Search Results (81)

Non-Intrusive Load Monitoring (NILM) represents a powerful approach for energy disaggregation, which enables detailed insights into energy consumption patterns without requiring extensive sensor deployment. While significant advances have been achieved in residential NILM applications, commercial and industrial buildings remain largely underexplored despite their substantial contribution to global energy consumption. This study addresses this gap by developing and evaluating multiple artificial intelligence approaches for energy disaggregation across residential, commercial, and industrial buildings under a unified experimental protocol. We implement and compare several AI-based models, including Vision Transformer (ViT), Variational Autoencoder (VAE), Random Forest (RF), and custom architectures inspired by TimeGPT and Prophet, alongside traditional baseline methods. The proposed framework is validated using three benchmark datasets representing residential (AMPds), commercial (COmBED), and industrial (IMDELD) environments. Experimental results demonstrate that architecture–load interactions, rather than model complexity alone, are the primary determinants of disaggregation accuracy: the ViT-small configuration achieves superior performance for complex industrial loads with R² values exceeding 0.94, Random Forest proves most effective for finite-state commercial HVAC systems with R² up to 0.97, and the Prophet-inspired model excels in capturing seasonal patterns in residential appliances. These findings provide evidence-based guidelines for selecting appropriate AI models based on load characteristics, signal-to-noise ratio, and building type, contributing to the practical deployment of NILM in heterogeneous building environments. Full article

Recent revisions of personality disorder (PD) classifications have moved from categorical diagnoses toward dimensional models, raising renewed questions about the nosological status and clinical utility of borderline personality disorder (BPD). This narrative review traces the development of the borderline construct from early descriptions of patients positioned between neurosis and psychosis, through its theoretical consolidation within the concept of borderline personality organization, to the operationalization of BPD in DSM-III and subsequent diagnostic revisions. A central section summarizes contemporary controversies regarding the validity and utility of BPD features. Arguments for abandoning the diagnosis emphasize the absence of a distinct borderline factor in factor analytic studies, the tendency of the construct to capture fluctuating symptoms and patterns of behaviour rather than stable maladaptive personality traits, the stigmatizing and non-selective use of the label, and the lack of disorder-specific treatment approaches. In contrast, converging evidence supports the view that core borderline symptoms frequently function as markers of general PD pathology and of the severity of impairments in self and interpersonal functioning. The paper integrates the concept of the borderline level of personality functioning, conceptualizing borderline pathology as a dynamic dimension of dysfunction with potential transient regressions, and links this concept to the Level of Personality Functioning (LPF, Criterion A) within the DSM 5 Alternative Model for Personality Disorders (AMPD). Retaining borderline pathology as a dimension may support contemporary PD assessment by offering a clinically recognizable marker of overall dysfunction, a guide for rating severity, an indicator of personality structure and need for psychotherapy, without disrupting continuity with an extensive clinical and research tradition. Full article

Elucidating the molecular mechanisms underlying beef quality differences is crucial for precision breeding of high-quality cattle. In this study, we first characterized the myofibrillar morphology of high-quality (H group) and low-quality (L group) beef samples using hematoxylin–eosin (HE) staining. Transcriptomic and metabolomic analyses were then conducted to reveal the molecular regulatory basis of quality variation. HE staining revealed highly significant differences in muscle fiber area and diameter between H and L groups (p < 0.01), along with significant differences in muscle fiber density (p < 0.05), but no significant differences in muscle fiber perimeter. Furthermore, by focusing on five core metabolic pathways shared across the transcriptome and metabolome datasets, 30 differentially expressed genes (DEGs) and 14 differentially accumulated metabolites (DAMs) were identified. Pearson correlation analysis revealed synergistic regulation between DEGs and DAMs: AMPD2 modulates umami flavor by regulating inosine accumulation via the purine metabolism pathway; ACOX3 promotes unsaturated fatty acid synthesis and intramuscular fat deposition through carbohydrate metabolism; genes in the glycolysis/gluconeogenesis pathway maintain post-slaughter muscle pH homeostasis, thereby influencing beef tenderness. Collectively, this study integrates morphological and molecular evidence to elucidate the multi-level basis of beef quality formation, providing key candidate genes, metabolites, and pathways for molecular breeding. These findings offer comprehensive theoretical and technical support for the sustainable development of the premium beef industry. Full article

