Publications by authors named "N Ojeda"

Aim: To describe the cortical brain development and full-IQ performance in middle school age children after extremely preterm (EPT) birth considering discrete white matter abnormalities (WMA). In addition, to assess possible early motor predictors of cortical brain development and full-IQ in children born EPT with and without discrete WMA diagnosed at 10 years.

Methods: T1-weighted MRI images from fifty-one children born before 27 weeks' gestation and 40 full-term born controls (M=10.

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Background: Perinatal infection is a major risk factor for diffuse white matter injury (dWMI), which remains the most common form of neurological disability among very preterm infants. The disease primarily targets oligodendrocytes (OL) lineage cells in the white matter but also involves injury and/or dysmaturation of neurons of the gray matter. This study aimed to investigate whether neuroinflammation preferentially affects the cellular compositions of the white matter or gray matter.

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Endocrine Disruptor Compounds (EDCs) in the aquatic environment have acquired pronounced relevance due to their toxic effect on the aquatic flora and fauna. Xenoestrogens are EDCs that possess estrogenic activity and, thus, disrupt normal estrogen signaling, affecting different functions, such as immune system processes. Two relevant xenoestrogens discarded into fresh and seawater are 4-nonylphenol (NP) and 17⍺-Ethynyl Estradiol (EE2).

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Prematurity has been related to altered brain structure and cognition, and so our aim was to describe them in the absence of major structural brain injury following low-risk preterm birth during adolescence and young adulthood. The sample consisted of 250 participants, 132 of whom were low-risk preterm (30-36 weeks' gestational age) and 118 were full-term individuals (37-42 weeks' gestational age), aged between 16 and 38 years old. All participants underwent an extensive neuropsychological assessment.

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Background: NOTCH3 encodes a transmembrane receptor critical for vascular smooth muscle cell function. NOTCH3 variants are the leading cause of hereditary cerebral small vessel disease (SVD). While monoallelic cysteine-involving missense variants in NOTCH3 are well-studied in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), patients with biallelic variants in NOTCH3 are extremely rare and not well characterised.

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