Coevolution of synchronous activity and connectivity in coupled chaotic oscillators

We investigate the coevolution dynamics of node activities and coupling strengths in coupled chaotic oscillators via a simple threshold adaptive scheme. The coupling strength is synchronous activity regulated, which in turn is able to boost the synchronization remarkably. In the case of weak coupling, the globally coupled oscillators present a highly clustered functional connectivity with a power-law distribution in the tail with γ≃3.1, while for strong coupling, they self-organize into a network with a heterogeneously rich connectivity at the onset of synchronization but exhibit rather sparse structure to maintain the synchronization in noisy environment. The relevance of the results is briefly discussed

HMS: A Hierarchical Mapping System for the Locator/ID Separation Network

The current Internet is facing serious scalability problems and the overloading of Internet Protocol (IP) addresses is regarded as an important reason. The Locator/ID Separation Protocol (LISP) is proposed as a network-based solution that separates IP addresses into Routing Locators (RLOCs) and Endpoint Identifiers (EIDs) to address the routing scalability problems. It is a critical challenge for LISP to design a scalable and efficient mapping system. In this paper, we propose a hierarchical mapping system (HMS). HMS consists of two levels with the bottom level maintaining the EID-to-RLOC mappings in an Autonomous System (AS) and the upper level storing the mappings between EID-prefixes and ASs in the global network. We adopt one-hop Distributed Hash Table (DHT) to organize EID-to-RLOC mappings in the bottom level and use a protocol like Border Gateway Protocol (BGP) to propagate EID-prefix-to-AS mappings in the upper level. HMS aggregates the prefixes in an AS and decreases the global mapping entries in the upper level. The evaluation results show that the number of mapping entries in HMS grows slower than the routing table size, which makes HMS scalable. In addition, the mobility in HMS does not cause mapping changes in the upper level. It makes HMS efficient in supporting host mobility. We estimate the map-requests sent to the mapping system, which show the load on HMS is small. Last, we compare HMS with LISP-TREE and LISP+ALT by quantitative analysis, in terms of resolution cost, and qualitative analysis. The results show that HMS has a good performance

An outbreak of aseptic meningitis caused by a distinct lineage of coxsackievirus B5 in China

SummaryIn 2009, an outbreak of aseptic meningitis caused by coxsackievirus B5 (CVB5) occurred in China. Epidemiological investigations of this outbreak revealed that the proportion of severe cases (14/43, 33%) was higher than in other outbreaks associated with CVB5 in China. Phylogenetic analysis of the entire VP1 sequences demonstrated that the CVB5 isolates from the severe cases form a distinct lineage belonging to genogroup E with the Shandong isolates of 2009. A substitution of serine (S) to asparagine (N) at amino acid 95 in the VP1 region may be a major virulence determinant for the virus. Our findings suggest that this new lineage of CVB5 is circulating in China. Further genetic studies are needed in order to gain a better insight into the genetic variability of CVB5 isolates and the relationship with pathogenicity

Probing electronic-vibrational dynamics of N2+ induced by strong-field ionization

The coupled electronic-vibrational dynamics of nitrogen ions induced by strong-field ionization is investigated theoretically to corroborate the recent transient X-ray K-edge absorption experiment [PRL 129, 123002 (2022)], where the population distribution of three electronic states in air lasing of N2+ was determined for the first time. By extending the ionization-coupling model to include the transient absorption, we successfully reproduce the time-resolved X-ray absorption spectra of nitrogen ions observed in the experiment. By identifying the contributions from different electronic states, the study provides different interpretation revealing the significant role of excited state A arising from the strong coupling between vibrational states in strong laser fields. It indicates that the electronic population inversion occurs at least for certain alignment of nitrogen molecules. The theory helps uncovering new features of absorption from forbidden transitions during ionization and confirming that the vibration coherence at each electronic channel induces the modulation of absorbance after strong field ionization. A new scheme is proposed to determine the population transfer at different probing geometry to avoid the spectral overlap. This work offers valuable insights into the intricate interplay between electronic and vibrational dynamics and helps to resolve the debate on nitrogen air lasing

