Shaping and Doping Metal-Organic Framework-Derived TiO2 to Steer the Selectivity of Photocatalytic CO2 Reduction toward CH4.

Steering selectivity in photocatalytic conversion of CO2, especially toward deep reduction products, is vital to energy and environmental goals yet remains a great challenge. In this work, we demonstrate a facet-dependent photocatalytic selective reduction of CO2 to CH4 in Cu-doped TiO2 catalysts exposed with different facets synthesized by a topological transformation from MIL-125 (Ti) precursors. The optimized round cake-like Cu/TiO2 photocatalyst mainly exposed with the (001) facet exhibited a high photocatalytic CO2 reduction performance with a CH4 yield of 40.36 µmol g-1 h-1 with a selectivity of 94.1%, which are significantly higher than those of TiO2 (001) (4.70 µmol g-1 h-1 and 52.6%, respectively), Cu/TiO2 (001 + 101) (18.95 µmol g-1 h-1 and 69.6%, respectively), and Cu/TiO2 (101) (14.73 µmol g-1 h-1 and 78.9%, respectively). The results of experimental and theoretical calculations demonstrate that the Cu doping dominating the promoted separation and migration efficiencies of photogenerated charges and the preferential adsorption on (001) facets synergistically contribute to the selective reduction of CO2 to CH4. This work highlights the significance of synergy between facet engineering and ion doping in the design of high-performance photocatalysts with respect to selective reduction of CO2 to multielectron products.

Coprococcus protects against high-fat diet-induced nonalcoholic fatty liver disease in mice.

AIMS: The incidence of nonalcoholic fatty liver disease (NAFLD) is increasing annually, leading to substantial medical and health burdens. Numerous studies have demonstrated the potential effectiveness of intestinal probiotics as a treatment strategy for NAFLD. Therefore, the objective of this study is to identify a probiotic for the treatment of NAFLD. METHODS AND RESULTS: In this study, blood and fecal samples were collected from 41 healthy volunteers and 44 patients diagnosed with NAFLD. Analysis of the 16S rDNA sequencing data and quantitative real-time PCR (RT-qPCR) revealed a significant reduction in the abundance of Coprococcus in NAFLD patients. Subsequent animal experiments demonstrated that Coprococcus was able to effectively reverse liver lipid accumulation, inflammation, and fibrosis induced by a high-fat diet (HFD) in mice. CONCLUSIONS: This study provides the first in vivo evidence that Coprococcus is a beneficial bacterium capable of preventing NAFLD and has the same probiotic effect in mice as Lactobacillus GG (LGG), a positive control. Therefore, Coprococcus has the potential to serve as a probiotic for the prevention and treatment of NAFLD in humans.

Phospholipase Dα6 and phosphatidic acid regulate gibberellin signaling in rice.

Phospholipase D (PLD) hydrolyzes membrane lipids to produce phosphatidic acid (PA), a lipid mediator involved in various cellular and physiological processes. Here, we show that PLDα6 and PA regulate the distribution of GIBBERELLIN (GA)-INSENSITIVE DWARF1 (GID1), a soluble gibberellin receptor in rice. PLDα6-knockout (KO) plants display less sensitivity to GA than WT, and PA restores the mutant to a normal GA response. PA binds to GID1, as documented by liposome binding, fat immunoblotting, and surface plasmon resonance. Arginines 79 and 82 of GID1 are two key amino acid residues required for PA binding and also for GID1's nuclear localization. The loss of PLDα6 impedes GA-induced nuclear localization of GID1. In addition, PLDα6-KO plants attenuated GA-induced degradation of the DELLA protein SLENDER RICE1 (SLR1). These data suggest that PLDα6 and PA positively mediate GA signaling in rice via PA binding to GID1 and promotion of its nuclear translocation.

Synergistic Effects of the Ni3B Cocatalyst and N Vacancy on g-C3N4 for Effectively Enhanced Photocatalytic N2 Fixation.

