8 research outputs found
Gut microbiota and its metabolites in Alzheimer’s disease: from pathogenesis to treatment
Introduction An increasing number of studies have demonstrated that altered microbial diversity and function (such as metabolites), or ecological disorders, regulate bowel–brain axis involvement in the pathophysiologic processes in Alzheimer’s disease (AD). The dysregulation of microbes and their metabolites can be a double-edged sword in AD, presenting the possibility of microbiome-based treatment options. This review describes the link between ecological imbalances and AD, the interactions between AD treatment modalities and the microbiota, and the potential of interventions such as prebiotics, probiotics, synbiotics, fecal microbiota transplantation, and dietary interventions as complementary therapeutic strategies targeting AD pathogenesis and progression. Survey methodology Articles from PubMed and china.com on intestinal flora and AD were summarized to analyze the data and conclusions carefully to ensure the comprehensiveness, completeness, and accuracy of this review. Conclusions Regulating the gut flora ecological balance upregulates neurotrophic factor expression, regulates the microbiota-gut-brain (MGB) axis, and suppresses the inflammatory responses. Based on emerging research, this review explored novel directions for future AD research and clinical interventions, injecting new vitality into microbiota research development
Charging and discharging electrochemical supercapacitors in the presence of both parallel leakage process and electrochemical decomposition of solvent
Simple models for electrochemical supercapacitors are developed to describe the charge-discharge behaviors in the presence of both voltage-independent parallel leakage process and electrochemical decomposition of solvent. The models are validated by experimental data collected using a symmetric two-electrode test cell with carbon powder as the electrode layer material and stainless steel as the current collector.Peer reviewed: YesNRC publication: Ye
Targetable Fluorescent Probe for Monitoring Exogenous and Endogenous NO in Mitochondria of Living Cells
Nitric oxide (NO) is a ubiquitous
cellular messenger molecule in
the cardiovascular, nervous, and immune systems. Mitochondrion is
the main area where endogenous NO is synthesized by inducible NOS
enzymes in mammalian cells. Thus, real-time monitoring NO in mitochondria
is very meaningful for NO chemical biology. Although a variety of
fluorescent probes for NO have been successfully developed, they are
not suited for detecting mitochondrial NO because none of them can
specifically localize in mitochondria. Herein, Mito-Rh-NO, the first
mitochondria-targetable “turn-on” fluorescent probe
for NO, has been developed through attaching a triphenylphosphonium
to a rhodamine spirolactam. The characteristics of this probe are
as following: (1) Mito-Rh-NO exhibits high sensitivity toward NO.
In solution, Mito-Rh-NO responds to NO by significant fluorescence
enhancement up to 60-fold, and its NO detection limit is as low as
4.0 nM. (2) The NO sensing of Mito-Rh-NO is highly selective, which
will not interfere with the other reactive oxygen and nitrogen species.
(3) Mito-Rh-NO has a low cytotoxic effect: after being treated with
10 ÎĽM Mito-Rh-NO for 24 h, the survival rate is higher than
90%. (4) Mito-Rh-NO specifically localizing in mitochondria: colocalization
experiment of Mito-Rh-NO and Rh 123, a typical mitotracker, shows
the merged fluorescent microcopy image with a high Pearson’s
colocalization coefficient 0.92 and overlap coefficient 0.99. (5)
Mito-Rh-NO demonstrates high applicability for real-time monitoring
of mitochondrial NO in live cells. Both the exogenous NO released
by the donor NOC13 and endogenous NO generated in cells under stimulation
have been visualized under confocal microscopy