Coexistence of distinct charge fluctuations in θ\theta-(BEDT-TTF)2_2X

Using the Lanczos exact-diagonalization and density-matrix renormalization group methods, we study the extended Hubbard model at quarter filling defined on the anisotropic triangular lattice. We focus on charge ordering (CO) phenomena induced by onsite and intersite Coulomb interactions. We determine the ground-state phase diagram including three CO phases, i.e., diagonal, vertical, and three-fold CO phases, based on the calculated results of the hole density and double occupancy. We also calculate the dynamical density-density correlation functions and find possible coexistence of the diagonal and three-fold charge fluctuations in a certain parameter region where the onsite and intersite interactions compete. Furthermore, the characteristic features of the optical conductivity for each CO phase are discussed.Comment: 9 pages, 7 figure

Contribution of edible insects to improved food and nutrition security:a review

The consumption of insects “entomophagy” or insect-based foods is increasingly being recognised as an emerging solution to promote diet diversification and address the multiple burden of malnutrition. Although several studies suggest edible insects as valuable nutrient sources, few have evaluated the effects of processing on nutrient bioavailability and bioaccessibility and provided actual evidence on human nutrition. Moreover, there is limited evidence of their actual contribution to improved food and nutrition security. Therefore, the review evaluated existing evidence on human interventions and the effects of processing methods on bioavailability and bioaccessibility of key nutrients since these directly influence food and nutrition security outcomes. Seven human efficacy studies have been conducted to date and these show limited observable effects on nutrition status therefore more research is required. Findings also suggest that the processing method, insect matrix, composition of the food matrix and interaction with other food components can influence nutrient bioavailability and bioaccessibility. Hence, these should be considered during formulation and upscaling for entomophagy and insect-based foods to be viable intervention strategies against malnutrition.</p

Activation of the beta interferon promoter by paramyxoviruses in the absence of virus protein synthesis

Conflicting reports exist regarding the requirement for virus replication in interferon (IFN) induction by paramyxoviruses. Our previous work has demonstrated that pathogen-associated molecular patterns capable of activating the IFN-induction cascade are not normally generated during virus replication, but are associated instead with the presence of defective interfering (DI) viruses. We demonstrate here that DIs of paramyxoviruses, including parainfluenza virus 5, mumps virus and Sendai virus, can activate the IFN-induction cascade and the IFN-β promoter in the absence of virus protein synthesis. As virus protein synthesis is an absolute requirement for paramyxovirus genome replication, our results indicate that these DI viruses do not require replication to activate the IFN-induction cascade

African inclusion in prostate cancer genomic studies provides the first glimpses into addressing health disparities through tailored clinical care

No abstract available.Funding for genomic support provided by the National Health and Medical Research Council (NHMRC) of Australia.http://wileyonlinelibrary.com/journal/ctm2am2024School of Health Systems and Public Health (SHSPH)SDG-03:Good heatlh and well-bein

