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Assessment and mapping of climate change impacts on spring wheat yield in Southern Saskatchewan using DSSAT and high-resolution RCM projections
Maternal aggression driven by the transient mobilisation of a dormant hormone-sensitive circuit
Abstract Aggression is a sexually dimorphic behaviour. In some species, including the laboratory mouse, it is robustly expressed in males – while females are not aggressive in the non-puerperal state. However, during nursing, females exhibit maternal aggression, a dramatic yet transient shift in their social behaviour repertoire. This phenotypic change occurring in adulthood presents an opportunity to investigate whether sex-biased behavioural programs depend on mono- or di-morphic neural circuits. While maternal hormones are known to elicit nursing, their role in maternal aggression, particularly regarding target sites and cellular mechanisms, remains unclear. Here, we show that a molecularly defined subset of mouse ventral premammillary (PMvDAT) neurons – with an established role in intermale aggression– transitions from quiescence to a hyperexcitable state during female lactation. The maternal hormones, prolactin and oxytocin, were found to excite these cells through pre- and post-synaptic electrophysiological actions. Gain- and loss-of-function experiments related to PMvDAT neuron activity bidirectionally influence maternal aggression, while PMvDAT neuron activation suppressed the expression of a competing social behaviour. This study identifies a sexually monomorphic neural substrate in mice capable of integrating hormonal cues, providing a likely mechanism that enables the transient access to a dormant behavioural program.
Link between the ESR2 (rs3020449) polymorphism and breast cancer risk in Bangladeshi women
Wearable interactive full-body motion tracking and haptic feedback network systems with deep learning
Correction: Purification and characterization of an antimicrobial compound against drug-resistant MRSA and VRE produced by Streptomyces levis strain HFM-2
Rising dengue risk with increasing El Niño–Southern Oscillation amplitude and teleconnections
Abstract Global climate variability has been linked with some of the largest dengue outbreaks, including the record-breaking 2023–2024 epidemic, but the understanding of their mechanism and evidence for their association is lacking. By incorporating reported dengue cases and climate data from 57 countries across the Americas and Asia from 1980 to 2024, we unpacked the global climate teleconnection and quantifying its impact on dengue cases. We revealed that the heterogeneity in the association between global climate variability and dengue cases across regions is affected by the strength and types of global climate teleconnections with temperature and precipitation. By controlling for the heterogeneity, 63% of the variation in dengue cases can be attributed to El Niño–Southern Oscillation fluctuations, with higher values in endemic regions. The 1982–83, 1997–98, 2015–16, and 2023–24 El Niño events were estimated to have induced an additional 0.2, 1.4, 4.1, and 9.6 million dengue cases, respectively, over regular seasonal patterns. Due to human-induced warming, El Niño events and teleconnections may cause a 39.0–81.7% increase in cumulative cases in 2020–2099. Our findings quantify the association between global climate variability and dengue epidemics and caution about the potential future risk.
Nurses crisis management during COVID-19 at individual and organizational levels in a qualitative single centre study in Poland
Tailored collagen binding of albumin-fused hyperactive coagulation factor IX dictates in vivo distribution and functional properties
Abstract The efficacy of hemophilia B (HB) replacement therapy is evaluated by coagulation factor IX (FIX) activity in plasma, although FIX bound to extravascular type IV collagen (Col4) also contributes to efficient hemostasis. Here, we investigated the impact of engineering FIX for improved (K5R) or reduced (K5A) Col4 binding on the pharmacokinetic properties of FIX Padua, fused to human serum albumin (HSAQMP) engineered for favorable neonatal Fc receptor (FcRn) engagement. Hyperactive features and extended plasma half-life in human FcRn expressing mice, attributed to FIX Padua and HSAQMP engineering, respectively, was confirmed. In HB mice, PaduaKA-HSAQMP exhibited negligible extravascular distribution and the highest plasma levels at early time points followed by the steepest decay. Conversely, PaduaKR-HSAQMP showed increased extravascular distribution and a 3-fold longer functional half-life (80 hours). These findings support the use of PaduaKA-HSAQMP and PaduaKR-HSAQMP as hyperactive short- or long-term therapeutics, respectively, with opportunities for tailored HB replacement therapy.
Low friction layer in sanitary products for reduced skin irritation
Abstract Sanitary napkins are essential during menstruation, but they can sometimes cause skin irritation due to friction. In this study, we propose a novel design: introducing a low-friction layer within the bulk of a sanitary napkin. Friction tests were conducted between an artificial skin block and sanitary napkin specimens with and without a low-friction layer. The strain distribution on the lateral side of the artificial skin block was experimentally measured. The friction coefficient and strain decreased when the low-friction layer was applied under loads greater than 1.96 N. The strain increased with normal load. Because lower strain on the skin correlates with reduced skin irritation, the use of a low-friction layer in sanitary napkins is expected to reduce skin irritation, particularly under high contact pressure.
