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I Bartók

Publications and source records attributed to I Bartók.

At least 19 recordsLinked to original sources
PubMed1995

Comparison of the binding of C3S and C3F to complement receptors types 1, 2, and 3.

The two common polymorphic variants of C3 are C3S/HAV4.1- and C3F/HAV4.1+. It was reported previously that erythrocytes coated with C3F rosetted more strongly with mononuclear cells than erythrocytes coated with C3S. We examined the binding of C3S/HAV4.1- and C3F/HAV4.1+ to complement receptors CR1, CR2, and CR3. The binding of 125I-labeled C3b dimers to erythrocyte CR1 was measured. Scatchard analysis showed a two-binding constant model with very similar binding constants for dimers prepared with C3S and C3F: for C3S Kd1 = 18.3 +/- 2 nM; Kd2 = 6.2 +/- 1 nM; for C3F Kd1 = 21.5 +/- 4 nM; Kd2 = 7.2 +/- 3 nM (mean +/- SEM). One-third of the binding sites were of the higher affinity. The rosetting of erythrocytes with different densities of iC3b, prepared from C3S or C3F, to CR2 on Raji cells was analyzed. The percentage of Raji cells rosetted was related to the coating dose of EC3bi: 400 molecules/cell = 9% rosettes; 5000 molecules/cell = 75%. The dose-response curves were very similar for C3S- and C3F-coated erythrocytes. CR3-dependent rosetting was studied in a similar manner by using neutrophils activated with f-met-leu-phe. CR3-dependent rosette formation with the indicator erythrocytes (600 to 6000 iC3b/cell) increased from 10% to 60% in a dose-dependent manner and was closely similar for C3S and C3F. Inhibition of CR2 and CR3 rosetting by fluid phase ligand was also studied. iC3b dimers (0.4 to 50 micrograms/ml) inhibited CR2-dependent rosetting in a dose-dependent manner but had no inhibitory effect on CR3-dependent rosetting. When the dimers were absorbed to fluorescent microspheres, they mediated phagocytic uptake of the microspheres in a CR3-dependent manner by neutrophils. CR3-dependent binding by activated neutrophils required surface-bound ligand.

Complement C3↗
PubMed1989

[Liver changes suggesting alpha-1-antitrypsin deficiency (a neglected disease)].

Liver needle biopsies of one hundred infants and children were examined. In fifteen of them the liver was normal. Of the 85 patients with liver disease three had liver changes due to severe alpha-1-antitrypsin (AAT) deficiency. In two cases fibrosis and inflammation of the portal fields could be seen. In the third case in addition to portal fibrosis and moderate periportal inflammation paucity of the intrahepatic bile ducts was found. Characteristic PAS-positive diastase resistant hepatocellular globules occurred only in one case but, using immunoperoxydase method, periportal hepatocytes showed AAT positivity in all three infants. Of 830 adult patients with liver cirrhosis 8 had PAS-positive diastase resistant AAT immunoreactive globules in the periseptal hepatocytes suggesting AAT deficiency, however, the serum AAT level and the phenotype of them were unknown. Investigation for AAT deficiency should be carried out in children and young adults with a history of neonatal liver disease and possibly in all patients with liver disease of uncertain etiology, especially in those with PAS-positive, AAT immunoreactive hepatocellular globules.

Biopsy↗
PubMed1989

Interaction between C3 and IL-2; inhibition of C3b binding to CR1 by IL-2.

We previously reported that C3 has a role in the enhancement of the IL-2 dependent proliferation of helper T cells. Because the IL-2R has a structural homology with the complement proteins, such as CR1 and CR2, we studied the possible ligand crossreactions on CR1 and IL-2-receptor, and the direct interaction between C3 and IL-2. While C3 has an enhancing effect on the IL-2 dependent proliferation of HT-2, a CR1-positive mouse T-cell line, the growth of the CTLL-16 line (CR1-negative) is not affected by C3. It has been proven that neither the insolubilized C3 nor the soluble C3b-like C3 react with the IL-2 binding epitope of the IL-2 receptor. However, using human RBC we have demonstrated that the binding of aggregated C3 to CR1 is inhibited by rIL-2, in a dose-dependent manner. When RBC were incubated with rIL-2 and FITC-labelled Fab-anti-CR1 simultaneously, there was no inhibition in the fluorescence intensity. As detected by ELISA, rIL-2 was bound to the same extent by insolubilized C3, C3b, and C3c, while C3d coat had lower binding capacity. The receptor-binding epitope of IL-2 is intact in the complex of complement proteins and rIL-2, as demonstrated by the binding of DMS1, a monoclonal antibody reacting with the receptor site of IL-2. It is strongly suggested that C3b may play a role in the growth of CR1 positive T cells.

