Results 131 to 140 of about 549,472 (306)

Microglia‐Targeted Biomimetic Tetrahedral Framework Nucleic Acid Nanovesicles for Synergistic Treatment of Sepsis‐Associated Encephalopathy

open access: yesAdvanced Science, EarlyView.
Sepsis‐associated encephalopathy (SAE) lacks effective therapies. We developed ME@FDsi, a biomimetic nanodrug using a tetrahedral framework nucleic acid to deliver disulfiram and siTNFα. It crosses the blood‐brain barrier, targets M1 microglia, inhibits pyroptosis and inflammation, and scavenges ROS.
Huimin Shi   +15 more
wiley   +1 more source

Rabbit models of heart disease. [PDF]

open access: yes, 2008
Human heart disease is a major cause of death and disability. A variety of animal models of cardiac disease have been developed to better understand the etiology, cellular and molecular mechanisms of cardiac dysfunction and novel therapeutic strategies ...
Bers, Donald M, Pogwizd, Steven M
core  

Multi‐Omics Insights Into the Mechanisms of Early Muscle Fiber Difference and Transformation Between Lean‐Type and Chinese Indigenous Pigs

open access: yesAdvanced Science, EarlyView.
Multi‐omics analyses uncover breed‐specific cis‐regulatory landscapes and higher‐order chromatin architectural differences that underlie early postnatal muscle fiber divergence in pigs. A super‐enhancer upstream of PPP3CB recruits MEF2C to activate PPP3CB transcription, while the PPP3CB–MEF2C positive feedback loop promotes oxidative muscle fiber ...
Shuailong Zheng   +8 more
wiley   +1 more source

Genital Hypertrophy [PDF]

open access: yesProceedings of the Royal Society of Medicine, 1935
openaire   +2 more sources

Mechanosensitive Piezo1/Osteocalcin/Irisin Axis Protects Against Disuse‐Induced Muscle Atrophy

open access: yesAdvanced Science, EarlyView.
Mechanical unloading suppresses bone Piezo1 expression, which reduces circulating undercarboxylated osteocalcin (unOCN). unOCN reduction subsequently exacerbates IMM‐induced Fndc5/Irisin decrease and drives severe muscle atrophy. Bone Piezo1 activation or exogenous osteocalcin/Irisin ameliorate muscle atrophy, while muscle‐specific Gprc6a or Fndc5 ...
Zhaolu Wang   +5 more
wiley   +1 more source

Short term creatine loading improves strength endurance even without changing maximal strength, RPE, fatigue index, blood lactate, and mode state

open access: yesAnais da Academia Brasileira de Ciências
Creatine is consumed by athletes to increase strength and gain muscle. The aim of this study was to evaluate the effects of creatine supplementation on maximal strength and strength endurance.
EDILSON TADEU F. FURTADO   +5 more
doaj   +1 more source

Hypertrophy

open access: yes, 2020
Justin Rich, Daniel Bell, Mostafa Elfeky
  +4 more sources

Biomimetic Bone Marrow Monocyte Membrane‐Fused Extracellular Vesicles for Targeted Therapy of Myocardial Infarction

open access: yesAdvanced Science, EarlyView.
This study develops a biomimetic delivery system (M‐hEV) by fusing monocyte membranes with extracellular vesicles for targeted therapy of damaged cardiac tissue. The system homes to injured myocardium through specific molecular pathways. In a myocardial infarction model, M‐hEV effectively accumulates in the heart, reduces infarct size, alleviates ...
Jiaxin Song   +10 more
wiley   +1 more source

Caveolin‐1 Stabilizes SERCA2 to Counteract Acute Kidney Injury via Suppression of Ca2+‐Dependent Endoplasmic Reticulum Stress in Distal Tubules

open access: yesAdvanced Science, EarlyView.
In AKI, initial kidney injury upregulates the expression of Cav‐1, which subsequently binds to and stabilizes SERCA2 via its scaffolding domain and through deubiquitination, thereby regulating Ca2+ homeostasis and ER stress. Conversely, Cav‐1 deficiency accelerates SERCA2 degradation, triggering Ca2+ overload and ER stress, and ultimately exacerbating ...
Yan Zhang   +19 more
wiley   +1 more source

CK2α Deficiency Drives Myocardial Fibrosis via Desmin‐Induced Mitochondrial Dysfunction

open access: yesAdvanced Science, EarlyView.
CK2α preserves mitochondrial homeostasis by phosphorylating Desmin to recruit Cryab, ensuring proper filament assembly. CK2α deficiency disrupts this interaction, causing mitochondrial dysfunction, metabolic shifts, bioenergetic failure, and oxidative stress—ultimately establishing a pro‐fibrotic environment that drives cardiac fibrosis.
Canjie Ma   +12 more
wiley   +1 more source

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