There is a long history of Toad venom in the treatment of cancer in China.Bufalin,extracted from Toad venom,is one of the biologically active compounds of anticancer.We elaborate the molecular mechanism of bufalin on anticancer activity from several aspects such as inducing cell apoptosis and differentiation,inhibitting cell proliferation and angiogenesis,enhancing the sensitivity of chemotherapeutics,which can provide the basis for in-depth study of Toad venom and its development and clinical medication.

Objective To investigate the status of Ureaplasma urealyticum (Uu) ,Mycoplasma hominis (Mh) and Chlamydia trachomatis(Ct) in patients with urogenital tract infection ,and to analyze the drug resistance of mycoplasma .Methods The myco‐plasma and its drug sensitivity of urogenital tract specimens were detected by culture‐identification‐susceptibility integration kit .Ct was detected by using immunochromatographic method .Results Among 497 cases of specimens ,there were 194 cases of simplex Uu infection (39 .0% ) ,9 cases of simplex Mh infection (1 .8% ) ,73 cases of Uu and Mh mixed infection (14 .7% ) ,and 54 cases of Ct infection (10 .9% ) .There were 38 cases of Ct and Uu mixed infection (7 .6% ) in the Ct positive specimens .The isolated myco‐plasmas were sensitive to doxycycline ,josamycin and minocycline ,but resistant to other drugs in varying degrees .Conclusion There are both simplex infection and mixed infection of chlamydia and mycoplasma in the patients with urogenital tract infection . The clinical use of antibiotics should be reasonable based on pathogen detection and drug susceptibility test results .

Objective In order to evaluate the efficacy of Diammonium Glycyrrhizinate in the treatment of chronic hepatitis B. Methods The randomized clinical trials(RCTs) that compared the efficacy of Diammonium Glycyrrhizinate and other kind of treatment in chronic hepatitis-B were chosen from CBM disks from 1995 to 2004 and CNKI from 1995 to 2004.A meta-analysis was employed to evaluate the results of these therapies. Results Twenty-four RCTs including 3201 cases were analyzed.Compared with control group,the total RR of efficiency rate of Diammonium Glycyrrhizinate group were 1.378(95%CI 1.243～1.529),showing significant difference(P

BACKGROUND: Islet transplantation is an effective method for the treatment of type 1 diabetes mellitus and parts of type 2 diabetes mellitus. However, its application is hindered by insufficient sources and immunologic rejection. Though transdifferentiation of pancreatic stem cells is at the starting step, it is thought to be the hopeful source for islet cell transplantation.OBJECTIVE: To look for a suitable cells-transplantation source for the treatment of diabetes mellitus. METHODS: The pancreatic ductal epithelial cells were separated from Kunming mice and cultured in DMEM/F12 medium supplemented with keratinocyte growth factor, hepatocyte growth factor and nicotinamide, etc. Samples were taken at different time points for light microscopy and electron microscope. The changes of CK-19 and PDX-1 were detected by immunocytochemistry at 1 and 16 days. The expressions of insulin and glucagon gene were detected by RT-PCR at 1 and 16 days. The physiologic function of these islet-like clusters was determined by dithizone staining and glucose stimulation at 21 days. RESULTS AND CONCLUSION: A large number of epitheliod cells were CK-19 immunoreactive positive and few of them were PDX-1 positive at 1 day after isolation, then CK-19 positive cells proliferated quickly and formed substantial plaques of epithelial cells in cobblestone pattern. At 16 days later, these cells begin to form islet-like clusters gradually, while most of them were PDX-1 immunoreactive positive. The analysis of mRNA by RT-PCR showed very low levels of insulin and glucagon mRNA in the starting materials but increase was found as the process of transdifferentiation. At 21 day differentiated islet-like clusters were stained red by dithizone. In those samples exposed to a stimulatory 15 mmol/L glucose, there was a 1.6-fold increase in insulin compared with to 5.6 mmol/L glucose (P < 0.05). Pancreatic ductal cells of adult Kunming mice could proliferate quickly and have the potency of transdifferentiation into islet-like clusters when cultured in vitro under appropriate conditions.

