Aerobic exercise improves verbal working memory sub-processes in adolescents: behavioral evidence from an N-back task.

Background: Studies on the effects of aerobic exercise on working memory (WM) have mainly concentrated on the overall effects, yet there is little knowledge on how moderate intensity aerobic exercise impacts the sub-processes of verbal WM (VWM) in adolescents. To address this gap, two experiments were conducted to explore the influence of aerobic exercise on the maintenance and updating sub-processes of VWM. Methods: In Experiment 1, a mixed experimental design of 2 (exercise habit: high vs. low) × 3 (memory load: 0-back vs. 1-back vs. 2-back) was used to compare VWM and its sub-processes in 40 adolescents. In Experiment 2, a 2 (group: intervention vs. control) × 3 (time point: pretest vs. 1st post-test vs. 18th post-test) × 3 (memory load: 0-back vs. 1-back vs. 2-back) mixed experimental design was used to investigate the acute and long-term effects of moderate intensity aerobic exercise on VWM and its sub-processes in 24 adolescents with low exercise habits. Results: The results of Experiment 1 showed that VWM performance and its sub-processes in the high exercise habit group were better than those in the low exercise habit group. The results of Experiment 2 showed that the effects of the long-term exercise intervention were superior to those of the acute exercise intervention, and both were superior to the pretest. Meanwhile, it was found that aerobic exercise intervention had a greater effect size on the updating sub-process of VWM. Conclusion: In conclusion, the results indicated that moderate intensity aerobic exercise could enhance the performance of VWM and its sub-processes in adolescents, and long-term intervention showed greater improvement effects compared to acute intervention, especially in the updating sub-process of VWM.

Neural network spectral relationship to improve an inherent optical properties data processing system for residual error correction.

The residual error was a critical indicator to measure the data quality of ocean color products, which allows a user to decide the valuable envisioned application of these data. To effectively remove the residual errors from satellite remote sensing reflectance (Rrs) using the inherent optical data processing system (IDAS), we expressed the residual error spectrum as an exponential plus linear function, and then we developed neural network models to derive the corresponding spectral slope coefficients from satellite Rrs data. Coupled with the neural network models-based spectral relationship, the IDAS algorithm (IDASnn) was more effective than an invariant spectral relationship-based IDAS algorithm (IDAScw) in reducing the effects of residual errors in Rrs on IOPs retrieval for our synthetic, field, and Chinese Ocean Color and Temperature Scanner (COCTS) data. Particularly, due to the improved spectral relationship of the residual errors, the IDASnn algorithm provided more accurate and smoother spatiotemporal ocean color product than the IDAScw algorithm for the open ocean. Furthermore, we could monitor the data quality with the IDASnn algorithm, suggesting that the residual error was exceptionally large for COCTS images with low effective coverage. The product effective coverage should be rigorously controlled, or the residual error should be accurately corrected before temporal and spatial analysis of the COCTS data. Our results suggest that an accurate spectral relationship of residual errors is critical to determine how well the IDAS algorithm corrects for residual error.

Adenosine A2a Receptor Regulates Autophagy Flux and Apoptosis to Alleviate Ischemia-Reperfusion Injury via the cAMP/PKA Signaling Pathway.

Exploring effective methods to lessen myocardial ischemia-reperfusion injury still has positive significance. The adenosine A2a receptor (A2aR) has played a crucial part in cardiac ischemia-reperfusion injury. Previous studies revealed that the adenosine A2a receptor regulated autophagy, but the specific mechanism in myocardial ischemia-reperfusion injury was still unclear. We established an ischemia-reperfusion model (30 min of ischemia and 2 h of reperfusion) in vivo and a model with oxygen-glucose deprivation for 6 h and reoxygenation for 18 h (OGDR) in vitro. The ischemia-reperfusion injury resulted in prolonged QTc interval, left ventricular systolic dysfunction, and myocardial infarction. In vitro model, we found that the OGDR-induced autophagosomes and apoptosis caused myocardial cell death, as evidenced by a significant increase in the generation of lactate dehydrogenase and creatine kinase-MB. Furthermore, overactivated autophagy with rapamycin showed an anti-apoptotic effect. The interaction between autophagy and apoptosis in myocardial ischemia-reperfusion injury was complex and variable. We discovered that the activation of adenosine A2a receptor could promote the expression of Bcl-2 to inhibit the levels of Beclin-1 and LC3II. The number of autophagosomes exceeded that of autolysosomes under OGDR, but the result reversed after A2aR activation. Activated A2aR with its agonist CGS21680 before reperfusion saved cellular survival through anti-apoptosis and anti-autophagy effect, thus improving ventricular contraction disorders, and visibly reducing myocardial infarction size. The myocardial protection of adenosine A2a receptor after ischemia may involve the cAMP-PKA signaling pathway and the interaction of Bcl-2-Beclin-1.

