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10.1016/j.psyneuen.2021.105295 http://scihub22266oqcxt.onion/10.1016/j.psyneuen.2021.105295 34119855!8172271!34119855     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Psychoneuroendocrinology 2021 ; 131 (ä): 105295 Nephropedia Template TP {{tp|p=34119855|t=2021. Interleukin-6 as potential mediator of long-term neuropsychiatric symptoms of COVID-19 |pdf=|usr=}}{{34119855}} gab.com Text Interleukin-6 as potential mediator of long-term neuropsychiatric symptoms of COVID-19 JO: Psychoneuroendocrinology http://www.kidney.de/pget.php?&tw=1&pmid=34119855 #FOAvip The majority of COVID-19 survivors experience long-term neuropsychiatric symptoms such as fatigue, sleeping difficulties, depression and anxiety. We propose that neuroimmune cross-talk via inflammatory cytokines such as interleukin-6 (IL-6) could underpin these long-term COVID-19 symptoms. This hypothesis is supported by several lines of research, including population-based cohort and genetic Mendelian Randomisation studies suggesting that inflammation is associated with fatigue and sleeping difficulties, and that IL-6 could represent a possible causal driver for these symptoms. Immune activation following COVID-19 can disrupt T helper 17 (T(H)17) and regulatory T (T(reg)) cell responses, affect central learning and emotional processes, and lead to a vicious cycle of inflammation and mitochondrial dysfunction that amplifies the inflammatory process and results in immuno-metabolic constraints on neuronal energy metabolism, with fatigue being the ultimate result. Increased cytokine activity drives this process and could be targeted to interrupt it. Therefore, whether persistent IL-6 dysregulation contributes to COVID-19-related long-term fatigue, sleeping difficulties, depression, and anxiety, and whether targeting IL-6 pathways could be helpful for treatment and prevention of long COVID are important questions that require investigation. This line of research could inform new approaches for treatment and prevention of long-term neuropsychiatric symptoms of COVID-19. Effective treatment and prevention of this condition could also help to stem the anticipated rise in depression and other mental illnesses ensuing this pandemic. Twit Text FOAVip Interleukin-6 as potential mediator of long-term neuropsychiatric symptoms of COVID-19 ????Psychoneuroendocrinology http://www.kidney.de/pget.php?&tw=1&pmid=34119855 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=34119855 #FOAvip English Wikipedia <ref>{{Cite pmid|34119855}}</ref> Interleukin-6 as potential mediator of long-term neuropsychiatric symptoms of COVID-19 #MMPMID34119855 Kappelmann N; Dantzer R; Khandaker GM Psychoneuroendocrinology 2021[Sep]; 131 (ä): 105295 PMID34119855show ga The majority of COVID-19 survivors experience long-term neuropsychiatric symptoms such as fatigue, sleeping difficulties, depression and anxiety. We propose that neuroimmune cross-talk via inflammatory cytokines such as interleukin-6 (IL-6) could underpin these long-term COVID-19 symptoms. This hypothesis is supported by several lines of research, including population-based cohort and genetic Mendelian Randomisation studies suggesting that inflammation is associated with fatigue and sleeping difficulties, and that IL-6 could represent a possible causal driver for these symptoms. Immune activation following COVID-19 can disrupt T helper 17 (T(H)17) and regulatory T (T(reg)) cell responses, affect central learning and emotional processes, and lead to a vicious cycle of inflammation and mitochondrial dysfunction that amplifies the inflammatory process and results in immuno-metabolic constraints on neuronal energy metabolism, with fatigue being the ultimate result. Increased cytokine activity drives this process and could be targeted to interrupt it. Therefore, whether persistent IL-6 dysregulation contributes to COVID-19-related long-term fatigue, sleeping difficulties, depression, and anxiety, and whether targeting IL-6 pathways could be helpful for treatment and prevention of long COVID are important questions that require investigation. This line of research could inform new approaches for treatment and prevention of long-term neuropsychiatric symptoms of COVID-19. Effective treatment and prevention of this condition could also help to stem the anticipated rise in depression and other mental illnesses ensuing this pandemic. |Animals[MESH] |Anxiety/epidemiology/etiology[MESH] |COVID-19/*complications/epidemiology/etiology/psychology[MESH] |Cohort Studies[MESH] |Depression/epidemiology/etiology[MESH] |Fatigue/epidemiology/etiology[MESH] |Humans[MESH] |Interleukin-6/metabolism/pharmacology/*physiology[MESH] |Mental Disorders/epidemiology/*etiology[MESH] |Neuroimmunomodulation/drug effects/physiology[MESH] |Post-Acute COVID-19 Syndrome[MESH] |SARS-CoV-2/physiology[MESH] |Sleep Wake Disorders/epidemiology/etiology[MESH]Interleukin-6 as potential mediator of long-term neuropsychiatric symp(epmc).pdf DeepDyve Pubget Overpricing