期刊：
International Immunopharmacology,2021年93(2):107411 ISSN：1567-5769
通讯作者：
Hu, Sihai;Long, Dingxin
作者机构：
[Wu, Xiaoxia; Hu, Sihai; Li, Zhenyu; Li, Yumeng; Hou, Yongli; Cao, Hui] Univ South China, Inst Pathogen Biol, Coll Med, Hengyang 421001, Peoples R China.;[Wang, Yan] Univ South China, Hosp 2, Operating Room, Hengyang 421001, Peoples R China.;[Long, Dingxin] Univ South China, Sch Publ Hlth, 28 West Changsheng Rd, Hengyang 421001, Hunan, Peoples R China.
通讯机构：
[Long, Dingxin] C;[Hu, Sihai] I;Institute of Pathogenic Biology, Medical College, University of South China, Hengyang 421001, China. Electronic address:;China School of Public Health, University of South China, Hengyang 421001, China. Electronic address:
关键词：
Chitosan nanoparticle;Immunopotentiators;Moucosal vaccine;NMB0315;Neisseria meningitidis serogroup B
摘要：
Neisseria meningitidis (N. meningitidis) is a human-specific pathogen and a major cause of meningitis and septicemia with a high case fatality rate. N. meningitidis may penetrate the nasopharyngeal mucosal membrane and cause severe meningitis, a mucosal immune response plays a key role in the defense against meningococcal infections. Our previous study demonstrated that N. meningitidis serogroup B 0315 (NMB0315) was a vaccine candidate against N. meningitidis serogroup B (NMB) through parenteral immunization. In this study, immunopotentiators (C48/80 or CpG-ODN) were loaded into chitosan nanoparticle (Chi NP) to form combination adjuvants (Chi-CpG NP and Chi-C48/80 NP) and adopted to enhance the immunogenicity of NMB0315 through intranasal immunization. The experimental results have indicated that both Chi-CpG NP and Chi-C48/80 NP are effective mucosal adjuvants for the induction of significantly higher rNMB0315-specific IgG, IgG1, IgG2a and sIgA antibodies. Meanwhile, Chi-CpG NP and Chi-C48/80 NP could change the ratio of IgG1/IgG2a, inducing a more balanced cellular/humoral immune response. Chi-CpG NP and Chi-C48/80 NP also boosted interleukin-4 (IL-4), interferon-γ (IFN-γ) and interleukin-17 A (IL-17A) production by splenocytes. The bactericidal antibodies have been detected in sera from mice immunized with rNMB0315+Chi-CpG NP and rNMB0315+Chi-C48/80 NP. Overall, the combination adjuvants could be applicable to the development of a mucosal vaccine against NMB.
摘要：
Purpose To study the effect of curcumin on proliferation and invasion of the human retinoblastoma cells and its potential mechanism. Methods A cell line of retinoblastoma (WERI-Rb-1) was treated with various concentrations of curcumin (0-40 mu M). Cell number was counted with CCK8 kit, and cell migration was assessed using the Transwell assay. Immunoblotting was performed to detect the proteins of metalloproteinase-2 (MMP-2), MMP-9 and vascular endothelial growth factor (VEGF) as well as nuclear translocation of nuclear factor-kappa B (NF-kappa B, p65). Results Proliferation and migration of WERI-Rb-1 cells were significantly inhibited by curcumin in a concentration-dependent manner (0-40 mu M). Protein expressions of MMP-2, MMP-9 and VEGF in the WERI-Rb-1 cells were also significantly inhibited by curcumin in a concentration-dependent manner (0-40 mu M). Furthermore, nuclear translocation of NF-kappa B (p65) was significantly inhibited by curcumin in time-dependent manner (6-24 h). Conclusion Curcumin inhibited proliferation and migration of WERI-Rb-1 cells, a cell line of human retinoblastoma, which might be through modulating NF-kappa B and its downstream proteins including VEGF, MMP-2, and MMP-9.
摘要：
This study aims to identify differentially expressed microRNAs (miRNAs) in gastric cancer by comparing gastric cancerous tissues with normal tissues, explore the potential roles.The miRNA expression microarray was employed on gastric cancer tissues, and apparently normal para-cancerous tissues from 3 patients undergoing radical surgery were matched. Quantitative RT-PCR was performed on the other 7 patients to validate the findings of the microarray. Furthermore, Gene Ontology (GO) analysis and enrichment analysis of KEGG Pathway were performed for 5 dysregulated candidate miRNAs, including 3 upregulated (miR-31-3p, miR-6736-3p, and miR-147b) and 2 downregulated (miR-3065-5p and miR-3921) miRNAs, in order to determine the role of miRNAs in tumorigenesis and development.Among these miRNAs, 17 miRNAs were found to be upregulated, and 19 miRNAs were found to be downregulated. The dysregulated expression of 5 candidate miRNAs, including miR-31-3p, miR-147b, miR-6736-3p, miR-3065-5p, and miR-3921, were verified by quantitative RT-PCR in the validation set. Among these miRNAs, miR-31-3p, miR-6736-3p, miR-3065-5p, and miR-3921 had 551 target gene intersections. The GO and KEGG Pathway analyses Revealed that miR-31-3p, miR-6736-3p, miR-3065-5p, and miR-3921 may participate in multiple pathophysiological processes, such as foreign substance metabolism and chemical carcinogenesis.The profile of differentially expressed miRNAs was successfully screened, and 4 miRNAs (i.e., miR-31-3p, miR-6736-3p, miR-3065-5p, and miR-3921) appeared to be involved in gastric carcinogenesis. These might serve as promising biomarkers for gastric cancer.
