[{"data":1,"prerenderedAt":-1},["ShallowReactive",2],{"_public_publisher_byId_2d57c82d-4443-4147-8cfa-da2ea3f8d991":3,"_public_publication_all{\"sortAscending\":false,\"sortField\":\"updateTime\",\"page\":0,\"size\":10,\"facet\":true,\"searchKey\":\"publisherId:2d57c82d-4443-4147-8cfa-da2ea3f8d991,\"}":81},{"code":4,"data":5,"meta":18},"SUCCESS",{"id":6,"createTime":7,"updateTime":8,"relativeEntities":9,"slug":10,"properties":11,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":20,"manageAffiliations":21,"indexDatabases":22,"url":38,"thumbnailPath":18,"statistic":39,"gsStatistic":18,"type":80,"analyzePriority":18},"2d57c82d-4443-4147-8cfa-da2ea3f8d991","2024-04-11T08:16:24.451+00:00","2025-11-21T10:00:10.749+00:00",[],"Clinical-Diabetes-and-Endocrinology",{"issn":12,"title":14},{"VOID":13},"2055-8260",{"EN":15},"Clinical Diabetes and Endocrinology","PUBLISHER","PENDING",null,0,[],[],[23],{"id":24,"indexDatabase":25,"url":35,"indexYears":36,"academicFieldIds":18,"indexDatabaseRanking":37},"8dfbd5a8-4800-4666-9cea-7e900e587fe7",{"id":26,"createTime":18,"updateTime":18,"relativeEntities":27,"label":28,"description":30,"key":32,"publicationTags":33,"standard":18},"3c7051d4-eb7d-4c57-a56b-36fc74c5d1e9",[],{"EN":29,"VI":29},"Scopus - Elsevier",{"EN":29,"VI":31},"Cơ sở dữ liệu Scopus thuộc Elsevier","scopus",[34],"SCOPUS","https:\u002F\u002Fwww.scopus.com\u002Fsourceid\u002F21100854011","","SCOPUS__Q3","https:\u002F\u002Flink.springer.com\u002Fjournal\u002F40842",{"impactFactor":19,"impactFactorByYear":40,"i10Index":49,"i10IndexLast5Year":50,"totalPublication":51,"totalPublicationByYear":52,"totalCitation":61,"totalCitationByYear":62,"totalCitationPerPublication":71,"totalCitationPerPublicationByYear":72,"hindexLast5Year":49,"hindex":49},{"2016":41,"2017":42,"2018":43,"2019":44,"2020":45,"2021":46,"2022":47,"2023":48},0.15,0.08,0.55,0.44,0.69,1.03,0.65,0.22,10,6,124,{"2015":53,"2016":54,"2017":54,"2018":55,"2019":49,"2020":56,"2021":57,"2022":58,"2023":59,"2024":60},13,11,16,19,18,9,5,7,259,{"2015":63,"2016":64,"2017":65,"2018":66,"2019":67,"2020":68,"2021":69,"2022":70},25,34,37,23,81,47,8,3,2.09,{"2015":73,"2016":74,"2017":75,"2018":76,"2019":77,"2020":78,"2021":44,"2022":79},1.92,3.09,3.36,1.44,8.1,2.47,0.33,"JOURNAL",{"meta":82,"data":84},{"total":83},"124",[85,385,534,624,775,830,1103,1367,1485,1736],{"id":86,"createTime":87,"updateTime":88,"relativeEntities":89,"slug":90,"properties":91,"entityType":103,"verifyStatus":104,"verifyTime":105,"verifyNote":106,"languages":107,"translateLanguages":109,"viewCount":19,"primaryUrl":111,"fullTextUrl":18,"authors":112,"publicationType":222,"publisherRelationship":223,"citationCount":19,"citationInfo":248,"publishDate":18,"publishYear":18,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":250,"openAccess":18,"references":251,"isForceReanalyzing":384},"9029290b-9163-4f7d-a96a-9122f7087bd2","2024-04-21T03:25:57.656+00:00","2026-09-05T09:21:39.437+00:00",[],"Comparison-of-therapeutic-effects-of-N-Acetylcysteine-with-pregabalin-in-improving-the-clinical-symptoms-of-painful-diabetic-neuropathy-a-randomized-double-blind-clinical-trial",{"openalex":92,"abstract":94,"title":96,"pm":99,"doi":101},{"VOID":93},"W4394951531",{"EN":95},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\n                \u003Cjats:title>Objectives\u003C\u002Fjats:title>\n                \u003Cjats:p>Painful diabetic neuropathy (PDN) is highly prevalent and annoyingly in patients with diabetes. The aim of this study was to investigate the effects of oral N-acetylcysteine (NAC) compared to pregabalin in PDN.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Methods\u003C\u002Fjats:title>\n                \u003Cjats:p>One hundred two eligible patients with type 2 diabetes and PDN were randomly recievied pregabalin (150 mg\u002Fday) or N-Acetylcysteine (NAC) (600 mg\u002F twice a day) for 8 weeks. Mean pain score, Sleep interference score (SIS), Patient Global Impression of Change (PGIC), Clinical Global Impression of Change (CGIC), and also, serum levels of total antioxidant capacity (TAC), total thiol groups (TTG), catalase activity (CAT), nitric oxide (NO), and malondialdehyde (MDA) were assessed at baseline and at the end of the study.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>NAC was well tolerated in all patients. The decrease in mean pain scores and increase in SIS was similar between two groups. More improvement in PGIC and CGIC from the baseline was reported in NAC group. NAC, significantly, decreased serum levels of MDA, and NO, but increased TAC, TTG, and CAT. Pregabalin, significantly, decreased serum levels of MDA, and NO and increased TAC.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Discussion\u003C\u002Fjats:title>\n                \u003Cjats:p>NAC is efficacious in alleviate symptoms of PDN which is probably related to its antioxidant effects.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Trial registration\u003C\u002Fjats:title>\n                \u003Cjats:p>The research protocol received approval from the Ethics Committee of Hamadan University of Medical Sciences (IR.UMSHA.REC.1397.137). The trial registry URL and number in Iranian Registry of Clinical Trials (IRCT): \u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" ext-link-type=\"uri\" xlink:href=\"https:\u002F\u002Fwww.irct.ir\u002Ftrial\u002F33313\">https:\u002F\u002Fwww.irct.ir\u002Ftrial\u002F33313\u003C\u002Fjats:ext-link>, IRCT20180814040795N2 (Registration date: 2019-01-21, Retrospectively registered)\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":97,"VI":98},"Comparison of therapeutic effects of N-Acetylcysteine with pregabalin in improving the clinical symptoms of painful diabetic neuropathy: a randomized, double-blind clinical trial","So sánh hiệu quả điều trị của N-acetylcysteine với pregabalin trong cải thiện các triệu chứng lâm sàng của bệnh thần kinh đái tháo đường gây đau: một thử nghiệm lâm sàng ngẫu nhiên, mù đôi",{"VOID":100},"38641841",{"VOID":102},"10.1186\u002Fs40842-024-00172-x","PUBLICATION","VERIFIED","2025-02-07T06:23:38.578+00:00","Auto 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A decade of diabetes research and development. Int J Diabetes Metab. 2000;8:88–92.",{"doi":255},"10.1159\u002F000497526",{"id":18,"text":257,"url":18,"identifiers":258},"Tandan R, Lewis GA, Krusinski PB, Badger GB, Fries TJ. Topical capsaicin in painful diabetic neuropathy: controlled study with long-term follow-up. Diabetes Care. 1992;15(1):8–14.",{"doi":259},"10.2337\u002Fdiacare.15.1.8",{"id":18,"text":261,"url":18,"identifiers":262},"Beck-Nielsen H, Groop LC. Metabolic and genetic characterization of prediabetic states. Sequence of events leading to non-insulin-dependent diabetes mellitus. J Clin Investig. 1994;94(5):1714-21.",{"doi":263},"10.1172\u002FJCI117518",{"id":18,"text":265,"url":18,"identifiers":266},"Fowler MJ. Microvascular and macrovascular complications of diabetes. Clin Diabetes. 2008;26(2):77–82.",{"doi":267},"10.2337\u002Fdiaclin.26.2.77",{"id":18,"text":269,"url":18,"identifiers":270},"Kahn CR. Insulin action, diabetogenes, and the cause of type II diabetes. Diabetes. 1994;43(8):1066–85.",{"doi":271},"10.2337\u002Fdiab.43.8.1066",{"id":18,"text":273,"url":18,"identifiers":274},"Naik AK, Tandan SK, Dudhgaonkar SP, Jadhav SH, Kataria M, Prakash VR, Kumar D. Role of oxidative stress in pathophysiology of peripheral neuropathy and modulation by N-acetyl-L-cysteine in rats. Eur J Pain. 2006;10(7):573–9.",{"doi":275},"10.1016\u002Fj.ejpain.2005.08.006",{"id":18,"text":277,"url":18,"identifiers":278},"Max M, Culnane M, Schafer S, Gracely R, Walther D, Smoller B, Dubner R. Amitriptyline relieves diabetic neuropathy pain in patients with normal or depressed mood. Neurology. 1987;37(4):589.",{"doi":279},"10.1212\u002FWNL.37.4.589",{"id":18,"text":281,"url":18,"identifiers":282},"Hicks J, Muller M, Panteghini M, Garry J. Consensus statement on the worldwide standardization of the hemoglobin A1C measurement: the American Diabetes Association, European Association for the Study of Diabetes, International Federation of Clinical Chemistry and Laboratory Medicine, and the International Diabetes Federation. Diabetes Care. 2007;30(9):2399.",{"doi":283},"10.2337\u002Fdc07-9925",{"id":18,"text":285,"url":18,"identifiers":286},"Group CS. Effect of treatment with capsaicin on daily activities of patients with painful diabetic neuropathy. Diabetes Care. 1992;15(2):159–65.",{"doi":287},"10.2337\u002Fdiacare.15.2.159",{"id":18,"text":289,"url":18,"identifiers":290},"Hosseini A, Abdollahi M. Diabetic neuropathy and oxidative stress: therapeutic perspectives. Oxid Med Cellular Longev. 2013;2013:168039. https:\u002F\u002Fdoi.org\u002F10.1155\u002F2013\u002F168039, https:\u002F\u002Fwww.hindawi.com\u002Fjournals\u002Fomcl\u002F2013\u002F168039\u002F.",{"doi":291},"10.1155\u002F2013\u002F168039",{"id":18,"text":293,"url":18,"identifiers":294},"Gonçalves NP, Vægter CB, Andersen H, Østergaard L, Calcutt NA, Jensen TS. Schwann cell interactions with axons and microvessels in diabetic neuropathy. Nat Rev Neurol. 2017;13(3):135–47.",{"doi":295},"10.1038\u002Fnrneurol.2016.201",{"id":18,"text":297,"url":18,"identifiers":298},"Sloan G, Shillo P, Selvarajah D, Wu J, Wilkinson ID, Tracey I, et al. A new look at painful diabetic neuropathy. Diabetes Res Clin Pract. 2018;144:177–91.",{"doi":299},"10.1016\u002Fj.diabres.2018.08.020",{"id":18,"text":301,"url":18,"identifiers":302},"Notartomaso S, Scarselli P, Mascio G, Liberatore F, Mazzon E, Mammana S, et al. N-Acetylcysteine causes analgesia in a mouse model of painful diabetic neuropathy. Mol Pain. 2020;16:1744806920904292.",{"doi":303},"10.1177\u002F1744806920904292",{"id":18,"text":305,"url":18,"identifiers":306},"Yüksel M, Bektaş H. Current Approaches in the Administration of Chronic Complications Related to Diabetes (Diyabete Bağlı Kronik Komplikasyonların Yönetiminde Güncel Yaklaşımlar). Turkiye Klinikleri J Nurs Sci. 2020;12(1):133–57. https:\u002F\u002Fdoi.org\u002F10.5336\u002Fnurses.2019-70201 , https:\u002F\u002Fwww.researchgate.net\u002Fprofile\u002FHicran-Bektas\u002Fpublication\u002F339897456_Current_Approaches_in_the_Administration_of_Chronic_Complications_Related_to_Diabetes\u002Flinks\u002F633fdc96ff870c55ce09f4a0\u002FCurrent-Approaches-in-the-Administration-of-Chronic-Complications-Related-to-Diabetes.pdf.",{"doi":307},"10.5336\u002Fnurses.2019-70201",{"id":18,"text":309,"url":18,"identifiers":310},"Rosenstock J, Tuchman M, LaMoreaux L, Sharma U. Pregabalin for the treatment of painful diabetic peripheral neuropathy: a double-blind, placebo-controlled trial. Pain. 2004;110(3):628–38.",{"doi":311},"10.1016\u002Fj.pain.2004.05.001",{"id":18,"text":313,"url":18,"identifiers":314},"Vinik AI, Nevoret M-L, Casellini C, Parson H. Diabetic neuropathy. Endocrinol Metab Clin. 2013;42(4):747–87.",{"doi":315},"10.1016\u002Fj.ecl.2013.06.001",{"id":18,"text":317,"url":18,"identifiers":318},"Lesser H, Sharma U, LaMoreaux L, Poole R. Pregabalin relieves symptoms of painful diabetic neuropathy: a randomized controlled trial. Neurology. 2004;63(11):2104–10.",{"doi":319},"10.1212\u002F01.WNL.0000145767.36287.A1",{"id":18,"text":321,"url":18,"identifiers":322},"Salas-Salvadó J, Martinez-Gonzalez M, Bullo M, Ros E. The role of diet in the prevention of type 2 diabetes. Nutr Metab Cardiovasc Dis. 2011;21:B32–48.",{"doi":323},"10.1016\u002Fj.numecd.2011.03.009",{"id":18,"text":325,"url":18,"identifiers":326},"Pitocco D, Tesauro M, Alessandro R, Ghirlanda G, Cardillo C. Oxidative stress in diabetes: implications for vascular and other complications. Int J Mol Sci. 2013;14(11):21525–50.",{"doi":327},"10.3390\u002Fijms141121525",{"id":18,"text":329,"url":18,"identifiers":330},"Vincent AM, Russell JW, Low P, Feldman EL. Oxidative stress in the pathogenesis of diabetic neuropathy. Endocr Rev. 2004;25(4):612–28.",{"doi":331},"10.1210\u002Fer.2003-0019",{"id":18,"text":333,"url":18,"identifiers":334},"Dodd S, Dean O, Copolov DL, Malhi GS, Berk M. N-acetylcysteine for antioxidant therapy: pharmacology and clinical utility. Exp Opin Biol Ther. 2008;8(12):1955–62.",{"doi":335},"10.1517\u002F14728220802517901",{"id":18,"text":337,"url":18,"identifiers":338},"Pieper GM, Siebeneich W. Oral administration of the antioxidant, N-acetylcysteine, abrogates diabetes-induced endothelial dysfunction. J Cardiovasc Pharmacol. 