Exposure memory and susceptibility to ambient PM2.5: A perspective from hepatic cholesterol and bile acid metabolism.

Both epidemiological and experimental studies increasingly show that exposure to ambient fine particulate matter (PM2.5) is related to the occurrence and development of chronic diseases, such as metabolic diseases. However, whether PM2.5 has "exposure memory" and how these memories affect chronic disease development like hepatic metabolic homeostasis are unknown. Therefore, we aimed to explore the effects of exposure transition on liver cholesterol and bile acids (BAs) metabolism in mice. In this study, C57BL/6 mice were exposed to concentrated ambient PM2.5 or filtered air (FA) in a whole-body exposure facility for an initial period of 10 weeks, followed by another 8 weeks of exposure switch (PM2.5 to FA and FA to PM2.5) comparing to non-switch groups (FA to FA and PM2.5 to PM2.5), which were finally divided into four groups (FF of FA to FA, PP of PM2.5 to PM2.5, PF of PM2.5 to FA, and FP of FA to PM2.5). Our results showed no significant difference in food intake, body composition, glucose homeostasis, and lipid metabolism between FA and PM2.5 groups after the initial exposure before the exposure switch. At the end of the exposure switch, the mice switched from FA to PM2.5 exposure exhibited a high sensitivity to late-onset PM2.5 exposure, as indicated by significantly elevated hepatic cholesterol levels and disturbed BAs metabolism. However, the mice switched from PM2.5 to FA exposure retained a certain memorial effects of previous PM2.5 exposure in hepatic cholesterol levels, cholesterol metabolism, and BAs metabolism. Furthermore, 18-week PM2.5 exposure significantly increased hepatic free BAs levels, which were completely reversed by the FA exposure switch. Finally, the changes in small heterodimeric partner (SHP) and nuclear receptor subfamily 5 group A member 2 (LRH1) in response to exposure switch mechanistically explained the above alterations. Therefore, mice switching from PM2.5 exposure to FA showed only a weak memory of prior PM2.5 exposure. In contrast, the early FA caused mice to be more susceptible to subsequent PM2.5 exposure.

PM2.5-induced cellular senescence drives brown adipose tissue impairment in middle-aged mice.

Airborne fine particulate matter (PM2.5) exposure is closely associated with metabolic disturbance, in which brown adipose tissue (BAT) is one of the main contributing organs. However, knowledge of the phenotype and mechanism of PM2.5 exposure-impaired BAT is quite limited. In the study, male C57BL/6 mice at three different life phases (young, adult, and middle-aged) were simultaneously exposed to concentrated ambient PM2.5 or filtered air for 8 weeks using a whole-body inhalational exposure system. H&E staining and high-resolution respirometry were used to assess the size of adipocytes and mitochondrial function. Transcriptomics was performed to determine the differentially expressed genes in BAT. Quantitative RT-PCR, immunohistochemistry staining, and immunoblots were performed to verify the transcriptomics and explore the mechanism for BAT mitochondrial dysfunction. Firstly, PM2.5 exposure caused altered BAT morphology and mitochondrial dysfunction in middle-aged but not young or adult mice. Furthermore, PM2.5 exposure increased cellular senescence in BAT of middle-aged mice, accompanied by cell cycle arrest, impaired DNA replication, and inhibited AKT signaling pathway. Moreover, PM2.5 exposure disrupted apoptosis and autophagy homeostasis in BAT of middle-aged mice. Therefore, BAT in middle-aged mice was more vulnerable to PM2.5 exposure, and the cellular senescence-initiated apoptosis, autophagy, and mitochondrial dysfunction may be the mechanism of PM2.5 exposure-induced BAT impairment.

Multifunctional Metasurfaces Enabled by Multifold Geometric Phase Interference.

