Journal articles: 'Air-blood barrier'

1

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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10

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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Seredenko, M. M., A. A. Moibenko, E. V. Rozova, and L. A. Grabovskii. "Changes in the air-blood barrier of the lungs during hyperthermia." Bulletin of Experimental Biology and Medicine 106, no. 2 (August 1988): 1189–92. http://dx.doi.org/10.1007/bf00840398.

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12

Conforti, Elena, Carla Fenoglio, Graziella Bernocchi, Ombretta Bruschi, and Giuseppe A. Miserocchi. "Morpho-functional analysis of lung tissue in mild interstitial edema." American Journal of Physiology-Lung Cellular and Molecular Physiology 282, no. 4 (April 1, 2002): L766—L774. http://dx.doi.org/10.1152/ajplung.00313.2001.

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Mild pulmonary interstitial edema was shown to cause fragmentation of interstitial matrix proteoglycans. We therefore studied compartmental fluid accumulation by light and electron microscopy on lungs of anesthetized rabbits fixed in situ by vascular perfusion after 0.5 ml · kg−1 · min−1 iv saline infusion for 180 min causing ∼6% increase in lung weight. Morphometry showed that a relevant portion (44%) of extravascular fluid is detected early in the alveolar septa, 85% of this fluid accumulating in the thick portion of the air-blood barrier. The arithmetic mean thickness of the barrier increased in interstitial edema from 1.06 ± 0.05 (SE) to 1.33 ± 0.06 μm. The harmonic mean thickness increased from 0.6 ± 0.03 to 0.86 ± 0.07 μm, mostly due to thickening of the thin portion causing an increase in gas diffusion resistance. Despite some structural damage, the air-blood barrier displays a relatively high structural resistance providing a safety factor against the development of severe edema. It is suggested that the increase in extra-alveolar perivascular space occurs as a consequence of fluid accumulation in the air-blood barrier.

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Schulze, Christine, Ulrich F. Schaefer, Matthias Voetz, Wendel Wohlleben, Cornel Venzago, and Claus-Michael Lehr. "Transport of Metal Oxide Nanoparticles Across Calu-3 Cell Monolayers Modelling the Air-Blood Barrier." EURO-NanoTox-Letters 3, no. 1 (December 1, 2011): 1–10. http://dx.doi.org/10.1515/entl-2015-0003.

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Abstract As inhalation is the major exposure route for nanoparticles, the question if inhaled particles can overcome the respiratory epithelial barrier and hence enter the body is of great interest. Here, we adapted the for soluble substances well established Calu-3 in vitro air-blood barrier model to the use of nanoparticle transport testing. As the usually used filter supports hindered particle transport due to their small pore size, supports with a pore size of 3 μm had to be used. On those filters, barrier and transport characteristics of the cells were tested and culture conditions changed to obtain optimal conditions. Functionality was confirmed with transport experiments with polystyrene model particles prior to testing of industrially relevant engineered metal oxide particles. Except for CeO2 nanoparticles, no transport across the epithelial barrier model could be detected. Paracellular permeability and barrier function was not affected by any of the nanoparticles, except for ZrO2.

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Barni, Sergio, Franco Bernini, and Paola De Piceis Polver. "Ultrastructural changes of the air-blood barrier in the lung of Rana esculenta during natural hibernation." Amphibia-Reptilia 17, no. 2 (1996): 141–47. http://dx.doi.org/10.1163/156853896x00171.

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AbstractPossible changes of the air-blood barrier in naturally hibernating frogs were examined by transmission electron microscopy and measured with an eye-piece micrometer under light microscopy. During hibernation a reduction of the "alveolar" air-space and a folding of the air-blood barrier were noticed: the thickness of the latter in the deep lung septa was double that seen in the active phase, as a consequence of deeper changes of the interstitial and surface epithelial components. An increase in electron-dense multilamellar bodies inside the pneumocyte cytoplasm was also observed. These morphological characteristics are indicative of a hypofunctionality in the lung respiratory components and may be related to a decrease in oxygen consumption during this quiescent phase of the annual life cycle.

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15

West, John B. "Comparative physiology of the pulmonary blood-gas barrier: the unique avian solution." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 297, no. 6 (December 2009): R1625—R1634. http://dx.doi.org/10.1152/ajpregu.00459.2009.

