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Antarctic krill (Euphausia superba) is Earth's most abundant wild animal, and its enormous biomass is vital to the Southern Ocean ecosystem. Here, we report a 48.01-Gb chromosome-level Antarctic krill genome, whose large genome size appears to have resulted from inter-genic transposable element expansions. Our assembly reveals the molecular architecture of the Antarctic krill circadian clock and uncovers expanded gene families associated with molting and energy metabolism, providing insights into adaptations to the cold and highly seasonal Antarctic environment. Population-level genome re-sequencing from four geographical sites around the Antarctic continent reveals no clear population structure but highlights natural selection associated with environmental variables. An apparent drastic reduction in krill population size 10 mya and a subsequent rebound 100 thousand years ago coincides with climate change events. Our findings uncover the genomic basis of Antarctic krill adaptations to the Southern Ocean and provide valuable resources for future Antarctic research.
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Euphausiacea , Genoma , Animales , Relojes Circadianos/genética , Ecosistema , Euphausiacea/genética , Euphausiacea/fisiología , Genómica , Análisis de Secuencia de ADN , Elementos Transponibles de ADN , Evolución Biológica , Adaptación FisiológicaRESUMEN
BACKGROUND: Indoor environmental factors, such as pet ownership, presence of cockroaches, mattress quality, fuel usage (gas or electricity), use of biomass for cooking and heating, exposure to tobacco smoke or household molds can significantly affect the sleep quality of children with chronic cough. However, data regarding the effects of indoor environmental conditions on sleep in this population are limited. This study aimed to assess the prevalence of abnormal sleep behaviors and to establish associations between indoor environmental factors and sleep behaviors among children with chronic cough in Wuxi, China. METHODS: A cross-sectional design was employed in this study, involving children aged 3-18 years. Data on sociodemographic factors, allergies, home environmental exposures, and sleep characteristics of the participants were collected using paper-based questionnaires. The association between indoor environmental factors and sleep behaviors in children with chronic cough was analyzed using logistic regression models. RESULTS: The findings demonstrated that the prevalence of chronic cough among children in Wuxi was 15.50%. The chronic cough group exhibited a significantly higher incidence of eczema, wheezing, rhinitis, food allergy, and nasosinusitis than the non-chronic cough group. In addition, children with chronic cough also tended to have a family history of sleep disorders and adenoid hypertrophy (P < 0.01). After adjusting for confounding factors, a significant association was observed between bruxism (teeth grinding) and chronic cough (sometimes: odds ratio [OR] = 1.04; confidence interval [CI] = 1.01-1.08; always: OR = 1.11; CI = 1.04-1.19; P < 0.01). Among children with chronic cough, recent home decoration was associated with sleepwalking (OR = 1.04; CI = 1.00-1.07; P < 0.05), mold exposure was associated with bruxism (OR = 1.15; CI = 1.0-1.31; P < 0.05), and carpet use at home was associated with apnea (OR = 1.09; CI = 1.02-1.17; P < 0.05), twitching during sleep (OR = 1.13; CI = 1.00-1.27; P < 0.01) and morning headache (OR = 1.14; CI = 1.05-1.23; P < 0.01). CONCLUSION: Children with chronic cough are more prone to some abnormal sleep behaviors than children without chronic cough. Household decoration within a year, household mold exposure, and carpet use were all significantly positively associated with abnormal sleep behaviors in children with chronic cough. Our study provides novel insights into the impact of the indoor environment on children's sleep and the occurrence of chronic cough, offering guidance for tailored health promotion programs for families.
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Contaminación del Aire Interior , Tos Crónica , Trastornos del Sueño-Vigilia , Adolescente , Niño , Preescolar , Femenino , Humanos , Masculino , Contaminación del Aire Interior/efectos adversos , China/epidemiología , Tos Crónica/epidemiología , Tos Crónica/etiología , Estudios Transversales , Exposición a Riesgos Ambientales/efectos adversos , Modelos Logísticos , Prevalencia , Factores de Riesgo , Trastornos del Sueño-Vigilia/epidemiología , Trastornos del Sueño-Vigilia/etiologíaRESUMEN
The ancestors of marine mammals once roamed the land and independently committed to an aquatic lifestyle. These macroevolutionary transitions have intrigued scientists for centuries. Here, we generated high-quality genome assemblies of 17 marine mammals (11 cetaceans and six pinnipeds), including eight assemblies at the chromosome level. Incorporating previously published data, we reconstructed the marine mammal phylogeny and population histories and identified numerous idiosyncratic and convergent genomic variations that possibly contributed to the transition from land to water in marine mammal lineages. Genes associated with the formation of blubber (NFIA), vascular development (SEMA3E), and heat production by brown adipose tissue (UCP1) had unique changes that may contribute to marine mammal thermoregulation. We also observed many lineage-specific changes in the marine mammals, including genes associated with deep diving and navigation. Our study advances understanding of the timing, pattern, and molecular changes associated with the evolution of mammalian lineages adapting to aquatic life.
