Search

Deep learning has been shown to be useful to detect breast cancer metastases by analyzing whole slide images of sentinel lymph nodes. However, it requires extensive scanning and analysis of all the lymph nodes slides for each case. Our deep learning study focuses on breast cancer screening with only a small set of image patches from any sentinel lymph node, positive or negative for metastasis, to detect changes in tumor environment and not in the tumor itself. We design a convolutional neural network in the Python language to build a diagnostic model for this purpose. The excellent results from this preliminary study provided a proof of concept for incorporating automated metastatic screen into the digital pathology workflow to augment the pathologists' productivity. Our approach is unique since it provides a very rapid screen rather than an exhaustive search for tumor in all fields of all sentinel lymph nodes., Comment: 9 pages, 3 figures, 5 tables

We have designed a single-pixel camera with imaging around corners based on computational ghost imaging. It can obtain the image of an object when the camera cannot look at the object directly. Our imaging system explores the fact that a bucket detector in a ghost imaging setup has no spatial resolution capability. A series of experiments have been designed to confirm our predictions. This camera has potential applications for imaging around corner or other similar environments where the object cannot be observed directly.

SIRT1 inhibitors cambinol and Ex527 are used for treatment in several breast cancer cell lines, including T47D, TB549, MDA-MB-231 and MDA-MB-468. Stem cell markers, SOX-2 and Nanog, are significantly decreased in SIRT1 inhibitor treated cancer cells by qRT-PCR and western blot in T47D cell line. The ALDH positive cells in MDA-MB-231 cell line are significant reduced from 29% to 3.2% with Adeflour assay, and the CD44 expression is significantly reduced in CD44/CD24 flow cytometry analysis. Using qRT-PCR, SIRT1 inhibitors significantly down regulate vimentin (-3.7 folds), N-cadherin and smooth muscle actin (-2.7 folds) and up regulate the gene of E-cadherin, indicating SIRT1 inhibitors can block the epithelial mesenchymal transformation (EMT) of breast cancer. SIRT1 inhibitors can completely block TGF-beta induced EMT. SIRT1 inhibitors can significantly (60-70%) block the cancer cell invasion and migration in several triple negative breast cancer cell lines. SIRT1 inhibitors can significantly reduce the mammosphere formation in T47D cells. Immunohistochemistry performed on breast cancer specimens shows the correlation between cancer stem cell markers and SIRT1 overexpression. SIRT1 inhibitors can inhibit cell proliferation on all tested breast cancer cell lines, and can induce significant cell apoptosis in T47D cells. Cell cycle analysis shows tumor cells are blocked at G1 to S phase. The molecular mechanism of SIRT1 inhibitors in blocking EMT and reducing cancer stem cells is likely associated with blocking the Wnt pathway. Several down stream target genes of Wnt pathway, such as cyclin D1, c-Myc and c-Jun, are significantly down regulated after using SIRT1 inhibitor cambinol, and the changes are more significant in TGF-beta stimulated cancer cells. Beta-catenin is significantly reduced including the active beta-catenin, and the decreasing beta-catenin protein may be related to the decreased Dvl proteins., The original document contains color images.

Clearly new breast cancer models are necessary in developing novel therapies. To address this challenge, we examined mammary tumor formation in the Syrian hamster using the chemical carcinogen N-methyl-N-nitrosourea (MNU). A single 50 mg/kg intraperitoneal dose of MNU resulted in a 60% incidence of premalignant mammary lesions, and a 20% incidence of mammary adenocarcinomas. Two cell lines, HMAM4A and HMAM4B, were derived from one of the primary mammary tumors induced by MNU. The morphology of the primary tumor was similar to a high-grade poorly differentiated adenocarcinoma in human breast cancer. The primary tumor stained positively for both HER-2/neu and pancytokeratin, and negatively for both cytokeratin 5/6 and p63. When the HMAM4B cell line was implanted subcutaneously into syngeneic female hamsters, tumors grew at a take rate of 50%. A tumor derived from HMAM4B cells implanted into a syngeneic hamster was further propagated in vitro as a stable cell line HMAM5. The HMAM5 cells grew in female syngeneic hamsters with a 70% take rate of tumor formation. These cells proliferate in vitro, form colonies in soft agar, and are aneuploid with a modal chromosomal number of 74 (the normal chromosome number for Syrian hamster is 44). To determine responsiveness to the estrogen receptor (ER), a cell proliferation assay was examined using increasing concentrations of tamoxifen. Both HMAM5 and human MCF-7 (ER positive) cells showed a similar decrease at 24 h. However, MDA-MB-231 (ER negative) cells were relatively insensitive to any decrease in proliferation from tamoxifen treatment. These results suggest that the HMAM5 cell line was likely derived from a luminal B subtype of mammary tumor. These results also represent characterization of the first mammary tumor cell line available from the Syrian hamster. The HMAM5 cell line is likely to be useful as an immunocompetent model for human breast cancer in developing novel therapies. (C) 2011 Elsevier Ireland Ltd. All rights re

