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Biomedical subjects

H Rauch

Publications and source records attributed to H Rauch.

43 records · Page 3Linked to original sources

[Problems of the ectoparasite control in the Mongolian People's Republic].

The co-operation between G.D.R. and M.P.R. in the field of control of ectoparasites in farm animals is described. The problems under the specific conditions of the M.P.R. in the control of the principal parasitoses of economic importance such as hypodermosis, mange, tick infestations, oestrosis, vermipsyllosis, gasterophilosis and wohlfahrtiosis are analysed. The successfully applied hypodermosis control program represents the base for further systematic, state-directed strategic measures in controlling of ectoparasitoses.

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Inverse relationship between net electric charge on the antigen and that on the sensitized cell in cellular immune response: demonstration with basic encephalitogen of the brain.

An inverse relationship exists between the net-electrical charge of immunogens and the antibodies elicited (1). The cellular basis of the net charge phenomenon has been established for both positively and negatively charged immunogens, by cell separation techniques over columns of opposite charge (7, 8). To establish whether this phenomenon can be extended to include cell-mediated immunity, the response to basic encephalitogenic protein (BE) which induces experimental allergic encephalomyelitis (EAE) was now investigated. Lymph node cells from sensitized strain 13 guinea pigs were fractionated over positively and negatively charged columns and compared to unfractionated cell populations in two assay systems: (a) in vitro response to BE in terms of lymphocyte transformation and (b) the passive transfer of EAE to unsensitized syngeneic recipients. The response was found to be confined to the fraction of cells eluted from glass bead columns, namely, the more negative cells. Cells eluted from poly-L-lysine-coated glass bead columns (i.e., positive cells) were devoid of the capacity to respond to this antigen either in vivo or in vitro. It was previously established that thymocytes rather than bone marrow cells account for the inverse charge phenomenon as assayed by T-helper-cell function in in vivo antibody production (8). We have now extended the inverse charge effect to include cell-mediated immune response of the delayed hypersensitivity type.

Animals↗

Fractionation of functional lymphocytes sensitized to basic encephalitogen on derivatized collagen and gelatin gels.

The lymph node cells of basic encephalitogen (BE)-sensitized guinea pigs were fractionated on derivatized collagen and gelatin gels. The population of cells specifically reactive to this antigen can be isolated from derivatized gelatin gels and retain their viability and functionality as assayed in vitro. The specific binding of BE-sensitized cells to BE-derivatized gels comprised between 1 and 2% of the cells applied per plate. The ratio of sensitized cells bound to non-sensitized cells bound ranged between 4 and 6. The viability and functionality of adherent cells detached from collagen gels after enzymatic degradation were impaired. In contrast, the responses obtained with the adherent cell population released from the gelatin gels, by melting at 37 degrees C, were equal or greater than those of the original unfractionated lymph node cell cultures. Furthermore, it was possible to obtain a nonadherent cell population which was virtually completely depleted of the capacity to respond to the sensitizing antigen.

Animals↗

Toxic milk, a new mutation affecting cooper metabolism in the mouse.

Toxic milk, tx, a new autosomal recessive mutation in mice is described. Litters produced by mutant females display a syndrome including poor growth, hypopigmentation, tremors, and ultimately death at two weeks of age. These features, consistent with copper deficiency, are attributed to failure in gestational hepatic copper accumulation exacerbated by subsistence on milk with greatly reduced copper content. Such infants can be rescued by foster-nursing on normal dams or by administered of supplemental cooper. Mutants themselves amass extraordinarily large concentrations of hepatic copper that ultimately leads to liver disease. Erroneous hepatic copper metabolism is further evidenced by reduced ceruloplasmin activity.

Animals↗