Comprehensive identification, characterization, and expression analysis of the MORF gene family in Brassica napus.

BACKGROUND: RNA editing in chloroplast and mitochondrion transcripts of plants is an important type of post-transcriptional RNA modification in which members of the multiple organellar RNA editing factor gene family (MORF) play a crucial role. However, a systematic identification and characterization of MORF members in Brassica napus is still lacking. RESULTS: In this study, a total of 43 MORF genes were identified from the genome of the Brassica napus cultivar "Zhongshuang 11". The Brassica napus MORF (BnMORF) family members were divided into three groups through phylogenetic analysis. BnMORF genes distributed on 14 chromosomes and expanded due to segmental duplication and whole genome duplication repetitions. The majority of BnMORF proteins were predicted to be localized to mitochondria and chloroplasts. The promoter cis-regulatory element analysis, spatial-temporal expression profiling, and co-expression network of BnMORF genes indicated the involvement of BnMORF genes in stress and phytohormone responses, as well as growth and development. CONCLUSION: This study provides a comprehensive analysis of BnMORF genes and lays a foundation for further exploring their physiological functions in Brassica napus.

Fractional exhaled nitric oxide in idiopathic pulmonary arterial hypertension and mixed connective tissue disease complicating pulmonary hypertension.

BACKGROUND: Fractional exhaled nitric oxide (FeNO) has been extensively studied in various causes of pulmonary hypertension (PH), but its utility as a noninvasive marker remains highly debated. The objective of our study was to assess FeNO levels in patients with idiopathic pulmonary arterial hypertension (IPAH) and mixed connective tissue disease complicating pulmonary hypertension (MCTD-PH), and to correlate them with respiratory functional data, disease severity, and cardiopulmonary function. METHODS: We collected data from 54 patients diagnosed with IPAH and 78 patients diagnosed with MCTD-PH at the Shanghai Pulmonary Hospital Affiliated to Tongji University. Our data collection included measurements of brain natriuretic peptide (pro-BNP), cardiopulmonary exercise test (CPET), pulmonary function test (PFT), impulse oscillometry (IOS), and FeNO levels. Additionally, we assessed World Health Organization functional class (WHO-FC) of each patient. RESULTS: (1) The fractional exhaled concentration of nitric oxide was notably higher in patients with IPAH compared to those with MCTD-PH. Furthermore, within the IPAH group, FeNO levels were found to be lower in cases of severe IPAH compared to mild IPAH (P = 0.024); (2) In severe pulmonary hypertension as per the WHO-FC classification, FeNO levels in IPAH exhibited negative correlations with FEV1/FVC (Forced Expiratory Velocity at one second /Forced Vital Capacity), MEF50% (Maximum Expiratory Flow at 50%), MEF25%, and MMEF75/25% (Maximum Mid-expiratory Flow between 75% and 25%), while in severe MCTD-PH, FeNO levels were negatively correlated with R20% (Resistance at 20 Hz); (3) ROC (Receiving operator characteristic curve) analysis indicated that the optimal cutoff value of FeNO for diagnosing severe IPAH was 23ppb; (4) While FeNO levels tend to be negatively correlated with peakPETO2(peak end-tidal partial pressure for oxygen) in severe IPAH, in mild IPAH they had a positive correlation to peakO2/Heart rate (HR). An interesting find was observed in cases of severe MCTD-PH, where FeNO levels were negatively correlated with HR and respiratory exchange ratio (RER), while positively correlated with O2/HR throughout the cardiopulmonary exercise test. CONCLUSION: FeNO levels serve as a non-invasive measure of IPAH severity. Although FeNO levels may not assess the severity of MCTD-PH, their significant makes them a valuable tool when assessing severe MCTD-PH.

Keratinocyte differentiation factor 1 enhances cervical cancer cell viability and migration by activating the PI3K/AKT pathway.

