Inhibitory effect of resveratrol on swimming motility and adhesion ability against Salmonella enterica serovar Typhimurium infection.

Salmonella enterica serovar Typhimurium (S. typhimurium) is a common Gram-negative foodborne pathogen that threatens public health and hinders the development of livestock industry. Resveratrol, an important component in grape fruits and seeds, has been shown to possess multiple biological activities, but its potential effects on S. typhimurium-mediated virulence have been rarely reported. In this study, we investigated the effect of resveratrol on S. typhimurium flagella -mediated virulence. The results showed that resveratrol significantly reduced the transcription of flagella genes and swimming motility of S. typhimurium, and also inhibited the transcription of T3SS-related virulence genes with varying degrees inhibiting bacterial growth. Simultaneously, resveratrol significantly reduced the adhesion of S. typhimurium to HeLa cells. Unfortunately, resveratrol does not improve the survival rate of S. typhimurium-infected mice, but it reduces the bacterial load in the liver and spleen of infected mice, and it also has a certain degree of anti-inflammatory activity. In summary, these results indicated that resveratrol has the potential to be developed as an alternative drug or antibacterial agent to prevent Salmonella infection.

Opponent Hitting Behavior Prediction and Ball Location Control for a Table Tennis Robot.

The hitting position and velocity control for table tennis robots have been investigated widely in the literature. However, most of the studies conducted do not consider the opponent's hitting behaviors, which may reduce hitting accuracy. This paper proposes a new table tennis robot framework that returns the ball based on the opponent's hitting behaviors. Specifically, we classify the opponent's hitting behaviors into four categories: forehand attacking, forehand rubbing, backhand attacking, and backhand rubbing. A tailor-made mechanical structure that consists of a robot arm and a two-dimensional slide rail is developed such that the robot can reach large workspaces. Additionally, a visual module is incorporated to enable the robot to capture opponent motion sequences. Based on the opponent's hitting behaviors and the predicted ball trajectory, smooth and stable control of the robot's hitting motion can be obtained by applying quintic polynomial trajectory planning. Moreover, a motion control strategy is devised for the robot to return the ball to the desired location. Extensive experimental results are presented to demonstrate the effectiveness of the proposed strategy.

Current and future potential distribution of the invasive scale Ceroplastes rusci (L., 1758) (Hemiptera: Coccidae) under climate niche.

BACKGROUND: The fig wax scale, Ceroplastes rusci is an invasive pest that feeds on more than 94 genera from 52 families that is spread across 60 countries, causing negative impacts to agriculture and forestry. Understanding the potential distribution of invasive species under climate change is crucial for the management and monitoring purposes. Thus, we predicted the potential distribution areas of C. rusci using Maximum Entropy (MaxEnt) based on the occurrence data and environmental variables under current and future climatic scenarios. RESULTS: Our results showed that the temperature annual range (Bio 7) and mean temperature of the warmest quarter (Bio 10) attributed to a higher contribution to the current model of the distribution of C. rusci. The potential distribution maps illustrated the main concentrated areas of C. rusci which included South America, Africa, Asia, and Oceania. In addition, potential range expansions or reductions were predicted under different future climate change scenarios, which showed that the total suitable areas of the fig wax scale presented an increasing trend until 2100. CONCLUSION: Our study provides significant data to understand the potential distribution of C. rusci around the world. It also serves as an early warning for the highly suitable habitat areas that even offers a platform to the currently non-infested regions or countries who are yet to develop monitoring strategies in response to the possible C. rusci outbreak. © 2022 Society of Chemical Industry.

First complete mitochondrial genome of the tribe Coccini (Hemiptera, Coccomorpha, Coccidae) and its phylogenetic implications.