The photocatalytic fixation of N2 is a promising technology for sustainable production of ammonia, while the unsatisfactory efficiency resulting from the low electron-transfer rate, narrow light absorption range, and limited active sites of the photocatalyst seriously hinder its application. Herein, we designed a noble metal-free Schottky junction photocatalyst constructed by g-C3N4 nanosheets with N vacancies (VN-CN) and metallic Ni3B nanoparticles (Ni3B/VN-CN) for N2 reduction to ammonia. The ammonia yield rate over the optimized Ni3B/VN-CN is 7.68 mM g-1 h-1, which is 6.7 times higher than that of pristine CN (1.15 mM g-1 h-1). The superior photocatalytic N2 fixation performance of Ni3B/VN-CN can be attributed not only to the formation of Schottky junctions between Ni3B and VN-CN, which facilitates the migration and separation of photogenerated electrons, but also to the incorporation of VN into g-C3N4, which enhances visible light absorption and improves electrical conductivity. More importantly, Ni3B nanoparticles can act as the cocatalyst, which provide more active sites for the adsorption and activation of N2, thereby improving the N2 reduction activity. This work provides an effective strategy of designing noble metal-free-based cocatalyst photocatalyst for sustainable and economic N2 fixation.

Relationship Between Prognostic Nutritional Index and New-Onset Atrial Fibrillation in Patients with Acute ST-Elevation Myocardial Infarction Following Percutaneous Coronary Intervention.

Multiple reports relate new-onset atrial fibrillation (NOAF) to poor clinical outcomes in patients with ST-elevation myocardial infarction (STEMI) who received percutaneous coronary intervention (PCI). The prognostic nutritional index (PNI) is a reliable indicator of immunonutritional-inflammatory status, and it is linked to clinical outcomes in cardiovascular disease patients. This research aims to explore the relationship between NOAF and PNI.Overall, 600 STEMI patients treated with PCI were recruited for this retrospective analysis. The patients were categorized into the NOAF group or sinus rhythm (SR) group. Logistic regression and receiver operating characteristic (ROC) curve analyses were conducted to assess PNI estimation. Lastly, the Kaplan-Meier curve was used to compare all-cause mortality between both groups.The combined NOAF incidence in PCI-treated STEMI patients was 7.7%. PNI was independently correlated with NOAF using multivariate regression analyses (odds ratio [OR], 0.824; 95% confidence interval [CI], 0.750-0.906; P < 0.001). In ROC curve analyses, the best PNI threshold value for predicting NOAF was 40.1, with sensitivity, and specificity of 76.09% and 71.30%, respectively area under the curve, 0.787; 95% CI, 0.752-0.819; P < 0.001). After a median of 41-month follow-up, the Kaplan-Meier curve revealed that the NOAF patients displayed an elevated all-cause death incidence compared with SR patients, with a log-rank of P = 0.005.This study demonstrated that PNI is an independent predictor of NOAF in STEMI patients during hospitalization after PCI, which is strongly correlated with a poor outcome upon discharge.

Ni3B as p-Block Element-Modulated Cocatalyst for Efficient Photocatalytic CO2 Reduction.

Due to the multiple electron and proton transfer processes involved, the photogenerated charges are easily recombined during the photocatalytic reduction of CO2, making the generation of the eight-electron product CH4 kinetically more difficult. Herein, Ni3B nanoparticles modulated by p-block element were combined with TiO2 nanosheets to construct a novel Schottky junction photocatalyst (Ni3B/TiO2) for the selective photocatalytic conversion of CO2 to CH4. The formed Ni3B/TiO2 photocatalyst with Schottky junction ensures a transfer pathway of photogenerated electrons from TiO2 to Ni3B, which facilitates the accumulation of electrons on the surface of Ni3B and subsequently improves the activity of photocatalytic CO2 reduction to CH4. The optimized Ni3B/TiO2 Schottky junction shows an improved CH4 yield of 30.03 µmol g-1 h-1, which was much higher than those of TiO2 (1.62 µmol g-1 h-1), NiO/TiO2 (2.44 µmol g-1 h-1), and Ni/TiO2 (4.3 µmol g-1 h-1). This work demonstrated that the introduction of p-block elements can alleviate the scaling relationship effect of pure metal cocatalysts to a certain extent, and the modified Ni3B can be used as a promising new cocatalyst to effectively improve the selective photocatalytic of CO2 to CH4.