BACKGROUND: The aim of This study is to investigate the effects of Keratinocyte differentiation factor 1 (KDF1) on cervical cancer cells and the underlying mechanisms. METHODS: The Gene Expression Profiling Interactive Analysis database was used to analyse KDF1 expression in cervical cancer and paracancerous tissue samples. The correlation between the expression of KDF1 and clinicopathological features was also analysed. Cervical cancer cells (HeLa cells) with KDF1 overexpression or knockdown were constructed. Reverse transcription polymerase chain reaction was used to detect the mRNA expression of KDF1 in cervical cancer tissues and cells. In different treatment groups of cervical cancer cells, protein expression of KDF1, cell viability, invasion, and migration were subsequently confirmed by western blotting, CCK-8 assay, transwell assay, and wound healing assay, respectively. A PI3K inhibitor (LY294002) was used to detect the effect of KDF1 on the phosphoinositide 3-kinase (PI3K)/Protein Kinase B (AKT) pathway. RESULTS: KDF1 was highly expressed in cervical cancer tissues and cell lines (p < 0.01), and was significantly associated with poor prognosis (p < 0.05). Knockdown of KDF1 in HeLa cells resulted in a significant decrease in cell proliferation, migration, and invasion, as well as phosphorylated PI3K (P-PI3K) and p-AKT levels (p < 0.01). However, KDF1 overexpression activated the PI3K/AKT pathway and significantly enhanced the malignant biological behaviour of cervical cancer cells (p < 0.01). Additionally, the PI3K inhibitor reduced the proliferation, invasion, and migration of HeLa cells overexpressing KDF1 (p < 0.01). CONCLUSION: KDF1 enhances cervical cancer viability and migration by activating the PI3K/AKT pathway, and may serve as a therapeutic target for patients with cervical cancer.

Cervical cancer is the fourth most common cancer in women worldwide and the leading cause of cancer-related deaths. Keratinocyte differentiation factor 1 (KDF1) is a protein-coding gene containing an unknown functional domain (DUF4656).In the present study, we detected the expression of KDF1 in cervical cancer tissues and cells. Furthermore, we investigated the effects of KDF1 on the proliferation, invasion, and migration of cervical cancer cells and the downstream mechanisms of KDF1.KDF1 promotes cervical cancer cell proliferation, invasion, and migration by activating the PI3K/AKT pathway, and KDF1 may be a biomarker for the treatment of cervical cancer.

Trends in weight change patterns across life course among US adults, 1988-2018: population-based study.

BACKGROUND: To examine trends in weight change patterns from young adulthood through midlife to late adulthood and their sex and racial/ethnic disparities among US adults from 1988 to 2018. METHODS: A total of 48,969 participants from the National Health and Nutrition Examination Survey 1988-1994 and 2001-2018 were included. RESULTS: The age-adjusted prevalence of stable non-obesity between young adulthood and midlife declined significantly from 84.1% (95 CI, 82.9-85.3%) in 1988-1994 to 68.7% (67.1-70.2%) in 2013-2018, and between midlife and late adulthood from 71.2% (69.2-73.1%) to 52.4% (50.5-54.2%). The magnitude of increase in the prevalence of weight gain from young adulthood to midlife (from 10.8% [9.9-11.6%] in 1988-1994 to 21.2% [20-22.3%] in 2013-2018; P < 0.001 for trend) was greater than that from midlife to late adulthood (from 14.1% [12.9-15.3%] to 17.2% [16.2-18.1%]; P = 0.002 for trend). The magnitude of increase in the prevalence of stable obesity from young adulthood to midlife (from 3.9% [3.1-4.8%] in 1988-1994 to 9.2% [8.2-10.3%] in 2013-2018; P < 0.001 for trend) was smaller than that from midlife to late adulthood (from 11.2% [10.1-12.2%] to 24.8% [23.3-26.3%]; P < 0.001 for trend). The declining trends in the prevalence of stable non-obesity and increasing trends in the prevalence of weight gain and stable obesity from young adulthood through midlife to late adulthood were also observed for all sex and race/ethnicity subgroups. The magnitude of decrease in the prevalence of stable non-obesity, and the magnitude of increase in the prevalence of weight gain from young adulthood through midlife to late adulthood were greater in men than in women (all P for interaction < 0.01). Weight gain patterns for those aged ≥ 65 years were substantially different from the younger age groups. CONCLUSIONS: More young people born in later years are encountering obesity and accumulate greater obesity exposure across their lives than young people born in earlier years.

The ATP Synthase γ Subunit ATPC1 Regulates RNA Editing in Chloroplasts.