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Adaptación Fisiológica , Evolución Molecular , Genoma , Genómica , Mamíferos/fisiología , Filogenia , Termogénesis/genética , Animales , Factores de Transcripción NFI/genética , Factores de Transcripción NFI/metabolismo , Selección Genética , Semaforinas/genética , Semaforinas/metabolismo , Proteína Desacopladora 1/genética , Proteína Desacopladora 1/metabolismoRESUMEN
As spent batteries can be considered as alternative raw sources of electrode materials; the development of regeneration techniques for spent graphite becomes key to realizing economic and environmental sustainability. Herein, the reutilization of small spent graphite particles is domonstrated due to their special structural characteristics, which may directly contribute to the improvement of lithiation kinetics and high-rate charging during long-term cycling. Such intrinsic defects and external cracked channels may be introduced by the aging of intrinsic bulk structure and exfoliation of surface structure. On account of these potential advantages, a carbonized polypyrrole layer on sieved small graphite particles is developed to obtain superior rate performance. The coated amorphous/graphitic layer could repair the exposed edge and basal plane, and significantly facilitate Li ion diffusion during fast charging. Moreover, the enhanced performance may favor the improved homogeneity of current density distribution during fast charging, which is confirmed by a porous electrode model. The regenerated graphite with a disorder/order coating layer could effectively regulate the Li+ transport channel, exhibiting a high specific capacity at high-rate charging (102.7 mAh g-1 at 4 C after 500 cycles) without severe Li plating. This work provides an opportunity to utilize spent graphite in fast-charging batteries.
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SiOx suspension is regarded as an attractive anolyte for high-energy-density Li-ion slurry flow batteries. However, the poor electronic conductivity and non-negligible volume variation of SiOx greatly hinder its practical applications. Herein, these issues are successfully addressed by rationally designing a trifunctional interface with mixed electron/ion and hard/soft modulated properties on SiOx surface via H-bonding interactions. The interface comprises a lithiated polymer layer (LiPN) interfused with functionalized single-walled carbon nanotubes. Carbon nanotubes work as electrical tentacles to enhance the multiscale electron conduction. The LiPN layer with transferable Li-ions facilitates ion transport. In addition, the LiPN layer employs lithiated rigid polyacrylic acid as a framework to provide mechanical support and soft nafion as a buffer to accommodate volume change, which maintains the structural integrity of SiOx . Hence, SiOx @LiPN/S anolytes exhibit significantly improved rate and cycle performances. Specially, the interface enables the anolytes to load more active particles (30 wt%) or less conductive additives (0.4 wt%). The semi-solid pouch cells based on high-active-content anolytes with stable cyclability are first demonstrated and the flow cell using low-conductive-content anolytes displays a high volumetric capacity of 207 Ah L-1 . This strategy paves a novel approach for optimizing semi-solid electrodes for high-performance Li-ion slurry flow batteries.
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PURPOSE: Allergic rhinitis (AR) is an independent risk factor for sleep disorders in children, including abnormal sleep behaviors. We investigated the occurrence of abnormal sleep behaviors in children with AR to determine indoor environmental risk factors affecting sleep. METHODS: This case-control study collected the sleep status and characteristics of the indoor environment of children aged 3-14 years with and without AR using a questionnaire. The differences between the two groups were compared using the Mann-Whitney U test, chi-square test, and Fisher's exact test. The indoor environmental factors affecting sleep behavior were analyzed using logistic regression analysis. RESULTS: Children with AR (n=427) had a higher probability of snoring (8.7 % vs. 2.9 %; P < 0.001), mouth breathing (14.1 % vs. 5.2 %; P < 0.001), restless sleep (6.6 % vs. 4.1 %; P = 0.047), sleep talking (3.3 % vs. 1.1 %; P = 0.003), and hyperhidrosis (16.4 % vs. 8.5 %; P < 0.001) than those without AR (n=1046). Emulsion wall paint (odds ratio (OR) = 2.779; 95 % confidence interval (CI), 1.332-5.796; P = 0.006) and tobacco exposure in early infancy (OR = 2.065; 95 % CI 1.079-3.950; P = 0.029) were associated with hyperhidrosis. CONCLUSION: Children with AR are more likely to have abnormal sleep behaviors than those without, including snoring, mouth breathing, restless sleep, sleep talking, and hyperhidrosis. Emulsion paint wall and tobacco smoke exposure in early infancy had a twofold higher risk of hyperhidrosis during sleep.