The integration of omics technologies, including genomics, proteomics, metabolomics, and microbiomics, has transformed sports science, particularly soccer, by providing new opportunities to optimize player performance, reduce injury risk, and enhance recovery. This systematic literature review was conducted in accordance with PRISMA 2020 guidelines and structured using the PICOS/PECOS framework. Comprehensive searches were performed in PubMed, Scopus, and Web of Science up to August 2025. Eligible studies were peer-reviewed original research involving professional or elite soccer players that applied at least one omics approach to outcomes related to performance, health, recovery, or injury prevention. Reviews, conference abstracts, editorials, and studies not involving soccer or omics technologies were excluded. A total of 139 studies met the inclusion criteria. Across the included studies, a total of 19,449 participants were analyzed. Genomic investigations identified numerous single-nucleotide polymorphisms (SNPs) spanning key biological pathways. Cardiovascular and vascular genes (e.g., ACE, AGT, NOS3, VEGF, ADRA2A, ADRB1–3) were associated with endurance, cardiovascular regulation, and recovery. Genes related to muscle structure, metabolism, and hypertrophy (e.g., ACTN3, CKM, MLCK, TRIM63, TTN-AS1, HIF1A, MSTN, MCT1, AMPD1) were linked to sprint performance, metabolic efficiency, and muscle injury susceptibility. Neurotransmission-related genes (BDNF, COMT, DRD1–3, DBH, SLC6A4, HTR2A, APOE) influenced motivation, fatigue, cognitive performance, and brain injury recovery. Connective tissue and extracellular matrix genes (COL1A1, COL1A2, COL2A1, COL5A1, COL12A1, COL22A1, ELN, EMILIN1, TNC, MMP3, GEFT, LIF, HGF) were implicated in ligament, tendon, and muscle injury risk. Energy metabolism and mitochondrial function genes (PPARA, PPARG, PPARD, PPARGC1A, UCP1–3, FTO, TFAM) shaped endurance capacity, substrate utilization, and body composition. Oxidative stress and detoxification pathways (GSTM1, GSTP1, GSTT1, NRF2) influenced recovery and resilience, while bone-related variants (VDR, P2RX7, RANK/RANKL/OPG) were associated with bone density and remodeling. Beyond genomics, proteomics identified markers of muscle damage and repair, metabolomics characterized fatigue- and energy-related signatures, and microbiomics revealed links between gut microbial diversity, recovery, and physiological resilience. Evidence from omics research in soccer supports the potential for individualized approaches to training, nutrition, recovery, and injury prevention. By integrating genomics, proteomics, metabolomics, and microbiomics data, clubs and sports practitioners may design precision strategies tailored to each player’s biological profile. Future research should expand on multi-omics integration, explore gene–environment interactions, and improve representation across sexes, age groups, and competitive levels to advance precision sports medicine in soccer. Full article

Introduction: Personality disorders are enduring, maladaptive patterns that impair social and vocational functioning. The DSM-5 Alternative Model for Personality Disorders (AMPD) distinguishes Criterion A (personality functioning: identity, self-direction, empathy, intimacy) from Criterion B (maladaptive trait domains: negative affectivity, detachment, antagonism, disinhibition, psychoticism). We frame this study within Criterion B, supporting the use of a dimensional approach that complements (rather than replaces) normative models like the Five-Factor Model (FFM) and addresses cross-cultural gaps amid Saudi Arabia’s rapid sociocultural change such as the reforms associated with Vision 2030. Given Saudi Arabia’s collectivist orientation and evolving sociocultural norms under Vision 2030, the dimensional approach of the AMPD Criterion B offers a culturally sensitive lens for capturing personality pathology beyond Western-centric diagnostic models. Aim: We aimed to examine how PID-5-BF maladaptive trait domains vary across key sociodemographic factors in Saudi adults. Subjects and Methods: This was a quantitative, cross-sectional analytical study conducted among Saudi adults using the PID-5-BF Convenience sampling was performed via the dissemination of an online survey; we aimed for 377 participants and obtained 343 completed responses (~91% of the target sample). For trait assessment, we used the PID-5-BF; analyses compared domains across sociodemographic groups. Results: Females showed a higher negative affect; participants ≤ 30 years exhibited higher psychoticism than those >40; and single individuals reported lower detachment and psychoticism than their married peers. Conclusions: Gender, age, and marital status are associated with differences in maladaptive trait expression, supporting the need for culturally tailored screening and interventions in Saudi mental health services. These findings should be interpreted with caution given the fact that WhatsApp-based convenience sampling was used, which may bias the results as the respondents were more likely to live in urban areas, be educated, and be technologically proficient. Full article

