Angiotensin-converting enzyme (ACE) gene polymorphism in type II diabetic patients with increased albumin excretion rate

Approximately one in three patients with diabetes is at risk of developing kidney disease, despite current methods of treatment. It has long been suspected that diabetic kidney disease has a genetic basis, but this has been difficult to prove. Polymorphisms of the angiotensin-converting enzyme (ACE) gene have been shown to be related to the occurrence of nephropathy in type I diabetic patients. This study showed that there was no association in the ACE genotype frequency and increased albumin excretion rate in type II diabetic patients.     

Are there any successful men from criminogenic backgrounds?

In the Cambridge Study in Delinquent Development, a prospective longitudinal survey of 411 London males, a vulnerable group of 63 boys from criminogenic backgrounds was defined on the basis of the best nonbehavioral predictors of delinquency at age 8-10 (low family income, large family size, convicted parents, low intelligence, and poor parental child-rearing behavior). These males were followed up to age 32, and the more successful men were defined according to criteria such as the absence of convictions and of other deviant behavior, good relationships with wives and children, and good accommodation and employment histories. Hence, "success" here refers to satisfactory social adjustment. The more successful men were those who had been neurotic at age 10, those who had few or no friends at age 8, those without convicted parents or behavior problem siblings, those with mothers who had a high opinion of their sons, and those who did not spend their leisure time with their fathers. At age 8-10 they were already better behaved and less daring than those later judged as the unsuccessful men. There was some tendency for shyness to act as a protective factor against delinquency for non-aggressive boys but as an aggravating factor for aggressive boys.     

The human leucocyte P30 antigen: properties and assessment of value as a clonal marker

FMC3 and FMC29 are monoclonal antibodies which react with a 30,000 Dalton molecule expressed on the lymphocyte surface membrane. The molecule is a protein which does not appear to be N-glycosylated. The antigen, which is also expressed intracellularly, does not appear to be a marker of differentiation or maturation. Polyclonal cell populations, such as peripheral blood lymphocytes, show a bimodal distribution of surface antigen density, whilst monoclonal cell populations analysed quantitatively showed unimodal antigen density distributions. This suggests the antigen may be a clonal marker.     

Opiate induced feeding is not dependent on the hippocampus

It has been shown that spreading depression of the hippocampus can elicit feeding, and that several opioid peptides elicit spreading depression when injected into the hippocampus. To determine whether such depression is the primary mechanism by which opiates induce feeding, we tested the feeding effects of naloxone, an opiate antagonist, and butorphanol tartrate, a kappa-sigma agonist, on feeding in rats with and without hippocampal lesions. Naloxone tended to reduce intake approximately equally in the two groups. Similarly, the doses of butorphanol that increased intake in sham rats were equally effective in lesioned rats. It was concluded that the hippocampus is not the major structure mediating opiate-induced feeding.     

Cervical specimen order and performance measures of Chlamydia trachomatis diagnostic testing

The orders of three endocervical specimens of 3,561 women for Chlamydia trachomatis testing were randomized to determine whether test performance measures of two nucleic acid amplification tests and a DNA probe were affected by swab order. Specimen collection order did not appear to affect the diagnostic accuracy of these tests.     

Prostaglandin E2 receptor subtype 2 (EP2) regulates microglial activation and associated neurotoxicity induced by aggregated α-synuclein

Background  

The pathogenesis of idiopathic Parkinson's disease (PD) remains elusive, although evidence has suggested that neuroinflammation characterized by activation of resident microglia in the brain may contribute significantly to neurodegeneration in PD. It has been demonstrated that aggregated α-synuclein potently activates microglia and causes neurotoxicity. However, the mechanisms by which aggregated α-synuclein activates microglia are not understood fully.     

Diverged evolution of recent equine-2 influenza (H3N8) viruses in the Western Hemisphere

Summary.  We reported previously that equine-2 influenza A virus (H3N8) had evolved into two genetically and antigenically distinct “Eurasian” and “American” lineages. Phylogenetic analysis, using the HA1 gene of more recent American isolates, indicated a further divergence of these viruses into three evolution lineages: A South American lineage, a Kentucky lineage, and a Florida lineage. These multiple evolution pathways were not due to geographic barriers, as viruses from different lineages co-circulated. For the Kentucky lineage, the evolution rate was estimated to be 0.89 amino acid substitutions per year, which agreed with the previously estimated rate of 0.8. For the South American lineage, the evolution rate was estimated to be only 0.27 amino acid substitutions per year. This low evolution rate was probably due to a unique alternating Ser138 to Ala138 substitutions at antigenic site A. For the Kentucky lineage, there was a preference for sequential nonsynonymous substitutions at antigenic site B, which was also a “hot spot” for amino acid substitutions. Convalescent sera had minimal cross-reactivity to viruses of different lineages, indicating antigenic distinctions among these viruses. In contrast to human H3N2 viruses, our results suggested that the evolution of equine-2 influenza virus resembled the multiple evolution pathways of influenza B virus. Accepted December 14, 2000 Received September 19, 2000     

Prion protein accumulation and neuroprotection in hypoxic brain damage

The function of the normal conformational isoform of prion protein, PrP(C), remains unclear although lines of research have suggested a role in the cellular response to oxidative stress. Here we investigate the expression of PrP(C) in hypoxic brain tissues to examine whether PrP(C) is in part regulated by neuronal stress. Cases of adult cerebral ischemia and perinatal hypoxic-ischemic injury in humans were compared with control tissues. PrP(C) immunoreactivity accumulates within neuronal processes in the penumbra of hypoxic damage in adult brain, and within neuronal soma in cases of perinatal hypoxic-ischemic injury, and in situ hybridization analysis suggests an up-regulation of PrP mRNA during hypoxia. Rodents also showed an accumulation of PrP(C) in neuronal soma within the penumbra of ischemic lesions. Furthermore, the infarct size in PrP-null mice was significantly greater than in the wild type, supporting the proposed role for PrP(C) in the neuroprotective adaptive cellular response to hypoxic injury.