Effect of dietary threonine supplementation on tyrosine toxicity in the rat

The objective of this study was to determine the effect of threonine supplementation on tyrosine metabolism in rats fed a low protein diet with excess tyrosine. The growth retardation and the development of eye and paw lesions that occur in rats ingesting a basal plus 3% or 5% L-tyrosine diet could be alleviated partially by the addition of 0.5% or 1.0% L-threonine to the diet. An increased blood tyrosine level in rats fed excess tyrosine was also lowered by threonine supplementation. In tyrotoxic conditions, the activities of liver tyrosine transaminase (EC 2.6.1.5) and threonine dehydratase (EC 4.2.9.16) were elevated, but p-hydroxyphenyl pyruvic acid oxidase (EC 1.13.11.27) which is also intimately associated with tyrosine toxicity was found to be inactivated. Furthermore, biosyn thesis of ascorbic acid in liver was significantly lowered in this condition. However, addition of L-threonine in the diet, not only could cure the signs developed due to excess tyrosine, but also could affect the levels of enzymes studied

Transformations in Early Historic and Early Medieval India: Excavations at Paithan, Maharashtra 1996-1999.

Transformations in Early Historic and Early Medieval India: Excavations at Paithan, Maharashtra 1996-1999 (Delhi: Archaeological Survery of India and British Association for South Asian Studies, 2015)

Identification of a Plasmodium falciparum phospholipid transfer protein.

Infection of erythrocytes by the human malaria parasite Plasmodium falciparum results in dramatic modifications to the host cell, including changes to its antigenic and transport properties and the de novo formation of membranous compartments within the erythrocyte cytosol. These parasite-induced structures are implicated in the transport of nutrients, metabolic products, and parasite proteins, as well as in parasite virulence. However, very few of the parasite effector proteins that underlie remodeling of the host erythrocyte are functionally characterized. Using bioinformatic examination and modeling, we have found that the exported P. falciparum protein PFA0210c belongs to the START domain family, members of which mediate transfer of phospholipids, ceramide, or fatty acids between membranes. In vitro phospholipid transfer assays using recombinant PFA0210 confirmed that it can transfer phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, and sphingomyelin between phospholipid vesicles. Furthermore, assays using HL60 cells containing radiolabeled phospholipids indicated that orthologs of PFA0210c can also transfer phosphatidylcholine, phosphatidylinositol, and phosphatidylethanolamine. Biochemical and immunochemical analysis showed that PFA0210c associates with membranes in infected erythrocytes at mature stages of intracellular parasite growth. Localization studies in live parasites revealed that the protein is present in the parasitophorous vacuole during growth and is later recruited to organelles in the parasite. Together these data suggest that PFA0210c plays a role in the formation of the membranous structures and nutrient phospholipid transfer in the malaria-parasitized erythrocyte

Avelumab in European patients (pts) with metastatic Merkel cell carcinoma (mMCC): Experience from an ad-hoc expanded access program (EAP)

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日本イエズス会版『サルヴァトル・ムンヂ』ポルトガル語全訳注 : 第一誡「御一体のデウスを敬ひ,貴み奉るべし」に関わる10の尋問

A new method for the preparation of the synthon (±)-2,6,7,7a-tetrahydro-1β-hydroxy-4-formyl-7aβ-methylindene (1,a) for the total synthesis of steroids in both (±) and (+) forms, starting from the known β-ketoester, (±)-methyl 1β-t-butoxy-5,6,7,7a-tetrahydro-7aβ-methyl-5-keto-4-indancarboxylate (2,a) has been described. An alternative route to (1,a) has been investigated. Although the compound, (±)-1β-hydroxy-5,6,7,7a-tetrahydro-7aβ-methyl-5-keto-4-methoxymethylindan (2,b) could not be prepared, interesting pathways leading to two unexpected products, (±)-5,6,7,7a-tetrahydro-4,7a-dimethyl-5H-indene-1,5-dione and (±)-2,6-diketo-3-methyltricyclo-(5,2,1,0)decan-8-ol (3 and 4), were encountered during an attempted annelation reaction of the ketone, N-diethylamino-5-methoxypentan-3-one (6), with 2-methylcyclopentan-1,3-dione (5). Trapping of the intermediate, (±)-3a,4,5,6,7,7a-hexahydro-3a-hydroxy-4-methylene-7a-methylindene-1,5-dione (7), through the formation of the adduct, (±)-3a,4,5,6,7,7a-hexahydro-3a-hydroxy-4-(1', 3'-diketo-2'-methylcyclopentano-2'-methylene)-7a-methylindene-1,5-dione (8), established the mechanism of the formation of the products (3 and 4)