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Two opposing selective pressures have shaped the evolution of the structure of the blood-gas barrier in air breathing vertebrates. The first pressure, which has been recognized for 100 years, is to facilitate diffusive gas exchange. This requires the barrier to be extremely thin and have a large area. The second pressure, which has only recently been appreciated, is to maintain the mechanical integrity of the barrier in the face of its extreme thinness. The most important tensile stress comes from the pressure within the pulmonary capillaries, which results in a hoop stress. The strength of the barrier can be attributed to the type IV collagen in the extracellular matrix. In addition, the stress is minimized in mammals and birds by complete separation of the pulmonary and systemic circulations. Remarkably, the avian barrier is about 2.5 times thinner than that in mammals and also is much more uniform in thickness. These advantages for gas exchange come about because the avian pulmonary capillaries are unique among air breathers in being mechanically supported externally in addition to the strength that comes from the structure of their walls. This external support comes from epithelial plates that are part of the air capillaries, and the support is available because the terminal air spaces in the avian lung are extremely small due to the flow-through nature of ventilation in contrast to the reciprocating pattern in mammals.

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Maina, John N., and John B. West. "Thin and Strong! The Bioengineering Dilemma in the Structural and Functional Design of the Blood-Gas Barrier." Physiological Reviews 85, no. 3 (July 2005): 811–44. http://dx.doi.org/10.1152/physrev.00022.2004.

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In gas exchangers, the tissue barrier, the partition that separates the respiratory media (water/air and hemolymph/blood), is exceptional for its remarkable thinness, striking strength, and vast surface area. These properties formed to meet conflicting roles: thinness was essential for efficient flux of oxygen by passive diffusion, and strength was crucial for maintaining structural integrity. What we have designated as “three-ply” or “laminated tripartite” architecture of the barrier appeared very early in the evolution of the vertebrate gas exchanger. The design is conspicuous in the water-blood barrier of the fish gills through the lungs of air-breathing vertebrates, where the plan first appeared in lungfishes (Dipnoi) some 400 million years ago. The similarity of the structural design of the barrier in respiratory organs of animals that remarkably differ phylogenetically, behaviorally, and ecologically shows that the construction has been highly conserved both vertically and horizontally, i.e., along and across the evolutionary continuum. It is conceivable that the blueprint may have been the only practical construction that could simultaneously grant satisfactory strength and promote gas exchange. In view of the very narrow allometric range of the thickness of the blood-gas barrier in the lungs of different-sized vertebrate groups, the measurement has seemingly been optimized. There is convincing, though indirect, evidence that the extracellular matrix and particularly the type IV collagen in the lamina densa of the basement membrane is the main stress-bearing component of the blood-gas barrier. Under extreme conditions of operation and in some disease states, the barrier fails with serious consequences. The lamina densa which in many parts of the blood-gas barrier is <50 nm thin is a lifeline in the true sense of the word.

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Fakhri, Yadolah. "Association Between Fine Particulate Matter (PM2.5) and the Reproductive System: A Narrative Review." Journal of Clinical and Nursing Research 6, no. 3 (May 30, 2022): 190–96. http://dx.doi.org/10.26689/jcnr.v6i3.3761.

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In the last two decades, the issue on exposure to air pollution, especially fine particulate matter (PM2.5), and its health effects has been a global concern. PM2.5 can enter the bronchi, lung cells, and subsequently the body, thus causing adverse health effects. One of these health effects include damage to the reproductive system. However, this has not gained much attention. In addition, PM2.5 contain toxic compounds, such as heavy metals or PAHs, which can cross various barriers, including epithelial barrier and blood-testis barrier, causing hormonal disorders in both, men and women, thus resulting in infertility. In this review, an attempt was made to provide useful information about effects of PM2.5 on the reproductive system.

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Al-Kadhomiy, N. K., and G. M. Hughes. "Histological study of different regions of the skin and gills in the mudskipper, Boleophthalmus boddarti with respect to their respiratory function." Journal of the Marine Biological Association of the United Kingdom 68, no. 3 (August 1988): 413–22. http://dx.doi.org/10.1017/s0025315400043319.

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Gills are the typical respiratory organ of fish in their usual habitat of well-aerated water. The transition from water- to air-breathing required many modifications to the structural and physiological adaptations of the gas-exchange surfaces, i.e. gill, skin, swimbladder and other accessory organs of the alimentary canal. The skin is particularly important among air-breathing fish. This histological study showed varying degrees of adaptation of parts of the skin from different body regions, paying particular attention to the water/blood barrier. The results suggest a general importance in gas exchange in the following order: gill, inner operculum, nasal, body and outer opercular skin, as indicated by increasing thickness of the water/blood barrier.

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Bao, Jun, Shanjun Tan, Wenkui Yu, Zhiliang Lin, Yi Dong, Qiyi Chen, Jialiang Shi, et al. "The Effect of Peritoneal Air Exposure on Intestinal Mucosal Barrier." Gastroenterology Research and Practice 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/674875.

