bluuebunny/crossref_metadata_2025_split huggingface dataset:
Smart youth: sociodemographic factors, usage patterns, and self-reported vs. actual smartphone addiction among secondary school students
Authors: Rękas Magdalena , Burzyńska Joanna 
Published: April 2024

AbstractBackgroundSmartphone addiction is a growing social problem especially in young mobile users. This study investigated indicators of smartphone use, smartphone addiction, and their associations with demographic and behavior-related variables in young people.Methods460 participants were secondary school students (Mage= 17,10, SDage= 0.92, 51.1% males, 52.4% high school students), took part in an anonymous questionnaire consisting of the following elements: the Mobile Phone Addiction Assessment Questionnaire (KBUTK), original questions regarding problematic smartphones usage, along with a subjective assessment of the use of such devices. Logistic regression model using forward stepwise method was used to characterize a typical smartphone user. Smartphone addiction was measured using KBUTK. Multiple logistic regression analysis was performed to determine factors associated with smartphone addiction.ResultsA total of 460 participants admitted to using a smartphone. Gender, age, type of school, place of living influenced the ways respondents used their smartphones. Being female (OR = 5.80;p< 0.0001), sixteen-year-old (OR = 0,41;p= 0.0456), and student of technical school (OR = 2.66;p= 0.0025) turned out to be the characteristics of a typical smartphone user. 21.7% of adolescents considered themselves addicted to smartphones, 22.2% admitted that they had problems with face-to-face relationships and girls significantly more often than boys (61.8% vs. 51.5%) neglected home or school duties as a result of using a smartphone. The overall rate of smartphone addiction was significantly higher (p< 0.0001) among girls (2.31 pts) than boys (2.03 pts), and correlated positively with the perception of being a smartphone addict (rho= 0.223;p< 0.0001). Addiction to smartphones was also significantly more common among students of technical schools, and respondents living in blocks of flats.ConclusionsThe way adolescents used smartphones differed depending on gender, age and type of school. Interventions for reducing the negative effects of smartphone use should take into account these context, as well as education both adolescents and their parents.
Antiretroviral therapy retention, adherence, and clinical outcomes among postpartum women with HIV in Nigeria
Authors: Young Clara M. , Chang Charlotte A. , Sagay Atiene S. , Imade Godwin , Ogunsola Olabanjo O. , Okonkwo Prosper , Kanki Phyllis J. 
Published: April 2024

AbstractWhile research involving pregnant women with HIV has largely focused on the antepartum and intrapartum periods, few studies in Nigeria have examined the clinical outcomes of these women postpartum. This study aimed to evaluate antiretroviral therapy retention, adherence, and viral suppression among postpartum women in Nigeria. This retrospective clinical data analysis included women with a delivery record at the antenatal HIV clinic at Jos University Teaching Hospital between 2013 and 2017. Descriptive statistics quantified proportions retained, adherent (≥95% medication possession ratio), and virally suppressed up to 24 months postpartum. Among 1535 included women, 1497 met the triple antiretroviral therapy eligibility criteria. At 24 months, 1342 (89.6%) women remained in care, 51 (3.4%) reported transferring, and 104 (7.0%) were lost to follow-up. The proportion of patients with ≥95% medication possession ratio decreased from 79.0% to 69.1% over the 24 months. Viral suppression among those with results was 88.7% at 24 months, but <62% of those retained had viral load results at each time point. In multiple logistic regression, predictors of loss to follow-up included having a more recent HIV diagnosis, higher gravidity, fewer antenatal care visits, and a non-hospital delivery. Predictors of viral non-suppression included poorer adherence, unsuppressed/missing baseline viral load, lower baseline CD4+ T-cell count, and higher gravidity. Loss to follow-up rates were lower and antiretroviral therapy adherence rates similar among postpartum women at our study hospital compared with other sub-Saharan countries. Longer follow-up time and inclusion of multiple facilities for a nationally representative sample would be beneficial in future studies.
Differential antigenic imprinting effects between influenza H1N1 hemagglutinin and neuraminidase in a mouse model
Authors: Lv Huibin , Teo Qi Wen , Lee Chang-Chun D. , Liang Weiwen , Choi Danbi , Mao Kevin J. , Bruzzone Roberto , Wilson Ian A. , Wu Nicholas C. , Mok Chris K. P. 
Published: April 2024