Geometric phase is frequently used in artificially designed metasurfaces; it is typically used only once in reported works, leading to conjugate responses of two spins. Supercells containing multiple nanoantennas can break this limitation by introducing more degrees of freedom to generate new modulation capabilities. Here, we provide a method for constructing supercells for geometric phases using triple rotations, each of which achieves a specific modulation function. The physical meaning of each rotation is revealed by stepwise superposition. Based on this idea, spin-selective holography, nanoprinting, and their hybrid displays are demonstrated. As a typical application, we have designed a metalens that enables spin-selective transmission, allowing for high-quality imaging with only one spin state, which can serve as a plug-and-play chiral detection device. Finally, we analyzed how the size of supercells and the phase distribution inside it can affect the higher order diffraction, which may help in designing supercells for different scenarios.

Midterm Surgical Outcomes for ALCAPA Repair in Infants and Children.

BACKGROUND: Surgical correction of an anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) has been associated with excellent survival during recent years. The purpose of this study was to evaluate the effectiveness of reimplantation of the coronary artery and to investigate the recovery of postoperative cardiac and mitral valve (MV) function. METHODS: From 2005 to 2015, 80 patients who had ALCAPA received surgical correction. Among them, 49 were infants. The median patient age was 7.8 months. Operative strategies included reimplantation of the coronary artery in 71 patients, the Takeuchi procedure in another 7 patients, and coronary artery ligation in the remaining 2 patients. RESULTS: There were 11 hospital deaths and 2 late deaths. Six patients required intraoperative or postoperative mechanical circulatory support. A significant improvement in the ejection fraction (EF) and shortening fraction (SF) was present in all surviving patients at discharge, at a 3-month follow-up and at a 1-year follow-up. MV function improved gradually after surgical repair with no late secondary intervention. CONCLUSIONS: The repair of ALCAPA can be accomplished by establishment of a dual-coronary system, which offers an acceptable mortality rate and will rarely require a second surgery. Left ventricular (LV) recovery is a progressive process, especially for infants with impaired LV function. Concomitant MV annuloplasty is safe and reliable and can be performed as necessary in patients with moderate or severe mitral valve regurgitation.

Surgical and Transcatheter Treatments in Children with Congenital Aortic Stenosis.

BACKGROUND: For patients with congenital aortic valve stenosis (AVS), comprehensive analysis of surgical aortic valvuloplasty (SAV) or balloon dilation (BD) is scarce and remains controversial. METHODS: This study reviewed AVS data (aortic peak gradient, aortic insufficiency, and survival and reoperation) for patients who were suitable for biventricular repair at our center in 2008 to 2018. Patients were categorized into two subgroups based on age (≤3 or >3 months). RESULTS: A total of 194 patients were treated, including 124 with SAV and 70 with BD. Resulting data revealed that residual aortic gradient at discharge was worse for BD (p = 0.001). While for patients younger than 3 months, the relief of AVS was comparable between the two groups (p = 0.624). There was no significant difference in time-related survival between the two groups (log-rank p = 0.644). Multivariate analysis demonstrated that preoperative left ventricular end-diastolic dimension predicted early death (p = 0.045). Survival in the two groups after 10 years was 96.8% in SAV and 95.7% in BD (p = 0.644). Freedom from reoperation after 10 years was 58.1% in SAV and 41.8% in BD patients (p = 0.01). There was no significant difference in freedom from reoperation between SAV and BD in patients younger than 3 months (p = 0.84). Multivariate analysis indicated that residual aortic peak gradient was predictive of reoperation (p = 0.038). CONCLUSION: Both methods achieved excellent survival outcomes at our center. SAV achieved superior gradient reduction and minimized the necessity for reoperation. For patients younger than 3 months, BD rivaled SAV both in aortic stenosis relief and freedom from reoperation.

Outcomes of Arch Reintervention for Recurrent Coarctation in Young Children.

