fatty acid salt
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2021 ◽  
Vol 54 ◽  
pp. 101746
Author(s):  
Yingqiang Zhu ◽  
Puzhen Li ◽  
Xiantao Feng ◽  
Dongsheng Sun ◽  
Tianwen Fang ◽  
...  

Foods ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2747
Author(s):  
Alessandro Micarelli ◽  
Sandro Malacrida ◽  
Giacomo Strapazzon ◽  
Simona Mrakic-Sposta ◽  
Beatrice Micarelli ◽  
...  

The aim of the present scoping review was to evaluate the impact of experimental meal loads or observational diet changes/habits on taste tests in both healthy subjects and patients. A systematic search performed in PubMed, Scopus, and Institute for Scientific Information (ISI) Web of Science electronic databases retrieved, respectively 2981, 6258, and 7555 articles from January 2000 to December 2020. A total of 17 articles were included for full-text review. Literature results were stratified according to the observational/interventional approach, the involvement of healthy subjects or patients, the taste test, and the meal/dietary changes. The present scoping review reinforced the notions postulating that certain taste tests (for example focusing on fatty acid, salt, or sugar) might be specifically influenced by the nutritional intervention and that other ones might be susceptible to a wide span of changes beyond the extent of tastant included in the specific food changes. This could also depend on the inhomogeneity of literature trend: The short duration of the intervention or the random type of meal load, unsuitability of the taste test chosen, and the presence of underlying disorders. Future studies for a better comprehension of taste tests reliability in relation to specific food changes are thus to be fostered.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Teruyuki Hara ◽  
Atsunori Sonoi ◽  
Takuya Handa ◽  
Masayuki Okamoto ◽  
Eri Kaneko ◽  
...  

AbstractCandidiasis-causing Candida sp. forms biofilms with various oral bacteria in the dentures of the elderly, making it harder to kill and remove the microorganism due to the extracellular polymeric substances. We found that biofilms on dentures can effectively be removed by immersion in an unsaturated fatty acid salt solution. Using optical coherence tomography to observe the progression of biofilm removal by the fatty acid salt solution, we were able to determine that the removal was accompanied by the production of gaps at the interface between the biofilm and denture resin. Furthermore, microstructural electron microscopy observations and time-of-flight secondary ion mass spectrometry elucidated the site of action, revealing that localization of the fatty acid salt at the biofilm/denture-resin interface is an important factor.


2021 ◽  
Author(s):  
Siriorn Boonyawanich ◽  
Pinanong Tanikkul ◽  
Pornpanna Thenchartanan ◽  
Nipon Pisutpaisal

Abstract Non-degradable polymer waste enlarged over increasing of human population. This badly affected on environmental pollution and biosphere changing. Polyhydroxyalkanoates (PHAs), an eco-friendly biopolymer, were substituted for conventional- or petrochemical-derived polymer. They are reserve carbon energy produced from diversity of microorganisms in granular under limited nutrient for bacterial growth (e.g. nitrogen and phosphorus). Pseudomonas aeruginosa TISTR 1287 was used to catalyze emulsified palm oil to produce valuable PHAs. The highest yield of PHAs production (0.65 g/L, 38.0%) was obtained in MSM supplemented with 0.75% (v/w) emulsified palm oil after 72-hr cultivation, which was a few lower than that produced by Pseudomonas putida TISTR 1522 (0.95 g/L, 40.15%) cultivated in 1% (w/v) fatty acid salt for after 24-hr cultivation. The intracellular PHAs were detected by staining with Nile red . The characters of intracellular PHAs examined by Transmission Electron Microscope (TEM) exhibited that PHAs accumulate in white and roundish-shaped granules with 0.2-0.5 m m diameter inside the cells, about 2-3 granules per rod-shaped bacterium cell. These optimizations were successfully demonstrated high content of intracellular PHAs accumulation in P. aeruginosa TISTR 1287 by utilization of emulsified palm oil.


2020 ◽  
Author(s):  
Deepak Sumbria ◽  
Engin Berber ◽  
Barry T Rouse

This report evaluates a dietary manipulation approach to suppress the severity of ocular infections caused by herpes simplex virus infection. The virus causes chronic damage to the cornea that results from a T cell orchestrated inflammatory reaction to the infection. Lesion severity can be limited if cells with regulatory activity predominate over proinflammatory T cells and non-lymphoid inflammatory cells. In this report, we show that this outcome can be achieved by including the short chain fatty acid salt sodium propionate (SP) in the drinking water. Animals given the SP supplement developed significantly reduced ocular lesions than those receiving no supplement. Corneas and lymphoid organs contained fewer CD4 Th1 and Th17 T cells, neutrophils and macrophages than controls, but a higher frequency of regulatory T cells (Treg) was present. The inclusion of SP in cultures to induce CD4 T cell subsets in-vitro reduced the magnitude of Th1 and Th17 responses but expanded Treg induction. Diet manipulation was an effective approach to limit the severity of viral immuno-inflammatory lesions and may be worth exploring as a means to reduce the impact of herpetic lesions in humans. IMPORTANCE Herpetic lesions are a significant problem in several persons and they are difficult to control with therapeutics. Our studies show that the severity of herpetic lesions in a mouse model can be diminished by changing the diet to include increased levels of SCFA which acts to inhibit the involvement of inflammatory T cells. We suggest that changing the diet to include higher levels of SCFA might be a useful approach to reduce the impact of recurrent herpetic lesions in humans.


Animals ◽  
2020 ◽  
Vol 10 (7) ◽  
pp. 1154 ◽  
Author(s):  
Xiujing Dou ◽  
Nan Gao ◽  
Di Yan ◽  
Anshan Shan

Inflammatory bowel disease (IBD) develops as a result of complicated interactions between genetic susceptibility, excessive innate immunity, and environmental factors, which are mainly related to the gut microbiota. The present study aimed to elucidate the protective effects and underlying mechanisms of a short-chain fatty acid salt, sodium butyrate, on colonic inflammation induced by dextran sulfate sodium (DSS) in mice. Pretreatment with sodium butyrate attenuated colitis, as demonstrated by the decreased disease activity index (DAI), colon length shortening, spleen tumidness, and histopathology scores, while maintaining intestinal barrier integrity, as observed by H&E staining and electron microscopy. 16S rRNA sequence analysis revealed that sodium butyrate caused a remarkable alteration of the gut microbiota. Bacteroides, Lachnospiraceae, the Lachnospiraceae NK4A136 group, and Ruminiclostridium 6 presented dramatic differences after sodium butyrate supplementation. This work verifies that sodium butyrate can improve mouse colitis via microbe–host interactions by regulating the microbial community. Taken together, the findings demonstrate that sodium butyrate shows great potential as a probiotic agent for ameliorating colitis.


2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Jingxuan Sun ◽  
Boyu Yuan ◽  
Yancheng Wu ◽  
Yuhong Gong ◽  
Wenjin Guo ◽  
...  

Alzheimer’s disease (AD) is a common neurodegenerative disease. Aβ plays an important role in the pathogenesis of AD. Sodium butyrate (NaB) is a short-chain fatty acid salt that exerts neuroprotective effects such as anti-inflammatory, antioxidant, antiapoptotic, and cognitive improvement in central nervous system diseases. The aim of this study is to research the protective effects of NaB on neurons against Aβ toxicity and to uncover the underlying mechanisms. The results showed that 2 mM NaB had a significant improvement effect on Aβ-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury. In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF. Therefore, NaB protects N2a cells from Aβ-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.


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