A colorimetric sensor based on multiple elements doped carbon dot nanozyme for rapid detection of 1-naphthol in human urine samples.

The residual carbaryl in crops can cause serious damage to the human kidney and nervous system after entering the human body, which may be metabolized to 1-naphthol (1-NAP) and excreted through urine. 1-NAP is often used as the biomarker for carbaryl exposure, so the intake or leakage of carbaryl can be monitored by detecting the concentration of 1-NAP. Herein, Co, N, P ternary co-doped carbon dots (CoNP-CDs) derived from vitamin B12 were synthesized by a facile hydrothermal method. CoNP-CDs exhibited oxidase-like activity and excellent peroxidase-like activity, which was attributed to the Fenton-like reaction of Co2+/Co3+ and the presence of pyrrole N and P elements, which together provided multiple active sites for chromogenic substrates. Due to the dual enzyme-like activity of CoNP-CDs, hydroxyl radicals (OH) and superoxide radicals (O2-) were generated during the catalytic process, which could rapidly oxidize colorless 3,3',5,5'-tetramethyl benzidine (TMB) to blue oxidation products (oxTMB). The α-carbon in 1-NAP can be attacked by OH, and the catalytic oxidation process of TMB can be inhibited by the consumption of OH, so that the blue color of the solution became lighter. Based on this principle, a smartphone-assisted colorimetric sensing platform was constructed for the detection of 1-NAP, and which resulted in a linear range of 1.07-37.3 µM and a visual detection limit of 0.68 µM. Moreover, the colorimetric sensing system showed satisfactory recoveries in the detection of human urine samples. The colorimetric sensing system owned the advantages of fast response, strong selectivity and simple operation, and provided a potential strategy for the on-site detection of 1-NAP.

Magnetic solid extraction of PCBs in the fruit juices based on polyaniline-modified CoFe2O4@Ti3C2 composite.

Polychlorinated biphenyls (PCBs) have been known pollutants, which are ubiquitous in various matrix, even in some food products and beverages like fruit juices. It is of great importance to develop efficient and simple method to detect them in such matrix. In this work, an effective magnetic composite integrating the advantages of the magnism of CoFe2O4, hydrophilicity and multisites of Ti3C2 and high adsorption properties of polyaniline (CoFe2O4@Ti3C2@PANI) was designed and synthesized. CoFe2O4@Ti3C2@PANI-based magnetic solid-phase extraction coupled with gas chromatography-tandem mass spectrometry was established for determination of nine PCBs in fruit juices. The developed method achieved low detection limits of 0.4-0.8 ng L-1. The established method was validated with three beverages and achieved good spiked recoveries ranging from 77.2 % to 104.7 %. These findings exhibited that the established method was very simple, efficient, and credible for the analysis of PCBs in food, environmental, and other fields.

Dual COF functionalized magnetic MXene composite for enhancing magnetic solid phase extraction of thiophene compounds from oilfield produced waters prior to GC-MS/MS analysis.

In this study, a novel COFTABT@COFTATp modified magnetic MXene composite (CoFe2O4 @Ti3C2 @COFTABT@COFTATp) was synthesized by Schiff base reaction and irre-versible enol-keto tautomerization, and employed to establish a sensitive monitoring method for six thiophene compounds in oilfield produced water samples based on magnetic solid-phase extraction (MSPE) prior to gas chromatography coupled with a triple quadruple mass spectrometer (GC-MS/MS). The designed magnetic materials exhibited unexpected enrichment ability to target thiophene compounds and achieved good extraction efficiencies ranging from 83 % to 98 %. The developed MSPE/GC-MS/MS method exhibited good linearity in the range of 0.001-100 µg L-1, and obtained lower limits of detection ranging from 0.39 to 1.9 ng L-1. The spiked recoveries of thiophene compounds obtained in three oilfield produced water samples were over the range of 96.26 %-99.54 % with relative standard deviations (RSDs) less than 3.7 %. Notably, benzothiophene, 4-methyldibenzothiophene and 4,6-dimethyldibenzothiophene were detected in three oilfield-produced water samples. Furthermore, the material still kept favorable stability after six recycling experiments. The adsorption kinetics, adsorption isotherms as well as adsorption thermodynamics of thiophene compounds were investigated in detail to provide insight into the mechanisms. Overall, the present work contributed a promising strategy for designing and synthesizing new functionalized materials for the enrichment and detection of typical pollutants in the environment.

