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Träfflista för sökning "WFRF:(Siddiq A) srt2:(2020-2023)"

Sökning: WFRF:(Siddiq A) > (2020-2023)

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1.
  • Kanai, M, et al. (författare)
  • 2023
  • swepub:Mat__t
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2.
  • Kousathanas, A, et al. (författare)
  • Whole-genome sequencing reveals host factors underlying critical COVID-19
  • 2022
  • Ingår i: Nature. - : Springer Science and Business Media LLC. - 1476-4687 .- 0028-0836. ; 607:7917, s. 97-
  • Tidskriftsartikel (refereegranskat)abstract
    • Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease.
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4.
  • Nawaz, Saima, et al. (författare)
  • Polyaniline inside the pores of high surface area mesoporous silicon as composite electrode material for supercapacitors
  • 2022
  • Ingår i: RSC Advances. - : ROYAL SOC CHEMISTRY. - 2046-2069. ; 12:27, s. 17228-17236
  • Tidskriftsartikel (refereegranskat)abstract
    • Mesoporous silicon (mSi) obtained by the magnesiothermic reduction of mesoporous silica was used to deposit polyaniline (PANI) in its pores, the composite was tested for its charge storage application for high performance supercapacitor electrodes. The mesoporous silica as confirmed by Small Angle X-ray Scattering (SAXS) has a Brunauer-Emmett-Teller (BET) surface area of 724 m(2)g(-1) and mean pore size of 5 nm. After magnesiothermic reduction to mSi, the BET surface area is reduced to 348 m(2)g(-1) but the mesoporousity is retained with a mean pore size of 10 nm. The BET surface area of mesoporous silicon is among the highest for porous silicon prepared/reduced from silica. In situ polymerization of PANI inside the pores of mSi was achieved by controlling the polymerization conditions. As a supercapacitor electrode, the mSi-PANI composite exhibits better charge storage performance as compared to pure PANI and mesoporous silica-PANI composite electrodes. Enhanced electrochemical performance of the mSi-PANI composite is attributed to the high surface mesoporous morphology of mSi with a network structure containing abundant mesopores enwrapped by an electrochemically permeable polyaniline matrix.
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