Objective Compare the value of multislice CT perfusion imaging (MSCTPI)?color brain atlas (CBA)?visual evoked potential mapping (VEP-M) in the diagnosis of acute cerebral infarction.Methods After routine CT was performed,the 27 cases of acute cerebral infarction underwent MSCTPI?CBA?and VEP-M respectively.Results The examination of MSCTPI showed that abnormal perfusion changes were in accordance with clinical symptoms;the examination of CBA showed that in 32 scale local high power shadow presented on the power of ??? of lesion;the examination of VEP-M showed the prolongation of latency of P100?degrade of amplitude on the lesion of the chart,the power of the lesion degraded obviously on the map of distribution of power,and distribution asymmetry.Conclusion Combined use of MSCTPI?CBA?VEP-M in the diagnosis of acute cerebral infarction can remedy the defects and improve diagnostic rate of acute cerebral infarction further.

BACKGROUND: It is pointed in some experiment that acidic peptide improves learning and memory of model rat with Alzheimer disease (AD) by inhibiting the synthesis of toxic compounds of nitric oxide (NO).OBJECTIVE: Animal model with Alzheimer disease was established to observe the changes in the levels of NO, nitric oxide synthase (NOS) and acetylcholinesterase (AChE) treated with acidic peptide of various dose concentration.DESIGN: Randomized control and single experiment.SETTING: Teaching-Research Room of Biochemistry and Molecular Biology of Basic Medical College of Zhengzhou University.MATERIALS: The experiment was performed in 2nd Research Room and Experimental Animal Room of Teaching-Research Room of Biochemistry and Molecular Biology of Basic Medical College of Zhengzhou University.Totally 100 SD male rats were selected and some of them were excluded due to retarded response in step down test. Totally 84 rats were included in the experiment and randomized into 7 groups, named normal control,model group, physiological saline group (PS group), Piracetam group, acidic peptide groups of 15, 30 and 60 mg/kg, 12 rats in each group. Acidic peptide was a new small molecular peptide separated from bovine brain and is tripeptide composed of three glutamic acids.METHODS: Except normal control, in the rest groups, after 1 week routine breeding, cerebral stereotactic microinjection was used to inject 5 μg ibotenic acid in hippocampus of rats to destroy bilateral Meynert's nucleus basalis to establish AD model. In normal control and model group, no medication was applied. In PS group, physiological saline was used for gastric perfusion. In piracetam group, piracetam of 0.3 g/kg was used for gastric perfusion and in acidic peptide groupsof 15, 30 and 60 mg/kg,acidic peptide of 15, 30 and 60 mg/kg was applied for gastric perfusion successively, continuously for 20 days, once per day, 2 mL/time. On the expiration of gastric perfusion, the rats were sacrificed after anesthetized and the brain was collected on ice plate to prepare tissue homogenate. After centrifugated at 1 000 r/minute, 4℃ for 10 minutes, the supernatant was collected to assay the levels of NO, NOS and AChE with NO, NOS and AChE kits successively.MAIN OUTCOME MEASURES: Levels of NO, NOS and AChE in brain of rat in each groupRESULTS: Totally 84 rats were employed in the experiment and all entered result analysis. Comparison of levels of NO, NOS and AChE in rat brain of each group: compared with model group, NO levels in acidic peptide groups of 15, 30 and 60 mg/kg were reduced remarkably[(1.95±0.20), (1.39±0.10), (1.25±0.07), (1.00±0.04) mmoL/kg, P ＜ 0.05],NOS levels were reduced remarkably [(4.53±0.18), (3.39±0.09), (3.10±0.06),(2.97±0.06) μmol/kg, P ＜ 0.05] and AChE did not change remarkably[(0.67±0.12), (0.71±0.11), (0.72±0.08), (0.72±0.07) mmol/L, P ＞ 0.05].CONCLUSION: Acidic peptide reduces significantly the synthesis of NO and NOS in brain of AD rat, but it dose not affect AChE activity remarkably. It is suggested that acidic peptide improves learning and memory of rat with Alzheimer disease probably by inhibiting the synthesis of toxic compound of NO or its toxicity.

