Size-segregated characteristics of water-soluble oxidative potential in urban Xiamen: Potential driving factors and implications for human health.

Oxidative potential (OP), defined as the ability of particulate matter (PM) to generate reactive oxygen species (ROS), has been considered as a potential health-related metric for PM. Particles with different sizes have different OP and deposition efficiencies in the respiratory tract and pose different health risks. In this study, size-segregated PM samples were collected at a coastal urban site in Xiamen, a port city in southeastern China, between August 2020 and September 2021. The water-soluble constituents, including inorganic ions, elements and organic carbon, were determined. Total volume-normalized OP based on the dithiothreitol assay was highest in spring (0.241 ± 0.033 nmol min-1 m-3) and lowest in summer (0.073 ± 0.006 nmol min-1 m-3). OP had a biomodal distribution with peaks at 0.25-0.44 µm and 1.0-1.4 µm in spring, summer, and winter and a unimodal pattern with peak at 0.25-0.44 µm in fall, which were different from the patterns of redox-active species. Variations in the seasonality of fine and coarse mode OP and their correlations with water-soluble constituents showed that the size distribution patterns of OP could be attributed to the combined effects of the size distributions of transition metals and redox-active organics and the interactions between them which varied with emissions, meteorological conditions and atmospheric processes. Respiratory tract deposition model indicated that the deposited OP and the toxic elements accounted for 47.9 % and 36.8 % of their measured concentrations, respectively. The highest OP doses and the excess lifetime carcinogenic risk (ELCR) were found in the head airway (>70 %). However, the size distributions of OP deposition and ELCR in the respiratory tract were different, with 63.9 % and 49.4 % of deposited ELCR and OP, respectively, coming from PM2.5. Therefore, attention must be paid to coarse particles from non-exhaust emissions and road dust resuspension.

Therapeutic Potential of Kaempferol against Sleep Deprivation-Induced Cognitive Impairment: Modulation of Neuroinflammation and Synaptic Plasticity Disruption in Mice.

Sleep deprivation (SD) has led to a rise in cognitive impairment (CI) cases. Kaempferol (KMP), known for its anti-inflammatory and antiapoptotic properties, holds promise in countering SD-induced CI. Experimental validation using a sleep-deprived CI model confirmed KMP's efficacy in mitigating CI. Immunofluorescence investigations emphasized diminished activation of astrocytes and reduced the proliferation of microglia in the hippocampus of mice subjected to SD. Subsequently, network pharmacological analyses were conducted and found that KMP may be closely related to the mitogen-activated protein kinase (MAPK) pathway in SD-induced CI. The influence of KMP on the MAPK pathway was verified by the observed decrease in the expression of phosphorylated JNK (p-JNK) and p38 (p-p38). Analyzing hippocampal AMPARS and NMDARS expression indicated KMP's ability to enhance GluA1 phosphorylation (Ser831 and Ser845) and GluN2A levels. Patch clamp assays demonstrated heightened excitatory transmitter transmission in the hippocampus, suggesting KMP's positive influence. Overall, KMP combats neuroinflammation via MAPK inhibition, augments synaptic function, and addresses learning and memory dysfunction in sleep-deprived mice.

Visible-Light-Mediated Annulation/Thiolation of 2-Isocyanobiaryls with Disulfides to Organoylthiophenanthridines Derivatives.

A visible-light-induced annulation/thiolation of 2-isocyanobiaryls with dialkyl(aryl)disulfides has been established, delivering a sustainable and atom-economic route to 6-organoylthiophenanthridines with wild functional group tolerance and good to excellent yields under oxidant-, base-, and transition-metal-free conditions.

The dualistic model of passion and the service quality of five-star hotel employees during the COVID-19 pandemic.

Given the generally stressful job demands of the hospitality industry during the COVID-19 pandemic, understanding the work passion and emotions of hotel employees is particularly important. Based on the conservation of resources theory and the job demands-resources model, this study develops a multiple mediation model to investigate how frontline hotel employees with different types of work passion choose emotional labor strategies under the effects of the COVID-19 pandemic and the impact of different choices on their service quality. A two-stage survey using data from 206 frontline employees of five-star hotels in China explored how work passion influences emotional labor and thereby affects emotional expression as well as service quality. The results showed emotional labor partially mediates the relationship between work passion and emotional expression, which in turn mediates the relationship between emotional labor and service quality during the COVID-19 pandemic. The theoretical and practical implications of this study are discussed.

