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Biomedical subjects

D Bernuau

Publications and source records attributed to D Bernuau.

51 records · Page 3Linked to original sources
PubMed1985

Liver perisinusoidal fibrosis in BB rats with or without overt diabetes.

Perisinusoidal fibrosis is a vascular lesion observed in the liver of type I diabetic patients. To investigate whether this liver lesion is secondary to hyperglycemia or whether it represents a separate collagen vascular disorder, the authors studied the structure of liver sinusoids in genetically susceptible BB rats in which a spontaneous diabetes develops similar to human type I diabetes. Seven diabetic insulin-treated BB rats, 7 nondiabetic BB rats, and 6 control non-BB rats were studied. Histologic abnormalities of the collagen network were detected on trichrome-stained sections. Perisinusoidal collagen fibers were quantified ultrastructurally by the point-counting method. All control non-BB rats had normal livers; 86% of the diabetic as well as 71% of the nondiabetic BB rats displayed localized sinusoidal thickening corresponding ultrastructurally to perisinusoidal fibrosis; in these abnormal rats the percentage of collagen fibers per sinusoid unit was significantly higher than that in controls. Fibrous septa (2 diabetic and 5 nondiabetic BB rats) and liver nodulation (3 diabetic and 1 nondiabetic BB rats) were also observed. Perisinusoidal fibrosis is a frequent liver vascular abnormality in a strain of rats genetically predisposed to the development of type I diabetes. The lesion is independent of the presence of diabetes. These observations suggest that liver perisinusoidal fibrosis in patients with type I diabetes might be linked to a genetic abnormality rather than to hyperglycemia per se.

Animals↗
PubMed1984

Peliosis-like ultrastructural changes of the hepatic sinusoids in human chronic hypervitaminosis A: report of three cases.

In addition to hypertrophy of Ito cells and perisinusoidal fibrosis, previously unrecognized ultrastructural abnormalities of the hepatic sinusoids were observed in three patients with chronic hypervitaminosis A: 1) large areas of communication between the sinusoidal lumina and the perisinusoidal spaces, allowing extravasation of blood cells; 2) marked dilation of the perisinusoidal spaces; and 3) swelling and clarification of endothelial cells. Most of these changes, along with some other sinusoidal barrier alterations previously reported in chronic hypervitaminosis A (i.e., bleb formation on the sinusoidal membrane of the hepatocytes and the presence of multiple cellular layers lining the sinusoids), are strikingly similar to those observed in peliosis hepatis. The present findings suggest that sinusoidal barrier abnormalities might constitute a major event in the pathophysiology of vitamin A-induced liver injury as well as of peliosis hepatis.

Adult↗
PubMed1984

In situ ultrastructural detection and quantitation of liver mononuclear phagocytes in contact with hepatocytes in chronic type B hepatitis.

An ultrastructural cytochemical method for detection of endogenous peroxidase was used to quantify the mononuclear phagocytes present in areas of tissue injury, i.e., in membrane contacts with hepatocytes, in liver biopsies from 12 patients with chronic type B hepatitis; 10 of them exhibited stable disease activity of various degrees of severity, and the other two displayed acutely exacerbated disease activity. Results were compared with those for three patients with acute type B hepatitis. The total percentage of mononuclear phagocytes was higher in patients with chronic hepatitis with stable high disease activity than in patients with stable low disease activity (31.3 +/- 7.4 versus 15.6 +/- 4.7%, p less than 0.01). Furthermore, in the former group of patients, recently recruited macrophages were significantly more frequent than in patients with low disease activity (11.6 +/- 4.0 versus 3.5 +/- 3.6%, p less than 0.01), and macrophages often displayed a markedly hypertrophied cytoplasm with numerous phagolysosomes, suggestive of an activated state. On the other hand, no significant differences in the percentage of the other leukocytes in contact with hepatocytes (lymphocytes, plasmocytes, and polymorphonuclear leukocytes) were noted between patients with high and low disease activity. In the three biopsies obtained from two patients with chronic hepatitis with acute exacerbation of disease activity, the profile of the leukocytes in contact with hepatocytes strikingly resembled the one observed in the three patients with acute type B hepatitis. In both instances, mononuclear phagocytes were rare, and a higher proportion of lymphocytes was observed than in patients with stable chronic liver disease activity. These results suggest that the mechanisms of hepatocyte necrosis in chronic type B hepatitis may differ from that in acute hepatitis due to this virus. Although lymphocyte-mediated mechanisms are likely to be predominant during acute episodes of hepatocyte necrosis, mechanisms mediated by mononuclear phagocytes might play a significant role in the low grade of hepatocyte necrosis characteristic of stable chronic type B hepatitis.

