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Oxidation-reduction sensitive interaction of a cellular 50-kDa protein with an RNA hairpin in the 5' noncoding region of the poliovirus genome.

Genetic and biochemical analyses of the 5' noncoding region of poliovirus have indicated the importance of this region in both translation and amplification of the viral RNA. The role of the cellular machinery required for these events is just beginning to be revealed. Using an RNA gel retention assay, we have identified a cellular 50-kDa protein that forms a specific complex with a stable stem-loop structure present in the viral 5' noncoding region. The formation of the RNA-protein complex is dependent on the availability of free sulfhydryl groups in the protein. The possible involvement of this RNA-protein complex in the regulation of viral gene expression is discussed.

Base Sequence↗

Analysis of the nitrous oxide reduction genes, nosZDFYL, of Achromobacter cycloclastes.

The structural gene, nosZ, for the monomeric N2O reductase has been cloned and sequenced from the denitrifying bacterium Achromobacter cycloclastes. The nosZ gene encodes a protein of 642 amino acid residues and the deduced amino acid sequence showed homology to the previously derived sequences for the dimeric N2O reductases. The relevant DNA region of about 3.6 kbp was also sequenced and found to consist of four genes, nosDFYL based on the similarity with the N2O reduction genes of Pseudomonas stutzeri. The gene product of A. cycloclastes nosF (299 amino acid residues) has a consensus ATP-binding sequence, and the nos Y gene encodes a hydrophobic protein (273 residues) with five transmembrane segments, suggesting the similarity with an ATP-binding cassette (ABC) transporter which has two distinct domains of a highly hydrophobic region and ATP-binding sites. The nosL gene encodes a protein of 193 amino acid residues and the derived sequence showed a consensus sequence of lipoprotein modification/processing site. The expression of nosZ gene in Escherichia coli cells and the comparison of the translated sequences of the nosDFYL genes with those of bacterial transport genes for inorganic ions are discussed.

Alcaligenes↗

Alteration of oxide reductive and haemostatic factors in type 2 diabetics.

OBJECTIVE: To assess any pathogenic role of radical activity and haemostatic alteration in the early cardiovascular disease of microalbuminuric type 2 diabetics (non-insulin dependent). DESIGN: A selected cohort of type 2 diabetics was identified, divided according to urinary albumin excretion and compared with a healthy control group depending on some haemostatic factors and radical activity. SETTING: All the subjects were studied as outpatients. SUBJECTS: Eighty diabetics and 84 healthy controls were interviewed and underwent blood tests to exclude standard cardiovascular risk factors before follow up. MAIN OUTCOME MEASURES: The subjects were males, age range 43-55 years, and divided according to albumin excretion (microalbuminuria > 30-200 mg L-1; normoalbuminuria < 15 mg L-1). The mean duration of diabetes referred by the patients was 9.3 years in albuminuric and 11.1 years in normoalbuminuric patients with a good control of plasma glucose level. Neither the diabetics nor the control group showed clinical evidence of renal and cardiovascular diseases. RESULTS: Microalbuminuric patients presented elevated malondialdehyde concentration, glutathione peroxidase activity, phospholipidic fatty acid levels, fibrinogen, plasminogen activator inhibitor, tissue plasminogen activator and von Willebrand factor compared with normoalbuminuric patients and controls. More collagen was required in microalbuminuric diabetics than in normoalbuminurics and controls. CONCLUSIONS: Our results confirm that both free radical activity and changes in haemostatic factors can be observed in type 2 diabetes and particularly in patients with albuminuria. Our very selected series with short duration, good control of diabetes and lack of clinical evidence of cardiovascular disease may suggest that these abnormalities develop earlier and may be associated with, and/or implicated in, the pathogenesis of microvascular complications which can be related to a higher and early cardiovascular morbidity and mortality rate in microalbuminuric diabetics.

Adult↗