Regulated cell death pathways in cardiomyopathy.

Heart disease is a worldwide health menace. Both intractable primary and secondary cardiomyopathies contribute to malignant cardiac dysfunction and mortality. One of the key cellular processes associated with cardiomyopathy is cardiomyocyte death. Cardiomyocytes are terminally differentiated cells with very limited regenerative capacity. Various insults can lead to irreversible damage of cardiomyocytes, contributing to progression of cardiac dysfunction. Accumulating evidence indicates that majority of cardiomyocyte death is executed by regulating molecular pathways, including apoptosis, ferroptosis, autophagy, pyroptosis, and necroptosis. Importantly, these forms of regulated cell death (RCD) are cardinal features in the pathogenesis of various cardiomyopathies, including dilated cardiomyopathy, diabetic cardiomyopathy, sepsis-induced cardiomyopathy, and drug-induced cardiomyopathy. The relevance between abnormity of RCD with adverse outcome of cardiomyopathy has been unequivocally evident. Therefore, there is an urgent need to uncover the molecular and cellular mechanisms for RCD in order to better understand the pathogenesis of cardiomyopathies. In this review, we summarize the latest progress from studies on RCD pathways in cardiomyocytes in context of the pathogenesis of cardiomyopathies, with particular emphasis on apoptosis, necroptosis, ferroptosis, autophagy, and pyroptosis. We also elaborate the crosstalk among various forms of RCD in pathologically stressed myocardium and the prospects of therapeutic applications targeted to various cell death pathways.

Crosstalk between PML and p53 in response to TGF-ß1: A new mechanism of cardiac fibroblast activation.

Cardiac fibrosis is a common pathological cardiac remodeling in a variety of heart diseases, characterized by the activation of cardiac fibroblasts. Our previous study uncovered that promyelocytic leukemia protein (PML)-associated SUMO processes is a new regulator of cardiac hypertrophy and heart failure. The present study aimed to explore the role of PML in cardiac fibroblasts activation. Here we found that PML is significantly upregulated in cardiac fibrotic tissue and activated cardiac fibroblasts treated with transforming growth factor-ß1 (TGF-ß1). Gain- and loss-of-function experiments showed that PML impacted cardiac fibroblasts activation after TGF-ß1 treatment. Further study demonstrated that p53 acts as the transcriptional regulator of PML, and participated in TGF-ß1 induced the increase of PML expression and PML nuclear bodies (PML-NBs) formation. Knockdown or pharmacological inhibition of p53 produced inhibitory effects on the activation of cardiac fibroblasts. We further found that PML also may stabilize p53 through inhibiting its ubiquitin-mediated proteasomal degradation in cardiac fibroblasts. Collectively, this study suggests that PML crosstalk with p53 regulates cardiac fibroblasts activation, which provides a novel therapeutic strategy for cardiac fibrosis.

Diagnostic value of multiple b-value diffusion-weighted imaging in discriminating the malignant from benign breast lesions.

OBJECTIVE: The conventional breast Diffusion-weighted imaging (DWI) was subtly influenced by microcirculation owing to the insufficient selection of the b values. However, the multiparameter derived from multiple b-value exhibits more reliable image quality and maximize the diagnostic accuracy. We aim to evaluate the diagnostic performance of stand-alone parameter or in combination with multiparameter derived from multiple b-value DWI in differentiating malignant from benign breast lesions. METHODS: A total of forty-one patients diagnosed with benign breast tumor and thirty-eight patients with malignant breast tumor underwent DWI using thirteen b values and other MRI functional sequence at 3.0 T magnetic resonance. Data were accepted mono-exponential, bi-exponential, stretched-exponential, aquaporins (AQP) model analysis. A receiver operating characteristic curve (ROC) was used to evaluate the diagnostic performance of quantitative parameter or multiparametric combination. The Youden index, sensitivity and specificity were used to assess the optimal diagnostic model. T-test, logistic regression analysis, and Z-test were used. P value < 0.05 was considered statistically significant. RESULT: The ADCavg, ADCmax, f, and α value of the malignant group were lower than the benign group, while the ADCfast value was higher instead. The ADCmin, ADCslow, DDC and ADCAQP showed no statistical significance. The combination (ADCavg-ADCfast) yielded the largest area under curve (AUC = 0.807) with sensitivity (68.42%), specificity (87.8%) and highest Youden index, indicating that multiparametric combination (ADCavg-ADCfast) was validated to be a useful model in differentiating the benign from breast malignant lesion. CONCLUSION: The current study based on the multiple b-value diffusion model demonstrated quantitatively multiparametric combination (ADCavg-ADCfast) exhibited the optimal diagnostic efficacy to differentiate malignant from benign breast lesions, suggesting that multiparameter would be a promising non-invasiveness to diagnose breast lesions.