1998;32(1):101–5.",{"doi":339},"10.1097\u002F00005344-199807000-00016",{"id":18,"text":341,"url":18,"identifiers":342},"Kamboj SS, Chopra K, Sandhir R. Neuroprotective effect of N-acetylcysteine in the development of diabetic encephalopathy in streptozotocin-induced diabetes. Metab Brain Dis. 2008;23(4):427.",{"doi":343},"10.1007\u002Fs11011-008-9104-7",{"id":18,"text":345,"url":18,"identifiers":346},"Heidari N, Sajedi F, Mohammadi Y, Mirjalili M, Mehrpooya M. Ameliorative Effects Of N-Acetylcysteine As Adjunct Therapy On Symptoms Of Painful Diabetic Neuropathy. J Pain Res. 2019;12:3147.",{"doi":347},"10.2147\u002FJPR.S228255",{"id":18,"text":349,"url":18,"identifiers":350},"Fishbane S. N-acetylcysteine in the prevention of contrast-induced nephropathy. Clin J Am Soc Nephrol. 2008;3(1):281–7.",{"doi":351},"10.2215\u002FCJN.02590607",{"id":18,"text":353,"url":18,"identifiers":354},"Horst A, Kolberg C, Moraes MS, Riffel APK, Finamor IA, Belló-Klein A, et al. Effect of N-acetylcysteine on the spinal-cord glutathione system and nitric-oxide metabolites in rats with neuropathic pain. Neurosci Lett. 2014;569:163–8.",{"doi":355},"10.1016\u002Fj.neulet.2014.03.063",{"id":18,"text":357,"url":18,"identifiers":358},"Dyck PJ, Litchy WJ, Lehman K, Hokanson J, Low P, O’Brien P. Variables influencing neuropathic endpoints: the Rochester diabetic neuropathy study of healthy subjects. Neurology. 1995;45(6):1115–21.",{"doi":359},"10.1212\u002FWNL.45.6.1115",{"id":18,"text":361,"url":18,"identifiers":362},"Hallynck T, Soep HH, Thomis J, Boelaert J, Daneels R, Fillastre JP, et al. Prediction of creatinine clearance from serum creatinine concentration based on lean body mass. Clin Pharmacol Ther. 1981;30(3):414–21.",{"doi":363},"10.1038\u002Fclpt.1981.181",{"id":18,"text":365,"url":18,"identifiers":366},"Sałat K, Gdula-Argasińska J, Malikowska N, Podkowa A, Lipkowska A, Librowski T. Effect of pregabalin on contextual memory deficits and inflammatory state-related protein expression in streptozotocin-induced diabetic mice. Naunyn-Schmiedeberg’s Arch Pharmacol. 2016;389(6):613–23.",{"doi":367},"10.1007\u002Fs00210-016-1230-x",{"id":18,"text":369,"url":18,"identifiers":370},"Aşcı S, Demirci S, Aşcı H, Doğuç DK, Onaran İ. Neuroprotective effects of pregabalin on cerebral ischemia and reperfusion. Balkan Med J. 2016;33(2):221.",{"doi":371},"10.5152\u002Fbalkanmedj.2015.15742",{"id":18,"text":373,"url":18,"identifiers":374},"Ezeriņa D, Takano Y, Hanaoka K, Urano Y, Dick TP. N-acetyl cysteine functions as a fast-acting antioxidant by triggering intracellular H2S and sulfane sulfur production. Cell Chem Biol. 2018;25(4):447-59. e4.",{"doi":375},"10.1016\u002Fj.chembiol.2018.01.011",{"id":18,"text":377,"url":18,"identifiers":378},"Li J, Xu L, Deng X, Jiang C, Pan C, Chen L, et al. N-acetyl-cysteine attenuates neuropathic pain by suppressing matrix metalloproteinases. Pain. 2016;157(8):1711–23.",{"doi":379},"10.1097\u002Fj.pain.0000000000000575",{"id":18,"text":381,"url":18,"identifiers":382},"Aldini G, Altomare A, Baron G, Vistoli G, Carini M, Borsani L, Sergio F. N-Acetylcysteine as an antioxidant and disulphide breaking agent: the reasons why. Free Radic Res. 2018;52(7):751–62.",{"doi":383},"10.1080\u002F10715762.2018.1468564",false,{"id":386,"createTime":387,"updateTime":388,"relativeEntities":389,"slug":390,"properties":391,"entityType":103,"verifyStatus":104,"verifyTime":388,"verifyNote":106,"languages":402,"translateLanguages":18,"viewCount":19,"primaryUrl":403,"fullTextUrl":18,"authors":404,"publicationType":222,"publisherRelationship":424,"citationCount":19,"citationInfo":447,"publishDate":18,"publishYear":18,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":449,"openAccess":18,"references":450,"isForceReanalyzing":384},"6a228f1e-7edb-44b9-b55b-af149d549a7a","2024-04-21T03:11:33.553+00:00","2025-02-27T03:05:27.019+00:00",[],"Sodium-bicarbonate-and-intubation-in-severe-diabetic-ketoacidosis-are-we-too-quick-to-dismiss-them-",{"openalex":392,"abstract":394,"title":396,"pm":398,"doi":400},{"VOID":393},"W4394795727",{"EN":395},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>Management of diabetic ketoacidosis (DKA) has internationally established guidelines. However, management of severe, refractory DKA with multiple contributors to acidosis, and management of DKA in patients with altered mentation, remain ambiguous. Use of sodium bicarbonate and intubation in DKA are unpopular treatment practices, but warrant consideration in these unique clinical scenarios. This paper describes a 61-year-old Sri Lankan female who presented with severe DKA, seizures and altered level of consciousness. In her case, the acidosis was secondary to DKA, hyperlactatemia, hyperchloraemic acidosis and acute kidney injury (AKI). Intravenous sodium bicarbonate was used in the management of acidosis. She was intubated due to altered level of consciousness with inadequate respiratory drive to compensate for metabolic acidosis. The outcome in her case was favorable. Intravenous sodium bicarbonate in DKA should be considered for patients with severe, refractory acidosis with hemodynamic instability, hyperkalemia and compounding acidosis due to normal anion gap acidosis or AKI. Intubation should be considered for patients with obtunded mentation unable to achieve respiratory compensation and obtunded mentation where reversal of DKA is unlikely to improve consciousness. Both strategies should be personalized with consideration of individual risk vs benefit.\u003C\u002Fjats:p>",{"EN":397},"Sodium bicarbonate and intubation in severe diabetic ketoacidosis: are we too quick to dismiss them?",{"VOID":399},"38616273",{"VOID":401},"10.1186\u002Fs40842-024-00171-y",[108],"https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-024-00171-y",[405],{"id":406,"sortIndex":19,"researcher":18,"roles":407,"affiliations":408,"properties":417,"displayName":421,"givenName":18,"familyName":18},"fc5cb39f-90b4-431c-9918-d1be875eaef5",[],[409],{"id":410,"sortIndex":19,"affiliation":411,"properties":18},"785bdc81-b2f1-453b-92a2-6079b06acf3e",{"id":410,"createTime":18,"updateTime":18,"relativeEntities":412,"slug":18,"properties":413,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":416,"statistic":18},[],{"title":414},{"VI":415},"Professorial Medical Unit, National Hospital of Sri Lanka, Colombo, Sri Lanka",[],{"orcid":418,"title":420,"openalex":422},{"VOID":419},"https:\u002F\u002Forcid.org\u002F0000-0002-0725-1238",{"EN":421},"Manudi Vidanapathirana",{"VOID":423},"A5034383812",{"url":18,"publisher":425,"properties":444},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":426,"slug":10,"properties":427,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":430,"manageAffiliations":431,"indexDatabases":432,"url":38,"thumbnailPath":18,"statistic":439,"gsStatistic":18,"type":80,"analyzePriority":18},[],{"issn":428,"title":429},{"VOID":13},{"EN":15},[],[],[433],{"id":24,"indexDatabase":434,"url":35,"indexYears":36,"academicFieldIds":18,"indexDatabaseRanking":37},{"id":26,"createTime":18,"updateTime":18,"relativeEntities":435,"label":436,"description":437,"key":32,"publicationTags":438,"standard":18},[],{"EN":29,"VI":29},{"EN":29,"VI":31},[34],{"impactFactor":19,"impactFactorByYear":440,"i10Index":49,"i10IndexLast5Year":50,"totalPublication":51,"totalPublicationByYear":441,"totalCitation":61,"totalCitationByYear":442,"totalCitationPerPublication":71,"totalCitationPerPublicationByYear":443,"hindexLast5Year":49,"hindex":49},{"2016":41,"2017":42,"2018":43,"2019":44,"2020":45,"2021":46,"2022":47,"2023":48},{"2015":53,"2016":54,"2017":54,"2018":55,"2019":49,"2020":56,"2021":57,"2022":58,"2023":59,"2024":60},{"2015":63,"2016":64,"2017":65,"2018":66,"2019":67,"2020":68,"2021":69,"2022":70},{"2015":73,"2016":74,"2017":75,"2018":76,"2019":77,"2020":78,"2021":44,"2022":79},{"issue":445,"volume":446},{"VOID":245},{"VOID":247},{"total":19,"publishYear":18,"statisticByYear":448},{},[],[451,455,459,462,466,469,473,477,481,485,489,493,497,500,504,508,512,516,520,523,526,530],{"id":18,"text":452,"url":18,"identifiers":453},"Dhatariya KK, Vellanki P. Treatment of Diabetic Ketoacidosis (DKA)\u002FHyperglycemic Hyperosmolar State (HHS): Novel Advances in the Management of Hyperglycemic Crises (UK Versus USA). Curr Diab Rep. 2017;17(5):33. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs11892-017-0857-4.PMID:28364357;PMCID:PMC5375966.",{"doi":454},"10.1007\u002Fs11892-017-0857-4.PMID:28364357;PMCID:PMC5375966",{"id":18,"text":456,"url":18,"identifiers":457},"Savage MW, Dhatariya KK, Kilvert A, Rayman G, Rees JA, Courtney CH, Hilton L, Dyer PH, Hamersley MS. for the Joint British Diabetes Societies Joint British Diabetes Societies guideline for the management of diabetic ketoacidosis. Diabetic Med. 2011;28:508–15. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fj.1464-5491.2011.03246.x.",{"doi":458},"10.1111\u002Fj.1464-5491.2011.03246.x",{"id":18,"text":460,"url":18,"identifiers":461},"Directorate of Non-Communicable Diseases, Ministry of Health Sri Lanka. National Guideline for Management of Diabetes for Secondary and Tertiary Healthcare Level 2021. https:\u002F\u002Fwww.ncd.health.gov.lk\u002Fimages\u002Fpdf\u002Fcirculars\u002Ffinal_dm_DM_for_secondary_and_tertiary__health_care_providers_feb3rd.pdf. Accessed 21 May 2023.",{},{"id":18,"text":463,"url":18,"identifiers":464},"Gabriel Wardi, Sarah Holgren, Arnav Gupta, Julia Sobel, Aaron Birch, Alex Pearce, Atul Malhotra, Christopher Tainter. A REVIEW OF BICARBONATE USE IN COMMON CLINICAL SCENARIOS. The Journal of Emergency Medicine,2023. ISSN 0736–4679. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.jemermed.2023.04.012.https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fbooks\u002FNBK560723\u002F.",{"doi":465},"10.1016\u002Fj.jemermed.2023.04.012.",{"id":18,"text":467,"url":18,"identifiers":468},"Diabetic ketoacidosis: management. BMJ Best Practice. https:\u002F\u002Fbestpractice.bmj.com\u002Ftopics\u002Fen-us\u002F162\u002Fmanagement-approach. Accessed 21 May 2023.",{},{"id":18,"text":470,"url":18,"identifiers":471},"Jaber S, et al. Sodium bicarbonate therapy for patients with severe metabolic acidaemia in the intensive care unit (BICAR-ICU): a multicenter, open-label, randomized controlled, phase 3 trial. The Lancet. 2018;V392(i10141):P31-40. https:\u002F\u002Fdoi.org\u002F10.1016\u002FS0140-6736(18)31080-8.",{"doi":472},"10.1016\u002FS0140-6736(18)31080-8",{"id":18,"text":474,"url":18,"identifiers":475},"Zhang Z, Zhu C, Mo L, Hong Y. Effectiveness of sodium bicarbonate infusion on mortality in septic patients with metabolic acidosis. Intensive Care Med. 2018;44(11):1888–95. https:\u002F\u002Fdoi.org\u002F10.1007\u002Fs00134-018-5379-2. (Epub 2018 Sep 25 PMID: 30255318).",{"doi":476},"10.1007\u002Fs00134-018-5379-2",{"id":18,"text":478,"url":18,"identifiers":479},"Lo KB, Garvia V, Stempel JM, Ram P, Rangaswami J. Bicarbonate use and mortality outcome among critically ill patients with metabolic acidosis: A meta analysis. Heart Lung. 2020 Mar-Apr;49(2):167–174. doi: https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.hrtlng.2019.10.007. Epub 2019 Nov 14. PMID: 31733880.",{"doi":480},"10.1016\u002Fj.hrtlng.2019.10.007",{"id":18,"text":482,"url":18,"identifiers":483},"Lutterman JA, Adriaansen AA, van ’t Laar A. Treatment of severe diabetic ketoacidosis. A comparative study of two methods. Diabetologia. 