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Topological Dirac and Weyl semimetals not only host quasiparticles analogous to the elementary fermionic particles in high-energy physics, but also have a non-trivial band topology manifested by gapless surface states, which induce exotic surface Fermi arcs1,2 . Recent advances suggest new types of topological semimetal, in which spatial symmetries protect gapless electronic excitations without high-energy analogues3–11 . Here, using angle-resolved photoemission spectroscopy, we observe triply degenerate nodal points near the Fermi level of tungsten carbide with space group $$P\bar{6}m2$$ P6̄m2 (no. 187), in which the low-energy quasiparticles are described as three-component fermions distinct from Dirac and Weyl fermions. We further observe topological surface states, whose constant-energy contours constitute pairs of ‘Fermi arcs’ connecting to the surface projections of the triply degenerate nodal points, proving the non-trivial topology of the newly identified semimetal state. Triply degenerate electronic structure—three-component fermions—protected by crystal symmetries is observed in tungsten carbide. The observed Fermi arcs associated with the surface states provide evidence of the non-trivial topology of the states.

In quantum field theory, Lorentz invariance leads to three types of fermion—Dirac, Weyl and Majorana. Although the existence of Weyl and Majorana fermions as elementary particles in high-energy physics is debated, all three types of fermion have been proposed to exist as low-energy, long-wavelength quasiparticle excitations in condensed-matter systems. The existence of Dirac and Weyl fermions in condensed-matter systems has been confirmed experimentally, and that of Majorana fermions is supported by various experiments. However, in condensed-matter systems, fermions in crystals are constrained by the symmetries of the 230 crystal space groups rather than by Lorentz invariance, giving rise to the possibility of finding other types of fermionic excitation that have no counterparts in high-energy physics. Here we use angle-resolved photoemission spectroscopy to demonstrate the existence of a triply degenerate point in the electronic structure of crystalline molybdenum phosphide. Quasiparticle excitations near a triply degenerate point are three-component fermions, beyond the conventional Dirac–Weyl–Majorana classification, which attributes Dirac and Weyl fermions to four- and two-fold degenerate points, respectively. We also observe pairs of Weyl points in the bulk electronic structure of the crystal that coexist with the three-component fermions. This material thus represents a platform for studying the interplay between different types of fermions. Our experimental discovery opens up a way of exploring the new physics of unconventional fermions in condensed-matter systems.

AbstractIn this paper, we introduce a diffuse interface model for describing the dynamics of mixtures involving multiple (two or more) phases. The coupled hydrodynamical system is derived through an energetic variational approach. The total energy of the system includes the kinetic energy and the mixing (interfacial) energies. The least action principle (or the principle of virtual work) is applied to derive the conservative part of the dynamics, with a focus on the reversible part of the stress tensor arising from the mixing energies. The dissipative part of the dynamics is then introduced through a dissipation function in the energy law, in line with Onsager's principle of maximum dissipation. The final system, formed by a set of coupled time-dependent partial differential equations, reflects a balance among various conservative and dissipative forces and governs the evolution of velocity and phase fields. To demonstrate the applicability of the proposed model, a few two-dimensional simulations have been carried out, including (1) the force balance at the three-phase contact line in equilibrium, (2) a rising bubble penetrating a fluid-fluid interface, and (3) a solid particle falling in a binary fluid. The effects of slip at solid surface have been examined in connection with contact line motion and a pinch-off phenomenon.

The matrix proteins (M) of many enveloped RNA viruses mediate virus assembly and budding. However, it remains poorly understood how M are involved in virus budding and how they interact with envelope proteins. Here, we show that the expression level of Nipah (NiV) M in particles produced by the host cells deviates from a gamma distribution and does not reflect that of the host cells, indicating assembly of the NiV-M in the process. Our data reveal that NiV-M affects the circularity of the particles while the NiV envelope proteins do not. The organization of NiV envelope proteins on the membrane of the particles is similar to those that do not express NiV-M, suggesting that NiV-M does not directly interact with the envelope proteins during assembly and budding.

