The role of solar and geomagnetic activity in endothelial activation and inflammation in the NAS cohort.
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ABSTRACT:
SUBMITTER: Schiff JE
PROVIDER: S-EPMC9321765 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundShort-term geomagnetic disturbances (GMD) driven by the quasi-periodic 11-year cycle of solar activity have been linked to a broad range of adverse health effects, including cardiovascular diseases (CVD) and total deaths. We conducted a large epidemiological study in 263 U.S. cities to assess the effects of GMD on daily deaths of total, CVD, myocardial infarction (MI), and stroke.MethodsWe employed a two-step meta-analysis approach, in which we estimated city-specific and season-stratified mortality risk associated with a GMD parameter (Kp index) in 263 U.S. cities. In addition, sensitivity analysis was performed to assess whether effect modification of particulate matter (PM2.5) in the prior day changed Kp index effects on daily deaths after adjusting for confounders.ResultsWe found significant association between daily GMD and total, CVD, and MI deaths. The effects were even stronger when we adjusted the models for 24-h PM2.5 for different seasons. For example, in the winter and fall one standard deviation of z-score Kp index increase was associated with a 0.13 and 0.31% increase in total deaths, respectively (Winter: p = 0.01, 95% CI: 0.02 to 0.24; Fall: p = 0.00001; 95% CI: 0.23 to 0.4), without adjusting for PM2.5. The effects of GMD on total deaths were also observed in spring and summer in the models without PM2.5 (p = 0.00001). When the models were adjusted for PM2.5 the total deaths increased 0.47% in winter (p = 0.00001, 95% CI: 0.3 to 0.65) and by 0.23% in fall (p = 0.001, 95% CI: 0.09 to 0.37). The effects of GMD were also significant associated with MI deaths and CVD. No positive significant association were found between Kp and stroke. The GMD effects on deaths were higher than for 24 h-PM2.5 alone, especially in spring and fall.ConclusionOur results suggest that GMD is associated with total, CVD and MI deaths in 263 U. S cities. Increased mortality in the general population during GMD should be further investigated to determine whether those human physiological dynamics driven by variations in solar activity can be related to daily clinical cardiovascular observations.
| S-EPMC6739933 | biostudies-literature
Project description:Magnetic clouds (MCs) are transient magnetic structures giving the strongest southward magnetic field (Bz south) in the solar wind. The sheath regions of MCs may also carry a southward magnetic field. The southward magnetic field is responsible for space-weather disturbances. We report a comprehensive analysis of MCs and Bz components in their sheath regions for 1995 to 2017. 85% of 303 MCs contain a south Bz up to 50 nT. Sheath Bz during the 23 years may reach as high as 40 nT. MCs of the strongest magnetic magnitude and Bz south occur in the declining phase of the solar cycle. Bipolar MCs depend on the solar cycle in their polarity, but not in the occurrence frequency. Unipolar MCs show solar-cycle dependence in their occurrence frequency, but not in their polarity. MCs with the highest speeds, the largest total- B magnitudes, and sheath Bz south originate from source regions closer to the solar disk center. About 80% of large Dst storms are caused by MC events. Combinations of a south Bz in the sheath and south-first MCs in close succession have caused the largest storms. The solar-cycle dependence of bipolar MCs is extended to 2017 and now spans 42 years. We find that the bipolar MC Bz polarity solar-cycle dependence is given by MCs that originated from quiescent filaments in decayed active regions and a group of weak MCs of unclear sources, while the polarity of bipolar MCs with active-region flares always has a mixed Bz polarity without solar-cycle dependence and is therefore the least predictable for Bz forecasting.Electronic supplementary materialThe online version of this article (10.1007/s11207-018-1356-8) contains supplementary material, which is available to authorized users.
