Tropospheric ozone

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Petr75
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Re: Tropospheric ozone

Post by Petr75 » Sat Oct 03, 2020 8:21 am

O3

2009 Jun 24
CNR, Institute of Clinical Physiology, Pisa, Italy
Ozone and cardiovascular injury
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2706799/

Abstract

Air pollution is increasingly recognized as an important and modifiable determinant of cardiovascular diseases in urban communities. The potential detrimental effects are both acute and chronic having a strong impact on morbidity and mortality. The acute exposure to pollutants has been linked to adverse cardiovascular events such as myocardial infarction, heart failure and life-threatening arrhythmias. The long-terms effects are related to the lifetime risk of death from cardiac causes. The WHO estimates that air pollution is responsible for 3 million premature deaths each year. The evidence supporting these data is very strong nonetheless, epidemiologic and observational data have the main limitation of imprecise measurements. Moreover, the lack of clinical experimental models makes it difficult to demonstrate the individual risk..


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MS

2020 Sep 2
Nuffield Department of Clinical Neurology, University of Oxford, UK
Vascular disease and multiple sclerosis: a post-mortem study exploring their relationships
https://pubmed.ncbi.nlm.nih.gov/32875311/

Abstract

Vascular comorbidities have a deleterious impact on multiple sclerosis clinical outcomes but it is unclear whether this is mediated by an excess of extracranial vascular disease (i.e. atherosclerosis) and/or of cerebral small vessel disease or worse multiple sclerosis pathology. To address these questions, a study using a unique post-mortem cohort wherein whole body autopsy reports and brain tissue were available for interrogation was established. Whole body autopsy reports were used to develop a global score of systemic vascular disease that included aorta and coronary artery atheroma, cardiac hypertensive disease, myocardial infarction and ischaemic stroke. The score was applied to 85 multiple sclerosis cases (46 females, age range 39 to 84 years, median 62.0 years) and 68 control cases. Post-mortem brain material from a subset of the multiple sclerosis (n = 42; age range 39-84 years, median 61.5 years) and control (n = 39) cases was selected for detailed neuropathological study. For each case, formalin-fixed paraffin-embedded tissue from the frontal and occipital white matter, basal ganglia and pons was used to obtain a global cerebral small vessel disease score that captured the presence and/or severity of arteriolosclerosis, periarteriolar space dilatation, haemosiderin leakage, microinfarcts, and microbleeds. The extent of multiple sclerosis-related pathology (focal demyelination and inflammation) was characterized in the multiple sclerosis cases. Regression models were used to investigate the influence of disease status on systemic vascular disease and cerebral small vessel disease scores and, in the multiple sclerosis group, the relationship between multiple sclerosis-related pathology and both vascular scores. We show that: (i) systemic cardiovascular burden, and specifically atherosclerosis, is lower and cerebral small vessel disease is higher in multiple sclerosis cases that die at younger ages compared with control subjects; (ii) the association between systemic vascular disease and cerebral small vessel disease is stronger in patients with multiple sclerosis compared with control subjects; and (iii) periarteriolar changes, including periarteriolar space dilatation, haemosiderin deposition and inflammation, are key features of multiple sclerosis pathology outside the classic demyelinating lesion. Our data argue against a common primary trigger for atherosclerosis and multiple sclerosis but suggest that an excess burden of cerebral small vessel disease in multiple sclerosis may explain the link between vascular comorbidity and accelerated irreversibility disability.

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2020 Sep 30
Cardiac Autonomic Modulation Is Different in Terms of Clinical Variant of Multiple Sclerosis
https://pubmed.ncbi.nlm.nih.gov/33008032/
Last edited by Petr75 on Fri Dec 04, 2020 8:22 am, edited 4 times in total.

