Frailty Predicts Dementia and Death in Older Adults Living in Long-Term Care.

OBJECTIVES: To investigate how the accumulation of deficits traditionally related and not traditionally related to dementia predicts dementia and mortality. DESIGN: A retrospective cohort study with up to 9 years of follow-up. SETTING AND PARTICIPANTS: Long-term care residents aged ≥65 with or without dementia. METHODS: Frailty indices based on health deficit accumulation were constructed. The FI-t consisted of 27 deficits traditionally related to dementia; the FI-n consisted of 27 deficits not traditionally related to dementia; the FI-a consisted of all 54 deficits taken from the FI-t and the FI-n. RESULTS: In this long-term care sample (n = 29,758; mean age = 84.6 ± 8.0; 63.8% female), 91% of the residents had at least 1 impairment in activities of daily living, 61% had a diagnosis of dementia, and the vast majority were frail (53% had FI-a > 0.2). Residents with dementia had a higher FI-t compared with those without dementia (0.278 ± 0.110 vs. 0.272 ± 0.108), whereas residents without dementia had a higher FI-n (0.143 ± 0.082 vs. 0.136 ± 0.079). Within 9 years, 97% of the sample had died; a 0.01 increase of the FI-a was associated with a 4% increase of the mortality risk, adjusting for age, sex, admission year, stay length, and dementia type. Residents who developed dementia after admission to long-term care had higher baseline FI-t and FI-a (P's < .003) than those who remained without dementia. CONCLUSIONS AND IMPLICATIONS: Frailty is highly prevalent in older adults living in long-term care, irrespective of the presence or absence of dementia. Accumulation of deficits, either traditionally related or unrelated to dementia, is associated with risks of death and dementia, and more deficits increases the probability. Our findings have implications for improving the quality of care of older adults in long-term care, by monitoring the degree of frailty at admission, managing distinct needs in relation to dementia, and enhancing frailty level-informed care and services.

Low-dose naltrexone for post-COVID fatigue syndrome: a study protocol for a double-blind, randomised trial in British Columbia.

INTRODUCTION: A significant proportion of individuals suffering from post COVID-19 condition (PCC, also known as long COVID) can present with persistent, disabling fatigue similar to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and post-viral fatigue syndromes. There remains no clear pharmacological therapy for patients with this subtype of PCC, which can be referred to as post-COVID fatigue syndrome (PCFS). A low dose of the opioid antagonist naltrexone (ie, low-dose naltrexone (LDN)) has emerged as an off-label treatment for treating fatigue and other symptoms in PCC. However, only small, non-controlled studies have assessed LDN in PCC, so randomised trials are urgently required. METHODS AND ANALYSIS: A prospective, randomised, double-blind, parallel arm, placebo-controlled phase II trial will be performed to assess the efficacy of LDN for improving fatigue in PCFS. The trial will be decentralised and open to eligible individuals throughout the Canadian province of British Columbia (BC). Participants will be recruited through the province-wide Post-COVID-19 Interdisciplinary Clinical Care Network (PC-ICCN) and research volunteer platform (REACH BC). Eligible participants will be 19-69 years old, have had a confirmed or physician-suspected SARS-CoV-2 infection at least 3 months prior and meet clinical criteria for PCFS adapted from the Institute of Medicine ME/CFS criteria. Individuals who are taking opioid medications, have a history of ME/CFS prior to COVID-19 or history of significant liver disease will be excluded. Participants will be randomised to an LDN intervention arm (n=80) or placebo arm (n=80). Participants in each arm will be prescribed identical capsules starting at 1 mg daily and follow a prespecified schedule for up-titration to 4.5 mg daily or the maximum tolerated dose. The trial will be conducted over 16 weeks, with assessments at baseline, 6, 12 and 16 weeks. The primary outcome will be fatigue severity at 16 weeks evaluated by the Fatigue Severity Scale. Secondary outcomes will include pain Visual Analogue Scale score, overall symptom severity as measured by the Patient Phenotyping Questionnaire Short Form, 7-day step count and health-related quality of life measured by the EuroQol 5-Dimension questionnaire. ETHICS AND DISSEMINATION: The trial has been authorised by Health Canada and approved by The University of British Columbia/Children's and Women's Health Centre of British Columbia Research Ethics Board. On completion, findings will be disseminated to patients, caregivers and clinicians through engagement activities within existing PCC and ME/CFS networks. Results will be published in academic journals and presented at conferences. TRIAL REGISTRATION NUMBER: NCT05430152.

