Enrichment of Ventilation Air Methane (VAM) with Carbon Fiber Composites

Treatment of ventilation air methane (VAM) with cost-effective technologies has been an ongoing challenge due to its high volumetric flow rate with low and variable methane concentrations. In this work, honeycomb monolithic carbon fiber composites were developed and employed to capture VAM with a large-scale test unit at various conditions such as VAM concentration, ventilation air (VA) flow rate, temperature, and purging fluids. Regardless of inlet VAM concentrations, methane was captured at almost 100%. To regenerate the composites, the initial vacuum swing followed by combined temperature and vacuum swing adsorption (TVSA) was applied. It was found that initial vacuum swing is a control step for the final methane concentration having 5 or 11 times the VAM enrichment by one-step adsorption, which is, to our knowledge, the best performance achieved in VAM enrichment technologies worldwide. Five-time enriched VAM can be utilized as a principle fuel for lean burn turbine. Also, it can be further enriched by second step adsorption to more than 25% which then can be used for commercially available gas engines. In this way, the final product can be out of the methane explosive range (5–15%)

Enrichment of Ventilation Air Methane (VAM) with Carbon Fiber Composites

Treatment of ventilation air methane (VAM) with cost-effective technologies has been an ongoing challenge due to its high volumetric flow rate with low and variable methane concentrations. In this work, honeycomb monolithic carbon fiber composites were developed and employed to capture VAM with a large-scale test unit at various conditions such as VAM concentration, ventilation air (VA) flow rate, temperature, and purging fluids. Regardless of inlet VAM concentrations, methane was captured at almost 100%. To regenerate the composites, the initial vacuum swing followed by combined temperature and vacuum swing adsorption (TVSA) was applied. It was found that initial vacuum swing is a control step for the final methane concentration having 5 or 11 times the VAM enrichment by one-step adsorption, which is, to our knowledge, the best performance achieved in VAM enrichment technologies worldwide. Five-time enriched VAM can be utilized as a principle fuel for lean burn turbine. Also, it can be further enriched by second step adsorption to more than 25% which then can be used for commercially available gas engines. In this way, the final product can be out of the methane explosive range (5–15%)

Image_1_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.jpeg

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

Image_2_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.jpeg

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

Image_4_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.jpeg

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

Image_5_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.jpeg

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

DataSheet_1_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.csv

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

Image_3_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.jpeg

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

Table_1_Splicing factor SRSF1 is essential for CD8 T cell function and host antigen-specific viral immunity.csv

Cytotoxic CD8 T cells are crucial for the host antigen-specific immune response to viral pathogens. Here we report the identification of an essential role for the serine/arginine-rich splicing factor (SRSF) 1 in CD8 T cell homeostasis and function. Specifically, SRSF1 is necessary for the maintenance of normal CD8 T lymphocyte numbers in the lymphoid compartment, and for the proliferative capacity and cytotoxic function of CD8 T cells. Furthermore, SRSF1 is required for antigen-specific IFN-γ cytokine responses in a viral infection challenge in mice. Transcriptomics analyses of Srsf1-deficient T cells reveal that SRSF1 controls proliferation, MAP kinase signaling and IFN signaling pathways. Mechanistically, SRSF1 controls the expression and activity of the Mnk2/p38-MAPK axis at the molecular level. Our findings reveal previously unrecognized roles for SRSF1 in the physiology and function of cytotoxic CD8 T lymphocytes and a potential molecular mechanism in viral immunopathogenesis.</p

Original data set

Please find the original MRI data in the MRI data file, and the histology image in the Histology file. All MRI data (referring to the .dat binary files) was from a 3 T clinical MR system (Tim Trio, Siemens, Erlangen, Germany) without using external ECG trigger and respiratory motion sensor. The data can be loaded, viewed, and analyzed with MATLAB 2013a (Mathworks Inc., Natick, MA, USA). After MR scan, all mice were re-anaesthetized and sacrificed by rapid excision of the heart. The heart was then rinsed in 0.9% NaCl, frozen and manually sectioned into 5-6 short-axis slices with thickness of ~1.5 mm from apex to base. The slices were incubated with 0.1% triphenyltetrazolium chloride (TTC) for 15 minutes, and photographed with a digital camera and prepared for further analysis (referring to the histology image)