Reference

Application of chitin and chitosan to pharmaceutical preparations

Application of chitin and chitosan to pharmaceutical preparations. Nagai, Tsuneji; Sawayanagi, Yoichi; Nambu, Naoki (Fac. Pharm. Sci., Hoshi Univ., Tokyo, Japan). Chitin, Chitosan, Relat. Enzymes, [Proc. Jt. U.S.-Jpn. Semin. Adv. Chitin, Chitosan, Relat. Enzymes], 21-39. Edited by: Zikakis, John P. Academic: Orlando, Fla. (English) 1984. CODEN: 53NUA7. DOCUMENT TYPE: Conference CA Section: 63 (Pharmaceuticals) Directly compressed tablets contg. chitin [1398-61-4] or chitosan [9012-76-4], sustained-release prepns. of water-sol. drugs with chitosan, and dissoln. properties and bioavailability of poorly sol. drugs from ground mixts. with chitin or chitosan were reported. The fluidity of combined powders with chitin and chitosan was greater than that with cryst. cellulose. Tablets contg. <60% chitin or chitosan passed the disintegration test of the Japanese Pharmacopeia X. Chitin and chitosan had better lubricating properties than cryst. cellulose. A zero-order controlled release was obtained for a water-sol. drug from tablets contg. chitosan in the Japanese Pharmacopeia X disintegration medium No. 1 (pH 1.2), and in the disintegration medium No. 2 (pH 6.8) following exposure to No. 1. The size of crystals of poorly sol. drugs decreased when ground in mixt. with chitin or chitosan, and the dissoln. rate of such poorly sol. drugs was significantly greater than that from phys. mixt. or intact ones. The ground mixt. of phenyltoin [57-41-0]-chitosan gave an enhanced bioavailability of phenytoin in beagle dogs.

Damage of Purkinje cell axons following chronic phenytoin administration: an animal model of distal axonopathy

Damage of Purkinje cell axons following chronic phenytoin administration: an animal model of distal axonopathy. Volk, B.; Kirchgaessner, N. (Dep. Neuropathol., Inst. Pathol., Freiburg D-7800, Fed. Rep. Ger.). Acta Neuropathol., 67(1-2), 67-74 (English) 1985. CODEN: ANPTAL. ISSN: 0001-6322. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) The chronic administration of diphenylhydantoin (phenytoin)(DPH) [57-41-0] in a liq. diet to male mice (C57/BL6J) with serum DPH levels of 25-40 mg/mL led to a severe axonopathy of Purkinje cell axons. The alterations were located mainly in the deep cerebellar nuclei, the projection of Purkinje cell axons, and consisted of perisomatic presynaptic segments with accumulation of neurofilaments and augmentation of the smooth endoplasmic reticulum. The chronic DPH administration to mice represents a new model of DPH-induced encephalopathy and of distal axonopathy of cerebellar neurons.