How does physical activity improve adolescent resilience? Serial indirect effects via self-efficacy and basic psychological needs.

Background: Resilience is vital for improving mental health and well-being during adolescence, which is an important yet vulnerable period. Previous research has indicated that physical activity enhances individual resilience. However, limited studies have examined underlying psychological mechanisms between them. The current study aimed to investigate the effect of physical activity on adolescent resilience via self-efficacy and basic psychological needs. Methods: A cross-sectional survey was conducted with 1,732 high school students aged 16 to 20 years old (mean age: 16.51 ± 0.77 years), with nearly equal number of boys (47.63%) and girls (52.37%). They each completed the Physical Exercise Questionnaire, Basic Psychological Needs in Exercise Scale, General Self-Efficacy Scale, and Resilience Scale, respectively. A serial indirect model was constructed to examine how physical activity influences resilience. Results: Structural equation model analysis revealed that physical activity significantly and directly predicted resilience. When self-efficacy and basic psychological needs were included in the model, both direct and indirect effects were observed. Specifically, the positive relationship between physical activity and resilience was partially mediated by self-efficacy and basic psychological needs. In addition, basic psychological needs and self-efficacy were found to serially mediate the direct relathonship between physical activity and resilience. Conclusions: The present study provides novel theoretical insights into sports psychology by establishing a link between basic psychological needs and self-efficacy. The findings have implications for school administrators and physical education instructors in designing targeted interventions to promote adolescent resilience. These interventions may involve creating supportive environment conductive to fulfilling students' basic psychological needs, implementing strategies to enhance self-efficacy beliefs, and providing opportunities for skill development and mastery experiences in sports and physical activities.

The involvement of ADAR1 in chronic unpredictable stress-induced cognitive impairment by targeting DARPP-32 with miR-874-3p in BALB/c mice.

Introduction: Chronic stress exposure is the main environmental factor leading to cognitive impairment, but the detailed molecular mechanism is still unclear. Adenosine Deaminase acting on double-stranded RNA1(ADAR1) is involved in the occurrence of chronic stress-induced cognitive impairment. In addition, dopamine and Adenosine 3'5'-monophosphate-regulated phospho-protein (DARPP-32) gene variation affects cognitive function. Therefore, we hypothesized that ADAR1 plays a key role in chronic stress-induced cognitive impairment by acting on DARPP-32. Methods: In this study, postnatal 21-day-old male BALB/c mice were exposed to chronic unpredictable stressors. After that, the mice were treated with ADAR1 inducer/inhibitor. The cognitive ability and cerebral DARPP-32 protein expression of BALB/c mice were evaluated. In order to explore the link between ADAR1 and DARPP-32, the effects of ADAR1 high/low expression on DARPP-32 protein expression in vitro were detected. Results: ADAR1 inducer alleviates cognitive impairment and recovers decreased DARPP-32 protein expression of the hippocampus and prefrontal cortex in BALB/c mice with chronic unpredictable stress exposure. In vivo and in vitro studies confirm the results predicted by bio-informatics; that is, ADAR1 affects DARPP-32 expression via miR-874-3p. Discussion: The results in this study demonstrate that ADAR1 affects the expression of DARPP-32 via miR-874-3p, which is involved in the molecular mechanism of pathogenesis in chronic unpredictable stress-induced cognitive impairment. The new findings of this study provide a new therapeutic strategy for the prevention and treatment of stress cognitive impairment from epigenetics.

Identification of Crucial Genes and Key Functions in Type 2 Diabetic Hearts by Bioinformatic Analysis.