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Hiperhidrosis , Rinitis Alérgica , Trastornos de la Transición Sueño-Vigilia , Estudios de Casos y Controles , Niño , Emulsiones , Humanos , Respiración por la Boca , Factores de Riesgo , Sueño , RonquidoRESUMEN
Between the winter of 2018 and the end of 2019, there has been an epidemic of adenovirus infection in southern China, including Zhejiang Province. The number of children suffering from adenovirus pneumonia (AP) has significantly increased. AP can be accompanied by Mycoplasma pneumoniae in children. This study aimed to investigate the association of M. pneumoniae and identify the risk factors for coinfection on hospitalized patients with AP. The patients were classified into two groups by etiologic analysis (single AP and AP with M. pneumoniae coinfection groups). The clinical manifestations, clinical medication, and laboratory and imaging findings of the two groups were compared and analyzed. The coinfection group (n = 125) had a significantly longer duration of fever than the single AP group (n = 171; P = 0.03). Shortness of breath (P = 0.023) and pulmonary imaging findings, such as pulmonary consolidation, atelectasis, pleural effusion, and multilobe lesions (P < 0.05), were more common in the coinfection group. The patients with coinfection had more severe symptoms, significantly longer hospitalization time and an increased proportion of using glucocorticoids and/or immunoglobulin needing oxygen inhalation (P < 0.05). The incidence of AP with M. pneumoniae coinfection is high. The prolonged fever duration and pulmonary imaging findings could be used as prediction factors to predict M. pneumoniae coinfection in children with AP. Patients with AP coinfected with MP may easily develop severe illness. Hence, a reasonable change in the treatment is necessary.
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Infecciones por Adenoviridae , Coinfección , Neumonía por Mycoplasma , Neumonía Viral , Adenoviridae , Infecciones por Adenoviridae/epidemiología , Niño , Coinfección/epidemiología , Humanos , Mycoplasma pneumoniae , Neumonía por Mycoplasma/epidemiologíaRESUMEN
The aim of this study was to explore the regulating effects of hyperoside (Hyp) on lipid metabolism in high-fat diet mice. The high-fat diet mouse model was established by high-fat diet induction. After 5 weeks of Hyp intragastric administration in high-fat diet mice, the serum lipid levels before and after Hyp administration were measured by the corresponding kits. The tissue structure of mouse liver was observed by HE staining before and after Hyp administration. The changes of intestinal flora and transcriptome were measured by Illumina platforms. Liquid chromatography-mass spectrometry (LC-MS) was used to determine non-targeted metabolites. The results showed that Hyp significantly reduced lipid levels in the high-fat diet mice and effectively restored the external morphology and internal structure of liver tissue. Hyp changed the species composition of the intestinal flora in high-fat diet mice, increased the abundance of beneficial flora such as Ruminococcus, and decreased the abundance of harmful flora such as Sutterella. Combined multi-omics analysis revealed that the effect of retinoic acid on lipid metabolism was significant in the high-fat diet mice treated with Hyp, while the increase of retinoic acid content was significantly negatively correlated with the expression of genes such as cyp1a2 and ugt1a6b, positively correlated with AF12 abundance, and significantly negatively correlated with unidentified_Desulfovibrionaceae abundance. These results suggest that Hyp may modulate the abundance of AF12, unidentified_Desulfovibrionaceae and inhibit the expression of genes such as cyp1a2 and ugt1a6b, thus increasing the content of retinoic acid and regulating lipid metabolism in the high-fat diet mice.
