Plastic waste are introduced into the environment inevitably and their exposure in the environment causes deterioration in mechanical and physicochemical properties and leads to the formation of plastic fragments, which are considered as microplastics when their size is < 5 mm. In recent years, microplastic pollution has been reported in all kinds of environments worldwide and is considered a potential threat to the health of ecosystems and humans. However, knowledge on the environmental degradation of plastics and the formation of microplastics is still limited. In this review, potential hotspots for the accumulation of plastic waste were identified, major mechanisms and characterization methods of plastic degradation were summarized, and studies on the environmental degradation of plastics were evaluated. Future research works should further identify the key environmental parameters and properties of plastics affecting the degradation in order to predict the fate of plastics in different environments and facilitate the development of technologies for reducing plastic pollution. Formation and degradation of microplastics, including nanoplastics, should receive more research attention to assess their fate and ecological risks in the environment more comprehensively.
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http://dx.doi.org/10.1016/j.envpol.2021.116554 | DOI Listing |
Endocr Relat Cancer
January 2025
S Dehm, Masonic Cancer Center, University of Minnesota, Minneapolis, United States.
Treatment for castration-resistant prostate cancer (CRPC) primarily involves the suppression of androgen receptor (AR) activity using androgen receptor signaling inhibitors (ARSIs). While ARSIs have extended patient survival, resistance inevitably develops. Mechanisms of resistance include genomic aberrations at the AR locus that reactivate AR signaling, or lineage plasticity that drives emergence of AR-independent phenotypes.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA.
Background: Vascular dysfunction, blood-brain barrier (BBB) dysregulation, and neuroinflammation are thought to participate in Alzheimer`s disease (AD) pathogenesis, though the mechanism is poorly understood. Among pathways of interest, AD pathology appears to affect vascular endothelial growth factor-A (VEGFA) signaling in a bidirectional manner. Higher VEGF levels are thought to have a protective role and slow cognitive decline.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Background: Aging is a time-dependent deterioration of physiological functions that occurs in both humans and animals. Within the brain, aging cells gradually become dysfunctional through a complex interplay of intrinsic and extrinsic factors, ultimately leading to behavioral deficits and enhanced risk of neurodegenerative diseases such as Alzheimer's disease (AD). The characteristics of normal aging are distinct from those associated with age-related diseases and it is important to understand the processes that contribute to this pathological divergence.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neuroscience Institute Cavalieri Ottolenghi, Orbassano, Italy.
Background: Understanding the neuronal mechanisms of learning and memory is one of the major goals in neurophysiology and neuropsychology. Disorders related to memory consolidation are often the consequences of dynamic plasticity changes, which may lead to a reduction in spine number and density, impairing neural networks. Sleep is one of the major physiological prerequisites for memory consolidation, especially during NREM sleepwhen glymphatic system clearance takes place, too.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indiana University, Bloomington, IN, USA.
Background: The roles of Aβ in the pathogenesis of Alzheimer 's disease (AD) include disruption of synaptic communication/function and synaptic plasticity mechanisms thought to underlie learning and memory. Exactly how these abnormal processes arise is incompletely understood, but evidence suggests that dysregulation of intracellular Ca levels is involved in alterations of neuronal excitability, synaptic remodeling, and neurodegeneration in AD. Our lab has focused on the potential involvement of voltage-gated potassium channels (VGKCs) in these processes, particularly Kv1.
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