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Biomedical subjects

H Popper

Publications and source records attributed to H Popper.

At least 163 records · Page 9Linked to original sources
PubMed1977

Chimpanzee livers after infection with human hepatitis viruses A and B: Ultrastructural studies.

Electron microscopical studies were carried out on coded liver biopsy specimens from chimpanzees inoculated with human hepatitis A or B virus. Hepatitis B was recognized by the presence of hepatitis B core particles in hepatocellular nuclei. Hepatitis A was characterized by unidentified large, dense, and more irregular heterochromatin-like particles in hepatocellular nuclei coincidental with peak aminotransferase activities. As type A hepatitis illness became manifest in the chimpanzees, mitochondrial cristae were curled and attenuated, and clusters of endoplasmic reticulum were tightly packed. In contrast, the livers in viral hepatitis B showed mainly hypertrophy of tubular smooth endoplasmic reticulum. This suggested different pathogenetic mechanisms in A and B chimpanzee viral hepatitis.

Animals↗
PubMed1976

Modification of chronic hepatitis-B virus infection in chimpanzees by administration of an interferon inducer.

Chimpanzees chronically infected with hepatitis-B virus showed transient changes in several markers of infection when treated with the interferon inducer polyriboinosinic-polyribocytidylic acid-poly-l-lysine carboxymethyl cellulose. Serum Dane-particle-associated D.N.A. polymerase, e antigen and hepatitis-B surface antigen, and intrahepatic hepatitis-B surface and core antigens diminished during treatment. Defective (D.N.A.-polymerase-negative) Dane particles increased in titre transiently during treatment; these may play a role in the modulation of hepatitis-B virus infection. Humoral immune responses in chronic hepatitis-B carrier chimps were unaffected. Interferon inducers (or exogenous interferon) may be useful for the treatment of chronic hepatitis-B virus infection.

Animals↗
PubMed1976

Release of prostaglandins by bradykinin as an intrinsic mechanism of its algesic effect.

1. The release of PGs from the isolated perfused rabbit ear was measured by means of a radioimmunoassay. 2. Bradykinin in dose dependent amounts released mainly PGE (presumably PGE1) and in much smaller amounts also PGF. 3. Bradykinin released similar amounts of PGE in innervated and chronically denervated ears. 4. Indomethacin completely prevented the PGE release by bradykinin. 5. ACh showed a much lower efficacy than bradykinin in releasing PGE and PGF. Synthetic substance P was devoid of any PGE releasing action. 6. It is concluded that bradykinin increases its own algesic action by a concomitant rapid stimulation of the PGE synthesis, thus providing a mechanism for the facilitation of its own algesic action.

Acetylcholine↗
PubMed1976

Vitamin A-containing lipocytes and formation of type III collagen in liver injury.

Hepatocellular necrosis in carbon tetracholride-induced injury of rats is associated with an accumulation of lipocytes (perisinusoidal cells or Ito cells) containing fat droplets and giving vitamin A fluorescence. In the subsequent formation of connective tissue septa, transitional cells having morphologic characteristics of lipocytes and fibroblasts are abundant and are associated with the appearance of type III collage-. The features suggest that the lipocyte is the precursor of the fibroblasts responsible for parenchymal fibrillogenesis and under these conditions forms type III collagen. The process is a postulated link between hepatocellular necrosis and fibrosis.

Animals↗
PubMed1976

Vinyl chloride-associated liver disease.

Although polyvinyl chloride has been produced from vinyl chlride monomer for more than 40 years, recognition of toxicity among vinyl chloride polymerization workers is more recent. In the mid 1960s, workers involved in cleaning polymerization tanks were found to have acro-osteolysis. In 1974, the same population of workers was found to be at risk for an unusual type of hepatic fibrosis and angiosarcoma of the liver. We describe two cases of vinyl chloride-associated liver injury, one of hepatic fibrosis and one of angiosarcoma. Histologic features of these lesions are similar to the hepatic fibrosis and angiosarcomas resulting from chronic exposure to inorganic arsenicals. Preliminary studies suggest that the toxicity of vinyl chloride may result from formation, during high-dose exposure, of active metabolites by mixed function oxidases of the liver. Epidemiologic studies indicate an increased incidence not only of liver disease, but also of cancers of the brain, lung, and possibly other organs.

Adult↗
PubMed1976

Hepatitis.

Explore the source record for details and available documents.

Chemical and Drug Induced Liver Injury↗
PubMed1976

The pathology of viral hepatitis types A and B in chimpanzees. A comparison.

