Plate : persistent memory management for nonvolatile main memory

Over the past few years, nonvolatile memory has actively been researched and developed. Therefore, studying operating system (OS) designs predicated on the main memory in the form of a nonvolatile memory and studying methods to manage persistent data in a virtual memory are crucial to encourage the widespread use of nonvolatile memory in the future. However, the main memory in most computers today is volatile, and replacing highcapacity main memory with nonvolatile memory is extremely cost-prohibitive. This paper proposes an OS structure for nonvolatile main memory. The proposed OS structure consists of three functions to study and develop OSs for nonvolatile main memory computers. First, a structure, which is called plate, is proposed whereby persistent data are managed assuming that nonvolatile main memory is present in a computer. Second, we propose a persistent-data mechanism to make a volatile memory function as nonvolatile main memory, which serves as a basis for the development of OSs for computers with nonvolatile main memory. Third, we propose a continuous operation control using the persistent-data mechanism and plates. This paper describes the design and implementation of the OS structure based on the three functions on The ENduring operating system for Distributed EnviRonment and describes the evaluation results of the proposed functions

Her yol Roma'ya varmaz!

Taha Toros Arşivi, Dosya Adı: Taha Torosİstanbul Kalkınma Ajansı (TR10/14/YEN/0033) İstanbul Development Agency (TR10/14/YEN/0033

Optimization of prediction methods for risk assessment of pathogenic germline variants in the Japanese population

Predicting pathogenic germline variants (PGVs) in breast cancer patients is important for selecting optimal therapeutics and implementing risk reduction strategies. However, PGV risk factors and the performance of prediction methods in the Japanese population remain unclear. We investigated clinicopathological risk factors using the Tyrer-Cuzick (TC) breast cancer risk evaluation tool to predict BRCA PGVs in unselected Japanese breast cancer patients (n = 1, 995). Eleven breast cancer susceptibility genes were analyzed using target-capture sequencing in a previous study; the PGV prevalence in BRCA1, BRCA2, and PALB2 was 0.75%, 3.1%, and 0.45%, respectively. Significant associations were found between the presence of BRCA PGVs and early disease onset, number of familial cancer cases (up to third-degree relatives), triple-negative breast cancer patients under the age of 60, and ovarian cancer history (all P < .0001). In total, 816 patients (40.9%) satisfied the National Comprehensive Cancer Network (NCCN) guidelines for recommending multigene testing. The sensitivity and specificity of the NCCN criteria for discriminating PGV carriers from noncarriers were 71.3% and 60.7%, respectively. The TC model showed good discrimination for predicting BRCA PGVs (area under the curve, 0.75; 95% confidence interval, 0.69-0.81). Furthermore, use of the TC model with an optimized cutoff of TC score ≥0.16% in addition to the NCCN guidelines improved the predictive efficiency for high-risk groups (sensitivity, 77.2%; specificity, 54.8%; about 11 genes). Given the influence of ethnic differences on prediction, we consider that further studies are warranted to elucidate the role of environmental and genetic factors for realizing precise prediction

Loss of SMAD4 From Colorectal Cancer Cells Promotes CCL15 Expression to Recruit CCR1(+) Myeloid Cells and Facilitate Liver Metastasis.

[Background & Aims]Loss of the tumor suppressor SMAD4 correlates with progression of colorectal cancer (CRC). In mice, colon tumors that express CCL9 recruit CCR1+ myeloid cells, which facilitate tumor invasion and metastasis by secreting matrix metalloproteinase 9. [Methods]We used human CRC cell lines to investigate the ability of SMAD4 to regulate expression of CCL15, a human ortholog of mouse CCL9. We used immunohistochemistry to compare levels of CCL15 and other proteins in 141 samples of human liver metastases. [Results]In human CRC cell lines, knockdown of SMAD4 increased CCL15 expression, and overexpression of SMAD4 decreased it. SMAD4 bound directly to the promoter region of the CCL15 gene to negatively regulate its expression; transforming growth factor-β increased binding of SMAD4 to the CCL15 promoter and transcriptional repression. In livers of nude mice, SMAD4-deficient human CRC cells up-regulated CCL15 to recruit CCR1+ cells and promote metastasis. In human tumor samples, there was a strong inverse correlation between levels of CCL15 and SMAD4; metastases that expressed CCL15 contained 3-fold more CCR1+cells than those without CCL15. Patients with CCL15-expressing metastases had significantly shorter times of disease-free survival than those with CCL15-negative metastases. CCR1+ cells in the metastases expressed the myeloid cell markers CD11b and myeloperoxidase, and also matrix metalloproteinase 9. [Conclusions]In human CRC cells, loss of SMAD4 leads to up-regulation of CCL15 expression. Human liver metastases that express CCL15 contain higher numbers CCR1+ cells; patients with these metastases have shorter times of disease-free survival. Reagents designed to block CCL15 recruitment of CCR1+ cells could prevent metastasis of CRC to liver

Time course changes of ¹⁰B concentration in 6 tissues.

<p>¹⁰B concentration in the heart, blood, brain, liver, kidney, lungs, and tumor of PC3 tumor-bearing mice were measured by ICP-AES instrument at 2 and 4 hour after intraperitoneal injection of 250 mg/kg BPA.</p

Ki67 staining on PC3 xenograft specimens.

<p>Xenograft tissues of mice (Group 1: untreated control and Group 4: BPA-mediated BNCT) were stained with Ki67, SMa-actin, and DAPI (A:DAPI B:Ki67 C:SMa-actin D:Mixed). Quantification of Ki67-positive cells was shown.</p

TUNEL staining on PC3 xenograft specimens.

<p>Xenograft tissues of mice (Group 1: untreated control and Group 4: BPA-mediated BNCT) were stained with TUNEL and the number of apoptotic cells was quantified. White arrows indicate TUNEL+ cells.</p