Methylation alterations of imprinted genes in different placental diseases.

BACKGROUND: Imprinted genes play important functions in placentation and pregnancy; however, research on their roles in different placental diseases is limited. It is believed that epigenetic alterations, such as DNA methylation, of placental imprinting genes may contribute to the different pathological features of severe placental diseases, such as pre-eclampsia (PE) and placenta accreta spectrum disorders (PAS). RESULTS: In this study, we conducted a comparative analysis of the methylation and expression of placental imprinted genes between PE and PAS using bisulfite sequencing polymerase chain reaction (PCR) and quantitative PCR, respectively. Additionally, we assessed oxidative damage of placental DNA by determining 8-hydroxy-2'-deoxyguanosine levels and fetal growth by determining insulin-like growth factor 2 (IGF2) and cortisol levels in the umbilical cord blood using enzyme-linked immunosorbent assay. Our results indicated that methylation and expression of potassium voltage-gated channel subfamily Q member 1, GNAS complex locus, mesoderm specific transcript, and IGF2 were significantly altered in both PE and PAS placentas. Additionally, our results revealed that the maternal imprinted genes were significantly over-expressed in PE and significantly under-expressed in PAS compared with a normal pregnancy. Moreover, DNA oxidative damage was elevated and positively correlated with IGF2 DNA methylation in both PE and PAS placentas, and cortisol and IGF2 levels were significantly decreased in PE and PAS. CONCLUSIONS: This study suggested that DNA methylation and expression of imprinted genes are aberrant in both PE and PAS placentas and that PE and PAS have different methylation profiles, which may be linked to their unique pathogenesis.

Characterization of a novel SCN5A mutation associated with long QT syndrome and arrhythmogenic right ventricular cardiomyopathy in a family.

Sudden cardiac death represents a significant diagnostic challenge for forensic pathologists, particularly in inherited arrhythmia syndromes or cardiomyopathies resulting from genetic defects. Molecular autopsies can reveal the underlying molecular etiology in such cases. In this study, we investigated a family with a history of sudden cardiac death to elucidate the molecular basis responsible for sudden cardiac death. The proband underwent a comprehensive forensic examination. Family members received thorough clinical evaluations, including electrocardiogram, Holter monitoring, echocardiography, and cardiac magnetic imaging. Whole exome sequencing and genetic analysis were performed on the deceased and her parents. In addition, Western blotting and patch-clamp recordings were employed to evaluate the expression and function of the mutant protein in vitro. Forensic examination diagnosed arrhythmogenic right ventricular cardiomyopathy (ARVC) as the cause of sudden death. Genetic analysis identified a novel missense mutation in SCN5A (p.V1323L), which was assessed as likely pathogenic by the ACMG guideline. Another family member carrying the mutation manifested long QT syndrome and mild cardiac fibrosis. The cellular electrophysiological study demonstrated that the mutation resulted in an enhanced late sodium current, suggesting it was a gain-of-function mutation. This study characterizes a novel SCN5A mutation that putatively causes long QT syndrome and may contribute to the development of ARVC. Our work expands the pathogenic spectrum of SCN5A variants and underscores the importance of molecular autopsy in sudden death cases, especially in those with suspected genetic disorders.

A scalable Li-Al-Cl stratified structure for stable all-solid-state lithium metal batteries.

Sulfides are promising electrolyte materials for all-solid-state Li metal batteries due to their high ionic conductivity and machinability. However, compatibility issues at the negative electrode/sulfide electrolyte interface hinder their practical implementation. Despite previous studies have proposed considerable strategies to improve the negative electrode/sulfide electrolyte interfacial stability, industrial-scale engineering solutions remain elusive. Here, we introduce a scalable Li-Al-Cl stratified structure, formed through the strain-activated separating behavior of thermodynamically unfavorable Li/Li9Al4 and Li/LiCl interfaces, to stabilize the negative electrode/sulfide electrolyte interface. In the Li-Al-Cl stratified structure, Li9Al4 and LiCl are enriched at the surface to serve as a robust solid electrolyte interphase and are diluted in bulk by Li metal to construct a skeleton. Enabled by its unique structural characteristic, the Li-Al-Cl stratified structure significantly enhances the stability of negative electrode/sulfide electrolyte interface. This work reports a strain-activated phase separation phenomenon and proposes a practical pathway for negative electrode/sulfide electrolyte interface engineering.

