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The liver has a complex cellular composition and a remarkable regenerative capacity. The primary cell types in the liver are two parenchymal cell populations, hepatocytes and cholangiocytes, that perform most of the functions of the liver and that are helped through interactions with non-parenchymal cell types comprising stellate cells, endothelia and various hemopoietic cell populations. The regulation of the cells in the liver is mediated by an insoluble complex of proteins and carbohydrates, the extracellular matrix, working synergistically with soluble paracrine and systemic signals. In recent years, with the rapid development of genetic sequencing technologies, research on the liver's cellular composition and its regulatory mechanisms during various conditions has been extensively explored. Meanwhile breakthroughs in strategies for cell transplantation are enabling a future in which there can be a rescue of patients with end-stage liver diseases, offering potential solutions to the chronic shortage of livers and alternatives to liver transplantation. This review will focus on the cellular mechanisms of liver homeostasis and how to select ideal sources of cells to be transplanted to achieve liver regeneration and repair. Recent advances are summarized for promoting the treatment of end-stage liver diseases by forms of cell transplantation that now include grafting strategies.
Assuntos
Humanos , Fígado/cirurgia , Hepatócitos/transplante , Células-Tronco/metabolismo , Hepatopatias/cirurgiaRESUMO
The evolution concept of decompensated cirrhosis rebuilds the clinical staging system for decompensated cirrhosis, which changes the focus from the pattern of disease progression to refining the status of acute decompensation onset and proposing "recompensation" of decompensated cirrhosis. During the process, factors such as portal hypertension and systemic inflammatory changes can affect the clinical outcome of decompensated cirrhotic patients. Significantly, more evidence is warranted to elucidate the clinical characteristics and potential mechanisms of achieving "recompensation" after etiology control, such as in viral hepatitis patients.
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Liver cirrhosis is the end stage of chronic liver disease and as the disease progresses to decompensated stage cirrhosis, the mortality rate of patients’ increases significantly. The goal of controlling the etiology or treatment in decompensated stage cirrhosis is to improve the liver function of patients, stabilize the disease condition or reverse decompensation, reduce the recurrence of decompensated events and reduce the mortality rate. However, presently, there are few studies on the reversal of cirrhotic decompensation/ re-compensation. Moreover, the effect of prophylactic treatment on re-compensation, evaluation indicators and duration of re-compensation, structure of hepatic lobules and whether microvessels can be reconstructed are unclear, so require further research.
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Inherited metabolic liver disease is a kind of metabolic disorders caused by the interactions between host and environmental factors because of genetic defects. The incidence of inherited metabolic liver disease is low and its clinical manifestations are complex and diverse, which initiates difficulties in clinical diagnosis. In addition, hereditary hemochromatosis and Wilson's disease are common types of metabolic abnormalities, often seem in clinical practice, and early diagnosis and treatment can improve the prognosis. Benign recurrent intrahepatic cholestasis in cholestatic liver disease is a benign phenotype of progressive familial intrahepatic cholestasis and progressive familial intrahepatic cholestasis type 3 can progress to adulthood with a poor outcome. The incidence of Gilbert’s syndrome is higher in congenital metabolic diseases, and the prognosis is good in absence of special treatment but most importantly, it should be differentiated from Crigler-Najjar syndrome and Dubin-Johnson syndrome. Presently the general characteristic of inherited metabolic liver disease in Chinese population is still vague.
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Liver fibrosis/cirrhosis is a common pathological outcome of chronic hepatic diseases, and an accurate assessment of the degree of liver fibrosis has an important reference value in a definite diagnosis, treatment decision-making, clinical outcome monitoring, and prognostic evaluation. Two quantitative assessment techniques are widely used at present: the quantitative assessment technique based on liver biopsy is the gold standard for identifying the exact liver fibrosis stage and evaluating the progression and reversion of liver fibrosis; the noninvasive quantitative assessment technique based on imaging technology plays an important role in dynamic monitoring and prognostic prediction of liver fibrosis due to its repeatability. This article summarizes the development and application of these two quantitative assessment techniques to provide guidance for clinical practice.
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Objective To evaluate the clinical value of Sharp-van der Heijde score (SHS)in rheumatoid arthritis (RA).Methods Clinical and X-ray of hands data in 200 patients with RA met the ACR criteria were collected in this study.Clinical DAS28,anti-cyclic citrullinated peptide antibody (aCCP)and imaging SHS were used to evaluate the activity of RA quantitatively before and after treatment.Results A moderate correlation existed between SHS and DAS28 (r s =0.61,P =0.00),but there was no significant cor-relation either between SHS and aCCP (r s = -0.1 5,P =0.03)or between aCCP and DAS28 (r s =0.14,P =0.05 ).Significant differences before and after treatment was existed in SHS (t=24.27,P =0.00)and DAS28 (t=1 5.98,P =0.00)respectively.And there was a moderate correlation between the difference in SHS before and after treatment and aCCP (r s =0.66,P =0.00).Conclu-sion The SHS,DAS28 and the aCCP in RA are closely related.Combination of three methods will help to develop the clinical pro-grams,evaluate the efficacy and prognosis.
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Aim: To investigate the pathological changes in NTBC[2-(2-nitro-4-trifluoro-methyl-benzoyl) -1,3 cy-clohexanedione]-induced hepatic injury in mice and in the repopulation of adult hepatocytes in Fah~(-/-) mouse. Methods: Autogenous hepatic injuries in Fah~(-/-) mice were induced by the treatment of NTBC. Injection of hepatocytes obtained from wild-type mice to spleen were transplanted into the Fah~(-/-) mice. Then, changes to body weight and the likelihood of the transplanted Fah~(-/-) mice, and hepatic immunohistochemistry were ob-served. In addition, pathological changes to liver damage induced by NTBC treatment were analyzed under HE-staining microscopy and electron microscopy. Results: The surviving Fah~(-/-) mice subjected to hepatocyte trans-plantation were found to be healthy and in stable body weight. liver repopulation reached to 90% in the 8th week. Repopulating hepatocytes caused no alteration to histological structure of the recipient liver, and subacute hepatic injury occurred in the Fah~(-/-) mice after NTBC treatment. Electronic microscopy observations indicated that necrosis in the hepatocytes occurred at early stage and that apoptosis gradually appeared. It was also shown both necrosis and apoptosis co-existed in the same samples of interest at the following stages of the induced liver injury. Conclusion: Transplanted hepatocytes proliferated in Fah~(-/-) mice allow 90% of the hepatocytic repopula- tion. Repopulation renders normal hepatic function and structure in the recipient Fah~(-/-) mice, as a model of liver repopulation, could be applicable in study of stem cell derived hepatic cells in transplantation assay.