Type 2 diabetes (T2D) patients with SARS-CoV-2 infection hospitalized develop an acute cardiovascular syndrome. It is urgent to elucidate underlying mechanisms associated with the acute cardiac injury in T2D hearts. We performed bioinformatic analysis on the expression profiles of public datasets to identify the pathogenic and prognostic genes in T2D hearts. Cardiac RNA-sequencing datasets from db/db or BKS mice (GSE161931) were updated to NCBI-Gene Expression Omnibus (NCBI-GEO), and used for the transcriptomics analyses with public datasets from NCBI-GEO of autopsy heart specimens with COVID-19 (5/6 with T2D, GSE150316), or dead healthy persons (GSE133054). Differentially expressed genes (DEGs) and overlapping homologous DEGs among the three datasets were identified using DESeq2. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes analyses were conducted for event enrichment through clusterProfile. The protein-protein interaction (PPI) network of DEGs was established and visualized by Cytoscape. The transcriptions and functions of crucial genes were further validated in db/db hearts. In total, 542 up-regulated and 485 down-regulated DEGs in mice, and 811 up-regulated and 1399 down-regulated DEGs in human were identified, respectively. There were 74 overlapping homologous DEGs among all datasets. Mitochondria inner membrane and serine-type endopeptidase activity were further identified as the top-10 GO events for overlapping DEGs. Cardiac CAPNS1 (calpain small subunit 1) was the unique crucial gene shared by both enriched events. Its transcriptional level significantly increased in T2D mice, but surprisingly decreased in T2D patients with SARS-CoV-2 infection. PPI network was constructed with 30 interactions in overlapping DEGs, including CAPNS1. The substrates Junctophilin2 (Jp2), Tnni3, and Mybpc3 in cardiac calpain/CAPNS1 pathway showed less transcriptional change, although Capns1 increased in transcription in db/db mice. Instead, cytoplasmic JP2 significantly reduced and its hydrolyzed product JP2NT exhibited nuclear translocation in myocardium. This study suggests CAPNS1 is a crucial gene in T2D hearts. Its transcriptional upregulation leads to calpain/CAPNS1-associated JP2 hydrolysis and JP2NT nuclear translocation. Therefore, attenuated cardiac CAPNS1 transcription in T2D patients with SARS-CoV-2 infection highlights a novel target in adverse prognostics and comprehensive therapy. CAPNS1 can also be explored for the molecular signaling involving the onset, progression and prognostic in T2D patients with SARS-CoV-2 infection.

KCOSS: an ultra-fast k-mer counter for assembled genome analysis.

MOTIVATION: The k-mer frequency in whole genome sequences provides researchers with an insightful perspective on genomic complexity, comparative genomics, metagenomics and phylogeny. The current k-mer counting tools are typically slow, and they require large memory and hard disk for assembled genome analysis. RESULTS: We propose a novel and ultra-fast k-mer counting algorithm, KCOSS, to fulfill k-mer counting mainly for assembled genomes with segmented Bloom filter, lock-free queue, lock-free thread pool and cuckoo hash table. We optimize running time and memory consumption by recycling memory blocks, merging multiple consecutive first-occurrence k-mers into C-read, and writing a set of C-reads to disk asynchronously. KCOSS was comparatively tested with Jellyfish2, CHTKC and KMC3 on seven assembled genomes and three sequencing datasets in running time, memory consumption, and hard disk occupation. The experimental results show that KCOSS counts k-mer with less memory and disk while having a shorter running time on assembled genomes. KCOSS can be used to calculate the k-mer frequency not only for assembled genomes but also for sequencing data. AVAILABILITYAND IMPLEMENTATION: The KCOSS software is implemented in C++. It is freely available on GitHub: https://github.com/kcoss-2021/KCOSS. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

An Effective Knowledge Transfer Approach for Multiobjective Multitasking Optimization.

Multiobjective multitasking optimization (MTO), which is an emerging research topic in the field of evolutionary computation, was recently proposed. MTO aims to solve related multiobjective optimization problems at the same time via evolutionary algorithms. The key to MTO is the knowledge transfer based on sharing solutions across tasks. Notably, positive knowledge transfer has been shown to facilitate superior performance characteristics. However, how to find more valuable transferred solutions for the positive transfer has been scarcely explored. Keeping this in mind, we propose a new algorithm to solve MTO problems. In this article, if a transferred solution is nondominated in its target task, the transfer is positive transfer. Furthermore, neighbors of this positive-transfer solution will be selected as the transferred solutions in the next generation, since they are more likely to achieve the positive transfer. Numerical studies have been conducted on benchmark problems of MTO to verify the effectiveness of the proposed approach. Experimental results indicate that our proposed framework achieves competitive results compared with the state-of-the-art MTO frameworks.

Evaluation of the correlation between infrared thermal imaging-magnetic resonance imaging-pathology of microwave ablation of lesions in rabbit lung tumors.