Clearly new breast cancer models are necessary in developing novel therapies. To address this challenge, we examined mammary tumor formation in the Syrian hamster using the chemical carcinogen N-methyl-N-nitrosourea (MNU). A single 50 mg/kg intraperitoneal dose of MNU resulted in a 60% incidence of premalignant mammary lesions, and a 20% incidence of mammary adenocarcinomas. Two cell lines, HMAM4A and HMAM4B, were derived from one of the primary mammary tumors induced by MNU. The morphology of the primary tumor was similar to a high-grade poorly differentiated adenocarcinoma in human breast cancer. The primary tumor stained positively for both HER-2/neu and pancytokeratin, and negatively for both cytokeratin 5/6 and p63. When the HMAM4B cell line was implanted subcutaneously into syngeneic female hamsters, tumors grew at a take rate of 50%. A tumor derived from HMAM4B cells implanted into a syngeneic hamster was further propagated in vitro as a stable cell line HMAM5. The HMAM5 cells grew in female syngeneic hamsters with a 70% take rate of tumor formation. These cells proliferate in vitro, form colonies in soft agar, and are aneuploid with a modal chromosomal number of 74 (the normal chromosome number for Syrian hamster is 44). To determine responsiveness to the estrogen receptor (ER), a cell proliferation assay was examined using increasing concentrations of tamoxifen. Both HMAM5 and human MCF-7 (ER positive) cells showed a similar decrease at 24 h. However, MDA-MB-231 (ER negative) cells were relatively insensitive to any decrease in proliferation from tamoxifen treatment. These results suggest that the HMAM5 cell line was likely derived from a luminal B subtype of mammary tumor. These results also represent characterization of the first mammary tumor cell line available from the Syrian hamster. The HMAM5 cell line is likely to be useful as an immunocompetent model for human breast cancer in developing novel therapies. (C) 2011 Elsevier Ireland Ltd. All rights re

A recent blast-movement study conducted at the Rain mine, in north-central Nevada, found that on average 4.0-6.6 ft horizontal movement occurred per blast, resulting in an estimated ore dilution ranging from 3-10%. The consequences of rock movement due to blasting are of considerable concern to a growing number of Nevada open pit disseminated gold mines. The procedure developed to determine the dilution figures and a preliminary site-specific blast movement characterisation are discussed. Results indicate that blast-related ore dilution can be minimised based on a systematic study of rock movement at a particular mine., A recent blast-movement study conducted at the Rain mine, in north-central Nevada, found that on average 4.0-6.6 ft horizontal movement occurred per blast, resulting in an estimated ore dilution ranging from 3-10%. The consequences of rock movement due to blasting are of considerable concern to a growing number of Nevada open pit disseminated gold mines. The procedure developed to determine the dilution figures and a preliminary site-specific blast movement characterisation are discussed. Results indicate that blast-related ore dilution can be minimised based on a systematic study of rock movement at a particular mine.

The results are presented of a survey by questionnaire sent to 35 mines, of which 27 responded. The deposits mined were mainly sediment-hosted, with seven volcanic-related, four skarns, two sinter and one intrusion-hosted. At 21 of the mines the gold was disseminated, with very poor visible distinction between ore and waste boundaries. Details are given of the various bench heights, blasthole patterns, burdens and spacings, blasthole diameters, explosives, powder factors and initiation patterns used and the fragmentation, rock displacement and grade control achieved., The results are presented of a survey by questionnaire sent to 35 mines, of which 27 responded. The deposits mined were mainly sediment-hosted, with seven volcanic-related, four skarns, two sinter and one intrusion-hosted. At 21 of the mines the gold was disseminated, with very poor visible distinction between ore and waste boundaries. Details are given of the various bench heights, blasthole patterns, burdens and spacings, blasthole diameters, explosives, powder factors and initiation patterns used and the fragmentation, rock displacement and grade control achieved.