Soft scale insects (Hemiptera, Coccidae) are important pests of various agricultural and horticultural crops and ornamental plants. They have negative impacts on agriculture and forestry. The tribe Coccini represents one of the most ancient evolutionary lineages of soft scale insects. However, no complete Coccini mitochondrial genome (mitogenome) is available in public databases. Here, we described the complete mitogenome of Coccushesperidum L., 1758. The 15,566 bp mitogenome of C.hesperidum had a high A+T content (83.4%) and contained a typical set of 37 genes, with 13 protein-coding genes (PCGs), 22 transfer RNA genes (tRNAs) and two ribosomal RNA genes (rRNAs). Only seven tRNAs had the typical clover-leaf secondary structure and the remaining tRNAs lacked the DHU arm, TψC arm or both. Moreover, a comparative analysis of all reported scale insect mitogenomes from GenBank database was performed. The mitogenomes of scale insects showed high similarities in base composition and A+T content. Additionally, our phylogenetic analysis confirmed the monophyly of Coccomorpha and revealed that the archaeococcoids were the most basal lineage within Coccomorpha, while Ericeruspela and Didesmococcuskoreanus, belonging to Coccidae, were often mixed with Aclerdidae, making Coccidae a paraphyletic group. These findings expand the mitogenome database of scale insects and provide new insights on mitogenome evolution for future studies across different insect groups.

Case report: Varicella-zoster virus infection triggering progressive encephalomyelitis with rigidity and myoclonus.

Progressive encephalomyelitis with rigidity and myoclonus (PERM) is a rare neurological disease of unknown etiology, and most patients with PERM are positive for anti-glycine receptor (GlyR) antibody. In this case study, we report a clinical case of a varicella-zoster virus-infected patient who developed anti-GlyR antibody-positive PERM. He initially suffered from herpes zoster and gradually developed symptoms of impaired brainstem functions including hoarse voice and dysphagia, accompanied by paroxysmal sympathetic hyperactivity. The patient also suffered from severe spasms, which were easily triggered by external stimuli. Glycine receptor antibodies were then found to be positive in serum and cerebrospinal fluid, and the diagnosis of PERM was confirmed. Methylprednisolone and gamma globulin treatments were given, and spasms were improved after treatment. Unfortunately, the patient's family insisted on automatic discharge and the patient passed away several days later.

The multifaceted role of ferroptosis in kidney diseases.

Ferroptosis, a form of cell death caused by the excessive accumulation of iron-dependent lipid peroxides. Studies over the last decade have identified multiple pathways that affect the sensitivity of cells to ferroptosis. Renal diseases, the tenth leading cause of death in the world, has been affecting the life of people for a long time. Numerous studies have shown that ferroptosis is inextricably linked to damage to kidney cells. Here, we review the pathophysiological features of the kidney, the basic pathways of ferroptosis, and the mechanisms of ferroptosis-induced kidney injury. It is proposed a promising outlook for the treatment of renal diseases by influencing ferroptosis.

JAML promotes acute kidney injury mainly through a macrophage-dependent mechanism.

Although macrophages are undoubtedly attractive therapeutic targets for acute kidney injury (AKI) because of their critical roles in renal inflammation and repair, the underlying mechanisms of macrophage phenotype switching and efferocytosis in the regulation of inflammatory responses during AKI are still largely unclear. The present study elucidated the role of junctional adhesion molecule-like protein (JAML) in the pathogenesis of AKI. We found that JAML was significantly upregulated in kidneys from 2 different murine AKI models including renal ischemia/reperfusion injury (IRI) and cisplatin-induced AKI. By generation of bone marrow chimeric mice, macrophage-specific and tubular cell-specific Jaml conditional knockout mice, we demonstrated JAML promoted AKI mainly via a macrophage-dependent mechanism and found that JAML-mediated macrophage phenotype polarization and efferocytosis is one of the critical signal transduction pathways linking inflammatory responses to AKI. Mechanistically, the effects of JAML on the regulation of macrophages were, at least in part, associated with a macrophage-inducible C-type lectin-dependent mechanism. Collectively, our studies explore for the first time to our knowledge new biological functions of JAML in macrophages and conclude that JAML is an important mediator and biomarker of AKI. Pharmacological targeting of JAML-mediated signaling pathways at multiple levels may provide a novel therapeutic strategy for patients with AKI.

Patulin Induces Acute Kidney Injury in Mice through Autophagy-Ferroptosis Pathway.

