ABSTRACT
The apparition and the breakage of esophageal varices et the level of cardioesophageal junction in the portal hypertension still represents a problem of pathological surgery. The presence of these varicose dilatations in this region is due to an important zone of porto-caval anastomoses. Angioarhitectonical study of lower abdominal esophagus represents a disputed problem in the specialty literature. The hypothesis of south American anatomist F. C. Carvalho (1966) looks to be the best model that could explain the appear of cardioesophageal varices. Studies realized in the past within the Anatomy Department of Medicine "Carol Davila" Bucharest tried to demonstrate the validity of Carvalho's theory, and the results of these researches are exposed in the present paper.
Subject(s)
Esophageal and Gastric Varices/pathology , Portal Vein/abnormalities , Vascular Fistula/pathology , Venae Cavae/abnormalities , Autopsy , Esophageal and Gastric Varices/etiology , Esophagus/blood supply , Humans , Hypertension, Portal/complications , Hypertension, Portal/pathology , Models, Anatomic , Vascular Fistula/complicationsABSTRACT
Differences in the susceptibility to paralytogenic infection with Coxsackie A10 virus were found in neonate and suckling mice belonging to A2G, ICR-K and CBA strains and ICR-K/CBA and CBA/ICR-K hybrids in the F1 generation. At the first passage in vivo the more susceptible strains selected paralytogenic viral particles from among the cytopathogenic and non-pathogenic Coxsackie A10 virus populations. The differences in susceptibility could not be related either with the humoral immune response to virus or to the rate of fixation of virus on the neonate mouse muscle cell receptors. These differences are, however, in agreement with the data concerning the synthesis of interferon in the striated muscle, the lots with greater resistance to viral infection being also those which synthesize interferon in higher concentrations. The hybrids resulting from the parental strains more susceptible to virus, presented a resistance superior to that of the parents.
Subject(s)
Coxsackievirus Infections/microbiology , Age Factors , Animals , Animals, Newborn , Antibody Formation , Cells, Cultured , Coxsackievirus Infections/immunology , Enterovirus/immunology , Enterovirus/pathogenicity , Female , Immunoglobulins/analysis , Interferons/analysis , Male , Mice , Mice, Inbred CBA , Mice, Inbred ICR , Muscles/analysis , Spleen , Virus CultivationABSTRACT
Sera from 75 children hospitalized with a clinical diagnosis of acute respiratory virus disease were tested by hemagglutination-inhibition as regards influenza A2 and B antibody shifts. In 48 patients there was an antibody shift during the clinical evolution of the disease (against influenza A2 in 34, B-- in 11, A2 and B in 3cases). A significant proportion of sera with antibody shift associated with a decrease of serum IgG levels and with an increase of serum IgM and IgA levels.
