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Biomedical subjects

T L Hayes

Publications and source records attributed to T L Hayes.

69 records · Page 4Linked to original sources
PubMed1967

Tribolium castaneum: morphology of "aureate" revealed by the scanning electron microscope.

Counts of setae in "aureate" (au), spontaneous autosomal recessive mutation of good penetrance and viability, show that the au gene causes a three-fold increase in setation over the normal in the visible abdominal sternites but not in the membranous wings of the tenebrionid flour beetle Tribolium castaneum. Micrographs taken with the scanning electron microscope demonstrate that the au gene increases setation throughout the body.

Animals↗
PubMed1966

Electron microscopy of living insects.

Electron micrographs of living specimens of the various developmental stages of the insect Tribolium confusum have been obtained with a scanning electron microscope. In most cases the specimens resumed their normal activity after being examined with the electron microscope and under went metamorphosis into the next stage.

Animals↗
PubMed1966

Particle-size distribution of very low density plasma lipoproteins during fat absorption in man.

The size distributions of electrophoretically isolated subfractions of the very low density human plasma lipoproteins have been determined using electron microscopy. The primary and secondary particles observed in plasma of normal subjects after fat ingestion appear to have similar size distributions. Particles produced by corn oil feeding can be fixed by the osmium tetroxide reaction while those produced by butter fat feeding could not be fixed or made visible by this technique. Good agreement between particle size as measured by electron microscopy and particle size as predicted by ultra-centrifugal analysis was obtained.

Blood Protein Electrophoresis↗
PubMedDate not supplied

Evaluation of neutralized chemical agent identification sets (CAIS) for skin injury with an overview of the vesicant potential of agent degradation products.

Vesication and skin irritation studies were conducted in hairless guinea-pigs to determine the vesicant and skin irritation potential of chemically-neutralized Chemical Agent Identification Sets (CAIS). The CAIS are training items that contain chemical warfare-related material--sulfur mustard (HD), nitrogen mustard (HN) or lewisite (L)--and were declared obsolete in 1971. Animals were dosed topically with 'test article'--neat HD, 10% agent/chloroform solutions or product solutions (waste-streams) from neutralized CAIS--and evaluated for skin-damaging effects (gross and microscopic). Product solutions from the chemical neutralization of neat sulfur mustard resulted in microvesicle formation. All agent-dosed (HD or agent/chloroform solutions) sites manifested microblisters as well as other histopathological lesions of the skin. Waste-streams from the neutralization of agent (agent/chloroform or agent/charcoal) were devoid of vesicant activity. Cutaneous effects (erythema and edema) were consistent with the skin-injurious activity associated with the neutralizing reagent 1,3-dichloro-5,5-dimethylhydantoin (DCDMH). Chemical neutralization of CAIS was effective in eliminating/reducing the vesicant property of CAIS containing agent in chloroform or agent on charcoal but was inefficient in reducing the vesicant potential of CAIS containing neat sulfur mustard.

Animals↗
PubMedDate not supplied

Nonphosphorylated neurofilament protein and calbindin immunoreactivity in layer III pyramidal neurons of human neocortex.

Subpopulations of pyramidal neurons in the neocortex have been shown to contain nonphosphorylated neurofilament protein (NPNFP) and calbindin D28K (Morrison et al., 1987; Campbell and Morrison, 1989; Hof et al., 1990; Kobayashi et al., 1990; Hof and Morrison, 1991; Mesulam and Geula, 1991). However, it is not known what relations, if any, exist between the pyramidal neurons containing each of these proteins. In this study, the expression of NPNFP and calbindin immunoreactivity was compared in six regions of human neocortex. Characteristic laminar patterns of immunoreactivity for each protein were seen in most regions examined, and both NPNFP- and calbindin-labeled pyramidal neurons were found in layer III. However, the pyramidal neurons labeled with NPNFP and calbindin differed in several respects. First, the sublaminar distribution of NPNFP-labeled pyramids within layer III differed across regions, ranging from an even distribution throughout the layer in a visual association region (area 18) to a predominance of labeled neurons in the deep half of that layer in a higher association region (area 20). The distribution of calbindin-immunoreactive pyramidal neurons also varied regionally, but in a different manner than that of the NPNFP-labeled neurons. Second, in every region examined, the average size of NPNFP-labeled layer III pyramids was greater than that of calbindin-immunoreactive pyramids. However, there was substantial regional heterogeneity in the extent to which the size distributions of neurons in each of the two populations overlapped. Third, in the regions in which NPNFP- and calbindin-immunoreactive neurons were most similar in size, the amount of colocalization (as identified by double-labeling studies) was also greatest. Similarly, in the regions in which there was minimal overlap in the size of the NPNFP- and the calbindin-immunoreactive neurons, there was minimal colocalization. These regional characteristics of NPNFP- and calbindin-immunoreactive layer III pyramidal neurons have implications for the involvement of these neuronal populations in Alzheimer's disease.

Adult↗