Immunological and morphological consequences of vasectomy in the rabbit.

Cell-mediated immunity to spermatozoa was detected in vitro 6--18 months after vasectomy in the rabbit. The autoimmunity was accompanied by aspermatogenic orchitis in the testes and epididymides.     

Purification of canine myocardial mitochondrial creatine kinase

Summary Mitochondrial creatine kinase, purified for the first time, is a dimeric molecule with a mol.wt of 82,000 and does not hybridize with M or B subunits or react to their specific antiserum. A specific antiserum to the mitochondrial form was developed which does not cross-react with the B or M subunits. Thus, the mitochondrial form is biochemically and immunologically unique.Supported in part by the Special Center of Research in Ischemic Heart Disease (1 P17 HL 17646).I thank Ann Grace for her technical assistance and Ava Ysaguirre for typing the mansucript.     

No evidence for preservation of somatostatin-containing neurons after intrastriatal injections of quinolinic acid

Intrastriatal injections of excitotoxic amino acids and their analogues (for example kainate and ibotenate) elicit a pattern of neuronal degeneration that is similar in many respects to that observed in Huntington's disease. In this disease there is a progressive degeneration of most types of intrinsic neuron but somatostatin and neuropeptide Y levels are increased 3-5-fold. This may be attributed to the selective preservation of a sub-class of striatal aspiny neurons, in which these two peptides are co-localized together with the enzyme NADPH-diaphorase. Beal et al. reported recently that following intrastriatal injections of quinolinic acid in rats, medium-sized aspiny neurons were selectively preserved and they suggested that quinolinic acid which is found in human brain might cause the neuronal degeneration seen in Huntington's disease. We have used immunocytochemical and enzyme histochemical techniques to examine this selective toxicity but find no evidence to support this finding. We conclude that there are substantial differences between the immunocytochemical changes detected in postmortem Huntington's disease brain and those following quinolinic-acid-induced degeneration.     

Molecular mechanism for the production of multiple forms of MM creatine kinase

Incubation of human, canine or rabbit MM creatine kinase with carboxypeptidase-N or B resulted in the production of 2 additional enzyme forms with increased anodal migration on polyacrylamide gels. The C-terminal amino acid of tissue MM creatine kinase from all 3 species was shown to be lysine, a specific substrate for carboxypeptidase-N and B.     

Essay Review: The Historicity of Sound and Hearing

This paper investigates the extent of overseas migration by British chemists over the period 1887–1971. Notwithstanding the ‘brain drain’ alarms of the 1960s, overseas employment was characteristic of some 19% of British chemists’ careers throughout our period, though its nature changed considerably. Our study examines the overseas employment histories of four cohorts of members of the [Royal] Institute of Chemistry in the ‘Chemists’ Database’ at the Open University. Those employed abroad were not only highly qualified but also both geographically mobile and occupationally versatile. Over the period, the pattern of chemists’ migration was broadly similar to that of British migration trends more generally. Except in the interwar years, chemists’ rate of migration was relatively constant. However, the length of time they spent abroad declined markedly over the period: long-term migration became less characteristic than short-term overseas employment for purposes of career development. From the late nineteenth century, British chemists staffed the Empire, but also found employment in the expanding US economy. After 1945, chemists’ destinations shifted more markedly towards North America, including Canada, and later also to Europe. Our work thus provides a new perspective on the dynamics of scientists’ migration and contributes to studies on the brain drain.     

An SCN9A channelopathy causes congenital inability to experience pain

The complete inability to sense pain in an otherwise healthy individual is a very rare phenotype. In three consanguineous families from northern Pakistan, we mapped the condition as an autosomal-recessive trait to chromosome 2q24.3. This region contains the gene SCN9A, encoding the alpha-subunit of the voltage-gated sodium channel, Na(v)1.7, which is strongly expressed in nociceptive neurons. Sequence analysis of SCN9A in affected individuals revealed three distinct homozygous nonsense mutations (S459X, I767X and W897X). We show that these mutations cause loss of function of Na(v)1.7 by co-expression of wild-type or mutant human Na(v)1.7 with sodium channel beta(1) and beta(2) subunits in HEK293 cells. In cells expressing mutant Na(v)1.7, the currents were no greater than background. Our data suggest that SCN9A is an essential and non-redundant requirement for nociception in humans. These findings should stimulate the search for novel analgesics that selectively target this sodium channel subunit.