9 research outputs found

    Characteristics of selenite bioreduction by Shewanella oneidensis MR-1 with redox mediators

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    Accelerating the selenite reduction rate is important in selenite bioreduction by microorganism process. This study investigates the impact of redox mediators (α-AQS, AQS, 1,5-AQDS and AQDS) on bioreduction of selenite by Shewanella oneidensis MR-1 and optimizes the bioreduction conditions with Shewanella oneidensis MR-1 and AQDS. The selenium particles obtained from cultures are analyzed using Zeta potential analyzer. The results suggest that all four tested redox mediators are able to accelerate the reduction of selenite by Shewanella oneidensis MR-1, and AQDS is the best. The optimum conditons are AQDS concentration of 0.2 mmol/L pH of 8.0 and temperature of 30 ℃. Selenite is completely removed after 48 h bioreduction by Shewanella oneidensis MR-1 with optimum conditons. Bigger size selenium nanoparticles (SeNPS) can be obtained with AQDS. AQDS may influence the composition and content of the organic layer covering around selenium nanoparticles (SeNPs). This study could provide a foundation for particle application in selenite biodegradation

    Amelioration of Experimental Autoimmune Encephalomyelitis in Alzheimer’s Disease Mouse Models: A Potential Role for Aβ

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    Emerging data have highlighted the coexistence of multiple sclerosis (MS) and Alzheimer’s disease (AD), both of which are common central nervous system degenerative diseases with a heavy burden on patients, their families, and society. However, it is unclear how MS progresses under an AD pathological background. We aimed to address the question of how MS progresses under an AD pathological background. We induced the experimental autoimmune encephalomyelitis (EAE) model of MS in two types of AD mouse models, Tg6799 and APP/PS1 mice. We found that, compared with wild-type mice, the clinical symptoms of EAE were significantly ameliorated in APP/PS1 mice but not in Tg6799 mice. Moreover, a much lower level of serum Aβ was observed in Tg6799 mice. EAE clinical symptoms in Tg6799 and C57BL/6J mice were ameliorated by intraperitoneal injection of Aβ42. Peripheral administration of Aβ42 peptides was able to inhibit Th17 development in vivo, which is likely to occur through the inhibition of IL-6 production in dendritic cells. Our findings revealed that AD and EAE could coexist in the same mouse, and Aβ residing in peripheral circulation likely plays an anti-inflammatory role in preventing EAE progression. These findings reveal the potential benefit of Aβ, one of the supervillains of AD, at least in certain contexts

    DMKN knockdown inhibits proliferation and invasion in advanced melanoma cell lines.

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    The dmkn gene (A) and protein (B) levels in DMKN-shRNA-transduced cells (shDMKN) compare to that in lentivirus-scrambled control (NC). Analysis of cell invasion by using a modified Boyden Chamber assay. in lentivirus control and DMKN-shRNA-transfected in the C8161 and MUM-2B cell lines. Microscopic picture of invaded cells (C) represents Bar graph (D) and the number of cells invaded the matrigel. (E) Relative cell viability of shDMKN (red line) or NC (black line) cells. Cell proliferation values are presented as the mean SEM of three independent tests. Values are as mean ± SEM, n = 3, **p < 0.001 for NC. The grouping of western blot gel cropped from different parts of the same gel. During the invasion assay, the leftover supernatants on the upper chamber of the transwell insert were collected from all the treatments of both cells.</p

    Rhamnose Displays an Anti-obesity Effect through Stimulating Adipose Dopamine Receptors and Thermogenesis

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    The imbalance between energy intake and energy expenditure leads to the prevalence of obesity world-widely. Strategy to simultaneously limit energy intake and promote energy expenditure will serve as a powerful mean for new obesity treatment. Here, we identified Rhamnose as a non-nutritive sweetener to promote adipose thermogenesis and energy expenditure. Rhamnose promotes cAMP production and PKA activation through dopamine receptor D1 in adipose tissue. As a result, Rhamnose administration promotes UCP1dependent thermogenesis and ameliorates obesity in mice. Thus, we have demonstrated a Rhamnose-dopamine receptor D1-PKA axis critical for thermogenesis and Rhamnose may serve as a new therapeutic molecular diet against obesity.</p

    The full-length gels are included in this study.

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    To discover vulnerabilities associated with dermokine (DMKN) as a new trigger of the epithelial-mesenchymal transition (EMT) -driven melanoma, we undertook a genome-wide genetic screening using transgenic. Here, we showed that DMKN expression could be constitutively increased in human malignant melanoma (MM) and that this correlates with poor overall survival in melanoma patients, especially in BRAF-mutated MM samples. Furthermore, in vitro, knockdown of DMKN inhibited the cell proliferation, migration, invasion, and apoptosis of MM cancer cells by the activation of ERK/MAPK signaling pathways and regulator of STAT3 in downstream molecular. By interrogating the in vitro melanoma dataset and characterization of advanced melanoma samples, we found that DMKN downregulated the EMT-like transcriptional program by disrupting EMT cortical actin, increasing the expression of epithelial markers, and decreasing the expression of mesenchymal markers. In addition, whole exome sequencing was presented with p.E69D and p.V91A DMKN mutations as a novel somatic loss of function mutations in those patients. Moreover, our purposeful proof-of-principle modeled the interaction of ERK with p.E69D and p.V91A DMKN mutations in the ERK-MAPK kinas signaling that may be naturally associated with triggering the EMT during melanomagenesis. Altogether, these findings provide preclinical evidence for the role of DMKN in shaping the EMT-like melanoma phenotype and introduced DMKN as a new exceptional responder for personalized MM therapy.</div
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