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V Welch

Publications and source records attributed to V Welch.

40 records · Page 3Linked to original sources
PubMed1993

Ovine myeloencephalitis-leukomyelomalacia associated with a Sarcocystis-like protozoan.

Bilateral pelvic limb paresis developed in 7 of 15 10-month-old Blueface Leicester ram lambs on a mixed enterprise farm in the North of England. Clinical signs were principally mild to severe paresis of the pelvic limbs. Two mildly affected lambs recovered. Multifocal spinal cord white matter edema and necrosis, glial nodules, and mild to moderate nonsuppurative encephalomyelitis were the principal findings in 3 severely paretic lambs examined histologically. Protozoan bodies (12.7-23.0 microns) that stained immunocytochemically for Sarcocystis epitopes were in spinal cord glial cells of 2 of 3 lambs. Protozoa did not react immunocytochemically with anti-Toxoplasma gondii or Neospora canium antisera. Serology indicated there was recent exposure to Sarcocystis spp. in some surviving lambs. These cases resembled those in previous reports of paresis due to an unidentified Sarcocystis-like protozoan in sheep (ovine protozoan myeloencephalitis) in the British Isles, the USA, France, Australia, and New Zealand.

Animals↗
PubMed1991

Importance of bile acid structure in amelioration of griseofulvin-induced murine protoporphyric hepatopathy.

This study investigated the effects of bile acid structure on griseofulvin-induced murine hepatopathy and explored the mechanism(s) of cholestasis in this model of protoporphyria. Mice were fed pulverized chow with cholate, chenodeoxycholate, or ursodeoxycholate, with or without griseofulvin. After 1 to 4 weeks, bile flow, bile acid excretion and composition, biliary protoporphyrin excretion, hepatic protoporphyrin contents, liver histology, and griseofulvin plasma concentrations were determined. Additionally, bile acid absorption was measured. Griseofulvin induced a progressive increase in liver weight, hepatic protoporphyrin content, and histopathologic evidence of cholestasis. Biliary protoporphyrin excretion increased and pigmented gallbladder microliths developed. Bile flow and bile acid excretion fell in relation to liver weight but not in relation to body weight. Cholic acid augmented biliary protoporphyrin excretion, markedly reduced hepatic protoporphyrin content, and obviated the development of intrahepatic biliary thrombi. Ursodeoxycholate and chenodeoxycholate both reduced biliary protoporphyrin excretion. This was associated with bile acid compositional changes, particularly a fall in cholic acid. Although histopathologic abnormalities were not altered, these bile acids reduced hepatic protoporphyrin contents. Bile acid treatments with griseofulvin all increased bile flow and bile acid excretion relative to controls, but differences in the relationship of bile flow to bile acid structure on protoporphyrin disposition. They document biliary excretion as the principal mode of cholic acid amelioration of griseofulvin-induced hepatopathy. They also suggest distinctive roles for griseofulvin and protoporphyrin in the generation of the cholestasis.

Absorption↗