PubMed Health⌕ Search

Biomedical subjects

H Popper

Publications and source records attributed to H Popper.

At least 109 records · Page 6Linked to original sources
PubMed1982

Reduction of carrageenan- bradykinin- and histamine-induced acute inflammation by experimental eosinophilia in rats.

An examination was made of the effects of eosinophilia on acute inflammation. Sprague Dawley rats were infected with Trichinella spiralis larvae which resulted in a blood eosinophilia. Groups of rats with the induced eosinophilia, and untreated rats without the eosinophilia, were treated with carrageenan, bradykinin or histamine in the hind paw to induce local inflammation. Paw oedema induced by carrageenan as a measure of the inflammation was much reduced in those rats with an eosinophilia, and slightly but significantly reduced in the site treated with histamine or bradykinin. Though other anti-inflammatory factors may have participated, it is believed that the reduction in inflammation was due to the eosinophils. Pretreatment of the rat paws with an eosinophil chemotactic factor tetrapeptide (ECF-A) caused no chemotaxis and therefore no effect on histamine-induced oedema.

Animals↗
PubMed1981

Review of four cases of childhood hepatic angiosarcoma--elevated environmental arsenic exposure in one case.

Four cases of childhood hepatic angiosarcoma (HAS), representing the malignant form of infantile hemangioendothelioma, are described. The morphologic appearance of childhood HAS differs from the adult form in the following features: the associated presence of benign infantile hemangioendothelioma; the presence of dysontogenetic features; and an altered appearance of the angiosarcoma itself. It is postulated for these cases that the benign infantile hemangioendothelioma progressed to the malignant angiosarcoma. One of the four cases had exposure to elevated levels of arsenic in the environment that may have contributed to this progression. This latter case adds to published reports associating arsenic exposure with increased risk for hepatic angiosarcoma.

Arsenic↗
PubMed1981

Arsenic-related hepatic angiosarcoma.

Data from several small autopsy series in German vintners in the 1940s and 1950s and a number of case reports have previously suggested that arsenic is a cause of hepatic angiosarcoma (HAS). In a nationwide review of deaths from HAS in the United States, we identified seven cases with a history of prolonged use of Fowler's solution (inorganic potassium arsenite), which provide further support for the association of arsenic exposure and HAS. An epidemiologic study of a cohort of individuals treated long-term with Fowler's solution might confirm this association.

Adult↗
PubMed1981

Substance P in the argentaffin carcinoid of the caecum: biochemical and biological characterization.

An argentaffin carcinoid tumour of the caecum which contained serotonin (167 micrograms/g) and consisted predominantly of EC1-cells, was analysed for the presence of peptides using immunohistochemical, biochemical and pharmacological methods. A very high content of 3.9 micrograms/g of immunoreactive substance P was found. The distribution of cells staining positively for substance P matched that of cells containing serotonin. While some immunoreactive somatostatin (3.2 ng/g) was present in the tumour, neurotensin, glucagon, gastrin, and motilin were not found. Part of the substance P immunoreactivity measured most likely represents authentic substance P: it behaved like substance P in two chromatographic systems and in two bioassays, and its activity on the guinea pig ileum was abolished by specific tachyphylaxis towards substance P.

Carcinoid Tumor↗
PubMed1981

A histochemical and biochemical study of a liposarcoma with several aspects on the development of fat synthesis.

The report describes a case of lipocytic and lipoblastic liposarcoma, morphologically to be classified as well-differentiated. A considerable number of liopoblastic areas with the mass of the tumour proper which contain large amounts of glycogen are interspersed. These immature lipocytes reproduce the histogenesis of normal white fat. The quantity of glycogen-storing lipoblastic cells nearly equals that of the fat-storing lipocytic cells. Acid mucopolysaccharides are seen in only small areas of tumour. Histochemical staining as well as biochemical investigations, show that the majority of tumour fat consists of triglycerides, followed by cholesterol esters. There are also small amounts of free cholesterol, phospholipids, free fatty acids and a further fraction, which seems to be a glycerol ether. There exist differences in the quantitative content of cholesterol, phospholipids and triglycerides of tumour fat compared to normal fat. No significant difference exists between the fatty acids in tumour fat and those in normal fat outside of the tumour.

Cell Differentiation↗
PubMed1981

Persistent non-A, non-B hepatitis in experimentally infected chimpanzees.

