International Autoimmune Hepatitis Group Report: review of criteria for diagnosis of autoimmune hepatitis

The hepatic stellate cell has surprised and engaged physiologists, pathologists, and hepatologists for over 130 years, yet clear evidence of its role in hepatic injury and fibrosis only emerged following the refinement of methods for its isolation and characterization. The paradigm in liver injury of activation of quiescent vitamin A-rich stellate cells into proliferative, contractile, and fibrogenic myofibroblasts has launched an era of astonishing progress in understanding the mechanistic basis of hepatic fibrosis progression and regression. But this simple paradigm has now yielded to a remarkably broad appreciation of the cell's functions not only in liver injury, but also in hepatic development, regeneration, xenobiotic responses, intermediary metabolism, and immunoregulation. Among the most exciting prospects is that stellate cells are essential for hepatic progenitor cell amplification and differentiation. Equally intriguing is the remarkable plasticity of stellate cells, not only in their variable intermediate filament phenotype, but also in their functions. Stellate cells can be viewed as the nexus in a complex sinusoidal milieu that requires tightly regulated autocrine and paracrine cross-talk, rapid responses to evolving extracellular matrix content, and exquisite responsiveness to the metabolic needs imposed by liver growth and repair. Moreover, roles vital to systemic homeostasis include their storage and mobilization of retinoids, their emerging capacity for antigen presentation and induction of tolerance, as well as their emerging relationship to bone marrow-derived cells. As interest in this cell type intensifies, more surprises and mysteries are sure to unfold that will ultimately benefit our understanding of liver physiology and the diagnosis and treatment of liver disease.

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Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver

The structure and function of mitochondrial respiratory-chain enzyme proteins were studied postmortem in the substantia nigra of nine patients with Parkinson's disease and nine matched controls. Total protein and mitochondrial mass were similar in the two groups. NADH-ubiquinone reductase (Complex I) and NADH cytochrome c reductase activities were significantly reduced, whereas succinate cytochrome c reductase activity was normal. These results indicated a specific defect of Complex I activity in the substantia nigra of patients with Parkinson's disease. This biochemical defect is the same as that produced in animal models of parkinsonism by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and adds further support to the proposition that Parkinson's disease may be due to an environmental toxin with action(s) similar to those of MPTP.

Mitochondrial complex I deficiency in Parkinson's disease.

Mise a jour: anatomopathologie, anomalies immunologiques et pathogenese, tests de laboratoire, manifestations cliniques et troubles associes, evolution, traitement

Primary biliary cirrhosis.

https://aasldpubs.onlinelibrary.wiley.com/doi/epdf/10.1002/hep.22906

Primary Biliary Cirrhosis

Determinants of progression to cirrhosis or fibrosis in pure alcoholic fatty liver.

Primary biliary cirrhosis: identification of two major m2 mitochondrial autoantigens

A controlled trial of prednisolone treatment in primary biliary cirrhosis. Three-year results.

To even the most casual observer, the elderly are a very heterogeneous population. Some individuals remain fit and active into their ninth or tenth decades, whilst others show evidence of infirmity during their early sixties in the absence of an acute physical illness. This dissociation of biological and chronological age represents a continuum bounded by, in the parlance of contemporary gerontology, the terms 'fit' and 'frail' [1]. The lack of an agreed operational definition, however, has resulted in conflict and confusion in the gerontological literature. We propose a definition which, we believe, describes these extremes.

/pdf/who-are-the-frail-elderly-5g10lcuu05.pdf

Who are the frail elderly

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/hep.1840050115

O.F.W. James

Papers

Determinants of progression to cirrhosis or fibrosis in pure alcoholic fatty liver.

Primary biliary cirrhosis: identification of two major m2 mitochondrial autoantigens

A controlled trial of prednisolone treatment in primary biliary cirrhosis. Three-year results.

Who are the frail elderly

Insulin action in cirrhosis