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Biomedical subjects

H J Roberts

Publications and source records attributed to H J Roberts.

At least 19 recordsLinked to original sources
PubMed1992

AIDS in Belle Glade.

Explore the source record for details and available documents.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Pentachlorophenol-associated aplastic anemia, red cell aplasia, leukemia and other blood disorders.

Aplastic anemia, pure red cell aplasia, leukemia, lymphoma and other hematologic disorders have followed exposure to products containing the pesticide pentachlorophenol (PCP). Information in a 25-year compilation of documented case reports is summarized, involving industrial and home exposure and accidental poisoning in a nursery. The potential hematologic, mutagenic and carcinogenic effects of PCP and its dioxin-dibenzofuran contaminants also are reviewed. Owing to widespread contamination of the environment by PCP products, and latent periods of up to several decades after exposure before these disorders become manifest clinically, it is necessary to consider their etiologic or contributory role. These issues continue to surface in toxic tort litigation relative to causation.

Adolescent↗
PubMed1989

Meiosis in trisomic female mice with Robertsonian translocations. I. Prophase pairing.

The prophase oocytes of two murine Robertsonian translocation (Rb) trisomies of chromosomes 16 and 19 were investigated using electron microscopy and a whole-cell micro-spreading technique after silver staining. About 20% of fetuses of each type were trisomic. They were obtained by mating animals heterozygous for two Rb's, monobrachially homologous for either chromosome 16 or 19, to an entirely acrocentric stock. Because of the almost inevitable prenatal mortality of the trisomic embryos, their fetal ovaries were "rescued" by an in vitro method for prophase studies. Analysis of the recovered oocytes showed frequent, close pairing associations of the three trisomic axes and evidence suggesting that the closely apposed axes coincided with the side-by-side formation of parallel, complete, true synaptonemal complexes; hence, the cytogenetic dogma that pairing is always two-by-two was contradicted. The presence of two parallel complexes has implications for crossing-over recombination. Triple associations of axes were found in almost half the trisomy 19 (Ts19) and in about 70% of the trisomy 16 (Ts16) prophases. The extent of triple associations varied and was greater in Ts16 than in Ts19 oocytes. Other relevant observations concerned the proportions of univalents and of univalence of the trisomic axes (21% in Ts16 and 46% in Ts19) and the distinctive, thickened appearance of all univalent axes. The pairing behaviour observed in balanced heterozygotes confirms what appears to be nonhomologous pairing and synaptic adjustment within the short-arm axes of the Rb trivalents.

Animals↗
PubMed1988

A cell-type-specific abnormality of cell proliferation in mutant (curly tail) mouse embryos developing spinal neural tube defects.

The mouse mutant curly tail (ct) provides a model system for studies of neurulation mechanisms. 60% of ct/ct embryos develop spinal neural tube defects (NTD) as a result of delayed neurulation at the posterior neuropore whereas the remaining 40% of embryos develop normally. In order to investigate the role of cell proliferation during mouse neurulation, cell cycle parameters were studied in curly tail embryos developing spinal NTD and in their normally developing litter-mates. Measurements were made of mitotic index, median length of S-phase and percent reduction of labelling index during a [3H]thymidine pulse-chase experiment. These independent measures of cell proliferation rate indicate a reduced rate of proliferation of gut endoderm and notochord cells in the neuropore region of embryos developing spinal NTD compared with normally developing controls. The incidence of cell death and the relative frequency of mitotic spindle orientations does not differ consistently between normal and abnormal embryos. These results suggest a mechanism of spinal NTD pathogenesis in curly tail embryos based on failure of normal cell proliferation in gut endoderm and notochord.

Animals↗
PubMed1983

Undernutrition of weanling and adult rats: effects on operant responding.

In the rat, brain growth is most vulnerable to undernutrition during the suckling period. Undernutrition at that stage also produces lasting effects on behaviour and it is often assumed that these are due to disturbances of brain growth. The proposal that this may not necessarily be so was explored by testing the behaviour of rats which had been undernourished at later stages of life and which, therefore, would be expected to show little or no deficit in brain growth. Rats were undernourished either immediately after weaning (25-67 days) or in adulthood (80-134 days) and were tested 3-4 months later on variable interval and variable ratio schedules of reinforcement with food as the reward. Their behaviour on these schedules was similar to that of rats undernourished during the suckling period: both groups responded or tended to respond at a higher rate than controls. Hence, it is possible that undernutrition at any stage in life may make animals more responsive to food when deprived subsequently. A cognitive mechanism for this change in behaviour is suggested.

Animals↗