the apoptosis of tumor cells. (5) Pretreatment of tumor cells with CDDP or ADM resulted in the increased vulnerability of tumor cells to CD3AK-mediated killing, the enhancement of CD3AK-mediated cytotoxicity by CDDP was relative to the increased expression of ICAM-1, HLA-ABC on tumor cell membrane.

Objective To observe the effect of healthy education on BMD and the risk of bone fracture in pa- tients with primary osteoporosis.Methods 628 patients with primary osteoporosis were randomly divided into two groups under the same conditions,and healthy education were conducted in treated group but were not conducted in control group.Two years later,BMD and the rates of bone fractures were collected and analysed.Results Compared with control groups,the bone loss was significantly lower at the feroral neck,Ward's triangle and the great trochanter,and the risk of bone fractures was remarkably reduced in treated group(P

AIM: To observe the effect of osthole on tricalcium phosphate (TCP) particles-induced calvarial osteolysis in vivo.METHODS:Male ICR mice were randomly divided into sham group , TCP group and osthole group .A mouse calvarial model of osteolysis was established by TCP particles .On the second postoperative day , osthole (20 mg/kg) was locally injected into the calvarium under the periosteum 3 times a week.Two weeks after osthole treatment , blood and calvaria were collected to determine the level of bone turnover markers such as alkaline phosphatase ( ALP) , osteocalcin and tartrate-resistant acid phosphatase ( TRACP) .The periosteum was performed to examine the release of tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and IL-1βby ELISA.The calvaria was obtained for histological and molecular analyses.RESULTS:Data from HE and TRACP staining revealed that osthole prevented TCP particles-induced obvious increase in osteoclastogenesis and resorption area in the metaphysis of mouse calvaria .Osthole treatment increased ALP ac-tivity and osteocalcin level , and dncreased the activity of TRACP in the mouse serum compared with TCP group .Further-more, TCP particles-induced the releases of TNF-α, IL-6 and IL-1βwere significantly suppressed by osthole treatment .In addition, Western blot demonstrated that endoplasmic reticulum ( ER) stress markers such as glucose-regulated protein 78 (GRP78) and CAAT/enhancer binding protein homologous protein (CHOP) were significantly up-regulated in TCP parti-cles-implanted calvarial mice , indicating that TCP particles triggered an ER stress response in the mouse calvarial osteolysis model , which obviously attenuated by osthole .CONCLUSION:Osthole inhibits TCP particles-induced calvarial osteolysis in mice, which is mediated by inhibition of ER stress signaling pathway .

AIM: To investigate the protective effect of Ginkgo biloba extract (GBE) on diabetic testis and explore its possible mechanism. METHODS: Testicular structure of streptozotocin-induced diabetic rats was observed under light microscopy (LM) and transmission electron microscopy (TEM). Content of malondialdehyde (MDA), NO_2~-/NO_3~- and activity of superoxide dismutase (SOD), nitric oxide synthase (NOS) were determined in testicular homogenate. RESULTS: In diabetic rats, it was manifestated as deformation of seminiferous tubule, atrophy and shedding of germinal epithelium under LM, while expansion of smooth endoplasmic reticulum, formation of fatty vacuoles and decrease of lysosome obviously in the cytoplasm of sertoli cell under TEM, the injury of testicular tissue was improved by GBE. Compared with diabetic rats, activity of SOD increased while activity of tNOS and iNOS, content of MDA and NO_2~-/NO_3~- decreased in GBE-treated rats. CONCLUSION: GBE could effectively prevent the development of diabetic testis and the effect may be partly achieved by resisting lipid peroxidation,restraining the activity of testicular tissue iNOS and reducing the pathological alterations of NO. [