scholarly journals Novel Options of Decellularization Solutions for Lung Tissue/Organ Engineering

Author(s):  
T. Tsuchiya ◽  
T. Obata ◽  
H. Sengyoku ◽  
R. Doi ◽  
G. Hatachi ◽  
...  
Author(s):  
M. G. Williams ◽  
C. Corn ◽  
R. F. Dodson ◽  
G. A. Hurst

During this century, interest in the particulate content of the organs and body fluids of those individuals affected by pneumoconiosis, cancer, or other diseases of unknown etiology developed and concern was further prompted with the increasing realization that various foreign particles were associated with or caused disease. Concurrently particularly in the past two decades, a number of methods were devised for isolating particulates from tissue. These methods were recently reviewed by Vallyathan et al. who concluded sodium hypochlorite digestion was both simple and superior to other digestion procedures.


Author(s):  
Jerrold L. Abraham

Inorganic particulate material of diverse types is present in the ambient and occupational environment, and exposure to such materials is a well recognized cause of some lung disease. To investigate the interaction of inhaled inorganic particulates with the lung it is necessary to obtain quantitative information on the particulate burden of lung tissue in a wide variety of situations. The vast majority of diagnostic and experimental tissue samples (biopsies and autopsies) are fixed with formaldehyde solutions, dehydrated with organic solvents and embedded in paraffin wax. Over the past 16 years, I have attempted to obtain maximal analytical use of such tissue with minimal preparative steps. Unique diagnostic and research data result from both qualitative and quantitative analyses of sections. Most of the data has been related to inhaled inorganic particulates in lungs, but the basic methods are applicable to any tissues. The preparations are primarily designed for SEM use, but they are stable for storage and transport to other laboratories and several other instruments (e.g., for SIMS techniques).


Author(s):  
Daniel C. Pease

It is reasonable to think that phospholipid micelles should be visible and identifiable in electron micrographs of ultrathin sections if only they can be preserved throughout the embedding process. The development of highly polar, water-containing, aminoplastic embedments has made this a likely possibility. With this in mind, an investigation of the lecithin-secreting, Type II pneumocytes of the lung is underway.Initially it has been easiest to recognize phospholipid micelles in lung tissue fixed first with glutaraldehyde, and then secondarily exposed to osmium tetroxide. However, the latter is not a necessary concomitant for micellar preservation. Conventional uranyl acetate and lead citrate staining is finally applied. Importantly, though, the micelles have been most easily seen in tissue embedded in 507. glutaraldehyde polymerized with urea, as described in detail by D.C. Pease and R.G. Peterson (J. Ultra- struct. Res., 41, 133, 1972). When oriented appropriately, the micellar units are seen as tiny, bilayer plates.


Author(s):  
J. D. Shelburne ◽  
Peter Ingram ◽  
Victor L. Roggli ◽  
Ann LeFurgey

At present most medical microprobe analysis is conducted on insoluble particulates such as asbestos fibers in lung tissue. Cryotechniques are not necessary for this type of specimen. Insoluble particulates can be processed conventionally. Nevertheless, it is important to emphasize that conventional processing is unacceptable for specimens in which electrolyte distributions in tissues are sought. It is necessary to flash-freeze in order to preserve the integrity of electrolyte distributions at the subcellular and cellular level. Ideally, biopsies should be flash-frozen in the operating room rather than being frozen several minutes later in a histology laboratory. Electrolytes will move during such a long delay. While flammable cryogens such as propane obviously cannot be used in an operating room, liquid nitrogen-cooled slam-freezing devices or guns may be permitted, and are the best way to achieve an artifact-free, accurate tissue sample which truly reflects the in vivo state. Unfortunately, the importance of cryofixation is often not understood. Investigators bring tissue samples fixed in glutaraldehyde to a microprobe laboratory with a request for microprobe analysis for electrolytes.


2020 ◽  
Vol 13 ◽  
Author(s):  
Kun Xiao ◽  
Fei Zhao ◽  
WenJie Xie ◽  
Jian Ding ◽  
XiaoAn Gong ◽  
...  

Objective: To explore and investigate the molecular mechanism of TLR4 mediated T cell immune effect in transfusion-induced acute injury based on SLIT2/ROBO4 signaling pathway. Methods: Sixty C57/BL6 male mice (Wild type, WT) aged 8 to 10 weeks were randomly divided into 5 groups: 1) normal type WT, 2) LPS control group of WT type lipopolysaccharide, 3) WT type TRALI group (LPS + MHC-I mAb), 4) (TLR4 antibody) lipopolysaccharide LPS control group, 5) (TLR4 antibody) TRALI group (LPS + MHC-I mAb). Mice were dosed with LPS (0.1 mg / kg), and MHC-I mAb (2 mg / kg) was injected into the tail vein 24 hours later for modeling. After 2 hours, mice were sacrificed and experimental samples were collected. HE staining was performed to detect pathological features. The myeloperoxidase (MPO) activity and the level of IL-2, IL-6, TNF, IFN-γ, IL-17A as well as IL-10 were measured in the lung tissue homogenate supernatant. Blood, spleen single cell suspension and bronchoalveolar lavage fluid (BALF) were collected to detect the ratio of Treg and Th17 cells by flow cytometry, respectively. RT-PCR and WB indicated the mRNA or protein expression of CDH5 (Cadherin-5), SLIT2 and ROBO4 in mouse lung tissue and pulmonary vascular tissue respectively. Results: TLR4 mAb treatment decreases the pathological features of LPS induced ALI model in vivo. And so does the MPO activity as well as the level of proinflammatory factors in the lung tissue. TLR4 exerts its function through the changes of Treg/Th17 ratio via SLIT2/ROBO4 signaling pathway and downregulating CDH5 and SETSIP in ALI model. Conclusion: TLR4 mediates immune response in LPS induced ALI model through SLIT2/ROBO4 signaling pathway.


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