Relevant bibliographies by topics / Air-blood barrier

Academic literature on the topic 'Air-blood barrier'

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Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Air-blood barrier"

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Simionescu, Maya. "Cellular components of the air-blood barrier." Journal of Cellular and Molecular Medicine 5, no. 3 (July 2001): 320–21. http://dx.doi.org/10.1111/j.1582-4934.2001.tb00167.x.

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Fu, Anchen, Mingyang Chang, Haiyan Zhu, Hongrui Liu, Danhong Wu, and Hulie Zeng. "Air-blood barrier (ABB) on a chip." TrAC Trends in Analytical Chemistry 159 (February 2023): 116919. http://dx.doi.org/10.1016/j.trac.2023.116919.

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Elliott, Rebekah Omarkhail, and Mei He. "Unlocking the Power of Exosomes for Crossing Biological Barriers in Drug Delivery." Pharmaceutics 13, no. 1 (January 19, 2021): 122. http://dx.doi.org/10.3390/pharmaceutics13010122.

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Since the 2013 Nobel Prize was awarded for the discovery of vesicle trafficking, a subgroup of nanovesicles called exosomes has been driving the research field to a new regime for understanding cellular communication. This exosome-dominated traffic control system has increased understanding of many diseases, including cancer metastasis, diabetes, and HIV. In addition to the important diagnostic role, exosomes are particularly attractive for drug delivery, due to their distinctive properties in cellular information transfer and uptake. Compared to viral and non-viral synthetic systems, the natural, cell-derived exosomes exhibit intrinsic payload and bioavailability. Most importantly, exosomes easily cross biological barriers, obstacles that continue to challenge other drug delivery nanoparticle systems. Recent emerging studies have shown numerous critical roles of exosomes in many biological barriers, including the blood–brain barrier (BBB), blood–cerebrospinal fluid barrier (BCSFB), blood–lymph barrier (BlyB), blood–air barrier (BAB), stromal barrier (SB), blood–labyrinth barrier (BLaB), blood–retinal barrier (BRB), and placental barrier (PB), which opens exciting new possibilities for using exosomes as the delivery platform. However, the systematic reviews summarizing such discoveries are still limited. This review covers state-of-the-art exosome research on crossing several important biological barriers with a focus on the current, accepted models used to explain the mechanisms of barrier crossing, including tight junctions. The potential to design and engineer exosomes to enhance delivery efficacy, leading to future applications in precision medicine and immunotherapy, is discussed.
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Khadzhieva, M. B., A. S. Gracheva, A. V. Ershov, Yu V. Chursinova, V. A. Stepanov, L. S. Avdeikina, O. A. Grebenchikov, et al. "Biomarkers of Air-Blood Barrier Damage In COVID-19." General Reanimatology 17, no. 3 (July 3, 2021): 16–31. http://dx.doi.org/10.15360/1813-9779-2021-3-2-0.

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The search for sensitive and specific markers enabling timely identification of patients with a life-threatening novel coronavirus infection (COVID-19) is important for a successful treatment.The aim of the study was to examine the association of molecular biomarkers of air-blood barrier damage, surfactant proteins SP-A and SP-D and Club cell protein CC16, with the outcome of patients with COVID-19.Materials and methods. A cohort of 109 patients diagnosed with COVID-19 was retrospectively divided into two groups. Group 1 comprised survivor patients discharged from the ICU (w=90). Group 2 included the patients who did not survive (w=19). Association of disease outcome and SP-A, SP-D, and CC16 levels in blood serum, clinical, and laboratory data were examined taking into account the day of illness at the time of biomaterial collection.Results. The non-survivors had higher SP-A (from days 1 to 10 of symptoms onset) and lower CC16 (from days 11 to 20 of symptoms onset) levels vs survivors discharged from ICU. No significant differences in SP-D levels between the groups were found.Conclusion. According to the study results, the surfactant protein SP-A and Club cell protein CC16 are associated with increased COVID-19 mortality.
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Bajanowski, T., and B. Brinkmann. "Thickness of the air-blood tissue barrier in infants." International Journal of Legal Medicine 113, no. 6 (October 17, 2000): 332–37. http://dx.doi.org/10.1007/s004149900103.