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Dieta Alta en Grasa , Metabolismo de los Lípidos , Animales , Ratones , Dieta Alta en Grasa/efectos adversos , Citocromo P-450 CYP1A2/metabolismo , Citocromo P-450 CYP1A2/farmacología , Multiómica , Hígado , Lípidos/farmacología , Tretinoina/metabolismo , Tretinoina/farmacología , Ratones Endogámicos C57BLRESUMEN
Exercise preconditioning (EP) provides protective effects for acute cardiovascular stress; however, its mechanisms need to be further investigated. Autophagy is a degradation pathway essential for myocardium health. Therefore, we investigated whether intermittent myocardial ischemia-hypoxia affected Beclin1 and whether the changes in autophagy levels contribute to EP-induced early myocardial protective effects. Rats were trained on a treadmill using an EP model (four cycles of 10 minutes of running/10 minutes of rest). Exhaustive exercise (EE) was performed to induce myocardial injury. Cardiac troponin I (cTnI) and ischemia-hypoxia staining were used to evaluate myocardial injury and protection. Double-labeled immunofluorescence staining and western blot analysis were employed to examine related markers. EP attenuated the myocardial ischemic-hypoxic injury induced by EE. Compared with the control (C) group, the dissociations of Beclin1/Bcl-2 ratio and Beclin1 expression were both higher in all other groups. Compared with the C group, PI3KC3 and the LC3-II/LC3-I ratio were higher in all other groups, whereas LC3-II was higher in the EE and EEP + EE groups. p62 was higher in the EE group than in the C group but lower in the EEP + EE group than in the EE group. We concluded that EP increases Beclin1 via intermittent myocardial ischemia-hypoxia and induces autophagy, which exerts early myocardial protective effects and reduces the myocardial ischemic-hypoxic injury induced by exhaustive exercise.
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Beclina-1/metabolismo , Isquemia Miocárdica/prevención & control , Miocardio/metabolismo , Condicionamiento Físico Animal/métodos , Animales , Autofagia , Western Blotting , Modelos Animales de Enfermedad , Masculino , Isquemia Miocárdica/fisiopatología , Miocardio/patología , Ratas , Ratas Sprague-DawleyRESUMEN
BACKGROUND: Sleep-disordered breathing (SDB) is a common syndrome in children, related to their immune responses, cardiovascular function, and neurocognitive function. This study aimed to determine the prevalence of SDB among children in Wuxi, China, and to evaluate the protective and risk factors of SDB in children. METHODS: A cross-sectional study was conducted on children attending different schools across Wuxi, China, aged 3-14 years old. Of a total of 5630 questionnaires distributed to the parents of the children, 3997 (71.0%) were deemed to be valid. The data on the general sociodemographic factors, children's allergy and sleep characteristics, and the parents' sleep characteristics were also collected. The Paediatric Sleep Questionnaire (PSQ) score was used to identify children at high risk of SDB. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated by logistic regression. RESULTS: The prevalence of SDB in this cohort was 13.4% (N = 534). SDB prevalence significantly differed in children with asthma (28.2% vs. 12.8%, P < 0.001), eczema (19.0% vs. 10.0%, P < 0.001), urticaria (16.4% vs. 12.9%, P < 0.01) and rhinitis (21.4% vs. 10.7%, P < 0.001). No significant differences were found in SDB prevalence with respect to pillow material or quilt material. On multivariate logistic regression analysis, asthma (OR 1.986 (95% CI 1.312-3.007), P < 0.01), eczema (OR 1.675 (95% CI 1.377-2.037), P < 0.001), rhinitis (OR 1.998 (95% CI 1.635-2.441), suffered from familial sleep sickness (OR 2.416 (95% CI 1.975-2.955), P < 0.001) and whose mothers slept for a shorter duration (6 h-8 h: OR 1.370 (95% CI 1.089-1.724), P < 0.01; <6 h: OR 3.385(95% CI 2.098-5.461), P < 0.001) increased the odds of having SDB. The incidence of SDB significantly decreased with children's age (6-11 years old: 0R 0.768 (95% CI 0.597-0.989), P < 0.05; 12-14 years old: OR 0.691 (95% CI 0.530-0.901), P < 0.01). CONCLUSION: The results of this study demonstrated that atopic diseases (asthma, eczema, and rhinitis) and family sleep habits were risk factors for SDB in children in Wuxi, China.
