There were some samples collected from the Antarctic soil and South Ocean water for isolation of microorganisms and screening of their antitumor bioactivity by lethality bioassay using brine shrimp and a flow cytometric bioassay.There were 259 stains were isolated from the samples,11% of the Antarctic microorganisms showed strong antitumor activity.This result showed that the Antarctic microorganisms have a good potential in bioactive metabolites researching.

Aim To observe the effects of active com-ponent of Radix Isatidis ( ACRI ) on anti-anoxia and anti-fatigue in mice and investigate its possible mecha-nism. Methods Based on the weights, the mice were randomly divided into 5 groups: blank control group, ACRI 25, 50 and 100 mg·kg-1 groups, positive drug ( American ginseng liquid) control group 3 mL·kg-1 . Drugs were administered to the mice for about 14 con-secutive days, and during the experiment general situa-tions of mice were observed. The experiment of bearing hypoxia at normal pressure and the experiment of swim-ming while weight-bearing were conducted to study the effect of ACRI on anti-anoxia and anti-fatigue in mice. Then the superoxide dismutase ( SOD ) activities, the content of maleic dialdehyde ( MDA ) of mice serum and liver and blood urea nitrogen, blood lactic acid, liver glycogen were detected, in order to investigate its mechanism. Results ACRI decreased the growth rate of body weight in mice significantly, obviously pro-longed the survival time of anoxic mice at normal pres-sure and the swimming time of loaded mice, enhanced the SOD activities of mice blood and liver, decreased the MDA content of mice blood and liver, increased the content of liver glycogen, and decreased the blood urea nitrogen and blood lactic acid in mice after swim-ming. Conclusion ACRI has the anti-anoxia and anti-fatigue functions.

Aim To explore the mechanism of insulin in combination with selenium preventing myocardial apoptosis in diabetic cardiomyopathy rats .Methods SD rats ( n =50 ) were randomly divided into five groups: control , diabetic cardiomyopathy ( DCM ) , DCM with insulin treatment , DCM with selenium treat-ment, and DCM with insulin and selenium combination treatment .The cell apoptosis was observed by TUNEL . The levels of Bcl-2, caspase-3, PARP, Cbl-b and p38 MAPK were examined by Western blot .The inter-actions of Cbl-b-p38 MAPK and Ku70-Bax were detec-ted by immunoprecipitation .Results Insulin in com-bination with selenium synergistically inhibited apopto-sis, up-regulated Cbl-b, down-regulated p38MAPK ex-pressions and increased the interactions of Cbl-b-p38MAPK and Ku70-Bax.Conclusion Insulin and selenium synergistically inhibit myocardial apoptosis by regulating Cbl-b-inhibited p38 MAPK and preventing Bax translocation .

AIM:To investigate the effect of insulin and selenium in combination on the apoptosis and the ex-pression of Ku70, acetylated Ku70, Bax and cytochrome C in myocardial cells of the rats with diabetic cardiomyopathy (DCM), and to explore the mechanism of insulin and selenium in their synergistic anti-DCM effect.METHODS:SD rats (n=50) were randomly grouped into control, DCM, DCM with insulin treatment (DCM+In) group, DCM with selenium treatment (DCM+Se) group, and DCM with insulin and selenium combination treatment (DCM+In+Se) group.Mito-chondrial membrane potential ( MMP) was measured by flow cytometry .The cell apoptosis was observed by terminal-deoxy-nucleotidyl transferase mediated nick end labeling (TUNEL).The levels of Ku70, Bax and cytochrome C were examined by Western blot .The acetylation status of Ku 70 was detected by co-immunoprecipitation .RESULTS: The rats in DCM group showed marked cell apoptosis compared with the control rats .The levels of Ku70 and acetylated Ku70 declined sig-nificantly compared with control group .Bax significantly translocated from cytoplasm into mitochondria and cytochrome C translocated from mitochondria into cytoplasm compared with control group .Compared with DCM +In group or DCM +Se group, insulin and selenium in combination significantly inhibited the apoptosis , down-regulated Ku70 and acetylated Ku70 levels, and prevented Bax and cytochrome C translocation .CONCLUSION: Insulin and selenium synergistically inhibits myocardial apoptosis by regulating Ku 70 acetylation and inhibiting Bax translocation .

