Tropospheric ozone

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Petr75
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Posts: 975
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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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( Question for you:
In what hours are you the most deaths? :confused: Petr)

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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 Sat Oct 24, 2020 2:29 am, edited 3 times in total.

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Petr75
Family Elder
Posts: 975
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic

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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Petr75
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Posts: 975
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic

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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Petr75
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Posts: 975
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic

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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Petr75
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Posts: 975
Joined: Sat Oct 19, 2013 10:17 am
Location: Czech Republic

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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