{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T18:43:51Z","timestamp":1777920231070,"version":"3.51.4"},"reference-count":21,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[1985,7,1]],"date-time":"1985-07-01T00:00:00Z","timestamp":489024000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Vet Pathol"],"published-print":{"date-parts":[[1985,7]]},"abstract":"<jats:p>Pelger-Hu\u00ebt anomaly was diagnosed in a young male cat on the basis of persistent nuclear hyposegmentation of blood granulocytes, absence of clinical disease or feline leukemia virus infection, and demonstration of genetic transmission of the anomaly. Neutrophils, eosinophils, basophils, and monocytes had significantly less nuclear segmentation when compared to similar leukocyte types from a control cat. On smears of bone marrow, megakaryocytes also appeared hyposegmented. A test mating with an unaffected queen produced a litter of five kittens (three males, two females). One male and one female kitten had the Pelger-Hu\u00ebt trait on examination of blood smears. Autosomal dominant transmission of this anomaly is suspected based on these findings.<\/jats:p>","DOI":"10.1177\/030098588502200412","type":"journal-article","created":{"date-parts":[[2017,1,11]],"date-time":"2017-01-11T15:17:32Z","timestamp":1484147852000},"page":"370-374","source":"Crossref","is-referenced-by-count":24,"title":["Pelger-Hu\u00ebt Anomaly in Cats"],"prefix":"10.1177","volume":"22","author":[{"given":"K. 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