Objective To discuss the surgery methods and clinical curative effect of application of nickel titanium memory alloy embracing device fixed femoral fractures inside wall of bone block.Methods The clinical data of 27 patients on the application of nickel titanium memory alloy embracing device fixed femoral fractures inside wall with bone block were retrospectively analyzed.There were 9 cases of male and 18 cases offemale.They were 69 ~89 years old,average 76.2 years.And there were 19 cases on the left side of inside wall and 8 cases on the right side. Curative effect evaluation was conducted according to the Evans-Jensen norm and the improved Harris standard. Results Postoperative follow-up loss in 2 cases,and 24 cases received follow-up for 6 ~20 months,which had an average of 14.15 months and follow-up rate was 92.3%.Three cases died respectively because of acute heart failure, cerebral hemorrhage and cor pulmonale.Patients at the time of the last follow-up had Harris mean score(80 ~97), including the optimal 19 cases,fine 4 cases and poor in 1 case,and the excellent rate was 95.8%.Conclusion Sur-gery method of nickel titanium memory alloy embracing device fixed femoral fractures inside wall of bone has reliable fixation,and can restore the biomechanical balance and decrease complications,etc.It allows early functional exercise of hip part in load conditions to obtain ideal therapeutic effect.

Objective To investigate the relationship between spinal neuronal microRNA 212 (miR-212) and phosphorylation of cAMP response element-binding protein (CREB) in a mouse model of bone cancer pain (BCP).Methods Thirty-two male SPF C3H/HeJ mice, aged 4-6 weeks, weighing 20-25 g, were randomly divided into 4 groups (n=8 each) using a random number table: sham operation group (group S), BCP group, BCP + intrathecal negative control locked nucleic acid (LNA) group (group BC) , and BCP + intrathecal miR-212 antisense LNA group (group BL).After the mice were anesthetized with intraperitoneal pentobarbital sodium, 20 μl of α minimal essential medium containing NCTC 2472 cells 2×105 was injected directly into the medullary cavity of the distal femur.In BC and BL groups, negative control LNA and miR-212 antisense LNA 12 pmol/5 μl were intrathecally injected, respectively, once a day for 7 consecutive days, starting from day 14 after inoculation.In S and BCP groups, the equal volume of DNAse/RNAse-free water was given instead.The number of spontaneous flinches (NSF) and mechanical paw withdrawal threshold (MWT) were measured on 1 day before inoculation and 4, 7, 10, 14 and 21 days after inoculation.The mice of each group were sacrificed after measurement of pain threshold on 21 days after inoculation, and the lumbar enlargement segments of the spinal cord were harvested to detect the expression of phosphorylated CREB (p-CREB) and CREB using Western blot.Results Compared with group S, the MWT was significantly decreased, and the NSF was increased on 7-21 days after inoculation, and the expression of p-CREB was up-regulated in BCP, BC and BL groups.Compared with group BCP, the MWT was significantly increased, and the NSF was decreased on 21 days after inoculation, and the expression of p-CREB was down-regulated in group BL, and no significant change was found in the parameters mentioned above in BC group.There was no significant difference in the expression of CREB between the four groups.Conclusion Spinal neuronal miR-212 is involved in the maintenance of BCP probably by promoting phosphorylation of CREB in mice.

Post-stroke cognitive impairment (PSCI) is a series of syndromes caused by stroke, involving impairment of one or more cognitive functions, such as attention, language function, executive function, visuospatial cognition, episodic memory and working memory, etc. The traditional treatment methods of PSCI include drug therapy and cognitive training. The treatment modalities are limited and the maintenance effect is not good. Therefore, an auxiliary treatment method is urgently needed to improve its therapeutic effect. Transcranial direct current stimulation (tDCS) is a safe and mature non-invasive brain stimulation technique, which generates weak direct current (1-2 mA) through electrodes placed on the scalp to change the resting membrane potential of neurons, regulate the excitability of the cerebral cortex, so as to achieve the purpose of treatment. This article reviews the effect of tDCS on PSCI, and hopes to provide reference and guidance for its rehabilitation treatment.

Objective: Elsibucol is a metabolically stable derivative of probucol with the properties of anti-oxidation, anti-inflammation and anti-proliferation. We want to explore the effect of elsibucol on abdominal aorta injury in hypercholesterolemia rabbits. Methods: A total of 45 male New Zealand rabbits were divided into 3 groups: Control group, the rabbits were fed by high cholesterol diet, Elsibucol group, the rabbits received high cholesterol diet with 1% elsibucol and Probucol group, the rabbits received high cholesterol diet with 1% probucol.n=15 in each group. All animals were treated for 2 weeks followed by the procedure of abdominal aortic balloon injury and then, drug therapy was continued for 10 weeks. The area and load of atherosclerosis in abdominal aorta were evaluated by IVUS, the amount of macrophages in plaque were observed by immunohistochemistry, mRNA and protein expressions of MCP-1, MMP-9 were examined by RT-PCR and immunohistochemistry. Results: Compared with Control group, Elsibucol group showed decreased blood LDL-C and oxidative stress, decreased amount of macrophages and lower expression of inlfammatory factors in atherosclerosis plaque, reduced plaque area and load, allP<0.01. Compared with Probucol group, Elsibucol group presented even lower plaque area and load, allP<0.01. Conclusion: Elsibucol inhibits the progress of atherosclerosis in experimental rabbits via regulating blood lipids, anti-inlfammation and anti-oxidation.