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McElroy, Mary C., Helen R. Harty, Gayle E. Hosford, Gráinne M. Boylan, Jean-François Pittet, and Timothy J. Foster. "Alpha-Toxin Damages the Air-Blood Barrier of the Lung in a Rat Model of Staphylococcus aureus-Induced Pneumonia." Infection and Immunity 67, no. 10 (October 1, 1999): 5541–44. http://dx.doi.org/10.1128/iai.67.10.5541-5544.1999.

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ABSTRACT We have shown that injury to alveolar epithelial type I cells may account, in part, for damage to the air-blood barrier of the lung in a rat model of Staphylococcus aureus pneumonia. We have also shown that alpha-toxin is an important cause of damage to the air-blood barrier; however, our data suggest that the toxin is not acting directly on alveolar type I cells.
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Johansson, Barbro B. "Cerebral air embolism and the blood-brain barrier in the rat." Acta Neurologica Scandinavica 62, no. 4 (January 29, 2009): 201–9. http://dx.doi.org/10.1111/j.1600-0404.1980.tb03027.x.

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Tsuda, Akira, Thomas C. Donaghey, Nagarjun V. Konduru, Georgios Pyrgiotakis, Laura S. Van Winkle, Zhenyuan Zhang, Patricia Edwards, Jessica-Miranda Bustamante, Joseph D. Brain, and Phillip Demokritou. "Age-Dependent Translocation of Gold Nanoparticles across the Air–Blood Barrier." ACS Nano 13, no. 9 (August 9, 2019): 10095–102. http://dx.doi.org/10.1021/acsnano.9b03019.

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Ko, Myung-Ah, Jung Hwa Lee, and Sang-Beom Jeon. "Ischemic Penumbra and Blood–Brain Barrier Disruption in Cerebral Air Embolism." American Journal of Respiratory and Critical Care Medicine 201, no. 3 (February 1, 2020): 369–70. http://dx.doi.org/10.1164/rccm.201809-1620im.

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Zagorul'ko, A. K., A. A. Birkun, G. V. Kobozev, and L. G. Safronova. "Correlation of ultrastructure of the air-blood barrier and surfactant activity." Bulletin of Experimental Biology and Medicine 106, no. 5 (November 1988): 1637–41. http://dx.doi.org/10.1007/bf00840866.

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Dissertations / Theses on the topic "Air-blood barrier"

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BENGALLI, ROSSELLA DANIELA. "In vitro models of the respiratory barrier: a case study on zinc oxide nanoparticles." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2015. http://hdl.handle.net/10281/69760.