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Re: Tropospheric ozone

Post by Petr75 » Tue Oct 06, 2020 10:55 pm

O3

2020 Aug 16
Hebei Medical University, Shijiazhuang, Hebei, Department of Neurology, Hebei General Hospital, China
The association between ambient air pollution and blood lipids: A longitudinal study in Shijiazhuang, China
https://pubmed.ncbi.nlm.nih.gov/32889259/

Abstract

Background: Few studies have explored the associations between ambient air pollution and blood lipid levels. This study aimed to fill this knowledge gap based on a routine health examination cohort in Shijiazhuang, China.

Methods: We included 7063 participants who took the routine health examination for 2-3 times at Hebei General Hospital from January 2016 to December 2018. Individual serum levels of cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and high-density lipoprotein cholesterol (HDL-C) were measured. Their three-month average exposure to air pollution prior to the routine health examinations was estimated using inverse distance weighted method. We used linear mixed-effects regression models to examine the associations between air pollution and levels of blood lipids while controlling for age, gender, body mass index (BMI), smoking, alcohol drinking, temperature, humidity, with a random effect for each individual.

Results: Particles with diameters ≤2.5 μm and ≤10 μm (PM2.5 and PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2) and ozone (O3) were all positively associated with TC, TG, and LDL-C and negatively associated with HDL-C, in single pollutant models. Each 10 μg/m3 increment of 3-month average PM2.5 was associated with 0.65% [95% confidence interval (CI): 0.03%-1.28%], 0.56% (95%CI: 0.33%-0.79%) and 0.63% (95%CI: 0.35%-0.91%) increment in TG, TC, and LDL-C, and 0.91% (95%CI: 0.68%-1.13%) decrease in HDL-C. In two-pollutant models, the effects of gaseous pollutants on blood lipids were weakened, while those of PMs were strengthened. Stronger associations were presented in the elderly (≥60 years) and overweight/obese (BMI ≥ 24) participants.

Conclusions: Ambient air pollution had significantly adverse effects on blood lipid levels, especially in overweight/obese and elderly individuals.

Capsule: Significant associations between increased air pollution and worse blood lipid levels were found, especially in overweight/obese and elderly individuals.
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MS

19 November 2018
nature.com
Lipoprotein markers associated with disability from multiple sclerosis
https://www.nature.com/articles/s41598- ... 8375a140ed

Abstract

Altered lipid metabolism is a feature of chronic inflammatory disorders. Increased plasma lipids and lipoproteins have been associated with multiple sclerosis (MS) disease activity. Our objective was to characterise the specific lipids and associated plasma lipoproteins increased in MS and to test for an association with disability. Plasma samples were collected from 27 RRMS patients (median EDSS, 1.5, range 1–7) and 31 healthy controls. Concentrations of lipids within lipoprotein sub-classes were determined from NMR spectra. Plasma cytokines were measured using the MesoScale Discovery V-PLEX kit. Associations were tested using multivariate linear regression. Differences between the patient and volunteer groups were found for lipids within VLDL and HDL lipoprotein sub-fractions (p < 0.05). Multivariate regression demonstrated a high correlation between lipids within VLDL sub-classes and the Expanded Disability Status..

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Re: Tropospheric ozone

Post by Petr75 » Fri Oct 09, 2020 10:59 am

O3

Ambient Air Pollution Associations with Retinal Morphology in the UK Biobank
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7405693/
(.. formation of ground-level ozone.)

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An acute exposure to ozone impairs human olfactory functioning
https://pubmed.ncbi.nlm.nih.gov/30007872/
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MS

Jul-Sep 2020
Department of Neurology, Medical University of Vienna, Vienna, Austria
Inner nuclear layer and olfactory threshold are interlinked and reflect inflammatory activity in multiple sclerosis
https://pubmed.ncbi.nlm.nih.gov/32922831/

Abstract

Background: Retinal inner nuclear layer (INL) and olfactory threshold (OT) are associated with inflammatory activity in multiple sclerosis (MS).

Objective: The study aims to investigate (a) whether there is an association of INL and OT in MS and (b) if changes in INL and OT follow a time pattern in relation to MS relapse.

