Clinical surgical teaching is an important course of undergraduate teaching.Aiming at the problem of disconnection between operation and case in traditional video teaching and observing teaching in operation room,a new model of live surgery teaching based on case teaching was launched:intraoperative diagnosis and preoperative medical history collection were combined;intraoperative surgical anatomy and similar comparative study;teaching surgery were combined with pathology and postoperative adjuvant therapy.Through the questionnaire it was found that all of the students were satisfied with live surgery teaching,96.5％ of the students believed the model would contribute to their understanding of textbook knowledge and memory,and 94.8％ of the students thought the model could improve their interest in clinical learning.

MicroRNAs are endogenously expressed non-coding RNAs, which are composed of approximately 18 nucleotides to 25 nucleotides. Mature microRNAs regulate gene expression by base pairing with the 3'-untranslated region of target mRNAs. These mature microRNAs can degrade target mRNAs or inhibit translation. This process is a type of post-transcriptional regulation of gene ex-pression. Studies have shown that microRNAs are important in physiological and pathological processes, such as cell proliferation, cell differentiation, and cell death. This article provides an overview of the function of microRNAs in the regulation of macrophages.

Objective To explore the clinical outcome of individuals with Clinical High Risk (CHR) for psychosis and its relationship with Theory of Mind (ToM) function.Methods The Structured Interview for Prodromal Symptoms/Scale of Prodromal Syndromes (SIPS/SOPS) was applied to assess prodromal psychosis.The Reading the mind in the Eyes and faux pas Task were conducted to assess the function of Theory of Mind among the individuals of clinical high risk of psychosis.All participants had completed the 2-year follow-up.Conversion was determined using the criteria of presence of psychotic symptoms (POPS).According to the outcome,CHR individuals were divided into conversion group (n=20) and no-conversion group (n=50).The baseline clinical symptom characteristics and Theory of Mind were compared between groups.Results There was no significant difference in clinical symptom characteristics among individuals with CHR (P＞0.05).In the faux pas text,there were significant differences in Faux Pas Detection (P=0.01),Faux Pas Understanding (P=0.01) and Faux Pas Total (P=0.02) but not in control stories and the Reading the Mind in the Eyes Test between convertors and non-convertors (P＞0.05).Conclusion The ToM disability in clinical high risk population increases risk for conversion to psychosis.

Objective To investigate the effectiveness of electromyography-triggered stimulation on the hand function post stroke.Methods 40 stroke patients were divided into electromyography-triggered stimulation group and neuromuscular electric stimulation group.They were assessed with Fugl-Meyer Assessment (FMA), active range of motion of wrist extension (WE-AROM) and modified Barthel index (MBI) before and 6 weeks after treatment. Results The scores of all the assessments improved in both groups after treatment (P<0.001),and improved more in the electromyography-triggered stimulation group than in the neuromuscular electric stimulation group (P<0.05).Conclusion Compared with neuromuscular electrical stimulation, electromyography-triggered stimulation may further improve the hand function post stroke

Objective To investigate the role of PDR1 gene in azole-resistant Candida glabrata (C.glabrata).Methods Thirty-eight clinical isolates of C.glabrata were collected from five different hospitals.The minimal inhibitory concentrations (MIC) of azole antifungals including fluconazole,itraconazole and voriconazole against C.glabrata were determined by broth microdilution.Sequencing and amplification of PDR1 gene was achieved by real-time quantitative polymerase chain reaction (PCR).The mutation was cloned into an expression plasmid and then transferred into C.glabrata.The efflux of rhodamine 6G and drug sensitivity test were performed,and expressions of CDR1 and CDR2 were examined to verify function of mutation.Results Among these 38 isolates of C.glabrata,17 were resistant to at least one of azole antifungals.Moreover,mutations of PDR1 gene existed in every resistant isolates.Results of phenotyping test showed that in the isolate that expressed PDR1P927S,the expression of CDR1 and CDR2 were increased by 20.53 and 4.03 fold,respectively.And the fluorescence intensity of rhodamine 6G was decreased to 0.62 in efflux experiment.Conclusion P927S mutation of PDR1 gene could induce azole resistance of C.glabrata by increasing the expressions of CDR1 and CDR2,which results in drug resistance due to enhanced effect of efflux pump.

