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Biomedical subjects

R L Peters

Publications and source records attributed to R L Peters.

At least 19 recordsLinked to original sources

Histopathologic observations in weanling B6C3F1 mice and F344/N rats and their adult parental strains.

Weanling Fischer 344/N (F344) rats and the first filial hybrid of C57BL/6 x C3H (B6C3F1) mice and retired breeders from the parental stocks of these strains were monitored over a 5-yr-period by examining the histopathology of selected organs and comparing those results to viral and mycoplasmal serology and the intestinal tract bacterial flora of each animal on an individual basis. Serology gave no evidence of viral infection, but Mycoplasma arthriditis antibodies were detected. Reactivity of serum of adult C57BL/6 female mice with control cells or media (tissue culture, TC) was seen in a significant number of mice. TC reactivity correlated positively with lymphoid perivascular infiltrates, predominantly of the lungs, suggesting an allergic response in development of the lesions. Other lesions of note consisted of Harderian gland inflammation of rats, focal necrotizing lesions of the liver of both species, and thickening of the pleura and adjacent pulmonary interstitium of weanling rats. Embolization of bacteria from the gastrointestinal tract to the liver was considered a possible cause of the liver necrosis in both species. Although lesions of the lung and Harderian gland of the rats are similar to those caused by known viral agents, the cause of the latter could not be determined as these animals were negative for viral antibodies and the former was considered to be related to incomplete pulmonary development in the young rat. Features differentiating the lesions observed in animals of this survey from those caused by viral infection are discussed.

Aging

Risk lesions in cirrhosis and development of hepatocellular carcinoma: an autopsy study.

Non-neoplastic morphologic changes in various types of cirrhosis were evaluated in relationship to the presence or absence of hepatocellular carcinoma (HCC), using autopsy livers from Hokuriku (Japan) and Los Angeles (USA). Macronodular cirrhosis was closely related to HCC in B-viral cirrhosis, alcoholic cirrhosis and cirrhosis of uncertain type. Liver cell dysplasia was most frequently seen in cases with and without HCC in B-viral cirrhosis but was significantly more frequent with HCC in cases of alcoholic cirrhosis and cirrhosis of uncertain type. Nodular bulging activity within regenerative nodules was closely related to HCC in alcoholic cirrhosis. A positive relationship between HCC and Mallory bodies was found in non-alcoholic cirrhosis. These data suggest that patients with macronodular cirrhosis, liver cell dysplasia, nodular bulging activity and Mallory bodies may have an increased risk of developing, or having HCC dependent on the etiology of cirrhosis. The geography and race differences had some relationship to the incidence of HCC.

Autopsy

Effects of sodium tetradecyl sulfate endoscopic variceal sclerotherapy on the esophagus. A prospective clinical and histopathologic study.

A prospective clinical, endoscopic, and histopathologic study of the esophagus was carried out in 24 patients with advanced liver disease who underwent esophageal variceal sclerotherapy (EVS) and who eventually came to autopsy. Patients were arbitrarily divided into three groups: acute (group I), intermediate (group II), and chronic (group III) based on the interval between the first EVS and death. EVS with sodium tetradecyl sulphate (STS) initially produced thrombosis with varying degrees of necrosis and inflammation followed by ulceration, recanalization, and eventually fibrosis with obliteration of varices. Recurrent variceal hemorrhage (VH) leading to death was highest in the acute group since all patients died of uncontrollable VH (100%); it ranged between 50-60% in both the intermediate and chronic groups. Despite variceal obliteration, recurrent hemorrhage developed in the chronic group due to gastric varices or other venous channels in the esophagus or stomach. Additionally, we describe findings not previously reported, such as the presence of sclerosant outside the varices after intravariceal injection, thrombosis of gastric varices after esophageal injections, and the development of muscular wall thickening.

Adult

Alpha-1-antitrypsin deficiency in adults.

A clinicopathological examination was carried out on eight adult patients with alpha-1-antitrypsin (ATT) deficiency. Phenotyping confirmed five patients with PiMZ, two patients with PiZ-, and one patient with PiZZ. Cirrhosis was found in six of the patients, four of whom had a history of excessive ethanol consumption. Hepatitis B surface antigen was positive in two patients with cirrhosis. Dysplastic change was present in four patients, although no neoplasia in the liver was found in all patients. All patients had periodic acid-Schiff positive and diastase resistant inclusions of hepatocytes, which were identified as ATT by indirect immunoperoxidase stain. The possibility of the combined effects of ATT inclusions and such harmful stimuli such as alcohol or viral hepatitis infection may render the hepatocytes more susceptible to damage, and may contribute to development of cirrhosis.

Adult

Pathologic features of the liver in acquired immune deficiency syndrome (AIDS).