Objective: Genetic and environmental factors influence the expression of personality pathology and subsequent treatment efforts. This study associates genetics with a contemporary nosology of personality pathology represented in the Alternative Model for Personality Disorders (AMPD). We hypothesized traits from Criterion B of the AMPD would differ between genotypes of the catechol-O-methyltransferase (COMT) polymorphism (rs4680/Val158Met variation), given this genetic marker’s role in the metabolism of dopamine and norepinephrine, especially in the prefrontal cortex. Methods: The Personality Inventory for DSM-V (PID-5) was used to quantify personality traits, and the Genomind platform was used to identify the genotypes of the Val158Met COMT polymorphism in 84 psychiatric outpatients. Results: One of the five Criterion B personality domains and three of the twenty-five traits were significantly different among genotypes. Met/Met carriers had significantly higher pathological scores on the broad domain of negative affect and specific traits of perceptual dysregulation and separation insecurity, while the Val/Val carriers had significantly higher scores on the restricted affectivity trait. The COMT Val158Met polymorphism’s association with personality pathology was sexually dimorphic, with the two domains and nine traits significantly different across genotypes in males, but no differences were found in females. A substantial improvement in the regression of domains/traits score when gene–sex interactions were included further confirmed the dimorphism, e.g., the R-squared (adjusted) for the psychoticism improved from 0.03 (p = 0.15) to 0.19 (p < 0.001). Conclusions: Findings offer preliminary support for a link, potentially dimorphic across sexes, between the COMT Val158Met polymorphism and personality pathology as represented by the AMPD. Full article

Background/Objectives: High fructose consumption is a significant risk factor for glomerular podocyte injury. This study aimed to identify the underlying mechanism of fructose-induced podocyte injury and explore the protective effect of the natural polyphenol morin. Methods: In vivo, high-fructose-diet-fed rats were used to evaluate podocyte injury through ultrastructural structure analysis, urinary albumin-to-creatinine ratio (UACR), and synaptopodin expression. In vitro, adenosine 5′-monophosphate deaminase (AMPD) expression and activity, mitochondrial function, and glycolytic flux were measured in mouse podocyte clone-5 (MPC5) exposed to 5 mM fructose, with molecular docking and siRNA interference assays validating morin’s regulatory role. Results: High fructose significantly increased AMPD activity in the purine nucleotide cycle (PNC), leading to mitochondrial dysfunction and a compensatory activation of glycolysis in podocytes. Morin effectively mitigated podocyte injury and suppressed the upregulation of AMPD activity, potentially through targeting AMPD2, as evidenced by molecular docking, which demonstrated a strong binding affinity between morin and AMPD2. Similarly, AMPD2 knockdown markedly alleviated mitochondrial impairment and glycolysis activation, confirming the pivotal role of AMPD2 in fructose-induced podocyte injury. In high-fructose-diet-fed rats, morin substantially improved ultrastructural damage, as shown by reduced podocyte foot process effacement, decreased UACR, restored glomerular synaptopodin expression, and suppressed AMPD activity in the renal cortex. Conclusions: Morin alleviated high-fructose-induced podocyte injury by inhibiting AMPD activity in the PNC, highlighting AMPD2 as a potential therapeutic target for podocyte injury caused by high fructose intake. This study provides novel mechanistic insights into how morin counteracts mitochondrial energy disturbance in podocyte injury. Full article

Third-wave cognitive-behavioral therapies (CBT3) have progressively shifted the focus of psychotherapy from symptom reduction to process-based and transdiagnostic mechanisms of change, emphasizing self-identification as a core dimension. Within this evolution, the Self-Identification Program (SIP) represents a conceptual and clinical advancement particularly relevant to mood disorders, where maladaptive self-identification, rumination, and self-judgment play central roles. SIP directly targets dysfunctional self-identification—the reification of transient and maladaptive mental contents as defining features of a self—through a framework integrating the three levels of CBT3: mindfulness (CBT3.1), loving/kindness and compassion (CBT3.2), and deconstructive insight into the nature of a self (CBT3.3). Theoretically, SIP aligns with dimensional psychiatry (AMPD, HiTOP, RDoC) and recent advances in behavioral linguistics (Relational Frame Theory) and psychotherapy (Process-Based Behavioral Therapy). By integrating linguistic, affective, and neuroscientific perspectives, SIP bridges contextual behavioral science and contemplative practice, offering a unified, process-based model of identity transformation. Clinically, SIP extends CBT3 beyond mindfulness and loving/kindness and/or compassion training to specifically address the mechanism by which self-identification becomes a source of suffering—namely, the mistaken identification with an independent and permanent self. In doing so, SIP provides a novel, mechanistically grounded pathway toward enduring change in depressive and bipolar spectrum disorders. Full article