ANO7 African-ancestral genomic diversity and advanced prostate cancer

DATA AVAILABILITY : The data used in this study will be made available on request.BACKGROUND : Prostate cancer (PCa) is a significant health burden for African men, with mortality rates more than double global averages. The prostate specific Anoctamin 7 (ANO7) gene linked with poor patient outcomes has recently been identified as the target for an African-specific protein-truncating PCa-risk allele. METHODS : Here we determined the role of ANO7 in a study of 889 men from southern Africa, leveraging exomic genotyping array PCa case-control data (n = 780, 17 ANO7 alleles) and deep sequenced whole genome data for germline and tumour ANO7 interrogation (n = 109), while providing clinicopathologically matched European-derived sequence data comparative analyses (n = 57). Associated predicted deleterious variants (PDVs) were further assessed for impact using computational protein structure analysis. RESULTS : Notably rare in European patients, we found the common African PDV p.Ile740Leu (rs74804606) to be associated with PCa risk in our case-control analysis (Wilcoxon rank-sum test, false discovery rate/FDR = 0.03), while sequencing revealed co-occurrence with the recently reported African-specific deleterious risk variant p.Ser914* (rs60985508). Additional findings included a novel protein-truncating African-specific frameshift variant p.Asp789Leu, African-relevant PDVs associated with altered protein structure at Ca2+ binding sites, early-onset PCa associated with PDVs and germline structural variants in Africans (Linear regression models, −6.42 years, 95% CI = −10.68 to −2.16, P-value = 0.003) and ANO7 as an inter-chromosomal PCa-related gene fusion partner in African derived tumours. CONCLUSIONS : Here we provide not only validation for ANO7 as an African-relevant protein-altering PCa-risk locus, but additional evidence for a role of inherited and acquired ANO7 variance in the observed phenotypic heterogeneity and African-ancestral health disparity.The National Health and Medical Research Council (NHMRC) of Australia; Ideas Grant; USA Congressionally Directed Medical Research Programs (CDMRP) Prostate Cancer Research Program (PCRP) Idea Development Award; HEROIC Consortium Award and the Petre Foundation via the University of Sydney Foundation, Australia. Open Access funding enabled and organized by CAUL and its Member Institutions.http://www.nature.com/pcan/hj2024School of Health Systems and Public Health (SHSPH)SDG-03:Good heatlh and well-bein

Alterations in the epigenetic machinery associated with prostate cancer health disparities

DATA AVAILABILITY STATEMENT : Data used in this study were published by Jaratlerdsiri et al., 2022, and made accessible via the European Genome-Phenome Archive (EGA; https://ega-archive.org, accessed on 1 June 2022) under study accession EGAS00001006425 and dataset accession EGAD00001009067 (Southern African Prostate Cancer Study, SAPCS) and EGAD00001009066 (Garvan/St. Vincent’s Prostate Cancer Study).SUPPLEMENTARY MATERIALS : FIGURE S1: Optimal cluster number identification; FIGURE S2: Consensus heatmap for variant data overlapping epigenetic machinery genes based on results from ten multi-omics integrative clustering algorithms with the assigned cluster numbers of (A) k = 3 and (B) k = 8; FIGURE S3: Silhouette plot quantifying Sample Similarity based on results from ten multi-omics integrative clustering algorithms with the assigned cluster numbers of (A) k = 3 and (B) k = 8; FIGURE S4: Mutational burden in African- and European-derived tumors; FIGURE S5: Damaging variant mutational burden in African- and European-derived tumors; TABLE S1: Patient Summary or African and European Study participants; TABLE S2: SuperPaths and their associated pathways included in this Study for their relationship to epigenetic processes; TABLE S3: List of genes assigned to Epigenetic Process Group 1 (chromatin organization and regulation); TABLE S4: List of genes assigned to Epigenetic Process Group 2 (histone modifications); TABLE S5: List of genes assigned to Epigenetic Process Group 3 (DNA methylation); TABLE S6: List of genes assigned to Epigenetic Process Group 4 (RNA regulation); TABLE S7: List of genes assigned to Epigenetic Process Group 5 (epigenetic