Background & Aims: Alcohol consumption exacerbates liver injury in chronic hepatitis C, and enhanced mitochondrial oxidative stress is one possible mechanism. The aim of this study was to determine whether hepatitis C virus core protein and alcohol-inducible cytochrome P450 2E1 contribute to reactive oxygen species production and cytotoxicity in human hepatoma cells. Methods: Huh-7 cells expressing core protein, cytochrome P450 2E1, or both were exposed to 0.1 mmol/L tertiary butyl hydroperoxide, tumor necrosis factor @a, and/or 25 mmol/L ethanol. Cytotoxicity, reactive oxygen species production, glutathione content, and mitochondrial membrane potential were measured. Results: Expression of core/cytochrome P450 2E1 synergistically enhanced cell death induced by either tertiary butyl hydroperoxide or tumor necrosis factor @a. After tertiary butyl hydroperoxide treatment, total reactive oxygen species production was increased more than 3-fold compared with cells that did not express core and cytochrome P450 2E1. Mitochondrial depolarization and reduced glutathione depletion occurred as well, and cell death was prevented by inhibition of mitochondrial permeability transition or caspase activity. Confocal microscopy showed that the mitochondria themselves were the origin of the reactive oxygen species. In the absence of core/cytochrome P450 2E1 expression, mitochondrial changes and cell death did not occur. Ethanol treatment further decreased mitochondrial reduced glutathione content and exacerbated mitochondrial reactive oxygen species production, depolarization, and cell death. All these effects were prevented by the antioxidant N-acetylcysteine. Conclusions: Mitochondrial reactive oxygen species production is induced by hepatitis C virus core and cytochrome P450 2E1, resulting in a reduction of mitochondrial antioxidant capacity and sensitivity to oxidants and tumor necrosis factor @a. Alcohol further depletes mitochondrial reduced glutathione, which exacerbates depolarization and cell death. Sensitization of mitochondria to oxidative insults is thus a potential mechanism for alcohol-related exacerbation of liver injury in chronic hepatitis C.

Reperfusion of ATP-depleted tissues after warm or cold ischemia causes pH-dependent necrotic and apoptotic cell death. In hepatocytes and other cell types as well, the mechanism underlying this reperfusion-induced cell death involves onset of the mitochondrial permeability transition (MPT). Opening of permeability transition (PT) pores in the mitochondrial inner membrane initiates the MPT, an event blocked by cyclosporin A (CsA) and pH less than 7.4. Thus, both acidotic pH and CsA prevent MPT-dependent reperfusion injury. Glycine also blocks reperfusion-induced necrosis but acts downstream of PT pore opening by stabilizing the plasma membrane. After the MPT, ATP availability from glycolysis or other source determines whether cell injury after reperfusion progresses to ATP depletion-dependent necrosis or ATP-requiring apoptosis. Thus, apoptosis and necrosis after reperfusion share a common pathway, the MPT. Cell injury progressing to either necrosis or apoptosis by shared pathways can be more aptly termed necrapoptosis.

Background & Aims: Activation of Fas or tumor necrosis factor receptor 1 (TNF-R1) on hepatocytes leads to apoptosis, which requires mitochondria activation. The pro-death Bcl-2 family protein, Bid, mediates this pathway by inducing mitochondrial releases of cytochrome c and other apoptotic factors. How Bid activates mitochondria has been studied in vitro with isolated mitochondria. We intended to study the mechanisms in intact hepatocytes so that findings could be made in a proper cellular context and would be more physiologically relevant. Methods: Hepatocytes were isolated from wild-type and bid-deficient mice and treated with anti-Fas or TNF-@a. Mechanisms of mitochondria activation were dissected with genetic, biochemical, and morphologic approaches. Results:bid-deficient hepatocytes were much more resistant to apoptosis. Bid was required for permeability transition and mitochondria depolarization in addition to the previously defined release of cytochrome c. Permeability transition inhibitors cyclosporin A and aristolochic acid could inhibit mitochondria activation effectively, but not as much as the deletion of the bid gene, and they could not inhibit Bak oligomerization. In addition, mitochondria depolarization also could be induced by caspases, whose activation was mainly dependent on Bid. Conclusions: Bid may activate mitochondria by 2 mechanisms, one is related to permeability transition and the other is related to Bak oligomerization. Bid can further affect mitochondria potentials by indirectly regulating caspase activity. This in vivo study provides novel findings not previously disclosed by in vitro studies, and indicates the importance of several mechanisms in contributing Bid-mediated mitochondria dysfunction that could be potential cellular targets of intervention.

