Diabetes mellitus is a metabolic disease characterized by long-term hyperglycaemia, which leads to microangiopathy and macroangiopathy and ultimately increases the mortality of diabetic patients. Endothelial dysfunction, which has been recognized as a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy, is characterized by a reduction in NO bioavailability. Oxidative stress, which is the main pathogenic factor in diabetes, is one of the major triggers of endothelial dysfunction through the reduction in NO. In this review, we summarize the four sources of ROS in the diabetic vasculature and the underlying molecular mechanisms by which the pathogenic factors hyperglycaemia, hyperlipidaemia, adipokines and insulin resistance induce oxidative stress in endothelial cells in the context of diabetes. In addition, we discuss oxidative stress-targeted interventions, including hypoglycaemic drugs, antioxidants and lifestyle interventions, and their effects on diabetes-induced endothelial dysfunction. In summary, our review provides comprehensive insight into the roles of oxidative stress in diabetes-induced endothelial dysfunction. 

pdf/the-role-of-oxidative-stress-in-diabetes-mellitus-induced-1h7v4lwqhz.pdf

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

Abstract Background Adipose tissue-derived adipokines are involved in various crosstalk between adipose tissue and other organs. Omentin1, a novel adipokine, exerts vital roles in the maintenance of body metabolism, insulin resistance and the like. However, the protective effect of omentin1 in myocardial ischemia (MI)-induced heart failure (HF) and its specific mechanism remains unclear and to be elucidated. Methods The model of MI-induced HF mice and oxygen glucose deprivation (OGD)-injured cardiomyocytes were performed. Mice with overexpression of omentin1 were constructed by a fat-specific adeno-associated virus (AAV) vector system. Results We demonstrated that circulating omentin1 level diminished in HF patients compared with healthy subjects. Furthermore, the fat-specific overexpression of omentin1 ameliorated cardiac function, cardiac hypertrophy, infarct size and cardiac pathological features, and also enhanced SIRT3/FOXO3a signaling in HF mice. Additionally, administration with AAV-omentin1 increased mitochondrial fusion and decreased mitochondrial fission in HF mice, as evidenced by up-regulated expression of Mfn2 and OPA1, and downregulation of p-Drp1(Ser616). Then, it also promoted PINK1/Parkin-dependent mitophagy. Simultaneously, treatment with recombinant omentin1 strengthened OGD-injured cardiomyocyte viability, restrained LDH release, and enhanced the mitochondrial accumulation of SIRT3 and nucleus transduction of FOXO3a. Besides, omentin1 also ameliorated unbalanced mitochondrial fusion-fission dynamics and activated mitophagy, thereby, improving the damaged mitochondria morphology and controlling mitochondrial quality in OGD-injured cardiomyocytes. Interestingly, SIRT3 played an important role in the improvement effects of omentin1 on mitochondrial function, unbalanced mitochondrial fusion-fission dynamics and mitophagy. Conclusion Omentin1 improves MI-induced HF and myocardial injury by maintaining mitochondrial dynamical homeostasis and activating mitophagy via upregulation of SIRT3/FOXO3a signaling. This study provides evidence for further application of omentin1 in cardiovascular diseases from the perspective of crosstalk between heart and adipose tissue. 

/pdf/omentin1-ameliorates-myocardial-ischemia-induced-heart-1hux0pat.pdf

Omentin1 ameliorates myocardial ischemia-induced heart failure via SIRT3/FOXO3a-dependent mitochondrial dynamical homeostasis and mitophagy

Bacterial infection-related diseases are major public safety issues leads to millions of deaths annually. Herein, a porous sulfur doped graphitic carbon nitride (g-SCN) for ecofriendly, metal-free and low systemic toxicity were synthesized. Sulfur doping enables to broaden the absorption spectrum and promote the photocarriers separation for photocatalysis enhancement. Moreover, sulfur element will coordinate with nitrogen, changing the electronic state and endowing g-SCN with the property of nanozyme. More importantly, we established different models and confirmed that S-N-C coordination is the source of peroxidase (POD)-like activity through theory and experiment. The increased specific surface area of g-SCN, ascribing to the porous structure, makes it easier to trap bacteria. With the synergistic effect of photocatalysis and nanozyme, the prepared g-SCN has the ability to kill both gram-negative and gram-positive bacterium, with an antibacterial efficiency up to 100%. This work provides innovative synergistic strategy for constructing nanomaterials for highly efficient antibacterial therapy. 

Construction of S-N-C bond for boosting bacteria-killing by synergistic effect of photocatalysis and nanozyme

Constructing the heterojunction by using covalent organic frameworks (COFs) is an effective way to promote photocatalytic activity. Herein, we designed and constructed different ratios of PDI/COFs hybrid materials by solvothermal method, denoted as PDI/TAPB-PDA (TAPB = 1,3,5-tris(4-aminophenyl)benzene, PDA = terephthaldehyde) composite. Although the construction of the heterojunction can destroy the long-range order of the TAPB-PDA COF structure to varying degrees, it does not affect the photocatalytic performance of PDI/TAPB-PDA composite. The optimal composite PDI/TAPB-PDA-5 with an initial molar ratio of PDI to TAPB-PDA COF of 32:1 has the highest photocatalytic performance for Cr(VI) reduction. The fitted first-order kinetic reaction rate k of PDI/TAPB-PDA-5 was 12.3 and 3.6 times that of PDI and TAPB-PDA COF, respectively. The superior photocatalytic activity of PDI/TAPB-PDA composite can be attributed to the broadened light absorption range and enhanced separation and transfer of carriers. The construction of composite materials between imine-linked COFs and dye PDI with excellent photocatalytic performance provides the possibility and affordability for realizing the practical application of expensive COFs-based catalysts. 