The associations of particulate matter short-term exposure and serum lipids are modified by vitamin D status: A panel study of young healthy adults.

Particulate matter (PM) exposure is associated to the adverse change in blood lipids. Vitamin D is beneficial to lipid metabolism, but whether vitamin D levels modifies the impact of air pollutants on lipids is unclear. The purpose of the study was to investigate if vitamin D modifies the associations of PM and serum lipids in young healthy people. From December 2017 to January 2018, a panel study with five once weekly follow-ups was conducted on 88 healthy adults aged 21.09 (1.08) (mean (SD)) years on average in Guangzhou, China. We measured serum lipids, serum 25-hydroxyvitamin D (25(OH)D) concentrations (440 blood samples in total), mass concentrations of particulate matter with diameters ≤2.5 µm (PM2.5), ≤1.0 µm (PM1.0), and ≤0.5 µm (PM0.5), and number concentrations of particulate matter with diameters ≤0.2 µm (PN0.2) and ≤0.1 µm (PN0.1) at each follow-up. Linear mixed-effect models were applied to assess the interaction of vitamin D and size-fractionated PM short-term exposure on four lipid metrics. We found the interactions between 25(OH)D and size-fractionated PM exposure on blood lipids in different lags (lag 3 days and 4 days). An interquartile range increase in PM2.5, PM1.0, PM0.5 were significantly associated with increments of 12.30%, 12.99%, and 13.66% in triglycerides (TGs) at lag 4 days at vitamin D levels <15 ng/mL group, respectively. Similar results were found for PN0.2, PN0.1 and low-density lipoprotein cholesterol (LDL-C). All the associations between size-fractionated PM and blood lipids were found null statistically significant in vitamin D levels ≥15 ng/mL group.

Circulating Irisin Level as a Biomarker for Pure Aortic Stenosis and Aortic Valve Calcification.

Irisin, a myokine mainly secreted by skeletal and cardiac muscles, is actively involved in cardiovascular diseases. However, whether irisin is associated with aortic stenosis remains unknown. Two hundred ninety-three severe AS patients who underwent transcatheter aortic valve implantation were enrolled and followed-up for 35 months on average. Enzyme-linked immunosorbent assay (ELISA) was applied to measure circulating irisin levels. Patients were divided into two groups based on the median plasma irisin level. We found that high plasma irisin levels were independently associated with pure aortic stenosis (PAS) after adjusting for age, body mass index, history of peripheral vascular disease, and creatinine (OR = 3.015, 95% CI 1.775-5.119, P < 0.001). ROC curve analysis showed a significant predictive value of irisin for PAS (AUC = 0.647, 95% CI 0.583-0.711, P < 0.001). The severity of aortic valve calcification was negatively associated with plasma irisin levels (P < 0.05). In conclusion, irisin is an independent predictor for PAS and is negatively associated with the severity of aortic valve calcification.

Dietary l-carnitine regulates liver lipid metabolism via simultaneously activating fatty acid ß-oxidation and suppressing endoplasmic reticulum stress in large yellow croaker fed with high-fat diets.

Dietary l-carnitine (LC) is a nutritional factor that reduces liver lipid content. However, whether dietary LC can improve lipid metabolism via simultaneous activation of mitochondrial fatty acid (FA) ß-oxidation and suppression of endoplasmic reticulum (ER) stress is still unknown. Large yellow croaker were fed with a high-fat diet (HFD) supplemented with dietary LC at 0, 1·2 or 2·4 ‰ for 10 weeks. The results indicated that a HFD supplemented with LC reduced the liver total lipid and TAG content and improved serum lipid profiles. LC supplementation administered to this fish increased the liver antioxidant capacity by decreasing serum and liver malondialdehyde levels and enhancing the liver antioxidant capacity, which then relieved the liver damage. Dietary LC increased the ATP dynamic process and mitochondrial number, decreased mitochondrial DNA damage and enhanced the protein expression of mitochondrial ß-oxidation, biogenesis and mitophagy. Furthermore, dietary LC supplementation increased the expression of genes and proteins related to peroxisomal ß-oxidation and biogenesis. Interestingly, feeding fish with LC-enriched diets decreased the protein levels indicative of ER stress, such as glucose-regulated protein 78, p-eukaryotic translational initiation factor 2a and activating transcription factor 6. Dietary LC supplementation downregulated mRNA expression relative to FA synthesis, reduced liver lipid and relieved liver damage through regulating ß-oxidation and biogenesis of mitochondria and peroxisomes, as well as the ER stress pathway in fish fed with HFD. The present study provides the first evidence that dietary LC can improve lipid metabolism via simultaneously promoting FA ß-oxidation capability and suppressing the ER stress pathway in fish.