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Background: In the last decade, nanoparticles (NPs) have brought a huge revolution in the many fields, especially in toxicology studies. Their small size (diameter lower than 100 nm) consent them to have unique chemical and physical properties, which, besides their positive impact in industrial use, may induce adverse health effects too. The production and the emission of zinc oxide nanoparticles (nZnO) is highly increased during the last years, for their industrial, cosmetic, anti-microbial and biomedical applications. Several in vitro and in vivo studies have shown that nZnO are toxic to different mammalian cells inducing inflammation, oxidative stress and systemic effects. However, many questions about the mechanisms of nZnO induced toxicity are still unanswered. Inhalation is the major way of entry and NPs, for their small dimension, can evade the clearance of the respiratory tree and reach the alveoli. NPs can exert their effects through two routes: 1) they may translocate across the air-blood barrier (ABB) and directly enter the endothelial cells; 2) they may induce the epithelial cells to release inflammatory mediators, which subsequently promote the release of endothelial dysfunction markers from the endothelium. According to the REACH regulation (No 1907/2006/EC) and the 3Rs (Refinement, Reduction, Replacement) principle, in vitro alternative strategies are needed to test new chemical compounds, such as NPs. Thus, the choice of an appropriate in vitro model becomes crucial for the evaluation of NPs-induced effects. Co-cultures on Transwell inserts represent a useful tool for the study of NPs effects on different cells. With this model, systemic effects are evaluable, as well as cells exposure to the air-liquid interface (ALI), a more suitable exposure scenario. The aim of this work was to evaluate the effects of nZnO, especially potential effects on inflammation and endothelial dysfunction, using different new in vitro models that mimic the respiratory barrier. Methods and results: Cytotoxicity and biological effects (inflammatory and cellular stress response) on monocultures of human epithelial alveolar cells (NCI-H441) have been tested. A co-culture, composed of epithelial lung cells and human endothelial microvascular pulmonary cells (HPMEC-ST1.6R), and a tri-culture adding monocytes, have been set-up. The results obtained have shown that nZnO (20 µg/ml) have a cytotoxic effect on monocultures, while at the lower dose (10 µg/ml) they do not affect the ABB integrity. However, nZnO induce inflammatory response and the release of soluble adhesion molecules from the endothelial cells in the co-culture system. These data showed for the first time that nZnO are able to induce endothelial inflammation and dysfunction in a 3D-in vitro model of the ABB in which the cells are not directly exposed to nZnO, but the release of inflammatory mediators is regulated by the overlaying epithelium that receives NPs. Furthermore, we observed that the addition of immune cells in the tri-culture modulated the cellular response to nZnO. Finally, a third different system was set-up in order to compare nZnO effects in submerged and ALI conditions. A co-culture of alveolar macrophages and epithelial cells have been set-up and exposed to nZnO suspension or aerosol. This experimental approach has shown that different ways of NPs administration influence the cellular response, demonstrating that cells are more sensitive to nZnO when they are exposed to the ALI system. Conclusions: This research evidenced that the crosstalk between different cells of the respiratory epithelium is crucial when NPs toxicity has to be evaluated. Different in vitro ABB are useful tools to understand the mechanisms of NPs-induced effects, especially their inflammatory potential and their effects on the cardiovascular system. Moreover, NPs administration too has a pivotal role in the biological outcomes occurring at NPs exposure.
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Suwannasual, Usa. "Investigating the Mechanisms involved in Traffic-Generated Air Pollution–Mediated Disruption of the Blood-Brain Barrier in a Wild Type Mouse Model using a Pharmaceutical Intervention Approach." Thesis, University of North Texas, 2020. https://digital.library.unt.edu/ark:/67531/metadc1707379/.