Patulin (PAT) is a common mycotoxin, widely found in cereals, seafood, nuts, and especially in fruits and their products. Exposure to this mycotoxin has been reported to induce kidney injury. However, the possible mechanism remains unclear. In our study, short-term high-dose intake of PAT caused acute kidney injury (AKI) in mice. We performed high-throughput transcriptional sequencing to identify differentially expressed genes (DEGs) between the treatment and control groups. The ferroptosis signaling pathway had the highest enrichment, suggesting ferroptosis is involved in PAT-induced AKI. Further, the existence of ferroptosis and autophagy was confirmed by observing the changes of mitochondria morphology and the formation of autophagosomes by electron microscopy. And the expression of solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), p62, nuclear receptor coactivator 4 (NCOA4), and ferritin heavy chain 1 (FTH1) were downregulated, whereas acyl-CoA synthase long-chain family member 4 (ACSL4), transferrin (TF), LC3, and ferritin light chain (FTL) expression were upregulated in PAT-exposed mice. These results suggested autophagy-dependent ferroptosis occurred in the animal model. This view has also been confirmed in the human renal tubular epithelial cell (HKC) experiments. Autophagy inhibitor 3-methyladenine (3MA) attenuated PAT-induced ferroptosis and the iron contents in HKC cells. Simultaneous autophagy-dependent ferroptosis can be inhibited by ferroptosis inhibitors ferrostatin-1 (Fer-1) and desferrioxamine (DFO). In general, this study provides a new perspective for exploring the new mechanism of acute kidney injury caused by PAT.

Inhibitory effect of hederagenin on Streptococcus pneumoniae pneumolysin in vitro.

Streptococcus pneumoniae is an important pathogen that causes otitis media, pneumonia, meningitis and bacteremia. As an important virulence factors of S. pneumoniae, pneumolysin (PLY) can penetrate cell membranes and lead to cell lysis and inflammation, which is one of the main causes of infection and damage of S. pneumoniae. Therefore, using pneumolysin as a target to study its inhibitors can provide a new treatment strategy for pneumococcal disease. This study analyzed the inhibitory effect of the natural compound hederagenin on PLY in vitro. The results show that hederagenin has great potential as a new strategy for the treatment of pneumococcal diseases.

The Updates of Podocyte Lipid Metabolism in Proteinuric Kidney Disease.

BACKGROUND: Podocytes, functionally specialized and terminally differentiated glomerular visceral epithelial cells, are critical for maintaining the structure and function of the glomerular filtration barrier. Podocyte injury is considered as the most important early event contributing to proteinuric kidney diseases such as obesity-related renal disease, diabetic kidney disease, focal segmental glomerulosclerosis, membranous nephropathy, and minimal change disease. Although considerable advances have been made in the understanding of mechanisms that trigger podocyte injury, cell-specific and effective treatments are not clinically available. SUMMARY: Emerging evidence has indicated that the disorder of podocyte lipid metabolism is closely associated with various proteinuric kidney diseases. Excessive lipid accumulation in podocytes leads to cellular dysfunction which is defined as lipotoxicity, a phenomenon characterized by mitochondrial oxidative stress, actin cytoskeleton remodeling, insulin resistance, and inflammatory response that can eventually result in podocyte hypertrophy, detachment, and death. In this review, we summarize recent advances in the understanding of lipids in podocyte biological function and the regulatory mechanisms leading to podocyte lipid accumulation in proteinuric kidney disease. KEY MESSAGES: Targeting podocyte lipid metabolism may represent a novel therapeutic strategy for patients with proteinuric kidney disease.

Molecular Mechanism of Palmitic Acid on Myocardial Contractility in Hypertensive Rats and Its Relationship with Neural Nitric Oxide Synthase Protein in Cardiomyocytes.