OBJECTIVES: To evaluate the outcomes of reintervention for postrepair recoarctation in young children. METHODS: Between January 2011 and December 2020, all consecutive patients aged ≤3 years who were treated for postrepair recoarctation were included. Recoarctations were classified into two morphological types by three-dimensional imaging. Two methods, namely, surgical repair and balloon angioplasty (BA), were used to treat recoarctation. RESULTS: This study included 50 patients with a median age of 10.5 months (range, 2.0-36.0 months) and a mean weight of 9.3 ± 3.1 kg. Hypoplastic recoarctation occurred most frequently in patients who had undergone patch aortoplasty at initial repair (p = 0.001). No hospital mortality occurred, and all patients achieved an increased diameter (p < 0.001) and a decreased pressure gradient (p < 0.001) at the recoarctation site immediately after reintervention. The median follow-up time after reintervention was 3.5 years (range, 16.0 days-9.6 years). Late mortality occurred in four patients (8.0%): two in the surgical group and two in the BA group (chi-square test= 0.414, p = 0.520). There was no difference in arch reobstruction after reintervention between the surgical and BA groups (chi-square test = 1.383, p = 0.240). Recoarctation with a hypoplastic morphology was the leading risk factor for arch reobstruction after reintervention (hazard ratio, 6.552; 95% confidence interval, 2.045-20.992; p = 0.002). CONCLUSION: Reintervention for recoarctation has favorable early outcomes in young children. However, late mortality is not rare, and arch reobstruction is common during close follow-up. For young children, recoarctation with hypoplastic morphology is the leading risk factor for reobstruction, while the choice of reintervention method exerts little effect on the outcomes of arch reintervention.

PM2.5 increases mouse blood pressure by activating toll-like receptor 3.

BACKGROUND AND AIMS: Plenty of literature has documented that fine particulate matter (PM2.5) exposure is related to blood pressure (BP) elevation. Vascular dysfunction is the initiation of cardiovascular diseases, such as hypertension. This thesis set out to assess the role of Toll-like receptor 3 (TLR3) in the increase in BP induced by PM2.5. METHODS: C57BL/6 and TLR3 deficient (TLR3-/-) male mice were randomly allocated to filtered air chamber or real-world inhaled concentrated PM2.5 chamber. BP was evaluated using non-invasive BP recordings. After euthanasia, the aortas and small mesenteric arteries (SMAs) were isolated, and vascular tone was measured using a wire myograph. Leucocytes were detached to assess myeloid-derived suppressor cells using flow cytometry. siRNA transfection was performed to silence TLR3 expression in the human vascular endothelial cells incubated with PM2.5. The gene expression levels of inflammation, adhesion molecules, and oxidative stress in the aortas were assessed by quantitative PCR. RESULTS: Exposure to PM2.5 increased mouse BP, and TLR3 deficiency protected against PM2.5 exposure-induced BP increase. Additionally, the injury of vascular function in the aortas and SMAs was inhibited in TLR3-/- mice. The intercellular adhesion molecule-1 (ICAM-1) was attenuated in TLR3-/- mice, accompanied by the inhibition of inflammatory and oxidized genes of the aortas, such as F4/80, interleukin-6, interleukin-1 beta, and NADPH oxidase 4. In vitro, the enhanced mRNA expression of genes encoding inflammation, oxidative stress, and ICAM-1 by PM2.5 was inhibited by TLR3 silence as well. CONCLUSIONS: PM2.5 exposure increased BP via TLR3 activation and impaired vascular function.

Ambient fine particulate matter exposure disrupts placental autophagy and fetal development in gestational mice.

Recent studies have shown that some adverse pregnancy outcomes, especially intrauterine growth restriction (IUGR), are associated with gestational exposure to ambient fine particulate matter (PM2.5). However, potential mechanism remains to be elucidated. In the present study, pregnant C57BL/6 mice were randomly assigned to be exposed to either filtered air or ambient PM2.5 in the gestation period via a concentrated whole-body exposure system. We found that gestational PM2.5 exposure exerted no effect on implantation, preterm delivery, as well as fetal resorption and death. However, in utero fetal exposure to PM2.5 showed a significant reduction in body weight and crown-rump length on GD13 and GD18. Meanwhile, maternal blood sinusoid in placenta was markedly reduced along with abnormal expression of placental nutrient transporters and growth hormone in dams exposed to PM2.5. Additional tests showed gestational PM2.5 exposure decreased autophagy-related protein levels and inhibited autophagy flux mainly on GD15. Correspondingly, AMPK/mTOR signaling pathway, a critical negative regulator of autophagy, was activated in placenta on GD15 by PM2.5 exposure as well. These findings provide evidences that placental developmental disorder caused by autophagy inhibition might be an important mechanism for the growth restriction caused by PM2.5 exposure.