Covalent organic framework-functionalized magnetic MXene nanocomposite for efficient pre-concentration and detection of organophosphorus and organochlorine pesticides in tea samples before gas chromatography-triple quadrupole mass spectrometry analysis.

In this study, a hydrophobic covalent organic framework-functionalized magnetic composite (CoFe2O4@Ti3C2@TAPB-TFTA) with a high specific area with 1,3,5-tris(4-aminophenyl)benzene (TAPB) and 2,3,5,6-tetrafluoroterephthalaldehyde (TFTA) was designed and synthesized through Schiff base reaction. An efficient magnetic solid-phase extraction method was established and combined with gas chromatography-triple quadrupole mass spectrometry to sensitively determine 10 organochlorine and organophosphorus pesticides in tea samples. The established method exhibited good linearity in the range of 0.05-120 µg/L and had low limits of detection (0.013-0.018 µg/L). The method was evaluated with tea samples, and the spiked recoveries of pesticides in different tea samples reached satisfactory values of 85.7-96.8%. Moreover, the adsorption of pesticides was spontaneous and followed Redlich-Peterson isotherm and pseudo-second-order kinetic models. These results demonstrate the sensitivity, effectiveness, and reliability of the proposed method for monitoring organochlorine and organophosphorus pesticides in tea samples, providing a preliminary basis for researchers to reasonably design adsorbents for the efficient extraction of pesticides.

Taxonomic identification and life cycle comparison of two populations of the monostromatic green algae Monostroma nitidum.

Monostroma nitidum, a monostromatic green algae (MGA) with high economic value, is distributed worldwide. Life cycle often serves as a fundamental criterion for taxonomic classification. Most researchers consider the life cycle of M. nitidum to involve dimorphic alternation of generations, although the possibility of a monomorphic asexual life cycle remains unclear. In this study, tufA and 18S rDNA sequences were employed as molecular markers, complemented by morphological analysis, to classify and identify MGA in two distinct habitats: Hailing Island reefs (YJ) and Naozhou Island reefs (ZJ). The results of tufA and 18S rDNA sequence analysis revealed that all samples from YJ and ZJ clustered to the same branch (M. nitidum clade) with high bootstrap support and genetic distances of less than 0.000 and 0.005, respectively. However, morphological observations indicated significant differences in the external morphology of the YJ and ZJ samples, although both initially exhibited a filament-blade form during early development. The life cycle of the ZJ samples exhibited typical dimorphic alternation of generations, whereas the YJ samples only produced biflagellate asexual gametes with negative phototaxis. Gametes of the YJ samples directly developed into new gametophytes without undergoing the sporophyte stage. Consequently, the YJ and ZJ samples were classified as monomorphic asexual and dimorphic sexual M. nitidum, respectively. These findings provide evidence supporting the monomorphic asexual life cycle of M. nitidum for the classification of MGA.

Adipose transplantation improves metabolism and atherosclerosis but not perivascular adipose tissue abnormality or vascular dysfunction in lipodystrophic Seipin/Apoe null mice.

Adipose dysfunction in lipodystrophic SEIPIN deficiency is associated with multiple metabolic disorders and increased risks of developing cardiovascular diseases, such as atherosclerosis, cardiac hypertrophy, and heart failure. Recently, adipose transplantation has been found to correct adipose dysfunction and metabolic disorders in lipodystrophic Seipin knockout mice; however, whether adipose transplantation could improve lipodystrophy-associated cardiovascular consequences is still unclear. Here, we aimed to explore the effects of adipose transplantation on lipodystrophy-associated metabolic cardiovascular diseases in Seipin knockout mice crossed into atherosclerosis-prone apolipoprotein E (Apoe) knockout background. At 2 months of age, lipodystrophic Seipin/Apoe double knockout mice and nonlipodystrophic Apoe knockout controls were subjected to adipose transplantation or sham operation. Seven months later, mice were euthanized. Our data showed that although adipose transplantation had no significant impact on endogenous adipose atrophy or gene expression, it remarkably increased plasma leptin but not adiponectin concentration in Seipin/Apoe double knockout mice. This led to significantly reduced hyperlipidemia, hepatic steatosis, and insulin resistance in Seipin/Apoe double knockout mice. Consequently, atherosclerosis burden, intraplaque macrophage infiltration, and aortic inflammatory gene expression were all attenuated in Seipin/Apoe double knockout mice with adipose transplantation. However, adipocyte morphology, macrophage infiltration, or fibrosis of the perivascular adipose tissue was not altered in Seipin/Apoe double knockout mice with adipose transplantation, followed by no significant improvement of vasoconstriction or relaxation. In conclusion, we demonstrate that adipose transplantation could alleviate lipodystrophy-associated metabolic disorders and atherosclerosis but has an almost null impact on perivascular adipose abnormality or vascular dysfunction in lipodystrophic Seipin/Apoe double knockout mice.NEW & NOTEWORTHY Adipose transplantation (AT) reverses multiply metabolic derangements in lipodystrophy, but whether it could improve lipodystrophy-related cardiovascular consequences is unknown. Here, using Seipin/Apoe double knockout mice as a lipodystrophy disease model, we showed that AT partially restored adipose functionality, which translated into significantly reduced atherosclerosis. However, AT was incapable of reversing perivascular adipose abnormality or vascular dysfunction. The current study provides preliminary experimental evidence on the therapeutic potential of AT on lipodystrophy-related metabolic cardiovascular diseases.

