Aluminum Molecular Ring Meets Deep Eutectic Solvents: Adaptive Assembly and Optical Behavior.

Different from the previous neutral reaction solvent system, this work explores the synthesis of Al-oxo rings in ionic environments. Deep eutectic solvents (DESs) formed by quaternary ammonium salts hydrogen bond acceptor (HBA) and phenols hydrogen bond donor (HBD) further reduce the melting point of the reaction system and provide an ionic environment. Further, the quaternary ammonium salt was chosen as the HBA because it contains a halogen anion that matches the size of the central cavity of the molecular ring. Based on this thought, five Al8 ion pair cocrystals were synthesized via "DES thermal". The general formula is Q+ ⊂ {Cl@[Al8(BD)8(µ2-OH)4L12]} (AlOC-180-AlOC-185, Q+ = tetrabutylammonium, tetrapropylammonium, 1-butyl-3-methylimidazole; HBD = phenol, p-chlorophenol, p-fluorophenol; HL = benzoic acid, 1-naphthoic acid, 1-pyrenecarboxylic acid, anthracene-9-carboxylic acid). Structural studies reveal that the phenol-coordinated Al molecular ring and the quaternary ammonium ion pair form the cocrystal compounds. The halogen anions in the DES component are confined in the center of the molecular ring, and the quaternary ammonium cations are located in the organic shell. Such an adaptive cocrystal binding pattern is particularly evident in the structures coordinated with low-symmetry ligands such as naphthoic acid and pyrene acid. Finally, the optical behavior of these cocrystal compounds is understood from the analysis of crystal structure and theoretical calculation.

A Simple Molten Salt Route to Crystalline ß-MoB2 Nanosheets with High Activity for the Hydrogen Evolution Reaction.

Molybdenum borides have been of interest due to their potential applications as electrocatalysts for the hydrogen evolution reaction (HER). As one of the common molybdenum borides, ß-MoB2 is deemed to exhibit low electrocatalytic activity due to the presence of puckered B layers, and improvement of its behavior is hindered by the lack of convenient synthetic methods. Herein, we report the synthesis of crystalline ß-MoB2 for the first time via the simple reaction of MoCl3 and B at 850 °C in LiCl-KCl. The as-prepared ß-MoB2 sample was shown to exhibit a nanosheet structure with a large Brunauer-Emmett-Teller surface area of 48 m2/g. Such ß-MoB2 nanosheets exhibit promising HER activity in acidic medium with an overpotential of 187 mV at a current density of 10 mA/cm2 and a Tafel slope of 49.3 mV/decade, which is much better than that of the known bulk ß-MoB2 and even close to the results of α-MoB2 that is commonly recognized as the best molybdenum boride electrocatalyst for HER. The high HER activity of ß-MoB2 nanosheets results from the large surface area that allows more active sites to be exposed, which compensates for the disadvantage arising from the intrinsic structure of ß-MoB2.

Enhanced Adsorption and Separation of Xenon over Krypton via an Unsaturated Calcium Center in a Metal-Organic Framework.

Krypton (Kr) and xenon (Xe) are nowadays widely applied in technical and industrial fields. Separating and collecting highly pure Xe from nuclear facilities are necessary and urgent. However, the technology is limited due to the inert nature of Xe and other interferential factors. In this work, a calcium-based metal-organic framework, Ca-SINAP-1, which comprises a three-dimensional microporous framework with a suitable pore width, was researched for xenon and krypton separation through both experimental and theoretical methods. Ca-SINAP-1, synthesized in solvothermal and gamma ray conditions, features accessible open-metal sites, exhibits a high Xe/Kr selectivity of 10.32, and owns a Xe adsorption capacity of 2.87 mmol/g at room temperature (1.0 bar). Particularly, its excellent chemical stability (from pH 2 to 13) and thermal stability (up to 550 °C), as well as radiation-resistance (up to 400 kGy ß irradiations), render this material a promising candidate for radioactive inert gases treatment.