RNA editing is the process of modifying RNA molecules by inserting, deleting, or substituting nucleotides. In flowering plants, RNA editing occurs predominantly in RNAs encoded by the organellar genomes of mitochondria and chloroplasts, and the main type of editing involves the substitution of cytidine with uridine at specific sites. Abnormal RNA editing in plants can affect gene expression, organelle function, plant growth, and reproduction. In this study, we report that ATPC1, the gamma subunit of ATP synthase in Arabidopsis chloroplasts, has an unexpected role in the regulation of editing at multiple sites of plastid RNAs. The loss of function of ATPC1 severely arrests chloroplast development, causing a pale-green phenotype and early seedling lethality. Disruption of ATPC1 increases the editing of matK-640, rps12-i-58, atpH-3'UTR-13210, and ycf2-as-91535 sites while decreasing the editing of rpl23-89, rpoA-200, rpoC1-488, and ndhD-2 sites. We further show that ATPC1 participates in RNA editing by interacting with known multiple-site chloroplast RNA editing factors, including MORFs, ORRM1, and OZ1. The transcriptome in the atpc1 mutant is profoundly affected, with a pattern of defective expression of chloroplast development-related genes. These results reveal that the ATP synthase γ subunit ATPC1 is involved in multiple-site RNA editing in Arabidopsis chloroplasts.

Long-term variability of impulse oscillometry and spirometry in stable COPD and asthma.

BACKGROUND: While optimizing spirometry is a challenge for lung function labs, long-term variability if any between IOS (impulse oscillometry) parameters and spirometry is not clearly known in stable COPD (chronic obstructive pulmonary disease) and chronic asthma. The forced oscillation technique is increasingly employed in routine lung function testing. Our aim in this study was to determine the variability in oscillometric parameters between clinic visits over weeks or months in two patient groups during a period of clinical stability. Moreover, the research assessed relationships between IOS parameters long-term variability and COPD severity. METHODS: We used data from 73 patients with stable COPD and 119 patients with stable asthma at the Shanghai Pulmonary Hospital Affiliated to Tongji University. Patients were included if they had three or more clinic visits where spirometry and IOS were performed during a clinically stable period. Data recorded from the first three visits were used. The standard deviation (SDbv), the coefficient of variation (COV), intraclass correlation coefficient (ICC) and the coefficient of repeatability (COR) were calculated, Wilcoxon Mann-Whitney test was used for data that did not conform to normality of distributions, Kruskal Wallis test was used to compare with multiple groups, post hoc comparison was analyzed by Bonferroni, Spearman correlation coefficients for non-parametric data, the multiple regression analyses to determine the relationship between long-term variability and airflow obstruction. RESULTS: (1) The repeatability of IOS resistance parameters with ICC values > 0.8 was high in COPD and asthma. ICC values of IOS resistance parameters were higher than IOS reactance parameters; (2) the repeatability of spirometry parameters with ICC values < 0.8 was lower than IOS resistance parameters in different GOLD (the Global Initiative for Chronic Obstructive Lung Disease) stages, the higher the stage the worse the repeatability; (3) the severity of airflow obstruction was correlated with long-term variability of R5 (R at 5 Hz) (P < 0.05) in GOLD4, not with long-term variability of R20 (R at 20 Hz) (P > 0.05) and R5-R20 (P > 0.05). CONCLUSION: IOS resistance parameters have good long-term repeatability in asthma and COPD. Additionally, repeatability of spirometry parameters is lower than IOS resistance parameters in different GOLD stages.

Catheter ablation of atrial tachycardia originated from the left atrial epicardium.

A patient was referred with frequent atrial tachycardia (AT) attacks. Activation mapping showed that the left atrium (LA) roof was earlier activated with a broad region, and right atrial activation was delayed. The far-field A wave corresponding to the pulmonary artery area was advanced with failed ablation. Therefore, the AT could be left atrial epicardial origin, which was further confirmed by the successful ablation at earliest activated site at the epicardium.

Variation of PetCO2 during incremental exercise and severity of IPAH and CTEPH.