regulation of gene expression); TABLE S8: MOVICS clustering results; TABLE S9: Statistical Summary for tumor mutational burden (per Mb) based on all coding variants in epigenetic machinery genes in African- and European-derived tumors; TABLE S10: Statistical Summary for tumor mutational burden (per Mb) based only on damaging variants (as per functional impact prediction) in epigenetic machinery genes in African- and European-derived tumors; TABLE S11: Independent test of epigenetic cancer Subtype (ECS) and Small Somatic mutation to compare mutation frequency; TABLE S12: Independent test of epigenetic cancer Subtype (ECS) and Structural variation to compare Structural variation frequency; TABLE S13: Clinical Summary based on hierarchical clustering results, with epigenetic cancer Subtype (ECS) as the grouping variable; TABLE S14: Top features, posterior probability, and rank order for joint analysis of Small Somatic mutation, Somatic Structural variant, and Somatic copy number alteration data identified by iClusterBayes; TABLE S15: Clinical Summary based on hierarchical clustering results for Somatic copy number alteration data only, with epigenetic copy number cancer Subtype (EcnCS) as the grouping variable.African ancestry is a significant risk factor for aggressive prostate cancer (PCa), with southern African ethnicity conferring a nearly 3-fold increased global risk for associated mortality. It is well understood that epigenetic alterations drive PCa initiation and progression, coupled with somatic alterations in genes encoding epigenetic enzymes. However, differences in the somatic alterations in these genes in African- versus European-derived prostate tumors and how they may contribute to PCa health disparities has yet to be investigated, which forms the objective of this study. With current PCa care almost exclusively based on and tailored for men of European ancestry, the identification of African-specific novel PCa epigenetic cancer drivers (n = 18), including therapeutic potential (6/18), offers clinical significance with the possibility of improving healthcare approaches and health outcomes for men of African ancestry.Prostate cancer is driven by acquired genetic alterations, including those impacting the epigenetic machinery. With African ancestry as a significant risk factor for aggressive disease, we hypothesize that dysregulation among the roughly 656 epigenetic genes may contribute to prostate cancer health disparities. Investigating prostate tumor genomic data from 109 men of southern African and 56 men of European Australian ancestry, we found that African-derived tumors present with a longer tail of epigenetic driver gene candidates (72 versus 10). Biased towards African-specific drivers (63 versus 9 shared), many are novel to prostate cancer (18/63), including several putative therapeutic targets (CHD7, DPF3, POLR1B, SETD1B, UBTF, and VPS72). Through clustering of all variant types and copy number alterations, we describe two epigenetic PCa taxonomies capable of differentiating patients by ancestry and predicted clinical outcomes. We identified the top genes in African- and European-derived tumors representing a multifunctional “generic machinery”, the alteration of which may be instrumental in epigenetic dysregulation and prostate tumorigenesis. In conclusion, numerous somatic alterations in the epigenetic machinery drive prostate carcinogenesis, but African-derived tumors appear to achieve this state with greater diversity among such alterations. The greater novelty observed in African-derived tumors illustrates the significant clinical benefit to be derived from a much needed African-tailored approach to prostate cancer healthcare aimed at reducing prostate cancer health disparities.The US Congressionally Directed Medical Research Programs (CDMRP) Prostate Cancer Research Program (PCRP) Idea Development Award, the Health Equity Research Outcomes Integrity Consortium (HEROIC) Award, the National Health and Medical Research Council (NHMRC) of Australia Project Grant and Ideas Grants, a Cancer Association of South Africa (CANSA) Development Gran, the National Research Foundation of South Africa andthe Petre Foundation, Australia.https://www.mdpi.com/journal/cancershj2023School of Health Systems and Public Health (SHSPH

