The association between sleep deprivation and the risk of cardiovascular diseases: A systematic meta­analysis.

Globally, sleep deprivation is a concerning health issue associated with an increased risk of cardiovascular diseases (CVDs). The present study aimed to explore the association between short-term sleep and the risk of CVDs, taking into consideration sex and age groups. A comprehensive review was conducted by assembling cohort studies that are available in the PubMed, Cochrane Library, and Embase databases. Individuals with ≤5 or ≤6 h of sleep per day were considered as sleep-deprived subjects. To minimize potential bias, two reviewers thoroughly evaluated the selected articles. Relevant data were extracted, and pooled odds ratios (ORs) or relative risks (RRs) were calculated using a random-effects model. In total, 18 cohort studies involving adult subjects were included in the present analysis. The pooled results strongly indicated that sleep deprivation was associated with a greater risk of CVDs [RR: 1.09, 95% confidence interval (CI): 1.02-1.16, P=0.009]. However, when the pooled analysis was stratified by sex and age, the following results were observed: short-term sleep women (RR: 1.06, 95% CI: 0.96-1.17, P=0.27), short-term sleep men (RR: 1.07, 95% CI: 0.97-1.17, P=0.17); ≥18 years-old sleep-deprived population (RR: 1.09, 95% CI: 1.00-1.17, P=0.04), ≥40 years-old sleep-deprived population (RR: 1.09, 95% CI: 0.98-1.22, P=0.11), and subjects with co-existing diseases, such as diabetes and hyperlipidemia (RR: 1.06, 95% CI: 0.94-1.20, P=0.32). In conclusion, short-term sleep is associated with the increased risk of CVDs. Among subjects who were aged ≥18 years-old, there was a strong association with the development of CVDs compared with those who were aged ≥40 years-old. Furthermore, men were at a higher risk of CVDs than women. Adequate sleep (7-8 h per day) may play a role in improving cardiac health. The results of the present study may provide valuable support for further research in public health, highlighting the correlation between sleep deprivation and the risk of CVDs.

Channel power equalization based on joint optimization of EDFA and ROADM configuration in open optical network.

Deterioration of the signal-to-noise ratio (SNR) is an important challenge in ultra-long multi optical line system (OLS) optical transmission systems. The non-uniform gain and cascading of the Erbium-doped fiber amplifier (EDFA) lead to SNR deterioration in transmission systems. In this paper, we propose two channel power equalization methods based on joint optimization of EDFA and Reconfigurable optical add-drop multiplexer (ROADM) configurations: 1) reinforcement learning (RL)-based channel power equalization (RL-PE) and 2) covariance matrix adaptive evolution strategy (CMA-ES) channel power equalization (CMA-PE). The simulation results indicate that the power equalization effect was improved by 1.9 dB through the CMA-PE method, while the RL-PE method led to a 1.5 dB improvement in an ultra-long 80-channel 7-OLS transmission system.

Detecting Key Factors of Grasshopper Occurrence in Typical Steppe and Meadow Steppe by Integrating Machine Learning Model and Remote Sensing Data.

Grasshoppers mainly threaten natural grassland vegetation and crops. Therefore, it is of great significance to understand the relationship between environmental factors and grasshopper occurrence. This paper studies the spatial distribution and key factors of grasshopper occurrence in two grass types by integrating a machine learning model (Maxent) and remote sensing data within the major grasshopper occurrence areas of Inner Mongolia, China. The modelling results demonstrate that the typical steppe has larger suitable area and more proportion for grasshopper living than meadow steppe. The soil type, above biomass, altitude and temperature mainly determine the grasshopper occurrence in typical steppe and meadow steppe. However, the contribution of these factors in the two grass types is significantly different. In addition, related vegetation and meteorological factors affect the different growing stages of grasshoppers between the two grass types. This study clearly defines the different effects of key environmental factors (meteorology, vegetation, soil and topography) for grasshopper occurrence in typical steppe and meadow steppe. It also provides a methodology to guide early warning and precautions for grasshopper pest prevention. The findings of this study will be helpful for future management measures, to ensure grass ecological environment security and the sustainable development of grassland.

Circular RNA circRNF169 functions as a miR-30c-5p sponge to promote cellular senescence.