AbstractUnderstanding how immune history influences influenza immunity is essential for developing effective vaccines and therapeutic strategies. This study investigates the antigenic imprinting of influenza hemagglutinin (HA) and neuraminidase (NA) using a mouse model with sequential infection by four seasonal H1N1 strains. Our findings reveal that, among pre-2009 H1N1 strains, the extent of infection history correlates with the restriction of antibody responses to antigenically drifted HA, but not NA. This suggests the mouse model failed to recapitulate NA imprinting in humans, likely due to the difference in NA immunodominance hierarchy between humans and mice. Nevertheless, pre-existing antibodies induced by infection with pre-2009 influenza virus impeded both functional HA and NA antibody responses against a 2009 pandemic H1N1 strain. Overall, this study provides insights into antigenic imprinting for influenza virus, as well as the limitations of using mouse models for studying antigenic imprinting.ImportanceInfluenza viruses continue to pose a significant threat to human health, with vaccine effectiveness being a persistent concern. One important factor is the individual immune history can influence subsequent antibody responses. While many studies have focused on how pre-existing antibodies influence the induction of anti-HA antibodies after influenza virus infections or vaccinations, the impact on anti-NA antibodies has been less extensively investigated. In this study, using a mouse model, we highlighted within the pre-2009 H1N1 strains, a greater extent of immune history negatively affected anti-HA antibodies but positively influenced anti-NA antibody responses. However, for the 2009 pandemic H1N1 strain, which underwent with antigenic shift, both anti-HA and anti-NA antibody responses have been impeded by the antibodies induced by pre-2009 H1N1 virus infection. These findings have important implications for enhancing our understanding of antigenic imprinting on anti-HA and anti-NA antibody response and for developing more effective vaccination strategies.
Efficient fine-tuning of endothelial gene expression by a single Tyrosine to Phenylalanine point mutation in theVE-cadheringene
Authors: Garnier Olivia , Jeanneret Florian , Durand Aude , Fertin Arnold , Berndt Sarah , Carpentier Gilles , Battail Christophe , Martin Donald K. , Vilgrain Isabelle 
Published: April 2024

AbstractCancer and inflammation are associated with vascular diseases that affect endothelial cells (ECs) and alter gene expression. We aimed at understanding whether the site Y685in the cytoplasmic domain of VE-cadherin triggers epigenetic programmingin vivo. Using our knock-in mice carrying the Y685F VE-cadherin mutation, RNA sequencing from lung ECs identified 884 differentially expressed genes (DEG) involved in processes such as cell-cell adhesion, vascular development, and angiogenesis. The 30 DEGs include 22 down-regulated genes (genes encoding cell signalling enzymes, anion transport and lipid metabolism) and 8 up-regulated genes, including the endothelial-specific S1PR1. Analysis of the VEGF/VEGFR2 signaling pathway shows a significant decrease in the expression of pY1173VEGFR2 whereas VEGF remains constant, this was consistent with impaired migration, proliferation and protrusive properties of ECsin vitro. Co-immunoprecipitation experiments showed that c-Src and Y685F-VE-cadherin association which was enhanced in KI compared to WT, resulting in increased in Y685F-VE-cadherin phosphorylation at site Y731. As a consequence, its partner β-catenin translocates to the nucleus. CHIPS assay showed that FOXF1 binds to thes1pr1promoter, leading to increased expression of the S1PR1. In vivo, in the lung vasculature, this process was associated with increased vessel wall thickness and reduced fibrosis. Overall, our findings provide a novel transcriptomic profile triggered by Y685F-VE-cadherin ECs for potential insights into therapeutic targets to envisage normalisation of the tumor vasculature.
An investigation into the patterns of occupancy and detection of two endemic montane bird species, in Southern Western Ghats, India
Authors: Pop Paul 
Published: April 2024