Methods: We assessed INL by optical coherence tomography and OT by Sniffin' Sticks in three different cohorts: a cross-sectional MS cohort (n = 260), a longitudinal, 3-year cohort of MS (n = 141) and healthy controls (n = 30), and a longitudinal, 24-weeks cohort with acute MS relapse (n = 28) and stable MS controls (n = 27).

Results: Cross-sectionally, INL and OT were strongly correlated with number but not localization of relapse in the previous 12 months and INL correlated with OT. Longitudinally, INL was thicker and OT score was lower short term in times of relapse activity, but not long term and independent of relapse localization. In acute MS relapse, INL and OT were altered compared with stable MS, again, independent of relapse localization resolving over 12-24 weeks with faster approximation to stable MS after escalation of disease-modifying treatment.

Conclusions: INL and OT are interlinked markers of short-term inflammatory activity, following a nearly congruent time pattern and independent of relapse localization, possibly reflecting a proinflammatory state within the central nervous system.

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Re: Tropospheric ozone

Post by Petr75 » Fri Oct 16, 2020 12:06 pm

O3

2017 Nov 21
Department of Chemistry, SUNY College of Environmental Science and Forestry, Syracuse
Ozone exposure is associated with acute changes in inflammation, fibrinolysis, and endothelial cell function in coronary artery disease patients
https://pubmed.ncbi.nlm.nih.gov/29157250/

Abstract

Background: Air pollution is a major risk factor for cardiovascular disease, of which ozone is a major contributor. Several studies have found associations between ozone and cardiovascular morbidity, but the results have been inconclusive. We investigated associations between ozone and changes across biological pathways associated with cardiovascular disease...
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MS

2020 Sep 16
Department of Neuroimmunology of Federal Center of Brain and Neurotechnology of the Federal Medical-Biological Agency of Russia, Moscow
Hyperhomocysteinemia and Endothelial Dysfunction in Multiple Sclerosis
https://pubmed.ncbi.nlm.nih.gov/32947812/

Abstract

Endothelial dysfunction is recognized as one of the leading factors in the pathogenesis of diseases of the central nervous system of various etiologies. Numerous studies have shown the role of hyperhomocysteinemia in the development of endothelial dysfunction and the prothrombogenic state. The most important condition in the development of multiple sclerosis (MS) is a dysregulation of the blood-brain barrier (BBB) and transendothelial leukocyte migration. It has been proven that homocysteine also contributes to the damage of neurons by the mechanism of excitotoxicity and the induction of the apoptosis of neurons. These processes can be one of the factors of neurodegenerative brain damage, which plays a leading role in the progression of MS. This review describes the pleiotropic effect of homocysteine on these processes and its role in MS pathogenesis.

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Re: Tropospheric ozone

Post by Petr75 » Thu Oct 22, 2020 12:13 am

O3

2015 Jul 6
Department of Neurobiology and Anatomy , West Virginia School of Medicine , Morgantown , West Virginia
Ozone exposure initiates a sequential signaling cascade in airways involving interleukin-1beta release, nerve growth factor secretion, and substance P upregulation
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4491938/


Abstract

Previous studies demonstrated that interleukin-1β (IL-1β) and nerve growth factor (NGF) increase synthesis of substance P (SP) in airway neurons both after ozone (O3) exposure and by direct application. It was postulated that NGF mediates O3-induced IL-1β effects on SP. The current study specifically focused on the influence of O3 on IL-1β, NGF, and SP levels in mice bronchoalveolar lavage fluid (BALF) and whether these mediators may be linked in an inflammatory-neuronal cascade in vivo. The findings showed that in vivo O3 exposure induced an increase of all three proteins in mouse BALF and that O3-induced elevations in both NGF and SP are mediated by the inflammatory cytokine IL-1β. Further, inhibition of NGF reduced O3 induced increases of SP in both the lung BALF and lung tissue, demonstrating NGF serves as a mediator of IL-1β effects on SP. These data indicate that IL-1β is an early mediator of O3-induced rise in NGF and subsequent SP release in mice in vivo.

