What informs the process of remembering and forgetting? Is it merely about our capability to store and retrieve experiences in a purely functional sense? What about ′collective memories′, not just ...those of the individual - how do these manifest themselves in the passages of time? The authors present a new, fascinating insight into the social psychology of experience drawing upon a number of classic works (particularly by Frederick Bartlett, Maurice Halbwachs & Henri Bergson) to help develop their argument. The significance of their ideas for developing a contemporary psychology of experience is illustrated with material from studies focused on settings at home and at work, in public and commercial organizations where remembering and forgetting are matters of concern, involving language and text based communication, objects and place. As their argument unfolds, the authors reveal that memories do not solely reside in a linear passage of time, linking past, present and future, nor do they soley rest within the indidvidual′s conciousness, but that memory sits at the very heart of ′lived experience′; whether collective or individual, the vehicle for how we remember or forget is linked to social interaction, object interaction and the different durations of living that we all have. It is very much connected to the social psychology of experience.
We have updated the catalogue of common and well‐documented (CWD) human leukocyte antigen (HLA) alleles to reflect current understanding of the prevalence of specific allele sequences. The original ...CWD catalogue designated 721 alleles at the HLA‐A, ‐B, ‐C, ‐DRB1, ‐DRB3/4/5, ‐DQA1, ‐DQB1, and ‐DPB1 loci in IMGT (IMmunoGeneTics)/HLA Database release 2.15.0 as being CWD. The updated CWD catalogue designates 1122 alleles at the HLA‐A, ‐B, ‐C, ‐DRB1, ‐DRB3/4/5, ‐DQA1, ‐DQB1, ‐DPA1 and ‐DPB1 loci as being CWD, and represents 14.3% of the HLA alleles in IMGT/HLA Database release 3.9.0. In particular, we identified 415 of these alleles as being ‘common’ (having known frequencies) and 707 as being ‘well‐documented’ on the basis of ~140,000 sequence‐based typing observations and available HLA haplotype data. Using these allele prevalence data, we have also assigned CWD status to specific G and P designations. We identified 147/151 G groups and 290/415 P groups as being CWD. The CWD catalogue will be updated on a regular basis moving forward, and will incorporate changes to the IMGT/HLA Database as well as empirical data from the histocompatibility and immunogenetics community. This version 2.0.0 of the CWD catalogue is available online at cwd.immunogenomics.org, and will be integrated into the Allele Frequencies Net Database, the IMGT/HLA Database and National Marrow Donor Program's bioinformatics web pages.
COVID-19 affects millions of patients worldwide, with clinical presentation ranging from isolated thrombosis to acute respiratory distress syndrome (ARDS) requiring ventilator support. Neutrophil ...extracellular traps (NETs) originate from decondensed chromatin released to immobilize pathogens, and they can trigger immunothrombosis. We studied the connection between NETs and COVID-19 severity and progression. We conducted a prospective cohort study of COVID-19 patients (n = 33) and age- and sex-matched controls (n = 17). We measured plasma myeloperoxidase (MPO)-DNA complexes (NETs), platelet factor 4, RANTES, and selected cytokines. Three COVID-19 lung autopsies were examined for NETs and platelet involvement. We assessed NET formation ex vivo in COVID-19 neutrophils and in healthy neutrophils incubated with COVID-19 plasma. We also tested the ability of neonatal NET-inhibitory factor (nNIF) to block NET formation induced by COVID-19 plasma. Plasma MPO-DNA complexes increased in COVID-19, with intubation (P < .0001) and death (P < .0005) as outcome. Illness severity correlated directly with plasma MPO-DNA complexes (P = .0360), whereas Pao2/fraction of inspired oxygen correlated inversely (P = .0340). Soluble and cellular factors triggering NETs were significantly increased in COVID-19, and pulmonary autopsies confirmed NET-containing microthrombi with neutrophil-platelet infiltration. Finally, COVID-19 neutrophils ex vivo displayed excessive NETs at baseline, and COVID-19 plasma triggered NET formation, which was blocked by nNIF. Thus, NETs triggering immunothrombosis may, in part, explain the prothrombotic clinical presentations in COVID-19, and NETs may represent targets for therapeutic intervention.