ABSTRACTMontecincla fairbanki(Palani Laughingthrush) andSholicola albiventris(White-bellied Sholakili) are avian species found only in a few high-altitude sky islands of the Southern Western Ghats. A taxonomic revision has resulted in the need for better resolution of species biology, especially their distribution, and factors affecting their distribution. The current study was an attempt to address this, by repeated surveys at plantation sites in the northern landscape of Idukki district (Kerala), and occupancy modelling. Around 96% of the sites surveyed were occupied byM. fairbankiand ∼52% byS. albiventris. Model-averaged site-averaged occupancy probability (ψ) ofM. fairbankiis 0.8618 (0.6659-0.9229), and ofS. albiventris, it is 0.4543 (0.1358-0.9972). Model-, site-, and survey-averaged detection probability (p) ofM. fairbankiis 0.6554 (0.5171-0.7341), and ofS. albiventris, it is 0.5731 (0.4102-0.7939). This confirms the hypothesis thatS. albiventrishas lower occupancy and detection probability compared toM. fairbanki. There is likely no effect on ψ of one species by the presence of the other, but there is likely a positive effect on p of one species, by the occupancy or detection of the other. Most significant effects on ψ ofM. fairbankiwere from the exclusive presence of dirt roads, elevation, slope, and visibility, and forS. albiventris, it was fromLantana camara, elevation, and understorey height. Most significant effects on p ofM. fairbankiwere from windy weather, sky conditions, time of surveys, and survey number, whereas forS. albiventris, they were from neutral weather, and survey number. Of the interactive effects hypothesized, significant evidence was found for the increase of ψ as a function of elevation, and the reduction of ψ in the presence of the invasiveL. camara(only forS. albiventris). The insights gained from this baseline study will be useful for further hypotheses testing and conservation efforts.
The ANKS3/BICC1 protein complex is a master post-transcriptional regulator ofNPHP1ciliopathy-gene transcripts
Authors: Mahuzier Alexia , Odye Gweltas , Grampa Valentina , Bizet Albane , Viau Amandine , Ryan Rebecca , Mehraz Manon , Blisnick Thierry , Clark Euan , Henry Charline , Piedagnel Rémi , Silbermann Flora , Hayot Gaelle , De grande Line , Kahn Agathe , Plaza Jean-Marc , Krug Pauline , Knebelmann Bertrand , Muller Florian , Bastin Philippe , Sailer Andreas W. , Saint-Mezard Pierre , Jeanpierre Cécile , Hoffmann Sigrid , Benmerah Alexandre , Lelongt Brigitte , Delous Marion , Saunier Sophie 
Published: April 2024

AbstractCiliopathies are a class of multi-systemic genetic diseases characterized by ciliary dysfunction. Here, we report a novelANKS3variant in patients with a renal ciliopathy known as nephronophthisis (NPH) associated with hepatic defects. ANKS3 is an ankyrin and sterile alpha motif domain-containing protein that interacts with many NPH proteins as well as with BICC1, an RNA-binding protein involved in renal cystic diseases. The pathogenic effect of theANKS3mutation was validated in the zebrafish mutant and knock-in rat model, the latter showing urine concentration defect and tubular dilatations similar to NPH patients. In addition, cilia morphology and function as well as epithelialization of kidney tubular cells was affected by loss or mutation ofANKS3. Finally, our results evidenced that these classically renal ciliopathy-associated phenotypes were linked to the negative regulation of BICC1 by ANKS3 which binds to transcripts of the major NPH geneNPHP1and mediates their decay through the AGO2-RISC complex and recruitment into P-bodies. Altogether, our findings suggest that the ANKS3/BICC1 complex is a key post-transcriptional regulator ofNPHP1transcript stability, providing another level of regulation of cilium biogenesis and kidney homeostasis, as well as an unusual mechanism leading to NPH-related ciliopathies.
Predicting immunotherapy response in advanced bladder cancer: a meta-analysis of six independent cohorts
Authors: Boll Lilian Marie , de Oca Sergio Vázquez Montes , Camarena Marta E. , Castelo Robert , Bellmunt Joaquim , Perera-Bel Júlia , Mar Albà M. 
Published: April 2024

ABSTRACTAdvanced bladder cancer patients show very variable responses to immune checkpoint inhibitors (ICIs) and effective strategies to predict response are still lacking. Here we integrate mutation and gene expression data from 707 advanced bladder cancer patients treated with anti-PD-1/anti-PD-L1 to build highly accurate predictive models. We find that, in addition to tumor mutational burden (TMB), enrichment in the APOBEC mutational signature, and the abundance of pro-inflammatory macrophages, are major factors associated with the response. Paradoxically, patients with high immune infiltration do not show an overall better response. We show that this can be explained by the activation of immune suppressive mechanisms in a large portion of these patients. In the case of non-immune-infiltrated cancer subtypes, we uncover specific variables likely to be involved in the response. Our findings provide novel information for advancing precision medicine in patients with advanced bladder cancer treated with immunotherapy.
KIRA6 is an effective and versatile mast cell inhibitor of IgE-mediated activation
Authors: Wunderle Veronika , Wilhelm Thomas , Boukeileh Shatha , Goßen Jonas , Margreiter Michael A. , Sakurov Roman , Capellmann Sandro , Schwoerer Maike , Ahmed Nabil , Bronneberg Gina , Arock Michel , Martin Christian , Schubert Thomas , Levi-Schaffer Francesca , Rosetti Giulia , Tirosh Boaz , Huber Michael 
Published: April 2024

