Quercetin Ameliorates Myocardial Injury in Diabetic Rats by Regulating Autophagy and Apoptosis through AMPK/mTOR Signaling Pathway.

A high-glucose environment is involved in the progression of diabetes mellitus (DM). This study aims to explore the regulatory effects of quercetin (QUE) on autophagy and apoptosis after myocardial injury in rats with DM. The type 2 DM rat models were constructed using low-dose streptozotocin (STZ) treatment combined with a high-carbohydrate (HC) diet in vivo. Compared with the control group, the body weight was decreased, whereas blood pressure, blood glucose, and the LVW/BW ratio were increased in the diabetic group. The results showed that the myocardial fibers were disordered in the diabetic group. Moreover, we found that the myocardial collagen fibers, PAS-positive cells, and apoptosis were increased, whereas the mitochondrial structure was destroyed and autophagic vacuoles were significantly reduced in the diabetic group compared with the control group. The expression levels of autophagy-related proteins LC3 and Beclin1 were decreased, whereas the expression levels of P62, Caspae-3, and Bax/Bcl-2 were increased in the diabetic group in vitro and in vivo. Moreover, QUE treatment alleviated the cellular oxidative stress reaction under high-glucose environments. The results of immunoprecipitation (IP) showed that the autophagy protein Beclin1 was bound to Bcl-2, and the binding capacity increased in the HG group, whereas it decreased after QUE treatment, suggesting that QUE inhibited the binding capacity between Beclin1 and Bcl-2, thus leading to the preservation of Beclin1-induced autophagy. In addition, the blood pressure, blood glucose, and cardiac function of rats were improved following QUE treatment. In conclusion, QUE suppressed diabetic myocardial injury and ameliorated cardiac function by regulating myocardial autophagy and inhibition of apoptosis in diabetes through the AMPK/mTOR signaling pathway.

Evidence-based systematic review of removal of peripheral arterial catheter in critically ill adult patients.

OBJECTIVE: To evaluate and summarize literature pertaining to evidence of peripheral arterial catheterization in adults, and to provide a reference for clinical practice. METHODS: We undertook a systematic review of literature on the removal of peripheral arterial manometric catheters in adult patients from various sources such as UpToDate, BMJ, National Institute for Health and Care Excellence (NICE), Medlive, Cochrane Library, Joanna Briggs Institute (JBI) Evidence-based Health Care Center Database, CINAHL, PubMed, Wanfang Data, VIP, and other databases. The retrieval time was set as from the establishment of the database till August 30, 2021. We screened the studies that fulfilled the inclusion criteria, evaluated their quality, and retrieved and summarized such articles. RESULTS: The review included 8 articles: 1 clinical decision, 3 guidelines, 2 evidence summaries, 1 systematic review, and 1 expert consensus. In all, 17 pieces of strong evidence were collected and extracted based on the following 5 dimensions: assessment of removal timing, preparation before removal, removal procedure, compression time, and key points after removal. CONCLUSIONS: The removal of a peripheral arterial manometry catheter requires careful consideration by medical professionals. In order to increase the removal standardization rate and decrease the incidence of clinical complications, standardized procedures and training need to be developed.

"Floating Catalytic Foam" with prominent heat-induced convection for the effective photocatalytic removal of antibiotics.

Immobilized photocatalysts represent a promising candidate for the wastewater treatments due to their good reusability, high stability and low eco-risk. Mass transfer within the immobilized catalytic bed is a crucial process that determines the contacting, adsorption, and degradation kinetics in the photodegradation. In this study, a floating catalytic foam (FCF) with a prominent pumping effect was designed to promote mass transfer. The polyurethane foam immobilized with rGO/TiO2/ultrathin-g-C3N4 photocatalyst (PRTCN) was prepared by a simple dip-coating and Uv-light aging process. It was found that the hydrophilic-hydrophobic interfaces could not only contribute to the floating of the catalyst but also establish a temperature gradient across the floating immobilized catalyst. In addition, the temperature gradient induced convection could serve as a built-in pump to effectively promote the diffusion and adsorption of target antibiotic molecules during the photocatalytic process. Therefore, the PRTCN demonstrated a high photodegradation and mineralization efficiency with excellent reusability and anti-interference capability. Moreover, the photodegradation mechanism and the intermediates' toxicity of norfloxacin were detailly investigated by ultra-high resolution electrospray time-of-flight mass spectrometry, density functional theory simulation and ECOSAR estimation. This work proposed a facile and sustainable strategy to enhance the mass transfer problem on immobilized photocatalysts, which could promote the application of the immobilized photocatalysts in the real water-treatment scenarios.