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Background. Damage of the intestinal mucosa barrier may result in intestinal bacterial and endotoxin translocation, leading to local and systemic inflammation. The present study was designed to investigate whether peritoneal air exposure induces damage of intestinal mucosal barrier.Methods. Sprague-Dawley rats (weighing 210 to 230 g) were randomized into five groups (6/group): a control group, a sham group, and three exposure groups with peritoneal air exposure for 1, 2, and 3 h, respectively. At 24 h after surgery, blood and terminal ileum were sampled. The serum D-lactate levels were determined using an ELISA kit. The intestinal permeability was determined by measuring the intestinal clearance of FITC-dextran (FD4). The histopathological changes in terminal ileum were also assessed.Results. Compared with the controls, peritoneal air exposure caused an increase in both serum D-lactate level and intestinal FD4 clearance, which were proportional to the length of peritoneal air exposure and correlated to Chiu’s scores, indices for intestinal mucosal injury. Edema and inflammatory cells were also observed in mucosa and submucosa of ileum in three exposure groups.Conclusions. Peritoneal air exposure could induce damage to the intestinal mucosal barrier, which is proportional to the time length of peritoneal air exposure.

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Metcalfe, Su M. "LIF and the lung’s stem cell niche: is failure to use LIF to protect against COVID-19 a grave omission in managing the pandemic?" Future Virology 15, no. 10 (October 2020): 659–62. http://dx.doi.org/10.2217/fvl-2020-0340.

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Beretta, Egidio, Francesca Lanfranconi, Gabriele Simone Grasso, Manuela Bartesaghi, Hailu Kinfu Alemayehu, Lorenza Pratali, Bruna Catuzzo, Guido Giardini, and Giuseppe Miserocchi. "Air blood barrier phenotype correlates with alveolo-capillary O 2 equilibration in hypobaric hypoxia." Respiratory Physiology & Neurobiology 246 (December 2017): 53–58. http://dx.doi.org/10.1016/j.resp.2017.08.006.

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Kreyling, Wolfgang G., Stephanie Hirn, Winfried Möller, Carsten Schleh, Alexander Wenk, Gülnaz Celik, Jens Lipka, et al. "Air–Blood Barrier Translocation of Tracheally Instilled Gold Nanoparticles Inversely Depends on Particle Size." ACS Nano 8, no. 1 (December 30, 2013): 222–33. http://dx.doi.org/10.1021/nn403256v.

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Bräuner, Elvira Vaclavik, Jann Mortensen, Peter Møller, Alfred Bernard, Peter Vinzents, Peter Wåhlin, Marianne Glasius, and Steffen Loft. "Effects of Ambient Air Particulate Exposure on Blood–Gas Barrier Permeability and Lung Function." Inhalation Toxicology 21, no. 1 (January 2009): 38–47. http://dx.doi.org/10.1080/08958370802304735.

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Fridman, Gregory, Marie Peddinghaus, Manjula Balasubramanian, Halim Ayan, Alexander Fridman, Alexander Gutsol, and Ari Brooks. "Blood Coagulation and Living Tissue Sterilization by Floating-Electrode Dielectric Barrier Discharge in Air." Plasma Chemistry and Plasma Processing 26, no. 4 (June 15, 2006): 425–42. http://dx.doi.org/10.1007/s11090-006-9024-4.

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Fridman, Gregory, Marie Peddinghaus, Manjula Balasubramanian, Halim Ayan, Alexander Fridman, Alexander Gutsol, Ari Brooks, and Gary Friedman. "Blood Coagulation and Living Tissue Sterilization by Floating-Electrode Dielectric Barrier Discharge in Air." Plasma Chemistry and Plasma Processing 27, no. 1 (November 5, 2006): 113–14. http://dx.doi.org/10.1007/s11090-006-9038-y.

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Zhang, Dan, Chichi Li, Jian Zhou, Yuanlin Song, Xiaocong Fang, Jiaxian Ou, Jing Li, and Chunxue Bai. "Autophagy protects against ischemia/reperfusion-induced lung injury through alleviating blood–air barrier damage." Journal of Heart and Lung Transplantation 34, no. 5 (May 2015): 746–55. http://dx.doi.org/10.1016/j.healun.2014.12.008.

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Huang, Longfei, Lijuan Yang, Jianfang Liu, and Xiaojuan Cao. "Comparative Histological Analysis of Intestines of Loach, Grass Carp and Catfish Provide Insights into Adaptive Characteristics in Air-Breathing Fish." Croatian Journal of Fisheries 78, no. 2 (June 1, 2020): 91–98. http://dx.doi.org/10.2478/cjf-2020-0009.

