How breaking a sweat affects mood: The mediating role of self-efficacy between physical exercise and emotion regulation ability.

OBJECTIVE: This study investigates the association between physical exercise and emotion regulation abilities among college students, introducing self-efficacy as a mediating variable to analyze the pathway mechanism through which physical exercise affects emotion regulation abilities. METHODS: A cross-sectional study design was employed, utilizing a stratified random sampling method to survey three colleges in Jiangsu Province, China. Physical Activity Rating Scale, Physical Activity Self-efficacy Scale, and Emotional Intelligence Scale were used to measure the college student population. Regression analysis and mediation tests assessed whether self-efficacy mediates the relationship between physical exercise and college students' emotion regulation abilities. A total of 5,430 valid questionnaires were collected. RESULTS: The distribution of college students' physical activities was 77.0% for low, 13.1% for medium, and 9.3% for high levels. Physical activities were significantly and positively correlated with self-efficacy and emotional management abilities (r = 0.298,0.105;P<0.01), and self-efficacy was significantly and positively correlated with emotional management abilities (r = 0.322, P<0.01). Situational motivation and subjective support under self-efficacy were 0.08 and 0.255, respectively, and the adjusted R2 was 0.107. Self-efficacy played a fully mediating role between physical activities and emotional management abilities, with a total effect value of 0.032. The values of the direct and indirect effects were 0.003 and 0.029, accounting for 8.95% and 90.74% of the total effect, respectively. CONCLUSION: The physical exercise behavior of college students is primarily characterized by low intensity. Physical exercise among college students can positively predict their ability to regulate emotions. Self-efficacy fully mediates the relationship between physical exercise and emotion regulation ability among college students. College students can indirectly influence their ability to regulate emotions through physical exercise and self-efficacy.

Influence of physical exercise on negative emotions in college students: chain mediating role of sleep quality and self-rated health.

Background: Negative emotions in college students are a significant factor affecting mental health, with suicide behaviors caused by negative emotions showing an annual increasing trend. Existing studies suggest that physical exercise is essential to alleviate negative feelings, yet the intrinsic mechanisms by which it affects negative emotions have not been fully revealed. Objective: Negative emotions in college students represent a significant issue affecting mental health. This study investigates the relationship between physical exercise and negative emotions among college students, incorporating sleep quality and self-rated health (SRH) as mediators to analyze the pathway mechanism of how physical exercise affects students' negative emotions. Methods: A cross-sectional study design was utilized, employing online questionnaires for investigation. The scales included the Physical Activity Rating Scale-3 (PARS-3), the Depression Anxiety Stress Scales-21 (DASS-21), the Pittsburgh Sleep Quality Index (PSQI), and the 12-Item Short Form Health Survey (SF-12), resulting in the collection of 30,475 valid questionnaires, with a validity rate of 91%. Chain mediation tests and Bootstrap methods were applied for effect analysis. Results: The proportions of university students engaged in low, medium, and high levels of physical exercise were 77.6, 13.1, and 9.3%, respectively. The proportions of students experiencing "very severe" levels of stress, anxiety, and depression were 4.5, 10.9, and 3.6%, respectively. Physical exercise was significantly positively correlated with self-rated health (r = 0.194, p < 0.01), significantly negatively correlated with sleep quality (r = -0.035, p < 0.01), and significantly negatively correlated with stress, anxiety, and depression (r = -0.03, p < 0.01; r = -0.058, p < 0.01; r = -0.055, p < 0.01). Sleep quality was significantly negatively correlated with self-rated health (r = -0.242, p < 0.01). Mediation effect testing indicated that sleep quality and self-rated health partially mediated the relationship between physical exercise and negative emotions, with total effect, total direct effect, and total indirect effect values of -1.702, -0.426, and - 1.277, respectively. Conclusion: College students primarily engage in low-intensity physical activity. Sleep quality and self-rated health mediate the impact of physical exercise on students' negative emotions. A certain level of physical activity can directly affect students' emotional states and indirectly influence their negative emotions via sleep and self-rated health. Regular engagement in physical activities primarily positively impacts emotional states by enhancing mood stability and overall emotional resilience.

HCP5, as the sponge of miR-1291, facilitates AML cell proliferation and restrains apoptosis via increasing PIK3R5 expression.

