The Implementation of One Opportunistic Routing in Wireless Networks

In the paper, it proposes an optimization framework addressing fairness issues for opportunity routing in wireless mesh networks, where we use network coding to ease the routing problem. We propose a distributed heuristic algorithm in the case when scheduling is determined by MAC, and discuss the suitability of our algorithm through simulations. It is found that in most situations our algorithm has better performances than the single-path algorithm and the classical network coding which is based opportunity algorithm MORE

Bis[μ-4-methyl-2-(2-pyridyl­methyl­sulfan­yl)pyrimidine-κN 1]bis­[(trifluoro­methanesulfonato-κO)silver(I)]

In the centrosymmetric dinuclear title complex, [Ag2(CF3SO3)2(C11H11N3S)2], the AgI atom is coordinated by two N atoms from two 4-methyl-2-(2-pyridyl­methyl­sulfan­yl)pyrimidine ligands and one O atom from a trifluoro­methane­sulfonate anion in a distorted T-type coordination geometry. The ligand adopts a bidentate bridging coordination mode through one pyridyl N atom and one pyrimidine N atom. In the crystal structure, π–π inter­actions are present between adjacent pyrimidine rings, with a centroid-to-centroid distance of 3.875 (7) Å

Extracting the number of type-B Goldstone modes and the dynamical critical exponent for a type of scale-invariant states

A generic scheme is proposed to perform a finite-entanglement scaling analysis for scale-invariant states, which appear to be highly degenerate ground states arising from spontaneous symmetry breaking with type-B Goldstone modes. This allows us to extract the number of type-B Goldstone modes and the dynamical critical exponent, in combination with a finite block-size scaling analysis, from numerical simulations of quantum many-body systems in the context of tensor network representations. The number of type-B Goldstone modes is identical to the fractal dimension, thus reflecting an abstract fractal underlying the ground state subspace. As illustrative examples, we investigate the spin-$s$ Heisenberg ferromagnetic model, the $\rm{SU}(3)$ ferromagnetic model and the $\rm{SO}(4)$ spin-orbital model.Comment: 14 pages, 24 figures, 11 table

ErbB4 Preserves Blood-Brain Barrier Integrity via the YAP/PIK3CB Pathway After Subarachnoid Hemorrhage in Rats

Studies have suggested that blood-brain barrier (BBB) disruption contributes to the pathogenesis of early brain injury after subarachnoid haemorrhage (SAH). Activation of the receptor tyrosine kinase ErbB4 can cause intramembrane proteolysis and release a soluble intracellular domain (ICD) that modulates transcription in the nucleus. This study was carried out to investigate the potential roles of ErbB4 in preserving BBB integrity after experimental SAH, as well as the underlying mechanisms of its protective effects. Endovascular perforation was used to prepare a rat SAH model. The SAH grade, neurological score, brain edema and BBB permeability were evaluated after surgery. Immunohistochemistry was used to determine the localization of ErbB4 and yes-associated protein (YAP). ErbB4 activator Nrg1 isoform β1 (Nrg1β1), Specific ErbB4 siRNA, YAP siRNA and PIK3CB specific inhibitor TGX 221 were used to manipulate the proposed pathway. The expression levels of ErbB4 ICD and YAP were markly increased after SAH. Double immunohistochemistry labeling showed that ErbB4 and YAP were expressed in endothelial cells and neurons. Activation of ErbB4 by Nrg1β1 (dosage 150 ng/kg) treatment promoted the neurobehavioral deficit, alleviated the brain water content and reduced albumin leakage 24 and 72 h after SAH. ErbB4 activation significantly promoted YAP and PIK3CB activity and increased the expression of tight junction proteins Occludin and Claudin-5. Depletion of ErbB4 aggravated neurological impairment and BBB disruption after SAH. The beneficial effects of ErbB4 activation were abolished by YAP small-interfering RNA and specific PIK3CB inhibitor. Activation of ErbB4 improved neurological performance after SAH through the YAP/PIK3CB signaling pathway, this neuroprotective effects may associated with BBB maintenance

