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To identify latent self-management profiles in people living with HIV (PLWH) with dyslipidemia and factors associated with profile membership, thereby facilitating targeted clinical intervention. A cross-sectional survey was conducted from December 2024 to June 2025 among 333 PLWH with dyslipidemia at Nanjing Second Hospital. Data were collected via sociodemographic/disease-related questionnaire, the HIV Self-Management Scale (HIVSMS), and the Health Literacy Management Scale (HLMS). Latent profile analysis (LPA) was performed in Mplus 8.3, and multinomial logistic regression was used to examine factors associated with profile membership. Fit indices (entropy = 0.993) supported a three-profile solution: low self-management-low social support-seeking (C1, 42.3%), moderate self-management-stable (C2, 37.8%), and high self-management-emotion regulation dominant (C3, 19.8%). Seeking social support was relatively low across profiles. Compared with C1, C2 membership was significantly associated with higher education and income, lipid-lowering medication use (OR 3.735, 95% CI 1.597-8.736), and CD4 350-500 cells/μL, and was less likely among participants with VL >1000 copies/mL or chronic comorbidities (all P < 0.05). Compared with C1, C3 membership was significantly associated with HIV infection duration ≥5 years, higher education and income, CD4 >500 cells/μL, and higher HDL-C, and was less likely among those with VL >1000 copies/mL (OR 0.037, 95% CI 0.004-0.380) or chronic comorbidities (all P < 0.05). Compared with C2, C3 membership was independently associated with higher health literacy (HL) (OR 1.038 per point, 95% CI 1.012-1.064) and was less likely among those with LDL-C ≥3 mmol/L (P < 0.05). We identified three distinct self-management profiles among PLWH with dyslipidemia. Profile membership was significantly associated with HL and socioeconomic, HIV-related, lipid-related, and comorbidity factors, supporting the need for profile-tailored strategies to improve self-management. Show less

Social connectedness promotes healthy aging and is associated with lower risk for psychological disorders and cognitive decline. However, little is known about the mechanisms underlying these relationships, and whether different network features are associated with unique health benefits. We used comprehensive data from 386 community-dwelling older adults with and without cognitive impairment to test the relationship between psychological and cognitive function and their personal social networks. Data were collected using a multisite sampling strategy, and included detailed social network interviews and comprehensive measures of episodic memory, executive function, and language. Longitudinal effects were evaluated using a subsample at high-risk for decline, having either at least one copy of APOE ε4 or a current diagnosis of impairment ( The online version contains supplementary material available at 10.1038/s41598-026-44571-9. Show less

Cadmium (Cd) is a potent neurotoxic heavy metal associated with cerebral oxidative disturbances. The beta-lactam antibiotic ceftriaxone has been known to modulate the expression of GLT-1, the primary glutamate transporter. This research has been framed to evaluate the potential neurodefensive activity of ceftriaxone against cadmium chloride (CdCl Show less

Intercellular communication is governed by the spatiotemporal dynamics of protein complexes at the cell-cell interface. However, conventional static interaction models fail to incorporate key physical constraints, such as steric hindrance, spatial compartmentalization, and dimensionality reduction that regulate complex assembly in vivo. To bridge the gap between static network topology and dynamic systems biology, we developed a multi-scale computational framework. We first identified a highly conserved, Fibroblast Growth Factor Receptor 1 (FGFR1)-centered cell adhesion and signaling motif by analyzing a diverse set of human cell-cell interfaces. We then constructed a multi-layer spatial stochastic simulator to recapitulate and interrogate the dynamic behavior of this network motif at cell-cell interfaces. Atomic-resolution structural models of the protein complexes within the motif were further generated using AlphaFold to define interaction rules for the stochastic simulations by categorizing binding interfaces. Our results show that the structural arrangement of cell-cell adhesion complexes controls how FGFR1 receptors cluster at the cell-cell interface, effectively dividing the membrane into distinct functional microdomains. Competition from decoy receptors further regulates this process by capturing receptors before they can participate in signaling. Even small changes in binding affinity can therefore alter receptor organization and disrupt normal signal transduction, which may contribute to human disease. By integrating macro-scale interactomics, atomic-level structural bioinformatics, and mesoscale stochastic modeling, this study reveals how structural interaction rules, combined with spatial constraints, shape the formation and function of intercellular signaling networks. Show less

