Cerebral small vessel disease (SVD) is an important subtype of cerebrovascular disease. It is also one of the major reasons for resulting in vascular cognitive impairment or dementia in the elderly. SVD is a small arteriovenous lesion in subcortex caused by a variety of causes, mainly causing subcortical lacunar infarction, white matter damage, microblecds and other pathological changes. There is evidence that vascular endothelial function and blood-brain barrier damage may result in small vessel structures and perivascular changes, which may be the initial factors.of causing SVD. Genetic susceptibility is also one of the risk factors that can not be ignored.

Objective To construct a set of evaluation index system for medical research project,to make the work justice and fairness,to manage the research work scientificly and standardized,to promote scientific research and hospital development closely,so as to better serve the society.Methods Based on the literature review,semi structure interview method and current medical research project evaluation index system and related management methods,a preliminary index system was formed.Using the Delphi method to carry out two rounds anonymous questionnaire consulting,the medical research project acceptance evaluation index system was finalized.Results The evaluation index system of medical research projects includes 5 first-level indexes and 21 second-level indexes.Ranking from high to low is based on the weight coefficient of the size.Conclusions Through the establishment of the index system of medical scientific research projects,the project acceptance management work has become scientifically planned,which guide scientific research project productive and improving the scientific management level and technological innovation ability.

Based on the background of knowledge economy,factors which have affected the social status of a person can be divided into five levels: physical fitness,technical ability,mental capacity,potential energy and recombination energy.This article analyzes the educational style of medical students by using five-level-ability model which judges a person from the economic angle.It aims at providing constructive opinions on innovation,enhancement and improvement of modern medical education.

Objective To investigate the application value of the XT-4000i blood cell analyzer in body fluid cell count.Methods 113 cases of body fluid specimen were collected in the hospitalized patients from September 2013 to February 2014.Then RBC and WBC counts in the collected specimens were detected whitin 1 h by XT-4000i blood cell analyzer and the manual detection method, the RBC count values were divided into 3 levels:L1 100~1 000 ×106/L,L2 1 001 ×106 ~100 000 ×106/L and L3 > 100 000 × 106/L;WBC count values were divided into 2 levels:L1 1~50×106/L and L2 >50×106/L.The correlation between the two kinds of test methods was analyzed.Results The results of RBC and WBC counts detected by the XT-4000i blood cell analyzer and the manual method had a higher correlation.The correlation coefficients were 0.931,0.996,0.865,0.942 and 0.988.Conclusion The XT-4000i blood cell analyzer can be applied in clinical fluids cell count.

Objective To investigate the effects and mechanisms of prostaglandin E2 receptor subtype 3 (EP3) on transforming growth factor β1 (TGF-β1)-induced mouse mesangial cells damage. Methods Primary mouse mesangial cells were separated and cultured. Three siRNAs were synthesized and transfected into mesangial cells for silencing EP3 by LipofectamineTM 2000 and the best one was chosen. MCs were grouped into: (1)control group; (2)TGF-β1 (10 μg/L) group; (3)NC-siRNA plus TGF-β1 (10 μg/L) group; (4) EP3-siRNA group; (5)EP3-siRNA plus TGF-β1 (10 μg/L). Then the proliferation of MCs was evaluated by CCK-8 assay. The expression of PGE2 and cAMP in cell supernatant were detected by ELISA. The mRNA and protein expression of fibronectin (FN), connective tissue growth factor (CTGF), cyclooxygenase-2 (COX2), membrane-bound prostaglandin E2 synthase 1 (mPGES1) were detected by real - time quantitative PCR and Western blotting. The phosphorylation of p38 MAPK and ERK1/2 was decected by Western blotting. Results Compared with control group, the cell proliferation induced by TGF-β1 was increased (P<0.05), the expression of PGE2 and cAMP were improved, mRNA and protein expression of FN, CTGF, COX2 and mPGES1 were up-regulated (all P<0.05). Compared with TGF-β1 group, the cell proliferation in EP3-siRNA plus TGF-β1 group was reduced, the expression of FN, CTGF, COX2 and mPGES1 mRNA and protein were downregulated (all P<0.05), the phosphorylation of ERK1/2, p38 MAPK were also declined (P<0.05). Conclusion EP3-siRNA may reduce TGF-β1-induced cell damage through upregulating the expression of cAMP, repressing the activity of ERK1/2 and p38 MAPK, inhibiting the expression of COX2 mPGES1 and PGE2 by feedback, then decreased the expression of FN and CTGF.