1979;17(1):17–21. https:\u002F\u002Fdoi.org\u002F10.1007\u002FBF01222972. PMID: 38163.",{"doi":484},"10.1007\u002FBF01222972",{"id":18,"text":486,"url":18,"identifiers":487},"Lever E, Jaspan JB. Sodium bicarbonate therapy in severe diabetic ketoacidosis. Am J Med. 1983;75(2):263–8. https:\u002F\u002Fdoi.org\u002F10.1016\u002F0002-9343(83)91203-2. (PMID: 6309004).",{"doi":488},"10.1016\u002F0002-9343(83)91203-2",{"id":18,"text":490,"url":18,"identifiers":491},"Hale PJ, Crase J, Nattrass M. Metabolic effects of bicarbonate in the treatment of diabetic ketoacidosis. Br Med J (Clin Res Ed). 1984;289(6451):1035–8. https:\u002F\u002Fdoi.org\u002F10.1136\u002Fbmj.289.6451.1035.PMID:6091840;PMCID:PMC1443021.",{"doi":492},"10.1136\u002Fbmj.289.6451.1035.PMID:6091840;PMCID:PMC1443021",{"id":18,"text":494,"url":18,"identifiers":495},"Morris LR, Murphy MB, Kitabchi AE. Bicarbonate therapy in severe diabetic ketoacidosis. Ann Intern Med. 1986;105(6):836–40. https:\u002F\u002Fdoi.org\u002F10.7326\u002F0003-4819-105-6-836. (PMID: 3096181).",{"doi":496},"10.7326\u002F0003-4819-105-6-836",{"id":18,"text":498,"url":18,"identifiers":499},"Gamba G, Oseguera J, Castrejón M, Gómez-Pérez FJ. Bicarbonate therapy in severe diabetic ketoacidosis. A double blind, randomized, placebo controlled trial. Rev Invest Clin. 1991;43(3):234–8 PMID: 1667955.",{},{"id":18,"text":501,"url":18,"identifiers":502},"Okuda Y, Adrogue HJ, Field JB, Nohara H, Yamashita K. Counterproductive effects of sodium bicarbonate in diabetic ketoacidosis. J Clin Endocrinol Metab. 1996;81(1):314–20. https:\u002F\u002Fdoi.org\u002F10.1210\u002Fjcem.81.1.8550770. PMID: 8550770.",{"doi":503},"10.1210\u002Fjcem.81.1.8550770",{"id":18,"text":505,"url":18,"identifiers":506},"Viallon A, Zeni F, Lafond P, Venet C, Tardy B, Page Y, Bertrand JC. Does bicarbonate therapy improve the management of severe diabetic ketoacidosis? Crit Care Med. 1999;27(12):2690–3. https:\u002F\u002Fdoi.org\u002F10.1097\u002F00003246-199912000-00014. (PMID: 10628611).",{"doi":507},"10.1097\u002F00003246-199912000-00014",{"id":18,"text":509,"url":18,"identifiers":510},"Robertshaw H. Diabetic ketoacidosis and bicarbonate therapy. Crit Care. 2000;3:4308. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fccf-2000-4308.",{"doi":511},"10.1186\u002Fccf-2000-4308",{"id":18,"text":513,"url":18,"identifiers":514},"Duhon B, Attridge RL, Franco-Martinez AC, Maxwell PR, Hughes DW. Intravenous sodium bicarbonate therapy in severely acidotic diabetic ketoacidosis. Ann Pharmacother. 2013;47(7–8):970–5. https:\u002F\u002Fdoi.org\u002F10.1345\u002Faph.1S014. Epub 2013 PMID: 23737516.",{"doi":515},"10.1345\u002Faph.1S014",{"id":18,"text":517,"url":18,"identifiers":518},"Chua HR, Schneider A, Bellomo R. Bicarbonate in diabetic ketoacidosis – a systematic review. Ann Intensive Care. 2011;1(1):23. https:\u002F\u002Fdoi.org\u002F10.1186\u002F2110-5820-1-23.PMC3224469.",{"doi":519},"10.1186\u002F2110-5820-1-23.PMC3224469",{"id":18,"text":521,"url":18,"identifiers":522},"Ozturk Z, Kilic A, Ozdemir G, Savas Erdeve S, Cetinkaya S. Sodium bicarbonate is safe but not useful in the management of severe diabetic ketoacidosis. Annals of Medical Research. 2023;30(4):474–80 Retrieved from https:\u002F\u002Fwww.annalsmedres.org\u002Findex.php\u002Faomr\u002Farticle\u002Fview\u002F4408.",{},{"id":18,"text":524,"url":18,"identifiers":525},"Lizzo JM, Goyal A, Gupta V. Adult Diabetic Ketoacidosis. [Updated 2022]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023. Available from: https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fbooks\u002FNBK560723\u002F.",{},{"id":18,"text":527,"url":18,"identifiers":528},"Gallo de Moraes A, Surani S. Effects of diabetic ketoacidosis in the respiratory system. World J Diabetes. 2019;10(1):16–22. doi: https:\u002F\u002Fdoi.org\u002F10.4239\u002Fwjd.v10.i1.16. PMID: 30697367; PMCID: PMC6347653.https:\u002F\u002Fwww.ncbi.nlm.nih.gov\u002Fpmc\u002Farticles\u002FPMC6347653\u002F.",{"doi":529},"10.4239\u002Fwjd.v10.i1.16",{"id":18,"text":531,"url":18,"identifiers":532},"Hallett A, Modi A, Levy N. Developments in the management of diabetic ketoacidosis in adults: implications for anaesthetists.British Journal of Anaesthesia. 2016; v16, i1.p 8–14. DOI: https:\u002F\u002Fdoi.org\u002F10.1093\u002Fbjaceaccp\u002Fmkv006.",{"doi":533},"10.1093\u002Fbjaceaccp\u002Fmkv006",{"id":535,"createTime":536,"updateTime":537,"relativeEntities":538,"slug":539,"properties":540,"entityType":103,"verifyStatus":104,"verifyTime":537,"verifyNote":106,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":549,"fullTextUrl":18,"authors":550,"publicationType":222,"publisherRelationship":596,"citationCount":18,"citationInfo":18,"publishDate":621,"publishYear":622,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":623,"openAccess":18,"references":18,"isForceReanalyzing":384},"75f4751c-223b-4112-b4dc-a9dbfce9ce1a","2024-01-02T02:48:07.747+00:00","2025-02-26T08:13:04.738+00:00",[],"Thyroid-nodule-update-on-diagnosis-and-management",{"abstract":541,"title":543,"references":545,"doi":547},{"EN":542},"Thyroid nodules are common. The clinical importance of thyroid nodules is related to excluding malignancy (4.0 to 6.5% of all thyroid nodules), evaluate their functional status and assess for the presence of pressure symptoms. Incidental thyroid nodules are being diagnosed with increasing frequency in the recent years with the use of newer and highly sensitive imaging techniques. The high prevalence of thyroid nodules necessitates that the clinicians use evidence-based approaches for their assessment and management. New molecular tests have been developed to help with evaluation of malignancy in thyroid nodules. This review addresses advances in thyroid nodule evaluation, and their management considering the current guidelines and supporting evidence.",{"EN":544},"Thyroid nodule update on diagnosis and management",{"VOID":546},"Haugen BR, Alexander EK, Bible KC, et al. 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer: The American Thyroid Association Guidelines Task Force on Thyroid Nodules and Differentiated Thyroid Cancer. Thyroid. 2016;26(1):1–133.\nTunbridge WM, Evered DC, Hall R, et al. The spectrum of thyroid disease in a community: the Whickham survey. Clin Endocrinol (Oxf). 1977;7(6):481–93.\nHegedus L. Clinical practice. The thyroid nodule. N Engl J Med. 2004;351(17):1764–71.\nDean DS, Gharib H. Epidemiology of thyroid nodules. Best Pract Res Clin Endocrinol Metab. 2008;22(6):901–11.\nDavies L, Welch HG. Current thyroid cancer trends in the United States. JAMA Otolaryngol Head Neck Surg. 2014;140(4):317–22.\nLi N, Du XL, Reitzel LR, Xu L, Sturgis EM. Impact of enhanced detection on the increase in thyroid cancer incidence in the United States: review of incidence trends by socioeconomic status within the surveillance, epidemiology, and end results registry, 1980–2008. Thyroid. 2013;23(1):103–10.\nWerk Jr EE, Vernon BM, Gonzalez JJ, Ungaro PC, McCoy RC. Cancer in thyroid nodules. A community hospital survey. Arch Intern Med. 1984;144(3):474–6.\nBelfiore A, Giuffrida D, La Rosa GL, et al. High frequency of cancer in cold thyroid nodules occurring at young age. Acta Endocrinol (Copenh). 1989;121(2):197–202.\nLin JD, Chao TC, Huang BY, Chen ST, Chang HY, Hsueh C. Thyroid cancer in the thyroid nodules evaluated by ultrasonography and fine-needle aspiration cytology. Thyroid. 2005;15(7):708–17.\nTan GH, Gharib H. Thyroid incidentalomas: management approaches to nonpalpable nodules discovered incidentally on thyroid imaging. Ann Intern Med. 1997;126(3):226–31.\nGharib H, Papini E. Thyroid nodules: clinical importance, assessment, and treatment. Endocrinol Metab Clin North Am. 2007;36(3):707–35. vi.\nCastro MR, Gharib H. Continuing controversies in the management of thyroid nodules. Ann Intern Med. 2005;142(11):926–31.\nGharib H, Papini E, Garber JR, et al. American Association of Clinical Endocrinologists, American College of Endocrinology, and Associazione Medici Endocrinologi Medical Guidelines for Clinical Practice for the Diagnosis and Management of Thyroid Nodules - 2016 Update. Endocr Pract. 2016;22(5):622–39.\nTan GH, Gharib H, Reading CC. Solitary thyroid nodule. Comparison between palpation and ultrasonography. Arch Intern Med. 1995;155(22):2418–23.\nSingh S, Singh A, Khanna AK. Thyroid incidentaloma. Indian J Surg Oncol. 2012;3(3):173–81.\nBoelaert K, Horacek J, Holder RL, Watkinson JC, Sheppard MC, Franklyn JA. Serum thyrotropin concentration as a novel predictor of malignancy in thyroid nodules investigated by fine-needle aspiration. J Clin Endocrinol Metab. 2006;91(11):4295–301.\nHaymart MR, Repplinger DJ, Leverson GE, et al. Higher serum thyroid stimulating hormone level in thyroid nodule patients is associated with greater risks of differentiated thyroid cancer and advanced tumor stage. J Clin Endocrinol Metab. 2008;93(3):809–14.\nCostante G, Filetti S. Early diagnosis of medullary thyroid carcinoma: is systematic calcitonin screening appropriate in patients with nodular thyroid disease? Oncologist. 2011;16(1):49–52.\nGharib H, Papini E, Paschke R. Thyroid nodules: a review of current guidelines, practices, and prospects. Eur J Endocrinol. 2008;159(5):493–505.\nElisei R, Bottici V, Luchetti F, et al. Impact of routine measurement of serum calcitonin on the diagnosis and outcome of medullary thyroid cancer: experience in 10,864 patients with nodular thyroid disorders. J Clin Endocrinol Metab. 2004;89(1):163–8.\nNiccoli P, Wion-Barbot N, Caron P, et al. Interest of routine measurement of serum calcitonin: study in a large series of thyroidectomized patients. The French Medullary Study Group. J Clin Endocrinol Metab. 1997;82(2):338–41.\nCostante G, Meringolo D, Durante C, et al. Predictive value of serum calcitonin levels for preoperative diagnosis of medullary thyroid carcinoma in a cohort of 5817 consecutive patients with thyroid nodules. J Clin Endocrinol Metab. 2007;92(2):450–5.\nMachens A, Hoffmann F, Sekulla C, Dralle H. Importance of gender-specific calcitonin thresholds in screening for occult sporadic medullary thyroid cancer. Endocr Relat Cancer. 2009;16(4):1291–8.\nChambon G, Alovisetti C, Idoux-Louche C, et al. The use of preoperative routine measurement of basal serum thyrocalcitonin in candidates for thyroidectomy due to nodular thyroid disorders: results from 2733 consecutive patients. J Clin Endocrinol Metab. 2011;96(1):75–81.\nToledo SP, Lourenco Jr DM, Santos MA, Tavares MR, Toledo RA, Correia-Deur JE. Hypercalcitoninemia is not pathognomonic of medullary thyroid carcinoma. Clinics (Sao Paulo). 2009;64(7):699–706.\nErdogan MF, Gursoy A, Kulaksizoglu M. Long-term effects of elevated gastrin levels on calcitonin secretion. J Endocrinol Invest. 2006;29(9):771–5.\nWang TS, Ocal IT, Sosa JA, Cox H, Roman S. Medullary thyroid carcinoma without marked elevation of calcitonin: a diagnostic and surveillance dilemma. Thyroid. 2008;18(8):889–94.\nDora JM, Canalli MH, Capp C, Punales MK, Vieira JG, Maia AL. Normal perioperative serum calcitonin levels in patients with advanced medullary thyroid carcinoma: case report and review of the literature. Thyroid. 2008;18(8):895–9.\nSuh I, Vriens MR, Guerrero MA, et al. Serum thyroglobulin is a poor diagnostic biomarker of malignancy in follicular and Hurthle-cell neoplasms of the thyroid. 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AACE\u002FACE disease state commentary: molecular diagnostic testing of thyroid nodules with indeterminate cytopathology. Endocr Pract. 2014;20(4):360–3.\nBauer DC, Rodondi N, Stone KL, Hillier TA. Thyroid hormone use, hyperthyroidism and mortality in older women. Am J Med. 2007;120(4):343–9.\nAuer J, Scheibner P, Mische T, Langsteger W, Eber O, Eber B. Subclinical hyperthyroidism as a risk factor for atrial fibrillation. Am Heart J. 2001;142(5):838–42.