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This study investigated whether oxLDL and/or angiotensin (Ang) II signaling pathways mediate traffic-generated air pollution- exposure induced alterations in blood-brain barrier (BBB) integrity and permeability in a healthy wild type (C57Bl/6) mouse model; additionally, whether these outcomes are exacerbated by a high fat-diet investigated. An environmentally relevant concentration of a mixture of vehicle engine exhaust (MVE) was used. To investigate the hypotheses, 12 wk old male C57Bl/6 mice on either a high fat (HF) or low fat (LF) diet were randomly assigned to inhalational exposure of either filtered-air (FA) or 30 µg PM/m3 diesel exhaust + 70 µg PM/m3 gasoline exhaust (MVE) for 6 hr/day for 30 days. Additionally, we examined mechanisms involved in MVE-mediated alterations BBB integrity using a novel BBB co-culture in vitro model, consisting of mouse primary cerebral vascular endothelial cells on an apical transwell and astrocytes in the basal compartment, which was treated with plasma from the mice on our exposure study. Our in vivo exposure study results showed that MVE inhalation resulted in increased circulating plasma oxLDL and Ang II, compared to FA controls. Additionally, we observed increased cerebral microvascular expression of oxLDL receptors, LOX-1 and CD-36, and Ang II receptor subtype 1 (AT1) in MVE-exposed C57Bl/6 mice, which was further exacerbated with consumption of an HF diet. Increased signaling of both Ang II and oxLDL was associated with decreased BBB integrity, as evidenced by the concurrent reduction in expression of tight junction (TJ) protein claudin-5 and increased permeability of sodium fluorescein (Na-F) from the blood into the cerebral parenchyma. Our results suggest that possible mechanisms involved in oxLDL and/or Ang II-mediated alterations in BBB integrity include oxidative stress and upregulated expression and activity of matrix metalloproteinase (MMP)-9, which is associated with degradation of TJ proteins in the BBB. Our in vitro BBB co-culture results confirm our in vivo findings, as we observe increased BBB permeability (TEER) and decreased integrity (decreased expression of TJ proteins) in the endothelial (apical) layer when treated with plasma from MVE-exposed mice, which was further exacerbated when treated with plasma from MVE-exposed mice on an HF diet. Pre-treatment of the endothelial cells with the AT1 receptor antagonist, Losartan, prior to applying plasma, resulted in attenuation of the alterations observed in endothelial integrity in the BBB co-culture treated with plasma from either MVE+LF or MVE+HF animals. These results suggest Ang II – AT1 signaling mediate, at least in part, the alterations in the BBB integrity observed after exposure to MVE. Moreover, we observed that treatment of the endothelial (apical) layer with plasma from MVE-exposed animals resulted in increased production of inflammatory mediators interleukin-6 (IL-6) and transforming growth factor-β in the astrocyte media (basal compartment). Additionally, these same astrocytes also displayed increased production of angiotensin-converting enzyme (ACE) and also AT1 receptor mRNA expression, while showing decreased expression of the aryl hydrocarbon receptor (AhR) and glutathione peroxidase (GPx). Collectively, these results suggest that exposure to the ubiquitous environmental air pollutant, vehicle engine emissions, results in increased oxLDL and Ang II signaling in the cerebral microvasculature, which is associated with decreased vessel integrity and increased oxidative stress and inflammatory signaling in the CNS. The observed detrimental outcomes are even further exacerbated when coupled with the consumption of an HF diet.
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Kletting, Stephanie [Verfasser], and Claus-Michael [Akademischer Betreuer] Lehr. "A new cell line-based coculture model of the human air-blood barrier to evaluate the interaction with aerosolized drug carriers / Stephanie Kletting ; Betreuer: Claus-Michael Lehr." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/1114735035/34.

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Kühn, Anna Michele [Verfasser], and Claus-Michael [Akademischer Betreuer] Lehr. "Immortalization of human alveolar epithelial cells : towards a cell line expressing functional tight junctions for modelling the air-blood barrier in vitro / Anna Michele Kühn. Betreuer: Claus-Michael Lehr." Saarbrücken : Saarländische Universitäts- und Landesbibliothek, 2016. http://d-nb.info/110979021X/34.

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Bur, Michael [Verfasser]. "Pulmonary epithelial cells as model to investigate in vivo drug absorption across the human air-blood barrier / von Michael Bur." 2007. http://d-nb.info/985721006/34.

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Schulze, Christine [Verfasser]. "Transport of metal oxide nanoparticles across the human air-blood barrier : interactions with physiologically relevant media and proteins / von Christine Schulze." 2010. http://d-nb.info/1010621416/34.

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Costa, Ana Margarida Martins Maia da. "Establishment of a three-dimensional in vitro model of air-blood barrier to assess the translocation of nanoparticles targeted to the lung." Doctoral thesis, 2018. https://hdl.handle.net/10216/113112.

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Costa, Ana Margarida Martins Maia da. "Establishment of a three-dimensional in vitro model of air-blood barrier to assess the translocation of nanoparticles targeted to the lung." Tese, 2018. https://hdl.handle.net/10216/113112.

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Books on the topic "Air-blood barrier"

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Biology and regulation of blood-tissue barriers. New York, N.Y: Springer Science+Business Media, 2012.

