Numerical investigation on the core thermal hydraulic behavior of pool-type sodium-cooled fast reactor (SFR)

A thorough understanding of the reactor core thermal hydraulic behavior is essential for the design and safety analysis of Sodium-cooled Fast Reactors (SFR). Due to the application of hexagonal subassembly, the core thermal hydraulic behavior is significantly affected by the flow field within the subassemblies, the inter-wrapper region and the hot pool. Analysis of the core thermal hydraulic behavior requires a model coupling the three regions mentioned above, which has been identified as one of the thermal hydraulic challenges in SFR. In the present study, a 3D model that covers the three regions was developed for the core of the China Experimental Fast Reactor (CEFR) with the Computational Fluid Dynamic (CFD) code, Fluent. The inter-wrapper region and the hot pool were modeled in detail, while the subassemblies were modeled with a special porous medium model. The core thermal hydraulics behavior under steady state was studied, more specifically, information for the flow field distribution at the core outlet, the inter-wrapper flow and the duct wall temperature distribution was obtained. Under steady state, liquid sodium in the inter-wrapper region is supplied by the inner region of the hot pool. And it enters the inter-wrapper region from the core outer region and returns back to the hot pool inner region from the core central region. The inter-wrapper flow is cooled by non-fuel subassemblies and heated up by fuel subassemblies. For non-fuel subassembly, the ratio of the total heat transfer rate between the inter-wrapper flow and the subassemblies to the heat generated within subassemblies could reaches 96%; for fuel subassemblies, the maximum ratio of the total heat transfer rate between the inter-wrapper flow and the subassemblies to the heat generated within subassemblies is 2.45%. Significant temperature gradients have been observed on the duct wall, with maximum values of 156.69 K/m in the vertical direction and 2,196.00 K/m in the circumferential direction. The largest temperature gradient appears on the duct of subassemblies adjacent to the transition region of fuel subassemblies and non-fuel subassemblies

Association of Cardiometabolic Disease With Cancer in the Community

BACKGROUND: Obesity and cardiometabolic dysfunction have been associated with cancer risk and severity. Underlying mechanisms remain unclear. OBJECTIVES: The aim of this study was to examine associations of obesity and related cardiometabolic traits with incident cancer. METHODS: FHS (Framingham Heart Study) and PREVEND (Prevention of Renal and Vascular End-Stage Disease) study participants without prevalent cancer were studied, examining associations of obesity, body mass index (BMI), waist circumference, visceral adipose tissue (VAT) and subcutaneous adipose tissue depots, and C-reactive protein (CRP) with future cancer in Cox models. RESULTS: Among 20,667 participants (mean age 50 years, 53% women), 2,619 cancer events were observed over a median follow-up duration of 15 years. Obesity was associated with increased risk for future gastrointestinal (HR: 1.30; 95% CI: 1.05-1.60), gynecologic (HR: 1.62; 95% CI: 1.08-2.45), and breast (HR: 1.32; 95% CI: 1.05-1.66) cancer and lower risk for lung cancer (HR: 0.62; 95% CI: 0.44-0.87). Similarly, waist circumference was associated with increased risk for overall, gastrointestinal, and gynecologic but not lung cancer. VAT but not subcutaneous adipose tissue was associated with risk for overall cancer (HR: 1.22; 95% CI: 1.05-1.43), lung cancer (HR: 1.92; 95% CI: 1.01-3.66), and melanoma (HR: 1.56; 95% CI: 1.02-2.38) independent of BMI. Last, higher CRP levels were associated with higher risk for overall, colorectal, and lung cancer (P < 0.05 for all). CONCLUSIONS: Obesity and abdominal adiposity are associated with future risk for specific cancers (eg, gastrointestinal, gynecologic). Although obesity was associated with lower risk for lung cancer, greater VAT and CRP were associated with higher lung cancer risk after adjusting for BMI

Supplementary file 1 from The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor in &lt;i&gt;Drosophila&lt;/i&gt; Imaginal Tissues

&lt;p&gt;Supplementary file 1&lt;/p&gt;</jats:p

Supplemental materials and methods and figure legends from The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor in &lt;i&gt;Drosophila&lt;/i&gt; Imaginal Tissues

