Results 171 to 180 of about 889,444 (319)

Inflammation Unchecked: Concurrent Kawasaki Disease and Stevens‐Johnson Syndrome in an 18‐Month‐Old Child

open access: yes
Arthritis Care &Research, EarlyView.
Catherine Deffendall   +6 more
wiley   +1 more source

G3BP1 Succinylation at K413 is Critical for Cardiac Function by Modulating PI3K‐AKT‐mTOR Signal Axis

open access: yesAdvanced Science, EarlyView.
Schematic illustrating the impact of G3BP1 succinylation at K413 on cardiac function. In the healthy human heart, G3BP1 succinylation maintains homeostatic mTOR signaling. In patients with dilated cardiomyopathy (DCM) and heart failure (HF), G3BP1 de‐succinylation induces RagA expression and disrupts the binding of the TSC1/2 complex, leading to the ...
Yuan Zhang   +9 more
wiley   +1 more source

Abfraction lesions: etiology, diagnosis, and treatment options

open access: yes, 2016
Marcelle M Nascimento,1 Deborah A Dilbone,1 Patricia NR Pereira,1 Wagner R Duarte,2,3 Saulo Geraldeli,1 Alex J Delgado1 1Department of Restorative Dental Sciences, Division of Operative Dentistry, 2Department of Periodontology, College of Dentistry ...
Pereira PN   +5 more
core  

T Cell Exhaustion in Cancer Immunotherapy: Heterogeneity, Mechanisms, and Therapeutic Opportunities

open access: yesAdvanced Science, EarlyView.
T cell exhaustion limits immunotherapy efficacy. This article delineates its progression from stem‐like to terminally exhausted states, governed by persistent antigen, transcription factors, epigenetics, and metabolism. It maps the exhaustion landscape in the TME and proposes integrated reversal strategies, providing a translational roadmap to overcome
Yang Yu   +7 more
wiley   +1 more source

Carboranyl‐Curcuminoids for the Neutron Capture‐Based Treatment of Amyloid Aggregates in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
The 10B‐enriched monocarbonyl analog of curcumin (BMAC) 10B‐9 enables site‐specific Boron Neutron Capture Therapy (BNCT) on amyloid‐β (Aβ) fibrils. Neutron irradiation induces histidine oxidation and fibril destabilization, as revealed by 1H‐NMR and FESEM analyses.
Sebastiano Micocci   +13 more
wiley   +1 more source

Insights into genetic susceptibility in the etiology of spontaneous preterm birth

open access: yes, 2015
Sasha E Parets,1 Anna K Knight,2 Alicia K Smith,1,2 1Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA, USA; 2Genetics and Molecular Biology Program, Emory University, Atlanta, GA, USA Abstract: Preterm ...
Knight AK, Parets SE, Smith AK
core  

Etiology of Acute Pancreatitis

open access: yes
Acute Pancreatitis is an inflammatory condition of the pancreas which is characterized by abdominal pain and elevated pancreatic enzymes in the blood. Acute pancreatitis is one of the leading gastrointestinal cause of hospitalization in the United States.
Casey, Kevin
core   +1 more source

Dose‐Dependent Reprogramming of Chromatin Accessibility by SOX4 Drives the Transcriptional Response to Iron Overload

open access: yesAdvanced Science, EarlyView.
This study demonstrates that iron overload triggers widespread chromatin compaction and transcriptional repression in human granulosa cells, recapitulating features of endometriosis. The epigenetic reprogramming is orchestrated by a TFEB‐SOX4‐SWI/SNF axis, with SOX4 acting as a central, dosage‐sensitive regulator.
Feifei Li   +15 more
wiley   +1 more source

Epithelial TRIM27 Inhibits Intestinal Inflammation in Ulcerative Colitis by the USP7/TRIM27‐IKK Double Negative‐Feedback

open access: yesAdvanced Science, EarlyView.
ABSTRACT The E3 ubiquitin ligase tripartite motif 27 (TRIM27) is a negative regulator of NF‐κB activation and the innate immune response, and TRIM27 deficiency significantly impairs dextran sulfate sodium (DSS)‐induced colitis. The function of TRIM27 in intestinal epithelial cells (IECs), the mechanism by which TRIM27 inhibits the NF‐κB pathway and its
Weimin Xu   +10 more
wiley   +1 more source

BIN1 and ALDH1B1 Deficiency in Colonic Smooth Muscle Drives Mitochondrial Dysfunction and Fibrosis in Slow‐Transit Constipation

open access: yesAdvanced Science, EarlyView.
Slow‐transit constipation (STC) is a disabling motility disorder with unclear smooth‐muscle mechanisms. Spatial proteomic analysis of STC patient colon reveals both the central pathogenic role of smooth muscle cells (SMCs) in STC and novel regulators of intestinal motility, BIN1 and ALDH1B1.
Jianbo Liu   +10 more
wiley   +1 more source

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