Brain vital signs as a quantitative measure of cognition: Methodological implementation in a care home environment.

Introduction: Managing cognitive function in care homes is a significant challenge. Individuals in care have a variety of scores across standard clinical assessments, such as the Mini-Mental Status Exam (MMSE), and many of them have scores that fall within the range associated with dementia. A recent methodological advance, brain vital sign monitoring through auditory event-related potentials, provides an objective and sensitive physiological measurement to track abnormalities, differences, or changes in cognitive function. Taking advantage of point-of-care accessibility, the current study evaluated the methodological feasibility, the assessment of whether a particular research method can be successfully implemented, of quantitatively measuring cognition of care home residents using brain vital signs. Secondarily, the current study examined the relationship between brain vital signs, specifically the cognitive processing associated N400 component, and MMSE scores in care home residents. Materials and methods: Brain vital signs used the established N100 (auditory sensation), P300 (basic attention), and N400 (cognitive processing) event-related potential (ERP) components. A total of 52 residents were enrolled, with all participants evaluated using the MMSE. Participants were assigned into homogeneous groups based on their MMSE scores, and were categorized into low (n = 14), medium (n = 17), and high (n = 13) MMSE groups. Both brain vital sign measures and underlying ERP waveforms were examined. Statistical analyses used partial least squares correlation (PLS) analyses in which both MMSE and age were included as factors, as well as jackknife approaches, to test for significant brain vital sign changes. Results: The current study successfully measured and analyzed standardized, quantifiable brain vital signs in a care home setting. ERP waveform data showed specific N400 changes between MMSE groups as a function of MMSE score. PLS analyses confirmed significant MMSE-related and age-related differences in the N400 amplitude (p < 0.05, corrected). Similarly, the jackknife approach emphasized the N400 latency difference between the low and high MMSE groups. Discussion and conclusion: It was possible to acquire brain vital signs measures in care home residents. Additionally, the current study evaluated brain vital signs relative to MMSE in this group. The comparison revealed significant decreasing in N400 response amplitude (cognitive processing) as a function of both MMSE score and age, as well as a slowing of N400 latency. The findings indicate that objective neurophysiological measures of impairment are detectable in care home residents across the span of MMSE scores. Direct comparison to MMSE- and age-related variables represents a critical initial step ahead of future studies that will investigate relative improvements in sensitivity, validity, reliability and related advantages of brain vital sign monitoring.

Abnormal expression of PRKAG2-AS1 in endothelial cells induced inflammation and apoptosis by reducing PRKAG2 expression.

PRKAG2 is required for the maintenance of cellular energy balance. PRKAG2-AS1, a long non-coding RNA (lncRNA), was found within the promoter region of PRKAG2. Despite the extensive expression of PRKAG2-AS1 in endothelial cells, the precise function and mechanism of this gene in endothelial cells have yet to be elucidated. The localization of PRKAG2-AS1 was predominantly observed in the nucleus, as revealed using nuclear and cytoplasmic fractionation and fluorescence in situ hybridization. The manipulation of PRKAG2-AS1 by knockdown and overexpression within the nucleus significantly altered PRKAG2 expression in a cis-regulatory manner. The expression of PRKAG2-AS1 and its target genes, PRKAG2b and PRKAG2d, was down-regulated in endothelial cells subjected to oxLDL and Hcy-induced injury. This finding suggests that PRKAG2-AS1 may be involved in the mechanism behind endothelial injury. The suppression of PRKAG2-AS1 specifically in the nucleus led to an upregulation of inflammatory molecules such as cytokines, adhesion molecules, and chemokines in endothelial cells. Additionally, this nuclear suppression of PRKAG2-AS1 facilitated the adherence of THP1 cells to endothelial cells. We confirmed the role of nuclear knockdown PRKAG2-AS1 in the induction of apoptosis and inhibition of cell proliferation, migration, and lumen formation through flow cytometry, TUNEL test, CCK8 assay, and cell scratching. Finally, it was determined that PRKAG2-AS1 exerts direct control over the transcription of PRKAG2 by its binding to their promoters. In conclusion, downregulation of PRKAG2-AS1 suppressed the proliferation and migration, promoted inflammation and apoptosis of endothelial cells, and thus contributed to the development of atherosclerosis resulting from endothelial cell injury.

