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A robust generalized labeled multi-Bernoulli (GLMB) filter is presented to perform multitarget tracking (MTT) with unknown non-stationary heavy-tailed measurement noise (HTMN). The HTMN is modeled as a multivariate Student’s t-distribution with unknown and time-varying mean. The proposed filter relaxes the restrictive assumption that the mean of HTMN is zero, and can effectively deal with MTT under the condition that the mean of HTMN is unknown and time-varying. The variational Bayesian (VB) approximation is applied in the GLMB filtering framework with the augmented state. The marginal likelihood function is obtained via minimizing the Kullback-Leibler divergence by the variational lower bound. The simulation results demonstrate that the proposed filter can effectively track multiple targets in both linear and nonlinear scenarios when the mean of HTMN is unknown and time-varying.

In accordance with the cerium-lanthanum ratio of fluorocerium ores in the mineralogy of the Baiyun Ebo process, the (Ce,La)CO3F grains were synthesised by hydrothermal method using pure material to simulate bastnaesite minerals, and used as NH3-SCR denitrification catalysts. The activity results showed that the synthetic (Ce,La)CO3F was roasted at 500&#730C, and the NOx conversion was 27% at 200&#730C. The NH3-SCR catalytic activity of the synthesised (Ce,La)CO3F was improved by loaded transition metal Mn. The best catalyst was found to be produced by impregnating (Ce,La)CO3F with 1 mol/L manganese nitrate solution, with a NOx conversion of 80% at 250&#730C. The loading of Mn resulted in the appearance of numerous well-dispersed MnOx species on the catalyst surface, the dispersion of Ce7O12 species was also greatly enhanced, and the reduction in grain size indicated that Mnn+ entered into the (Ce,La)CO3F lattice causing lattice shrinkage. The number of acidic sites on the catalyst surface and the redox capacity were enhanced. The amount of Ce3+ in the catalyst was also enhanced by the introduction of Mnn+, but the proportion of adsorbed oxygen decreased, which indicated that the introduction of Mnn+ was detrimental to the increase in the proportion of adsorbed oxygen. The reaction mechanisms of the (Ce,La)CO3F and Mn/(Ce,La)CO3F catalysts were investigated by in-situ Fourier transform infrared spectroscopy (FTIR). The results showed that catalysts followed the E-R and L-H mechanisms. When loaded with Mn, the main reactive species in the L-H mechanism were the (ad) species on the Br&#248nsted acidic site and the O-Ce3+-O-NO, O-Mn3+-O-NO species. The main reactive species for the E-R mechanism were NH3/ (ad) species and NO. The (ad) species on the Br&#248nsted acidic sites act as the main reactive NH3 (g) adsorbing species, bonded to the Ce4+ in the carrier (Ce,La)CO3F to participate in the acid cycle reaction. The introduction of Mnn+ increases the number of Br&#248nsted acidic sites on the catalyst surface, and acts as an adsorption site for NO, to react with NO to generate more monodentate nitrate species, to participate in the redox cycle reactions. The above results indicated that Mnn+ and (Ce,La)CO3F have a good mutual promotion effect, which makes the loaded catalyst have excellent performance, which provides a theoretical basis for the high value utilization of bastnaesite.

Background: Due to the high nursing pressure of patients with Cerebral hemorrhage and the general shortage of clinical nurses, nursing support workers often participate in clinical nursing work, but the influence of nursing support workers' participation on the negative emotion, quality of life and life satisfaction of patients with intracerebral hemorrhage is unknown. Methods: A total of 107 ICH patients admitted to our hospital from January 2022 to March 2022 were enrolled, including 60 patients receiving conventional care (CG control group) and 47 patients receiving nursing support worker participation (RG research group). All patients were recorded with self-perceived Burden Scale (SPBS), Hamilton Depression Scale (HAMD), Quality of Life Scale (SF-36), Somatic Self rating Scale (SSS), Patient self-care ability assessment scale（Barthel）and Satisfaction with life scale (SWLS) scores. Results: Patients with high negative emotion were more willing to participate in clinical nursing work (P). Nursing support workers involved in cerebral hemorrhage patients can alleviate negative emotions, improve life quality, improve nursing satisfaction (P). Conclusion: The participation of nursing support workers can alleviate the negative emotions of ICH patients, enhance their self-management ability, and improve their life quality.

Objective. The accelerate loss of skeletal muscle mass, strength, and function, named sarcopenia, is a progressive and generalised skeletal muscle disorder, and it is always associated with increased outcomes including falls, frailty, and disability. Diabetes mellitus is associated with significant muscle and physical complications. We aimed at clarifying the changes and risk factors of skeletal muscle mass and strength in elderly with type 2 diabetes. Methods. The study consisted of patients with type 2 diabetes ( n = 120 ) and an older general population ( n = 126 ). The skeletal muscle mass and muscle strength, as well as the serum levels of chronic inflammation, oxidative stress, homocysteine, and insulin-like factor-1 were assessed, and the correlation and regression analysis were conducted to evaluate outcomes. Results. T2DM patients exhibited lower muscle strength compared with the non-T2DM subjects ( P < 0.01 ). Among T2DM patients, serum IGF-1 levels were positively correlated with muscle strength ( r = 0.255 , P < 0.01 ) and muscle mass ( r = 0.209 , P < 0.05 ), levels of 8-OHdG were inversely correlated with muscle strength ( r = − 0.252 , P < 0.01 ), and there was a negative association between HCY and muscle mass ( r = − 0.185 , P < 0.05 ). Muscle mass and strength of patients with higher education level were significantly higher than those with lower education level ( P < 0.05 ), in male patients, muscle mass and muscle strength were significantly lower in smokers ( P < 0.01 ), and muscle mass was lower in chronic drinkers ( P < 0.05 ). Conclusions. These findings suggest that diabetic patients may be more susceptible to sarcopenia at an older age. And it also provides evidences that among elderly with diabetes mellitus, oxidative damage and HCY as well as IGF-1 are important predictors of age-dependent sarcopenia.