PURPOSE: This study aimed to evaluate the correlation between infrared thermal imaging-magnetic resonance imaging (MRI)-pathology of microwave ablation (MWA) of lesions in rabbit lung tumors. MATERIALS AND METHODS: MR-guided MWA was performed in nine VX2 tumor-bearing rabbits. Infrared thermal imaging, postoperative MRI, and pathological presentation were obtained and analyzed. The differences between the infrared thermal imaging-MRI-pathology of MWA were compared. RESULTS: The center of the ablated lesion exhibited a high signal on T1-Vibe, and an isointense envelope was observed; the center of the ablated lesion exhibited a low signal on fat-suppressed turbo spin-echo T2-weighted imaging (TSE-T2WI-FS) and bands of high signal surrounding it compared with before MWA. No statistically significant difference existed between the maximum diameter of the central low-signal area of the ablation zone on TSE-T2WI-FS after MWA, the high-signal area of the ablation zone on T1-Vibe after MWA, and the maximum diameter of the pathological coagulation necrosis area, as well as between the maximum diameter of the isointense signal area peripheral to the ablation zone on T1-Vibe after MWA, the high-signal area peripheral to the ablation zone on TSE-T2WI-FS, the maximum diameter at the 41°C isothermal zone on infrared thermal imaging, and the maximum diameter of the pathological thermal injury zone. CONCLUSIONS: MWA of malignant lung tumors had specific MRI characteristics that were comparable with postoperative pathology. Infrared thermal imaging combined with MRI can be used to evaluate the extent of thermal damage to lung VX2 tumors.

Epidermal growth factor promotes stromal cells migration and invasion via up-regulation of hyaluronate synthase 2 and hyaluronan in endometriosis.

OBJECTIVE: To investigate the role(s) of hyaluronan synthase 2 (HAS2) and hyaluronan in disease progression of endometriosis and epidermal growth factor (EGF)-induced motility changes of endometriotic cells. DESIGN: A case-control experimental study and in vitro primary cell culture study. SETTING: University hospital-affiliated research centers. PATIENTS: A total of 21 women with stage I/II endometriosis, 33 women with stage III/IV endometriosis with endometrioma, and 32 women without endometriosis were included in our study. INTERVENTIONS: Serum, eutopic endometrial tissues, and/or ectopic endometriotic tissues were collected. Primary eutopic endometrial stromal cells (EuESCs) and ectopic ovarian endometriotic stromal cells (OvESCs) were isolated and cultured from women with ovarian endometrioma, and then treated with or without EGF. MAIN OUTCOME MEASURES: The concentrations of EGF and hyaluronan in serum were analyzed by enzyme-linked immunosorbent assay. The expressions and localizations of EGF receptor (EGFR), phosphorylated-(p)EGFR, HAS2, and hyaluronan receptor CD44 in tissues were examined by immunohistochemistry. The mRNA and protein levels of HAS2 in EuESCs and OvESCs were examined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot, respectively, and the concentrations of hyaluronan in conditioned medium were examined by enzyme-linked immunosorbent assay (ELISA). Cell motility was evaluated by transwell migration/invasion assays. RESULTS: Serum EGF and hyaluronan concentrations were higher in women with stage III/IV endometriosis than in women with stage I/II or without endometriosis. EGFR, pEGFR, HAS2, and CD44 were immunolocalized in eutopic endometrium and ectopic endometriotic lesions, and the expressions of pEGFR and HAS2 were elevated in ectopic endometriotic lesions compared to eutopic endometrium. Treatment with EGF upregulated HAS2 and hyaluronan expression as well as cell migration and invasion in both EuESCs and OvESCs, and pharmaceutical blocking of EGFR abolished these effects. In addition, knockdown of HAS2 by small interfering RNA attenuated both basal and EGF-induced hyaluronan expression and cell motility changes. Notably, ERK1/2 and AKT signaling pathways were shown to be downstream of EGF in regulating HAS2 and hyaluronan expression as well as cell migration and invasion. CONCLUSION: EGF increased the expression of endometriosis-associated hyaluronan and its synthase HAS2, both of which mediated EGF-induced stromal cell migration and invasion in women with endometriosis.

Upregulation of S100A6 in patients with endometriosis and its role in ectopic endometrial stromal cells.

