Miracle-dz/UniFAR-FTUs huggingface dataset:
Trajectories of adaptive and disturbed identity dimensions in adolescence: developmental associations with self-esteem, resilience, symptoms of depression, and borderline personality disorder features

To advance our understanding of adolescents’ identity formation and how it may play into their psychological functioning, this study investigated developmental trajectory classes of adaptive and disturbed dimensions of identity formation, and whether adolescents belonging to different trajectory classes develop differently on self-esteem, resilience, symptoms of depression, and borderline personality disorder (BPD) features. Three-wave longitudinal data from 2,123 Flemish adolescents was used (54.2% girls; Mage = 14.64, range = 12–18 at T1). Results pointed to four trajectory classes of identity formation: adaptive identity, identity progression, identity regression, and diffused identity. The adaptive identity class presented with stable high levels of self-esteem and resilience, and stable low levels of symptoms of depression and BPD, whereas opposite results were obtained for the diffused identity class. The identity progression class reported an increase in self-esteem and resilience as well as a decrease in symptoms of depression and BPD, whereas opposite results were obtained for the identity regression class. These results emphasize that adaptive and disturbed dimensions of identity formation are closely related to markers of well-being and psychopathology among adolescents, and could help identify adolescents with an increased risk for negative psychological functioning or increased opportunity for positive psychological functioning.
Inhibition of ferroptosis alleviates high-power microwave-induced myocardial injury

Background The use of high-power microwave (HPM) in our daily live is becoming more and more widespread, but the safety has also caused our concern. And ferroptosis is a newly discovered modality that can regulate cell death in recent years. The aim of our study was to demonstrate whether ferroptosis is an important cause of myocardial injury caused by HPM. And whether myocardial injury caused by HPM can be alleviated by inhibiting ferroptosis. Methods We verified the extent of myocardial damage by different doses of HPM through in vivo and in vitro assays, respectively. In addition, GPX4 was knocked down and overexpressed in cardiac myocytes to verify the altered sensitivity of cardiac myocytes to HPM. Finally, the therapeutic effect of Fer-1 and tanshinoneIIA on myocardial injury caused by HPM was verified in in vivo and in vitro assays. Results We found that cardiac tissue and cardiomyocyte injury in mice gradually increased with increasing HPM dose, while ferroptosis markers were consistent with the injury trend. Gpx4 had an important role in ferroptosis in cardiomyocytes caused by HPM. Finally, tanshinoneIIA and Fer-1 could attenuate the damage of cardiac tissues and cardiomyocytes caused by HPM. Conclusions In conclusion, our study found that ferroptosis, a novel mode of cell death, is present in myocardial injury caused by HPM. Moreover, tanshinone, a drug already in clinical use, can significantly reduce myocardial injury caused by HPM, which is promising to provide new therapeutic ideas for myocardial injury caused by HPM.
Weak Solutions for Boundary-Value Problems with Nonlinear Fractional Differential Inclusions

This paper deals with the existence of solutions, under the Pettis inte- grability assumption, for a class of boundary value problems for fractional differential inclusions involving nonlinear integral conditions. Our results are based on the tech- nique of measures of weak noncompactness and a fixed point theorem of Monch type.
Depression and quality of life among Macau residents in the 2022 COVID-19 pandemic wave from the perspective of network analysis