\nBiondi B, Cooper DS. The clinical significance of subclinical thyroid dysfunction. Endocr Rev. 2008;29(1):76–131.\nOrlandi A, Puscar A, Capriata E, Fideleff H. Repeated fine-needle aspiration of the thyroid in benign nodular thyroid disease: critical evaluation of long-term follow-up. Thyroid. 2005;15(3):274–8.\nIllouz F, Rodien P, Saint-Andre JP, et al. Usefulness of repeated fine-needle cytology in the follow-up of non-operated thyroid nodules. Eur J Endocrinol. 2007;156(3):303–8.\nOertel YC, Miyahara-Felipe L, Mendoza MG, Yu K. 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Highly accurate diagnosis of cancer in thyroid nodules with follicular neoplasm\u002Fsuspicious for a follicular neoplasm cytology by ThyroSeq v2 next-generation sequencing assay. Cancer. 2014;120(23):3627–34.\nMoon HJ, Kwak JY, Kim EK, et al. The role of BRAFV600E mutation and ultrasonography for the surgical management of a thyroid nodule suspicious for papillary thyroid carcinoma on cytology. Ann Surg Oncol. 2009;16(11):3125–31.\nGharib H, Papini E, Paschke R, et al. American Association of Clinical Endocrinologists, Associazione Medici Endocrinologi, and EuropeanThyroid Association Medical Guidelines for Clinical Practice for the Diagnosis and Management of Thyroid Nodules. Endocr Pract. 2010;16 Suppl 1:1–43.\nCobin RH, Gharib H, Bergman DA, et al. AACE\u002FAAES medical\u002Fsurgical guidelines for clinical practice: management of thyroid carcinoma. American Association of Clinical Endocrinologists. American College of Endocrinology. 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Impact of pregnancy on prognosis of differentiated thyroid cancer: clinical and molecular features. Eur J Endocrinol. 2014;170(5):659–66.\nSchneider AB, Ron E, Lubin J, Stovall M, Gierlowski TC. Dose–response relationships for radiation-induced thyroid cancer and thyroid nodules: evidence for the prolonged effects of radiation on the thyroid. J Clin Endocrinol Metab. 1993;77(2):362–9.\nCurtis RE, Rowlings PA, Deeg HJ, et al. Solid cancers after bone marrow transplantation. N Engl J Med. 1997;336(13):897–904.\nPacini F, Vorontsova T, Demidchik EP, et al. Post-Chernobyl thyroid carcinoma in Belarus children and adolescents: comparison with naturally occurring thyroid carcinoma in Italy and France. J Clin Endocrinol Metab. 1997;82(11):3563–9.\nShibata Y, Yamashita S, Masyakin VB, Panasyuk GD, Nagataki S. 15 years after Chernobyl: new evidence of thyroid cancer. Lancet. 2001;358(9297):1965–6.\nHemminki K, Eng C, Chen B. Familial risks for nonmedullary thyroid cancer. 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is the acute or chronic inflammation of the pituitary gland. The spectrum of hypophysitis has expanded in recent years with the addition of two histologic subtypes and recognition as a complication of treatment with immune checkpoint inhibitors. Despite the increased number of published cases, the pathogenesis of hypophysitis is poorly understood, and treatment strategies are diverse and controversial. The diagnosis of hypophysitis generally requires histopathologic confirmation. The presentation and clinical course of hypophysitis varies. Hypophysitis can resolve spontaneously, relapse may occur, and some cases can be refractory to treatment.",{"EN":785},"Hypophysitis: Evaluation and Management",{"EN":36},{"VOID":788},"Chan WB, Cockram CS. Panhypopituitarism in association with interferon-alpha treatment. Singapore Med J. 2004;45:93–4.\nConcha LB, Carlson HE, Heimann A, Lake-Bakaar GV, Paal AF. Interferon-induced hypopituitarism. Am J Med. 2003;114:161–3.\nRidruejo E, Christensen AF, Mando OG. 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The engagement of CTLA-4 on primary melanoma cell lines induces antibody-dependent cellular cytotoxicity and TNF-alpha production. J Transl Med. 2013;11:108.\nFaje A, Ma J, Wang X, Swearingen B, Tritos NA, Nachtigall L, Zhang X, Klibanski A: Cytotoxic T-lymphocyte antigen-4 gene expression in human pituitary adenomas. ENDO 2015, abstract.\nKuehn HS, Ouyang W, Lo B, Deenick EK, Niemela JE, Avery DT, Schickel JN, Tran DQ, Stoddard J, Zhang Y, et al. Immune dysregulation in human subjects with heterozygous germline mutations in CTLA4. Science. 2014;345:1623–7.\nSchubert D, Bode C, Kenefeck R, Hou TZ, Wing JB, Kennedy A, Bulashevska A, Petersen BS, Schaffer AA, Gruning BA, et al. Autosomal dominant immune dysregulation syndrome in humans with CTLA4 mutations. Nat Med. 2014;20:1410–6.\nGarred P, Michaelsen TE, Aase A. The IgG subclass pattern of complement activation depends on epitope density and antibody and complement concentration. Scand J Immunol. 1989;30:379–82.\nMichaelsen TE, Garred P, Aase A. Human IgG subclass pattern of inducing complement-mediated cytolysis depends on antigen concentration and to a lesser extent on epitope patchiness, antibody affinity and complement concentration. Eur J Immunol. 1991;21:11–6.\nBruhns P, Iannascoli B, England P, Mancardi DA, Fernandez N, Jorieux S, Daeron M. Specificity and affinity of human Fcgamma receptors and their polymorphic variants for human IgG subclasses. Blood. 2009;113:3716–25.",{"VOID":790},"10.1186\u002Fs40842-016-0034-8","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-016-0034-8",[793],{"id":794,"sortIndex":19,"researcher":18,"roles":795,"affiliations":796,"properties":805,"displayName":807,"givenName":18,"familyName":18},"9de735c4-e079-48f3-aa33-a739f3050c2c",[554],[797],{"id":798,"sortIndex":19,"affiliation":799,"properties":18},"06fa607e-cf72-4b09-a0e9-5109df21d99d",{"id":798,"createTime":18,"updateTime":18,"relativeEntities":800,"slug":18,"properties":801,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":804,"statistic":18},[],{"title":802},{"VI":803},"Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, USA",[],{"title":806},{"VI":807},"Alexander Faje",{"url":18,"publisher":809,"properties":18},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":810,"slug":10,"properties":811,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":814,"manageAffiliations":815,"indexDatabases":816,"url":38,"thumbnailPath":18,"statistic":823,"gsStatistic":18,"type":80,"analyzePriority":18},[],{"issn":812,"title":813},{"VOID":13},{"EN":15},[],[],[817],{"id":24,"indexDatabase":818,"url":35,"indexYears":36,"academicFieldIds":18,"indexDatabaseRanking":37},{"id":26,"createTime":18,"updateTime":18,"relativeEntities":819,"label":820,"description":821,"key":32,"publicationTags":822,"standard":18},[],{"EN":29,"VI":29},{"EN":29,"VI":31},[34],{"impactFactor":19,"impactFactorByYear":824,"i10Index":49,"i10IndexLast5Year":50,"totalPublication":51,"totalPublicationByYear":825,"totalCitation":61,"totalCitationByYear":826,"totalCitationPerPublication":71,"totalCitationPerPublicationByYear":827,"hindexLast5Year":49,"hindex":49},{"2016":41,"2017":42,"2018":43,"2019":44,"2020":45,"2021":46,"2022":47,"2023":48},{"2015":53,"2016":54,"2017":54,"2018":55,"2019":49,"2020":56,"2021":57,"2022":58,"2023":59,"2024":60},{"2015":63,"2016":64,"2017":65,"2018":66,"2019":67,"2020":68,"2021":69,"2022":70},{"2015":73,"2016":74,"2017":75,"2018":76,"2019":77,"2020":78,"2021":44,"2022":79},"2016-09-06",[37],{"id":831,"createTime":832,"updateTime":833,"relativeEntities":834,"slug":835,"properties":836,"entityType":103,"verifyStatus":104,"verifyTime":833,"verifyNote":106,"languages":847,"translateLanguages":18,"viewCount":19,"primaryUrl":848,"fullTextUrl":18,"authors":849,"publicationType":222,"publisherRelationship":967,"citationCount":134,"citationInfo":991,"publishDate":18,"publishYear":18,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":993,"openAccess":18,"references":994,"isForceReanalyzing":384},"893c2ea1-7c53-43b5-b3c8-4667abc783f0","2024-04-17T20:10:41.874+00:00","2025-02-24T13:52:26.198+00:00",[],"Multidisciplinary-intensive-lifestyle-intervention-improves-markers-of-nonalcoholic-fatty-liver-disease-NAFLD-in-patients-with-type-1-diabetes-and-obesity-a-retrospective-matched-cohort-study",{"openalex":837,"abstract":839,"title":841,"pm":843,"doi":845},{"VOID":838},"W4365148145",{"EN":840},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:sec>\n                \u003Cjats:title>Background\u003C\u002Fjats:title>\n                \u003Cjats:p>The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing among patients with type 1 diabetes (T1D) paralleling the increasing prevalence of obesity among this population. However, little is known about the impact of intensive lifestyle intervention (ILI) on NAFLD in patients with T1D.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Methods\u003C\u002Fjats:title>\n                \u003Cjats:p>Using Hepatic Steatosis Index (HSI), a noninvasive surrogate predictor of NAFLD, we retrospectively evaluated 88 adult patients with T1D and obesity after one year of participating in a 12-week ILI program in real-world clinical practice. Using the NAFLD guidelines of the American Association for the Study of Liver Diseases (AASLD), we excluded 11 participants. We matched the remaining ILI cohort (age 43 ± 12 years, females 65%, diabetes duration 22 ± 9 years, A1C 8.2 ± 0.9%, body weight 101 ± 17 kg, BMI 35.3 ± 4.9 kg\u002Fm\u003Cjats:sup>2\u003C\u002Fjats:sup>) in 1:1 ratio with a similar cohort of patients with T1D and obesity who received standard diabetes care (SC) at the same practice and during the same period. Matching criteria included: sex, age, BMI, A1C and duration of T1D. HSI [8 + ALT\u002FAST + BMI (+ 2 if female, + 2 if T2D)] was calculated at baseline and after 12 months of intervention.\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Results\u003C\u002Fjats:title>\n                \u003Cjats:p>At baseline, HSI was similar between the two cohorts (46.2 ± 6.1 in the ILI cohort and 44.9 ± 5.7 in the SC cohort). After 12 months, the ILI group lost an average of 5.6 ± 2.7 kg (5.8%, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05) while the SC group maintained their baseline body weight (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001 between groups). HSI decreased significantly from baseline in the ILI group (-2.7 ± 1.1, p = 0.01), but did not change in the SC group (0.6 ± 0.9, p = 0.53, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.001 between groups). Percentage of patients with high likelihood of NAFLD diagnosis decreased from 100% at baseline to 88.3% in the ILI group, and was 10.4% less compared to SC (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.01). Total daily insulin dose decreased in the ILI cohort compared to the SC cohort (-6.1 ± 4.2 versus 1.34 ± 4.3 units\u002Fday, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.01).\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>\u003Cjats:sec>\n                \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n                \u003Cjats:p>Twelve weeks of ILI improved HSI and decreased total daily insulin requirements in patients with T1D and obesity at one year. Short-term ILI should be implemented in the management of NAFLD for obese patients with type 1 diabetes.