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Periodontitis is a chronic inflammatory and destructive disease caused by periodontal microbial infection and mediated by host immune response. As the main cause of loosening and loss of teeth in adults, it is considered to be one of the most common and serious oral diseases in the world. The co-existence of periodontitis and systemic chronic inflammatory diseases such as rheumatoid arthritis, psoriasis, inflammatory bowel disease, diabetes and so on is very common. It has been found that interleukin-17A (IL-17A) secreted by various innate and adaptive immune cells can activate a series of inflammatory cascade reactions, which mediates the occurrence and development of periodontitis and related systemic chronic inflammatory diseases. In this work, we review the role of IL-17A in the pathomechanisms of periodontitis and related systemic chronic inflammatory diseases, and briefly discuss the therapeutic potential of cytokine targeted agents that modulate the IL-17A signaling. A deep understanding of the possible molecular mechanisms in the relationship between periodontitis and systemic diseases will help dentists and physicians update their clinical diagnosis and treatment ideas.

Denitrification is an important part of the nitrogen cycle and the key step to removal of nitrogen in surface-flow wetlands. In this study, we explored space–time analysis with high-throughput sequencing to elucidate the relationships between denitrifying bacteria community structures and environmental factors during different seasons. Our results showed that along the flow direction of different processing units, there were dynamic changes in physical and chemical indicators. The bacterial abundance indexes (ACEs) in May, August, and October were 686.8, 686.8, and 996.2, respectively, whereas the Shannon-Weiner indexes were 3.718, 4.303, and 4.432, respectively. Along the flow direction, the denitrifying bacterial abundance initially increased and then decreased subsequently during the same months, although diversity tended to increase. The abundance showed similar changes during the different months. Surface flow wetlands mainly contained the following denitrifying bacteria genus: unclassified Bacteria (37.12%), unclassified Proteobacteria (18.16%), Dechloromonas (16.21%), unranked environmental samples (12.51%), unclassified Betaproteobacteria (9.73%), unclassified Rhodocyclaceae (2.14%), and Rhodanobacter (1.51%). During different seasons, the same unit showed alternating changes, and during the same season, bacterial community structures were influenced by the second genus proportion in different processing units. ACEs were strongly correlated with temperature, dissolved oxygen, and pH. Bacterial diversity was strongly correlated with temperature, electrical conductivity, pH, and oxidation reduction potential. Denitrifying bacteria are greatly affected by environmental factors such as temperature and pH.

Background: Reward expectation is an important motivation for aggression. However, despite substantial progress in behavioral studies related to reward expectation in aggression, the neural basis underlying this process remains unclear. Methods: To investigate the brain correlates of aggressive reward expectation, we developed the Harm–Gain Task (HGT). In this task, participants were informed that they could gain money by causing harm to another person and were instructed to evaluate their satisfaction with the anticipated monetary reward. Additionally, we designed a questionnaire to measure participants’ moral disengagement concerning aggressive decision-making in the HGT. Thirty-four healthy Chinese university students completed the HGT while in the scanner, and their functional images were acquired using a 3.0-T Siemens Tim Trio scanner. Data from two participants were excluded from the analysis due to excessive head motion. Finally, data from 32 participants (15 males, Mage = 19.97 years, SDage = 2.07 years) were included in the analyses. Results: Findings show that during the reward expectation phase of the HGT, (1) relative to the baseline condition, the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), and middle cingulate cortex (MCC) were significantly activated. Conversely, activation in the bilateral dorsolateral prefrontal cortex (DLPFC), bilateral inferior parietal lobule (IPL), and bilateral lateral temporal cortex (LTC) was attenuated. (2) As the monetary amount raised, activation in the OFC and ACC significantly increased, while activation in the DLPFC, IPL, and LTC significantly decreased. (3) As the monetary amount raised, the heightened activation in the OFC and ACC was significantly correlated with participants’ aggressive behavior and moral disengagement scores. Conclusions: The results provide preliminary evidence regarding neural correlates in aggressive reward expectation, promoting further exploration of the cognitive neural mechanisms underlying aggression.

Positive outcome expectancy is a crucial cognitive factor influencing aggression, yet its neural basis remains unclear. Therefore, the present study combined voxel-based morphometry (VBM) with a resting-state functional connectivity (RSFC) analysis to investigate the brain correlates of positive outcome expectancy in aggression in young people. In the VBM analysis, multiple linear regression was conducted to explore the relationship between individual differences in aggressive positive outcome expectancy and regional gray matter volume (GMV) among 325 undergraduate students. For the RSFC analysis, seed regions were selected based on the results of the VBM analysis. Subsequently, multiple linear regression was employed to examine whether a significant correlation existed between individual differences in aggressive positive outcome expectancy and the RSFC of seed regions with other brain regions in 304 undergraduate students. The findings indicated that aggressive positive outcome expectancy was positively correlated with GMV in the posterior cingulate cortex (PCC), right temporoparietal junction (TPJ), and medial prefrontal cortex (MPFC). Moreover, it was also positively associated with RSFC between the PCC and the left dorsolateral prefrontal cortex (DLPFC). The prediction analysis indicated robust relationships between aggressive positive outcome expectancy and the GMV in the PCC, right TPJ, as well as the RSFC between the PCC and the left DLPFC. Our research provides the initial evidence for the neural basis of positive outcome expectancy in aggression, suggesting the potential role of the PCC as a hub in its neural network.

