Search

Because people do not consider the requirement of communication in the construction of power line, that resulting in the poor channel environment and the orthogonality between the sub-carriers are damaged. Meanwhile, the symbol offset will occur in the receiving terminal, which will cause the inter symbol interference, so it has very important significance to estimate and compensate the frequency offset and symbol offset for OFDM symbol effectively. According to the special frame structure of G3-PLC, this paper uses the double correlation detection method to compensate the frequency offset and symbol offset of the OFDM system. At last, the algorithm is confirmed by Monte Carlo approach. The results indicate that the synchronization algorithm used in this paper can be very good to compensate for the frequency offset and symbol offset of the system, and the algorithm is very simple and has strong adaptability to the channel.

Background Percutaneous coronary intervention (PCI) is the main treatment for acute coronary syndrome (ACS), but some patients may experience recurrent major cardiovascular events (MACE) after the treatment. Recent studies have shown that lysophospholipid metabolites such as lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA), which are important components of oxidized low-density lipoprotein and low-density lipoprotein, can promote the formation and rupture of atherosclerotic plaques. However, it remains unclear whether lysophospholipid metabolites can be used to predict the occurrence of MACE following PCI in patients with ACS. Objective To investigate the predictive value of lysophospholipids for MACE following PCI in patients with ACS. Methods The study included patients with ACS who underwent PCI at Beijing Anzhen Hospital, Capital Medical University from June 2017 to September 2019. Baseline data of the patients were collected, and targeted metabolomics was performed to detect phospholipids and lysophospholipids. Patients were followed up at 1, 3, 6, 9, and 12 months post-enrollment, and then every 6 months thereafter, through outpatient visits and telephone consultations to record the occurrence of MACE. Principal component analysis (PCA) score plots were used to analyze the metabolic profiles and inter-group distributions of lysophospholipids between the non-MACE and MACE groups. A partial least squares-discriminant analysis (PLS-DA) with variable importance in projection (VIP) plots was utilized to assess the differential metabolites of lysophospholipids between the groups. The importance of each phospholipid and lysophospholipid metabolite was ranked using the random forest accuracy decrease diagram. Monte Carlo cross-validation was applied to construct the receiver operating characteristic (ROC) curve for the multivariable random forest models composed of different numbers of metabolites, and the area under the curve (AUC) was calculated to select key lysophospholipid metabolites associated with MACE. The accuracy of the predictive models was assessed using permutation tests. Results Participants included 212 cases of patients, with an average follow-up of 3 years. Patients were divided into the MACE group (n=29) and the non-MACE group (n=183) based on whether MACE occurred during the follow-up period. There was no statistically significant difference in baseline data between the two groups (P>0.05). The PCA score plot revealed a distinct distribution of MACE and non-MACE group samples, indicating significant differences in the lysophospholipid metabolite profiles. Integrated analysis identified significant changes in LPA, oxidized lysophosphatidylcholine (LPC-O), LPE, LPI, and LPS. Monte Carlo cross-validation was used to construct a predictive model for MACE using the top 13 ranked lipid metabolites [mainly including 10 lysophospholipid metabolites (LPA 16: 0, LPA 18: 1, LPC-O 16: 0, LPC 16: 0, LPG 18: 2, LPC 18: 0, LPE 20: 3, LPE 22: 6, LPG 18: 1, LPS 20: 4) and 3 phospholipid metabolites (PA 16: 0-18: 0, PA 16: 0-20: 4, PA 16: 0-18: 1) ]. The ROC curve indicated that the model had an AUC of 0.934 (95%CI=0.793-0.998) for predicting MACE. Conclusion Abnormal expression of lysophospholipids metabolites in preoperative serum is closely correlated with the risk of recurrent MACE following PCI in patients with ACS. This exhibits significant predictive efficacy and clinical value for MACE following PCI in patients with ACS.