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AbstractAccessory respiratory is generally accepted to have evolved independently on numerous occasions in adaption to aquatic hypoxia in freshwater habitats. In general, the air-breathing organ in fish is believed to be structurally modified to supplement respiration. In this study, intuitive evidence for elaborate structural modifications of the intestine, an air-breathing organ in mud loach (Misgurnus anguillicaudatus), compared with two other obligate aquatic breathers, grass carp (Ctenopharyngodon idellus) and yellow catfish (Pelteobagrus fulvidraco), were directly provided by histological and morphometric methods. As a result, a sharply decreasing height of mucosal folds and thickness of muscularis were manifested in loach intestine from its anterior to posterior region. Compared with grass carp and yellow catfish, loach had the smallest ratios of mucosal fold height/muscularis thickness to intestinal lumen radius in the posterior intestine. These suggested that the posterior intestine is the air-breathing location for the loach. Furthermore, length density of capillary (0.46±0.05 μm−2) in the posterior intestine of the loach was significantly higher than those of grass carp and yellow catfish. Meanwhile, diffusion distance of air-blood barrier (1.34±0.04 μm) in the posterior intestine of the loach was significantly smaller than those of the other two fish species. In summary, the characteristics of highly vascularized, short diffusion distance of air-blood barrier, thinned and flattened made the posterior intestine a perfect air-breathing location for the loach.

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Mokhtar, Doaa M., Manal T. Hussein, Marwa M. Hussein, Enas A. Abd-Elhafez, and Gamal Kamel. "New Insight into the Development of the Respiratory Acini in Rabbits: Morphological, Electron Microscopic Studies, and TUNEL Assay." Microscopy and Microanalysis 25, no. 3 (February 14, 2019): 769–85. http://dx.doi.org/10.1017/s1431927619000059.

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AbstractThis study investigated the histomorphological features of developing rabbit respiratory acini during the postnatal period. On the 1st day of postnatal life, the epithelium of terminal bronchiole consisted of clear cells which intercalated between few ciliated and abundant non-ciliated (Clara) cells. At this age, the rabbit lung was in the alveolar stage. The terminal bronchioles branched into several alveolar ducts, which opened into atria that communicated to alveolar sacs. All primary and secondary inter-alveolar septa were thick and showed a double-capillary network (immature septa). The primitive alveoli were lined largely by type-I pneumocytes and mature type-II pneumocytes. The type-I pneumocytes displayed an intimate contact with the endothelial cells of the blood capillaries forming the blood–air barrier (0.90 ± 0.03 µm in thickness). On the 3rd day, we observed intense septation and massive formation of new secondary septa giving the alveolar sac a crenate appearance. The mean thickness of the air–blood barrier decreased to reach 0.78 ± 0.14 µm. On the 7th day, the terminal bronchiole epithelium consisted of ciliated and non-ciliated cells. The non-ciliated cells could be identified as Clara cells and serous cells. New secondary septa were formed, meanwhile the inter-alveolar septa become much thinner and the air–blood barrier thickness was 0.66 ± 0.03 µm. On the 14th day, the terminal bronchiole expanded markedly and the pulmonary alveoli were thin-walled. Inter-alveolar septa become much thinner and single capillary layers were observed. In the 1st month, the secondary septa increased in length forming mature cup-shaped alveoli. In the 2nd month, the lung tissue grew massively to involve the terminal respiratory unit. In the 3rd month, the pulmonary parenchyma appeared morphologically mature. All inter-alveolar septa showed a single-capillary layer, and primordia of new septa were also observed. The thickness of the air–blood barrier was much thinner; 0.56 ± 0.16 µm. TUNEL assay after birth revealed that the apoptotic cells were abundant and distributed in the epithelium lining of the pulmonary alveoli and the interstitium of the thick interalveolar septa. On the 7th day, and onward, the incidence of apoptotic cells decreased markedly. This study concluded that the lung development included two phases: the first phase (from birth to the 14th days) corresponds to the period of bulk alveolarization and microvascular maturation. The second phase (from the 14th days to the full maturity) corresponds to the lung growth and late alveolarization.

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Namba, Y., S. S. Kurdak, Z. Fu, O. Mathieu-Costello, and J. B. West. "Effect of reducing alveolar surface tension on stress failure in pulmonary capillaries." Journal of Applied Physiology 79, no. 6 (December 1, 1995): 2114–21. http://dx.doi.org/10.1152/jappl.1995.79.6.2114.