Background In the summer of 2022, Macau experienced a surge of COVID-19 infections (the 618 COVID-19 wave), which had serious effects on mental health and quality of life (QoL). However, there is scant research on mental health problems and QoL among Macau residents during the 618 COVID-19 wave. This study examined the network structure of depressive symptoms (hereafter depression), and the interconnection between different depressive symptoms and QoL among Macau residents during this period. Method A cross-sectional study was conducted between 26th July and 9th September 2022. Depressive symptoms were measured with the 9-item Patient Health Questionnaire (PHQ-9), while the global QoL was measured with the two items of the World Health Organization Quality of Life-brief version (WHOQOL-BREF). Correlates of depression were explored using univariate and multivariate analyses. The association between depression and QoL was investigated using analysis of covariance (ANCOVA). Network analysis was used to evaluate the structure of depression. The centrality index “Expected Influence” (EI) was used to identify the most central symptoms and the flow function was used to identify depressive symptoms that had a direct bearing on QoL. Results A total 1,008 participants were included in this study. The overall prevalence of depression was 62.5% (n = 630; 95% CI = 60.00–65.00%). Having depression was significantly associated with younger age (OR = 0.970; p < 0.001), anxiety (OR = 1.515; p < 0.001), fatigue (OR = 1.338; p < 0.001), and economic loss (OR = 1.933; p = 0.026). Participants with depression had lower QoL F (1, 1,008) =5.538, p = 0.019). The most central symptoms included PHQ2 (“Sad Mood”) (EI: 1.044), PHQ4 (“Fatigue”) (EI: 1.016), and PHQ6 (“Guilt”) (EI: 0.975) in the depression network model, while PHQ4 (“Fatigue”), PHQ9 (“Suicide”), and PHQ6 (“Guilt”) had strong negative associations with QoL. Conclusion Depression was common among Macao residents during the 618 COVID-19 wave. Given the negative impact of depression on QoL, interventions targeting central symptoms identified in the network model (e.g., cognitive behavioral therapy) should be developed and implemented for Macau residents with depression.
Atypical developmental trajectories of white matter microstructure in prenatal alcohol exposure: Preliminary evidence from neurite orientation dispersion and density imaging

Introduction Fetal alcohol spectrum disorder (FASD), a life-long condition resulting from prenatal alcohol exposure (PAE), is associated with structural brain anomalies and neurobehavioral differences. Evidence from longitudinal neuroimaging suggest trajectories of white matter microstructure maturation are atypical in PAE. We aimed to further characterize longitudinal trajectories of developmental white matter microstructure change in children and adolescents with PAE compared to typically-developing Controls using diffusion-weighted Neurite Orientation Dispersion and Density Imaging (NODDI). Materials and methods Participants: Youth with PAE (n = 34) and typically-developing Controls (n = 31) ages 8–17 years at enrollment. Participants underwent formal evaluation of growth and facial dysmorphology. Participants also completed two study visits (17 months apart on average), both of which involved cognitive testing and an MRI scan (data collected on a Siemens Prisma 3 T scanner). Age-related changes in the orientation dispersion index (ODI) and the neurite density index (NDI) were examined across five corpus callosum (CC) regions defined by tractography. Results While linear trajectories suggested similar overall microstructural integrity in PAE and Controls, analyses of symmetrized percent change (SPC) indicated group differences in the timing and magnitude of age-related increases in ODI (indexing the bending and fanning of axons) in the central region of the CC, with PAE participants demonstrating atypically steep increases in dispersion with age compared to Controls. Participants with PAE also demonstrated greater increases in ODI in the mid posterior CC (trend-level group difference). In addition, SPC in ODI and NDI was differentially correlated with executive function performance for PAE participants and Controls, suggesting an atypical relationship between white matter microstructure maturation and cognitive function in PAE. Discussion Preliminary findings suggest subtle atypicality in the timing and magnitude of age-related white matter microstructure maturation in PAE compared to typically-developing Controls. These findings add to the existing literature on neurodevelopmental trajectories in PAE and suggest that advanced biophysical diffusion modeling (NODDI) may be sensitive to biologically-meaningful microstructural changes in the CC that are disrupted by PAE. Findings of atypical brain maturation-behavior relationships in PAE highlight the need for further study. Further longitudinal research aimed at characterizing white matter neurodevelopmental trajectories in PAE will be important.
Staphylococcus aureus increases Prostaglandin E2 secretion in cow neutrophils by activating TLR2, TLR4, and NLRP3 inflammasome signaling pathways