Regulatory mechanisms of long non-coding RNAs on mitochondrial function in congestive heart failure.

Congestive heart failure (CHF) is a multifaceted cardiovascular condition that imposes significant economic and social burdens on society, while also presenting a dearth of efficacious treatment modalities. Long non-coding RNAs (lncRNAs) possess the ability to influence the pathophysiological mechanisms underlying cardiac disease through their regulation of gene transcription, translation, and post-translational modifications. Additionally, certain lncRNAs can be encoded by the mitochondrial genome, hence impacting mitochondrial function. The heart relies heavily on mitochondrial oxidative phosphorylation for approximately 95 % of its ATP production. Consequently, the primary determinant linking mitochondrial dysfunction to heart failure is the impairment of cardiac energy supply resulting from mitochondrial injury. Cardiac dysfunction can arise as a result of various factors, including metabolic disease, disturbances in calcium homeostasis, oxidative stress, apoptosis, and mitochondrial phagocytosis, all of which are facilitated by mitochondrial damage. Currently, an increasing body of research indicates that lncRNA plays a significant role in the regulation of mitochondrial activity, hence impacting heart failure. As a result, the goal of this paper is to propose new ideas and targets for clinical research and therapy of heart failure by reviewing recent research on the regulatory mechanism of mitochondrial function by novel lncRNAs.

The power of microdroplet photochemistry.

This study presents compelling evidence demonstrating that irradiation of the air-solution interface, whether achieved through the spraying of microdroplets into the air or by bubbling air through a solution, significantly accelerates the rate of photochemical reactions by orders of magnitude compared to identical reaction conditions in bulk solutions. We propose this approach as a novel and versatile method for harnessing solar energy in chemical transformations.

Morning blood pressure surge and intracranial atherosclerotic plaque characteristics: a high-resolution magnetic resonance vessel wall imaging study.

OBJECTIVE: To investigate the relationship between morning blood pressure surge (MBPS) and intracranial atherosclerotic plaque burden and vulnerability. METHODS: A total of 267 ischaemic stroke patients were retrospectively analysed. Sleep-trough and prewaking MBPS were calculated from ambulatory blood pressure monitoring (ABPM). Plaque characteristics, including intraplaque haemorrhage (IPH), maximum wall thickness (max WT), and stenosis degree, were obtained from high-resolution MR vessel wall imaging (HR-vwMRI). Linear and logistic regression were used to detect the association. RESULTS: Subjects with the top tertile of sleep-trough MBPS (≥15.1 mmHg) had a lower prevalence (9.1% vs. 19.6%, P = .029) of severe stenosis (≥70%) than others. Subjects within the top tertile of prewaking MBPS (≥7.6 mmHg) had a lower percentage of IPH (27.3% vs. 40.4%, P = .035) than others. After adjusting for stroke risk factors (age, sex, diabetes, hyperlipidaemia, hyperhomocysteinaemia, smoking, and family stroke history) and 24-h mean systolic blood pressure, 10 mmHg sleep-trough MBPS increment was associated with 0.07mm max WT reduction, and the top tertile MBPS group was associated with a lower chance of severe stenosis (odd ratio = 0.407, 95% CI, 0.175-0.950). Additionally, an increased prewaking MBPS is associated with a lower incidence of IPH, with OR = 0.531 (95% CI, 0.296-0.952). Subgroup analysis demonstrated that the positive findings could only be seen in non-diabetic subjects. CONCLUSION: Increment of MBPS is negatively associated with intracranial atherosclerotic plaque burden and vulnerability, and this relationship remains significant in the non-diabetic subgroup. ADVANCES IN KNOWLEDGE: This study provided evidence that MBPS was associated with the intracranial atherosclerotic plaque burden and vulnerability on HR-vwMRI.

