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| 1 | Park7 interacts with p47phox to direct NADPH oxidase- dependent ROS production and protect against sepsis显示文摘 | Wenjun Liu Hailong Wu Lili Chen Yankai Wen Xiaoni Kong Wei-Qiang Gao | 2015 | Cell Research2015，25，6： | 5 |
| 2 | Association of assisted reproductive technology, germline de novo mutations and congenital heart defects in a prospective birth cohort study显示文摘Emerging evidence suggests that children conceived through assisted reproductive technology(ART)have a higher risk of congenital heart defects(CHDs)even when there is no family history.De novo mutation(DNM)is a well-known cause of sporadic congenital diseases;however,whether ART procedures increase the number of germline DNM(gDNM)has not yet been well studied.Here,we performed whole-genome sequencing of 1137 individuals from 160 families conceived through ART and 205 families conceived spontaneously.Children conceived via ART carried 4.59 more gDNMs than children conceived spontaneously,including 332 paternal and 1.26 maternal DNMs,after correcting for parental age at conception,cigarette smoking,alcohol drinking,and exercise behaviors.Paternal DNMs in offspring conceived via ART are characterized by C>T substitutions at CpG sites,which potentially affect protein-coding genes and are significantly associated with the increased risk of CHD.In addition,the accumulation of non-coding functional mutations was independently associated with CHD and 87.9% of the mutations were originated from the father.Among ART offspring,infertility of the father was associated with elevated paternal DNMs;usage of both recombinant and urinary follicle-stimulating hormone and high-dosage human chorionic gonadotropin trigger was associated with an increase of maternal DNMs.In sum,the increased gDNMs in offspring conceived by ART were primarily originated from fathers,indicating that ART itself may not be a major reason for the accumulation of gDNMs.Our findings emphasize the importance of evaluating the germline status of the fathers in families with the use of ART. | Cheng Wang Hong Lv Xiufeng Ling Hong Li Feiyang Diao Juncheng Dai Jiangbo Du Ting Chen Qi Xi Yang Zhao Kun Zhou Bo Xu Xiumei Han Xiaoyu Liu Meijuan Peng Congcong Chen Shiyao Tao Lei Huang Cong Liu Mingyang Wen Yangqian Jiang Tao Jiang Chuncheng Lu Wei Wu Di Wu Minjian Chen Yuan Lin Xuejiang Guo Ran Huo Jiayin Liu Hongxia Ma Guangfu Jin Yankai Xia Jiahao Sha Hongbing Shen Zhibin Hu | 2021 | Cell Research2021，31，8： | 2 |
| 3 | Freeway Slope Stability E- valuation Based on Multi -Level Fuzzy Neural Network 显示文摘 | Wu Yankai Sang Xiansong Niu Bin | 2012 | Advanced Materials Research2012，430，： | 1 |
| 4 | Vaccination with the repeat β-hCG C-terminal peptide carried by heat shock protein-65 (HSP65) for inducing antitumor effects显示文摘 | Jie Yang Yankai Zhang Huaqian Wang Zhenqiu Gao Zeyu Wang Bin Liu Xiuhua Zhang Mingzhu Du Xiao Huang Maolei Xu Jie Wu Taiming Li Jingjing Liu Rongyue Cao | 2012 | Tumor Biology2012，，： | 1 |
| 5 | Application of Advance Geologic Prediction to the Observational Construction of Rail- way Tunnels显示文摘 | LIAO YanKai DAI JianLing WU Zhi | | Modem Tunnelling Technology0，52，1： | 1 |
| 6 | Profiles of metabolic gene expression in the white adipose tissue, liver and hypothalamus in leptin knockout(Lep^(△I14/△I14)) rats显示文摘Leptin deficiency is principally linked to metabolic disorders. Leptin knockout(Lep^(△I14/△I14) Sprague Dawley rats created by CRISPR/Cas9 is a new model to study metabolic disorders. We used a whole rat genome oligonucleotide microarray to obtain tissue-specific gene expression profiles of the white adipose tissue, liver and hypothalamus in Lep^(△I14/△I14))and wild-type(WT) rats. We found 1,651 differentially expressed(enriched) genes in white adipose tissue,916 in the liver, and 306 in the hypothalamus in the Lep^(△I14/△I14) rats compared to WT. Gene ontology category and KEGG pathway analysis of the relationships among differentially expressed genes showed that these genes were represented in a variety of functional categories, including fatty acid metabolism, molecular transducers and cellular processes. The reliability of the data obtained from microarray was verified by quantitative real-time PCR on 14 representative genes. These data will contribute to a greater understanding of different metabolic disorders, such as obesity and diabetes. | Leijian Guan Kaixuan Xu Shuyang Xu Ningning Li Xinru Wang Yankai Xia Di Wu | 2017 | The Journal of Biomedical Research2017，31，6： | 1 |