BACKGROUND AND OBJECTIVE: End-tidal PCO2 (PetCO2) patterns during exercise testing as well as ventilatory equivalents for CO2 have been reported for different pulmonary vascular diseases but seldomly for the significant differences in exercise response depending on the etiology of pulmonary hypertension. We aimed to compare PetCO2 change pattern in IPAH and CTEPH with varying severity during incremental cardiopulmonary exercise testing (CPET). METHODS: 164 IPAH patients and 135 CTEPH patients referred to Shanghai Pulmonary Hospital between 2012 and 2019 were retrospectively recruited into the study. All patients performed CPET and also underwent right-heart catheterization (RHC). Forty-four healthy subjects also performed CPET and were included as controls. RESULTS: PetCO2 was significantly lower in IPAH and CTEPH patients as compared to normal subjects. Moreover, the PetCO2 did not rise, in fact fell from rest to anaerobic threshold (AT), then further decreased until peak in both IPAH and CTEPH. PetCO2 value at rest, unloaded, AT and peak were proportionately reduced as the World Health Organization functional class (WHO-Fc) increased in both IPAH and CTEPH patients. The PETCO2 in IPAH patients had significant differences during all phases of exercise between WHO-Fc I-II and III-IV subgroup. CTEPH also demonstrated significant difference except for PetCO2 at peak. PetCO2 values were significantly higher in IPAH during all phases of exercise as compared to CTEPH patients (all P < 0.001). PeakVO2%pred correlated significantly with PetCO2 at rest (r = 0.477, P < 0.001), AT (r = 0.609, P < 0.001) and peak exercise (r = 0.576, P < 0.001) in IPAH. N-terminal natriuretic peptide type-B (NT-proBNP) also correlated markedly with PetCO2, with a correlation coefficient of - 0.326 to - 0.427 (all P < 0.001). Additionally, PetCO2 at rest, at AT and at peak correlated positively with peakVO2%pred and showed an inverse correlation with NT-proBNP in CTEPH patients (all P < 0.05). CONCLUSIONS: PetCO2 during exercise in IPAH and CTEPH patients was significantly different from normal subjects. Moreover, PetCO2 values were significantly higher in IPAH during all phases of exercise as compared to CTEPH patients (all P < 0.001). PetCO2 was progressively more abnormal with increasing disease severity according to peakVO2%pred and WHO-Fc.

Cardiac Computed Tomography-Based Epicardial Adipose Tissue Assessment Reveals Association With Electroanatomical Voltage Mapping in Patients With Atrial Fibrillation.

BACKGROUND: Epicardial adipose tissue (EAT) around the left atrium (LA) can change the electric conduction of the LA, potentially leading to atrial fibrillation (AF). AIM: The aim of this study was to evaluate whether an association existed between EAT and the electrophysiological properties of adjacent atrial myocardium in patients with AF. METHOD: A total of 201 consecutive patients referred for initial AF catheter ablation were prospectively included. A preprocedural computed tomography scan was performed to assess total and LA-EAT parameters. Detailed point-by-point voltage mapping using an electroanatomical mapping system was realised to assess the LA low-voltage zone (LVZ), defined as an area with bipolar electrograms ≤0.5 mV during sinus rhythm. RESULTS: Ninety-one (91) patients (45.3%) presented at least one LVZ. They had a significantly more severe AF pattern (p=0.04) than patients without LVZ, and little difference existed with regard to other clinical variables. Patients with LVZ presented significantly more total EAT volume (162.4±71.3 mL vs 135.5±57.2 mL; p=0.03) and LA-EAT volume (26.4±15.9 mL vs 20.9±10.5 mL; p<0.01) than no-LVZ patients. Multivariable logistic regression analyses revealed total EAT volume index to be an independent predictor of the presence of LVZ (odds ratio [OR] 1.01; 95% confidence interval [CI] 1.01-1.04; p<0.01) and LA-EAT percentage to be an independent predictor of severe LVZ (OR 1.34; 95% CI 1.18-1.64; p<0.001). CONCLUSIONS: The EAT volume and its distribution around the LA may indicate the presence and severity of LVZ. The assessment of the volume of EAT and its distribution may lead to better risk stratification in patients with AF.

Emotional Stress Induces Structural Plasticity in Bergmann Glial Cells via an AC5-CPEB3-GluA1 Pathway.