Objective To investigate the mechanisms of fluconazole resistance in clinical and experimental induced isolates of C.glabrata.Methods Efflux of rhodamine 6G was performed to evaluate the effects of efflux pumps.The expression levels of transporter genes CDR1,CDR2,SNQ2 and ERG11 were examined by real-time RT-PCR.Meanwhile,sequence of PDR1 was determined by PCR based DNA sequencing.Results Efflux pumps of all fluconazole-resistant isolates had stronger effects than that of susceptible isolates,consistently with significant upregulation of CDR1,but no obvious difference was found in CDR2 or SNQ2.Also,no notable change in the expression level of ERG11 between susceptible and resistant isolates.PDR1 mutations existed in both clinical and experimental induced isolates of C.glabrata,among which P927S,L543P and S947L haven't been reported previously.Conclusion Mutations of PDR1 were induced by fluconazole both in vivo andin vitro,which will result in overexpression of CDR1 and strengthen the effect of efflux pump.

Aim To investigate the effect of ASX (trans-astaxanthin)on the expressions of NF-κB p65 , iNOS and TNF-αin the hippocampus and the prefron-tal cortex of chronic alcohol mice.Methods 40 mice were randomly divided into control group,7 d,14 d, 21 d,28 d alcohol-treated group,the mice were given alcohol preference testing on day of 6,13,20,27. Mice were subjected to alcohol withdrawal for one day after testing.In order to determine the exact time point of cognitive memory impairment in mice after alcohol consumption,they were given morris water maze test after alcohol preference testing. The other 40 mice were randomly divided into control group, alcohol group and ASX group (20,40,80 mg·kg-1 ).After chronic ASX administration, mice were given one probe trial of 60 s in which the platform was removed from the pool to evaluate escape latency,the number of times the animal crossed the previous location of the platform,time spent in the target quadrant,and swim-ming speed.The expressions of NF-κB p65 ,iNOS and TNF-αwere detected by western blotting after behav-ioral testing.Results The mice showed an obvious al-cohol-related phenomenon on 2 1 and 28 days after al-cohol treatment,and escape latency significantly in-creased,entries in target quadrant and duration in tar-get quadrant significantly decreased with increasing drinking days and withdrawal times.The results also suggested that 2 1 days chronic ASX treatment reversed this learning deficit.Moreover,the expression of NF-κB p65 ,iNOS and TNF-αin the hippocampus were significantly increased after 2 1 d alcohol treatment (P<0.001),and pretreatment with ASX (40,80 mg· kg-1 ) could obviously inhibit these changes (P <0.001);Parallel to these changes in the hippocam-pus,the level of NF-κB p65 ,iNOS and TNF-αwere also increased in the prefrontal cortex (P<0.001 ), however,only ASX (80 mg · kg-1 ) administration could inhibit the increase (P<0.05 ).Conclusion These results indicate that ASX pretreatment can pro-tect against alcohol-induced memory impairment via the inhibition of NF- κB p65 ,iNOS and TNF-αexpres-sions in hippocampus and prefrontal cortex.