\n\u003C\u002Fjats:p>\n              \u003C\u002Fjats:sec>",{"EN":842},"Multidisciplinary intensive lifestyle intervention improves markers of nonalcoholic fatty liver disease (NAFLD) in patients with type 1 diabetes and obesity: a retrospective matched-cohort study",{"VOID":844},"37046323",{"VOID":846},"10.1186\u002Fs40842-023-00150-9",[108],"https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-023-00150-9",[850,869,886,903,920,935,950],{"id":851,"sortIndex":19,"researcher":18,"roles":852,"affiliations":853,"properties":862,"displayName":866,"givenName":18,"familyName":18},"21861656-62ea-4df7-9b9c-fe435f126028",[],[854],{"id":855,"sortIndex":19,"affiliation":856,"properties":18},"9f1abb4c-acaf-4e7e-96f5-676ff070e022",{"id":855,"createTime":18,"updateTime":18,"relativeEntities":857,"slug":18,"properties":858,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":861,"statistic":18},[],{"title":859},{"VI":860},"Joslin Diabetes Center, Boston, MA 02215, USA",[],{"orcid":863,"title":865,"openalex":867},{"VOID":864},"https:\u002F\u002Forcid.org\u002F0000-0003-3864-7494",{"EN":866},"Shaheen Tomah",{"VOID":868},"A5031226271",{"id":870,"sortIndex":134,"researcher":18,"roles":871,"affiliations":872,"properties":879,"displayName":883,"givenName":18,"familyName":18},"9b1d7f56-f019-427e-b07f-9c5bf4ed18b4",[],[873],{"id":855,"sortIndex":19,"affiliation":874,"properties":18},{"id":855,"createTime":18,"updateTime":18,"relativeEntities":875,"slug":18,"properties":876,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":878,"statistic":18},[],{"title":877},{"VI":860},[],{"orcid":880,"title":882,"openalex":884},{"VOID":881},"https:\u002F\u002Forcid.org\u002F0000-0002-3978-6384",{"EN":883},"TAREQ SALAH",{"VOID":885},"A5089617066",{"id":887,"sortIndex":150,"researcher":18,"roles":888,"affiliations":889,"properties":896,"displayName":900,"givenName":18,"familyName":18},"a53ebafb-92a2-406e-9676-0477dd16fc3a",[],[890],{"id":855,"sortIndex":19,"affiliation":891,"properties":18},{"id":855,"createTime":18,"updateTime":18,"relativeEntities":892,"slug":18,"properties":893,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":895,"statistic":18},[],{"title":894},{"VI":860},[],{"orcid":897,"title":899,"openalex":901},{"VOID":898},"https:\u002F\u002Forcid.org\u002F0000-0002-4998-9708",{"EN":900},"Marwa Al‐Badri",{"VOID":902},"A5075337962",{"id":904,"sortIndex":70,"researcher":18,"roles":905,"affiliations":906,"properties":913,"displayName":917,"givenName":18,"familyName":18},"b432d433-af47-4c7f-a5c3-5b6bc3349aff",[],[907],{"id":855,"sortIndex":19,"affiliation":908,"properties":18},{"id":855,"createTime":18,"updateTime":18,"relativeEntities":909,"slug":18,"properties":910,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":912,"statistic":18},[],{"title":911},{"VI":860},[],{"orcid":914,"title":916,"openalex":918},{"VOID":915},"https:\u002F\u002Forcid.org\u002F0000-0002-5281-6728",{"EN":917},"SHILTON E. 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Non-alcoholic fatty liver disease, obesity and the metabolic syndrome. Best Pract Res Clin Gastroenterol. 2014;28(4):637–53.",{"doi":998},"10.1016\u002Fj.bpg.2014.07.008",{"id":18,"text":1000,"url":18,"identifiers":1001},"Younes R, Bugianesi E. NASH in Lean Individuals. Semin Liver Dis. 2019;39(1):86–95.",{"doi":1002},"10.1055\u002Fs-0038-1677517",{"id":18,"text":1004,"url":18,"identifiers":1005},"Singh A, Le P, Lopez R, Alkhouri N. The utility of noninvasive scores in assessing the prevalence of nonalcoholic fatty liver disease and advanced fibrosis in type 1 diabetic patients. Hep Intl. 2018;12(1):37–43.",{"doi":1006},"10.1007\u002Fs12072-017-9840-z",{"id":18,"text":1008,"url":18,"identifiers":1009},"Chillaron JJ, Flores Le-Roux JA, Benaiges D, Pedro-Botet J. Type 1 diabetes, metabolic syndrome and cardiovascular risk. Metabolism. 2014;63(2):181–7.",{"doi":1010},"10.1016\u002Fj.metabol.2013.10.002",{"id":18,"text":1012,"url":18,"identifiers":1013},"Targher G, Bertolini L, Padovani R, Rodella S, Zoppini G, Pichiri I, et al. Prevalence of non-alcoholic fatty liver disease and its association with cardiovascular disease in patients with type 1 diabetes. J Hepatol. 2010;53(4):713–8.",{"doi":1014},"10.1016\u002Fj.jhep.2010.04.030",{"id":18,"text":1016,"url":18,"identifiers":1017},"Mantovani A, Mingolla L, Rigolon R, Pichiri I, Cavalieri V, Zoppini G, et al. Nonalcoholic fatty liver disease is independently associated with an increased incidence of cardiovascular disease in adult patients with type 1 diabetes. Int J Cardiol. 2016;225:387–91.",{"doi":1018},"10.1016\u002Fj.ijcard.2016.10.040",{"id":18,"text":1020,"url":18,"identifiers":1021},"Targher G, Mantovani A, Pichiri I, Mingolla L, Cavalieri V, Mantovani W, et al. Nonalcoholic fatty liver disease is independently associated with an increased incidence of chronic kidney disease in patients with type 1 diabetes. Diabetes Care. 2014;37(6):1729–36.",{"doi":1022},"10.2337\u002Fdc13-2704",{"id":18,"text":1024,"url":18,"identifiers":1025},"Vendhan R, Amutha A, Anjana RM, Unnikrishnan R, Mohan V. Clinical profile of nonalcoholic Fatty liver disease among young patients with type 1 diabetes mellitus seen at a diabetes speciality center in India. Endocrine Practice. 2014;20(12):1249–57.",{"doi":1026},"10.4158\u002FEP14044.OR",{"id":18,"text":1028,"url":18,"identifiers":1029},"Raza S, Rajak S, Upadhyay A, Tewari A, Anthony SR. Current treatment paradigms and emerging therapies for NAFLD\u002FNASH. Front Biosci (Landmark Ed). 2021;26(2):206–37.",{"doi":1030},"10.2741\u002F4892",{"id":18,"text":1032,"url":18,"identifiers":1033},"Pandyarajan V, Gish RG, Alkhouri N, Noureddin M. Screening for Nonalcoholic Fatty Liver Disease in the Primary Care Clinic. Gastroenterology Hepatology. 2019;15(7):357–65.",{},{"id":18,"text":1035,"url":18,"identifiers":1036},"Anstee QM, Targher G, Day CP. Progression of NAFLD to diabetes mellitus, cardiovascular disease or cirrhosis. Nat Rev Gastroenterol Hepatol. 2013;10(6):330.",{"doi":1037},"10.1038\u002Fnrgastro.2013.41",{"id":18,"text":1039,"url":18,"identifiers":1040},"Piazzolla VA, Mangia A. Noninvasive Diagnosis of NAFLD and NASH. Cells. 2020;9(4):1005.",{"doi":1041},"10.3390\u002Fcells9041005",{"id":18,"text":1043,"url":18,"identifiers":1044},"Lee JH, Kim D, Kim HJ, Lee CH, Yang JI, Kim W, et al. Hepatic steatosis index: a simple screening tool reflecting nonalcoholic fatty liver disease. Dig Liver Dis. 2010;42(7):503–8.",{"doi":1045},"10.1016\u002Fj.dld.2009.08.002",{"id":18,"text":1047,"url":18,"identifiers":1048},"Hamdy O, Mottalib A, Morsi A, El-Sayed N, Goebel-Fabbri A, Arathuzik G, et al. Long-term effect of intensive lifestyle intervention on cardiovascular risk factors in patients with diabetes in real-world clinical practice: a 5-year longitudinal study. BMJ Open Diabetes Res Care. 2017;5(1):e000259.",{"doi":1049},"10.1136\u002Fbmjdrc-2016-000259",{"id":18,"text":1051,"url":18,"identifiers":1052},"Hamdy O, Carver C. The Why WAIT program: improving clinical outcomes through weight management in type 2 diabetes. Curr DiabRep. 2008;8(5):413–20.",{},{"id":18,"text":1054,"url":18,"identifiers":1055},"Chalasani N, Younossi Z, Lavine JE, Charlton M, Cusi K, Rinella M, et al. The diagnosis and management of nonalcoholic fatty liver disease: Practice guidance from the American Association for the Study of Liver Diseases. Hepatology. 2018;67(1):328–57.",{"doi":1056},"10.1002\u002Fhep.29367",{"id":18,"text":1058,"url":18,"identifiers":1059},"Hegazy MA, Samy MA, Tawfik A, Naguib MM, Ezzat A, Behiry ME. 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Obesity (Silver Spring). 2019;27(9):1385-7.",{"doi":1071},"10.1002\u002Foby.22559",{"id":18,"text":1073,"url":18,"identifiers":1074},"Desmet VJ, Roskams T. Cirrhosis reversal: a duel between dogma and myth. J Hepatol. 2004;40(5):860–7.",{"doi":1075},"10.1016\u002Fj.jhep.2004.03.007",{"id":18,"text":1077,"url":18,"identifiers":1078},"Sviklane L, Olmane E, Dzerve Z, Kupcs K, Pirags V, Sokolovska J. Fatty liver index and hepatic steatosis index for prediction of non-alcoholic fatty liver disease in type 1 diabetes. J Gastroenterol Hepatol. 2018;33(1):270–6.",{"doi":1079},"10.1111\u002Fjgh.13814",{"id":18,"text":1081,"url":18,"identifiers":1082},"Nd AM. Non-Alcoholic Fatty Liver Disease, an Overview. Integr Med (Encinitas). 2019;18(2):42–9.",{},{"id":18,"text":1084,"url":18,"identifiers":1085},"TOMAH S, SALAH T, AL-BADRI M, DHAVER SE, CURRY MP, JIANG Z, et al. 1105-P: Moderate-to-Advanced Liver Fibrosis Is Common in Patients with Type 1 Diabetes (T1D) and Nonalcoholic Fatty Liver Disease (NAFLD). Diabetes. 2022;71(Supplement_1).",{"doi":1086},"10.2337\u002Fdb22-1105-P",{"id":18,"text":1088,"url":18,"identifiers":1089},"Kabisch S, Bäther S, Dambeck U, Kemper M, Gerbracht C, Honsek C, et al. Liver Fat Scores Moderately Reflect Interventional Changes in Liver Fat Content by a Low-Fat Diet but Not by a Low-Carb Diet. Nutrients. 2018;10(2):157.",{"doi":1090},"10.3390\u002Fnu10020157",{"id":18,"text":1092,"url":18,"identifiers":1093},"Kabisch S, Markova M, Hornemann S, Sucher S, Pivovarova-Ramich O, Machann J, et al. Liver fat scores do not reflect interventional changes in liver fat content induced by high-protein diets. Sci Rep. 2021;11(1):8843.",{"doi":1094},"10.1038\u002Fs41598-021-87360-2",{"id":18,"text":1096,"url":18,"identifiers":1097},"Keating SE, Parker HM, Hickman IJ, Gomersall SR, Wallen MP, Coombes JS, et al. NAFLD in clinical practice: Can simple blood and anthropometric markers be used to detect change in liver fat measured by (1) H-MRS? Liver Int. 2017;37(12):1907–15.",{"doi":1098},"10.1111\u002Fliv.13488",{"id":18,"text":1100,"url":18,"identifiers":1101},"Kantartzis K, Rettig I, Staiger H, Machann J, Schick F, Scheja L, et al. An extended fatty liver index to predict non-alcoholic fatty liver disease. Diabetes Metab. 2017;43(3):229–39.",{"doi":1102},"10.1016\u002Fj.diabet.2016.11.006",{"id":1104,"createTime":1105,"updateTime":1106,"relativeEntities":1107,"slug":1108,"properties":1109,"entityType":103,"verifyStatus":104,"verifyTime":1106,"verifyNote":106,"languages":1124,"translateLanguages":18,"viewCount":19,"primaryUrl":1125,"fullTextUrl":18,"authors":1126,"publicationType":222,"publisherRelationship":1178,"citationCount":19,"citationInfo":1202,"publishDate":1205,"publishYear":1203,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":1206,"openAccess":18,"references":1207,"isForceReanalyzing":384},"1a5c0db0-6795-4776-b307-47e338568cb2","2024-04-18T19:12:15.892+00:00","2025-02-23T05:15:07.737+00:00",[],"Vehicle-ergonomics-contributing-to-a-diabetic-foot-ulcer",{"mag":1110,"pmc":1112,"openalex":1114,"abstract":1116,"title":1118,"pm":1120,"doi":1122},{"VOID":1111},"2984472483",{"VOID":1113},"6839194",{"VOID":1115},"W2984472483",{"EN":1117},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\n\u003Cjats:sec>\n\u003Cjats:title>Background\u003C\u002Fjats:title>\n\u003Cjats:p>Diabetes mellitus continues to be a rising concern in the United States. It affects an estimated 9.4% of the population and approximately 1.5 million Americans are diagnosed annually. Approximately 85% of diabetic foot ulcers are associated with diabetic peripheral neuropathy and an infected diabetic foot ulcer is often the first sign of diabetes. There are countless studies within the literature that investigate how insensate feet and the manifestation of a foot ulcer further decrease quality of life and increase risk for mortality. Literature focuses on gait and kinematics that contribute to the formation of a diabetic foot ulcer. While pressure and shear forces are etiologic factors that may lead to the formation of diabetic foot ulcers, the position of the foot while driving an automobile has been ignored as a possible risk factor.\u003C\u002Fjats:p>\n\u003C\u002Fjats:sec>\n\u003Cjats:sec>\n\u003Cjats:title>Case presentation\u003C\u002Fjats:title>\n\u003Cjats:p>The clinical case will describe the events of healing a neuropathic diabetic foot ulcer beyond the standard of care treatment plan. It is one of the first case reports to describe vehicle ergonomics as an etiologic factor contributing to a diabetic foot ulcer. Once the patient becomes aware of the unnecessary source of pressure, education and care is provided to manage this likely source of daily pressure to the neuropathic foot.\u003C\u002Fjats:p>\n\u003C\u002Fjats:sec>\n\u003Cjats:sec>\n\u003Cjats:title>Conclusion\u003C\u002Fjats:title>\n\u003Cjats:p>The article emphasizes the importance of a complete assessment, including nontraditional factors, which may lead to diabetic complications.