Results 101 to 110 of about 2,337,421 (248)

QRICH1 Disrupts Endoplasmic Reticulum Homeostasis and Amplifies NF‐κB Signaling in Periodontal Ligament Stem Cells to Exacerbate Diabetic Periodontitis

open access: yesAdvanced Science, EarlyView.
QRICH1 has been established as a key factor contributing to impaired osteogenic potential and accelerated apoptosis of PDLSCs in diabetic periodontitis. QRICH1 not only significantly enhances UPR‐associated apoptotic signaling but also amplifies NF‐κB‐mediated inflammatory responses. Its inhibition restores osteogenic capacity and reduces alveolar bone
Han Li   +9 more
wiley   +1 more source

Hypoxic stress in diabetic pregnancy contributes to impaired embryo gene expression and defective development by inducing oxidative stress

open access: yes, 2005
We have shown that neural tube defects (NTD) in a mouse model of diabetic embryopathy are associated with deficient expression of Pax3, a gene required for neural tube closure. Hyperglycemia-induced oxidative stress is responsible.
Jung, Sung-Kwon   +4 more
core   +1 more source

An Audit of Neural Tube Defects in the Republic Of Ireland for 2012-2015

open access: yes, 2018
Neural tube defects (NTD) are potentially preventable in two-thirds of cases by periconceptional maternal Folic Acid (FA) supplementation. A national audit for the years 2009-11 showed no decline in NTD rates over twenty years.
Delany, V   +4 more
core  

Gut Microbial Release of Ferulic Acid From Germinated Quinoa Alleviates Obesity‐Associated Cognitive Impairment by Activating Hippocampal Mitophagy Associated with PINK1/Parkin Pathway

open access: yesAdvanced Science, EarlyView.
Liberation of ferulic acid by gut microbial feruloyl esterase mediates cognitive enhancement of germinated quinoa (GQF) on obese mice. Ferulic acid enriched in GQF is released by gut microbes Roseburia hominis and R. intestinalis and subsequently mediates the neuroprotective effects of GQF on obesity‐induced cognitive decline by activating hippocampal ...
Yongli Lan   +11 more
wiley   +1 more source

A Second Pathogenic Protein, PolyGN2C‐iso2, Reveals a Dual‐Protein Pathology in Neuronal Intranuclear Inclusion Disease

open access: yesAdvanced Science, EarlyView.
This study reveals that NOTCH2NLC transcript variant 2 generates PolyGN2C‐iso2, an aggregating protein present within intranuclear inclusions of NIID patient tissues. A novel mouse model expressing PolyGN2C‐iso2 recapitulates white matter abnormalities and cognitive deficits, mechanistically linked to mitochondrial dysfunction. These findings support a
Kang Zhang   +22 more
wiley   +1 more source

Global prevention of neural tube defects [PDF]

open access: yes
Tuesday, October 17, 2017 at 1:00 p.m.Neural tube defects are serious birth defects of the brain and spine. They are a major cause of death and lifelong disability worldwide.

core  

Estudo clínico de pacientes com defeitos de fechamento do tubo neural na cidade de Florianópolis, no período de 01/01/2000 a 31/12/2004. [PDF]

open access: yes, 2005
Trabalho de Conclusão de Curso - Universidade Federal de Santa Catarina. Curso de Medicina.
Batista, Luana Graziela.
core  

Ultrasound‐Activated Piezoelectric Neuroimmune Hydrogel Orchestrates Neurogenesis‐Macrophage Crosstalk in Diabetic Wound Healing

open access: yesAdvanced Science, EarlyView.
In this work, we design an ultrasound‐activated piezoelectric hydrogel platform (AOEF@AP5+US) that reprograms neurogenesis‐macrophage crosstalk as an integrated strategy to overcome the intertwined barriers of chronic inflammation, peripheral neuropathy, and impaired regeneration in diabetic wounds.
Kai Wang   +13 more
wiley   +1 more source

Neural Tube Defects

open access: yes, 2018
Neural tube defects (NTDs) and hemivertebra represent major congenital abnormalities of the cranial vault and the fetal spine.NTDs are the consequence of a failed closure of the cranial and/or the caudal neural tube.
Frusca T.   +5 more
core   +1 more source

Trafficking Deficiency of TMEM175 Variants in Parkinson's Disease Pathogenesis and the Prospects of Precision Medicine

open access: yesAdvanced Science, EarlyView.
This study identifies that the PD‐associated TMEM175‐L156P variant disrupts lysosomal ion channel trafficking by causing aberrant endoplasmic reticulum retention. A “chaperone–agonist” bifunctional small molecule restores TMEM175‐L156P lysosomal localization and channel function, thereby alleviating PD‐relevant cellular phenotypes and highlighting a ...
Ting Luo   +17 more
wiley   +1 more source

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