Impact of autoantibodies against the M2-muscarinic acetylcholine receptor on clinical outcomes in peripartum cardiomyopathy patients with standard treatment.

OBJECTIVES: To evaluate the impact of autoantibodies against the M2-muscarinic receptor (anti-M2-R) on the clinical outcomes of patients receiving the standard treatment for peripartum cardiomyopathy (PPCM). METHODS: A total of 107 PPCM patients who received standard heart failure (HF) treatment between January 1998 and June 2020 were enrolled in this study. According to anti-M2-R reactivity, they were classified into negative (n = 59) and positive (n = 48) groups, denoted as the anti-M2-R (-) and anti-M2-R (+) groups. Echocardiography, 6-min walk distance, serum digoxin concentration (SDC), and routine laboratory tests were performed regularly for 2 years. The all-cause mortality, cardiovascular mortality, and rehospitalisation rate for HF were compared between the two groups. RESULTS: A total of 103 patients were included in the final data analysis, with 46 in the anti-M2-R (+) group and 57 in the anti-M2-R (-) group. Heart rate was lower in the anti-M2-R (+) group than in the anti-M2-R (-) group at the baseline (102.7 ± 6.1 bpm vs. 96.0 ± 6.4 bpm, p < 0.001). The initial SDC was higher in the anti-M2-R (+) group than in the anti-M2-R (-) group with the same dosage of digoxin (1.25 ± 0.45 vs. 0.78 ± 0.24 ng/mL, p < 0.001). The dosages of metoprolol and digoxin were higher in the anti-M2-R (-) patients than in the anti-M2-R (+) patients (38.8 ± 4.6 mg b.i.d. vs. 27.8 ± 5.3 mg b.i.d., p < 0.0001, respectively, for metoprolol; 0.12 ± 0.02 mg/day vs. 0.08 ± 0.04 mg/day, p < 0.0001, respectively, for digoxin). Furthermore, there was a greater improvement in cardiac function in the anti-M2-R (-) patients than in the anti-M2-R (+) patients. Multivariate analysis identified negativity for anti-M2-R as the independent predictor for the improvement of cardiac function. Rehospitalisation for HF was lower in the anti-M2-R (-) group, but all-cause mortality and cardiovascular mortality were the same. CONCLUSIONS: There were no differences in all-cause mortality or cardiovascular mortality between the two groups. Rehospitalisation rate for HF decreased in the anti-M2-R (-) group. This difference may be related to the regulation of the autonomic nervous system by anti-M2-R.

Detection of major loci associated with the variation of 18 important agronomic traits between Solanum pimpinellifolium and cultivated tomatoes.

Wild species can be used to improve various agronomic traits in cultivars; however, a limited understanding of the genetic basis underlying the morphological differences between wild and cultivated species hinders the integration of beneficial traits from wild species. In the present study, we generated and sequenced recombinant inbred lines (RILs, 201 F10 lines) derived from a cross between Solanum pimpinellifolium and Solanum lycopersicum tomatoes. Based on a high-resolution recombination bin map to uncover major loci determining the phenotypic variance between wild and cultivated tomatoes, 104 significantly associated loci were identified for 18 agronomic traits. On average, these loci explained ~39% of the phenotypic variance of the RILs. We further generated near-isogenic lines (NILs) for four identified loci, and the lines exhibited significant differences for the associated traits. We found that two loci could improve the flower number and inflorescence architecture in the cultivar following introgression of the wild-species alleles. These findings allowed us to construct a trait-locus network to help explain the correlations among different traits based on the pleiotropic or linked loci. Our results provide insights into the morphological changes between wild and cultivated tomatoes, and will help to identify key genes governing important agronomic traits for the molecular selection of elite tomato varieties.

Atomic Scale Stability of Tungsten-Cobalt Intermetallic Nanocrystals in Reactive Environment at High Temperature.