Abstract: If γ(x)=x+iA(x),tan −1‖A′‖∞<ω<π/2,S ω0 ={z∈C}| |argz|<ω, or, |arg(-z)|<ω} We have proved that if φ is a holomorphic function in S ω0 and $$\left| {\varphi (z)} \right| \leqslant \frac{C}{{\left| z \right|}}$$ , denotingT f (z)= ∫ϕ(z-ζ)f(ζ)dζ, ∀f∈C 0(γ), ∀z∈suppf, where Cc(γ) denotes the class of continuous functions with compact supports, then the following two conditions are equivalent:

This paper presents a theory of Clifford algebra-valued martingales on a σ-finte measure space, with respect to a pseudoaccretive weight. A novel dual pair system of Haar functions associated with the Clifford martingale is constructed, and Littlewood-Paley estimates are established. The dual pair system of Clifford Haar functions is used to give a new proof of the boundedness of the Cauchy principal value integral on Lipschitz surfaces, and of the Clifford-valued T(b) theorem.

Without Abstract:

Single-crystalline La_0.5Ca_0.5MnO₃ nanowires have been successfully prepared by a hydrothermal method at low temperature. X-Ray diffraction (XRD) results show that the La_0.5Ca_0.5MnO₃ nanowires have an orthorhombic perovskite structure without any other impurity phase. Transmission electron microscopy (TEM) images demonstrate that the as-synthesized samples are made up of a large quantity of nanowires with lengths ranging from several to several tens of micrometers and uniform diameter (~80 nm). High-resolution transmission electron microscopy (HRTEM) images reveal that the nanowires with very clean surfaces grow along [100]. The result of magnetic measurements indicates that the nanowires have an enhanced T_c due to the shrinkage of the unit cell volume.

Single-crystalline La0.5Ca0.5MnO3nanowires have been successfully prepared by a hydrothermal method at low temperature. X-Ray diffraction XRD results show that the La0.5Ca0.5MnO3nanowires have an orthorhombic perovskite structure without any other impurity phase. Transmission electron microscopy TEM images demonstrate that the as-synthesized samples are made up of a large quantity of nanowires with lengths ranging from several to several tens of micrometers and uniform diameter ∼80 nm. High-resolution transmission electron microscopy HRTEM images reveal that the nanowires with very clean surfaces grow along 100. The result of magnetic measurements indicates that the nanowires have an enhanced Tcdue to the shrinkage of the unit cell volume.

Summary: A transcatheter double-blade valvotome for cutting a stenotic pulmonary valve has been devised. The valvotome consists of a retractable rhomboid structure at its tip, with a blade on each side of its proximal half. By tugging the extended blades from the pulmonary artery to the right ventricle it is possible to tear the stenotic valve. After animal experiments proved the feasibility and safety of this method, it was used in three children with pulmonary stenosis. The results were encouraging.

Because of the National Acute Spinal Cord Injury Studies (NASCIS), high-dose methylprednisolone became the standard of care for the acute spinal cord injury. In the NASCIS, there was no mention regarding the possibility of acute corticosteroid myopathy that high-dose methylprednisolone may cause. The dosage of methylprednisolone recommended by the NASCIS 3 is the highest dose of steroids ever being used during a 2-day period for any clinical condition. We hypothesize that it may cause some damage to the muscle of spinal cord injury patients. Further, steroid myopathy recovers naturally and the neurological improvement shown in the NASCIS may be just a recording of this natural motor recovery from the steroid myopathy, instead of any protection that methylprednisolone offers to the spinal cord injury. To our knowledge, this is the first discussion considering the possibility that the methylprednisolone recommended by NASCIS may cause acute corticosteroid myopathy.

La dysfonction endothéliale a été décrite chez les patients porteurs d’anticorps anti-phospholipides (aPL). Cependant, il n’est pas établi si les cellules endothéliales circulantes (CECs) – qui sont relarguées par l’endothélium lésé – peuvent identifier les patients à risque de thrombose. Ainsi, notre objectif était d’étudier l’association entre les CECs et les évènements thrombotiques chez les patients porteurs d’aPL et atteints de maladies auto-immunes associées.

Modeling the outbreak of a novel epidemic, such as coronavirus disease 2019 (COVID-19), is crucial for estimating its dynamics, predicting future spread and evaluating the effects of different interventions. However, there are three issues that make this modeling a challenging task: uncertainty in data, roughness in models, and complexity in programming. We addressed these issues by presenting an interactive individual-based simulator, which is capable of modeling an epidemic through multi-source information fusion., (© 2020 The Author(s).)