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D Senitzer

Publications and source records attributed to D Senitzer.

42 records · Page 3Linked to original sources
PubMed1975

Hyperglycemia in the NZB/NZW F1 hybrid mouse.

Both the NZW and NZB mice exhibit an elevated fasting blood sugar level when compared to Swiss white mice. The NZB/NZW F1 hybrid mouse shows still a higher fasting serum glucose level than either of its parental strains. The elevated glucose level is noted very early in the animals' life, long before definitive signs or symptoms of pathology are evident, and remains elevated at least until the fortieth week of life, the last testing period in our series before sacrificing the aminals. There are two major peaking periods for the glucose levels, namely at 4-10 weeks of age and then again at 31-40 weeks of age. These age periods correspond to the very young animal and to the animal that is beyond its prime and most likely sick and near the end of its lifespan due to the animals' inherent disease processes. The NZB and NZB/NZW F1 hybrid succumb to their disease processes at approximately 8-10 months of age. The NZW usually lives until 18 months. The questions are raised: does the altered immunologic state in the NZB and/or the NZB/NZW F1 hybrid produce the elevated blood sugar levels and the pancreatic histopathology or is it the early hyperglycemic condition coupled with pancreatic pathology which are in some measure instrumental in producing the lesions discussed and observed, in the beginning of the three to four month period of age, in the various organs? Is there a relationship between the hyperglycemic condition and the immune state or are these independent phenomena in a genetically "mixed up" mouse?

Animals↗
PubMed1972

Deoxyribonucleic acid of Anaplasma marginale.

Deoxyribonucleic acid from isolated marginal bodies and calf erythrocytes infected with Anaplasma marginale is found to be double stranded and to contain 51 moles per cent guanine plus cytosine.

Anaplasma↗
PubMedDate not supplied

Autoimmune mechanisms in the pathogenesis of rheumatic fever.

The etiologic agent of acute rheumatic fever is the group A streptococcus; however, its role in the pathogenesis of this disease is not well understood. Epidemiologic and immunologic evidence suggests that there is a population at risk and that the nature of the host response to streptococcal antigens and the physicochemical nature of the streptococcal antigens all play a significant role in determining the natural history of the disease process. Furthermore, the genetic control of the interaction of the host with the streptococci is clearly involved in a set of events--as yet obscure--that result in acute rheumatic fever. Neither antibody-mediated nor cell-mediated hypersensitivity reactions have been demonstrated in vivo or in vitro that wholly reproduce the characteristics of this disease. Additional studies of the regulation of the immune response and of human immunogenetics are essential for gaining further insight into the pathogenesis of acute rheumatic fever.

Animals↗