The livers of 26 adult males with acquired immune deficiency syndrome (AIDS) were reviewed. The occurrence of portal tracts with diminished lymphocytes, probably reflecting generalized exhaustion of the lymphoid system, was a characteristic morphologic change, and was found in all cases. Kupffer cell hyperplasia was also a frequent finding and probably reflected generalized infection(s). Punched-out clusters of foamy histiocytes filled with acid-fast bacilli, typical for infection with Mycobacterium avium intracellulare (MAC), were found in three patients. In addition, MAC was cultured from two livers without the foamy histiocytic changes. Chronic viral hepatitis (three cases) and deposition of polarizable materials (one case) in the liver might be related to unusual habits of patients with AIDS. In conclusion, livers from patients with AIDS disclosed several kinds of lesions reflecting underlying or associated conditions in AIDS, but these did not contribute to the cause of death in our patients.

Acquired Immunodeficiency Syndrome

The kinetics of the flash-induced P515 response in relation to the H+-permeability of the membrane bound ATPase in spinach chloroplasts.

The effect of dicyclohexylcarbodiimide (DCCD) on the kinetics of the flash-induced P515 response and on the activity of the ATPase was investigated in isolated spinach chloroplasts. It was found that after the addition of 5 X 10(-8)mol DCCD the rate of ATP hydrolysis induced by a period of 60 sec illumination was decreased to less than 5% of its original value. At this concentration, hardly any effect, if at all, could be detected on the kinetics of the flash-induced P515 response, neither in dark-adapted nor in light-activated chloroplasts. It was concluded that the presence of concentrations of DCCD, sufficiently high to affect the ATPase activity, does not affect the kinetics of the flash-induced P515 response. Since DCCD decreases the H+ permeability of the membrane-bound ATPase, it was concluded that this permeability coefficient for protons is not an important factor in the regulation of the flash-induced membrane potential and, therefore, does not affect the kinetics of the flash-induced P515 response.

Adenosine Triphosphatases

Liver allograft. Its use in chronic active hepatitis with macronodular cirrhosis, hepatitis B surface antigen.

A patient suffering from chronic active hepatitis with macronodular cirrhosis, positive for hepatitis B surface antigen (HBsAg), was treated with an orthotopic liver allograft. The HBs antigenemia, as measured with several precipitation tests and by complement fixation, became negative after transplantation and remained so for about 2 1/2 months. During the interval, very low titers of the antigen were detectable by radioimmunoassay. At about three months after transplantation, she had an attack of acute hepatitis, at which time HBsAg became detectable by all tests. She recovered, but progressive liver disease developed during the remaining 1 1/2 years of her life. She died of disseminated nocardiosis and candidiasis with deteriorating hepatic function. The homograft at autopsy showed no evidence of rejection, but was the site of chronic active liver disease, although of a different pathologic pattern than that affecting her native liver. The differences in histology may reflect the influence of chronic immunosuppression on the features of chronic active hepatitis.

Adult

Enzyme-linked immunosorbent assay for detection of antibodies to murine hepatitis virus.

An enzyme-linked immunosorbent assay was developed for the detection of antibodies to murine hepatitis virus. A high prevalence of antibody to murine hepatitis virus was found by the enzyme-linked immunosorbent assay in colonies with a low prevalence of complement-fixing antibodies. Murine hepatitis virus strain A59 was found to be broadly reactive as an enzyme-linked immunosorbent assay antigen.

Age Factors

Hepatocellular carcinoma in the U.S.A., etiologic considerations. Localization of hepatitis B antigens.

The serologic and tissue markers of hepatitis B virus (HBV) were studied in 50 patients in whom hepatocellular carcinoma (HCC) was confirmed at autopsy. Serologic and tissue markers included serum hepatitis B surface antigen (HBsAg), tissue HBsAg, tissue hepatitis core antigen (HBcAg), and serum antibody to HBcAg (anti-HBc). Twenty-two patients had HCC arising in alcoholic cirrhosis; 2 of the 22 (9.1%) had one or more of the HBV tissue and serologic markers. This infection rate is similar to the rate of 7.9% observed in 63 control alcoholic cirrhotic patients without HCC. In contrast, 15 of 20 (75.0%) patients with HCC in nonalcoholic chronic active liver disease showed evidence of active HBV infection. One of 8 patients with HCC in normal liver had serum HBV markers. This result indicates that there is an extremely high prevalence of HBV infection among HCC patients with nonalcoholic chronic liver disease in the U.S.A. The prevalence of HBV infection in these patients is as high as that observed in Asia and Africa. Thus, it can be concluded that the lower prevalence rate of active HBV infection in HCC patients in the U.S.A. is the result of statistical dilution of HCC-B-viral disease by the large numbers of the alcoholic cirrhotic patients with HCC, and that if chronic active hepatitis type B were as common in the United States as it is in Africa and Asia, the frequency of occurrence of HCC might also be as high.

Adult