LRENet: a location-related enhancement network for liver lesions in CT images.

Objective. Liver cancer is a major global health problem expected to increase by more than 55% by 2040. Accurate segmentation of liver tumors from computed tomography (CT) images is essential for diagnosis and treatment planning. However, this task is challenging due to the variations in liver size, the low contrast between tumor and normal tissue, and the noise in the images. APPROACH: In this study, we propose a novel method called location-related enhancement network (LRENet) which can enhance the contrast of liver lesions in CT images and facilitate their segmentation. LRENet consists of two steps: (1) locating the lesions and the surrounding tissues using a morphological approach and (2) enhancing the lesions and smoothing the other regions using a new loss function. MAIN RESULTS: We evaluated LRENet on two public datasets (LiTS and 3Dircadb01) and one dataset collected from a collaborative hospital (Liver cancer dateset), and compared it with state-of-the-art methods regarding several metrics. The results of the experiments showed that our proposed method outperformed the compared methods on three datasets in several metrics. We also trained the Swin-Transformer network on the enhanced datasets and showed that our method could improve the segmentation performance of both liver and lesions. SIGNIFICANCE: Our method has potential applications in clinical diagnosis and treatment planning, as it can provide more reliable and informative CT images of liver tumors.

Continuous ammonia synthesis from water and nitrogen via contact electrification.

We synthesized ammonia (NH3) by bubbling nitrogen (N2) gas into bulk liquid water (200 mL) containing 50 mg polytetrafluoroethylene (PTFE) particles (~5 µm in diameter) suspended with the help of a surfactant (Tween 20, ~0.05 vol.%) at room temperature (25 °C). Electron spin resonance spectroscopy and density functional theory calculations reveal that water acts as the proton donor for the reduction of N2. Moreover, isotopic labeling of the N2 gas shows that it is the source of nitrogen in the ammonia. We propose a mechanism for ammonia generation based on the activation of N2 caused by electron transfer and reduction processes driven by contact electrification. We optimized the pH of the PTFE suspension at 6.5 to 7.0 and employed ultrasonic mixing. We found an ammonia production rate of ~420 µmol L-1 h-1 per gram of PTFE particles for the conditions described above. This rate did not change more than 10% over an 8-h period of sustained reaction.

Physiological phenotypes have optimal values relevant to healthy aging: sweet spots deduced from the Canadian Longitudinal Study on Aging.

Previous observations on a group of exceptionally healthy "Super-Seniors" showed a lower variance of multiple physiological measures relevant for health than did a less healthy group of the same age. The finding was interpreted as the healthier individuals having physiological measurement values closer to an optimal level, or "sweet spot." Here, we tested the generalizability of the sweet-spot hypothesis in a larger community sample, comparing differences in the variance between healthier and less healthy groups. We apply this method to the Canadian Longitudinal Study on Aging (CLSA) comprehensive cohort of 30,097 participants aged 45 to 85 years with deep phenotype data. Data from both sexes and four age ranges were analyzed. Five instruments were used to represent different aspects of health, physical, and cognitive functioning. We tested 231 phenotypic measures for lower variance in the most healthy vs. least healthy quartile of each sex and age group, as classified by the five instruments. Segmented regression was used to determine sex-specific optimal values. One hundred forty-two physiological measures (61%) showed lower variance in the healthiest than in the least healthy group, in at least one sex and age group. The difference in variance was most significant for hemoglobin A1c and was also significant for many body composition measurements, but not for bone mineral density. Ninety-four phenotypes showed a nonmonotonic relationship with health, consistent with the idea of a sweet spot; for these, we determined optimal values and 95% confidence intervals that were generally narrower than the ranges of current clinical reference intervals. These findings for sweet spot discovery validate the proposed approach for identifying traits important for healthy aging.

