Why reducing the cosmic sound horizon alone can not fully resolve the Hubble tension

The mismatch between the locally measured expansion rate of the universe and the one inferred from the cosmic microwave background measurements by Planck in the context of the standard ΛCDM, known as the Hubble tension, has become one of the most pressing problems in cosmology. A large number of amendments to the ΛCDM model have been proposed in order to solve this tension. Many of them introduce new physics, such as early dark energy, modifications of the standard model neutrino sector, extra radiation, primordial magnetic fields or varying fundamental constants, with the aim of reducing the sound horizon at recombination r⋆. We demonstrate here that any model which only reduces r⋆ can never fully resolve the Hubble tension while remaining consistent with other cosmological datasets. We show explicitly that models which achieve a higher Hubble constant with lower values of matter density Ωmh2 run into tension with the observations of baryon acoustic oscillations, while models with larger Ωmh2 develop tension with galaxy weak lensing data.

Why reducing the cosmic sound horizon can not fully resolve the Hubble tension

The mismatch between the locally measured expansion rate of the universe and the one inferred from the cosmic microwave background measurements by Planck in the context of the standard ΛCDM, known as the Hubble tension, has become one of the most pressing problems in cosmology. A large number of amendments to the ΛCDM model have been proposed in order to solve this tension. Many of them introduce new physics, such as early dark energy, modifications of the standard model neutrino sector, extra radiation, primordial magnetic fields or varying fundamental constants, with the aim of reducing the sound horizon at recombination r*. We demonstrate here that any model which only reduces r* can never fully resolve the Hubble tension while remaining consistent with other cosmological datasets. We show explicitly that models which operate at lower matter density Ωmh2 run into tension with the observations of baryon acoustic oscillations, while models operating at higher Ωmh2 develop tension with galaxy weak lensing data.

Anchoring of actin to the plasma membrane enables tension production in the fission yeast cytokinetic ring

The cytokinetic ring generates tensile force that drives cell division, but how tension emerges from the relatively disordered ring organization remains unclear. Long ago, a musclelike sliding filament mechanism was proposed, but evidence for sarcomeric order is lacking. Here we present quantitative evidence that in fission yeast, ring tension originates from barbed-end anchoring of actin filaments to the plasma membrane, providing resistance to myosin forces that enables filaments to develop tension. The role of anchoring was highlighted by experiments on isolated fission yeast rings, where sections of ring became unanchored from the membrane and shortened ∼30-fold faster than normal. The dramatically elevated constriction rates are unexplained. Here we present a molecularly explicit simulation of constricting partially anchored rings as studied in these experiments. Simulations accurately reproduced the experimental constriction rates and showed that following anchor release, a segment becomes tensionless and shortens via a novel noncontractile reeling-in mechanism at about the velocity of load-free myosin II. The ends are reeled in by barbed end–anchored actin filaments in adjacent segments. Other actin anchoring schemes failed to constrict rings. Our results quantitatively support a specific organization and anchoring scheme that generate tension in the cytokinetic ring.

Anchoring of actin to the plasma membrane enables tension production in the fission yeast cytokinetic ring

The cytokinetic ring generates tensile force that drives cell division, but how tension emerges from the relatively disordered ring organization remains unclear. Long ago a muscle-like sliding filament mechanism was proposed, but evidence for sarcomeric order is lacking. Here we present quantitative evidence that in fission yeast ring tension originates from barbed-end anchoring of actin filaments to the plasma membrane, providing resistance to myosin forces which enables filaments to develop tension. The role of anchoring was highlighted by experiments on isolated fission yeast rings, where sections of ring unanchored from the membrane and shortened ~30-fold faster than normal [Mishra M., et al. (2013) Nat Cell Biol 15(7):853-859]. The dramatically elevated constriction rates are unexplained. Here we present a molecularly explicit simulation of constricting partially anchored rings as studied in these experiments. Simulations accurately reproduced the experimental constriction rates, and showed that following anchor release a segment becomes tensionless and shortens via a novel non-contractile reeling-in mechanism at about the load-free myosin-II velocity. The ends are reeled in by barbed-end-anchored actin filaments in adjacent segments. Other actin anchoring schemes failed to constrict rings. Our results quantitatively support a specific organization and anchoring scheme that generates tension in the cytokinetic ring.

Asymmetric Tug-of-War leads to Cooperative Transport of a Cargo by Multiple Kinesins

How cargoes move within a crowded cell—over long distances and at speeds that are nearly the same as when moving on an unimpeded pathway—has long been mysterious. Through an in vitro gliding assay, which involves measuring nanometer displacement and piconewtons of force, we have evidence that when kinesins, a cytoplasmic molecular motor, operate in small groups, from 2-10, they can communicate among themselves through an asymmetric tug-of-war by inducing tension (up to 4 pN) on the cargo. Surprisingly, the primary role of approximately one-third of kinesins is to develop tension, which instantaneously slows forward motion but helps increase cargo run length. These hindering kinesins fall off rapidly when experiencing a forward tug. Occasionally, they may be ripped off from their anchors by other driving kinesins working in tandem. Furthermore, with roadblocks on the microtubule, multiple kinesins cooperate to overcome impediments. Hence, kinesin may employ an asymmetric tug-of-war and a cooperative motion to navigate through cellular environment.

Cyclic Load Protocol for Anchored Nonstructural Components and Systems

This work is motivated by the need to investigate the cyclic load response of restrained (via anchorage or other) nonstructural components and systems (NCSs). For this purpose, a load protocol is developed for capturing the behavior of the restraining element when subjected to seismic loading. The protocol incorporates numerical analyses of buildings designed to respond nonlinearly under design earthquake events, analysis of secondary systems located in these buildings and rainflow counting of time history results extracted from these analyses. Secondary system response results are used to develop tension and shear load protocols. Protocol statistics are presented and envisioned to be useful in anchor or other restraint system qualification tests.

Design of Tension Control System of Fiberglass Winding Machine Based on Fuzzy Logic Control Algorithm

Winding tension is one of the most important factors that affects the winding products' quality. This paper introduces a method to develop tension control system based on data acquisition card, and presents the block diagram of the system which actuators are AC servomotors. In order to meet the demands on tension control system, such as good stability, strong robust and etc., this paper proposes a tension control method which is based on the fuzzy control theory.

Assembly of fibronectin fibrils by fibroblasts cultured within an attached collagen lattice

Dupuytren's disease is characterized by a contraction of the palmar fascia resulting in irreversible flexion of the affected digits. Collagen lattices provide a model system for studying the cellular mechanisms of tissue contraction. Fibroblasts cultured within an attached collagen lattice resemble the myofibroblasts present in the diseased tissue. They form bundles of actin microfilaments, assemble fibronectin fibrils and form a specialized transmembrane association (fibronexus) linking the two filament systems. In addition, fibroblasts cultured in an attached collagen lattice will develop tension which results in rapid lattice retraction upon mechanical release from the underlying substratum. In this study we examined fibronectin fibril assembly in an attached collagen lattice and the potential role these fibrils play in tension development.