Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
9,566
result(s) for
"Mitchell, K."
Sort by:
The potential of emerging bio-based products to reduce environmental impacts
The current debate on the sustainability of bio-based products questions the environmental benefits of replacing fossil- by bio-resources. Here, we analyze the environmental trade-offs of 98 emerging bio-based materials compared to their fossil counterparts, reported in 130 studies. Although greenhouse gas life cycle emissions for emerging bio-based products are on average 45% lower (−52 to −37%; 95% confidence interval), we found a large variation between individual bio-based products with none of them reaching net-zero emissions. Grouped in product categories, reductions in greenhouse gas emissions ranged from 19% (−52 to 35%) for bioadhesives to 73% (−84 to −54%) for biorefinery products. In terms of other environmental impacts, we found evidence for an increase in eutrophication (369%; 163 to 737%), indicating that environmental trade-offs should not be overlooked. Our findings imply that the environmental sustainability of bio-based products should be evaluated on an individual product basis and that more radical product developments are required to reach climate-neutral targets.
Publication
AIM2 inflammasome mediates hallmark neuropathological alterations and cognitive impairment in a mouse model of vascular dementia
Chronic cerebral hypoperfusion is associated with vascular dementia (VaD). Cerebral hypoperfusion may initiate complex molecular and cellular inflammatory pathways that contribute to long-term cognitive impairment and memory loss. Here we used a bilateral common carotid artery stenosis (BCAS) mouse model of VaD to investigate its effect on the innate immune response—particularly the inflammasome signaling pathway. Comprehensive analyses revealed that chronic cerebral hypoperfusion induces a complex temporal expression and activation of inflammasome components and their downstream products (IL-1β and IL-18) in different brain regions, and promotes activation of apoptotic and pyroptotic cell death pathways. Polarized glial-cell activation, white-matter lesion formation and hippocampal neuronal loss also occurred in a spatiotemporal manner. Moreover, in AIM2 knockout mice we observed attenuated inflammasome-mediated production of proinflammatory cytokines, apoptosis, and pyroptosis, as well as resistance to chronic microglial activation, myelin breakdown, hippocampal neuronal loss, and behavioral and cognitive deficits following BCAS. Hence, we have demonstrated that activation of the AIM2 inflammasome substantially contributes to the pathophysiology of chronic cerebral hypoperfusion-induced brain injury and may therefore represent a promising therapeutic target for attenuating cognitive impairment in VaD.
Journal Article
Chronic cerebral hypoperfusion: a critical feature in unravelling the etiology of vascular cognitive impairment
Vascular cognitive impairment (VCI) describes a wide spectrum of cognitive deficits related to cerebrovascular diseases. Although the loss of blood flow to cortical regions critically involved in cognitive processes must feature as the main driver of VCI, the underlying mechanisms and interactions with related disease processes remain to be fully elucidated. Recent clinical studies of cerebral blood flow measurements have supported the role of chronic cerebral hypoperfusion (CCH) as a major driver of the vascular pathology and clinical manifestations of VCI. Here we review the pathophysiological mechanisms as well as neuropathological changes of CCH. Potential interventional strategies for VCI are also reviewed. A deeper understanding of how CCH can lead to accumulation of VCI-associated pathology could potentially pave the way for early detection and development of disease-modifying therapies, thus allowing preventive interventions instead of symptomatic treatments.
Journal Article
Chemical cover : smells and poisons
\"Many mammals, reptiles, fish, and amphibians produce chemicals in their bodies in order to ward off predators. Some manufacture poisons or smelly or painful substances in their own bodies. Others acquire these chemicals through their diet. Engaging text and eye-catching photographs invite readers to delve into the world of stinky sprays, poisonous skin, and slimy goo in order to understand how animals use these chemicals to defend themselves.\"-- Publisher's description.
Book
The role of inflammasomes in vascular cognitive impairment
There is an increasing prevalence of Vascular Cognitive Impairment (VCI) worldwide, and several studies have suggested that Chronic Cerebral Hypoperfusion (CCH) plays a critical role in disease onset and progression. However, there is a limited understanding of the underlying pathophysiology of VCI, especially in relation to CCH. Neuroinflammation is a significant contributor in the progression of VCI as increased systemic levels of the proinflammatory cytokine interleukin-1β (IL-1β) has been extensively reported in VCI patients. Recently it has been established that CCH can activate the inflammasome signaling pathways, involving NLRP3 and AIM2 inflammasomes that critically regulate IL-1β production. Given that neuroinflammation is an early event in VCI, it is important that we understand its molecular and cellular mechanisms to enable development of disease-modifying treatments to reduce the structural brain damage and cognitive deficits that are observed clinically in the elderly. Hence, this review aims to provide a comprehensive insight into the molecular and cellular mechanisms involved in the pathogenesis of CCH-induced inflammasome signaling in VCI.
Journal Article
Aging-associated sensory decline and Alzheimer’s disease
Multisensory decline is common as people age, and aging is the primary risk of Alzheimer’s Disease (AD). Recent studies have begun to shed light on the possibility that age-related sensory decline could accelerate AD pathogenesis, or be a prodromal indicator of AD. Sensory impairments, specifically in taste and smell, often emerge before cognitive symptoms in AD, indicating their potential as early biomarkers. Olfactory dysfunction has been frequently associated with AD and may offer valuable insights into early detection. Hearing impairment is significantly associated with AD, but its causal impact on AD progression remains unclear. The review also discusses visual and tactile deficits in AD, including retinal thinning and changes in tactile perception, highlighting their links to disease progression. Focusing on molecular mechanisms, the review explores the roles of amyloid-β (Aβ) accumulation and tau protein pathology in sensory decline and their bidirectional relationship with AD. In summary, the evidence presented conclusively supports advocating for an integrated approach to understanding AD and sensory decline, to enhance early detection, implementing preventive strategies, and developing therapeutic interventions for AD. This approach underscores the significance of sensory health in addressing neurodegenerative diseases, particularly AD.
Journal Article