Genetic Heterogeneity ; Humans ; Magnetic Resonance Imaging ; methods ; Neoplasms ; diagnosis ; genetics ; pathology ; Positron-Emission Tomography ; methods ; Tomography, X-Ray Computed ; methods

0.05).The degreeⅢ～Ⅳthrombocytopenia was more common in group A than in group B,but the degreeⅢ～Ⅳhypolekocytosis and phlebitis was more serious in group B.Conclusion NC and GC for treating refractory metastatic breast cancer have a high response rate and tolerable side effects.

Objective To summarize the methods of diagnosis and results of surgical treatment of pancreatic insulinoma. Methods The clinical data of 137 patients with insulinoma treated in our hospital during the past twenty-six years were reviewed retrospectively.Results There were 77 males and 60 females. All of them were characterized by the Whipple′s triad. The sensitivity of ultrasonography, CT and MRI for localization was 35.1%, 67.9% and 58.1% respectively. One hundred and tweenty-six patients underwent operation. Of them, 102 cases had tumor enucleation, 4 cases had pancreaticoduodenectomy, 16 cases had distal panreatectomy, and the other 4 cases had only laparotomy. Of the 122 patients, who underwent resection, the tumor was benign in 118(96.7%) and malignant in 4(3.3%). The diameter of the tumor was less than 2cm in 86.9% of cases. In 98.4% of cases the tumors were single and in 1.6% of cases were multiple. 13.1% of the tumors located in the head, 46.7% in the body, and 40.2% in the tail.Conclusions Whipple′s triad and the measurement of fasting glucose, IRI, IGR, C-peptide, and proinsulin levels contribute to the diagnosis of insulinoma. However, the preoperative tumor localization is still difficult. Tumor enucleation is the technique of choice when feasible. Patients in whom tumor localization is unsuccessful at operation should be carefully evaluated to be certain of the diagnosis, and in general should not undergo blind resection.

Objective To explore the inhibitory effects of Corilagin on the production of proinflammatory cytokines in microglia induced by radiation. Methods The cytotoxicity of Corilagin was measured by MTT assay. Microglia BV-2 cells were irradiated 0 or 32 Gy after pretreated with Corilagin for 12 hours. Realtime-PCR was used to detect the mRNA levels of inflammatory cytokines, such as IL-1β,TNF-α on several time-points. The content of nitric oxide (NO) was determined with nitrate reductase method. The translocation of NF-κB was measured by Western blot and immunocytochemical stain.Confocal microscopy was used to observe the expression of Iba-1 and Nemo. Results No cytotoxicity was detected on BV-2 cells with 1-10 μg/ml Corilagin. Iba-1 expression in microglia cells was activated by irradiation, the expression levels of inflammatory cytokines, such as IL-1β, TNF-α and NO were also elevated. Whereas, the production of IL-1 β, TNF-α in activated microglia cells was significantly inhibited with 5 μg/mL corilagin ( tIL-1β = 6. 341, tTNF-α = 3.41 1, tNO = 3. 134, P ＜ 0. 05 ). Corilagin significantly inhibited the expression of Nemo and the translocation of NF-κB p65. Conclusion Corilagin could inhibit the activation of irradiated microglia cells and down-regulate the expression of inflammatory cytokines, via inhibition of the NF-κB signaling pathway.

Aim The effect of tetrandrine on TGF-?1 mRNA expression in glomerulosclerosis rat was observed. Methods The rats were randomly divided into four groups, such as the normal control group (sham operative rat), glomerulosclerosis model group,tetrandrine group and amlodipine group. The expression of TGF-?1 mRNA was analyzed by Northern blot hybridization. Results The expressions of TGF-?1 mRNA in two treating groups were much lower than untreated model group. There were no difference between these two treating groups. Conclusion Tetrandrine can decrease the expression of TGF-?1 mRNA in glomerulosclerosis rat induced by unilateral renctomy plus adriamycin.