•NETs contribute to microthrombi through platelet-neutrophil interactions in COVID-19 ARDS.•nNIF blocks NETs induced by COVID-19 plasma and represents a potential therapeutic intervention in COVID-19.
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Amino acid residues 90–120 of the prion protein (PrP) are likely to be critical for the conversion of PrPc to PrPsc in the transmissible spongiform encephalopathies. We raised 10 monoclonal ...antibodies against the 90–120 amino acid region, mapped the epitope specificity of these anti‐PrP antibodies, and investigated the expression of epitopes recognized by the antibodies in both PrPc and PrPsc. Four out of five of the anti‐PrP antibodies raised in a prion knockout mouse immunized with the linear peptide of PrP90–120 could detect PrPsc in ‘native’ and denatured forms and PrPc in normal cells, as well as recognize epitopes within PrP93–112 residues. In contrast, the other six anti‐PrP reagents, including five raised from the two knockout mice immunized with conformationally modified PrP90–120 peptide, could detect PrPc and recognize epitopes within PrP93–107 residues. Four of these reagents could also detect denatured PrPsc on western blots but not PrPsc plaques in brain tissue. The results indicate that residues PrP93–102 are exposed in PrPc but are buried upon conversion to the PrPsc isoform. Furthermore, PrP103–107 residues are partially buried in PrPsc while only the PrP107–112 epitope remains exposed, suggesting that the region PrP93–112 undergoes conformational changes during its conversion to PrPsc.
Triple treatment with elexacaftor, tezacaftor, and ivacaftor in patients with cystic fibrosis who had one Phe508del allele and a minimal-function mutation resulted in sustained improvement in FEV
1
, ...sweat chloride concentration, and the number of pulmonary exacerbations.
Data Intensive Computing refers to capturing, managing, analyzing, and understanding data at volumes and rates that push the frontiers of current technologies. The challenge of data intensive ...computing is to provide the hardware architectures and related software systems and techniques which are capable of transforming ultra-large data into valuable knowledge. Handbook of Data Intensive Computing is written by leading international experts in the field. Experts from academia, research laboratories and private industry address both theory and application. Data intensive computing demands a fundamentally different set of principles than mainstream computing. Data-intensive applications typically are well suited for large-scale parallelism over the data and also require an extremely high degree of fault-tolerance, reliability, and availability. Real-world examples are provided throughout the book. Handbook of Data Intensive Computing is designed as a reference for practitioners and researchers, including programmers, computer and system infrastructure designers, and developers. This book can also be beneficial for business managers, entrepreneurs, and investors.
Tumour necrosis factor (TNF) α is involved in the pathogenesis of established lymphoproliferative disease. Serum levels of TNFα and its soluble receptors are above normal values in B-cell chronic ...lymphocytic leukaemia (B-CLL) and they are valuable prognostic markers in lymphoma patients. The production of TNFα is genetically controlled. Altered synthesis of TNFα has been associated with polymorphisms at the TNF gene cluster (i.e. TNFA, TNFB and LTB). In the present study, we evaluated the prevalence of the known high TNFα- and TNFβ- producing alleles TNF1, TNF2 of the TNFA gene, TNFB1, TNFB2 alleles of the TNFB gene and of the polymorphic alleles TNFd1, d2, d3, d4 and d5 of the microsatellite TNFd in patients with B-CLL, non-Hodgkin's lymphoma (NHL) and Hodgkin's disease (HD). This study demonstrates that there is no difference in the frequency of the tested TNF alleles between normal controls and cohorts of patients with lymphoproliferative disease. These results indicate that TNF alleles are not genetic predisposing factors in the development of these diseases.
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Dostopno za:
DOBA, IJS, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
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