Light distribution in human lung tissue at 413.1 nm in vitro

Author(s):  
Zhiwei Huang ◽  
Chee T. Chia ◽  
Cheong Hoong Diong ◽  
Sing Lee ◽  
Wei-Ming Zheng ◽  
...  
Allergy ◽  
1986 ◽  
Vol 41 (5) ◽  
pp. 319-326 ◽  
Author(s):  
H. Bergstrand ◽  
B. Lundquist ◽  
B.-Å. Petersson

2015 ◽  
Vol 6 (12) ◽  
pp. 6971-6979 ◽  
Author(s):  
Ahsan R. Akram ◽  
Nicolaos Avlonitis ◽  
Annamaria Lilienkampf ◽  
Ana M. Perez-Lopez ◽  
Neil McDonald ◽  
...  

A fluorescently labelled ubiquicidin peptide enables bacterial detection in human lung tissuein vitro.


2021 ◽  
Vol 11 (2) ◽  
pp. 360-369
Author(s):  
Caide Xie ◽  
Tianjing Zhao ◽  
Liang Fang

In order to explore the high-resolution CT findings of leukemia pulmonary infiltration and chemotherapy outcomes and the in vitro study of human lung tissue, this paper selected a total of 120 clinically or surgically confirmed leukemia patients at the designated hospital of the study from December 2014 to December 2018, and divided them into three groups according to the random number table method: pulmonary infiltration group, chemotherapy outcome group and in vitro study group, with 40 cases in each group. The CT imaging features of the three groups of patients were observed and summarized respectively; the anomalous evaluation indexes of pulmonary parenchyma tissue abnormalities included CT halo sign, air crescent sign, lung segment consolidation, bronchial vascular bundle and nodules; the CT abnormalities such as thickening of the interlobular septum, bronchial interstitial thickening, nodular shadow, ground glassy change, and air cavity consolidation were selected as observation indicators. The results show that all cases have multiple solid nodules or multiple plaques, varying in number, size and distribution, in which 13 cases have multiple patchy shadows, 9 cases have multiple knots and 11 cases have multiple plaques and nodules; lesions are mainly distributed along the bronchial vessels in 21 cases, and 9 cases are along the center of the small leaves and 5 cases are randomly distributed; there are 13 cases that have frosted glass, in which 4 cases with pleural effusion, 9 cases with mold infection, show multiple patchy shadows with halo signs and layered mold balls. In summary, leukemia pulmonary infiltration has polymorphic high-resolution CT findings and chemotherapy outcomes; high-resolution CT imaging and in vitro studies of human lung tissue have important clinical and pathological research value for leukemia infiltration and chemotherapy outcome. The results of this study provide a reference for the further researches on high-resolution CT findings of pulmonary infiltration and chemotherapy outcomes and in vitro studies of human lung tissue.


1993 ◽  
Vol 41 (6) ◽  
pp. 851-866 ◽  
Author(s):  
S M Morris ◽  
P J Stone ◽  
G L Snider

Much of the experimental evidence supporting the hypothesis that pulmonary emphysema results from an imbalance between elastases and anti-elastases in the lung comes from animal models. The present study was designed to examine the effects on human lung tissue of the two elastases that have been most widely used to produce these animal models. Lung tissue was exposed in vitro to human neutrophil elastase (HNE) or porcine pancreatic elastase (PPE). Although both enzymes solubilized protein at similar rates, PPE solubilized elastin five times faster than did HNE. Ultrastructurally, HNE-exposed tissue exhibited fewer damaged elastic fibers as well as some fibers that were damaged at the edges, whereas the interior of the fiber appeared intact. Elastic fibers showing damage only at the periphery were not seen in tissue exposed to PPE. Immunocytochemical studies in which antibodies to HNE and PPE were applied to thin sections of Lowicryl-embedded tissue indicated that both of these elastases could be detected in association with elastic fibers, but only in areas of the fiber that showed morphological evidence of elastase injury. Both HNE and PPE removed fibronectin from basement membranes (as determined by loss of binding of fibronectin antibodies after exposure to elastase), but neither elastase was detected on basement membrane. Loss of epithelial cells usually accompanied elastic fiber damage by HNE but not PPE.


