Objective: To interview the role of CGRP to hepatic microcirculation in acute liver injury induced by coneanavalin A(Con A). Methods: Sixty Kunming rats were divided into three groups randomly(n=20), acute liver injury was established by injection with 20 mg/kg Con A through the tail vein. A saline control group was established by injection with saline. In CGRP-administered group, CGRP was given to rats 30 min before Con A injected. Ten mice in each group were used to observe the average liver blood flow volume and concentration by laser-doppler flow-instrument, and the other ten rats were observed the hepatic microcirculation velocity in vivo by an inverted microscope. Liver damage was assessed by histological evaluation after the rat had been killed. Results: Compared to the injury group, the average liver blood flow volume and velocity were significantly increased in CGRP-administered group, meanwhile, the pathological injury was markedly alleviated, whereas the blood concentration was almost the same. Conclusion: CGRP can decrease the dysfunction of hepatic microcirculation by means of improving the tissue perfusion, and alleviate the pathological damage during acute liver injury.

Objective To study the effect of bcl-2 antisense oligodexynucleotides on the apoptosis in human small-cell lung cancer cell line NCI-H69. Methods Cultured cells were divided into 4 groups: antisense oligodexynucleotides(ASODN), sense oligodexynucleotides (SODN), nonsense oligodexynucleotides (NSODN) and control.The different bcl-2 oligodexynucleotides was transfected into corresponding cells using oligofectamine.The expression of bcl-2 was examined by Western blot.The apoptosis rates were measured by flow cytometry (FCM).Results The bcl-2 expression in ASODN group was significantly inhibited compared to the control group, SODN and NSODN groups, but it was not obviously inhibited in SODN and NSODN groups.The apoptosis rate of ASODN group in different concentration was (9.97±1.54) %, (15.28±1.73) % and (21.41±1.85) % respectively, it was significantly higher than that of the control group (F = 7.19-15.48,q = 5.21-7.98, P ＜0.01). Conclusion The bcl-2 ASODN could enhance cell apoptosis rate in small-cell lung cancer by blocking bcl-2 gene effectively.

Objective To investigate the value of multislice spiral CT(MSCT,)in interventional therapy of the hepatocellular carcinoma(HCC)emphasising on transcatheter hepanc arterial chemoembolization(TACE).Methods MSCT were performed in 60 cases of HCC before interventional procedure,CT findings of hepatic artery phase,portal venous phase and hepatic venous phase were observed respectively,among which CTA were done in 15 cases,and the anatomy of celiacartery and its branches were observed in 45 cases.The schemes of interventional therapy were worked out according to the findings of MSCT.Results MSCT showed 250 lesions,10 cases of tumor thrombosis in portal vein and 19 cases of hepatic arterioportal shunt.There was no significant difference between MSCT and digital subtraction angiography(DSA)in positive rate of in showing number of tumor or tumor thrombosis in portal vein(P＞0.05),but the 3D construction of celiac artery branches in CTA was better than that in DSA,while angles between celiac artery and abdominal aorta in MSCT were more convenient than that in DSA.MSCT showed 5 eases of hepatic artery original abnormality,according to that in DSA.Conclusion MSCT is of importance for guidance of interventional therapy of hepatocellular carcinoma.

Parkinson's disease (PD) is a common neurological degenerative diseases.Neuron degeneration process is irreversible;therefore,the correct diagnosis is critical and reliable biomarkers are urgently needed.With the development of molecular biology,some nonspecific biomarker detection methods,such as metabolomics,have been used in the study ofPD.Metabonomics provides a technology and a new technical platform for testing comprehensive metabolites of PD.Metabonomics is very important for biomarker screening in PD.In this paper,the concept,research methods and research progress of metabonomics in PD are reviewed.

