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| http://dx.doi.org/10.1007/s10815-022-02561-6 | DOI Listing |
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Space exploration and risk of Parkinson's disease: a perspective review.
NPJ Microgravity
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Department of Biological Science, Boise State University, Boise, ID, 83725, USA.
Systemic mitochondrial dysfunction, dopamine loss, sustained structural changes in the basal ganglia including reduced tyrosine hydroxylase, and altered gait- these effects observed in space-flown animals and astronauts mirrors Parkinson's disease (PD). Evidence of mitochondrial changes in space-flown human cells, examined through the lens of PD, suggests that spaceflight-induced PD-like molecular changes are important to monitor during deep space exploration. These changes, may potentially elevate the risk of PD in astronauts.
View Article and Find Full Text PDFA self-assembled fluorescent nanoprobe recognized by FA1 site for specifically selecting HSA: Its applications in hemin detection, cell imaging and fluorescent tracing drug delivery.
Bioorg Chem
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Pancreas Center, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, State Key Laboratory of Druggability Evaluation and Systematic Translational Medicine, Tianjin Key Laboratory of Digestive Cancer, Tianjin's Clinical Research Center for Cancer, Tianjin 300060, China. Electronic address:
As naturally essential biomacromolecule, HSA has become diagnostic indicators for various diseases and universal carriers for anticancer drug delivery, therefore, fluorescence detection and labeling for HSA possess significant application value in the biomedical field. In this paper, hydrazide Schiff base fluorescent probe NDQC was designed and synthesized, which self-assembled into nanoparticles in aqueous solution system and demonstrated excellent selectivity and sensitivity towards HSA. Through displacement assay and molecular docking simulation, the binding of NDQC with HSA in FA1 site was demonstrated, thereby no obvious fluorescence signal presented for homologous protein BSA due to their structural differences in binding site.
View Article and Find Full Text PDFCorrection: IFI6 depletion inhibits esophageal squamous cell carcinoma progression through reactive oxygen species accumulation via mitochondrial dysfunction and endoplasmic reticulum stress.
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Department of Thoracic Surgery, Shanghai Tongji Hospital Affiliated With Tongji University, Shanghai, 200065, P. R. China.
Mitochondrial DNA lineages determine tumor progression through T cell reactive oxygen signaling.
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Center for Mitochondrial and Epigenomic Medicine, The Children's Hospital of Philadelphia, Philadelphia, PA 19104.
Mitochondrial DNA (mtDNA) is highly polymorphic, and host mtDNA variation has been associated with altered cancer severity. To determine the basis of this mtDNA-cancer association, we analyzed conplastic mice with the C57BL/6J (B6) nucleus but two naturally occurring mtDNA lineages, and , where mitochondria generate more oxidative phosphorylation (OXPHOS)-derived reactive oxygen species (mROS). In a cardiac transplant model, Foxp3+ T regulatory (Treg) cells supported long-term allograft survival, whereas Treg cells failed to suppress host T effector (Teff) cells, leading to acute rejection.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
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Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Sodium glucose transporter 2 inhibitor (SGLT2i) is the latest guideline-directed medical therapy for patients with heart failure, as it has demonstrated favorable cardiovascular outcomes in heart failure (HF) patients with or without diabetes. Furthermore, SGLT2i has effectively improved cognitive function in older adults with diabetes and HF. However, the effects of SGLT2i on cognitive function and brain mitochondrial function in rats with ischemic HF have never been investigated.
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