Results 41 to 50 of about 449,811 (276)

LRRC4 Orchestrates AP2A1‐Containing Clathrin‐Coated Vesicles to Disrupt Mitochondrial Cristae and Restrict Glioblastoma Progression

open access: yesAdvanced Science, EarlyView.
LRRC4 suppresses GBM by regulating AP2A1‐containing Golgi‐derived clathrin‐coated vesicles. Low LRRC4 allows cytoplasmic AP2A1 to maintain mitochondrial fission‐fusion, MICOS integrity, and OXPHOS, promoting proliferation and invasion. High LRRC4 redirects AP2A1‐containing Golgi‐derived clathrin‐coated vesicles to mitochondria, disrupts MICOS, enhances
Yang Li   +5 more
wiley   +1 more source

A Patient With Thiamine Deficiency Exhibiting Muscle Edema Suggested by MRI

open access: yesFrontiers in Neurology, 2018
Myalgia is sometimes observed in patients with thiamine-deficiency neuropathy. However, the detailed mechanism(s) underlying muscular manifestations have been poorly elucidated.
Kenichiro Murate   +9 more
doaj   +1 more source

An audit of the changes in thiamine levels during higher caloric nutritional rehabilitation of adolescent patients hospitalised with a restrictive eating disorder

open access: yesJournal of Eating Disorders, 2020
Background Routine supplementation of thiamine in patients with restrictive eating disorders prior to initiation of nutritional rehabilitation, is an example of a clinical guideline based on expert opinion rather than evidence-based recommendations. This
Elizabeth Parker   +7 more
doaj   +1 more source

Long Noncoding RNA PCALRx Interacts with Pyruvate Carboxylase to Drive Multi‐Organ Developmental Toxicity in Zebrafish Embryos Exposed to Amoxicillin

open access: yesAdvanced Science, EarlyView.
Embryonic amoxicillin exposure disrupts multi‐organ development in zebrafish larvae through a lncRNA–metabolic enzyme regulatory axis. PCALRx associates with pyruvate carboxylase, promotes PC protein ubiquitination, and impairs mitochondrial energy metabolism, while vitamin B1 partially restores PC‐centered metabolic function and developmental outcomes.
Yixue Yao   +5 more
wiley   +1 more source

Thiamine Deficiency in the Aged [PDF]

open access: yes, 2006
We experienced 8 patients (5 males and 3 females;39~67 yrs,mean:57.9 yrs) with beriberi neuropathy, and 2 patients (a 77 year-old-female and a 64 year-old-male) with Wernicke encephalopathy for the past 4 years. All 8 beriberi patients showed disturbance
中川, 広人, 栗山, 勝
core   +1 more source

Thiamine Allocation and Deficiency Status Throughout the Life Cycle of Cod

open access: yesEcology and Evolution
Several wild bird and fish species across the Northern Hemisphere have been shown to episodically be thiamine deficient. This may lead to mass‐mortality events, especially in offspring.
Marc M. Hauber   +6 more
doaj   +1 more source

Stress Hyperglycemia Drives CD4+ T Cell PANoptosis and Postoperative Organ Injury via Monocyte‐Derived Succinate

open access: yesAdvanced Science, EarlyView.
High glucose is linked to reduced succinate dehydrogenase activity in CD14+ monocytes, accompanied by succinate accumulation and extracellular release. Extracellular succinate exacerbates mitochondrial ROS production and mtDNA release in CD4+ T cells. Cytosolic mtDNA then activates Z‐DNA binding protein 1 (ZBP1) and engages ZBP1‐associated inflammatory
Shuai Zhao   +11 more
wiley   +1 more source

Metabolic Acidosis and Thiamine Deficiency [PDF]

open access: yesMayo Clinic Proceedings, 1999
We describe a 19-year-old patient who was receiving home parenteral nutrition in whom lactic acidosis developed. A review of her home parenteral nutrition formula revealed the absence of multivitamins, most significantly thiamine. After thiamine administration, the acidosis resolved, and the patient experienced pronounced clinical improvement ...
S A, Romanski, M M, McMahon
openaire   +2 more sources

A Case of Multiple Mitochondrial Dysfunctions Syndrome 1 and Review of the Literature

open access: yesAmerican Journal of Medical Genetics Part A, EarlyView.
ABSTRACT Multiple mitochondrial dysfunctions syndrome 1 (MMDS1, MIM #605711) due to NFU1 gene defects is an ultra‐rare autosomal recessive inborn error of metabolism associated with reduced function of NFU1 iron–sulfur cluster (ISC) scaffold protein.
Charles R. DiFalco   +6 more
wiley   +1 more source

L‐Cysteine and N‐Acetylcysteine Supplementation Improves Clinical Outcome in a Patient With COXPD10

open access: yesAmerican Journal of Medical Genetics Part A, EarlyView.
ABSTRACT MTO1 is a nuclear gene that encodes a mitochondrial protein essential for modifying mitochondrial transfer RNAs (tRNAs) and stabilizing codon‐anticodon interactions to ensure accurate and efficient mitochondrial protein synthesis and oxidative phosphorylation.
Nishitha R. Pillai   +5 more
wiley   +1 more source

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