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Biomedical subjects

R Sowinski

Publications and source records attributed to R Sowinski.

At least 55 records · Page 3Linked to original sources
PubMed1976

Necrotic myelopathy (myelomalacia) in rats with allergic encephalomyelitis treated with tilorone.

Necrosis of the spinal cord was produced by administering tilorone to rats before or during the incubation period of experimental allergic encephalomyelitis (EAE). Under slected conditions of dose and timing, the drug delayed onset of clinical signs but did not prevent progression to paralysis. The lymphocytic component of the inflammatory lesions was reduced, but this was accompanied by a dramatic increase of monocytes in the spinal cord, followed by softening (myelomalacia). This new variant of EAE simulates necrotic myelopathy in man. The similarity provides support for an autoimmune etiology of the latter. Furthermore, the inverse relation between lymphocytic cuffs around vessels and massive monocytic infiltration of the cord adds to the growing evidence that lymphocytic cuffs protect the neural parenchyma by "vascular blockade."

Animals↗
PubMed1975

Choroid plexus isografts in rats.

Choroid plexuses from adult rats were grafted to the kidneys of other rats of the same inbred strain. Almost all the grafts survived and exhibited a multiloculated pattern of choroidal papillae. Mild but progressive enlargement of the locules was probably caused by secretion of cerebrospinal fluid. Cyclophosphamide, a drug which damages the normally situated plexus, had similar but milder effects on the plexus implants. Isografts should prove useful for other studies of choroid plexus structure and function.

Animals↗
PubMed1975

Do neurological signs occur in experimental allergic encephalomyelitis in the absence of inflammatory lesions of the central nervous system?.

Guinea pigs with paralysis or other severe neurological signs of experimental allergic encephalomyelitis (EAE) always exhibited typical histological inflammatory lesions. A few animals inoculated with either the encephalitogenic emulsion or only the control adjuvant emulsion had mild weakness or slowness but no histologic lesion. In some instances, these signs were explained by coincidental non-neural disease or trauma. Therefore, such mild clinical signs cannot be considered pathognominic of EAE. Reports from the literature suggesting that animals have developed clinical signs without histological lesions in EAE are considered invalid because of the nonspecificity of clinical signs, the occurrence of intercurrent diseases, the inadequacy or incorrect timing of histologic evaluations, and the lack of controls for specificity of the signs. There is no basis for the supposition that autoimmunity can cause major neurological signs in the absence of inflammatory lesions in the nervous system.

Animals↗
PubMed1975

The role of the adrenal in relapses of experimental allergic encephalomyelitis.

Adrenalectomy shortly after onset of clinical signs of experimental allergic encephalomyelitis (EAE) was uniformly lethal to rats within 2 days. If adrenalectomy was postponed until the third to fifth day of signs, most of the rats survived and experienced a complete or incomplete remission followed by a relapse. The success of adrenalectomy in inducing relapses suggests that spontaneous relapses in EAE are related to adrenal homeostatic mechanisms whereby paralysis, nonspecific stress, increased corticosteroids, immunosuppression, recovery from paralysis, decreased stress, corticosteroids and reimmunization follow each other in logical order. However, the failure of adrenalectomy to induce relapses in EAE produced with aqueous inoculum or by passive transfer with lymphoid cells suggests that relapses are related to the persistent antigenic depot from water-in-oil inocula, rather than being an inherent part of the immunopathologic process.

Adrenal Glands↗
PubMed1975

Allergic encephalomyelitis in the reputedly resistant Brown Norway strain of rats.

Brown Norway (BN) rats are much less susceptible to experimental allergic encephalomyelitis (EAE) than Lewis rats. Nevertheless, BN rats developed severe EAE, even paralysis, when immunized with rat spinal cord and carbonyl iron adjuvant. Complete Freund's adjuvant (CFA) was much less effective. The use of both CFA and pertussis vaccine with rat cord was moderately, but not consistently, effective. Guinea pig spinal cord was weakly encephalitogenic to BN rats with all adjuvant combinations. We were not able to produce EAE in BN rats with purified myelin basic protein from either rat or guinea pig. Inoculations directly into lymph nodes or into the blood stream proved that the low susceptibility of BN rats was not due to lack of absorption from the site of inoculation, but may be related to peculiarities of processing antigen in draining lymph nodes. The severity of EAE in F1 hybrids was intermediate between the BN and Lewis parental strains when tested with an immunizing procedure of appropriate strength. The fact that F1 hybrids were less reactive than Lewis mandates modification of the theory that susceptibility to EAE is inherited through a single autosomal dominant gene.