Gradient-Pattern Micro-Grooved Wicks Fabricated by the Ultraviolet Nanosecond Laser Method and Their Enhanced Capillary Performance.

Capillary-gradient wicks can achieve fast or directional liquid transport, but they face fabrication challenges by traditional methods in terms of precise patterns. Laser processing is a potential solution due to its high pattern accuracy, but there are a few studies on laser-processed capillary-gradient wicks. In this paper, capillary step-gradient micro-grooved wicks (CSMWs) were fabricated by an ultraviolet nanosecond pulsed laser, and their capillary performance was studied experimentally. The CSMWs could be divided into three regions with a decreasing capillary radius. The equilibrium rising height of the CSMWs was enhanced by 124% compared to the non-gradient parallel wick. Different from the classical Lucas-Washburn model describing a uniform non-gradient wick, secondary capillary acceleration was observed in the negative gradient direction of the CSMWs. With the increase in laser power and the decrease in scanning speed, the capillary performance was promoted, and the optimal laser processing parameters were 4 W-10 mm/s. The laser-enhanced capillary performance was attributed to the improved hydrophilicity and reduced capillary radius, which resulted from the increased surface roughness, protrusion morphology, and deep-narrow V-shaped grooves induced by the high energy density of the laser. Our study demonstrates that ultraviolet pulsed laser processing is a highly efficient and low-cost method for fabricating high-performance capillary gradient wicks.

Research Advances of Engineered Exosomes as Drug Delivery Carrier.

Exosomes are nanoscale vesicles secreted by living cells that have similar membrane composition to parental cells and carry a variety of proteins, lipids, and nucleic acids. Therefore, exosomes have certain biological activities and play an important role in intercellular communication. On the basis of its potential as a carrier for drug delivery systems, exosomes have been engineered to compensate for the shortage of natural exosomes through various engineering strategies for improving drug delivery efficiency, enhancing targeting to tissues and organs, and extending the circulating half-life of exosomes. This review focuses on the engineered exosomes loading drugs through different strategies, discussions on exosome surface modification strategies, and summarizes the advantages and disadvantages of different strategies. In addition, this review provides an overview of the recent applications of engineered exosomes in a number of refractory and relapsable diseases. This review has the potential to provide a reference for further research and development of engineered exosomes.

A Wireless Neural Stimulator IC for Cortical Visual Prosthesis.

We propose a 0.25 × 0.25 × 0.3 mm (~0.02 mm3) optically powered mote for visual cortex stimulation to restore vision. Up to 1024 implanted motes can be individually addressed. The complete StiMote system was confirmed fully functional when optically powered and cortex stimulation was confirmed in-vivo with a live rat brain.

Hyperhomocysteinaemia Promotes Doxorubicin-Induced Cardiotoxicity in Mice.

