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| 1 | 急性肾损伤诊断与分类专家共识显示文摘近几十来.临床和基础的研究工作者们针对急性肾功能衰竭(ARF)进行了广泛的研究,尽管我们在该疾病的生理和发病机制方面都取得了长足的进步,但如何将这些知识用于临床,改进ARF患者预后方面的工作却做得十分有限。ARF是由多种病因导致、可发生在各种临床情况之下(儿童或成人、门诊或住院、ICU或非ICU患者)的一种复杂的肾功能紊乱,其临床表现既可以是血肌酐水平的轻微升高,也可以是无尿性肾功能衰竭。 | RL Mehta JA Kellum S Shah B Molitoris C Ronco D Warnock A Levin 王欣 | 2006 | 中华肾脏病杂志2006，22，11： | 348 |
| 2 | Iron and liver fibrosis: Mechanistic and clinical aspects显示文摘Liver fibrosis is characterised by excessive deposition of extracellular matrix that interrupts normal liver functionality. It is a pathological stage in several untreated chronic liver diseases such as the iron overload syndrome hereditary haemochromatosis, viral hepatitis, alcoholic liver disease, non-alcoholic fatty liver disease, non-alcoholic steatohepatitis and diabetes. Interestingly, regardless of the aetiology, iron-loading is frequently observed in chronic liver diseases. Excess iron can feed the Fenton reaction to generate unquenchable amounts of free radicals that cause grave cellular and tissue damage and thereby contribute to fibrosis. Moreover, excess iron can induce fibrosis-promoting signals in the parenchymal and non-parenchymal cells, which accelerate disease progression and exacerbate liver pathology. Fibrosis regression is achievable following treatment, but if untreated or unsuccessful, it can progress to the irreversible cirrhotic stage leading to organ failure and hepatocellular carcinoma, where resection or transplantation remain the only curative options. Therefore,understanding the role of iron in liver fibrosis is extremely essential as it can help in formulating iron-related diagnostic, prognostic and treatment strategies. These can be implemented in isolation or in combination with the current approaches to prepone detection, and halt or decelerate fibrosis progression before it reaches the irreparable stage. Thus, this review narrates the role of iron in liver fibrosis. It examines the underlying mechanisms by which excess iron can facilitate fibrotic responses. It describes the role of iron in various clinical pathologies and lastly,highlights the significance and potential of iron-related proteins in the diagnosis and therapeutics of liver fibrosis. | Kosha J Mehta Sebastien Je Farnaud Paul A Sharp | 2019 | World Journal of Gastroenterology2019，25，5： | 39 |
| 3 | Acute Kidney Injury:Global Health Alert显示文摘Acute kidney injury(AKI) is increasingly prevalent in developing and developed countries and is associated with severe morbidity and mortality.Most etiologies of AKI can be prevented by interventions at the individual,community,regional and in-hospital levels.Effective measures must include community-wide efforts to increase an awareness of the devastating effects of AKI and provide guidance on preventive strategies,as well as early recognition and management.Efforts should be focused on minimizing causes of AKI,increasing awareness of the importance of serial measurements of serum creatinine in high risk patients,and documenting urine volume in acutely ill people to achieve early diagnosis;there is as yet no definitive role for alternative biomarkers.Protocols need to be developed to systematically manage prerenal conditions and specific infections.More accurate data about the true incidence and clinical impact of AKI will help to raise the importance of the disease in the community,increase awareness of AKI by governments,the public,general and family physicians and other health care professionals to help prevent the disease.Prevention is the key to avoid the heavy burden of mortality and morbidity associated with AKI. | Philip Kam Tao Li Emmanuel A Burdmann Ravindra L Mehta | 2013 | 肾脏病与透析肾移植杂志2013，22，1： | 14 |