This study was aimed to summarize the adverse drug reaction (ADR) caused by the toxicity of Tripterygium Wilfordiiand its preparations, in order to explore possible relationship betweenTripterygium Wilfordiifactors and reported ADR. Relevant articles on toxicity ofTripterygium Wilfordiiand its preparations were systematically searched in 5 databases, including the Pubmed, CNKI,Wanfang Data, VIP Data and Sinomed from the database was established until Feb 25th, 2014. And then, the randomized controlled trials (RCTs) were systematically collected, analyzed and summarized. The results showed that there were 260 RCTs with 13301 patients included. The outcome of data analysis showed that ADR rates of digestive system and reproductive system of RCT1 and RCT2 were different. ADR rates (per hundred people) in RCT1 and RCT2 were as follows: digestive system were 14.73 and 12.26, reproductive system were 8.25 and 8.00, liver was 6.50 and 5.66, kidneys were 6.79 and 3.03, blood system were 6.73 and 6.50, cardiovascular system were 2.35 and 0.67, skin and mucous system were 11.42 and 4.78, respectively. Articles on rheumatoid arthritis (RA) of both RCT1 and RCT2 were the highest, which occupied 22.17% in RCT1 and 63.16% in RCT2. The corresponding ADR rates were 34.18 and 27.26. The standard deviation (SD) of 7 disease types, which were RA, IgA nephropathy, nephritis, nephrotic syndrome (NS), diabetic nephropathy, psoriasis, lichen and rashes, as well as uterine fibroids, was 8.69 in RCT1. The SD of RA, IgA nephropathy, psoriasis, lichen and rashes was 7.11 in RCT2. It was concluded that the possible ADR distribution ofTripterygium Wilfordiiand its preparations were the highest in the digestive system, reproductive system and liver. Besides, different diseases (i.e., RA, nephritis, NS, and etc.) had huge differences with their correspondent ADR rates. Therefore, it was suggested that specific measures should be taken to select the appropriateTripterygium Wilfordiipreparation, protect the stomach and liver during the application ofTripterygium Wilfordiiand its preparations. During medication, attentions should be paid to the reaction of patients. Stop the medication when necessary to minimize ADR rates to the lowest.

Objective To investigate the anti-inflammatory effect of C1q/ tumor necrosis factor (TNF)-related protein 9 (CTRP9) in RAW264.7 mouse macrophage cells treated with oxidized low density lipoprotein (oxLDL),and to explore its mechanism.Methods RAW264.7 mouse macrophage cells were divided into three groups:the control group,the oxLDL group (treated with oxLDl) and the gCTRP9-oxLDL group (pretreated with recombinant globular domain of CTRP9 and stimulated by oxLDL).Foam cells were detected by oil red O staining.Western blot was used to detect the expressions of pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and monocyte chemoattractant protein 1 (MCP-1).In addition,the expression levels of NF-κB p65 in cytoplasm and nucleus proteins extraction were both determined.Results The relative levels of MCP-1 and NF-κB were increased in the oxLDL group as compared with the control group (1.66±0.09 vs.1.03±0.10,0.52±0.11 vs.1.03±0.06,both P＜0.05).The expression levels of TNF-α and MCP-1 were decreased in gCTRP9+oxLDL group as compared with the oxLDL group (both P＜0.05).The expression level of NF κB p65 in nucleus 2 and 8 h after treatment was lower in the gCTRP9+oxLDL group than in the oxLDL group (1.03±0.06 vs.0.17±0.10,0.31±0.03,both P＜0.05).Conclusions oxLDL may induce the expressions of inflammatory cytokines of TNF α and MCP-1 in macrophage ceils.gCTRP9 pretreatment could reduce the oxLDL-induced pro inflammatory effect and nuclear factor κB translocation may be involved in this process,which suggests that gCTRP9 may play a protective role in anti inflammatory and anti-atherosclerosis.