The relationship between formal and informal finance is uncertain. They serve as substitute for high-quality borrowers but are complement for low-quality borrowers. As formal financial institutions expand, they may concentrate on high-quality borrowers or diversify among borrowers of different qualities. Using unique survey data from Chinese private firms, we are allowed to investigate the relationship for a group of borrowers who were considered as low-quality. We find that formal financial development imposes a crowd-in effect for private firms’ informal financing, especially in East China. There is heterogeneity between East and West China. We document that the crowd-in effect is greater for private firms with bank access or of large size.

Given the global epidemic of obesity, numerous strategies have been employed in the management of metabolic syndrome (MS) in this population. A meta-analysis was designed in the present investigation to evaluate the benefits of tea extract (TE) supplementation in MS in obesity.We conducted searches of published literature in MEDLINE, PsycINFO, Scopus, EMBASE, and the Cochrane Central Register of Controlled Trials (CENTRAL) databases from inception in 1985 to May 2017. Randomized controlled trials (RCTs) which studied TE consumption in obesity with MS were analyzed. Results were summarized using weighted mean differences (WMDs), standardized mean differences (SMDs) or odds ratio (OR) by suitable effect model.Sixteen eligible randomized controlled trials, including 1090 subjects were identified. Benefits were demonstrated on reduction of Body Mass Index (BMI) (SMD, -0.27; 95% CI, -0.40 to -0.15, P 0.0001) and blood glucose (SMD, -0.22; 95% CI, -0.34 to -0.10, P = 0.0003), and increasing high-density lipoprotein (HDL) (SMD, 0.18; 95% CI, 0.01 to 0.35, P = 0.03). Limited benefits without significance were observed on blood pressure and other anthropometric, cholesterol, and biochemistry outcomes. All-cause adverse events were minimal (0.99; 95% CI: 0.55, 1.77, P = 0.97).This meta-analysis suggests that consumption of TE supplementation in the obese with MS has beneficial effects on improvement of lipid and glucose metabolism, as well as in the facilitation of weight loss.

Peptide-based nanofibres are a versatile class of tunable materials with applications in optoelectronics, sensing and tissue engineering. However, the understanding of the nanofibre surface at the molecular level is limited. Here, a series of homologous dilysine–diphenylalnine tetrapeptides were synthesised and shown to self-assemble into water-soluble nanofibres. Despite the peptide nanofibres displaying similar morphologies, as evaluated through atomic force microscopy and neutron scattering, significant differences were observed in their ability to support sensitive primary neurons. Contact angle and labelling experiments revealed that differential presentation of lysine moieties at the fibre surface did not affect neuronal viability; however the mobility of phenylalanine residues at the nanofibre surface, elucidated through solid- and gel-state NMR studies and confirmed through tethered bilayer lipid membrane experiments, was found to be the determining factor in governing the suitability of a given peptide as a scaffold for primary neurons. This work offers new insights into characterising and controlling the nanofibre surface at the molecular level., The mobility of hydrophobic moieties at a peptide nanofibre surface determines its suitability as a scaffold for sensitive primary cells.

Meat color is the primary criterion by which consumers evaluate meat quality. However, there are a few candidate genes and molecular markers of meat color that were reported for pig molecular breeding. The purpose of the present study is to identify the candidate genes affecting meat color and provide the theoretical basis for meat color molecular breeding. A total of 306 Suhuai pigs were slaughtered, and meat color was evaluated at 45 min and 24 h after slaughter by CIELAB color space. All individuals were genotyped using GeneSeek GGP-Porcine 80K SNP BeadChip. The genomic estimated breeding values (GEBVs), heritability, and genetic correlation of meat color were calculated by DMU software. The genome-wide association studies (GWASs) and the fixation index (F

In accordance with the cerium-lanthanum ratio of fluorocerium ores in the mineralogy of the Baiyun Ebo process, pure substances such as Ce(NO3)3·6H2O, La(NO3)3·6H2O were used to synthesize (Ce,La)CO3F grains to simulate bastnaesite minerals by hydrothermal method, and used as NH3-SCR denitrification catalysts. After being roasted at a series of different temperatures, the catalyst surface produced a well-crystallised Ce7O12 species as the active component for denitrification. The activity results showed that the synthetic (Ce,La)CO3F was roasted at 500°C, and the NOx conversion was 27% at 200°C. The NH3-SCR catalytic activity of the synthesised (Ce,La)CO3F was improved by loaded transition metal Mn. The best catalyst was found to be produced by impregnating (Ce,La)CO3F with 1 mol/L manganese nitrate solution, with a NOx conversion of 80% at 250°C. The physicochemical properties were analysed using XRD, BET, H2-TPR, NH3-TPD and XPS. The loading of Mn resulted in the appearance of numerous well-dispersed MnOx species on the catalyst surface, the dispersion of Ce7O12 species was also greatly enhanced, and the reduction in grain size indicated that Mnn+ entered into the (Ce,La)CO3F lattice causing lattice shrinkage. The number of acidic sites on the catalyst surface and the redox capacity were enhanced. The amount of Ce3+ in the catalyst was also enhanced by the introduction of Mnn+, but the proportion of adsorbed oxygen decreased, which indicated that the introduction of Mnn+ was detrimental to the increase in the proportion of adsorbed oxygen. The reaction mechanisms of the (Ce,La)CO3F and Mn/(Ce,La)CO3F catalysts were investigated by in-situ Fourier transform infrared spectroscopy (FTIR), to provide theoretical guidance for the specific reaction pathways of bastnaesite in the NH3-SCR reaction. The results showed that catalysts followed both the E-R and L-H mechanisms throughout the reaction process. When loaded with Mn, the main reactive species in the L-H mechanism were the NH4+(ad) species on the Brønsted acidic site and the O-Ce3+-O-NO, O-Mn3+-O-NO species. The main reactive species for the E-R mechanism were NH3/NH4+(ad) species on the Brønsted/Lewis acidic sites and NO. The NH4+ (ad) species on the Brønsted acidic sites act as the main reactive NH3(g) adsorbing species, bonded to the Ce4+ in the carrier (Ce,La)CO3F to participate in the acid cycle reaction. The introduction of Mnn+ increases the number of Brønsted acidic sites on the catalyst surface, and acts as an adsorption site for NO, to react with NO to generate more monodentate nitrate species, to participate in the redox cycle reactions. The above results indicated that Mnn+ and (Ce,La)CO3F have a good mutual promotion effect, which makes the loaded catalyst have excellent performance, which provides a theoretical basis for the high value utilization of bastnaesite.

