|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Impacts of different methylprednisolone administration routes in patients with sudden hearing loss or Meniere’s disease显示文摘Background:Evidence suggests that glucocorticoids are important in the treatment of sudden hearing loss(SHL)and Meniere’s disease(MD).However,different glucocorticoid administration methods may have a significant impact on treatment outcomes.Objective:This study aimed to investigate effects of different glucocorticoid administration methods on sudden hearing loss and Meniere’s disease.Methods:In this study,glucocorticoids were administered orally in 18 patients,by retroauricular injection in 15 patients and by intratympanic injection in 15 patients.White blood cell(WBC)count,serum Kt,fasting plasma glucose(FPG),body temperature,heart rate and blood pressure were used to evaluate effects of glucocorticoids on patients with hearing loss.Visual analog scale(VAS)of pain and sleep disorders were also surveyed,and pure tone audiometry(PTA)results were compared among groups to evaluate efficacy of different glucocorticoids administration methods.Result:WBC count,heart rate and blood pressure were higher in patients taking oral glucocorticoids,while body temperature,serum Kt and FPG levels did not change in all three groups.However,patients who received intratympanic injection of glucocorticoids experienced more pain,while those taking oral glucocorticoids reported more sleep impairment.Treatment efficacy on hearing loss was not significantly different among the three groups.Conclusion:These findings suggest that systemic glucocorticoid administration can result in greater whole body responses than local administration,but with similar hearing treatment efficacy. | Dan Chen Zhipeng Li Qilin Zhou Yubin Chen Luoying Yang Jingqian Tan Xiangli Zeng Peng Li | 2020 | Journal of Otology2020，15，4： | 4 |
| 2 | Nuclear Envelope Protein MAN1 Regulates the Drosophila Circadian Clock via Period显示文摘Almost all organisms exhibit ~24-h rhythms, or circadian rhythms, in a plentitude of biological processes.These rhythms are driven by endogenous molecular clocks consisting of a series of transcriptional and translational feedback loops. Previously, we have shown that the inner nuclear membrane protein MAN1 regulates this clock and thus the locomotor rhythm in flies, but the mechanism remains unclear. Here, we further confirmed the previous findings and found that knocking down MAN1 in the pacemaker neurons of adult flies is sufficient to lengthen the period of the locomotor rhythm. Molecular analysis revealed that knocking down MAN1 led to reduced m RNA and protein levels of the core clock gene period(per),likely by reducing its transcription. Over-expressing per rescued the long period phenotype caused by MAN1 deficiency whereas per mutation had an epistatic effect on MAN1, indicating that MAN1 sets the pace of the clock by targeting per. | Bei Bu Weiwei He Li Song Luoying Zhang | 2019 | Neuroscience Bulletin2019，35，6： | 2 |
| 3 | Four new dibenzocyclooctadiene lignansfrom Schisandra rubriflora显示文摘 | LI H M LUOY M PU J X | 2008 | Helvetica Chimica Acta2008，91，： | 1 |
| 4 | Experimental investigation on heat transfer from a heated rod with a helically wrapped wire inside a square vertical channel to water atsupercritical pressures显示文摘 | Li H Wang H LuoY etal | 2009 | Nuclear Engineering and Design2009，239，10： | 1 |
| 5 | Low temperature fabrication of efficient porous carbon counter electrode for dye-sensitized solar cells显示文摘 | LI K LUOY H | 2009 | Electro- chemistry Communications2009，11，1： | 1 |
| 6 | Tau Accumulation and Defective Autophagy:A Common Pathological Mechanism Underlying Repeat-Expansion-Induced Neurodegenerative Diseases?显示文摘Repetitive DNA tracts(microsatellites)occur thousands of times throughout the human genome,and their expansion is known to cause many diseases.Expansion of CAG repeats encoding poly glutamine(polyQ)tracts is a pathological cause of nine neurodegenerative diseases:spinal and bulbar muscular atrophy,Huntington’s disease,dentatorubropallidoluysian atrophy,and six autosomal dominant forms of spinocerebellar ataxia(SCA1,2,3,6,7,and 17)[1]. | Li Song Luoying Zhang | 2020 | Neuroscience Bulletin2020，36，12： | 1 |
| 7 | Synthesis of 5-benzoylac-enaphthene in the presence of Lewis acidic ionic liq-uids 显示文摘 | Chen M Li D LuoY | 2011 | Journal of Industrial and Engineering Chem-istry (Amsterdam Netherlands)2011，17，1： | 1 |
| 8 | Binding sensitivity of adefovir to the polymerase from different genotypes of HBV: molecular modeling, docking and dynamics simulation studies显示文摘 | Jing LI Yun D1 Xian LIU Qian-cheng SHEN Ai-long HUANG Ming-yue ZHENG Xiao-min LUOI Hua-liang JIANG | 2013 | Acta Pharmacologica Sinica2013，34，2： | 1 |
| 9 | Structure and properties of poly (vinyl chloride)/halloysite nanotubes nanoeomposites 显示文摘 | LiuC LuoY F Jia Z X Li S Q Guo B C Jia D M | 2012 | Journal of Macromolecular Science PartB: Physics2012，51，5： | 1 |
| 10 | Wide dissemination of multidrug-resistant Shigella isolates in China显示文摘 | ZhangW LuoY Li J | 2011 | J Antimicrob Chemother2011，66，11： | 1 |
