Biocompatibility of Polyimide Fibers with Human Gastric Cells In Vitro

Author(s):  
Xiaoyue Wang ◽  
Jianwei Gao ◽  
Jie Zhang
2017 ◽  
Vol 19 (12) ◽  
pp. e12771 ◽  
Author(s):  
Anis Rageh Al-Maleki ◽  
Mun Fai Loke ◽  
Sook Yin Lui ◽  
Nur Siti Khadijah Ramli ◽  
Yalda Khosravi ◽  
...  

1992 ◽  
Vol 14 ◽  
pp. S156-S161 ◽  
Author(s):  
Shinichi Ota ◽  
Yasuo Hata ◽  
Hideyuki Hiraishi ◽  
Hiroyuki Mutoh ◽  
Akira Terano ◽  
...  

1990 ◽  
Vol 12 ◽  
pp. S32-S38 ◽  
Author(s):  
Tetsuo Arakawa ◽  
Atsushi Nakamura ◽  
Takashi Fukuda ◽  
Kazuhide Higuchi ◽  
Hajime Nakamura ◽  
...  

2021 ◽  
Vol 22 (11) ◽  
pp. 5650
Author(s):  
Samantha A. Whiteside ◽  
Mahi M. Mohiuddin ◽  
Sargon Shlimon ◽  
Jaspreet Chahal ◽  
Chad W. MacPherson ◽  
...  

Helicobacter pylori is a prevalent bacterium that can cause gastric ulcers and cancers. Lactic acid bacteria (LAB) ameliorate treatment outcomes against H. pylori, suggesting that they could be a source of bioactive molecules usable as alternatives to current antibiotics for which resistance is mounting. We developed an in vitro framework to compare the anti-H. pylori properties of 25 LAB and their secretions against H. pylori. All studies were done at acidic and neutralized pH, with or without urea to mimic various gastric compartments. Eighteen LAB strains secreted molecules that curtailed the growth of H. pylori and the activity was urea-resistant in five LAB. Several LAB supernatants also reduced the urease activity of H. pylori. Pre-treatment of H. pylori with acidic LAB supernatants abrogated its flagella-mediated motility and decreased its ability to elicit pro-inflammatory IL-8 cytokine from human gastric cells, without reverting the H. pylori-induced repression of other pro-inflammatory cytokines. This study identified the LAB that have the most anti-H. pylori effects, decreasing its viability, its production of virulence factors, its motility and/or its ability to elicit pro-inflammatory IL-8 from gastric cells. Once identified, these molecules can be used as alternatives or complements to current antibiotics to fight H. pylori infections.


The gastric ulcers in these experiments were produced by the injection of gastrotoxic serum. In a form er communication (1) it was demonstrated that the serum, formed by immunising the rabbit with the gastric cells of the guinea-pig or with those of another rabbit, on injection into the guinea-pig's peritoneum produced general symptoms of intoxication and patches of necrosis in the mucous membrane of the stomach. In two later communications (2) and (3) the reactions of gastrotoxin in vitro and its precise mode of action in corpore were demonstrated.


1984 ◽  
Vol 58 (3) ◽  
pp. 230-238 ◽  
Author(s):  
Yasuko Rikihisa ◽  
Thomas Letonja ◽  
Nancy Pratt ◽  
Young Chin Lin

1998 ◽  
Vol 275 (2) ◽  
pp. G322-G330 ◽  
Author(s):  
Evan R. Kokoska ◽  
Gregory S. Smith ◽  
Andrew B. Wolff ◽  
Yashwant Deshpande ◽  
Christopher L. Rieckenberg ◽  
...  

We have developed an in vitro model of adaptive cytoprotection induced by deoxycholate (DC) in human gastric cells and have shown that pretreatment with a low concentration of DC (mild irritant, 50 μM) significantly attenuates injury induced by a damaging concentration of DC (250 μM). This study was undertaken to assess the effect of the mild irritant on changes in intracellular Ca2+ and to determine if these perturbations account for its protective action. Protection conferred by the mild irritant was lost when any of its effects on intracellular Ca2+ were prevented: internal Ca2+ store release via phospholipase C and inositol 1,4,5-trisphosphate sustained Ca2+ influx through store-operated Ca2+ channels or eventual Ca2+ efflux. We also investigated the relationship between Ca2+accumulation and cellular injury induced by damaging concentrations of DC. In cells exposed to high concentrations of DC, sustained Ca2+ accumulation as a result of extracellular Ca2+ influx, but not transient changes in intracellular Ca2+ content, appeared to precede and induce cellular injury. We propose that the mild irritant disrupts normal Ca2+ homeostasis and that this perturbation elicits a cellular response (involving active Ca2+ efflux) that subsequently provides a protective action by limiting the magnitude of intracellular Ca2+ accumulation.


Author(s):  
P.L. Moore

Previous freeze fracture results on the intact giant, amoeba Chaos carolinensis indicated the presence of a fibrillar arrangement of filaments within the cytoplasm. A complete interpretation of the three dimensional ultrastructure of these structures, and their possible role in amoeboid movement was not possible, since comparable results could not be obtained with conventional fixation of intact amoebae. Progress in interpreting the freeze fracture images of amoebae required a more thorough understanding of the different types of filaments present in amoebae, and of the ways in which they could be organized while remaining functional.The recent development of a calcium sensitive, demembranated, amoeboid model of Chaos carolinensis has made it possible to achieve a better understanding of such functional arrangements of amoeboid filaments. In these models the motility of demembranated cytoplasm can be controlled in vitro, and the chemical conditions necessary for contractility, and cytoplasmic streaming can be investigated. It is clear from these studies that “fibrils” exist in amoeboid models, and that they are capable of contracting along their length under conditions similar to those which cause contraction in vertebrate muscles.


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