Search results

Filter

Filetype

Your search for "*" yielded 465284 hits

The turn to history in international law and the sources doctrine : Critical approaches and methodological imaginaries

Expanding now familiar debates about the impact of the 'historical turn' upon the field of international law, this article considers some of the different ways in which 'turn to history' scholars have confronted the methodological and theoretical tensions arising from the central, yet paradoxical, role occupied by the sources doctrine in international law. We suggest that the anxiety over the sour

Epilepsy in immigrants and Swedish-born : A cohort study of all adults 18 years of age and older in Sweden

Purpose: We aimed to study the association between country of birth and incident epilepsy in several immigrant groups using Swedish-born individuals as referents. Method: The study population included all adults aged 18 years and older in Sweden, living and deceased, 6,690,598 in the first-generation and 6,683,125 in the second-generation sub-study. Epilepsy was defined as having at least one regi

Consumption of Fish and Long-chain n-3 Polyunsaturated Fatty Acids Is Associated With Reduced Risk of Colorectal Cancer in a Large European Cohort

Background & Aims: There is an unclear association between intake of fish and long-chain n-3 polyunsaturated fatty acids (n-3 LC-PUFAs) and colorectal cancer (CRC). We examined the association between fish consumption, dietary and circulating levels of n-3 LC-PUFAs, and ratio of n-6:n-3 LC-PUFA with CRC using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) coh

Effect of Oxygen Therapy on Cardiovascular Outcomes in Relation to Baseline Oxygen Saturation

Objectives: The aim of this study was to determine the effect of supplemental oxygen in patients with myocardial infarction (MI) on the composite of all-cause death, rehospitalization with MI, or heart failure related to baseline oxygen saturation. A secondary objective was to investigate outcomes in patients developing hypoxemia. Background: In the DETO2X-AMI (Determination of the Role of Oxygen

Flera svenska fall av infektion med rävens dvärgbandmask

Alveolar echinococcosis (AE) caused by the fox tapeworm Echinococcus multilocularis is a zoonosis presenting with focal liver lesions and has a poor prognosis without treatment. The disease is common in Central and Eastern Europe but has been highly unusual in Sweden. A suspicion of AE usually arises through radiology and the diagnosis may be confirmed by histology and/or serological antibody dete

Diversity buffers winegrowing regions from climate change losses

Agrobiodiversity—the variation within agricultural plants, animals, and practices—is often suggested as a way to mitigate the negative impacts of climate change on crops [S. A. Wood et al., Trends Ecol. Evol. 30, 531–539 (2015)]. Recently, increasing research and attention has focused on exploiting the intraspecific genetic variation within a crop [Hajjar et al., Agric. Ecosyst. Environ. 123, 261–

Soil moisture and hydrology projections of the permafrost region-a model intercomparison

This study investigates and compares soil moisture and hydrology projections of broadly used land models with permafrost processes and highlights the causes and impacts of permafrost zone soil moisture projections. Climate models project warmer temperatures and increases in precipitation (P) which will intensify evapotranspiration (ET) and runoff in land models. However, this study shows that most

WNT5A-induced activation of the protein kinase C substrate MARCKS is required for melanoma cell invasion

WNT5A is a well-known mediator of melanoma cell invasion and metastasis via its ability to activate protein kinase C (PKC), which is monitored by phosphorylation of the endogenous PKC substrate myristoylated alanine-rich c-kinase substrate (MARCKS). However, a possible direct contribution of MARCKS in WNT5A-mediated melanoma cell invasion has not been investigated. Analyses of melanoma patient dat

Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of alzheimer's disease

Increased oxidative stress is implicated in the pathogenesis of Alzheimer's disease (AD). A large body of evidence suggests that mitochondrial dysfunction and increased reactive oxygen species occur prior to amyloid-β (Aβ) deposition. Coenzyme Q10 (CoQ10), a component of the mitochondrial electron transport chain, is well characterized as a neuroprotective antioxidant in animal models and human tr

Accumulation of cellular prion protein within dystrophic neurites of amyloid plaques in the Alzheimer's disease brain