Roles of flavonoids in ischemic heart disease: Cardioprotective effects and mechanisms against myocardial ischemia and reperfusion injury.

BACKGROUND: Flavonoids are extensively present in fruits, vegetables, grains, and medicinal plants. Myocardial ischemia and reperfusion (MI/R) comprise a sequence of detrimental incidents following myocardial ischemia. Research indicates that flavonoids have the potential to act as cardioprotective agents against MI/R injuries. Several specific flavonoids, e.g., luteolin, hesperidin, quercetin, kaempferol, and puerarin, have demonstrated cardioprotective activities in animal models. PURPOSE: The objective of this review is to identify the cardioprotective flavonoids, investigate their mechanisms of action, and explore their application in myocardial ischemia. METHODS: A search of PubMed database and Google Scholar was conducted using keywords "myocardial ischemia" and "flavonoids". Studies published within the last 10 years reporting on the cardioprotective effects of natural flavonoids on animal models were analyzed. RESULTS: A total of 55 natural flavonoids were identified and discussed within this review. It can be summarized that flavonoids regulate the following main strategies: antioxidation, anti-inflammation, calcium modulation, mitochondrial protection, ER stress inhibition, anti-apoptosis, ferroptosis inhibition, autophagy modulation, and inhibition of adverse cardiac remodeling. Additionally, the number and position of OH, 3'4'-catechol, C2=C3, and C4=O may play a significant role in the cardioprotective activity of flavonoids. CONCLUSION: This review serves as a reference for designing a daily diet to prevent or reduce damages following ischemia and screening of flavonoids for clinical application.

Insight into the mechanisms of activity promotion and SO2 resistance over Fe-doped Ce-W oxide catalyst for NOx reduction.

Ceria-based catalysts for the selective catalytic reduction of NOx with NH3 (NH3-SCR) are always subject to deactivation by sulfur poisoning. In this study, Fe-doped Ce-W mixed oxides, which were synthesized by the co-precipitation method, improved the SCR activity and SO2 durability at low temperatures of undoped Ce-W oxides. The improved low-temperature activity was mainly due to the enhancement of redox properties at low temperatures and more active oxygen species, together with the adsorption and activation of more abundant NOx species, facilitating the "fast SCR" reaction. In the presence of SO2, doping with Fe species effectively prevented sulfate deposition on the CeW catalyst, due to the interaction between Fe, Ce, and W species inducing electron transfer among different metal sites and altering the electron distribution. The competitive adsorption behavior between NO and SO2 was changed by Fe doping, in which the adsorption and oxidation of SO2 were restrained. Besides, the elevated NO oxidation accelerated the decomposition of ammonium bisulfate, causing the SCR reaction to not be greatly suppressed. Hence, Fe-doped Ce-W oxides catalysts showed excellent sulfur resistance. This study provides an in-depth understanding of efficient Ce-based catalysts for SO2-tolerance strategies.

Hydrothermal Aging Treatment Activates V2O5/TiO2 Catalysts for NOx Abatement.

Thermal stability is crucial for the practical application of deNOx catalysts. Vanadia-based catalysts are widely applied for the selective catalytic reduction of NOx with NH3 (NH3-SCR). Generally, hydrothermal aging at high temperatures induces the deactivation of deNOx catalysts. However, in this work, a remarkable increase in low- and medium-temperature NH3-SCR activity was observed for a V2O5/TiO2 catalyst after hydrothermal aging treatment, especially at 750 °C for 16 h. After the vanadia-based catalyst was hydrothermally treated at 750 °C, the specific surface area decreased and the surface VOx density and surface V ratio increased significantly. Therefore, the aged catalyst presented more abundant polymeric vanadyl species than the fresh one. Furthermore, the redox capability was improved markedly after hydrothermal treatment due to the strong interaction of vanadia and titania, contributing to the NH3-SCR reaction. 750 °C is the optimal temperature to activate the V2O5/TiO2 catalyst, improving the SCR performance significantly. This study provides an in-depth understanding of vanadia-based catalysts for practical applications.

AVE 0991 attenuates cardiac hypertrophy through reducing oxidative stress.