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MS

2020 Sep 23
Unit of Neurology & Neurorehabilitation, IRCCS Neuromed, Italy
Interleukin-1β Alters Hebbian Synaptic Plasticity in Multiple Sclerosis
https://pubmed.ncbi.nlm.nih.gov/32977401/

Abstract

In multiple sclerosis (MS), inflammation alters synaptic transmission and plasticity, negatively influencing the disease course. In the present study, we aimed to explore the influence of the proinflammatory cytokine IL-1β on peculiar features of associative Hebbian synaptic plasticity, such as input specificity, using the paired associative stimulation (PAS). In 33 relapsing remitting-MS patients and 15 healthy controls, PAS was performed on the abductor pollicis brevis (APB) muscle. The effects over the motor hot spot of the APB and abductor digiti minimi (ADM) muscles were tested immediately after PAS and 15 and 30 min later. Intracortical excitability was tested with paired-pulse transcranial magnetic stimulation (TMS). The cerebrospinal fluid (CSF) levels of IL-1β were calculated. In MS patients, PAS failed to induce long-term potentiation (LTP)-like effects in the APB muscle and elicited a paradoxical motor-evoked potential (MEP) increase in the ADM. IL-1β levels were negatively correlated with the LTP-like response in the APB muscle. Moreover, IL-1β levels were associated with synaptic hyperexcitability tested with paired-pulse TMS. Synaptic hyperexcitability caused by IL-1β may critically contribute to alter Hebbian plasticity in MS, inducing a loss of topographic specificity.

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Re: Tropospheric ozone

Post by Petr75 » Fri Oct 30, 2020 12:17 pm

O3


Published online 2016 Mar 23
Inflammasome, IL-1 and inflammation in ozone-induced lung injury
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4858604/

..Alveolar macrophages accumulate lipids upon cigarette smoke exposure resembling foamy macrophages and release spontaneously the IL-1α and IL-1β cytokines [40]. This was not investigated upon ozone exposure.

Ozone induction of other members of the IL-1 family proteins such as IL-18, IL-33, IL-36 or IL-38 with inflammatory properties have so far not been investigated..

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MS

2020 Oct 20
Autoimmune Diseases Research Center, Shiraz University of Medical Sciences, Shiraz, Iran
Elevated IL-38 Serum Levels in Newly Diagnosed Multiple Sclerosis and Systemic Sclerosis Patients
https://pubmed.ncbi.nlm.nih.gov/33080590/

Abstract

Objective: Interleukin (IL)-38 is a newly discovered member of the IL-1 cytokine family with a proposed anti-inflammatory profile. We studied the probable role of this cytokine in the pathogenesis of two autoimmune diseases: multiple sclerosis (MS) and systemic sclerosis (SSc).

Subjects and methods: A total of 87 MS patients and 86 SSc patients (40 new and recently untreated cases and 46 treated cases) were selected for this study. Eighty-seven and 80 age- and sex-matched healthy subjects were included as controls for MS and SSc, respectively. Clinical and paraclinical features of the patients were recorded at the time of sampling. Serum IL-38 was measured by ELISA.

Results: Levels of serum IL-38 did not significantly differ between the total MS or SSc patients compared to controls. However, levels of IL-38 were significantly higher in newly diagnosed patients of MS (206.43 ± 38.97 pg/mL, p < 0.0001) than in those previously treated (158.04 ± 39.45 pg/mL). Similarly, new/recently untreated cases of SSc patients showed increased IL-38 levels (185.19 ± 36.27 pg/mL, p = 0.001) compared to treated patients (166.82 ± 33.08 pg/mL). IL-38 levels in newly diagnosed MS patients (p = 0.007) and new/recently untreated SSc patients (p = 0.032) were significantly higher than those in healthy controls.

Conclusion: The higher serum levels of IL-38 in new or recently untreated cases of MS and SSc patients than in treated patients and healthy controls suggest the possible role of this cytokine in the development of these diseases or as part of a feedback loop to attenuate the inflammatory conditions in early stages of these diseases.