Remaining Useful Life Prediction of Rolling Bearings Based on Multi-scale Permutation Entropy and ISSA-LSTM.

The performance of bearings plays a pivotal role in determining the dependability and security of rotating machinery. In intricate systems demanding exceptional reliability and safety, the ability to accurately forecast fault occurrences during operation holds profound significance. Such predictions serve as invaluable guides for crafting well-considered reliability strategies and executing maintenance practices aimed at enhancing reliability. In the real operational life of bearings, fault information often gets submerged within the noise. Furthermore, employing Long Short-Term Memory (LSTM) neural networks for time series prediction necessitates the configuration of appropriate parameters. Manual parameter selection is often a time-consuming process and demands substantial prior knowledge. In order to ensure the reliability of bearing operation, this article investigates the application of three advanced techniques-Maximum Correlation Kurtosis Deconvolution (MCKD), Multi-Scale Permutation Entropy (MPE), and Long Short-Term Memory (LSTM) recurrent neural networks-for the prediction of the remaining useful life (RUL) of rolling bearings. The improved sparrow search algorithm (ISSA) is employed for configuring parameters in the Long Short-Term Memory (LSTM) network. Each technique's principles, methodologies, and applications are comprehensively reviewed, offering insights into their respective strengths and limitations. Case studies and experimental evaluations are presented to assess their performance in RUL prediction. Findings reveal that MCKD enhances fault signatures, MPE captures complexity, and LSTM excels in modeling temporal patterns. The root mean square error of the prediction results is 0.007. The fusion of these techniques offers a comprehensive approach to RUL prediction, leveraging their unique attributes for more accurate and reliable predictions.

An improved method for the synthesis and formation mechanism of M2B10H14 based on the reactions of B10H14 with MNH2BH3 (M = Na, K).

An efficient method for the synthesis of M2B10H14 (M = Na and K) has been developed. The two possible formation mechanisms of the B10H142- anion are proposed, in which the NH2BH3- anion acts as a proton abstractor and a hydride donor. Furthermore, the B10H13- and B10H15- intermediates were detected.

STING promotes ferroptosis through NCOA4-dependent ferritinophagy in acute kidney injury.

Ferroptosis in tubules has been implicated in the pathogenesis of acute kidney injury (AKI), whereas the regulatory mechanism remains unclear. The stimulator of interferon genes (STING) is previously recognized as a critical mediator of innate immunity via a DNA-sensing pathway and has been increasingly linked to lipid peroxidation, a hallmark of ferroptosis. Herein we investigated the role and the underlying mechanism of STING in AKI models established by ischemia/reperfusion (IR) in C57BL mice. The expression level of STING was predominantly increased in tubules of kidney after IR treatment. Besides, STING deficiency markedly alleviated IR-induced lipid peroxidation, tissue damage and renal dysfunction. Consistently, in vitro experiments demonstrated that the increase in ferroptotic cell death, lipid ROS production and the decrease in GSH peroxidase 4 (GPX4) expression in renal tubular cells subjected to ferroptosis agonist or hypoxia/reoxygenation intervention were all mitigated by genetic deficiency or pharmacological inhibition of STING, while all exacerbated by STING overexpression. Further, these detrimental effects of STING overexpression relied on the induction of ferritinophagy, i.e. autophagic degradation of ferritin, leading to iron overload. Mechanistically, STING mediated the initiation of ferritinophagy through interacting with nuclear receptor coactivator 4 (NCOA4), a fundamental receptor for the transfer of ferritin into lysosome. Collectively, STING contributes to ferroptosis during ischemic AKI through facilitating NCOA4-mediated ferritinophagy and shows the potential as a promising therapeutic choice for AKI.

Green Production of Biomass-Derived Carbon Materials for High-Performance Lithium-Sulfur Batteries.