Ambient fine particulate matter exposure disrupts circadian rhythm and oscillation of the HPA axis in a mouse model.

Emerging evidence supports that exposure to ambient fine particulate matter (PM2.5) is associated with the metabolic syndrome. As the main neuroendocrine axis in mammals, the hypothalamic-pituitary-adrenal (HPA) axis's circadian rhythm (CR) plays an essential role in regulating metabolic homeostasis. Our previous studies found that ambient PM2.5 exposure caused CR disorder of the critical enzymes involved in lipid metabolism in mouse liver and adipose tissues. However, the impact of ambient PM2.5 exposure on the HPA axis is not fully illustrated yet. Male C57BL/6 mice were randomly exposed to ambient PM2.5 or filtered air for ten weeks via a whole-body exposure system. Rhythmic oscillations of clock genes in the hypothalamus and adrenal gland were characterized. The effects of ambient PM2.5 exposure on clock gene expression and rhythmic expression of molecules related to glucocorticoid synthesis were also examined. Firstly, a more robust CR of clock genes was demonstrated in the adrenal gland than that in the hypothalamus. Secondly, PM2.5 exposure significantly inhibited the expression of Clock at ZT8 in the hypothalamus. However, both circadian oscillation and expression levels of Bmal1, Cry1, Cry2, and Rorα were increased significantly by ambient PM2.5 exposure in the adrenal gland. Moreover, abnormal rhythmic oscillation patterns of corticotropin-releasing hormone and adrenocorticotropic hormone were observed after ambient PM2.5 exposure, with no change at the expression levels. Finally, the expression of Cyp11b1 was markedly decreased at ZT0 in the adrenal gland of PM2.5 exposed mice. Our findings provide new insights into the ambient PM2.5 exposure-induced metabolic syndrome from the perspective of CR disturbances.

Anomalous left coronary artery from pulmonary artery repair: Outcomes from the European Congenital Heart Surgeons Association Database.

INTRODUCTION: We sought to determine the surgical outcomes of patients with anomalous origin of the left coronary artery from the pulmonary artery (ALCAPA) enrolled in the European Congenital Heart Surgeons Association (ECHSA) database. MATERIALS AND METHODS: From 1999 to 2019, 907 patients with ALCAPA underwent surgical repair and were included in the current study. The primary outcome was in-hospital mortality. Secondary outcomes included frequency and results of concomitant mitral valve surgery and postoperative mechanical circulatory support (MCS). RESULTS: The overall in-hospital mortality was 6% (54/907) and was significantly higher in neonates (p = .01), patients with lower body surface area (BSA) (p = .01), and those requiring postoperative MCS (p = .001). Associated mitral valve surgery was performed in 144 patients (15.9%) and was associated with longer cardiopulmonary bypass (CPB) and aortic cross-clamp times (AOX) (p ≤ .0001) but was not significantly related to an increase in in-hospital mortality. Postoperative MCS was required in 66 patients (7.3%). These patients were younger (p ≤ .001), had a lower BSA (p ≤ .001), and required a longer CPB (p ≤ .001) and AOX time (p ≤ .001). CONCLUSIONS: ALCAPA repair can be achieved successfully, and with low surgical risk. Concomitant mitral valve procedures can be performed without increasing operative mortality. The use of MCS remains a valuable option, especially in younger patients.

Midterm Outcomes of Surgical Repair of Partial Anomalous Pulmonary Venous Connection to SVC.