Cell Line↗
PubMed1989

Ultrastructure of the Ito cells in liver disease associated with fibrosis.

The ultrastructure of Ito cells was examined in percutaneous needle liver biopsies of 36 patients. In three cases the liver was normal. Four specimens showed mild or moderate fatty degeneration. In the rest of the liver samples various types of fibrosis were seen: in four cases portal, in ten centrilobular, in eight periportal fibrosis and in five cases cirrhosis. In the normal liver Ito cells occurred not only in the Disse spaces but also in the walls of the terminal hepatic venules. In livers showing portal fibrosis the ultrastructure of Ito cells was similar to that seen in the normal liver. In the fibrotic areas of liver samples showing centrilobular or periportal fibrosis or cirrhosis Ito cells localized inside the fibrotic tissue and along the border between the connective tissue and hepatocytes. These interstitial Ito cells contained few lipid, abundant rough endoplasmic reticulum with dilated tubules filled by a flocculant material, well developed Golgi complexes and often bundles of 5 nm thick filaments with densities. These cells also known as activated Ito cells were in places surrounded by immature collagen fibrils and basement membrane fragments. There was a close contact between activated Ito cells and lymphocytes. The ultrastructure of Ito cells localizing in non-fibrotic areas did not differ from that seen in normal liver lobules. These observations suggest that Ito cells are related to fibroblasts and myofibroblasts and play an important role in the pathogenesis of liver fibrosis in humans.

Biopsy, Needle↗
PubMed1989

[Ultrastructure of Ito cells in fibrotic liver diseases].

Authors have studied the ultrastructure of Ito-cells in percutane needle-biopsy samples of hepatic tissue from 36 patients. In 3 samples no alteration was found, in four only moderate steatosis occurred without fibrosis. In four samples portal, in ten centrilobular and in five periportal fibrosis was detected, while in five samples cirrhosis was pointed out. In the intact liver, Ito-cells occur not only in the spaces of Disse but also in the wall of the central vein. In portal fibrosis Ito-cells were similar in location and structure to those in the non-fibrotic liver. In centrilobular and periportal fibroses as well as in cirrhosis Ito-cells in the fibrotic parenchyma areas were either localized in the accumulated connective tissue or at the border of connective tissue and hepatocytes. These interstitial Ito-cells contained small amount of lipid, abundant dilated rough endoplasmic reticulum filled with a flocculent material, well-developed Golgi-complex and often bundles of 5 nm thick filaments with dense territories. Close to the Ito-cells immature collagen-fibrils and basement membrane-fragments were seen. A close relationship was pointed out between activated Ito-cells and lymphocytes. In parenchyma areas away from fibrotic foci the structure of Ito-cells was comparable to that of Ito-cells in intact hepatic lobules. Observations suggest that Ito-cells are related to fibroblasts and myofibroblasts and play a role in the pathogenesis of fibrosis occurring in human liver diseases.

Cytoplasm↗
PubMed1984

A case of liver cirrhosis with alpha-1-antitrypsin globules and hepatitis B surface antigen seropositivity.

PAS staining, immunohistochemical examination and electron microscopy revealed presence of alpha-1-antitrypsin (AAT) globules in the hepatocytes of a HBsAg and anti-HBc seropositive female patient diseased of liver cirrhosis. The possible causes of cirrhosis are briefly analysed and the diagnostic importance of PAS-positive, amylase-resistant hepatocellular inclusions is discussed. Apart from the case reported, only two of 509 cirrhotic livers of adults, examined either by biopsy or post mortem, demonstrated similar characteristic PAS-positive globules. This indicates that in the population group (135,000 persons) referred for health care to the hospital where the examinations were done, AAT deficiency has played a negligible role in the development of liver cirrhosis in adults.

Female↗
PubMed1983

Fine structure of perisinusoidal cells in developing human and mouse liver.