Oxidative stress acts as an essential culprit factor in the development of stroke and Alzheimer’s disease. Norcepharadione B possesses various pharmacologic features as an extract obtained from Houttuynia cordata. Nevertheless, the anti-apoptotic and neuroprotective characteristics of norcepharadione B remain unclear. In this study, the neuronal protection effect provided by norcepharadione B against injury caused by hydrogen peroxide (H2O2) in HT22 cell as well as the fundamental mechanism was systematically explored. The neurotoxicity assays of hippocampal cells, which were co-cultured with H2O2, showed that norcepharadione B had the ability to insulate the toxicity induced by H2O2 with significant reduced cell apoptosis. Besides, norcepharadione B potentiated the activity of superoxide dismutase (SOD), increased the level of glutathione (GSH), and decreased malondialdehyde content. The H2O2-induced apoptotic protein Bax was suppressed, and the anti-apoptotic protein Bcl-2 was boosted by norcepharadione B. Norcepharadione B promoted Akt phosphorylation and further upregulated heme oxygenase (HO-1) in cells exposed to oxidative stress. However, the inductive effect of HO-1 by norcepharadione B was shut off via the PI3K/Akt inhibitor LY294002. Furthermore, 2-h incubation with H2O2 substantially increased cell volume in HT22 cells, while norcepharadione B effectively alleviated such effect by interrupting the activation of VSOR Cl− channel. Collectively, our data revealed protective properties of norcepharadione B in resisting oxidative stress induced by H2O2 through elevation of HO-1 in the dependence of PI3K/Akt and in inhibiting H2O2-induced cell swelling by VSOR Cl− channel obstruction in HT22 cells. Impact statement Norcepharadione B is an aporphine alkaloid compound extracted from Chinese herb Houttuynia cordata. It was well known for its anti-inflammatory, anti-cancer, and anti-platelet aggregation outcomes. Our study demonstrated that Norcepharadione B protected hippocampal neurons against oxidative stress and the resultant cell apoptosis upon H2O2 exposure. Meanwhile, Norcepharadione B also substantially reduced cell swelling induced by H2O2 via inhibiting VSOR Cl− channel in neurons. These findings uncovered the potential mechanisms of Norcepharadione B in protecting neuron apoptosis under oxidative stress and propose that Norcepharadione B may serve as a favorable herb medicine for restoring neuronal injury in the pathogenesis of stroke together with other neurodegenerative diseases.

Significance The factors that regulate RNA polymerase II (Pol II) elongation rate and processivity are poorly understood. Here, we show that the Paf1 complex (Paf1C) modulates Pol II elongation rate, and loss of Paf1 results in accumulation of Ser5P in the first 20 to 30 kb of gene bodies, coinciding with reduction of histone H2B ubiquitylation specifically within this region. Moreover, reduced elongation rates provoked by Paf1 depletion resulted in defects in Pol II processivity and premature termination of transcription. Paf1 ablation did not impact the recruitment of other key elongation factors, suggesting that Paf1C function may be mechanistically distinguishable from each of these factors. Our data pinpoint Paf1C as a key modulator of Pol II elongation rates across mammalian genes., Elongation factor Paf1C regulates several stages of the RNA polymerase II (Pol II) transcription cycle, although it is unclear how it modulates Pol II distribution and progression in mammalian cells. We found that conditional ablation of Paf1 resulted in the accumulation of unphosphorylated and Ser5 phosphorylated Pol II around promoter-proximal regions and within the first 20 to 30 kb of gene bodies, respectively. Paf1 ablation did not impact the recruitment of other key elongation factors, namely, Spt5, Spt6, and the FACT complex, suggesting that Paf1 function may be mechanistically distinguishable from each of these factors. Moreover, loss of Paf1 triggered an increase in TSS-proximal nucleosome occupancy, which could impose a considerable barrier to Pol II elongation past TSS-proximal regions. Remarkably, accumulation of Ser5P in the first 20 to 30 kb coincided with reductions in histone H2B ubiquitylation within this region. Furthermore, we show that nascent RNA species accumulate within this window, suggesting a mechanism whereby Paf1 loss leads to aberrant, prematurely terminated transcripts and diminution of full-length transcripts. Importantly, we found that loss of Paf1 results in Pol II elongation rate defects with significant rate compression. Our findings suggest that Paf1C is critical for modulating Pol II elongation rates by functioning beyond the pause-release step as an “accelerator” over specific early gene body regions.