Circular RNAs (circRNAs), characterized as single-stranded closed circular RNA molecules, have been established to exert pivotal functions in various biological or pathological processes. Nonetheless, the effects and underlying mechanisms concerning circRNAs on the aging and aging-related diseases remain elusive. We herein compared the expression patterns of circRNAs in young and senescent mouse embryonic fibroblasts (MEFs), and uncovered that circRNF169 was dramatically up-regulated in senescent MEFs compared with that in young MEFs. Therefore, we further digged into the role and potential mechanisms of circRNF169 in the senescence of MEFs. The results of senescence-associate-ß-galactosidase staining and BrdU incorporation assay showed that silencing of circRNF169 significantly delayed MEFs senescence and promoted cell proliferation, while ectopic expression of circRNF169 exhibited the opposite effects. Moreover, the dual-luciferase reporter assay confirmed that circRNF169 acted as an endogenous miR-30c-5p sponge, which accelerated cellular senescence by sequestering and inhibiting miR-30c-5p activity. Taken together, our results suggested that circRNF169 exerted a crucial role in cellular senescence through sponging miR-30c-5p and represented a promising target for aging intervention.

Rapid Test Method for Multi-Beam Profile of Phased Array Antennas.

The measurement of the phased array antenna (PAA) is completely different from the traditional antenna, due to its multi beam patterns. Usually, each beam pattern of the PAA needs a separate measurement, which makes the overall time extremely long. Thus, the traditional method can no longer meet the efficiency and cost requirements of new PAA measurement. In this paper, a pattern reconstruction method is proposed which significantly reduce the measurement time of multi-beam PAAs. With the known array element patterns (AEP) and theoretical weighted port excitation of the beams, any beam pattern can be predicted by measuring only a certain beam pattern, due to the element excitation coefficient (including the matching, mutual coupling, and manufacturing factors, etc.) of the specific PAA being calculated. The approach has low reconstruction error in term of beam pointing accuracy, side lobe, and co-polar and cross-polar patterns while being validated for large scanning range. Through theoretical derivation and experiments, the effectiveness of the method is verified, and the testing efficiency of the phased array antenna can be improved by 10 times or even more.

Metabolomics Analysis of Hippocampus and Cortex in a Rat Model of Traumatic Brain Injury in the Subacute Phase.

Traumatic brain injury (TBI) is a complex and serious disease as its multifaceted pathophysiological mechanisms remain vague. The molecular changes of hippocampal and cortical dysfunction in the process of TBI are poorly understood, especially their chronic effects on metabolic profiles. Here we utilize metabolomics-based liquid chromatography coupled with tandem mass spectrometry coupled with bioinformatics method to assess the perturbation of brain metabolism in rat hippocampus and cortex on day 7. The results revealed a signature panel which consisted of 13 identified metabolites to facilitate targeted interventions for subacute TBI discrimination. Purine metabolism change in cortical tissue and taurine and hypotaurine metabolism change in hippocampal tissue were detected. Furthermore, the associations between the metabolite markers and the perturbed pathways were analyzed based on databases: 64 enzyme and one pathway were evolved in TBI. The findings represented significant profiling changes and provided unique metabolite-protein information in a rat model of TBI following the subacute phase. This study may inspire scientists and doctors to further their studies and provide potential therapy targets for clinical interventions.

Cd exposure-induced growth retardation involves in energy metabolism disorder of midgut tissues in the gypsy moth larvae.

Cadmium, a common environmental contaminant in both terrestrial and aquatic ecosystems, presented a serious hazard to growth and development of phytophagous insects. For better understanding the toxicology of Cd exposure on phytophagous insects, the physiological and molecular mechanisms underlying the energy metabolism disorder in midgut tissue of gypsy moth larvae fed on Cd-amended artificial diets (3.248 or 44.473 mg Cd/kg fresh food) were investigated. Our results showed that compared with control, Cd exposure at both two levels triggered detriment effects on growth indexes, and with the increase of exposure concentrations, the adverse effects were significantly exacerbated. Larval growth and nutritional indexes (except approximate digestibility) showed a strong positive correlation, indicating that growth retardation in the gypsy moth larvae under Cd stress was tightly related to the food utilization. The key genes at mRNA level in glycolysis/gluconeogenesis, citrate cycle pathway and starch/sucrose metabolism pathway also presented a significant and positive correlation with growth indexes, once again demonstrating that energy metabolism was the key factor that controls the growth and development of the gypsy moth larvae under Cd stress. Antioxidant system collapse and oxidative damage, a chief cause of histopathological alterations in midgut tissue, consist of the physiological basis of energy metabolism disorder in Cd-treated gypsy moth larvae. Together, these results suggest that histopathological alterations or oxidative damage of tissue structure significant disturbed physiological functions of midgut tissue in gypsy moth larvae exposed to Cd stress, as reflected via food utilization or energy metabolism disorder, and eventually resulted in larval growth retardation.