Hyperammonemia in a pregnant woman with citrullinemia type I: a case report and literature review.

BACKGROUND: Citrullinemia type I (CTLN1) is a rare urea cycle disorder (UCD) with few adult cases described so far. Diagnosis of late-onset CTLN1 is difficult, and delayed treatment may increase the risk of severe hyperammonemia. Pregnancy is an important risk factor for women with CTLN1. However, the clinical manifestations of CTLN1 in a pregnant woman may be mistaken for pregnancy side effects and ultimately delay a timely diagnosis. CASE PRESENTATION: A 34-year-old woman developed vomiting and disturbance of consciousness after 12 weeks of gestation. A blood test showed hyperammonemia (454 µg/dL) with normal liver function tests. She fell into a deep coma, and her serum ammonia level increased to 800 µg/dL. Continuous renal replacement therapy (CRRT) was administered as a diagnostic treatment for UCD and serum ammonia. This patient's case was complicated by co-infection; her dependents decided to withdraw life support and the patient died. She was diagnosed with CTLN1 by analyses of plasma amino acids, urinary orotic acid, and second-generation gene sequencing. DISCUSSION AND CONCLUSION: When a patient displays symptoms of emesis and disturbance of consciousness in early pregnancy, blood ammonia should be monitored, and UCD should be considered, particularly for patients with hyperammonemia in the absence of severe liver function abnormalities.

Inhibition of miR-188-5p alleviates hepatic fibrosis by significantly reducing the activation and proliferation of HSCs through PTEN/PI3K/AKT pathway.

Persistent hepatic damage and chronic inflammation in liver activate the quiescent hepatic stellate cells (HSCs) and cause hepatic fibrosis (HF). Several microRNAs regulate the activation and proliferation of HSCs, thereby playing a critical role in HF progression. Previous studies have reported that miR-188-5p is dysregulated during the process of HF. However, the role of miR-188-5p in HF remains unclear. This study investigated the potential role of miR-188-5p in HSCs and HF. Firstly, we validated the miR-188-5p expression in primary cells isolated from liver of carbon tetrachloride (CCl4 )-induced mice, TGF-ß1-induced LX-2 cells, livers from 6-month high-fat diet (HFD)-induced rat and 4-month HFD-induced mice NASH models, and human non-alcoholic fatty liver disease (NAFLD) patients. Furthermore, we used miR-188-5p inhibitors to investigate the therapeutic effects of miR-188-5p inhibition in the HFD + CCl4 induced in vivo model and the potential role of miR-188-5p in the activation and proliferation of HSCs. This present study reported that miR-188-5p expression is significantly increased in the human NAFLD, HSCs isolated from liver of CCl4 induced mice, and in vitro and in vivo models of HF. Mimicking the miR-188-5p resulted in the up-regulation of HSC activation and proliferation by directly targeting the phosphatase and tensin homolog (PTEN). Moreover, inhibition of miR-188-5p reduced the activation and proliferation markers of HSCs through PTEN/AKT pathway. Additionally, in vivo inhibition of miR-188-5p suppressed the HF parameters, pro-fibrotic and pro-inflammatory genes, and fibrosis. Collectively, our results uncover the pro-fibrotic role of miR-188-5p. Furthermore, we demonstrated that miR-188-5p inhibition decreases the severity of HF by reducing the activation and proliferation of HSCs through PTEN/AKT pathway.

Chronic Toxic Effects of Flutolanil on the Liver of Zebrafish ( Danio rerio).