Objective To evaluate the role of phosphatase and tensin homolog deleted on ehromo-some ten (PTEN) protein in sevoflurane postconditioning-induced mitigation of focal cerebral ischemia-reperfusion (I/R) injury via activating PI3K/Akt pathway in rats.Methods One hundred and eight Sprague-Dawley rats,aged 2-3 months,weighing 250-280 g,were randomly assigned into 6 groups (n =18 each) using a random number table:sham operation group (group S),group I/R,I/R + sevoflurane postconditioning group (group I/R + S),I/R + normal saline group (group I/R + NS),I/R + selective PTEN inhibitor pic group (group I/R + P),and I/R + pic + sevofluraue postconditioning group (group I/R + P+ S).Focal cerebral I/R was induced by right middle cerebral artery occlusion (MCAO).The animals were anesthetized with intraperitoneal chloral hydrate.In I/R + P and I/R + P + S group,pic 20 μg/100 g (0.4 ml/100 g) was injected intraperitoneally every 3 h for 4 times before MCAO,and the equal volume of normal saline was given instead of pic in I/R + NS group.The rats in all sevoflurane postconditioning groups inhaled 2.5 ％ sevoflurane for 30 min starting from the onset of reperfusion,and the rats in the other groups inhaled oxygen for 30 min instead.At 24 h of reperfusion,neurological deficit scores (NDSs) were measured and the rats were then sacrificed.Their brains were removed for determination of infarct size (by TTC),cell apoptosis (by TUNEL),and expression of phosphorylated PTEN (p-PTEN) protein and phosphorylated Akt (p-Akt) (by Western blot).Apoptosis index was calculated.Results Compared with S group,the NDSs,percentage of cerebral infarct size and apoptosis index were significantly increased,and the expression of p-Akt and p-PTEN protein was up-regulated in the other 5 groups.Compared with I/R and I/R + NS groups,the NDSs,percentage of cerebral infarct size and apoptosis index were significantly decreased,and the expression of p-Akt and p-PTEN protein was up-regulated in I/R + S,I/R + P and I/R + P + S groups.There were no significant changes in the parameters mentioned above between I/R + S,I/R + P and I/R + P + S groups,and between I/R and I/R + NS groups.Conclusion Sevoflurane postconditioning can activate PI3K/Akt pathway via inhibiting PTEN protein,thus mitigating focal cerebral I/R injury in rats.

Objective To study the effect of the recombinant matrilysin (rMMP-7) and its antisense oligonucleotide transfected by liposome (LIPO-MAON) on the proliferation of lung adenocarcinoma cell line A549 and human umbilical vein endothelial cells (HUVEC). Methods Antisense oligonucleotide of matrilysin was constructed by liposome transfection. The proliferation of HUVEC and A549 was detected by MTT assay in case of rMMP-7 or LIPO-MAON existence. The expression of MMP-7 mRNA in both HUVEC and A549 was examined by semi-quantitative RT-PCR assay. Results The proliferation of both HUVEC and A549 cell line was accelerated by high level of rMMP-7 (0.75, 1.0 ?g/ml), and the inhibited proliferation was only found in A549 cell line treated with high concentration of LIPO-MAON (7.5, 10 nmol/ml), but not in HUVEC. By RT-PCR assay, no expression of MMP-7 mRNA was found in HUVEC; however, enhanced or decreased expression of mRNA were found when A549 cell line was treated respectively with rMMP-7 or LIPO-MAON (P