Effects of prior anterior cruciate ligament reconstruction on clinical outcomes associated with total knee arthroplasty: A protocol of retrospective analysis.

BACKGROUND: The argument on the clinical effects of previous anterior cruciate ligament (ACL) reconstruction on total knee arthroplasty (TKA) remains to be resolved. The aim of the current study was to compare operative and postoperative outcomes of patients undergoing TKA after ACL reconstruction with a matched cohort of control subjects having primary osteoarthritis and no history of ligament reconstruction. METHODS: This study was performed and reported in accordance with the Strengthening the Reporting of Observational studies in Epidemiology checklist. The institutional review board approval of our hospital was obtained for the study. The ACL and control groups were matched 1:1 using a caliper width of 0.1 for the propensity score through nearest neighbor matching. Written informed consent was obtained from all subjects participating in the trial. The primary outcome measure was postoperative complications. Secondary outcome measures included operative time, tourniquet time, intraoperative complications, Oxford Knee Score, range of motion, and Western Ontario and McMaster Universities index. RESULTS: This study had limited inclusion and exclusion criteria and a well-controlled intervention. We hypothesized that prior ACL reconstruction had a negative impact on the operative and postoperative outcomes of TKA. TRIAL REGISTRATION: This study protocol was registered in Research Registry (researchregistry5598).

Proteomics Analysis of Brain Tissue in a Rat Model of Ischemic Stroke in the Acute Phase.

Background: Stroke is a leading health issue, with high morbidity and mortality rates worldwide. Of all strokes, approximately 80% of cases are ischemic stroke (IS). However, the underlying mechanisms of the occurrence of acute IS remain poorly understood because of heterogeneous and multiple factors. More potential biomarkers are urgently needed to reveal the deeper pathogenesis of IS. Methods: We identified potential biomarkers in rat brain tissues of IS using an iTRAQ labeling approach coupled with LC-MS/MS. Furthermore, bioinformatrics analyses including GO, KEGG, DAVID, and Cytoscape were used to present proteomic profiles and to explore the disease mechanisms. Additionally, Western blotting for target proteins was conducted for further verification. Results: We identified 4,578 proteins using the iTRAQ-based proteomics method. Of these proteins, 282 differentiated proteins, comprising 73 upregulated and 209 downregulated proteins, were observed. Further bioinformatics analysis suggested that the candidate proteins were mainly involved in energy liberation, intracellular protein transport, and synaptic plasticity regulation during the acute period. KEGG pathway enrichment analysis indicated a series of representative pathological pathways, including energy metabolite, long-term potentiation (LTP), and neurodegenerative disease-related pathways. Moreover, Western blotting confirmed the associated candidate proteins, which refer to oxidative responses and synaptic plasticity. Conclusions: Our findings highlight the identification of candidate protein biomarkers and provide insight into the biological processes involved in acute IS.

Metabolomics analysis of the hippocampus in a rat model of traumatic brain injury during the acute phase.

