A renal resistance-index value of at least 80 reliably identifies patients with renal-artery stenosis in whom angioplasty or surgery will not improve renal function, blood pressure, or kidney survival.
Previous studies on the frequency of intestinal mast cells and eosinophils in patients with inflammatory bowel disease yielded conflicting results. In the present morphometric study, we quantified mast cells and eosinophils in the lamina propria by histological and immunohistochemical methods in 64 patients suffering from Crohn's disease (33 cases) or ulcerative colitis (31 cases), and in 29 controls. Histological data from 206 biopsies were related to the presence of mucosal inflammation and clinical parameters. The number of eosinophils was increased in patients with inflammatory bowel conditions (mean +/- SE: 331 +/- 44/mm2) as compared to controls (258 +/- 27/mm2), and was dependent on disease activity and drug treatment. Mean mast cell numbers did not differ between patients and controls. However, a reduced mast cell number was found in toluidine blue-stained sections of actively inflamed tissue areas (143 +/- 16/mm2, versus 206 +/- 18/mm2 in non-inflamed tissue). Immunohistochemical studies using antibodies against the granule proteins tryptase and chymase suggest that this decrease in mast cell numbers is due to mast cell degranulation. The present data show that the number of intestinal mast cells and eosinophils is altered in patients with inflammatory bowel diseases, suggesting that both cell types are involved in the pathogenesis of chronic intestinal inflammation.
The telomere hypothesis of cancer initiation indicates that telomere shortening initiates cancer by induction of chromosomal instability. To test whether this hypothesis applies to human hepatocellular carcinoma (HCC), we analyzed the telomere length of hepatocytes in cytological smears of fine-needle biopsies of liver tumors from patients with cirrhosis (n ؍ 39). The tumors consisted of 24 HCC and 15 regenerative nodules as diagnosed by combined histological and cytological diagnostics. In addition, we analyzed the telomere length of hepatocytes in HCC and surrounding noncancerous liver tissue within individual patients in another cohort of 10 patients with cirrhosis. Telomere length analysis of hepatocytes was correlated with tumor pathology and ploidy grade of the tumors, which was analyzed by cytophotometry. Telomeres were significantly shortened in hepatocytes of HCC compared to hepatocytes in regenerative nodules or surrounding noncancerous liver tissue. Hepatocyte telomere shortening in HCC was independent of the patient's age. There was no overlap in mean telomere lengths of individual samples when comparing HCC with regenerative nodules or noncancerous surrounding liver. Within the HCC group, telomeres were significantly shorter in hepatocytes of aneuploid tumors compared to diploid tumors. In conclusion, our data suggest that the telomere hypothesis of cancer initiation applies to human HCC and that cell type-specific telomere length analysis might indicate the risk of HCC development. (HEPATOLOGY 2004;40:80 -86.) L iver cirrhosis is the major risk factor for the development of hepatocellular carcinoma (HCC), and the incidence of HCC in cirrhotic patients is 3% to 6% annually. 1-3 One of the common features of human epithelial cancer is the prevalence of chromosomal instability (CIS). 4 As in other epithelial cancers, HCCs show a high incidence of CIS. 5 A current hypothesis is that telomere shortening and loss of telomere function play a role in the induction of CIS. 6,7 The main function of telomeres is the capping of chromosomal ends. 8 Due to the "end-replication problem" of DNA polymerase, telomeres shorten during each round of cell division. 9 Telomere shortening limits the proliferative capacity of primary human cells to a finite number of cell divisions 10 and appears to restrain the regenerative capacity of tissues and organs in aging and chronic diseases. 7 In the liver, hepatocyte telomere shortening has been linked to cirrhosis formation. 11 When telomeres reach a critically short length, they lose capping function, resulting in chromosomal fusions. 12 When cells with fused chromosomes enter the cell cycle, these fusions will be disrupted during mitosis, resulting in the breakage of chromosomes and chromosomal gains and losses. 13 This phenomenon has been termed the fusion-bridge-breakage cycle and might contribute to the induction of CIS and cancer in the aged. 13 In line with this hypothesis, the initiation of cancer is increased by telomere shortening in telomerase-deficient mice. 1...
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