Introduction In clinical settings, dairy cows are often attacked by pathogenic bacteria after delivery, especially Staphylococcus aureus (S. aureus). Neutrophils have long been regarded as essential for host defense against S. aureus. Prostaglandin E2 (PGE2) can additionally be used as an inflammatory mediator in pathological conditions to promote the repair of inflammatory injuries. However, whether S. aureus can promote the accumulation of PGE2 after the infection of neutrophils in cows and its mechanism remain unclear. Lipoprotein is an important immune bioactive ingredient of S. aureus. Methods In this study, the changes in neutrophils were monitored in dairy cows infected with wild-type S. aureus (SA113) and an S. aureus lipoprotein-deficient strain (Δlgt); meanwhile, we established whether pattern recognition receptors mediate this process and whether S. aureus lipoproteins are necessary for causing the release of PGE2 from cow neutrophils. Results The results showed that Δlgt was less effective than SA113 in inducing the production of IL-1β, IL-6, IL-8, IL-10, and PGE2 within neutrophils; furthermore, TLR2, TLR4, and NLRP3 receptors were found to mediate the inducible effect of lipoprotein on the above inflammation mediators and cytokines, which depended on MAPK and Caspase-1 signaling pathways. In addition, TLR2, TLR4, and NLRP3 inhibitors significantly inhibited PGE2 and cytokine secretion, and PGE2 was involved in the interaction of S. aureus and neutrophils in dairy cows, which could be regulated by TLR2, TLR4, and NLRP3 receptors. We also found that S. aureus was more likely to be killed by neutrophils when it lacked lipoprotein and TLR2, TLR4, and NLRP3 were involved, but PGE2 seemed to have no effect. Discussion Taken together, these results suggest that lipoprotein is a crucial component of S. aureus in inducing cytokine secretion by neutrophils as well as killing within neutrophils, which could be accomplished by the accumulation of PGE2 by activating MAPK and the Caspase-1 signaling pathways through TLR2, TLR4, and NLRP3 receptors. These results will contribute to a better understanding of the interaction between S. aureus and host immune cells in dairy cows.
Bridging event-related potentials with behavioral studies in motor learning

Behavioral approaches and electrophysiology in understanding human sensorimotor systems have both yielded substantial advancements in past decades. In fact, behavioral neuroscientists have found that motor learning involves the two distinct processes of the implicit and the explicit. Separately, they have also distinguished two kinds of errors that drive motor learning: sensory prediction error and task error. Scientists in electrophysiology, in addition, have discovered two motor-related, event-related potentials (ERPs): error-related negativity (ERN), and feedback-related negativity (FRN). However, there has been a lack of interchange between the two lines of research. This article, therefore, will survey through the literature in both directions, attempting to establish a bridge between these two fruitful lines of research.
Synchronization of Two Motion Control Axes Under Adaptive Feedforward Control

In this paper, motion synchronization of two d-c motors, or motion control axes, under adaptive feedforward control is considered. The adaptive feedforward control system for each axis consists of a proportional feedback controller, an adaptive disturbance compensator and an adaptive feedforward controller. If the two adaptive systems are left uncoupled, a disturbance input applied to one of the two axes will cause a motion error in the disturbed axis only, and the error becomes the synchronization error. To achieve a better synchronization, a coupling controller, which responds to the synchronization error, i.e., the difference between the two motion errors, is introduced. In this case, when a disturbance input is applied to one axis, the motion errors appear in the undisturbed axis as well as in the disturbed axis. The motion error in the undisturbed axis is introduced by the coupling controller and the adaptive feedforward controller. The adaptive synchronization problem is formulated and analyzed in the continuous time domain first, and then in the discrete time domain. Stability conditions are obtained. Effectiveness of the adaptive synchronization controller is demonstrated by simulation.
BMI1 fine-tunes gene repression and activation to safeguard undifferentiated spermatogonia fate

