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H Popper

Publications and source records attributed to H Popper.

At least 37 records · Page 2Linked to original sources
PubMed1988

Studies of prototype live hepatitis A virus vaccines in primate models.

We have prepared two prototype live hepatitis A virus (HAV) vaccines by serial passage of the HM-175 strain of HAV in African green monkey kidney cells. Passage 21 (P-21) HM-175 virus shows evidence of attenuation for chimpanzees but not for marmosets; passage 32 (P-32) HM-175 virus shows evidence of attenuation for both species. Animals that received P-32 HAV had fewer elevations in levels of liver enzyme activity and evidence of less virus replication in the liver and excretion of virus in stool than did those that received wild-type virus. The P-21 and P-32 viruses were highly immunogenic in both species. The information provided by this study will aid in the development of a live HAV vaccine.

Alanine Transaminase↗
PubMed1988

Chronic hepatitis D virus (HDV) infection in hepatitis B virus carrier chimpanzees experimentally superinfected with HDV.

Chimpanzees that were chronic hepatitis B virus carriers and that were superinfected with hepatitis D virus (HDV) apparently developed acute, self-limited type D hepatitis. Reevaluation with a sensitive hybridization-based assay using RNA probes specific for the HDV genome, however, demonstrated that greater than 50% of these animals still had detectable signs of ongoing HDV replication an average of 2.4 y (range, 1-6.4 y) after inoculation. The only positive marker for the presence of HDV was serum HDV RNA; HDV antigen was undetectable in both serum and the liver by an immunoblot assay and immunofluorescence, respectively. Because the detected amount of viral genome was very low, the previous failure to identify the chronic HDV carrier state in the chimpanzee can be attributed to the lower sensitivity of previously described assays.

Animals↗
PubMed1988

The diagnostic significance of periportal hepatic necrosis and inflammation.

In this review the several types of cell damage and cell death which may be found in liver biopsy specimens are defined. We describe the different processes which occur at the portal/parenchymal or septal/parenchymal interface, viz. periportal spillover, periportal hepatitis, classic or lymphocytic piecemeal necrosis and biliary piecemeal necrosis. The diagnostic implications of these lesions in relation to the clinicopathological diagnosis and prognosis in various liver diseases are discussed.

Diagnosis, Differential↗
PubMed1988

Pulmonary exchange of solutes during experimental lung lavage in pigs.

Unilateral continuous lung lavage in a nonregenerating system (3,000 ml isotonic cristalloid) was done in 12 pigs for 270 min. The concentration of substances in serum and fluid was measured. Half-time (t1/2) of exchange and permeability constants (P) were determined. In the fluid Na+ decreased significantly (t1/2 = 107 min, P = 7.8 x 10(-7]. Urea increased significantly, reaching serum level after 270 min (t1/2 = 109.1 min, P = 6.18 x 10(-6]. Ca2+ (t1/2 = 36.7 min, P = 4.1 x 10(-7] PO4 = (t1/2 = 173.3 min, P = 1.1 x 10(-7], and creatinine (t1/2 = 55.2 min, P = 6.2 x 10(-7] also increased markedly but did not reach serum level. The adjustment to serum concentration may be prevented by interaction between diffusion, active transport or Donnan's equilibria. K+ increased almost linearly, documented by the long half-time (t1/2 = 7,835.2 min, P = 7.7 x 10(-7] and did not reach serum level. The calculated limit value was higher than the serum level. Active transport systems or influx of K+ from cellular compartments rather than from the serum might be involved in its linear kinetics. Total protein (t1/2 = 61.5 min, P = 2.06 x 10(-9] and albumin (t1/2 = 58.8 min, P = 1.7 x 10(-9] increased initially but levelled far below the serum value. The low P indicates a lack of significant permeation. Initial increase may be due to washout of the epithelial lining fluid compartment. There was minimal transfer of lavage fluid into the organism (10-20 ml/30 min). Serum concentrations were not affected by the lavage.

Animals↗
PubMed1988

Evolution of hepatocellular carcinoma associated with chronic hepatitis B virus infection in Alaskan Eskimos.