AbstractIncidents of IgE-mediated, mast cell (MC)-driven allergic diseases are constantly rising and there is an urgent need for the development of novel pharmacological MC stabilizers. Allergen/antigen (Ag)-triggered activation of MCs via crosslinking of the high-affinity receptor for IgE (FcεRI) is regulated, amongst others, by the coordinated action of various cytosolic tyrosine kinases of the SRC family, e.g. LYN and FYN, which exert positive as well as negative functions. We report that KIRA6, an inhibitor developed for the endoplasmic reticulum (ER) stress sensor IRE1α, suppresses IgE-mediated pro-inflammatory MC activation by inhibiting both LYN and FYN. KIRA6 dose-dependently and effectively attenuates Ag-stimulated early signaling (e.g. substrate tyrosine phosphorylation, Ca2+mobilization, and activation of MAPK pathways) as well as effector functions such as degranulation and pro-inflammatory cytokine production/secretion in murine bone marrow-derived MCs (BMMCs). Moreover, Ag-triggered bronchoconstriction in anex vivomodel of precision-cut lung slices (PCLS), and IgE-mediated stimulation of human MCs were repressed by KIRA6. To get in-depth inside into KIRA6 interaction with three MC-relevant tyrosine kinases, LYN, FYN, and KIT, and to elicit the potential of KIRA6 structure to serve as pharmacophore for the development of respective single-, dual-, or triple-specificity inhibitors, we modeled and evaluated the binding of KIRA6 on the three kinases by applying homology modeling and molecular dynamics simulations, as well as MM GBSA calculations. We found that KIRA6 has a high propensity to bind the inactive state of LYN, FYN, and KIT with comparable affinities. In conclusion, our data suggest the use of novel inhibitors based on the KIRA6 pharmacophore as effective MC stabilizers to improve treatment of pro-inflammatory diseases with MC involvement in need of effective pharmacological interventions.
Importin α4 deficiency induces psychiatric disorder-related behavioral deficits and neuroinflammation in mice
Authors: Sakurai Koki , Morita Makiko , Aomine Yoshiatsu , Matsumoto Mitsunobu , Moriyama Tetsuji , Kasahara Emiko , Sekiyama Atsuo , Otani Mayumi , Oshima Rieko , Loveland Kate L. , Yamada Masami , Yoneda Yoshihiro , Oka Masahiro , Hikida Takatoshi , Miyamoto Yoichi 
Published: April 2024

ABSTRACTImportin α4, which is encoded by theKpna4gene, is a well characterized nuclear-cytoplasmic transport factor known to mediate transport of transcription factors including NF-κB. Here, we report thatKpna4knock-out (KO) mice exhibit psychiatric disorder-related behavioral abnormalities such as anxiety-related behaviors, deceased social interaction and sensorimotor gating deficits. Contrary to a previous study predicting attenuated NF-κB activity as a result ofKpna4deficiency, we observed a significant increase in expression levels of NF-κB genes and pro-inflammatory cytokines such asTNFα,Il1βorIl-6in the Prefrontal Cortex or Basolateral Amygdala of the KO mice. Moreover, examination of inflammatory responses in primary cells revealed thatKpna4deficient cells have an increased inflammatory response, which was rescued by addition of not only full-length, but also a nuclear transport deficient truncation mutant of importin α4, suggesting contribution of its non-transport functions. Furthermore, RNAseq of sorted adult Microglia and Astrocytes and subsequent transcription factor analysis suggested increases in Polycomb repressor complex 2 (PRC2) activity inKpna4KO cells. Taken together, importin α4 deficiency induces psychiatric disorder-related behavioral deficits in mice, along with an increased inflammatory response and possible alteration of PRC2 activity in glial cells.
Familiarity modulates preference for joint feeding with conspecifics in rats
Authors: Wada Reo , Kamijo Makiko , Katsu Noriko , Hakataya Shiomi , Okanoya Kazuo , Koda Hiroki 
Published: April 2024

