umin.ac.jp/ctr Identifier: C000000412.

ABSTRACT. Most metabolic diseases in dairy cows occur during the peripartum period and are suggested to be derived from fatty liver initially developed during the nonlactating stage. Fatty liver is induced by hepatic uptake of nonesterified fatty acids that are released in excess by adipose tissues attributable to negative energy balance. The fatty accumulation leads to impairment of lipoprotein metabolism in the liver, and the impairment in turn influences other metabolic pathways in extrahepatic tissues such as the steroid hormone production by the corpus luteum. Detailed understanding of the impaired lipoprotein metabolism is crucial for elucidation of the mechanistic bases of the development of fatty liver and fatty liver-related peripartum diseases. This review summarizes results on evaluation of lipoprotein lipid and protein concentrations and enzyme activity in cows with fatty liver and those with ketosis, left displacement of the abomasum, milk fever, downer syndrome and retained placenta. Obtained data strongly suggest that decreases in serum concentrations of apolipoprotein B-100, apolipoprotein A-I and apolipoprotein C-III, a reduction in activity of lecithin:cholesterol acyltransferase and induction of haptoglobin and serum amyloid A are intimately related to the development of fatty liver and fatty liver-related diseases. Moreover, determination of the apolipoprotein concentrations and enzyme activity during the peripartum period is useful for early diagnoses of these diseases. KEY WORDS: apolipoprotein, bovine, estrogen receptor, fatty liver, protein kinase C.J. Vet. Med. Sci. 64(4): 293-307, 2002 PREFACE AND SCOPE OF THIS REVIEW Control of metabolic diseases, including ketosis, left displacement of the abomasum (LDA), milk fever and downer cow syndrome are crucially important for modern dairy husbandry, because their occurrence is intimately related to extensive feeding and management of dairy cows and also because high-yielding cows are particularly susceptible to such diseases. Affected cows, even after recovery from those metabolic diseases, have high incidences of reproductive and infectious diseases. Most metabolic diseases occur during the peripartum period (2 to 4 weeks from parturition) and are suggested to be caused by fatty liver (hepatic lipidosis) initially developed during the nonlactating stage. Fatty liver is a condition in which triglycerides (TG) accumulate in the liver. As a logical consequence, the TG accumulation results in impaired metabolism of lipoproteins, most of which are produced by the liver. Lipoproteins have a role in the transport of lipids between the liver and extrahepatic tissues. Impairment of lipoprotein metabolism is linked to disturbances of other metabolic pathways in extrahepatic tissues, for example, the steroid hormone production in the corpus luteum. Studies on impaired lipoprotein metabolism are therefore prerequisite to elucidate the mechanistic bases of the development of fatty liver and fatty liver-related diseases. Lipoproteins consist of lipids a...

A widespread occurrence of Ca +-dependent protein kinase was shown in various tissues and phyla of the animal kingdom. Phosphatidylserine appeared to be more effective than calmodulin in supporting the Ca2+-dependent phosphotransferase activity. The phospholipid-sensitive Ca2+-dependent protein kinase activity, distributed in both the cytosolic and particulate fractions, was not inhibited by trifluoperazine, a specific inhibitor of calmodulin-sensitive, Ca2+_ dependent reactions or processes. The enzyme activity levels, compared to those of cyclic AMP-dependent and cyclic GMPdependent protein kinases, were exceedingly high in certain tissues (such as brain and spleen) and exhibited a much-greater disparity among tissues. The Ka for Ca2+ was about 100 gM in the presence of phosphatidylserine; the value was as low as 2

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A steep dose-response curve between 40 and 48 Gy using a daily dose of 12 Gy delivered in one week was identified for stage IB NSCLC in SBRT using RTRT.

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