[Objective]To forecast the sponge mechanism mediated by LOC389023 in patients with intractable temporal lobe epilepsy(TLE),through investigating the expression of microRNA interacted with dipeptidyl peptidase 10(DPP10)and LOC389023.[Methods]The expression of DPP10 and Kv4.3 were detected in 15 temporal neocortex from patients with brain trauma (control group)and in 26 temporal neocortex from patients with intractable TLE(epilepsy group)by western blot(WB)and immunohisto?chemical(IHC)staining. The location of DPP10 and voltage dependent potassium channel 4.3(Kv4.3)was detected by immunofluo?rescent(IF)staining. The interaction between DPP10 and Kv4.3 was testified by co-immunoprecipitation(Co-IP). The expression of microRNA obtained by softwares(miRanda,Pita,TargetScan and miRDB)was detected by qPCR.[Results]IHC and WB showed an increased expression of DPP10(P<0.05)and a decreased expression of Kv4.3(P<0.05)in the epilepsy group. IF showed that the DPP10 and the Kv4.3 co-expressed in the membrane and the cytoplasm of neurons. Co-IP showed obvious interaction between the DPP10 and the Kv4.3.Five microRNA(miR-32-5p,miR-140-5p,miR-367-3p,miR-25-3p,miR-4325)were obtained by soft?wares. No significant differences in the expression of miR-32-5p and miR-4325 were found between epilepsy group and control group by qPCR(P>0.05). But decreased expression of LOC389023 and miR-140-5p and increased expression of miR-25-3p and miR-367-3p were found in epilepsygroup compared to control group (P < 0.05).[Conclusion]miR-25-3p and miR-367-3p may be regulated by LOC389023 through the sponge mechanism followed by altered expression of DPP10 in intractable temporal lobe epilepsy.

Objective By analyzing the characteristics of PI system in the US,especially its advantages,to learn the ways and means in the cultivation of postgraduates' innovative ability.Combined with the current situation of medical postgraduate training in China,some countermeasures in line with the actual situation of our country and the cultivation characteristics of medical graduate students' innovative ability were proposed.Methods Conducting literature review by using the CNKI and logging on to the official website of relevant agencies to collect and summarize related research data.Results Concrete suggestions from four aspects were proposed:Encourage medical graduate students to participate in scientific and technological research,well-planning of scientific research resources,optimizing and perfecting the mentor-mentee system and constructing a reasonable mechanism for achievement distribution.Conclusions The PI system in American scientific research field can be used for reference in the form and content of cultivating the innovative ability of medical postgraduates in China.

OBJECTIVE: To investigate the effect of bactericidal/permeability-increasing protein(BPI) on the outcome of sepsis in mice and its possible mechanism. METHODS: Sepsis was induced by injection of 2x10(6) colony-formed unit E. coli J5 via the tail vein. BPI of 5 mg/kg or equal volume of normal saline(NS) were injected intravenously at the same time. Endotoxin and TNFalpha levels in serum were assayed using a chromogenic limulus amebocyte lysate test and ELISA respectively. RESULTS: Seventy-two hour survival rate of septic mice was significantly higher in the BPI group (15/18) than in the NS group(8/18, P<0.01). Serum endotoxin levels in the BPI group (1.3+/-0.3 and 0.7+/-0.4 &mgr;g/L) were significantly lower than those in the NS group (3.9+/-0.8 and 2.5+/-0.9 &mgr; g/L, P<0.01) 0.5 and 1 hour following injection of bacteria respectively. The peak levels of serum tumor necrosis factor-alpha(TNFalpha)in the BPI group (1.9+/-0.6 &mgr;g/L) were also markedly lower than those in the NS group (3.8+/-0.8 &mgr;g/L, P<0.01) 1.5 hours following bacterial injection. But there was no significant difference in blood bacterial count between the BPI and NS groups 0.5, 1.5 and 3.0 hours after injection of bacteria. CONCLUSIONS: BPI has a marked protective effect on E. coli sepsis, which might be related to its action against bacterial endotoxin and its inhibition of TNFalpha production in sepsis.

Objective To investigate the effects of hydrochloride fasudil on inflammation and secondary brain injury in rats after intracerebral hemorrhage (ICH).Methods One hundred and seventeen male Wistar rats were randomly divided into normal group (n=9),sham-operated group (n=36),ICH group (n=36) and hydrochloride fasudil treatment group (ICH/HF,n=36).ICH was caused by injecting non-anticoagulant autologous arterial blood into the right caudate nucleus,3 mg HF was dissolved in 2 mL 0.9％ saline solution and administrated intraperitioneally once daily (12 mg/kg/d) since 12 h ofICH onset.Rats in the sham-operated group and ICH group received an equal volume of normal saline.On one,3,7 and 14 d ofICH induction,Bederson method was used to score neurological deficits in rats;interleukin (IL)-6 and tumor necrosis factor (TNF)-α levels in serum were detected by enzyme-linked immunosorbent assay (ELISA).Brain edema was measured by comparing wet and dry brain weights.Inflammatory cell infiltration around the hematoma was visualized using hematoxylin and eosin,and changes in neuronal morphology were detected by Nissl staining.Immunohistochemistry method was used to detect the expressions of Caspase-3 and Bcl-2.Results (1) The neurological deficit scale scores on one and 3 d ofICH in the ICH/HF group were significantly decreased as compared with those in the ICH group (P＜0.05).(2) Serum IL-6 (except 14 d of ICH) and TNF-α levels in ICH/HF group were significantly decreased as compared with those in the ICH group (P＜0.05).(3) Brain water contents at each time point in ICH/HF group were significantly decreased as compared with those in the ICH group (P＜0.05).(4) HE staining showed the sizes of hematoma on one and 3 d ofICH in the ICH/HF group and ICH group were consistent;but ICH/HF group had smaller hematomas on 7 d of ICH,and disappeared hematoma and glial cell hyperplasia on 14 d of ICH.Mass neutrophils infiltration developed in the perihematomal areas of the ICH and ICH/HF groups;however,neutrophils infiltration in the ICH/HF group ([20.56±6.37] cells/field) was significantly decreased as compared with that in the ICH group ([41.50±8.91] cells/field) on one d of ICH (P＜0.05).(5) Nissl staining showed neuron death and loss in the perihematomal areas on one,3 and 7 d of ICH in the ICH group;but ICH/HF group had significantly increased neuron number as compared with the ICH group (P＜0.05).(6) The Caspase-3 expression on 3 and 7 d ofICH in the ICH/HF group was significantly decreased as compared with that in the ICH group (P＜0.05);the Bcl-2 expressions at each time point in the ICH/HF group was significantly increased as compared with that in the ICH group (P＜0.05).Conclusion HF exerts neuroprotective effects in ICH rat models by decreasing serum IL-6 and TNF-α levels,reducing neutrophils infiltration and neuronal necrosis around the hematoma,restraining the cell apoptosis through down-regulating Caspase-3 and up-regulating expression of Bcl-2,alleviating the brain edema,and improving the neurological outcome.