Introduction: Spermatogenesis is sustained by the homeostasis of self-renewal and differentiation of undifferentiated spermatogonia throughout life, which is regulated by transcriptional and posttranscriptional mechanisms. B cell-specific Moloney murine leukemia virus integration site 1 (BMI1), one of spermatogonial stem cell markers, is a member of Polycomb repressive complex 1 (PRC1) and important to spermatogenesis. However, the mechanistic underpinnings of how BMI1 regulates spermatogonia fate remain elusive. Methods: We knocked down BMI1 by siRNA to investigate the role of BMI1 in undifferentiated spermatogonia. Differentially expressed genes were identified by RNA-seq and used for KEGG pathway analysis. We performed ChIP-seq analysis in wild type and BMI1 knockdown cells to explore the underlying molecular mechanisms exerted by BMI1. BMI1-associated alterations in repressive histone modifications were detected via Western blotting and ChIP-seq. Furthermore, we performed mass spectrometry and Co-immunoprecipitation assays to investigate BMI1 co-factors. Finally, we demonstrated the genomic regions occupied by both BMI1 and its co-factor. Results: BMI1 is required for undifferentiated spermatogonia maintenance by both repressing and activating target genes. BMI1 preserves PI3K-Akt signaling pathway for spermatogonia proliferation. Decrease of BMI1 affects the deposition of repressive histone modifications H2AK119ub1 and H3K27me3. BMI also positively regulates H3K27ac deposited genes which are associated with proliferation. Moreover, we demonstrate that BMI1 interacts with Sal-like 4 (SALL4), the transcription factor critical for spermatogonia function, to co-regulate gene expression. Discussion: Overall, our study reveals that BMI1 safeguards undifferentiated spermatogonia fate through multi-functional roles in regulating gene expression programs of undifferentiated spermatogonia.
Critical gaps in nanoplastics research and their connection to risk assessment

Reports of plastics, at higher levels than previously thought, in the water that we drink and the air that we breathe, are generating considerable interest and concern. Plastics have been recorded in almost every environment in the world with estimates on the order of trillions of microplastic pieces. Yet, this may very well be an underestimate of plastic pollution as a whole. Once microplastics (<5 mm) break down in the environment, they nominally enter the nanoscale (<1,000 nm), where they cannot be seen by the naked eye or even with the use of a typical laboratory microscope. Thus far, research has focused on plastics in the macro- (>25 mm) and micro-size ranges, which are easier to detect and identify, leaving large knowledge gaps in our understanding of nanoplastic debris. Our ability to ask and answer questions relating to the transport, fate, and potential toxicity of these particles is disadvantaged by the detection and identification limits of current technology. Furthermore, laboratory exposures have been substantially constrained to the study of commercially available nanoplastics; i.e., polystyrene spheres, which do not adequately reflect the composition of environmental plastic debris. While a great deal of plastic-focused research has been published in recent years, the pattern of the work does not answer a number of key factors vital to calculating risk that takes into account the smallest plastic particles; namely, sources, fate and transport, exposure measures, toxicity and effects. These data are critical to inform regulatory decision making and to implement adaptive management strategies that mitigate risk to human health and the environment. This paper reviews the current state-of-the-science on nanoplastic research, highlighting areas where data are needed to establish robust risk assessments that take into account plastics pollution. Where nanoplastic-specific data are not available, suggested substitutions are indicated.
Haemophilus influenzae carriage and antibiotic resistance profile in Belgian infants over a three-year period (2016–2018)