Flutolanil is a broad-spectrum amide fungicide that is widely used to prevent fungal pathogens in agriculture. However, its usage may have a potential environmental impact on organisms. So far, few literatures have investigated the chronic toxicity of flutolanil at concentrations relevant to environmental conditions in the nontarget aquatic organisms. This study was aimed at evaluating whether the long-term exposure of flutolanil affects oxidative stress, immune response, and apoptosis in the liver of zebrafish ( Danio rerio). The results showed that the activity of catalase (CAT) was significantly decreased in the liver in all flutolanil-treated groups. Interestingly, the malondialdehyde (MDA) contents were remarkably increased following the flutolanil exposure. Deoxyribonucleic acid (DNA) damage was increased with a concentration-dependent manner. The transcription level of genes involved in apoptosis and the immune system were significantly altered following flutolanil chronic exposure in zebrafish liver. Furthermore, the caspase-3 enzyme activity was significantly increased. Taken together, this study demonstrated that the resulting effects on oxidative stress, immune toxicity, and apoptosis may be responsible for the pathological alterations in zebrafish liver after flutolanil exposure at concentrations relevant to environmental conditions, advancing the knowledge of pesticide environmental risk assessment.

HAND1 loss-of-function mutation associated with familial dilated cardiomyopathy.

BACKGROUND: The basic helix-loop-helix transcription factor HAND1 is essential for cardiac development and structural remodeling, and mutations in HAND1 have been causally linked to various congenital heart diseases. However, whether genetically compromised HAND1 predisposes to dilated cardiomyopathy (DCM) in humans remains unknown. METHODS: The whole coding region and splicing junctions of the HAND1 gene were sequenced in 140 unrelated patients with idiopathic DCM. The available family members of the index patient carrying an identified mutation and 260 unrelated ethnically matched healthy individuals used as controls were genotyped for HAND1. The functional effect of the mutant HAND1 was characterized in contrast to its wild-type counterpart by using a dual-luciferase reporter assay system. RESULTS: A novel heterozygous HAND1 mutation, p.R105X, was identified in a family with DCM transmitted as an autosomal dominant trait, which co-segregated with DCM in the family with complete penetrance. The nonsense mutation was absent in 520 control chromosomes. Functional analyses unveiled that the mutant HAND1 had no transcriptional activity. Furthermore, the mutation abolished the synergistic activation between HAND1 and GATA4, another crucial cardiac transcription factors that has been associated with various congenital cardiovascular malformations and DCM. CONCLUSIONS: This study firstly reports the association of HAND1 loss-of-function mutation with increased susceptibility to DCM in humans, which provides novel insight into the molecular mechanisms underpinning DCM.

Case report: First Chinese patient with family partial lipodystrophy type 6 due to novel compound heterozygous mutations in the LIPE gene.

Background: Family partial lipodystrophy (FPLD) is a rare autosomal dominant disease characterized by disorders of variable body fat loss associated with metabolic complications. FPLD6 has only been reported in a limited number of cases. Here, we reported a Chinese FPLD6 patient with compound heterozygous mutations in the lipase E, hormone-sensitive type (LIPE) gene. Case presentation: A 20-year-old female patient presented with hypertriglyceridemia, diabetes mellitus, hepatomegaly, and hepatic steatosis. Subcutaneous fat was significantly diminished in her face, abdomen, and limbs. The patient was assessed by detailed clinical and biochemical examinations. A liver biopsy showed severe lipodystrophy. In addition, there were retinal changes, peripheral nerve damage, and renal tubular injury. Sequencing was performed on extracted DNA. Genetic analysis revealed that the patient had compound heterozygous mutations in the LIPE gene: c.2497_250ldel (p.Glu833LysfsTer22) and c.2705del (p.Ser902ThrfsTer27) heterozygous mutations. Verification revealed that this mutation was inherited from her father and mother, respectively, and that they formed newly discovered compound heterozygous mutations occurring in the LIPE gene, causing FPLD6. Conclusion: We reported the first case of FPLD6 in China. Gene analysis demonstrated compound heterozygous mutations in LIPE in this patient. Our case emphasizes the importance of genetic testing in young patients with severe metabolic syndromes.

Case report: The use of metagenomic next-generation sequencing to diagnose Lemierre's syndrome caused by lost root canal fillings in a 33-year-old patient with metabolic syndrome.