OBJECTIVE: It is aimed at investigating the mechanism of palmitic acid (PA) on myocardial contractility in hypertensive rats and its relationship with myocardial neural nitric oxide synthase (nNOS) protein. METHODS: The rats were randomly divided into sham operation group and hypertensive group, with thirty rats in each group, to prepare angiotensin II-induced hypertensive model rats. The blood pressure of rats was measured by the multianimal multichannel tail cuff noninvasive blood pressure system of Kent Coda, USA. The Ionoptix single-cell contraction detection system was used to detect myocardial cells. ATP level of left ventricular cardiomyocytes was determined by luminescence method, and protein was measured by Western blot. RESULTS: Compared with the sham group, systolic blood pressure and diastolic blood pressure were increased in the hypertensive group over 4 weeks; PA increased the contractility of left ventricular cardiomyocytes in normal rats, but not in hypertensive rats, and PA increased the intracellular ATP level of rats in the sham group but not in the hypertension group. In the hypertension group, the expression of nNOS in the cardiomyocytes was significantly increased, and specific nNOS inhibitor S-methyl-L-thiocitrulline (SMTC) was found to restore the positive inotropic effect of PA in the myocardium of the hypertension group. PA was supplemented after using CPT-1 inhibitor etomoxir (ETO); it was found that ETO inhibited the positive inotropic effect of PA on left ventricular cardiomyocytes in the sham group, and PA was supplemented after using SMTC and ETO, it was found that SMTC + ETO could inhibit the positive inotropic effect of PA on left ventricular cardiomyocytes in myocardium of hypertensive rats. CONCLUSION: PA could increase the contractility of healthy cardiomyocytes, but had no obvious positive effect on the cardiomyocytes of hypertensive rats, PA enhanced the contractility of cardiomyocytes by increasing ATP level in them, and the inhibitory effect of PA on myocardial contractility in hypertensive rats may be related to the increased nNOS and CPT-1 in cardiomyocytes.

Complete chloroplast genome features and phylogenetic analysis of Eruca sativa (Brassicaceae).

Eruca sativa Mill. (Brassicaceae) is an important edible vegetable and a potential medicinal plant due to the antibacterial activity of its seed oil. Here, the complete chloroplast (cp) genome of E. sativa was de novo assembled with a combination of long PacBio reads and short Illumina reads. The E. sativa cp genome had a quadripartite structure that was 153,522 bp in size, consisting of one large single-copy region of 83,320 bp and one small single-copy region of 17,786 bp which were separated by two inverted repeat (IRa and IRb) regions of 26,208 bp. This complete cp genome harbored 113 unique genes: 79 protein-coding genes, 30 tRNA genes, and four rRNA genes. Forty-nine long repetitive sequences and 69 simple sequence repeats were identified in the E. sativa cp genome. A codon usage analysis of the E. sativa cp genome showed a bias toward codons ending in A/T. The E. sativa cp genome was similar in size, gene composition, and linearity of the structural region when compared with other Brassicaceae cp genomes. Moreover, the analysis of the synonymous (Ks) and non-synonymous (Ka) substitution rates demonstrated that protein-coding genes generally underwent purifying selection pressure, expect ycf1, ycf2, and rps12. A phylogenetic analysis determined that E. sativa is evolutionarily close to important Brassica species, indicating that it may be possible to transfer favorable E. sativa alleles into other Brassica species. Our results will be helpful to advance genetic improvement and breeding of E. sativa, and will provide valuable information for utilizing E. sativa as an important resource to improve other Brassica species.

Patulin induces pyroptosis through the autophagic-inflammasomal pathway in liver.

Patulin (PAT), a kind of mycotoxin, is produced by many common fungi in fruit and vegetable-based products. It has been shown to cause hepatotoxicity. However, the possible mechanisms are not completely elucidated. The present study aimed to characterize the role of autophagic-inflammasomal pathway on pyroptosis induced by PAT. In mouse livers, PAT induced pyroptosis, and increased inflammation through the activation of NLRP3 inflammasome. In liver cells, we noticed that PAT induced pyroptotic cell death, which was confirmed by the activation of GSDMD, caspase-1, the release of LDH, and the result of PI/Hoechst assay. In addition, PAT-induced pyroptosis was dependent upon the activation of NLRP3 inflammasome and the release of cathepsin B. Cells had less expression of caspase-1 and IL-1ß protein levels after treated by NLRP3 inhibitor MCC950 or cathepsin B inhibitor CA-074Me. The expression of GSDMD and IL-1ß protein levels were also decrease after treated by caspase-1 inhibitor Ac-YVAD-cmk. Moreover, autophagy inhibitor 3-methyladenine (3-MA) attenuated PAT-induced increase in cytoplasmic cathepsin B expression, and subsequent LDH release, the activation of NLRP3 inflamosomes, pyroptotic cell death, and inflammation. These findings suggested that PAT-induced pyroptosis maybe through autophagy-cathepsin B-inflammasomal pathway in the liver. These results provide new mechanistic insights into PAT-induced hepatotoxicity.

Elevation of JAML Promotes Diabetic Kidney Disease by Modulating Podocyte Lipid Metabolism.

