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  • 1
    In: Journal of Occupational Health, Wiley, Vol. 44, No. 6 ( 2002-11), p. 429-432
    Type of Medium: Online Resource
    ISSN: 1341-9145 , 1348-9585
    Language: English
    Publisher: Wiley
    Publication Date: 2002
    detail.hit.zdb_id: 1340985-2
    detail.hit.zdb_id: 2075956-3
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  • 2
    Online Resource
    Online Resource
    Wiley ; 2021
    In:  Liver International Vol. 41, No. 9 ( 2021-09), p. 2132-2138
    In: Liver International, Wiley, Vol. 41, No. 9 ( 2021-09), p. 2132-2138
    Abstract: Tufting enteropathy (TE) is a rare congenital disorder often caused by mutations in the gene encoding epithelial cell adhesion molecule (EpCam). The disease leads to diarrhoea, intestinal failure and dependence on total parenteral nutrition (TPN). These patients often have liver impairments, but the pathology and mechanism of the damage are not well understood. We evaluated liver biopsies from TE patients to understand the pathophysiology. Methods We identified three patients with TE who underwent liver biopsy. Two normal controls and 45 patients on TPN secondary to short gut syndrome were selected for comparison (five were age‐ and TPN duration matched to the TE patients). Results We found that all TE patients showed a complete loss of EpCam expression in enterocytes and biliary epithelial cells, while the normal and TPN groups show basolateral expression. Histologically TE patients showed ductopenia, which was not seen in control groups. E‐cadherin and β‐catenin are normally located along the lateral membrane of biliary epithelial cells. However, they were relocated to the apical membrane in TE patients, indicating a defect in the apical‐basal polarity of cholangiocytes. We examined hepatic reparative cells and found near absence of hepatic progenitor cells and intermediate hepatobiliary cells with mild reactive ductular cells in TE patients. Conclusion Our findings show that TE is associated with disrupted polarity of cholangiocyte and ductopenia. We demonstrate for the first time a role of EpCam in the maintenance of integrity of biliary epithelium. We also provided evidence for a disrupted development of hepatic reparative cells.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2124684-1
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  • 3
    In: Journal of Occupational Health, Wiley, Vol. 45, No. 1 ( 2003-01), p. 43-52
    Abstract: Uptake of Cadmium in Meals from the Digestive Tract of Young Non‐smoking Japanese Female Volunteers: Yuriko Kikuchi, et al. Department of Preventive Medicine and Public Health, School of Medicine, Keio University Objectives To estimate rates of cadmium (Cd) uptake from the digestive tract and changes in Cd in biological specimens after intake of Cd mainly in rice. Methods Twenty‐five young non‐smoking Japanese female volunteers (20–23 in age) were recruited and a 20‐d experimental study was conducted. With polished rice containing 0.004 ppm and 0.340 ppm of Cd, Meal L and Meal H were prepared. Approximately 12% of total Cd in Meal L and 92% of total Cd in Meal H originated in rice. The volunteers ate Meal L for 11 d to achieve a stable intake‐output balance of Cd. Fifteen of the 25 volunteers ate Meal H on the 12 th day (Group D1), and the remaining 10 ate Meal H on the 12 th , 13 th and 14 th day (Group D3). All 25 subjects then resumed the consumption of Meal L to the end of the study (20 th day). All meals, feces and urine were collected during the study, and Cd intake from the daily meals (Cd‐I), Cd in feces (Cd‐F) and Cd in urine (Cd‐U) were determined. For measurement of Cd in blood (Cd‐B), venous blood was collected from all volunteers on the day before the study and again on the 12 th and 20 th day; venous blood was also collected from 4–8 volunteers at additional time points. Results Mean Cd‐I was 4.51 µg/d (range: 1.85–6.93) or 48.48 µg/d (range: 27.98–56.27) when they ate Meal L or Meal H. Cd‐F and Cd‐B exhibited faster responses to the change in Cd‐I than did Cd‐U. The Cd uptake rate, defined as (1‐Cd‐F excess /Cd‐I excess ) (Fig. 1), was 47.2% (range: –9.4–83.3%) in Group D1 and 36.6% (range: –9.2– 73.5%) in Group D3, and the Cd balance rate, defined as (1‐Cd‐F output /Cd‐I intake ), was 23.9% (range: –4.0–37.7%) in Group D1 and 23.7% (range: –8.2–56.9%) in Group D3. Conclusions Cd‐F and Cd‐B are better biological monitoring parameters for assessing change in Cd‐I than Cd‐U. The Cd uptake and Cd balance rates appeared to be higher than those in previous papers when ingested Cd mainly originated in rice.
    Type of Medium: Online Resource
    ISSN: 1341-9145 , 1348-9585
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 1340985-2
    detail.hit.zdb_id: 2075956-3
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  • 4
    In: Pediatric Transplantation, Wiley, Vol. 18, No. 2 ( 2014-03)
    Abstract: HCV infection is the leading cause of liver transplantation in the adult population in the United States. HCV infection occurs in 0.2–0.4% of the pediatric population and progression to HCC is uncommon. Liver transplantation for HCV in children is rare. In this report, we present a case of pediatric patient with HCV and multifocal HCC at the age of 13 who underwent successful liver transplantation. While good graft function was initially observed, at one month after transplant, he experienced significant hepatitis C recurrence. He was treated with low‐accelerating dose regimen antiviral therapy of PEG‐IFN and RBV , followed by addition of a protease inhibitor, boceprevir, which led to viral clearance. To our knowledge, this is the first case report describing the post‐transplant course of a child transplanted for HCV and HCC , and the first pediatric case report on using the triple therapy for management of post‐liver transplant recurrence of HCV . This case report demonstrates the need for increased vigilance of surveillance for HCC during childhood.
    Type of Medium: Online Resource
    ISSN: 1397-3142 , 1399-3046
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2014
    detail.hit.zdb_id: 2008614-3
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