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Biomedical subjects

A Saltzman

Publications and source records attributed to A Saltzman.

At least 55 records · Page 3Linked to original sources
PubMed1991

Tin compounds inhibit the plasma cell response to metallic tin. Transfer of inhibition by parabiosis.

Injection of metallic tin powder causes intense proliferation of plasma cells in draining lymph nodes of Lewis rats. Pretreatment orally with soluble tin salts prevents this response to subsequently injected metallic tin. In the present work, pretreatment with tin salts by parenteral injection was just as effective as addition to the drinking water. This new approach made the following experiments possible. Poorly soluble tin compounds were found to be inhibitory when injected parenterally. Tin salts injected parenterally into one of two rats joined in parabiotic union prevented the plasma cell response to metallic tin in both parabionts. The transfer of the inhibitory effect via the cross-circulating blood represents significant progress toward understanding the mechanisms involved. The evidence suggests the possibility that tin salts elicit an intermediary substance or process that is responsible for inhibition of the plasma cell response to metallic tin.

Animals↗
PubMed1991

Accelerated response to reinoculation in experimental allergic encephalomyelitis: histopathologic study.

Experimental allergic encephalomyelitis (EAE) was induced in Lewis rats by the injection of spinal cord tissue or myelin basic protein and adjuvants (Freund's or carbonyl iron or pertussis vaccine), or by adoptive immunization. After an interval of five to 12 weeks, the recovered rats were reinoculated by a different route and usually with a different adjuvant. The onset of the second attack was determined by the histologic detection of EAE lesions at intervals during the incubation period. In each of ten experiments, the second attack of EAE occurred one or two days earlier than in naive controls injected at the same time. Residual EAE lesions left over from the first attack could not explain the findings in the reinoculated rats. The accelerated response to the second inoculation may be related to the anamnestic response of classical immunology or to residual damage to the blood-brain barrier. Resistance to a second attack was not encountered in this histopathologic study.

Adjuvants, Immunologic↗
PubMed1991

Anaphylaxis is enhanced by increased absorption of antigen in postinflammatory state.

Hemagglutinating antibodies and cell-mediated immunity are increased when antigens are injected intraperitoneally (i.p.) into rats during the healing phase of a chemical peritonitis. In the present work, the anaphylactogenic effects of either sensitization or challenge were increased when any of three different antigens were injected i.p. in the postinflammatory state. The postinflammatory state made it possible to sensitize rats for anaphylaxis without any adjuvants at all. Lymph nodes draining the peritoneal cavity had evidence of enhanced absorption of inoculum in the postinflammatory state.

Adrenal Glands↗
PubMed1991

Accelerated response to reinoculation in experimental allergic encephalomyelitis: clinical study.

An attack of experimental allergic encephalomyelitis is generally thought to confer resistance to a second attack. Nevertheless, some authors have produced second attacks, sometimes with an anamnestic shortening of the incubation period. In addition, second attacks of experimental allergic encephalomyelitis with accelerated onsets following reinoculation were found in every experiment when histopathologic rather than clinical criteria were employed. In the present work, we found that clinical signs with accelerated onset were also found in each experiment provided that the first attack was produced with the aid of Freund's complete adjuvant and provided that the reinoculation stimulus was the highly potent combination of rat spinal cord and carbonyl iron. Whatever the potency of the reinoculation, and regardless of the occurrence of an accelerated onset, the eventual outcome was a decreased severity and mortality of the second attack of experimental allergic encephalomyelitis. The new data demonstrate that accelerated onset is not necessarily an indication of increased severity.

Adjuvants, Immunologic↗
PubMed1991

Cloning and expression of the human substance K receptor and analysis of its role in mitogenesis.

The primary structure of the human substance K receptor was established from the sequences of complementary DNA clones isolated from a human jejunal complementary DNA library. It consists of 398 amino acids, including seven putative transmembrane regions. The gene for the human substance K receptor was localized to chromosome region 10p13-10q23, a region with frequent chromosomal abnormalities. The human substance K receptor was expressed in transfected NIH-3T3 cells lacking endogenous substance K receptors, and Scatchard analysis of 125I-labeled substance K binding indicates approximately 100,000 receptors/cell with a single dissociation constant of 12 nM. Covalent cross-linking experiments utilizing 125I-substance K and three different chemical cross-linking reagents (disuccinimidyl suberate, disuccinimidyl tartrate, or 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide-HCl) demonstrate an apparent molecular weight of 45,000, consistent with little or no N-linked glycosylation. The binding of substance K to its receptor on transfected cells led to a rapid increase in the production of total inositol phosphates and the release of Ca2+ from internal stores. Growth of the cells transfected with the human substance K receptor is stimulated by the addition of substance K to the medium to a level similar to 10% serum. Therefore, the human substance K receptor can function as a growth factor receptor when expressed in mouse 3T3 cells.

Amino Acid Sequence↗
PubMed1990

Encephalitogenicity for rats of myelin basic protein without the aid of water-in-oil emulsions.