Sleep deprivation (SD) impairs information processing through alterations of prefrontal cortex (PFC) function, yet the molecular underpinnings of this process remain poorly understood. We previously showed that SD disrupts sensorimotor gating by elevating prefrontal levels of the neurosteroid allopregnanolone (AP), a positive allosteric modulator of GABA-A receptors. Here we identify a complementary, mechanistically independent process whereby SD alters GABA-A currents in the PFC of mice and rats. SD reduced membrane expression of the chloride exporter KCC2, leading to intracellular chloride accumulation and a depolarizing shift in GABA-A receptor reversal potential that weakened GABAergic inhibition. Pharmacological normalization of chloride homeostasis with bumetanide fully rescued SD-induced deficits in sensorimotor gating and information encoding. SD also upregulated BDNF, and intra-PFC antagonism of its receptor TrkB restored KCC2 expression and normalized information processing, identifying BDNF-TrkB signaling as an upstream driver of chloride dysregulation. Notably, blocking AP synthesis rescued behavioral deficits without correcting chloride imbalance, confirming mechanistic independence. Finally, combined administration of AP and a KCC2 blocker produced information-processing deficits akin to those induced by SD. These findings identify TrkB-dependent disruption of prefrontal chloride homeostasis as a druggable mechanism underlying sleep loss-induced cognitive dysfunction. Show less

Cardiovascular and renal diseases exhibit a close bidirectional interaction, which often leads to the development of cardio-renal syndrome (CRS)-a clinical condition in which cardiac dysfunction further aggravates renal injury. Type I CRS is characterized by acute kidney injury secondary to acute heart failure, and this sub-type is closely related to elevated morbidity and mortality in patients with coronary artery disease (CAD). Despite the availability of traditional biomarkers, there is an unmet need for more sensitive indicators to identify high-risk patients for Type I CRS in CAD patients. The apolipoprotein B (ApoB)/apolipoprotein A1 (ApoA1) ratio has emerged as a promising predictor of cardiovascular risk, yet its role in CRS remains unclear. This study aimed to evaluate the association between the ApoB/ApoA1 ratio and Type I CRS in patients with CAD, and to assess its value as a biomarker for identifying high-risk patients. A retrospective cohort study was carried out on 269 CAD patients complicated with heart failure who were hospitalized in our hospital from 2022 to 2024. According to the estimated glomerular filtration rate (eGFR) results, the enrolled patients were divided into two subgroups: the simple heart failure (SHF) group and the type I CRS group. Data on demographics, clinical history, biochemical measurements, echocardiographic and coronary angiography assessments, and renal function were collected. A multivariable logistic regression model was used to assess the association between the ApoB/ApoA1 ratio and CRS, adjusting for potential confounders. Correlation analyses were performed to explore the relationships between key variables and the occurrence of type I CRS. A multivariable logistic regression model was used to assess the association between the ApoB/ApoA1 ratio and CRS. Furthermore, a receiver operating characteristic (ROC) curve was constructed to evaluate the predictive accuracy of the ApoB/ApoA1 ratio for type I CRS. A total of 269 patients were enrolled. Significant differences were observed between the simple heart failure (SHF) group and the CRS group in terms of age, history of diabetes mellitus, levels of triglycerides (TG), apolipoprotein A1 (apo-A1), apolipoprotein B (apo-B), ApoB/ApoA1 ratio, and serum creatinine (Scr). Patients in the CRS group were older, had a higher proportion of diabetes mellitus, higher levels of TG, apo-B, and Scr, a higher ApoB/ApoA1 ratio, but lower levels of apo-A1 compared to the SHF group. Multivariable logistic regression analysis identified age and the ApoB/ApoA1 ratio as independent risk factors for CRS. The receiver operating characteristic (ROC) curve analysis showed that the ApoB/ApoA1 ratio had a moderate level of predictive accuracy for Type I CRS, with an area under the curve (AUC) of 0.782. The ApoB/ApoA1 ratio is moderately associated with the risk of developing Type I CRS in patients with CAD. This ratio could serve as a clinically relevant biomarker for early identification of in-hospital Type I CRS risk in CAD patients with acute heart failure, potentially aiding in the implementation of early and targeted interventions to improve patient outcomes. Show less