| 7 | A nomogram predicting clinical pregnancy in the first fresh embryo transfer for women undergoing in vitro fertilization and intracytoplasmic sperm injection(IVF/ICSI) treatments显示文摘The extent to which factors affect the probability of clinical pregnancy in the first fresh embryo transfer after assisted conception is unknown.In order to examine the predictors of clinical pregnancy,a retrospective cohort study was launched between January 1,2013 and December 31,2016 in four infertility clinics including 19837 in vitro fertilization and intracytoplasmic sperm injection(IVF/ICSI)fresh cycles with known outcomes and relevant records.A multivariable logistic regression was used to select the most significant predictors in the final nomogram for predicting clinical pregnancy.Furthermore,the model was validated by an independent validation set and the performance of the model was evaluated by the receiver operating characteristic(ROC)curves along with the area under the ROC curve(AUC)and calibration plots.In a training set including 17854 participants,we identified that female age,tubal factor,number of embryos transferred,endometrial thickness and number of good-quality embryos were independent predictors for clinical pregnancy.We developed a nomogram using these five factors and the predictive ability was 0.66 for AUC(95%CI=0.64−0.68),which was independently validated in the validation set(AUC=0.66,95%CI=0.65−0.68).Our results show that some specific factors can be used to provide infertile couples with an accurate assessment of clinical pregnancy following assisted conception and facilitate to guide couples and clinicians. | Fang Wu Feng Liu Yichun Guan Jiangbo Du Jichun Tan Hong Lv Qun Lu Shiyao Tao Lei Huang Kun Zhou Yankai Xia Xinru Wang Hongbing Shen Xiufeng Ling Feiyang Diao Zhibin Hu Guangfu Jin | 2019 | The Journal of Biomedical Research2019，33，6： | 1 |
| 8 | Neuroprotection of a cocktail therapy involving anti-intercellular adhesion molecule 1 antibody and insulin-like growth factor 1 in treatment of cerebral ischemia/reperfusion injury in cats Nuclear magnetic resonance examination and pathological validatio显示文摘BACKGROUND: The pathophysiological mechanisms of ischemia are extremely complicated. It is difficult to confirm and maintain the therapeutic effects if only one neuroprotective agent is used. It is hypothesized that a cocktail therapy involving a combined application of neuroprotective agents is feasible and offers excellent therapeutic potential. OBJECTIVE: To evaluate the neuroprotective effects of a cocktail therapy of insulin-like growth factor 1 (IGF1) combined with anti-intercellular adhesion molecule 1 (ICAM1) antibody in the treatment of cerebral ischemia/reperfusion injury using medical imaging, pathology, and functional neurological deficit scoring techniques. DESIGN, TIME AND SETTING: This randomized, controlled, neuroimaging analysis of function and pathological observation was performed at the Laboratory of Molecular Imaging, Second Hospital, Hebei Medical University between September 2006 and December 2007. MATERIALS: Transient middle cerebral artery occlusion (MCAO) was induced in 24 healthy adult cats. Anti-ICAM1 antibody and IGF1 were sourced from the Shanghai Kangcheng Biological Product Co., Ltd., China. Stereotaxic apparatus was purchased from the Center for Medical Apparatus and Instruments, Shandong Liaocheng People’s Hospital, China. The in situ apoptosis kit was provided by the Beijing Zhongshan Biotechnique Co., Ltd., China. METHODS: Twenty-four cat models of MCAO were randomly divided into four groups (n = 6): control, IGF1, anti-ICAM1 antibody and cocktail therapy. Following a 2-hour ischemia and subsequent lateral cerebral ventricular puncture, 100 μg IGF1(cerebral ventricular), 100 μg anti-ICAM1 antibody (i.v.), 50 μg IGF1(lateral cerebral ventricular) + 50 μg anti-ICAM1 antibody (i.v.), and 100 μg physiological saline (i.v.) were administered to the IGF1, anti-ICAM1 antibody, cocktail therapy and control groups, respectively. On the following day, the same administration was performed again. MAIN OUTCOME MEASURES: Pathological observation of the cerebral dura mater tissue surrounding the MCAO target site was performed by electron microscopy. At days 3 and 7 following MCAO induction, the volume of the cerebral infarction was measured by Philips functional neurological deficit scoring and nuclear magnetic resonance imaging. RESULTS: Pathological observation revealed that the control group exhibited a great number of swollen neurons, glial cells and vascular endothelial cells, and showed severely injured mitochondria with an absence of the double membrane structure. The same phenomena were partially alleviated