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We previously showed that when pulmonary capillaries are exposed to high transmural pressures, stress failure of the blood-gas barrier occurs. It has been suggested that the surface tension of the alveolar lining layer may protect against stress failure because at high transmural pressures the capillaries bulge into the alveolar spaces. To test this hypothesis, we abolished the gas-liquid surface tension of the alveoli by filling rabbit lungs with normal saline. The lungs were then perfused at capillary transmural pressures of 32.5 or 52.5 cmH2O for 1 min with autologous blood, the blood was washed out with a saline-dextran mixture (3 min), and the lungs were fixed for electron microscopy with buffered glutaraldehyde; all perfusions were done at the same pressure. The frequency of breaks was measured in the capillary endothelial layer, alveolar epithelial layer, and basement membranes, and the data were compared with those in air-filled lungs at the same capillary transmural pressure and lung volume. We found that the frequency of breaks in the endothelium was not significantly different between air and saline filling and that there were fewer breaks in the outer boundary of the epithelial cells. By contrast, after saline filling, a larger number of breaks were seen in the inner boundary of the epithelium. The frequency of disruptions of the inner boundary of the epithelium was closely correlated with the volume of edema fluid collected at the trachea during the perfusion. These breaks in the inner boundary of the epithelium had not previously been seen in air-filled lungs exposed to the same pressures. The results suggest that abolishing the surface tension of the alveolar lining layer removes support from parts of the blood-gas barrier when the capillaries are subjected to a high transmural pressure but that not all portions of the barrier are subjected to the same forces.

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Salomon, Johanna Jessica, and Carsten Ehrhardt. "Organic cation transporters in the blood–air barrier: expression and implications for pulmonary drug delivery." Therapeutic Delivery 3, no. 6 (June 2012): 735–47. http://dx.doi.org/10.4155/tde.12.51.

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Meng, Ge, Jian Zhao, He‐Mei Wang, Ri‐Gao Ding, Xian‐Cheng Zhang, Chun‐Qian Huang, and Jin‐Xiu Ruan. "Cell Injuries of the Blood‐Air Barrier in Acute Lung Injury Caused by Perfluoroisobutylene Exposure." Journal of Occupational Health 52, no. 1 (January 2010): 48–57. http://dx.doi.org/10.1539/joh.l9047.

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Palestini, Paola, Chiara Calvi, Elena Conforti, Rossella Daffara, Laura Botto, and Giuseppe Miserocchi. "Compositional changes in lipid microdomains of air-blood barrier plasma membranes in pulmonary interstitial edema." Journal of Applied Physiology 95, no. 4 (October 2003): 1446–52. http://dx.doi.org/10.1152/japplphysiol.00208.2003.

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We evaluated in anesthetized rabbits the compositional changes of plasmalemmal lipid microdomains from lung tissue samples after inducing pulmonary interstitial edema (0.5 ml/kg for 3 h, leading to ∼5% increase in extravascular water). Lipid microdomains (lipid rafts and caveolae) were present in the detergent-resistant fraction (DRF) obtained after discontinuous sucrose density gradient. DRF was enriched in caveolin-1, flotillin, aquaporin-1, GM1, cholesterol, sphingomyelin, and phosphatidylserine, and their contents significantly increased in interstitial edema. The higher DRF content in caveolin, flotillin, and aquaporin-1 and of the ganglioside GM1 suggests an increase both in caveolar domains and in lipid rafts, respectively. Compositional changes could be ascribed to endothelial and epithelial cells that provide most of plasma membrane surface area in the air-blood barrier. Alterations in lipid components in the plasma membrane may reflect rearrangement of floating lipid platforms within the membrane and/or lipid translocation from intracellular stores. Lipid traffic could be stimulated by the marked increase in hydraulic interstitial pressure after initial water accumulation, from approximately -10 to 5 cmH2O, due to the low compliance of the pulmonary tissue, in particular in the basement membranes and in the interfibrillar substance. Compositional changes in lipid microdomains represent a sign of cellular activation and suggest the potential role of mechanotransduction in response to developing interstitial edema.

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Bengalli, Rossella, Paride Mantecca, Marina Camatini, and Maurizio Gualtieri. "Effect of Nanoparticles and Environmental Particles on a Cocultures Model of the Air-Blood Barrier." BioMed Research International 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/801214.

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Exposure to engineered nanoparticles (NPs) and to ambient particles (PM) has increased significantly. During the last decades the application of nano-objects to daily-life goods and the emissions produced in highly urbanized cities have considerably augmented. As a consequence, the understanding of the possible effects of NPs and PM on human respiratory system and particularly on the air-blood barrier (ABB) has become of primary interest. The crosstalk between lung epithelial cells and underlying endothelial cells is indeed essential in determining the effects of inhaled particles. Here we report the effects of metal oxides NPs (CuO and TiO2) and of PM on anin vitromodel of the ABB constituted by the type II epithelial cell line (NCI-H441) and the endothelial one (HPMEC-ST1.6R). The results demonstrate that apical exposure of alveolar cells induces significant modulation of proinflammatory proteins also in endothelial cells.

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Bengalli, R., M. Gualtieri, M. Camatini, C. Urani, and P. Mantecca. "Effects of zinc oxide nanoparticles on an in vitro model of the air–blood barrier." Toxicology Letters 221 (August 2013): S241. http://dx.doi.org/10.1016/j.toxlet.2013.05.593.