Stress alters brain function by modifying the structure and function of neurons and astrocytes. The fine processes of astrocytes are critical for the clearance of neurotransmitters during synaptic transmission. Thus, experience-dependent remodeling of glial processes is anticipated to alter the output of neural circuits. However, the molecular mechanisms that underlie glial structural plasticity are not known. Here we show that a single exposure of male and female mice to an acute stress produced a long-lasting retraction of the lateral processes of cerebellar Bergmann glial cells. These cells express the GluA1 subunit of AMPA-type glutamate receptors, and GluA1 knockdown is known to shorten the length of glial processes. We found that stress reduced the level of GluA1 protein and AMPA receptor-mediated currents in Bergmann glial cells, and these effects were absent in mice devoid of CPEB3, a protein that binds to GluA1 mRNA and regulates GluA1 protein synthesis. Administration of a ß-adrenergic receptor blocker attenuated the reduction in GluA1, and deletion of adenylate cyclase 5 prevented GluA1 suppression. Therefore, stress suppresses GluA1 protein synthesis via an adrenergic/adenylyl cyclase/CPEB3 pathway, and reduces the length of astrocyte lateral processes. Our results identify a novel mechanism for GluA1 subunit plasticity in non-neuronal cells and suggest a previously unappreciated role for AMPA receptors in stress-induced astrocytic remodeling.SIGNIFICANCE STATEMENT Astrocytes play important roles in synaptic transmission by extending fine processes around synapses. In this study, we showed that a single exposure to an acute stress triggered a retraction of lateral/fine processes in mouse cerebellar astrocytes. These astrocytes express GluA1, a glutamate receptor subunit known to lengthen astrocyte processes. We showed that astrocytic structural changes are associated with a reduction of GluA1 protein levels. This requires activation of ß-adrenergic receptors and is triggered by noradrenaline released during stress. We identified adenylyl cyclase 5, an enzyme that elevates cAMP levels, as a downstream effector and found that lowering GluA1 levels depends on CPEB3 proteins that bind to GluA1 mRNA. Therefore, stress regulates GluA1 protein synthesis via an adrenergic/adenylyl cyclase/CPEB3 pathway in astrocytes and remodels their fine processes.

Cardiopulmonary exercise testing and pulmonary function testing for predicting the severity of CTEPH.

BACKGROUND: Cardiopulmonary exercise testing (CPET) and pulmonary function testing (PFT) are noninvasive methods to evaluate the respiratory and circulatory systems. This research aims to evaluate and monitor chronic thromboembolic pulmonary hypertension (CTEPH) noninvasively and effectively by these two methods. Moreover, the research assesses the predictive value of CPET and PFT parameters for severe CTEPH. METHODS: We used data from 86 patients with CTEPH (55 for test set, and 31 for validation set) at the Shanghai Pulmonary Hospital Affiliated to Tongji University. The clinical, PFT and CPET data of CTEPH patients of different severity classified according to pulmonary artery pressure (PAP) (mm Hg) were collected and compared. Logistic regression analysis was performed to appraise the predictive value of each PFT and CPET parameter for severe CTEPH. The performance of CPET parameters for predicting severe CTEPH was determined by receiver operating characteristic (ROC) curves and calibration curves. RESULTS: Data showed that minute ventilation at anaerobic threshold (VE @ AT) (L/min) and oxygen uptake at peak (VO2 @ peak) (mL/kg/min) were independent predictors for severe CTEPH classified according to PAP (mm Hg). Additionally, the efficacy of VE @ AT (L/min) and VO2 @ peak (mL/kg/min) in identifying severe CTEPH was found to be moderate with the area under ROC curve (AUC) of 0.769 and 0.740, respectively. Furthermore, the combination of VE @ AT (L/min) and VO2 @ peak (mL/kg/min) had a moderate utility value in identifying severe CTEPH with the AUC of 0.843. CONCLUSION: Our research suggests that CPET and PFT can noninvasively and effectively evaluate, monitor and predict the severity of CTEPH.

Dexmedetomidine Preconditioning Protects Cardiomyocytes Against Hypoxia/Reoxygenation-Induced Necroptosis by Inhibiting HMGB1-Mediated Inflammation.

