Effect of High Magnesium and Astragaloside IV on Vascular Endothelial Cells.

Percutaneous coronary intervention (PCI) is the main treatment for patients with severe coronary vascular stenosis. However, In-stent neo-atherosclerosis (ISNA) is an important clinical complication in patients after PCI, which is mainly caused by a persistent inflammatory response and endothelial insufficiency. In the cardiovascular field, magnesium-based scaffolds stand out due to their properties. Magnesium plays a key role in regulating cardiovascular physiology. Magnesium deficiency can promote endothelial cell dysfunction, which contributes to the formation of atherosclerosis. Since astragaloside IV (AS­IV) has been proven to have potent cardioprotective effects, we asked whether high levels of magnesium cooperate with AS­IV might have effects on endothelial function and ISNA. We performed in vitro experiments on endothelial cells. Being treated with different concentrations of magnesium or/and AS-IV, the cell growth and migration were detected by CCK-8 and wound healing assay, respectively. The pro-inflammatory factors tumor necrosis factor α (TNF-α) and interleukin 6 (IL-6), adhesion molecule vascular cell adhesion molecule-1 (VCAM-1), and NF-kB were determined by qRT-PCR, ELISA kits or western blot. Results showed that high magnesium and AS-IV improved endothelial function, including promoting cell migration and decreasing the content of TNF-α, IL-6, VCAM-1, and NF-kB. With the supplement of AS-IV, additive magnesium maintains cell proliferation, migration, and function of endothelial cells. In conclusion, these findings suggest that high magnesium and AS­IV could improve vascular endothelial dysfunction. Early detection and treatment for neo-atherosclerosis may be of great clinical significance for improving stent implantation efficacy and long-term prognosis.

Understanding Sorafenib-Induced Cardiovascular Toxicity: Mechanisms and Treatment Implications.

Tyrosine kinase inhibitors (TKIs) have been recognized as crucial agents for treating various tumors, and one of their key targets is the intracellular site of the vascular endothelial growth factor receptor (VEGFR). While TKIs have demonstrated their effectiveness in solid tumor patients and increased life expectancy, they can also lead to adverse cardiovascular effects including hypertension, thromboembolism, cardiac ischemia, and left ventricular dysfunction. Among the TKIs, sorafenib was the first approved agent and it exerts anti-tumor effects on hepatocellular carcinoma (HCC) and renal cell carcinoma (RCC) by inhibiting angiogenesis and tumor cell proliferation through targeting VEGFR and RAF. Unfortunately, the adverse cardiovascular effects caused by sorafenib not only affect solid tumor patients but also limit its application in curing other diseases. This review explores the mechanisms underlying sorafenib-induced cardiovascular adverse effects, including endothelial dysfunction, mitochondrial dysfunction, endoplasmic reticulum stress, dysregulated autophagy, and ferroptosis. It also discusses potential treatment strategies, such as antioxidants and renin-angiotensin system inhibitors, and highlights the association between sorafenib-induced hypertension and treatment efficacy in cancer patients. Furthermore, emerging research suggests a link between sorafenib-induced glycolysis, drug resistance, and cardiovascular toxicity, necessitating further investigation. Overall, understanding these mechanisms is crucial for optimizing sorafenib therapy and minimizing cardiovascular risks in cancer patients.

Research status of pathogenesis of anxiety or depression after percutaneous coronary intervention and Traditional Chinese Medicine intervention.

ETHNIC PHARMACOLOGICAL RELEVANCE: Anxiety or depression after percutaneous coronary intervention (PCI) is a common clinical disease. Currently, conventional pharmacotherapy primarily involves the administration of anxiolytic or antidepressant medications in conjunction with anticoagulants, antiplatelet agents, and other cardiovascular drugs. However, challenges such as drug dependence, adverse reactions and related concerns persist in the treatment of this disease. Numerous pertinent studies have demonstrated that Traditional Chinese Medicine (TCM) exhibits significant therapeutic efficacy and distinctive advantages in managing post-PCI anxiety or depression. AIM OF THIS REVIEW: This review attempted to summarize the characteristics of TCM for treating anxiety or depression after PCI, including single Chinese herbs, Chinese medicine monomers, compound TCM prescriptions, TCM patented drugs, and other TCM-related treatment methods, focusing on the analysis of the relevant mechanism of TCM treatment of this disease. METHODS: By searching the literature on treating anxiety or depression after PCI with TCM in PubMed, Web of Science, CNKI, and other relevant databases, this review focuses on the latest research progress of TCM treatment of this disease. RESULTS: In the treatment of anxiety or depression after PCI, TCM exerts significant pharmacological effects such as anti-inflammatory, antioxidant, anti-anxiety or anti-depression, cardiovascular and cerebrovascular protection, and neuroprotection, mainly by regulating the levels of related inflammatory factors, oxidative stress markers, neurotransmitter levels, and related signaling pathways. TCM has a good clinical effect in treating anxiety or depression after PCI with individualized treatment. CONCLUSIONS: TCM has terrific potential and good prospects in the treatment of anxiety or depression after PCI. The main direction of future exploration is the study of the mechanism related to Chinese medicine monomers and the large sample clinical study related to compound TCM prescriptions.

