Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cytotoxicity of liver natural killer cells against regenerating hepatocytes has been reported as a possible mechanism of regeneration failure in fulminant hepatitis. An augmenter of liver regeneration (ALR) inhibits liver natural killer cell activity in rats. In this study, we measured hepatic expression of ALR mRNA, blood levels of ALR, and peripheral blood natural killer cell activity in patients with various types of acute liver disease to investigate the relationship between failure of liver regeneration and hepatic natural killer cells. Hepatic ALR mRNA expression was higher in liver disease patients than in non-liver disease controls, and a correlation was found between serum ALR values and hepatic levels of ALR mRNA. In acute liver injury, the serum ALR level also showed a negative correlation with NK activity. ALR was produced by and released from the liver at the time of hepatic injury. Our findings suggest that ALR may protect against failure of regeneration by inhibition of hepatic natural killer cell activity in acute liver injury.
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PMID:Augmenter of liver regeneration (ALR) may promote liver regeneration by reducing natural killer (NK) cell activity in human liver diseases. 1068 Jun 66

Human cytomegalovirus (HCMV) is a widespread pathogen, the most common congenital viral infection, and the leading cause of infant hepatitis syndrome. In this study, serum samples were collected from 20 HCMV-infected infants with hepatitis and 25 controls. Of the 25 infants in the control group, 5 were infected with HCMV but without hepatitis, 10 had hepatitis but no HCMV infection, and 10 were healthy. Proteomic expression in the serum was detected by WCX2 chips and surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS), to identify serum protein biomarkers in infants with hepatitis syndrome resulting from HCMV. Fifteen protein peaks were distinctly different among the four groups in the mass range from 2,000 to 20,000 Da. Of these 15 peaks, 4 at 4,349.8, 5,808.7, 7,935.6, and 8,885.9 Da were significantly different between the congenital HCMV-infected infants with hepatitis and the controls. Five peaks were distinctly up-regulated in the infants with HCMV infection (3,266.8, 5,638.5, 5,909.1, 7,771.4, and 15,835.6 Da) compared to those without HCMV infection. Two proteins at 4,600.1 and 5,704.3 were up-regulated in infants with HMCV infection but no hepatitis. Four protein peaks were markedly different (7,567.0, 13,744.8, 15,100.7, and 15,915.0 Da) between the infants with hepatitis and the other controls. Comparison of the differentially expressed proteins' properties with those available on an international database suggest that specific serum proteins such as the augmenter of liver regeneration, pre-albumin, and haptoglobin closely related to liver function, and cytokines such as beta-defensins 31 and 8, and macrophage-derived chemokine, among others, are involved in HMCV infection and the pathogenesis of HMCV-induced hepatitis in infants.
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PMID:Serum proteomics with SELDI-TOF-MS in congenital human cytomegalovirus hepatitis. 1770 91

The aim of the present study was to establish a quantitative method for the measurement of serum human augmenter of liver regeneration (hALR) using competitive inhibition that is applicable in the clinic. A monoclonal antibody to hALR was used as the primary antibody and the pure hALR protein was used as a standard for competition with Eu3+-labeled hALR (Eu3+-hALR) to plot a standard curve. Serum samples from 90 patients with various liver diseases due to hepatitis B virus (HBV) infection were used for a competitive reaction with Eu3+-hALR. A regression analysis of the results was performed using the standard curve to calculate the serum concentration of hALR. The minimum detectable value using direct competitive measurement established by Eu3+-hALR was 1 ng/ml, with a positive linear correlation within the range of 200 ng/ml. In the sera of the 90 patients, the hALR level in the severe hepatitis group was the highest, followed by that in the acute hepatitis group. The serum hALR levels in the cirrhosis and chronic hepatitis groups were significantly higher compared with those in the normal control groups (P<0.01). The direct competitive measurement method of serum hALR established in the present study has high sensitivity, specificity, stability and reliability, meets clinical requirements and may be used as potential index in clinical tests.
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PMID:Establishment and primary clinical application of competitive inhibition for measurement of augmenter of liver regeneration. 2434 71

Augmenter of liver regeneration (ALR), produced and released by hepatocytes, has cytoprotective and immunoregulatory effects on liver injury, and has been used in many experimental applications. However, little attention has been paid to the effects of ALR on concanavalin A (Con A)-induced hepatitis. The purpose of this paper is to explore the protective effect of ALR on Con A-induced hepatitis and elucidate potential mechanisms. We found that the ALR pretreatment evidently reduced the amount of ALT and AST in serum. In addition, pro-inflammatory cytokines, chemokines and iNOS were suppressed. ALR pretreatment also decreased CD4(+), CD8(+) T cell infiltration in liver. Besides, we observed that ALR pretreatment was capable of suppressing the activation of several signaling pathways in Con A-induced hepatitis. These findings suggest that ALR can obviously weaken Con A-induced hepatitis and ALR has some certain immune regulation function.
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PMID:Augmenter of liver regeneration (ALR) restrains concanavalin A-induced hepatitis in mice. 2708 79