Genetic determinants of monocyte splicing are enriched for disease susceptibility loci
Abstract Insights into variation in monocyte context-specific splicing and transcript usage are limited. Here, we perform paired gene and transcript QTL mapping across distinct immune states using RNA sequencing data of monocytes isolated from a cohort of 185 healthy Europeans incubated alone or in the presence of interferon gamma (IFN-γ) or lipopolysaccharide (LPS). We identify regulatory variants for 5749 genes and 8727 transcripts, with 291 context-specific transcript QTL colocalizing with GWAS loci. Notable disease relevant associations include IFN-γ specific transcript QTL at COVID-19 severity locus rs10735079, where allelic variation modulates context-specific splicing of OAS1 , and at rs4072037, a risk allele for gastro-esophageal cancer, which associates with context-specific splicing of MUC1 . We use DNA methylation data from the same cells to demonstrate overlap between methylation QTL and causal context-specific expression QTL, permitting inference of the direction of effect. Finally, we identify a subset of expression QTL that uncouple genes from proximally acting regulatory networks, creating ‘co-expression QTL’ with different allele-specific correlation networks. Our findings highlight the interplay between context and genetics in the regulation of the monocyte gene expression and splicing, revealing putative mechanisms of diverse disease risk alleles including for COVID-19 and cancer.
Selective agonists of KIR and NKG2A to evade missing self response of natural killer cells
Abstract Immune rejection is one of the most serious challenges in allogeneic transplantation, including allogeneic induced pluripotent stem cell (allo-iPSC)-derived cell therapy. Beta-2-Microglobulin gene-knockout, human leukocyte antigen (HLA) class I-deficient iPSCs can evade immune rejection by host T cells, which occurs due to HLA mismatches. However, natural killer (NK) cells recognize HLA class Ⅰ-deficient cells and reject them, which is known as the missing-self response. Introducing chimeric HLA-E protein to HLA class Ⅰ-deficient iPSCs suppresses the missing-self response of NK cells expressing the inhibitory receptor NKG2A; however, technology to suppress NKG2A-negative NK cells is still required. Here, we developed novel agonists for the other inhibitory receptor, killer immunoglobulin receptor (KIR), on NK cells. We found that antibodies that bind to activating KIR enhance NK cell activation and developed selective agonists for inhibitory KIRs (KIR2DL1, KIR2DL2/3, and KIR3DL1). Introducing these selective inhibitory KIR agonists on T cells and HLA class Ⅰ-deficient iPSCs allowed them to evade immune rejection by NK cells. Additionally, we identified an NKG2A-selective agonist as an alternative to chimeric HLA-E, which stimulates the activating receptor NKG2C. This technology enhances immune tolerance in allo-iPSCs and facilitates the development of various iPSC-derived regenerative medicines.
Arctic Sea Route access reshapes global shipping carbon emissions
Investigation of new Helicobacter pylori variants among cagA positive strains using MLST typing method in Iraq
Immunogenicity of fractional and standard dose COVID-19 vaccine boosters among healthy adults in Indonesia: twenty four month follow-up from a randomised controlled trial
Severe obstructive sleep apnea phenotypes by cluster analysis based on multiple organs function
Pvf1-Pvr-mediated crosstalk between trachea and gut guides intestinal stem cell migration to promote gut regeneration
A deep learning model for epidermal growth factor receptor prediction using ensemble residual convolutional neural network
Circumpolar spread of avian influenza H5N1 to southern Indian Ocean islands
Abstract Since 2020, the outbreak of high pathogenicity avian influenza (HPAI) H5N1 virus clade 2.3.4.4b has turned into the largest documented panzootic 1,3. Here, we describe its arrival into the Indian Ocean sub-Antarctic archipelagos of Crozet and Kerguelen, where we first detected the virus in October 2024 in dead southern elephant seals. While the panzootic is ongoing, it has already caused unprecedented mortalities of marine mammals and seabirds. We collected brain swabs from seal and seabird carcasses and obtained 25 novel HPAI H5N1 2.3.4.4b sequences. Using phylogeographic analyses, we show that there have been independent introductions of the virus to Crozet and Kerguelen islands, most likely from the distant South Georgia islands in the Southern Atlantic, and not from the more nearby coasts of South Africa. Our results point to a year-long gap in genomic surveillance in the sub-Antarctic region. Locally, our analyses show that the virus is transmitted between different species. Our serological analyses show that some southern elephant seal had mounted an anti-H5 antibody response. Through its circumpolar spread to the Indian Ocean, HPAI H5N1 2.3.4.4b moves closer to Australia, which remains free from infections with this strain, and represents a major threat to the sub-Antarctic wildlife.