A uniqueness result for a Schrödinger–Poisson system with strong singularity

In this paper, we consider the following Schrödinger–Poisson system with strong singularity −∆u + φu = f(x)u , x ∈ Ω, −∆φ = u 2 , x ∈ Ω, u > 0, x ∈ Ω, u = φ = 0, x ∈ ∂Ω, where Ω ⊂ R3 is a smooth bounded domain, γ > 1, f ∈ L 1 (Ω) is a positive function (i.e. f(x) > 0 a.e. in Ω). A necessary and sufficient condition on the existence and uniqueness of positive weak solution of the system is obtained. The results supplement the main conclusions in recent literature

A uniqueness result for a Schrödinger-Poisson system with strong singularity

In this paper, we consider the following Schrödinger–Poisson system with strong singularity −∆u + φu = f(x)u , x ∈ Ω, −∆φ = u 2 , x ∈ Ω, u > 0, x ∈ Ω, u = φ = 0, x ∈ ∂Ω, where Ω ⊂ R3 is a smooth bounded domain, γ > 1, f ∈ L 1 (Ω) is a positive function (i.e. f(x) > 0 a.e. in Ω). A necessary and sufficient condition on the existence and uniqueness of positive weak solution of the system is obtained. The results supplement the main conclusions in recent literature

Oxidative stress-mediated activation of extracellular signal-regulated kinase contributes to mild cognitive impairment-related mitochondrial dysfunction

Mild cognitive impairment (MCI) occurs during the pre-dementia stage of Alzheimer’s disease (AD) and is characterized by a decline in cognitive abilities that frequently represents a transition between normal cognition and AD dementia. Its pathogenesis is not well understood. Here, we demonstrate the direct consequences and potential mechanisms of oxidative stress, mitochondrial dynamic and functional defects in MCI-derived mitochondria. Using cytoplasmic hybrid (cybrid) cell model in which mitochondria from MCI or age-matched non-MCI subjects were incorporated into a human neuronal cell line depleted of endogenous mitochondrial DNA, we evaluated the mitochondrial dynamics and functions, as well as the role of oxidative stress in the resultant cybrid lines. We demonstrated increased expression levels of mitofusin 2 (Mfn2) is markedly induced by oxidative stress in MCI-derived mitochondria along with aberrant mitochondrial functions. Inhibition of oxidative stress rescues MCI-impaired mitochondrial fusion/fission balance as shown by the suppression of Mfn2 expression, attenuation of abnormal mitochondrial morphology and distribution, and improvement in mitochondrial function. Furthermore, blockade of MCI related stress-mediated activation of extracellular signal-regulated kinase (ERK) signaling not only attenuates aberrant mitochondrial morphology and function but also restores mitochondrial fission and fusion balance, in particular inhibition of overexpressed Mfn2. Our results provide new insights into the role of the oxidative stress-ERK-Mfn2 signal axis in MCI-related mitochondrial abnormalities, indicating that the MCI phase may be targetable for the development new therapeutic approaches that improve mitochondrial function in age-related neurodegeneration

Inhibition of ERK-DLP1 signaling and mitochondrial division alleviates mitochondrial dysfunction in Alzheimer's disease cybrid cell

Mitochondrial dysfunction is an early pathological feature of Alzheimer’s disease (AD). The underlying mechanisms and strategies to repair it remain unclear. Here, we demonstrate for the first time the direct consequences and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in AD. Using cytoplasmic hybrid (cybrid) neurons with incorporated platelet mitochondria from AD and age-matched non-AD human subjects into mitochondrial DNA (mtDNA)-depleted neuronal cells, we observed that AD cybrid cells had significant changes in morphology and function; such changes associate with altered expression and distribution of dynamin-like protein (DLP1) and mitofusin 2 (Mfn2). Treatment with antioxidant protects against AD mitochondria-induced extracellular signal-regulated kinase (ERK) activation and mitochondrial fission-fusion imbalances. Notably, inhibition of ERK activation not only attenuates aberrant mitochondrial morphology and function but also restores the mitochondrial fission and fusion balance. These effects suggest a role of oxidative stress-mediated ERK signal transduction in modulation of mitochondrial fission and fusion events. Further, blockade of the mitochondrial fission protein DLP1 by a genetic manipulation with a dominant negative DLP1 (DLP1K38A), its expression with siRNA-DLP1, or inhibition of mitochondrial division with mdivi-1 attenuates mitochondrial functional defects observed in AD cybrid cells. Our results provide new insights into mitochondrial dysfunction resulting from changes in the ERK-fission/fusion (DLP1) machinery and signaling pathway. The protective effect of mdivi-1 and inhibition of ERK signaling on maintenance of normal mitochondrial structure and function holds promise as a potential novel therapeutic strategy for AD