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Cheng, C. Yan. Biology and regulation of blood-tissue barriers. New York, N.Y: Springer Science+Business Media, 2012.

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Book chapters on the topic "Air-blood barrier"

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Pinkerton, Kent E., Peter Gehr, Alejandro Castañeda, and James D. Crapo. "Architecture and Cellular Composition of the Air–Blood Tissue Barrier." In Comparative Biology of the Normal Lung, 105–17. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-12-404577-4.00009-6.

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Young, Tamara L., Katherine E. Zychowski, Jesse L. Denson, and Matthew J. Campen. "Blood-brain barrier at the interface of air pollution-associated neurotoxicity and neuroinflammation." In Role of Inflammation in Environmental Neurotoxicity, 295–337. Elsevier, 2019. http://dx.doi.org/10.1016/bs.ant.2018.10.010.

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Kwon, Minkyung, and Jose L. Diaz-Gomez. "Respiratory Physiology in Critical Illness." In Mayo Clinic Critical and Neurocritical Care Board Review, edited by Eelco F. M. Wijdicks, James Y. Findlay, William D. Freeman, and Ayan Sen, 3–9. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190862923.003.0001.

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The practice of critical care medicine requires detailed knowledge of the practical aspects of respiratory physiology, including lung mechanics, the physiology of hypoxia, and the control of breathing. Before the lungs can enable gas exchange, air must move from the upper airway down a series of branching small airways and reach the alveoli. In the walls of the alveoli, capillaries form a dense network and receive blood flowing from the pulmonary artery before it flows to the pulmonary vein. Between the capillary network and the alveoli lies a thin blood-gas barrier through which oxygen and carbon dioxide move, chiefly by simple diffusion.
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Maher, Barbara A. "Airborne Magnetite- and Iron-Rich Pollution Nanoparticles: Potential Neurotoxicants and Environmental Risk Factors for Neurodegenerative Disease, Including Alzheimer’s Disease." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210006.

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Fewer than 5% of Alzheimer’s disease (AD) cases are demonstrably directly inherited, indicating that environmental factors may be important in initiating and/or promoting the disease. Excess iron is toxic to cells; iron overload in the AD brain may aggressively accelerate AD. Magnetite nanoparticles, capable of catalyzing formation of reactive oxygen species, occur in AD plaques and tangles; they are thought to form in situ, from pathological iron dysfunction. A recent study has identified in frontal cortex samples the abundant presence of magnetite nanoparticles consistent with high-temperature formation; identifying therefore their external, not internal source. These magnetite particles range from ∼10 to 150 nm in size, and are often associated with other, non-endogenous metals (including platinum, cadmium, cerium). Some display rounded crystal morphologies and fused surface textures, reflecting cooling and crystallization from an initially heated, iron-bearing source material. Precisely-matching magnetite ‘nanospheres’ occur abundantly in roadside air pollution, arising from vehicle combustion and, especially, frictional brake-wear. Airborne magnetite pollution particles <∼200 nm in size can access the brain directly via the olfactory and/or trigeminal nerves, bypassing the blood-brain barrier. Given their toxicity, abundance in roadside air, and nanoscale dimensions, traffic-derived magnetite pollution nanoparticles may constitute a chronic and pernicious neurotoxicant, and hence an environmental risk factor for AD, for large population numbers globally. Olfactory nerve damage displays strong association with AD development. Reported links between AD and occupational magnetic fields (e.g., affecting welders, machinists) may instead reflect inhalation exposure to airborne magnetic nanoparticles.
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Hajirasouliha, Farzaneh, and Dominika Zabiegaj. "Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences." In Environmental Emissions. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.92451.