| 11 | Novel heterozygous USH1C mutation impacts hair cell mechanotransduction and causes progressive hearing loss显示文摘Hearing loss is one of the most common sensory disorders worldwide,affecting approximately 466 million people,including 34 million children[1].Genetic mutations accounts for approximately 60%of inherited hearing loss cases[2,3].These genetic changes result in a wide variety of clinical manifestations,ranging from nonsyndromic hearing loss(NSHL)to over 400 syndromes involving hearing loss and from mild adult-onset hearing loss to profound congenital deafness,covering the entire spectrum of Mendelian inheritance. | Yanyan Jia Gaogan Jia Luo Guo Nan Song Yu-Meng Wang Luoying Jiang Yilai Shu Yan Chen Shujia Zhu Huawei Li Wenyan Li | 2024 | Science Bulletin2024，69，2： | 0 |
| 12 | Functional characterization of novel NPRL3 mutations identified in three families with focal epilepsy显示文摘Focal epilepsy accounts for 60% of all forms of epilepsy, but the pathogenic mechanism is not well understood. In this study,three novel mutations in NPRL3(nitrogen permease regulator-like 3), c.937_945del, c.1514dup C and 6,706-bp genomic DNA(g DNA) deletion, were identified in three families with focal epilepsy by linkage analysis, whole exome sequencing(WES) and Sanger sequencing. NPRL3 protein is a component of the GATOR1 complex, a major inhibitor of m TOR signaling. These mutations led to truncation of the NPRL3 protein and hampered the binding between NPRL3 and DEPDC5, which is another component of the GATOR1 complex. Consequently, the mutant proteins enhanced m TOR signaling in cultured cells, possibly due to impaired inhibition of m TORC1 by GATOR1. Knockdown of nprl3 in Drosophila resulted in epilepsy-like behavior and abnormal synaptic development. Taken together, these findings expand the genotypic spectrum of NPRL3-associated focal epilepsy and provide further insight into how NPRL3 mutations lead to epilepsy. | Shiyue Du Sheng Zeng Li Song Hongying Ma Rui Chen Junyu Luo Xu Wang Tingbin Ma Xuan Xu Hao Sun Ping Yi Jifeng Guo Yaling Huang Mugen Liu Tao Wang Wei-Ping Liao Luoying Zhang Jing Yu Liu Beisha Tang | 2023 | Science China(Life Sciences)2023，66，9： | 0 |
| 13 | LncRNA KCNQ1OT1:Molecular mechanisms and pathogenic roles in human diseases显示文摘Long non-coding RNAs(lncRNAs)exhibit a length more than 200 nucleotides and they are characterized by non-coding RNAs(ncRNA)not encoded into proteins.Over the past few years,the role and development of lncRNAs have aroused the rising attention of researchers.To be specific,KCNQ1OT1,the KCNQ1 opposite strand/antisense transcript 1,is clearly classified as a regulatory ncRNA.KCNQ1OT1 is capable of interacting with miRNAs,RNAs and proteins,thereby affecting gene expression and various cell functions(e.g.,cell proliferation,migration,epithelialemesenchymal transition(EMT),apoptosis,viability,autophagy and inflammation).KCNQ1OT1 is dysregulated in a wide range of human diseases(e.g.,cardiovascular disease,cancer,diabetes,osteoarthritis,osteoporosis and cataract),and it is speculated to act as a therapeutic target for treating various human diseases.On the whole,this review aims to explore the biological functions,underlying mechanisms and pathogenic roles of KCNQ1OT1 in human diseases. | Fangqi Xia Yaqi Wang Mengzhen Xue Leiqi Zhu Dengke Jia Yue Shi Yan Gao Luoying Li Yuanyang Li Silong Chen Guangfu Xu Ding Yuan Chengfu Yuan | 2022 | Genes & Diseases2022，9，6： | 0 |
| 14 | Time-restricted feeding is an intervention against excessive dark-phase sleepiness induced by obesogenic diet显示文摘High-fat diet(HFD)-induced obesity is a growing epidemic and major health concern.While excessive daytime sleepiness(EDS)is a common symptom of HFD-induced obesity,preliminary findings suggest that reduced wakefulness could be improved with time-restricted feeding(TRF).At present,however,the underlying neural mechanisms remain largely unknown.The paraventricular thalamic nucleus(PVT)plays a role in maintaining wakefulness.We found that chronic HFD impaired the activity of PVT neurons.Notably,inactivation of the PVT was sufficient to reduce and fragment wakefulness during the active phase in lean mice,similar to the sleep-wake alterations observed in obese mice with HFD-induced obesity.On the other hand,enhancing PVT neuronal activity cons olidated wakefulness in mice with HFD-induced obesity.We observed that the fragmented wakefulness could be eliminated and reversed by TRF.Furthermore,TRF prevented the HFD-induced disruptions on synaptic transmission in the PVT,in a feeding duration-dependent manner.Collectively,our findings demonstrate that ad libitum access to a HFD results in inactivation of the PVT,which is critical to impaired nocturnal wakefulness and increased sleep,while TRF can prevent and reverse diet-induced PVT dysfunction and excessive sleepiness.We establish a link between TRF and neural activity,through which TRF can potentially serve as a lifestyle intervention against diet/obesity-related ED S. | Xu Wang Keke Xing Mengge He Ting He Xinkuan Xiang Tao Chen Luoying Zhang Haohong Li | 2023 | National Science Review2023，10，1： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员