Results 311 to 320 of about 9,625,606 (401)

The Mechanism of Postoperative Tetany in Graves' Disease

open access: bronze, 1989
Tsukasa Murakami   +4 more
openalex   +2 more sources

Atrial Fibroblasts‐Derived Extracellular Vesicles Exacerbate Atrial Arrhythmogenesis

open access: yesAdvanced Science, EarlyView.
Exosome miR‐224‐5p derived from angiotensin II‐treated atrial fibroblasts creates a substrate for AF by promoting atrial electrical remodeling. Increased exosome miR‐224‐5p enhances AF susceptibility by inhibiting CACNA1c expression and decreasing ICa current of atrial cardiomyocytes.
Yue Yuan   +13 more
wiley   +1 more source

Alternative Models for Anticancer Drug Discovery From Natural Products Using Binary Tumor‐Microenvironment‐on‐a‐Chip

open access: yesAdvanced Science, EarlyView.
This study presents a binary tumor‐microenvironment‐on‐a‐chip (T‐MOC) system incorporating multicellular tumor spheroids (MCTs) as an alternative preclinical platform to evaluate the efficacy of anticancer natural products. The T‐MOC model reproduces in vivo drug delivery barriers and physiological conditions, enabling morphological analysis to predict
Youngwon Kim   +7 more
wiley   +1 more source

Acute Pericarditis Associated With Graves' Disease: A Case Report. [PDF]

open access: yesCureus
Estrela Santos M   +4 more
europepmc   +1 more source

FOXM1 Protects Against Myocardial Ischemia‐Reperfusion Injury in Rodent and Porcine Models by Suppressing MKRN1‐Dependent LKB1 Ubiquitination

open access: yesAdvanced Science, EarlyView.
FOXM1 maintains mitochondrial bioenergetic function by inhibiting MKRN1‐mediated ubiquitination of LKB1 in cardiomyocytes. Loss of FOXM1 in cardiomyocytes results in upregulation of MKRN1, which enhances LKB1 ubiquitination and disrupts AMPK signaling and energy metabolism pathways. Conversely, FOXM1 overexpression preserves mitochondrial bioenergetics
Shuai Song   +17 more
wiley   +1 more source

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