Amyloid plaques, a well-known hallmark of Alzheimer's disease (AD), are formed by aggregated β-amyloid (Aβ). The cellular prion protein (PrPc) accumulates concomitantly with Aβ in amyloid plaques. One type of amyloid plaque, classified as a neuritic plaque, is composed of an amyloid core and surrounding dystrophic neurites. PrPc immunoreactivity reminiscent of dystrophic neurites is observed in ne

Degradation of Alzheimer's amyloid fibrils by microglia requires delivery of CIC-7 to lysosomes

Incomplete lysosomal acidification in microglia inhibits the degradation of fibrillar forms of Alzheimer's amyloid β peptide (fAβ). Here we show that in primary microglia a chloride transporter, ClC-7, is not delivered efficiently to lysosomes, causing incomplete lysosomal acidification. ClC-7 protein is synthesized by microglia but it is mistargeted and appears to be degraded by an endoplasmic re

Synapses, synaptic activity and intraneuronal Aβ in Alzheimer's disease

β-Amyloid peptide accumulation plays a central role in the pathogenesis of Alzheimer's disease. Aberrant β-amyloid buildup in the brain has been shown to be present both in the extracellular space and within neurons. Synapses are important targets of β-amyloid, and alterations in synapses better correlate with cognitive impairment than amyloid plaques or neurofibrillary tangles. The link between β

Effects of synaptic modulation on β-amyloid, synaptophysin, and memory performance in Alzheimer's disease transgenic mice

Accumulation of β-amyloid (Aβ) and loss of synapses are hallmarks of Alzheimer's disease (AD). How synaptic activity relates to Aβ accumulation and loss of synapses is a current topic of major interest. Synaptic activation promotes Aβ secretion, and chronic reduction of synaptic activity reduced Aβ plaques in an AD transgenic mouse model. This suggested beneficial effects of reducing synaptic acti

Dementia

Dementia is a decline in cognitive function that impairs a person's previous level of social and occupational function. Dementia is a very common medical condition that can result from diverse causes. Dementias are classified based on common clinical, genetic, and neuropathological features. The most common cause of dementia is Alzheimer's disease. Other major classes of disorders that cause demen

Dysregulation of the mTOR pathway mediates impairment of synaptic plasticity in a mouse model of Alzheimer's disease

Background: The mammalian target of rapamycin (mTOR) is an evolutionarily conserved Ser/Thr protein kinase that plays a pivotal role in multiple fundamental biological processes, including synaptic plasticity. We explored the relationship between the mTOR pathway and β-amyloid (Ab)-induced synaptic dysfunction, which is considered to be critical in the pathogenesis of Alzheimer's disease (AD). Met

Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer's disease

The aberrant accumulation of aggregated β-amyloid peptides (Aβ) as plaques is a hallmark of Alzheimer's disease (AD) neuropathology and reduction of Ab has become a leading direction of emerging experimental therapies for the disease. The mechanism(s) whereby Aβ is involved in the pathophysiology of the disease remain(s) poorly understood. Initially fibrils, and subsequently oligomers of extracell

Co-occurrence of Alzheimer's disease β-amyloid and tau pathologies at synapses

Although β-amyloid (Aβ) plaques and tau neurofibrillary tangles are hallmarks of Alzheimer's disease (AD) neuropathology, loss of synapses is considered the best correlate of cognitive decline in AD, rather than plaques or tangles. How pathological Aβ and tau aggregation relate to each other and to alterations in synapses remains unclear. Since aberrant tau phosphorylation occurs in amyloid precur

Synaptic activity reduces intraneuronal Aβ, promotes APP transport to synapses, and protects against Aβ-related synaptic alterations

A central question in Alzheimer's disease research is what role synaptic activity plays in the disease process. Synaptic activity has been shown to induce β-amyloid peptide release into the extracellular space, and extracellular β-amyloid has been shown to be toxic to synapses. We now provide evidence that the well established synaptotoxicity of extracellular β-amyloid requires β-secretase process