Model of a multiverse providing the dark energy of our universe

It is shown that the dark energy presently observed in our universe can be regarded as the energy of a scalar field driving an inflation-like expansion of a multiverse with ours being a subuniverse among other parallel universes. A simple model of this multiverse is elaborated: Assuming closed space geometry, the origin of the multiverse can be explained by quantum tunneling from nothing; subuniverses are supposed to emerge from local fluctuations of separate inflation fields. The standard concept of tunneling from nothing is extended to the effect that in addition to an inflationary scalar field, matter is also generated, and that the tunneling leads to an (unstable) equilibrium state. The cosmological principle is assumed to pertain from the origin of the multiverse until the first subuniverses emerge. With increasing age of the multiverse, its spatial curvature decays exponentially so fast that, due to sharing the same space, the flatness problem of our universe resolves by itself. The dark energy density imprinted by the multiverse on our universe is time-dependent, but such that the ratio $w{=}\varrho/(c^2p)$ of its mass density and pressure (times $c^2$) is time-independent and assumes a value $-1{+}\epsilon$ with arbitrary $\epsilon{>}0$. $\epsilon$ can be chosen so small, that the dark energy model of this paper can be fitted to the current observational data as well as the cosmological constant model.Comment: 32 pages, 4 figure

Structural impairment patterns in peripapillary retinal fiber layer and retinal ganglion cell layer in mitochondrial optic neuropathies

AIM: To evaluate the structural injure patterns in peripapillary retinal fiber layer (pRNFL), retinal ganglion cell layer (RGCL) and their correlations to visual function in various mitochondrial optic neuropathies (MON) to offer help to their differential diagnosis. METHODS: Totally 32 MON patients (60 eyes) were recruited within 6mo after clinical onsets, including 20 Leber hereditary optic neuropathy (LHON) patients (37 eyes), 12 ethambutol-induced optic neuropathy (EON) patients (23 eyes), and 41 age-gender matched healthy controls (HC, 82 eyes). All subjects had pRNFL and RGCL examinations with optic coherence tomography (OCT) and visual function tests. RESULTS: In the early stages of MON, the temporal pRNFL thickness decreased (66.09±22.57 μm), but increased in other quadrants, compared to HC (76.95±14.81 μm). The other quadrants remaining stable for LHON and EON patients besides the second hour sector of pRNFL thickness reduced and the temporal pRNFL decreased (56.78±15.87 μm) for EON. Total macular thickness in MON reduced remarkably (279.25±18.90 μm; P=0.015), which mainly occurring in the inner circle (3 mm diameter of circle) and the nasal temporal sectors in the outer circle (5.5 mm diameter of circle), in contrast to those in HC. RGCL thickness reduced in each sector of the macula (61.90±8.73 μm; P≤0.001). It strongly showed the correlationship of best corrected visual acuity (R=0.50, P=0.0003) and visual field injury (R=0.54, P=0.0002) in MON patients. CONCLUSION: OCT is a potential tool for detecting structural alterations in the optic nerves of various MON. Different types of MON may have different damage patterns

Recent developments in the immunopathology of COVID-19

There has been an important change in the clinical characteristics and immune profile of Coronavirus disease 2019 (COVID-19) patients during the pandemic thanks to the extensive vaccination programs. Here, we highlight recent studies on COVID-19, from the clinical and immunological characteristics to the protective and risk factors for severity and mortality of COVID-19. The efficacy of the COVID-19 vaccines and potential allergic reactions after administration are also discussed. The occurrence of new variants of concerns such as Omicron BA.2, BA.4, and BA.5 and the global administration of COVID-19 vaccines have changed the clinical scenario of COVID-19. Multisystem inflammatory syndrome in children (MIS-C) may cause severe and heterogeneous disease but with a lower mortality rate. Perturbations in immunity of T cells, B cells, and mast cells, as well as autoantibodies and metabolic reprogramming may contribute to the long-term symptoms of COVID-19. There is conflicting evidence about whether atopic diseases, such as allergic asthma and rhinitis, are associated with a lower susceptibility and better outcomes of COVID-19. At the beginning of pandemic, the European Academy of Allergy and Clinical Immunology (EAACI) developed guidelines that provided timely information for the management of allergic diseases and preventive measures to reduce transmission in the allergic clinics. The global distribution of COVID-19 vaccines and emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants with reduced pathogenic potential dramatically decreased the morbidity, severity, and mortality of COVID-19. Nevertheless, breakthrough infection remains a challenge for disease control. Hypersensitivity reactions (HSR) to COVID-19 vaccines are low compared to other vaccines, and these were addressed in EAACI statements that provided indications for the management of allergic reactions, including anaphylaxis to COVID-19 vaccines. We have gained a depth knowledge and experience in the over 2 years since the start of the pandemic, and yet a full eradication of SARS-CoV-2 is not on the horizon. Novel strategies are warranted to prevent severe disease in high-risk groups, the development of MIS-C and long COVID-19