11 research outputs found
Growth and Thyroid Function in Children With In Utero Exposure to Dioxin: A 5-Year Follow-Up Study
DIAGNOSIS OF URINARY BLADDER RUPTURE USING ULTRASOUND CONTRAST CYSTOGRAPHY: IN VITRO MODEL AND TWO CASE-HISTORY REPORTS
Analysis of energy intensity trend as a tool for long-term forecasting of energy consumption
The role of heat shock proteins in inflammatory injury induced by cold stress in chicken hearts
Prevention of allograft rejection in heart transplantation through concurrent gene silencing of TLR and Kinase signaling pathways
Neurotoxic Vulnerability Underlying Schizophrenia Spectrum Disorders
Neurotoxic vulnerability that putatively contributes to the etiopathogenesis of schizophrenia spectrum disorders encompasses perinatal adversity, genetic linkage, epigenetic disadvantage and neurodegenerative propensities that affect both symptom domains, positive, negative and cognitive, and biomarkers of the disorder. Molecular and cellular apoptosis/excitotoxicity that culminates in regional brain loss, reductions in reelin expression, trophic disruption, perinatal adversity, glycogen synthase kinase-3 dysregulation and various instances of oxidative stress all influence the final end-point disorder. The existence of prodromal psychotic phases, structural-functional aspects of regional neuroimaging, dopamine signal overexpression and psychosis propensity provide substance for neurodegenerative influences. The pathophysiology of schizophrenia spectrum disorder encompasses the destruction of normal functioning of the neurotrophins, in particular brain-derived neurotrophic factor (BDNF), dyskinesia of necessary movements, and metabolic-metabolomic and proteomic markers. Neurotoxic accidents combined with genetic susceptibility appears to play a role in interfering normal neurodevelopment or in the tissue-destructive neurodegeneration or both, thereby elevating the eventual risk for disorder tendencies and eventual expression