A note on “Jacobi elliptic function solutions for the modified Korteweg–de Vries equation”

AbstractThe recently published paper “Jacobi elliptic function solutions for the modified Korteweg–de Vries equation” [J. King Saud Univ. Sci. 25 (2013) 271–274] is analyzed. We show that these Jacobi elliptic function solutions obtained by the authors do not satisfy the original modified Korteweg–de Vries equation

Protective effects of cysteine analogues on acute myocardial ischemia: novel modulators of endogenous H2S production

The current study was designed to evaluate the pharmacologic effects of three novel cysteine-containing compounds: S-propyl-l-cysteine (SPC), S-allyl-l-cysteine (SAC), and S-propargyl-l-cysteine (SPRC) on H(2)S production and antioxidant defenses in an acute myocardial infarction (MI) rat model. The enzymatic activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx), as well as glutathione redox status and malonaldehyde (MDA) content, also were determined. All three compounds were found to preserve SOD and GPx activities and also tissue GSH levels while reducing the formation of the lipid peroxidation product MDA in ventricular tissues. With immunfluorescence assays, we observed the expression of CSE and Mn-SOD. The morphologic changes of the cardiac cells are seen with both light and electron microscopy. The corresponding pathologic alterations were characterized mainly as loss of adherence between cardiac myocytes and swollen or ruptured mitochondria at the ultrastructural level. Propargylglycine, a selective inhibitor of CSE, abolished the protective effects of each compound used in the current model. Our study provides novel evidence that SPC, SAC, and SPRC have cardioprotective effects in MI by reducing the deleterious effects of oxidative stress by modulating the endogenous levels of H(2)S and preserving the activities of antioxidant defensive enzymes like SOD

Recent updates in click and computational chemistry for drug discovery and development

Drug discovery is a costly and time-consuming process with a very high failure rate. Recently, click chemistry and computer-aided drug design (CADD) represent popular areas for new drug development. Herein, we summarized the recent updates in click and computational chemistry for drug discovery and development including clicking to effectively synthesize druggable candidates, synthesis and modification of natural products, targeted delivery systems, and computer-aided drug discovery for target identification, seeking out and optimizing lead compounds, ADMET prediction as well as compounds synthesis, hopefully, inspires new ideas for novel drug development in the future

A Simplification for Exp-Function Method When the Balanced Nonlinear Term Is a Certain Product

The Exp-function method plays an important role in searching for analytic solutions of many nonlinear differential equations. In this paper, we prove that the balancing procedure in the method is unnecessary when the balanced nonlinear term is a product of the dependent variable under consideration and its derivatives. And in this case, the ansatz of the method can be simplified to be with less parameters so as to be easy to calculate

Comment on “New Exact Solutions to the KdV-Burgers-Kuramoto Equation with the Exp-Function Method”

We point out in this paper that the claims made by Kim et al. in the commented paper are incorrect and no new exact solution was obtained

S-propargyl-cysteine protects both adult rat hearts and neonatal cardiomyocytes from ischemia/hypoxia injury: the contribution of the hydrogen sulfide-mediated pathway

In this study, we determined the cardioprotective effects of S-propargyl-cysteine (SPRC), a structural analog of S-allylcysteine (SAC), using in vivo models of acute myocardial infarction (MI) and in vitro hypoxic cardiomyocytes models. MI was created in rats by ligating the left anterior descending coronary artery. Plasma enzymes levels and cystathionine-γ-lyase (CSE) activities were determined. Primary cultures of newborn rats' cardiomyocytes were injured by hypoxia for 6 h. Cell viabilities were measured with the thiazolyl blue assay. RT-PCR and western blot analysis revealed the expression of CSE in both models. The protective effects of SPRC were associated with an observed reduction in infarct size (20.8 ± 2.4% vs. 36.0 ± 1.3%), decreased plasma enzymes levels and reduced malondialdehyde levels when compared to the MI vehicle group (P < 0.05); cardiac function was also improved. SPRC increased CSE activity and plasma H2S concentration by 1.6-fold and 1.3-fold, respectively, in MI rats. Decreased cell viability (64.5 ± 5.4%) in hypoxic cardiomyocytes could be rescued with use of SPRC (81.0 ± 3.1%). Similarly, mRNA and protein expression of CSE were upregulated in the SPRC group. Treatment with the CSE inhibitor propargylglycine abolished the protective effects of SPRC. Our study provides novel evidence that SPRC is protective in myocardial infarctions via a H2S-related pathway

Co-effects of m6A and chromatin accessibility dynamics in the regulation of cardiomyocyte differentiation

