Linked to major volcanic eruptions around 536 and 540 CE, the onset of the Late Antique Little Ice Age has been described as the coldest period of the past two millennia. The exact timing and spatial extent of this ex...
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Linked to major volcanic eruptions around 536 and 540 CE, the onset of the Late Antique Little Ice Age has been described as the coldest period of the past two millennia. The exact timing and spatial extent of this exceptional cold phase are, however, still under debate because of the limited resolution and geographical distribution of the available proxy archives. Here, we use 106 wood anatomical thin sections from 23forest sites and 20 tree species in both hemispheres to search for cell-level fingerprints of ephemeral summer cooling between 530 and 550 CE. After cross-dating and double-staining, we identified 89Blue Rings(lack of cell wall lignification), nine Frost Rings(cell deformation and collapse), and 93Light Rings(reduced cell wall thickening) in the Northern Hemisphere. Our network reveals evidence for the strongest temperature depression between mid-July and early-August 536 CE across North America and Eurasia, whereas more localised cold spells occurred in the summers of 532, 540–43, and548 CE. The lack of anatomical signatures in the austral trees suggests limited incursion of stratospheric volcanic aerosol into the Southern Hemisphere extra-tropics, that any forcing was mitigated by atmosphere-ocean dynamical responses and/or concentrated outside the growing season, or a combination of factors. Our findings demonstrate the advantage of wood anatomical investigations over traditional dendrochronological measurements, provide a benchmark for Earth system models, support cross-disciplinary studies into the entanglements of climate and history, and question the relevance of global climate averages.
Atherosclerotic carotid stenosis is an important risk factor for stroke. Carotid plaques(CPs) causing stroke may present a distinct type of molecular pathology compared with transient ischemic attack( TIA)-associated ...
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Atherosclerotic carotid stenosis is an important risk factor for stroke. Carotid plaques(CPs) causing stroke may present a distinct type of molecular pathology compared with transient ischemic attack( TIA)-associated or asymptomatic plaques. We compared the gene expression profiles of CPs from stroke patients( n =12) and asymptomatic patients( n =9),both with similar risk factors and severity of carotid stenosis(>70%). Sixty probes showed over 1.5-fold expression difference at 5% false discovery rate. Functional clustering showed enrichment of genes in 51 GO categories and seven pathways, the most significant of which relate to extracellular-matrix interaction, PPAR gamma signaling, scavanger receptor activity, and lysosomal activity. Differential expression of ten genes was confirmed in an extended replication group(n=43), where the most significant expression differences were found in CD36( 2.1-fold change, p =0.005), CD163( 1.7-fold change, p =0.007) and FABP4(2.2-fold change, p=0.015). These include four genes not previously linked to plaque destabilization: GLUL(2.2-fold change,p=0.016), FUCA1(2.2-fold change, p=0.025), IL1RN(1.6-fold change, p=0.034), and S100A8(2.5-fold change, p=0.047). Strong correlations were found to plaque ulceration, plaque hemorrhage, and markers of apoptosis and proliferation(activated caspase 3, TUNEL, and Ki67). Protein expression of these genes was confirmed by immunohistochemistry and was found in the atheromatous areas of CPs critical for plaque destabilization. This study presents a comprehensive transcriptional analysis of stroke-associated CPs and demonstrates a significant transcriptome difference between stroke-associated and asymptomatic CPs. Followup studies on the identified genes are needed to define whether they could be used as biomarkers of symptomatic CPs or have a role in plaque destabilization.
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