AbstractRats are highly social mammals that form social groups of various sizes. Interestingly, they are known to show prosocial behaviors, and are socially tolerant of other conspecifics as they feed together, but the specificity of their prosociality has not been fully understood. Here, we investigated what degree rats showed social choice, i.e., preferential joint feeding even with unfamiliar animals by performing a simple feeding site choice task. In the task, subjects were tested to choose between the feeding site where they fed with other rats (social option) or the other site where they could feed alone (solitary option). The results showed that social option choices increased particularly when the partner was a single non-cagemate rat. This result means that high social preference for other individuals occurs spontaneously, even when they are feeding with unfamiliar non-cagemates. This high degree of social tolerance would lead to the suppression of aggressive behavior as well as enhancement of affiliative relationships even in situations when the rats met with unfamiliar conspecifics for the first time.HighlightsRats are highly socially tolerant mammals as they feed with conspecifics together.We explored how the presence of conspecifics affects feeding site choices in rats.Social choices increased when the partners were non-cagemates.Social choices decreased as the number of non-cagemates increased.Joint feeding with a single non-cagemate is observed particularly frequently.
Data-centric AI approach for automated wildflower monitoring
Authors: Schouten Gerard , Michielsen Bas S.H.T. , Gravendeel Barbara 
Published: April 2024

AbstractBoth researchers and policy makers are in need of standards and tools that help understanding and assessing natural capital. Wildflowers are a major component of our natural capital; they play an essential role in ecosystems, improve soil health, supply food and medicines, and curb climate change. In this paper, we present the Eindhoven Wildflower Dataset (EWD) as well as a PyTorch object detection model that is able toidentifyandcountwildflowers. EWD, collected over two entire flowering seasons and expert annotated, contains 2002 top-view images of flowering plants captured ‘in the wild’ in five different landscape types (roadsides, urban green spaces, cropland, weed-rich grassland, marshland). It holds a total of 65571 annotations for 160 species belonging to 31 different families of flowering plants and serves as a reference dataset for automating wildflower monitoring. To ensure consistent annotations, we define specific floral count units (largely based on inflorescences) and provide extensive annotation guidelines. With a 0.82 mAP (@IoU > 0.50) score the presented baseline model, trained with a balanced subset of EWD, is to the best of our knowledge superior in its class. Our approach empowers automated quantification of wildflower richness and abundance and encourages the development of standards for AI-based wildflower monitoring. The annotated EWD dataset is publicly available on the DataverseNL research data repository, and the code to train and run the baseline model is supplied as supplementary material.
Understanding the characteristic behavior of the wild-type and mutant protein structure of FLT3 protein by computational methods
Authors: Younus Saleena , Tatli Özge , Nasimian Ahmad , Kazi Julhash U. , Rönnstrand Lars 
Published: April 2024

AbstractFLT3 emerges as a commonly mutated protein with significant prognostic implications in acute myeloid leukemia (AML). Point mutations or deletions in the tyrosine kinase domain (TKD) at the activation loop and internal tandem duplications (ITD) in the juxtamembrane (JM) region (and less commonly in the TKD) are the primary mutations that occur in the FLT3 protein. Besides, AML treatment with tyrosine kinase inhibitor drugs may result in the acquisition of TKD mutations in the FLT3-ITD structure. All these mutations will induce activation of the kinase activity of FLT3 protein leading to activation of downstream signaling pathways. Therefore, finding better therapeutics against each of these mutant FLT3 proteins is crucial in the treatment of AML. This study aims to comprehend the characteristic behavior of TKD mutants (C and F in Y842), ITD mutants, and the combination of ITD with TKD mutations (C and F in Y842) in the FLT3 protein through computational approaches, including Molecular Dynamic (MD) simulation, cluster analysis, and machine learning techniques. The MD simulation studies revealed the alterations in the optimized state, flexibility, and compactness nature between FLT3-WT and mutated FLT3 proteins and identified significant changes in the point mutants, ITD, and the combined ITD and TKD mutated FLT3 protein structures. Cluster analysis also confirmed that these mutations significantly impact the overall flexibility of the protein structures, especially in the point-mutated structures of FLT3-Y842C and FLT3-ITD-Y842F. These findings emphasize the diverse protein conformations of mutated structures of the FLT3 protein, contributing to the deregulation of FLT3 protein function, and identified these mutated proteins as promising therapeutic targets in the treatment of AML.