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Neurological and functional outcomes of 32 patients with hemorrhagic brainstem cavernous malformations: a practical guide for surgical planning.
J Neurosurg
January 2025
1Department of Neurosurgery, ASST Cremona, Italy.
Objective: Brainstem cavernous malformations (BSCMs) were once considered inoperable. Microsurgical resection now represents a valuable option for treating patients with hemorrhagic or symptomatic lesions. The aim of this study was to provide a practical guide for surgical planning by analyzing postoperative neurological and functional outcomes.
View Article and Find Full Text PDFIntroduction: This study aimed to evaluate the predictive validity and discriminatory ability of clinical outcomes, inflammatory activity, oxidative and vascular damage, and metabolic mechanisms for detecting significant improve maximum heart rate after physical activity training in individuals with psychiatric disorders and obesity comorbid using a longitudinal design and transdiagnostic perspective.
Methods: Patients with major depressive disorder, bipolar disorder and, schizophrenia and with comorbid obesity (n = 29) were assigned to a 12-week structured physical exercise program. Peripheral blood biomarkers of inflammation, oxidative stress, vascular mechanisms, and metabolic activity, as well as neurocognitive and functional performance were assessed twice, before and after intervention.
Base of Skull & Spinal Canal Narrowing in an Adolescent with Autosomal Recessive Hypophosphatemic Rickets Type 2.
Calcif Tissue Int
January 2025
Department of Paediatric Endocrinology, Alder Hey Children's Hospital, Liverpool, UK.
Autosomal recessive hypophosphatemic rickets type 2 (ARHR2) is an uncommon hereditary form of rickets characterised by chronic renal phosphate loss and impaired bone mineralisation. This results from compound heterozygous or homozygous pathogenic variants in ectonucleotide pyrophosphatase/phosphodiesterase 1 (ENPP1), a key producer of extracellular inorganic pyrophosphate (PPi) and an inhibitor of fibroblast growth factor23 (FGF23). ENPP1 deficiency impacts FGF23 and increases its activity.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Indiana University School of Medicine, Stark Neurosciences Research Institute, Department of Neurology, Indianapolis, IN, USA.
Background: Diagnosis of Alzheimer's disease (AD) via MRI is costly and can be limited by regional availability. With the recent advancements and discovery of amyloid in the retina, diagnosis of AD and the effect of AD pathology on the retina is becoming well characterized. However, the prevalence of vascular contributions to cognitive impairment and dementia (VCID) and its effects on the retina are less well known.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Brain endothelial cell (EC) stress, including that induced by vascular amyloid β (Aβ) deposits in cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), contributes to cerebral blood flow impairment, blood brain barrier (BBB) damage, neurovascular unit dysfunction, microhemorrhages and hypoperfusion, precipitating neurodegeneration and neuroinflammation processes. Epidemiological and experimental evidence suggests that hyperhomocysteinemia (Hhcy) contributes to increasing AD risk as well as CAA pathology. However, the cellular and molecular mechanisms through which Aβ and Hhcy drive EC and BBB dysfunction, whether the molecular effects of these challenges are additive or independent, and possible therapeutic strategies, remain to be determined.
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