Serum primates

Neuringer, M., M. M. Sandstrom et al. (2004). Nutritional manipulation of primate retinas, I Effects of lutein or zeaxanthin supplements on serum and macular pigment in xanthophyll-free rhesus monkeys. Invest. Ophthalmol. Vis. Sci. 45(9) 3234-3243. 

Typical side effects are constitutional in nature, including a flu-like syndrome within 6 hours after dosing in more than 30% of patients that tends to resolve upon continued administration. Other potential adverse effects include thrombocytopenia, granulocytopenia, elevation in serum aminotransferase levels, induction of autoantibodies, nausea, fatigue, headache, arthralgias, rash, alopecia, anorexia, hypotension, and edema. Severe neuropsychiatric side effects may occur. Absolute contraindications to therapy are psychosis, severe depression, neutropenia, thrombocytopenia, symptomatic heart disease, decompensated cirrhosis, uncontrolled seizures, and a history of organ transplantation (other than liver). Alfa interferons are abortifacient in primates and should not be administered in pregnancy. 

S. Keller, M.T. Tang, J.Y. Tso, M. Vasquez, and N. Tsurushita. 2004. Engineered human IgG antibodies with longer serum half-lives in primates. J. Biol. Chem. 279 6213-6216. 

Serum and Tissue Lipids. A decrease in circulating cholesterol and triglyceride levels is also associated with DEHP exposure in rats (Bell 1982 Dostal et al. 1987a Eagon et al. 1994 Mocchiutti and Bernal 1997 Oishi 1989a Poon et al. 1997 Rhodes et al. 1986), but not in primates (Rhodes et al. 1986). 

P5. Parks, J. S., and Rudel, L. L., Metabolism of the serum amyloid A proteins (SAA) in high-density lipoproteins and chylomicrons of nonhuman primates (vervet monkey). Am. /. Pathol. 112, 243-249 (1983). 

Anthony et al., 1997) cause significant reductions in serum TC and triglyceride (TG). In non-human primates, dietary genistein, the isoflavone significantly reduces plasma LDL and VLDL cholesterol levels (Anthony et al., 1997). 

Ascorbic acid is a vitamin in primates. In most other animals, it can be synthesized by a branch of the glucoronic acid pathway (Chapter 18). It is apparently not changed into any coenzyme in the human being and participates as a vitamin in a reducing capacity in several biochemical reactions. These include the post-translational hydroxylation of proline in collagen biosynthesis (Chapter 8) and in tyrosine metabolism (Chapter 20). Ascorbic acid is oxidized to dehydroascorbic acid, a diketo derivative of ascorbate. Scurvy is a deficiency disease caused by a shortage of dietary ascorbic acid. In children, this results in defective bone formation in adults, extensive bleeding occurs in a number of locations. Scurvy is to be suspected if serum ascorbic acid levels fall below 1 jug/mL. 

DEFICIENCY Man, other primates, and guinea pigs cannot synthesize vitamin C. Nor is it stored in the b y. Hence, the need for continued replenishment, and the development of scurvy with lack of vitamin C, In scurvy, there are swollen gums and easy bniisability, coinciding with defective collagen formation. Serum levels of ascorbic acid may be tested for diagnosis. 

The classical column procedures for the preparation of lysozyme are difficult to use with high viscosity solutions such as serum. A batch method was developed based on affinity chromatography using deami-nated chitin [82]. The method was found to give a one-step purification of nearly theoretical amounts in tissue homogenates tested. These included tissue homogenates from humans, primates, avian egg white and plants. The use of a chitin-coated cellulose affinity column for purification of lysozyme has also been described [83]. 

TTV has not been shown by electron microscopy. Up to now, the virus could only be demonstrated in the serum due to the presence of TTV DNA. A total of 16 genotypes have now been differentiated. (564) Recently, a TTV isolate from non-human primates could be identified the authors named it s-TTV. Overall, 10.5% of Japanese patients with liver disease were found to be infected with s-TTV, whereby two different genotypes were classified. (557) There have also been reports of TTV-like mini virus DNA, which are detectable in a large number of patients. (558) TTV can replicate in various tissues, although changes in the liver are only mild. (565)... 

Allantoin is the catabolic end product of purines in most mammals. It is formed by the action of the enzyme uricase on urate. Humans and other primates lack uricase and excrete urate as the final product of purine metabolism. However, small amounts of allantoin are present in human serum. Some authors demonstrated that free radical attack on urate generates allantoin. Therefore small amounts of allantoin detected in human serum may provide a marker of free radical activity in vivo. 

ENll Bankson, D., Rifai, N., Henderson, M., Klein, R. and Raghunathun, T. (1991). Dietary fat and the polyunsaturated/saturated fat ratio influences serum lipids in old, female, non-human primates. Clin. Chem. 37, 929, Abstr. 93. 

Dipropylacetic acid (40) protected rats against picrotoxin and pentetrazole.88 The chelating agent D-penicillamine (41) markedly reduced seizures in P. Papio baboons, a primate with high serum Zn levels.89... 

Comparison of sequences of the same protein in different species yields a wealth of information about evolutionary pathways. Genealogical relations between species can be inferred from sequence differences between their proteins. We can even estimate the time at which two evolutionary lines diverged, thanks to the clocklike nature of random mutations, For example, a comparison of serum albumins found in primates indicates that human beings and African apes diverged 5 million years ago, not 30 million years ago as was once thought. Sequence analyses have opened a new perspective on the fossil record and the pathway of human evolution. 

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