Lithium-sulfur batteries (LSBs) with a high energy density have been regarded as a promising energy storage device to harness unstable but clean energy from wind, tide, solar cells, and so on. However, LSBs still suffer from the disadvantages of the notorious shuttle effect of polysulfides and low sulfur utilization, which greatly hider their final commercialization. Biomasses represent green, abundant and renewable resources for the production of carbon materials to address the aforementioned issues by taking advantages of their intrinsic hierarchical porous structures and heteroatom-doping sites, which could attribute to the strong physical and chemical adsorptions as well as excellent catalytic performances of LSBs. Therefore, many efforts have been devoted to improving the performances of biomass-derived carbons from the aspects of exploring new biomass resources, optimizing the pyrolysis method, developing effective modification strategies, or achieving further understanding about their working principles in LSBs. This review firstly introduces the structures and working principles of LSBs and then summarizes recent developments in research on carbon materials employed in LSBs. Particularly, this review focuses on recent progresses in the design, preparation and application of biomass-derived carbons as host or interlayer materials in LSBs. Moreover, outlooks on the future research of LSBs based on biomass-derived carbons are discussed.

Impacts of the zero mark-up policy on hospitalization expenses of T2DM and cholecystolithiasis inpatients in SC province, western China: an interrupted time series analysis.

Background: Since 2009, a series of ambitious health system reforms have been launched in China, including the zero mark-up drug policy (ZMDP); the policy was intended to reduce substantial medicine expenses for patients by abolishing the 15% mark-up on drugs. This study aims to evaluate the impacts of ZMDP on medical expenditures from the perspective of disease burden disparities in western China. Method: Two typical diseases including Type 2 diabetes mellitus (T2DM) in internal medicine and cholecystolithiasis (CS) in surgery were selected from medical records in a large tertiary level-A hospital in SC Province. The monthly average medical expenses of patients from May 2015 to August 2018 were extracted to construct an interrupted time series (ITS) model to evaluate the impact of policy implementation on the economic burden. Results: A total of 5,764 cases were enrolled in our study. The medicine expenses for T2DM patients maintained a negative trend both before and after the intervention of ZMDP. It had declined by 74.3 CNY (P < 0.001) per month on average in the pre-policy period and subsequently dropped to 704.4 CNY (P = 0.028) immediately after the policy. The level change of hospitalization expenses was insignificant (P = 0.197), with a reduction of 677.7 CNY after the policy, while the post-policy long-term trend was significantly increased by 97.7 CNY (P = 0.035) per month contrasted with the pre-policy period. In addition, the anesthesia expenses of T2DM patients had a significant increase in the level under the impact of the policy. In comparison, the medicine expenses of CS patients significantly decreased by 1,014.2 CNY (P < 0.001) after the policy, while the total hospitalization expenses had no significant change in level and slope under the influence of ZMDP. Furthermore, the expenses of surgery and anesthesia for CS patients significantly increased by 320.9 CNY and 331.4 CNY immediately after the policy intervention. Conclusion: Our study indicated that the ZMDP has been an effective intervention to reduce the excessive medicine expenses for both researched medical and surgical diseases, but failed to show any long-term advantage. Moreover, the policy has no significant impact on relieving the overall hospitalization burden for either condition.

Codon usage bias of Venezuelan equine encephalitis virus and its host adaption.

Venezuelan equine encephalitis virus (VEEV) is an emerging zoonotic virus in the alphavirus genus. It can be transmitted to humans due to spillover from equid-mosquito cycles. The symptoms caused by VEEV include fever, headache, myalgia, nausea, and vomiting. It can also cause encephalitis in severe cases. The evolutionary features of VEEV are largely unknown. In this study, we comprehensively analyzed the codon usage pattern of VEEV by computing a variety of indicators, such as effective number of codons (ENc), codon adaptation index (CAI), relative synonymous codon usage (RSCU), on 130 VEEV coding sequences retrieved from GenBank. The results showed that the codon usage bias of VEEV is relatively low. ENc-GC3s plot, neutrality plot, and CAI-ENc correlation analyses supported that translational selection plays an important role in shaping the codon usage pattern of VEEV whereas the mutation pressure has a minor influence. Analysis of RSCU values showed that most of the preferred codons in VEEV are C/G-ended. Analysis of dinucleotide composition found that all CG- and UA-containing codons are not preferentially used. Phylogenetic analysis showed that VEEV isolates can be clustered into three genera and evolutionary force affects the codon usage pattern. Furthermore, a correspondence analysis (COA) showed that aromaticity and hydrophobicity as well as geographical distribution also have certain effects on the codon usage variation of VEEV, suggesting the possible involvement of translational selection. Overall, the codon usage of VEEV is comparatively slight and translational selection might be the main factor that shapes the codon usage pattern of VEEV. This study will promote our understanding about the evolution of VEEV and its host adaption, and might provide some clues for preventing the cross-species transmission of VEEV.

ALDH2 attenuates ischemia and reperfusion injury through regulation of mitochondrial fusion and fission by PI3K/AKT/mTOR pathway in diabetic cardiomyopathy.