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Human health has been affected adversely by air pollution as a serious environmental challenge. Ambient (outdoor) air pollution mainly resulted from human activities (e.g., fuel combustion, heat generation, industrial facilities) causes 4.2 million deaths every year. Moreover, each year, 3.8 million people die from indoor air pollution which means household exposure to smoke from fuels and dirty cook stoves. They are the risks of stroke, heart attack, lung disease, or cancer that resulted from air pollution which assaults our brain, heart, and lungs using its invisible weapons named particulate matter (PM). These inhalable particles are of a nanoscale or microscale size. Upon inhalation, the air with its components enters the human body through the respiratory system. The lungs are the responsible organs for gas exchange with blood. Inhaled particles, such as silica, organic compounds, and metallic dusts, have toxic effects on our pulmonary system. For example, the accumulation of nanoparticles in the kidneys, liver, spleen, and central nervous system through the penetration of the epithelial barriers in the lungs has been observed. The purpose of this chapter is to describe the toxic effects of air particles on the different organs in the human body and to introduce some of the adverse effects of air pollution on human health.
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Hajirasouliha, Farzaneh, and Dominika Zabiegaj. "Effects of Environmental Emissions on the Respiratory System: Secrets and Consequences." In Environmental Emissions. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.92451.

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Human health has been affected adversely by air pollution as a serious environmental challenge. Ambient (outdoor) air pollution mainly resulted from human activities (e.g., fuel combustion, heat generation, industrial facilities) causes 4.2 million deaths every year. Moreover, each year, 3.8 million people die from indoor air pollution which means household exposure to smoke from fuels and dirty cook stoves. They are the risks of stroke, heart attack, lung disease, or cancer that resulted from air pollution which assaults our brain, heart, and lungs using its invisible weapons named particulate matter (PM). These inhalable particles are of a nanoscale or microscale size. Upon inhalation, the air with its components enters the human body through the respiratory system. The lungs are the responsible organs for gas exchange with blood. Inhaled particles, such as silica, organic compounds, and metallic dusts, have toxic effects on our pulmonary system. For example, the accumulation of nanoparticles in the kidneys, liver, spleen, and central nervous system through the penetration of the epithelial barriers in the lungs has been observed. The purpose of this chapter is to describe the toxic effects of air particles on the different organs in the human body and to introduce some of the adverse effects of air pollution on human health.
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González-Maciel, Angélica, Rafael Reynoso-Robles, Ricardo Torres-Jardón, Partha S. Mukherjee, and Lilian Calderón-Garcidueñas. "Combustion-Derived Nanoparticles in Key Brain Target Cells and Organelles in Young Urbanites: Culprit Hidden in Plain Sight in Alzheimer’s Disease Development." In Advances in Alzheimer’s Disease. IOS Press, 2021. http://dx.doi.org/10.3233/aiad210005.

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Millions of children and young adults are exposed to fine particulate matter (PM2.5) and ozone, associated with Alzheimer’s disease (AD) risk. Mexico City (MC) children exhibit systemic and brain inflammation, low cerebrospinal fluid (CSF) Aβ1-42, breakdown of nasal, olfactory, alveolar-capillary, duodenal, and blood-brain barriers, volumetric and metabolic brain changes, attention and short-term memory deficits, and hallmarks of AD and Parkinson’s disease. Airborne iron-rich strongly magnetic combustion-derived nanoparticles (CDNPs) are present in young urbanites’ brains. Using transmission electron microscopy, we documented CDNPs in neurons, glia, choroid plexus, and neurovascular units of young MC residents versus matched clean air controls. CDNPs are associated with pathology in mitochondria, endoplasmic reticulum (ER), mitochondria-ER contacts (MERCs), axons,and dendrites. There is a significant difference in size and numbers between spherical CDNPs (>85%) and the angular, euhedral endogenous NPs (<15%). Spherical CDNPs (dogs 21.2 ± 7.1 nm in diameter versus humans 29.1 ± 11.2 nm, p = 0.002) are present in neurons, glia, choroid plexus, endothelium, nasal and olfactory epithelium, and in CSF at significantly higher in numbers in MC residents (p < 0.0001). Degenerated MERCs, abnormal mitochondria, and dilated ER are widespread, and CDNPs in close contact with neurofilaments, glial fibers, and chromatin are a potential source for altered microtubule dynamics, mitochondrial dysfunction, accumulation and aggregation of unfolded proteins, abnormal endosomal systems, altered insulin signaling, calcium homeostasis, apoptotic signaling, autophagy, and epigenetic changes. Highly oxidative, ubiquitous CDNPs constitute a novel path into AD pathogenesis. Exposed children and young adults need early neuroprotection and multidisciplinary prevention efforts to modify the course of AD at early stages.
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Conference papers on the topic "Air-blood barrier"