Objective To explore the association between HLA-Cw alleles with systemic lupuserythematosus. Methods Polymerase chain reaction-sequence specific primer method was used to analyze thedistribution of HLA-Cw01-08 alleles among 108 patients with SLE and 102 healthy controls. The allelefrequencies was compared between various patient groups and the control population. Results The frequencyof HLA-Cw07 alleles in patients with SLE was significantly increased in patients with SLE. Conclusion Theresults indicate that HLA-Cw07 may be the susceptible alleles or may be closely linked to the susceptiblegenes for SLE.

Objective To determine the mRNA levels of microRNA-223 (miR-223) and NLRP3 in-flammasome components [Nod-like receptor pyrin domain-containing protein 3 (NLRP3), apoptosis-associated speck-like protein containing a CARD (ASC) and caspase-1] in peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus (SLE) and to explore its clinical significance. Methods Real time polymerase chain reaction (PCR) was used to detect the mRNAlevels of miR-223 and NLRP3 inflam-masome components in PBMCs from 35 SLE patients, 30 healthy controls and 20 SLE patients after treatment, and then their correlations with clinical and laboratory parameters [anti-double-stranded deoxyribon-ucleic acid (dsDNA) antibody, anti-nucleosome antibody (AnuA), erythrocyte sedi-mentation rate (ESR)] were evaluated. Data were analyzed using t test or x2 test and Pearson test was used for correlation analysis. Results Com-pared with healthy controls, mRNA levels of miR-223 and Caspase-1 were higher in the PBMCs from SLE patients [(1.17 ±0.15) vs (0.68 ±0.14), t=2.416, P=0.0186; (1.89 ±0.13) vs (1.32 ±0.13), t=3.123, P=0.0027], but the NLRP3 and ASC mRNA expression levels were in the opposite [(0.64 ±0.05) vs (0.98 ±0.06), t=4.442, P<0.01;(0.98±0.08) vs (1.32±0.12), t=2.391, P=0.0198]. Correlation analysis results showed that there was a negative correlation of mRNA levels between the miR-223 and NLRP3 (r=-0.7849, P<0.05), but the miR-223 had no correlation with ASC and caspase-1. The mRNA levels of miR-223 was positively correlated with anti-dsDNA antibody, SLEDAI and ESR (r=0.7035, 0.6923, 0.6873, all P values<0.05), but had no correlation with AnuA. After treatment, the mRNA expression of miR-223 and caspase-1 in PBMCs from SLE patients was significantly reduced [(1.30±0.22) vs (0.79±0.11), t=2.07, P=0.0453; (2.05±0.19) vs (1.50±0.11), t=2.471, P=0.0183], while the mRNA level of NLRP3 increased [(0.69 ±0.08) vs (0.94 ±0.07); t=2.445, P=0.0193]. There was no significant difference in the expression of miR-223 mRNA in PBMCs between lupus nephritis (LN) patients and SLE patients without renal impairment. Conclusion miR-223 and caspase-1 are highly ex-pressed in the PBMCs from patients with SLE, while the mRNA of NLRP3 and ASC is in low expression. The mRNA expression of miR-223 is negatively correlated with NLRP3 and disease activity. Expression of miR-223 mRNA decreases significantly after treatment. So miR-223 may play an important role in the pathogenesis of SLE.