Variational quantum eigensolver with linear depth problem-inspired ansatz for solving portfolio optimization in finance

Great efforts have been dedicated in recent years to explore practical applications for noisy intermediate-scale quantum (NISQ) computers, which is a fundamental and challenging problem in quantum computing. As one of the most promising methods, the variational quantum eigensolver (VQE) has been extensively studied. In this paper, VQE is applied to solve portfolio optimization problems in finance by designing two hardware-efficient Dicke state ansatze that reach a maximum of 2n two-qubit gate depth and n^2/4 parameters, with n being the number of qubits used. Both ansatze are partitioning-friendly, allowing for the proposal of a highly scalable quantum/classical hybrid distributed computing (HDC) scheme. Combining simultaneous sampling, problem-specific measurement error mitigation, and fragment reuse techniques, we successfully implement the HDC experiments on the superconducting quantum computer Wu Kong with up to 55 qubits. The simulation and experimental results illustrate that the restricted expressibility of the ansatze, induced by the small number of parameters and limited entanglement, is advantageous for solving classical optimization problems with the cost function of the conditional value-at-risk (CVaR) for the NISQ era and beyond. Furthermore, the HDC scheme shows great potential for achieving quantum advantage in the NISQ era. We hope that the heuristic idea presented in this paper can motivate fruitful investigations in current and future quantum computing paradigms.Comment: 21 pages, 20 figure

Inhibition of ERK-DLP1 signaling and mitochondrial division alleviates mitochondrial dysfunction in Alzheimer's disease cybrid cell

Mitochondrial dysfunction is an early pathological feature of Alzheimer’s disease (AD). The underlying mechanisms and strategies to repair it remain unclear. Here, we demonstrate for the first time the direct consequences and potential mechanisms of mitochondrial functional defects associated with abnormal mitochondrial dynamics in AD. Using cytoplasmic hybrid (cybrid) neurons with incorporated platelet mitochondria from AD and age-matched non-AD human subjects into mitochondrial DNA (mtDNA)-depleted neuronal cells, we observed that AD cybrid cells had significant changes in morphology and function; such changes associate with altered expression and distribution of dynamin-like protein (DLP1) and mitofusin 2 (Mfn2). Treatment with antioxidant protects against AD mitochondria-induced extracellular signal-regulated kinase (ERK) activation and mitochondrial fission-fusion imbalances. Notably, inhibition of ERK activation not only attenuates aberrant mitochondrial morphology and function but also restores the mitochondrial fission and fusion balance. These effects suggest a role of oxidative stress-mediated ERK signal transduction in modulation of mitochondrial fission and fusion events. Further, blockade of the mitochondrial fission protein DLP1 by a genetic manipulation with a dominant negative DLP1 (DLP1K38A), its expression with siRNA-DLP1, or inhibition of mitochondrial division with mdivi-1 attenuates mitochondrial functional defects observed in AD cybrid cells. Our results provide new insights into mitochondrial dysfunction resulting from changes in the ERK-fission/fusion (DLP1) machinery and signaling pathway. The protective effect of mdivi-1 and inhibition of ERK signaling on maintenance of normal mitochondrial structure and function holds promise as a potential novel therapeutic strategy for AD

Comparative genomics reveals insights into avian genome evolution and adaptation

Birds are the most species-rich class of tetrapod vertebrates and have wide relevance across many research fields. We explored bird macroevolution using full genomes from 48 avian species representing all major extant clades. The avian genome is principally characterized by its constrained size, which predominantly arose because of lineage-specific erosion of repetitive elements, large segmental deletions, and gene loss. Avian genomes furthermore show a remarkably high degree of evolutionary stasis at the levels of nucleotide sequence, gene synteny, and chromosomal structure. Despite this pattern of conservation, we detected many non-neutral evolutionary changes in protein-coding genes and noncoding regions. These analyses reveal that pan-avian genomic diversity covaries with adaptations to different lifestyles and convergent evolution of traits

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Global Asymptotic Stability of a Predator-Prey Model with Modified Leslie-Gower and Holling-Type II Schemes

We study the predator-prey model proposed by Aziz-Alaoui and Okiye (Appl. Math. Lett. 16 (2003) 1069–1075) First, the structure of equilibria and their linearized stability is investigated. Then, we provide two sufficient conditions on the global asymptotic stability of a positive equilibrium by employing the Fluctuation Lemma and Lyapunov direct method, respectively. The obtained results not only improve but also supplement existing ones