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Biomedical subjects

K M Fischer

Publications and source records attributed to K M Fischer.

11 recordsLinked to original sources
PubMed1998

Expanded (CAG)n, (CGG)n and (GAA)n trinucleotide repeat microsatellites, and mutant purine synthesis and pigmentation genes cause schizophrenia and autism.

Unstable (CAG)n trinucleotide repeat microsatellites are hypothesized to cause schizophrenia. The (CAG)n microsatellite of dominant spinal cerebellar ataxia type 1 (SCA1) is a candidate schizophrenia gene. Autism results from expansions of (CGG)n and (GAA)n trinucleotide repeat stretches at fragile X syndrome (FRAXA), and the recessive Friedreich's ataxia (FA). Dominant ataxia genes may cause schizophrenia and recessive ataxia genes may cause autism. Syndromes with autism show purine synthesis defects (PSDs) and/or pigmentation defects (PDs). Autism is caused by very lengthy expansions of (CAG)n, (CGG)n and (GAA)n repeats, while schizophrenia results from much smaller (CAG)n and (CGG)n repeat expansions.

Animals↗
PubMed1992

Transgenic domestic animals provide an animal model for rheumatoid arthritis.

Production of transgenic domestic animals by microinjection of egg nuclei has permitted the introduction of exogenous genes into the transgenic animal. Pursell et al (1) report severe synovitis, cardiomegaly, dermatitis, renal disease and gastric ulcers in pigs with an expressed bovine growth hormone transgene. I have hypothesized that rheumatoid arthritis (RA) is a disease with initial symptoms to the gamete (2, 3). This hypothesis is supported by data showing a reduced rate of RA in women using oral contraceptives (4, 5) and remission of RA in pregnancy (6). RA in animals resulting from trauma to the gamete would be consistent with this hypothesis. This paper hypothesizes that some of the pathology associated with genetic engineering of livestock can be attributed to a rheumatoid arthritis-like spectrum of symptoms. This systemic reaction could be sufficiently similar to human RA to permit the transgenic pig to serve as an animal model of the disease.

Animals↗
PubMed1991

Hypothesis: tobacco use is a risk factor in rheumatoid arthritis.

Rheumatoid arthritis (RA) has been described in 3000-5000 year-old skeletal remains from North America by Rothschild, Turner and DeLuca (1). RA was first described unambiguously in Europeans in 1800 (1). Tobacco was introduced into Europe from the New World in the 1600s, and Rothschild, Turner and DeLuca include tobacco among variables that could be responsible for the appearance of RA in Europe. Primary and secondary exposure to tobacco smoke could be etiological, along with other causal variables. Tokuhata found cigarette smoking correlated with reduced fertility in women (2). I have hypothesized that RA is a disease with initial symptoms to the gamete and gonad (3). The hypothesis predicts a significant positive correlation between primary and secondary exposure to smoking and RA.

Arthritis, Rheumatoid↗
PubMed1985

Systemic lupus erythematosus and human development.

The symptoms of systemic lupus erythematosus (SLE) suggest that the manifestations of the disorder are related to known or plausible control mechanisms in embryogenesis. It is suggested that homo sapiens has, in the course of evolution, developed novel processes controlling development.

Embryonic and Fetal Development↗
PubMed1978

Sequential changes of T- and B-cells, virus antigen expression and primary histologic tumor diagnosis in virus-induced lymphomagenesis of mice.

T- and B-cell counts, estimation of Ig receptor fluidity, and expression of virus-coded antigens were correlated with histological findings during the development of virus-induced mouse lymphoma. Tested were BALB/c mice after infection with the strongly oncogenic Moloney leukemia virus (MLV), the moderately oncogenic (in BALB/c mice) Gross passage A virus (GLV-A), and the essentially non-oncogenic Gross 3T3 tissue culture virus (GLV-T). Methods included immunofluorescence microscopy with antisera against T-cells, B-cells and MLV intact virus, routine histology, and electron microscopy. Following time sequence of changes was observed in mice with oncogenic MLV- and GLV-A infection but not in GLV-T infection: Significant decrease of Ig receptor fluidity and expression of virus antigen were observed already at the initial investigation, i.e. 2 weeks post virus infection. This was followed by significant decreases in percent T-cells 5--8 weeks later, accompanied by histologic atrophy of the thymus and of thymus-dependent regions of lymphatic tissues. Another 2--8 weeks after the decrease in percent T-cells occurred, the first lymphomatous foci became obvious in the thymus. Clinically overt and generalized lymphoma was diagnosed at 20--30 weeks post virus infection. Ultrastructurally, some changes in the arrangement and quantity of cytoplasmic microfilaments were noted in proliferating lymphoblasts and in lymphoma cells. It is concluded, that the described changes were related to the oncogenic potential of mouse C-type RNA viruses and not just to virus infection per se.

AKR murine leukemia virus↗