Objective: We previously elucidated that long non-coding RNA Promoter of CDKN1A Antisense DNA damage Activated RNA (PANDAR) as a p53-dependent oncogene to promote cisplatin resistance in ovarian cancer (OC). Intriguingly, high level of p53-independent PANDAR was found in cisplatin-resistant patients with p53 mutation. Here, our study probed the new roles and the underlying mechanisms of PANDAR in p53-mutant OC cisplatin-resistance. Methods: A2780 and A2780-DDP cells were served as OC cisplatin-sensitive and cisplatinresistant cells. HO-8910PM cells were subjected to construct chemotherapy-induced extracellular vesicles (Chemo-EVs). Transmission electron microscopy (TEM) and nanoparticle tracking analysis were employed to evaluate Chemo-EVs. Cell viability was assessed using cell counting kit-8 and colony formation assays. Cell apoptosis was assessed using Annexin V and propidium iodide staining. The relationships between PANDAR, serine and arginine-rich premRNA splicing factor 9 (SRSF9) were verified by RNA immunoprecipitation and fluorescence in situ hybridization. Tumor xenograft experiment was employed to evaluate the effects of PANDAR-Chemo-EVs on OC cisplatin-resistance in vivo. Immunofluorescent staining and immunohistochemistry were performed in tumor tissue. Results: PANDAR level increased in OC patients with p53-mutation. PANDAR efflux enacted via exosomes under cisplatin conditions. Additionally, exosomes from OC cell lines carried PANDAR, which significantly increased cell survival and chemoresistance in vitro and tumor progression and metastasis in vivo. During cisplatin-induced stress, SRSF9 was recruited to nuclear bodies by increased PANDAR and muted apoptosis in response to cisplatin. Besides, SRSF9 significantly increased the ratio of SIRT4/SIRT6 mRNA in OC. Conclusion Cisplatin-induced exosomes transfer PANDAR and lead to a rapid adaptation of OC cell survival through accumulating SRSF9 following cisplatin stress exposure.

Objective: We previously elucidated that long non-coding RNA Promoter of CDKN1A Antisense DNA damage Activated RNA (PANDAR) as a p53-dependent oncogene to promote cisplatin resistance in ovarian cancer (OC). Intriguingly, high level of p53-independent PANDAR was found in cisplatin-resistant patients with p53 mutation. Here, our study probed the new roles and the underlying mechanisms of PANDAR in p53-mutant OC cisplatin-resistance. Methods: A2780 and A2780-DDP cells were served as OC cisplatin-sensitive and cisplatinresistant cells. HO-8910PM cells were subjected to construct chemotherapy-induced extracellular vesicles (Chemo-EVs). Transmission electron microscopy (TEM) and nanoparticle tracking analysis were employed to evaluate Chemo-EVs. Cell viability was assessed using cell counting kit-8 and colony formation assays. Cell apoptosis was assessed using Annexin V and propidium iodide staining. The relationships between PANDAR, serine and arginine-rich premRNA splicing factor 9 (SRSF9) were verified by RNA immunoprecipitation and fluorescence in situ hybridization. Tumor xenograft experiment was employed to evaluate the effects of PANDAR-Chemo-EVs on OC cisplatin-resistance in vivo. Immunofluorescent staining and immunohistochemistry were performed in tumor tissue. Results: PANDAR level increased in OC patients with p53-mutation. PANDAR efflux enacted via exosomes under cisplatin conditions. Additionally, exosomes from OC cell lines carried PANDAR, which significantly increased cell survival and chemoresistance in vitro and tumor progression and metastasis in vivo. During cisplatin-induced stress, SRSF9 was recruited to nuclear bodies by increased PANDAR and muted apoptosis in response to cisplatin. Besides, SRSF9 significantly increased the ratio of SIRT4/SIRT6 mRNA in OC. Conclusion Cisplatin-induced exosomes transfer PANDAR and lead to a rapid adaptation of OC cell survival through accumulating SRSF9 following cisplatin stress exposure.