Catalyst design plays vital roles in structurally relevant reactions. Revealing the catalyst structure and chemistry in the reactive environment at the atomic scale is imperative for the rational design of catalysts as well as the investigation of reaction mechanisms, while in situ characterization at the atomic scale at high temperature is still a great challenge. Here, tracking intermetallic Co7W6 nanocrystals with a defined structure and a high melting point by environmental aberration-corrected transmission electron microscopy in combination with in situ synchrotron X-ray absorption spectroscopy, we directly present the structural and chemical stability of the Co7W6 nanocrystals in methane, carbon monoxide, and hydrogen at temperatures of 700-1100 °C. The evidence is in situ and in real time with both atomic scaled resolution and collective information. The results are helpful in revealing the mechanism of structural-specified synthesis of single-walled carbon nanotubes. This research offers an example of systematic investigation at the atomic scale on catalysts under reactive conditions. Such catalysts presenting high structural stability may also find applications in other structure-specific synthesis.

Identification and characterization analysis of sulfotransferases (SOTs) gene family in cotton (Gossypium) and its involvement in fiber development.

BACKGROUND: Sulfotransferases (SOTs) (EC 2.8.2.-) play a crucial role in the sulphate conjugation reaction involved in plant growth, vigor, stress resistance and pathogen infection. SOTs in Arabidopsis have been carried out and divided into 8 groups. However, the systematic analysis and functional information of SOT family genes in cotton have rarely been reported. RESULTS: According to the results of BLASTP and HMMER, we isolated 46, 46, 76 and 77 SOT genes in the genome G. arboreum, G. raimondii, G. barbadense and G. hirsutum, respectively. A total of 170 in 245 SOTs were further classified into four groups based on the orthologous relationships comparing with Arabidopsis, and tandem replication primarily contributed to the expansion of SOT gene family in G. hirsutum. Expression profiles of the GhSOT showed that most genes exhibited a high level of expression in the stem, leaf, and the initial stage of fiber development. The localization analysis indicated that GhSOT67 expressed in cytoplasm and located in stem and leaf tissue. Additionally, the expression of GhSOT67 were induced and the length of stem and leaf hairs were shortened after gene silencing mediated by Agrobacterium, compared with the blank and negative control plants. CONCLUSIONS: Our findings indicated that SOT genes might be associated with fiber development in cotton and provided valuable information for further studies of SOT genes in Gossypium.

Measurement and decomposition of income-related inequality in self-rated health among the elderly in China.

BACKGROUND: Population ageing in China has brought increasing attention to the health inequalities of the elderly. The purpose of this paper is to measure income-related health inequality among the elderly in China and decompose its causes. METHODS: The data are from the China Health and Retirement Longitudinal Study (CHARLS) survey in 2013, which contains 6176 individuals aged 60 years and above. A multiple linear regression model was used to analyze the influencing factors of self-rated health (SRH) among the elder people. Furthermore, the corrected concentration index were used to measure income-related health inequality. Wagstaff-type decomposition analysis was employed to explore the cause of inequality. The measurement and decomposition of health inequality was also performed separately in the male and female subgroups. RESULTS: Most elderly declared their health status as "fair" (51.33%) or "poor" (21.88%). Income, gender, residence, region, health insurance and other factors had significant association with SRH (P < 0.05). The corrected concentration index (CCI) was 0.06, indicating pro-rich inequality in health among the elderly. Decomposition analyses revealed that the main contributors to health inequality included income, residence, region, health insurance, and employment. For female elderly, most of the inequality was due to residence (50.78%) and income (49.51%); for male elderly, most of the inequality was due to insurance (38.65%) and income (22.26%); for the total sample, employment had a negative contribution to health inequality (- 25.83%). CONCLUSION: The findings confirm a high proportion of elderly with poor SRH, and health inequality in the Chinese. Some socioeconomic strategies should be conducted to reduce this health inequality among the elderly, such as reducing income disparities, consolidating health insurance schemes, and narrowing urban-rural and regional gaps. Older females with low incomes in rural areas are a vulnerable subgroup and warrant targeted policy attention.

Templated Synthesis of Single-Walled Carbon Nanotubes with Specific Structure.