Peroxisome proliferator-activated receptor gamma (PPARγ) is a master regulator of adipogenesis and lipogenesis. To understand its roles in fiber formation and fat deposition in skeletal muscle, we successfully generated muscle-specific overexpression of PPARγ in two pig models by random insertion and CRISPR/Cas9 transgenic cloning procedures. The content of intramuscular fat was significantly increased in PPARγ pigs while had no changes on lean meat ratio. PPARγ could promote adipocyte differentiation by activating adipocyte differentiating regulators such as FABP4 and CCAAT/enhancer-binding protein (C/EBP), along with enhanced expression of LPL, FABP4, and PLIN1 to proceed fat deposition. Proteomics analyses demonstrated that oxidative metabolism of fatty acids and respiratory chain were activated in PPARγ pigs, thus, gathered more Ca2+ in PPARγ pigs. Raising of Ca2+ could result in increased phosphorylation of CAMKII and p38 MAPK in PPARγ pigs, which can stimulate MEF2 and PGC1α to affect fiber type and oxidative capacity. These results support that skeletal muscle-specific overexpression of PPARγ can promote oxidative fiber formation and intramuscular fat deposition in pigs.

Background: With the aggravation of social competition and work burden pressure, the health condition of the middle-aged and above population in China has declined significantly. Frailty can be used as a criterion for evaluating a person's unhealthy state. However, there is limited data on the prevalence and related factors of frail status in Chinese middle-aged and older people.The objective of this study was to explore the correlation between frail status, chronic diseases, abnormal physical examination indicators among middle-aged and older populations.Methods: Participants were 9,985 community-dwelling adults over the age of 40 years living in China. Data were from the 2015 China Health and Retirement Longitudinal Survey which was a nationally representative sample and frailty phenotype was based on Fried frailty criteria. We analyzed the demographics of participants and multivariate-adjusted related factors for frail and pre-frail population.Results: The overall prevalence of frailty and pre-frailty was 3.1% (95% CI: 2.8, 3.5) and 53.66% (95% CI: 52.7, 54.6) among the general Chinese population aged 40 years or older. Hypertension (OR: 1.8, 95% CI: 1.3, 2.593), pain (OR: 1.8, 95% CI: 1.3, 2.5), and hip fracture (OR: 2.2, 95% CI: 1.1, 4.4) were associated with prevalent frailty. Relative factors for frailty also included increased cystatin C (OR: 4.5, 95% CI: 3.0, 6.7) and glycated hemoglobin (OR: 1.2, 95% CI: 1.1, 1.4), as well as decreased peak expiratory flow (OR: 0.993, 95% CI: 0.991, 0.994).Conclusions: Fried-defined frailty and pre-frailty are highly prevalent in the Chinese population over 40 years older. Hypertension, pain, hip fracture, low education, and underweight are major related factors for frailty. The decrease in peak expiratory flow and the increase in cystatin C and glycated hemoglobin are good indicators for detecting frailty. Thus, frailty is an increasingly common condition and will become a major important health issue for people over middle age.

To solve the problem of multi-target tracking with heavy-tailed process noise and measurement noise, a Student's t mixture $\delta$ -generalized labeled multi-Bernoulli ( $\delta$ -GLMB) filter is proposed for nonlinear systems. A third-degree Spherical-Radial rule is utilized to calculate the probability density functions of the prediction and update of target states for nonlinear multi-target models. The performance of the proposed Student's t mixture $\delta$ -GLMB filter for nonlinear systems is compared with the Sequential Monte Carlo $\delta$ -GLMB (SMC- $\delta$ -GLMB) filter through simulation experiments. Simulation results demonstrated that the proposed filter can achieve a good trade-off between efficiency and tracking accuracy.

PPARγ is a master regulator of adipogenesis and lipogenesis. To understand its roles in fat deposition and fiber formation in skeletal muscle, we successfully generated muscle-specific overexpression of PPARγ by pig cloning procedures. The content of intramuscular fat was significantly increased in PPARγ transgenic pigs while the muscle mass as lean percentage of body weight was not changed. The proteomics analysis demonstrated oxidative metabolism of fatty acids and respiratory chain were increased in PPARγ pigs. Furthermore, expressions of oxidative muscle fiber-related genes such as MyHC1 and TNNT1 were enhanced. CAMK2, MEF2 and PGC1α were also significantly increased in skeletal muscle of PPARγ pigs, indicating that Ca2+-sensitive phosphatases and kinases may play an important role in the switch of muscle fiber types when PPARγ activity is elevated in skeletal muscle. The results support skeletal muscle-specific overexpression of PPARγ can promote oxidative fiber formation and intramuscular fat deposition in pigs.

Chloride channels represent a group of potential drug targets; their blockers showed significant protecting effect on impaired cells by modulating apoptosis, autophagy, and other cell signals. However, clinical drugs with chloride channel inhibitory properties have not yet been developed. Natural product extract becomes an underlying candidate satisfied the clinical requirements for its low toxicity, low cost, and abundant sources. Here, a fluorescence-based EYFP-H148Q/I153L-HeLa cell line model was constructed by molecular cloning and verified by real-time polymerase chain reaction and Western blotting assay. By using this chloride channel blocker screening model, seven hit compounds chosen from 6988 natural compounds showed the channel blocking activity. Then the hit compounds were further validated by electrophysiological patch-clamp analysis. Our study preliminarily identified PC-4 as a new chloride channel inhibitor and demonstrated the reliability and sensitivity of fluorescence-based high throughput screening technologies for discovery of biologically active compounds from natural herbal compounds.

