, 2-[3,5-bis(N-trimellitimidoyl)-phenyl] benzimidazole (DIDA-i) and 2-[3,5-bis(N-trimellitimidoyl)-phenyl] 5-methyl benzimidazole (DIDA-ii) from the condensation of 5-(2-benzimidazole)-1,3-phenylenediamine (DABI(A)) and 5-(5-methyl-2benzimidazole)-1,3-phenylenediamine (DABI(B)) with trimellitic anhydride in glacial acetic acid were synthesized, respectively. 1,3-bis(N-trimellitimidoyl)benzene (DIDA-iii, as a reference) was also synthesized in a similar manner to study the properties of the its structure. Three series of aromatic poly(amide-imide)s were prepared by triphenyl phosphite-activated polycondensation from diimide-dicarboxylic

acid DIDA-i, DIDA-ii, and the reference monomer DIDA-iii with various aromatic diamines. The polymers were obtained in quantitative yields with inherent viscosities between 0.46 SB203580 and 0.81 dL g(-1). The effects of the benzimidazole pendent groups on the polymer properties, such as solubility and thermal stability were investigated by comparison of the polymers. The polymers bearing benzimidazole pendent groups exhibited thermal stability and good solubility in common polar solvents higher than the reference polymers. (C) 2009 Wiley Periodicals, Inc. J Appl Polym Sci 114: 185-192, 2009″
“Background: Biotin, a water-soluble vitamin,

is used as a co-factor by enzymes involved in carboxylation reactions. It functions as the carboxyl carrier for biotin-dependent carboxylases. These enzymes catalyze AZD8055 gluconeogenesis, fatty acid metabolism and amino acid catabolism, Ferroptosis activation thus biotin

plays an essential role in maintaining metabolic homeostasis. Biotinidase deficiency is an inherited metabolic disorder characterized by neurological and cutaneous symptoms, treated by oral administration of the vitamin biotin. In central Anatolia marriages between relatives are very common (26%).

Infants and Methods: We screened 34,378 infants born in four cities in central Anatolia during the one-year period beginning February 2006 for deficiency of the enzyme biotinidase. A simple calorimetric screening procedure was used to detect the presence or absence of biotinidase activity on the same blood-soaked filter paper cards used for screening for phenylketonuria. Positive samples were confirmed with a quantitative method.

Results: One newborn infant with partial biotinidase deficiency (10-30% of mean normal serum activity) was identified during the 12-month pilot study. The estimated incidence of partial biotinidase deficiency in central Anatolia is approximately 1:34,378; this ratio was the same in findings from Istanbul (1:33,307).

Conclusions: Like children with profound biotinidase deficiency, children with partial biotinidase deficiency arc symptom-free at birth. However, the subsequent occurrence of symptoms of profound biotinidase deficiency in our patient with partial deficiency suggests that biotin therapy for this condition may be warranted.