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Síndromes de la Apnea del Sueño , Adolescente , Niño , Preescolar , China/epidemiología , Estudios Transversales , Humanos , Prevalencia , Factores de Riesgo , Sueño , Síndromes de la Apnea del Sueño/epidemiología , Síndromes de la Apnea del Sueño/etiología , Encuestas y CuestionariosRESUMEN
Hemocyanin, a multifunctional oxygen-carrying protein, has critical effects on immune defense in crustaceans. To explore the role of hemocyanin in anti-pathogen mechanism, effects of Vibrio harveyi (V. harvey) and Staphyloccocus aureus (S. aureus) on hemocyanin synthesis and innate immune responses were investigated in Litopenaeus vannamei (L. vannamei) during infection in vivo. Results showed that 105 and 106â¯cells mL-1V. harveyi and 106â¯cells mL-1S. aureus significantly affected plasma hemocyanin concentration, hepatopancreas hemocyanin mRNA and subunits expressions, plasma phenol oxidase (PO), hemocyanin-derived PO (Hd-PO), antibacterial, and bacteriolytic activities during the experiment under bacterial stress, while these parameters did not change remarkably in control group. The concentration of hemocyanin in plasma fluctuated, with a minimum at 12â¯h and a maximum at 24â¯h. Moreover, the expression of hemocyanin mRNA peaked at 12â¯h, while the level of hemocyanin p75 and p77 subunits reached maximum at 24â¯h. Besides, plasma PO and Hd-PO activities peaked at 24â¯h, and antimicrobial and bacteriolytic activities peaked at 12â¯h and 24â¯h, respectively. In addition, 105â¯cells mL-1S. aureus had no significant effect on the synthesis of hemocyanin and prophenoloxidase activating (pro-PO) system, but significantly increased antimicrobial activity at 12â¯h and bacteriolytic activity at 24â¯h. Therefore, these results suggest that the hemocyanin synthesis was initiated after invasion of pathogen, and the newly synthesized hemocyanin, acted as an immune molecule, can exerts PO activity to regulate the immune defense in L. vannamei in vivo.
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Hemocianinas/biosíntesis , Inmunidad Innata , Penaeidae/inmunología , Staphylococcus aureus/fisiología , Vibrio/fisiología , Animales , Femenino , Masculino , Penaeidae/microbiología , Distribución AleatoriaRESUMEN
The role of autophagy in the cardioprotection conferred by ischemic preconditioning (IPC) has been well described. This study aimed to investigate the changes in autophagy levels during the cardioprotective effects initiated by exercise preconditioning (EP).Rats were randomly divided into 4 groups: group C (control), group EP, group EE (exhaustive exercise), and group EP + EE (EP pretreatment at 0.5 hours before EE). The EP protocol included 4 periods of 10 minutes of treadmill running each at 30 m/minute with intervening 10 minute periods of rest. Hematoxylin-basic fuchsin-picric acid (HBFP) staining and plasma levels of cardiac troponin I (cTnI) were used to evaluate the ischemia-hypoxia injury in rat myocardium. Alteration levels in several autophagy proteins in the left ventricular myocardium were analyzed by Western blot. The phasic alterations of autophagy levels during EP-initiated cardioprotective phase were also examined.Compared with group C, the ischemia-hypoxia positive areas and IOD value in HBFP-staining and cTnI plasma levels increased significantly in group EE. Compared with group EE, the ischemia-hypoxia injury was markedly attenuated in group EP + EE. Compared with group C, the LC3-II/LC3-I ratio, a marker of autophagosome formation, was reduced in group EE, but the LC3-II/LC3-I ratio remained unaltered in group EP + EE. Furthermore, the LC3-II/LC3-I ratio increased significantly at 2 hours during the cardioprotective phase after EP.These results suggest that the activated autophagy level during the EP-initiated cardioprotective phase may be partly involved in the cardioprotective effects by maintaining a normal autophagy basal level during the subsequent exhaustive exercise in rat myocardium.
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Autofagia/fisiología , Precondicionamiento Isquémico Miocárdico/métodos , Proteínas Asociadas a Microtúbulos/metabolismo , Isquemia Miocárdica , Miocardio/metabolismo , Condicionamiento Físico Animal/fisiología , Animales , Autofagosomas/metabolismo , Vasos Coronarios , Isquemia Miocárdica/metabolismo , Isquemia Miocárdica/fisiopatología , Isquemia Miocárdica/prevención & control , Ratas , Ratas Sprague-Dawley , Troponina I/sangreRESUMEN
High-throughput (HTP) material design is an emerging field and has been proved to be powerful in the prediction of novel functional materials. In this work, an HTP effort has been carried out for thermoelectric chalcogenides with diamond-like structures on the newly established Materials Informatics Platform (MIP). Specifically, the relaxation time is evaluated by a reliable yet efficient method, which greatly improves the accuracy of HTP electrical transport calculations. The results show that all the compounds may have power factors over 10 µW/cm·K2 if fully optimized. A new series of diamond-like chalcogenides with an atomic ratio of 1:2:4 possess relatively higher electrical transport properties among all the compounds investigated. One particular compound, CdIn2Te4, and its variations have been verified experimentally with a peak ZT over 1.0. Further analysis reveals the existence of general conductive networks and the similar Pisarenko relations under the same anion sublattice, and the transport distribution function is found to be a good indicator for the power factors for the compounds investigated. This work demonstrates a successful case study in HTP material screening.