The different skeletal muscle fiber types exhibit distinctively different physiological and metabolic properties, and have been linked to both human metabolic diseases and meat quality traits in livestock. Circular RNAs (circRNAs) are a new class of endogenous RNA regulating gene expression, but regulatory mechanisms of skeletal muscle fibers involved in circRNAs remain poorly understood. Here, we constructed circRNA expression profiles of three fast-twitch biceps femoris (Bf) and three slow-twitch soleus (Sol) muscles in pigs using RNA-seq and identified 16,342 distinct circRNA candidates. Notably, 242 differentially expressed (DE) circRNAs between Bf and Sol muscles were identified, including 105 upregulated and 137 downregulated circRNAs, and are thus potential candidates for the regulation of skeletal muscle fiber conversion. Moreover, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of host genes of DE circRNAs revealed that host genes were mainly involved in skeletal muscle fiber-related GO terms (e.g., muscle contraction, contractile fiber part, and Z disk) and skeletal muscle fiber-related signaling pathways (e.g., AMPK and cGMP-PKG). We also constructed co-expression networks of DE circRNA-miRNA-mRNA using previously acquired high-throughput sequencing mRNA and miRNA data, from which 112 circRNA-miRNA and 95 miRNA-mRNA interactions were identified. Multiple circRNAs essentially serve as a sponge for miR-499-5p, which is preferentially expressed in slow-twitch muscle and reduces the severity of Duchenne muscular dystrophy (DMD). Taken together, a series of novel candidate circRNAs involved in the growth and development of porcine skeletal muscle was identified. Furthermore, they provide a comprehensive circRNA resource for further in-depth research on the regulatory mechanisms of circRNA in the formation of skeletal muscle fiber, and may provide insights into human skeletal muscle diseases.

BackgroundFibroblast growth factor 21 (FGF21) may play a role in the development of chronic kidney disease (CKD). We therefore investigated the relationship of plasma FGF21 levels with kidney function and albuminuria in the Multi-Ethnic Study of Atherosclerosis (MESA).MethodsThe analysis included 5724 MESA participants ages 45-84 years between 2000 and 2002, free of clinically apparent cardiovascular disease (CVD). Participants were followed up in person at four additional clinic visits over 10 years. Plasma FGF21 levels were measured at baseline examination by enzyme-linked immunosorbent assay. Kidney function was assessed by estimated glomerular filtration rate (eGFR). Outcomes were urinary albumin:creatinine ratio (UACR) progression, incident CKD by eGFR (reaching eGFR 5%/year).ResultsAt baseline, higher FGF21 levels, assessed as both continuous and categorical quartile variables, were significantly associated with lower eGFR and higher UACR, after adjusting for demographic, socioeconomic and other confounding factors [adjusted mean differences of -2.63 mL/min/1.73m2 in eGFR and 0.134 in log normally transformed UACR (mg/g) for the highest FGF21 quartile compared with the lowest quartile, all P 0.05).ConclusionsOur study does not support a role of FGF21 as a biomarker for predicting kidney function decline or albuminuria in adults free of clinically apparent CVD at baseline.

In this letter, an ultra-thin microwave metamaterial for ultra-broadband radar cross section (RCS) reduction is presented. In the unit cell, an impedance surface pattern with two split-square-loops is proposed to achieve broadband absorption and polarization conversion. Two FR-4 dielectric substrates are above and below the resistive pattern. This design exhibits 85% absorption from 3.8 to 19.2 GHz under normal incidence. The fractional bandwidth of 134% is realized by multiple resonances. The polarization conversion rate (PCR) of the design is above 0.3 in the operating frequency band. The proposed concept is proved by full-wave simulation and experimental measurements. The performance under oblique incidence are investigated. The surface current has been illustrated to analyze the absorption mechanism. This design is ultra-thin (0.079λL at the lowest operating frequency) with ultra-broadband RCS reduction performance and provides an alternative to the stealth application of satellite solar panels.

Fibroblast growth factor 21(FGF21) is a pivotal regulator of energy metabolism, which is currently being assessed as a potential drug target for the treatment of insulin-resistant conditions. However, the cellular mechanisms by which FGF21 affects myogenesis remain unclear. In this study, we explored the function of FGF21 in myogenesis both in vitro and in vivo. Our experiments showed for the first time that FGF21 promotes myoblast differentiation and serves as a switch of molecular transformation from anaerobic myofibers to aerobic myofibers via the FGF21-SIRT1-AMPK-PGC1α axis. Furthermore, we employed the Dual-Luciferase Reporter Assay System and Electrophoretic Mobility Shift Assay (EMSA) and demonstrated that MYOD, a major myogenic transcription factor, binds directly to the promoter region of Fgf21, leading to the activation of Fgf21 expression in mouse C2C12 myoblasts. Our study revealed a novel mechanism of myogenesis and muscle fiber transformation and indicated that FGF21 serves as a vital regulator of muscle development and important contributor to the pathogenesis of myopathy. J. Cell. Physiol. 232: 1893-1906, 2017. © 2016 Wiley Periodicals, Inc.