2016 ◽  
Vol 84 (5) ◽  
pp. 1438-1445 ◽  
Author(s):  
Joseph G. Graham ◽  
Caylin G. Winchell ◽  
Richard C. Kurten ◽  
Daniel E. Voth

Coxiella burnetiiis an intracellular bacterial pathogen that causes human Q fever, an acute debilitating flu-like illness that can also present as chronic endocarditis. Disease typically occurs following inhalation of contaminated aerosols, resulting in an initial pulmonary infection. In human cells,C. burnetiigenerates a replication niche termed the parasitophorous vacuole (PV) by directing fusion with autophagosomes and lysosomes.C. burnetiirequires this lysosomal environment for replication and uses a Dot/Icm type IV secretion system to generate the large PV. However, we do not understand howC. burnetiievades the intracellular immune surveillance that triggers an inflammatory response. We recently characterized human alveolar macrophage (hAM) infectionin vitroand found that avirulentC. burnetiitriggers sustained interleukin-1β (IL-1β) production. Here, we evaluated infection ofex vivohuman lung tissue, defining a valuable approach for characterizingC. burnetiiinteractions with a human host. Within whole lung tissue,C. burnetiipreferentially replicated in hAMs. Additionally, IL-1β production correlated with formation of an apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC)-dependent inflammasome in response to infection. We also assessed potential activation of a human-specific noncanonical inflammasome and found that caspase-4 and caspase-5 are processed during infection. Interestingly, although inflammasome activation is closely linked to pyroptosis, lytic cell death did not occur followingC. burnetii-triggered inflammasome activation, indicating an atypical response after intracellular detection. Together, these studies provide a novel platform for studying the human innate immune response toC. burnetii.


1982 ◽  
Vol 63 (2) ◽  
pp. 219-221 ◽  
Author(s):  
V. Y. Lee ◽  
J. Margaret Hughes ◽  
J. P. Seale ◽  
Diana M. Temple

1. Macroscopically normal human lung tissue was obtained from operative specimens removed for lung cancer and challenged with antigen or calcium ionophore. The release of histamine and slow-reacting substances was measured by fluorimetric and bioassay techniques respectively. 2. Benoxaprofen, a drug with inhibitory effects on the lipoxygenase and cyclo-oxygenase pathways, caused a dose-related reduction of release of slow-reacting substances without affecting histamine release. 3. These results with human lung tissue in vitro suggest that benoxaprofen may be used to investigate the role of slow-reacting substances in experimental and clinical asthma.


2021 ◽  
Author(s):  
Alejandro Peralta-Garcia ◽  
Mariona Torrens-Fontanals ◽  
Tomasz Maciej Stepniewski ◽  
Judit Grau-Expósito ◽  
David Perea ◽  
...  

Since the start of the COVID-19 outbreak, pharmaceutical companies and research groups have focused on the development of vaccines and antiviral drugs against SARS-CoV-2. Here, we apply a drug repurposing strategy to identify potential drug candidates that are able to block the entrance of the virus into human cells. By combining virtual screening with in vitro pseudovirus assays and antiviral assays in Human Lung Tissue (HLT) cells, we identify entrectinib as a promising antiviral drug. We found that part of the antiviral action of entrectinib is mediated by a non-specific mechanism, likely occurring at the viral membrane level. Such a profile could provide entrectinib with protection against the development of drug resistance by emerging SARS-CoV-2 variants.


2021 ◽  
Author(s):  
E.A. Rosado-Olivieri ◽  
B. Razooky ◽  
H.-H. Hoffmann ◽  
R. De Santis ◽  
C.M. Rice ◽  
...  

AbstractSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of the global COVID-19 pandemic and the lack of therapeutics hinders pandemic control1–2. Although lung disease is the primary clinical outcome in COVID-19 patients1–3, how SARS-CoV-2 induces tissue pathology in the lung remains elusive. Here we describe a high-throughput platform to generate tens of thousands of self-organizing, nearly identical, and genetically matched human lung buds derived from human pluripotent stem cells (hPSCs) cultured on micropatterned substrates. Strikingly, in vitro-derived human lung buds resemble fetal human lung tissue and display in vivo-like proximo-distal coordination of alveolar and airway tissue differentiation whose 3D epithelial self-organization is directed by the levels of KGF. Single-cell transcriptomics unveiled the cellular identities of airway and alveolar tissue and the differentiation of WNThi cycling alveolar stem cells, a human-specific lung cell type4. These synthetic human lung buds are susceptible to infection by SARS-CoV-2 and endemic coronaviruses and can be used to track cell type-dependent susceptibilities to infection, intercellular transmission and cytopathology in airway and alveolar tissue in individual lung buds. Interestingly, we detected an increased susceptibility to infection in alveolar cells and identified cycling alveolar stem cells as targets of SARS-CoV-2. We used this platform to test neutralizing antibodies isolated from convalescent plasma that efficiently blocked SARS-CoV-2 infection and intercellular transmission. Our platform offers unlimited, rapid and scalable access to disease-relevant lung tissue that recapitulate key hallmarks of human lung development and can be used to track SARS-CoV-2 infection and identify candidate therapeutics for COVID-19.


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