Lattice distortion inducing exciton splitting and coherent quantum beating in CsPbI3 perovskite quantum dots

Anisotropic exchange-splitting in semiconductor quantum dots (QDs) results in bright-exciton fine-structure-splitting (FSS) important for quantum information processing. Direct measurement of FSS usually requires single/few QDs at liquid-helium temperatures, because of its sensitivity to QD size and shape, whereas measuring and controlling FSS at an ensemble-level seem to be impossible unless all the dots are made to be nearly the same. Here we report strong bright-exciton FSS up to 1.6 meV in solution-processed CsPbI3 perovskite QDs, manifested as quantum beats in ensemble-level transient absorption at liquid-nitrogen to room temperatures. The splitting is robust to QD size and shape heterogeneity, and increases with decreasing temperature, pointing towards a mechanism associated with orthorhombic distortion of perovskite lattice. Effective-mass-approximation calculations reveal an intrinsic "fine-structure gap" that agrees well with the observed FSS. This gap stems from an avoided crossing of bright-excitons confined in orthorhombically-distorted QDs that are bounded by the pseudocubic {100} family of planes

Unveiling the link between systemic inflammation markers and cognitive performance among older adults in the US: A population-based study using NHANES 2011–2014 data

Purpose: This study aimed to evaluate the association between systemic inflammation markers and cognitive performance among older US adults. Methods: This cross-sectional study assessed 3,632 older participants from the 2011–2014 National Health and Nutrition Examination Survey (NHANES). The main analysis included participants aged over 60 years. Systemic inflammation markers were quantified by calculating the composite inflammation indicators from the blood routine count, and cognitive performance was assessed using Consortium to Establish a Registry for Alzheimer\u27s Disease (CERAD) test, Animal Fluency test (AFT), and Digit Symbol Substitution test (DSST). Results: There were 2,743 individuals enrolled in the current analysis. The overall mean age was 64.9 years and 48.7 % were males. The levels of SIRI and PIV were significant negative associated with scores of CERAD, CERAD delayed recall, and DSST in the unadjusted models. Moreover, SII were significant negative associated with scores of CERAD and CERAD delayed recall. After adjusting the covariates of demographics, lifestyle factors, history of chronic diseases and BMI, significant negative association were observed between systematic inflammation markers and cognitive performance. Additionally, a progressive and significant decrease in the score of cognitive performance assessments with the increased levels of SIRI, SII, and PIV were respectively observed. Finally, the correlation between systemic inflammation markers and cognitive performance were evidenced in the sensitive analysis. Conclusion: Findings support a strong inverse correlation between systemic inflammation markers and cognitive performance, suggesting that addressing inflammation could be a promising avenue for enhancing cognitive health and mitigating age-related cognitive decline

Mechanism of METTL14-mediated ERα m6A regulation of endometrial cancer metastasis

Background and purpose: Aberrant N6-methyladenosine (m6A) modification caused by dysregulation of methyltransferase-like factor 14 (METTL14) plays an important role in the progression of various cancers, and it is unclear whether it is involved in the endometrial cancer (EC) progression. This study aimed to investigate the role of aberrant m6A modification caused by dysregulation of METTL14 in EC invasion and metastasis. Methods: Ninety-six EC patients who underwent curative surgery in Qinghai Provincial People’s Hospital from 2017 to 2021 were enrolled. RNA (70 pairs) or proteins (10 pairs) were isolated from frozen tissues for real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR) or immunoblot analysis to assess METTL14 expression in EC. The expression of METTL14 and its correlation with clinicopathological features of EC were assessed. The biological effects of METTL14 in EC were determined in vitro and in vivo. Methylated RNA immunoprecipitation sequencing (MeRIP-seq) combined with RNA sequencing (RNA-seq), and following m6A dot blot, MeRIP-RTFQ-PCR, RIP-RTFQ-PCR or dual luciferase reporter assays were employed to screen and validate the candidate targets of METTL14. Results: The mRNA expression and protein levels of METTL14 were significantly downregulated in EC compared with matched adjacent tissues. Compared with the METTL14 high expression group, the METTL14 low expression group had a significant increase in International Federation of Gynecology and Obstetrics (FIGO) stage, infiltration depth, lymphovascular invasion, lymph node metastasis and the number of cases of tumor metastasis (P<0.05). Functionally, METTL14 inhibited the proliferation and invasive capacity of EC cells in vitro and in vivo. Mechanistically, METTL14-mediated demethylation of m6A resulted in post-transcriptional repression of estrogen receptor alpha (ERα). Furthermore, compared with METTL14, ERα induced oncogenic behavior of tumors. Conclusion: METTL14 attenuates ERα expression in EC cells in a m6A-dependent manner, thereby inhibiting tumor metastasis and invasion

