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Biomedical subjects

Z Schaff

Publications and source records attributed to Z Schaff.

At least 127 records · Page 7Linked to original sources
PubMed1975

[Scanning electron microscopic study of human bronchial mucosa under normal and pathological conditions].

Scanning electronmicroscopic picture of the normal human bronchial mucosa and alterations of it in chronic bronchitis are described. According to the author's findings in chronic bronchitis the regular arrangement of cilia disappears, the number of them decreases and they become shortened with a club-like formation on the end. Focal destruction of the cilia can also be seen. In the epithelium of the mucosa number of the cells without cilia increases. This is a consequence of the destruction of the cilia on one hand, and increase of the number of mucus secreting goblet cells on the other. Alterations of the bronchial mucosa in chronic bronchitis revealed by scanning electron microscopy may play an important part in the pathogenesis and persistence of chronic bronchitis of different origine.

Aged↗
PubMed1975

[Electron microscopic study of cytoplasmic crystals in liver damages caused by alcoholism].

Liver biopsy of 50 patients with liver disease of alcoholic etiology was examined electronmicroscopically. In every stage of the disease presence of intramitochondrial paracrystalloids was revealed. Hyalin of alcoholic origin of fibrillar structure was seen in cases of alcoholic hepatitis. By the electronmicroscopic examination of three cases of alcoholic fatty liver a special form of cytoplasmatic paracristalloid inclusion could be seen. This inclusion consists of membranless parallely lying fibrills. Changing the plain of the preparats containing inclusions by the aid of a goniometer the structure of the inclusions appeared in a form of "honey-comb". Inclusion in the question can not be regarded identical neither with intramitochondrial inclusions nor with the fibrills of the so called alcoholic hyalin. Formation and function of these inclusions are as yet unknown.

Adult↗
PubMedDate not supplied

HLA class I antigens on the hepatocyte membrane during recovery from acute hepatitis B virus infection and during interferon therapy in chronic hepatitis B virus infection.

In a chimpanzee model of acute type B hepatitis, at the time of onset of hepatitis B virus replication and before the development of immunity to hepatitis B virus, interferon is present in the plasma. This is followed by an increase in the display of HLA class I, but not class II proteins, on the hepatocyte membrane. In chronic hepatitis B virus infection, there is a low density of HLA class I protein display on the infected hepatocyte. Administration of alpha-interferon enhances HLA display and in many cases is followed by a transaminase elevation, seroconversion of HBe antigen to antibody and disappearance of hepatitis B virus DNA from serum, changes implying clearance of infected hepatocytes. Successful response to interferon therapy may be predicted by a rapidly rising serum beta 2-microglobulin, a component of the HLA class I molecule, during the first 2 weeks of therapy, before the rise in transaminases.

Acute Disease↗
PubMedDate not supplied

Hepatic inclusions during interferon therapy in chronic viral hepatitis.

Two types of cytomembranous abnormalities were identified for the first time in liver biopsies from patients with chronic active type B hepatitis during treatment with recombinant alpha-interferon. Tubuloreticular inclusions were present in the hepatic endothelial cells, Kupffer cells and perisinusoidal cells of liver biopsies from both patients, and they were absent in liver biopsies obtained before treatment. Cylindrical confronting lamellae, having "test tube" or "ring-shape" forms were observed in the cytoplasm both of Kupffer cells and macrophages in the second liver biopsy of one of the patients. The findings suggest that interferon can be involved in the pathogenesis of both cytomembranous abnormalities, but that additional biological factors may play a role in formation of the cylindrical confronting lamellae.

Adult↗
PubMedDate not supplied

Hepatitis viruses and hepatocarcinogenesis.

Hepatocellular carcinoma (HCC) is among the most frequent malignancies worldwide. Hepatitis viruses, such as the hepatitis B virus (HBV) and hepatitis C virus (HCV) are undoubtedly listed in the etiology of HCC. Studies show that, in the near future, viral hepatitis will carry increasing weight in the etiology of HCC. This review briefly discusses the known carcinogenic effects of HBV and HCV in the light of experimental and human studies. The data show that viral proteins may directly interfere with gene products responsible for cell proliferation and cell growth. Many other signal transduction cascades may be affected as well. Direct integration of HBV viral sequences into the host genome increases the genomic instability. The genomic imbalance allows the development and survival of malignant clones bearing defected genomic information. HBV and HCV infection induces indirect and direct mechanisms through cellular damage, increased regeneration and cell proliferation, therefore enhancing the development of HCC.

Hepatitis B↗