The function of mitochondrial fusion and fission is one of the important factors causing ischemia-reperfusion (I/R) injury in diabetic myocardium. Aldehyde dehydrogenase 2 (ALDH2) is abundantly expressed in heart, which involved in the regulation of cellular energy metabolism and stress response. However, the mechanism of ALDH2 regulating mitochondrial fusion and fission in diabetic myocardial I/R injury has not been elucidated. In the present study, we found that the expression of ALDH2 was downregulated in rat diabetic myocardial I/R model. Functionally, the activation of ALDH2 resulted in the improvement of cardiac hemodynamic parameters and myocardial injury, which were abolished by the treatment of Daidzin, a specific inhibitor of ALDH2. In H9C2 cardiomyocyte hypoxia-reoxygenation model, ALDH2 regulated the dynamic balance of mitochondrial fusion and fission and maintained mitochondrial morphology stability. Meanwhile, ALDH2 reduced mitochondrial ROS levels, and apoptotic protein expression in cardiomyocytes, which was associated with the upregulation of phosphorylation (p-PI3KTyr458, p-AKTSer473, p-mTOR). Moreover, ALDH2 suppressed the mitoPTP opening through reducing 4-HNE. Therefore, our results demonstrated that ALDH2 alleviated the ischemia and reperfusion injury in diabetic cardiomyopathy through inhibition of mitoPTP opening and activation of PI3K/AKT/mTOR pathway.

Mass balance, metabolic disposition, and pharmacokinetics of a novel selective inhibitor of PI3Kδ [14C] SHC014748M in healthy Chinese subjects following oral administration.

PURPOSE: SHC014748M is a potent, novel selective PI3Kδ isoform inhibitor and is proposed for the treatment of non-Hodgkin lymphoma and chronic lymphocytic leukemia/small lymphocytic lymphoma. This study investigated the pharmacokinetics, mass balance, metabolism and excretion of SHC014748M in Chinese male subjects following a single oral dose of 150 mg (100 µCi) [14C] SHC014748M. METHODS: Six healthy Chinese male subjects administrated an oral suspension of 150 mg (100 µCi) [14C] SHC014748M and the samples of blood, urine and feces were collected for measuring. Liquid chromatography-tandem mass spectrometry and liquid scintillation counter were utilized to obtain mass balance and the pharmacokinetic data. RESULTS: The median Tmax for [14C]-radioactivity was 1.6 ± 0.5 h after the oral administration of [14C] SHC014748M and the mean Cmax was 3863 ± 354 ng Eq./mL in plasma, while the mean Cmax, t1/2 values and AUC0-∞ values for total radioactivity in whole blood were 2466 ± 518 ng Eq./mL, 32.2 ± 30.5 h and 66,236 ± 44,232 h * ng Eq./mL, respectively. Fecal excretion was proposed as the predominant elimination route, accounting for a mean of 90.68 ± 11.38% of the administered dose, whereas the mean urine excretion was 6.00 ± 1.48% within 336 h post-dose. The proposed major metabolic pathway of [14C] SHC014748M in the human body were as follows: (I) monooxidation, (II) glucuronide acid conjugation, and (III) monoxide-hydrogenation. CONCLUSIONS: SHC014748M was absorbed, metabolized and excreted with unchanged SHC014748M as its main circulating component in plasma following oral administration. In addition, it was speculated that fecal excretion was the principal excretion pathway; meanwhile, monohydroxy, glucuronide conjugation, oxygen, and hydrogenation were the major clearance pathways of SHC014748M through urine and/or feces. TRIAL REGISTRATION: The trial registration number: CTR20202505.

Research progress on microRNA in gout.

Gout is a common form of arthritis caused by the deposition of sodium urate crystals in the joints and tissues around them. MicroRNAs (miRNAs) are noncoding RNAs that have been shown to be involved in regulating the pathogenesis of gout through multiple cellular signaling pathways, which may be potential targets for the treatment of gout. In this review, we systematically discuss the regulatory roles of related miRNAs in gout, which will provide help for the treatment of gout and miRNAs is expected to become a potential biomarker for gout diagnosis.

When liquid-liquid phase separation meets viral infections.