BACKGROUND: Few reports concern the effects of dendritic cells-a kind of antigen presenting cells, and interleukin-10 (IL-10) on airway hyperreactivity or inflammation. OBJECTIVE: To construct mice IL-10 recombinant adenovirus vector Ad-mIL-10 to acquire the dendritic cells modified by mIL-10, which can provide a foundation for the further study. METHODS: Mouse IL-10 (mIL-10) gene comprise of enzyme cutting spot was synthesized according to the mIL-10 gene sequence and multiclone spot of adenovirus vector, connected to pMD18-T vector and sequenced. MIL-10 was subcloned to BD Adeno-X~(TM) vector, packed and augmented in HEK 293 cells, following determine the protein expression, and the vector was transfected to mice bone marrow-derived dendritic cells. RESULTS AND CONCLUSION: Recombinant adenovirus vector Ad-mIL-10 was successfully synthesized, packed and augmented, which could highly express protein IL-10. Bone marrow-derived dendritic cells were successfully cultured and transduced in vitro. It suggested that it is feasible to transfect mice dendritic cells by Ad-mIL-10 adenovirus vector. The study can provide more sufficient theoretic evidence for the possibility of correlative gene therapy.

To explore the protective effect of adenovirus mediated IGF-Ⅰgene(Ad-IGF-Ⅰ)transfer on non-obese diabetic(NOD)mice. The results showed that the incidence of diabetes and degree of insulitis were significantly reduced in mice receiving Ad-IGF- Ⅰ . Treatment with Ad-IGF- Ⅰ significantly decreased apoptosis rate,expression of Fas and caspase-3, and increased expression of Bcl-xl. This study indicates the potential of IGF- Ⅰ gene therapy in protecting NOD mice from insulitis and apoptosis.

Objective To investigate the protective effect of c-jun N-terminal kinase (JNK)inhibitor SP600125 against acute liver failure in mice.Methods Fifty-five male C57/BL6 mice were divided into control group (n =30) and SP600125 group (n =25).The animals were given an intraperitoneal injection of D-galactosamine (D-GalN,400 mg/kg body weight)/lipopolysaccharide (LPS,30 μg/kg body weight).The control group and SP600125 group were given 10％ dimethyl sulfoxide (15 mL/kg body weight) or SP600125 (75 mg/kg body weight) subcutaneously 12 h and 1 h before D-GalN/LPS administration,respectively.D GalN/LPS induced mouse JNK activation was detected by immunohistochemistry for phospho JNK (p-JNK).D-GalN/LPS induced mouse liver cell apoptosis was detected by immunohistochemistry for Caspase-3 and TdT-mediated-dUTP nick endlabeling (TUNEL).Serum alanine transaminase (ALT) level was tested to assess liver injury.Survival rate of mice within 24 h after D-GalN/LPS administration was observed.The comparison between groups was done by t test and survival rate was analyzed by Kaplan-Meier method.Results JNK activity in liver tissues,as indicated by observation of p-JNK positive cells by immunohistochemistry,was diminished 4 h after D-GalN/LPS administration in SP600125 group.Reduced Caspase-3 activity was observed 6 h after D-GalN/LPS administration in SP600125 group (as indicated in immunohistochemistry by Caspase-3 positive cells).Mice in SP600125 group showed significantly lower TUNEL-positive cell count than control group (43.0±24.5 vs 194.7±73.8; t=9.743,P=0.000).Serum ALT level 6 h after D-GalN/LPS administration was (24.0±54.7) U/L in SP600125 group,which was significantly lower than that in control group [(1234.4±478.4) U/L; t=4.734,P=0.0015].SP600125 also significantly improved the survival rate within 24 h after D-GalN/LPS administration (4/5 vs 1/10； x2=5.225,P=0.0223).Conclusions JNK inhibitor SP600125 exerts protective effects against D-GalN/LPS induced acute liver failure in mice by suppressing JNK activation and hepatocyte apoptosis.