Doxorubicin, a widely used chemotherapeutic drug in clinical oncology, causes a series of cardiac side effects referred to as doxorubicin-induced cardiotoxicity. Hyperhomocysteinaemia is an independent risk factor for multiple cardiovascular diseases. However, whether hyperhomocysteinaemia contributes to doxorubicin-induced cardiotoxicity is currently unknown. In this study, we explored the pathogenic effects of hyperhomocysteinaemia induced by dietary methionine supplementation (2% wt/wt in rodent chow) in a mouse model of doxorubicin-induced cardiotoxicity. Our data showed that methionine supplementation doubled serum homocysteine levels, inducing mild hyperhomocysteinaemia. Doxorubicin at a cumulative dosage of 25 mg/kg body weight led to significant weight loss and severe cardiac dysfunction, which were further exacerbated by methionine-induced mild hyperhomocysteinaemia. Doxorubicin-induced cardiac atrophy, cytoplasmic vacuolisation, myofibrillar disarray and loss, as well as cardiac fibrosis, were also exacerbated by methionine-induced mild hyperhomocysteinaemia. Additional folic acid supplementation (0.006% wt/wt) prevented methionine-induced hyperhomocysteinaemia and inhibited hyperhomocysteinaemia-aggravated cardiac dysfunction and cardiomyopathy. In particular, hyperhomocysteinaemia increased both serum and cardiac oxidative stress, which could all be inhibited by folic acid supplementation. Therefore, we demonstrated for the first time that hyperhomocysteinaemia could exacerbate doxorubicin-induced cardiotoxicity in mice, and the pathogenic effects of hyperhomocysteinaemia might at least partially correlate with increased oxidative stress and could be prevented by folic acid supplementation. Our study provides preliminary experimental evidence for the assessment of hyperhomocysteinaemia as a potential risk factor for chemotherapy-induced cardiotoxicity in cancer patients.

Transcriptome analysis reveals the molecular mechanisms of adaptation to high temperatures in Gracilaria bailinae.

Global warming causes great thermal stress to macroalgae and those species that can adapt to it are thought to be better able to cope with warmer oceans. Gracilaria bailinae, a macroalgae with high economic and ecological values, can survive through the hot summer in the South China Sea, but the molecular mechanisms underlying its adaptation to high temperatures are unclear. To address this issue, the present study analyzed the growth and transcriptome of G. bailinae after a 7-day exposure to 15°C (LT: low temperature), 25°C (MT: middle temperature), and 35°C (HT: high temperature). Growth analysis showed that the HT group had the highest relative growth rate (RGR = 2.1%) with the maximum photochemical quantum yield of PSII (F v/F m = 0.62) remaining within the normal range. Transcriptome analysis showed more differentially expressed genes (DEGs) in the comparison between MT and HT groups than in that between MT and LT, and most of these DEGs tended to be downregulated at higher temperatures. The KEGG pathway enrichment analysis showed that the DEGs were mainly enriched in the carbohydrate, energy, and lipid metabolisms. In addition, the genes involved in NADPH and ATP synthesis, which are associated with photosynthesis, the Calvin cycle, pyruvate metabolism, and the citrate cycle, were downregulated. Downregulation was also observed in genes that encode enzymes involved in fatty acid desaturation and alpha-linolenic acid metabolism. In summary, G. bailinae regulated the synthesis of NADPH and ATP, which are involved in the above-mentioned processes, to reduce unnecessary energy consumption, and limited the synthesis of enzymes in the metabolism of unsaturated fatty acids and alpha-linolenic acid to adapt to high environmental temperatures. The results of this study improve our understanding of the molecular mechanisms underlying the adaptation of G. bailinae to high temperatures.

Severe hypertriglyceridemia caused by Gpihbp1 deficiency facilitates vascular remodeling through increasing endothelial activation and oxidative stress.

Hypertriglyceridemia (HTG) is an independent risk factor for atherosclerosis. However, its impact on non-atherosclerotic cardiovascular diseases remains largely unknown. Glycosylphosphatidylinositol anchored high-density lipoprotein binding protein 1 (GPIHBP1) is essential for the hydrolysis of circulating triglycerides and loss of functional GPIHBP1 causes severe HTG. In this study, we used Gpihbp1 knockout (GKO) mice to investigate the potential effects of HTG on non-atherosclerotic vascular remodeling. We compared the aortic morphology and gene expressions between three-month-old and ten-month-old GKO mice and their age-matched wild-type controls. We also conducted similar comparisons between GKO mice and wild-type controls in an angiotensin II (AngII)-induced vascular remodeling model. Our data showed that the intima-media wall of ten-month-old GKO mice but not three-month-olds was significantly thickened compared to wild-type controls. Moreover, ten-month-old GKO mice but not three-month-olds had increased aortic macrophage infiltration and perivascular fibrosis, along with increased endothelial activation and oxidative stress. Similarly, the AngII-induced vascular remodeling, as well as endothelial activation and oxidative stress, were also exacerbated in the GKO mice compared to wild-type controls. In conclusion, we demonstrated that severe HTG caused by Gpihbp1 deficiency could facilitate the onset and progression of non-atherosclerotic vascular remodeling through endothelial activation and oxidative stress in mice.

