�ber das Karyogramm der menschlichen Leber unter normalen und pathologischen Bedingungen

Altmann, H. W.; Loeschke, K; Schenck, Karl

doi:10.1007/bf00958971

Cited by 37 publications

(4 citation statements)

References 22 publications

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“…6,22 However, all studies of DNA content in LCC suffer from certain difficulties. First, because of methodOur hypothesis submits that in chronic liver disease, a population of hepatocytes is driven by persistent hepatocellu-ological constraints, the studies have exclusively examined isolated nuclei or mononuclear hepatocytes; consequently lar injury and regeneration toward terminal differentiation and polyploidization 42,[48][49][50] and that the programmed mecha-the data obtained refer only to nuclear, and not to cellular, ploidy. In addition, the normal liver grows in a quasiclonal nisms of cell division inherent to these processes are then disregulated and disrupted.…”

Section: Discussionmentioning

confidence: 99%

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

1997

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Liver cell dysplasia is the term originally applied by AnLarge cell change (LCC), characterized by cellular enthony et al. 1 in 1973 to cytologically atypical hepatocytes largement, nuclear pleomorphism and hyperchromasia, showing cellular enlargement, nuclear pleomorphism with and multinucleation of hepatocytes, is a common lesion hyperchromasia, and multinucleation. In their study, this in cirrhotic livers, but its nature, significance, and pathoalteration was uncommon in normal livers and occasionally genesis remain uncertain. Therefore, we assessed the noted in cirrhotic livers, particularly with chronic hepatitis prognostic value of LCC as a marker of subsequent hepato-B infection, but was most prevalent in cirrhotic livers bearing cellular carcinoma (HCC) through a case-control study hepatocellular carcinoma (HCC). Because of this relationthat compared pretransplant liver biopsy specimens from ship, liver cell dysplasia, later termed large cell dysplasia, 37 cirrhotic liver transplant recipients with HCC to speciwas proposed to represent a premalignant change.1 mens from a control group of recipients without HCC, Over the succeeding 25 years, however, this proposal has matched for sex, age ({5 years), and cause of cirrhosis.been contested, and other workers have concluded that large LCC was identified in 16 (43%) of the study and 7 (19%) cell dysplasia instead represents a regenerative or degeneraof the control group biopsy specimens. By matched-pair tive phenomenon. Evidence has been marshalled to support analysis, LCC conveyed a moderately increased risk of both sides of this controversy, but much of the data are later HCC with an estimated odds ratio of 3.3 (95% CI, conflicting or circumstantial in nature, and no consensus has 1.2-15; P Å .038). However, a pathology review of 45 been reached as to the nature or significance of the alteration. HCCs showed adjoining LCC in only 12 (27%) and didBecause of this lingering uncertainty, the pathogenetically not suggest a morphological transition or a histogenetic noncommittal term large cell change (LCC) is now recomassociation between the two lesions. LCC hepatocytes dismended as an alternative designation.2 played a low proliferative rate by Ki-67 or proliferating The controversy over LCC poses a practical conundrum: cell nuclear antigen immunostaining (labeling indices of Should it receive special notice as a potential precursor of 0.27 and 0.73) but showed a greater degree of apoptosis malignancy, or should it be dismissed as an inconsequential than normal hepatocytes (labeling indices of 1.9 and 0.23; marker of chronic liver injury? To address this issue, we P Å .03) To reconcile these findings, we propose that LCC evaluated three different aspects of LCC. First, we performed derives from derangements in the hepatocyte's normal a case-control study to evaluate whether the presence of LCC process of polyploidization. Such derangements, possibly presaged any increased risk for the subsequent presence of caused by chronic inflammation-induced DNA damage, HCC...

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Section: Discussionmentioning

confidence: 99%

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

1997

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“…96 Autoradiographic studies have shown that in rats liver cell proliferation decreases postnatally to a value of õ0.1% of hepatocytes simultaneously in the cell cycle during adolescence. 97 Keeping in mind the increase of binuclear and tetraploid hepatocytes in human liver as a function of age 73,98 it appears that a sustained ability for proliferation exists in the human liver at old age, at least for a fraction of hepatocytes. Because cellular proliferation in the liver is induced by liver cell loss 99 liver cell proliferation as a cause of foci formation may be thought of above all in cirrhotic livers.…”

Section: Aidmentioning

confidence: 99%

Defects of the respiratory chain in the normal human liver and in cirrhosis during aging

