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Biomedical subjects

H Popper

Publications and source records attributed to H Popper.

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

Cytochrome P-450 in the activation and inactivation of carcinogens.

The capacity of isolate mouse liver microsomes to alter the mutagenicity for bacteria of the primary carcinogen N-methyl-N'-nitro-N-nitrosoguanisine (MNNG) and the secondary one dimethylnitrosamine (DMN) was studied. Microsomal activation of DMN and inactivation of MNNG were decreased by protein- and protein-cholinedeficient diets and were increased by pretreatment with microsomal enzyme inducers. The decrease and increase paralleled the content of cytochrome P-450 present in the different microsomal preparations. With human liver microsomes of differing cytochrome P-450 contents similar correlation was obtained, whereas normal rat liver microsomes did not activate or inactivate DMN or MNNG. Oxidative demethylation of DMN by mouse liver microsomes and the activation of DMN to a mutagen followed similar kinetics. Both reactions were inhibited by carbon monoxide and the inhibition was maximally reversed by monochromatic light at 450 nm. These observations indicate that at least some carcinogens are activated or inactivated by the unspecific cytochrome P-450 dependent enzyme system, suggesting that the extent of this biotransformation may be one factor influencing human carcinogenesis.

Animals↗
PubMed1975

Experimental infection of chimpanzees with hepatitis A virus.

The susceptibility of chimpanzees to viral hepatitis type A was examined with immine electron microscopy. Of four seronegative infant chimpanzees, two were inoculated with a hepatitis A acute-phase stool filtrate rich in 27 nm virus-like hepatitis A antigen (HA Ag) particles, and two were inoculated with an HA Ag-negative preinfection stool filtrate. One of each pair of chimpanzees was inoculated intravenously, the other orally. One month later both chimpanzees that had received the HA Ag-positive filtrate developed biochemical, histologic, and clinical evidence of acute viral hepatitis. HA Ag particle (27 nm) were detected in their stools by immune electron microscopy; particle shedding followed a pattern similar to that in human volunteers. Immune electron microscopy also showed that antibody HA Ag had developed in the convalescent-phase sera of the infected chimpanzees. Control animals remained free of illness at this time but did develop hepatitis three to five weeks after exposure to the two infected chimpanzee-. The infectious inoculum was titrated in two additional seronegative chimpanzees. It was concluded that hepatitis a can be successfully transmitted to seronegative chimpanzees. Moreover, these studies provide further evidence that the 27-nm virus-like HA Ag particle is the etiologic agent of viral hepatitis type A.

Animals↗
PubMed1975

Effects of steroid hormones on replication of murine sarcoma virus in mouse embryo cultures.

The androgenic steroid hormone, testosterone, inhibited focus formation by the murine Moloney sarcoma virus in mouse embryo cells. The inhibition of focus formation was enhanced by cyclic AMP. Although focus formation was inhibited, there was no inhibition of viral replication. The glucogenic adrenal corticosteroids, cortisol and dexamethasone, and 17-beta-estradiol and progesterone did not affect focus formation by MuSV(M).

Adrenal Cortex Hormones↗
PubMed1975

Clinical pathologic correlation in viral hepatitis. The effect of the virus on the liver.

In clinical pathologic correlations, including the potential effect of the virus on the liver, the morphologic features of the various stages of viral hepatitis are the firm information available today. With acute hepatitis being an inflammatory reaction to cell injury and necrosis, and chronic hepatitis being sustained inflammation, correlation with clinical features and functional defects is good in acute hepatitis and less so in the chronic stages. The pathogenesis of the diseases-including cell necrosis, inflammation, fibrosis, and cirrhosis formation-is reasonably well understood, and this knowledge assists both in prognosis and in monitoring of therapy. The localization of the components of the hepatitis B antigen and their effects, including the nature of the immune response, is the most exciting aspect of the clinical pathologic problem. Today's interpretations offer, at best, a working hypothesis promising further understanding of the evolution of the disease.

Acute Disease↗