Aim To study effects of berberine on the proliferation a nd differentiation of HL-60 cells. Methods Cell inhibitory effec t was determined by growthcurve method and colony formation.Cell differentiation was analyzed by cytomorphological changes, NBT reduction and cell surface antig en.Cell cycle was analyzed by flow cytometry.Results The growth o f HL-60 cells was significantly inhibited by berberine in a time and dose-depe ndent manner.1,2,4,8 mg?L -1 berberine induced differentiation of HL-60 c ells: Morphological evaluation indicated that the berberine-treated cells exhibited granulation appearance; NBT reduction was significantly increase d; expression of CD11b increased obviously. Flow cytometry analysis showed that berberine arrested HL-60 cells in G 0/G 1 phase, the percent of the cells in S phase decreased.Conclusion Berberine can induce differentiatio n and growth inhibition of HL-60 cells

Objective To observe the serum levels of homocysteine (Hcy) and hypersensitivity C-reactive protein(hs-CRP) in elderly patients with cerebral infarction and to investigate their relationship and clinical significance by National Institutes of Health Stroke Scale (NIHSS).Methods The serum levels of Hcy and hs-CRP were by enzymatic cycling method and scattering turbidimetry in the elderly patients ( 116 cases with cerebral infarction and 100 cases of healthy control).Those 116 cases with cerebral infarction were divided into three groups by the degree of NIHSS.The three groups were compared with each other.Results The levels of serum Hcy and hs-CRP in elderly patients with cerebral infarction were significantly higher than that of healthy control group ( t =6.97,P ＜0.01 ; t =14.96,P ＜0.01 ).There has significant difference among those three groups with cerebral infarction by comparing with each other( F =23.49,P ＜0.05; F =28.19,P ＜0.05).A positive correlation was found between Hcy and degree of NIHSS( r=0.54,P ＜0.05),and between hs-CRPand degree of NIHSS( r =0.58,P ＜0.05).Conclusions Serum levels of Hcy and hs-CRP are correlated with the occurrence of cerebral infarction and its severity.There has positive clinical significance to evaluate the effect of cerebral infarction by measuring the serum levels of Hcy and hs-CRP dynamic.

Shape-memory polymers(SMPs) can retain a temporary shape after pre-deformation at an elevated temperature and subsequent cooling to a lower temperature.When reheated,the original shape can be recovered.The development of the research on polyolefin,polyurethanes,polyester and some other shape-memory polymers were introduced and their applications in medical equipment were reviewed.

Objective To establish the DNA fingerprint of microflora of some intestinal diseases such as ulcerative colitis (UC),acute gastroenteritis (AG) and irritable bowel syndrome (IBS),and analyze the structural characteristics of such fingerprints. Methods Thirty seven patients with intestinal diseases,definitely diagnosed by coloscopy as UC (20 cases),IBS (6 cases) and AG (11 cases),and 11 healthy people as control were involved in the present study. The total DNA was extracted from the fecal samples,and enterobacterial repetitive intergenic consensus sequence-polymerase chain reaction (ERIC-PCR) was used to set up the DNA fingerprint of intestinal microflora. The differences existed among the fingerprint profiles of intestinal microflora were compared. Results The numbers of DNA bands were obviously less in UC patients than in IBS and AG patients and healthy subjects,implying that significant differences existed in the intestinal microflora among UC and AG patients and healthy subjects. The principal band of DNA fingerprint in 17 UC patients appeared at 0.7kb,and 2 main DNA bands existed at 0.8kb and 1.1kb in AG patients,while no principal band was found in the DNA fingerprint of the IBS patients and healthy subjects. Conclusions It is likely that a single principal microflora is presented in the intestinal tissue of UC patients,which might be responsible for the morbidity of UC.