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Cevik, Nihal Gunes, Nurcan Orhan, Canan Ugur Yilmaz, Nadir Arican, Bulent Ahishali, Mutlu Kucuk, Mehmet Kaya, and Akin Savas Toklu. "The effects of hyperbaric air and hyperbaric oxygen on blood–brain barrier integrity in rats." Brain Research 1531 (September 2013): 113–21. http://dx.doi.org/10.1016/j.brainres.2013.07.052.

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Zagorul'ko, A. K., A. A. Birkun, E. E. Fisik, and L. G. Safronova. "Changes in surfactant activity and ultrastructure of the air-blood barrier in experimental alcohol poisoning." Bulletin of Experimental Biology and Medicine 109, no. 5 (May 1990): 649–53. http://dx.doi.org/10.1007/bf00839892.

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Yao, Xiao-Hong, Tao Luo, Yu Shi, Zhi-Cheng He, Rui Tang, Pei-Pei Zhang, Jun Cai, et al. "A cohort autopsy study defines COVID-19 systemic pathogenesis." Cell Research 31, no. 8 (June 16, 2021): 836–46. http://dx.doi.org/10.1038/s41422-021-00523-8.

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AbstractSevere COVID-19 disease caused by SARS-CoV-2 is frequently accompanied by dysfunction of the lungs and extrapulmonary organs. However, the organotropism of SARS-CoV-2 and the port of virus entry for systemic dissemination remain largely unknown. We profiled 26 COVID-19 autopsy cases from four cohorts in Wuhan, China, and determined the systemic distribution of SARS-CoV-2. SARS-CoV-2 was detected in the lungs and multiple extrapulmonary organs of critically ill COVID-19 patients up to 67 days after symptom onset. Based on organotropism and pathological features of the patients, COVID-19 was divided into viral intrapulmonary and systemic subtypes. In patients with systemic viral distribution, SARS-CoV-2 was detected in monocytes, macrophages, and vascular endothelia at blood–air barrier, blood–testis barrier, and filtration barrier. Critically ill patients with long disease duration showed decreased pulmonary cell proliferation, reduced viral RNA, and marked fibrosis in the lungs. Permanent SARS-CoV-2 presence and tissue injuries in the lungs and extrapulmonary organs suggest direct viral invasion as a mechanism of pathogenicity in critically ill patients. SARS-CoV-2 may hijack monocytes, macrophages, and vascular endothelia at physiological barriers as the ports of entry for systemic dissemination. Our study thus delineates systemic pathological features of SARS-CoV-2 infection, which sheds light on the development of novel COVID-19 treatment.

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Frost, Timothy S., Linan Jiang, and Yitshak Zohar. "Pharmacokinetic Analysis of Epithelial/Endothelial Cell Barriers in Microfluidic Bilayer Devices with an Air–Liquid Interface." Micromachines 11, no. 5 (May 25, 2020): 536. http://dx.doi.org/10.3390/mi11050536.

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As the range of applications of organs-on-chips is broadening, the evaluation of aerosol-based therapies using a lung-on-a-chip model has become an attractive approach. Inhalation therapies are not only minimally invasive but also provide optimal pharmacokinetic conditions for drug absorption. As drug development evolves, it is likely that better screening through use of organs-on-chips can significantly save time and cost. In this work, bio-aerosols of various compounds including insulin were generated using a jet nebulizer. The aerosol flows were driven through microfluidic bilayer devices establishing an air–liquid interface to mimic the blood–air barrier in human small airways. The aerosol flow in the microfluidic devices has been characterized and adjusted to closely match physiological values. The permeability of several compounds, including paracellular and transcellular biomarkers, across epithelial/endothelial cell barriers was measured. Concentration–time plots were established in microfluidic devices with and without cells; the curves were then utilized to extract standard pharmacokinetic parameters such as the area under the curve, maximum concentration, and time to maximum concentration. The cell barrier significantly affected the measured pharmacokinetic parameters, as compound absorption through the barrier decreases with its increasing molecular size. Aerosolizing insulin can lead to the formation of fibrils, prior to its entry to the microfluidic device, with a substantially larger apparent molecular size effectively blocking its paracellular transport. The results demonstrate the advantage of using lung-on-a-chip for drug discovery with applications such as development of novel inhaled therapies.

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Sapich, Sandra, Marius Hittinger, Remi Hendrix-Jastrzebski, Urska Repnik, Gareth Griffiths, Tobias May, Dagmar Wirth, Robert Bals, Nicole Schneider-Daum, and Claus-Michael Lehr. "Murine Alveolar Epithelial Cells and Their Lentivirus-mediated Immortalisation." Alternatives to Laboratory Animals 46, no. 2 (May 2018): 73–89. http://dx.doi.org/10.1177/026119291804600207.

