Advances in veterinary science and comparative medicine最新文献

{"title":"Hereditary conjugated hyperbilirubinemia in Wistar rats: a model for the study of ATP-dependent hepatocanalicular organic anion transport.","authors":"P L Jansen, R P Oude Elferink","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"175-95"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multiple drug resistance.","authors":"C R Leveille, A S Moore","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"31-59"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18901593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Equine fasting hyperbilirubinemia.","authors":"L R Engelking","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>It appears that different mechanisms responsible for fasting hyperbilirubinemia may be operative in different mammalian species (and subspecies). An increase in bilirubin production does not seem to occur in the horse, but a decrease in the hepatic uptake of bilirubin has been supported by a number of studies. Even though the delay in plasma elimination could also result from a decrease in hepatic blood flow, this possibility does not seem to play a major role since the hepatic uptake of compounds with low intrinsic hepatic clearance (e.g., ICG and bilirubin) appear to be affected more during fasting than those with higher clearances (e.g., BSP, bile acid, antipyrine, acetaminophen, and lidocaine) (Table I). Other possibilities such as a decrease in the affinity of hepatocellular membrane carriers involved in the uptake of these compounds or altered content of intracellular proteins involved in cellular transport or storage of bilirubin have not been investigated in horses. Competition with free fatty acids for these carrier-mediated events seems likely, particularly because horses and ponies experience high degrees of hyperlipidemia during fasting. However, studies that have explored the competition hypothesis, while not entirely negative, do not fully support it as being the sole mechanism responsible for this phenomenon. Hepatocellular UDPGT activities have not been adequately investigated in horses, but it is apparent that intraduodenal infusion of glucose is effective in reducing fasting hyperbilirubinemia and also in increasing biliary bilirubin excretion. It therefore seems possible that UDP-glucose and UDPGA levels in the livers of horses could be reduced during fasting, thus resulting in substrate depletion for the conjugating enzymes. As pointed out by Freedland et al. (1991), it is also possible that the horse, like the Bolivian squirrel monkey, might also have a relatively high apparent Km and low Vmax for UDPGT, thus resulting in high steady-state levels of plasma bilirubin, particularly during fasting. Although little is known about the cause of equine fasting hyperbilirubinemia and the subtle factors that may be modulating slight changes in the production, hepatocellular uptake, binding, conjugation, and/or biliary excretion of this pigment, it is known that it can be rapidly reversed by refeeding native hay. Perhaps one direction for future research could point toward more fully exploring what aspects of feeding are responsible for reversing this intriguing physiological phenomenon.</p>","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"115-25"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261433","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Animal models of copper toxicosis.","authors":"M L Schilsky,&nbsp;I Sternlieb","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"357-77"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Animal models of pigment gallstones.","authors":"R V Rege,&nbsp;L G Dawes,&nbsp;J D Ostrow","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"257-87"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Avian fatty liver hemorrhagic syndrome: a comparative review.","authors":"R J Hansen,&nbsp;R L Walzem","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Metabolic fatty liver syndromes occur in a variety of species including chickens, humans, cows, and cats. Both energy excess and deficit appear to initiate the accumulation of liver fat. Although the conditions preceding the onset of liver steatosis vary, all syndromes share a common basis in altered lipid utilization, lipoprotein assembly, and secretion. Laying hens and humans appear to develop fatty livers under similar metabolic conditions of energy excess. This similarity and the additional structural requirements inherent in yolk deposition make the laying hen an exciting model in which to study lipoprotein synthesis, assembly, and secretion. The overfed hen provides additional insights into the effects of nutrition and hormones on these same processes. Within this model it may be possible to distinguish the effects of altered gene expression versus altered physical properties (lipids) and postranslational processing (proteins) in mediating the observed responses.</p>","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"451-68"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biliary atresia in lampreys.","authors":"J H Youson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The preceding pages have described an organism that is far removed from mammals on the taxonomic scale of vertebrates but one that has proven to have a unique and most useful system for studies of liver function and, in particular, bile product transport and excretion. It is also an organism in which iron loading can be studied in the liver and other organs and tissues. Many of the events that occur in this animal during its life cycle with regard to bile pigment metabolism as normal programmed phenomena are unparalleled among the vertebrates. In the larval (ammocoete) period of lampreys, there is an intrahepatic gallbladder and a biliary tree that is well equipped for the storage, transport, and elimination of bile products into the intestine for ultimate excretion with the feces. The importance of the patency of these bile ducts to bile excretion is illustrated in one species of lampreys in which the bile ducts of young ammocoetes become infested with larval nematodes to a degree that bile pigment regurgitation into the blood results in a green serum that is identified as biliverdin. Despite having serum levels of biliverdin that would be toxic to humans, these individuals live a complete larval life. The larvae of all lamprey species undergo a phase of metamorphosis in which they transform into adults. During this phase the larval gallbladder, the bile canaliculi of the hepatocytes, and all the intrahepatic bile ducts completely regress in a developmental process called lamprey biliary atresia. The epithelium of the extrahepatic common bile duct transforms and expands into a caudal portion of the endocrine pancreas of the adult. Many of the events of lamprey biliary atresia resemble events occurring during experimental and pathological conditions of mammalian cholestasis, including disruption to the bile-blood barrier (intercellular junctions), accumulation of bile components in the cytoplasmic inclusions, and alteration of the distribution of membrane enzymes in hepatocytes. Regression of the bile ducts and ductules is accompanied by a periductular fibrosis that seems to be a product of activity by lipocytes (Ito cells). The regurgitation of bile products into the interstitial tissue of the liver during early biliary atresia may be the stimulus for both inflammatory (granulomatous) and autoimmune responses. There are no bile ducts in adults lampreys, yet they seem to show no immediate consequences of the absence of an exocrine mechanism for the elimination of bile products.(ABSTRACT TRUNCATED AT 400 WORDS)</p>","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"197-255"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic cell transplantation.","authors":"A A Demetriou,&nbsp;M Holzman,&nbsp;A D Moscioni,&nbsp;J Rozga","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"313-32"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Animal models in liver research: iron overload.","authors":"T C Iancu","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"379-401"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol cholelithiasis.","authors":"B I Cohen,&nbsp;E H Mosbach","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":75456,"journal":{"name":"Advances in veterinary science and comparative medicine","volume":"37 ","pages":"289-312"},"PeriodicalIF":0.0,"publicationDate":"1993-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19261439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}