Objective To observe the clinical effects of phosphocreatine treatment on left ventricular function and on amino-terminal pro-brain natriuretic peptide (NT-proBNP) level in elderly patients with chronic heart failure. Methods In our department, the 172 elderly patients with chronic heart failure were randomly divided into treatment group and control group (n= 86, each).The control group received routine anti-heart failure treatment. The treatment group received conventional therapy plus creatine phosphate sodium for 4 weeks. The cardiac function was evaluated and the NT-proBNP level was measured in all subjects. Results Four weeks after treatment, the improvements of left ventricular ejection fraction (LVEF), left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic dimension (LVEDD) were better in treatment group than in control group (all P＜0.05). The plasma NT-proBNP level decreased significantly in treatment group as compared with control group [before treatment: (956.4 ± 644.2) pmol/L and (973.6 ±639.8) pmol/L; after treatment: (414. 5 ± 163.8 ) pmol/L and ( 719.3 ± 477. 5 ) pmol/L, all P＜0. 05]. Conclusions Phosphocreatine could improve left ventricular function and decrease plasma NT-proBNP level in elderly patients with chronic heart failure.

The basic course of medical specialty is an important part of medical education. There are few studies on effective teaching of basic courses of medical specialty. Based on the course of Pharmacology, this paper discusses the connotation, influencing factors and strategies of effective teaching of basic courses of medical specialty. The factors influencing the effective teaching of basic courses of medical specialty are multiple, that mainly includes four dimensions: students, teachers, course resources and teaching environment. Strategies to improve teaching effect include strengthening the idea of education, positioning goals hierarchically, optimizing curriculum structure, and innovating education platform.

Objective To determine the effect of Mycobacterium tuberculosis spp. inducing transformation of THP-1 cells to epithelioid cells (EC) and the involved signaling pathways and their regulations. Methods THP-1 cells infection models respectively infected with M. tuberculosis strains H37Rv, bovis and phlei were established. Indirect immunofluorescent staining assays were used to detect the expressions of monocyte/macrophage differentiation antigen CD115 and EC differentiation antigen CD82 of the THP-1 cells before or after infection. By Sandwich ELISA Kits, the phosphorylation levels of p38MAPK, Akt1 and STAT3 of the THP-1 cells before or after infection were measured. The alterations of CD115 and CD82 expression levels were examined when the associated signaling pathways were blocked with specific blocking agents. Results CD115 expression was weakened and CD82 expression was strongly increased in all the THP-1 cells infected with the three strains. A temporal up-regulation of the p38MAPK phoshporylation level but no obvious alteration of Akt and STAT3 phosphorylation levels after THP-1 cells infected by strain H37Rv or bovis. The THP-1 cells infected with anyone of the three strains continuously expressed CD115 after MAPK, PI3K/Akt or JAK/STAT of the cells was blocked. Although JAK/STAT was blocked, the THP-1 cells respectively infected with the three different strains still expressed CD82. However, CD82 expressed in THP-1 cells infected by the strain H37Rv or bovis was disappeared when p38MAPK and PI3K/Akt pathways of the cells were blocked. Conclusion Strain H37Rv and bovis can induce the infected THP-1 cells transforming to EC and p38MAPK and PI3K/Akt signaling pathways participate and regulate the transformation procedure. Of the two signaling pathways p38MAPK seems to be more important.

[ ABSTRACT] AIM:To investigate the effect of oxidized low-density lipoprotein ( ox-LDL) on autophagy in mac-rophages and the underlying molecular mechanisms.METHODS:RAW264.7 macrophages were pretreated with 2 mg/L anti-CD36 monoclonal antibody (anti-CD36 mAb), 5 μmol/L diphenyleneiodonium (DPI), 3 mmol/L 3-methyladenine (3-MA) or 1μmol/L rapamycin for 1 h and then treated with ox-LDL (100 mg/L) for 12 h.The viability of the cells was measured by MTT assay.The activities of lactic dehydrogenase ( LDH) in the medium and nicotinamide adenine dinucleoti-de phosphate ( NADPH) oxidase, superoxide dismutase ( SOD) in the cells as well as the levels of intracellular reactive ox-ygen species ( ROS) and malondialdehyde ( MDA) were determined to characterize the membrane integrity and the oxida-tive stress, respectively.The protein levels of beclin-1 and microtubule-associated protein 1 light chain 3-II ( LC3-II) , 2 important molecular markers of autophagy, were examined by Western blotting.RESULTS:ox-LDL induced autophagy in
RAW264.7 macrophages as assessed by upregulation of beclin-1 and LC3-II.Similar to 3-MA, an autophagy inhibitor, an-ti-CD36 mAb significantly inhibited the ox-LDL-induced upregulation of beclin-1 and LC3-II.Anti-CD36 mAb suppressed the ox-LDL-induced oxidative stress as revealed by decreased NADPH oxidase activation, ROS and MDA generation as well as increased SOD activity.Similar results were observed in the cells pretreated with DPI, a NADPH oxidase inhibitor.Mo-reover, DPI significantly inhibited the ox-LDL-induced upregulation of beclin-1 and LC3-II.Inaddition, the decrease in the cell viability and increase in LDH release induced by ox-LDL were promoted by 3-MA and blocked by rapamycin ( an auto-phagy inducer).CONCLUSION: ox-LDL induces autophagy in RAW264.7 macrophages, which may be involved in CD36-mediated ox-LDL uptake and subsequent activation of oxidative stress, and moderate activation of autophagy may pro-tect macrophages from ox-LDL-induced injury.