Lipid accumulation in podocytes is a major determinant of diabetic kidney disease (DKD) and identification of potential therapeutic targets by mediating podocyte lipid metabolism has clinical importance. This study was to elucidate the role of JAML (junctional adhesion molecule-like protein) in the pathogenesis of DKD. We first confirmed the expression of JAML in podocytes and found that podocyte-specific deletion of Jaml ameliorated podocyte injury and proteinuria in two different models of diabetic mice. We further demonstrated a novel role of JAML in regulating podocyte lipid metabolism through SIRT1-mediated SREBP1 signaling. Similar results were also found in mice with adriamycin-induced nephropathy. Importantly, we observed a higher expression of JAML in glomeruli from subjects with DKD and other types of proteinuric kidney diseases, and the level of JAML was correlated with lipid accumulation and glomerular filtration rate, suggesting that JAML may be an attractive therapeutic target for proteinuric kidney disease.

Prevalence and association of medication nonadherence with major adverse cardiovascular events in patients with myocardial infarction.

Current study was to evaluate the prevalence of guideline recommended medications adherence in myocardial infarction (MI) patients postpercutaneous coronary intervention (PCI) and the association of medication nonadherence and major adverse cardiovascular events (MACEs).MI patients who underwent PCI in the last 12 months were enrolled. Demographic and clinical characteristics were collected and guideline recommended medications were evaluated. Patients were divided into with and without MACEs groups.Compared to patients without MACEs, those with MACEs were older (54.8 ±â€Š16.4 vs 51.1 ±â€Š15.2 years), more likely to be smoker (40.2% vs 31.9%), have higher body mass index (BMI; 25.0 ±â€Š6.1 vs 23.8 ±â€Š5.7 kg/m), diabetes (47.5% vs 37.8%), ischemic stroke (34.4% vs 25.6%), and estimated lower glomerular filtration rate (85.4 ±â€Š9.6 vs 92.6 ±â€Š10.7 mL/minute/1.73 m). Patients with MACEs were also more likely to present with ST-elevation MI (STEMI; 54.1% vs 48.4%) and to undergo urgent PCI (62.3% vs 56.3%). Furthermore, patients with MACEs were less likely to adhere to dual antiplatelet therapy (77.9% vs 85.9%), renin-angiotensin system inhibitor (62.3% vs 69.7%), and beta-blocker (69.7% vs 72.8%) treatment. In unadjusted model, medication nonadherence was associated with 2-fold higher odds of MACEs. After adjustment for demographics, risk factors, comorbidities, and peri-PCI characteristics, medications nonadherence remained independently associated with MACEs, with odds ratio of 1.40 (95% confidence interval: 1.29-1.87).Medications adherence rate among MI patients post-PCI is suboptimal in China, which is independently associated with MACEs.

Baicalin Protects against Thrombin-Induced Cell Injury in Human Umbilical Vein Endothelial Cells.

Thrombin plays a pivotal role in the pathogenesis of atherosclerosis. Baicalin, an active flavonoid compound, was shown to attenuate the development of atherosclerosis, but the mechanism remains elusive. In the present study, the role and mechanism of baicalin in thrombin-induced cell injury was investigated in human umbilical vein endothelial cells (HUVECs). Our results showed that baicalin significantly reduced thrombin-induced apoptosis of HUVECs. Additional experiments showed that baicalin inhibited thrombin-induced NF-κB activation and PAR-1 expression. In addition, baicalin decreased thrombin-induced PAR-1 expression by inhibiting ERK pathway. These results indicated that baicalin has protective effects on thrombin-induced cell injury in HUVECs possibly through inhibition of PAR-1 expression and its downstream NF-κB activation, which was mediated by ERK1/2 activation.

Silencing of junctional adhesion molecule-like protein attenuates atherogenesis and enhances plaque stability in ApoE-/- mice.