Single-walled carbon nanotubes (SWNTs) have shown great potential in various applications attributed to their unique structure-dependent properties. Therefore, the controlled preparation of chemically and structurally pristine SWNTs is a crucial issue for their advanced applications (e.g., nanoelectronics) and has been a great challenge for two decades. Epitaxial growth from well-defined seeds has been shown to be a promising strategy to control the structure of SWNTs. Segments of carbon nanotubes, including short pipes from cutting of preformed nanotubes and caps from opening of fullerenes or cyclodehydrogenation of polycyclic hydrocarbon precursors, have been used as the seeds to grow SWNTs. Single-chirality SWNTs were obtained with both presorted chirality-pure SWNT segments and end caps obtained from polycyclic hydrocarbon molecules with designed structure. The main challenges of nanocarbon-segment-seeded processes are the stability of the seeds, yield, and efficiency. Catalyst-mediated SWNT growth is believed to be more efficient. The composition and morphology of the catalyst nanoparticles have been widely reported to affect the chirality distribution of SWNTs. However, chirality-specific SWNT growth is hard to achieve by alternating catalysts. The specificity of enzyme-catalyzed reactions brings us an awareness of the essentiality of a unique catalyst structure for the chirality-selective growth of SWNTs. Only catalysts with the desired atomic arrangements in their crystal planes can act as structural templates for chirality-specific growth of SWNTs. We have developed a new family of catalysts, tungsten-based intermetallic compounds, which have high melting points and very special crystal structures, to facilitate the growth of SWNTs with designed chirality. By the use of W6Co7 catalysts, (12,6) SWNTs were directly grown with purity higher than 92%. Both high-resolution transmission electron microscopy measurements and density functional theory simulations show that the selective growth of (12,6) tubes is due to a good structural match between the carbon atom arrangement around the nanotube circumference and the metal atom arrangement of (0 0 12) planes in the catalyst. Similarly, (16,0) SWNTs exhibit a good structural match to the (116) planes of the W6Co7 catalyst. By optimization of the chemical vapor deposition (CVD) conditions, zigzag (16,0) SWNTs, which are generally known as a kinetically unfavorable species in CVD growth, were obtained with a purity of ∼80%. Generally speaking, the chirality-specific growth of SWNTs is realized by the cooperation of two factors: the structural match between SWNTs and the catalysts makes the growth of SWNTs with specific chirality thermodynamically favorable, and further manipulation of the CVD conditions results in optimized growth kinetics for SWNTs with this designed chirality. We expect that this advanced epitaxial growth strategy will pave the way for the ultimate goal of chirality-specified growth of SWNTs and will also be applicable in the controlled preparation of other nanomaterials.

Hydrothermal route upcycling surgical masks into dual-emitting carbon dots as ratiometric fluorescent probe for Cr (VI) and corrosion inhibitor in saline solution.

Exploration effective route to convert plastic waste into valuable carbon dots with bifunction of metal fluorescence monitoring and corrosion protection in seawater is promising. Herein, using "white-pollution" polypropylene surgical masks as a single precursor, dual-emitting carbon dots (CDs) with excellent ratiometric fluorescent sensitivity and corrosion inhibitor efficiency were fabricated with high yield (∼100 %) by a one-pot in situ acid oxidation hydrothermal strategy without post-treatment and organic solvents. Chemical, structural, morphological, optical properties and the Cr (VI) detection and Cu inhibition mechanism of the synthesized CDs had been systematically studied. Furthermore, a dual-response-OFF proportional fluorescent probe had been developed for the detection of the analyte Cr (VI) with a low detection limit of 24 nM. Additionally, the corrosion inhibition efficiency of the prepared CDs reached approximately 94.01 % for Cu substrate in 3.5 wt% NaCl electrolyte under a CDs concentration of 200 mg/L, which is higher than that of most previous reports.

Adipose-derived miRNAs as potential biomarkers for predicting adulthood obesity and its complications: A systematic review and bioinformatic analysis.