Plasmon-gating photoluminescence in graphene/GeSi quantum dots hybrid structures

The ability to control light-matter interaction is central to several potential applications in lasing, sensing, and communication. Graphene plasmons provide a way of strongly enhancing the interaction and realizing ultrathin optoelectronic devices. Here, we find that photoluminescence (PL) intensities of the graphene/GeSi quantum dots hybrid structures are saturated and quenched under positive and negative voltages at the excitation of 325 nm, respectively. A mechanism called plasmon-gating effect is proposed to reveal the PL dependence of the hybrid structures on the external electric field. On the contrary, the PL intensities at the excitation of 405 and 795 nm of the hybrid structures are quenched due to the charge transfer by tuning the Fermi level of graphene or the blocking of the excitons recombination by excitons separation effect. The results also provide an evidence for the charge transfer mechanism. The plasmon gating effect on the PL provides a new way to control the optical properties of graphene/QD hybrid structures

Association of abnormal lung function and its subtypes with arterial stiffness: A longitudinal cohort study

BACKGROUND: Prior studies have reported the cross-sectional relationship between lung function and arterial stiffness, while the longitudinal association remains unclear to date. This study aimed to investigate whether abnormal lung function and its subtypes at baseline are associated with increased arterial stiffness using a cohort. METHODS AND RESULTS: This was a secondary analysis extracting 2461 participants from Beijing Health Management Cohort as baseline and annually followed for development of arterial stiffness. Abnormal lung function was defined by forced expiratory volume in 1s \u3c 80% of the predicted value, forced vital capacity of the predicted value, or forced expiratory volume in 1s/ forced vital capacity ratio \u3c 70%. Increased arterial stiffness was determined by brachial-ankle pulse wave velocity ≥ 1400 cm/s. Cox proportional hazards model was used to calculate the hazard ratio and population attributable fraction. The mean age was 42.8±8.1 years, and 444 (18.0%) cases developed increased arterial stiffness during a median follow-up of 3.0 years. The adjusted hazard ratio (95% CI) of arterial stiffness was 1.47 (95% CI, 1.10–1.96) for abnormal lung function, with a population attributable fraction of 3.9% (95% CI, 0.8–7.1). Of subtypes, only obstructive ventilatory dysfunction was significantly associated with arterial stiffness (adjusted hazard ratio, 2.06 [95% CI, 1.27–3.36]), not restricted ventilatory dysfunction (adjusted hazard ratio, 0.95 [95% CI, 0.54–1.65]). Consistent results were observed on multiple sensitivity analyses. CONCLUSIONS: Our study indicated a longitudinal association of abnormal lung function with increased arterial stiffness using a large cohort, especially for the obstructive ventilatory dysfunction

MAPK1 promotes the metastasis and invasion of gastric cancer as a bidirectional transcription factor