in the IGF1 and anti-ICAM1 antibody groups, and the most obvious alleviation of injuries was in the cocktail therapy group. At day 6 following MCAO establishment, the cocktail therapy group exhibited the smallest cerebral infarction volumes among the four groups (F = 71.322, P < 0.01). At days 3 and 7 following MCAO induction, the F value of Philips functional neurological deficit scoring was 10.398 and 14.430, respectively (P < 0.01); however, the best neurological functional recovery was in the cocktail therapy group. CONCLUSION: A cocktail therapy of IGF1 combined with anti-ICAM1 antibody produces better neuroprotective effects than IGF1 or anti-ICAM1 alone, as judged by injury to mitochondria and swelling in and around neurons and glial cells. | Huaijun Liu Liqun Yan Yaping Hou Shuochun Wu Dan He Linfang Li Yankai Wu BoyuanHuang Fei Yang | 2008 | Neural Regeneration Research2008，3，12： | 0 |
| 9 | A systematic review of the impacts of exposure to micro-and nano-plastics on human tissue accumulation and health显示文摘Micro-and nano-plastics(MNPs)pollution has become a pressing global environmental issue,with growing concerns regarding its impact on human health.However,evidence on the effects of MNPs on human health remains limited.This paper reviews the three routes of human exposure to MNPs,which include ingestion,inhalation,and dermal contact.It further discusses the potential routes of translocation of MNPs in human lungs,intestines,and skin,analyses the potential impact of MNPs on the homeostasis of human organ systems,and provides an outlook on future research priorities for MNPs in human health.There is growing evidence that MNPs are present in human tissues or fluids.Lab studies,including in vivo animal models and in vitro human-derived cell cultures,revealed that MNPs exposure could negatively affect human health.MNPs exposure could cause oxidative stress,cytotoxicity,disruption of internal barriers like the intestinal,the air–blood and the placental barrier,tissue damage,as well as immune homeostasis imbalance,endocrine disruption,and reproductive and developmental toxicity.Limitedly available epidemiological studies suggest that disorders like lung nodules,asthma,and blood thrombus might be caused or exacerbated by MNPs exposure.However,direct evidence for the effects of MNPs on human health is still scarce,and future research in this area is needed to provide quantitative support for assessing the risk of MNPs to human health. | Yudong Feng Chen Tu Ruijie Li Di Wu Jie Yang Yankai Xia Willie J.G.M.Peijnenburg Yongming Luo | 2023 | Eco-Environment & Health2023，2，4： | 0 |
| 10 | Metabolic modulation of acetaminophen-induced hepatotoxicity by osteopontin显示文摘Induction of osteopontin(OPN),a well-known pro-inflammatory molecule,has been observed in acetaminophen(APAP)-induced hepatotoxicity.However,the precise cell source for OPN induction and its role during APAP-induced hepatotoxicity has not been fully explored.By employing a hepatotoxic mouse model induced by APAP overdose,we demonstrate that both serum and hepatic OPN levels were significantly elevated in response to APAP treatment.Our in vivo and in vitro studies clearly indicated that the induced expression of hepatic OPN was mainly located in necrosis areas and produced by dying or dead hepatocytes.Functional experiments showed that OPN deficiency protected against the APAP-induced liver injury by inhibiting the toxic APAP metabolism via reducing the expression of the cytochrome P450 family 2 subfamily E member 1(CYP2E1).Interestingly,this inhibition of CYP2E1 expression did not occur in unfasted Opn−/−mice,but was significant in fasted Opn−/−mice and maintained for 2hours after APAP challenge in fasted Opn−/−mice.In addition,despite the early protective role of OPN deficiency on APAP-induced hepatotoxicity,OPN deficiency retarded injury resolution by sensitizing hepatocytes to apoptosis and impairing liver regeneration.Finally,we demonstrated that a siRNA-mediated transient hepatic Opn knockdown could sufficiently and significantly protect animals from APAP-induced hepatotoxicity and death.In conclusion,this study clearly defines the cell source of OPN induction in response to APAP treatment,provides a novel insight into the metabolic role of OPN to APAP overdose,and suggests an Opn-targeted therapeutic strategy for the treatment or prevention of APAP-induced hepatotoxicity. | Yankai Wen Chenchen Wang Jinyang Gu Chang Yu Kaixia Wang Xuehua Sun Yun Sun Hailong Wu Ying Tong Qiang Xia Xiaoni Kong | 2019 | Cellular & Molecular Immunology2019，16，5： | 0 |
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