Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mange caused by Sarcoptes scabiei var. vulpes appeared among red foxes (Vulpes vulpes) in Scandinavia (south-west Finland) for the first time in this century in 1967. The disease was most probably introduced by foxes crossing the Gulf of Finland from Estonia. The mange epizootic spread northwards through Finland and reached Sweden in late 1975, when mangy foxes appeared in the northern part of the country. In 1984, mange was observed in most parts of Sweden. The disease was observed to spread rapidly in boreal areas, whereas it spread more slowly in agricultural areas. Mortality due to mange was very high. The duration of the disease before death due to emaciation has been shown experimentally to be over 90 days. An outbreak of fox mange among Arctic foxes (Alopex lagopus) occurred in 1986. The local population of Arctic foxes was caught and successfully treated. The following year, treated foxes were caught again and no signs of disease were found. Sporadic cases of fox mange have also been diagnosed in lynx (Lynx lynx), pine marten (Martes martes) and domestic dogs. Single cases have been observed in other species: wolf (Canis lupus), mountain hare (Lepus timidus), domestic cat and horse. No cases of sarcoptic mange have been recorded in the badger (Meles meles). At present, although fox mange occurs as an epizootic in local populations, the number of foxes has increased again in many parts of Sweden.
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PMID:Sarcoptic mange in Swedish wildlife. 130 57

A suppression of hepatic ethoxyresorufin-O-deethylase (EROD) activity was reported recently in large-sized Atlantic tomcod (Microgadus tomcod) from the St. Lawrence Estuary (SLE; QC, Canada), possibly related to chronic exposure to persistent contaminants and/or to emaciation. In the present study, hepatic concentrations of organochlorine contaminants and biological responses were measured in female tomcods from three estuaries located on the Canadian east coast: The SLE, the Miramichi (ME), and the Richibucto (RE) Rivers Estuaries (NB, Canada). Tomcods from the SLE had higher hepatic concentrations of organochlorine contaminants than tomcods from the ME and RE. For example, concentrations of polychlorinated biphenyls (PCBs, lipid wt) were 2.5 to 4 times higher, and concentrations of mirex and chlordanes were 6 times higher, in tomcods from the SLE than in tomcods from the other sites. Concentrations of polycyclic aromatic hydrocarbons (PAHs) metabolites in the bile did not differ among sites. The pattern of biological responses differed markedly between the SLE and the two other sites. Tomcods from the SLE had 1.5 times higher concentrations of DNA adducts and 2 times higher rates of hepatocellular proliferation, but 20 times lower hepatic EROD activity, than tomcods from the ME and RE. Lipid content was not correlated with EROD activity, indicating that low hepatic lipid content alone does not cause suppression of EROD activity in Atlantic tomcod. In contrast, for the three sites combined, EROD activity decreased as concentrations of PCBs increased. Within sites, hepatic PCB concentrations increased as lipid content decreased. This study supports the hypothesis that low EROD activity in SLE tomcods is related to chronic exposure to organochlorine contaminants.
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PMID:Low hepatic ethoxyresorufin-O-deethylase activity correlates with high organochlorine concentrations in Atlantic tomcod from the Canadian east coast. 1626 47

We report a patient with systemic lupus erythematosus (SLE) who developed progressive emaciation and postprandial abdominal pain with a 27-year history of corticosteroid treatment. The patient was diagnosed as having intestinal angina based on computed tomography that showed severe stenosis of the superior mesenteric artery (SMA) in addition to complete occlusion of the celiac and inferior mesenteric arteries. Histopathology of the SMA and abdominal aorta showed atherosclerosis with no vasculitis or thrombus formation. Intestinal angina should actively be considered as a possible cause of recurrent abdominal pain in SLE patients, particularly in those with a long history of disease.
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PMID:Intestinal angina due to atherosclerosis in a 45-year-old systemic lupus erythematosus patient. 2093 Apr 50