The fine structure of hepatic perisinusoidal cells was studied in human fetuses and in mouse embryos and fetuses. The perisinusoidal cells differed in structure from the sinusoidal lining cells, and occasionally mitosis of perisinusoidal cells was observed suggesting that these cells are independent and self-proliferating at the stage of development studied. Unlike perisinusoidal cells of the normal mature liver, those of the developing liver contained only sparse and small lipid droplets. They possessed a well developed rough endoplasmic reticulum and Golgi complex, and many microtubules. Collagen fibrils appeared in close proximity to perisinusoidal cells. In perisinusoidal cells of the mouse liver development of the rough endoplasmic reticulum and Golgi complex, accumulation of microtubules and increase of collagen fibrils progressed with the time of gestation. The thick cytoplasmic processes of the perisinusoidal cells frequently encircled the sinusoids, and 5-6 nm thick filaments appeared at the cell periphery. Perisinusoidal cells and hepatocytes were frequently linked by junctional elements. These findings strongly suggest that the perisinusoidal cells are responsible for the production of type III collagen. Also they may indicate that these cells reinforce the sinusoides, influence the sinusoidal blood flow by contractile activity and participate in the maintenance of the parenchymal organisation in the developing liver.

Animals↗
PubMed1982

Postnatal development of perisinusoidal cells in the porcine liver.

The ultrastructure of perisinusoidal (PS) cells was studied in the liver of young pigs 1-28 days after birth. In immature animals these cells have long cytoplasmic processes often surrounding almost the entire sinusoid. In their close vicinity newly formed collagen filaments are found. While in the adult pig the PS cell cytoplasm is almost totally occupied by a large lipid droplet, in the young animal it contained only a few small lipid droplets, accompanied by a well-developed granular endoplasmic reticulum and Golgi-apparatus, microtubules and filaments 5-6 nm in diameter. The latter formed bundles with patchy dark areas. Findings indicate that during early postnatal development the function of PS cells is protein synthesis, perhaps for the production of reticulum fibres rather than fat or vitamin-A storage. In addition, PS cells by containing contractile elements may regulate the width of the sinusoids.

Animals↗
PubMed1981

Clinicopathological studies of liver cirrhosis and hepatocellular carcinoma in a general hospital.

Clinicopathological studies of 181 patients with liver cirrhosis undergoing autopsy in the pathology department of a municipal hospital between 1973 and 1976 are reported. The main etiological types were alcoholic (25.4 per cent), HBsAg positive (14.9 per cent), and cryptogenic cirrhosis (54.7 per cent). Four patients had multifactorial and secondary biliary cirrhosis and one patient had congestive cirrhosis. The morphological characteristics of the condition and the age and sex distribution of the patients were analyzed in each etiological group. Hepatocellular carcinoma occurred in 28.7 per cent of the cases, most frequently in association with HBsAg positive cirrhosis. Hepatocellular atypia was significantly more frequent in HBsAg positive than in other etiological types of cirrhosis and significantly more frequent in cases associated with hepatocellular carcinoma than in those not associated with it.

Aged↗
PubMed1981

[Not Available].

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History, Early Modern 1451-1600↗
PubMed1980

Focal nodular hyperplasia of the liver and hepatic cell adenoma in women on oral contraceptives.

The article reports on the respective occurrence of focal nodular hyperplasia and hepatic cell adenoma in the liver of two women on oral contraceptives. The hepatic cell adenoma showed serious vascular lesions, including peliosis hepatis. Both tumors were removed surgically, and the patients are well. A possible relationship between oral contraception and benign hepatic tumor genesis is discussed under consideration of the pertinent literary data.

Adult↗
PubMed1979

Ultrastructure of the hepatic perisinusoidal cells in man and other mammalian species.

Perisinusoidal (P.S.) cells occurring in the spaces of Disse in the livers of normal cats, dogs, miniature pigs, albino rats, human adults and children were examined by electron microscopy. The ultrastructural details of the P.S. cells and their topographic relationships with hepatocytes, sinusoidal lining cells and reticulum fibers are described. Species differences between P.S. cells were primarily a dissimilarity in lipid content: the main ultrastructural features were the same in all species studied. The P.S. cells of the rat liver displayed only low endocytotic activity, and no phagosome formation following intravenous administration of horseradish peroxidase. The close topographic relationship of the P.S. cells with the intralobular reticulum fibers was reminiscent of the intimate connection between fibroblasts and collagen fibers, or, in cat liver, of the reticulum cell--reticulum fiber association seen in lymphoid organs. Fibroblasts were not found inside the hepatic lobules. These findings support the conclusion that the reticulum fibers of hepatic lobules are produced by perisinusoidal cells which, however, display also other functions.

Adult↗