Occupational risk of human parvovirus B19 infection for school and day-care personnel during an outbreak of erythema infectiosum.

Human parvovirus B19, the cause of erythema infectiosum, has recently been associated with adverse fetal outcomes. During a large outbreak of erythema infectiosum in Connecticut, a survey was conducted on 571 (90%) of 634 school and day-care personnel to determine the risk of acquiring B19 infection. Serologic evidence of B19 infection was determined by using an enzyme-linked immunosorbent assay. Of the school and day-care personnel, 58% had evidence of previous B19 infection. The minimal rate of B19 infection in susceptible personnel during the outbreak was 19%. The risk was increased for teachers and day-care providers who had contact with younger children and with greater numbers of ill children. These results suggest that B19 infection is an occupational risk for school and day-care personnel.

Oligodendrocytes repel axons and cause axonal growth cone collapse.

We have examined the interactions between axons regenerating from dorsal root ganglia (DRGs) derived from newborn rats and oligodendrocytes cultured by three different techniques. Cultures examined after 2 days have a profuse outgrowth of axons from the DRGs, forming a dense mat on the culture surface. However, the axons avoid growing on oligodendrocytes; axons are seen all around these cells, but do not grow over them. We have also performed time-lapse video studies of the interactions between axonal growth cones and oligodendrocytes. Axons grow normally until their growth cone comes into direct contact with an oligodendrocyte, following which the growth cone remains motile for 30-60 min, but without making any progress over the cell. The growth cone then suddenly collapses, and the axon retracts, leaving a thin strand in contact with the cell. After this a new growth cone is usually elaborated and the process repeated. Oligodendrocytes are therefore inhibitory to axonal growth, and this may partially explain the failure of axons to regenerate in the mammalian central nervous system.

Estimation of lipase activity by the diffusion plate method.

A diffusion plate method for the assay of the activity of lipases in large series of samples was worked out. When using this method the maximum deviation was found to be +/- 3.8%.

Deacylation of acetylated amino acids by the esterase from Mycobacterium phlei.

In addition to typical acetyl esters, acetic ester acetyl-hydrolase from Mycobacterium phlei can degrade aliphatic acetylated amino acids under suitable conditions.

Utilization of a lipid substrate for submerged fermentation of Streptomyces albus.

When investigating the effect of aeration on the utilization of a lipid substrate from the cultivation broth and production of salinomycin in Streptomyces albus it was demonstrated that a higher aeration results in a better utilization of soya oil and a higher production of the antibiotic.

Central pontine myelinolysis in association with Hodgkin's lymphoma.

Central pontine myelinolysis was found histologically in a young man who died with Hodgkin's lymphoma. Clinically he had developed a progressive peripheral sensory deficit, ataxia, quadriparesis, dysarthria, incontinence and drowsiness. This is the fifth case reported in the British literature. The pathogenesis and aetiology of this primary demyelinating disease are considered.

Experimental contribution to the pathogenesis of spina bifida.

Reopening of the central canal in 3-day-old chick embryos results in the development of a typical myeloschisis within 5 min. Focal continuity between the ectoderm and neural tissue at the site of experimentally induced spina bifida (SB) may be achieved in 2 hr and increases in consecutive hours. In 24 hr a secondary neuro-ectodermal junction at the site of SB is fully formed and can be misinterpreted as evidence of a failure of the neural tube to close. Therefore the continuity between ectoderm and neural tube to close. The detachment of the notochord from the open portion of the spinal cord is a secondary phenomenon.

Pathogenesis of trypan-blue-induced spina bifida.

Congenital malformations induced in rats by the application of trypan blue were studied at variable times of their development of congenital malformations is a continuous process of structural and functional adaptation of the development embryo to focal tissue degeneration and necrosis (cell death). The primary degeneration is a transitory phenomenon, because the dead cells are phagocytosed by surviving cells. However, the damage triggers off the process of abnormal development.

Pathogenesis of diastematomyelia and spina bifida.

Three cases of spina bifida (SB) associated with diastematomyelia (DM) are described and possible differences in pathogenesis are discussed. The frequent simultaneous occurrence of both malformations and the possibility that the cord can be split above, at the level of or below the SB indicate a common pathogenesis for SB and DM. Splitting of the cord symmetrically, asymmetrically, bilateraly or even antero-posteriorly can be explained only by the existence of a destructive phenomenon which is responsible for the bifurcation of the neural tube or its anlage. The existence of such a phenomenon indicates that myelocele can develop due to re-opening of a previously closed neural tube. Meningocele may be a manifestation of early embryonic antero-posterior DM in which the anterior tubule develops into an almost normal spinal cord, whereas the posterior tubule provides the wall of the cystic sac of meningocele in which most or all the neural tissue undergoes fibrous replacement.