Adipose tissue is the first and primary target organ of obesity and the main source of circulating miRNAs in patients with obesity. This systematic review aimed to analyze and summarize the generation and mechanisms of adipose-derived miRNAs and their role as early predictors of various obesity-related complications. Literature searches in the PubMed and Web of Science databases using terms related to miRNAs, obesity, and adipose tissue. Pre-miRNAs from the Human MicroRNA Disease Database, known to regulate obesity-related metabolic disorders, were combined for intersection processing. Validated miRNA targets were sorted through literature review, and enrichment analysis using the Kyoto Encyclopedia of Genes and Genomes via the KOBAS online tool, disease analysis, and miRNA transcription factor prediction using the TransmiR v. 2.0 database were also performed. Thirty miRNAs were identified using both obesity and adipose secretion as criteria. Seventy-nine functionally validated targets associated with 30 comorbidities of these miRNAs were identified, implicating pathways such as autophagy, p53 pathways, and inflammation. The miRNA precursors were analyzed to predict their transcription factors and explore their biosynthesis mechanisms. Our findings offer potential insights into the epigenetic changes related to adipose-driven obesity-related comorbidities.

Dysfunction of Akt/FoxO3a/Atg7 regulatory loop magnifies obesity-regulated muscular mass decline.

BACKGROUND: Myoprotein degradation accelerates in obese individuals, resulting in a decline in muscular mass. Atg7 plays a crucial role in regulating protein stability and function through both autophagy-dependent and independent pathways. As obesity progresses, the expression of Atg7 gradually rises in muscle tissue. Nonetheless, the precise impact and mechanism of Atg7 in promoting muscle mass decline in obesity remain uncertain. The study aimed to elucidate the role and underly mechanism of Atg7 action in the context of obesity-induced muscle mass decline. METHODS: In this study, we established a murine model of high-fat diet-induced obesity (DIO) and introduced adeno-associated virus delivery of short hairpin RNA to knock down Atg7 (shAtg7) into the gastrocnemius muscle. We then examined the expressions of Atg7 and myoprotein degradation markers in the gastrocnemius tissues of obese patients and mice using immunofluorescence and western blotting techniques. To further investigate the effects of Atg7, we assessed skeletal muscle cell diameter and the myoprotein degradation pathway in C2C12 and HSkMC cells in the presence or absence of Atg7. Immunofluorescence staining for MyHC and western blotting were utilized for this purpose. To understand the transcriptional regulation of Atg7 in response to myoprotein degradation, we conducted luciferase reporter assays and chromatin immunoprecipitation experiments to examine whether FoxO3a enhances the transcription of Atg7. Moreover, we explored the role of Akt in Atg7-mediated regulation and its relevance to obesity-induced muscle mass decline. This was accomplished by Akt knockdown, treatment with MK2206, and GST pulldown assays to assess the interaction between Atg7 and Akt. RESULTS: After 20 weeks of being on a high-fat diet, obesity was induced, leading to a significant decrease in the gastrocnemius muscle area and a decline in muscle performance. This was accompanied by a notable increase in Atg7 protein expression (p < 0.01). Similarly, in gastrocnemius tissues of obese patients when compared to nonobese individuals, there was a significant increase in both Atg7 (p < 0.01) and TRIM63 (p < 0.01) levels. When palmitic acid was administered to C2C12 cells, it resulted in increased Atg7 (p < 0.01), LC3Ⅱ/Ⅰ (p < 0.01), and p62 levels (p < 0.01). Additionally, it promoted FoxO3a-mediated transcription of Atg7. The knockdown of Atg7 in the gastrocnemius partially reversed DIO-induced muscle mass decline. Furthermore, when Atg7 was knocked down in C2C12 and HSkMC cells, it mitigated palmitic acid-induced insulin resistance, increased the p-Akt/Akt ratio (p < 0.01), and reduced TRIM63 (p < 0.01). Muscular atrophy mediated by Atg7 was reversed by genetic knockdown of Akt and treatment with the p-Akt inhibitor MK2206. Palmitic acid administration increased the binding between Atg7 and Akt (p < 0.01) while weakening the binding of PDK1 (p < 0.01) and PDK2 (p < 0.01) to Akt. GST pulldown assays demonstrated that Atg7 directly interacted with the C-terminal domain of Akt. CONCLUSION: The consumption of a high-fat diet, along with lipid-induced effects, led to the inhibition of Akt signaling, which, in turn, promoted FoxO3a-mediated transcription, increasing Atg7 levels in muscle cells. The excess Atg7 inhibited the phosphorylation of Akt, leading to a cyclic activation of FoxO3a and exacerbating the decline in muscle mass regulated by obesity. Consequently, Atg7 serves as a regulatory point in determining the decline in muscle mass induced by obesity.