\u003C\u002Fjats:p>\n\u003C\u002Fjats:sec>",{"EN":1119},"Vehicle ergonomics contributing to a diabetic foot ulcer",{"VOID":1121},"31720006",{"VOID":1123},"10.1186\u002Fs40842-019-0089-4",[108],"https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-019-0089-4",[1127,1146,1163],{"id":1128,"sortIndex":19,"researcher":18,"roles":1129,"affiliations":1130,"properties":1139,"displayName":1143,"givenName":18,"familyName":18},"10315db1-007f-463f-a0c9-a35e951b8c84",[],[1131],{"id":1132,"sortIndex":19,"affiliation":1133,"properties":18},"fbf1f369-f141-4f56-9029-48d677498a5d",{"id":1132,"createTime":18,"updateTime":18,"relativeEntities":1134,"slug":18,"properties":1135,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1138,"statistic":18},[],{"title":1136},{"EN":1137},"Department of Internal Medicine, Division of Metabolism, Endocrinology, and Diabetes, University of Michigan Hospital and Health System, Domino’s Farms Lobby G, Suite 1500, 24 Frank Lloyd Wright Drive, Ann Arbor, MI, 48106, USA",[],{"orcid":1140,"title":1142,"openalex":1144},{"VOID":1141},"https:\u002F\u002Forcid.org\u002F0000-0003-2624-4006",{"EN":1143},"Christine Jarocki",{"VOID":1145},"A5009905061",{"id":1147,"sortIndex":134,"researcher":18,"roles":1148,"affiliations":1149,"properties":1156,"displayName":1160,"givenName":18,"familyName":18},"825a127c-6dde-4d08-8bd1-986f7535181f",[],[1150],{"id":1132,"sortIndex":19,"affiliation":1151,"properties":18},{"id":1132,"createTime":18,"updateTime":18,"relativeEntities":1152,"slug":18,"properties":1153,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1155,"statistic":18},[],{"title":1154},{"EN":1137},[],{"orcid":1157,"title":1159,"openalex":1161},{"VOID":1158},"https:\u002F\u002Forcid.org\u002F0000-0002-2561-9243",{"EN":1160},"Brian M. Schmidt",{"VOID":1162},"A5082160803",{"id":1164,"sortIndex":150,"researcher":18,"roles":1165,"affiliations":1166,"properties":1173,"displayName":1175,"givenName":18,"familyName":18},"b1f588df-6a2c-4820-9e23-4cafb16996cb",[],[1167],{"id":1132,"sortIndex":19,"affiliation":1168,"properties":18},{"id":1132,"createTime":18,"updateTime":18,"relativeEntities":1169,"slug":18,"properties":1170,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1172,"statistic":18},[],{"title":1171},{"EN":1137},[],{"title":1174,"openalex":1176},{"EN":1175},"Crystal M. Holmes",{"VOID":1177},"A5032131225",{"url":18,"publisher":1179,"properties":1198},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1180,"slug":10,"properties":1181,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1184,"manageAffiliations":1185,"indexDatabases":1186,"url":38,"thumbnailPath":18,"statistic":1193,"gsStatistic":18,"type":80,"analyzePriority":18},[],{"issn":1182,"title":1183},{"VOID":13},{"EN":15},[],[],[1187],{"id":24,"indexDatabase":1188,"url":35,"indexYears":36,"academicFieldIds":18,"indexDatabaseRanking":37},{"id":26,"createTime":18,"updateTime":18,"relativeEntities":1189,"label":1190,"description":1191,"key":32,"publicationTags":1192,"standard":18},[],{"EN":29,"VI":29},{"EN":29,"VI":31},[34],{"impactFactor":19,"impactFactorByYear":1194,"i10Index":49,"i10IndexLast5Year":50,"totalPublication":51,"totalPublicationByYear":1195,"totalCitation":61,"totalCitationByYear":1196,"totalCitationPerPublication":71,"totalCitationPerPublicationByYear":1197,"hindexLast5Year":49,"hindex":49},{"2016":41,"2017":42,"2018":43,"2019":44,"2020":45,"2021":46,"2022":47,"2023":48},{"2015":53,"2016":54,"2017":54,"2018":55,"2019":49,"2020":56,"2021":57,"2022":58,"2023":59,"2024":60},{"2015":63,"2016":64,"2017":65,"2018":66,"2019":67,"2020":68,"2021":69,"2022":70},{"2015":73,"2016":74,"2017":75,"2018":76,"2019":77,"2020":78,"2021":44,"2022":79},{"issue":1199,"volume":1200},{"VOID":245},{"VOID":1201},"5",{"total":19,"publishYear":1203,"statisticByYear":1204},2019,{},"2019-12-01",[37],[1208,1211,1215,1219,1223,1227,1231,1235,1239,1242,1246,1250,1254,1258,1262,1266,1270,1274,1278,1282,1286,1290,1294,1298,1301,1305,1308,1312,1315,1319,1323,1326,1330,1333,1337,1341,1345,1349,1353,1357,1361,1364],{"id":18,"text":1209,"url":18,"identifiers":1210},"National Diabetes Statistics Report. 2017 [cited 17 September 2019]. Available from: \nhttps:\u002F\u002Fwww.cdc.gov\u002Fdiabetes\u002Fpdfs\u002Fdata\u002Fstatistics\u002Fnational-diabetes-statistics-report.pdf",{},{"id":18,"text":1212,"url":18,"identifiers":1213},"Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. Jama. 2005;293(2):217–28.",{"doi":1214},"10.1001\u002Fjama.293.2.217",{"id":18,"text":1216,"url":18,"identifiers":1217},"Armstrong DG, Boulton AJM, Bus SA. Diabetic foot ulcers and their recurrence. N Engl J Med. 2017;376(24):2367–75.",{"doi":1218},"10.1056\u002FNEJMra1615439",{"id":18,"text":1220,"url":18,"identifiers":1221},"Boyko EJ, Ahroni JH, Smith DG, Davignon D. Increased mortality associated with diabetic foot ulcer. Diabetic Med. 1996;13(11):967–72.",{"doi":1222},"10.1002\u002F(SICI)1096-9136(199611)13:11\u003C967::AID-DIA266>3.0.CO;2-K",{"id":18,"text":1224,"url":18,"identifiers":1225},"Boulton AJ. The pathogenesis of diabetic foot problems: an overview. Diabetic Med. 1996;13(Suppl 1):S12–6.",{"doi":1226},"10.1002\u002Fdme.1996.13.s1.12",{"id":18,"text":1228,"url":18,"identifiers":1229},"Boulton AJ. The pathway to foot ulceration in diabetes. Med Clin North Am. 2013;97(5):775–90.",{"doi":1230},"10.1016\u002Fj.mcna.2013.03.007",{"id":18,"text":1232,"url":18,"identifiers":1233},"Boulton AJ, Malik RA, Arezzo JC, Sosenko JM. Diabetic somatic neuropathies. Diabetes Care. 2004;27(6):1458–86.",{"doi":1234},"10.2337\u002Fdiacare.27.6.1458",{"id":18,"text":1236,"url":18,"identifiers":1237},"Pop-Busui R, Boulton AJ, Feldman EL, Bril V, Freeman R, Malik RA, et al. Diabetic neuropathy: a position statement by the American Diabetes Association. Diabetes Care. 2017;40(1):136–54.",{"doi":1238},"10.2337\u002Fdc16-2042",{"id":18,"text":1240,"url":18,"identifiers":1241},"National Institute of Neurological Disorders and Stroke: Peripheral Neuropathy Fact Sheet. 2019 [cited 17 September 2019]. Available from: \nhttps:\u002F\u002Fwww.ninds.nih.gov\u002FDisorders\u002FPatient-Caregiver-Education\u002FFact-Sheets\u002FPeripheral-Neuropathy-Fact-Sheet",{},{"id":18,"text":1243,"url":18,"identifiers":1244},"Albers JW, Pop-Busui R. Diabetic neuropathy: mechanisms, emerging treatments, and subtypes. Curr Neurol Neurosci Rep. 2014;14(8):473.",{"doi":1245},"10.1007\u002Fs11910-014-0473-5",{"id":18,"text":1247,"url":18,"identifiers":1248},"Bansal V, Kalita J, Misra UK. Diabetic neuropathy. Postgrad Med J. 2006;82:95–100.",{"doi":1249},"10.1136\u002Fpgmj.2005.036137",{"id":18,"text":1251,"url":18,"identifiers":1252},"Boulton AJ. Diabetic neuropathy: is pain God's greatest gift to mankind? Semin Vasc Surg. 2012;25(2):61–5.",{"doi":1253},"10.1053\u002Fj.semvascsurg.2012.04.009",{"id":18,"text":1255,"url":18,"identifiers":1256},"Almurdhi MM, Reeves ND, Bowling FL, Boulton AJ, Jeziorska M, Malik RA. Reduced lower-limb muscle strength and volume in patients with type 2 diabetes in relation to neuropathy, intramuscular fat, and vitamin D levels. Diabetes Care. 2016;39(3):441–7.",{"doi":1257},"10.2337\u002Fdc15-0995",{"id":18,"text":1259,"url":18,"identifiers":1260},"Bus SA, Maas M, Michels RP, Levi M. Role of intrinsic muscle atrophy in the etiology of claw toe deformity in diabetic neuropathy may not be as straightforward as widely believed. Diabetes Care. 2009;32(6):1063–7.",{"doi":1261},"10.2337\u002Fdc08-2174",{"id":18,"text":1263,"url":18,"identifiers":1264},"Allan J, Munro W, Figgins E. Foot deformities within the diabetic foot and their influence on biomechanics: a review of the literature. Prosthetics Orthot Int. 2016;40(2):182–92.",{"doi":1265},"10.1177\u002F0309364615592705",{"id":18,"text":1267,"url":18,"identifiers":1268},"Andersen H. Motor dysfunction in diabetes. Diabetes Metab Res Rev. 2012;28(Suppl 1):89–92.",{"doi":1269},"10.1002\u002Fdmrr.2257",{"id":18,"text":1271,"url":18,"identifiers":1272},"Yavuz M, Ersen A, Hartos J, Lavery LA, Wukich DK, Hirschman GB, et al. Temperature as a causative factor in diabetic foot ulceration: a call to revisit ulcer Pathomechanics. J Am Podiatr Med Assoc. 2018.",{"doi":1273},"10.7547\u002F17-131",{"id":18,"text":1275,"url":18,"identifiers":1276},"Schmidt BM, Allison S, Wrobel JS. Describing normative foot temperatures in patients with diabetes-related peripheral neuropathy. J Diabetes Sci Technol. 2019:1932296819864664.",{"doi":1277},"10.1177\u002F1932296819864664",{"id":18,"text":1279,"url":18,"identifiers":1280},"Meyr AJ SKE. Diabetic Driving Studies – Part 1: Brake Response Time in Diabetic Drivers With Lower Extremity Neuropathy. J Foot Ankle Surg. 2017;56:568–72.",{"doi":1281},"10.1053\u002Fj.jfas.2017.01.042",{"id":18,"text":1283,"url":18,"identifiers":1284},"Sansosti SKE, AJ LEM. Diabetic Driving Studies – Part 2: A Comparison of Brake Response Time Between Drivers With Diabetes With and Without Lower Extremity Sensorimotor Neuropathy. J Foot Ankle Surg. 2017;56:573–6.",{"doi":1285},"10.1053\u002Fj.jfas.2017.01.043",{"id":18,"text":1287,"url":18,"identifiers":1288},"Perazzolo M, Reeves ND, Bowling FL, Boulton AJM, Raffi M, Marple-Horvat DE. Altered accelerator pedal control in a driving simulator in people with diabetic peripheral neuropathy. Diabetic Med. 2019.",{"doi":1289},"10.1111\u002Fdme.13957",{"id":18,"text":1291,"url":18,"identifiers":1292},"Sansosti LE, Greene T, Hasenstein T, Berger M, Meyr AJ. U.S. State Driving Regulations Relevant to Foot and Ankle Surgeons. J Foot Ankle Surg. 2017;56(3):522–42.",{"doi":1293},"10.1053\u002Fj.jfas.2017.01.022",{"id":18,"text":1295,"url":18,"identifiers":1296},"Rajput B, Abboud RJ. The inadequate effect of automobile seating on foot posture and callus development. Ergonomics. 2007;50(1):131–7.",{"doi":1297},"10.1080\u002F00140130601032614",{"id":18,"text":1299,"url":18,"identifiers":1300},"National Highway Traffic Safety Administration:HYBRID III Fiftieth Percentile Male. 2014 [cited 16 September 2019]. Available from: \nhttp:\u002F\u002Fwww.nhtsa.gov.edgesuite-staging.net\u002FResearch\u002FHybrid+III+50th+Percentile+Male\u002F",{},{"id":18,"text":1302,"url":18,"identifiers":1303},"American Diabetes Association. Obesity Management for the Treatment of Type 2 Diabetes: Standards of Medical Care in Diabetes-2019. Diabetes care. 2019;42(Suppl 1):S81-s9.",{"doi":1304},"10.2337\u002Fdc19-S008",{"id":18,"text":1306,"url":18,"identifiers":1307},"Blana, E. Driving simulator validation studies: a literature review. University of Leeds 1996.",{},{"id":18,"text":1309,"url":18,"identifiers":1310},"Casutt G, Martin M, Keller M, Jancke L. The relation between performance in on-road driving, cognitive screening and driving simulator in older healthy drivers. Transp Res F. 2013.",{"doi":1311},"10.1016\u002Fj.trf.2013.12.007",{"id":18,"text":1313,"url":18,"identifiers":1314},"Hoskins AH, El-Gindy M. Technical report: Literature survey on driving simulator validation studies. International Journal of Heavy Vehicle Systems. 2006. [2], 241–252.",{},{"id":18,"text":1316,"url":18,"identifiers":1317},"Meuleners LB, Fraser M. A validation study of driving errors using a driving simulator. Transp Res F. 2015.",{"doi":1318},"10.1016\u002Fj.trf.2014.11.009",{"id":18,"text":1320,"url":18,"identifiers":1321},"Sahami S, Sayed S. How drivers adapt to drive in driving simulator, and what is the impact of practice scenario on the research? Transportation Research Part F. 2013. [16]:41–52.",{"doi":1322},"10.1016\u002Fj.trf.2012.08.003",{"id":18,"text":1324,"url":18,"identifiers":1325},"Yubin Xi JB, Paul Venhovens, Patrick Rosopa, John DesJardins, Shayne McConomy, Leah Belle, Nathalie Drouin, Sarah Hennessy, Kevin Kopera, Jeremy McKee, Stephanie Tanner, Constance, Truesdail KL, Loren Staplin. Understanding the Automotive Pedal Usage and Foot Movement Characteristics of Older Drivers. SAE Technical Paper. 2018.",{},{"id":18,"text":1327,"url":18,"identifiers":1328},"Sahil Garg SB, Shashank Gupta. Analysis of Automotive Control Pedals Ergonomics through Mathematical Modelling Based on Human Anthropometry. SAE Technical Paper. 