Objective To study the effect of glycyrrhizin(GL) on the gene expression of high mobility group protein 1 (HMGB1) in hippocampus and serum.To evaluate the effect on the expression of neuron-specific nuclear-binding protein (Neu-N) in the hippocampus CA1,CA3 regions in the chronic stage of an immature rat epilepsy model.Methods Fifty-two 21 day-old SD rats were randomly divided into control group,model group Ⅰ and model group Ⅱ according to the random table method.Model group Ⅰ was induced epilepsy by kainic acid (KA),and the model group Ⅱ was pretreated with GL by intraperitoneal injection at 30 min before KA injection.According to the different observation time points,each group was divided into 4 subgroups:3 h,12 h,24 h and 7 d.Model group Ⅱ was divided into 3 subgroups:10 mg/kg,50 mg/kg,100 mg/kg,according to the different doses of GL.There were 3 animals in each subgroup.Score was performed according to the Racine score,and quantitative real-time polymerase chain reaction and Western blot were applied to detect the mRNA and protein expression of HMGB1 in the acute phase.Enzyme-linked immunosorbent assay(ELISA) was applied to measure the expression of HMGB1 in blood;immunohistochemical was applied to measure the expression of Neu-N in hippocampus in the chronic phase(7 d).Results Compared with model group Ⅰ,seizure onset time was obviously prolonged in model group Ⅱ [(24.08 ± 1.98) min vs.(33.39 ± 2.66) min],and the difference was statistically significant (t =9.231,P ＜0.05);Comparing KA model group Ⅰ with control group,the gene expression of HMGB1 significantly increased,and reached a peak at the time of 12 h (H =10.532,P ＜ 0.05),but the protein expression of HMGB1 was changed obviously and there was no significant difference (H =5.227,P ＞0.05).The expression of HMGB1 in the serum also significantly increased,especially at 12 h (H =6.897,P ＜0.05).At the time of 12 h after KA injection,the gene expression of HMGB1 in the hippocampus was significantly decreased in model group Ⅱ compared with model group Ⅰ (H =10.721,P ＜0.05) (especially in the 100 mg/kg model group).Also,the expression of HMGB1 in the scrum was obviously decreased (H =6.967,P ＜ 0.05) (especially in the 100 mg/kg model group).At the time of 7 d after KA injection,hippocampal neuron loss in model group.Ⅰ was significantly reduced compared with control group (P ＜ 0.05),and hippocampal neuron loss in model group Ⅱ was evidently decreased compared with model group Ⅰ (P ＜ 0.05),(especially in the 100 mg/kg model group in CA1,50 mg/kg model group in CA3).Conclusions In the immature rat temporal lobe epilepsy model,GL may have neuroprotective by inhibiting the synthesis and release of HMGB1,inhibiting inflammation further to restrain the loss of neurons in the chronic phase.

The adhesion of leukocytes to vascular endothelium is crucial for the generation of inflammatory responses. The selectins and ?2-integrin (Mac-1) play a major role in the process. Recently, it was reported that RO-heparin can inhibit selectin-mediated leukocyte adhesion. The effect of RO-heparin on the Mac-1-mediated neutrophils adhesion were further tested. The results showed that RO-heparin could effectively inhibit neutrophils binding to ICAM-1, adhering to COS-7 cells expressing human ICAM-1, and adhering to human umbilical vein endothelial cells (HUVECs) under static and flow conditions. The findings suggest that the effect of RO-heparin on leukocyte adhesion is mainly due to its inhibition on the interaction between selectins or Mac-1 and their ligands and that RO-heparin might be useful in preventing inflammation diseases.

Objective To evaluate the cellular toxic and release of pharmaceutical dressing.Method Following the State standard GB/T14233.2-2005.the L929 cellular merphology was observed by inveded microscopy after 72h and proliferation of the cells was examined using mitochondrial function(MTT)assay.Relative growth rate (RGR)was calculated and cytotoxicity grade was evaluated by absorbency(OD)data.With PBS7.4 as dissolution media,and(32±0.5)℃as dissolution temperature,the release rate was determined with UV method with the determination wavelength of 288 nm and the dissolved liquid in 1/6,1/2,1,3,16,24,36 and 48 h.Results The average cell RGR of the pharmaceutical dressing is 91.25%and reaches 1 cytotoxicity grade.L929 cellular morphology is normal.Pharmaceutical dressing release accord to Higuchi equation,and the simulated equation is M_t/M_∞=0.3271t~(0.239).Conclusions Biologic compatibility of the pharmaceutical dressing is good,and the release of levofloxacin from the pharmaceutical dressing is sustained in vitro.