Myocardial ischemia/reperfusion (I/R) injury is a serious threat to the health of people around the world. Recent evidence has indicated that high-mobility group box-1 (HMGB1) is involved in I/R-induced inflammation, and inflammation can cause necroptosis of cells. Interestingly, dexmedetomidine (DEX) has anti-inflammatory properties. Therefore, we speculated that DEX preconditioning may suppress H/R-induced necroptosis by inhibiting expression of HMGB1 in cardiomyocytes. We found that hypoxia/reoxygenation (H/R) significantly increased cellular damage, as measured by cell viability (100 ± 3.26% vs. 53.33 ± 3.29, p < 0.01), CK-MB (1 vs. 3.25 ± 0.26, p < 0.01), cTnI (1 vs. 2.69 ± 0.31, p < 0.01), inflammation as indicated by TNF-α (1 ± 0.09 vs. 2.57 ± 0.12, p < 0.01), IL-1ß (1 ± 0.33 vs. 3.87 ± 0.41, p < 0.01) and IL-6 (1 ± 0.36 vs. 3.60 ± 0.45, p < 0.01), and necroptosis, which were accompanied by significantly increased protein levels of HMGB1. These changes [cellular damage as measured by cell viability (53.33 ± 3.29% vs. 67.59 ± 2.69%, p < 0.01), CK-MB (3.25 ± 0.26 vs. 2.27 ± 0.22, p < 0.01), cTnI (2.69 ± 0.31 vs. 1.90 ± 0.25, p < 0.01), inflammation as indicated by TNF-α (2.57 ± 0.12 vs. 1.75 ± 0.15, p < 0.01), IL-1ß (3.87 ± 0.41 vs. 2.09 ± 0.36, p < 0.01) and IL-6 (3.60 ± 0.45 vs. 2.21 ± 0.39, p < 0.01), and necroptosis proteins] were inhibited by DEX preconditioning. We also found that silencing expression of HMGB1 reinforced the protective effects of DEX preconditioning and overexpression of HMGB1 counteracted the protective effects of DEX preconditioning. Thus, we concluded that DEX preconditioning inhibits H/R-induced necroptosis by inhibiting expression of HMGB1 in cardiomyocytes.

Cholecystectomy versus central obesity or insulin resistance in relation to the risk of nonalcoholic fatty liver disease: the third US National Health and Nutrition Examination Survey.

BACKGROUND: Cholecystectomy, central obesity, and insulin resistance (IR) are established risk factors for nonalcoholic fatty liver disease (NAFLD). We aimed to examine the relative contributions and combined association of cholecystectomy and central obesity/IR with NAFLD risk. METHODS: We conducted a cross-sectional analysis of data from the third National Health and Nutrition Examination Survey (NHANES III), in which ultrasonography was performed. Odds ratios (ORs) and 95% confidence intervals for NAFLD were estimated using logistic regression. RESULTS: Cholecystectomy associated with a higher prevalence of NAFLD compared with gallstones among both centrally obese and non-centrally-obese subjects. Gallstones associated with a higher prevalence of NAFLD only in the presence of central obesity. In centrally obese participants, the OR increased from 2.67 (2.15-3.32) for participants without gallstone disease to 6.73 (4.40-10.29) for participants with cholecystectomy. In participants with cholecystectomy, the OR increased from 2.57 (1.35-4.89) for participants without central obesity to 6.73 (4.40-10.29) for centrally obese counterparts. We observed a modest increase in the risk of NAFLD with cholecystectomy compared with a large increase in the risk with IR or metabolic syndrome. CONCLUSION: The magnitude of the NAFLD risk contributed by cholecystectomy was similar to central obesity in combined analyses. The magnitude of the association with IR or metabolic syndrome was greater than with cholecystectomy.

Non-HDL cholesterol and LDL cholesterol in the dyslipidemic classification in patients with nonalcoholic fatty liver disease.

