Organs-on-a-Chip

Bioprinting ◽  
2021 ◽  
pp. 155-182
Author(s):  
Kenneth Douglas

Abstract: This chapter explores organs-on-a-chip, miniaturized bioprinted organ tissues enclosed in a microfluidic housing (microfluidics refers to very small-scale plumbing) that can mimic functions of human physiology or disease and are particularly effective when multiple tissue types—for example, lung, heart, and liver—can interact on the same chip. The chapter sets forth the historical evolution of organs-on-a-chip and instances several studies. In one investigation, experimenters found a totally unexpected result in which a drug produced an inflammation of lung tissue that in turn led to toxic results in nearby heart tissue. In another inquiry, researchers focused on a bioprinted, functional, airway-on-a-chip to characterize inflammatory diseases such as asthma and chronic obstructive lung disease and vet potential medications for their treatment. Their work included quantitative comparisons of normal lung tissue and asthmatic lung tissue to a variety of insults, including household dust mites.

1984 ◽  
Vol 66 (5) ◽  
pp. 585-590 ◽  
Author(s):  
J. A. M. Raaijmakers ◽  
G. K. Terpstra ◽  
A. J. Van Rozen ◽  
A. Witter ◽  
J. Kreukniet

1. Muscarinic cholinergic receptors have been identified and characterized by radioligand binding studies in human peripheral lung tissue. The tissue was obtained at thoracotomy of 12 patients, of whom four had chronic obstructive lung disease. 2. The radioligand l-quinuclidinyl[phenyl-4-3H]benzilate (3H-QNB) was used to label the muscarinic cholinergic receptors. Binding was saturable, protein dependent and showed a high affinity and stereospecificity. Specific binding could be inhibited by agonists and antagonists; molar inhibition constants determined for the agents used were of the same order of magnitude as those reported for 3H-QNB inhibition in various tissues of laboratory animals. Inhibition experiments with agonists resulted in Hill slopes which were significantly different from unity, indicating multiple binding sites. The stable GTP analogue guanyl-5′-imidodiphosphate had no effect on the Hill slopes of agonists or antagonists. 3. The number of binding sites was significantly less in lung tissue from patients with chronic obstructive lung disease.


2021 ◽  
Vol 42 (3) ◽  
pp. 56-71
Author(s):  
Tae Hyeon Kim ◽  
Won Kyung Yang ◽  
Su Won Lee ◽  
Seung Hyung Kim ◽  
Yee Ran Lyu ◽  
...  

Objectives: This study is aimed to evaluate the protective effects of GGX on lung injury of Chronic Obstructive Lung Disease (COPD) mice model. Materials and Methods: C57BL/6 mice were challenged with lipopolysaccharide (LPS) and cigarette smoke extract (CSE) and then treated with vehicle only (Control group), dexamethasone 3 ㎎/㎏ (Dexa group), gam-gil-tang 200 ㎎/㎏ (GGT group), GGX 100, 200, and 400 ㎎/㎏ (GGX group). After sacrifice, its bronchoalveolar lavage fluid (BALF) or lung tissue was analyzed with cytospin, Enzyme-Linked Immunosorbent Assay (ELISA), real-time polymerase chain reaction (PCR) and hematoxylin & eosin (H&E), and Masson’s trichrome staining. Results: In the COPD model, GGX significantly inhibited the increase of neutrophils, TNF-α, IL-17A, CXCL-1, MIP2 in BALF and TNF-α, IL-1β, IL-10 mRNA expression in lung tissue. It also decreased the severity of histological lung injury. Conclusion: This study suggests the usability of GGX for COPD patients by controlling lung tissue injury.


Respiration ◽  
1981 ◽  
Vol 41 (1) ◽  
pp. 25-32 ◽  
Author(s):  
J. Hutsebaut ◽  
G. Scano ◽  
P. Garcia-Herreros ◽  
S. Degré ◽  
A. De Coster ◽  
...  

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