Background: Lemierre's syndrome is a rare and serious complication of pharyngitis with an estimated annual incidence of 1 in 100,000 people worldwide. It is characterized by septic thrombophlebitis of the internal jugular vein with metastatic infection, usually after oropharyngeal infection. Rare cases of Lemierre's syndrome have been reported to be caused by odontogenic infection. Case report: A 33-year-old male visited our hospital with symptoms of fever and sore throat for 16 days. The other symptoms included pain in his left neck and shoulder. In addition, metabolic syndrome was diagnosed based on waist circumference, diabetes, and hyperlipidemia. Fusobacterium necrophorum bacteria was detected using the metagenomic next-generation sequencing (mNGS) technique. The enhanced computerized tomography (CT) scan showed thrombosis of the left proximal jugular vein and brachiocephalic vein. Based on these observations, Lemierre's syndrome was diagnosed. The etiology was that the fillings in the root canal tooth were lost with no blood or pain about 2 weeks before the onset. The patient recovered after treatment with antibiotics and blood purification. Conclusion: Lemierre's syndrome should be evaluated for patients with fever, sore throat, and neck pain. If the loss of fillings from root canal therapy occurs, especially for those with metabolic syndrome, we should be aware of the possibility of this disease. Furthermore, the mNGS test can be used as a crucial supplementary diagnostic tool for patients with undetermined fever.

Plant natural product-based pesticides in crop protection: semi-synthesis, mono-crystal structures and agrochemical activities of osthole ester derivatives, and study of their toxicology against Tetranychus cinnabarinus (Boisduval).

BACKGROUND: Owing to large amounts of synthetic pesticides being extensively and unreasonably used for crop protection, currently, resistance and negative impacts on human health and environment safety have appeared. Therefore, development of potential pesticide candidates is highly urgent. Herein, a series of ester derivatives of osthole were designed and synthesized as pesticidal agents. RESULTS: Six spatial configurations of 4'-(p-toluenoyloxy)osthole (4b), 4'-(m-fluorobenzoyloxy)osthole (4f), 4'-(p-fluorophenylacetyloxy)osthole (4m), 4'-(3'',4''-methylenedioxybenzoyloxy)osthole (4q), 4'-formyloxyosthole (4u) and 4'-acetyloxyosthole (4v) were determined by X-ray mono-crystal diffraction. Compounds 4b, 4'-(p-chlorobenzoyloxy)osthole (4g), 4'-(m-chlorobenzoyloxy)osthole (4h), 4'-(p-bromobenzoyloxy)osthole (4i) and 4'-(2''-chloropyridin-3''-ylcarbonyloxy)osthole (4p) showed higher insecticidal activity than toosendanin against Mythimna separata Walker; notably, compound 4b displayed 1.8 times insecticidal activity of the precursor osthole. Against Tetranychus cinnabarinus Boisduval, compounds 4g and 4h showed 3.3 and 2.6 times acaricidal activity of osthole, and good control effects in the glasshouse. Scanning electron microscopy assay demonstrated that compound 4g can damage the cuticle layer of T. cinnabarinus resulting in death. CONCLUSION: Compounds 4g and 4h can be further studied as lead pesticidal agents for the management of M. separata and T. cinnabarinus. These results will pave the way for application of osthole derivatives as agrochemicals. © 2024 Society of Chemical Industry.

PARP9 affects myocardial function through TGF-ß/Smad axis and pirfenidone.