Objective To study the effect of pioglitazone(PIO) on AdipoR1 and cholesterol ester(CE) in foam cells derived from THP-1-derived macrophages.Methods THP-1-derived macrophages were incubated with increasing concentrations of PIO for 24 hours.After co-cultured with low density lipoprotein(LDL),the accumulation of cholesterol in macrophages was measured by fluorescence spectrophotometric method.The lipid peroxide within cells was detected by TBARS method,the foam cells were observed by oil red staining.AdipoR1 levels were determined by Western blot.Results Compared with the ox-LDL group (0 μmol/L),oil red O-positive cells of the PIO protective groups were greatly reduced.TC,CE,MDA of the PIO protective groups were also obviously decreased.TC (53.6 ± 1.2) μg/mg,CE (30.2 ± 3.6) μg/mg,MDA (3.42 ± 0.06) μg/mg of 5 μμ mol/L PIO group were lower than those of 0μmol/L PIO group[(98.2 ± 3.5),(65.5 ± 6.5),(8.50 ± 1.21)] μg/mg (P ＜ 0.05).TC (25.6 ± 1.8) μg/mg,CE (22.5 ± 4.5) μg/mg,MDA (1.90 ± 0.42) μg/mg of 50 μmol/L PIO group.TC (16.8 ± 2.2) μg/mg,CE(5.9 ± 1.4) μg/mg,MDA (0.65 ± 0.05) μg/mg of 100μmol/L PIO group.Concomitantly,PIO significantly increased AdipoR1 protein expresion,AdipoR1 of 5μmol/L PIO group(0.06±0.05) was higher than that of 0μmol/L PIO group(0.03 ±0.07).AdipoR1 of 50μmol/L PIO group(0.11 ±0.07) was higher than that of 5μmol/L PIO group (0.06 ± 0.05).AdipoR1 of 100 μmol/L PIO group (0.40 ± 0.05) was obviously higher than that of 50 μ mol/L PIO group (0.11 ± 0.07).Conclusion PIO inhibited THP-1-derived formation by up-regulation the expression of AdipoR1,which may play an important role in the development and progression of atherosclerosis.

Objective To construct the eukaryotic expression vector pEGFP-N1/IL-37b and analyze the expression of IL-37 gene in THP-1 cells. Methods Total RNA was extracted from human peripheral blood mononuclear cells ( PB-MCs) and the coding region of IL-37b gene was amplified by RT-qPCR. Then, the gene was cloned into pEGFP-N1 eu-karyotic expression vector. After transfected the recombinant plasmid into THP-1 cells, the expression of IL-37 was detec-ted by RT-qPCR and Western blot. Results Double restriction enzyme digestion and gene sequencing showed that IL-37b gene was correctly inserted into the eukaryotic expression vector pEGFP-N1. RT-qPCR and Western blot showed that the IL-37 expression level was increased significantly (P<0. 01) after transfection in THP-1 cells. Conclusions We successful-ly constructed a novel anti-inflammatory cytokine IL-37 eukaryotic expression vector pEGFP-N1/IL-37b, which lays a foun-dation for further study on IL-37 functions and its association with related diseases.

AIM:To investigate the effect of phosphodiesterase 4 (PDE4) inhibitor rolipram on the levels of cyclic adenosine monophosphate (cAMP), protein kinase A (PKA), cAMP response element-binding protein (CREB), phosphorylated CREB (p-CREB) and brain-derived neurotrophic factor (BDNF) in the hippocampus and the prefrontal cortex (PFC) of alcoholism model mice.METHODS:The mice (n=60) were randomly divided into control group , con-trol+rolipram group, alcoholism model group, and alcohol +rolipram (0.1, 0.5 and 1 mg/kg) groups.The mice were given alcohol preference test on days 6, 13, 20 and 27.After the test, the mice received withdrawal of alcohol for 1 d.On day 28, the mice were given behavior test of depression , and after the test, the mice were sacrificed.The cAMP levels in the hippocampus and PFC were detected by ELISA , and the protein levels of PKA , CREB, p-CREB and BDNF were detec-ted by Western blot.RESULTS:The mice showed an obvious drinking phenomenon (P<0.01), and the immobility time of forced swimming test and tail suspension test was significantly increased (P<0.01), with increasing drinking days and withdrawal times .However , chronic treatment with rolipram for 28 d reversed this phenomenon .Moreover , the cAMP lev-els in the hippocampus and PFC were significantly decreased after 28 d alcohol treatment ( P<0.01 ) , and pretreatment with rolipram (1 mg/kg) obviously reversed this decrease (P<0.01).Parallel to these changes of cAMP , the protein lev-els of PKA, p-CREB and BDNF were also decreased in the hippocampus and PFC (P<0.01), and 28 d rolipram adminis-tration inhibited the decreased cAMP , PKA, p-CREB and BDNF levels in the hippocampus .Moreover, 28 d rolipram ad-ministration also reversed decreased cAMP , PKA and p-CREB in the PFC.CONCLUSION:Rolipram treatment protects against alcohol-induced depression-like behaviors , and also reduces alcohol drinking .These effects may be related to PDE4-cAMP-PKA-CREB-BDNF pathway .