HDAC6 inhibitor ACY-1215 improves neuropathic pain and its comorbidities in rats of peripheral nerve injury by regulating neuroinflammation.

The fact that neuropathic pain (NP) has no effective therapy and is frequently accompanied by psychiatric comorbidities is well established. Aberrant neuroinflammation plays an important role in the development and maintenance of NP. HDAC6 inhibitors have been demonstrated to ameliorate mechanical allodynia brought on by chemotherapy and peripheral nerve damage. However, its pharmacological mechanisms and its effects on NP-related mental disorders have not been fully elucidated. The present study was dedicated to exploring the effects of ACY-1215 (a specific HDAC6 inhibitor) on neuroinflammation and behavioral abnormalities associated with NP. In this work, spinal nerve ligation (SNL) was performed as an NP model on rats. Mechanical allodynia, cognitive impairment, and depressive-like behavior caused by SNL were attenuated by continuous intraperitoneal injection of ACY-1215. Moreover, ACY-1215 administration suppressed SNL-induced neuroinflammatory responses (including microgliosis, the elevation of pro-inflammatory factors IL-1ß and TNF-α) in ligation of the ipsilateral spinal dorsal horn (iSDH), hippocampus (HPC) and prefrontal cortex (PFC). Mechanistically, MyD88-dependent pro-inflammatory pathways (MyD88/NF-κB and MyD88/ERK) were activated in the iSDH following SNL and were inhibited by ACY-1215. Moreover, ACY-1215 enhanced the acetylation modification of MyD88 and inhibited the SNL-induced elevation of MyD88 without affecting its transcription in the iSDH. These findings suggest that pharmacological inhibition of HDAC6 can ameliorate NP and its psychiatric complications through modulating neuroinflammation, in part by blocking the MyD88-mediated pro-inflammatory pathways. The possible mechanism is that ACY-1215 prevents the elevation of MyD88 reactivity by increasing its acetylation level. Notably, neither SNL nor ACY-1215 significantly altered MyD88 expression in HPC and PFC, indicating differentiated pro-inflammatory mechanisms in the supraspinal neural regions.

Valproic acid mitigates spinal nerve ligation-induced neuropathic pain in rats by modulating microglial function and inhibiting neuroinflammatory response.

Spinal inflammation is a pathophysiological state of neuropathic pain (NP). The subsequent microglial activation and neuroinflammatory response are contributing factors for long-lasting behavioral hypersensitivity. Valproic acid (VPA), a histone deacetylase inhibitor, has promising anti-inflammatory and neuroprotective properties for clinical use in the treatment of neurological disorders. However, the underlying mechanisms of its effects on NP have not been determined. This study aimed to clarify the possible mechanisms by which VPA alleviates NP in rat models induced by spinal nerve ligation (SNL). Intraperitoneal injection of VPA (300 mg/kg) efficiently attenuated mechanical allodynia in rats with NP. VPA exerted anti-inflammatory effects by downregulating proinflammatory cytokines (tumor necrosis factor-α, cytokines interleukin-1ß, cytokines interleukin-6; TNF-α, IL-1ß, and IL-6) and upregulating anti-inflammatory cytokines (transforming growth factor-ß, cytokines interleukin-10, cytokines interleukin-4; TGF-ß, IL-10 and IL-4). Additionally, VPA suppressed spinal microgliosis and promoted the polarization of microglia towards the M2 phenotype to further ameliorate spinal neuroinflammation. VPA also exerted neuroprotective effects by decreasing spinal cell apoptosis. The anti-inflammatory and neuroprotective effects may have depended on changes in nuclear histone deacetylase 3 (HDAC3) expression following VPA treatment. Moreover, VPA treatment inhibited nuclear factor-κB (NF-κB) p65 nuclear expression and upregulated acetylated the signal transducer and activator of transcription 1 (STAT1). In addition, VPA suppressed SNL-induced phosphorylation of Janus Kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3). Taken together, our results demonstrate that VPA is a promising anti-inflammatory agent suitable for NP therapy that regulates microglial function and suppresses spinal neuroinflammation via the STAT1/NF-κB and JAK2/STAT3 signaling pathways.