Abstract Background Cardiomyocyte growth and differentiation rely on precise gene expression regulation, with epigenetic modifications emerging as key players in this intricate process. Among these modifications, N6-methyladenosine (m6A) stands out as one of the most prevalent modifications on mRNA, exerting influence over mRNA metabolism and gene expression. However, the specific function of m6A in cardiomyocyte differentiation remains poorly understood. Results We investigated the relationship between m6A modification and cardiomyocyte differentiation by conducting a comprehensive profiling of m6A dynamics during the transition from pluripotent stem cells to cardiomyocytes. Our findings reveal that while the overall m6A modification level remains relatively stable, the m6A levels of individual genes undergo significant changes throughout cardiomyocyte differentiation. We discovered the correlation between alterations in chromatin accessibility and the binding capabilities of m6A writers, erasers, and readers. The changes in chromatin accessibility influence the recruitment and activity of m6A regulatory proteins, thereby impacting the levels of m6A modification on specific mRNA transcripts. Conclusion Our data demonstrate that the coordinated dynamics of m6A modification and chromatin accessibility are prominent during the cardiomyocyte differentiation

Learning to Attack Real-World Models for Person Re-identification via Virtual-Guided Meta-Learning

Recent advances in person re-identification (re-ID) have led to impressive retrieval accuracy. However, existing re-ID models are challenged by the adversarial examples crafted by adding quasi-imperceptible perturbations. Moreover, re-ID systems face the domain shift issue that training and testing domains are not consistent. In this study, we argue that learning powerful attackers with high universality that works well on unseen domains is an important step in promoting the robustness of re-ID systems. Therefore, we introduce a novel universal attack algorithm called ``MetaAttack'' for person re-ID. MetaAttack can mislead re-ID models on unseen domains by a universal adversarial perturbation. Specifically, to capture common patterns across different domains, we propose a meta-learning scheme to seek the universal perturbation via the gradient interaction between meta-train and meta-test formed by two datasets. We also take advantage of a virtual dataset (PersonX), instead of real ones, to conduct meta-test. This scheme not only enables us to learn with more comprehensive variation factors but also mitigates the negative effects caused by biased factors of real datasets. Experiments on three large-scale re-ID datasets demonstrate the effectiveness of our method in attacking re-ID models on unseen domains. Our final visualization results reveal some new properties of existing re-ID systems, which can guide us in designing a more robust re-ID model. Code and supplemental material are available at \url{https://github.com/FlyingRoastDuck/MetaAttack_AAAI21}

PDGF-BB is involved in HIF-1α/CXCR4/CXCR7 axis promoting capillarization of hepatic sinusoidal endothelial cells

Background: The activation of HIF-1α/CXCR4 pathway in liver sinusoidal endothelial cells (LSECs) could downregulate CXCR7, leading to the capillarization of LSECs to promote hepatic fibrosis. However, the mechanism between CXCR4 and CXCR7 is still undefined. The aim is to investigate the role of PDGF-BB in the dedifferentiation of LSECs and hepatic stellate cells (HSCs) activation. Methods: The activation of HIF-1α/CXCR4 pathway in two kinds of liver fibrosis models were observed. The effects of HIF-1α, CXCR4, PDGF-BB on the dedifferentiation of LSECs were investigated by using the inhibitors of HIF-1α, CXCR4 or PDGFR-β separately or transfecting with a CXCR4 knockdown lentiviral vector. In addition, the relationship between LSECs and HSCs was demonstrated by co-culture of LSECs and HSCs using the transwell chamber. Results: CXCR4 upregulation and CXCR7 downregulation were accompanied by LSECs capillarization and HSCs activation both in CCl4-induced and BDL-induced fibrotic liver. In vitro, downregulation of HIF-1α significantly descreased CXCR4 and CD31 expression, and enhanced the expressions of CXCR7, CD44 and LYVE1. Downregulation of CXCR4 in LSECs significantly downregulated PDGF-BB, PDGFR-β and CD31, and enhanced CXCR7, CD44 and LYVE1 expression, while the expression of HIF-1α did not change significantly. STI571, a PDGF receptor inhibitor, could significantly downregulate PDGFR-β and increase the expression of CXCR7 to inhibit the dedifferentiation of LSECs. In addition, alleviateion the dedifferentiation of LSECs could decrease the expression of PDGFR-β of HSCs, then inhibiting the activation of HSCs. Conclusions: This study revealed that HIF-1α/CXCR4/PDGF-BB/CXCR7 axis promoted the dedifferentiation of LSECs, consequently triggering HSCs activation and liver fibrosis