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In this study, we describe the isolation and immortalisation of primary murine alveolar epithelial cells (mAEpC), as well as their epithelial differentiation and barrier properties when grown on Transwell® inserts. Like human alveolar epithelial cells (hAEpC), mAEpC transdifferentiate in vitro from an alveolar type II (ATII) phenotype to an ATI-like phenotype and exhibit features of the air–blood barrier, such as the establishment of a thin monolayer with functional tight junctions (TJs). This is demonstrated by the expression of TJ proteins (ZO-1 and occludin) and the development of high transepithelial electrical resistance (TEER), peaking at 1800ω•cm2. Transport across the air–blood barrier, for general toxicity assessments or preclinical drug development, is typically studied in mice. The aim of this work was the generation of novel immortalised murine lung cell lines, to help meet Three Rs requirements in experimental testing and research. To achieve this goal, we lentivirally transduced mAEpC of two different mouse strains with a library of 33 proliferation-promoting genes. With this immortalisation approach, we obtained two murine alveolar epithelial lentivirus-immortalised (mAELVi) cell lines. Both showed similar TJ protein localisation, but exhibited less prominent barrier properties (TEERmax ~250Ω•cm2) when compared to their primary counterparts. While mAEpC demonstrated their suitability for use in the assessment of paracellular transport rates, mAELVi cells could potentially replace mice for the prediction of acute inhalation toxicity during early ADMET studies.

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Kasper, Jennifer Y., Lisa Feiden, Maria I. Hermanns, Christoph Bantz, Michael Maskos, Ronald E. Unger, and C. James Kirkpatrick. "Pulmonary surfactant augments cytotoxicity of silica nanoparticles: Studies on an in vitro air–blood barrier model." Beilstein Journal of Nanotechnology 6 (February 20, 2015): 517–28. http://dx.doi.org/10.3762/bjnano.6.54.

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The air–blood barrier is a very thin membrane of about 2.2 µm thickness and therefore represents an ideal portal of entry for nanoparticles to be used therapeutically in a regenerative medicine strategy. Until now, numerous studies using cellular airway models have been conducted in vitro in order to investigate the potential hazard of NPs. However, in most in vitro studies a crucial alveolar component has been neglected. Before aspirated NPs encounter the cellular air–blood barrier, they impinge on the alveolar surfactant layer (10–20 nm in thickness) that lines the entire alveolar surface. Thus, a prior interaction of NPs with pulmonary surfactant components will occur. In the present study we explored the impact of pulmonary surfactant on the cytotoxic potential of amorphous silica nanoparticles (aSNPs) using in vitro mono- and complex coculture models of the air–blood barrier. Furthermore, different surface functionalisations (plain-unmodified, amino, carboxylate) of the aSNPs were compared in order to study the impact of chemical surface properties on aSNP cytotoxicity in combination with lung surfactant. The alveolar epithelial cell line A549 was used in mono- and in coculture with the microvascular cell line ISO-HAS-1 in the form of different cytotoxicity assays (viability, membrane integrity, inflammatory responses such as IL-8 release). At a distinct concentration (100 µg/mL) aSNP–plain displayed the highest cytotoxicity and IL-8 release in monocultures of A549. aSNP–NH2 caused a slight toxic effect, whereas aSNP–COOH did not exhibit any cytotoxicity. In combination with lung surfactant, aSNP–plain revealed an increased cytotoxicity in monocultures of A549, aSNP–NH2 caused a slightly augmented toxic effect, whereas aSNP–COOH did not show any toxic alterations. A549 in coculture did not show any decreased toxicity (membrane integrity) for aSNP–plain in combination with lung surfactant. However, a significant augmented IL-8 release was observed, but no alterations in combination with lung surfactant. The augmented aSNP toxicity with surfactant in monocultures appears to depend on the chemical surface properties of the aSNPs. Reactive silanol groups seem to play a crucial role for an augmented toxicity of aSNPs. The A549 cells in the coculture seem to be more robust towards aSNPs, which might be a result of a higher differentiation and polarization state due the longer culture period.

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Viola, Hannah, Kendra Washington, Cauviya Selva, Jocelyn Grunwell, Rabindra Tirouvanziam, and Shuichi Takayama. "A High‐Throughput Distal Lung Air–Blood Barrier Model Enabled By Density‐Driven Underside Epithelium Seeding." Advanced Healthcare Materials 10, no. 15 (June 26, 2021): 2100879. http://dx.doi.org/10.1002/adhm.202100879.