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Fridman, G., M. Peddinghaus, H. Ayan, A. Fridman, M. Balasubramanian, A. Gutsol, A. Brooks, and G. Friedman. "Blood coagulation and living tissue sterilization by floating-electrode dielectric barrier discharge in air." In The 33rd IEEE International Conference on Plasma Science, 2006. ICOPS 2006. IEEE Conference Record - Abstracts. IEEE, 2006. http://dx.doi.org/10.1109/plasma.2006.1707305.

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Zamprogno, Pauline, Simon Wüthrich, Sven Achenbach, Janick D. Stucki, Nina Hobi, Nicole Schneider-Daum, Claus-Michael Lehr, et al. "Lung-on-a-chip with a biological, stretchable membrane: New generation of in-vitro air-blood barrier model." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa1904.

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Hendrix, Remi, Stephanie Kletting, Cristiane Carvalho-Wodarz, Nicole Schneider-Daum, and Claus-Michael Lehr. "LSC Abstract – Modeling the air-blood barrier in healthy and disease state to evaluate safety and efficacy of inhaled (nano)medicines." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pp116.

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Shafahi, Maryam, and Kambiz Vafai. "Thermal Modeling of the Human Eye as a Porous Structure." In ASME 2009 Heat Transfer Summer Conference collocated with the InterPACK09 and 3rd Energy Sustainability Conferences. ASMEDC, 2009. http://dx.doi.org/10.1115/ht2009-88138.

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Human eye is one of the most sensitive parts of the body when exposed to radiation effects. Since there is no barrier (such as skin) to protect the eye against the absorption of the external thermal waves, radiation can readily interact with cornea. On the other hand, lack of blood flow in the interior part of the eye makes it more vulnerable compared to other organs even in the case of weak heat interaction. Further, blood flow circulation alone cannot establish thermal equilibrium between the eye and body organs effectively. There are limitations in measuring human eye temperature profile experimentally due to the required invasive procedures in monitoring the inner layers. Therefore, there is a need to develop an accurate model to represent the eye structure and energy transport through it. Thermal modeling of the eye is important to investigate the effect of external heat sources as well as in predicting the abnormalities within the eye. Modeling of heat transport through the human eye has been the subject of interest for years, but the application of porous media models in this field is new and will be one of the themes of this study. In this work, iris/sclear is considered as a porous medium and energy transport is modeled using the tissue local thermal equilibrium equations. The eye is assumed to include six different parts: cornea, anterior chamber, posterior chamber, iris/sclera, lens and vitreous. A two-dimensional finite element simulation will be performed. Results are shown in terms of transient corneal surface temperature, isothermal lines in different regions and local temperature of pupillary axis. Effects of external radiation sources, convection coefficient of the surrounding air, blood temperature, blood convection coefficient and ambient temperature on different regions of the eye are also investigated.
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Javadpour, Sina, Fereidoon Delfanian, and Khaled Saadeddin. "Numerical Simulations of Airborne Particle Removal Rates for Air-Ventilated Spaces of Different Obstacle Setups." In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-67004.

