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Biomedical subjects

A Segal

Publications and source records attributed to A Segal.

At least 181 records · Page 10Linked to original sources
PubMed1975

Ultrastructural and immunohistochemical study of the human kidney in Argentine haemorrhagic fever.

In six lethal cases of Argentine Haemorrhagic Fever (AHF) a disease caused by Junin virus, kidney samples were studied by means of immunofluorescent and electron microscopic techniques.--The ultrastructural studies showed that the distal and collecting tubes presented a large number of virus like intracytoplasmic particles. Those particles were present in the lumen of the endoplasmic reticulum cisternae and showed two distinct morphological aspects. Some of them were of high electron density and contained a few granules. The others were larger in size, electron lucid, and contained a variable number of ribosome like granules. Both types of particles originated from the endoplasmic reticulum wall by a process of budding. The presence of these particles was coincident with a severe cell damage which lead to necrosis and desquamation; and with large quantities of Junin virus antigen as demonstrated by immunofluorescence.--On the basis of these observations it is assumed that in AHF the cell damage is due to direct viral replication within the affected cells.

Antigens, Viral↗
PubMed1975

Ultrastructural and immunohistochemical studies in five cases of Argentine hemorrhagic fever.

Ultrastructural and immunohistochemical studies on tissues from five patients with Argentine hemorrhagic fever revealed previously undetected lesions caused by the viral infection. Two types of particle were seen in the cells of all organs examined. The particles had some characteristics similar to those described for arenaviruses. However, the virus-like particles were intracellular, had a single membrane, and apparently originated by a process of budding into the endoplasmic reticulum cisternae. Intranuclear bodies and three types of cytopolasmic change were observed in conjunction with the virus-like particles; Antigenic determinants of Junin virus were demonstrated in cells of all organs examined. Immunohistochemical experiments also indicated alterations in the cellular mechanisms of protein synthesis. Until now the pathogenesis of human diseases produced by arenaviruses has not been established. The results of this study suggest that in Argentine hemorrhagic fever the virus is responsible for a direct pathogenic action.

Adult↗
PubMed1975

The identification of phorbolol myristate acetate as a new metabolite of phorbol myristate acetate in mouse skin.

Aspects of the metabolism of phorbol myristate acetate (PMA) in mouse skin were investigated. Phorbolol myristate acetate (PHMA), a potential metabolite of PMA in mouse skin, was prepared from PMA by NaBH4 reduction of the C-5 carbonyl group of PMA to a secondary alcohol. The structure of PHMA was assigned on the basis of spectral and chemical evidence. PHMA had an inflammatory effect in mouse skin equal to or slightly less than PMA, on the basis of the dermal infiltration of lymphocytes and neutrophils and interfollicular epidermal hyperplasia. Application of PHMA and PMA to mouse skin resulted in equal increases in numbers of interfollicular epidermal basal layer mitotic cells after 28 hr. PHMA was found to be nearly as effective as PMA in increasing the incorporation of [3H]thymidine into interfollicular epidermal basal layer cells after 28 hr. When tritiated PMA was applied to mouse skin, PHMA was identified as a metabolite. PHMA was present in about 1.7% of the amount of PMA. When tritiated PHMA was applied to mouse skin, PMA was not detected as a metabolite in the mouse skin extracts.

Animals↗
PubMed1975

Immunopathologic and morphologic studies of skeletal muscle in Chagas' disease.

Skeletal muscle biopsies from 21 individuals infected with Trypanosoma cruzi were studied my means of immunofluorescence, ultrastructural immunochemical, light and electron microscopic, and histochemical procedures. In 12 cases, definite morphologic alterations were found. These alterations were coincident with the presence of circulating antibodies against the plasma membrane of striated muscle fibers and endothelial cells (EVI antibodies). In almost all cases the lesions also presented autologous immunoglobulins bound to the plasma membrane of muscle fibers and endothelial cells. Interstitial inflammatory exudate was not observed in the diseased muscle. On the basis of these observations, it is suggested that the EVI antibody is related to some of the pathogenetic mechanism of skeletal muscle damage in Chagas' disease.

Adenosine Triphosphatases↗
PubMed1975

Immunological studies in Rockland mice infected with T. cruzi. Development of antinuclear antibodies.

The existence of antinuclear antibodies (ANA) and their relationship with anti-Trypanosoma cruzi specific agglutinins was studied in Rockland mice inoculated with 10(5), 10(4) or 10(3) epimastigotes and 2 X 10(5) trypomastigotes of T. cruzi. ANA and anti-T. cruzi agglutinins were detected at the same time in groups of mice receiving 10(5) culture forms, while in those groups of mice receiving 10(4) parasites agglutinins were established earlier than ANA which were present only at low titres. Positive serology and ANA were also detected in mice infected with trypomastigotes. Neither specific agglutinins nor ANA were found in groups of mice receiving 10(3) parasites probably because the number of parasites inoculated was too low to infect them. ANA were not found in not infected mice. ANA induced in mice by T. cruzi infection seem to be related to the amount of parasites inoculated and thus with the degree of the subsequent infection. Immunopathologic studies carried out in mice infected with trypomastigotes showed the presence of nodular deposits of gamma globulin in the kidneys, suggesting the possibility of an immune complex disease : the light and electron microscopic studies of the kidneys showed in the glomeruli an increase of the mesangium, hypercellularity and thickened basement membranes.

Animals↗
PubMed1971

Modulation of glutamine synthetase adenylylation and deadenylylation is mediated by metabolic transformation of the P II -regulatory protein.

Earlier studies showed that two protein components, P(I) and P(II), are concerned with the adenylylation and deadenylylation of Escherichia coli glutamine synthetase (EC 6.3.1.2). P(I) by itself catalyzes both adenylylation and deadenylylation, but its activity is modulated by the P(II)-protein and by glutamine, 2-oxoglutarate, ATP, and UTP, The P(II)-protein exists in two forms: one form, P(II)-AT, stimulates P(I)-catalyzed adenylylation activity in the absence of glutamine and makes this activity very sensitive to inhibition by 2-oxoglutarate; it does not affect deadenylylation activity. The other form, P(II)-DA, stimulates adenylylation only if glutamine is present, and also stimulates the deadenylylation activity of P(I), which is then dependent upon the presence of ATP and 2-oxoglutarate. Conversion of P(II)-AT to P(II)-DA requires the presence of UTP, ATP, and 2-oxoglutarate; it is catalyzed by an enzyme present in P(I) preparations. UTP may be directly involved in this conversion since P(II)-DA fractions reisolated by filtration through Sephadex G-100 contain small quantities of a bound uridine derivative that lacks the gamma-phosphoryl group of UTP. The activity of P(II)-DA, but not of P(II)-AT, is destroyed by treatment with snake-venom phosphodiesterase. ATP and 2-oxoglutarate apparently function as allosteric effectors for the conversion of P(II)-AT to P(I)-DA.

Adenine Nucleotides↗