2017.",{"doi":1329},"10.4271\u002F2017-26-0252",{"id":18,"text":1331,"url":18,"identifiers":1332},"Crandall JR, Martin P G, Bass C R, Pilkey W D, Dischinger, P C Burgess A R, O'Quinn T D, Schmidhauser C B. Foot and Ankle Injury: The Role of Driver Antrhopometry, Footwear, and Pedal Controls. Annual Proceedings of the Association for the Advancement of Automotive Medicine 1996.",{},{"id":18,"text":1334,"url":18,"identifiers":1335},"Morrison S, Colberg SR, Parson HK, Vinik AI. Relation between risk of falling and postural sway complexity in diabetes. Gait Posture 2012;35:662–668. pmid:22269128",{"doi":1336},"10.1016\u002Fj.gaitpost.2011.12.021",{"id":18,"text":1338,"url":18,"identifiers":1339},"Brown SJ, Handsaker JC, Bowling FL, Boulton AJ, Reeves ND. Diabetic peripheral neuropathy compromises balance during daily activities. Diabetes Care 2015;38:1116–1122. pmid:25765355.",{"doi":1340},"10.2337\u002Fdc14-1982",{"id":18,"text":1342,"url":18,"identifiers":1343},"Chihuri S, Mielenz TJ, DiMaggio CJ, Betz ME, DiGuiseppi C, Jones VC, et al. Driving cessation and health outcomes in older adults. J Am Geriatr Soc. 2016;64(2):332–41.",{"doi":1344},"10.1111\u002Fjgs.13931",{"id":18,"text":1346,"url":18,"identifiers":1347},"Choi M, Lohman MC, Mezuk B. Trajectories of cognitive decline by driving mobility: evidence from the health and retirement study. Int J Geriatr Psychiatry. 2014;29(5):447–53.",{"doi":1348},"10.1002\u002Fgps.4024",{"id":18,"text":1350,"url":18,"identifiers":1351},"Fonda SJ, Wallace RB, Herzog AR. Changes in driving patterns and worsening depressive symptoms among older adults. J Gerontol Ser B Psychol Sci Soc Sci. 2001;56(6):S343–51.",{"doi":1352},"10.1093\u002Fgeronb\u002F56.6.S343",{"id":18,"text":1354,"url":18,"identifiers":1355},"Marottoli RA, Mendes de Leon CF, Glass TA, Williams CS, Cooney LM Jr, Berkman LF, et al. Driving cessation and increased depressive symptoms: prospective evidence from the New Haven EPESE. Established Populations for Epidemiologic Studies of the Elderly. J Am Geriatr Soc. 1997;45(2):202–6.",{"doi":1356},"10.1111\u002Fj.1532-5415.1997.tb04508.x",{"id":18,"text":1358,"url":18,"identifiers":1359},"Ragland DR, Satariano WA, MacLeod KE. Driving cessation and increased depressive symptoms. J Gerontol A Biol Sci Med Sci. 2005;60(3):399–403.",{"doi":1360},"10.1093\u002Fgerona\u002F60.3.399",{"id":18,"text":1362,"url":18,"identifiers":1363},"Badescu SV, Tataru C, Kobylinska L, Georgescu EL, Zahiu DM, Zagrean AM, et al. The association between diabetes mellitus and depression. J Med Life. 2016;9(2):120–5.",{},{"id":18,"text":1365,"url":18,"identifiers":1366},"Natovich R, Kushnir T, Harman-Boehm I, Margalit D, Siev-Ner I, Tsalichin D, et al. Cognitive dysfunction: part and parcel of the diabetic foot. Diabetes Care.",{},{"id":1368,"createTime":1369,"updateTime":1370,"relativeEntities":1371,"slug":1372,"properties":1373,"entityType":103,"verifyStatus":104,"verifyTime":1370,"verifyNote":106,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1382,"fullTextUrl":18,"authors":1383,"publicationType":222,"publisherRelationship":1457,"citationCount":18,"citationInfo":18,"publishDate":1482,"publishYear":1483,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":1484,"openAccess":18,"references":18,"isForceReanalyzing":384},"acd99283-4b28-4707-b2ed-c81da5459648","2023-12-11T07:05:45.701+00:00","2025-02-23T01:47:23.880+00:00",[],"Study-of-single-nucleotide-polymorphism-of-vascular-endothelium-factor-in-patients-with-differentiated-thyroid-cancer",{"abstract":1374,"title":1376,"references":1378,"doi":1380},{"EN":1375},"Genetic alterations and high levels of the vascular endothelial growth factor (VEGF) are presumptive risk factors for differentiated thyroid cancer (DTC). This work aims to study the presence of − 634G\u002FC polymorphism of vascular endothelial growth factor (rs2010963) and its’ serum level in patients with DTC and comparing these results with those of the control subjects. The study was a retrograde case–control study that included seventy patients with DTCin addition to seventy apparently healthy control subjects. Blood sample was taken and subjected to study of − 634G\u002FC VEGF polymorphism (rs2010963) by real time PCR and measurement of its’ plasma level by immunoassay kit (ELISA). Regarding genotyping of VEGFA − 634G\u002FC (rs2010963) polymorphism, there was significant increase in CG and GG genotypes (28.6%, 18.6% respectively) among patients compared to control subjects (20.0%, 4.3% respectively) and significant increase in CC genotype in control subjects (75.7%) compared to patients (52.9%), P = 0.001. The VEGF mean ± SD level was significantly elevated in patients compared to control subjects (1215.81 ± 225.78 versus 307.16 ± 91.81, P = 0.006). Moreover, there was significant increase in VEGF levels in patients with CG and GG genotypes (1295.9 ± 68.74, 1533.08 ± 109.95, respectively) compared to patients with CC genotype (1061 163.25), P = 0.001). There was significant increase in GG and CG genotypes in patients with DTC compared to control subjects which may suggest a predisposing role for these genotypes in development of DTC. Moreover, there was significant increase in serum level of vascular endothelial growth factor in patients with GG and CG genotypes which may reflect the mechanism of these genotypes in development of DTC.",{"EN":1377},"Study of single nucleotide polymorphism of vascular endothelium factor in patients with differentiated thyroid cancer",{"VOID":1379},"Saenko VA, Rogounovitch TI. 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Association between single nucleotide variants of vascular endothelial growth factor A and the risk of thyroid carcinoma and nodular goiter in a Han Chinese population. Oncotarget. 2017;8(9):15838–45.\nHe H, Li W, Liyanarachchi S, Srinivas M, Wang Y, Akagi K, Wu D, Wang Q, Jin V, Symer DE, Shen R, Phay J, Nagy R, et al. Multiple functional variants in long-range enhancer elements contribute to the risk of SNP rs965513 in thyroid cancer. Proc Natl Acad Sci U S A. 2015;112:6128–33.\nWeis SM, Cheresh DA. Tumor angiogenesis: molecular pathways and therapeutic targets. Nat Med. 2011;17(11):1359–70.\nWang Z, Dabrosin C, Yin X, Fuster MM, Arreola A, Rathmell WK, et al. Broad targeting of angiogenesis for cancer prevention andtherapy. Semin Cancer Biol. 2015;35 Suppl:S224-43.\nKammerer PW, Toyoshima T, Eletr S, Kämmerer P, Kuhr K, Al-Nawas B, Brieger J. Single nucleotide polymorphisms of the vascular endothelial growth factor gene associated with incidence of oral squamous cell carcinoma. J Oral Pathol Med. 2010;39:786–92.\nYang PW, Hsieh MS, Huang YC, Hsieh CY, Chiang TH, Lee JM. Genetic variants of EGF and VEGF predict prognosis of patients with advanced esophageal squamous cell carcinoma. PLoS One. 2014;9:e100326.\nVincenti V, Cassano C, Rocchi M, Persico G. Assignment of the vascular endothelial growth factor gene to human chromosome 6p21.3. Circulation. 1996;93:1493–5.\nLiu W, Dong Z, Hu R, Wang C. Association of vascular endothelial growth factor (VEGF) gene polymorphisms with gastric cancer and its development, prognosis, and survival. Technol Cancer Res Treat. 2018;17:1533034617753810.\nYu W, Jiang X, Bai T, Lv X, Chang F. Association between + 936 C > T gene polymorphism of vascular endothelial growth factor and lung cancer: a meta-analysis. Cancer Biomark. 2014;14:483–92.\nMaeda A, Nakata M, Yasuda K, Yukawa T, Saisho S, Okita R, et al. Influence of vascular endothelial growth factor single nucleotide polymorphisms on non-small cell lung cancer tumor angiogenesis. Oncol Rep. 2013;29:39–44.\nJain L, Vargo CA, Danesi R, Sissung TM, Price DK, Venzon D, et al. The role of vascular endothelial growth factor SNPs as predictive and prognostic markers for major solid tumors. Mol Cancer Ther. 2009;8(9):2496–508.\nWatson CJ, Webb NJ, Bottomley MJ, Brenchley PE. Identification of polymorphisms within the vascular endothelial growth factor (VEGF) gene: correlation with variation in VEGF protein production. Cytokine. 2000;12(8):1232–5. https:\u002F\u002Fdoi.org\u002F10.1006\u002Fcyto.2000.0692. PMID: 10930302.\nSkrypnik D, Mostowska A, Jagodziński PP, Bogdański P. Association of rs699947 (-2578 C\u002FA) and rs2010963 (-634 G\u002FC) single nucleotide polymorphisms of the VEGF gene, VEGF-A and leptin serum level, and cardiovascular risk in patients with excess body mass: a case-control study. J Clin Med. 2020;9(2):469. https:\u002F\u002Fdoi.org\u002F10.3390\u002Fjcm9020469. PMID: 32046348; PMCID: PMC7073834.\nKhosroshahi NS, Pouladi N, Shavali M, Ghafouri F, Abdolahi S, Feizi MA. Association of – 634 G > C VEGF-A polymorphism in thyroid cancer patients in Northwest of Iran. Meta Gene. 2019;22:100611. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.mgene.2019.100611.\nTuttle RM, Haugen B, Perrier ND. Updated American Joint Committee on cancer\u002Ftumor-node-metastasis staging system for differentiated and anaplastic thyroid cancer (eighth edition): what changed and why? Thyroid. 2017;27(6):751–6.\nPasieka Z, Stępień H, Komorowski J, Kołomecki K, Kuzdak K. Evaluation of the Levels of bFGF, VEGF, sICAM-1, and sVCAM-1 in Serum of Patients with Thyroid Cancer Molecular Staging of Cancer. 2003;162. ISBN: 978-3-642-63945-6.\nFellmer PT, Sato K, Tanaka R, Okamoto T, Kato Y, Kobayashi M, et al. 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Cancer Biother Radiopharm. 2005;20:648–61. https:\u002F\u002Fdoi.org\u002F10.1089\u002Fcbr.2005.20.648.\nLewy-Trenda I, Wierzchniewska-Ławska A. Expression of vascular endothelial growth factor (VEGF) in hu-man thyroid tumors. Pol J Pathol. 2002;53:129–32.\nBunone G, Vigneri P, Mariani L, Butó S, Collini P, Pilotti S, Pierotti MA, Bongarzone I. Expression of angiogenesis stimulators and inhibitors in human thyroid tumors and correlation with clinical pathological features. Am J Pathol. 1999;155:1967–76.\nMelaccio A, Sgaramella LI, Pasculli A, Di Meo G, Gurrado A, Prete FP, Vacca A, Ria R, Testini M. Prognostic and therapeutic role of angiogenic microenvironment in thyroid cancer. Cancers (Basel). 2021;13(11):2775. https:\u002F\u002Fdoi.org\u002F10.3390\u002Fcancers13112775.\nSalajegheh A, Kasem RS, Gopalan K, Nassiri V, William MR, Lam R. Single nucleotide polymorphisms and mRNA expression of VEGF-A in papillary thyroid carcinoma: potential markers for aggressive phenotypes. 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IRF1 inhibits the proliferation and metastasis of colorectal cancer by suppressing the RAS-RAC1 pathway. Cancer Manag Res. 2019;11:369.\nStoltz KP, Jondle CN, Pulakanti K, Sylvester PA, Urrutia R, Rao S, Tarakanova VL. Tumor suppressor interferon regulatory factor 1 selectively blocks expression of endogenous retrovirus. Virology. 2019;526:52–60.\nTamura T, Yanai H, Savitsky D, Taniguchi T. The IRF family transcription factors in immunity and oncogenesis. Annu Rev Immunol. 2008;26:535–84.\nSafavi A, Azizi F, Jafari R, Chaibakhsh S, Safavi AA. Thyroid cancer epidemiology in Iran: a time trend study. Asian Pac J Cancer Prev. 2016;17(1):407–12.\nBelletti B, Ferraro P, Arra C, Baldassarre G, Bruni P, Staibano S, et al. Modulation of in vivo growth of thyroid tumor-derived cell lines by sense and antisense vascular endothelial growth factor gene. Oncogene. 1999;18:4860–9.\nGood DJ, Polverini PJ, Rastinejad F, Le Beau MM, Lemons RS, Frazier WA, Bouck NP. A tumor suppressor-dependent inhibitor of angiogenesis is immunologically and functionally indistinguishable from a fragment of thrombospondin. Proc Natl Acad Sci USA. 1990;87:6624–8. https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.87.17.6624.\nHaytaoglu G, Kuzu F, Arpaci D, et al. Correlation of vascular endothelial growth factor and vascular endothelial growth factor receptor-1 levels in serum and thyroid nodules with histopathological and radiological variables. J Lab Physicians. 