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Re: Tropospheric ozone

Post by Petr75 » Mon Nov 02, 2020 11:24 am

2020 Aug
Department of Labor and Environmental Hygiene, Shenyang Medical College, China
The Impact of Air Pollution on Hospitalization for Cardiovascular and Cerebrovascular Disease in Shenyang, China
https://pubmed.ncbi.nlm.nih.gov/33083324/

Abstract

Background: The aim of this study was to investigate the overall impact of PM2.5, PM10, NO2, SO2, CO, and O3 on the admission of cardiovascular and cerebrovascular disease.

Conclusion: Short-term exposure to ambient air pollution (NO2, O3, and PM10) may be associated with an increased risk of daily cardiovascular and cerebrovascular admission, which may provide reliable evidence for further understanding of the potential adverse effects of air pollution on cardiovascular and cerebrovascular diseases.
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MS

2020 Oct 22
Multiple Sclerosis Clinical Care and Research Centre, Department of Neuroscience, Reproductive Science and Odontostomatology, Federico II University, Naples, Italy
The Framingham cardiovascular risk score and 5-year progression of multiple sclerosis
https://pubmed.ncbi.nlm.nih.gov/33091222/

Abstract

Background: Cardiovascular risk factors and comorbidities can affect the prognosis of multiple sclerosis (MS). The Framingham risk score is an algorithm that can estimate the 10-year risk of developing macrovascular disease.

Objective: To evaluate possible association between the Framingham risk score at baseline, and MS relapses, disability and disease-modifying therapy (DMT) choices over 5-year follow-up.

Methods: This is a retrospective cohort study including 251 MS subjects. At baseline, we calculated the Framingham risk score considering the following variables: age, sex, diabetes, smoking, systolic blood pressure, and body mass index. MS outcomes including relapses, disability and treatments were collected over 5 years. Cox proportional regression models were employed to estimate hazard ratios (HR).

Results: 1-point increase in the Framingham risk score was associated with 31% higher risk of relapse (HR=1.31; 95%CI=1.03, 1.68), 19% higher risk of reaching of EDSS 6.0 (HR=1.19; 95%CI=1.05, 3.01), and 62% higher risk of DMT escalation (HR=1.62; 95%CI=1.22, 3.01).

Conclusions: Higher cardiovascular risk was associated with higher risk of relapses, disability, and DMT escalation in MS. Early identification, correction and treatment of cardiovascular comorbidities should be carefully considered within MS management.
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2020 Oct 21
Developmental venous anomalies in patients with multiple sclerosis: is that a coincidence or an ancillary finding?
https://pubmed.ncbi.nlm.nih.gov/33083936/

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Re: Tropospheric ozone

Post by Petr75 » Sun Nov 15, 2020 4:13 am

O3

2020 Oct 26
Section of Environmental Health, Department of Public Health, University of Copenhagen, Denmark
Telomere length in newborns is associated with exposure to low levels of air pollution during pregnancy
https://pubmed.ncbi.nlm.nih.gov/33120230/

bstract

Telomere length (TL) is a biomarker of biological aging that may be affected by prenatal exposure to air pollution. The aim of this study was to assess the association between prenatal exposure to air pollution and TL in maternal blood cells (leukocytes), placenta and umbilical cord blood cells, sampled immediately after birth in 296 Danish mother-child pairs from a birth cohort. Exposure data was obtained using the high-resolution and spatial-temporal air pollution modeling system DEHM-UBM-AirGIS for PM2.5, PM10, SO2, NH4+, black carbon (BC), organic carbon (OC), CO, O3, NO2, and NOx at residential and occupational addresses of the participating women for the full duration of the pregnancy. The association between prenatal exposure to air pollutants and TL was investigated using distributed lag models. There were significant and positive associations between TL in umbilical cord blood cells and prenatal exposure to BC, OC, NO2, NOx, CO, and O3 during the second trimester. TL in umbilical cord blood was significantly and inversely associated with prenatal exposure to PM2.5, BC, OC, SO2, NH4+, CO and NO2 during the third trimester. There were similar inverse associations between TL from umbilical cord blood cells and air pollution exposure at the residential and occupational addresses. There were weaker or no associations between air pollution exposure and TL in placenta tissue and maternal blood cells. In conclusion, both the second and third trimesters of pregnancy are shown to be sensitive windows of exposure to air pollution affecting fetal TL.

