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      • Transient expression of ZBTB32 in anti-viral CD8 <sup>+</sup> T cells limits the magnitude of the effector response and the generation of memory

        Shin, Hyun Mu,Kapoor, Varun N.,Kim, Gwanghun,Li, Peng,Kim, Hang-Rae,Suresh, M.,Kaech, Susan M.,Wherry, E. John,Selin, Liisa K.,Leonard, Warren J.,Welsh, Raymond M.,Berg, Leslie J. Public Library of Science 2017 PLoS pathogens Vol.13 No.8

        <▼1><P>Virus infections induce CD8<SUP>+</SUP> T cell responses comprised of a large population of terminal effector cells and a smaller subset of long-lived memory cells. The transcription factors regulating the relative expansion versus the long-term survival potential of anti-viral CD8<SUP>+</SUP> T cells are not completely understood. We identified ZBTB32 as a transcription factor that is transiently expressed in effector CD8<SUP>+</SUP> T cells. After acute virus infection, CD8<SUP>+</SUP> T cells deficient in ZBTB32 showed enhanced virus-specific CD8<SUP>+</SUP> T cell responses, and generated increased numbers of virus-specific memory cells; in contrast, persistent expression of ZBTB32 suppressed memory cell formation. The dysregulation of CD8<SUP>+</SUP> T cell responses in the absence of ZBTB32 was catastrophic, as <I>Zbtb32</I><SUP><I>-/-</I></SUP> mice succumbed to a systemic viral infection and showed evidence of severe lung pathology. We found that ZBTB32 and Blimp-1 were co-expressed following CD8<SUP>+</SUP> T cell activation, bound to each other, and cooperatively regulated Blimp-1 target genes <I>Eomes</I> and <I>Cd27</I>. These findings demonstrate that ZBTB32 is a key transcription factor in CD8<SUP>+</SUP> effector T cells that is required for the balanced regulation of effector versus memory responses to infection.</P></▼1><▼2><P><B>Author summary</B></P><P>CD8<SUP>+</SUP> T lymphocytes are essential for immune protection against viruses. In response to an infection, these cells are activated, proliferate, and generate antiviral effector cells that eradicate the infection. Following this, the majority of these effector cells die, leaving a small subset of long-lived virus-specific memory T cells. Our study identifies a transcription factor, ZBTB32, that is required for the regulation of CD8<SUP>+</SUP> T cell responses. In its absence, antiviral CD8<SUP>+</SUP> T cell numbers increase to abnormally high levels, and generate an overabundance of memory T cells. When this dysregulated response occurs following infection with a virus that cannot be rapidly eliminated by the immune system, the infected animals die from immune-mediated tissue damage, indicating the importance of this pathway.</P></▼2>

      • Design and simulation of resonance based DC current sensor

        Santhosh Kumar, B.V.M.P.,Suresh, K.,Varun Kumar, U.,Uma, G.,Umapathy, M. Techno-Press 2010 Interaction and multiscale mechanics Vol.3 No.3

        A novel resonance based proximity DC current sensor is proposed. The sensor consists of a piezo sensed and actuated cantilever beam with a permanent magnet mounted at its free end. When the sensor is placed in proximity to a wire carrying DC current, resonant frequency of the beam changes with change in current. This change in resonant frequency is used to determine the current through the wire. The structure is simulated in micro and meso scale using COMSOL Multi physics software and the sensor is found to be linear with good sensitivity.

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        Assessment of functional outcome of patients undergoing surgery for chronic pancreatitis: A prospective study

        Pagadala Naga Balaji Nitesh,Vutukuru Venkatarami Reddy,Sivarama Krishna Gavini,Suresh Vaikkakara,Chandramaliteeswaran Chandraha,Musunuru Bramheswara Rao,Dasari Varun 한국간담췌외과학회 2020 Annals of hepato-biliary-pancreatic surgery Vol.24 No.2

        Backgrounds/Aims: This study was done with the aim of assessing impact of surgery for chronic pancreatitis on exocrine and endocrine functions, quality of life and pain relief of patients. Methods: 35 patients of chronic pancreatitis who underwent surgery were included. Exocrine function assessed with fecal fat globule estimation and endocrine function assessed with glycated haemoglobin (HbA1C), fasting plasma glucose (FPG), Insulin and C-peptide levels. Percentage (%) beta cell function by homeostatic model assessment (HOMA) was determined using web-based calculator. Quality of life (QOL) and pain assessment was done using Short form survey (SF-36) questionnaire and Izbicki scores respectively. Follow up done till 3 months following surgery. Results: Endocrine insufficiency was noted in 13 (37%) patients in the postoperative period compared to 17 (49%) patients preoperatively (p=0.74). Exocrine insufficiency was detected in 11 (32%) patients postoperatively compared to 8 (23%) patients preoperatively, with denovo insufficiency noted in 3 (8%) patients (p<0.05). The mean Izbicki score at 3 months postoperatively was remarkably lower compared to preoperative score (29.3±14.3 vs. 60.6±12.06; p<0.05). QOL at 3 months following surgery for chronic pancreatitis was significantly better than preoperative QOL (50.24±22.16 vs. 69.48±20.81; p<0.05). Conclusions: Significant pain relief and improvement in quality of life among patients of chronic pancreatitis following surgery. However, worsening of exocrine function with only clinical improvement of endocrine function was also noted.

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