OBJECTIVES: We explore midterm results after surgical treatment of partial anomalous pulmonary venous connection (PAPVC) to superior vena cava (SVC) in our institution. METHODS: From 2008 to 2017, 78 patients underwent surgical repair for PAPVC to SVC. Patients were divided into three groups based on surgical techniques: Single-patch repair (n = 20, group A), double-patch repair (n = 31, group B), and Warden repair (n = 27, group C). Their median age was 1.9 years (range: 3 months-13.8 years); median weight was 11.4 kg (range: 4.4-39.7 kg). Clinical, electrocardiographic and echocardiographic were available for all patients. RESULTS: There were no early or late mortality. The mean follow-up duration was 1.8 ± 2.1 years (range: 0.6 months to 8 years). No pulmonary venous obstruction occurred and no residual left-to-right shunts sustained during the follow-up. Reoperation for SVC obstruction was required: 1 (5.3%) in group A, 1 (3.2%) in group B, and 2 (7.4%) in group C (p = 0.78). Four patients (3 in group B, 1 in group C, p = 0.7) presented transient rhythm disturbance at discharge and one patient in group B remains nonsinus rhythm during follow-up. Pacemaker was not required in all patients. CONCLUSION: PAPVC to SVC can be safely managed by multiple techniques. Careful manipulation nearby sinus node must be emphasized during double-patch repair to prevent injury of sinus node. Obstruction of postoperative SVC stenosis should be paid attention to after Warden procedure. For young patients, operation should not be performed that early, but until preschool age.

Novel Focus of Sin Nombre Virus in Peromyscus eremicus Mice, Death Valley National Park, California, USA.

The deer mouse (Peromyscus maniculatus) is the primary reservoir for Sin Nombre virus (SNV) in the western United States. Rodent surveillance for hantavirus in Death Valley National Park, California, USA, revealed cactus mice (P. eremicus) as a possible focal reservoir for SNV in this location. We identified SNV antibodies in 40% of cactus mice sampled.

Public Health Response to Aedes aegypti and Ae. albopictus Mosquitoes Invading California, USA.

Aedes aegypti and Ae. albopictus mosquitoes, primary vectors of dengue and chikungunya viruses, were recently detected in California, USA. The threat of potential local transmission of these viruses increases as more infected travelers arrive from affected areas. Public health response has included enhanced human and mosquito surveillance, education, and intensive mosquito control.

Isolation and characterization of a Sca-1+/CD31- progenitor cell lineage derived from mouse heart tissue.

BACKGROUND: Myocardial infarction remains the leading cause of mortality in developed countries despite recent advances in its prevention and treatment. Regenerative therapies based on resident cardiac progenitor cells (CPCs) are a promising alternative to conventional treatments. However, CPCs resident in the heart are quite rare. It is unclear how these CPCs can be isolated and cultured efficiently and what the effects of long-term culture in vitro are on their 'stemness' and differentiation potential, but this is critical knowledge for CPCs' clinical application. RESULTS: Here, we isolated stem cell antigen-1 positive cells from postnatal mouse heart by magnetic active cell sorting using an iron-labeled anti-mouse Sca-1 antibody, and cultured them long-term in vitro. We tested stemness marker expression and the proliferation ability of long-term cultured Sca-1+ cells at early, middle and late passages. Furthermore, we determined the differentiation potential of these three passages into cardiac cell lineages (cardiomyocytes, smooth muscle and endothelial cells) after induction in vitro. The expression of myocardial, smooth muscle and endothelial cell-specific genes and surface markers were analyzed by RT-PCR and IF staining. We also investigated the oncogenicity of the three passages by subcutaneously injecting cells in nude mice. Overall, heart-derived Sca-1+ cells showed CPC characteristics: long-term propagation ability in vitro, non-tumorigenic in vivo, persistent expression of stemness and cardiac-specific markers, and multipotent differentiation into cardiac cell lineages. CONCLUSIONS: Our research may bring new insights to myocardium regeneration, for which even a small number of biopsy-derived CPCs could be enriched and propagated long term in vitro to obtain sufficient seed cells for cell injection or cardiac tissue engineering.

Contactless vital signs monitoring in macaques using a mm-wave FMCW radar.