Objective To investigate the effect of Zuogui Jiangtang Jieyu Formula(左归降糖解郁方,ZJJF)on hippocampal neuron apoptosis in diabetic rats with depression and to ascertain whether its mechanism involves the regulation of JNK signaling pathway. Methods(i)A total of 72 specific pathogen-free(SPF)grade male Sprague Dawley(SD)rats were randomly divided into six groups,with 12 rats in each group:control,model,metformin(Met,0.18 g/kg)+fluoxetine(Flu,1.8 mg/kg),and the high-,medium-,and low-ZJJF dosages(ZJJF-H,20.52 g/kg;ZJJF-M,10.26 g/kg;ZJJF-L,5.13 g/kg)groups.All groups except control group were injected once via the tail vein with streptozotocin(STZ,38 mg/kg)combined with 28 d of chronic unpredictable mild stress(CUMS)to establish diabetic rat models with de-pression.During the CUMS modeling period,treatments were administered via gavage,with control and model groups receiving an equivalent volume of distilled water for 28 d.The effi-cacy of ZJJF in reducing blood sugar and alleviating depression was evaluated by measuring fasting blood glucose,insulin,and glycated hemoglobin levels,along with behavioral assess-ments,including the open field test(OFT),forced swim test(FST),and sucrose preference test(SPT).Hippocampal tissue damage and neuronal apoptosis were evaluated using hema-toxylin-eosin(HE)staining and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling(TUNEL)staining.Apoptosis-related proteins Bax,Bcl-2,caspase-3,and the ex-pression levels of JNK/Elk-1/c-fos signaling pathway were detected using Western blot and real-time quantitative polymerase chain reaction(RT-qPCR).(ii)To further elucidate the role of JNK signaling pathway in hippocampal neuronal apoptosis and the pharmacological ef-fects of ZJJF,an additional 50 SPF grade male SD rats were randomly divided into five groups,with 10 rats in each group:control,model,SP600125(SP6,a JNK antagonist,10 mg/kg),ZJJF(20.52 g/kg),and ZJJF(20.52 g/kg)+Anisomycin(Aniso,a JNK agonist,15 mg/kg)groups.Ex-cept for control group,all groups were established as diabetic rat models with depression,and treatments were administered via gavage for ZJJF and intraperitoneal injection for SP6 and Aniso for 28 d during the CUMS modeling period.Behavioral changes in rats were evaluated through the OFT,FST,and SPT,and hippocampal neuron damage and apoptosis were ob-served using HE staining,Nissl staining,TUNEL staining,and transmission electron mi-croscopy(TEM).Changes in apoptosis-related proteins and JNK signaling pathway in the hippocampal tissues of rats were also analyzed. Results(i)ZJJF significantly reduced the high blood glucose,insulin,and glycated he-moglobin levels in model rats(P<0.01).It increased autonomous activity and decreased de-spair-like behaviors(P<0.01),improved the pathological damage of hippocampal neurons,increased the number of neuronal nuclei(P<0.01),and reduced the number of mechanocytes,vacuolar cells,and apoptotic neurons(P<0.05,P<0.01,and P<0.01,respec-tively).ZJJF down-regulated the expression levels of pro-apoptotic proteins Bax and caspase-3(P<0.01),up-regulated the anti-apoptotic protein Bcl-2(P<0.01),and significantly inhibit-ed the overexpression of phosphorylated JNK(p-JNK),Elk-1,and c-fos(P<0.01).(ii)SP6 in-creased autonomous activity and reduced despair time in model rats(P<0.05),although it had no significant effects on sucrose preference(P>0.05).It increased the number of Nissl bodies in hippocampal neurons(P<0.01),reduced the protein expression levels of Bax(P<0.01)and caspase-3(P<0.05),and decreased the number of apoptotic neurons(P<0.05).SP6 also increased the expression level of Bcl-2(P<0.01),and inhibited the high expression levels of p-JNK,Elk-1,and c-fos(P<0.01,P<0.01,and P<0.05,respectively),suggesting that hip-pocampal neuronal apoptosis in diabetic rats with depression is associated with abnormal ac-tivation of JNK signaling pathway.Compared with ZJJF group,ZJJF+Aniso group showed a decrease in sucrose preference(P<0.05)and an increase in despair time(P<0.01)with more notable hippocampal neuronal damage.This group also exhibited a decrease in expression level(P<0.01)Bcl-2 and an increase in expression levels of Bax,caspase-3,p-JNK,Elk-1,and c-fos(P<0.01,P<0.05,P<0.05,P<0.01,and P<0.05,respectively),indicating that the antidepressant effects of ZJJF,its improvement of neuronal apoptosis,and regulation of JNK signaling molecules could all be reversed by a specific JNK agonist. Conclusion ZJJF exerts a significant hypoglycemic effect and ameliorates the apoptosis of hippocampal neurons by inhibiting the activation of JNK signaling pathway,which is a promising formula for the treatment of diabetic depression in clinical settings.