摘要：
Listeria ivanovii subsp. ivanovii is an intracellular bacterium distributed widely in nature, causing the listeriosis in ruminants and humans. Previous researches had isolated 116 strains of L. ivanovii subsp. ivanovii from wild rodents and pikas of different regions in China, and the predominant sequence types were ST1 and ST2. In this study, we first investigated the biological characteristics and virulence of these two clonal strains including motility, metabolism and virulence in cells and mouse model. The results demonstrated the ST1 strains exhibited motility, wide metabolic activity and hypervirulence, whereas the ST2 strains showed non-motility, relative lower metabolic activity and virulence. Considering the transmissible ability from wild rodents and pikas to ecological environment, the L. ivanovii subsp. ivanovii with potential pathogenicity to humans and ruminants should be monitored.
摘要：
Introduction: This meta-analysis aimed to explore the preventive effects of combined statin and antihypertensive therapy on major cardiovascular outcomes in patients with hypertension. Methods: PubMed, Embase, and the Cochrane Library databases and reference lists of published studies were systematically searched throughout October 9, 2019. Studies designed as randomized controlled trials and investigating the effects of combined statin and antihypertensive therapy versus antihypertensive therapy alone were included. Data abstraction and quality of included studies were assessed by 2 independent authors. The summary results were calculated using relative risks (RRs) with 95% CIs employing a random-effects model. Results: A total of 8 randomized controlled trials including 38,618 patients were finally enrolled. The summary RRs indicated that the combined therapy significantly reduced the risk of major adverse cardiovascular events compared with antihypertensive therapy alone (RR 0.79; 95% CI 0.71–0.88; p < 0.001). Furthermore, the patients in the combined therapy group also experienced less myocardial infarction (RR 0.67; 95% CI 0.53–0.84; p = 0.001) and stroke risks (RR 0.82; 95% CI 0.72–0.94; p = 0.005), while no significant difference was observed between combined therapy and antihypertensive therapy alone regarding cardiac death (RR 0.96; 95% CI 0.84–1.08; p = 0.465) and all-cause mortality (RR 0.95; 95% CI 0.86–1.04; p = 0.277). Conclusion: These findings suggested that combined statin and antihypertensive therapy was associated with more cardiovascular benefits compared with antihypertensive therapy alone.
期刊：
American Journal of Human Genetics,2019年105(1):166-176 ISSN：0002-9297
通讯作者：
Shen, Lu;Jin, Peng
作者机构：
[Tian, Yun; Sun, Qi-Ying; Yi, Fang; Tang, Bei-Sha; Zhou, Ya-Fang; Xu, Hong-Wei] Cent S Univ, Xiangya Hosp, Dept Geriatr, Changsha 410008, Hunan, Peoples R China.;[Zeng, Sheng; Jiao, Bin; Liu, Zhen; Chen, Zhao; Jiang, Hong; Zhou, Chao-Jun; Yan, Xin-Xiang; Hou, Xuan; Guo, Ji-Feng; Tang, Bei-Sha; Long, Hong-Yu; Wang, Jun-Ling; Shen, Lu] Cent S Univ, Xiangya Hosp, Dept Neurol, Changsha 410008, Hunan, Peoples R China.;[Tian, Yun; Tang, Bei-Sha; Shen, Lu] Cent S Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha 410008, Hunan, Peoples R China.;[Xia, Kun; Hu, Zheng-Mao; Huang, Wen; Duan, Ran-Hui] Cent S Univ, Sch Life Sci, Ctr Med Genet, Changsha 410008, Hunan, Peoples R China.;[Kong, Ha Eun; Li, Yujing; Shafik, Andrew Mark; Allen, Emily G.; Jin, Peng] Emory Univ, Sch Med, Dept Human Genet, Whitehead Res Bldg,Room 305A,615 Michael St, Atlanta, GA 30322 USA.
通讯机构：
[Shen, Lu] C;[Jin, Peng] E;Cent S Univ, Xiangya Hosp, Dept Neurol, Changsha 410008, Hunan, Peoples R China.;Cent S Univ, Xiangya Hosp, Natl Clin Res Ctr Geriatr Disorders, Changsha 410008, Hunan, Peoples R China.;Emory Univ, Sch Med, Dept Human Genet, Whitehead Res Bldg,Room 305A,615 Michael St, Atlanta, GA 30322 USA.