Acute Disease↗
PubMed1982

Ultrastructural aspects of the liver perisinusoidal space in diabetic patients with and without microangiopathy.

To determine whether abnormalities of the perisinusoidal space of Disse are present in the liver of diabetic patients with microangiopathy, an ultrastructural stereologic study of the space of Disse was performed in six insulin-treated diabetics with severe performed in six insulin-treated diabetics with severe proliferative retinopathy and six insulin-treated diabetics with normal fluorescein angiography, six patients with familial unconjugated hyperbilirubinemia were studied as controls. No patient had clinical and/or biochemical hepatic abnormalities and none suffered from any of the pathologic conditions known to be associated with collagenization of the perisinusoidal space. In control patients, the space of Disse of liver sinusoids contained occasional small deposits of collagen fibers. The relative volume of these fibers per unit of sinusoid represented 2.63 +/- 0.82%. In all diabetic patients with retinopathy, marked deposition of collagen fibers within the perisinusoidal space was constantly observed, a finding confirmed by ultrastructural stereologic analysis which showed that the relative volume of collagen fibers per unit of sinusoid represented 7.33 +/- 1.44% and differed significantly from control patient values (P less than 0.001). On the contrary, the relative volume of collagen fibers within the space of Disse in diabetic patients without retinopathy (3.95 +/- 2.96%) did not differ significantly from control patient values. These findings demonstrate that collagenization of the space of Disse is positively correlated with the presence of diabetic microangiopathy. Ultrastructural examination of the liver sinusoids might constitute a sensitive and useful approach for detecting the early changes of the microcirculation in diabetic patients.

Adult↗
PubMed1982

A quantitative ultrastructural analysis of the leukocytes in contact with hepatocytes in chronic active hepatitis, with a cytochemical detection of mononuclear phagocytes.

In an attempt to characterize in vivo the immune cells cytotoxic to hepatocytes in patients with chronic active hepatitis (CAH), a quantitative ultrastructural analysis of leukocytes in close contact with hepatocytes was performed in 13 patients with untreated HBsAg-negative CAH. Mononuclear phagocytes were identified by detection of endogenous peroxidase. Of the leukocytes, 8.3-4.1% were mononuclear phagocytes, 12.5-25.8% were large lymphocytes with a prominent secretory apparatus, assumed to represent mostly killer cells (T-cytotoxic cells and/or null cells), 12.2-56.8% were small lymphocytes poor in cytoplasmic organelles, and 0-45.8% were plasma cells. Patients with high serum transaminase levels had significantly more mononuclear phagocytes (P less than 0.001) and significantly fewer plasma cells (P less than 0.001) and small lymphocytes (P less than 0.001) than patients with lower disease activity. The profile of the leukocytes in contact with hepatocytes in these CAH patients suggests that mononuclear phagocyte-mediated mechanisms play an important role in hepatocyte necrosis in vivo.

Adolescent↗
PubMed1981

Ultrastructural lesions of bile ducts in primary biliary cirrhosis. A comparison with the lesions observed in graft versus host disease.