Hepatocellular carcinoma (HCC) associated with chronic hepatitis B virus (HBV) infection in Yupik Eskimos in southwestern Alaska, detected in early stages as a result of screening, appears to be more frequently associated with variants of chronic portal inflammation in the noninvolved liver than with fully developed cirrhosis, otherwise common in HBV-associated HCC from other geographic areas. Of 38 patients diagnosed with HCC since 1969, adequate tissue was available from both the tumor and nontumorous liver in 17. Of the 17 specimens, 14 had chronic portal inflammation and three had advanced cirrhosis; 12 of the 14 were from hepatitis B surface antigen carriers. These 12 cases were studied in detail to examine the features accompanying the development of HCC unobscured by cirrhotic transformation. In the noninvolved parenchyma they included hepatocytic nodules as apparent precursors to HCC and, as markers of phenotypic alterations, dysplastic hepatocytes and hepatitis B surface antigen-laden ground-glass hepatocytes. The latter were observed in eight instances and often accumulated in nodules. Parenchyma within 1 mm of the HCC exhibited increased confluent hyperplasia and frequently conspicuous necroinflammation associated with pericellular and periductular fibrosis, which contributed, in addition to fibrous connections between displaced and heavily inflamed portal tracts, to the capsule that was forming in all cases to varying degrees in the pericarcinomatous region. The HCC was uniformly trabecular and in a few specimens, a continuous transition from hyperplasia and dysplasia near the periphery of the tumor to increasing anaplasia in the center could be made out in addition to pressure effects of the HCC. The pericarcinomatous changes, including hyperplasia progressing to neoplasia and necroinflammation, are also observed in experimental models, particularly the woodchuck HCC induced by a hepadna virus related to HBV. Coordinated morphologic and molecular biologic studies on such animal models and on human HCC detected by screening, as for instance in Eskimos, neither complicated by cirrhosis, should elucidate the direction of the evolution of the HCC and the postulated promoting role of the inflammation.

Adolescent↗
PubMed1988

Relation between hepatocellular carcinoma and persistent hepatitis B infection.

Epidemiologic studies indicate a close association between hepatocellular carcinoma (HCC) and chronic hepatitis B virus (HBV) infection. HCC, a most frequent malignancy, is far more common in the Far East and Africa than in the West and may be the first to be greatly eliminated because of prevention of HBV infection by vaccination. The conceptual integration of epidemiologic observations, morphologic studies of the human precursor stages and investigations of animal infections by hepadna viruses with biologic and genomic similarity to HBV as well as with clinical and molecular biologic studies contribute to the understanding of the hepatocarcinogensis. In the woodchuck model after laboratory infection, HCC develops regularly without external cocarcinogen in permanent surface antigen carriers. The hypothesis is presented that an episodic necroinflammation in the carrier stage may act as an endogenous cocarcinogen or promoter in that previous integration of hepadna viral DNA in the host chromosone may become disorganized, which induces the clonal development of HCC. This hypothesis may become important in the management of the carrier stage.

Carcinoma, Hepatocellular↗
PubMed1988

[Pulmonary involvement in tuberous sclerosis].

The authors present a case of tuberous sclerosis with marked pulmonary involvement, confirmed by both radiological and pathological studies. The radiological manifestations and basic pathology of this rare condition are reviewed with emphasis on differential diagnosis.

Adult↗
PubMed1988

Non-A, non-B hepatitis-related hepatocellular carcinoma in a chimpanzee.

Epidemiology has indicated the possible association of non-A, non-B hepatitis (NANBH) with hepatocellular carcinoma (HCC) in man, but there are no means for confirmation. Chimpanzees are recognized models for studying hepatitis B and NANBH, and may become carriers of both. The first case of HCC to be reported in chimpanzees was found after longitudinal study of a hepatitis B-free chimpanzee 7 years after inoculation with human plasma from a patient reported to have chronic NANBH.

Animals↗
PubMed1987

Primary liver cancer in Alaskan natives. 1980-1985.

The authors reviewed the cases of 19 Alaskan Natives (15 men, four women) with primary hepatocellular carcinoma (HCC) diagnosed during 1980-1985. Of these 19 patients, 16 were seropositive for hepatitis B surface antigen (HBsAg). Alpha-fetoprotein (AFP) was elevated in 15 patients (all were HBsAg positive). The patients ranged in age from 8 to 80 years old. Of the 19 patients, 16 were Eskimo, 13 of whom were Yupik. The annual age-adjusted (world standard) incidence of HCC for all Alaskan Natives was 9.3/100,000 for men and 2.2/100,000 for women. The tumor was resected in seven patients; six showed no recurrence of cancer 1 to 4 years after surgery. Histologic evaluation in 18 patients revealed trabecular type of HCC in 15 and acinar HCC in two others. In 16 specimens in which nontumorous liver could be studied, only six had evidence of cirrhosis; ten others showed variants of chronic persistent hepatitis.