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Viola, Hannah, Kendra Washington, Cauviya Selva, Jocelyn Grunwell, Rabindra Tirouvanziam, and Shuichi Takayama. "A High‐Throughput Distal Lung Air–Blood Barrier Model Enabled By Density‐Driven Underside Epithelium Seeding." Advanced Healthcare Materials 11, no. 1 (January 2022): 2102450. http://dx.doi.org/10.1002/adhm.202102450.

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Jackson, George, Courtney Mankus, Jonathan Oldach, Matthew Child, Maureen Spratt, Helena Kandarova, Seyoum Ayehunie, and Patrick Hayden. "A triple cell co-culture model of the air–blood barrier reconstructed from primary human cells." Toxicology Letters 221 (August 2013): S138. http://dx.doi.org/10.1016/j.toxlet.2013.05.270.

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Bengalli, Rossella, Maurizio Gualtieri, Laura Capasso, Chiara Urani, and Marina Camatini. "Impact of zinc oxide nanoparticles on an in vitro model of the human air-blood barrier." Toxicology Letters 279 (September 2017): 22–32. http://dx.doi.org/10.1016/j.toxlet.2017.07.877.

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Beretta, Egidio, Francesca Lanfranconi, Gabriele Simone Grasso, Manuela Bartesaghi, Hailu Kinfu Alemayehu, and Giuseppe Miserocchi. "Reappraisal of DLCO adjustment to interpret the adaptive response of the air-blood barrier to hypoxia." Respiratory Physiology & Neurobiology 238 (April 2017): 59–65. http://dx.doi.org/10.1016/j.resp.2016.08.009.

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Naota, Misaki, Akinori Shimada, Takehito Morita, Yuko Yamamoto, Kenichiro Inoue, and Hirohisa Takano. "Caveolae-mediated Endocytosis of Intratracheally Instilled Gold Colloid Nanoparticles at the Air–Blood Barrier in Mice." Toxicologic Pathology 41, no. 3 (August 23, 2012): 487–96. http://dx.doi.org/10.1177/0192623312457271.

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Tolkach, P. G., V. A. Basharin, S. V. Chepur, A. N. Gorshkov, and D. T. Sizova. "Ultrastructural Changes in the Air—Blood Barrier of Rats in Acute Intoxication with Furoplast Pyrolysis Products." Bulletin of Experimental Biology and Medicine 169, no. 2 (June 2020): 270–75. http://dx.doi.org/10.1007/s10517-020-04866-x.

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Zagorul'ko, A. K., and E. E. Fisik. "Ultrastructural morphology of the air-blood barrier and surfactant in experimental pneumonia superposed on alcohol poisoning." Bulletin of Experimental Biology and Medicine 111, no. 1 (January 1991): 103–7. http://dx.doi.org/10.1007/bf00841254.

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Kasper, Jennifer Y., Maria I. Hermanns, Ronald E. Unger, and C. James Kirkpatrick. "A responsive human triple-culture model of the air-blood barrier: incorporation of different macrophage phenotypes." Journal of Tissue Engineering and Regenerative Medicine 11, no. 4 (June 15, 2015): 1285–97. http://dx.doi.org/10.1002/term.2032.

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Zheng, Lu P., Rui Sheng Du, and Barbara E. Goodman. "Effects of acute hyperoxic exposure on solute fluxes across the blood-gas barrier in rat lungs." Journal of Applied Physiology 82, no. 1 (January 1, 1997): 240–47. http://dx.doi.org/10.1152/jappl.1997.82.1.240.

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Zheng, Lu P., Rui Sheng Du, and Barbara E. Goodman.Effects of acute hyperoxic exposure on solute fluxes across the blood-gas barrier in rat lungs. J. Appl. Physiol. 82(1): 240–247, 1997.—We investigated effects of acute hyperoxia on solute transport from air space to vascular space in isolated rat lungs. Air spaces were filled with Krebs-Ringer bicarbonate solution containing fluorescein isothiocyanate-labeled dextran (FD-20; mol wt 20,000) and either22Na+and [14C]sucrose, ord-[14C]glucose andl-[3H]glucose. Apparent permeability-surface area products for tracers over time (up to 120 min) were calculated for isolated perfused lungs from control rats (room air) and rats exposed to >95% O2 for 48 or 60 h immediately postexposure. After O2 exposures, mean fluxes for [14C]sucrose and FD-20 were significantly higher than in room-air control lungs. However, amiloride-sensitive Na+ and actived-glucose fluxes were unchanged after hyperoxic exposure. Therefore, it is unlikely that decreases in net solute transport in this lung-injury model contributed to pulmonary edema resulting from O2 toxicity. Increased net solute transport shown to help resolve pulmonary edema after acute hyperoxic exposure must therefore begin during the recovery period. In summary, our data show increases in passive solute fluxes but no changes in active solute fluxes immediately after acute hyperoxic lung injury.

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Journal articles on the topic 'Air-blood barrier'

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