Folic acid and zinc improve hyperuricemia by altering the gut microbiota of rats with high-purine diet-induced hyperuricemia

A high-purine diet can cause hyperuricemia and destroy the microbial composition of the gut microbiota. Both folic acid and zinc significantly reduce uric acid levels and alleviate hyperuricemia. However, whether the underlying mechanisms are associated with the regulation of the gut microbiota remain unknown. To explore alterations of the gut microbiota related to folic acid and zinc treatment in rats with hyperuricemia in our study. A hyperuricemic rat model was established with a high-purine diet. The effects of folic acid and zinc on uric acid levels were evaluated. Alterations of the gut microbiota related to hyperuricemia and the treatments were evaluated by sequencing using the Illumina MiSeq system. The results demonstrated that uric acid levels dropped observably, and the activities of adenosine deaminase (ADA) and xanthine oxidase (XOD) were downregulated after folic acid or zinc intervention. 16S rRNA gene sequencing-based gut microbiota analysis revealed that folic acid and zinc enhanced the abundance of probiotic bacteria and reduced that of pathogenic bacteria, thus improving intestinal barrier function. PICRUST analysis indicated that folic acid and zinc restored gut microbiota metabolism. These findings indicate that folic acid and zinc ameliorate hyperuricemia by inhibiting uric acid biosynthesis and stimulating uric acid excretion by modulating the gut microbiota. Thus, folic acid and zinc may be new and safe therapeutic agents to improve hyperuricemia

A novel trifunctional IgG-like bispecific antibody to inhibit HIV-1 infection and enhance lysis of HIV by targeting activation of complement

BACKGROUND: The complement system is not only a key component of innate immunity but also provides a first line of defense against invading pathogens, especially for viral pathogens. Human immunodeficiency virus (HIV), however, possesses several mechanisms to evade complement-mediated lysis (CoML) and exploit the complement system to enhance viral infectivity. Responsible for this intrinsic resistance against complement-mediated virolysis are complement regulatory membrane proteins derived from the host cell that inherently downregulates complement activation at several stages of the cascade. In addition, HIV is protected from complement-mediated lysis by binding soluble factor H (fH) through the viral envelope proteins, gp120 and gp41. Whereas inhibition of complement activity is the desired outcome in the vast majority of therapeutic approaches, there is a broader potential for complement-mediated inhibition of HIV by complement local stimulation. PRESENTATION OF THE HYPOTHESIS: Our previous studies have proven that the complement-mediated antibody-dependent enhancement of HIV infection is mediated by the association of complement receptor type 2 bound to the C3 fragment and deposited on the surface of HIV virions. Thus, we hypothesize that another new activator of complement, consisting of two dsFv (against gp120 and against C3d respectively) linked to a complement-activating human IgG1 Fc domain ((anti-gp120 × anti-C3d)-Fc), can not only target and amplify complement activation on HIV virions for enhancing the efficiency of HIV lysis, but also reduce the infectivity of HIV through blocking the gp120 and C3d on the surface of HIV. TESTING THE HYPOTHESIS: Our hypothesis was tested using cell-free HIV-1 virions cultivated in vitro and assessment of virus opsonization was performed by incubating appropriate dilutions of virus with medium containing normal human serum and purified (anti-gp120 × anti-C3d)-Fc proteins. As a control group, viruses were incubated with normal human serum under the same conditions. Virus neutralization assays were used to estimate the degree of (anti-gp120 × anti-C3d)-Fc lysis of HIV compared to untreated virus. IMPLICATIONS OF THE HYPOTHESIS: The targeted complement activator, (anti-gp120 × anti-C3d)-Fc, can be used as a novel approach to HIV therapy by abrogating the complement-enhanced HIV infection of cells

A new treatment for neurogenic inflammation caused by EV71 with CR2-targeted complement inhibitor