Associaton of Retinol Binding Protein 4 (RBP4) Levels With Hyperuricemia: A Cross-Sectional Study in a Chinese Population.

Background: There are few studies on predictive biomarkers for hyperuricemia, and the predictive value of these biomarkers tends to be poor. Additionally, no reports have described the predictive value of retinol binding protein 4 (RBP4) for hyperuricemia. Purpose: This study was performed to evaluate the value of RBP4 for predicting the risk of hyperuricemia in a general population, determine whether RBP4 could be used alone or in combination with other factors to predict the risk of hyperuricemia in the general population, and establish an optimum predictive model. Methods: We conducted a population-based cross-sectional survey in 2018, involving a questionnaire, physical examination, and laboratory testing. We enrolled 2303 individuals by stratified random sampling, and 2075 were included in the data analysis after applying the eligibility criteria. Results: Serum RBP4 level had a highly significant association with hyperuricemia (P<0.001). After adjusting for potential confounders, logistic regression indicated that the risk of hyperuricemia was highest in the highest RBP4 quartile (odds ratio: 7.9, 95% confidence interval [CI]: 4.18-14.84, compared to the lowest quartile). The area under the receiver operating characteristic (ROC) curve (AUC) for RBP4 was 0.749 (95% CI: 0.725-0.774, P<0.001), which was higher than that for all the other predictors assessed. The optimum model for predicting hyperuricemia in the general population consisted of RBP4, sex (male), body mass index, serum creatinine, high-sensitivity C-reactive protein, fasting blood glucose, insulin, and alcohol consumption. The AUC was 0.804 (95% CI: 0.782-0.826, P<0.001). Conclusions: RBP4 is strongly associated with hyperuricemia, and its predictive value was higher than that of traditional predictors.

Elevated N-terminal pro C-type natriuretic peptide is associated with mortality in patients undergoing transcatheter aortic valve replacement.

BACKGROUND: Unlike N-terminal pro-B-type natriuretic peptide (NT-proBNP), which have been extensively studied, little is known about the role of N-terminal pro-C-type natriuretic peptide (NT-proCNP) for predicting survival post transcatheter aortic valve replacement (TAVR). METHODS: A total of 309 patients were included in the analysis. Patients were grouped into quartiles (Q1-4) according to the baseline NT-proCNP value. Blood for NT-proCNP analysis was obtained prior to TAVR procedure. The primary endpoint was mortality after a median follow-up of 32 months. Multivariable Cox proportional hazards regression models analyzed prognostic factors. The predictive capability was compared between NT-proBNP and NT-proCNP using receiver operator curve (ROC) analysis. RESULTS: A total of 309 subjects with the mean age of 76.8 ± 6.3 years, among whom 58.6% were male, were included in the analysis. A total of 58 (18.8%) patients died during follow-up. Cox multivariable analyses indicated society of thoracic surgeons (STS)-score was a strong independent predictor for mortality (hazard ratio (HR) 1.08, 95% confidential interval (CI) 1.05-1.12, P < 0.001). Elevated NT-proCNP was associated with a higher risk of cardiovascular mortality (HR 1.02, 95% CI 1.00-1.03, P = 0.025) and All-cause mortality (HR 1.01, 95% CI 1.00-1.03, P = 0.027), whereas NT-proBNP showed a small effect size on mortality. ROC analysis indicated that NT-proCNP was superior to NT-proBNP for TAVR risk evaluation in patients with left ventricular ejection fraction (LVEF) < 50% [(Area under the curve (AUC)-values of 0.79 (0.69; 0.87) vs. 0.59 (0.48; 0.69), P = 0.0453]. CONCLUSIONS: NT-proCNP and STS-Score were the independent prognostic factors of mortality among TAVR patients. Furthermore, NT-proCNP was superior to NT-proBNP for TAVR risk evaluation in patients with LVEF < 50%. Trial registration NCT02803294, 16/06/2016.