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BACKGROUND: Late exercise preconditioning (LEP) is confirmed to have a protective effect on acute cardiovascular stress. However, the mechanisms by which mitophagy participates in exercise preconditioning (EP)-induced cardioprotection remain unclear. LEP may involve mitophagy mediated by the receptors PARK2 gene-encoded E3 ubiquitin ligase (Parkin) and BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (Bnip3) to scavenge damaged mitochondria. METHODS: Our EP protocol involved four 10-minute periods of running, separated by 10-minute recovery intervals, plus a period of exhaustive running at 24 hours after EP. We assessed this late protective effect by injection of the autophagy inhibitor wortmannin, transmission electron microscopy, laser scanning confocal microscopy, and other molecular biotechnology methods; we simultaneously detected related markers, analyzed the specific relationships between mitophagy proteins, and assessed mitochondrial translocation. RESULTS: Exhaustive exercise (EE) causes serious injuries to cardiomyofibrils, inducing hypoxia-ischemia and changing the ultrastructure. EE fails to clear excessively generated mitochondria to link with LC3 accumulation. After EP, increased autophagy levels at 30 minutes were converted to mitophagy within 24 hours. We found that LEP significantly suppressed EE-induced injuries, which we confirmed by observing decreased levels of the mitochondria-localized proteins COX4/1 and TOM20. LEP to exhaustion caused mitochondrial degradation by increasing the efficiency of LC3-outer mitochondrial membrane translocation in a Parkin-mediated manner, in which activated protein kinase and TOM70 may play both key roles. However, we did not observe mitophagy to be associated with Bnip3 mediation in LEP-induced cardioprotection. However, Bnip3 may play a role in inducing mitochondrial LC3-II increases. Wortmannin had no effect on LC3 translocation; instead, it influenced LC3-I to convert to LC3-II. Thus, suppressing mitophagy led to the attenuation of EP-induced cardioprotection.
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Cardiopatías/prevención & control , Proteínas de la Membrana/metabolismo , Mitocondrias Cardíacas/metabolismo , Proteínas Mitocondriales/metabolismo , Mitofagia , Miocardio/metabolismo , Condicionamiento Físico Animal/métodos , Ubiquitina-Proteína Ligasas/metabolismo , Proteínas Quinasas Activadas por AMP/metabolismo , Animales , Autofagia/efectos de los fármacos , Cardiopatías/genética , Cardiopatías/metabolismo , Cardiopatías/patología , Masculino , Proteínas Asociadas a Microtúbulos/metabolismo , Mitocondrias Cardíacas/efectos de los fármacos , Mitocondrias Cardíacas/ultraestructura , Proteínas del Complejo de Importación de Proteínas Precursoras Mitocondriales , Mitofagia/efectos de los fármacos , Miocardio/ultraestructura , Esfuerzo Físico , Transporte de Proteínas , Ratas Sprague-Dawley , Receptores Citoplasmáticos y Nucleares/metabolismo , Transducción de Señal , Factores de Tiempo , Wortmanina/farmacologíaRESUMEN
The cardiac effects of exercise preconditioning (EP) are well established; however, the mechanisms involving cardiac ATP-sensitive potassium channel (KATP channel) subunits and autophagy are yet to be fully established. The present work aims to investigate the alterations of cardiac KATP channel subunits Kir6.2, SUR2A, and autophagy-related LC3 during the late cardioprotective phase of EP against exhaustive exercise-induced myocardial injury. Rats run on treadmill for four running time intervals, each with 10 minutes running and rest. Exhaustive exercise was performed 24 h after EP. Cardiac biomarkers, cTnI and NT-proBNP, along with the histological stain, were served as indicators of myocardial injury. Cardiac KATP channel subunits Kir6.2 and SUR2A were analyzed in this study, and autophagy was evaluated by LC3. The results revealed that EP reduced the exhaustive exercise-induced high level of serum cTnI and myocardial ischemia/hypoxia; however, it did not reveal any changes in the serum NT-proBNP level or cardiac BNP. Cardiac SUR2A mRNA significantly upregulated during the exhaustive exercise. The high levels of Kir6.2, SUR2A, LC3IIpuncta and LC3II turnover observed after exhaustive exercise were signiï¬cantly mitigated by EP in the late phase. These results suggest that EP alleviates myocardial injury induced by exhaustive exercise through the downregulation of cardiac KATP channels and autophagy.