Ferritinophagy activation and sideroflexin1-dependent mitochondrial iron overload contribute to patulin-induced cardiac inflammation and fibrosis.

Patulin (PAT) is a mycotoxin that is commonly present throughout the ecosystem where fungi grow and mainly contaminates food, soil, and water. PAT was found to be cardiotoxic in previous studies. However, the detailed mechanism has not been fully elucidated. The present study aimed to explore the role and underlying mechanism of ferroptosis in PAT-induced cardiac injury. Here, we confirmed in vivo and in vitro that ferroptosis is involved in PAT-induced myocardial inflammation and fibrosis. Mice exposed to PAT (1 and 2 mg/kg body weight/day for 14 days) exhibited myocardial inflammation and fibrosis along with disrupted iron homeostasis, elevated lipid peroxidation, depletion of glutathione peroxidase 4, and abnormal mitochondrial morphology. When primary neonatal rat cardiomyocytes (NRCMs) and H9c2 cells were exposed to PAT, ferroptosis was initiated in a dose-dependent manner, and this process could be significantly attenuated by ferrostatin-1. Mechanistically, we found that nuclear receptor coactivator (NCOA) 4, a master regulator of ferritinophagy, bound to and degraded ferritin in response to PAT treatment, thereby releasing large amounts of ferrous iron and further leading to sideroflexin (SFXN) 1-dependent mitochondrial iron overload. Conversely, knockdown of NCOA4 or SFXN1 with small interfering RNAs could effectively ameliorate ferroptotic cell death, cellular or mitochondrial iron overload and lipid peroxides accumulation. Furthermore, myocardial inflammation and fibrosis in PAT-exposed mice was alleviated by the mitochondrial iron chelator deferiprone. Overall, our findings underscore that ferritinophagy activation and SFXN1-dependent mitochondrial iron overload play critical roles in PAT-induced myocardial ferroptosis and consequent cardiotoxicity.

The pathogenesis of aging-induced left atrial appendage thrombus formation and cardioembolic stroke in mice is influenced by inflammation-derived matrix metalloproteinases.

Elderly people without atrial fibrillation (AF) still have a high incidence of cardioembolic stroke, suggesting that thrombus formation within the left atrial appendage (LAA) may also occur in an AF-independent manner. In the present study, we explored the potential mechanisms for aging-induced LAA thrombus formation and stroke in mice. We monitored stroke events in 180 aging male mice (14-24 months) and assessed left atrium (LA) remodeling by echocardiography at different ages. Mice that had stroke were implanted with telemeters to confirm AF. Histological features of LA and LAA thrombi were examined, as well as collagen content, expression of matrix metalloproteinases (MMPs), and leukocyte density in the atria at different ages, in mice with or without stroke. Also, the effects of MMP inhibition on stroke incidence and atrial inflammation were tested. We detected 20 mice (11 %) with stroke, 60 % of which were within 18-19 months of age. Although we did not detect AF in mice with stroke, we detected the presence of LAA thrombi, suggesting that stroke originated from the hearts of these mice. Compared with 18-month-old mice without stroke, 18-month-old stroke mice had enlarged LA with a very thin endocardium, that was associated with less collagen and heightened MMP expression in the atria. During aging, we found that the expression of mRNAs for atrial MMP7, MMP8, and MMP9 peaked at 18 months, which closely correlated with reductions in collagen content and the time-window for cardioembolic stroke in these mice. Treatment of mice with an MMP inhibitor at 17-18 months of age reduced atrial inflammation and remodeling, and stroke incidence. Taken together, our study demonstrates that aging-induced LAA thrombus formation occurs through a mechanism involving upregulation of MMPs and breakdown of collagen, and that treatment with an MMP inhibitor may be effective as a treatment strategy for this heart condition.

Hyperhomocysteinemia Promotes Cardiac Hypertrophy in Hypertension.

