Results 101 to 110 of about 1,701,334 (266)

Gut microbiome and aging—A dynamic interplay of microbes, metabolites, and the immune system

open access: yesFEBS Letters, EarlyView.
Age‐dependent shifts in microbial communities engender shifts in microbial metabolite profiles. These in turn drive shifts in barrier surface permeability of the gut and brain and induce immune activation. When paired with preexisting age‐related chronic inflammation this increases the risk of neuroinflammation and neurodegenerative diseases.
Aaron Mehl, Eran Blacher
wiley   +1 more source

Epigenetic blind spots – the role of DNA methylation dynamics in stem cell‐based models of embryogenesis

open access: yesFEBS Letters, EarlyView.
Embryo‐like structures (stembryos) are an innovative tool, but they are hindered by experimental variability and limited developmental potential. DNA methylation is crucial for mammalian development, but its status in stembryo models is poorly characterized.
Sara Canil   +4 more
wiley   +1 more source

The human gut microbiome across the life course

open access: yesFEBS Letters, EarlyView.
Despite significant individual variation and continuous change throughout life, the human gut microbiome follows some life stage‐specific trends. This article provides a brief overview of how gut microbiome composition shifts across different phases of life. Created in BioRender. Özkurt, E. (2026) https://BioRender.com/8q4nrnc.
Alise J. Ponsero   +4 more
wiley   +1 more source

Degradation mechanism of the von Willebrand factor A2 domain by nattokinase

open access: yesFEBS Letters, EarlyView.
Nattokinase, a natto‐derived protease, exhibits potent antithrombotic effects. This study demonstrates that nattokinase directly cleaves the von Willebrand factor (vWF) A2 domain in vitro. Unlike the native regulator ADAMTS13, nattokinase degrades folded vWF independently of shear stress.
Ryuichi Hyakumoto   +3 more
wiley   +1 more source

Microbiome‐blood–brain barrier interactions in aging — mechanisms and therapeutic potential

open access: yesFEBS Letters, EarlyView.
Aging reshapes the gut microbiome (↓SCFA‐producing commensals; ↑pro‐inflammatory outputs), shifting circulating metabolites (↓SCFAs; ↑LPS, ↑TMAO, ↑PAA) that act at the BBB to increase nonspecific transcytosis, alter transport, and promote astrocyte reactivity, heightening brain vulnerability.
Daniel Cuervo‐Zanatta   +3 more
wiley   +1 more source

Ultrasound and adverse effects [PDF]

open access: yesUltrasound in Obstetrics & Gynecology, 2002
H, Kieler   +4 more
openaire   +2 more sources

The therapeutic opportunities and pitfalls of using iron ion chelators to treat neurodegenerative diseases

open access: yesFEBS Letters, EarlyView.
Although too much iron in the brain promotes neurodegeneration, iron ion chelators have had mixed effects in clinical trials. This review explains why; some chelators do not render the iron redox‐inactive (e.g., L1) whereas others do (e.g., desferrioxamine).
Barry Halliwell
wiley   +1 more source

The role of miR‐335‐5p in the redifferentiation of BRAF p.V600E thyroid cancers

open access: yesMolecular Oncology, EarlyView.
The BRAF p.V600E mutation promotes thyroid cancer dedifferentiation and radioiodine resistance. Using a network approach, we identified miR‐335‐5p as a key regulator of BRAF‐mutated thyroid tumors. Restoring miR‐335‐5p increased thyroid‐specific gene expression and iodine uptake in cells and organoids.
Valeria Pecce   +11 more
wiley   +1 more source

Dimethyl fumarate combined with cisplatin at subcytotoxic doses sensitizes cervical cancer toward ferroptosis and apoptosis through GSH restriction and p53 (re)activation

open access: yesMolecular Oncology, EarlyView.
Dimethyl fumarate (DMF) reduces growth of HPV‐positive cervical cancer spheroids and induces ferroptosis in cervical cancer cells via blocking SLC7A11/Glutathione (GSH) axis. Combination of subcytotoxic doses of DMF and cisplatin (CDDP) further suppresses spheroid growth and drives cell death in 2D culture models.
Carolina Punziano   +6 more
wiley   +1 more source

Differential expression of cancer‐related genes supports prediction of poor response to first‐line treatments in T‐ALL pediatric patients with high minimal residual disease

open access: yesMolecular Oncology, EarlyView.
In the present work, we have identified a transcriptional signature based on the differential expression of six genes (BCL2&MAST4, HSH2D&LAT2, METRN&PITPNM2) that would facilitate the early detection of T‐cell acute lymphoblastic leukemia (T‐ALL) patients prone to a poor treatment response and could be implemented at diagnosis, along with other risk ...
Antonio Lahera   +11 more
wiley   +1 more source

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