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Autofagia/fisiología , Hipoxia/metabolismo , Canales KATP/metabolismo , Isquemia Miocárdica/metabolismo , Condicionamiento Físico Animal/efectos adversos , Animales , Cardiotónicos/metabolismo , Masculino , Proteínas Asociadas a Microtúbulos/metabolismo , Isquemia Miocárdica/fisiopatología , Miocitos Cardíacos/metabolismo , Péptido Natriurético Encefálico/sangre , Fragmentos de Péptidos/sangre , Condicionamiento Físico Animal/fisiología , Canales de Potasio de Rectificación Interna/metabolismo , Ratas , Ratas Sprague-Dawley , Receptores de Sulfonilureas/metabolismo , Troponina I/sangreRESUMEN
The atmospheric oxidation mechanism of 2-methylnaphthalene (2-MN) initiated by OH radicals is investigated by using quantum chemistry at BH&HLYP/6-311++G(2df,2p) and ROCBS-QB3 levels and kinetic calculations by transient state theory and unimolecular reaction theory coupled with master equation (RRKM-ME). This reaction is mainly initiated by OH additions, forming adducts Rn (2-MN-n-OH, n = 1-8). The fates of R1 and R3, representing the α- and ß-adducts, are examined. The fates of R1 and R3 are found to be drastically different. In the atmosphere, R1 reacts with O2via O2 addition to the C2 position to form R1-2OO-a/s, which will undergo a bimolecular reaction with the atmospheric NO or unimolecular isomerization via intramolecular H-shifts, of which the latter is found to be dominant and accounts for the formation of dicarbonyl compounds observed in experimental studies. The role of the tricyclic radical intermediates formed from the ring-closure of R1-2OO is rather limited because their formation is endothermic and reversible, being contrary to the important role of the analogous bicyclic radical intermediates in the oxidation of benzenes. On the other hand, the fate of R3 is similar to that of the benzene-OH adduct, and the tricyclic intermediates will play an important role. An oxidation mechanism is proposed based on the theoretical predictions, and the routes for the experimentally observed products are suggested and compared.
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PURPOSE: To examine the role of calcitonin gene-related peptide (CGRP) in cardioprotection of short-term and long-term exercise preconditioning (EP). METHODS: Male Sprague-Dawley rats were, respectively, subjected to continuous intermittent treadmill training 3 days or 3 weeks as short-term or long-term EP protocols. The myocardial injury induced by isoproterenol (ISO) was performed 24 hours after short-term and long-term EP. The myocardial injury was evaluated in terms of the serum cardiac troponin levels and the hematoxylin-basic fuchsin-picric acid staining. Additionally, serum CGRP levels, CGRP expression in the dorsal root ganglion (DRG), and heart were analyzed as possible mechanisms to explain short-term and long-term EP-induced cardioprotection. RESULTS: Both short-term and long-term EP markedly attenuated the isoproterenol-induced myocardial ischemia with lower serum cardiac troponin levels. Short-term EP does not alter serum CGRP levels and CGRP expression in the DRG and heart. Long-term EP significantly increases serum CGRP levels and CGRP expression in the DRG and heart. CONCLUSIONS: The results indicate that short-term EP does not increase the synthesis and release of CGRP. Therefore, the cardioprotective effect of short-term EP does not involve CGRP adaptation. Furthermore, long-term EP increases CGRP synthesis in the DRG and promotes CGRP release in the blood and heart. Hence, CGRP may play an important role in the cardioprotective effect of long-term EP.
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Péptido Relacionado con Gen de Calcitonina/metabolismo , Precondicionamiento Isquémico Miocárdico/métodos , Isquemia Miocárdica/prevención & control , Condicionamiento Físico Animal/fisiología , Animales , Péptido Relacionado con Gen de Calcitonina/sangre , Péptido Relacionado con Gen de Calcitonina/genética , Isoproterenol/toxicidad , Masculino , Ratas , Ratas Sprague-Dawley , Factores de Tiempo , Troponina/sangreRESUMEN
BACKGROUND: Exercise preconditioning (EP) can provide powerful protection to the heart. Evidence supports the contention that EP directly enhances myocardial tolerance to ischaemia through a protein kinase C (PKC)-mediated mechanism. However, studies investigating the role of isoform-specific PKC after EP are lacking. METHODS AND RESULTS: In this study, a male Sprague-Dawley rat model of EP was established (4 periods of 30 m/min for 10 min exercise then a 10 min rest at 0% grade treadmill exercise). Rats were subjected to exhaustive exercise to induce myocardial injury. Chelerythrine (5 mg/kg) was injected before EP to investigate the role of PKC in EP. EP was found to attenuate exhaustive exercise-induced myocardial injury in both of EP's 2 protective phases, especially the latter phase. After EP, PKCε was markedly upregulated, and PKCε was translocated to myocardial intercalated disks, and p-PKCε(Ser729) was translocated to the myocardial cytomembrane. Even though PKCε was markedly upregulated and translocated to intercalated disks during exhaustive exercise, p-PKCε(Ser729) was mainly distributed in the cytoplasm. A chelerythrine injection before EP did not suppress the activation of PKC and the protection of EP. CONCLUSIONS: These results indicate that PKCε plays an important role in EP-mediated protection of the myocardium during exhaustive exercise-induced myocardial injury, and that a chelerythrine injection during exercise is not suitable for demonstrating the role of PKCε.