Hyperhomocysteinemia (HHcy) is positively linked with several cardiovascular diseases; however, its role and underlying mechanisms in pathological cardiac hypertrophy are still unclear. Here, we focused on the effects and underlying mechanisms of HHcy in hypertensive cardiac hypertrophy, one of the most common and typical types of pathological cardiac hypertrophy. By a retrospective analysis of the association between HHcy and cardiac hypertrophy in a hypertensive cohort, we found that the prevalence of HHcy was higher in patients with hypertrophy and significantly associated with the presence of cardiac hypertrophy after adjusting for other conventional risk factors. In mice, HHcy induced by a methionine (2% wt/wt) diet feeding significantly promoted cardiac hypertrophy as well as cardiac inflammation and fibrosis induced by 3-week angiotensin ІІ (AngІІ) infusion (1000 ng/kg/min), while folic acid (0.006% wt/wt) supplement corrected HHcy and attenuated AngII-stimulated cardiac phenotypes. Mechanistic studies further showed that homocysteine (Hcy) exacerbated AngII-stimulated expression of Calcineurin and nuclear factor of activated T cells (NFAT), which could be attenuated by folic acid both in mice and in neonatal rat cardiomyocytes. Moreover, treatment with cyclosporin A, an inhibitor of Calcineurin, blocked Hcy-stimulated Calcineurin-NFAT signaling and hypertrophy in neonatal rat cardiomyocytes. In conclusion, our study indicates that HHcy promotes cardiac hypertrophy in hypertension, and Calcineurin-NFAT pathway might be involved in the pro-hypertrophic effect of Hcy.

Characterization of the Complete Chloroplast Genome of Four Species in Callerya.

BACKGROUND: Callerya reticulata (Bentham) Schot, Callerya dielsiana (Harms) P.K. Loc ex Z. Wei & Pedley, Callerya nitida var. hirsutissima (Z. Wei) X.Y. Zhu, and Callerya nitida (Bentham) R. Geesink, which belongs to the Leguminosae family, are important medicinal plants in China. The genus Callerya includes 26 species, 18 species are distributed in China, and the vine stems of some species are used as traditional medicinal herbs because they have important pharmacological activity. Due to the high similarity of appearance, it is difficult to identify them in the market by appearance alone. Therefore, circulating of Callerya-related materia medica on the market is confusing, sometimes even leading to drug safety problems. It is urgent to develop molecular methods for their identification. OBJECTIVE: To sequence and analyze the complete chloroplast (cp) genomes of C. reticulata, C. dielsiana, C. nitida var. hirsutissima, and C. nitida and to analyze their cp genome differences as a basis for seeking easier DNA barcoding for their identification. METHOD: After using Illumina high-throughput sequencing and nanopore sequencing to obtain the genome data, some bioinformatics software was used to assembly and analyze the molecular structure of cp genomes. RESULTS: The complete cp genomes of the four species were circular molecules, which ranged from 130 435 to 132 546 bp, and GC contents ranged from 33.89% to 34.89%. Each of them includes a large single-copy region, a small single-copy region, and without large inverted repeat regions. CONCLUSIONS: These results suggested that highly variable regions of the four cp genomes would provide useful plastid markers, which could be used as a potential genomic resource to resolve phylogenetic questions and provide a reference for mining specific DNA barcodes of these species. HIGHLIGHTS: Our study provided highly effective molecular markers for subsequent phylogenetic analysis, species identification, and biogeographic analysis of Callerya.

Low-Dose Gallic Acid Administration Does Not Improve Diet-Induced Metabolic Disorders and Atherosclerosis in Apoe Knockout Mice.

Diets rich in polyphenols are known to be beneficial for cardiovascular health. Gallic acid (GA) is a plant-derived triphenolic chemical with multiple cardio-protective properties, such as antiobesity, anti-inflammation, and antioxidation. However, whether GA could protect against atherosclerotic cardiovascular diseases is still not defined. Here, we investigated the effects of low-dose GA administration on diet-induced metabolic disorders and atherosclerosis in the atherosclerosis-prone apolipoprotein E (Apoe) knockout mice fed on a high-fat Western-type diet (WTD) for 8 weeks. Our data showed that GA administration by oral gavage at a daily dosage of 20 mg/kg body weight did not significantly ameliorate WTD-induced hyperlipidemia, hepatosteatosis, adipogenesis, or insulin resistance; furthermore, GA administration did not significantly ameliorate WTD-induced atherosclerosis. In conclusion, our data demonstrate that low-dose GA administration does not elicit significant health effect on diet-induced metabolic disorders or atherosclerosis in the Apoe knockout mice. Whether GA could be beneficial for atherosclerotic cardiovascular diseases therefore needs further exploration.