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MS

15 April 2020
sciencedirect.com
Association between shorter leukocyte telomeres and multiple sclerosis
https://www.sciencedirect.com/science/a ... 2819306745

Highlights

• Age‐ and sex‐adjusted telomere lengths in MS cases is significantly shorter than in healthy controls
• Telomere shortening is not correlated with clinical disability
• Is telomere shortening is the cause or the consequence of MS?

Abstract

Relative telomere length (TL) is regarded as a biomarker of biological age. Accelerated immune aging, as represented by TL reduction, has been demonstrated in autoimmune diseases, including multiple sclerosis (MS). However, it is still unresolved whether telomere shortening is the cause or the consequence of the pathogenic events underlying autoimmunity.

Assessing TL in whole blood DNA samples in 138 MS patients and 120 healthy controls showed reduced TL in patients as compared with controls There seems to be a prelude of accelerated telomere shortening, which may increase the risk for development of MS.

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Re: Tropospheric ozone

Post by Petr75 » Mon Nov 16, 2020 12:47 pm

O3


31 October 2019
frontiersin.org
Ozone Pollution: A Major Health Hazard Worldwide
https://www.frontiersin.org/articles/10 ... 02518/full

..Day et al. found that an increase in 24-h or 2-week average exposure to ozone was associated with increased p-selectin (a soluble plasma marker of platelet activation), suggesting that ozone exposure increases the risk of thrombosis (21). Wang et al. found that increased ambient ozone exposure was associated with increased rate of carotid wall thickness progression and risk of new plaque formation in healthy adults (52). Jia et al. showed that ambient ozone exposure within several minutes can decrease heart rate variability in the healthy elderly subjects, suggesting that a dysfunction of cardiac autonomic nervous system may be involved ..

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MS

2020 Oct 6
University Hospital Schleswig-Holstein, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany
Platelets as Mediators of Neuroinflammation and Thrombosis
https://pubmed.ncbi.nlm.nih.gov/33123127/

Abstract

Beyond platelets function in hemostasis, there is emerging evidence to suggest that platelets contribute crucially to inflammation and immune responses. Therefore, considering the detrimental role of inflammatory conditions in severe neurological disorders such as multiple sclerosis or stroke, this review outlines platelets involvement in neuroinflammation. For this, distinct mechanisms of platelet-mediated thrombosis and inflammation are portrayed, focusing on the interaction of platelet receptors with other immune cells as well as brain endothelial cells. Furthermore, we draw attention to the intimate interplay between platelets and the complement system as well as between platelets and plasmatic coagulation factors in the course of neuroinflammation. Following the thorough exposition of preclinical approaches which aim at ameliorating disease severity after inducing experimental autoimmune encephalomyelitis (a counterpart of multiple sclerosis in mice) or brain ischemia-reperfusion injury, the clinical relevance of platelet-mediated neuroinflammation is addressed. Thus, current as well as future propitious translational and clinical strategies for the treatment of neuro-inflammatory diseases by affecting platelet function are illustrated, emphasizing that targeting platelet-mediated neuroinflammation could become an efficient adjunct therapy to mitigate disease severity of multiple sclerosis or stroke associated brain injury.

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2017 May 22
Prediction of disease activity in models of multiple sclerosis by molecular magnetic resonance imaging of P-selectin
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5468646/

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Re: Tropospheric ozone

Post by Petr75 » Wed Dec 09, 2020 11:06 am

Maybe I have it - activated carbon applies to O3, so I'm testing the Nano FFP2 Carbon respirator.
But briefly, so I don't know what and how. So far so good. ;)
Big black drape ...