| S-EPMC6190751 | biostudies-literature
Project description:Observations performed by the Earth Observing System Microwave Limb Sounder instrument on board the Aura satellite from 2004 to 2009 (2004 to 2014) were used to investigate the 27?day solar rotational cycle in mesospheric OH (O3) and the physical connection to geomagnetic activity. Data analysis was focused on nighttime measurements at geomagnetic latitudes connected to the outer radiation belts (55°N/S-75°N/S). The applied superposed epoch analysis reveals a distinct 27?day solar rotational signal in OH and O3 during winter in both hemispheres at altitudes >70?km. The OH response is positive and in-phase with the respective geomagnetic activity signal, lasting for 1-2?days. In contrast, the O3 feedback is negative, delayed by 1?day, and is present up to 4?days afterward. Largest OH (O3) peaks are found at ~75?km, exceeding the 95% significance level and the measurement noise of <2% (<0.5%), while reaching variations of +14% (-7%) with respect to their corresponding background. OH at 75?km is observed to respond to particle precipitation only after a certain threshold of geomagnetic activity is exceeded, depending on the respective OH background. The relation between OH and O3 at 75?km in both hemispheres is found to be nonlinear. In particular, OH has a strong impact on O3 for relatively weak geomagnetic disturbances and accompanying small absolute OH variations (<0.04?ppb). In contrast, catalytic O3 depletion is seen to slow down for stronger geomagnetic variations and OH anomalies (0.04-0.13?ppb), revealing small variations around -0.11?ppm.
| S-EPMC5054829 | biostudies-other
Project description:BackgroundThe mechanisms by which exposure to particulate matter might increase risk of cardiovascular morbidity and mortality are not fully known. However, few existing studies have investigated the potential role of particle radioactivity. Naturally occurring radionuclides attach to particulate matter and continue to release ionizing radiation after inhalation and deposition in the lungs. We hypothesize that exposure to particle radioactivity increases biomarkers of inflammation.MethodsOur repeated-measures study included 752 men in the greater Boston area. We estimated regional particle radioactivity as a daily spatial average of gross beta concentrations from five monitors in the study area. We used linear mixed-effects regression models to estimate short- and medium-term associations between particle radioactivity and biomarkers of inflammation and endothelial dysfunction, with and without adjustment for additional particulate air pollutants.ResultsWe observed associations between particle radioactivity on C-reactive protein (CRP), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1), but no associations with fibrinogen. An interquartile range width increase in mean 7-day particle radioactivity (1.2 × 10 Bq/m) was associated with a 4.9% increase in CRP (95% CI = 0.077, 9.9), a 2.8% increase in ICAM-1 (95% CI = 1.4, 4.2), and a 4.3% increase in VCAM-1 (95% CI = 2.5, 6.1). The main effects of particle radioactivity remained similar after adjustment in most cases. We also obtained similar effect estimates in a sensitivity analysis applying a robust causal model.ConclusionRegional particle radioactivity is positively associated with inflammatory biomarkers, indicating a potential pathway for radiation-induced cardiovascular effects.
| S-EPMC7269805 | biostudies-literature
Project description:Endothelial inflammation and damage are the main drivers of cardiovascular risk/disease. Endothelial repair is mediated in part by recruitment of bone marrow endothelial progenitor/endothelial colony forming cells (EPC/ECFC). People with HIV (PWH) have increased cardiovascular risk and the impact of infection in endothelial repair is not well defined. The low frequencies and challenges to in vitro isolation and differentiation of EPC/ECFC from PBMCs had made it difficult to study their role in this context. We hypothesized that HIV driven inflammation induces phenotypic changes that reflects the impact of infection. To test this hypothesis, we evaluated expression of markers of trafficking, endothelial differentiation, and angiogenesis, and study their association with biomarkers of inflammation in a cohort of PWH. In addition, we investigated the relationship of circulating endothelial progenitors and angiogenic T cells, a T cell subset with angiogenic function. Using a flow cytometry approach, we identified two subsets of circulating progenitors LIN4-CD45-CD34+ and LIN4-CD45dimCD34+ in PWH. We found that the phenotype but not frequencies were associated with biomarkers of inflammation. In addition, the percentage of LIN4-CD45dimCD34+ was associated with serum levels of lipids. This data may provide a new tool to better address the impact of HIV infection in endothelial inflammation and repair.