Subcutaneous fat deposition critically impacts duck meat quality and feed efficiency. We monitored growth and fat deposition in ducks from 30 to 70 days, performed transcriptomics on adipose tissue, and established an in vitro duck preadipocyte model to assess Fat deposition peaked at 50 days. Show less

Pesticides are essential for modern agriculture but raise concerns about potential neurodevelopmental consequences, leading to bans in some countries. This study aimed to investigate the long-term effects of prenatal exposure to chlorpyrifos (CPF) on behavior and DNA methylation, considering genetic susceptibility via the apolipoprotein E ( Show less

Psilocybin is studied as innovative medication in anxiety, substance abuse and treatment-resistant depression. Animal studies show that psychedelics promote neuronal plasticity by strengthening synaptic responses and protein synthesis. However, the exact molecular and cellular changes induced by psilocybin in the human brain are not known. Here, we treated human cortical neurons derived from induced pluripotent stem cells with the 5-HT2A receptor agonist psilocin - the psychoactive metabolite of psilocybin. We analyzed how exposure to psilocin affects gene expression, neuronal morphology, synaptic markers and neuronal function. Psilocin provoked a 5-HT2A-R-mediated augmentation of BDNF abundance. Transcriptomic profiling identified gene expression signatures priming neurons to neuroplasticity. On a morphological level, psilocin induced enhanced neuronal complexity and increased expression of synaptic proteins, in particular in the postsynaptic compartment. Consistently, we observed an increased excitability and enhanced synaptic network activity in neurons treated with psilocin. In conclusion, exposure of human neurons to psilocin might induce a state of enhanced neuronal plasticity, which could explain why psilocin is beneficial in the treatment of neuropsychiatric disorders where synaptic dysfunctions are discussed. Show less

Methadone maintenance treatment (MMT) is one of the major pharmacotherapies for opioid use disorder. The underlying mechanisms of addiction and the treatment response are only partially understood. The study's main goal was to identify differential DNA CpG methylation that occurred in response to MMT. Toward this goal, we have conducted a longitudinal epigenome-wide study of blood samples from 64 patients at the beginning and after 1-3 years of MMT, using a linear mixed model. A total of 1881 differentially methylated probes (DMPs) were identified (FDR < 0.05), controlling for sex, age, estimates of blood cell proportions, and the first two principal components based on genome-wide SNP genotypes. Among the genes annotated to the top DMPs are The study provides preliminary insight into the epigenetic effect of MMT. Future studies will have to confirm the DMPs, assess their impact on gene expression, and determine their clinical relevance. Show less

Exercise as a non-pharmacological measure is important to increase the brain plasticity hence improving cognitive performance as well as mental health. This narrative review describes in depth the hierarchical multiscale processes of neuroplasticity to exercise, including the presence of neurotrophic factor regulation, cellular metabolic adaptations and neurotransmitter remodeling, up to the structure and functional reorganization of brain networks as seen through neuroimaging, and concluding with adaptive cognitive and behavioral outcomes. We further investigate the role of personal variations in genetic time and social environments in moderating the neuroplasticity of exercise. Furthermore, the review identifies the importance of combining multimodal visualization methods with computational models in generating accurate workout prescriptions and their potential of translation into clinical and educational practice. Lastly, the research problems and "grand challenges" are addressed, with a focus on the importance of exercise as a pleiotropic behavior-intervention and its general implications to the area of promoting brain health. Show less