Individual skeletal muscles in the animal body are heterogeneous, as each is comprised of different fiber types. Type I muscle fibers are rich with mitochondria, and have high oxidative metabolisms while type IIB fibers have few mitochondria and high glycolytic metabolic capacity. Peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α), a transcriptional co-activator that regulates mitochondrial biogenesis and respiratory function, is implicated in muscle fiber-type switching. Over-expression of PGC-1α in transgenic mice increased the proportion of red/oxidative type I fiber. During pig muscle growth, an increased number of type I fibers can give meat more red color. To explore the roles of PGC-1α in regulation of muscle fiber type conversion, we generated skeletal muscle-specific PGC-1α transgenic mice and pig. Ectopic over-expression of PGC-1α was detected in both fast and slow muscle fibers. The transgenic animals displayed a remarkable amount of red/oxidative muscle fibers in major skeletal muscle tissues. Skeletal muscles from transgenic mice and pigs have increased expression levels of oxidative fiber markers such as MHC1, MHC2x, myoglobin and Tnni1, and decreased expressions of glycolytic fiber genes (MHC2a, MHC2b, CASQ-1 and Tnni2). The genes responsible for the TCA cycle and oxidative phosphorylation, cytochrome coxidase 2 and 4, and citrate synthase were also increased in the transgenic mice and pigs. These results suggested that transgenic over-expressed PGC-1α significantly increased muscle mitochondrial biogenesis, resulting in qualitative changes from glycolytic to oxidative energy generation. The transgenic animals also had elevated levels of PDK4 and PPARγ proteins in muscle tissue, which can lead to increased glycogen deposition and fatty acid oxidation. Therefore, the results support a significant role of PGC-1α in conversion of fast glycolytic fibers to slow and oxidative fiber through enhanced mitochondrial respiration and fatty acid oxidation, and transgenic over-expression of PGC-1α in skeletal muscle leads to more red meat production in pigs.

Oxidative stress acts as an essential culprit factor in the development of stroke and Alzheimer’s disease. Norcepharadione B possesses various pharmacologic features as an extract obtained from Houttuynia cordata. Nevertheless, the anti-apoptotic and neuroprotective characteristics of norcepharadione B remain unclear. In this study, the neuronal protection effect provided by norcepharadione B against injury caused by hydrogen peroxide (H(2)O(2)) in HT22 cell as well as the fundamental mechanism was systematically explored. The neurotoxicity assays of hippocampal cells, which were co-cultured with H(2)O(2), showed that norcepharadione B had the ability to insulate the toxicity induced by H(2)O(2) with significant reduced cell apoptosis. Besides, norcepharadione B potentiated the activity of superoxide dismutase (SOD), increased the level of glutathione (GSH), and decreased malondialdehyde content. The H(2)O(2)-induced apoptotic protein Bax was suppressed, and the anti-apoptotic protein Bcl-2 was boosted by norcepharadione B. Norcepharadione B promoted Akt phosphorylation and further upregulated heme oxygenase (HO-1) in cells exposed to oxidative stress. However, the inductive effect of HO-1 by norcepharadione B was shut off via the PI3K/Akt inhibitor LY294002. Furthermore, 2-h incubation with H(2)O(2) substantially increased cell volume in HT22 cells, while norcepharadione B effectively alleviated such effect by interrupting the activation of VSOR Cl(−) channel. Collectively, our data revealed protective properties of norcepharadione B in resisting oxidative stress induced by H(2)O(2) through elevation of HO-1 in the dependence of PI3K/Akt and in inhibiting H(2)O(2)-induced cell swelling by VSOR Cl(−) channel obstruction in HT22 cells. IMPACT STATEMENT: Norcepharadione B is an aporphine alkaloid compound extracted from Chinese herb Houttuynia cordata. It was well known for its anti-inflammatory, anti-cancer, and anti-platelet aggregation outcomes. Our study demonstrated that Norcepharadione B protected hippocampal neurons against oxidative stress and the resultant cell apoptosis upon H(2)O(2) exposure. Meanwhile, Norcepharadione B also substantially reduced cell swelling induced by H(2)O(2) via inhibiting VSOR Cl(−) channel in neurons. These findings uncovered the potential mechanisms of Norcepharadione B in protecting neuron apoptosis under oxidative stress and propose that Norcepharadione B may serve as a favorable herb medicine for restoring neuronal injury in the pathogenesis of stroke together with other neurodegenerative diseases.

Apolipoprotein A-I (apoA-I), the main protein constituent of HDLs, increases insulin synthesis and insulin secretion in pancreatic beta cells. ApoA-I also accepts cholesterol that effluxes from cells expressing ATP-binding cassette transporter A1 (ABCA1) and ATP-binding cassette transporter G(1) (ABCG1). Mice with conditional deletion of ABCA1 and ABCG1 in beta cells [beta-double knockout (DKO) mice] have increased islet cholesterol levels and reduced glucose-stimulated insulin secretion (GSIS). The project asks whether metabolic pathways are dysregulated in beta-DKO mouse islets and whether this can be corrected, and GSIS improved, by treatment with apoA-I. beta-DKO mice were treated with apoA-I or PBS, and islets were isolated for determination of GSIS. Total RNA was extracted from beta-DKO and control mouse islets for microarray analysis. Metabolic pathways were interrogated by functional enrichment analysis. ApoA-I treatment improved GSIS in beta-DKO but not control mouse islets. Plasma lipid and lipoprotein levels and islet cholesterol levels were also unaffected by treatment with apoA-I. Cholesterol metabolism, glucose metabolism, and inflammation pathways were dysregulated in beta-DKO mouse islets. This was not corrected by treatment with apoA-I. In summary, apoA-I treatment improves GSIS by a cholesterol-independent mechanism, but it does not correct metabolic dysregulation in beta-DKO mouse islets.-Hou, L., Tang, S., Wu, B. J., Ong, K.-L., Westerterp, M., Barter, P. J., Cochran, B. J., Tabet, F., Rye, K.-A. Apolipoprotein A-I improves pancreatic beta-cell function independent of the ATP-binding cassette transporters ABCA1 and ABCG1.