2019;11(1):51–7.",{"VOID":1381},"10.1186\u002Fs40842-022-00146-x","https:\u002F\u002Fclindiabetesendo.biomedcentral.com\u002Farticles\u002F10.1186\u002Fs40842-022-00146-x",[1384,1399,1414,1429,1444],{"id":1385,"sortIndex":19,"researcher":18,"roles":1386,"affiliations":1387,"properties":1396,"displayName":1398,"givenName":18,"familyName":18},"61aef792-e086-4a22-bb16-85d7d35456b7",[554],[1388],{"id":1389,"sortIndex":19,"affiliation":1390,"properties":18},"d9a8cefa-0d02-4012-a1ae-59793e183386",{"id":1389,"createTime":18,"updateTime":18,"relativeEntities":1391,"slug":18,"properties":1392,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1395,"statistic":18},[],{"title":1393},{"VI":1394},"Internal Medicine Department, Mansoura Faculty of Medicine, Mansoura University, Mansoura, Egypt",[],{"title":1397},{"VI":1398},"Mohamad Mohsen Motawea",{"id":1400,"sortIndex":134,"researcher":18,"roles":1401,"affiliations":1402,"properties":1411,"displayName":1413,"givenName":18,"familyName":18},"48daabf5-2aa3-4f18-98c0-cdb8bd660b25",[554],[1403],{"id":1404,"sortIndex":19,"affiliation":1405,"properties":18},"3bfba9ca-a165-411a-bd70-92c6cc064402",{"id":1404,"createTime":18,"updateTime":18,"relativeEntities":1406,"slug":18,"properties":1407,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1410,"statistic":18},[],{"title":1408},{"VI":1409},"Clinical Pathology Department, Mansoura faculty of Medicine, Mansoura University, Mansoura, Egypt",[],{"title":1412},{"VI":1413},"Maysaa El Sayed Zaki",{"id":1415,"sortIndex":150,"researcher":18,"roles":1416,"affiliations":1417,"properties":1426,"displayName":1428,"givenName":18,"familyName":18},"f492de25-8cbd-49b6-acdf-7e377a47f673",[554],[1418],{"id":1419,"sortIndex":19,"affiliation":1420,"properties":18},"144c23bf-a08d-44f3-9997-e58ba058223f",{"id":1419,"createTime":18,"updateTime":18,"relativeEntities":1421,"slug":18,"properties":1422,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1425,"statistic":18},[],{"title":1423},{"VI":1424},"Oncology Department, Mansoura Faculty of Medicine, Mansoura University, Mansoura, Egypt",[],{"title":1427},{"VI":1428},"Maha Saif",{"id":1430,"sortIndex":70,"researcher":18,"roles":1431,"affiliations":1432,"properties":1441,"displayName":1443,"givenName":18,"familyName":18},"3bda0874-7a58-47fb-bff6-460fc1273390",[554],[1433],{"id":1434,"sortIndex":19,"affiliation":1435,"properties":18},"cc003856-9786-4556-b86d-9d956488a9e1",{"id":1434,"createTime":18,"updateTime":18,"relativeEntities":1436,"slug":18,"properties":1437,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1440,"statistic":18},[],{"title":1438},{"VI":1439},"Clinical Pathology Department, Assuit Faculty of Medicine, Assuit University, Assiut, Egypt",[],{"title":1442},{"VI":1443},"Asmaa Osama BS Osman",{"id":1445,"sortIndex":185,"researcher":18,"roles":1446,"affiliations":1447,"properties":1454,"displayName":1456,"givenName":18,"familyName":18},"7253e39a-b4c9-47dd-8a9d-f62df86059d8",[554],[1448],{"id":1389,"sortIndex":19,"affiliation":1449,"properties":18},{"id":1389,"createTime":18,"updateTime":18,"relativeEntities":1450,"slug":18,"properties":1451,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":1453,"statistic":18},[],{"title":1452},{"VI":1394},[],{"title":1455},{"VI":1456},"Aml Mohamed Nada",{"url":1382,"publisher":1458,"properties":1477},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":1459,"slug":10,"properties":1460,"entityType":16,"verifyStatus":17,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":19,"subjectFields":1463,"manageAffiliations":1464,"indexDatabases":1465,"url":38,"thumbnailPath":18,"statistic":1472,"gsStatistic":18,"type":80,"analyzePriority":18},[],{"issn":1461,"title":1462},{"VOID":13},{"EN":15},[],[],[1466],{"id":24,"indexDatabase":1467,"url":35,"indexYears":36,"academicFieldIds":18,"indexDatabaseRanking":37},{"id":26,"createTime":18,"updateTime":18,"relativeEntities":1468,"label":1469,"description":1470,"key":32,"publicationTags":1471,"standard":18},[],{"EN":29,"VI":29},{"EN":29,"VI":31},[34],{"impactFactor":19,"impactFactorByYear":1473,"i10Index":49,"i10IndexLast5Year":50,"totalPublication":51,"totalPublicationByYear":1474,"totalCitation":61,"totalCitationByYear":1475,"totalCitationPerPublication":71,"totalCitationPerPublicationByYear":1476,"hindexLast5Year":49,"hindex":49},{"2016":41,"2017":42,"2018":43,"2019":44,"2020":45,"2021":46,"2022":47,"2023":48},{"2015":53,"2016":54,"2017":54,"2018":55,"2019":49,"2020":56,"2021":57,"2022":58,"2023":59,"2024":60},{"2015":63,"2016":64,"2017":65,"2018":66,"2019":67,"2020":68,"2021":69,"2022":70},{"2015":73,"2016":74,"2017":75,"2018":76,"2019":77,"2020":78,"2021":44,"2022":79},{"pages":1478,"volume":1480},{"VOID":1479},"1-7",{"VOID":1481},"8","2022-12-15",2022,[37],{"id":1486,"createTime":1487,"updateTime":1488,"relativeEntities":1489,"slug":1490,"properties":1491,"entityType":103,"verifyStatus":104,"verifyTime":1488,"verifyNote":106,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1500,"fullTextUrl":18,"authors":1501,"publicationType":222,"publisherRelationship":1708,"citationCount":18,"citationInfo":18,"publishDate":1733,"publishYear":1734,"citationAnalyzeStatus":17,"lastCitationAnalyze":18,"indexDatabases":1735,"openAccess":18,"references":18,"isForceReanalyzing":384},"e74aaf42-1f4a-49d9-b2df-3440e076102a","2023-11-28T05:17:34.395+00:00","2025-02-22T21:03:09.826+00:00",[],"Potential-association-of-LMNA-associated-generalized-lipodystrophy-with-juvenile-dermatomyositis",{"abstract":1492,"title":1494,"references":1496,"doi":1498},{"EN":1493},"Juvenile dermatomyositis (JDM) is an auto-immune muscle disease which presents with skin manifestations and muscle weakness. At least 10% of the patients with JDM present with acquired lipodystrophy. Laminopathies are caused by mutations in the lamin genes and cover a wide spectrum of diseases including muscular dystrophies and lipodystrophy. The p.T10I LMNA variant is associated with a phenotype of generalized lipodystrophy that has also been called atypical progeroid syndrome. A previously healthy female presented with bilateral proximal lower extremity muscle weakness at age 4. She was diagnosed with JDM based on her clinical presentation, laboratory tests and magnetic resonance imaging (MRI). She had subcutaneous fat loss which started in her extremities and progressed to her whole body. At age 7, she had diabetes, hypertriglyceridemia, low leptin levels and low body fat on dual energy X-ray absorptiometry (DEXA) scan, and was diagnosed with acquired generalized lipodystrophy (AGL). Whole exome sequencing (WES) revealed a heterozygous c.29C > T; p.T10I missense pathogenic variant in LMNA, which encodes lamins A and C. Muscle biopsy confirmed JDM rather than muscular dystrophy, showing perifascicular atrophy and perivascular mononuclear cell infiltration. Immunofluroscence of skin fibroblasts confirmed nuclear atypia and fragmentation. This is a unique case with p.T10I LMNA variant displaying concurrent JDM and AGL. This co-occurrence raises the intriguing possibility that LMNA, and possibly p.T10I, may have a pathogenic role in not only the occurrence of generalized lipodystrophy, but also juvenile dermatomyositis. Careful phenotypic characterization of additional patients with laminopathies as well as individuals with JDM is warranted.",{"EN":1495},"Potential association of LMNA-associated generalized lipodystrophy with juvenile dermatomyositis",{"VOID":1497},"Bingham A, Mamyrova G, Rother KI, Oral E, Cochran E, Premkumar A, Kleiner D, James-Newton L, Targoff IN, Pandey JP, Carrick DM, Sebring N, O'Hanlon TP, Ruiz-Hidalgo M, Turner M, Gordon LB, Laborda J, Bauer SR, Blackshear PJ, Imundo L, Miller FW, Rider LG. Childhood myositis heterogeneity study G. Predictors of acquired lipodystrophy in juvenile-onset dermatomyositis and a gradient of severity. Medicine (Baltimore). 2008;87:70–86.\nLebastchi J, Ajluni N, Neidert A, Oral EA. A report of three cases with acquired generalized lipodystrophy with distinct autoimmune conditions treated with Metreleptin. J Clin Endocrinol Metab. 2015;100:3967–70.\nAjluni N, Meral R, Neidert AH, Brady GF, Buras E, McKenna B, DiPaola F, Chenevert TL, Horowitz JF, Buggs-Saxton C, Rupani AR, Thomas PE, Tayeh MK, Innis JW, Omary MB, Conjeevaram H, Oral EA. Spectrum of disease associated with partial lipodystrophy: lessons from a trial cohort. Clin Endocrinol. 2017;86:698–707.\nGarg A, Subramanyam L, Agarwal AK, Simha V, Levine B, D'Apice MR, Novelli G, Crow Y. Atypical progeroid syndrome due to heterozygous missense LMNA mutations. J Clin Endocrinol Metab. 2009;94:4971–83.\nMory PB, Crispim F, Kasamatsu T, Gabbay MA, Dib SA, Moises RS. Atypical generalized lipoatrophy and severe insulin resistance due to a heterozygous LMNA p.T10I mutation. Arquivos brasileiros de endocrinologia e metabologia. 2008;52:1252–6.\nHussain I, Patni N, Ueda M, Sorkina E, Valerio CM, Cochran E, Brown RJ, Peeden J, Tikhonovich Y, Tiulpakov A, Stender SRS, Klouda E, Tayeh MK, Innis J, Meyer A, Lal P, Godoy-Matos AF, Teles MG, Adams-Huet B, Rader DJ, Hegele RA, Oral EA, Garg A A Novel Generalized Lipodystrophy-associated Progeroid Syndrome due to recurrent heterozygous LMNA p.T10I Mutation. J Clin Endocrinol Metab. 2017;103(3);1005-14.\nCardona-Hernandez R, Suarez-Ortega L, Torres M. Difficult to manage diabetes mellitus associated with generalized congenital lipodystrophy. Report of two cases. Anales de pediatria (Barcelona, Spain : 2003). 2011;74:126–30.\nCsoka AB, Cao H, Sammak PJ, Constantinescu D, Schatten GP, Hegele RA. Novel Lamin a\u002FC gene (LMNA) mutations in atypical progeroid syndromes. J Med Genet. 2004;41:304–8.\nKwan R, Brady GF, Brzozowski M, Weerasinghe SV, Martin H, Park MJ, Brunt MJ, Menon RK, Tong X, Yin L, Stewart CL, Omary MB. Hepatocyte-specific deletion of mouse Lamin a\u002FC leads to male-selective steatohepatitis. Cellular and molecular gastroenterology and hepatology. 2017;4:365–83.\nTaranum S, Vaylann E, Meinke P, Abraham S, Yang L, Neumann S, Karakesisoglou I, Wehnert M, Noegel AA. LINC complex alterations in DMD and EDMD\u002FCMT fibroblasts. Eur J Cell Biol. 2012;91:614–28.\nGreenberg SA, Pinkus JL, Amato AA. Nuclear membrane proteins are present within rimmed vacuoles in inclusion-body myositis. Muscle Nerve. 2006;34:406–16.\nKomaki H, Hayashi YK, Tsuburaya R, Sugie K, Kato M, Nagai T, Imataka G, Suzuki S, Saitoh S, Asahina N, Honke K, Higuchi Y, Sakuma H, Saito Y, Nakagawa E, Sugai K, Sasaki M, Nonaka I, Nishino I. Inflammatory changes in infantile-onset LMNA-associated myopathy. Neuromuscular disorders : NMD. 2011;21:563–8.\nMoraitis E, Foley AR, Pilkington CA, Manzur AY, Quinlivan R, Jacques TS, Phadke R, Compeyrot-Lacassagne S. Infantile-onset LMNA-associated muscular dystrophy mimicking juvenile idiopathic inflammatory myopathy. J Rheumatol. 2015;42:1064–6.\nLuo YB, Mitrpant C, Johnsen R, Fabian V, Needham M, Fletcher S, Wilton SD, Mastaglia FL. Investigation of splicing changes and post-translational processing of LMNA in sporadic inclusion body myositis. Int J Clin Exp Pathol. 2013;6:1723–33.\nQuijano-Roy S, Mbieleu B, Bonnemann CG, Jeannet PY, Colomer J, Clarke NF, Cuisset JM, Roper H, De Meirleir L, D'Amico A, Ben Yaou R, Nascimento A, Barois A, Demay L, Bertini E, Ferreiro A, Sewry CA, Romero NB, Ryan M, Muntoni F, Guicheney P, Richard P, Bonne G, Estournet B. De novo LMNA mutations cause a new form of congenital muscular dystrophy. Ann Neurol. 2008;64:177–86.\nMiller FW, Cooper RG, Vencovsky J, Rider LG, Danko K, Wedderburn LR, Lundberg IE, Pachman LM, Reed AM, Ytterberg SR, Padyukov L, Selva-O’ Callaghan A, Radstake TR, Isenberg DA, Chinoy H, Ollier WE, O'Hanlon TP, Peng B, Lee A, Lamb JA, Chen W, Amos CI, Gregersen PK. Genome-wide association study of dermatomyositis reveals genetic overlap with other autoimmune disorders. 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