Attention deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder with a complex and not fully understood etiology. Increasing evidence suggests that neurotrophic factors involved in neurodevelopment and synaptic plasticity, as well as hormones of the hypothalamic-pituitary-adrenal (HPA) axis that regulate the stress response, may contribute to the pathophysiology of ADHD. This cross-sectional study aimed to compare children diagnosed with ADHD and healthy controls with respect to serum levels of brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neurotrophin-3 (NT-3), adrenocorticotropic hormone (ACTH), and cortisol. A total of 80 children aged 6-18 years with a diagnosis of ADHD and 81 healthy controls were included in the study. The severity of ADHD symptoms was assessed using the Conners' Parent Rating Scale-Short Version (CPRS-SV). Serum levels of biochemical parameters were measured using commercially available electrochemiluminescence immunoassay and enzyme-linked immunosorbent assay kits. Compared with the healthy control group, the ADHD group exhibited significantly higher serum levels of BDNF, GDNF, VEGF, ACTH, and cortisol, whereas NT-3 levels did not differ between the groups. These group differences remained statistically significant after controlling for potential confounding variables. Correlation analyses revealed no significant associations between neurotrophic factors, hypothalamic-pituitary-adrenal (HPA) axis hormones, and CPRS-SV subscale scores. The present findings indicate that neurotrophic factors and hormones related to the hypothalamic-pituitary-adrenal (HPA) axis are altered in medication-naïve children and adolescents with ADHD. The absence of a direct correlation between neurotrophic factors and HPA axis hormones suggests that these systems may contribute to the pathophysiology of ADHD through parallel yet partially independent and complex mechanisms. Future longitudinal and multimodal studies are warranted to elucidate the dynamic interactions between stress-related neuroendocrine processes and neurodevelopmental pathways in ADHD. Show less

In recent years, the global incidence of Non-Suicidal Self-Injury (NSSI) has risen, posing a significant challenge in public health. Adolescents are the main group affected. A cross-sectional study was conducted using a self-administered questionnaire to collect data from 6,311 adolescents in Hefei, China. This study employed the Compositional Isotemporal Substitution Model (CISM, a statistical method that estimates health effects of replacing time in one behavior with another while accounting for the interdependent, compositional nature of 24-h time-use data) to examine the impact of Screen Time (ST), Non-Screen-based Sedentary Time (NSST), Physical Activity, and Sleep Time on NSSI among adolescents. Compositional logistic regression analysis revealed that, relative to the remaining behavioral components, higher Light Physical Activity (LPA) ( The findings highlight those reasonably allocating adolescents' daily activities, reducing ST, can help lower the risk of NSSI among adolescents. Show less

Older adults increasingly rely on digital health resources, yet evidence regarding the relationship between eHealth literacy (eHL) and 24-hour movement behaviors (24-HMB), including physical activity (PA), sedentary behavior (SB), and sleep, remains underexplored. This study examined the associations between eHL and 24-HMB in Chinese older adults and examined self-efficacy as a potential mediator and moderator. Using a convenience sampling approach, 564 community-dwelling older adults (aged 60-74 years) were recruited from four urban Chinese cities via an online survey. A total of 553 valid cases were retained for analyses. eHL was assessed using the eHealth Literacy Scale-Web 3.0, and self-efficacy was assessed using a validated Self-Efficacy Scale. PA and SB were assessed objectively using ActiGraph GT3X+ accelerometers over three consecutive days (two weekdays and one weekend day). Sleep duration was derived from accelerometer-based estimates anchored by daily sleep logs. Multiple linear regression analyses were conducted to examine associations, and mediation and moderation were tested using PROCESS macro (Model 4 and Model 1, respectively), adjusting for age, sex, and education. After adjustment for covariates ( In this cross-sectional, urban, device-using sample of older adults, higher eHL was associated with a more favorable 24-HMB profile, particularly higher LPA and lower SB, while associations with sleep duration were weaker. Self-efficacy showed modest indirect associations consistent with partial mediation for PA and SB and also acted as a moderator of several associations. Given the observational design and modest effect sizes, findings should be interpreted cautiously and require confirmation in longitudinal or experimental studies with more representative sampling and improved sleep assessment. Show less