摘要：
Neuronal intranuclear inclusion disease (NIID) is a slowly progressing neurodegenerative disease characterized by eosinophilic intranuclear inclusions in the nervous system and multiple visceral organs. The clinical manifestation of NIID varies widely, and both familial and sporadic cases have been reported. Here we have performed genetic linkage analysis and mapped the disease locus to 1p13.3-q23.1; however, whole-exome sequencing revealed no potential disease-causing mutations. We then performed long-read genome sequencing and identified a large GGC repeat expansion within human-specific NOTCH2NLC. Expanded GGC repeats as the cause of NIID was further confirmed in an additional three NIID-affected families as well as five sporadic NIID-affected case subjects. Moreover, given the clinical heterogeneity of NIID, we examined the size of the GGC repeat among 456 families with a variety of neurological conditions with the known pathogenic genes excluded. Surprisingly, GGC repeat expansion was observed in two Alzheimer disease (AD)-affected families and three parkinsonism-affected families, implicating that the GGC repeat expansions in NOTCH2NLC could also contribute to the pathogenesis of both AD and PD. Therefore, we suggest defining a term NIID-related disorders (NIIDRD), which will include NIID and other related neurodegenerative diseases caused by the expanded GGC repeat within human-specific NOTCH2NLC.
作者机构：
[Feng Shu-Jun; Tang Xin-Ying] Univ South China, Peoples Hosp Chenzhou 1, Dept Cardiol, Chenzhou 423000, Peoples R China.;[Tang Zhi-Han; Li Tao-Hua; Tang Wei] Univ South China, Inst Cardiovasc Dis, Key Lab Arteriosclerol Hunan Prov, Hengyang 421001, Peoples R China.;[Tang Zhi-Han] Univ Calgary, Hlth Sci Ctr, Dept Biochem & Mol Biol, Libin Cardiovasc Inst Alberta, 3330 Hosp Dr NW, Calgary, AB T2N 4N1, Canada.;[Wang Ying] Henan Univ Sci & Technol, Dept Cardiol, Affiliated Hosp 2, Luoyang 471000, Peoples R China.;[Tang Wei] Univ South China, Med Coll, Class 2014, Hengyang 421001, Peoples R China.
通讯机构：
[Kuang Ze-Min] C;Capital Med Univ, Dept Hypertens, Beijing Anzhen Hosp, Beijing 100029, Peoples R China.
关键词：
Red yeast rice;Xuezhikang;Atherosclerotic cardiovascular disease;Endothelial cells;Molecular mechanism
摘要：
Atherosclerotic cardiovascular disease (ASCVD) is the deadliest disease in the world, with endothelial injury occurring throughout the course of the disease. Therefore, improvement in endothelial function is of essential importance in the prevention of ASCVD. Red yeast rice (RYR), a healthy traditional Chinese food, has a lipid modulation function and also plays a vital role in the improvement of endothelial reactivity and cardiovascular protection; thus, it is significant in the prevention and treatment of ASCVD. This article reviews the molecular mechanisms of RYR and its related products in the improvement of endothelial function in terms of endothelial reactivity, anti-apoptosis of endothelial progenitor cells, oxidative stress alleviation and anti-inflammation.
摘要：
Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide. Thyroid hormone receptor interactor 13 (TRIP13) has been reported to promote nonhomologous end joining (NHEJ). However, the role of TRIP13 in the molecular pathogenesis of HCC remains to be elucidated. The aim of the present study was to investigate the role and potential mechanism of TRIP13 in HCC. Real-time PCR and western blotting were used to detect the expression of TRIP13 in 47 paired HCC and adjacent liver tissues. The Cancer Genome Atlas (TCGA) database was used to collect TRIP13 expression data in HCC. Loss-of-function siRNA assays were performed to alter TRIP13 expression. Cell proliferation, migration and invasion capabilities were investigated using CCK-8, wound healing and Transwell assays, while cell cycle distribution and apoptosis were assessed using flow cytometry. The expression of TRIP13 was upregulated in HCC tissues and cell lines. We analyzed the association between TRIP13 expression and patient prognosis. Patients with higher TRIP13 expression had significantly shorter survival periods compared with patients with lower TRIP13 expression. CCK-8, wound healing and Transwell assays revealed that TRIP13 downregulation inhibited the proliferation, migration and invasion of HCC cells. TRIP13 downregulation resulted in increased apoptosis and cell cycle arrest at S-phase. Finally, we found that loss of TRIP13 reduced the expression of cellular NHEJ proteins such as KU70, KU80 and PRKDC, and these results suggest that loss of TRIP 13 impairs the NHEJ repair process in HCC cells. Collectively, these results provide evidence that TRIP13 may act as a tumor promoter during HCC development and could serve as a potential therapeutic target for this disease.