Cardiac arrhythmias are often linked to the overactivity of cardiac fibroblasts (CFs). Investigating the impact of poly (ADP-ribose) polymerase 9 (PARP9) on Angiotensin II (Ang II)-induced fibroblast activation and the therapeutic effects of pirfenidone (PFD) offers valuable insights into cardiac arrhythmias. This study utilized weighted gene co-expression network analysis (WGCNA), differential gene expression (DEG) analysis, protein-protein interaction (PPI), and receiver operating characteristic (ROC) analysis on the GSE42955 dataset to identify the hub gene with a significant diagnostic value. The ImmuCellAI tool revealed an association between PARP9 and immune cell infiltration. Our in vitro assessments focused on the influence of PFD on myofibroblast differentiation, transforming growth factor-beta (TGF-ß) expression, and Ang II-induced proliferation and migration in CFs. Additionally, we explored the impact on fibrosis markers and the TGF-ß/Smad signaling pathway in the context of PARP9 overexpression. Analysis of the GSE42955 dataset revealed PARP9 as a central gene with high clinical diagnostic value, linked to seven types of immune cells. The in vitro studies demonstrated that PFD significantly mitigates Ang II-induced CF proliferation, migration, and fibrosis. It also reduces Ang II-induced PARP9 expression and decreases fibrosis markers, including TGF-ß, collagen I, collagen III, and α-SMA. Notably, PARP9 overexpression can partially counteract PFD's inhibitory effects on CFs and modify the expression of fibronectin, CTGF, α-SMA, collagen I, collagen III, MMP2, MMP9, TGF-ß, and p-Smad2/3 in the TGF-ß/Smad signaling pathway. In summary, our findings suggest that PFD effectively counteracts the adverse effects of Ang II-induced CF proliferation and fibrosis, and modulates the TGF-ß/Smad signaling pathway and PARP9 expression. This identifies a potential therapeutic approach for managing myocardial fibrosis.

Cycloastragenol inhibits adipogenesis and fat accumulation in vitro and in vivo through activating Hedgehog signaling.

In this study, we investigated the effect of cycloastragenol (CAG), a triterpenoid isolated from Astragalus membranaceus roots, on regulating the adipogenesis and fat accumulation in vitro and in vivo. During the adipogenesis of 3T3-L1 cells, CAG inhibited lipid accumulation and the expression of key adipogenic factors, proliferator-activated receptor γ (PPARγ) and CCAAT enhancer binding protein α (C/EBPα) and increased the expression of Gli1, a key mediator in Hedgehog (Hh) signaling. In HFD-induced animal experiment, CAG significantly reduced body weight gain without affecting brown fat weight. In addition, CAG regulated the expression of PPARγ, C/EBPα, and Gli1 in visceral white adipose tissue (vWAT). We also confirmed the inhibitory effect of CAG on specifically targeting white adipose tissue (WAT) formation in stromal vascular fraction (SVF) cell differentiation. Taken together, these results suggest that CAG may be a potent phytochemical preventing adipogenesis and obesity via Hh signaling. Supplementary Information: The online version contains supplementary material available at 10.1007/s10068-023-01403-0.

Curcumol metabolized by rat liver S9 fraction and orally administered in mouse suppressed the proliferation of colon cancer in vitro and in vivo.

Following 3R (reduction, refinement, and replacement) principles, we employed the rat liver S9 fraction to mimic liver metabolism of curcumol having high in vitro IC50 on cancer cells. In HCT116 and HT29 colon cancer cells, the metabolites of curcumol by S9 fraction exerted more enhanced activity in inducing cell cycle arrest and apoptosis via regulating the expression of cyclin D1, CDK1, p21, PARP and Bcl-2 than curcumol. In addition, oral administration of curcumol at 4 mg/kg BW significantly suppressed the development of colon tumor induced by azoxymethane/dextran sulfate sodium, and induced cell cycle arrest and apoptosis in tumor tissues. In mass analysis, curcumenol and curzerene were identified as the metabolites of curcumol by S9 fraction metabolism. Taken together, curcumol metabolites showed the enhanced suppressive effect on colon cancer, suggesting that S9 fraction can be considered as simple, fast, and bio-mimicking platform for the screening of chemical libraries on different chronic diseases.

A 2-decade bibliometric analysis of epigenetics of cardiovascular disease: from past to present.

