59 research outputs found

    Slip-rate on the Main Köpetdag (Kopeh Dagh) strike-slip fault, Turkmenistan, and the active tectonics of the South Caspian

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    We provide the first measurement of strike-slip and shortening rates across the 200-km-long right-lateral strike-slip Main Köpetdag Fault (MKDF) in Turkmenistan. Strike-slip and shortening components are accommodated on parallel structures separated by ∼10 km. Using Infra-red-stimulated luminescence and reconstruction of offset alluvial fans we find a right-lateral rate of 9.1 ± 1.3 mm/yr averaged over 100 ± 5 ka, and a shortening rate of only ∼0.3 mm/yr averaged over 35 ± 4 ka across the frontal thrust, though additional shortening is likely to be accommodated locally by folding and faulting, and regionally within the eastern Caspian lowlands to its south. The MKDF is estimated to have ∼35 km of cumulative right-lateral slip which, if these geological measurements are correct, would accumulate in only 3–5 Ma at the rate we have determined, suggesting that the present tectonic configuration started within that time period. We use the MKDF slip-rate to form a velocity triangle, from which we estimate the Iran-South Caspian and Eurasia-South Caspian shortening rates, and show that the South Caspian Basin moves at 10.4 ± 1.1 mm/yr in direction 333° ± 5 relative to Eurasia and at 4.8 ± 0.8 mm/yr in direction 236° ± 14 relative to Iran. In contrast to both the eastern Köpetdag and the Caspian lowlands the MKDF has little recent or historical seismicity. The rapid slip-rate estimated here suggests that it is a zone of high earthquake hazard

    Whole-genome sequencing reveals host factors underlying critical COVID-19

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    Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 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

    Stabilization of axisymmetric liquid bridges through vibration-induced pressure fields

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    Previous theoretical studies have indicated that liquid bridges close to the Plateau-Rayleigh instability limit can be stabilized when the upper supporting disk vibrates at a very high frequency and with a very small amplitude. The major effect of the vibration-induced pressure field is to straighten the liquid bridge free surface to compensate for the deformation caused by gravity. As a consequence, the apparent Bond number decreases and the maximum liquid bridge length increases. In this paper, we show experimentally that this procedure can be used to stabilize millimeter liquid bridges in air under normal gravity conditions. The breakup of vibrated liquid bridges is examined experimentally and compared with that produced in absence of vibration. In addition, we analyze numerically the dynamics of axisymmetric liquid bridges far from the Plateau-Rayleigh instability limit by solving the Navier-Stokes equations. We calculate the eigenfrequencies characterizing the linear oscillation modes of vibrated liquid bridges, and determine their stability limits. The breakup process of a vibrated liquid bridge at that stability limit is simulated too. We find qualitative agreement between the numerical predictions for both the stability limits and the breakup process and their experimental counterparts. Finally, we show the applicability of our technique to control the amount of liquid transferred between two solid surfaces
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