Enhanced photocatalytic Cr(VI) reduction performance by novel PDI/COFs composite

Nanozymes, as innovative materials, have demonstrated remarkable potential in the field of electrochemical biosensors. This article provides an overview of the mechanisms and extensive practical applications of nanozymes in electrochemical biosensors. First, the definition and characteristics of nanozymes are introduced, emphasizing their significant role in constructing efficient sensors. Subsequently, several common categories of nanozyme materials are delved into, including metal-based, carbon-based, metal-organic framework, and layered double hydroxide nanostructures, discussing their applications in electrochemical biosensors. Regarding their mechanisms, two key roles of nanozymes are particularly focused in electrochemical biosensors: selective enhancement and signal amplification, which crucially support the enhancement of sensor performance. In terms of practical applications, the widespread use of nanozyme-based electrochemical biosensors are showcased in various domains. From detecting biomolecules, pollutants, nucleic acids, proteins, to cells, providing robust means for high-sensitivity detection. Furthermore, insights into the future development of nanozyme-based electrochemical biosensors is provided, encompassing improvements and optimizations of nanozyme materials, innovative sensor design and integration, and the expansion of application fields through interdisciplinary collaboration. In conclusion, this article systematically presents the mechanisms and applications of nanozymes in electrochemical biosensors, offering valuable references and prospects for research and development in this field.

Nanozyme-Enhanced Electrochemical Biosensors: Mechanisms and Applications.

ABSTRACT Introduction Chronic metabolism-related diseases are challenging clinical problems. Omentin-1 is mainly expressed in stromal vascular cells of adipose tissue and can also be expressed in airway goblet cells, mesothelial cells, and vascular cells. Omentin-1 has been found to exert important anti-inflammatory, antioxidative and anti-apoptotic roles and to regulate endothelial dysfunction. Moreover, omentin-1 also has protective effects against cancer, atherosclerosis, type 2 diabetes mellitus, and bone metabolic diseases. The current review will discuss the therapeutic potential of omentin-1. Areas covered This review summarizes the biological actions of omentin-1 and provides an overview of omentin-1 in metabolic-related diseases. The relevant literature was derived from a PubMed search spanning 1998–2021 using these search terms: omentin-1, atherosclerosis, diabetes mellitus, bone, cancer, inflammation, and oxidative stress. Expert opinion As a novel adipocytokine, omentin-1 is a promising therapeutic target in metabolic-related diseases. Preclinical animal studies have shown encouraging results. Moreover, circulating omentin-1 has excellent potential as a noninvasive biomarker. In the future, strategies for regulating omentin-1 need to be investigated further in clinical trials in a large cohort.

Omentin-1: a newly discovered warrior against metabolic related diseases

Regulation of Functional Groups Enable the Metal-free PDINH/GO Advisable Antibacterial Photocatalytic Therapy

Determining the optimum span of a solar greenhouse

High energy density materials (HEDM) are the subject of an extensive research effort in relation to the use of these compounds as components of rocket propellants, powders, and formulations of high-performance explosives. Hexanitrohexaazaisowurtzitane (HNIW, i.e., CL-20) has received much attention in these research fields for its specific impulse, burning rate, ballistics, and detonation velocity. In this paper, the development and performances of the explosives from the first to the fourth generation are briefly summarized, and the synthesis status of the fourth-generation explosive, HNIW, is reviewed. The key issues that restrict the development of industrial amplification synthesis of HNIW are analyzed, and the potential directions of development are proposed. It is pointed out that to synthesize new and efficient catalysts is the key to making the cost-effective manufacturing of CL-20 a reality.

/pdf/research-progress-and-key-issues-of-hydrodebenzylation-of-2dlt656x.pdf

Research Progress and Key Issues of Hydrodebenzylation of Hexabenzylhexaazaisowurtzitane (HBIW) in the Synthesis of High Energy Density Material Hexanitrohexaazaisowurtzitane (HNIW)

Breast cancer is one of the most common cancers endangering women's health. SRY-related high-mobility-group box 6 (SOX6) is associated with many cancers, though its role has not been reported in breast cancer. Here, we aimed to explore the expression and function of SOX6 in breast cancer. On the basis of the analysis of SOX6 in The Cancer Genome Atlas, Cancer Cell Line Encyclopedia and Genotype-Tissue Expression databases, we revealed that SOX6 was downregulated in breast cancer, and we verified the results at the cellular level by means of western blotting and quantitative real-time PCR. When SOX6 was overexpressed, the proliferation of breast cancer cells was inhibited, and apoptosis was promoted. Moreover, the methylation level of the SOX6 promoter in breast cancer was significantly higher than that in normal tissues. 5'-Aza-2'-deoxycytidine reversed the high level of methylation that was caused by decreased expression of SOX6. This evidence suggests that SOX6 is a tumor suppressor gene associated with breast cancer. This study could provide a new target for breast cancer treatment.

SRY-related high-mobility-group box 6 suppresses cell proliferation and is downregulated in breast cancer.

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