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Re: Tropospheric ozone

Post by Petr75 » Tue Dec 29, 2020 12:01 am

Petr75 wrote:
Wed Feb 01, 2017 12:34 am
Yes good question but ozone been there before:
Volcanic activity, fires..


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source http://www.neurology.org/content/61/10/ ... nsion.html




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just speculation
June 12, 2019
Rice University
Old ice and snow yields tracer of preindustrial ozone
https://www.sciencedaily.com/releases/2 ... 141340.htm

Using rare oxygen molecules trapped in air bubbles in old ice and snow, U.S. and French scientists have answered a long-standing question: How much have "bad" ozone levels increased since the start of the Industrial Revolution?

"We've been able to track how much ozone there was in the ancient atmosphere," said Rice University geochemist Laurence Yeung, the lead author of a study published online today in Nature. "This hasn't been done before, and it's remarkable that we can do it at all."

Researchers used the new data in combination with state-of-the-art atmospheric chemistry models to establish that ozone levels in the lower atmosphere, or troposphere, have increased by an upper limit of 40% since 1850.

"These results show that today's best models simulate ancient tropospheric ozone levels well," said Yeung. "That bolsters our confidence in their ability to predict how tropospheric ozone levels will change in the future."

The Rice-led research team includes investigators from the University of Rochester in New York, the French National Center for Scientific Research's (CNRS) Institute of Environmental Geosciences at Université Grenoble Alpes (UGA), CNRS's Grenoble Images Speech Signal and Control Laboratory at UGA and the French Climate and Environmental Sciences Laboratory of both CNRS and the French Alternative Energies and Atomic Energy Commission (CEA) at the Université Versailles-St Quentin.

"These measurements constrain the amount of warming caused by anthropogenic ozone," Yeung said. For example, he said the most recent report from the Intergovernmental Panel on Climate Change (IPCC) estimated that ozone in Earth's lower atmosphere today is contributing 0.4 watts per square meter of radiative forcing to the planet's climate, but the margin of error for that prediction was 50%, or 0.2 watts per square meter.

"That's a really big error bar," Yeung said. "Having better preindustrial ozone estimates can significantly reduce those uncertainties.

"It's like guessing how heavy your suitcase is when there's a fee for bags over 50 pounds," he said. "With the old error bars, you'd be saying, 'I think my bag is between 20 and 60 pounds.' That's not good enough if you can't afford to pay the penalty."

Ozone is a molecule that contains three oxygen atoms. Produced in chemical reactions involving sunlight, it is highly reactive, in part because of its tendency to give up one of its atoms to form a more stable oxygen molecule. The majority of Earth's ozone is in the stratosphere, which is more than five miles above the planet's surface. Stratospheric ozone is sometimes called "good" ozone because it blocks most of the sun's ultraviolet radiation, and is thus essential for life on Earth.

The rest of Earth's ozone lies in the troposphere, closer to the surface. Here, ozone's reactivity can be harmful to plants, animals and people. That's why tropospheric ozone is sometimes called "bad" ozone. For example, ozone is a primary component of urban smog, which forms near ground level in sunlit-driven reactions between oxygen and pollutants from motor vehicle exhaust. The Environmental Protection Agency considers exposure to ozone levels greater than 70 parts per billion for eight hours or longer to be unhealthy.

"The thing about ozone is that scientists have only been studying it in detail for a few decades," said Yeung, an assistant professor of Earth, environmental and planetary sciences. "We didn't know why ozone was so abundant in air pollution until the 1970s. That's when we started to recognize how air pollution was changing atmospheric chemistry. Cars were driving up ground-level ozone."

While the earliest measurements of tropospheric ozone date to the late 19th century, Yeung said those data conflict with the best estimates from today's state-of-the-art atmospheric chemistry models.

"Most of those older data are from starch-paper tests where the paper changes colors after reacting with ozone," he said. "The tests are not the most reliable -- the color change depends on relative humidity, for example -- but they suggest, nevertheless, that ground-level ozone could have increased up to 300% over the past century. In contrast, today's best computer models suggest a more moderate increase of 25-50%. That's a huge difference....

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