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Biomedical subjects

S Levine

Publications and source records attributed to S Levine.

At least 559 records · Page 31Linked to original sources
PubMed1975

Interferon action II. Membrane-bound alkaline ribonuclease activity in chick embryo cells manifesting interferon-mediated interference.

Membrane fractions from chick embryo cells manifesting viral interference mediated by interferon or poly(I)-poly(C) contain high levels of an alkaline ribonuclease. Enhanced RNase activity is not observed when inhibitors of cell protein or RNA synthesis are present during interferon treatment, or when heterologous interferon is used. The RNase associated with comparable membrane fractions from cells treated with mock-interferon is about 1/10 as active, and shows qualitative differences. In principle, divergent views of interferon action may be reconciled to a common mode of action by postulating that viral interference results from a newly induced or activated RNase of cellular origin and proper specificity that acts to reduce the accumulation and functional capacity of newly synthesized viral RNAs, particularly mRNA. Previous data in support of interferon's acting to inhibit virion-derived transcription in vivo are now interpreted as demonstrating enhanced degradation of viral transcripts (mRNA).

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

Development of circadian periodicity in base and stress levels of corticosterone.

Base and stress levels of corticosterone were assessed at 4-h intervals over a 24-h period in male and female rats at age 18, 22, and 26 days. A significant periodicity in base levels of corticosterone is present at 22 days of age; however, a rhythm in stress values does not appear until age 26 days. At age 26 days the pattern of the circadian periodicity in both base and stress concentrations of corticosterone resembles that of the mature rhythm.

Animals↗
PubMed1975

Ventilatory response to drug-induced hypermetabolism.

Previous workers have demonstrated that an increase in minute ventilation accompanies tissue hypermetabolism induced by uncouplers of oxidative phosphorylation. The mechanism of this increase in minute ventilation has not been established. Accordingly, 2.5 mg/kg of 2,4-dinitrophenol (DNP) or 8-15 mg/kg of ethyl methylene blue (EMB) were infused into chloralose-anesthetized mongrel dogs; Vo2 increased 105 plus or minus 3% and VE INCREASED 107 PLUS OR MINUS 14%. Heads of vagotomized dogs were then perfused entirely with normal unchanging blood. Spinal cord remained intact. (The carotid bodies lay within the region of the perfused head.) Ventilatory responses of these head-perfused animals to breathing low oxygen and to breathing high CO2 gas mixtures were greatly attenuated. However, when DNP or EMB was infused into the body, VO2 increased 114 plus or minus 23% and VE increased 123 plus or minus 22%. When similar doses of DNP or emb were selectively administered to the head, increases in VE were limited to 21 plus or minus 6%. It is concluded that a major portion of the stimulus to ventilation, which accompanies infusion of DNP or of EMB, arises in tissues other than arterial chemoreceptors and brain. Presumably, this ventilatory stimulus is transmitted to the respiratory center via afferent pathways of the cervical spinal cord.

Animals↗
PubMed1975

Nonperipheral chemoreceptor stimulation of ventilation by cyanide.

To assess the ventilatory responses elicited by changes of tissue hypoxia, sodium cyanide (0.12 mg/kg-min for 10 min) was infused into the upper abdominal aorta of anesthetized dogs. These infusions produced decreases in oxygen consumption, increases in arterial lactate concentration, and increases in arterial lactate/pyruvate ratio. Coincident with these metabolic changes of hypoxia, minute ventilation (VE) increased 228 +/- SE 36% and arterial PCO2 decreased 21 +/- SE 2 mmHg; therefore, pH increased both in arterial blood in and cisternal cerebrospinal fluid. Following infusion of cyanide into the abdominal aorta, small quantities of cyanide (48 +/- SE 14 mumol/liter) appeared in carotid arterial blood. To evaluate the possibility that the observed increases in VE were due to stimulation of peripheral arterial chemoreceptors by the recirculating cyanide, the carotid and aortic chemoreceptors were denervated in four dogs. Nonetheless, after intra-aortic infusion of sodium cyanide (1.2 mg/kg), ventilation in these chemodenervated animals again increased considerably (154 +/- SE 36%). In order to explore the possibility that cyanide infusion can stimulate ventilation by an extracranial mechanism, heads of vagotomized dogs (including the carotid bodies) were perfused entirely by donor dogs. The intra-aortic infusion of sodium cyanide (0.9 mg/kg) into these head-perfused animals still caused large increases in VE (163 +/- SE 19%). It is concluded that intra-aortic cyanide infusions stimulate VE by an extracranial mechanism other than the carotid and aortic chemoreceptors.

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

Studies on the immunochemical composition of human thoracic duct lymph of patients with rheumatoid arthritis and polymyositis.

Analysis of immunoglobulins, autoantibodies and third component of complement was carried out on the thoracic duct lymph of 6 patients with rheumatoid arthritis and 2 patients with polymyositis. It was found that the distribution of these immunoproteins between lymph and serum reflected the distribution of total protein and did not appear to be dependent on molecular size. There was no significant difference in the distribution of the macromolecule IgM as compared to the other immunoglobulins. IgD was an exception with an unanticipated and unexplained lower concentration in lymph and higher serum to lymph ratio when compared to the other immunoglobulins.

Adult↗
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↗
PubMed1975

The location of regions in guinea pig and bovine myelin basic proteins which induce experimental allergic encephalomyelitis in Lewis rats.

Myelin basic proteins and peptides derived from them by limited cleavage with pepsin were tested for their ability to induce experimental allergic encephalomyelitis (EAE) in Lewis rats. The encephalitogenicity of the weakly active bovine protein was found to be associated with both halves of the molecule, peptides (1-88) and (89-169). Of the four smaller derivates of peptide (1-88), peptides (1-36), (43-88), (1-42), and (37-88), only the last two were active. This demonstrated that the overlap region consisting of residues 37-42 (sequence Asp-Ser-Leu-Gly-Arg-Phe) constitutes an encephalitogenic determinant. Of the two smaller derivatives of peptide (89-169), peptides (111-169) and (89-152), only the last was active. This indicated that the second encephalitogenic determinant begins between residues 88 and 111 and ends before residue 153. This region contains the sequence Leu-Ser-Leu-Ser-Arg-Phe (residues 108-113), which is strikingly similar to that of the first encephalitogenic determinant. Studies involving the extremely encephalitogenic guinea pig protein demonstrated that virtually all of the activity was recovered in the peptides corresponding to bovine peptides (37-88) and (43-88). These peptides, but not those comprising the remainder of the protein, were active in inhibiting the passive transfer of EAE with lymph node cells from donors immunized with guinea pig spinal cord.

Amino Acid Sequence↗