The histologic manifestations in the livers of chimpanzees inoculated with hepatitis A and B virus were compared with each other and correlated with biochemical, serologic, and virologic observations. Both types of hepatitis reveal alterations similar to those seen in human hepatitis, but the lesions--particularly the hepatocellular necrosis--are far milder. Hepatitis Type A in chimpanzees is a disease of short incubation period and duration. The hepatocytic alterations are mainly restricted to the periportal areas, and the parenchymal changes are less severe than the portal inflammation. The lesions correlated well with biochemical changes, the presence of virus in the liver, and its shedding in the stool. In contrast, experimental Type B hepatitis has a long incubation period and longer duration, involves the entire lobular parenchyma, and is, if anything, more severe in the lobular centers while portal inflammation is less conspicuous. Biochemical alterations and presence of virus in the liver correlate with these lesions, and the antibody response is similar to that seen in man. The chimpanzee is a useful model for studying the pathogenesis of viral hepatitis; additional study of serial morphologic events may contribute to our understanding of the clinical differences between hepatitis Type A and Type B.

Animals↗
PubMed1975

Alterations of liver and spleen among workers exposed to vinyl chloride.

Preliminary review of hepatic biopsy and autopsy specimens obtained from workers engaged for prolonged periods in the polymerization of vinyl chloride indicates a fibrotic precursor lesion in the liver. It is the only lesion in some instances but also was found in the uninvolved liver of patients with angiosarcoma and in two instances in liver biopsy specimens obtained before angiosarcoma developed. This precursor stage is characterized by a conspicuous subcapsular fibrosis, a nonpathognomonic progressive portal fibrosis, and a borderline increase of intralobular connective tissue, all associated with focal stimulation of sinusoidal lining cells and hepatocytes. This precursor stage is often accompanied by splenomegaly with enlarged Malpighian follicles and in some instances by portal hypertension requiring portacaval shunt because of variceal hemorrhage. The portal hypertension is explained by increased splenic blood flow in the face of nondistensible fibrotic portal tracts as well as Glisson's capsule. Transition to angiosarcoma is preceded by focal dilatation of sinusoids with even greater activation but dedifferentiation of their lining cells. This lesion is presumably the result of stimulation of various hepatic as well as splenic cells by vinyl chloride or its metabolites. The demonstrated evolution is identical with that following prolonged exposure to inorganic arsenicals. It is postulated also that other instances of inconspicuous hepatic fibrosis associated with splenomegaly and often with portal hypertension, a combination designated as Banti's syndrome or "idiopathic portal hypertension," are the result of a toxic, possibly environmental agent, particularly since the disease is found with greater frequency in some parts of the world. The delineation of the fibrotic precursor stage in the liver may assist in the epidemiologic studies of the vinyl chloride-induced injury.

Arsenic Poisoning↗
PubMed1975

Pathology of angiosarcoma of the liver among vinyl chloride-polyvinyl chloride workers.

We described the histologic features of 13 hepatic angiosarcomas which developed in workers engaged in the polymerization of vinyl chloride to polyvinyl chloride. Although the histologic features varied considerably in different portions of the angiosarcoma in the same liver and in the angiosarcomas of the liver from different patients, many features were similar such as sinusoidal, papillary, and cavernous growth patterns coincident with the precursor lesions of proliferation and atypia of sinusoidal lining cells.

Hemangiosarcoma↗
PubMed1975

Vinyl-chloride-induced liver disease. From idiopathic portal hypertension (Banti's syndrome) to Angiosarcomas.

Histologic examination of liver tissue (eight autopsy and 18 biopsy specimens) and five spleens from 20 workers with vinyl chloride polymerization showed hepatic angiosarcomas in 15. In addition, a peculiar pattern of progressive portal-tract, inconspicuous intralobular and conspicuous capsular fibrosis was observed in the five workers without angiosarconma, in all the seven patients with angiosarcoma from whom tumor-free portions of the liver were available, and in two tumor-free biopsies from patients subsequently found to have angiosarcoma. The fibrosis was accompanied by splenomegaly. Hypertrophy and hyperplasia of both hepatocytes and hepatic and splenic mesenchymal cells were also seen. The histologic similarity to chronic inorganic arsenical poisoning, in which angiosarcomas also occur, and to idiopathic portal hypertension (Banti's syndrome) suggests that the latter syndrome at times results from unknown toxic, possible environmental, chemicals.

Autopsy↗