The effects of moral protective factors (e.g., moral cost) on aggression and the underlying mechanisms remain unclear. To address this issue, this study developed the Moral Cost of Aggression Questionnaire (MCAQ) and validated its psychometric properties in 516 college students (287 female; Mage = 19.77 years, SD = 1.61). Subsequently, the relationships among moral cost, positive outcome expectancies for aggression (POEA), and aggression were examined in 749 college students (330 females; Mage = 18.96 years, SD = 0.74). Mediation analysis indicated that POEA mediated the relationship between moral cost and aggression. This pattern of associations is consistent with the hypothesis that moral cost is negatively associated with aggression, in part through its link to lower subjective value of aggressive outcomes (i.e., lower POEA). This study provides a reliable and valid measure of the trait moral cost (MCAQ) and offers preliminary empirical support for a discounting mechanism in which moral cost is associated with reduced aggression via decreased POEA. These findings suggest that interventions targeting both moral cost and outcome valuation may be a useful direction for future research.

Purpose Temporomandibular joint osteoarthritis (TMJOA) is a common disease that negatively affects the life quality of human beings. Circadian rhythm acts an important role in life activities. However, whether the clock genes are rhythmic expressed in mandibular condylar chondrocytes, or the clock genes have an effect on the progression of TMJOA remains unknown. In this study, we aim to explore expression of clock genes and regulatory mechanism of TMJOA in rat mandibular condylar chondrocytes. Methods After synchronized by dexamethasone, the expression of core clock genes Per1 , Per2 , Clock , Cry1 , Cry2 and Bmal1 and cartilage matrix degrading factor gene Mmp13 were analyzed in mandibular condylar chondrocytes every 4 h with RT-qPCR. The mandibular condylar chondrocytes were stimulated with IL-1β, and expression of Per1 , Mmp13 , P65 and p-P65 was assessed by RT-qPCR and Western blot. Sh- Per1 lentivirus was used to assess the effect of clock gene Per1 in IL-1β-induced chondrocytes, and expression of Mmp13 , P65 and p-P65 was measured. After establishing a rat TMJOA model using unilateral anterior crossbite (UAC), micro-CT, H & E, Alcian Blue & Nuclear Fast Red and Safranin O & Fast Green, cartilage thickness was utilized to assess the damage of cartilage and subchondral bone. Immunohistochemistry of PER1, MMP13 and P65 was performed in condylar sections. Results All core clock genes and Mmp13 were rhythmically expressed. And Mmp13 expression curve was closed in phase and amplitude with Per1 . After stimulation with IL-1β, the expression of MMP13, PER1 and P65 and ratio of p-P65/P65 increased in condylar chondrocytes. After Per1 was down-regulated in condylar chondrocytes, the expression of MMP13 and P65 and ratio of p-P65/P65 decreased. Compared with the condyles of Sham group, the bony parameters of UAC group were significantly worse. The thickness of cartilage in UAC group significantly reduced. The modified Mankin scores and the expression of PER1, MMP13 and P65 in cartilage of UAC group significantly increased compared with Sham group. Conclusion Core clock genes and Mmp13 are rhythmic expressed in rat mandibular condylar chondrocytes. PER1 can regulate the expression of MMP13 through NF-κB pathway in IL-1β-induced mandibular condylar chondrocytes.

Cardiovascular diseases remain the leading cause of death worldwide. Maladaptive transcriptional programs drive the fibrosis, hypertrophy, and vascular inflammation that characterize these pathologies. Histone posttranslational modifications regulate these programs by remodeling chromatin accessibility and transcriptional output in cardiomyocytes, vascular cells, and immune cells. These modifications include methylation, acetylation, and metabolite‐derived acylations. While the enzymatic machinery of classical histone marks is increasingly well defined, the cell‐type‐specific integration of these regulators into dynamic cardiovascular networks remains incompletely understood. This narrative review summarizes experimental and human studies published up to early 2026. We examine how classical marks such as H3K27me3 and H3K9ac, alongside emerging metabolic sensors like histone lysine lactylation, shape core pathobiological programs, including oxidative stress responses, endothelial dysfunction, and extracellular matrix remodeling, across major cardiovascular syndromes. We further critically evaluate the enzymatic machinery and pharmacological strategies by contrasting broad‐spectrum histone deacetylase inhibition with precision approaches, including bromodomain inhibition and locus‐selective epigenome editing. Finally, we address translational constraints such as drug delivery and off‐target effects. We propose that single‐cell resolution and spatial multiomics will be essential to identify compartment‐specific targets and advance precision cardiovascular epigenetic therapeutics. This graphical summarizes how classical and emerging histone posttranslational modifications (PTMs), together with their chromatin regulators (writers, erasers, and readers), govern major pathobiological programs in cardiovascular disease. These programs include inflammation, oxidative and mitochondrial stress, fibrosis and extracellular matrix (ECM) remodeling, endothelial dysfunction, vascular smooth muscle cell (VSMC) phenotypic switching, and cardiac hypertrophy and remodeling. Across heart failure, atherosclerosis, myocardial infarction, myocardial ischemia–reperfusion injury, and hypertension, these shared yet context‐dependent chromatin programs contribute to disease phenotype and therapeutic translation. The figure also outlines the translational landscape, including targetable regulators, major translational constraints, and enabling technologies relevant to precision cardiovascular epigenetic therapeutics. This graphical was created by the authors using BioRender.com. No copyrighted third‐party published images or graphical elements were reproduced. Abbreviations: BET, bromodomain and extraterminal domain; ECM, extracellular matrix; HDAC, histone deacetylase; PTMs, posttranslational modifications; VSMC, vascular smooth muscle cell.