Objective:To analyze the long-term therapeutic effect of endoscopic submucosal dissection (ESD) on the treatment of early gastric cancer (EGC).Methods:We retrospectively reviewed EGC patients who underwent ESD at Cancer Hospital, Chinese Academy of Medical Sciences (CAMS), from January 2009 to December 2016. The incidence rates of local recurrence, synchronous cancer and heterogeneous cancer were analyzed. Kaplan-Meier method was used to analyze 5-years recurrence free survival (RFS) and 5-years disease special survival (DSS) of all patients.Results:A total of 255 EGC patients were enrolled in this study, included 175 differentiated early gastric cancer (D-EGC) patients and 80 undifferentiated early gastric cancer (UD-EGC) patients. Among them, 171 patients within the extended indication of ESD while 84 patients beyond the extended indication of ESD. Among the 225 patients, the incidence rates of local recurrence, synchronous cancer and heterogeneous cancer were 2.0%, 2.0% and 2.4%, respectively. The local recurrence rates of D-EGC group and UD-EGC group was 1.7% and 2.5%, respectively, without significant difference ( χ2=0.176, P=0.675). The incidence rates of synchronous and heterogenous cancer in the D-EGC group were 2.3% and 3.4%, higher than 1.2% and 0 of UD-EGC group, although there was no significant difference ( χ2=0.306, P=0.580 vs χ2=2.809, P=0.094). There were no significant differences in 5-years RFS (91.3% vs 95.9%, P=0.236) and 5-years DSS (100% vs 98.6%, P=0.156) between D-EGC group and UD-EGC group. Conclusions:The long-term outcome of ESD in the treatment of EGS is good. More attention should be paid to the occurrence of local recurrence and heterogeneous cancer in EGC patients undergo ESD. These patients still have a good long-tern outcome even undergoing ESD for more than once.

Objective:To analyze the long-term therapeutic effect of endoscopic submucosal dissection (ESD) on the treatment of early gastric cancer (EGC).Methods:We retrospectively reviewed EGC patients who underwent ESD at Cancer Hospital, Chinese Academy of Medical Sciences (CAMS), from January 2009 to December 2016. The incidence rates of local recurrence, synchronous cancer and heterogeneous cancer were analyzed. Kaplan-Meier method was used to analyze 5-years recurrence free survival (RFS) and 5-years disease special survival (DSS) of all patients.Results:A total of 255 EGC patients were enrolled in this study, included 175 differentiated early gastric cancer (D-EGC) patients and 80 undifferentiated early gastric cancer (UD-EGC) patients. Among them, 171 patients within the extended indication of ESD while 84 patients beyond the extended indication of ESD. Among the 225 patients, the incidence rates of local recurrence, synchronous cancer and heterogeneous cancer were 2.0%, 2.0% and 2.4%, respectively. The local recurrence rates of D-EGC group and UD-EGC group was 1.7% and 2.5%, respectively, without significant difference ( χ2=0.176, P=0.675). The incidence rates of synchronous and heterogenous cancer in the D-EGC group were 2.3% and 3.4%, higher than 1.2% and 0 of UD-EGC group, although there was no significant difference ( χ2=0.306, P=0.580 vs χ2=2.809, P=0.094). There were no significant differences in 5-years RFS (91.3% vs 95.9%, P=0.236) and 5-years DSS (100% vs 98.6%, P=0.156) between D-EGC group and UD-EGC group. Conclusions:The long-term outcome of ESD in the treatment of EGS is good. More attention should be paid to the occurrence of local recurrence and heterogeneous cancer in EGC patients undergo ESD. These patients still have a good long-tern outcome even undergoing ESD for more than once.

Background: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic β-cell senescence. However, targets and effective agents for preventing stearic acid-induced β-cell senescence are still lacking. Although melatonin administration can protect β-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse β-cells and elucidated the possible role of microRNAs in this process. Methods: β-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated β-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked β-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. Results: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and β-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced β-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected β-cells. Conclusion These data demonstrate that melatonin protects against stearic acid-induced β-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced β-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.