A hybrid variable selection and modeling strategy for the determination of target compounds in different spectral datasets.

In this paper, a hybrid technique is proposed to establish quantitative models for the determination of target compounds in different spectral datasets. The proposed hybrid method is the hybridization of interval partial least squares (iPLS) method with gradient descent (GD) algorithm. Here, the novelty of the proposed method is that the iPLS method is applied to variable selection and the GD algorithm is employed to establish quantitative models based on the selected optimal variables. In the application of the hybrid iPLS-GD method, the factors, i.e., the number of the interval for the iPLS method and the learning rate, the number of iterations for the GD method, that affect the quantitative accuracy of the method are optimized and determined. Then three spectral datasets, including the near-infrared spectroscopy (NIR) dataset, nuclear magnetic resonance (1H NMR) dataset and excitation-emission matrix fluorescence (EEM) dataset, are used to test and verify the performance of the iPLS-GD method. We compare the hybrid iPLS-GD method with the PLS and iPLS methods from the aspects of modeling ability and predictive ability. The results demonstrated that the iPLS-GD method can be used as an effective and promising tool for the determination of target compounds in complex samples in practice.

Exploring the Potential Mechanism of Shennao Fuyuan Tang for Ischemic Stroke Based on Network Pharmacology and Molecular Docking.

METHODS: Screen the biologically active components and potential targets of SNFYT through Traditional Chinese Medicine Systems Pharmacology (TCMSP), Traditional Chinese Medicines Integrated Database (TCMID), and related literature. In addition, DrugBank, OMIM, DisGeNET, and the Therapeutic Target Database were searched to explore the therapeutic targets of IS. The cross-targets of SNFYT potential targets and IS treatment targets were taken as candidate gene targets, and GO and KEGG enrichment analyses were performed on the candidate targets. On this basis, the SNFYT-component-target network and protein-protein interaction (PPI) network were constructed using Cytoscape 3.7.2. Finally, AutoDock was used to verify the molecular docking of core components and core targets. RESULTS: We screened out 95 potentially active components and 143 candidate targets. SNFYT-component-target network, PPI network, and Cytoscape analysis identified four core active ingredients and 14 core targets. GO enrichment analyzed 2333 biological processes, 79 cell components, and 149 molecular functions. There are 170 KEGG-related signal pathways (P < 0.05), including the IL-17 signal pathway, TNF signal pathway, and HIF-1 signal pathway. The molecular docking results of the core components and the core targets showed good binding power. CONCLUSIONS: SNFYT may achieve the effect of treating ischemic stroke through its anti-inflammatory effect through a signal pathway with core targets as the core.

Soluble Klotho-integrin ß1/ERK1/2 pathway ameliorates myocardial fibrosis in diabetic cardiomyopathy.

Soluble Klotho (sKL) is closely related to insulin resistance, which is a major factor in the progression of diabetic cardiomyopathy (DCM). The purpose of this study was to investigate the role of sKL in the regulation of DCM and the mechanism involved. A mouse model of type 2 diabetes was induced by high-fat diet and streptozotocin injection. An insulin-resistant cardiac fibroblast model was established by high glucose and high insulin. KL gene overexpression was achieved in vivo and vitro through transfection with an adenovirus-harboring KL-cDNA. Gene overexpression was used to evaluate the role of sKL in the pathophysiologic characteristics of DCM. Insulin-resistant cardiac fibroblasts reduced sKL expression and collagen deposition. Diabetic mice constructed by streptozotocin exhibited severe insulin resistance, inflammation, fibrosis, left ventricular dysfunction, and sKL downregulation. The overexpression of sKL mitigated insulin resistance and metabolic disturbance; inflammation, fibrosis, and upregulated collagen I/III content ratio in diabetic state were significantly reduced. Our findings were accompanied by notable moderation of cardiac function. Further, blunted phosphorylation of Akt was restored with sKL gene overexpression, and activated phosphorylation of extracellular signal-regulated kinase 1/2 in DCM was reduced. Our results suggest that sKL protein overexpression exerts a defensive measure by ameliorating selective insulin resistance in mouse DCM, thus revealing its underlying mechanism for potential human DCM treatment.