The Cellular Mechanism for Water Detection in the Mammalian Taste System

Initiation of drinking behavior relies on both internal state and peripheral water detection. While central neural circuits regulating thirst have been well studied, it is still unclear how mammals recognize external water. Here we show that acid-sensing taste receptor cells (TRCs) that were previously suggested as the sour taste sensors also mediate taste responses to water. Genetic silencing of these TRCs abolished water-evoked responses in taste nerves. Optogenetic self-stimulation of acid-sensing TRCs in thirsty animals induced robust drinking responses toward light even without water. This behavior was only observed when animals were water-deprived but not under food- or salt-depleted conditions, indicating that the hedonic value of water-evoked responses is highly internal-state dependent. Conversely, thirsty animals lacking functional acid-sensing TRCs showed compromised discrimination between water and nonaqueous fluids. Taken together, this study revealed a function of mammalian acid-sensing TRCs that provide a cue for external water

Global Intermittency and Collapsing Turbulence in the Stratified Planetary Boundary Layer

Direct numerical simulation of the turbulent Ekman layer over a smooth wall is used to investigate bulk properties of a planetary boundary layer under stable stratification. Our simplified configuration depends on two non-dimensional parameters: a Richardson number characterizing the stratification and a Reynolds number characterizing the turbulence scale separation. This simplified configuration is sufficient to reproduce global intermittency, a turbulence collapse, and the decoupling of the surface from the outer region of the boundary layer. Global intermittency appears even in the absence of local perturbations at the surface; the only requirement is that large-scale structures several times wider than the boundary-layer height have enough space to develop. Analysis of the mean velocity, turbulence kinetic energy, and external intermittency is used to investigate the large-scale structures and corresponding differences between stably stratified Ekman flow and channel flow. Both configurations show a similar transition to the turbulence collapse, overshoot of turbulence kinetic energy, and spectral properties. Differences in the outer region resulting from the rotation of the system lead, however, to the generation of enstrophy in the non-turbulent patches of the Ekman flow. The coefficient of the stability correction function from Monin-Obukhov similarity theory is estimated as (Formula presented.) in agreement with atmospheric observations, theoretical considerations, and results from stably stratified channel flows. Our results demonstrate the applicability of this set-up to atmospheric problems despite the intermediate Reynolds number achieved in our simulations. © 2014 The Author(s)

Effect of Chorda Tympani Nerve Transection on Salt Taste Perception in Mice

Effects of gustatory nerve transection on salt taste have been studied extensively in rats and hamsters but have not been well explored in the mouse. We examined the effects of chorda tympani (CT) nerve transection on NaCl taste preferences and thresholds in outbred CD-1 mice using a high-throughput phenotyping method developed in our laboratory. To measure taste thresholds, mice were conditioned by oral self-administration of LiCl or NaCl and then presented with NaCl concentration series in 2-bottle preference tests. LiCl-conditioned and control NaCl-exposed mice were given bilateral transections of the CT nerve (LiCl-CTX, NaCl-CTX) or were left intact as controls (LiCl-CNT, NaCl-CNT). After recovery from surgery, mice received a concentration series of NaCl (0–300 mM) in 48-h 2-bottle tests. CT transection increased NaCl taste thresholds in LiCl-conditioned mice and eliminated avoidance of concentrated NaCl in control NaCl-exposed mice. This demonstrates that in mice, the CT nerve is important for detection and recognition of NaCl taste and is necessary for the normal avoidance of high concentrations of NaCl. The results of this experiment also show that the method of high-throughput phenotyping of salt taste thresholds is suitable for detecting changes in the taste periphery in mouse genetic studies

Calcineurin and Protein kinase G regulate C. elegans behavioral quiescence during locomotion in liquid

<p>Abstract</p> <p>Background</p> <p>Most rhythmic motor behaviors in nature are episodic i.e. they alternate between different behavioral states, including quiescence. Electrophysiological studies in invertebrate behavioral switching, maintenance and quiescence have elucidated several neuronal mechanisms that generate a temporal pattern in behavior. However, the genetic bases of these processes are less well studied. We have previously uncovered a novel episodic behavior exhibited by <it>C. elegans </it>in liquid media where they alternate between distinct phases of rhythmic swimming and quiescence. Here, we have investigated the effect of several genes and their site of action on the behavioral quiescence exhibited in liquid by the nematode <it>C. elegans</it>.</p> <p>Results</p> <p>We have previously reported that high cholinergic signaling promotes quiescence and command interneurons are critical for timing the quiescence bout durations. We have found that in addition to command interneurons, sensory neurons are also critical for quiescence. We show that the protein phosphatase calcineurin homolog <it>tax-6 </it>promotes swimming whereas the protein kinase G homolog <it>egl-4 </it>promotes quiescence. <it>tax-6 </it>expression in the sensory neurons is sufficient to account for its effect. <it>egl-4 </it>also acts in multiple sensory neurons to mediate its effect on quiescence. In addition our data is consistent with regulation of quiescence by <it>egl-4 </it>acting functionally downstream of release of acetylcholine (ACh) by motor neurons.</p> <p>Conclusions</p> <p>Our study provides genetic evidence for mechanisms underlying the maintenance of a behavioral state operating at multiple neuronal levels through the activities of a kinase and a phosphatase. These results in a genetically tractable organism establish a framework for further dissection of the mechanism of quiescence during episodic behaviors.</p