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Introduction: The current study aimed to compare cytology using SurePath® (SP)‐LBC and biliary tissue histology (BTH) for the diagnosis of biliary disease. Methods: Between January 2014 and December 2016, 57 patients underwent endoscopic retrograde cholangiopancreatography for the diagnosis of biliary disease. Biliary cytological samples were processed using SP‐LBC and subsequently BTH was performed. A final diagnosis was confirmed by surgery (23 malignant cases) and clinical follow‐up (34 benign and malignant cases): 18 extrahepatic cholangiocarcinoma; 17 intrahepatic/hilar cholangiocarcinoma (intra/H‐CC); eight other malignant disease; and 14 benign biliary disease. The diagnoses made using SP‐LBC and BTH were classified into four categories: (1) benign; (2) indeterminate; (3) suspicious for malignancy/malignant; and (4) inadequate. In addition, diagnostic accuracy was compared between SP‐LBC and BTH. Results: Although 23% (13/57) of BTH samples were classified as inadequate, all SP‐LBC cases were classified as adequate. Among 43 malignant cases, 11 normal, four indeterminate and 28 suspicious for malignancy/malignant were found using SP‐LBC (26%, 9% and 65%, respectively), in contrast to 10 inadequate, nine normal, 10 indeterminate and 14 suspicious for malignancy/malignant observed using BTH (23%, 21%, 23%, and 33%, respectively). The identification of malignant cells was strikingly different between SP‐LBC and BTH. Furthermore, limited to intra/H‐CC, accuracy was significantly higher using SP‐LBC than using BTH (P < .001). Conclusions: SP‐LBC of the biliary tract is a useful and reliable method for diagnosing biliary malignant disease and has an advantage over BTH for detecting malignant cells and accurately diagnosing intra/H‐CC. [ABSTRACT FROM AUTHOR]

Studies have shown an association between periodontitis and serum cholesterol levels. We hypothesized that high dietary cholesterol could influence periodontitis as a result of proliferation of the junctional epithelium. Rats were divided into 4 groups. Two groups were fed a regular diet, and 2 groups were fed a high-cholesterol diet. One of each dietary group was treated with periodontitis-inducing agents (lipopolysaccharide and proteases), while the other was treated with pyrogen-free water. Feeding rats with a highcholesterol diet induced an increase in blood total cholesterol and a decrease in high-density lipoprotein cholesterol. Proliferation of the junctional epithelium with increasing bone resorption was promoted by the consumption of a high-cholesterol diet. High dietary cholesterol further increased the cell-proliferative activity of the junctional epithelium induced by lipopolysaccharide and proteases. These results suggest that high dietary cholesterol can initiate and augment periodontitis in the rat periodontitis model. [ABSTRACT FROM AUTHOR]

To investigate the characteristics of the numerical chromosome aberrations in liver metastasis of colorectal cancers, fluorescence in situ hybridization (FISH) for chromosomes 8, 18, 14/22, and 20 was performed in 18 specimens of primary regions and 18 of metastatic regions in liver metastasis of colorectal cancers compared with 15 of non-liver metastatic cancers. Among these numerical aberrations, the gain of chromosome 20, especially copy numbers exceeding three, was frequently observed in primary and metastatic cancers. Among these numerical aberrations, the gain of chromosome 20, especially copy numbers exceeding three, was frequently observed in primary and metastatic regions of liver metastasis groups compared with that of the non-liver metastasis group (P < 0.05). The incidences of gain of chromosome 20 in both regions of the liver metastasis group were higher than that of the non-liver metastasis group (P < 0.05). The gain of chromosome 20 is a frequent aberration in primary and metastatic regions in patients with liver metastatic colorectal cancers and may be available as a genetic marker for the diagnosis or prediction of liver metastasis. [ABSTRACT FROM AUTHOR]

Using indirect immunoperoxidase staining, we examined the distribution of blood group substances and related antigens, including Le(a), A, B, H type 2, and Le(x), in 87 carcinomas and 42 normal mucosal specimens of colon and rectum, as well as in metastatic lesions of 32 lymph nodes and 9 liver specimens. The compatible expression rate of A/B/H type 2 antigens was 33.3% (3/9) in proximal normal colon, but only 6.1% (2/33) in distal normal colon. Compatible expression was observed in 14 of 25 carcinomas in the proximal colon (56.0%), but these antigens in distal colon cancers reappeared with a high positive rate, 62.9% (39/62). The rate of H type 2 accumulation with the deletion of A and/or B antigens was 6.9% (6/87). Incompatible expression was not observed in colorectal cancer. Le(a) and Le(x) antigens were expressed in normal mucosa and primary carcinoma throughout the colon. Le(a) and Le(x) in primary carcinoma that showed A/B deletion with/without H type 2 accumulation was expressed more than in carcinoma with A/B/H type 2 compatible expression (88.2% vs 71.7% for Le(a); 94.1% vs 88.7% for Le(x), respectively). In 16 of 32 patients (50.0%), A/B/H type 2 antigen expression in metastatic lesions had disappeared or was decreased compared with that in primary carcinoma, followed by metastasis to regional lymph nodes. These results suggested that: (a) A/B/H type 2 blood group substances in the distal colon behave as tumor-associated antigens in colorectal carcinoma. (b) Most frequently, A/B/H type 2 antigens expressed in primary carcinoma were weakened or had disappeared in metastatic lymph nodes. Further investigation of the biological function of carbohydrate chains, such as those of blood group substances and related antigens on cancer cell surfaces may lead to a solution of the problem of the metastatic behavior of tumor cells. [ABSTRACT FROM AUTHOR]

Examines the relationship between the immunological background and the induction of inflammatory renal lesions by interleukin-12 (IL-12) in a high IgA (HIGA) strain of ddY mice. Characteristics of HIGA strain of ddY mice; Immunohistological analysis of infiltrative cells; Background of marked upregulated interferon-gamma productivity of CD4+ T cells.