[Pollution Characteristics and Multilevel Risk Assessments of Antibiotics in the Urban Rivers of Beijing, China].

To comprehensively assess the pollution characteristics and ecological risks of antibiotics in the rivers in Beijing, the concentrations of 35 common antibiotics belonging to four categories were quantified by using solid phase extraction combined with high-performance liquid chromatography-tandem mass spectrometry. The ecological risks of antibiotics were evaluated using the methods of risk quotient (RQ) and joint probability curves (JPCs). The results showed that a total of 33 antibiotics were detected in the surface water of ten rivers in Beijing, and the total concentrations of antibiotics ranged from N.D. to 1 573.57 ng·L-1. Sulfamethoxazole showed the highest concentration (N.D.-160.04 ng·L-1), followed by sulfadiazine (0.09-147.90 ng·L-1) and ofloxacin (0.28-94.72 ng·L-1). There were 16 antibiotics with a detection frequency greater than 50.0 %. The RQ method showed that there were 12 antibiotics with potential ecological risks. Tetracycline, clarithromycin, and trimethoprim showed the highest risks, with RQs of 3.99, 1.86, and 1.01, respectively. The risks of antibiotics at the outlets of wastewater treatment plants were higher than those in mainstream rivers. The PNEC exceedance rates of tetracycline, clarithromycin, and trimethoprim were above 2.3 %. Based on JPCs, the maximum risk product of clarithromycin was 1.66 %, and it showed low risks to 0.3 %-7.0 % of species. The risks of other antibiotics could be ignored. The detection frequency, distribution of concentrations, most sensitive species, and species sensitivity distribution of antibiotics had important impacts on the ecological risk assessment. Using the multilevel ecological risk assessment strategy can effectively avoid inadequate protection and overprotection and is also conducive to the hierarchical and zoning management of antibiotics throughout the region.

Research progress of circadian rhythm in cardiovascular disease: A bibliometric study from 2002 to 2022.

Background: Given that the circadian rhythm is intricately linked to cardiovascular physiological functions, the objective of this investigation was to employ bibliometric visualization analysis in order to scrutinize the trends, hotspots, and prospects of the circadian rhythm and cardiovascular disease (CVD) over the past two decades. Methods: A thorough exploration of the literature related to the circadian rhythm and CVD was conducted via the Web of Science Core Collection database spanning the years 2002-2022. Advanced software tools, including citespace and VOSviewer, were employed to carry out a comprehensive analysis of the co-occurrence and collaborative relationships among countries, institutions, journals, references, and keywords found in this literature. Furthermore, correlation mapping was executed to provide a visual representation of the data. Results: The present study encompassed a total of 3399 published works, comprising of 2691 articles and 708 reviews. The publications under scrutiny were primarily derived from countries such as the United States, Japan, and China. The most prominent research institutions were found to be the University of Vigo, University of Minnesota, and Harvard University. Notably, the journal Chronobiology International, alongside its co-cited publications, had the most substantial contribution to the research in this field. Following an exhaustive analysis, the most frequently observed keywords were identified as circadian rhythm, blood pressure, hypertension, heart rate, heart rate variability, and melatonin. Furthermore, a nascent analysis indicated that future research might gravitate towards topics such as inflammation, metabolism, oxidative stress, and autophagy, thereby indicating new directions for investigation. Conclusion: This analysis represents the first instance of bibliometric scrutiny pertaining to circadian rhythm and its correlation with cardiovascular disease (CVD) through the use of visualization software. Notably, this study has succeeded in highlighting the recent research frontiers and prominent trajectories in this field, thereby providing a valuable contribution to the literature.

Dietary supplementation with inulin improves burn-induced skeletal muscle atrophy by regulating gut microbiota disorders.

