Search

ZnS-based ZnMgSTe quaternary alloy layers have been grown by molecular beam epitaxy. The bandgap of ZnMgSTe has been estimated from the reflectance spectra, and it was found that it increases with increasing Mg content, while it decreases with increasing Te content. Nitrogen acceptor doping to Zn1-xMgxS1-yTey layers has also been investigated. The layers with Te content y>0.1 were found to be p-type, and the layer with the larger Te content exhibited lower resistivity. From these results, it seems that the ZnMgSTe quaternary alloy with appropriate composition possesses both a wide bandgap and p-type conductivity. [ABSTRACT FROM AUTHOR]

BACKGROUND: Upregulation of oligopeptide transport activity by dietary protein, certain dipeptides and amino acids has been reported in the rat intestine and a human intestinal cell line. OBJECTIVE: In this study, the pharmacokinetics of cefdinir were investigated after L-phenylalanine supplementation and a high-protein diet (HPD) in humans to explore changes in the activities of intestinal and renal oligopeptide transporters. METHODS: A normal-protein diet (NPD, 73.2 +/- 2.6 g/day), NPD + l-phenylalanine (7.5 g/day), or HPD (141.3 +/- 3.7 g/day) was given to six male healthy volunteers for 12 days followed by a single dose of cefdinir after an overnight fast in a randomized three-way crossover study with a 22-day washout. Blood and urine were collected over a 12-h period after administration of cefdinir. Concentrations of cefdinir in plasma and/or urine were measured by high-performance liquid chromatography. RESULTS: Plasma concentrations and urinary excretion of the drug did not change throughout the study. Physiological variables and laboratory values did not reveal any differences between the three periods except for serum and urinary nitrogen levels and serum triglyceride. DISCUSSION: A reason for the unchanged pharmacokinetics of cefdinir may be due to lower doses of L-phenylalanine and protein in humans than in animals when converting animal effective doses to humans. CONCLUSION: In humans, L-phenylalanine supplementation and HPD do not seem to upregulate intestinal and renal oligopeptide transport in the ranges of duration and dose examined. [ABSTRACT FROM AUTHOR]

Background: Upregulation of oligopeptide transport activity by dietary protein, certain dipeptides and amino acids has been reported in the rat intestine and a human intestinal cell line. Objective: In this study, the pharmacokinetics of cefdinir were investigated afterl-phenylalanine supplementation and a high-protein diet (HPD) in humans to explore changes in the activities of intestinal and renal oligopeptide transporters. Methods: A normal-protein diet (NPD, 73·2 ± 2·6 g/day), NPD + l-phenylalanine (7·5 g/day), or HPD (141·3 ± 3·7 g/day) was given to six male healthy volunteers for 12 days followed by a single dose of cefdinir after an overnight fast in a randomized three-way crossover study with a 22-day washout. Blood and urine were collected over a 12-h period after administration of cefdinir. Concentrations of cefdinir in plasma and/or urine were measured by high-performance liquid chromatography. Results: Plasma concentrations and urinary excretion of the drug did not change throughout the study. Physiological variables and laboratory values did not reveal any differences between the three periods except for serum and urinary nitrogen levels and serum triglyceride. Discussion: A reason for the unchanged pharmacokinetics of cefdinir may be due to lower doses ofl-phenylalanine and protein in humans than in animals when converting animal effective doses to humans. Conclusion: In humans,l-phenylalanine supplementation and HPD do not seem to upregulate intestinal and renal oligopeptide transport in the ranges of duration and dose examined. [ABSTRACT FROM AUTHOR]

An account is given of an unusual patient with acute sensory neuropathy, leading within a few weeks to almost generalized sensory loss. Generalized sensory deficits were involved in the face, tongue, and palate. He had a drug allergy from chemotherapy during an early stage of illness. An albuminocytological dissociation of the cerebrospinal fluid was noted in a few months. A sural nerve biopsy after 2 months showed a marked reduction of fibers, and extensive invasion of phagocytes throughout the endoneurium. This patient recovered poorly with profound sensory ataxia of the limbs and tongue. A possible explanation for the clinico-pathological findings may be that acute idiopathic polyradiculoneuritis (Guillain-Barré syndrome) and toxic neuropathy exert an etiological role in the extramedullary sensory system. [ABSTRACT FROM AUTHOR]

A 69 year old woman presented with cognitive impairment and supranuclear gaze palsy caused by paraneoplastic limbic/brain stem encephalitis associated with atypical medullary breast carcinoma. The cerebrospinal fluid from the patient harboured an anti-neuronal cell antibody against Ma2 antigen, but not against Ma1 or Ma3 antigen. Despite the antibody being restricted to the Ma2 antigen, the patient's cancer tissue expressed Ma1, Ma2, and Ma3 mRNAs. These results, and the expression of Ma2 mRNA in an atypical medullar breast carcinoma in another patient without paraneoplastic encephalitis, indicate that the induction of anti-Ma2 antibody depends on host immunoreponsiveness and not on the presence of the antigen itself in the cancer. [ABSTRACT FROM AUTHOR]