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The varieties of remembered experience: Moving memory beyond the bounded self
We review the contributions to this Special Issue that highlight the diverse ways in which memory takes place that go beyond the standard personal autobiographical memory and its reliance on internal imagery. We look at how contributors explore a highly individual memory of trauma and re-consider it as a complex, socially contested phenomenon. We next turn to a discussion of shared memory within dyads and then look at a contribution that examines bodily and gestural alignment during shared recollection among group members and/or families. From there, contributors raise considerations of collective memory in prisoner-of-war survivors and among football fans attending a World Cup event. The next contribution illustrates how collective forgetting creates social bonds in a similar manner to collective remembering. Finally, we show how the boundaries of memory are being stretched by digital technology through its influence on how we recall and share memories. Methodological innovations are also discussed
Author Correction: A HIF independent oxygen-sensitive pathway for controlling cholesterol synthesis (Nature Communications, (2023), 14, 1, (4816), 10.1038/s41467-023-40541-1)
\ua9 The Author(s) 2024.The original version of this Article contained errors in Figs. 2, 3, and 5. In the original Fig. 2e, the flow cytometry panel on the right (labelled “StD (24 hr) followed by 1% O2 (~16 hr)”), was inadvertently duplicated from the panel on the left (labelled “Concurrent StD and 1% O2 (~24 hr)”). In the original Fig. 3a, the flow cytometry panel on the right (labelled “Roxadustat”), was inadvertently duplicated from the panel on the left (labelled “DMOG”). In the original Fig. 5c, the labels did not properly communicate that both panels come from the same experiment and have the same controls. The following sentence has been added to the end of the legend for Fig. 5c: “The data depicted in the left and right panels originated from the same experiment and as such the control plots are the same in both.” Figures 2, 3, and 5 have been corrected in both the PDF and HTML versions of the Article. The original version of the Supplementary Information associated with this Article contained an error in Supplementary Fig. 5. In the original Supplementary Fig. 5a, the labels did not properly communicate that all three panels come from the same experiment and have the same control. The following sentence has been added to the end of the legend for Supplementary Fig. 5a: “The data depicted in the three panels originated from the same experiment and as such the control plot is the same in all panels”. The HTML has been updated to include a corrected version of the Supplementary Information
Current research into brain barriers and the delivery of therapeutics for neurological diseases: a report on CNS barrier congress London, UK, 2017.
This is a report on the CNS barrier congress held in London, UK, March 22-23rd 2017 and sponsored by Kisaco Research Ltd. The two 1-day sessions were chaired by John Greenwood and Margareta Hammarlund-Udenaes, respectively, and each session ended with a discussion led by the chair. Speakers consisted of invited academic researchers studying the brain barriers in relation to neurological diseases and industry researchers studying new methods to deliver therapeutics to treat neurological diseases. We include here brief reports from the speakers
HFE gene polymorphism defined by sequence based typing of the Brazilian population and a standardized nomenclature for HFE allele sequences
The HFE molecule controls iron uptake from gut, and defects in the molecule have been associated with iron overload, particularly in hereditary hemochromatosis. The HFE gene including both coding and boundary intronic regions were sequenced in 304 Brazilian individuals, encompassing healthy individuals and patients exhibiting hereditary or acquired iron overload. Six sites of variation were detected: i) H63D C > G in exon 2, ii) IVS2 (+4) T > C in intron 2, iii) a C > G transversion in intron 3, iv) C282Y G > A in exon 4, v) IVS4 (-44) T > C in intron 4, and vi) a new Guanine deletion (G > del) in intron 5, which were used for haplotype inference. Nine HFE alleles were detected and six of these were officially named on the basis of the HLA Nomenclature, defined by the WHO Nomenclature Committee for Factors of the HLA System, and published via the IPD-IMGT/HLA website. Four alleles, HFE*001, 002, 003 and 004 exhibited variation within their exon sequences
AMP-dependent kinase/mammalian target of rapamycin complex 1 signaling in T-cell acute lymphoblastic leukemia: therapeutic implications.
The mammalian target of rapamycin (mTOR) serine/threonine
kinase is the catalytic subunit of two multi-protein complexes,
referred to as mTORC1 and mTORC2. Signaling downstream
of mTORC1 has a critical role in leukemic cell biology by
controlling mRNA translation of genes involved in both cell
survival and proliferation. mTORC1 activity can be downmodulated
by upregulating the liver kinase B1/AMP-activated
protein kinase (LKB1/AMPK) pathway. Here, we have explored
the therapeutic potential of the anti-diabetic drug, metformin
(an LKB1/AMPK activator), against both T-cell acute lymphoblastic
leukemia (T-ALL) cell lines and primary samples
from T-ALL patients displaying mTORC1 activation. Metformin
affected T-ALL cell viability by inducing autophagy and
apoptosis. However, it was much less toxic against proliferating
CD4þ T-lymphocytes from healthy donors. Western blot
analysis demonstrated dephosphorylation of mTORC1 downstream
targets. Unlike rapamycin, we found a marked inhibition
of mRNA translation in T-ALL cells treated with metformin.
Remarkably, metformin targeted the side population of T-ALL
cell lines as well as a putative leukemia-initiating cell subpopulation
(CD34þ/CD7/CD4) in patient samples. In conclusion,
metformin displayed a remarkable anti-leukemic activity,
which emphasizes future development of LKB1/AMPK activators
as clinical candidates for therapy in T-ALL.
Leukemia (2012) 26, 91–100; doi:10.1038/leu.2011.269;
published online 4 October 201
Gene sequence variations of the platelet P2Y12 receptor are associated with coronary artery disease
<p>Abstract</p> <p>Background</p> <p>The platelet P2Y<sub>12 </sub>receptor plays a key role in platelet activation. The H2 haplotype of the P2Y<sub>12 </sub>receptor gene (<it>P2RY12</it>) has been found to be associated with maximal aggregation response to adenosine diphosphate (ADP) and with increased risk for peripheral arterial disease. No data are available on its association with coronary artery disease (CAD).</p> <p>Methods </p> <p>The H2 haplotype of the <it>P2RY12 </it>was determined in 1378 unrelated patients of both sexes selected according to the presence of significant coronary artery disease (CAD group) or having normal coronary angiogram at cardiac catheterization (CAD-free group). Significant coronary artery disease was angiographically determined, and was defined as a greater than 50% visually estimated luminal diameter stenosis in at least one major epicardial coronary artery.</p> <p>Results</p> <p>In the studied population 71.9% had CAD (n = 991) and 28.1% had normal coronary angiogram (n = 387). H2 haplotype carriers were more frequent in the CAD group (p = 0.03, OR = 1.36, 95%CI = 1.02–1.82). The H2 haplotype was significantly associated with CAD in non-smokers (p = 0.007, OR = 1.83 95%CI = 1.17–2.87), but not in smokers. The association remained significant after adjustment for other covariates (age, triglycerides, HDL, hypertension, diabetes) by multivariate logistic regression (p = 0.004, OR = 2.32 95%CI = 1.30–4.15).</p> <p>Conclusion</p> <p>Gene sequence variations of the P2Y<sub>12 </sub>receptor gene are associated with the presence of significant CAD, particularly in non-smoking individuals.</p
Human capital, percieved domestic institutional quality and entrepreneurship among highly skilled Chinese returnees
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