Lift enhancement of a butterfly-like flapping wing vehicle by reinforcement learning algorithm.

In order to enhance the take-off lift of a butterfly-like flapping wing vehicle (FWV), we implemented an integrated experimental platform and applied a reinforcement learning algorithm. The vehicle, which has a wingspan of 81 cm and is mounted on a stand with a force sensor, is driven by two servos that are powered and controlled wirelessly. To achieve the goal of enhancing take-off lift, we used a model-free, on-policy actor-critic proximal policy optimization algorithm. After 300 learning steps, the average aerodynamic lift force increased significantly from 0.044 N to 0.861 N. This enhanced lift force was sufficient to meet the take-off requirements of the vehicle without the need for any additional aids or airflow. Additionally, we observed a strong lift peak in the upstroke after analyzing the learning results. Further experiments showed that this lift peak is directly related to the elastic release of the wing twist and the opening and closing of the gap between the forewing and hindwing in the early stage of the upstroke. These findings were not easily predicted or discovered using traditional aerodynamic methods. This work provides valuable reinforcement learning experience for the future development of FWVs.

Mitochondrial quality control and its role in osteoporosis.

Mitochondria are important organelles that provide cellular energy and play a vital role in cell differentiation and apoptosis. Osteoporosis is a chronic metabolic bone disease mainly caused by an imbalance in osteoblast and osteoclast activity. Under physiological conditions, mitochondria regulate the balance between osteogenesis and osteoclast activity and maintain bone homeostasis. Under pathological conditions, mitochondrial dysfunction alters this balance; this disruption is important in the pathogenesis of osteoporosis. Because of the role of mitochondrial dysfunction in osteoporosis, mitochondrial function can be targeted therapeutically in osteoporosis-related diseases. This article reviews different aspects of the pathological mechanism of mitochondrial dysfunction in osteoporosis, including mitochondrial fusion and fission, mitochondrial biogenesis, and mitophagy, and highlights targeted therapy of mitochondria in osteoporosis (diabetes induced osteoporosis and postmenopausal osteoporosis) to provide novel targets and prevention strategies for the prevention and treatment of osteoporosis and other chronic bone diseases.

Outlook of Ferroptosis-Targeted Lipid Peroxidation in Cardiovascular Disease.

Lipid metabolism is a complex biochemical process that regulates normal cell activity and death. Ferroptosis is a novel mode of programmed cell death different from apoptosis, pyroptosis, and autophagy. Abnormal lipid metabolism may lead to lipid peroxidation and cell rupture death, which are regulated by lipoxygenase (LOX), long-chain acyl-coA synthases, and antioxidant enzymes. Alternatively, Fe2+ and Fe3+ are required for the activity of LOXs and ferroptosis, and Fe2+ can significantly accelerate lipid peroxidation in ferroptosis. Abnormal lipid metabolism is a certain risk factor for cardiovascular disease. In recent years, the important role of ferroptosis in developing cardiovascular disease has been increasingly reported. Reducing lipid accumulation could reduce the occurrence of ferroptosis, thus alleviating cardiovascular disease deterioration. This article reviews the relationship of lipid peroxidation to the general mechanism of ferroptosis and highlights lipid peroxidation as the common point of ferroptosis and cardiovascular disease.

Serum galactose-deficient immunoglobulin A1 in recurrent immunoglobulin a nephropathy after kidney transplantation: A meta-analysis.