Alaska↗
PubMed1987

Giant fibroma of the lung. A morphological study.

The authors report the case of a 78-year-old male patient with an inoperable giant lung tumour diagnosed 5 years prior to death. Fine needle cytological examination at that time was interpreted as indicative of malignancy. In the following years the tumour grew very slowly without signs of infiltration or metastatic spread. On radiological examination sharp limitation of the tumour was evident. Recurrent pleural effusions occurred and the patient died from cardiorespiratory insufficiency. Autopsy revealed a giant fibroma, well vascularized but without signs of malignancy. The diagnosis was confirmed by immunohistochemical and electron microscopic examinations.

Aged↗
PubMed1987

Malignant fibrous histiocytoma of the lung: prognosis and therapy of a rare disease. Report of two cases and review of the literature.

On the basis of 2 own patients and 18 cases reported in the literature, clinicopathological features of primary malignant fibrous histiocytoma of the lung are reviewed. Of the 20 patients (age-range: 14-75 yrs; 13 male, 7 female), 14 underwent resection. Recurrences were noted in 7 of them. 8 patients were free of disease at least 8 months postoperatively, one having undergone successful pulmonary metastasectomy. Postresection disease-free survival ranged from 8 months to 10 years. Adjuvant chemotherapy or irradiation (3/14) did not influence postoperative outcome. After chemotherapy, irradiation or conservative measures alone (6/20) survival did not exceed 12 months; remissions were not reported. The course was fatal within 12 months in 9/20 cases due to distant metastasis or local growth. 1 patient died of tumour-associated hypoglycemia. Age, sex, localization of the tumor and histologic subtype did not influence prognosis. Small tumors, asymtomatic at time of detection probably carry a better prognosis than larger ones.

Aged↗
PubMed1987

Histologic patterns of liver disease in hemophiliacs, with special reference to morphologic characteristics of non-A, non-B hepatitis.

In a retrospective study 157 liver specimens from hemophiliac patients (105 percutaneous needle and 12 wedge biopsies, 40 autopsy specimens) were read blindly and independently by four pathologists on the basis of a computer codable questionnaire asking for evaluation of individual histologic features, classification of the liver disease, and speculation on etiology. The majority of cases had histologic evidence of mild chronic viral hepatitis; 7.6% of all cases were classified as CAH, and an additional 7.6% as CPH by all four interpreters. A large number (40.8%) were on the borderline of CAH and CPH or CLH. These were classified as "possible CAH" because of a diagnosis of CAH by one to three of the pathologists. Although there was therefore some interobserver variability in the diagnostic labels applied to these cases, all four pathologists were strikingly similar in their identification of individual histologic features. Furthermore, on blind rereadings, each pathologist made the same diagnosis in more than 90% of readings. In this retrospective study, serologic data were not available in many cases. Thus, etiologic considerations were based purely on speculation from the histologic appearance. One case was identified as "definite" and 28 of 157 (18%) as "possible" HBV infection. Based on the assumption that some of the individual histologic criteria indeed might be in favor of NANB hepatitis, 21 cases (13%) were considered "definite" NANB, and "possible" NANB was suspected in 107 additional cases (68%). The addition of these figures makes clear that within the limitations of histologic assessment, double infections appear to be frequent in this setting.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy, Needle↗
PubMed1987

Hepatitis B virus produced by transfected Hep G2 cells causes hepatitis in chimpanzees.

We have reported that clonal cells derived from Hep G2 cells transfected with a plasmid containing hepatitis B virus (HBV) DNA secrete spherical and filamentous forms of hepatitis B surface antigen (HBsAg), core particles, and virions into the culture medium. Here we describe the development of typical hepatitis in two chimpanzees following intravenous inoculation with the medium in which the transfected cells had grown. The liver biopsies from these animals showed characteristic lesions in parenchyma and portal tracts, more conspicuous at an earlier time in the chimpanzee that had received a greater number of virions. The amount of HBsAg in the serum of one infected chimpanzee increased with time after the initial inoculation and then decreased concomitantly with the appearance of antibodies against HBsAg and core antigens. HBsAg remained detectable in the other animal throughout the course of the experiment. The levels of hepatitis B "e" antigen in both animals peaked at week 5, signifying the acute phase of the infection. The activities of serum enzymes that are markers for necroinflammation also increased. The hepatitis HBsAg subtype of the virions isolated from the patient whose DNA was cloned and then used for transfection of the Hep G2 cells was the same as that found in the chimpanzees. Furthermore, the restriction enzyme analysis of the viral DNA isolated from the chimpanzees was identical to the cloned DNA. Thus, HBV DNA-transfected Hep G2 cells can support the replication of virions that, in turn, produce hepatitis in chimpanzees.

