On the Dynamics of Starting Plumes

We explore the dynamics of starting plumes by analysis of a series of new small-scale laboratory experiments combined with a theoretical model for mass, momentum, and buoyancy conservation. We find that the head of the plume ascends with a speed which is approximately 0.6 times the characteristic speed of the fluid in the following steady plume, in accord with Turner (1962), and so the fluid released from the source eventually catches the head of the flow. On reaching the top of the plume it recirculates and mixes in the plume head. We estimate that approximately 0.61 ± 0.04 of the total buoyancy released from the source accumulates in the plume head, with the remainder in the following steady plume. Using measurements of the volume of the head, we estimate that a fraction 0.16 ± 0.08 of the volume of the head is entrained directly from the ambient, with the remainder of the fluid in the head being supplied by the following steady plume. These results imply that the buoyancy force exerted on the plume head plus the momentum flux supplied by the following plume exceeds the rate of change of momentum of the plume head even including the added-mass of the plume head. We propose that the difference is associated with a drag force resulting from the displacement of ambient fluid around the plume head. Using our experimental data, we estimate that the drag coefficient $C_d$ has a value 4.2 ± 1.4, with the range in values associated with the uncertainty in our estimate of entrainment of fluid directly into the plume head. As a test, the proposed model is shown to provide a reasonable description of a starting plume rising through a stratified environment in the region below the maximum height of rise of the associated steady plume, although above this point, the shape of the plume head changes and the model breaks down

D-branes in PP-wave light cone string field theory

The cubic interaction vertex and the dynamical supercharges are constructed for open strings ending on D7-branes, in light-cone superstring field theory in PP-wave background. In this context, we write down the symmetry generators in terms of the relevant group structure: SU(2) x SU(2) x SO(2) x SO(2), originating from the eight transverse directions in the PP-wave background and use the expressions to explicitly construct the vertex at the level of stringy zero modes. The results are further generalized to include all the stringy excitations as well.Comment: 30 pages, correction in eqn. (4.28), few equations (appendix), Comments (p.17-18) and a reference (no. 58) added, typo is corrected in eqn. (4.5

The ventilation of buildings and other mitigating measures for COVID-19: a focus on wintertime.

The year 2020 has seen the emergence of a global pandemic as a result of the disease COVID-19. This report reviews knowledge of the transmission of COVID-19 indoors, examines the evidence for mitigating measures, and considers the implications for wintertime with a focus on ventilation.This work was undertaken as a contribution to the Rapid Assistance in Modelling the Pandemic (RAMP) initiative, coordinated by the Royal Society

Autoinhibition of TBCB regulates EB1-mediated microtubule dynamics

Tubulin cofactors (TBCs) participate in the folding, dimerization, and dissociation pathways of the tubulin dimer. Among them, TBCB and TBCE are two CAP-Gly domain-containing proteins that interact and dissociate the tubulin dimer. Here we show how TBCB localizes at spindle and midzone microtubules during mitosis. Furthermore, the motif DEI/M-COO– present in TBCB, which is similar to the EEY/F-COO– element characteristic of EB proteins, CLIP-170, and α-tubulin, is required for TBCE–TBCB heterodimer formation and thus for tubulin dimer dissociation. This motif is responsible for TBCB autoinhibition, and our analysis suggests that TBCB is a monomer in solution. Mutants of TBCB lacking this motif are derepressed and induce microtubule depolymerization through an interaction with EB1 associated to microtubule tips. TBCB is also able to bind to the chaperonin complex CCT containing α-tubulin, suggesting that it could escort tubulin to facilitate its folding and dimerization, recycling or degradation

Unraveling the function of Arabidopsis thaliana OS9 in the endoplasmic reticulum-associated degradation of glycoproteins

In the endoplasmic reticulum, immature polypeptides coincide with terminally misfolded proteins. Consequently, cells need a well-balanced quality control system, which decides about the fate of individual proteins and maintains protein homeostasis. Misfolded and unassembled proteins are sent for destruction via the endoplasmic reticulum-associated degradation (ERAD) machinery to prevent the accumulation of potentially toxic protein aggregates. Here, we report the identification of Arabidopsis thaliana OS9 as a component of the plant ERAD pathway. OS9 is an ER-resident glycoprotein containing a mannose-6-phosphate receptor homology domain, which is also found in yeast and mammalian lectins involved in ERAD. OS9 fused to the C-terminal domain of YOS9 can complement the ERAD defect of the corresponding yeast Δyos9 mutant. An A. thaliana OS9 loss-of-function line suppresses the severe growth phenotype of the bri1-5 and bri1-9 mutant plants, which harbour mutated forms of the brassinosteroid receptor BRI1. Co-immunoprecipitation studies demonstrated that OS9 associates with Arabidopsis SEL1L/HRD3, which is part of the plant ERAD complex and with the ERAD substrates BRI1-5 and BRI1-9, but only the binding to BRI1-5 occurs in a glycan-dependent way. OS9-deficiency results in activation of the unfolded protein response and reduces salt tolerance, highlighting the role of OS9 during ER stress. We propose that OS9 is a component of the plant ERAD machinery and may act specifically in the glycoprotein degradation pathway

The ventilation of buildings and other mitigating measures for COVID-19: a focus on wintertime.

The year 2020 has seen the emergence of a global pandemic as a result of the disease COVID-19. This report reviews knowledge of the transmission of COVID-19 indoors, examines the evidence for mitigating measures, and considers the implications for wintertime with a focus on ventilation