Results 61 to 70 of about 74,343 (191)
Ferroptosis: The Demise of Cells Through Phospholipid Peroxidation
The relative abundance of peroxidation‐resistant monounsaturated fatty acids (MUFAs) vs. peroxidation‐sensitive polyunsaturated fatty acids (PUFAs) incorporated into phospholipid (PL) is a key determinant of ferroptosis sensitivity, as the peroxidation of PL PUFA acyl chains (PUFA‐PL) disrupts membrane integrity, causing ferroptotic cell death ...
Shaojie Cui, Jin Ye
wiley +1 more source
Immunometabolic and Spatiotemporal Control of Tissue‐Resident Memory T Cell Biology
Tissue‐resident memory T (TRM) cells in barrier tissues provide a frontline defense against invading pathogens. Immune (Signals 1–3) and nutrient (Signal 4) cues play an integral role in directing TRM formation and heterogeneity. The spatial and temporal organization of these signals establishes durable TRM cells across tissues, enabling diverse ...
Jana L. Raynor, Hongbo Chi
wiley +1 more source
An implementation of Deflate in Coq
The widely-used compression format "Deflate" is defined in RFC 1951 and is based on prefix-free codings and backreferences. There are unclear points about the way these codings are specified, and several sources for confusion in the standard. We tried to
AW Appel +9 more
core +1 more source
Coenzyme Q deficiency causes impairment of the sulfide oxidation pathway [PDF]
Coenzyme Q (CoQ) is an electron acceptor for sulfide‐quinone reductase (SQR), the first enzyme of the hydrogen sulfide oxidation pathway. Here, we show that lack of CoQ in human skin fibroblasts causes impairment of hydrogen sulfide oxidation ...
Barca, Emanuele +7 more
core +1 more source
Coenzyme Q supplementation in pulmonary arterial hypertension
Mitochondrial dysfunction is a fundamental abnormality in the vascular endothelium and smooth muscle of patients with pulmonary arterial hypertension (PAH). Because coenzyme Q (CoQ) is essential for mitochondrial function and efficient oxygen utilization
Jacqueline Sharp +8 more
doaj +1 more source
Inherited metabolic epilepsies–established diseases, new approaches
Abstract Inherited metabolic epilepsies (IMEs) represent the inherited metabolic disorders (IMDs) in which epilepsy is a prevailing component, often determining other neurodevelopmental outcomes associated with the disorder. The different metabolic pathways affected by individual IMEs are the basis of their rarity and heterogeneity.
Itay Tokatly Latzer, Phillip L. Pearl
wiley +1 more source
CoQ Regulates Brown Adipose Tissue Respiration and Uncoupling Protein 1 Expression
Coenzyme Q (CoQ, aka ubiquinone) is a key component of the mitochondrial electron transport chain (ETC) and membrane-incorporated antioxidant. CoQ10 deficiencies encompass a heterogeneous spectrum of clinical phenotypes and can be caused by hereditary ...
Ching-Fang Chang +6 more
doaj +1 more source
Under hyperglycemic conditions, mitochondrial dysfunction in retinal endothelial cells triggers excessive reactive oxygen species/reactive nitrogen species production, barrier protein degradation, and endothelial barrier breakdown in diabetic retinopathy.
Siyu Gui +12 more
wiley +1 more source
Efficient Certified Resolution Proof Checking [PDF]
We present a novel propositional proof tracing format that eliminates complex processing, thus enabling efficient (formal) proof checking. The benefits of this format are demonstrated by implementing a proof checker in C, which outperforms a state-of-the-
A Biere +29 more
core +3 more sources
Ferroptosis is driven by unrestricted peroxidation of polyunsaturated fatty acyl (PUFA) chains in membrane phospholipids. In triple‐negative breast cancer cells, lipid droplets (LDs) sequester dietary PUFAs, limiting their incorporation into membrane phospholipids, preventing mitochondrial damage, and reducing lipid peroxidation and ferroptosis.
Ana Kump +10 more
wiley +1 more source