Objective To explore the relationship and predictive function of blood urea nitrogen (BUN) level in association with major adverse cardiovascular event(MACE) subsequent to percutaneous coronary intervention(PCI) among patients diagnosed with acute coronary syndrome (ACS). Methods Between April 2017 and November 2017, ACS patients undergoing their initial PCI at the Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University were recruited. Following a 36-month follow-up period, 487 patients were included as 114 subjects experiencing MACE and 373 subjects without MACE. The Cox proportional hazards regression model was utilized to assess the risk ratio of MACE and its 95% confidence interval (CI) concerning BUN levels and ACS post-PCI. Additionally, the area under the receiver operating characteristic (ROC) curve (AUC) was applied to assess the predictive effect of BUN. Results After adjusting for confounding variables, Cox proportional hazards regression analysis revealed that the risk of MACE was approximately four times higher in the high BUN level group compared to the low BUN level group (OR=4.722,95% CI 1.716-12.993). Upon inclusion of BUN in both the basic prediction model and SCORE model for cardiovascular event risk, there was a significant increase in the AUC area (P＜ 0.001). Conclusions BUN levels can independently predict the risk of MACE following PCI in ACS patients, irrespective of traditional risk factors.

Purpose Obstructive sleep apnea (OSA) is a common sleep disorder that is influenced by various environmental and genetic factors. The potential associations of leptin and leptin receptor (LEPR) polymorphisms with OSA have been studied in different populations; however, the results remain inconclusive. The aim of this study was to examine the association between LEPR gene polymorphisms and OSA risk. Methods A total of 322 samples were used, including 226 OSA subjects and 96 controls. Targeted sequencing of the entire LEPR gene was performed in all subjects. Polysomnography was used to diagnose obstructive sleep apnea. The associations between variants and OSA were determined by multivariate regression analyses. Results Four single-nucleotide polymorphisms of LEPR were identified in all subjects. The genotype frequency of locus rs3790435 was significantly different between the OSA and control groups. Specifically, the variant genotype rs3790435 CC in LEPR was associated with a lower risk of OSA (OR 0.462, 95% CI 0.250-0.854, p = 0.014) in a recessive model after controlling for potential confounders. After BMI stratification, obese patients with this variant genotype were found to have a lower risk of developing OSA. Moreover, subjects with the rs3790435 CC genotype were found to have a statistically lower apnea-hypopnea index (AHI) and higher nadir oxygen saturation than the TT/CC genotypes without differences in plasma leptin levels. Conclusions Our study identified a novel variant of LEPR in patients with OSA, and specifically found an association between rs3790435 polymorphisms and OSA risk in Chinese Han subjects., Author(s): Juan Li [sup.1] , Song Yang [sup.1] , Xiaolu Jiao [sup.1] [sup.2] , Yunyun Yang [sup.1] [sup.2] , Haili Sun [sup.1] [sup.3] , Ming Zhang [sup.4] , Yunxiao Yang [...]

Endotherms recently expanding to cold environments generally exhibit strong physiological acclimation to sustain high body temperature. During this process, gut microbes likely play a considerable role in host physiological functions, including digestion and thermogenesis. The light-vented bulbul Pycnonotus sinensis represents one such species. It used to be restricted to the Oriental realm but expanded its distribution range north to the Palearctic areas during the past few decades. Here, we explored the seasonal dynamics of the resting metabolic rate (RMR) and microbiota for local and newly colonized populations of the species. Our results showed that the mass-adjusted RMR and body mass were positively correlated with latitude variations in both seasons. Consistently, the gut microbiota showed a corresponding variation to the northern cold environments. In the two northern populations, the alpha diversity decreased compared with those of the two southern populations. Significant differences were detected in dominant phyla, such as Firmicutes, Bacteroidetes, Proteobacteria, and Desulfobacterota in both seasons. The core microbiota showed geographic differences in the winter, including the elevated relative abundance of 5 species in northern populations. Finally, to explore the link between microbial communities and host metabolic thermogenesis, we conducted a correlation analysis between microbiota and mass-adjusted RMR. We found that more genera were significantly correlated with mass-adjusted RMR in the wintering season compared to the breeding season (71 vs. 23). These results suggest that microbiota of the lighted-vented bulbul linked with thermogenesis in diversity and abundance under northward expansion. [ABSTRACT FROM AUTHOR]