Role of Brain-Derived Neurotrophic Factor in Anxiety or Depression After Percutaneous Coronary Intervention.

Anxiety or depression after percutaneous coronary intervention (PCI) is one of the key clinical problems in cardiology that need to be solved urgently. Brain-derived neurotrophic factor (BDNF) may be a potential biomarker for the pathogenesis and treatment of anxiety or depression after PCI. This article reviews the correlation between BDNF and cardiovascular system and nervous system from the aspects of synthesis, release and action site of BDNF, and focuses on the latest research progress of the mechanism of BDNF in anxiety or depression after PCI. It includes the specific mechanisms by which BDNF regulates the levels of inflammatory factors, reduces oxidative stress damage, and mediates multiple signaling pathways. In addition, this review summarizes the therapeutic potential of BDNF as a potential biomarker for anxiety or depression after PCI.

Deep learning-based identification of spine growth potential on EOS radiographs.

OBJECTIVES: To develop an automatic computer-based method that can help clinicians in assessing spine growth potential based on EOS radiographs. METHODS: We developed a deep learning-based (DL) algorithm that can mimic the human judgment process to automatically determine spine growth potential and the Risser sign based on full-length spine EOS radiographs. A total of 3383 EOS cases were collected and used for the training and test of the algorithm. Subsequently, the completed DL algorithm underwent clinical validation on an additional 440 cases and was compared to the evaluations of four clinicians. RESULTS: Regarding the Risser sign, the weighted kappa value of our DL algorithm was 0.933, while that of the four clinicians ranged from 0.909 to 0.930. In the assessment of spine growth potential, the kappa value of our DL algorithm was 0.944, while the kappa values of the four clinicians were 0.916, 0.934, 0.911, and 0.920, respectively. Furthermore, our DL algorithm obtained a slightly higher accuracy (0.973) and Youden index (0.952) compared to the best values achieved by the four clinicians. In addition, the speed of our DL algorithm was 15.2 ± 0.3 s/40 cases, much faster than the inference speeds of the clinicians, ranging from 177.2 ± 28.0 s/40 cases to 241.2 ± 64.1 s/40 cases. CONCLUSIONS: Our algorithm demonstrated comparable or even better performance compared to clinicians in assessing spine growth potential. This stable, efficient, and convenient algorithm seems to be a promising approach to assist doctors in clinical practice and deserves further study. CLINICAL RELEVANCE STATEMENT: This method has the ability to quickly ascertain the spine growth potential based on EOS radiographs, and it holds promise to provide assistance to busy doctors in certain clinical scenarios. KEY POINTS: • In the clinic, there is no available computer-based method that can automatically assess spine growth potential. • We developed a deep learning-based method that could automatically ascertain spine growth potential. • Compared with the results of the clinicians, our algorithm got comparable results.

MicroRNA-specific therapeutic targets and biomarkers of apoptosis following myocardial ischemia-reperfusion injury.

MicroRNAs are single-stranded non-coding RNAs that participate in post-transcriptional regulation of gene expression, it is involved in the regulation of apoptosis after myocardial ischemia-reperfusion injury. For example, the alteration of mitochondrial structure is facilitated by MicroRNA-1 through the regulation of apoptosis-related proteins, such as Bax and Bcl-2, thereby mitigating cardiomyocyte apoptosis. MicroRNA-21 not only modulates the expression of NF-κB to suppress inflammatory signals but also activates the PI3K/AKT pathway to mitigate ischemia-reperfusion injury. Overexpression of MicroRNA-133 attenuates reactive oxygen species (ROS) production and suppressed the oxidative stress response, thereby mitigating cellular apoptosis. MicroRNA-139 modulates the extrinsic death signal of Fas, while MicroRNA-145 regulates endoplasmic reticulum calcium overload, both of which exert regulatory effects on cardiomyocyte apoptosis. Therefore, the article categorizes the molecular mechanisms based on the three classical pathways and multiple signaling pathways of apoptosis. It summarizes the targets and pathways of MicroRNA therapy for ischemia-reperfusion injury and analyzes future research directions.

K-N Bridge-Mediated charge separation in hollow g-C3N4 Frameworks: A bifunctional photocatalysts towards efficient H2 and H2O2 production.