BACKGROUND: Low-density lipoprotein cholesterol (LDL-C) always underestimates the true cholesterol burden in patients with nonalcoholic fatty liver disease (NAFLD). We aimed to compare LDL-C and non-high-density lipoprotein cholesterol (non-HDL-C) in the identification of high-risk dyslipidemic phenotypes in those with NAFLD. METHODS: We conducted a cross-sectional analysis using a cohort of 9560 apparently healthy Chinese adults who underwent comprehensive health checkups including abdominal ultrasonography. RESULTS: Among 3709 patients with NAFLD, the prevalence of abnormal LDL using LDL-C was 68.5%, whereas the prevalence was relatively lower when using non-HDL-C (55.9%). The concordance between non-HDL-C- and LDL-C-based diagnoses of abnormal LDL was similar in the hypertriglyceridemic (ҝ = 0.56; 95% CI 0.52-0.60) and normotriglyceridemic subgroups (ҝ = 0.47; 95% CI 0.44-0.51). Non-HDL-C detected fewer patients with abnormal LDL than LDL-C in normotriglyceridemic patients. However, non-HDL-C detected more patients with abnormal LDL than LDL-C in hypertriglyceridemic patients: 114 of the 1662 patients considered as abnormal LDL according to LDL-C fell into the normonon-HDL-C phenotype, whereas 204 of the 1662 patients considered as abnormal LDL according to non-HDL-C fell into the normoLDL-C phenotype. CONCLUSION: Among patients with NAFLD, LDL-C is superior to non-HDL-C in the detection of high-risk phenotypes in normotriglyceridemic patients, whereas non-HDL-C seems to be superior in hypertriglyceridemic patients.

Trends in cardiovascular risk factors among U.S. men and women with and without diabetes, 1988-2014.

BACKGROUND: Studies evidenced that reduction in cardiovascular disease (CVD) mortality in diabetic patients can be attributed to improvements in major CVD risk factors and evidence-based treatments. Furthermore, studies showed that the relative risk of CVD mortality associated with diabetes compared with non-diabetes is stronger in women than in men. Hence, we aimed to examine trends in CVD risk factors and intervention measures by sex and diabetic status. METHODS: Analysis of 5 distinct cross-sectional National Health and Nutrition Examination Surveys, 1988-1994, 1999-2002, 2003-2006, 2007-2010, and 2010-2014. Since detailed information on nontraditional risk factors such as sleep apnea was not available in each NHANES survey, traditional CVD risk factors including obesity, hypertension, and dyslipidemia were assessed in the study. To assess whether changes throughout the 27-year period differed by diabetes status, a logistic regression analysis was utilized to examine potential interaction effects between survey and diabetes. The similar process was repeated for sex. RESULTS: Means of all risk factors except body mass index and waist circumference decreased and the prevalence of antihypertensive and lipid-lowering medication use increased over time among diabetic and non-diabetic men and women. For both men and women, survey × diabetes status interaction terms for changes in HDL-cholesterol and triglyceride levels were not statistically significant, while the prevalence of antihypertensive and lipid-lowering medication use increased more in diabetic than in non-diabetic persons (all P < 0.001). For women, survey × diabetes status interaction terms indicated that compared with the first survey, total cholesterol, LDL-cholesterol, and non-HDL-cholesterol fallen more in diabetic than in non-diabetic persons (all P < 0.001). In the diabetic state, men experienced similar changes in means of all CVD risk factors and the prevalence of antihypertensive and lipid-lowering medication use as women (all P for interactions between survey and sex were >0.01). CONCLUSIONS: The major traditional CVD risk factors in diabetic men decreased to the same extent that they did for non-diabetic men. The magnitude of changes in the favorable trends in diabetic women was of similar or greater compared with those among non-diabetic women. Diabetic women had as good an improvement in CVD risk factors as diabetic men.

External Heavy-Atom Effect via Orbital Interactions Revealed by Single-Crystal X-ray Diffraction.

Enhanced spin-orbit coupling through external heavy-atom effect (EHE) has been routinely used to induce room-temperature phosphorescence (RTP) for purely organic molecular materials. Therefore, understanding the nature of EHE, i.e., the specific orbital interactions between the external heavy atom and the luminophore, is of essential importance in molecular design. For organic systems, halogens (e.g., Cl, Br, and I) are the most commonly seen heavy atoms serving to realize the EHE-related RTP. In this report, we conduct an investigation on how heavy-atom perturbers and aromatic luminophores interact on the basis of data obtained from crystallography. We synthesized two classes of molecular systems including N-haloalkyl-substituted carbazoles and quinolinium halides, where the luminescent molecules are considered as "base" or "acid" relative to the heavy-atom perturbers, respectively. We propose that electron donation from a π molecular orbital (MO) of the carbazole to the σ* MO of the C-X bond (π/σ*) and n electron donation to a π* MO of the quinolinium moiety (n/π*) are responsible for the EHE (RTP) in the solid state, respectively.