Athletic performance results from complex interactions between genetic and environmental factors. This review compiles and synthesizes available literature on polymorphic genes associated with endurance, power, and strength performance, as well as their links to injury susceptibility and chronic metabolic diseases. Endurance performance is modulated by ACE, PPARGC1A, HFE, UCP2, UCP3, CDKN1A, and PPARA, regulating mitochondrial biogenesis, oxygen utilization, and muscle fiber composition. Power performance involves ACTN3, MCT1, IGF1, AMPD1, AGT, and AGTR2, affecting anaerobic metabolism, lactate clearance, and fast-twitch fiber recruitment. Strength performance is influenced by AR, PPARG, ARK2N, MMS22L, LRPPRC, PHACTR1, and MTHFR, related to androgen signaling, muscle hypertrophy, and recovery. Injury-related genes (COL1A1, COL5A1, IL6, VEGFA, NOG) and metabolic risk genes (FTO, PPARG, ADRB3) further highlight the clinical relevance of genomics. Collectively, these insights support the application of genetic information to personalize training, enhance performance, prevent injuries, and guide exercise interventions to mitigate metabolic disease risk. Full article

300 healthy Chinese perch (Siniperca chuatsi) (34.35 ± 0.47 g) were randomly divided into five groups (P1–P5) fed diets supplemented with 0, 0.2, 0.4, 0.8, and 1.6 g/kg protease for 8 weeks. Compared to P1, protease supplementation significantly up-regulated endogenous pepsinogen genes (pga1 and pgc) and down-regulated the muscle deamination gene ampd. In comparison to P1, the expression level of the hepatic gene ast increased in P2, P3, and P5, while gdh elevated in P2 and P3 (p < 0.05). Compared to P1, the expression of feeding-related gene npy decreased while pomc increased in P2; agrp increased in P3; and pomc and cart decreased in P5, resulting in significant increases in feed intake in P2, P3, and P5 (p < 0.05). Glycolytic genes (gk and pk) and lipid metabolism gene pparα were up-regulated in P2, P3 and P5, while hsl increased in P3 but decreased in P5 (p < 0.05). P5 exhibited significantly improved weight gain rate, specific growth rate, protein efficiency ratio, and protein retention rate, alongside reduced feed conversion ratio compared with P1. Therefore, dietary 1.6 g/kg protease significantly enhances growth, improves feed efficiency, stimulates pepsinogen secretion, and modulates deamination, glycolytic, and lipid metabolism genes in Siniperca chuatsi. Full article

Biologically active peptides can be obtained with various research methods, depending on the starting material, biological activity, and intended use. To use the most efficient method, it is worth combining in silico and in vitro experiments. Among the tools that can support an in silico analysis are databases such as the Antimicrobial Peptide Database (AMPD) or BIOPEP-UWM. The aim of this study was to make an in silico hydrolysis of peptides with anticancer properties selected from the AMP database, using pepsin, trypsin, and chymotrypsin. Most peptides obtained had properties inhibiting ACE and dipeptidyl peptidase IV activity. Among the resulting peptides, those with the sequence AR, CF, ER, TF, IY, ER, AW, GF, TW, SK and IM are potentially resistant to peptidase from microbial action. An analysis of the peptides’ characteristics showed that peptides with the sequence AR, EK, ER and SK are well-soluble in water and have high affinity for protein and ligand binding. Peptides with the sequence TF, IL and PF are unstable. Thermostable peptides are PGL, IL, GL, IY, VF, PL, IM and QL. The results of the study may be used to design in vitro experiments. Full article

Exercise addiction is described in the literature as a compulsive behavior associated with adverse health symptoms. Currently, knowledge about the biological and social factors that trigger the development of this behavior is still lacking, and there are no published studies on genetic variants associated with the disorder. Because of this, we genotyped specific polymorphisms in the genes DRD1 (rs265981), DRD2 (rs1800497), BDNF (rs6265), HFE (rs1799945), ACTN3 (rs1815739), PPARA (rs4253778), PPARGC1A (rs8192678), and AMPD1 (rs17602729) to investigate whether they were associated with exercise addiction. In total, 469 men and women, comprising athletes and non-athletes between the ages of 18 and 50, were enrolled in the study. Each participant provided an oral swab sample for genetic analysis and completed the Negative Addiction Scale questionnaire that tests for physical exercise addiction. For the DRD2 polymorphism, there was a significant association of the GG genotype with asymptomatic participants and of the AA genotype with participants symptomatic for exercise addiction. Additionally, for the BDNF polymorphism, the CC genotype was associated with symptomatic participants, and the T allele was associated with asymptomatic individuals. However, all associations were found by evaluating the SNP individually, and this demonstrates the difficulty in studying variables related to behavioral phenotypes. Full article