Eukaryotic cells have both membranous and membraneless organelles. While the formation mechanism of membranous organelles is well understood, the formation mechanism of membraneless organelles remains unknown. Many biomolecules in the cytoplasm transition from the liquid phase to the agglutinated phase are known as liquid-liquid phase separation (LLPS). The biomolecular agglomerates' physical properties enable them to function as dynamic compartments that respond to external pressures and stimuli. Scientists have gradually recognized the importance of phase separation during viral infections. LLPS provides a powerful new framework for understanding the viral life cycle from viral replication to evasion of host immune surveillance. As a result, this review focuses on the progress of LLPS research in viral infection and immune regulation to provide clues for antiviral therapeutic strategies.

Mechanisms of Quercetin against atrial fibrillation explored by network pharmacology combined with molecular docking and experimental validation.

Atrial fibrillation (AF) is a common atrial arrhythmia for which there is no specific therapeutic drug. Quercetin (Que) has been used to treat cardiovascular diseases such as arrhythmias. In this study, we explored the mechanism of action of Que in AF using network pharmacology and molecular docking. The chemical structure of Que was obtained from Pubchem. TCMSP, Swiss Target Prediction, Drugbank, STITCH, Pharmmapper, CTD, GeneCards, DISGENET and TTD were used to obtain drug component targets and AF-related genes, and extract AF and normal tissue by GEO database differentially expressed genes by GEO database. The top targets were IL6, VEGFA, JUN, MMP9 and EGFR, and Que for AF treatment might involve the role of AGE-RAGE signaling pathway in diabetic complications, MAPK signaling pathway and IL-17 signaling pathway. Molecular docking showed that Que binds strongly to key targets and is differentially expressed in AF. In vivo results showed that Que significantly reduced the duration of AF fibrillation and improved atrial remodeling, reduced p-MAPK protein expression, and inhibited the progression of AF. Combining network pharmacology and molecular docking approaches with in vivo studies advance our understanding of the intensive mechanisms of Quercetin, and provide the targeted basis for clinical Atrial fibrillation treatment.

Positive correlations between plasma BPI level and MPO-DNA and S100A8/A9 in myocardial infarction.

Bactericidal/permeability-increasing protein (BPI) exhibits a number of important characteristics. RNA-seq analysis revealed that the BPI expression was increased in platelets of (non)ST-elevated myocardial infarction (NSTEMI/STEMI) patients. Activated platelets can induce NETosis which may be accompanied by the release of myeloperoxidase-DNA (MPO-DNA) and S100A8/A9. This study investigated the plasma BPI levels in myocardial infarction patients and its correlation with MPO-DNA and S100A8/A9. This prospective study recruited 80 control individuals, as well as 63 NSTEMI and 59 STEMI patients who were admitted to the First Affiliated Hospital of Bengbu Medical College for coronary angiography (CAG) and/or percutaneous coronary intervention (PCI) between May 1, 2020 and August 31, 2020. Demographic and clinical characteristics, clinical indicators, hs-CRP, IL-1ß, MPO-DNA (a circulated marker of NETs), circulating levels of S100A8/A9 and BPI were measured from each individual. The severity of coronary lesions was evaluated by the Gensini score, based on the results of the CAG. Pearson's or spearman's correlation was used to examine the correlation between BPI and the above-mentioned parameters, as well as the severity of coronary artery disease. Linear regression analysis was applied to identify the independent predictive factors of BPI. Received operating characteristic (ROC) curve analysis was used to evaluate the diagnostic efficacy of plasma BPI for MI. The plasma BPI levels increased by 8.76 times in the STEMI group and 5.38 times in the NSTEMI group compared to the control group. The plasma level of hs-CRP and IL-1ß in both STEMI and NSTEMI groups were also significantly higher than the control group. In addition, the plasma levels of MPO-DNA and S100A8/A9 in the STEMI and NSTEMI groups were significantly higher than the control group. Plasma levels of BPI were positively correlated with IL-1ß, hs-CRP, MPO-DNA and S100A8/A9. The correlation between BPI and the severity of coronary artery disease was also significant. The optimal cutoff value of plasma BPI was 35.1705 ng/ml for MI patients from the ROC curve analysis. Plasma BPI levels are increased in myocardial infarction patients and positively correlated with MPO-DNA and S100A8/A9. Plasma BPI level may serve as a potential biomarker of myocardial infarction.

A Modified Simple Method for Induction of Myocardial Infarction in Mice.