The aims of this study were to determine the prognostic value of primary tumor surgery and identify optimal candidates for such surgery among patients with seminoma and distant metastasis at diagnosis. We identified 521 patients with seminoma and distant metastasis at diagnosis between 2004 and 2014 from the Surveillance, Epidemiology, and End Results database. Among these patients, 434 had undergone surgery, whereas 87 had not. The prognostic value of primary tumor surgery was assessed by Kaplan-Meier methods, log-rank analyses, and multivariate Cox's proportional hazards model. Survival curves and forest plots were also plotted. Survival analysis indicated that patients who underwent surgery had a better 5-year overall survival and cancer-specific survival than those who did not. Multivariate analyses demonstrated that primary tumor surgery is an independent prognostic factor for overall survival and cancer-specific survival, along with age at diagnosis, M stage, and marital status. In addition, primary tumor surgery still had considerable prognostic value in the subgroup of patients with lymph node metastasis. Further, forest plots demonstrated that patients with M1a stage, N1 or N2-3 stage, and a younger age at diagnosis (<60 years) may benefit from primary tumor surgery. In conclusion, our findings indicate that primary tumor surgery is correlated with improved survival in patients with seminoma and distant metastasis. Furthermore, primary tumor surgery is an independent prognostic indicator for patients with seminoma and distant metastasis.

This paper studies the thesis of slip-sweep acquisition method in vibroseis exploring. First of all, it briefly describes slip-sweep acquisition in principle, operation and signal processing, compared with the bomb exploring and conventional cascaded sweep acquisition and analyzes the principle of vibroseis exploration in detail. Then the reason why harmonics generated is analyzed. Among the harmonics, high frequency harmonics is most serious. Based on extensive research on the theory and the numerical experiments, the paper assumes that the energy of the high frequency harmonics and that of the original stimulated signal into a linear relationship. According to this assumption, a mathematical model to filer out high frequency harmonics is established. After generating standard high frequency harmonics through frequency doubling and estimating the ratio of the energy of each harmonic and fundamental, the mathematical model perfectly matches actual seismic data processing, that is, an effective way of vibroseis data processing. Finally, the paper developed full procedures of slip-sweep vibroseis data processing and made all the programs. With a fast processing speed and obvious effect, the programs achieve good application; fully meet the industrial demand to process vibroseis data.

Background Laparoscopy-assisted distal gastrectomy (LADG) with D1+β lymph node dissection has become the most popular treatment for early gastric cancer in Asian countries. However, the same clinical advantages with this procedure as with LADG with D1+α lymph node dissection has not been shown. The aim of this study was to compare the outcome of LADG with D1+β to that of LADG with D1+α lymph node dissection. Methods During the period June 2002 through June 2006, LADG with D1+α lymph node dissection was performed in 54 patients, and LADG with D1+β lymph node dissection was performed in 42 patients. Surgical findings, clinicopathological data, postoperative course, complications, nutritional status, and blood analysis findings were compared between the two groups. Differences were analyzed with Mann–Whitney U test and chi-square test. Results Patients in the two groups were comparable with respect to age, sex, body mass index, and stage and pathological characteristics of gastric cancer. A significantly greater number of N2 lymph nodes were harvested by D1+β lymph node dissection than by D1+α dissection (5.9 vs. 2.7, P  < 0.01). However, no significances in the total number of retrieved lymph nodes (24.7 vs. 22.2) or perigastric lymph nodes dissected (18.9 vs. 19.4) were identified between the D1+β and D1+α groups. There was also no significant difference between the D1+α and D1+β groups with respect to operation time, blood loss, complication rate, time to first walking, first flatus, first eating, and first defecation, frequency of analgesics given, volume of food intake on postoperative day 7, weight loss, and postoperative hospital stay. Blood analysis showed there were no significant differences in white blood cell count, granulocyte count, lymphocyte count, levels of C-reactive protein, and serum albumin. Conclusions The short-term outcome of LADG with D1+β lymph node dissection is comparable to that of LADG with D1+α lymph node dissection. According to the oncological requirements, we can apply this operation as a minimally invasive surgery.