Evaluation of the effects of chitosan films as a replacement for conventional sulphur dioxide treatment of white wines
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TISSUE(S): Wine
PROVIDER: ST002267 | MetabolomicsWorkbench |
REPOSITORIES: MetabolomicsWorkbench
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Project description:Mammals display wide range of variation in their lifespan. Investigating the molecular networks that distinguish long- from short-lived species has proven useful to identify determinants of longevity. Here, we compared the liver of long-lived naked mole-rats (NMRs) and the phylogenetically closely related, shorter-lived, guinea pigs using an integrated omic approach. We found that NMRs livers display a unique expression pattern of mitochondrial proteins that result in distinct metabolic features of their mitochondria. For instance, we observed a generally reduced respiration rate associated with lower protein levels of respiratory chain components, particularly complex I, and increased capacity to utilize fatty acids. Interestingly, we show that the same molecular networks are affected during aging in both NMR and humans, supporting a direct link to the extraordinary longevity of both species. Finally, we identified a novel longevity pathway and validated it experimentally in the nematode C. elegans.
2018-06-21 | PXD008720 | Pride
Project description:Transcriptome of long-lived naked-mole rat (NMR) oligodendrocyte progenitor cells (OPCs) were compared with OPCs of other species.
2022-03-31 | E-MTAB-9160 | biostudies-arrayexpress
Project description:The naked mole-rat (NMR), Heterocephalus glaber, is a mouse-sized subterranean rodent native to East Africa. Research on NMRs is intensifying in an effort to gain leverage from their unusual physiology, long-life span and cancer resistance for the development of new theraputics. Few studies have attempted to explain the reasons behind the NMR’s cancer resistance, but most prominently Tian et al. reported that NMR cells produce high-molecular weight hyaluronan as a potential cause for the NMR’s cancer resistance. Tian et al. have shown that NMR cells are resistant to transformation by SV40 Large T Antigen (SV40LT) and oncogenic HRAS (HRASG12V), a combination of oncogenes sufficient to transform mouse and rat fibroblasts. We have developed a number of lentiviral vectors to deliver both these oncogenes and generated 106 different cell lines from five different tissues and eleven different NMRs, and report here that contrary to Tian et al.’s observation, NMR cells are susceptible to oncogenic transformation by SV40LT and HRASG12V. Our data thus point to a non-cell autonomous mechanism underlying the remarkable cancer resistance of NMRs. Identifying these non-cell autonomous mechanisms could have significant implications on our understanding of human cancer development.
2020-06-12 | E-MTAB-8932 | biostudies-arrayexpress
Project description:The detachment of epithelial cells, but not cancer cells, causes anoikis due to reduced energy production. Invasive tumor cells generate three splice variants of the metastasis gene osteopontin. The cancer-specific form osteopontin-c supports anchorage-independence through inducing oxidoreductases and upregulating intermediates/enzymes in the hexose monophosphate shunt, glutathione cycle, glycolysis, glycerol phosphate shuttle, and mitochondrial respiratory chain. Osteopontin-c signaling upregulates glutathione (consistent with the induction of the enzyme GPX-4), glutamine and glutamate (which can feed into the tricarboxylic acid cycle). Consecutively, the cellular ATP levels are elevated. The elevated creatine may be synthesized from serine via glycine and also supports the energy metabolism by increasing the formation of ATP. Metabolic probing with N-acetyl-L-cysteine, L-glutamate, or glycerol identified differentially regulated pathway components, with mitochondrial activity being redox dependent and the creatine pathway depending on glutamine. The effects are consistent with a stimulation of the energy metabolism that supports anti-anoikis. Our findings imply a synergism in cancer cells between osteopontin-a, which increases the cellular glucose levels, and osteopontin-c, which utilizes this glucose to generate energy. mRNA profiles of MCF-7 cells transfected with osteopontin-a, osteopontin-c and vector control were generated by RNA-Seq, in triplicate, by Illumina HiSeq.
2014-02-21 | E-GEOD-55193 | biostudies-arrayexpress
Project description: Not available
| S-BIAD10 | bioimages
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| S-EPMC8362223 | biostudies-literature
Project description:Background and hypothesisSchizophrenia involves microstructural changes in white matter (WM) tracts. Oxidative stress is a key factor causing WM damage by hindering oligodendrocyte development and myelin maturation. Uric acid (UA), an endogenous antioxidant, may protect against oxidative stress. We investigated the effect of UA on WM connectivity in antipsychotic-naive or -free patients with early- or chronic-stage schizophrenia.Study designA total of 192 patients with schizophrenia (122 recent-onset [ROS] and 70 chronic [CS]) and 107 healthy controls (HCs) participated in this study. Diffusion tensor imaging data and serum UA levels at baseline were obtained.Study resultsFractional anisotropy was lower in the widespread WM regions across the whole brain, and diffusivity measures were higher in both schizophrenia groups than in HCs. The CS group showed lower diffusivity in some WM tracts than the ROS or HC groups. The linear relationship of serum UA levels with axial and mean diffusivity in the right frontal region was significantly different between schizophrenia stages, which was driven by a negative association in the CS group. WM diffusivity associated with serum UA levels correlated with 8-week treatment responses only in patients with CS, suggesting UA to be protective against long-term schizophrenia.ConclusionsUA may protect against the WM damage associated with the progression of schizophrenia by reducing oxidative stress and supporting WM repair against oxidative damage. These results provide insights into the positive role of UA and may facilitate the development of novel disease-modifying therapies.