BACKGROUND: Traumatic brain injury (TBI) has increased in rank among traumatic injuries worldwide. Traumatic brain injury is a serious obstacle given that its complex pathology represents a long-term process. Recently, systems biology strategies such as metabolomics to investigate the multifactorial nature of TBI have facilitated attempts to find biomarkers and probe molecular pathways for its diagnosis and therapy. METHODS: This study included a group of 20 rats with controlled cortical impact and a group of 20 sham rats. We utilized mNSS tests to investigate neurological metabolic impairments on day 1 and day 3. Furthermore, we applied metabolomics and bioinformatics to determine the metabolic perturbation caused by TBI during the acute period in the hippocampus tissue of controlled cortical impact (CCI) rats. Notably, TBI-protein-metabolite subnetworks identified from a database were assessed for associations between metabolites and TBI by the dysregulation of related enzymes and transporters. RESULTS: Our results identified 7 and 8 biomarkers on day 1 and day 3, respectively. Additionally, related pathway disorders showed effects on arginine and proline metabolism as well as taurine and hypotaurine metabolism on day 3 in acute TBI. Furthermore, according to metabolite-protein database searches, 25 metabolite-protein pairs were established as causally associated with TBI. Further, bioinformation indicated that these TBI-associated proteins mainly take part in 5'-nucleotidase activity and carboxylic acid transmembrane transport. In addition, interweaved networks were constructed to show that the development of TBI might be affected by metabolite-related proteins and their protein pathways. CONCLUSION: The overall results show that acute TBI is susceptible to metabolic disorders, and the joint metabolite-protein network analysis provides a favorable prediction of TBI pathogenesis mechanisms in the brain. The signatures in the hippocampus might be promising for the development of biomarkers and pathways relevant to acute TBI and could further guide testable predictions of the underlying mechanism of TBI.

Ivabradine abrogates TNF-α-induced degradation of articular cartilage matrix.

Ivabradine is most commonly used for the treatment of worsening cardiac failure in patients who cannot tolerate the maximum dose of ß-blockers or in whom treatment with ß-blockers is contraindicated. While ivabradine is regarded as a highly selective "funny current" (If) inhibitor, the molecular mechanism behind the effect of this drug remains poorly understood. In the present study, we applied ivabradine in the context of osteoarthritis by treating primary human chondrocytes with tumor necrosis factor-α (TNF-α) and measuring degradation of the articular cartilage matrix as well as the expression of various enzymes and pro-inflammatory cytokines. Our results indicate that ivabradine significantly abrogated TNF-α-induced up-regulation of matrix metalloproteinase-3 (MMP-3), MMP-13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)-4, and ADAMTS-5 at both the gene and protein levels. Notably, ivabradine attenuated TNF-α-induced reduction of type II collagen and aggrecan at both the mRNA and protein levels. Also, we found that ivabradine inhibited the expression and secretion of interleukin-6 (IL-6) and interleukin-1ß (IL-1ß) as well as the production of reactive oxygen species (ROS). Mechanistically, our results indicate that ivabradine abolished the activation of nuclear factor (NF-κB) by inhibiting nuclear translocation of NF-κB p65. Knockdown of HCN2 enhanced the protective effects of ivabradine against TNF-α- induced degradation of both type II collagen and aggrecan, suggesting that the inhibitory effects of ivabradine in ECM degradation might be mediated by HCN2. Our findings demonstrate that ivabradine may indeed have a potential application in preventing excessive degradation of the articular cartilage matrix, thereby preventing the pathological development and progression of osteoarthritis.

Plasma metabolomics profiles in rats with acute traumatic brain injury.

Traumatic brain injury (TBI) is a major cause of mortality and disability worldwide. We validated the utility of plasma metabolomics analysis in the clinical diagnosis of acute TBI in a rat model of controlled cortical impact (CCI) using gas chromatography/mass spectrometry (GC/MS). Thirty Sprague-Dawley rats were randomly divided into two groups of 15 rats each: the CCI group and sham group. Blood samples were obtained from the rats within the first 24 h after TBI injury. GC/MS measurements were performed to evaluate the profile of acute TBI-induced metabolic changes, resulting in the identification of 45 metabolites in plasma. Principal component analysis, partial least squares-discriminant analysis, orthogonal partial least square discriminant analysis using hierarchical clustering and univariate/multivariate analyses revealed clear differences in the plasma metabolome between the acute CCI group and the sham group. CCI induced distinctive changes in metabolites including linoleic acid metabolism, amino acid metabolism, galactose metabolism, and arachidonic acid metabolism. Specifically, the acute CCI group exhibited significant alterations in proline, phosphoric acid, ß-hydroxybutyric acid, galactose, creatinine, L-valine, linoleic acid and arachidonic acid. A receiver operating characteristic curve analysis showed that the above 8 metabolites in plasma could be used as the potential biomarkers for the diagnosis of acute TBI. Furthermore, this study is the first time to identify the galactose as a biomarker candidate for acute TBI. This comprehensive metabolic analysis complements target screening for potential diagnostic biomarkers of acute TBI and enhances predictive value for the therapeutic intervention of acute TBI.