Background: Although junctional adhesion molecule-like protein (JAML) has recently been implicated in leukocyte recruitment during inflammation and wound repair, its role in atherosclerosis remains to be elucidated. Methods and results: First, we showed that JAML was strongly expressed in atherosclerotic plaques of cardiovascular patients. Similar results were obtained with atherosclerotic plaques of ApoE-/- mice. Co-immunofluorescence staining showed that JAML was mainly expressed in macrophages. Enhanced expression of JAML in cultured macrophages was observed following exposure of the cells to oxLDL. The functional role of JAML in atherosclerosis and macrophages function was assessed by interference of JAML with shRNA in vivo and siRNA in vitro Silencing of JAML in mice significantly attenuated atherosclerotic lesion formation, reduced necrotic core area, increased plaque fibrous cap thickness, decreased macrophages content and inflammation. In addition, histological staining showed that JAML deficiency promoted plaques to stable phenotype. In vitro, JAML siRNA treatment lowered the expression of inflammatory cytokines in macrophages treated with oxLDL. The mechanism by which JAML mediated the inflammatory responses may be related to the ERK/NF-κB activation. Conclusions: Our results demonstrated that therapeutic drugs which antagonize the function of JAML may be a potentially effective approach to attenuate atherogenesis and enhance plaque stability.

Tetramethylpyrazine analogue CXC195 protects against cerebral ischemia/reperfusion-induced apoptosis through PI3K/Akt/GSK3ß pathway in rats.

CXC195 showed strongest protective effects among the ligustrazine derivatives in cells and prevented apoptosis induced by H2O2 injury. We recently demonstrated that CXC195 protected against cerebral ischemia/reperfusion (I/R) injury by its antioxidant activity. However, whether the anti-apoptotic action of CXC195 is involved in cerebral I/R injury is unknown. Here, we investigated the role of CXC195 in apoptotic processes induced by cerebral I/R and the possible signaling pathways. Male Wistar rats were submitted to transient middle cerebral artery occlusion for 2h, followed by 24h reperfusion. CXC195 was injected intraperitoneally at 2h and 12h after the onset of ischemia. The number of apoptotic cells was measured by TUNEL assay, apoptosis-related protein cleaved caspase-3, Bcl-2, Bax and the phosphorylation levels of Akt and GSK3ß in ischemic penumbra were assayed by western blot. The results showed that administration of CXC195 at the doses of 3mg/kg and 10mg/kg significantly inhibited the apoptosis by decreasing the number of apoptotic cells, decreasing the level of cleaved caspase-3 and Bax, and increasing the level of Bcl-2 in rats subjected to I/R injury. Simultaneously, CXC195 treatment markedly increased the phosphorylation of Akt and GSK3ß. Blockade of PI3K activity by wortmannin, dramatically abolished its anti-apoptotic effect and lowered both Akt and GSK3ß phosphorylation levels. Our study firstly demonstrated that CXC195 protected against cerebral I/R injury by reducing apoptosis in vivo and PI3K/Akt/GSK3ß pathway involved in the anti-apoptotic effect.

HtrA1 downregulation induces cisplatin resistance in lung adenocarcinoma by promoting cancer stem cell-like properties.

Cisplatin (CDDP) resistance usually develops during lung adenocarcinoma (LAC) therapy. However, the comprehensive mechanisms remain largely unclear. In this study, we first established a CDDP-resistant LAC cell line-A549/CDDP from its parental cell line-A549. The results showed that CDDP resistance in A549/CDDP cells correlates with acquirement of cancer stem cell-like properties (increased percentage of CD133-expressing subpopulation, sphere formation and levels of some pluripotency-associated markers). HtrA1 expression at both mRNA and protein levels was reduced in CDDP-resistant A549/CDDP cells compared with that in A549 cells. Ectopic expression of HtrA1 in A549/CDDP cells reversed cancer stem cell-like properties and CDDP resistance. In A549 cells, stable knockdown of HtrA1 expression promoted cancer stem cell-like properties and CDDP insensitivity, however, these effects were blocked by inhibition of PI3K/Akt pathway using LY294002. Furthermore, HtrA1 knockdown could significantly stimulate PI3K/Akt signaling in A549 cells. In vivo studies, HtrA1 knockdown promoted tumorigenesis and conferred CDDP resistance in xenograft A549 tumors, which were reversed by intraperitoneal injection of LY294002. In conclusion, these results indicate that HtrA1 downregulation confers CDDP resistance by inducing cancer stem cell-like properties via PI3K/Akt-dependent pathway in A549 cells. Therefore, HtrA1 may be a potential target for overcoming CDDP resistance in LAC.