BACKGROUND: Acute myeloid leukemia (AML) is recognized as a hematological neoplasm with heterogenetic cytology and short-term outcome. HCP5 has been proven to be related with the pathogenesis of AML. However, the underlying mechanism of HCP5 in AML remains unclear. METHODS: Clinical profiles of AML patients were downloaded from TCGA and GTEx databases. LncBase and TargetScan online tools were utilized to predict potential targets, and dual-luciferase reporter assay was performed to verify the association between miR-1291 and HCP5 or PIK3R5. Cell Counting Kit 8 and flow cytometry tests were implemented to evaluate the effects of HCP5/miR-1291/PIK3R5 axis in AML cells. Quantitative RT-PCR and Western blot were conducted to detect the expression levels of genes. RESULTS: HCP5 and PIK3R5 were significantly increased in AML tissue samples compared with healthy controls. HCP5 facilitated AML cells viability and inhibited apoptosis. There was a positive relationship between HCP5 and PIK3R5, but miR-1291 negatively regulated PIK3R5. Overexpression of PIK3R5 enhanced the promoting effect of HCP5 in the development of AML, while weakened the suppression of miR-1291 to AML progression. CONCLUSION: Our findings manifested that HCP5 was remarkably upregulated in AML and upregulated HCP5 promoted the malignant behaviors of AML cells by mediating miR-1291/PIK3R5 axis, which would provide a new insight for the treatment of AML.

[Progress of enzyme in mitochondrial DNA repair system].

Mitochondrial DNA (mtDNA) encodes subunits of the mitochondrial electron transport system and the rRNAs and tRNAs required for constructing the mitochondrial translational machinery. Each subunit encoded by mtDNA is essential for normal oxidative phosphorylation. Thus, integrity of the mtDNA is crucial for the survival of organisms. It has long been held that there is no DNA repair in mitochondria. But in recent years,a number of repair factors have been found in mitochondrial extracts, suggesting the presence of DNA repair in mitochondria. This review summarized recent progress of enzyme in mitochondrial DNA repair processes.

Detection of mitochondrial DNA deletion by a modified PCR method in a 60Co radiation-exposed patient.

A new PCR based method was developed to detect deleted mitochondrial DNA (mtDNA). Peripheral blood cell DNA was obtained from a victim who was accidently exposed to a 60Co radiation source in 1990. Using the DNA as template, first PCR was performed to generate multiple products including true deletions and artifacts. The full length product was recovered and used as template of secondary PCR. The suspicious deletion product of mtDNA could be confirmed only if it was yielded by first PCR. Using either original primers or their nested primers, the suspicious deletion product was amplified and authenticated as a true deletion product. The template was recovered and determined to be a deletion by sequencing directly. The results show that a new mtDNA deletion, which spans 889 bp from nt 11688 to nt 12576, was detected in the peripheral blood cells of the victim. It indicates that this new PCR-based method was more efficient at detecting small populations of mtDNA deletion than other routine methods. MtDNA deletion was found in the victim, suggesting the relationship between the deletion and phenotypes of the disease.

Search for difference in aminoacylation of mitochondrial DNA-encoded wild-type and mutant human tRNALeu (UUR).

The pathogenetic mechanism of the most extensively investigated A3243G mutated tRNALeu(UUR) gene, which causes the MELAS encephalomyopathy, maternally inherited diabetes, or chronic progressive external ophlthalmoplegia, is still unresolved, despite the numerous investigations on the topic. Previous evidences presented in published work suggested that the mitochondrial DNA harboring A3243G mutation result decreases in the rates of mitochondrial protein synthesis. To search for differences in aminoacylation of mitochondrial DNA-encoded wild-type and mutant human tRNALeu(UUR), we have expressed and purified the two kinds of tRNAsLeu(UUR), and have expressed human mitochondrial leucyl-tRNA synthetase for in vitro assays of aminoacylation of wild-type and mutant human tRNALeu(UUR). The results indicate human mitochondrial tRNALeu(UUR) gene A3243G point mutant can remarkably reduce its aminoacylation, suggesting it could be one of the mechanisms that the mutation can produce in such clinical phenotypes.

[Effects of A3243G point mutation on aminoacylation of human mitochondrial tRNALeu(UUR)].

The wild-type and mutant-type human mitochondrial tRNALeu(UUR) genes were synthesized and transcribed in vitro with T7 RNA polymerase. The kinetic parameters of human mitochondrial leucyl-tRNA synthetase(mtLeuRS) were determined with wild-type and mutant-type human mitochondrial tRNALeu(UUR) respectively. The results show that the value of Km/Kcat of mtLeuRS for the mutant-type tRNALeu(UUR) is 63.9% as compared with the wild-type. Human mitochondrial tRNALeu(UUR) gene A3243G point mutant can remarkably reduce it's aminoacylation activity, suggesting it would be one of the mechanisms that the mutation could produce such clinical phenotypes.