Non-A, non-B (NANB) hepatitis was transmitted to six chimpanzees by intravenous inoculation of antihemophilic (factor VIII) materials, acute-phase chimpanzee liver, and chronic-phase plasma obtained from two NANB hepatitis-infected chimpanzees 10 and 16 months, respectively, after their inoculation. Five of six experimentally infected chimpanzees observed for more than one year demonstrated persistent or intermittent elevations in levels of serum alanine aminotransferase (ALT) indicative of continuing liver dysfunction. Liver biopsy specimens obtained from three chimpanzees with persistent elevations in levels of ALT were positive for hepatocyte cytoplasmic structures associated with NANB hepatitis for as long as 27 months after inoculation. Liver biopsy specimens obtained from four infected animals 13-30 months after inoculation also showed mild but persistent histopathologic lesions of undefined character. The detection of circulating immune complexes in one chimpanzee with persistent elevations in levels of ALT suggests that these complexes may be involved in the pathogenesis of NANB hepatitis.

Animals↗
PubMed1981

Non-A, non-B hepatitis in chimpanzees and marmosets.

Nine of 15 specimens of human origin thought to contain non-A, non-B hepatitis agents caused hepatitis in recipient chimpanzees. Two have been further characterized. One inoculum, designated strain F, has been reported to produce unique cytoplasmic changes detected by electron microscopy in liver biopsy specimens; the other, strain H, produced distinctive nuclear changes. It is not yet clear whether these two changes result from infection by different agents; they have been useful markers of non-A, non-B hepatitis in chimpanzees. Strain F was serially passaged six times in chimpanzees, and the infectivity titer of the strain F plasma was estimated to be less than 10(2)/ml. Strain H had an infectivity titer in chimpanzees of at least 10(6)/ml. Both the strain F and strain H agents have been successfully transmitted and serially passaged in marmosets. Although hepatitis was detected in a lower percentage of marmosets than chimpanzees given either the strain F or H inoculum, the infectivity titer of the strain H agent appeared to be greater than or equal to 10(8) marmoset infectious doses/ml.

Acute Disease↗
PubMed1981

Vinyl chloride-induced hepatic lesions in man and rodents. A comparison.

Histologic sequences in the liver of rodents exposed by inhalation to gaseous vinyl chloride were compared to the lesions in man exposed to the same agent, mainly in vinyl chloride polymerization plants. An identical sequence, starting with circumscribed proliferation of hepatocytes, soon followed by proliferation of a variety of sinusoidal cells and frequently associated with sinusoidal dilatation, progresses to intralobular and more frequently to trabecular angiosarcoma. Predominantly in young animals and rarely in man, hepatocellular carcinoma develops, but never cirrhosis. The sequence represents a dynamic process of competition between proliferating hepatocytes and sinusoidal cells, of hepatocytes with fibroplasia, between perisinusoidal fibrosis and sinusoidal dilatation, and of proliferation of various sinusoidal cells versus angiosarcoma. The great similarity in the evolution in man and rodents, rarely encountered in other experimental models, supports the prediction of human cancer from animal experiments. The precursor nodules differ from the nodules commonly observed in hepatocarcinogenesis by co-proliferation of sinusoidal cells. The differences in the reactions between man and rodents bespeak a strong fibroblastic reactivity in man. Most important, the precursor lesion of mixed hepatocellular and sinusoidal cell proliferation may be of diagnostic value, being superior to conventional hepatic tests in detection of some initial environmental lesions.

Animals↗
PubMed1981

Epidemiology of hepatic angiosarcoma in the United States: 1964-1974.

A nationwide survey of hepatic angiosarcoma (HAS) in the United States during the years 1964 through 1974 identified 168 cases. Of these, 42 cases (25%) were associated with known etiologic factors, such as vinyl chloride monomer exposure during preparation of poly(vinyl chloride), use of Thorotrast in angiography, exposure to inorganic arsenic, and treatment with androgenic-anabolic steroids; 126 cases (75%) are of uncertain etiology. HAS most often affects males (ratio of approximately 3:1), peaks in the sixth and seventh decades of life (somewhat earlier than other sarcomas of the liver) and appears to occur more often in the industrialized Northeast and Midwest (although reporting artifact may be a factor). There is an extraordinary relative risk for poly(vinyl chloride) polymerization workers; there may also be other chemical-industrial associations that require further investigation. Prospective epidemiologic studies of HAS should be considered as a means of identifying other causative factors (e.g., chemicals or drugs) related to HAS.

Adolescent↗