Elongin is an RNA polymerase II (RNAPII)-associated factor that has been shown to stimulate transcriptional elongation in vitro. The Elongin complex is thought to be required for transcriptional induction in response to cellular stimuli and to ubiquitinate RNAPII in response to DNA damage. Yet, the impact of the Elongin complex on transcription in vivo has not been well studied. Here, we performed comprehensive studies of the role of Elongin A, the largest subunit of the Elongin complex, on RNAPII transcription genome-wide. Our results suggest that Elongin A localizes to actively transcribed regions and potential enhancers, and the level of recruitment correlated with transcription levels. We also identified a large group of factors involved in transcription as Elongin A–associated factors. In addition, we found that loss of Elongin A leads to dramatically reduced levels of serine2-phosphorylated, but not total, RNAPII, and cells depleted of Elongin A show stronger promoter RNAPII pausing, suggesting that Elongin A may be involved in the release of paused RNAPII. Our RNA-seq studies suggest that loss of Elongin A did not alter global transcription, and unlike prior in vitro studies, we did not observe a dramatic impact on RNAPII elongation rates in our cell-based nascent RNA-seq experiments upon Elongin A depletion. Taken together, our studies provide the first comprehensive analysis of the role of Elongin A in regulating transcription in vivo. Our studies also revealed that unlike prior in vitro findings, depletion of Elongin A has little impact on global transcription profiles and transcription elongation in vivo.

Apolipoprotein A-I (apoA-I) is the major component of HDL and central to the ability of HDL to stimulate ATP-binding cassette transporter A1 (ABCA1)-dependent, antiatherogenic export of cholesterol from macrophage foam cells, a key player in the pathology of atherosclerosis. Cell-mediated modifications of apoA-I, such as chlorination, nitration, oxidation, and proteolysis, can impair its antiatherogenic function, although it is unknown whether macrophages themselves contribute to such modifications. To investigate this, human monocyte-derived macrophages (HMDMs) were incubated with human apoA-I under conditions used to induce cholesterol export. Two-dimensional gel electrophoresis and Western blot analysis identified that apoA-I is cleaved (∼20-80%) by HMDMs in a time-dependent manner, generating apoA-I of lower MW and isoelectric point. Mass spectrometry analysis identified a novel C-terminal cleavage site of apoA-I between Ser228-Phe229 Recombinant apoA-I truncated at Ser228 demonstrated profound loss of capacity to solubilize lipid and to promote ABCA1-dependent cholesterol efflux. Protease inhibitors, small interfering RNA knockdown in HMDMs, mass spectrometry analysis, and cathepsin B activity assays identified secreted cathepsin B as responsible for apoA-I cleavage at Ser228 Importantly, C-terminal cleavage of apoA-I was also detected in human carotid plaque. Cleavage at Ser228 is a novel, functionally important post-translational modification of apoA-I mediated by HMDMs that limits the antiatherogenic properties of apoA-I.-Dinnes, D. L. M., White, M. Y., Kockx, M., Traini, M., Hsieh, V., Kim, M.-J., Hou, L., Jessup, W., Rye, K.-A., Thaysen-Andersen, M., Cordwell, S. J., Kritharides, L. Human macrophage cathepsin B-mediated C-terminal cleavage of apolipoprotein A-I at Ser228 severely impairs antiatherogenic capacity.

Lipoproteins are supramolecular assemblies of proteins and lipids with dynamic characteristics critically linked to their biological functions as plasma lipid transporters and lipid exchangers. Among them, spherical high-density lipoproteins are the most abundant forms of high-density lipoprotein (HDL) in human plasma, active participants in reverse cholesterol transport, and associated with reduced development of atherosclerosis. Here, we employed elastic incoherent neutron scattering (EINS) and hydrogen-deuterium exchange mass spectrometry (HDX-MS) to determine the average particle dynamics and protein backbone local mobility of physiologically competent discoidal and spherical HDL particles reconstituted with human apolipoprotein A-I (apoA-I). Our EINS measurements indicated that discoidal HDL was more dynamic than spherical HDL at ambient temperatures, in agreement with their lipid-protein composition. Combining small-angle neutron scattering (SANS) with contrast variation and MS cross-linking, we showed earlier that the most likely organization of the three apolipoprotein A-I (apoA-I) chains in spherical HDL is a combination of a hairpin monomer and a helical antiparallel dimer. Here, we corroborated those findings with kinetic studies, employing hydrogen-deuterium exchange mass spectrometry (HDX-MS). Many overlapping apoA-I digested peptides exhibited bimodal HDX kinetics behavior, suggesting that apoA-I regions with the same amino acid composition located on different apoA-I chains had different conformations and/or interaction environments.

This paper proposes two nonlinear $\delta$ -generalized labeled the multi-Bernoulli ( $\delta$ -GLMB) filters by combining quadrature Kalman (QK) and cubature Kalman (CK) with $\delta-$ GLMB filter for nonlinear Gaussian mixture (GM) multi-target model. And the $\mathbf{QK}-\mathbf{GM}-\delta-\mathbf{GLMB}$ and $\mathbf{CK}-\mathbf{GM}-\delta-\mathbf{GLMB}$ filters are compared with other two existing nonlinear $\delta$ -GLMB tracking algorithms, which are respectively based on the Extended Kalman Filter (EKF) as well as the Unscented Kalman Filter (UKF), about tracking performance for multi-target tracking (MTT) in the case of different clutter densities as well as detection probabilities. Moreover, the GM implementation process of the four filters is compared with the SMC simulation process of the $\delta$ -GLMB filter in the nonlinear Gaussian model. Simulation consequences demonstrate that both the QK-GM $-\delta$ -GLMB and CK-GM $-\delta$ -GLMB filters are effective nonlinear tracking methods, and we can conclude that the QK-GM $-\delta$ -GLMB filter is a competitive approach that achieves better tracking performance at an acceptable time cost for mildly nonlinear multi-target motion scenarios.