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As a result of industrialization, human activities and consequently the time spent in indoor spaces has significantly increased. As airborne particles, especially those of relatively small sizes (less than 2 μm), can easily enter human respiratory tract and cross the thin air-blood barrier inside the lungs, necessary measures need to be taken to minimize exposure to these particles. In this study numerical simulations were done by coupling the “Laminar” and “Turbulent Flow” and the “Particle Tracing for Fluid Flow” interfaces in COMSOL Multiphysics to investigate the effects of obstacle setup on air flow profile and particle removal rate in a confined space of an air-ventilated office using 3D models. Particle tracing for fluid flow was used with a Newtonian formulation to simulate and trace particles with diameter of 0.5 μm and density of 1086 kg/m3. A total of 100,000 particles were simulated to reduce the uncertainty in particle concentration calculations and also to yield statistically more accurate results. Simulations were done for a control model with no obstacles, and 3 other models of different obstacle setups in a cubic room of 2.5 m * 4 m * 1 m with the same inlet and outlet configurations and a maximum interval of 180 minutes (3 hours). All cases had a monodisperse particle distribution, where particles were released transiently and evenly distributed through the entire space at the initial time step (t = 0 min). All models reached a steady-state stage after 180 minutes, with the remaining particles circulating and trapped. Analyzing the results revealed that a positive correlation exists between path-length and particle removal rate. Thus, it was concluded that an obstacle orientation and setup leading to increased flow path-length would greatly enhance the particle removal rate and pollutant dilution. Also, regions of recirculation and stagnation proved to have a negative impact on particle removal by trapping the particles and hence should be avoided in obstacle configuration.
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6

Mendoza, Eduardo, Jean-pierre Cooper, John W. Evangelista, Margaret Auerbach, and Özer Arnas. "On Demand Thermal Protection (ODTP): A New Approach for Designing Garments Exposed to Flash Flame Incidents." In ASME 2012 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/imece2012-87999.

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Abstract:
Soldiers, first responders and other high risk occupations such as power line technicians are routinely exposed to dangerous situations where severe burn injuries are possible. Standard flame resistant (FR) fabrics provide minimal burn protection when exposed to a flash flame incident. As a result, improvement in thermal protection is desperately needed and remains an ongoing subject of research and development. A simplified one dimensional physical model composed of a muscle layer, skin/fat layer, air gap(s) and fabric layer(s) is used to model heat transfer entering the body covered by a garment that is exposed to a flash flame. Heat transfer within the skin and muscle layers is modeled by combined conduction, metabolic heat generation and blood perfusion by a recently developed modification to the heat equation termed the bio-heat equation. Boundary conditions include a fixed temperature (core body temperature) at the inside of the muscle layer and combined convection and radiation from the flame on the outside of the fabric. The heat equation is solved by discretizing the domain in one dimension and using a finite volume approach to derive the finite difference equations. This model is an initial step to be used to provide an assessment of common FR garments with respect to both comfort in ambient conditions and protection during a flash flame. It also provides for parametric analysis to determine ideal thermo-physical properties, fabric thicknesses and layering for better protection during flash flame incidents. Estimates for time to burn injury from the numerical model is presented with experimental results using live mannequin flame tests (ASTMF-1930), standard vertical flame tests (ISO-17492) and a non-standard flame test with combined convection and radiation heat fluxes up to 85 kW/m2. The main effort of this study revolves around an initial working design for a dynamic garment termed On Demand Thermal Protection (ODTP). The primary focus of the design is the development of a thermistor circuit embedded in a protective garment to act as an electric sensor for rapidly deploying the necessary thermal protection that is needed as predicted by the numerical model instantaneously in the event of a flash flame incident. An initial prototype is being developed with a focus on designing the thermistor circuit to mechanically actuate protective components in a flash-flame environment. Concepts include rapidly releasing a pressurized flame retardant fluid through vinyl tubing sewn into a garment and deploying a protective barrier around the face and neck when the thermistor circuit detects a sudden change in heat transfer. A summary of the prototype along with experimental testing to date compared to the theoretical predictions from the model described above is presented.
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