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Biomedical subjects

M Richman

Publications and source records attributed to M Richman.

6 recordsLinked to original sources
PubMed1996

Olfactory marker protein (OMP) gene deletion causes altered physiological activity of olfactory sensory neurons.

Olfactory marker protein (OMP) is an abundant, phylogentically conserved, cytoplasmic protein of unknown function expressed almost exclusively in mature olfactory sensory neurons. To address its function, we generated OMP-deficient mice by gene targeting in embryonic stem cells. We report that these OMP-null mice are compromised in their ability to respond to odor stimull, providing insight to OMP function. The maximal electroolfactogram response of the olfactory neuroepithelium to several odorants was 20-40% smaller in the mutants compared with controls. In addition, the onset and recovery kinetics following isoamyl acetate stimulation are prolonged in the null mice. Furthermore, the ability of the mutants to respond to the second odor pulse of a pair is impaired, over a range of concentrations, compared with controls. These results imply that neural activity directed toward the olfactory bulb is also reduced. The bulbar phenotype observed in the OMP-null mouse is consistent with this hypothesis. Bulbar activity of tyrosine hydroxylase, the rate limiting enzyme of catecholamine biosynthesis, and content of the neuropeptide cholecystokinin are reduced by 65% and 50%, respectively. This similarity to postsynaptic changes in gene expression induced by peripheral olfactory deafferentation or naris blockade confirms that functional neural activity is reduced in both the olfactory neuroepithelium and the olfactory nerve projection to the bulb in the OMP-null mouse. These observations provide strong support for the conclusion that OMP is a novel modulatory component of the odor detection/signal transduction cascade.

Animals↗
PubMed1990

Mapping of the two mouse engrailed-like genes: close linkage of En-1 to dominant hemimelia (Dh) on chromosome 1 and of En-2 to hemimelic extra-toes (Hx) on chromosome 5.

The mouse genome contains two genes, En-1 and En-2, with sequence similarity to the engrailed gene of Drosophila. Using conventional linkage crosses, we have shown that En-1 maps approximately 0.28 cM distal to the dominant hemimelia (Dh) gene on chromosome 1 and that En-2 maps approximately 1.1 cM proximal to the hemimelic extra-toes (Hx) gene on chromosome 5. We have also shown by Northern blot analysis that En-1 transcripts in Dh homozygotes and En-2 transcripts in Hx homozygotes are of normal size and abundance. These data, in conjunction with previously published studies of the patterns of En-1 and En-2 expression in developing mouse embryos, suggest that Dh and Hx are very unlikely to be mutant alleles of En-1 or En-2, respectively. Instead, we suggest that En-1-Dh and En-2-Hx represent paralogous linkage groups that evolved following duplication of a common ancestral chromosome segment.

Animals↗
PubMed1989

Lack of host cellular immune response in eruptive molluscum contagiosum.

A lack of cellular immunity on the part of the host has been incriminated as the cause of the persistence of the cutaneous lesions of molluscum contagiosum. We present a patient in the eruptive phase of the disease, confirming the absence of T-lymphocyte and natural killer cell subsets in the base of these typical lesions, using a panel of monoclonal antibodies. We also report the observation of lipid material ultrastructurally (confirmed by osmium staining on fresh-frozen tissue), as well as cross-reactivity immunocytochemically of the antigens on these molluscum bodies with antigens normally present on macrophages, as defined by DAKO-macrophage monoclonal antibodies. We have considered the possible role of these findings in the lack of host cellular responsiveness in the eruptive phase of the disease.

Adult↗
PubMed1982

Effects of contact lens deformation on tear film pressures induced during blinking.

The pressures induced in a tear film between a contact lens and the eye during the initial stages of a blink are estimated by means of a flexible slider-bearing model. Calculations are made of the pressure distributions as functions of two nondimensional parameters, one of which is purely geometrical and the other involves the sliding velocity, the viscosity of the tear film, and the flexibility of the lens. For the dimensions and velocities which apply to a typical blink, it is found that the effects of soft lens deformation in reducing pressure can be significant, especially for small tear film thicknesses.

Blinking↗