BACKGROUND: The oxidation of low density lipoprotein (LDL) is a key influencing factor in the occurrence and development process of atherosclerosis. How is the merit of the method for the detection of the level of anti-serum oxidized LDL (ox-LDL) antibody on the evaluation of atherosclerotic plaque?OBJECTIVE: To study the method for the detection of serum anti-ox-LDL antibody in mice with apolipoprotein E (Apo-E) genetic defect to analyze the merits of serous level of anti-ox-LDL antibody on the evaluation of the area of atherosclerotic plaque in mice with Apo-E genetic defect.DESIGN: Single factor analysis of variance (a case-controlled study)SETTING: Laboratory of nutrition and metabolism diseases in a university.PARTICIPANTS: Mice with Apo-E genetic defect were grouped into positive group (series: C57B L/6J, n = 15), while normal mice were grouped into control group (series: C57BL/6J, n = 15).INTERVENTIONS: Mice of two groups were fed in separate cage on laminar flow shelf for free drinking and eating. The venous blood was drawn from the orbit of mice after 16 weeks for the separation of mice serum. The level of anti-ox-LDL antibody was detected by enzyme-linked immunosorbent assay (ELISA) in the separated serum from either mice with Apo-E genetic defect or normal mice. The area of atherosclerotic plaque was measured by image analysis after oil red O staining.MAIN OUTCOME MEASURES: ox-LDL level and atherosclerotic plaque area in mice with Apo-E genetic defect or normal mice.RESULTS: Anti-ox-LDL antibody level of mice with Apo-E genetic defect was[ (0. 079 ±0. 028)% ], which was significantly higher than [(0. 012± 0.001 )% ] of normal mice ( F= 10. 666, P ＜ 0.01 ). The area of atherosclerotic plaque of mice with Apo-E genetic defect was (26. 25 ± 9.20) %, which was also significantly higher than 0% of normal mice, and moreover, there was a significant correlation between these two factors ( r =0. 638, P ＜ 0.01).CONCLUSION: Serum level of anti-ox-LDL antibody in mice with Apo-E genetic defect is closely correlated with the area of atherosclerotic plaque,which is an important indicator for the generation of atherosclerosis in mice with Apo-E genetic defect.

The adhesion of leukocytes to vascular endothelium is crucial for the generation of inflammatory responses. The selectinsand β2-integrin (Mac-1) play a major role in the process. Recently, it was reported that RO-heparin can inhibit selectin-mediated leukocyte adhesion. The effect of RO-heparin on the Mac-1-mediated neutrophils adhesion were further tested. The results showed that RO-heparin could effectively inhibit neutrophils binding to ICAM-1, adhering to COS-7 cells expressing human ICAM-1, and adheringto human umbilical vein endothelial cells (HUVECs) under static and flow conditions. The findings suggest that the effect of RO-heparin on leukocyte adhesion is mainly due to its inhibition on the interaction between selectins or Mac-1 and their ligands and that RO-heparin might be useful in preventing inflammation diseases.

Objective To explore the possible risk factors that influence bone mineral density (BMD) in elderly men with type 2 diabetes. Methods A total of 80 elderly men with type 2 diabetes were included in this study. The BMD of lumbar vertebrae and femur were measured by dual-energy X-ray absorptiometry (DXA). And fasting blood and urine samples were taken to check the biochemical levels of bone metabolism and blood glucose. The correlations between BMD and other related factors were analyzed. Results In this group, the prevalence rates of osteoporosis and osteopenia were 18. 6% and 53.8%, respectively. Body mass and body mass index (BMI) were positively correlated with BMD at all sites (r=0. 202～0. 298, P<0. 05 or P<0. 01). However, age and glycosylated hemoglobin (HbAlc) were negatively correlated with BMD of lumbar and femoral neck (r=-0. 172～-0. 211 ,all P<0. 05). Leptin was not only positively correlated with the BMD of femoral neck and Ward's triangle, but also with body mass, BMI, fasting blood glucose (FBG), total cholesterol and HbAlc (r=0. 219 ～ 0. 509, P<0.05 or P<0.01). Using stepwise regression analysis, body mass was the predictor of BMD at all sites assessed, while the HbAlc and leptin levels could respectively influence BMD at femoral neck and Ward's triangle (r~2= 0. 196 ～ 0. 276, all P< 0. 01). Conclusions It may suggest that differential factors predict the variance of BMD at different sites in elderly men with type 2 diabetes.