Exploring group theory and topology for analyzing the structure of biology

The concepts of population and species play a fundamental role in biology. The existence and precise definition of higher-order hierarchies, such as division into species, is open to debate among biologists. First, we seek to show a fractal structure of species. We are able to define a species as a $p$-Sylow subgroup of a particular community in a single niche, confirmed by topological analysis. We named this model the patch with zeta dominance (PzDom) model. Next, the topological nature of the system is carefully examined and for testing purposes, species density data are used in conjunction with data derived from liquid-chromatography mass spectrometry of proteins. We confirm the induction of hierarchy and time through a one-dimensional probability space with certain topologies. For further clarification of induced fractals including the relation to renormalization in physics, a theoretical development is proposed based on a newly identified fact, namely that scaling parameters for magnetization exactly correspond to imaginary parts of the Riemann zeta function's nontrivial zeros. A master torus and a Lagrangian/Hamiltonian are derived expressing fractal structures as a solution for diminishing divergent terms in renormalization. We will also focus on an application of our developed model. We extend current PzDom model to the so-called exPzDom model to qualify population dynamics as a topological matter as a whole, not focusing on hierarchy. The indicators in the exPzDom model adhere well to the empirical dynamics of SARS-CoV-2 infected people and align appropriately with actual policies instituted by the Japanese government. In our patch with zeta dominance (PzDom) model or its extended version (exPzDom), calculations only require knowledge of the density of individuals over time

Coronavirus Diversification

Human coronaviruses (HCoVs) are of zoonotic origins, and seven distinct HCoVs are currently known to infect humans. While the four seasonal HCoVs appear to be mildly pathogenic and circulate among human populations, the other three designated SARS-CoV, MERS-CoV, and SARS-CoV-2 can cause severe diseases in some cases. The newly identified SARS-CoV-2, a causative virus of COVID-19 that can be deadly, is now spreading worldwide much more efficiently than the other two pathogenic viruses. Despite evident differences in these properties, all HCoVs commonly have an exceptionally large genomic RNA with a rather peculiar gene organization and have the potential to readily alter their biological properties. CoVs are characterized by their biological diversifications, high recombination, and efficient adaptive evolution. We are particularly concerned about the high replication and transmission nature of SARS-CoV-2, which may lead to the emergence of more transmissible and/or pathogenic viruses than ever before. Furthermore, novel variant viruses may appear at any time from the CoV pools actively circulating or persistently being maintained in the animal reservoirs, and from the CoVs in infected human individuals. In this review, we describe knowns of the CoVs and then mention their unknowns to clarify the major issues to be addressed. Genome organizations and sequences of numerous CoVs have been determined, and the viruses are presently classified into separate phylogenetic groups. Functional roles in the viral replication cycle in vitro of non-structural and structural proteins are also quite well understood or suggested. In contrast, those in the in vitro and in vivo replication for various accessory proteins encoded by the variable 3' one-third portion of the CoV genome mostly remain to be determined. Importantly, the genomic sequences/structures closely linked to the high CoV recombination are poorly investigated and elucidated. Also, determinants for adaptation and pathogenicity have not been systematically investigated. We summarize here these research situations. Among conceivable projects, we are especially interested in the underlying molecular mechanism by which the observed CoV diversification is generated. Finally, as virologists, we discuss how we handle the present difficulties and propose possible research directions in the medium or long term

Microstructured organic cavities with high-reflective flat reflectors fabricated by using a nanoimprint-bonding process

The integration of photonic microstructure into organic microcavities represents an effective strategy for manipulating eigenstates of cavity or polariton modes. However, well-established fabrication processes for microstructured organic microcavities are still lacking. In this study, we propose a nanoimprint-bonding process as a novel fabrication method for microstructured organic microcavities. This process relies on a UV nanoimprint technique utilizing two different photopolymer resins, enabling the independent fabrication of highly reflective reflectors and photonic microstructures without compromising the accuracy of each. The resulting organic microcavities demonstrate spatially localized photonic modes within dot structures and their nonlinear responses on the pumping fluence. Furthermore, a highly precise photonic band is confirmed within a honeycomb lattice structure, which is owing to the high quality factor of the cavity achievable with the nanoimprint-bonding process. Additionally, a topological edge state is also observable within a zigzag lattice structure. These results highlight the significant potential of our fabrication method for advancing organic-based photonic devices, including lasers and polariton devices