The overuse of carbapenems has driven the rise of carbapenem-resistant Pseudomonas aeruginosa (CRPA) and Enterobacterales (CRE), against which ceftazidime–avibactam (CAZ-AVI) offers an alternative treatment. This study phenotypically determined resistance profiles of P. aeruginosa (PA), Escherichia coli (EC), and Klebsiella pneumoniae (KP) clinical isolates to CAZ-AVI and investigated molecular resistance mechanisms genotypically. A total of 394 PA, 90 EC, and 84 KP isolates were collected from the American University of Beirut Medical Center. Antimicrobial susceptibility testing (AST) and whole-genome sequencing (WGS) were performed on 30 isolates per species. Results showed that 100% of KP, 63% of EC, and 100% of PA isolates were carbapenem-resistant. Among these, 73% of KP, 79% of EC, and 60% of PA were CAZ-AVI-resistant. WGS revealed diverse sequence types, plasmids, and antimicrobial resistance genes. Additionally, 100% of KP, 93% of EC, and 89% of PA isolates produced metallo-β-lactamases (MBLs). Mutations in ampD, ampR, and mexR were identified in CAZ-AVI-resistant, non-MBL-producing PA, whereas mutations in ompC, marR, and ampC were detected in CAZ-AVI-resistant, non-MBL-producing EC. While CAZ-AVI remains effective against most CRE and CRPA lacking MBLs, resistance to CAZ-AVI is multifactorial, commonly involving overexpression of efflux pumps and AmpC β-lactamases, loss of porin channels, and the presence of oxacillinases. Full article

APOBEC3B (A3B) has been implicated in host–virus interactions, but its role in SARS-CoV-2 infection is unclear. Here, we demonstrate that A3B is overexpressed in bronchoalveolar lavage fluid (BALF) cells from severe COVID-19 patients compared to those with mild disease. A3B knockdown in Caco-2 cells significantly reduces SARS-CoV-2 infectivity, likely through attenuation of the PKR-mediated integrated stress response, a pathway proposed to promote SARS-CoV-2. Single-cell RNA sequencing (scRNA-seq) data suggest that BALF cells from severe COVID-19 patients exhibit a repressed state for cellular translation, potentially mediated by eIF2α phosphorylation. However, in A549-ACE2 cells, SARS-CoV-2 does not activate PKR, but A3B knockdown still reduces SARS-CoV-2 infectivity, suggesting an alternative mechanism of action in different cellular contexts. To further investigate A3B’s role in severe COVID-19, we employed Geneformer, a transformer-based machine learning model, which predicted that A3B knockout would perturb AMPD2 (adenosine monophosphate deaminase 2), a key enzyme in purine metabolism and immune regulation. We validated this prediction using bulk RNA-seq and clinical scRNA-seq data, confirming that AMPD2 expression is downregulated in severe COVID-19 but restored upon A3B knockdown. Together, these findings suggest that A3B plays a proviral role in SARS-CoV-2 infection by modulating translational control and immune regulatory networks, warranting further studies to elucidate the underlying mechanistic details. Full article

Attachment styles and defense mechanisms are widely recognized as central components in personality development. However, few empirical studies have examined their combined contribution to maladaptive personality traits within the dimensional framework of the DSM-5 Alternative Model for Personality Disorders (AMPD). This study investigated the extent to which adult attachment styles and defense mechanisms predict the five AMPD maladaptive personality domains: negative affectivity, detachment, antagonism, disinhibition, and psychoticism. Data were collected from a community sample of 400 adults (190 males, 47.5%), aged 18 to 69 years (M = 36.96; SD = 11.59). Hierarchical multiple regression analyses were conducted for each maladaptive personality domain to examine the predictive roles of attachment styles and defense mechanisms. Our findings indicate that each maladaptive personality domain is associated with specific configurations of attachment styles and defense mechanisms. In conclusion, the findings suggest the relevance of assessing adult attachment styles and defensive functioning in clinical contexts in order to deepen the understanding of the individuals’ personality profiles. Full article