Current Issue : July - September Volume : 2016 Issue Number : 3 Articles : 5 Articles
Aims. To detect anatomical and intrinsic histopathological features of the ascending aorta and left ventricular (LV) myocardium\nand evaluate right ventricular (RV) function in fetuses with hypoplastic left heart syndrome (HLHS). Methods. Twenty-five fetuses\ndiagnosed with HLHS were followed up in the antenatal and postpartum periods. 12 necropsy heart specimens were analyzed\nfor morphological and histological changes. Results. Prenatal echocardiography and pathologic anatomy displayed the typical\ncharacteristics of HLHS as a severe underdevelopment of the LV in the form of mitral stenosis or atresia or as aortic atresia or\nstenosis, with a decreased ratio of aortic diameter to pulmonary artery diameter (median of 0.49 with a range of 0.24 to 0.69,\n...
Background: Staging of melanoma includes quantification of a proliferation index, i.e., presumed melanocytic\nmitoses of H&E stains are counted manually in hot spots. Yet, its reproducibility and prognostic impact increases\nby immunohistochemical dual staining for phosphohistone H3 (PHH3) and MART1, which also may enable fully\nautomated quantification by image analysis. To ensure manageable workloads and repeatable measurements in\nmodern pathology, the study aimed to present an automated quantification of proliferation with automated hot-spot\nselection in PHH3/MART1-stained melanomas.\nMethods: Formalin-fixed, paraffin-embedded tissue from 153 consecutive stage I/II melanoma patients was\nimmunohistochemically dual-stained for PHH3 and MART1. Whole slide images were captured, and the number\nof PHH3/MART1-positive cells was manually and automatically counted in the global tumor area and in a manually and\nautomatically selected hot spot, i.e., a fixed 1-mm2 square. Bland-Altman plots and hypothesis tests compared manual\nand automated procedures, and the Cox proportional hazards model established their prognostic impact.\nResults: The mean difference between manual and automated global counts was 2.9 cells/mm2 (P = 0.0071) and 0.23\ncells per hot spot (P = 0.96) for automated counts in manually and automatically selected hot spots. In 77 % of cases,\nmanual and automated hot spots overlapped. Fully manual hot-spot counts yielded the highest prognostic performance\nwith an adjusted hazard ratio of 5.5 (95 % CI, 1.3ââ?¬â??24, P = 0.024) as opposed to 1.3 (95 % CI, 0.61ââ?¬â??2.9, P = 0.47) for\nautomated counts with automated hot spots.\nConclusions: The automated index and automated hot-spot selection were highly correlated to their manual\ncounterpart, but altogether their prognostic impact was noticeably reduced. Because correct recognition of only\none PHH3/MART1-positive cell seems important, extremely high sensitivity and specificity of the algorithm is\nrequired for prognostic purposes. Thus, automated analysis may still aid and improve the pathologistsââ?¬â?¢ detection\nof mitoses in melanoma and possibly other malignancies....
We proposed a method for automatic detection of cervical cancer cells in images captured from thin liquid based cytology slides.\nWe selected 20,000 cells in images derived from 120 different thin liquid based cytology slides, which include 5000 epithelial cells\n(normal 2500, abnormal 2500), lymphoid cells, neutrophils, and junk cells.We first proposed 28 features, including 20 morphologic\nfeatures and 8 texture features, based on the characteristics of each cell type.We then used a two-level cascade integration system\nof two classifiers to classify the cervical cells into normal and abnormal epithelial cells. The results showed that the recognition\nrates for abnormal cervical epithelial cells were 92.7% and 93.2%, respectively, when C4.5 classifier or LR (LR: logical regression)\nclassifier was used individually; while the recognition rate was significantly higher (95.642%) when our two-level cascade integrated\nclassifier system was used.The false negative rate and false positive rate (both 1.44%) of the proposed automatic two-level cascade\nclassification system are also much lower than those of traditional Pap smear review....
Background: Serous carcinoma arising in adenomyosis and adenomyotic cyst is very rare. Only 3 serous carcinomas\nand 5 serous endometrial intraepithelial carcinomas (EIC) have been reported to date.\nMethods: We reviewed the clinicopathological features of 2 serous carcinoma in uterine adenomyosis and 1 serous\nEIC in adenomyotic cyst of the cervical stump.\nResults: Case 1 had an endometrial serous carcinoma in the uterine myometrium and the left ovary. A minor\ncomponent of benign endometrial glands with minimal endometrial stroma was found in the uterine mass\nand the surrounding myometrium. Case 2 showed 3 small foci of serous carcinoma, serous EIC and endometrial\nglandular dysplasia (EmGD) in the adenomyosis. Scanty serous carcinoma was present in the endometrium without\nevidence of myometrial invasion. The eutopic endometrium in both case 1 and 2 had no evidence of neoplastic\nchanges after complete examination. Case 3 had 3 microscopic serous EICs in the adenomyotic cysts of the\ncervical stump. One EIC lesion coexisted with EmGD. No cancer was found in the endocervical tube although\nthe preoperative endocervical biopsy showed a poorly differentiated endometrioid carcinoma. Immunohistochemistry\ndemonstrated that serous carcinoma in case 1 and EIC in all 3 cases showed a characteristic pattern of p53 and p16\nover expression, high Ki67 index, and lack of WT1, ER and PR staining. EmGD in case 1 and 3 had a similar staining\npattern except a lower Ki67 index and the presence of ER expression.\nConclusions: We believe that this case series may expand our recognition on serous carcinoma arising in uterine\nadenomyosis/adenomyotic cyst including extra-uterine spread and the potential synchronous growth of carcinomas in\neutopic endometrium....
Vitamin A is essential to mucosal immunity and cell differentiation. The fact that lack of it might involve chronic inflammation\nand increased risk of cancer has been reported. Little is known about the mechanism of vitamin A deficiency in the development\nof colitis and its influence on development of colorectal cancer. To determine the influence of vitamin A deficiency on colitis\nand colorectal cancer development, an experimental study using a colitis mouse model was performed. Dextran sulfate sodium\n(DSS) colitis was induced in vitamin A-deficient and vitamin A-supplemented mice. Further, colorectal carcinoma was induced\nby a combination of azoxymethane preinjection and DSS colitis. Results were compared between the two groups mainly by\nimmunohistochemical analysis. Colitis was more severe and recovery from colitis was slower in vitamin A-deficient mice than in\nvitamin A-supplemented mice. Compared with vitamin A-supplemented mice, vitamin A-deficient mice had decreases in colonic\nsubepithelial myofibroblasts and the ratio of mucosal IgA+/IgG+ cells, increases in CD11c+ dendritic cells, and a higher rate of\ndevelopment of colorectal carcinoma with colitis following azoxymethane. Vitamin A lipid droplets in subepithelial myofibroblasts\nwere decreased in vitamin A-deficient mice, suggesting alterations in colonic crypt niche function.Thus, vitamin A inhibited colitis\nand the development of colorectal cancer....
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