The induction of experimental allergic encephalomyelitis (EAE) with purified myelin basic protein (MBP) has, heretofore, required its incorporation in a water-in-oil emulsion or adsorption on particulate adjuvants. In the present work, the absorption of a saline solution of MBP from the peritoneal cavity into the mediastinal lymph nodes was increased by giving repeated inoculations or by pretreating rats with a peritoneal irritant. Under these conditions, the only adjuvant needed for production of EAE was aqueous pertussis vaccine which was injected separately a few hours or one day after the MBP. Pertussis vaccine was also necessary for production of EAE with intradermal injection of aqueous MBP. By injecting the aqueous MBP directly into pre-enlarged popliteal lymph nodes, it was possible to produce EAE without the pertussis vaccine. Thus, EAE can be induced in rats using MBP without the addition of Freund's adjuvant or pertussis vaccine.

Animals↗
PubMed1990

Peptides of myelin basic protein are encephalitogenic in rats without the aid of emulsions.

Immunization with peptides is usually done with the aid of Freund's adjuvant. Using peptides derived from myelin basic protein, we show that aqueous solutions can be antigenic (encephalitogenic in this instance) in Lewis rats. The first procedure involved multiple doses of aqueous peptide, increased absorption into the lymphatic system from the peritoneal cavity in the postinflammatory state, and the use of pertussis vaccine. Three different peptides containing the major encephalitogenic site were active in this system, with the activity somewhat proportional to the size of the fragment. The second procedure, the direct delivery of peptide to lymph nodes by percutaneous inoculation, was equally successful and did not require the use of pertussis vaccine.

Absorption↗
PubMed1990

Acute obstructive parasternal lymphedema produced in rats without surgery.

Although rat red blood cells (RBC) were altered by pretreatment with glutaraldehyde, they nonetheless were well absorbed into mediastinal lymphatics of Lewis rats after intraperitoneal injection. Unlike normal RBC, they did not pass freely through the draining mediastinal lymph nodes. Instead, clumps of free and phagocytosed glutaraldehyde-treated RBC distended and obstructed the afferent lymphatics and the sinuses of draining lymph nodes. The lymphatic obstruction caused edema in a clearly defined compartment of fatty connective tissue between the muscle layers of the ventral chest wall. The obstructive lymphedema interfered with the immunizing effect of small doses of sheep RBC injected intraperitoneally. This study emphasizes the potential utility of the rat's mediastinal lymphatics for studies of lymphatic leakage and obstruction.

Animals↗
PubMed1990

Lymphatic metastases from the peritoneal cavity are increased in the postinflammatory state.

Cell suspensions of chemically induced tumors (rhabdomyosarcoma) were transplanted into the peritoneal cavities of Lewis rats. In normal animals, the greater omentum was the main site of tumor growth, and transdiaphragmatic metastases to regional lymph nodes in the mediastinum were few and small. In animals during the healing phase of a chemical peritonitis, the greater omentum was fibrotic, shrunken, and inactivated. The loss of the scavenging function of the omentum was associated with wide dissemination of the tumor in the peritoneal cavity and increased access of the tumor to the lymphatic stomata on the peritoneal surface of the diaphragm. Number and size of transdiaphragmatic metastases in draining lymph nodes were greatly increased in this postinflammatory state.

Animals↗
PubMed1989

Suppression of experimental allergic encephalomyelitis in rats by mercuric chloride.

Brown-Norway (BN) rats are uniquely susceptible to development of autoimmune phenomena and enlargement of lymph nodes and spleen after repeated injections of mercuric chloride. Despite its ability to produce autoimmunity, HgCl2 inhibited the development in BN rats of experimental allergic encephalomyelitis (EAE), another autoimmune process. The inhibition by mercury was probably due to lack of the normal absorption and granulomatous reaction to the EAE inoculum in the enlarged lymph nodes draining the inoculation site. Lewis rats did not develop enlarged nodes from HgCl2 treatment. Lewis lymph nodes absorbed the EAE inoculum abundantly and developed an extensive granulomatous reaction despite the mercury treatment, and there was only a slight inhibition of EAE. Therefore, the ability of HgCl2 to produce lymphadenopathy in BN rats may be responsible for the inability of these rats to absorb the inoculated antigen. The mercury-induced failure of absorption was manifested as an inhibition of EAE in BN rats.

Animals↗
PubMed1989

The hyperacute form of allergic encephalomyelitis produced in rats without the aid of pertussis vaccine.

The hyperacute form of experimental allergic encephalomyelitis (EAE), characterized by a short incubation period, severe paralysis, high mortality, and abundant polymorphonuclear leukocytes and fibrin in the lesions, was produced in rats without the use of pertussis vaccine (previously considered an essential requirement) or Freund's adjuvant. Carbonyl iron or mineral oil without mycobacteria were effective adjuvants and whole rat spinal cord was the best antigen. Hyperacute EAE was produced in this manner in some Lewis rats, most dark agouti (DA) rats and most F1 hybrids of these two strains. Clinical signs were earlier in onset and more severe in the DA strain than in the Lewis strain in all adjuvant-antigen combinations that were tested. Dark agouti rats developed clinical signs in six days, histological lesions in five days, and localized EAE lesions could be induced in four days. The data support the hypothesis that hyperacute type lesions (neutrophils and fibrin) can be caused by an exceptionally strong immune response to neural antigen, whether that response is engendered by a particular adjuvant (pertussis vaccine) or by an unusual degree of genetic susceptibility (DA rats).