Intrahepatic bile duct destruction is a characteristic feature of primary biliary cirrhosis and hepatic graft versus host disease. Lymphocytotoxicity against antigens on the surface of biliary cells is one of the cell mediated immune mechanisms debated in the pathogenesis of persistent bile duct destruction during primary biliary cirrhosis. Immune complex injury has also been hypothesized. In graft versus host disease, damage to bile duct cells is also believed to be due to a cytotoxic reaction of the grafted lymphoid cells against the host histocompatibility antigens, and immune complex deposition is likely to occur. The aim in this comparative ultrastructural study of intrahepatic bile ducts in 10 patients with primary biliary cirrhosis and six patients with hepatic graft versus host disease was to investigate whether identical or different ultrastructural lesions were detected in both diseases. Features of conspicuous necrosis of biliary cells, including cytolysosomes, apoptosis, and basement membrane disruption, were observed in both diseases. Numerous lymphocytes established close membrane contacts with biliary cells, especially with the necrotic ones. They had cytoplasmic pseudopods, and some of them displayed a uropod or contained lysosomal vesicles. Abnormalities of the bile duct basement membrane, also observed in both diseases, included thickening or multilayering and numerous lucent areas of rarefaction often containing osmiophilic inclusions. The striking similarity of the ultrastructural lesions in both diseases provides an additional morphological argument to suggest that certain common pathogenic mechanisms might be involved in the destruction of bile ducts in primary biliary cirrhosis as well as in hepatic graft versus host disease.

Adolescent↗
PubMed1978

Hodgkin's disease: ultrastructural localization of intra-cytoplasmic immunoglobulins within malignant cells.

An immunoperoxidase technique has been applied to the detection of intracellular immunoglobulins at the light and ultrastructural levels in three untreated cases of Hodgkin's disease. The results are compared with those obtained in three treated cases. In both groups, 20-90% of malignant cells had intra-cytoplasmic immunoglobulins. There was no correlation between the percentage of immunoglobulin-containing cells and the histological type or the stage of the disease. At the ultrastructural level, immunoglobulins were constantly localized on cytoplasmic ribosomes, the later being either free in the cytoplasm or bound to the endoplasmic reticulum and to the external envelope of the perinuclear space. In addition, a very few malignant cells exhibited immunoglobulins within their perinuclear space and their endoplasmic reticulum. These results demonstrate that immunoglobulins in Hodgkin's malignant cells are present on the cellular sites of protein synthesis. They appear to be retained in their cytoplasm, and to be secreted only very occasionally. The significance of these findings as to the cellular origin of malignant cells in Hodgkin's disease is briefly discussed.

Adolescent↗
PubMed1976

[Lymph node pathology during dermatoses with circulating Sézary cells].

The authors reported 12 cases of patients with cutaneous involvment associated with the presence of Sezary cells in the peripheral blood and specific lymph node involvment. They classify these cases as partial, early segmentary types, advanced types and diffuse types. either leukemic or sarcomatous. This study, once again, suggests the possibility that the Sezary syndrome and mycosis fu ngoïdes are different expressions, either predominantly leukemic, or predominantly sarcomatous, of the same chronic malignant hemopathy of "T" lymphocytes.

Aged↗
PubMedDate not supplied

In situ cellular analysis of alpha-fetoprotein gene expression in regenerating rat liver after partial hepatectomy.

Cellular analysis of hepatic alpha-fetoprotein gene expression in normal adult rat and during regeneration induced by partial hepatectomy was performed at the cellular level by in situ hybridization using 35S-labeled complementary DNA probes and immunoperoxidase techniques. In normal adult rat liver sections, a few alpha-fetoprotein mRNA-cDNA hybrids are detected over all hepatocytes. No protein is detected with routine immunoperoxidase methods. However, after in vivo colchicine blockade of alpha-fetoprotein secretion, 10 to 20% alpha-fetoprotein-positive hepatocytes are observed. In regenerating livers, at 2,6 and 24 hr (before and at the time of the peak of DNA synthesis in the periportal zones), a rise of the nuclear signal level is observed selectively in periportal hepatocytes, without modification of the cytoplasmic signal. At 48 hr (when most hepatocytes have completed at least one replicative cycle), almost all hepatocytes throughout the liver lobule display a rise of the nuclear (2- to 3-fold) and cytoplasmic (1.5- to 2-fold) signal level compared to nonoperated rats. These data show that all hepatocytes in the adult liver express a small number of alpha-fetoprotein mRNA sequences; they appear to be translated in protein whose secretion can be blocked by colchicine. The moderate increase in alpha-fetoprotein gene expression induced by liver regeneration takes place in all hepatocytes, in apparently two distinct steps: a very early nuclear accumulation of alpha-fetoprotein mRNA sequences and a late cytoplasmic accumulation of alpha-fetoprotein mRNA molecules.

Animals↗