Tetrodotoxin-sensitive persistent current boosts the depolarization of retinal amacrine cells in goldfish

This study aims to resolve a paradox. Experiments measuring alpha band power report an event related decrease (desynchronization) in alpha activity, whereas those measuring evoked alpha report synchronization. During a recognition memory task with human subjects, we measured the evoked (phase locked) and induced (not phase locked) alpha response. The findings reveal that evoked alpha is due to a transient phase locking (at about 100-200 ms poststimulus) of three alpha sub-bands which can be observed only at parieto-occipital sites. In contrast, induced alpha shows a widespread pattern of desynchronization at most recording sites. Thus, opposite alpha responses occur within similar time windows. Evoked alpha synchronization may reflect cortical inhibition which serves to increase the signal to noise ratio for activation processes following immediately later.     

Concentration quenching of photoluminescent Ru(bpy) dispersed in a polysiloxane film containing 2,2′-bipyridine pendant groups in dependence of molecular distribution

The photoluminescent Ru(bpy) complex was dispersed in a polysiloxane film containing 2,2′-bipyridine (bpy) pendant groups. The unusually long photoluminescence lifetime of the Ru(bpy) (1,94 μs at 25°C) and the blue-shifted photoluminescent wavelength suggest a rigid polymer matrix. The fluorescence yield becomes lower with higher probe concentration, indicating concentration quenching. According to the analysis based on Stern-Volmer plots, the quenching obeys a mechanism composed of both static and dynamic processes. A statistical intermolecular distance distribution between the probes was used to interpret the results in terms of static and dynamic quenching. It is shown that in the present system the dispersed complexes diffuse slightly during the excited state.     

The kinetics of the oxidative polymerization of 2.6-xylenol with a copper-amine complex

It was found that the oxidative polymerization of 2.6-xylenol with a copper-amine complex proceeds via a mechanism similar to that of a MICHAELIS-MENTEN-type reaction, the steady state being maintained during the polymerization; the kinetics were studied. The LINEWEAVER-BURK plots showed linear relationships, supporting this mechanism. From the comparison of the kinetic constants it was concluded that oxygen not only takes part in the recycling step of the catalyst, but also promotes the catalytic action of the cuprous complex by being coordinated to the intermediate complex. K₁ values (the reciprocal of the MICHAELIS constant, K_m) vary with the amine-ligand species, but the reaction-rate constants (k₂) do not change, regardless of the ligands used. According to the kinetic formula, K₁ is proportional to the product of the formation constant of the complex between the copper-amine catalyst and the monomer (K′₁) by the rate constant of electron transfer (k_e). It is because of the K′₁ values that the apparent polymerization rate varies with the amine ligands in the region of relatively low monomer concentrations. It was found that, as the ligand ratio ([pyridine]/[Cu]) increases, i.e., as the selectivity for C? O coupling increases, the K₁ values become larger. The mechanism for the coupling selectivity is discussed in relation to the K₁ values.     

Identification of two mutations in a compound heterozygous child with dihydrolipoamide dehydrogenase deficiency

An infant girl with elevated blood lactate, pyruvate, and plasma branched-chain amino acids was diagnosed with dihydrolipoamide dehydrogenase (E3; dihydrolipoamide: NAD+ oxidoreductase, EC 1.8.1.4) deficiency. Activities of the pyruvate dehydrogenase complex and E3 from patient were 26 and 2% of controls in blood lymphocytes, and 11 and 14% in cultured skin fibroblasts, respectively. Western blot analysis demonstrated that the amount of E3 protein in fibroblasts from the patient and her father was about half of controls, while Northern blot analysis showed normal amounts of E3 RNA. DNA sequencing of cloned full-length E3 cDNAs from the patient revealed two mutations in separate alleles. One is a single base insertion of an extra adenine in the last codon of the leader peptide sequence (TAC-->TAAC) leading to a nonsense mutation which results in the premature termination of the precursor E3 polypeptide (Y35X). The other is a missense mutation due to substitution of guanine for adenine, causing an Arg-->Gly substitution at amino acid 460 of the mature protein (R460G) which triggers the loss of E3 activity probably by structural change in the E3 dimer. DNA sequencing of E3 cDNAs from the parents demonstrated that the nonsense mutation was inherited from the father and the missense mutation was inherited from the mother.      

No evidence of PEG1/MEST gene mutations in Silver‐Russell syndrome patients

Silver‐Russell syndrome (SRS) is characterized by prenatal and postnatal growth retardation with morphologic anomalies. Maternal uniparental disomy 7 has been reported in some SRS patients. PEG1/MEST is an imprinted gene on chromosome 7q32 that is expressed only from the paternal allele and is a candidate gene for SRS. To clarify its biological function and role in SRS, we screened PEG1/MEST abnormalities in 15 SRS patients from various standpoints. In the lymphocytes of SRS patients, no aberrant expression patterns of two splice variants (α and β) of PEG1/MEST were detected when they were compared with normal samples. Direct sequence analysis failed to detect any mutations in the PEG1/MEST α coding region, and there were no significant mutations in the 5′‐flanking upstream region containing the predicted promoter and the highly conserved human/mouse genomic region. Differential methylation patterns of the CpG island for PEG1/MEST α were normally maintained and resulted in the same pattern as in the normal control, suggesting that there was no loss of imprinting. These findings suggest that PEG1/MEST can be excluded as a major determinant of SRS. © 2001 Wiley‐Liss, Inc.     

A possible pathogenic role of CD8+ T cells and their derived cytokine, IL-16, in SLE

Current investigations into the role of CD8+ T cells and their derived cytokine, interleukin (IL)-16, in the induction of CD4+ T cell abnormalities in systemic lupus erythematosus (SLE) were reviewed and discussed on the basis of results mainly obtained in our laboratory.