Suicidal behavior in children and adolescents is a major global public health issue, and suicide is one of the leading causes of death in this age group. While psychosocial determinants of suicidality are well established, understanding its biological risk factors is crucial for targeted prevention and treatment. This review presents a narrative synthesis of recent literature examining current evidence on the biological mechanisms that contribute to youth suicidality. Genetic liability plays a substantial role, often interacting with environmental stressors. Key neurobiological factors include dysfunction of the serotonin system and impaired neuroplasticity, characterized by a glutamate-gamma-aminobutyric acid imbalance and reduced brain-derived neurotrophic factor. Psychosocial stress appears linked to these changes through several pathways, including dysregulation of the hypothalamic-pituitary-adrenal axis, chronic low-grade inflammation, oxidative stress, and activation of the kynurenine pathway. Neurodevelopmental conditions like autism spectrum disorders and attention deficit hyperactivity disorder, as well as sleep disturbances, may further increase risk. While therapeutic agents such as ketamine and lithium target these neurobiological systems, evidence for their anti-suicidal efficacy in youth remains limited, with only a small number of randomized controlled trials conducted in pediatric populations. Biological research offers valuable insights, but the use of varied study methods and a lack of longitudinal data complicate its translation into clinical practice. Future studies should employ integrative, developmentally informed models to elucidate causal mechanisms and inform more effective interventions. Show less

Major depressive disorder (MDD) is a highly prevalent psychiatric illness for which rapid-acting antidepressants such as ketamine provide only transient benefit. Because κ-opioid receptor (KOR) signaling contributes to stress-related dysphoria and impaired neuroplasticity, we examined whether KOR antagonism could prolong ketamine's antidepressant-like effects in a mouse model of adolescent chronic unpredictable stress (CUS). Male Show less

According to neuropsychiatric sequelae for cardiovascular pathology, carotid artery disease (CAD) represents a significant medical, social, and economic burden. Numerous efforts have been made to define reliable markers that can reflect the principal pathological event and the effect of employed therapeutic protocols, prognoses, and clinical outcomes of CAD. However, the potential role of the neurotrophin (NT) system has not yet been confirmed. This narrative review was conducted following a literature search of PubMed, which included all studies on NT system elements and CAD published over the last two decades, encompassing both animal and clinical investigations, regarding the potential use of NT system elements as biomarkers for neurotoxicity manifestations and therapeutic effectiveness in CAD. Still, the analysis presented in this review is not sufficient to reveal whether NT system elements can be considered as exploratory or standard biomarkers for the evaluation of CAD. Further research is essential to elucidate this dilemma. Show less

Kidney transplantation (KTx) corrects many uremia-related metabolic disturbances; however, dyslipidemia remains common in kidney transplant recipients and contributes to persistent cardiovascular risk. Lipoprotein(a) [Lp(a)] is a largely genetically determined proatherogenic lipoprotein that increases in advanced chronic kidney disease (CKD) and may decrease after restoration of renal function. Autotaxin (ATX), an enzyme involved in proinflammatory lipid signaling through the ATX-lysophosphatidic acid axis, has also been implicated in cardiovascular pathology, but its early post-transplant dynamics remain poorly characterized. In addition to quantitative lipid abnormalities, CKD is associated with high-density lipoprotein (HDL) dysfunction and reduced paraoxonase-1 (PON-1) activity; however, data on early post-transplant changes in PON-1 activity are limited. In this prospective observational study, lipid profile parameters, Lp(a) concentration, ATX activity, and PON-1 activity were assessed in 55 Caucasian patients with CKD stage 5, most of whom were dialysis-dependent, before and 2-3 weeks after KTx. All recipients received tacrolimus-based maintenance immunosuppression with corticosteroids and mycophenolate mofetil. After KTx, Lp(a) levels decreased by a median of 21% and ATX activity by 28% (both Show less

