{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:49:52Z","timestamp":1787014192997,"version":"build-2736575974"},"reference-count":42,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2019,2,7]],"date-time":"2019-02-07T00:00:00Z","timestamp":1549497600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["beva.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Equine Veterinary Journal"],"published-print":{"date-parts":[[2019,9]]},"abstract":"Summary<\/jats:title>\n \n Background<\/jats:title>\n Continuous digital hypothermia can prevent the development and progression of laminitis associated with sepsis but its effects on laminitis due to hyperinsulinaemia are unknown.<\/jats:p>\n <\/jats:sec>\n \n Objectives<\/jats:title>\n To determine the effects of continuous digital hypothermia on laminitis development in the euglycaemic hyperinsulinaemic clamp model.<\/jats:p>\n <\/jats:sec>\n \n Study design<\/jats:title>\n Randomised, controlled (within subject), blinded, experiment.<\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n Eight clinically normal Standardbred horses underwent laminitis induction using the euglycaemic hyperinsulinaemic clamp model (\n EHC<\/jats:styled-content>\n ). At initiation of the\n EHC<\/jats:styled-content>\n , one forelimb was continuously cooled (\n ICE<\/jats:styled-content>\n ), with the other maintained at ambient temperature (\n AMB<\/jats:styled-content>\n ). Dorsal lamellar sections (proximal, middle, distal) were harvested 48\u00a0h after initiation of the\n EHC<\/jats:styled-content>\n and were analysed using histological scoring (0\u20133) and histomorphometry. Cellular proliferation was quantified by counting epidermal cell nuclei staining positive with an immunohistochemical proliferation marker (\n TPX<\/jats:styled-content>\n 2).\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Severe elongation and disruption of\n SEL<\/jats:styled-content>\n with dermo\u2010epidermal separation (score of 3) was observed in all\n AMB<\/jats:styled-content>\n feet at one or more section locations, but was not observed in any\n ICE<\/jats:styled-content>\n sections. Overall 92% of the\n AMB<\/jats:styled-content>\n sections received the most severe histological score (grade 3) and 8% were grade 2, whereas\n ICE<\/jats:styled-content>\n sections were classified as either grade 1 (50%) or grade 2 (50%). Relative to\n AMB<\/jats:styled-content>\n feet,\n ICE<\/jats:styled-content>\n sections were 98% less likely to exhibit grades 2 or 3 (\n OR<\/jats:styled-content>\n : 0.02, 95%\n CI<\/jats:styled-content>\n 0.001, 0.365; P<0.01). Histomorphometry measurements of total and nonkeratinised primary epidermal lamellar length were significantly increased (P<0.01) in\n AMB<\/jats:styled-content>\n limbs compared with\n ICE<\/jats:styled-content>\n .\n TPX<\/jats:styled-content>\n 2 positive cell counts were significantly increased (P<0.01) in\n AMB<\/jats:styled-content>\n limbs compared with\n ICE<\/jats:styled-content>\n .\n <\/jats:p>\n <\/jats:sec>\n \n Main limitations<\/jats:title>\n Continuous digital hypothermia was initiated before recognition of laminitis and therefore the clinical applicability requires further investigation.<\/jats:p>\n <\/jats:sec>\n \n Conclusions<\/jats:title>\n \n Continuous digital hypothermia reduced the severity of laminitis in the\n EHC<\/jats:styled-content>\n model and prevented histological lesions compatible with lamellar structural failure.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1111\/evj.13072","type":"journal-article","created":{"date-parts":[[2019,1,13]],"date-time":"2019-01-13T06:54:36Z","timestamp":1547362476000},"page":"658-664","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Continuous digital hypothermia prevents lamellar failure in the euglycaemic hyperinsulinaemic clamp model of equine laminitis"],"prefix":"10.1111","volume":"51","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0250-5849","authenticated-orcid":false,"given":"S. M.","family":"Stokes","sequence":"first","affiliation":[{"name":"Australian Equine Laminitis Research Unit School of Veterinary Science the University of Queensland Gatton Queensland Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. K.","family":"Belknap","sequence":"additional","affiliation":[{"name":"Department of Veterinary Clinical Sciences College of Veterinary Medicine the Ohio State University Columbus Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9057-2093","authenticated-orcid":false,"given":"J. B.","family":"Engiles","sequence":"additional","affiliation":[{"name":"New Bolton Center Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Kennett Square Pennsylvania USA"},{"name":"New Bolton Center Pathobiology School of Veterinary Medicine University of Pennsylvania Kennett Square Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D.","family":"Stefanovski","sequence":"additional","affiliation":[{"name":"New Bolton Center Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Kennett Square Pennsylvania USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2820-8431","authenticated-orcid":false,"given":"F. 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