Inulin, as a prebiotic, could modulate the gut microbiota. Burn injury leads to gut microbiota disorders and skeletal muscle catabolism. Therefore, whether inulin can improve burn-induced muscle atrophy by regulating microbiota disorders remains unknown. This study aimed to clarify that inulin intake alleviates gut microbiota disorders and skeletal muscle atrophy in burned rats. Rats were divided into the sham group, burn group, prebiotic inulin intervention group, and pseudo-aseptic validation group. A 30% total body surface area (TBSA) third-degree burn wound on dorsal skin was evaluated in all groups except the sham group. Animals in the intervention group received 7 g/L inulin. Animals in the validation group received antibiotic cocktail and inulin treatment. In our study inulin intervention could significantly alleviate the burn-induced skeletal muscle mass decrease and skeletal myoblast cell apoptosis. Inulin intake increased the abundances of Firmicutes and Actinobacteria but decreased the abundance of Proteobacteria. The biosynthesis of amino acids was the most meaningful metabolic pathway distinguishing the inulin intervention group from the burn group, and further mechanistic studies have shown that inulin can promote the phosphorylation of the myogenesis-related proteins PI3K, AKT and P70S6K and activate PI3K/AKT signaling for protein synthesis. In conclusion, inulin alleviated burn induced muscle atrophy through PI3K/AKT signaling and regulated gut microbiota dysbiosis.

Inhibiting Rev-erbα-mediated ferroptosis alleviates susceptibility to myocardial ischemia-reperfusion injury in type 2 diabetes.

The complex progression of type-2 diabetes (T2DM) may result in increased susceptibility to myocardial ischemia-reperfusion (IR) injury. IR injuries in multiple organs involves ferroptosis. Recently, the clock gene Rev-erbα has aroused considerable interest as a novel therapeutic target for metabolic and ischemic heart diseases. Herein, we investigated the roles of Rev-erbα and ferroptosis in myocardial IR injury during T2DM and its potential mechanisms. A T2DM model, myocardial IR and a tissue-specific Rev-erbα-/- mouse in vivo were established, and a high-fat high glucose environment with hypoxia-reoxygenation (HFHG/HR) in H9c2 were also performed. After myocardial IR, glycolipid profiles, creatine kinase-MB, AI, and the expression of Rev-erbα and ferroptosis-related proteins were increased in diabetic rats with impaired cardiac function compared to non-diabetic rats, regardless of the time at which IR was induced. The ferroptosis inhibitor ferrostatin-1 decreased AI in diabetic rats given IR and LPO levels in cells treated with HFHG/HR, as well as the expression of Rev-erbα and ACSL4. The ferroptosis inducer erastin increased AI and LPO levels and ACSL4 expression. Treatment with the circadian regulator nobiletin and genetically targeting Rev-erbα via siRNA or CRISPR/Cas9 technology both protected against severe myocardial injury and decreased Rev-erbα and ACSL4 expression, compared to the respective controls. Taken together, these data suggest that ferroptosis is involved in the susceptibility to myocardial IR injury during T2DM, and that targeting Rev-erbα could alleviate myocardial IR injury by inhibiting ferroptosis.

Abnormalities of glucose and lipid metabolism in myocardial ischemia-reperfusion injury.

Myocardial ischemia-reperfusion injury is a common condition in cardiovascular diseases, and the mechanism of its occurrence involves multiple complex metabolic pathways and signaling pathways. Among these pathways, glucose metabolism and lipid metabolism play important roles in regulating myocardial energy metabolism. Therefore, this article focuses on the roles of glucose metabolism and lipid metabolism in myocardial ischemia-reperfusion injury, including glycolysis, glucose uptake and transport, glycogen metabolism and the pentose phosphate pathway; and triglyceride metabolism, fatty acid uptake and transport, phospholipid metabolism, lipoprotein metabolism, and cholesterol metabolism. Finally, due to the different alterations and development of glucose metabolism and lipid metabolism in myocardial ischemia-reperfusion, there are also complex interregulatory relationships between them. In the future, modulating the equilibrium between glucose metabolism and lipid metabolism in cardiomyocytes and ameliorating aberrations in myocardial energy metabolism represent highly promising novel strategies for addressing myocardial ischemia-reperfusion injury. Therefore, a comprehensive exploration of glycolipid metabolism can offer novel theoretical and clinical insights into the prevention and treatment of myocardial ischemia-reperfusion injury.