BACKGROUND: Cardiovascular disease (CVD) remains a major health killer worldwide, and the role of epigenetic regulation in CVD has been widely studied in recent decades. Herein, we perform a bibliometric study to decipher how research topics in this field have evolved during the past 2 decades. RESULTS: Publications on epigenetics in CVD produced during the period 2000-2022 were retrieved from the Web of Science Core Collection (WoSCC). We utilized Bibliometrix to build a science map of the publications and applied VOSviewer and CiteSpace to assess co-authorship, co-citation, co-occurrence, and bibliographic coupling. In total, 27,762 publications were included for bibliometric analysis. The yearly amount of publications experienced exponential growth. The top 3 most influential countries were China, the United States, and Germany, while the most cited institutions were Nanjing Medical University, Harbin Medical University, and Shanghai Jiao Tong University. Four major research trends were identified: (a) epigenetic mechanisms of CVD; (b) epigenetics-based therapies for CVD; (c) epigenetic profiles of specific CVDs; and (d) epigenetic biomarkers for CVD diagnosis/prediction. The latest and most important research topics, including "nlrp3 inflammasome", "myocardial injury", and "reperfusion injury", were determined by detecting citation bursts of co-occurring keywords. The most cited reference was a review of the current knowledge about how miRNAs recognize target genes and modulate their expression and function. CONCLUSIONS: The number and impact of global publications on epigenetics in CVD have expanded rapidly over time. Our findings may provide insights into the epigenetic basis of CVD pathogenesis, diagnosis, and treatment.

Trends in worldwide research on cardiac fibrosis over the period 1989-2022: a bibliometric study.

Background: Cardiac fibrosis is a hallmark of various end-stage cardiovascular diseases (CVDs) and a potent contributor to adverse cardiovascular events. During the past decades, extensive publications on this topic have emerged worldwide, while a bibliometric analysis of the current status and research trends is still lacking. Methods: We retrieved relevant 13,446 articles on cardiac fibrosis published between 1989 and 2022 from the Web of Science Core Collection (WoSCC). Bibliometrix was used for science mapping of the literature, while VOSviewer and CiteSpace were applied to visualize co-authorship, co-citation, co-occurrence, and bibliographic coupling networks. Results: We identified four major research trends: (1) pathophysiological mechanisms; (2) treatment strategies; (3) cardiac fibrosis and related CVDs; (4) early diagnostic methods. The most recent and important research themes such as left ventricular dysfunction, transgenic mice, and matrix metalloproteinase were generated by burst analysis of keywords. The reference with the most citations was a contemporary review summarizing the role of cardiac fibroblasts and fibrogenic molecules in promoting fibrogenesis following myocardial injury. The top 3 most influential countries were the United States, China, and Germany, while the most cited institution was Shanghai Jiao Tong University, followed by Nanjing Medical University and Capital Medical University. Conclusions: The number and impact of global publications on cardiac fibrosis has expanded rapidly over the past 30 years. These results are in favor of paving the way for future research on the pathogenesis, diagnosis, and treatment of cardiac fibrosis.

Bismuth nanoparticles and oxygen vacancies synergistically modified HNb3O8 nanosheets for enhanced photocatalytic N2 reduction towards NH3.

Due to the high stability of the N2 molecule and the low charge separation efficiency, the photocatalytic reduction of N2 to high-value chemicals (NH3) under mild conditions remains a great challenge. Herein, a composite photocatalyst (Bi/HNb3O8-Vo nanosheets) with Bi nanoparticles modified the HNb3O8-Vo nanosheets are designed for the conversion of N2 into NH3. In this design, the introduction of oxygen vacancies on the catalyst surface facilitates the formation of defective energy levels within the band gap of HNb3O8-Vo NS, which promotes the absorption of visible light, and enhances the charge carrier transport and separation. Bi nanoparticles co-catalyst not only facilitates the separation and migration of photogenerated charges, but also acts as reaction sites to adsorb and activate N2 molecule. Consequently, the optimized 5 % Bi/HNb3O8-Vo photocatalysts show a NH3 yield of 372.7 µmol/L g-1h-1 under full spectral irradiation without sacrificial agent, which is much higher than that of HNb3O8 NS (92.2 µmol/L g-1h-1). This work provides a new way for the design of efficient N2 reduction photocatalysts through the synergistic effect of surface vacancies and metal co-catalysts.

Correction to: 1,3,5,8­Tetrahydroxyxanthone suppressed adipogenesis via activating Hedgehog signaling in 3T3­L1 adipocytes.

[This corrects the article DOI: 10.1007/s10068-022-01130-y.].