Objective: We previously elucidated that long non-coding RNA Promoter of CDKN1A Antisense DNA damage Activated RNA (PANDAR) as a p53-dependent oncogene to promote cisplatin resistance in ovarian cancer (OC). Intriguingly, high level of p53-independent PANDAR was found in cisplatin-resistant patients with p53 mutation. Here, our study probed the new roles and the underlying mechanisms of PANDAR in p53-mutant OC cisplatin-resistance. Methods: A2780 and A2780-DDP cells were served as OC cisplatin-sensitive and cisplatinresistant cells. HO-8910PM cells were subjected to construct chemotherapy-induced extracellular vesicles (Chemo-EVs). Transmission electron microscopy (TEM) and nanoparticle tracking analysis were employed to evaluate Chemo-EVs. Cell viability was assessed using cell counting kit-8 and colony formation assays. Cell apoptosis was assessed using Annexin V and propidium iodide staining. The relationships between PANDAR, serine and arginine-rich premRNA splicing factor 9 (SRSF9) were verified by RNA immunoprecipitation and fluorescence in situ hybridization. Tumor xenograft experiment was employed to evaluate the effects of PANDAR-Chemo-EVs on OC cisplatin-resistance in vivo. Immunofluorescent staining and immunohistochemistry were performed in tumor tissue. Results: PANDAR level increased in OC patients with p53-mutation. PANDAR efflux enacted via exosomes under cisplatin conditions. Additionally, exosomes from OC cell lines carried PANDAR, which significantly increased cell survival and chemoresistance in vitro and tumor progression and metastasis in vivo. During cisplatin-induced stress, SRSF9 was recruited to nuclear bodies by increased PANDAR and muted apoptosis in response to cisplatin. Besides, SRSF9 significantly increased the ratio of SIRT4/SIRT6 mRNA in OC. Conclusion Cisplatin-induced exosomes transfer PANDAR and lead to a rapid adaptation of OC cell survival through accumulating SRSF9 following cisplatin stress exposure.

Objective:To investigate the relationships between hyperuricemia and the incidence risk for cardiometabolic abnormity in children.Methods:Data were obtained from School-based Cardiovascular and Bone Health Promotion Program. In 2017, a total of 15 391 children aged 6-16 years in Beijing were selected through stratified cluster sampling at baseline survey. Follow-up investigation was conducted in 2019. Logistic regression model was used to analyze the relationships of uric acid quartiles and change in uric acid levels with incidence risks for cardiometabolic abnormity (hypertension, hyperglycemia and dyslipidemia).Results:A total of 8 807 children (4 376 boys, 4 431 girls) were included in the analysis, the average age of the children was (11.1±3.3) years at baseline survey. The adjusted odds ratios ( ORs) and 95% confidence intervals ( CIs) of incidence risk for hypertension in the third and fourth quartiles of the UA were 1.39 (1.11-1.75) and 1.56 (1.19-1.81), respectively. The ORs and 95% CIs of risk for high LDL-C in the second, third and fourth quartiles were 1.88 (1.16-3.05),1.98 (1.23-3.17) and 2.25 (1.42-3.57). The uric acid level increased by one standard deviation, the risk increased by 17% for hypertension and 27% for high LDL-C. The uric acid level increased by 10 μmol/L, the risk increased by 2.1% for hypertension and 2.9% for high LDL-C. The gender-stratified analysis showed that the similar results. The ORs and 95% CIs were 1.32 (1.09-1.60) and 1.50 (1.05-2.16) for hypertension, 1.90 (1.38-2.60) and 2.96 (1.58-5.52) for high TC, 1.78 (1.26-2.51) and 2.84 (1.60-5.03) for high LDL-C in the groups of newly diagnosed hyperuricemia and persistent hyperuricemia. Conclusions:Higher uric acid level was associated with increased incidence risks for hypertension, abnormal TC and LDL-C. Maintaining optimal uric acid level by children might contribute to the early prevention of cardiovascular diseases.