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Biomedical subjects

G Tovey

Publications and source records attributed to G Tovey.

33 records · Page 2Linked to original sources
PubMed1985

Acute glandular fever-like illness in a patient with HTLV-III antibody.

A lymph node biopsy obtained from a patient with human T-cell lymphocytotropic virus III/lymphadenopathy-associated virus (HTLV-III/LAV) antibody, presenting with an acute glandular fever-like illness, was examined by electron microscopy. Numerous pathological changes were present in the biopsy, including hypertrophy of smooth endoplasmic reticulum, intracytoplasmic rod-like inclusions within the cisternae of endoplasmic reticulum, multivesicular bodies, test-tube and ring-shaped forms, and tubulo-reticular structures. Intranuclear and intracytoplasmic viral-like particles measuring 105-120 nm in diameter and small cytoplasmic particles measuring 50-70 nm in diameter were found in some degenerating lymph node cells. These pathological findings may reflect a host cell response to various pathological and viral stimuli resulting from immune deficiency owing to infection with HTLV-III/LAV.

Acute Disease↗
PubMed1985

The chemotherapy of rodent malaria, XXXIX. Ultrastructural changes following treatment with artemisinine of Plasmodium berghei infection in mice, with observations of the localization of [3H]-dihydroartemisinine in P. falciparum in vitro.

Ultrastructural changes were followed in Plasmodium berghei after the treatment of the mouse host with a single 10 mg kg-1 dose of artemisinine (qinghaosu). After 30 minutes, changes in the limiting and other membranes of the parasite were seen, together with alterations in ribosomal organization and endoplasmic reticulum. No changes were noted in digestive vacuoles or pigment, but nuclear membrane blebbing developed after one hour and segregation of the nucleoplasm after three hours. Further degenerative changes with disorganization and death occurred from eight hours onwards. The morphological changes in ribosomes and endoplasmic reticulum correlate in time with the depression in protein synthesis observed in P. falciparum in vitro. Similarly, the onset of nucleoplasmic segregation correlates with the development of nucleic acid synthesis inhibition. Tritiated reduced drug was shown to be localized in parasite membranes, indicating that changes in membrane integrity might precede the early depression of protein synthesis. Membrane association of artemisinine may be related to its amphipathic characteristics and similarity in some respects to a sterol.

Animals↗
PubMed1984

Persistent lymphadenopathy in homosexual men: a clinical and ultrastructural study.

Ultrastructural changes (tubuloreticular structures and tube and ring shaped forms) previously described in patients with acquired immunodeficiency syndrome (AIDS) are described for the first time in the lymph nodes and circulating lymphocytes of patients with persistent lymphadenopathy. These observations support the view that the persistent lymphadenopathy syndrome and AIDS are caused by the same transmissible agent(s).

Acquired Immunodeficiency Syndrome↗
PubMed1984

Intracytoplasmic inclusions in human hepatocytes in non-A, non-B hepatitis: an ultrastructural study.

An ultrastructural study was carried out on 114 liver biopsies obtained for diagnostic purposes from patients with various pathological disorders of the liver including hepatitis B-related liver disease, non-A, non-B hepatitis, alcoholic liver disease, fatty change, and cryptogenic cirrhosis. The opportunity was taken to evaluate the significance of intracytoplasmic crystalline structures found in the hepatocytes of nine patients with a variety of liver disorders. The cytoplasmic inclusions varied in size up to 2 microns in length and shape and were not limited by membranes. The presence of these inclusions cannot, however, be correlated either specifically with non-A, non-B hepatitis or with other known nonviral liver disease. The functional, physiological, and pathological significance of the crystalline structures remain to be elucidated.

Adult↗
PubMed1983

Non-A, non-B hepatitis in persistent carriers of hepatitis B virus.

There are reports in the literature that infection with hepatitis A virus in hepatitis B carriers can result in resolution of the carrier state. In an attempt to induce clearance of the carrier state of hepatitis B virus in two persistently infected chimpanzees, the chimpanzees were infused with documented non-A, non-B infectious material. Biochemical and histopathological evidence of hepatitis was accompanied by the unique abnormalities of endoplasmic reticulum associated with non-A, non-B hepatitis in the chimpanzees. Elevation of alanine aminotransferase was accompanied by fourfold reduction in one chimpanzee and sixfold reduction in the other in the plasma levels of HBV-associated DNA polymerase activity and simultaneously by twofold reduction in the concentration of hepatitis B surface antigen in both chimpanzees. A mediator may account for these changes in markers of hepatitis B virus infection, and this mechanism may also explain the occurrence of spontaneous regression in some persistently infected carriers. The significance of transient red cell anaemia in non-A, non-B hepatitis, which was observed in one of the chimpanzees, is yet to be established.

Alanine Transaminase↗
PubMed1982

Examination of crystalline arrays in non-A, non-B hepatitis.

Individual patients within crystalline arrays found in the endothelial cells of hepatic sinusoids in experimental non-A, non-B hepatitis were examined by the Markham rotation technique. The particles appeared to possess an outer structure with 16-18 divisions. The presence of the crystalline structures is probably a reflection of host cell response to infection.

Animals↗
PubMed1982

Non-A, non-B hepatitis: a case report.