| S-EPMC8165313 | biostudies-literature
Project description:RATIONALE:Microvascular inflammation and endothelial dysfunction secondary to unchecked activation of endothelium play a critical role in the pathophysiology of sepsis and organ failure. The intrinsic signaling mechanisms responsible for dampening excessive activation of endothelial cells are not completely understood. OBJECTIVE:To determine the central role of YAP (Yes-associated protein), the major transcriptional coactivator of the Hippo pathway, in modulating the strength and magnitude of endothelial activation and vascular inflammation. METHODS AND RESULTS:Endothelial-specific YAP knockout mice showed increased basal expression of E-selectin and ICAM (intercellular adhesion molecule)-1 in endothelial cells, a greater number of adherent neutrophils in postcapillary venules and increased neutrophil counts in bronchoalveolar lavage fluid. Lipopolysaccharide challenge of these mice augmented NF-?B (nuclear factor-?B) activation, expression of endothelial adhesion proteins, neutrophil and monocyte adhesion to cremaster muscle venules, transendothelial neutrophil migration, and lung inflammatory injury. Deletion of YAP in endothelial cells also markedly augmented the inflammatory response and cardiovascular dysfunction in a polymicrobial sepsis model induced by cecal ligation and puncture. YAP functioned by interacting with the E3 ubiquitin-protein ligase TLR (Toll-like receptor) signaling adaptor TRAF6 (tumor necrosis factor receptor-associated factor 6) to ubiquitinate TRAF6, and thus promoted TRAF6 degradation and modification resulting in inhibition of NF-?B activation. TRAF6 depletion in endothelial cells rescued the augmented inflammatory phenotype in mice with endothelial cell-specific deletion of YAP. CONCLUSIONS:YAP modulates the activation of endothelial cells and suppresses vascular inflammation through preventing TRAF6-mediated NF-?B activation and is hence essential for limiting the severity of sepsis-induced inflammation and organ failure.
| S-EPMC6014930 | biostudies-literature
Project description:AimsVolume overload and venous congestion are typically viewed as a consequence of advanced and of acute heart failure (HF) and renal failure (RF) although it is possible that hypervolaemia itself might be a critical intermediate in the pathophysiology of these diseases. This study aimed at elucidating whether peripheral venous congestion is sufficient to promote changes in inflammatory, neurohormonal, and endothelial phenotype similar to those observed in HF and RF.MethodsTo experimentally model peripheral venous congestion, we developed a new method (so-called venous stress test) and applied the methodology on 24 healthy subjects (14 men, age 35 ± 2 years). Venous arm pressure was increased to ∼30 mmHg above the baseline level by inflating a tourniquet cuff around the dominant arm (test arm). Blood and endothelial cells (ECs) were sampled from test and control arm (lacking an inflated cuff) before and after 75 min of venous congestion, using angiocatheters and endovascular wires. Magnetic beads coated with EC-specific antibodies were used for EC separation; amplified mRNA was analysed by Affymetrix HG-U133 Plus 2.0 Microarray.ResultsPlasma interleukin-6 (IL-6), endothelin-1 (ET-1), angiotensin II (AII), vascular cell adhesion molecule-1 (VCAM-1), and chemokine (C-X-C motif) ligand 2 (CXCL2) were significantly increased in the congested arm. A total of 3437 mRNA probe sets were differentially expressed (P < 0.05) in venous ECs before vs. after testing, including ET-1, VCAM-1, and CXCL2.ConclusionPeripheral venous congestion causes release of inflammatory mediators, neurohormones, and activation of ECs. Overall, venous congestion mimicked, notable aspects of the phenotype typical of advanced and of acute HF and RF.