Malignant peripheral nerve sheath tumor in an elderly patient with superficial spreading melanoma: A case report.

BACKGROUND: Malignant peripheral nerve sheath tumor (MPNST) is a type of spindle cell sarcoma originating from the peripheral nerve, which usually results in the corresponding nerve sign on magnetic resonance imaging (MRI). Patients with MPNST may also have neurofibromatosis type 1. CASE SUMMARY: A 78-year-old male was admitted to the hospital due to a tumor in his left knee. He had a previous history of superficial spreading melanoma on the left thigh. Color Doppler ultrasonography showed a hypoechoic mass in the subcutaneous soft tissues of the medial left knee with an abundant rich blood flow. Computed tomography scanning did not show obvious signs of bone destruction, but the skin adjacent to the tumor was slightly thickened. MRI examination revealed that the hypervascular lesion was well-circumscribed, lobulated, invaded the surrounding soft tissues and demonstrated heterogeneous enhancement but lacked an entering and exiting nerve sign. The MRI result indicated the invasiveness of the tumor. The patient underwent a left knee joint mass expanded resection and the first histopathological examination showed a MPNST with positive surgical margins. Therefore, the second extended resection was performed, and the patient had a good outcome in the short term. CONCLUSION: MRI is a useful technique for revealing the biological characteristics of MPNST and provides clinical support for evaluation of the surgical area before operation.

Mitochondrial Fatty Acid ß-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid ß-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. METHODS: Carnitine-depleted male Nile tilapia (initial weight: 4.29 ± 0.12 g; 3 mo old) were established by feeding them with mildronate diets (1000 mg/kg/d) for 6 wk. Zebrafish deficient in the carnitine palmitoyltransferase 1b gene (cpt1b) were produced by using CRISPR/Cas9 gene-editing technology, and their males (154 ± 3.52 mg; 3 mo old) were used for experiments. Normal Nile tilapia and wildtype zebrafish were used as controls. We assessed nutrient metabolism and energy homeostasis-related biochemical and molecular parameters, and performed 14C-labeled nutrient tracking and transcriptomic analyses. RESULTS: The mitochondrial FAO decreased by 33.1-88.9% (liver) and 55.6-68.8% (muscle) in carnitine-depleted Nile tilapia and cpt1b-deficient zebrafish compared with their controls (P < 0.05). Notably, glucose oxidation and muscle protein deposition increased by 20.5-24.4% and 6.40-8.54%, respectively, in the 2 fish models compared with their corresponding controls (P < 0.05). Accordingly, the adenosine 5'-monophosphate-activated protein kinase/protein kinase B-mechanistic target of rapamycin (AMPK/AKT-mTOR) signaling was significantly activated in the 2 fish models with inhibited mitochondrial FAO (P < 0.05). CONCLUSIONS: These data show that inhibited mitochondrial FAO in fish induces energy homeostasis remodeling and enhances glucose utilization and protein deposition. Therefore, fish with inhibited mitochondrial FAO could have high potential to utilize carbohydrate. Our results demonstrate a potentially new approach for increasing protein deposition through energy homeostasis regulation in cultured animals.

[Distribution characteristics of heavy metals in soil and its influence on greening plants in a main road of Lanzhou City, Northwest China]. / å °å·žå¸‚æŸäº¤é€šå¹²é“åœŸå£¤é‡é‡‘å±žåˆ†å¸ƒç‰¹å¾åŠå ¶å¯¹ç»¿åŒ–æ¤ç‰©çš„å½±å“.

To investigate the characteristics of heavy metal pollution caused by traffic and its potential ecological risks, we measured the amount of metal elements in samples collected from a traffic trunk road in Lanzhou City with atomic absorption spectrophotometer. The single factor index method and potential ecological risk index method were used to evaluate the degree of pollution and potential ecological risks, and then the effects of heavy metal pollution on chlorophyll and calcium (Ca) contents in greening plants were analyzed. The results showed that the amount of heavy metals including chromium (Cr), manganese (Mn), zinc (Zn), copper (Cu) and nickel (Ni) in the soils increased significantly, with Cr, Cu and Pb reaching moderate pollution level. The degree of potential ecological risk was Cu>Pb>Cr>Ni>Zn>Mn. Sophora japonica, Rosa chinesis, Prunus ceraifera, and Euonymus japonicas showed different accumulation effects on Pb, Mn, Zn, and Ni. The content of chlorophyll in the leaves of deciduous species S. japonica, R. chinesis and P. ceraifera was higher in the roadside sampling point than that in the control point, while the pattern was just the opposite in evergreen species E. japonicas and P. orientalis. Foliar Ca content of greening plants in the roadside sampling point was higher than that in the control point, suggesting that high chlorophyll and Ca contents might be beneficial to plant survival in the heavy metal contaminated area. Taken together, traffic operation led to the accumulation of heavy metals (Cr, Mn, Zn, Cu, and Ni) in the soil of the study area. S. japonica, R. chinesis, P. ceraifera and E. japonicas could accumulate Pb, Mn, Zn and Ni, which could be used as greening plants in soils polluted by those heavy metals.

