Engineering Papers⌕ Search

SEARCH · Engineering Papers

Results for “Network centrality”

Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24
All sourcesNASA NTRSDOE OSTI
DOE OSTI2023

Development of a Scalable Risk-informed Predictive Maintenance Cloud-based Strategy at Nuclear Power Plants

The fact that light-water reactor operation and maintenance costs are prohibitively expensive and contribute to the premature decommissioning of nuclear power plants is partly due to how the equipment is monitored. In recent years, cloud computing has emerged as a dominant technology, as its low cost, computing and storage adaptability, and ability to host applications across numerous virtual infrastructures potentially make it a cost-effective alternative to onsite storage and diagnostics. In this paper, a technological assessment is carried out on a provisional cloud deployment architecture for a nuclear power plant predictive monitoring system. This cloud-based monitoring system would enable maintenance and diagnostic analysts and other authorized plant users to remotely monitor equipment functionality, thus enabling early fault detection and effective predictive maintenance practices. To provide data processing and storage, sensor device networking, and database management, the Microsoft Azure cloud platform is utilized as part of the proposed cloud architecture; however, this analysis could be extended to other cloud computing service providers as well. The focus of this paper is on application of cloud resources for enabling predictive maintenance, identification of technological hurdles associated with moving to a cloud-computing-based architecture, and potential benefits from moving to a centralized cloud system.

46 INSTRUMENTATION RELATED TO NUCLEAR SCIENCE AND ↗
DOE OSTI2025

Multi-omics data compendium of pancreatic islet and β cell responses to pro-inflammatory cytokines

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 10 (Pck010)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 11 (Pck011)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 12 (Pck012)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 13 (Pck013)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 14 (Pck014)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 15 (Pck015)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 16 (Pck016)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 17 (Pck017)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 18 (Pck018)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 19 (Pck019)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 1 (Pck001)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 20 (Pck020)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 21 (Pck021)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 2 (Pck002)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 3 (Pck003)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗
DOE OSTI2025

Multi-omics data compendium: Data package 4 (Pck004)

In type 1 diabetes (T1D), autoimmune response and inflammation cause the death of pancreatic ß cells, leading to the body’s inability to produce insulin and maintain glucose homeostasis. This process is at least in part mediated by pro-inflammatory cytokines, such as interferon (IFN)a, IFN?, interleukin (IL)-1ß, and tumor necrosis factor (TNF)a, which induce ß-cell dysfunction and apoptosis. A deep understanding of the ß-cell signaling and regulatory networks induced by these cytokines could lead to the identification of therapeutic targets to prevent T1D development. To study cytokine-mediated islets/ß-cell signaling and regulatory networks, a variety of omics experiments have been conducted, including transcriptomics, epigenomics (DNA methylation, UMI-4C, ATAC-seq & ChIP-seq), proteomics (bottom-up, top-down, post-translational modification analysis), lipidomics, and metabolomics. The combination of these datasets can be instrumental in identifying signaling components and regulatory factors involved in ß-cell stress/death. Here, we aggregated these multiple omics datasets into a centralized location, providing a quality-controlled and statistically rigorous resource for investigators seeking to holistically study ß-cell regulation by pro-inflammatory cytokines.

Sarkar, Soumyadeep [Pacific Northwest National Lab↗