OBJECTIVETo explore the therapeutic effect of Jiawu Mufangji Decoction (JMD) in treating rats with adjuvant arthritis (AA) and its mechanism.

METHODSAA model rats induced by Freund's complete adjuvant were treated with JMD by gastrogavage starting from 18 days after modeling. On the 39th day, body weight, spleen and thymus index, and swelling degree of paw of the AA rats were measured, pathological changes of the ankle joint tissue were observed using HE staining, and serum levels of interleukin-1beta (IL-1beta) and tumor necrosis factor a (TNF-alpha) were determined by enzyme-linked immunosorbent assay (ELISA).

RESULTSJMD could relieve the symptoms of AA rats, decrease the paw swelling, improve the weight and spleen and thymus index, reduce the dropsy of joints and lymphocytes infiltration, inhibit the proliferation of synovium, and obviously lower the serum levels of interleukin-1beta and TNF-alpha.

CONCLUSIONThe therapeutic effect of JMD might be related to its action in down-regulating the serum levels of IL-1beta and tumor necrosis factor alpha.

Animals ; Arthritis, Experimental ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Immunosuppressive Agents ; therapeutic use ; Interleukin-1 ; blood ; Male ; Phytotherapy ; Rats ; Rats, Wistar ; Tumor Necrosis Factor-alpha ; metabolism

Objective:To investigate RNA interference and apoptosis induced by LPS in kidney epithelial cells through silencing C5aR gene with small hairpin RNA (shRNA).Methods:We construct the eukaryotic expression vector of small hairpin RNA targeting rat C5aR gene,and transfected RK3E cell by electroporation,after G418 selection,so we got the stable cell line expressing C5aR shRNA.The experiment was designed into 3 groups:①normal control group,RK3E cells without transfection;②negative control group,RK3E cells transfected with blank vector;③ experimental group,RK3E cells transfected with C5aR shRNA.After incubation with LPS for 12 h,the ratio of apoptosis was tested by flow cytometry,the level of mRNA was tested by RT-PCR,and binding of ~(125)I-rrC5a to RK3E cells stimulated with LPS were performed to examine the expression of C5aR in RK3E cells.Results:Compared with the normal control group and negative control group,in the experimental group the ratio of apoptosis was significantly decreased(P＜0.01),and the expression of C5aR mRNA was significantly inhibited(P＜0.01),and binding of ~(125)I-rrC5a to RK3E cells was significantly decreased also.Conclusion:Hairpin shRNA targeting C5aR gene can lead to obvious gene silence in vitro and inhibit the cell apoptosis induced by LPS in kidney epithelial cell.

CD46 is not only identified as a complement regulatory protein which protects host cells from complement attack, but also a new co-stimulatory molecule for human T cells. CD3/CD46 co-stimulation can induce a T-regulatory 1 cell (Tr1)-specific cytokine phenotype in human CD4(+) T cells. However, the role of CD46 as a co-stimulatory molecule in the modulation of the acquired immunity, such as transplant immunology, remains unclear. In this study, CD4(+) T cells were isolated from human CD46-transgenic C57BL/6 mice by magnetic-activated cell sorting, and further induced by anti-CD3, anti-CD28 and anti-CD46 antibodies respectively, and anti-CD3/anti-CD28 antibodies, anti-CD3/anti-CD46 antibodies, or the monoclonal antibody panel against CD3/CD28/CD46. The levels of interleukin-2 (IL-2), gamma-interferon (gamma-IFN), interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta) were detected in the supernatants of different groups. Suppression of allogeneic T cell proliferation were assessed by using mixed lymphocyte reaction (MLR) assay, in which monoclonal antibodies against CD46 were added to the culture. The results showed that CD3/CD28, CD3/CD46 and CD3/CD28/CD46 co-stimulation could significantly induce stronger proliferation of T cells than CD3 stimulation (P<0.05), and CD3/CD28/CD46 co-stimulation significantly increased the proliferation of T cells when compared with CD3/CD28 or CD3/CD46 co-stimulation (P<0.05 for each). IL-2 and gamma-IFN levels were much higher in CD3/CD28 co-stimulation group than in CD3, CD28, CD46 and CD3/CD46 groups (P<0.05 for each). IL-10 and TGF-beta levels were dramatically increased in CD3/CD46 co-stimulation group as compared with those in the CD3, CD28, CD46 and CD3/CD28 groups (P<0.05 for each). CD3/CD46 co-stimulation significantly inhibited the T cell proliferation and allogenic immune responses through the secretion of IL-10 and TGF-beta in MLR (P<0.05). These results suggested that CD3/CD46 can induce Tr1 cells to modulate allogenic immune responses, and it may become a novel target for the development of new therapeutic approach for T-cell-mediated diseases. CD46 plays an important role in regulating the T cell-mediated immune responses by bridging innate and acquired immunity.