Ultrastructural changes in a liver biopsy obtained for diagnostic purposes from a patient with suspected non-A, non-B hepatitis were consistent with hepatitis and included dilatation and disaggregation of the endoplasmic reticulum, hepatocyte disarray, and variations in mitochondrial size. In addition, some foci of hepatocytes showed atypical cytoplasmic changes including intranuclear cytoplasmic pseudo-inclusions, consisting basically of invaginations of the cytoplasmic mass into the nucleus, glycogen deposits in the same nuclei, and frequently accumulations of fat droplets. The mitochondria were generally pleomorphic, and occasionally the mitochondrial cristae were arranged longitudinally. Dilatation, hypertrophy, and distortion of the Golgi complexes were found in affected hepatocytes. Similar ultrastructural changes have previously been reported in human hepatocellular carcinoma as well as in carcinomas of other tissues.

Cell Nucleus↗
PubMed1982

Application of electron microscopy to the study of structural changes in the liver in non-A, non-B hepatitis.

Ultrastructural studies employing techniques such as alternative electron metal stain, high-angle tilting and high-voltage electron microscopy were carried out on liver biopsies obtained from chimpanzees infected with non-A, non-B hepatitis. Typical derangement of the endoplasmic reticulum leading to the formation of tubular structures in hepatocytes was observed. The use of potassium permanganate as an alternative stain revealed two features which have not been previously described. The first of these shows the wall of the tubular structures to be composed of a well-defined fibrillar-like meshwork with a periodicity of approximately 15 nm. The second feature is the demonstration of clusters of fibrin-like inclusions consisting of striated fibrils in the neighborhood of the tubular structures. The presence of intracytoplasmic fibrin may indicate non-specific morphological evidence of cell injury. Crystalline structures containing arrays of particles with an average size of 24 nm were also observed in the endoplasmic reticulum of endothelial cells of the hepatic sinusoids. Morphological differences between the crystalline lattice and the reticular arrangement, demonstrated with the use of high-angle tilting of the specimen in the electron microscopy suggest that the arrays may not be viral particules but a reflection of pathological response of the host cell.

Animals↗
PubMed1982

A study of ultrastructural alterations in experimental non-A, non-B hepatitis by electron-beam analysis.

An electron-beam X-ray microanalysis was carried out on sections of liver biopsy specimens obtained from chimpanzees infected with non-A, non-B hepatitis. The microanalysis was concentrated over areas where typical derangement of the endoplasmic reticulum, with the formation of tubular forms possessing walls with electron-dense central membrane, was visualized. These tubular structures are regarded as the most notable pathological alteration in affected hepatocytes. However, the electron-probe microanalysis showed no deviation of the energy spectrum when compared with the background or control analysis.

Animals↗
PubMed1981

Ultrastructural changes in the liver in experimental non-A, non-B hepatitis.

Factor VIII, a blood-clotting derivative prepared from pooled human plasma, previously shown to cause a short-incubation-period non-A, non-B hepatitis in patients and in chimpanzees, was studied further to establish the nature of the pathological lesions associated with this infection. Percutaneous liver biopsy specimens were examined in detail. Cytoplasmic changes in the hepatocytes were observed on the 7th day after inoculation in one instance and after 13 days in the second, and persisted in the biopsy specimens for 13 weeks after infection. Abnormalities in hepatocyte nuclei, including aggregates of irregularly shaped particles 15-20 nm in size, were observed about 1 week after the onset of the cytoplasmic changes. The ultrastructural changes are described and their nature and significance discussed. Attention is drawn to somewhat similar cytoplasmic and nuclear changes occurring in other disease entities.

Animals↗
PubMed1980

Further evidence of cellular changes associated with non-A, non-B hepatitis.

Two distinct types of ultrastructural changes were found in the hepatocytes of chimpanzees infected with two forms of non-A, non-B hepatitis. In the type of infection that was of long incubation, there was a marked cytoplasmic derangement of the endoplasmic reticulum, with the formation of tubules, but no pathological changes in the nuclei. In the short-incubation type of non-A, non-B hepatitis, induced experimentally in a chimpanzee that had recovered from the long-incubation type of infection, nuclear alterations were found together with the presence of aggregates of particles measuring 15--27 nm in diameter. Cytoplasmic tubules were not seen in this type of non-A, non-B infection.

Animals↗
PubMedDate not supplied

Unusual development of polyoma virus in the brains of two patients with the acquired immune deficiency syndrome (AIDS).

Two HIV-positive male patients presented with a variety of symptoms including hemiparesis, unsteadiness, progressive loss of vision and poor memory. There were multiple non-enhancing lesions shown by CT scan in the white matter of the cerebral hemispheres. Specimens obtained by burr-hole biopsy showed the features of progressive multifocal leucoencephalopathy (PML) in both cases. Electron microscopy demonstrated round and rod shaped particles of papovavirus in the nuclei and cytoplasm of oligodendrocytes and in processes of astrocytes where abnormal and florid modes of viral replication were seen. Additional features observed were viral particles suggestive of an enterovirus in Case 1 and, in both specimens, massive membrane proliferation within both nuclei and cytoplasm of infected cells together with the presence of tubuloreticular structures (TRS) in the cytoplasm of endothelial cells. At post-mortem, the brain of patient 2 showed PML and HIV encephalitis. The presence of HIV was confirmed by immunohistochemical methods. We suggest that in AIDS patients the abnormality of the immune system induced by HIV causes abnormal replication patterns of papovavirus in the brain. In addition, these cases confirm the frequent occurrence in AIDS patients of TRS, now considered to be a marker for HIV.

Acquired Immunodeficiency Syndrome↗