AVE 0991, the nonpeptide angiotensin-(1-7) (Ang-(1-7)) analog, is recognized as having beneficial cardiovascular effects. However, the mechanisms have not been fully elucidated. This study was designed to investigate the effects of AVE 0991 on cardiac hypertrophy and the mechanisms involved. Mice were underwent aortic banding to induce cardiac hypertrophy followed by the administration of AVE 0991 (20 mg kg·day (-1)) for 4 weeks. It was shown that AVE 0991 reduced left ventricular hypertrophy and improved heart function, characterized by decreases in left ventricular weight and left ventricular end-diastolic diameter, and increases in ejection fraction. Moreover, AVE 0991 significantly down-regulated mean myocyte diameter and attenuate the gene expression of the hypertrophic markers. Furthermore, AVE 0991 inhibited the expression of NOX 2 and NOX 4, meaning that AVE 0991 reduced oxidative stress of cardiac hypertrophy mice. Our data showed that AVE 0991 treatment could attenuate cardiac hypertrophy and improve heart function, which may be due to reduce oxidative stress.

Translation and validation of a Chinese version of the 8-item Morisky medication adherence scale in myocardial infarction patients.

RATIONALE, AIMS AND OBJECTIVES: Poor medication adherence is a major global public health challenge. A valid, reliable, cost-effective tool for measuring medication adherence would lead to a better understanding of non-adherence and lay the groundwork for interventions aimed at facilitating adherence to therapies. The aim of this study was to translate and evaluate the psychometric properties of the Chinese version of the 8-item Morisky medication adherence scale (C-MMAS-8) in Chinese myocardial infarction (MI) patients. METHODS: Psychometric testing of the C-MMAS-8 was conducted using a convenience sample of 176 MI patients recruited from four major hospitals in Guangzhou in southern China. Socio-demographic data, C-MMAS-8 and three subscales of the revised illness perception questionnaire (treatment control, personal control and illness coherence subscales) were administered to the MI patients. Thirty MI patients participated in a 4-week retest. RESULTS: The C-MMAS-8 demonstrated good internal consistency (Cronbach's α = 0.77) and test-retest reliability (r = 0.88, P < 0.001). Significant correlations with treatment control subscale (r = 0.32, P < 0.01), personal control subscale (r = 0.47, P < 0.01), and illness coherence subscale (r = 0.44, P < 0.01) of the revised illness perception questionnaire demonstrated good construct validity. CONCLUSIONS: The psychometric properties of the C-MMAS-8 are satisfactory.

The effect of a telephone follow-up intervention on illness perception and lifestyle after myocardial infarction in China: a randomized controlled trial.

BACKGROUND: Lifestyle modification is an integral component of cardiac secondary prevention, while it has been confirmed that myocardial infarction (MI) patients' health-related behaviors are heavily influenced by their illness perception. OBJECTIVES: To evaluate the effect of a telephone follow-up intervention for improving MI patients' illness perception and lifestyle. DESIGN: A randomized controlled trial, longitudinal research design was employed. SETTINGS: Cardiac care units in four major general hospitals in Guangzhou, China. PARTICIPANTS: Inclusion criteria were being diagnosed with an initial acute MI, being able to communicate orally in Mandarin or Cantonese and read in Chinese, and living in Guangzhou. Exclusion criteria were with continuing uncontrolled arrhythmias or heart failure, being illiteracy, or with a history of major psychiatric illness, exercise-induced asthma, uncontrolled diabetes, or evidence of dementia. METHOD: 124 patients admitted with the first acute MI were randomized to receive either routine care or routine care plus a telephone follow-up intervention, which consist of a pre-discharge education and three telephone follow-up instructions. Data were collected before discharge, at the 6th and the 12th week after discharge from hospital, respectively. RESULTS: At the 6th and the 12th week after discharge, patients in the intervention group had significantly positive perceptions about symptoms of MI (mean difference 3.27, 95% confidence interval 2.48-4.07, p<.001; mean difference 2.12, 95% confidence interval 1.34-2.89, p<.001 respectively) and how long their illness would last (mean difference -0.69, 95% confidence interval -0.91 to -0.47, p<.001; mean difference -0.74, 95% confidence interval -0.96 to -0.51, p<.001 respectively) compared with the control group. The intervention group also had more positive beliefs about the controllability (F=4.23, p=.04) and more improved beliefs about the causes of MI than the control group. Moreover, the intervention improved the patients' nutrition (F=5.16, p=.03) and physical activity at the 12-week follow-up (mean difference 0.37, 95% confidence interval 0.17-0.58, p<.001). CONCLUSION: This telephone follow-up intervention can result in improved illness perception and lifestyle after MI. It could be incorporated into current hospital treatment regimens for MI to improve patients' quality of life.