Mapping of the mouse 86-kDa heat-shock protein expressed gene (Hsp86-1) on chromosome 12 and related genes on chromosomes 3, 4, 9, and 11

The HSP86 gene family in BALB/c, AKR/J, C58/J, and NFS/N inbred mice comprises an intron-containing expressed gene and, depending on the strain, two to four other HSP86-related members that are apparently processed pseudogenes. The expressed gene locus, Hsp86-1, was identified by its sequence identity with the mouse HSP86 cDNA coding region together with the presence of an intron at the same position as in the homologous human gene. Hsp86-1 was mapped 11.6 cM from the immunoglobulin heavy chain gene IgH on Chromosome 12 using an intersubspecies backcross. Two of the other loci that were common to all inbred strains tested, designated Hsp86-ps1 and Hsp86-ps2, were mapped to positions on Chromosomes 11 and 3, respectively. An HSP86-related locus specific to NFS/N and C58/J mice, designated Hsp86-ps3, was mapped on Chromosome 9. Also, an HSP86-related locus that was unique to NFS/N mice, designated Hsp86-ps4, was mapped to Chromosome 4.     

Successful disinfection of trumpet mouthpieces using domestic steam disinfection

There have been numerous reports in the literature describing the diversity of microbial flora isolated from woodwind and brass instruments, with potential infection risks for players, especially when such instruments are shared. Steam disinfection has become established as a trusted method of decontamination; however, there have been no reports on the employment of this technology to disinfect parts of musical instruments, hence it was the aim of this study to examine the fate of bacterial and yeast pathogens on artificially contaminated trumpet mouthpieces and to evaluate whether such disinfection is an effective method of disinfection for such instrument parts. Trumpet mouthpieces were artificially contaminated with 18 microbial strains (17 bacteria from four genera (Enterococcus, Escherichia, Staphylococcus and Streptococcus) and one yeast (Candida)), each at an inoculum density of approximately 1·5 × 10⁷ colony forming units and subjected to a disinfection cycle. The experiment was repeated including 50% (v/v) sterile sputum as soil. No bacteria or yeast organisms were recovered post disinfection, including following recovery and with nonselective cultural enrichment techniques.     

Degradation of DNA and structure-activity relationship between bleomycins A2 and B2 in the absence of DNA repair.

The contribution of DNA repair to the net number of DNA breaks produced during chemical degradation of DNA was determined by using temperature-sensitive mutant cells deficient in ATP-dependent DNA ligase [poly(deoxyribonucleotide):poly(deoxyribonucleotide) ligase, EC 6.5.1.1]. In a very sensitive assay for determining lesions introduced into Saccharomyces cerevisiae DNAs, 2-14C- and 6-3H-prelabeled DNAs from ligase-proficient and ligase-deficient cells were sedimented together through precalibrated, isokinetic alkaline sucrose gradients. DNA ligation was slower after chemical degradation of DNA by bleomycin than after gamma irradiation. DNA breaks increased approximately linearly with drug concentrations, and were approximately equivalent for ligase-proficient and ligase-deficient cells. These results were unexpected because ligase-deficient, but not ligase-proficient, cells lacked the capacity to eliminate DNA breaks produced by bleomycin. The results indicated that DNA repair did not occur during the chemical degradation of DNA under the experimental conditions. Bleomycin B2 produced considerably more DNA breaks than bleomycin A2 over a range of concentrations in ligase-proficient cells, which tolerated higher numbers of DNA breaks in general than ligase-deficient cells. The chemical analogues are structurally identical except for their cationic C-terminal amine. The actual number of DNA breaks produced by bleomycin A2 or bleomycin B2, and not the concentration of bleomycin A2 or bleomycin B2 per se, determined the amount of cell killing. DNA repair is critical in quantitating DNA breaks produced by chemicals, but was ruled out as a factor in the higher DNA breakage by bleomycin B2 than bleomycin A2.     

A Short, Informal History of the Biological Sciences at Yale University

In May 2012, Yale University’s Graduate School of Arts and Sciences held a reunion for all who have received doctorates from Yale in the biological sciences. The proceedings began with two presentations on the history of biological research at Yale: one focused on the Medical School, and the other centered on the rest of the University. This essay is a lightly edited version of my account of the history of the biological sciences outside the Medical School.     

Enhanced K-cell activity in the peripheral blood of patients with malignant disease

Summary We have analysed the influence of human malignant, inflammatory and infectious disease on the capacity of peripheral lymphocytes to mediate antibody-dependent haemolysis. The application of an enzyme-like kinetic model for measurement of maximal cytotoxic function has permitted reproducible and sensitive determinations of the K-cell function. The results show that malignant disease is associated with enhancement of ADCC capacity.