Adjuvants, Immunologic↗
PubMed1975

Role of the kidney in development of cystitis and other toxic effects of cyclophosphamide.

Cystitis caused by excretion of cyclophosphamide (CY) metabolites in the urine was prevented by nephrectomy. There was a concomitant increase of CY lesions in brain, eye, and spleen due to the avoidance of urinary losses. Anuria caused by extra- or intrarenal obstruction, or by prerenal deviation of water, also prevented cystis; these procedures enhanced other CY lesions more than nephrectomy did. The data are interpreted to indicate significant production of active CY metabolites by the kidneys, a production which is eliminated by nephrectomy but not by other procedures.

Adrenalectomy↗
PubMed1975

Nuclear bodies produced in astrocytes by tilorone.

Large, eosinophilic, nonglycogenic nuclear inclusions were produced in the central nervous system by the drug tilorone. At the light microscope level, the inclusions occurred predominantly in astrocytes. Ultrastructurally, they were identical to the nuclear bodies described in many cell types under many conditions. The bodies were produced by tilorone in small numbers in the median eminence, a part of the hypothalamus that lacks a blood-brain barrier. They were produced in only 2 or 3 days in large numbers adjacent to zones of thermal or traumatic necrosis or in areas of inflammation. These facts, and the distribution of affected astrocytes, indicated that permeability factors and cerebrospinal fluid flow were involved in the development of the nuclear bodies. The large size and large number of nuclear bodies produced by tilorone should facilitate studies of this poorly understood nuclear organelle.

Animals↗
PubMed1974

A hemorrhagic diathesis with involvement of hypothalamus produced in rats by cyclophosphamide.

Large doses of cyclophosphamide caused a hemorrhagic diathesis related to bone marrow destruction and thrombocytopenia. Although several organs had hemorrhages, there was a striking predilection for the hypothalamus, ileum and mesentery of adult rats. The reasons for this localization are not known, but involvement of hypothalamus may be related to known functional effects of the drug on the neuroendocrine system. There were hemorrhages in choroid plexus, ciliary body and urinary bladder also, but these localizations were due to prior direct toxic injury to these structures by cyclophosphamide.

Animals↗
PubMed1973

Hyperacute allergic encephalomyelitis. A localized form produced by passive transfer and pertussis vaccine.

A hyperacute form of experimental allergic encephalomyelitis (EAE) has been produced previously by administering pertussis vaccine to rats actively immunized with neural antigen or given passive transfer of lymphoid cells from donors with EAE. Now, a localized form of hyperacute EAE has been produced within 1 day of passive transfer. The speed with which pertussis acts tends to exclude antibody production as the mechanism for conversion of EAE to the hyperacute form. With this rapid system, it has been found that pertussis, or its histamine-sensitizing factor, inhibited the host mononuclear cell component of the pervascular lesions. When the immune injury was sufficiently severe (high doses of donor EAE cells), the decrease in the number of mononuclear cells was accompanied by an increase in the amount of fibrin and the number of neutrophils in the lesions. This inverse relationship may be explained by the loss of the protective effect of mononuclear cells on vessels, a concept for which there is increasing evidence.

Acute Disease↗
PubMed1972

Inhibition of macrophage response to brain injury. A new effect of pertussis vaccine possibly related to histamine-sensitizing factor.

Intravenous injection of pertussis vaccine inhibited the outpouring of macrophages into a zone of thermal coagulation necrosis in the brain. The inhibition of this cellular reaction to injury was observed in rats and mice, and was especially notable in gerbils. It was not due to nonspecific stress or to endotoxin. A relationship of this new activity to pertussis vaccine's histamine-sensitizing factor was suggested by the use of partially purified extracts and heat-inactivated vaccines. There was a close parallel between the effects of pertussis vaccine on brain macrophages and on the spleen.

Animals↗
PubMed1971

Allergic encephalomyelitis: new form featuring polymorphonuclear leukocytes.

The passive transfer of allergic encephalomyelitis can be produced in a single day. In work described, the procedure was made to coincide with a transient drug-induced deficiency of lymphocytes. As a result, the lesions of this autoimmune disease contained a predominance of polymorphonuclear leukocytes instead of the usual mononuclear cells. Not only is this a new histologic form of the disease, but the ready recognition of polymorphonuclears as reactive cells provides a powerful new tool for investigating the roles of immunologically specific effector cells and nonspecific reactive cells in production of tissue damage.

Animals↗