Role of interleukin-15 in cardiovascular diseases.

Interleukin (IL)-15 is a recently identified cytokine, which belongs to the interleukin-2(IL-2) family, and plays an important role in innate and adaptive immunoreaction. Given the fact that the structure of IL-15 is partially similar to IL-2, they share some common biological effects, including immunoregulation. IL-2 was proven to protect cardiac function in mouse myocardial infarction models. Cardiovascular diseases (CVDs) dominate the cause of mortality worldwide. Besides atherosclerosis, inflammation is also widely involved in the pathogenesis of many CVDs including hypertension, heart failure (HF) and aneurysm. IL-15, as a pro-inflammatory cytokine, is up-regulated in some cardiovascular diseases, such as myocardial infarction and atherosclerosis. The current understanding of IL-15, including its signal pathway and cellular function, was described. Furthermore, IL-15 has a protective effect in myocardial infarction and myocarditis by decreasing cardiomyocyte death and improving heart function. The inhibited effect of IL-15 in ductus arteriosus (DA) should be focused on. IL-15 promoted atherogenesis. IL-15 may be a good target in treatment of cardiovascular diabetology. Finally, future research direction of IL-15 deserves attention. Since IL-15 plays several roles in CVDs, understanding the role of the IL-15/IL-15R system may provide a scientific basis for the development of new approaches that use IL-15 for the treatment of CVDs.

Efficacy of cattle encephalon glycoside and ignotin in patients with acute cerebral infarction: a randomized, double-blind, parallel-group, placebo-controlled study.

Cattle encephalon glycoside and ignotin (CEGI) injection is a compound preparation formed by a combination of muscle extract from healthy rabbits and brain gangliosides from cattle, and it is generally used as a neuroprotectant in the treatment of central and peripheral nerve injuries. However, there is still a need for high-level clinical evidence from large samples to support the use of CEGI. We therefore carried out a prospective, multicenter, randomized, double-blind, parallel-group, placebo-controlled study in which we recruited 319 patients with acute cerebral infarction from 16 centers in China from October 2013 to May 2016. The patients were randomized at a 3:1 ratio into CEGI (n = 239; 155 male, 84 female; 61.2 ± 9.2 years old) and placebo (n = 80; 46 male, 34 female; 63.2 ± 8.28 years old) groups. All patients were given standard care once daily for 14 days, including a 200 mg aspirin enteric-coated tablet and 20 mg atorvastatin calcium, both taken orally, and intravenous infusion of 250-500 mL 0.9% sodium chloride containing 40 mg sodium tanshinone IIA sulfonate. Based on conventional treatment, patients in the CEGI and placebo groups were given 12 mL CEGI or 12 mL sterile water, respectively, in an intravenous drip of 250 mL 0.9% sodium chloride (2 mL/min) once daily for 14 days. According to baseline National Institutes of Health Stroke Scale scores, patients in the two groups were divided into mild and moderate subgroups. Based on the modified Rankin Scale results, the rate of patients with good outcomes in the CEGI group was higher than that in the placebo group, and the rate of disability in the CEGI group was lower than that in the placebo group on day 90 after treatment. In the CEGI group, neurological deficits were decreased on days 14 and 90 after treatment, as measured by the National Institutes of Health Stroke Scale and the Barthel Index. Subgroup analysis revealed that CEGI led to more significant improvements in moderate stroke patients. No drug-related adverse events occurred in the CEGI or placebo groups. In conclusion, CEGI may be a safe and effective treatment for acute cerebral infarction patients, especially for moderate stroke patients. This study was approved by the Ethical Committee of Peking University Third Hospital, China (approval No. 2013-068-2) on May 20, 2013, and registered in the Chinese Clinical Trial Registry (registration No. ChiCTR1800017937).