Animals↗
PubMed1987

Detection of hepatitis A virus by extraction of viral RNA and molecular hybridization.

Hepatitis A virus (HAV) RNA was extracted from cell culture, serum, liver, and feces and then detected by molecular hybridization with cloned HAV cDNA. Hybridization was approximately 10-fold more sensitive than immune electron microscopy or radioimmunoassay was and less sensitive than was assays of HAV infectivity in primates or in cell culture. As little as 10(3) 50% infective doses of HAV, or approximately 0.1 pg of viral RNA, was detected by this method. Analysis of fecal specimens from an experimentally infected marmoset and an epidemic of hepatitis A showed that HAV excretion could often be detected later in the illness by hybridization than by radioimmunoassay. This technique should be widely applicable for detection and analysis of HAV RNA.

Animals↗
PubMed1987

Immunohistochemical and histochemical markers of primary lung cancer, lung metastases, and pleural mesotheliomas.

Sections of primary lung carcinomas, lung metastases, mesotheliomas, and lung metastases of some rare mesenchymal tumors were incubated with different cytokeratin (CK), vimentin, desmin, and tissue polypeptide antigen (TPA) antibodies and with antibodies reactive with different hormones (ACTH, PTH, alpha-HCG, Calcitonin CT), CEA, carcinoma-associated antigen (CA1), secretory component (SC), neuron-specific enolase (NSE), alpha-1-antitrypsin (alpha-1-AT), lysozyme (lyso), and S-100 protein (S 100). CK antibodies derived from a 49 kD (reactive with simple epithelia [SE]) and a 67 kD CK polypeptide fraction (reaction with complex epithelia [CE] were useful differentiation markers for the four major groups of lung carcinomas. In one half of small cell carcinomas a positive reaction with NSE antibodies was found. S 100 and SC were good markers for papillary and bronchioloalveolar adenocarcinomas, whereas CEA was less important because of its reactivity with different types of lung carcinomas. To discern clear cell carcinomas of lung and renal origin a positive reaction with vimentin antibodies (some renal but not lung types) and with CA1 (no renal but all lung types) seemed to be useful. All hormone antibodies were of no importance as markers for difficult differential diagnosis, because positive reactivities were found in cases from every major carcinoma group. In addition, a Ca2+-activated adenosine triphosphatase (ATPase) was found in mesotheliomas but not in papillary adenocarcinomas.

Adenocarcinoma↗
PubMed1986

The gastric juice aspiration syndrome (Mendelson syndrome). Aspects of pathogenesis and treatment in the pig.

The gastric juice aspiration syndrome (GJA-S, Mendelson syndrome) was studied experimentally in pigs. Following instillation of gastric juice into the right main bronchus necrosis of pneumocytes and bronchiolar epithelium occurred with activation of complement and a prostaglandin E releasing system (possibly the kinin system). Cell necrosis was followed by loss of surfactant and formation of hyaline membranes, rich in immunoglobulin M. The alveolar damage organized, resulting in intraalveolar and interstitial fibrosis. The causative agents were found to be both gastric hydrochloric acid and pepsin. Pretreatment with H2-, or acetylcholine-receptor-antagonists (cimetidine or pirenzepin) as well as buffering of the gastric juice to a neutral pH did not prevent lung fibrosis. If a mixture of aluminium hydroxide, magnesium carbonate and oxethazaine was added to the aspirate, development of lung fibrosis was prevented, but severe granulomatous reaction with foreign body giant cells within both lungs evolved. Kallikrein inhibitor, when administered intravenously not later than 3 min after artificial aspiration, protected the left lung completely and large areas of the right. If infused within 60-90 s complete protection of the left lung and the right upper lobe was achieved. In the majority of the animals a mild focal fibrosis developed in the right lower lobe; in one experiment both lungs were devoid of fibrotic areas. If Kallikrein inhibitor was infused 5 min prior to aspiration, lung fibrosis was not prevented.

Anesthesia, General↗