&lt;p&gt;Legends and methods.&lt;/p&gt;</jats:p

Data from The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor in &lt;i&gt;Drosophila&lt;/i&gt; Imaginal Tissues

&lt;div&gt;Abstract&lt;p&gt;Components of the SWI/SNF chromatin-remodeling complex are among the most frequently mutated genes in various human cancers, yet only SMARCB1/hSNF5, a core member of the SWI/SNF complex, is mutated in malignant rhabdoid tumors (MRT). How SMARCB1/hSNF5 functions differently from other members of the SWI/SNF complex remains unclear. Here, we use &lt;i&gt;Drosophila&lt;/i&gt; imaginal epithelial tissues to demonstrate that Snr1, the conserved homolog of human SMARCB1/hSNF5, prevents tumorigenesis by maintaining normal endosomal trafficking-mediated signaling cascades. Removal of Snr1 resulted in neoplastic tumorigenic overgrowth in imaginal epithelial tissues, whereas depletion of any other members of the SWI/SNF complex did not induce similar phenotypes. Unlike other components of the SWI/SNF complex that were detected only in the nucleus, Snr1 was observed in both the nucleus and the cytoplasm. Aberrant regulation of multiple signaling pathways, including Notch, JNK, and JAK/STAT, was responsible for tumor progression upon &lt;i&gt;snr1&lt;/i&gt;-depletion. Our results suggest that the cytoplasmic Snr1 may play a tumor suppressive role in &lt;i&gt;Drosophila&lt;/i&gt; imaginal tissues, offering a foundation for understanding the pivotal role of SMARCB1/hSNF5 in suppressing MRT during early childhood. &lt;i&gt;Cancer Res; 77(4); 862–73. ©2017 AACR&lt;/i&gt;.&lt;/p&gt;&lt;/div&gt;</jats:p

Supplementary table 1 from The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor in &lt;i&gt;Drosophila&lt;/i&gt; Imaginal Tissues

&lt;p&gt;Supplementary Table 1: The mRNA level changes of representative components or targets of JAK-STAT, JNK, and Notch signaling pathways in snr1-RNAi tumorous wing discs relative to control wildtype wing discs.&lt;/p&gt;</jats:p

The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor in <i>Drosophila</i> Imaginal Tissues

Abstract Components of the SWI/SNF chromatin-remodeling complex are among the most frequently mutated genes in various human cancers, yet only SMARCB1/hSNF5, a core member of the SWI/SNF complex, is mutated in malignant rhabdoid tumors (MRT). How SMARCB1/hSNF5 functions differently from other members of the SWI/SNF complex remains unclear. Here, we use Drosophila imaginal epithelial tissues to demonstrate that Snr1, the conserved homolog of human SMARCB1/hSNF5, prevents tumorigenesis by maintaining normal endosomal trafficking-mediated signaling cascades. Removal of Snr1 resulted in neoplastic tumorigenic overgrowth in imaginal epithelial tissues, whereas depletion of any other members of the SWI/SNF complex did not induce similar phenotypes. Unlike other components of the SWI/SNF complex that were detected only in the nucleus, Snr1 was observed in both the nucleus and the cytoplasm. Aberrant regulation of multiple signaling pathways, including Notch, JNK, and JAK/STAT, was responsible for tumor progression upon snr1-depletion. Our results suggest that the cytoplasmic Snr1 may play a tumor suppressive role in Drosophila imaginal tissues, offering a foundation for understanding the pivotal role of SMARCB1/hSNF5 in suppressing MRT during early childhood. Cancer Res; 77(4); 862–73. ©2017 AACR.</jats:p

Supplementary table 1 from The SWI/SNF Complex Protein Snr1 Is a Tumor Suppressor in &lt;i&gt;Drosophila&lt;/i&gt; Imaginal Tissues

&lt;p&gt;Supplementary Table 1: The mRNA level changes of representative components or targets of JAK-STAT, JNK, and Notch signaling pathways in snr1-RNAi tumorous wing discs relative to control wildtype wing discs.&lt;/p&gt;</jats:p