| 4 | Autophagy inhibition by chloroquine sensitizes HT-29 colorectal cancer cells to concurrent chemoradiation显示文摘AIM:To investigate whether the inhibition of autophagy by chloroquine(CQ)sensitizes rectal tumors to radiation therapy(RT)or concurrent chemoradiation(chemoRT).METHODS:In vitro,HCT-116 and HT-29 colorectal cancer(CRC)cell lines were treated as following:(1)PBS;(2)CQ;(3)5-fluorouracil(5-FU);(4)RT;(5)CQ and RT;(6)5-FU and RT;(7)CQ and 5-FU;and(8)5-FU and CQ and RT.Each group was then exposed to various doses of radiation(0-8 Gy)depending on the experiment.Cell viability and proliferative capacity were measured by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)and clonogenic assays.Clonogenic survivalcurves were constructed and compared across treatment groups.Autophagy status was determined by assessing the LC3-Ⅱto LC3-Ⅰratio on western blot analysis,autophagosome formation on electron microscopy and identification of a perinuclear punctate pattern with GFPlabeled LC3 on fluorescence microscopy.Cell cycle arrest and cell death were evaluated by FACS and AnnexinⅤanalysis.All experiments were performed in triplicate and statistical analysis was performed by the student’s t test to compare means between treatment groups.RESULTS:RT(2-8 Gy)induced autophagy in HCT-116and HT-29 CRC cell lines at 4 and 6 h post-radiation,respectively,as measured by increasing LC3-Ⅱto LC3-Ⅰratio on western blot.Additionally,electron microscopy demonstrated autophagy induction in HT-29 cells24 h following irradiation at a dose of 8 Gy.Drug treatment with 5-FU(25μmol/L)induced autophagy and the combination of 5-FU and RT demonstrated synergism in autophagy induction.CQ(10μmol/L)alone and in combination with RT effectively inhibited autophagy and sensitized both HCT-116 and HT-29 cells to treatment with radiation(8 Gy;P<0.001 and 0.00001,respectively).Significant decrease in clonogenic survival was seen only in the HT-29 cell line,when CQ was combined with RT at doses of 2 and 8 Gy(P<0.5 and P=0.05,respectively).There were no differences in cell cycle progression or Annexin V staining upon CQ addition to RT.CONCLUSION:Autophagy inhibition by CQ increases CRC cell sensitivity to concurrent treatment with 5-FU and RT in vitro,suggesting that addition of CQ to chemoRT improves CRC treatment response. | Caitlin A Schonewolf Monal Mehta Devora Schiff Hao Wu Bruce G Haffty Vassiliki Karantza Salma K Jabbour | 2014 | World Journal of Gastrointestinal Oncology2014，6，3： | 12 |
| 5 | Magnetic anchor guidance for endoscopic submucosal dissection and other endoscopic procedures显示文摘Endoscopic submucosal dissection(ESD) is a wellestablished, minimally invasive treatment for superficial neoplasms of the gastrointestinal tract. The universal adoption of ESD has been limited by its slow learning curve, long procedure times, and high risk of complications. One technical challenge is the lack of a second hand that can provide traction, as in conventional surgery. Reliable tissue retraction that exposes the submucosal plane of dissection would allow for safer and more efficient dissection. Magnetic anchor guided endoscopic submucosal dissection(MAGESD) has potential benefits compared to other current traction methods. MAG-ESD offers dynamic tissue retraction independent of the endoscope mimicking a surgeon's 'second hand'. Two types of magnets can be used: electromagnets and permanent magnets. In this article we review the MAG-ESD technology, published work and studies of magnets in ESD. We also review the use of magnetic anchor guidance systems in natural orifice transluminal endoscopic surgery and the idea of magnetic non-contact retraction using surface ferromagentization. We discuss the current limitations, the future potential of MAG-ESD and the developments needed for adoption of this technology. | Mohamed Mortagy Neal Mehta Mansour A Parsi Seiichiro Abe Tyler Stevens John J Vargo Yutaka Saito Amit Bhatt | 2017 | World Journal of Gastroenterology2017，23，16： | 12 |
| 6 | 血管紧张素转换酶抑制剂和血管紧张素受体拮抗剂的使用与2019冠状病毒疾病检测阳性之间的关系显示文摘血管紧张素转换酶抑制剂(angiotensin-converting enzyme inhibitor,ACEI)和血管紧张素受体拮抗剂(angiotensin receptor blocker,ARB)在2019新型冠状病毒疾病(coronavirus disease 2019,COVID-19)全球大流行背景下的作用备受争议。此类药物是治疗一些慢性病的必须药物,有建议停止使用这些药物. | Mehta N KalraA Nowacki AS Anjewierden S Han Z Bhat p Rubio AEC Jacob M Procop GW Harrington S Milinovich A Svensson LG Jehi L Young JB Chung MK 周卫(译) 叶鹏(校) | 2020 | 中华高血压杂志2020，28，5： | 9 |
| 7 | Surgical considerations for ‘intrinsic' brainstem gliomas: proposal of a modification in classification显示文摘 | Mehta VS Chandra PS Singh PK Garg A Rath GK | 2009 | 中国神经肿瘤杂志2009，7，3： | 9 |