S100 calcium-binding protein A6 (S100A6) is up-regulated in many malignancies and overexpression of S100A6 has been identified associated with proliferation, migration and invasion phenotype in several cancer cells. In the present study, we explored whether S100A6 plays a role in the development of endometriosis. Significantly higher levels of mRNA and protein expression of S100A6 were observed in ectopic endometrial tissues compared to eutopic and normal endometrial tissues. Silencing of S100A6 in ectopic endometrial stromal cells (ESCs) significantly inhibited cell viability, migration and invasion. Moreover, knockdown of S100A6 suppressed p38/MAPK activity in ectopic ESCs, which can be partially attenuated by CacyBP/SIP phosphorylation inhibitor. In conclusion, our results suggest that the abnormal expression of S100A6 may contribute to the pathogenesis of endometriosis and the S100A6/CacyBP/p38 signaling may provide as a promising treatment target.

7-ketocholesteryl-9-carboxynonanoate enhances ATP binding cassette transporter A1 expression mediated by PPARγ in THP-1 macrophages.

BACKGROUND: ATP binding cassette transporter A1 (ABCA1) is a member of the ATP-binding cassette transporter family. It plays an essential role in mediating the efflux of excess cholesterol. It is known that peroxisome proliferator-activated receptor gamma (PPARγ) promoted ABCA1 expression. We previously found 7-ketocholesteryl-9-carboxynonanoate (oxLig-1) upregulated ABCA1 partially through CD36 mediated signals. In the present study, we intended to test if PPARγ signally is involved in the upregulation mediated by oxLig-1. METHODS AND RESULTS: First, we docked oxLig-1 and the ligand-binding domain (LBD) of PPARγ by using AutoDock 3.05 and subsequently confirmed the binding by ELISA assay. Western blotting analyses showed that oxLig-1 induces liver X receptor alpha (LXRα), PPARγ and consequently ABCA1 expression. Furthermore, oxLig-1 significantly enhanced ApoA-I-mediated cholesterol efflux. Pretreatment with an inhibitor for PPARγ (GW9662) or/and LXRα (GGPP) attenuated oxLig-1-induced ABCA1 expression. Under PPARγ knockdown by using PPARγ-shRNA, oxLig-1-induced ABCA1 expression and cholesterol efflux in THP-1 macrophages was blocked by 62% and 25% respectively. CONCLUSIONS: These observations suggest that oxLig-1 is a novel PPARγ agonist, promoting ApoA-I-mediated cholesterol efflux from THP-1 macrophages by increasing ABCA1 expression via induction of PPARγ.

[The role of matrix metalloproteinases-9 and tissue inhibitor of metalloproteinaes-1 in chronic obstructive pulmonary disease].

OBJECTIVE: To evaluate the role of matrix metalloproteinases-9 (MMP-9) and tissue inhibitor of metalloproteinases-1 (TIMP-1) in the pathogenesis of chronic obstructive pulmonary disease (COPD). METHODS: Five milliliters of peripheral venous blood were extracted form 36 patients with COPD, subdivided into stable group (CS group, n = 12), exacerbation group (CE group, n = 12), and exacerbation group with glucocorticosteroids treatment (CE + G group, n = 12), and 12 normal controls. The peripheral blood mononuclear cells (PBMCs) were isolated and the mRNA expressions of MMP-9 and TIMP-1 therein in each group were measured by RT-PCR quantitative analysis. The MMP-2 and MMP-9 levels in the plasma were studied by gelatin zymography. The relationship between MMP and pulmonary function was evaluated. RESULTS: (1) The MMP-9 mRNA expression and MMP-9: TIMP-1 ratios in the samples obtained from patients with COPD were higher in comparison with those from the control group (all P < 0.05). (2) The MMP-9 levels in plasma were higher in the COPD groups than in the control group (P < 0.05). (3) In the COPD groups, the MMP-9 mRNA expression, MMP-9: TIMP-1 ratio, and MMP-9 level in plasma were negatively correlated with FEV(1.0)% of prediction (r = -0.789, P < 0.05; r = -0.53, P < 0.05; and r = -0.652, P < 0.05), and positively correlated with RV/TLC% (r = 0.375, P < 0.05; r = 0.44, P < 0.05; and r = 0.529, P < 0.05). CONCLUSION: MMP-9 and the imbalanced ratio of MMP-9: TIMP-1 may not only play a role in the pathogenesis of COPD, but also relate to FEV(1.0)% of prediction and RV/TLC%.