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Project description:Genome wide DNA methylation profiling of white blood cells in obese patients under two different diets (The American Heart Association's Diet and RESMENA diet (Zulet MA et al., Nutr Hosp. 2011 Jan-Feb;26(1):16-26. )) in order to reduce weight. The Illumina infinium HumanMethylation450 beadchip kit was used, which assayed 450,000 potential methylation sites. Bisulphite converted DNA from the 48 samples were hybridised to the Illumina Infinium 450 Human Methylation Beadchip.
2019-10-30 | E-MTAB-2372 | biostudies-arrayexpress
Project description:IntroductionTime-and dose-dependent adverse effects of amiodarone have not been described in cats. The primary aim of this retrospective multicenter cohort study was to report the type and frequency of clinical adverse effects and biochemical changes in cats receiving amiodarone chronically. The secondary aim was to report survival outcomes in this population of cats.MethodsMedical records were reviewed for signalment, arrhythmia diagnosis, presence of structural heart disease, systemic comorbidities and congestive heart failure at presentation, amiodarone dose, serial bloodwork results, adverse events, and survival outcome.ResultsThe study population included 27 client-owned cats (2016-2022). All cats had structural cardiac disease, and many were in congestive heart failure (17/27; 63%) at presentation. Amiodarone was most commonly prescribed for ventricular tachycardia (19/27, 70%), and it was administered once daily with a median [range] dose of 8.8 [4.515.2] mg/kg/day. There was a decrease in serum concentration of alanine transaminase between pretreatment values and values measured during the early amiodarone treatment window, 1-90 days (n = 16; p = 0.034). No statistical difference in serum concentration of alanine transaminase (n = 10; p = 0.799) was noted after 90 days of treatment compared to pretreatment. There was no change in hematocrit, neutrophil count, and serum concentration of alkaline phosphatase and total thyroxine during treatment in assessed cats. Ten cats (37%) had at least one episode of hyporexia or vomiting while receiving amiodarone. The median survival time for all-cause mortality was 441 days (95% confidence interval, 126-929 days); cats in which the primary therapeutic target was both supraventricular and concomitant ventricular tachyarrhythmias had at least a two-fold risk of dying compared to cats with supraventricular tachyarrhythmias alone (hazard ratio 12.9, 95% CI 1.86-89.8; p = 0.010).DiscussionAmiodarone was primarily used to treat ventricular arrhythmias. Transient gastrointestinal signs were reported in approximately one-third of the cats studied, but no clinically significant laboratory abnormalities were found in cats receiving amiodarone.
| S-EPMC11782268 | biostudies-literature
Project description:BackgroundBreastmilk stem cells (BSCs) have been reported to have potential benefits for infants. However, whether the BSCs could improve brain injury is unknown. A culture system for BSCs was established, and the roles of BSCs in treating white matter injury (WMI) were investigated in our study.MethodsBreastmilk samples were collected from healthy lactating women between days 1 and 5 after delivery. The BSCs were cultured in a specialized culture medium and then characterized through flow cytometry and immunofluorescence methods. A rat model with WMI was established by ligating the right carotid artery of Sprague-Dawley rats at postnatal day 3 (P3) and exposing the rats to 6% hypoxia for 2 h. Rats were categorized into sham, WMI with breastmilk cell (WMI + BC), and WMI with (WMI + NS) groups. In the WMI + BC group, 5 µL BCs (1 × 106) was injected into the lateral ventricle 24 h post-modeling. Four different stages of oligodendrocyte (OL) markers were observed. Long-term neurobehavioral evaluations were conducted using the Morris water maze test. The inflammatory cytokines and proportion of proinflammatory microglial cells were detected to study the mechanisms of BSC treatment.ResultsThe isolated BSCs expressed mesenchymal stem cell-positive markers, including CD105, CD73, CD29, CD166, CD44, and CD90. Meanwhile, the mesenchymal stem cell-negative markers, including HLA-DR, CD45, and CD79a, were also found in BSCs. The BSCs did not express pluripotent stem cell markers, including SOX2, Nanog, OCT4, SSEA4, and TRA-1-60. Immunofluorescence detection showed that BSCs expressed neural stem/progenitor cell markers, including Vimentin, Nestin, and A2B5. Following BSC treatment, pathological improvements were observed in WMI. The expressions of mature OLs markers myelin basic protein and myelin-associated glycoprotein were increased in the corpus callosum and periventricular areas. Meanwhile, the numbers of myelin sheath increased, and learning and memory abilities improved. Furthermore, a decrease in B7-2+/Iba1 + proinflammatory microglia and an increase in CD206+/Iba1 + anti-inflammatory microglia were observed. The mRNA expressions of proinflammatory factors (Il1b, Il6, Ifng, and Tnfa) and anti-inflammatory factors (Arg1 and Tgfb) decreased and increased, respectively.ConclusionOur findings suggest that BSCs can improve the maturation of OLs following WMI in newborn rats. The mechanisms may be attributed to the reduced proinflammatory microglia cells and factors as well as the increased anti-inflammatory microglia cells and factors.
| S-EPMC11887140 | biostudies-literature