Background: The Mitogen-activated protein kinase 1 (MAPK1) has both independent functions of phosphorylating histones as a kinase and directly binding the promoter regions of genes to regulate gene expression as a transcription factor. Previous studies have identified elevated expression of MAPK1 in human gastric cancer, which is associated with its role as a kinase, facilitating the migration and invasion of gastric cancer cells. However, how MAPK1 binds to its target genes as a transcription factor and whether it modulates related gene expressions in gastric cancer remains unclear. Results: Here, we integrated biochemical assays (protein interactions and chromatin immunoprecipitation (ChIP)), cellular analysis assays (cell proliferation and migration), RNA sequencing, ChIP sequencing, and clinical analysis to investigate the potential genomic recognition patterns of MAPK1 in a human gastric adenocarcinoma cell-line (AGS) and to uncover its regulatory effect on gastric cancer progression. We confirmed that MAPK1 promotes AGS cells invasion and migration by regulating the target genes in different directions, up-regulating seven target genes (KRT13, KRT6A, KRT81, MYH15, STARD4, SYTL4, and TMEM267) and down-regulating one gene (FGG). Among them, five genes (FGG, MYH15, STARD4, SYTL4, and TMEM267) were first associated with cancer procession, while the other three (KRT81, KRT6A, and KRT13) have previously been confirmed to be related to cancer metastasis and migration. Conclusion: Our data showed that MAPK1 can bind to the promoter regions of these target genes to control their transcription as a bidirectional transcription factor, promoting AGS cell motility and invasion. Our research has expanded the understanding of the regulatory roles of MAPK1, enriched our knowledge of transcription factors, and provided novel candidates for cancer therapeutics

IgG N-glycosylation cardiovascular age tracks cardiovascular risk beyond calendar age

The use of an altered immunoglobulin G (IgG) N-glycan pattern as an inflammation metric has been reported in subclinical atherosclerosis and metabolic disorders, both of which are important risk factors in cardiovascular health. However, the usable capacity of IgG N-glycosylation profiles for the risk stratification of cardiovascular diseases (CVDs) remains unknown. This study aimed to develop a cardiovascular aging index for tracking cardiovascular risk using IgG N-glycans. This cross-sectional investigation enrolled 1465 individuals aged 40–70 years from the Busselton Healthy and Ageing Study. We stepwise selected the intersection of altered N-glycans using feature-selection methods in machine learning (recursive feature elimination and penalized regression algorithms) and developed an IgG N-glycosylation cardiovascular age (GlyCage) index to reflect the deviation from calendar age attributable to cardiovascular risk. The strongest contributors to GlyCage index were fucosylated N-glycans with bisecting N-acetylglucosamine (GlcNAc) (glycan peak 6 (GP6), FA2B,) and digalactosylated N-glycans with bisecting GlcNAc (GP13, A2BG2). A one-unit increase of GlyCage was significantly associated with a higher Framingham ten-year cardiovascular risk (odds ratio (OR), 1.09; 95% confidence interval (95% CI): 1.05–1.13) and probability of CVDs (OR, 1.07; 95% CI: 1.01–1.13) independent of calendar age. Individuals with excessive GlyCage (exceeding a calendar age \u3e 3 years) had an increased cardiovascular risk and probability of CVDs, with adjusted ORs of 2.22 (95% CI: 1.41–3.53) and 2.71 (95% CI: 1.25–6.41), respectively. The area under curve (AUC) values of discriminating high cardiovascular risk and events were 0.73 and 0.65 for GlyCage index, and 0.65 and 0.63 for calendar age. The GlyCage index developed in this study can thus be used to track cardiovascular health using IgG N-glycosylation profiles. The distance between GlyCage and calendar age independently indicates the cardiovascular risk, suggesting that IgG N-glycosylation plays a role in the pathogenesis of CVDs. The generalization of the observed associations and the predictive capability of GlyCage index require external and longitudinal validation in other populations

Combined evaluation of arterial stiffness, glycemic control and hypertension for macrovascular complications in type 2 diabetes