et al. 1997

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cal studies of the respiratory chain complexes in these and Defects of the respiratory chain are a typical feature of mitochondrial diseases and occur also during normal aging other tissues [11][12][13][14][15][16][17] have revealed that aging is an inhomogeneous process at the cellular level leading to randomly diswhere they have been described in postmitotic tissues. The present study addresses the question of defect expression in tributed defects of cytochrome-c-oxidase (complex IV of the respiratory chain) and to intercellular and interorgan differthe normal and cirrhotic liver. Randomly distributed defects of complex III (ubiquinone-cytochrome-c-oxidoreductase) and ences of the defect manifestation.Recently a decline of respiratory rates with age was also of complex IV (cytochrome-c-oxidase) of the respiratory chain have been detected with age-related increasing frequency both reported for the human liver 18 both for unstimulated (state 4) and adenosine diphosphate-stimulated respiration (state in normal and cirrhotic livers. No defects were present for complex II (succinate-dehydrogenase) and complex V (adeno-3). In the last few years molecular genetic studies have revealed that mutations of mitochondrial DNA (mtDNA) such sine triphosphate-synthase) and in liver cell carcinomas. Sixty-one of 107 normal livers (57%) showed defects of the as deletions, duplications, point mutations in transfer RNAs (tRNAs), and structural genes are involved in the pathogenerespiratory chain. The defects occurred in advanced age (over 50 years) in 87%. In contrast 50 of 64 cirrhotic livers (78%) sis of mitochondrial diseases. [19][20][21][22] Similar mutations also accumulate with age although at a lesser degree both in huhad defects and approximately 60% occurred after age 50. The defects were caused by a loss of enzyme protein involving mans 23-38 and in animals. [39][40][41][42][43][44][45][46][47] The present study reports on a random defect pattern of the respiratory chain in normal and both nuclearly and mitochondrially coded subunits. Ninetyfour percent of the defects (n Å 275) involved complex IV cirrhotic livers during aging underlining that aging occurs primarily at the individual cellular level and that similar selectively. In 4% selective defects of complex III were found and combined defects of both complexes occurred in only pathogenetic mechanisms are involved in postmitotic fixed muscular tissue and in liver. Although the random defect 2%. In situ hybridization and polymerase chain reaction (PCR) studies for the detection of the common deletion (4.977 bp) pattern favors a stochastic process, molecular genetic analyses failed to reveal a pathogenetic role of various mutations and of various point mutations of mitochondrial DNA (mtDNA) revealed no consistent molecular genetic abnormali-of mtDNA. Loss of respiratory chain function is a typical feature of normal livers and to the 8th decade in patients with cirrhosis. The mitochondrial diseases. 1-3 To a lesser degree respiratory chain tissue probes were stored fr...

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Section: In Situ Hybridizationmentioning

confidence: 99%

Defects of the respiratory chain in the normal human liver and in cirrhosis during aging

Müller‐Höcker

1997

Hepatology

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cal studies of the respiratory chain complexes in these and Defects of the respiratory chain are a typical feature of mitochondrial diseases and occur also during normal aging other tissues 11-17 have revealed that aging is an inhomogeneous process at the cellular level leading to randomly dis-where they have been described in postmitotic tissues. The present study addresses the question of defect expression in tributed defects of cytochrome-c-oxidase (complex IV of the respiratory chain) and to intercellular and interorgan differ-the normal and cirrhotic liver. Randomly distributed defects of complex III (ubiquinone-cytochrome-c-oxidoreductase) and ences of the defect manifestation. Recently a decline of respiratory rates with age was also of complex IV (cytochrome-c-oxidase) of the respiratory chain have been detected with age-related increasing frequency both reported for the human liver 18 both for unstimulated (state 4) and adenosine diphosphate-stimulated respiration (state in normal and cirrhotic livers. No defects were present for complex II (succinate-dehydrogenase) and complex V (adeno-3). In the last few years molecular genetic studies have revealed that mutations of mitochondrial DNA (mtDNA) such sine triphosphate-synthase) and in liver cell carcinomas. Sixty-one of 107 normal livers (57%) showed defects of the as deletions, duplications, point mutations in transfer RNAs (tRNAs), and structural genes are involved in the pathogene-respiratory chain. The defects occurred in advanced age (over 50 years) in 87%. In contrast 50 of 64 cirrhotic livers (78%) sis of mitochondrial diseases. 19-22 Similar mutations also accumulate with age although at a lesser degree both in hu-had defects and approximately 60% occurred after age 50. The defects were caused by a loss of enzyme protein involving mans 23-38 and in animals. 39-47 The present study reports on a random defect pattern of the respiratory chain in normal and both nuclearly and mitochondrially coded subunits. Ninetyfour percent of the defects (n Å 275) involved complex IV cirrhotic livers during aging underlining that aging occurs primarily at the individual cellular level and that similar selectively. In 4% selective defects of complex III were found and combined defects of both complexes occurred in only pathogenetic mechanisms are involved in postmitotic fixed muscular tissue and in liver. Although the random defect 2%. In situ hybridization and polymerase chain reaction (PCR) studies for the detection of the common deletion (4.977 bp) pattern favors a stochastic process, molecular genetic analyses failed to reveal a pathogenetic role of various mutations and of various point mutations of mitochondrial DNA (mtDNA) revealed no consistent molecular genetic abnormali-of mtDNA. ties in microdissected respiratory chain defective liver cell MATERIALS AND METHODS areas. Single point mutations at nt 3243 and/or 5692 were found only in 7 of 18 microdissected probes from 6 patients. Investigations were performed on the following: 1) 107 resection specimens of ...

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�ber das Karyogramm der menschlichen Leber unter normalen und pathologischen Bedingungen

Cited by 37 publications

References 22 publications

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

Large cell change (liver cell dysplasia) and hepatocellular carcinoma in cirrhosis: Matched case-control study, pathological analysis, and pathogenetic hypothesis

Defects of the respiratory chain in the normal human liver and in cirrhosis during aging

Defects of the respiratory chain in the normal human liver and in cirrhosis during aging

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