Chronic stress induces sensorimotor, cognitive, and neuroendocrine alterations, particularly in females who exhibit heightened vulnerability to stress-related disorders. This study tested the hypothesis that chronic quetiapine administration during ongoing unpredictable chronic mild stress (UCMS) would attenuate stress-induced impairments in sensorimotor gating, recognition memory, and HPA-axis–related biochemical markers in female rats. Adult female Wistar rats were exposed to a 9-week UCMS paradigm, with quetiapine (10 mg/kg/day, i.p.) administered during the final 3 weeks. Behavioral outcomes were assessed using prepulse inhibition (PPI), startle reactivity, and the Novel Object Recognition (NOR) test. Serum and hippocampal corticosterone and BDNF levels were quantified by ELISA. Chronic stress significantly reduced PPI and recognition memory performance and increased serum and hippocampal corticosterone levels. Quetiapine treatment improved PPI and startle responsiveness, restored NOR discrimination index values, and partially attenuated stress-induced corticosterone elevations. Hippocampal BDNF levels were elevated in stressed animals and were modulated toward intermediate levels following quetiapine treatment. These findings indicate that chronic quetiapine administration mitigates behavioral and neuroendocrine alterations induced by prolonged stress in female rats. [Image: see text] The online version contains supplementary material available at 10.1007/s11011-026-01834-8. Show less

Osteoporosis (OP) is a metabolic bone disease characterized by low bone mineral density (BMD), and its pathogenesis involves endoplasmic reticulum (ER) stress-related cell death. This study aimed to identify diagnostic biomarkers associated with ER stress-related cell death in OP and explore their underlying mechanisms. The training dataset (GSE56815), validation dataset (GSE56814), and single-cell RNA sequencing (scRNA-seq) dataset (GSE147287) were downloaded. Differentially expressed genes (DEGs) between OP patients and controls were identified. Candidate genes were obtained by intersecting DEGs with ER stress-related genes and programmed cell death (PCD)-related genes. Machine learning was used to screen intersection genes, and biomarkers were determined via expression level analysis. Gene set enrichment analysis (GSEA), immune cell infiltration analysis, drug prediction and molecular docking, scRNA-seq analysis, key cell screening, cell communication analysis, and pseudotime analysis were performed. Finally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) were further conducted. A total of 28 candidate genes were obtained by intersection. CAMKK2 and DAPK3 were confirmed as biomarkers, and were consistently down-regulated in both datasets and verified by RT-qPCR. GSEA analysis revealed that biomarkers were enriched in cytokine-cytokine receptor interaction. Correlations between biomarkers and activated dendritic cells were found via immune cell infiltration analysis. Preliminary computational analyses indicated that drugs including calcitriol and danazol may potentially interact with the biomarkers in a stable manner. Bone marrow-derived mesenchymal stem cells (BM-MSCs) were identified as potential key cells via scRNA-seq analysis. Complex interactions involving BM-MSCs, such as ANGPTL4-CDH11 mediating BM-MSC self-communication, were revealed by cell communication analysis. Dynamic expression of biomarkers during BM-MSC differentiation was shown by pseudotime analysis: CAMKK2 fluctuated with differentiation stages, while DAPK3 shifted from high to low then high expression. CAMKK2 and DAPK3 were confirmed as diagnostic biomarkers for OP, providing insights into OP diagnosis and potential therapeutic targets. Show less