Heart rate (HR) and respiration rate (RR) play an important role in the study of complex behaviors and their physiological correlations in non-human primates (NHPs). However, collecting HR and RR information is often challenging, involving either invasive implants or tedious behavioral training, and there are currently few established simple and non-invasive techniques for HR and RR measurement in NHPs owing to their stress response or indocility. In this study, we employed a frequency-modulated continuous wave (FMCW) radar to design a novel contactless HR and RR monitoring system. The designed system can estimate HR and RR in real time by placing the FMCW radar on the cage and facing the chest of both awake and anesthetized macaques, the NHP investigated in this study. Experimental results show that the proposed method outperforms existing methods, with averaged absolute errors between the reference monitor and radar estimates of 0.77 beats per minute (bpm) and 1.29 respirations per minute (rpm) for HR and RR, respectively. In summary, we believe that the proposed non-invasive and contactless estimation method could be generalized as a HR and RR monitoring tool for NHPs. Furthermore, after modifying the radar signal-processing algorithms, it also shows promise for applications in other experimental animals for animal welfare, behavioral, neurological, and ethological research.

Gut microbiota linked to hydrocephalus through inflammatory factors: a Mendelian randomization study.

Background: The gut microbiota (GM) has been implicated in neurological disorders, but the relationship with hydrocephalus, especially the underlying mechanistic pathways, is unclear. Using Mendelian randomization (MR), we aim to discover the mediating role of inflammatory factors in the relationship between GM and hydrocephalus. Methods: After removing confounders, univariable and multivariable MR analyses were performed using summary statistics to assess the causal relationships between GM, inflammatory factors (IL-17A and IL-27), and types of hydrocephalus. Meta-analyses were used to reconcile the differences in MR results between different hydrocephalus sources. Finally, mediator MR analyses were applied to determine the mediating effect of inflammatory factors. Various sensitivity analysis methods were employed to ensure the reliability and stability of the results. Results: After correction for P-values, Firmicutes (phylum) (OR, 0.34; 95%CI, 0.17-0.69; P = 2.71E-03, P FDR = 2.44E-02) significantly reduced the risk of obstructive hydrocephalus. The remaining 18 different taxa of GM had potential causal relationships for different types of hydrocephalus. In addition, Firmicutes (phylum) decreased the risk of obstructive hydrocephalus by increasing levels of IL-17A (mediating effect = 21.01%), while Eubacterium ruminantium group (genus) increased the risk of normal-pressure hydrocephalus by decreasing levels of IL-27 (mediating effect = 7.48%). Conclusion: We reveal the connection between GM, inflammatory factors (IL-17A and IL-27), and hydrocephalus, which lays the foundation for unraveling the mechanism between GM and hydrocephalus.

Gestational exposure to PM2.5 disrupts fetal development by suppressing placental trophoblast syncytialization via progranulin/mTOR signaling.

Recent epidemiological and animal studies have indicated that ambient fine particulate matter (PM2.5) exposure during pregnancy is closely associated with intrauterine growth restriction (IUGR). However, the underlying mechanisms remain to be revealed. In this study, we found that gestational exposure to PM2.5 significantly decreased fetal weight and crown-rump length in mice, accompanied by insufficient placental trophoblast syncytialization and increased expression of progranulin (PGRN) in mice placenta. Administering PGRN neutralizing antibody to pregnant mice alleviated growth restriction and insufficient placental trophoblast syncytialization caused by PM2.5, accompanied with suppressed activation of the mTOR signaling pathway. Furthermore, in vitro experiments using human placental BeWo cells showed that 10 µg·mL-1 PM2.5 activated PGRN/mTOR signaling and suppressed forskolin-induced cell fusion, which was blocked by knockdown of PGRN. Taken together, our results demonstrated that PM2.5 exposure during pregnancy inhibited placental trophoblast syncytialization by activating PGRN/mTOR signaling, leading to abnormal placental development and IUGR. This study reveals a novel mechanism underlying the developmental toxicity of PM2.5 exposure during pregnancy.

Chronic Rhinosinusitis and Mental Health.