Treating High COD Dyeing Wastewater via a Regenerative Sorption-Oxidation Process Using a Nano-Pored Activated Carbon.

Nowadays, the structural complexity of dyes used in the textile industry and the widely adopted water-saving strategy in the dyeing processes often fail plants' biological wastewater treatment units due to chemical oxygen demand (COD) overload. To alleviate this problems, this study investigated a regenerable adsorption-oxidation process to treat dyeing wastewater with COD around 10,000 mg/dm3 using a highly nano-pored activated carbon (AC) as a COD adsorbent, followed by its regeneration using hydrogen peroxide as an oxidizing reagent. In addition to studying AC's COD adsorption and oxidation performance, its operational treatment conditions in terms of temperature and pH were assessed. The results firstly demonstrated that about 50-60% of the COD was consistently adsorbed during the repeated adsorption operation before reaching AC's maximum adsorption capacity (qmax) of 0.165 g-COD/g-AC. The optimal pH and temperature during adsorption were 4.7 and 25 °C, respectively. Secondly, AC regeneration was accomplished by using an initial peroxide concentration of 2.5% (by wt %) and EDTA-Fe of 2.12 mmole/dm3. The reuse of the regenerated ACs was doable. Surprisingly, after the first AC regeneration, the COD adsorption capacity of the regenerated AC even increased by ~7% with respect to the virgin AC. Thirdly, the results of a five-consecutive adsorption-regeneration operation showed that a total of 0.3625 g COD was removed by the 5 g AC used, which was equivalent to an adsorption capacity (q) of 0.0725 (= 0.3625/5) g-COD/g-AC during each adsorption stage. Based on the obtained results, a regenerable COD adsorption-oxidation process using a nano-pored AC to treat the high-textile-COD wastewater looks promising. Thus, a conceptual treatment unit was proposed, and its potential benefits and limitations were addressed.

Anthracycline-Induced Atrial Structural and Electrical Remodeling Characterizes Early Cardiotoxicity and Contributes to Atrial Conductive Instability and Dysfunction.

Aims: Cancer patients treated with anthracyclines are susceptible to atrial fibrillation (AF), while the mechanisms remain unclear. Due to sudden and unpredictable features, prediction of anthracycline-induced AF at early phase is difficult. Clinically, we tested whether anthracycline-induced early atrial remodeling in patients could be detected by echocardiography. Experimentally, we investigated the mechanisms of doxorubicin-induced atrial remodeling and AF in mice, and the protective effects of dexrazoxane and antioxidants. Methods and Results: Postsurgery breast cancer patients with an anthracycline-containing or anthracycline exclusion regimen were recruited for echocardiography before chemotherapy, and 3 and 6 months after chemotherapy. Mice were injected with doxorubicin or vehicle (5 mg/kg/week, 4 weeks), and left atrial diameter, electrical transmission, and AF inducibility were measured. Meanwhile, the level of reactive oxygen species (ROS), activity of antioxidant enzymes, cardiomyocyte size, vacuolization, inflammation, and fibrosis were also measured in mouse atria. The therapeutic effects of dexrazoxane and antioxidants on doxorubicin-induced changes in the aforementioned parameters were also determined. While ventricular parameters and functions were unchanged in cancer patients receiving anthracyclines before and after chemotherapy, left atrial reservoir and conduit function were decreased at 3 months postchemotherapy versus prechemotherapy. Doxorubicin-induced susceptibility to AF occurred in mice before onset of ventricular dysfunction. Doxorubicin-induced AF was via inducing structural remodeling (cardiomyocyte death, hypotrophy, and vacuolization) and electrical remodeling (reduction and redistribution of connexin 43) in atria, which was effectively prevented by dexrazoxane or antioxidants through inhibiting ROS generation or enhancing ROS elimination. Innovation and Conclusion: AF inducibility was induced after doxorubicin injection, which can be inhibited by repressing the ROS level. Antioxid. Redox Signal. 37, 19-39. The Clinical Trial Registration number is PJ-KS-KY-2019-73.