The development of bifunctional photocatalysts for enhancing hydrogen (H2) and hydrogen peroxide (H2O2) production from water is essential in addressing environmental and energy issues. However, the practical implementation of photocatalytic technology is still constrained by the inadequate separation of photo-generated charge carriers. Herein, potassium (K) atoms are introduced into the interlayers of graphitic carbon nitride (g-C3N4) with a hollow hexagonal structure (K-TCN) and are coordinated with N atoms in adjacent layers. The presence of K-N coordination serves as a layer bridge, facilitating the separation of charge carriers. The hollow hexagonal structure reduces the distance over which photogenerated electrons migrate to the surface, thereby enhancing the reaction kinetics. Consequently, the optimized K-TCN exhibits a dramatically improved photocatalytic H2 (941.6 µmol g-1h-1 with platinum (Pt) as the cocatalyst) and H2O2 (347.6 µmol g-1h-1) generation as compared to hollow g-C3N4 (TCN) and bulk g-C3N4 nanosheet (CN) without K-N bridge under visible light irradiation. The unique design holds promising potential for developing highly efficient bifunctional photocatalysts towards producing renewable fuels and value-added chemicals.

Progress in clinical characteristics of high myopia with primary open-angle glaucoma.

High myopia (HM) is a significant risk factor for the occurrence and progression of primary open-angle glaucoma (POAG). Identification with POAG in the HM population is an emergent challenge. Patients with HM have a significantly higher probability of complicating POAG than those without HM. When HM is associated with POAG, the changes to the fundus caused by both of them are confused with each other, making the diagnosis of early glaucoma difficult. This article reviews available researches on HM with POAG, summarizing the characteristics of the fundus structure such as epidemiology, intraocular pressure, optic disc, ganglion cell layer, retinal nerve fiber layer, vascular density, and visual field.

Gradient Cationic Vacancies Enabling Inner-To-Outer Tandem Homojunctions: Strong Local Internal Electric Field and Reformed Basic Sites Boosting CO2 Photoreduction.

The slow charge dynamics and large activation energy of CO2 severely hinder the efficiency of CO2 photoreduction. Defect engineering is a well-established strategy, while the function of common zero-dimensional defects is always restricted to promoting surface adsorption. In this work, a gradient layer of tungsten vacancies with a thickness of 3-4 nm is created across Bi2 WO6 nanosheets. This gradient layer enables the formation of an inner-to-outer tandem homojunction with an internal electric field, which provides a strong driving force for the migration of photoelectrons from the bulk to the surface. Meanwhile, W vacancies change the coordination environment around O and W atoms, leading to an alteration in the basic sites and the mode of CO2 adsorption from weak/strong adsorption to moderate adsorption, which ultimately decreases the formation barrier of the key intermediate *COOH and facilitates the conversion thermodynamics for CO2 . Without any cocatalyst and sacrificial reagent, W-vacant Bi2 WO6 shows an outstanding photocatalytic CO2 reduction performance with a CO production rate of 30.62 µmol g-1  h-1 , being one of the best catalysts in similar reaction systems. This study reveals that gradient vacancies as a new type of defect will show huge potential in regulating charge dynamics and catalytic reaction thermodynamics.

Altered Bacterial-Fungal Interkingdom Networks in the Guts of Ankylosing Spondylitis Patients.

Intestinal bacterial dysbiosis has been increasingly linked to ankylosing spondylitis (AS), which is a prototypic and best studied subtype of spondyloarthritis (SpA). Fungi and bacteria coexist in the human gut and interact with each other. Although they have been shown to contribute actively to health or disease, no studies have investigated whether the fungal microbiota in AS patients is perturbed. In this study, fecal samples from 22 AS patients, with clinical and radiographic assessments, and 16 healthy controls (HCs) were collected to systematically characterize the gut microbiota and mycobiota in AS patients by 16S rRNA gene- and ITS2-based DNA sequencing. Our results showed that the microbiota of AS patients was characterized by increased abundance of Proteobacteria and decreased Bacteroidetes, which was contributed by enrichment of Escherichia-Shigella, Veillonella, Lachnospiraceae NK4A136 group, and reduction of Prevotella strain 9, Megamona, and Fusobacterium. The gut mycobiota of AS patients was characterized by higher levels of Ascomycota, especially the class of Dothideomycetes, and decreased abundance of Basidiomycota, which was mainly contributed by the decease of Agaricales. Compared to HCs, decreased ITS2/16S biodiversity ratios and altered bacterial-fungal interkingdom networks were observed in AS patients. Compared with nonsteroidal anti-inflammatory drugs (NSAIDs), treating AS patients with biological agents induced obvious changes in the gut mycobiota, and this result was highly associated with disease activity indexes, including AS disease activity index (ASDAS) C-reactive protein (asCRP), erythrocyte sedimentation rate (ESR), and Bath AS disease activity index (BASDAI). In addition, altered mycobiota in AS patients was also found associated with the degree of radiographic damage. IMPORTANCE The human gut is colonized by diverse fungi (mycobiota), and fungi have long been suspected in the pathogenesis of SpA. Our study unraveled a disease-specific interkingdom network alteration in AS, suggesting that fungi, or the interkingdom interactions between bacteria and fungi, may play an essential role in AS development. However, our study is limited by sample size, and in-depth mechanism studies and additional large-scale investigations characterizing the gut mycobiome in AS patients are needed to form a foundation for research into the relationship between mycobiota dysbiosis and AS development.