Peripheral T-cell subsets in radiofrequency ablation for tumors from different origins.

BACKGROUNDS: Radiofrequency ablation (RFA) is known to destroy tumoral tissue and activate immune cells. This study aimed to investigate the impact of RFA on peripheral T-cell responses and its relationship with tumor origin and hepatitis status. METHODS: A retrospective analysis was conducted on 62 patients with various types of tumors, including hepatocellular carcinoma, colorectal cancer, lung cancer, breast cancer, and others, who underwent RFA treatment between June 2017 and December 2018. Blood samples were collected before and one day after RFA treatment. The peripheral T-cell subsets were measured by flow cytometry, and their changes were analyzed. RESULTS: The study found a decrease in the CD4+CD8-and CD4-CD8+ T-cell subsets after RFA, but no significant changes were observed in the populations of CD4+CD8+ and the CD4+CD8-/CD4-CD8+ ratio. Furthermore, no significant differences were observed in peripheral T-cell subsets concerning tumor type or hepatitis status. CONCLUSIONS: The study suggests that RFA treatment may have a short-term impact on peripheral T-cell responses, characterized by a decrease in certain T-cell subsets. However, these changes do not seem to be related to the tumor type or hepatitis status of the patients.

Noninvasive Detection of Skin Cancer by Imprint Desorption Electrospray Ionization Mass Spectrometry Imaging.

We report a technique for the noninvasive detection of skin cancer by imprint desorption electrospray ionization mass spectrometry imaging (DESI-MSI) using a transfer agent that is pressed against the tissue of interest. By noninvasively pressing a tape strip against human skin, metabolites, fatty acids, and lipids on the skin surface are transferred to the tape with little spatial distortion. Running DESI-MSI on the tape strip provides chemical images of the molecules on the skin surface, which are valuable for distinguishing cancer from healthy skin. Chemical components of the tissue imprint on the tape strip and the original basal cell carcinoma (BCC) section from the mass spectra show high consistency. By comparing MS images (about 150-µm resolution) of same molecules from the tape strip and from the BCC section, we confirm that chemical patterns are successfully transferred to the tape stripe. We also used the technique to distinguish cherry angiomas from normal human skin by comparing the molecular patterns from a tape strip. These results demonstrate the potential of the imprint DESI-MSI technique for the noninvasive detection of skin cancers as well as other skin diseases before and during clinical surgery.

Water Microdroplets-Initiated Methane Oxidation.

The special redox reactivity of water microdroplets causes "mild ignition" of methane gas to form methane oxygenates. The C(sp3)-H bond of methane can be activated by the hydroxyl radical (OH·) or the hydrogen radical (H·) across the air-water interface (AWI) of microdroplets to generate the methyl radical (CH3·). Once CH3· is formed, it undergoes free-radical reactions with O2 in the air, excessive OH· and H· across the AWI, and H2O2 present at the AWI and generated CH3· itself to produce methanol and other species. Production of the methanol and other oxygenates was confirmed by gas chromatography, mass spectrometry, and 1H- and 13C-nuclear magnetic resonance. Formic acid, acetic acid, ethanol, carbon dioxide, and methyl peroxide were also detected as methane oxidation byproducts. This water microdroplet-initiated oxidation process can be further enhanced under ultrasonication to yield 2.66 ± 0.77 mM methanol conversion from the methane gas in a single spray run for 30 min, with a selectivity of 19.2% compared with all other oxygenated species.