BACKGROUND: Enterovirus 71 (EV71), one of the most important neurotropic EVs, has caused death and long-term neurological sequelae in hundreds of thousands of young children in the Asia-Pacific region in the past decade. The neurological diseases are attributed to infection by EV71 inducing an extensive peripheral and central nervous system (CNS) inflammatory response with abnormal cytokine production and lymphocyte depletion induced by EV71 infection. In the absence of specific antiviral agents or vaccines, an effective immunosuppressive strategy would be valuable to alleviate the severity of the local inflammation induced by EV71 infection. PRESENTATION OF THE HYPOTHESIS: The complement system plays a pivotal role in the inflammatory response. Inappropriate or excessive activation of the complement system results in a severe inflammatory reaction or numerous pathological injuries. Previous studies have revealed that EV71 infection can induce complement activation and an inflammatory response of the CNS. CR2-targeted complement inhibition has been proved to be a potential therapeutic strategy for many diseases, such as influenza virus-induced lung tissue injury, postischemic cerebral injury and spinal cord injury. In this paper, a mouse model is proposed to test whether a recombinant fusion protein consisting of CR2 and a region of Crry (CR2-Crry) is able to specifically inhibit the local complement activation induced by EV71 infection, and to observe whether this treatment strategy can alleviate or even cure the neurogenic inflammation. TESTING THE HYPOTHESIS: CR2-Crry is expressed in CHO cells, and its biological activity is determined by complement inhibition assays. 7-day-old ICR mice are inoculated intracranially with EV71 to duplicate the neurological symptoms. The mice are then divided into two groups, in one of which the mice are treated with CR2-Crry targeted complement inhibitor, and in the other with phosphate-buffered saline. A group of mice deficient in complement C3, the breakdown products of which bind to CR2, are also infected with EV71 virus. The potential bioavailability and efficacy of the targeted complement inhibitor are evaluated by histology, immunofluorescence staining and radiolabeling. IMPLICATIONS OF THE HYPOTHESIS: CR2-Crry-mediated targeting complement inhibition will alleviate the local inflammation and provide an effective treatment for the severe neurological diseases associated with EV71 infection

Characterization and Genomic Analysis of SFPH2, a Novel T7virus Infecting Shigella

Shigellosis, caused by Shigella, is a major global health concern, with nearly 164.7 million cases and over a million deaths occurring annually worldwide. Shigella flexneri is one of the most common subgroups of Shigella with a high incidence of multidrug-resistance. The phage therapy approach is an effective method for controlling multidrug-resistant bacteria. However, only a few Shigella phages have been described to date. In this study, a novel lytic bacteriophage SFPH2 was isolated from a sewage sample obtained from a hospital in Beijing, China, using a multidrug-resistant S. flexneri 2a strain (SF2) isolated from the fecal sample of a dysentery patient. SFPH2 is a member of the Podoviridae virus family with an icosahedral capsid and a short, non-contractile tail. It was found to be stable over a wide range of temperatures (4–50°C) and pH values (pH 3–11). Moreover, SFPH2 could infect two other S. flexneri serotypes (serotypes 2 variant and Y). High-throughput sequencing revealed that SFPH2 has a linear double-stranded DNA genome of 40,387 bp with 50 open reading frames. No tRNA genes were identified in the genome. Comparative analysis of the genome revealed that the SFPH2 belongs to the subfamily Autographivirinae and genus T7virus. The genome shows high similarity with other enterobacterial T7virus bacteriophages such as Citrobacter phage SH4 (95% identity and 89% coverage) and Cronobacter phage Dev2 (94% identity and 92% coverage). A comparison of the fiber proteins showed that minor differences in the amino acid residues might specify different protein binding regions and determine host species. In conclusion, this is the first report of a T7virus that can infect Shigella; SFPH2 has a functional stability under a wide range of temperatures and pH values, showing the potential to be widely applied to control Shigella–associated clinical infections and reduce the transmission rates of S. flexneri serotype 2a and its variants in the environment