Objective To study the relationship between the expression of cytochrome c ( Cyt c) and programmed cell death 4 (PDCD4) in pancreatic cancer, and investigate the pathway of PDCD4 inducing the apoptosis of pancreatic cancer cells. Methods Pancreatic cancer specimens from 69 patients who received pancreatic resection from 1990 to 2002 in First Affiliated Hospital of China Medical University were collected. The expression of Cyt c in the 69 paraffin specimens of pancreatic cancer was detected by immunohistochemistry, and the expression of Cyt c in 8 samples of cold-preserved fresh pancreatic cancer and normal pancreatic tissues were detected by Western blot. The expression of PDCD4 and Cyt c in pancreatic cancer was analyzed by paired t test and chi-square test. Results Compared with normal pancreatic tissues, the expression of Cyt c in pancreatic cancer was significantly decreased. The positive expression rate of Cyt c in 69 samples of pancreatic cancer was 41% (28/69). The expression of Cyt c was positive in most patients with positive expression of PDCD4, and the expression of PDCD4 was negative in most patients with negative expression of Cyt c. The expression of PDCD4 and Cyt c was closely correlated with each other (χ2= 10.52, P < 0.05). Conclusions There is a close relationship between the expression of PDCD4 and Cyt c in pancreatic cancer. PDCD4 may induce the apoptosis of pancreatic cancer cells through mitochondrial pathway.

To study the effect of cholesterol and 25-OH-cholesterol on cholesterol metabolism in HepG2 cells and the effect of coptisine (Cop) extracted from Coptidis Rhizoma (CR) in reducing and regulating cholesterol. In this study, TC, TG, LDL-c and HDL-c were measured by biochemical analysis; mRNA and protein expressions of LDLR, HMGCR and CYP7A1 were detected by qRT-PCR and Western blot. According to the results, cholesterol and 25-OH-cholesterol inducing could decrease in mRNA and protein expressions of LDLR and CYP7A1, so as to increase TC and LDL-c contents. However, Cop could up-regulate mRNA and protein expressions of LDLR and CYP7A1 and down-regulate that of HMGCR, so as to reduce TC and LDL-c levels. These findings suggested that Cop has potential pharmacological activity for reducing cholesterol, and may reduce cholesterol by regulating mRNA and protein expressions of key genes involved in cholesterol metabolism, such as LDLR, CYP7A1 and HMGCR. This study laid a firm theoretical foundation for developing new natural drugs with the cholesterol-lowering activity.
Berberine ; analogs & derivatives ; pharmacology ; Cholesterol ; metabolism ; Cholesterol 7-alpha-Hydroxylase ; genetics ; metabolism ; Drugs, Chinese Herbal ; pharmacology ; Gene Expression Regulation, Enzymologic ; drug effects ; Hep G2 Cells ; Humans ; Hydroxymethylglutaryl CoA Reductases ; genetics ; metabolism ; Receptors, LDL ; genetics ; metabolism ; Triglycerides ; metabolism