[Health Impact Analysis of Fine Particulate Pollution from Vehicles in the Beijing-Tianjin-Hebei Region].

Vehicle exhaust emissions are posing an increasingly adverse impact on urban air quality. The emission characteristics analysis and health effect assessment of specific air pollution sources can provide scientific evidence for environmental air quality management. The characteristics and health effects of PM2.5 emissions from vehicles and economic losses caused by them in the Beijing-Tianjin-Hebei Region were analyzed from 2010 to 2020. From 2010 to 2020, PM2.5 emissions from vehicles in the Beijing-Tianjin-Hebei Region showed an annual increase at first, followed by a slow decrease. According to the emission sharing ratios of different vehicle types, heavy-duty trucks and buses were the main contributors to PM2.5, with a total contribution rate of over 65.27%. The emission characteristics of vehicle pollutants varied in different cities. The contribution rate of pollutants in Beijing decreased significantly, and the emission reduction in other cities was also dramatic. The evaluation results of the impact of PM2.5 emissions from vehicles on human health showed that the number of health endpoints in the Beijing-Tianjin-Hebei Region was on the rise. In 2020, PM2.5 pollution caused approximately 34337 premature deaths (95% CI:9025-57209), 45500 hospitalizations (95% CI:10800-80200), 282300 outpatients (95% CI:140500-416300), and 439000 people to fall ill (95% CI:160300-679200). Beijing had the largest number of patients that presented different health endpoints. The total health and economic losses caused by PM2.5 emissions from vehicles in 2010, 2015, and 2020 were 27.742 billion yuan (95% CI:8.616-44.643 billion yuan), 90.608 billion yuan (95% CI:28.476-144.050 billion yuan), and 129.965 billion yuan (95% CI:40.829-205.245 billion yuan), respectively. In addition, due to the differences in vehicle ownership, PM2.5 concentrations, population, and economic losses per case of health outcome, the health effects and economic losses varied in different cities within the region. Among these cities, Beijing, Tianjin, Baoding, and Tangshan were at higher health risks and suffered more economic losses. The results of this study will help reduce the adverse effects on health and economic losses caused by pollution discharge and provide scientific evidence for environmental protection authorities to implement targeted pollution prevention and control.

Variations of arterial compliance and vascular resistance due to plaque or infarct in a single vascular territory of the middle cerebral artery.

Background: Arterial compliance (AC) and vascular resistance (VR) are crucial for the regulation capacity of the vascular system. However, alterations of these features and hemodynamics due to atherosclerosis in a single intracranial artery territory have not been extensively investigated. Thus this study aimed to examine the AC, VR, and hemodynamic variations due to plaque and infarction in the middle cerebral artery (MCA). Methods: Patients with symptomatic MCA atherosclerosis were recruited. Both sides of the MCA were assessed and then classified according to the following scheme: group 0, without plaque; group 1, with plaque but without infarct; group 2, with plaque and infarct in the supplying territories. Data on AC, VR, blood flow, and pulsatility index (PI) were obtained based on 4D flow magnetic resonance imaging (MRI) and the Windkessel model. Results: A total of 63 patients were recruited. After 17 MCAs were excluded (occlusion, n=6; poor image quality, n=11), datasets on 109 MCAs were finally collected and classified into group 0 (n=39), group 1 (n=40), and group 2 (n=30). From groups 0 to 2, there was a decrease in AC (0.0060±0.0031 vs. 0.0052±0.0029 vs. 0.0026±0.0020 mL/mmHg) and an increase in VR [28.65±16.11 vs. 42.59±27.53 vs. 63.21±40.37 mmHg/(mL/s)]. Compared to group 1, group 2 had significantly decreased AC (0.0052±0.0029 vs. 0.0026±0.0020 mL/mmHg; P=0.003) and increased VR [42.59±27.53 vs. 63.21±40.37 mmHg/(mL/s); P=0.021]. From group 0 to group 2, there was a decrease in blood flow (179.29±73.57 vs. 125.11±59.04 vs. 92.05±48.79 mL/min; P<0.001). The PI varied significantly among the 3 groups (0.86±0.20 vs. 1.12±0.50 vs. 0.79±0.16; P<0.001), with group 1 having the highest PI. Conclusions: With the occurrence of plaque and infarct, AC and blood flow progressively decrease while VR increases. The PI was the highest in the group with plaque and without infarct. Assessments of vascular function and hemodynamics in a single artery territory can clarify comprehensive alterations in the cerebral vascular system (CVS).