Background Non-typeable Haemophilus influenzae has become increasingly important as a causative agent of invasive diseases following vaccination against H. influenzae type b. The emergence of antibiotic resistance underscores the necessity to investigate typeable non-b carriage and non-typeable H. influenzae (NTHi) in children. Methods Nasopharyngeal swab samples were taken over a three-year period (2016–2018) from 336 children (6–30 months of age) attending daycare centers (DCCs) in Belgium, and from 218 children with acute otitis media (AOM). Biotype, serotype, and antibiotic resistance of H. influenzae strains were determined phenotypically. Mutations in the ftsI gene were explored in 129 strains that were resistant or had reduced susceptibility to beta-lactam antibiotics. Results were compared with data obtained during overlapping time periods from 94 children experiencing invasive disease. Results Overall, NTHi was most frequently present in both carriage (DCC, AOM) and invasive group. This was followed by serotype “f” (2.2%) and “e” (1.4%) in carriage, and “b” (16.0%), “f” (11.7%), and “a” (4.3%) in invasive strains. Biotype II was most prevalent in all studied groups, followed by biotype III in carriage and I in invasive strains. Strains from both groups showed highest resistance to ampicillin (26.7% in carriage vs. 18.1% in invasive group). A higher frequency of ftsI mutations were found in the AOM group than the DCC group (21.6 vs. 14.9% – p = 0.056). Even more so, the proportion of biotype III strains that carried a ftsI mutation was higher in AOM compared to DCC (50.0 vs. 26.3% – p < 0.01) and invasive group. Conclusion In both groups, NTHi was most frequently circulating, while specific encapsulated serotypes for carriage and invasive group were found. Biotypes I, II and III were more frequently present in the carriage and invasive group. The carriage group had a higher resistance-frequency to the analyzed antibiotics than the invasive group. Interestingly, a higher degree of ftsI mutations was found in children with AOM compared to DCC and invasive group. This data helps understanding the H. influenzae carriage in Belgian children, as such information is scarce.
The efficacy and the safety of eltrombopag in pediatric patients with severe aplastic anemia: a systematic review

Background Acquired aplastic anemia (AAA) in pediatric patients is a rare disorder characterized by hypocellular bone marrow and pancytopenia. Eltrombopag, an oral thrombopoietin receptor agonist, provides a hematologic improvement in adults with severe aplastic anemia (SAA) refractory to immunosuppressive therapy (IST). The association of ELT and IST was approved by the US Food and Drug Administration (FDA) for adults and children ≥2 years of age as a first-line treatment for SAA. However, the effects of ELT on pediatric patients with SAA remain controversial and limited. Methods and findings We conducted a systematic review of the most recent literature from Pubmed, Web of Science, and Embase, published up to 20th December 2022, in order to evaluate the available evidence on the efficacy and safety of ELT added to IST for the treatment of SAA in the pediatric population. Conclusion Eltrombopag added to the IST has shown a good safety profile, without manifestations of excessive toxic effects, although not all the results obtained from our studies support the addition of ELT to the IST in the first-line treatment of children with SAA. Systematic Review Registration https://www.crd. york.ac. uk/prospero/, identifier: CRD42022325859.
Survivin inhibition with YM155 ameliorates experimental pulmonary arterial hypertension

Background: Imbalance between cell proliferation and apoptosis underlies the development of pulmonary arterial hypertension (PAH). Current vasodilator treatment of PAH does not target the uncontrolled proliferative process in pulmonary arteries. Proteins involved in the apoptosis pathway may play a role in PAH and their inhibition might represent a potential therapeutic target. Survivin is a member of the apoptosis inhibitor protein family involved in cell proliferation. Objectives: This study aimed to explore the potential role of survivin in the pathogenesis of PAH and the effects of its inhibition. Methods: In SU5416/hypoxia-induced PAH mice we assessed the expression of survivin by immunohistochemistry, western-blot analysis, and RT-PCR; the expression of proliferation-related genes (Bcl2 and Mki67); and the effects of the survivin inhibitor YM155. In explanted lungs from patients with PAH we assessed the expression of survivin, BCL2 and MKI67. Results: SU5416/hypoxia mice showed increased expression of survivin in pulmonary arteries and lung tissue extract, and upregulation of survivin, Bcl2 and Mki67 genes. Treatment with YM155 reduced right ventricle (RV) systolic pressure, RV thickness, pulmonary vascular remodeling, and the expression of survivin, Bcl2, and Mki67 to values similar to those in control animals. Lungs of patients with PAH also showed increased expression of survivin in pulmonary arteries and lung extract, and also that of BCL2 and MKI67 genes, compared with control lungs. Conclusion: We conclude that survivin might be involved in the pathogenesis of PAH and that its inhibition with YM155 might represent a novel therapeutic approach that warrants further evaluation.