| S-EPMC3924182 | biostudies-literature
Project description:Inflammation and endothelial activation play a pivotal role in development and progression of diabetic retinopathy (DR), a vision-threatening complication of diabetes mellitus (DM) and the leading cause of blindness in the working age population. Easily accessible and validated biomarkers for DR early diagnosis and progression are required for use in clinical trials: here, we reviewed the available literature to understand the association of circulating levels of selected markers of inflammation and endothelial activation with the presence of nonproliferative and proliferative DR (NPDR and PDR) and investigate the relationship between their systemic and ocular levels. We additionally provide data synthesis and perform statistical analysis for interpretation of the collected evidence. CRP, IL-1β, IL-6, TNFα, sICAM1, and sVCAM1 circulating levels were increased in subjects with DM compared to healthy individuals. Moreover, TNFα and sVCAM1 showed increasing systemic levels with DR presence and severity; circulating CRP increased with the transition from no DR to NPDR, whereas IL-6 was increased in PDR compared to NDPR stages. The relationship between ocular and systemic concentrations of these proteins remained unclear due to the low number of studies with matched sampling. In conclusion, the available data supports the use of systemic biomarkers of inflammation and endothelial activation to identify DM status and DR severity. These systemic biomarkers are likely reflecting an overall state of inflammation and vascular activation in different tissues of the body, including the eyes. Prospective, longitudinal datasets are required to validate these biomarkers as predictors of early DR presence, of DR progression, or for disease monitoring.
| S-EPMC8496421 | biostudies-literature
Project description:This long-term study examined relationships between solar and magnetic factors and the time course and lags of autonomic nervous system (ANS) responses to changes in solar and geomagnetic activity. Heart rate variability (HRV) was recorded for 72 consecutive hours each week over a five-month period in 16 participants in order to examine ANS responses during normal background environmental periods. HRV measures were correlated with solar and geomagnetic variables using multivariate linear regression analysis with Bonferroni corrections for multiple comparisons after removing circadian influences from both datasets. Overall, the study confirms that daily ANS activity responds to changes in geomagnetic and solar activity during periods of normal undisturbed activity and it is initiated at different times after the changes in the various environmental factors and persist over varying time periods. Increase in solar wind intensity was correlated with increases in heart rate, which we interpret as a biological stress response. Increase in cosmic rays, solar radio flux, and Schumann resonance power was all associated with increased HRV and parasympathetic activity. The findings support the hypothesis that energetic environmental phenomena affect psychophysical processes that can affect people in different ways depending on their sensitivity, health status and capacity for self-regulation.
| S-EPMC5805718 | biostudies-literature
Project description:Cerebral ischemia is associated with an acute inflammatory response that contributes to the resulting injury. The innate immunity receptor CD36, expressed in microglia and endothelium, and the pro-inflammatory cytokine interleukin-1β (IL-1β) are involved in the mechanisms of ischemic injury. Since CD36 has been implicated in activation of the inflammasome, the main source of IL-1β, we investigated whether CD36 mediates brain injury through the inflammasome and IL-1β. We found that active caspase-1, a key inflammasome component, is decreased in microglia of CD36-deficient mice subjected to transient middle cerebral artery occlusion, an effect associated with a reduction in brain IL-1β. Conditional deletion of CD36 either in microglia or endothelium reduced ischemic injury in mice, attesting to the pathogenic involvement of CD36 in both cell types. Application of an ischemic brain extract to primary brain endothelial cell cultures from wild type (WT) mice induced IL-1β-dependent endothelial activation, reflected by increases in the cytokine colony stimulating factor-3, a response markedly attenuated in CD36-deficient endothelia. Similarly, the increase in colony stimulating factor-3 induced by recombinant IL-1β was attenuated in CD36-deficient compared to WT endothelia. We conclude that microglial CD36 is a key determinant of post-ischemic IL-1β production by regulating caspase-1 activity, whereas endothelial CD36 is required for the full expression of the endothelial activation induced by IL-1β. The data identify microglial and endothelial CD36 as critical upstream components of the acute inflammatory response to cerebral ischemia and viable putative therapeutic targets.
| S-EPMC8187325 | biostudies-literature