BACKGROUND: Immunoglobulin A nephropathy (IgAN) is a main cause of end stage renal disease (ESRD). Many IgAN patients with ESRD accept kidney allograft for renal replacement. However, disease recurrence occurs after transplantation. Galactose-deficient immunoglobulin A1(Gd-IgA1) has been proved to be a crucial biomarker in the primary IgAN population. METHODS: This meta-analysis aimed to explore the association between serum Gd-IgA1 and IgAN recurrence after renal transplantation and was registered on PROSPERO: CRD42022356952; A literature search was performed and relevant studies were retrieved from the PubMed, Embase and Cochrane library databases from inception to April 27, 2023. The inclusion criteria were: 1) full-text studies; 2) patients with histological diagnosis of IgAN of their native kidneys who underwent kidney transplantation; 3) studies exploring the relationship between serum Gd-IgA1 and IgAN recurrence after kidney transplantation. The exclusion criteria were: 1) reviews, case reports, or non-clinical studies. 2) studies with insufficient original data or incomplete data. 3) studies with duplicated data. Study quality was assessed using Newcastle Ottawa Scale (NOS). Data were pooled using a random-effects model. RESULTS: 8 full-text studies including 515 patients were identified. The Newcastle-Ottawa Scale (NOS) score ranged from 6 to 8. The standard mean difference (SMD) of the level of Gd-IgA1 was significantly higher in recurrence group than in non-recurrence group (SMD = 0.50，95%CI = 0.15-0.85, p = 0.005). Furthermore, Gd-IgA1 levels were higher in recurrence patients than in non-recurrence in both Europe subgroup (SMD 0.45, 95%CI: 0.08-0.82, p = 0.02) and Asia subgroup (SMD 0.90, 95%CI: 0.10-1.70, p = 0.03). However, pretransplant Gd-IgA1 levels showed no significant difference between recurrence and non-recurrence group (SMD 0.46, 95%CI: 0.06-0.99, p = 0.08) in anther subgroup analysis while posttransplant Gd-IgA1 levels were significantly higher in recurrence population than in non-recurrence (SMD 0.57, 95%CI 0.21 to 0.92, p = 0.002). CONCLUSIONS: This meta-analysis showed that posttransplant serum Gd-IgA1 levels are associated with IgAN recurrence after kidney transplantation; however, pretransplant serum Gd-IgA1 levels are not.

Trim65 attenuates isoproterenol-induced cardiac hypertrophy by promoting autophagy and ameliorating mitochondrial dysfunction via the Jak1/Stat1 signaling pathway.

Pathological cardiac hypertrophy is a major cause of heart failure, and there is no effective approach for its prevention or treatment. The Trim family is a recently identified family of E3 ubiquitin ligases that regulate cardiac hypertrophy. Trim65, which is a member of the Trim family, previous studies have not determined whether Trim65 affects cardiac hypertrophy. In this study, the effects of Trim65 on isoproterenol (ISO)-induced cardiac hypertrophy and the underlying mechanisms were investigated. In contrast to C57BL/6 mice, Trim65-knockout (Trim65-KO) mice developed more severe myocardial hypertrophy, fibrosis and cardiac dysfunction after being intraperitoneally injected with ISO for 2 weeks. Transmission electron microscopy (TEM) revealed that the autophagic flux was inhibited, mitochondria were swollen, and mitochondrial cristae were lost or decreased in the myocardium of Trim65-KO mice. In vitro studies demonstrated that overexpression of Trim65 inhibited ISO-induced cardiomyocyte hypertrophy by increasing mitochondrial density and membrane potential, and the Stat1 inhibitor fludarabine attenuated the effect of Trim65 knockdown on ISO-induced cardiomyocyte hypertrophy by reducing Reactive oxygen species (ROS) production and increasing the mitochondrial density and membrane potential. Our findings provide the first link between Trim65 and mitochondria, and we found for the first time that Trim65 inhibits mitochondria-dependent apoptosis and autophagy via the Jak1/Stat1 signalling pathway, ultimately attenuating ISO-induced cardiac hypertrophy; this effect of Trim65 might be mediated via the regulation of Jak1 ubiquitination. Taking these findings together, we suggest that genes that are related to mitochondria-dependent apoptosis and that are associated with Trim65 could be promising therapeutic targets for cardiac hypertrophy.