Rev-erbs agonist SR9009 alleviates ischemia-reperfusion injury by heightening endogenous cardioprotection at onset of type-2 diabetes in rats: Down-regulating ferritinophagy/ferroptosis signaling.

The complex progression of type-2 diabetes (T2DM) results in inconsistent findings on myocardial susceptibility to ischemia-reperfusion (IR). IR injuries in multiple organs interconnect with ferroptosis. Targeting Rev-erbs might limit ferroptosis, with increasing attention turning to the application of circadian medicine against IR injuries. However, whether the Rev-erbs agonist SR9009 could mitigate diabetic IR injury remains unknown. Here, we investigated the susceptibility to IR at onset of T2DM in rats and its potential association between SR9009 and ferritinophagy/ferroptosis signaling. Onset of T2DM model was induced with a high-fat diet and the intraperitoneal injection of a low dose of streptozotocin. Myocardial IR model was established as well. Rats' general characteristics, cardiac function, glycolipid profiles, serum biochemistry, apoptosis index (AI) and morphological histology were observed and analyzed. Western blot and immunofluorescence (IF) were employed to evaluate the expression of ferritinophagy/ferroptosis signaling and its co-localization. Glycolipid profiles and cardiac diastolic function were significantly impaired in diabetic rats. CK-MB, AI levels and ferritinophagy/ferroptosis-related proteins expression decreased towards myocardial IR in diabetic rats compared to non-diabetic rats'. The ferroptosis inducer Erastin up-regulated SOD, MDA, and AI levels, as well as the expression of ferritinophagy/ferroptosis-related proteins in diabetic rats towards IR. Treatment with SR9009 down-regulated the degree of myocardial injury and ferritinophagy/ferroptosis-related proteins expression compared to diabetic rats treated with or without Erastin. Onset of T2DM activated endogenous cardioprotection against the susceptibility to myocardial IR injury, and SR9009 exogenously enhanced this endogenous mechanism and alleviated myocardial IR injury at onset of T2DM by down-regulating ferritinophagy/ferroptosis signaling.

A Rescue-Assistance Navigation Method by Using the Underground Location of WSN after Disasters.

A challenging rescue task for the underground disaster is to guide survivors in getting away from the dangerous area quickly. To address the issue, an escape guidance path developing method is proposed based on anisotropic underground wireless sensor networks under the condition of sparse anchor nodes. Firstly, a hybrid channel model was constructed to reflect the relationship between distance and receiving signal strength, which incorporates the underground complex communication characteristics, including the analytical ray wave guide model, the Shadowing effect, the tunnel size, and the penetration effect of obstacles. Secondly, a trustable anchor node selection algorithm with node movement detection is proposed, which solves the problem of high-precision node location in anisotropic networks with sparse anchor nodes after the disaster. Consequently, according to the node location and the obstacles, the optimal guidance path is developed by using the modified minimum spanning tree algorithm. Finally, the simulations in the 3D scene are conducted to verify the performance of the proposed method on the localization accuracy, guidance path effectiveness, and scalability.

Preparation and application of a beta-d-glucan microsphere conjugated protein A/G.

Antibodies (Abs) have been widely used in both immunodiagnostics and immunotherapy for the treatment of various diseases and, in recent years, scientific research applications. With the increasing use of Abs, there has been an urgent demand for low-cost and highly efficient purification methods. In this study, we present a novel formulation based on a ß-d-glucan particle loaded protein A/G (GP-protein A/G conjugates) by the carbodiimide method for the purification of immunoglobulin (IgG) antibodies. The prepared GP-protein A/G conjugates exhibit high stability and isolation efficiency. The microspheres also constitute an essential specialty reagent useful for isolating IgG from mammalian species such as goat, mouse and rabbit. Recovery of IgG showed that up to a purity of 92% was reached in the elution step. In addition, they has been shown to be important tools for molecular purification methods such as immunoprecipitation and co-immunoprecipitation. Taken together, these results suggest that the GP-protein A/G system has the potential to be used as a platform for purification techniques.