Importance: Chronic rhinosinusitis (CRS) has been associated with anxiety and depression, but the association of socioeconomic factors and temporality has yet to be fully explored. Objective: To determine the bidirectional risk of anxiety and depression for patients with CRS. Design, Setting, and Participants: This retrospective cohort study of the National Institutes of Health All of Us database from January 1, 2008, to December 31, 2018, included 2 cohorts of adult patients with and without CRS. The data were analyzed from July 1, 2023, through April 1, 2024. Patients were classified as having CRS if they had at least 2 diagnoses during the study period. Those with a diagnosis of CRS before the study period were excluded. Patients were propensity score matched (1:5) with patients without CRS for age, sex, race, and annual household income. Main Outcomes and Measures: The primary outcome was the development of anxiety and depression. Patients with CRS were counted as having the primary outcome if it occurred after the criteria for CRS diagnosis were fulfilled. Multivariate logistic regression and survival analysis were performed to determine the odds ratios (ORs) and hazard ratios (HRs) of anxiety and depression. A secondary survival analysis determined the risk of developing CRS between patients with anxiety and depression and controls. Results: Among 33 732 patients (23 382 [69.3%] female individuals; 510 [1.5%] Asian, 6002 [17.9%] Black or African American, 576 [1.7%] multiracial, and 26 036 [77.2%] White individuals), there were 28 110 controls and 5622 patients with CRS. Along with higher odds of having anxiety (OR, 4.39; 95% CI, 3.95-4.87) and depression (OR, 2.04; 95% CI, 1.86-2.24), patients with CRS were at an increased risk of developing anxiety (HR, 2.79; 95% CI, 2.47-3.15) and depression (HR, 1.40; 95% CI, 1.27-1.55) compared with controls. Additionally, patients with anxiety (HR, 2.37; 95% CI, 2.18-2.57) and depression (HR, 1.59; 95% CI, 1.46-1.72) were at an increased risk of developing chronic rhinosinusitis compared with controls. Conclusions and Relevance: In this population-based cohort study of adults with and without CRS, a bidirectional association between common psychiatric disorders and CRS was observed. Physicians and health care clinicians who treat patients with anxiety, depression, and CRS should be vigilant regarding these risks and screen patients appropriately.

An Organic Chiroptical Detector Favoring Circularly Polarized Light Detection from Near-Infrared to Ultraviolet and Magnetic-Field-Amplifying Dissymmetry in Detectivity.

Circularly polarized light detection has attracted growing attention because of its unique application in security surveillance and quantum optics. Here, through designing a chiral polymer as a donor, a high-performance circularly polarized light detector is fabricated, successfully enabling detection from ultraviolet (300 nm) to near-infrared (1100 nm). The chiroptical detector presents an excellent ability to distinguish right-handed and left-handed circularly polarized light, where dissymmetries in detectivity, responsivity, and electric current are obtained and then optimized. The dissymmetry in electric current can be increased from 0.18 to 0.23 once an external magnetic field is applied. This is a very rare report on the dissymmetry tunability by an external field in chiroptical detectors. Moreover, the chirality-generated orbital angular momentum is one of the key factors determining the performance of the circularly polarized light detection. Overall, the organic chiroptical detector presents excellent stability in detection, which provides great potential for future flexible and compact integrated platforms.

Ageing and Inflammation: What Happens in Periodontium?

Periodontitis is a chronic inflammatory disease with a high incidence and severity in the elderly population, making it a significant public health concern. Ageing is a primary risk factor for the development of periodontitis, exacerbating alveolar bone loss and leading to tooth loss in the geriatric population. Despite extensive research, the precise molecular mechanisms underlying the relationship between ageing and periodontitis remain elusive. Understanding the intricate mechanisms that connect ageing and inflammation may help reveal new therapeutic targets and provide valuable options to tackle the challenges encountered by the rapidly expanding global ageing population. In this review, we highlight the latest scientific breakthroughs in the pathways by which inflammaging mediates the decline in periodontal function and triggers the onset of periodontitis. We also provide a comprehensive overview of the latest findings and discuss potential avenues for future research in this critical area of investigation.