Objective To evaluate the effects of combination of dexmedetomidine and mild hypothermia on global cerebral ischemia-reperfusion (I/R) injury in neonatal rats.Methods Ninety-six neonatal Sprague-Dawley rats,aged 6-7 days,weighing 18-22 g,were randomly divided into 4 groups (n=24 each) using a random number table:I/R group,mild hypothermia group (group H),dexmedetomidine group (group D) and combination of dexmedetomidine and mild hypothermia group (group DH).Global cerebral ischemia was induced in rats anaesthetized with chloral hydrate by bilateral common carotid artery clamping (for 15 min) combined with hypotension followed by reperfusion.Dexmedetomidine 75 pg/kg was given intraperitoneally at 30 min before ischemia in D and DH groups,while the equal volume of normal saline was given in I/R and H groups.The temperature in the temporal muscle was maintained at 36.7-37.2℃ in I/R and D groups,and at 34.8-35.3℃ in H and DH groups.At 12,24 and 72 h of reperfusion,8 rats were randomly chosen in each group,and neurological deficit score (NDS) was determined.The animals were then sacrificed,and their brains were removed for determination of myeloperoxidase (MPO) activity (by spectrophotometry) and contents of tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) in brain tissues (using ELISA).Results Compared with I/R group,the NDS,MPO activity and contents of TNF-α and IL-6 were significantly decreased in the other three groups.The NDS,MPO activity and contents of TNF-α and IL-6 were significantly lower in DH group than in H or D group.Conclusion Dexmedetomidine can optimize cerebral protection providedby mild hypothermia against global cerebral I/R injury through inhibiting inflammatory responses in brain tissues of neonatal rats.

Objective To study the effect of 1,25-dihydroxyvitamin D3 on bone metabolism in diabetic rats and the related molecular mechanism.Methods A total of 45 healthy 6-8 weeks old male Sprague Dawley (SD) rats were treated with streptozotocin.The streptozotocin-induced diabetic rats were randomly assigned to diabetic group (DM),low dose vitamin D treated group(LD),and high dose vitamin D treated group(HD).Another 12 healthy SD rats were used as normol control group(NC).The rats in NC group and DM group were fed with 0.05 ml/d nut oil;those in the LD group and HD group were fed respectively with 0.03 and0.10 μg · kg-1 · d-1 1,25-dihydroxyvitamin D3 dissolved in 0.05 ml nut oil.12 weeks later,serum calcium,phosphorus,osteocalcin,type Ⅰ collagen cross-linked telopeptide (NTX),and 24 h urinary calcium were determined.Right femurs were harvested for pathohistological analysis by hematoxylin-eosin (HE) staining.Expressions of osteoprotegerin,receptor activator nuclear factor κB ligand (RANKL),core binding factor α1(Cbfa1) were detected by immunohistochemical staining.The osteoprotegerin,RANKL,Cbfa1,osteocalcin mRNA levels of bone tissue were performed by realtime quantitative reverse transcription polymerase chain reaction assay.Results (1) Compared with the NC group,serum calcium and 24 h urinary calcium in LD and HD groups were significantly higher (P＜0.05) ; 24 h urinary calcium in DM group was significantly higher than that in NC group (P ＜ 0.05).(2) Serum osteocalcin level in DM and LD groups was significantly lower than that in NC group (P＜0.05) ; there was no significant difference between the serum NTX levels of all groups (P＞0.05).(3) There was no significant difference in the mRNA expression of Cbfa1 in all groups (P＞0.05).The mRNA expression of osteocalcin in DM group was significantly lower than that in NC group (P ＜0.05).The mRNA expression of RANKL in DM group was significantly lower than that in NC group (P＜0.05) ; and that in LD and HD group was significantly higher than that in DM group (P＜0.05),and that in HD group was significantly higher than that in LD group (P＜0.05).The mRNA expression of osteoprotegerin in DM group was significantly lower than that in NC group (P＜0.05).The ratio of RANKL to osteoprotegerin in HD group was significantly higher than that in DM group (P＜0.05).Conclusions Vitamin D may promote bone metabolism in diabetic rats by up-regulating the expressions of osteocalcin and RANKL or in addition to other means.