Fatty acid-binding proteins (FABPs) influence cellular energy metabolism by regulating fatty acid kinetics. They also play a vital role in neuronal apoptosis following cerebral infarction. Resveratrol (RSV) has demonstrated neuroprotective effects in ischemic stroke; however, its regulatory impact on FABPs and associated pathways requires further investigation. This study aimed to explore the potential mechanisms by which RSV protects ischemic stroke neurons by regulating fatty acid metabolism. A weighted gene co-expression network analysis revealed significant enrichment of FABP5 in fatty acid metabolism-related pathways in rats with middle cerebral artery occlusion (MCAO). Modulating FABP5 expression level may influence post-infarction neuronal recovery. Molecular docking experiments demonstrated that RSV exhibited strong binding affinity with FABP5. In the MCAO-group of rats, administering different doses of RSV led to a significant decrease in cerebral infarct area and improved neurological function with increased RSV doses. Concurrently, the expression of FABP5 and neuron-specific enolase in brain tissue decreased, whereas the expression of the brain-derived neurotrophic factor increased and neuronal morphology improved. Further experiments using FABP5 overexpression and inhibition models revealed that FABP5 overexpression exacerbated neuronal apoptosis and suppressed the expression of adenosine monophosphate (AMP)-activated protein kinase (AMPK) protein, whereas FABP5 inhibition reduced neuronal apoptosis and enhanced AMPK protein expression. RSV downregulates FABP5 expression in cerebral infarction tissues and potentially mediates the AMPK-related pathways to ameliorate neuronal apoptosis. Show less

There are limited data on the dynamic changes in daily composition of movement behaviors (sleep; moderate-to-vigorous physical activity, MVPA; light physical activity, LPA; and sedentary time, SED) and their associations with body weight in postpartum women. The purpose of this study was to examine associations of reallocating time in one behavior to another with body weight, at different times in the first year postpartum. The study included 86 women who delivered a singleton infant at ≥37 weeks gestation. Physical activity and sleep were measured via actigraphy in early, mid-, and late postpartum. Body weight was measured at each timepoint. Isotemporal substitution models were used to examine the association of reallocating ten minutes of one behavior (MVPA, LPA, SED, or sleep) to another, with body weight. Participants spent most of their day in SED (~52-53%), followed by sleep (~30%), LPA (~12-13%), and then MVPA (~2%) throughout the first year postpartum. In early and mid-postpartum, but not late postpartum, reallocating 10 min of MVPA to LPA, SED, or sleep was associated with lower body weight (range: 3.07-4.03 kg lower). In early and late postpartum, reallocating 10 min of SED to LPA was associated with a lower body weight (4.03 kg and 1.04 kg, respectively). In participants who slept ≥7 h per day, reallocating sleep to LPA in early postpartum, and MVPA time to LPA in mid-postpartum was associated with lower body weight. In those who slept <7 h, no significant associations with body weight were found when reallocating time from one behavior to another. Encouraging LPA throughout the postpartum period may be beneficial for weight loss, and having enough sleep may be especially important for early to mid-postpartum. Future research examining the impact of changes in LPA on body weight in the postpartum period are needed, along with postpartum specific 24 h movement guidelines. Show less

Doxorubicin (Dox) is a potent cytotoxic medication, yet its adverse properties are undeniable obstacles to its clinical use. The objective of the existing research was to inspect the potential beneficial actions of lurasidone (Lura) against the neurotoxicity and cardiotoxicity triggered by Dox in rats. Sixty rats were equally allocated to four groups: Control group; Dox group; Lur (1 mg/kg) + Dox group; Lura (3 mg/kg) + Dox group. For 18 days, Lura (1 and 3 mg/kg) was given orally, starting 7 days before giving six doses of Dox (2.5 mg/kg every other day, i.p). Lura attenuated Dox-instigated cardiac injury as assured by the decrease in cardiac troponin-I (cTn-I), kg) and creatine kinase MB (CK-MB) levels. In addition, Lura remarkably declined Dox-triggered neuronal dysfunction, as confirmed by diminished anxiety and depression-alike behaviors in the open field (OFT) and forced swimming (FST) tests, respectively. Furthermore, Lura replenished cardiac and brain antioxidant markers, mitochondrial modulator, PGC-1α, and significantly decreased inflammatory mediators, miR34a-5p, and pro-apoptotic caspase-3 levels. In the brain, Lura also mitigated the induction of glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor-1 (Iba-1). In the same context, Lura pretreatment upregulated the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/phosphoinositide 3-kinase (PI Show less