Myocardial infarction (MI) represents one of the leading causes of death. MI models are widely used for investigating the pathomechanisms of post-MI remodeling and evaluation of novel therapeutics. Different methods (e.g., isoproterenol treatment, cryoinjury, coronary artery ligation, etc.) have been used to induce MI. Compared with isoproterenol treatment and cryoinjury, coronary artery ligation may better reflect the ischemic response and chronic remodeling after MI. However, traditional methods for coronary ligation in mice are technically challenging and require commercially available apparatus. The current study describes a simple and efficient process for induction of MI in mice with readily available materials. The mouse chest skin was cut open under stable anesthesia with a simplified anesthesia device made of centrifuge tubes. The heart was immediately externalized through the intercostal space after blunt separation of the pectoralis major and pectoralis minor. The left anterior descending branch (LAD) was ligated with a 6-0 suture 3 mm from its origin. Following LAD ligation, staining with 2,3,5-Triphenyltetrazolium chloride (TTC) indicated successful induction of MI and temporal changes of post-MI scar size. Meanwhile, survival analysis results showed overt mortality within 7 days after MI, mainly due to cardiac rupture. Moreover, post-MI echocardiographic assessment demonstrated successful induction of contractile dysfunction and ventricular remodeling. Once mastered, an MI model can be established in mice within 2-3 min with readily available materials.

Changes of Necroptosis in Irbesartan Medicated Cardioprotection in Diabetic Rats.

BACKGROUND: Diabetic cardiomyopathy (DCM) is strongly linked to microvascular disease, renin-angiotensin system (RAS) activation, cardiac inflammation and cell apoptosis. Irbesartan is an angiotensin II (Ang II) receptor antagonist in RAS system, which inhibited the conversion of Ang I into Ang II, while the specific mechanism is still obscure. OBJECTIVE: This study aims to investigate the expressions necroptosis RIP1-RIP3-MLKL pathway in myocardium of diabetic rats, and the protective action of irbesartan on myocardial damage. MATERIALS AND METHODS: In our study, 30 Sprague-Dawley rats were divided into 5 groups: CON4W, high glucose and high caloric (HC4W), diabetes mellitus 4 weeks (DM4W group), diabetes mellitus 8 weeks (DM8W group), and irbesartan diabetes 8 weeks (Ir DM8W group). RESULTS: We discovered that as diabetes progresses, the rats gradually lost weight, the HW/BW ratio were increased gradually, and the cardiac function became worse accompanied with the aggravation of inflammatory injury. Meanwhile, the myocardial fibers and cells were disordered, and the expression of positive substances, RIP1 and RIP3 increased significantly. The mRNA and protein levels of myocardial RIP1, RIP3 and MLKL were all increased with the progression of DM. After the intervention of irbesartan in diabetic rats, the cardiac function was improved, whereas inflammatory injury and HW/BW ratio were decreased. Also, the myocardial fibrosis injury was attenuated, and the PAS positive substances, RIP1 and RIP3 were significantly decreased. The curative effect of irbesartan was related to decreased myocardial RIP1, RIP3 and MLKL mRNA and protein levels. CONCLUSION: In conclusion, irbesartan has a cardioprotective effect on the diabetic rats, and its mechanism may be connected with inhibition of RIP1-RIP3-MLKL pathway.

Pharmacokinetic and pharmacodynamic evaluation of the new prolonged-release leuprorelin acetate microspheres for injection compared with Enantone® in healthy Chinese male volunteers.

PURPOSE: To compare the pharmacokinetics, pharmacodynamics and safety of the new prolonged-release leuprorelin acetate microspheres for injection (3.75 mg) with the reference product Enantone® (3.75 mg). METHOD: 48 healthy male volunteers were enrolled and randomly received a single 3.75 mg dose of the test drug or Enantone®. RESULTS: There were no significant differences in Cmax, AUC0-t and AUC0-48 between the test group and reference group (P > 0.05). The 90% confidence intervals of the two groups were 87.49%~112.74%, 97.15%~154.25%, and 80.85%~109.01%, respectively. Twenty-eight days after administration, both groups reached 100.0% castration level; there was no difference in the time from administration to reaching castration level between the two groups (P > 0.05); However, the difference between the two groups in the duration of castration level was statistically significant (P < 0.05). There were no major or serious adverse events, and the severity was mild to moderate. CONCLUSION: The pharmacokinetic characteristics of leuprorelin in two groups were consistent. The two groups exhibited similar inhibitory effects on testosterone and more subjects in the test group maintained a longer castration time than those in the reference group.

Corrigendum to "ALDH2 Overexpression Alleviates High Glucose-Induced Cardiotoxicity by Inhibiting NLRP3 Inflammasome Activation".

[This corrects the article DOI: 10.1155/2019/4857921.].