The role of ROS-induced pyroptosis in CVD.

Cardiovascular disease (CVD) is the number one cause of death in the world and seriously threatens human health. Pyroptosis is a new type of cell death discovered in recent years. Several studies have revealed that ROS-induced pyroptosis plays a key role in CVD. However, the signaling pathway ROS-induced pyroptosis has yet to be fully understood. This article reviews the specific mechanism of ROS-mediated pyroptosis in vascular endothelial cells, macrophages, and cardiomyocytes. Current evidence shows that ROS-mediated pyroptosis is a new target for the prevention and treatment of cardiovascular diseases such as atherosclerosis (AS), myocardial ischemia-reperfusion injury (MIRI), and heart failure (HF).

Understanding the Potential Function of Perivascular Adipose Tissue in Abdominal Aortic Aneurysms: Current Research Status and Future Expectation.

An abdominal aortic aneurysm (AAA) is a progressive dilatation of the vascular wall occurring below the aortic fissure, preferably occurring below the renal artery. The molecular mechanism of AAA has not yet been elucidated. In the past few decades, research on abdominal aortic aneurysm has been mainly focused on the vessel wall, and it is generally accepted that inflammation and middle layer fracture of the vessel wall is the core steps in the development of AAA. However, perivascular adipose tissue plays a non-negligible role in the occurrence and development of AAA. The position of PVAT plays a supporting and protective role on the vascular wall, but the particularity of the location makes it not only have the physiological function of visceral fat; but also can regulate the vascular function by secreting a large number of adipokines and cytokines. An abdominal aortic aneurysm is getting higher and higher, with a vascular rupture, low rescue success rate, and extremely high lethality rate. At present, there is no drug to control the progression or reverse abdominal aortic aneurysm. Therefore, it is critical to deeply explore the mechanism of abdominal aortic aneurysms and find new therapeutic ways to inhibit abdominal aortic aneurysm formation and disease progression. An abdominal aortic aneurysm is mainly characterized by inflammation of the vessel wall and matrix metalloprotein degradation. In this review, we mainly focus on the cytokines released by the perivascular adipose tissue, summarize the mechanisms involved in the regulation of abdominal aortic aneurysms, and provide new research directions for studying abdominal aortic aneurysms.

Oxidative stress impairs the Nur77-Sirt1 axis resulting in a decline in organism homeostasis during aging.

Sirt1 is an NAD+ -dependent deacetylase that protects against premature aging and cell senescence. Aging accompanied by oxidative stress leads to a decrease in Sirt1 levels and activity, but the regulatory mechanism that connects these events remains unclear. Here, we reported that Nur77, which shares similar biological pathways with Sirt1, was also decreased with age in multiple organs. Our in vivo and in vitro results revealed that Nur77 and Sirt1 decreased during aging and oxidative stress-induced cell senescence. Deletion of Nr4a1 shortened the lifespan and accelerated the aging process in multiple mouse tissues. Overexpression of Nr4a1 protected the Sirt1 protein from proteasomal degradation through negative transcriptional regulation of the E3 ligase MDM2. Our results showed that Nur77 deficiency markedly aggravated aging-related nephropathy and elucidated a key role for Nur77 in the stabilization of Sirt1 homeostasis during renal aging. We proposed a model wherein a reduction of Nur77 in response to oxidative stress promotes Sirt1 protein degradation through MDM2, which triggers cell senescence. This creates additional oxidative stress and provides positive feedback for premature aging by further decreasing Nur77 expression. Our findings reveal the mechanism by which oxidative stress reduces Sirt1 expression during aging and offers an attractive therapeutic strategy for targeting aging and homeostasis in organisms.