Combined influence of nonalcoholic fatty liver and body size phenotypes on diabetes risk.

BACKGROUND: We aimed to determine the association between nonalcoholic fatty liver disease (NAFLD) and diabetes risk among body size phenotypes which was based on cross-classification of body mass index (BMI) categories (normal or overweight/obesity) and metabolic status (metabolically health or metabolically at-risk). METHODS: We conducted a cross-sectional analysis using a cohort of 10,761 apparently healthy Chinese adults who underwent comprehensive health checkups including abdominal ultrasonography. Subjects were classified as metabolically at-risk by having any two of the following, consistent with the Adult Treatment Panel-III metabolic syndrome definition: (1) systolic/diastolic blood pressure ≥130/85 mmHg, (2) triglycerides ≥1.7 mmol/L, (3) fasting blood glucose ≥5.6 mmol/L, (4) HDL-cholesterol ≥1.0/1.3 mmol/L for men/women. RESULTS: Among participants without metabolically at-risk, multivariate-adjusted odds ratios (ORs) for diabetes from NAFLD compared with those without NAFLD in the normal-weight (BMI <23 kg/m(2)) and overweight/obese (BMI ≥23 kg/m(2)) group were 2.10 (1.85-3.93) and 1.85 (1.35-2.53), respectively. Among participants with metabolically at-risk, the significant association between NAFLD and diabetes was lost, regardless of obesity status. There were only 27.1% subjects with the presence of the three factors (overweight/obesity, NAFLD, and metabolically at-risk) occurring together, while the three factors occurring together was common (56.16%) in diabetic individuals. The multivariate-adjusted ORs for diabetes were 1.1 (0.61-1.98) for overweight/obesity, 2.23 (1.05-5.14) for NAFLD, and 8.04 (5.0-12.09) for metabolically at-risk. The OR for the presence of all the three factors occurring together was 23.22 (13.96-38.63). CONCLUSIONS: NAFLD was associated with diabetes risk among participants without metabolically at-risk. The clustering of overweight/obesity, NAFLD, and metabolically at-risk is common in diabetic subjects and strikingly and markedly increases the diabetes risk.

Polymerization-enhanced intersystem crossing: new strategy to achieve long-lived excitons.

For a singlet-triplet coupled molecular system, the efficiency of forward and reverse intersystem crossing processes can be enhanced by reducing the energy gap between the singlet and triplet excited states (ΔEST ), thus prolonging the exciton lifetimes. This has been proven beneficial for many emerging applications such as molecular luminescence, optoelectronics, and photonics. Here, a strategy is proposed to create small ΔEST by polymerizing fluorescent dye molecules, the efficacy of which is justified by density functional theory calculations and ultrafast spectroscopy. Thus, singlet-triplet exciton communication through polymerization-enhanced intersystem crossing is also proposed.

Aggregation-Induced Emission from Fluorophore-Quencher Dyads with Long-Lived Luminescence.

Aggregation-induced emission (AIE) is an important photophysical phenomenon in molecular materials and has found broad applications in optoelectronics, bioimaging, and chemosensing. Currently, the majority of reported AIE-active molecules are based on either propeller-shaped rotamers or donor-acceptor molecules with strong intramolecular charge-transfer states. Here, we report a new design motif, where a fluorophore is covalently tethered to a quencher, to expand the scope of AIE-active materials. The fluorophore-quencher dyad (FQD) is nonemissive in solutions due to photoinduced electron-transfer quenching but becomes luminescent in the solid state. The intrinsic emission lifetimes are found to be within the microseconds domain at both room and low temperatures. We performed single-crystal X-ray diffraction measurement for each of the FQDs as well as theoretical calculations to account for the possible origin of the long-lived AIE. These FQDs represent a new class of AIE-active molecules with potential applications in organic optoelectronics.