Adjuvants, Immunologic↗
PubMed1989

Inflammatory siderosis of the nervous system in rats.

Large intravenous doses of a relatively nontoxic iron polymaltose complex were taken up by liver and spleen and did not enter the central nervous system (CNS) of normal rats. When the injections were given during development of the inflammatory lesions of experimental allergic encephalomyelitis (EAE), many iron-laden macrophages entered vessels, perivascular cuffs and neural parenchyma. Iron polymaltose injected before the EAE lesions started to develop, or during the healing phase, did not enter the lesions. This model of CNS siderosis may be useful for studies on long-term effects of iron and for neuroimaging by nuclear magnetic resonance.

Animals↗
PubMed1988

The role of antigen absorption in the resistance of brown-Norway rats to experimental allergic encephalomyelitis.

The designation of Brown-Norway (BN) rats as resistant to experimental allergic encephalomyelitis (EAE) is an oversimplification. Lewis rats are susceptible and BN rats are usually resistant to EAE after inoculation with guinea pig spinal cord or basic protein in Freund's adjuvant. However, EAE can be produced in BN rats by immunizing with rat cord and carbonyl iron, a particulate adjuvant. In the present work, the possibility that susceptibility of BN rats under these conditions is due only to the special qualities of the adjuvant has been eliminated by producing EAE in them without any adjuvant at all, merely by increasing the absorption and processing of the rat cord antigen. The susceptibility of the F1 hybrids is intermediate with respect to guinea pig cord antigen but it was equal to or greater than either parental strain when tested with rat cord antigen. Histologic evidence that BN rats do not absorb or process neural antigen as well as other strains, and the augmentation of EAE by increasing the dose and absorption of the inoculum, suggest that antigen absorption, processing and presentation is a "bottleneck" for development of EAE in BN rats. Absorption and processing of antigen should be considered along with cellular response, inflammatory mediators and epitope dominance when analyzing susceptibility and resistance to EAE.

Adjuvants, Immunologic↗
PubMed1988

Transcription elongation factor SII interacts with a domain of the large subunit of human RNA polymerase II.

Genomic sequences for the large subunit of human RNA polymerase II corresponding to a part of the fifth exon were inserted into an expression vector at the carboxy-terminal end of the beta-galactosidase gene. The in-frame construct produced a 125-kilodalton fusion protein, containing approximately 10 kilodaltons of the large subunit of RNA polymerase II and 116 kilodaltons of beta-galactosidase. The purified bacterially produced fusion protein inhibited specific transcription from the adenovirus type 2 major late promoter, while beta-galactosidase had no effect. This effect of the fusion protein was during RNA elongation, not at the level of initiation, resembling the faithfully initiated but incomplete transcripts produced with purified factors in the absence of SII. Similarly, monoclonal antibody 2-7B, which reacts with the RNA polymerase II region represented in the fusion protein, inhibited specific transcription at the level of elongation in a whole-cell extract. Both monoclonal antibody 2-7B and the fusion protein, although unable to inhibit purified RNA polymerase II in a nonspecific transcription assay, selectively blocked the stimulation elicited by transcription elongation factor SII on the activity of the purified enzyme in vitro. This suggests that the fusion protein traps the SII in nonstimulatory interactions and that antibody 2-7B inhibits SII binding to RNA polymerase II. Thus, this suggests that an SII-binding contact required for specific RNA elongation resides within the fifth exon region of the largest RNA polymerase II subunit.

Amino Acid Sequence↗
PubMed1988

The topography of mercurial lymphadenopathy in brown Norway rats.

Injection of mercuric chloride caused a progressive systemic lymphadenopathy and splenomegaly in Brown Norway (BN) but not in Lewis rats, as reported by others. We studied the number, duration and route of HgCl2 treatments and the topography of the resultant lymphadenopathy, as well as its age and strain dependency. Five injections of HgCl2 increased three-fold the weight of the lymph nodes which became considerably heavier than the spleen. Weanling rats were less susceptible than adults. A regional lymphadenopathy could not be produced. However, a synergistic interaction was observed when the systemic effects of HgCl2 were added to the regional lymphadenopathy produced by injections of metal powders, such that the lymph node mass approached 2% of body weight.

Animals↗
PubMed1988

Retrosternal hemorrhage: an experimental model for study of lymphatic leakage.

Courtice and colleagues observed that blood injected into the peritoneal cavity of rats occasionally leaked from retrosternal lymphatics. The present work shows that this leakage is determined by volume as well as dose of inoculum. The uniform occurrence of visible retrosternal hemorrhage after injection of diluted blood suggests its use as a model for lymphatic leakage. Leakage was prevented when the blood was instilled during the healing phase of a chemical peritonitis.

Animals↗