Thiazolo[5,4-d]thiazole-Based Metal-Organic Framework for Catalytic CO2 Cycloaddition and Photocatalytic Benzylamine Coupling Reactions.

Metal-organic frameworks (MOFs) with permanent porosity and multifunctional catalytic sites constructed by two or more organic ligands are regarded as effective heterogeneous catalysts to improve certain organic catalytic reactions. In this work, a pillared-layer Zn-MOF (MOF-LS10) was constructed by 2,3,5,6-tetrakis(4-carboxyphenyl)pyrazine (H4TCPP) and 2,5-di(pyridin-4-yl)thiazolo[5,4-d]thiazole (DPTZTZ). After activation, MOF-LS10 has a permanent porosity and moderate CO2 adsorption capacity. The introduction of thiazolo[5,4-d]thiazole (TZTZ), a photoactive unit, into the framework endows MOF-LS10 with excellent photocatalytic performance. MOF-LS10 can not only efficiently catalyze the formation of cyclic carbonates from CO2 and epoxide substrates under mild conditions but also can photocatalyze benzylamine coupling at room temperature. In addition, we used another two ligands 1,2,4,5-tetrakis(4-carboxyphenyl)benzene (H4BTEB) and 1,4-di(pyridin-4-yl)benzene (DPB) to synthesize MOF-LS11 (constructed by BTEB4- and DPTZTZ) and MOF-LS12 (constructed by TCPP4- and DPB) in order to explore whether the pyrazine structural unit and the TZTZ structural unit synergistically catalyze the reaction. The electron paramagnetic resonance spectrum demonstrates that the superoxide radical (·O2-), generated by electron transfer from the MOF excited by light to the oxidant, is the main active substance of oxidation. The design and synthesis of MOF-LS10 provide an effective synthetic strategy for the development of versatile heterogeneous catalysts for various organic reactions and a wide range of substrates.

One-step Formation of Urea from Carbon Dioxide and Nitrogen Using Water Microdroplets.

Water (H2O) microdroplets are sprayed onto a graphite mesh covered with a CuBi2O4 coating using a 1:1 mixture of N2 and CO2 as the nebulizing gas. The resulting microdroplets contain urea [CO(NH2)2] as detected by both mass spectrometry and 13C nuclear magnetic resonance. This gas-liquid-solid heterogeneous catalytic system synthesizes urea in one step on the 0.1 ms time scale. The conversion rate reaches 2.7 mmol g-1 h-1 at 25 °C and 12.3 mmol g-1 h-1 at 65 °C, with no external voltage applied. Water microdroplets serve as the hydrogen source and the electron transfer medium for N2 and CO2 in contact with CuBi2O4. Water-gas and water-solid contact electrification are speculated to drive the reaction process. This strategy couples N2 fixation and CO2 utilization in an ecofriendly process to produce urea, converting a greenhouse gas into a value-added product.

Abnormal expression of PRKAG2-AS results in dysfunction of cardiomyocytes through regulating PRKAG2 transcription by interacting with PPARG.