| 8 | RTOG 0211:a phase 1/2 study of radiation therapy with concurrent gefitinib for newly diagnosed glioblastoma patients显示文摘PURPOSE: To determine the safety and efficacy of gefitinib,an epidermal growth factor receptor(EGFR) tyrosine kinase inhibitor,in combination with radiation for newly diagnosed glioblastoma(GBM) patients.METHODS AND MATERIALS: Between March 21,2002,and May 3,2004,Radiation Therapy Oncology Group(RTOG) 0211 enrolled 31 and 147GBM patients in the phase 1 and 2 arms,respectively.Treatment consisted of daily oral gefinitnib started at the time of conventional cranial radiation therapy(RT) and continued post RT for 18 months or until progression.Tissue microarrays from 68 cases were analyzed for EGFR expression.RESULTS: The maximum tolerated dose(MTD) of gefitinib was determined to be 500 mg in patients on non-enzyme-inducing anticonvulsant drugs(non-EIAEDs).All patients in the phase 2 component were treated at a gefitinib dose of 500 mg;patients receiving EIADSs could be escalated to 750 mg.The most common side effects of gefitinib in combination with radiation were dermatologic and gastrointestinal.Median survival was 11.5 months for patients treated per protocol.There was no overall survival benefit for patients treated with gefitinib + RT when compared with a historical cohort of patients treated with RT alone,matched by RTOG recursive partitioning analysis(RPA) class distribution.Younger age was significantly associated with better outcome.Per protocol stratification,EGFR expression was not found to be of prognostic value for gefitinib + RT-treated patients.CONCLUSIONS: The addition of gefitinib to RT is well tolerated.Median survival of RTOG 0211 patients treated with RT with concurrent and adjuvant gefitinib was similar to that in a historical control cohort treated with radiation alone. | Chakravarti A Wang M Robins HI Lautenschlaeger T Curran WJ Brachman DG Schultz CJ Choucair A Dolled-Filhart M Christiansen J Gustavson M Molinaro A Mischel P Dicker AP Bredel M Mehta M | 2013 | 中国神经肿瘤杂志2013，11，1： | 8 |
| 9 | Importance of fatigue and its measurement in chronic liver disease显示文摘The mechanisms of fatigue in the group of people with non-alcoholic fatty liver disease and non-alcoholic steatohepatitis are protean. The liver is central in the pathogenesis of fatigue because it uniquely regulates much of the storage, release and production of substrate for energy generation. It is exquisitely sensitive to the feedback controlling the uptake and release of these energy generation substrates. Metabolic contributors to fatigue, beginning with the uptake of substrate from the gut, the passage through the portal system to hepatic storage and release of energy to target organs (muscle and brain) are central to understanding fatigue in patients with chronic liver disease. Inflammation either causing or resulting from chronic liver disease contributes to fatigue, although inflammation has not been demonstrated to be causal. It is this unique combination of factors, the nexus of metabolic abnormality and the inflammatory burden of non-alcoholic fatty liver disease and non-alcoholic steatohepatitis that creates pathways to different types of fatigue. Many use the terms central and peripheral fatigue. Central fatigue is characterized by a lack of self-motivation and can manifest both in physical and mental activities. Peripheral fatigue is classically manifested by neuromuscular dysfunction and muscle weakness. Therefore, the distinction is often seen as a difference between intention (central fatigue) versus ability (peripheral fatigue). New approaches to measuring fatigue include the use of objective measures as well as patient reported outcomes. These measures have improved the precision with which we are able to describe fatigue. The measures of fatigue severity and its impact on usual daily routines in this population have also been improved, and they are more generally accepted as reliable and sensitive. Several approaches to evaluating fatigue and developing endpoints for treatment have relied of biosignatures associated with fatigue. These have been used singly or in combination and include: physical performance measures, cognitive performance measures, mood/behavioral measures, brain imaging and serological measures. Treatment with non-pharmacological agents have been shown to be effective in symptom reduction, whereas pharmacological agents have not been shown effective. | Lynn H Gerber Ali A Weinstein Rohini Mehta Zobair M Younossi | 2019 | World Journal of Gastroenterology2019，25，28： | 7 |