Background: Arterial stiffness, glycemic control and blood pressure are risk factors of macrovascular complications in type 2 diabetes. This study aimed to investigate the combined association of arterial stiffness, glycemic control and hypertension status with the occurrence of diabetic macrovascular complication. Methods: A total of 1870 patients of diabetes were enrolled from Beijing Health Management Cohort between 2008 and 2018 as baseline, and then followed for macrovascular complication onset. We proposed a composite risk score (0 – 4) by arterial stiffness severity, pool glycemic control and hypertension status. Cox model was used to estimate the hazard ratio (HR) and 95 % confidence interval (CI). Results: The mean age (SD) of this population was 59.90 (12.29) years. During a median follow-up of 4.0 years, 359 (19.2 %) patients developed macrovascular complication. Compared to the normal arterial stiffness and good glycemic control group, patients with severe arterial stiffness and pool glycemic control had the highest risk of macrovascular complications (HR: 2.73; 95 % CI: 1.42 – 5.25). Similarly, those of severe arterial stiffness and hypertension had the highest risk (HR: 2.69; 95 % CI: 1.61 – 4.50). Patients of the composite score \u3e 2 had a significantly increased risk of macrovascular complication. Conclusion: This study suggested the clinical importance of combined evaluation of arterial stiffness, glycemic control and hypertension status for the risk stratification and management of macrovascular complication of type 2 diabetes

Combined evaluation of arterial stiffness and blood pressure promotes risk stratification of peripheral arterial disease

Background: Previous studies have reported the separate association of arterial stiffness (AS) and blood pressure with peripheral arterial disease (PAD). Objectives: The aim of this study was to investigate the risk stratification capacity of AS on incident PAD beyond blood pressure status. Methods: A total of 8,960 participants from Beijing Health Management Cohort were enrolled at the first health visit between 2008 and 2018 and then followed until the incidence of PAD or 2019. Elevated AS was defined as brachial-ankle pulse-wave velocity (baPWV) \u3e 1,400 cm/s, including moderate stiffness (1,400 ≤ baPWV \u3c 1,800 cm/s) and severe stiffness (baPWV ≥ 1,800 cm/s). PAD was defined as ankle-brachial index \u3c 0.9. A frailty Cox model was used to calculate the HR, integrated discrimination improvement, and net reclassification improvement. Results: During follow-up, 225 participants (2.5%) developed PAD. After adjusting for confounding factors, the highest risk for PAD was observed in the group with elevated AS and blood pressure (HR: 2.253; 95% CI: 1.472-3.448). Among participants with ideal blood pressure and those with well-controlled hypertension, PAD risk was still significant for severe AS. The results remained consistent in multiple sensitivity analyses. In addition, baPWV significantly improved the predictive capacity for PAD risk beyond systolic and diastolic blood pressures (integrated discrimination improvement 0.020 and 0.190, net reclassification improvement 0.037 and 0.303). Conclusions: This study suggests the clinical importance of combined evaluation and control of AS and blood pressure for the risk stratification and prevention of PAD

Patterns of Convergence and Divergence Between Bipolar Disorder Type I and Type II: Evidence From Integrative Genomic Analyses

Aim: Genome-wide association studies (GWAS) analyses have revealed genetic evidence of bipolar disorder (BD), but little is known about the genetic structure of BD subtypes. We aimed to investigate the genetic overlap and distinction of bipolar type I (BD I) & type II (BD II) by conducting integrative post-GWAS analyses. Methods: We utilized single nucleotide polymorphism (SNP)-level approaches to uncover correlated and distinct genetic loci. Transcriptome-wide association analyses (TWAS) were then approached to pinpoint functional genes expressed in specific brain tissues and blood. Next, we performed cross-phenotype analysis, including exploring the potential causal associations between two BD subtypes and lithium responses and comparing the difference in genetic structures among four different psychiatric traits. Results: SNP-level evidence revealed three genomic loci, SLC25A17, ZNF184, and RPL10AP3, shared by BD I and II, and one locus (MAD1L1) and significant gene sets involved in calcium channel activity, neural and synapsed signals that distinguished two subtypes. TWAS data implicated different genes affecting BD I and II through expression in specific brain regions (nucleus accumbens for BD I). Cross-phenotype analyses indicated that BD I and II share continuous genetic structures with schizophrenia and major depressive disorder, which help fill the gaps left by the dichotomy of mental disorders. Conclusion: These combined evidences illustrate genetic convergence and divergence between BD I and II and provide an underlying biological and trans-diagnostic insight into major psychiatric disorders