The role of PRKAG2 in the maintenance of heart function is well established, but little is known about how PRKAG2 is regulated in cardiomyocytes. In this study, we investigated the role of the lncRNA PRKAG2-AS, which is present at the PRKAG2 promoter, in the regulation of PRKAG2 expression. PRKAG2-AS expression was predominantly nuclear, as determined by RNA nucleoplasmic separation and fluorescence in situ hybridization. Knockdown of PRKAG2-AS in the nucleus, but not the cytoplasm, significantly decreased the expression of PRKAG2b and PRKAG2d. Interestingly, we found that PRKAG2-AS and its target genes, PRKAG2b and PRKAG2d, were reduced in the hearts of patients with ischemic cardiomyopathy, suggesting a potential role for PRKAG2-AS in myocardial ischemia. Indeed, knockdown of PRKAG2-AS in the nucleus resulted in apoptosis of cardiomyocytes. We further elucidated the mechanism by which PRKAG2-AS regulates PRKAG2 transcription by identifying 58 PRKAG2-AS interacting proteins. Among them, PPARG was selected for further investigation based on its correlation and potential interaction with PRKAG2-AS in regulating transcription. Overexpression of PPARG, or its activation with rosiglitazone, led to a significant increase in the expression of PRKAG2b and PRKAG2d in cardiomyocytes, which could be attenuated by PRKAG2-AS knockdown. This finding suggests that PRKAG2-AS mediates, at least partially, the protective effects of rosiglitazone on hypoxia-induced apoptosis. However, given the risk of rosiglitazone in heart failure, we also examined the involvement of PRKAG2-AS in this condition and found that PRKAG2-AS, as well as PRKAG2b and PRKAG2d, was elevated in hearts with dilated cardiomyopathy (DCM) and that overexpression of PRKAG2-AS led to a significant increase in PRKAG2b and PRKAG2d expression, indicating that up-regulation of PRKAG2-AS may contribute to the mechanism of heart failure by promoting transcription of PRKAG2. Consequently, proper expression of PRKAG2-AS is essential for maintaining cardiomyocyte function, and aberrant PRKAG2-AS expression induced by hypoxia or other stimuli may cause cardiac dysfunction.

An assessment of O3-related health risks and economic losses in typical regions of China.

Introduction: As one of the key areas for air pollution prevention and control in China, the Fenwei Plain is experiencing serious near-surface O3 pollution, which is a key issue that needs to be solved urgently. Methods: Based on pollutant concentration monitoring data and meteorological and health data over the same period, this study analyzed the temporal and spatial characteristics, the relationships with meteorological factors of O3 pollution, and the health effects and economic losses caused by exposure to O3 pollution using environmental health risk and environmental value assessment methods in 11 cities on the Fenwei Plain in China from 2014 to 2020. Results: The results showed that O3 pollution has become increasingly serious on the Fenwei Plain in recent years. The annual average concentration of O3_8h_max showed an overall upwards trend, with an increase of 32.39% in 2020 compared to 2014. The mean concentrations observed in summer were the highest, followed by spring and autumn, and the lowest was in winter. The O3 concentration had a significant positive correlation with air temperature and sunshine hours. The evaluation results of the impact of air pollution on population health showed that the number of premature deaths caused by O3 pollution fluctuated and increased during 2014-2020. In 2020, the numbers of total, cardiovascular and respiratory deaths attributable to O3 pollution on the Fenwei Plain were 6,867 (95% CI: 3,739-9,965), 3,652 (95% CI: 1,363-5,905), and 1,257 (95% CI: 747-2,365), respectively, and the total number of premature deaths related to O3 exposure increased by 48.05% compared with 2014. The health and economic losses attributed to O3 pollution on the Fenwei Plain during the study period were 44.22 (95% CI: 22.17-69.18), 47.16 (95% CI: 23.64-73.77), 68.28 (95% CI: 34.27-106.31), 114.44 (95% CI: 57.42-177.76), 110.85 (95% CI: 55.45-172.52), 116.41 (95% CI: 58.24-180.74), and 116.81 (95% CI: 58.00-180.88) billion yuan, respectively. In Linfen City, the increasing rate of the number of premature deaths reached 283.39% because the O3 concentration increased greatly. Discussion: Due to high O3 concentrations and obvious population growth in Xi'an, the problems of premature death and health and economic losses attributed to O3 concentrations exceeding the standard value are prominent.