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10.1172/jci.insight.99276 http://scihub22266oqcxt.onion/10.1172/jci.insight.99276 C5931124!5931124 !29669944     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 263.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\29669944 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       JCI+Insight 2018 ; 3 (8 ): ä Nephropedia Template TP {{tp|p=29669944 |t=2018. Neutrophil subsets and their gene signature associate with vascular inflammation and coronary atherosclerosis in lupus |pdf=|usr=}}{{29669944 }} gab.com Text Neutrophil subsets and their gene signature associate with vascular inflammation and coronary atherosclerosis in lupus JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29669944 #FOAvip BACKGROUND: Systemic lupus erythematosus (SLE) is associated with enhanced risk of atherosclerotic cardiovascular disease not explained by Framingham risk score (FRS). Immune dysregulation associated to a distinct subset of lupus proinflammatory neutrophils (low density granulocytes; LDGs) may play key roles in conferring enhanced CV risk. This study assessed if lupus LDGs are associated with in vivo vascular dysfunction and inflammation and coronary plaque. METHODS: SLE subjects and healthy controls underwent multimodal phenotyping of vascular disease by quantifying vascular inflammation (18F-fluorodeoxyglucose-PET/CT [18F-FDG-PET/CT]), arterial dysfunction (EndoPAT and cardio-ankle vascular index), and coronary plaque burden (coronary CT angiography). LDGs were quantified by flow cytometry. Cholesterol efflux capacity was measured in high-density lipoprotein-exposed (HDL-exposed) radioactively labeled cell lines. Whole blood RNA sequencing was performed to assess associations between transcriptomic profiles and vascular phenotype. RESULTS: Vascular inflammation, arterial stiffness, and noncalcified plaque burden (NCB) were increased in SLE compared with controls even after adjustment for traditional risk factors. In SLE, NCB directly associated with LDGs and associated negatively with cholesterol efflux capacity in fully adjusted models. A neutrophil gene signature reflective of the most upregulated genes in lupus LDGs associated with vascular inflammation and NCB. CONCLUSION: Individuals with SLE demonstrate vascular inflammation, arterial dysfunction, and NCB, which may explain the higher reported risk for acute coronary syndromes. The association of LDGs and neutrophil genes with vascular disease supports the hypothesis that distinct neutrophil subsets contribute to vascular damage and unstable coronary plaque in SLE. Results also support previous observations that neutrophils may disrupt HDL function and thereby promote atherogenesis. TRIAL REGISTRATION: Clinicaltrials.gov NCT00001372FUNDING. Intramural Research Program NIAMS/NIH (ZIA AR041199) and Lupus Research Institute. Twit Text FOAVip Neutrophil subsets and their gene signature associate with vascular inflammation and coronary atherosclerosis in lupus ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=29669944 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29669944 #FOAvip English Wikipedia <ref>{{Cite pmid|29669944 }}</ref> Neutrophil subsets and their gene signature associate with vascular inflammation and coronary atherosclerosis in lupus #MMPMID29669944 Carlucci PM ; Purmalek MM ; Dey AK ; Temesgen-Oyelakin Y ; Sakhardande S ; Joshi AA ; Lerman JB ; Fike A ; Davis M ; Chung JH ; Playford MP ; Naqi M ; Mistry P ; Gutierrez-Cruz G ; Dell'Orso S ; Naz F ; Salahuddin T ; Natarajan B ; Manna Z ; Tsai WL ; Gupta S ; Grayson P ; Teague H ; Chen MY ; Sun HW ; Hasni S ; Mehta NN ; Kaplan MJ JCI Insight 2018[Apr]; 3 (8 ): ä PMID29669944 show ga BACKGROUND: Systemic lupus erythematosus (SLE) is associated with enhanced risk of atherosclerotic cardiovascular disease not explained by Framingham risk score (FRS). Immune dysregulation associated to a distinct subset of lupus proinflammatory neutrophils (low density granulocytes; LDGs) may play key roles in conferring enhanced CV risk. This study assessed if lupus LDGs are associated with in vivo vascular dysfunction and inflammation and coronary plaque. METHODS: SLE subjects and healthy controls underwent multimodal phenotyping of vascular disease by quantifying vascular inflammation (18F-fluorodeoxyglucose-PET/CT [18F-FDG-PET/CT]), arterial dysfunction (EndoPAT and cardio-ankle vascular index), and coronary plaque burden (coronary CT angiography). LDGs were quantified by flow cytometry. Cholesterol efflux capacity was measured in high-density lipoprotein-exposed (HDL-exposed) radioactively labeled cell lines. Whole blood RNA sequencing was performed to assess associations between transcriptomic profiles and vascular phenotype. RESULTS: Vascular inflammation, arterial stiffness, and noncalcified plaque burden (NCB) were increased in SLE compared with controls even after adjustment for traditional risk factors. In SLE, NCB directly associated with LDGs and associated negatively with cholesterol efflux capacity in fully adjusted models. A neutrophil gene signature reflective of the most upregulated genes in lupus LDGs associated with vascular inflammation and NCB. CONCLUSION: Individuals with SLE demonstrate vascular inflammation, arterial dysfunction, and NCB, which may explain the higher reported risk for acute coronary syndromes. The association of LDGs and neutrophil genes with vascular disease supports the hypothesis that distinct neutrophil subsets contribute to vascular damage and unstable coronary plaque in SLE. Results also support previous observations that neutrophils may disrupt HDL function and thereby promote atherogenesis. TRIAL REGISTRATION: Clinicaltrials.gov NCT00001372FUNDING. Intramural Research Program NIAMS/NIH (ZIA AR041199) and Lupus Research Institute. |Adult [MESH] |Atherosclerosis/complications/diagnostic imaging/*immunology/pathology [MESH] |Coronary Angiography/methods [MESH] |Coronary Artery Disease/complications/diagnostic imaging/*immunology/pathology [MESH] |Cross-Sectional Studies [MESH] |Female [MESH] |Healthy Volunteers [MESH] |Humans [MESH] |Inflammation/complications/*immunology/pathology [MESH] |Lupus Erythematosus, Systemic/complications/genetics/*immunology/pathology [MESH] |Male [MESH] |Middle Aged [MESH] |Neutrophils/*immunology/metabolism [MESH] |Phenotype [MESH] |Positron Emission Tomography Computed Tomography/methods [MESH] |Risk Factors [MESH]Neutrophil subsets and their gene signature associate with vascular in(epmc).pdf DeepDyve Pubget Overpricing