| 10 | Expression of genes that control core fucosylation in hepatocellular carcinoma: Systematic review显示文摘BACKGROUND Changes in N-linked glycosylation have been observed in the circulation of individuals with hepatocellular carcinoma. In particular, an elevation in the level of core fucosylation has been observed. However, the mechanisms through which core fucose is increased are not well understood. We hypothesized that a review of the literature and related bioinformatic review regarding six genes known to be involved in the attachment of core fucosylation, the synthesis of the fucosylation substrate guanosine diphosphate(GDP)-fucose, or the transport of the substrate into the Golgi might offer mechanistic insight into the regulation of core fucose levels.AIM To survey the literature to capture the involvement of genes regulating core Nlinked fucosylation in hepatocellular carcinoma METHODS The PubMed biomedical literature database was searched for the association of hepatocellular carcinoma and each of the core fucose-related genes and their protein products. We also queried The Cancer Genome Atlas Liver hepatocellular carcinoma(LIHC) dataset for genetic, epigenetic and gene expression changes for the set of six genes using the tools at cBioportal.RESULTS A total of 27 citations involving one or more of the core fucosylation-related genes(FPGT, FUK, FUT8, GMDS, SLC35 C1, TSTA3) and hepatocellular carcinoma were identified. The same set of gene symbols was used to query the371 patients with liver cancer in the LIHC dataset to identify the frequency of m RNA over or under expression, as well as non-synonymous mutations, copy number variation and methylation level. Although all six genes trended to moresamples displaying over expression relative to under-expression, it was noted that a number of tumor samples had undergone amplification of the genes of the de novo synthesis pathway, GMDS(27 samples) and TSTA3(78 samples). In contrast, the other four genes had undergone amplification in 2 or fewer samples.CONCLUSION Amplification of genes involved in the de novo pathway for generation of GDPfucose, GMDS and TSTA3, likely contributes to the elevated core fucose observed in hepatocellular carcinoma. | Pamela A Norton Anand S Mehta | 2019 | World Journal of Gastroenterology2019，25，23： | 3 |
| 11 | KIinefeIter综合征的诊断:新型甲基化特异性实时定量PCR显示文摘本文研究目的为设计一种基于额外X染色体(X-ch)检测的分子检测方法用于Klinefelter综合征的诊断。从26名47,XXY男性,2名46,XY/47,XXY男性,22名46,XY男性和15名46,XX的女性的外周血标本中提取DNA,并进行脱氨基处理。甲基化特异性的定量多聚酶链反应(MS-qpPCR)以非甲基化和甲基化的X染色体非活化特异性转录基因(XIST-U和XIST-M)拷贝为模板。X染色体二倍体通过XIST基因甲基化状态来判定。46,XY/47,XXY男性的嵌合程度通过核型分析和原位荧光杂交(FISH)的结果比较来判定。数据分析应用Roche LightCycler software v.3.5.3,包括通过拟合点分析和溶解曲线分析决定交叉点(CPs)。所有对照组女性和Ks患者均检测到X染色体二倍体,而对照组男性只表达XIST-M。XIST-U和IXIST-M的交叉点范围分别是(29.5-32.5,SD0.8)和(29-31,SD0.6)。嵌合度的检测极限为1%。根据2名47,XXY/46,XY患者的XIST-U/)(IST-M比值分析,计算出的嵌合率(1.8%和17.8%)与FISH结果(2.3%和15%)相当。从DNA脱氨基到最终数据分析的间隔小于9小时。本文得出结论:MS-qpPCR是一种敏感、特异及快速的X染色体二体检测方法,可以用于KS的筛查和诊断,甚至在低嵌合水平的47,XXY/46,XY患者也适用。 | Akanksha Mehta Anna Mielnik Peter N Schlegel Darius A Paduch | 2014 | Asian Journal of Andrology2014，16，5： | 2 |
| 12 | Noncanonical autophagy: one small step for LC3, one giant leap for immunity显示文摘 | Payal Mehta Jill Henault Roland Kolbeck Miguel A Sanjuan | 2014 | Current Opinion in Immunology2014，，： | 2 |
| 13 | Asynchronous Interference Mitigation in Cooperative Base Station Systems显示文摘 | ZHANG Hong-yuan MEHTA N B MOLISCJ A F | 2008 | IEEE Transactions on Wireless Communications2008，7，1： | 1 |
| 14 | Adwords and Generalized Online Matching显示文摘 | Mehta A Saberi A Vazirani U | 2007 | Journal of the ACM2007，54，5： | 1 |
| 15 | Improved thermodynamic parameters for prediction of structure hydrate equilibria 显示文摘 | MEHTA A P SLOAN E D | 1996 | AICHE J1996，42，7： | 1 |
| 16 | Constrictive pericarditis显示文摘 | Mehta A Mehta M Jain AC | 1999 | Clin Cardiol1999，22，5： | 1 |
| 17 | Medullary thyroid cancer: early detection and novel treatments显示文摘 | Roman S Mehta P Sosa J A | 2009 | Curr Opin Oncol2009，21，1： | 1 |
| 18 | Identification of Posttrans lationally Modified 18-Kilodalton Protein from Rice as Eukaryotic Translation Initiation Factor 5A显示文摘 | Mehta A M Saftner R A Mehta R A | 1994 | Plant Physiol1994，106，4： | 1 |
| 19 | A staged treatment plan for the management of Type II and Type IIIA open ealeaneus fractures显示文摘 | Mehta S Mirza A J Dunbar RP | 2010 | J Orthop Tranma2010，24，3： | 1 |
| 20 | Excitotoxicity: bridge tovarious triggers in neurodegenerative disorders 显示文摘 | Mehta A Prabhakar M Kumar P | 2013 | Eur JPharmacol2013，698，13： | 1 |
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