Asunto(s)
Isquemia Miocárdica/prevención & control , Miocardio/enzimología , Condicionamiento Físico Animal , Proteína Quinasa C-epsilon/metabolismo , Animales , Antineoplásicos/farmacología , Benzofenantridinas/farmacología , Citoplasma/enzimología , Citoplasma/patología , Activación Enzimática/efectos de los fármacos , Masculino , Isquemia Miocárdica/enzimología , Isquemia Miocárdica/patología , Miocardio/patología , Transporte de Proteínas/efectos de los fármacos , Ratas , Ratas Sprague-DawleyRESUMEN
The atmospheric oxidation mechanism of m-xylene (mX) initiated by the OH radical is investigated at M06-2X and ROCBS-QB3 levels, coupled with reaction kinetics calculations by using transition state theory and unimolecular RRKM-ME theory. The calculations show that the reaction between OH and mX is dominated by OH addition to the C2 and C4 positions, forming adducts mX-2-OH (R2) and mX-4-OH (R4). In the atmosphere, R2 and R4 react with O2 by irreversible H-abstraction to dimethylphenols or by reversible additions to bicyclic radical intermediates, which would recombine again with O2 to form bicyclic peroxy radicals, to bicyclic alkoxyl radicals by reacting with NO or HO2, and eventually to final products such as glyoxal, methylglyoxal, and their coproducts. The effects of reaction pressure and temperature are explored by RRKM-ME calculations. A mechanism at 298 K is proposed on the basis of current predictions and previous experimental and modeling results. The predicted product yields support the values in the SAPRC mechanism, even though the predicted yield of 1.0% for glyoxal is lower than the value of â¼11% from the experimental measurements.
RESUMEN
The atmospheric oxidation mechanism of toluene initiated by OH radical addition is investigated by quantum chemistry calculations at M06-2X, G3MP2-RAD, and ROCBS-QB3 levels and by kinetics calculation by using transition state theory and unimolecular reaction theory coupled with master equation (RRKM-ME). The predicted branching ratios are 0.15, 0.59, 0.05, and 0.14 for OH additions to ipso, ortho, meta, and para positions (forming R1-R4 adducts), respectively. The fate of R2, R4, and R1 is investigated in detail. In the atmosphere, R2 reacts with O2 either by irreversible H-abstraction to form o-cresol (36%), or by reversible recombination to R2-1OO-syn and R2-3OO-syn, which subsequently cyclize to bicyclic radical R2-13OO-syn (64%). Similarly, R4 reacts with O2 with branching ratios of 61% for p-cresol and 39% for R4-35OO-syn, while reaction of R1 and O2 leads to R1-26OO-syn. RRKM-ME calculations show that the reactions of R2/R4 with O2 have reached their high-pressure limits at 760 Torr and the formation of R2-16O-3O-s is only important at low pressure, i.e., 5.4% at 100 Torr. The bicyclic radicals (R2-13OO-syn, R4-35OO-syn, and R1-26OO-syn) will recombine with O2 to produce bicyclic alkoxy radicals after reacting with NO. The bicyclic alkoxy radicals would break the ring to form products methylglyoxal/glyoxal (MGLY/GLY) and their corresponding coproducts butenedial/methyl-substituted butenedial as proposed in earlier studies. However, a new reaction pathway is found for the bicyclic alkoxy radicals, leading to products MGLY/GLY and 2,3-epoxybutandial/2-methyl-2,3-epoxybutandial. A new mechanism is proposed for the atmospheric oxidation mechanism of toluene based on current theoretical and previous theoretical and experimental results. The new mechanism predicts much lower yield of GLY and much higher yield of butenedial than other atmospheric models and recent experimental measurements. The new mechanism calls for detection of proposed products 2,3-epoxybutandial and 2-methyl-2,3-epoxybutandial.