Results 141 to 150 of about 1,407,914 (310)

Oregon practitioner's manual

open access: yes, 2008
This archived document is maintained by the Oregon State Library as part of the Oregon Documents Depository Program. It is for informational purposes and may not be suitable for legal purposes.OrDocs shipping list 2009-15"A collaborative project ...

core  

TH/TRs–COL11A2 Axis Mediates Loss of a Differentiated Astrocyte State in Hypogyrified Brains

open access: yesAdvanced Science, EarlyView.
Using a gyrencephalic congenital hypothyroidism pig model, this study reveals cerebral atrophy and cortical hypogyrification. Single‐cell sequencing identifies astrocytes as major TH‐responsive cells, with the COL11A2‐enriched Astro‐2 state nearly absent.
Ying Zhang   +14 more
wiley   +1 more source

Usefulness of levels of 2-methylbutyrylglycine and 2-ethylhydracrylic acid in urine for diagnosing 2-methylbutyrylglycinuria

open access: yesOrphanet Journal of Rare Diseases
Background The congenital disease 2-methylbutyrylglycinuria involves defective isoleucine metabolism and is currently diagnosed based on elevated levels of 2-methylbutyrylcarnitine/isovalerylcarnitine C5 in blood, followed by analysis of 2 ...
Hao Liu   +6 more
doaj   +1 more source

A NEW OUTCOME MEASURE FOR COST-UTILITY ANALYSES OF SCREENING PROGRAMS [PDF]

open access: yes
In this paper we provide a new outcome measure for the cost-utility analyses of alternative screening programs of a particular disease. We show that for non-invasive screening programs satisfying plausible assumptions, QALYs can be replaced by a simpler ...
Carmen Herrero Blanco   +1 more
core  

Periostin‐CCL3 Feedforward Signaling Loop Promotes Cardiac Fibrosis and Cardiomyocyte Necroptosis in Arrhythmogenic Cardiomyopathy

open access: yesAdvanced Science, EarlyView.
POSTN‐CCL3 signaling forms a feed‐forward circuit between cardiomyocytes and cardiac myofibroblasts in arrhythmogenic cardiomyopathy. POSTN activates JNK/RIP3‐dependent necroptotic signaling and JNK/ETS2‐induced CCL3 expression in cardiomyocytes. In turn, CCL3‐CCR5 signaling in cardiac myofibroblasts activates NF‐κB/p65 and promotes POSTN expression ...
Tiantian Wu   +12 more
wiley   +1 more source

Microglial TSPAN4‐Dependent Migrasomes Promote Pathological Retinal Neovascularization via Immune‐Vascular Crosstalk

open access: yesAdvanced Science, EarlyView.
Combined high‐glucose and hypoxic stress switches microglia into a TSPAN4‐dependent migrasome‐producing state. These migrasomes deliver pro‐angiogenic signals to endothelial cells, activating HIF‐1α/VEGF signaling, disrupting vascular junctions, and fueling pathological neovascularization. This work uncovers migrasome‐mediated immune‐vascular crosstalk
Jingyi Xu   +12 more
wiley   +1 more source

P619: Three years of newborn screening for MPS1 in Ontario: Challenges of screening for the severe end of a disease continuum

open access: yesGenetics in Medicine Open
Melanie Lacaria   +6 more
doaj   +1 more source

Matrix Rigidity Mechanoprimes Microglia for Inflammation Through Cytoskeletal‐to‐Nuclear Signaling and 3D Spatio‐Epigenomic Remodeling

open access: yesAdvanced Science, EarlyView.
Pathological tissue rigidity mechanoprimes microglia by enhancing actin cytoskeleton–nucleus coupling and chromatin opening at rigidity‐responsive cis‐regulatory elements (mechanoCREs). Subsequent NF‐κB/p65 signaling converges on this permissive regulatory state to amplify inflammatory gene expression and microglial activation.
Yu Xuan Meng   +15 more
wiley   +1 more source

P506: Long-term results and challenges of newborn screening for classic homocystinuria in New York State

open access: yesGenetics in Medicine Open
Jing Xiao   +6 more
doaj   +1 more source

An Extracellular Pore‑Targeting Peptide Defines a Designable Allosteric Site in TRPV2

open access: yesAdvanced Science, EarlyView.
Structure‐guided peptide engineering yields Depiv2, a highly potent and subtype‐selective TRPV2 inhibitor that binds to the extracellular pore and remodels it into a closed, non‐conductive state. Depiv2 suppresses pathological cardiac hypertrophy, establishing the TRPV2 outer pore as a designable interface for selective peptide modulation.
Aiqin Zhu   +7 more
wiley   +1 more source

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