Aims Angiopoietin-like protein 8 (ANGPTL8) plays important roles in lipid metabolism, glucose metabolism, inflammation, and cell proliferation and migration. Clinical studies have indicated that circulating ANGPTL8 concentrations are increased in patients with hypertension and positively associated with blood pressure. ANGPTL8 deficiency ameliorates blood pressure in mice treated with chronic intermittent hypoxia. Currently, little is known regarding the pathophysiological role of the vascular smooth muscle cell (VSMC)-derived ANGPTL8 in hypertension and hypertensive cardiovascular remodelling. Methods and results Circulating ANGPTL8 concentrations, as determined by enzyme-linked immunosorbent assay, were significantly higher in hypertensive patients than in controls (524.51 ± 26.97 vs. 962.92 ± 15.91 pg/mL; P < 0.001). In hypertensive mice [angiotensin II (AngII) treatment for 14 days] and spontaneously hypertensive rats, ANGPTL8 expression was increased and predominantly located in VSMCs. In AngII-treated mice, systolic and diastolic blood pressure in Tagln-Cre-ANGPTL8fl/fl mice were approximately 15–25 mmHg lower than that in ANGPTL8fl/fl mice. AngII-induced vascular remodelling, vascular constriction, and increased expression of cell markers of proliferation (PCNA and Ki67) and migration (MMP-2 and MMP-9) were strikingly attenuated in Tagln-Cre-ANGPTL8fl/fl mice compared with ANGPTL8fl/fl mice. Furthermore, the AngII-induced increase in the heart size, heart weight, heart/body weight ratio, cardiomyocyte cross-sectional area, and collagen deposition was ameliorated in Tagln-Cre-ANGPTL8fl/fl mice compared with ANGPTL8fl/fl mice. In rat artery smooth muscle cells, ANGPTL8-short hairpin RNA decreased intracellular calcium levels and prevented AngII-induced proliferation and migration through the PI3K-Akt pathway, as shown using LY294002 (inhibitor of PI3K) and Akt inhibitor VIII. Conclusion This study suggests that ANGPTL8 in VSMCs plays an important role in AngII-induced hypertension and associated cardiovascular remodelling. ANGPTL8 may be a novel therapeutic target against pathological hypertension and hypertensive cardiovascular hypertrophy. [ABSTRACT FROM AUTHOR]

Abdominal aortic aneurysm (AAA) is a potentially life-threatening vascular disease primarily in the male elderly population, but there is a lack of approved medical therapies to prevent the progression and rupture of AAA. Activating Transcription Factor 4 (ATF4) has been established to be involved in cardiovascular diseases, such as heart failure and calcific aortic valve disease. However, the role of ATF4 in the pathogenesis of AAA remains unclear. We found that ATF4 expression was significantly increased in patients with AAA and mouse models of AAA and was mainly confined to macrophages in arteries. ATF4 knockdown significantly attenuated aneurysm formation in experimental mouse model of AAA, while ATF4 overexpression promoted the development of AAA. RNA sequencing suggested that ATF4 was strongly related to the biological function of acute inflammatory response. Macrophages-specific ATF4 knockout significantly reduced the incidence and development of AAA, and decreased M1 polarization of macrophages in mice. Sphingomyelin phosphodiesterase 3 (SMPD3), a regulator of inflammatory responses in monocytes/macrophages, has been identified as a target gene of ATF4 through RNA sequencing, ChIP sequencing, and standard ChIP analyses. ATF4 induces M1 polarization of macrophages through the activation of SMPD3, thereby promoting inflammatory responses. Together, these results suggest that ATF4 mediated macrophage M1 polarization by regulating the expression of target genes SMPD3, leading to an increased inflammatory response, which further promotes the formation and development of AAA. These findings suggest ATF4 may be a new therapeutic target for AAA.

Angiopoietin-like protein 8 (ANGPTL8) plays important roles in lipid metabolism, glucose metabolism, inflammation, and cell proliferation and migration. Clinical studies have indicated that circulating ANGPTL8 levels are increased in patients with thoracic aortic dissection (TAD). TAD shares several risk factors with abdominal aortic aneurysm (AAA). However, the role of ANGPTL8 in AAA pathogenesis has never been investigated. Here, we investigated the effect of ANGPTL8 knockout on AAA in ApoE-/- mice. ApoE-/-ANGPTL8-/- mice were generated by crossing ANGPTL8-/- and ApoE-/- mice. AAA was induced in ApoE-/- using perfusion of angiotensin II (AngII). ANGPTL8 was significantly up-regulated in AAA tissues of human and experimental mice. Knockout of ANGPTL8 significantly reduced AngII-induced AAA formation, elastin breaks, aortic inflammatory cytokines, matrix metalloproteinase expression, and smooth muscle cell apoptosis in ApoE-/- mice. Similarly, ANGPTL8 sh-RNA significantly reduced AngII-induced AAA formation in ApoE-/- mice. ANGPTL8 deficiency inhibited AAA formation, and ANGPTL8 may therefore be a potential therapeutic target for AAA., (© 2023 The Author(s).)