Modulation of vif-mRNA by HIV-1-SA1D2prox

Genomic RNA of HIV-1 contains localized structures critical for viral replication. Its structural analysis has demonstrated a stem-loop structure, SLSA1, in a nearby region of HIV-1 genomic splicing acceptor 1 (SA1). We have previously shown that the expression level of vif mRNA is considerably altered by some natural single-nucleotide variations (nSNVs) clustering in SLSA1 structure. In this study, besides eleven nSNVs previously identified by us, we totally found nine new nSNVs in the SLSA1-containing sequence from SA1, splicing donor 2, and through to the start codon of Vif that significantly affect the vif mRNA level, and designated the sequence SA1D2prox (142 nucleotides for HIV-1 NL4-3). We then examined by extensive variant and mutagenesis analyses how SA1D2prox sequence and SLSA1 secondary structure are related to vif mRNA level. While the secondary structure and stability of SLSA1 was largely changed by nSNVs and artificial mutations introduced to restore the original NL4-3 form from altered ones by nSNVs, no clear association of the two SLSA1 properties with vif mRNA level was observed. In contrast, when naturally occurring SA1D2prox sequences that contain multiple nSNVs were examined, we attained significant inverse correlation between the vif level and SLSA1 stability. These results may suggest that SA1D2prox sequence adapts over time, and also that the altered SA1D2prox sequence, SLSA1 stability, and vif level are mutually related. In total, we show here that the entire SA1D2prox sequence and SLSA1 stability critically contribute to the modulation of vif mRNA level

V3 Tip-Dependent Species Specificity of HIV-1 Env

Molecular interactions of the variable envelope gp120 subunit of HIV-1 with two cellular receptors are the first step of viral infection, thereby playing pivotal roles in determining viral infectivity and cell tropism. However, the underlying regulatory mechanisms for interactions under gp120 spontaneous variations largely remain unknown. Here, we show an allosteric mechanism in which a single gp120 mutation remotely controls the ternary interactions between gp120 and its receptors for the switch of viral cell tropism. Virological analyses showed that a G310R substitution at the tip of the gp120 V3 loop selectively abolished the viral replication ability in human cells, despite evoking enhancement of viral replication in macaque cells. Molecular dynamics (MD) simulations predicted that the G310R substitution at a site away from the CD4 interaction site selectively impeded the binding ability of gp120 to human CD4. Consistently, virions with the G310R substitution exhibited a reduced binding ability to human lymphocyte cells. Furthermore, the G310R substitution influenced the gp120-CCR5 interaction in a CCR5-type dependent manner as assessed by MD simulations and an infectivity assay using exogenously expressed CCR5s. Interestingly, an I198M mutation in human CCR5 restored the infectivity of the G310R virus in human cells. Finally, MD simulation predicted amino acid interplays that physically connect the V3 loop and gp120 elements for the CD4 and CCR5 interactions. Collectively, these results suggest that the V3 loop tip is a cis-allosteric regulator that remotely controls intra- and intermolecular interactions of HIV-1 gp120 for balancing ternary interactions with CD4 and CCR5

LDL-C/HDL-C Ratio Predicts Carotid Intima-Media Thickness Progression Better Than HDL-C or LDL-C Alone

High-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) are strong predictors of atherosclerosis. Statin-induced changes in the ratio of LDL-C to HDL-C (LDL-C/HDL-C) predicted atherosclerosis progression better than LDL-C or HDL-C alone. However, the best predictor of subclinical atherosclerosis remains unknown. Our objective was to investigate this issue by measuring changes in carotid intima-media thickness (IMT). A total of 1,920 subjects received health examinations in 1999, and were followed up in 2007. Changes in IMT (follow-up IMT/baseline IMT × 100) were measured by ultrasonography. Our results showed that changes in IMT after eight years were significantly related to HDL-C (inversely, P < 0.05) and to LDL-C/HDL-C ratio (P < 0.05). When the LDL-C/HDL-C ratios were divided into quartiles, analysis of covariance showed that increases in the ratio were related to IMT progression (P < 0.05). This prospective study demonstrated the LDL-C/HDL-C ratio is a better predictor of IMT progression than HDL-C or LDL-C alone

Collective Thomson scattering diagnostic with in situ calibration system for velocity space analysis in large helical device

A collective Thomson scattering (CTS) diagnostic with a ±3 GHz band around a 77 GHz gyrotron probe beam was developed to measure the velocity distribution of bulk and fast ions in high-temperature plasmas. We propose a new in situ calibration method for a CTS diagnostic system combined with a raytracing code. The method is applied in two situations for electron cyclotron emission in plasmas and in a CTS diagnostic with a modulated probe beam. Experimental results highlight the importance of refraction correction in probe and receive beams. The CTS spectrum is measured with the in situ calibrated CTS receiver and responds to fast ions originating from a tangential neutral beam with an energy of 170 keV and from a perpendicular beam with an energy of 60 keV, both in the large helical device. From a velocity space analysis model, the results elucidate the measured anisotropic CTS spectrum caused by fast ions. The calibration methods and analyses demonstrated here are essential for CTS, millimeter-wave diagnostics, and electron cyclotron heating required under fusion reactor conditions