A new optimization algorithm of sensor selection is proposed in this paper for decentralized large-scale multi-target tracking (MTT) network within a labeled random finite set (RFS) framework. The method is performed based on a marginalized δ-generalized labeled multi-Bernoulli RFS. The rule of weighted Kullback-Leibler average (KLA) is used to fuse local multi-target densities. A new metric, named as the label assignment (LA) metric, is proposed to measure the distance for two labeled sets. The lower bound of LA metric based mean square error between the labeled multi-target state set and its estimate is taken as the optimized objective function of sensor selection. The proposed bound is obtained by the information inequality to RFS measurement. Then, we present the sequential Monte Carlo and Gaussian mixture implementations for the bound. Another advantage of the bound is that it provides a basis for setting the weights of KLA. The coordinate descent method is proposed to compromise the computational cost of sensor selection and the accuracy of MTT. Simulations verify the effectiveness of our method under different signal-to- noise ratio scenarios.

The problem of blind image recovery using multiple blurry images of the same scene is addressed in this paper. To perform blind deconvolution, which is also called blind image recovery, the blur kernel and image are represented by groups of sparse domains to exploit the local and nonlocal information such that a novel joint deblurring approach is conceived. In the proposed approach, the group sparse regularization on both the blur kernel and image is provided, where the sparse solution is promoted by $\ell _{1}$ -norm. In addition, the reweighted data fidelity is developed to further improve the recovery performance, where the weight is determined by the estimation error. Moreover, to reduce the undesirable noise effects in group sparse representation, distance measures are studied in the block matching process to find similar patches. In such a joint deblurring approach, a more sophisticated two-step interactive process is needed in which each step is solved by means of the well-known split Bregman iteration algorithm, which is generally used to efficiently solve the proposed joint deblurring problem. Finally, numerical studies, including synthetic and real images, demonstrate that the performance of this joint estimation algorithm is superior to the previous state-of-the-art algorithms in terms of both objective and subjective evaluation standards. The recovery results of real captured images using unmanned aerial vehicles are also provided to further validate the effectiveness of the proposed method.

Background High density lipoprotein (HDL) infusions increase new blood vessel formation (angiogenesis) in rodents with ischemic injury. This study asks if increasing HDL levels by inhibiting cholesteryl ester transfer protein (CETP) activity increases angiogenesis in New Zealand White (NZW) rabbits with hindlimb ischemia. Methods and results NZW rabbits were maintained for 6weeks on chow or chow supplemented with 0.07% or 0.14% (wt/wt) of the CETP inhibitor, des-fluoro-anacetrapib. The left femoral artery was ligated after 2weeks of des-fluoro-anacetrapib treatment. The animals were sacrificed 4weeks after femoral artery ligation. Treatment with 0.07% and 0.14% (wt/wt) des-fluoro-anacetrapib reduced CETP activity by 63±12% and 81±8.6%, increased plasma apoA-I levels by 1.3±0.1- and 1.4±0.1-fold, and increased plasma HDL-cholesterol levels by 1.4±0.1- and 1.7±0.2-fold, respectively. Treatment with 0.07% and 0.14% (wt/wt) des-fluoro-anacetrapib increased the number of collateral arteries by 60±16% and 84±27%, and arteriole wall area in the ischemic hindlimbs by 84±16% and 94±13%, respectively. Capillary density in the ischemic hindlimb adductor muscle increased from 1.1±0.2 (control) to 2.1±0.3 and 2.2±0.4 in the 0.07% and 0.14% (wt/wt) des-fluoro-anacetrapib-treated animals, respectively. Incubation of HDLs from des-fluoro-anacetrapib-treated animals with human coronary artery endothelial cells at apoA-I concentrations comparable with their plasma levels increased tubule network formation. These effects were abolished by knockdown of scavenger receptor-B1 (SR-B1) and PDZK1, and pharmacological inhibition of PI3K/Akt. Conclusion Increasing HDL levels by inhibiting CETP activity is associated with increased collateral blood vessel formation in NZW rabbits with hindlimb ischemia in an SR-B1- and PI3K/Akt-dependent manner.

Objective— Angioplasty and stent implantation, the most common treatment for atherosclerotic lesions, have a significant failure rate because of restenosis. This study asks whether increasing plasma high-density lipoprotein (HDL) levels by inhibiting cholesteryl ester transfer protein activity with the anacetrapib analog, des-fluoro-anacetrapib, prevents stent-induced neointimal hyperplasia. Approach and Results— New Zealand White rabbits received normal chow or chow supplemented with 0.14% (wt/wt) des-fluoro-anacetrapib for 6 weeks. Iliac artery endothelial denudation and bare metal steel stent deployment were performed after 2 weeks of des-fluoro-anacetrapib treatment. The animals were euthanized 4 weeks poststent deployment. Relative to control, dietary supplementation with des-fluoro-anacetrapib reduced plasma cholesteryl ester transfer protein activity and increased plasma apolipoprotein A-I and HDL cholesterol levels by 53±6.3% and 120±19%, respectively. Non-HDL cholesterol levels were unaffected. Des-fluoro-anacetrapib treatment reduced the intimal area of the stented arteries by 43±5.6% ( P P P Conclusions— Inhibiting cholesteryl ester transfer protein activity in New Zealand White rabbits with iliac artery balloon injury and stent deployment increases HDL levels, inhibits vascular smooth muscle cell proliferation, and reduces neointimal hyperplasia in an scavenger receptor-B1, PDZ domain-containing protein 1– and phosphatidylinositol-3-kinase/Akt-dependent manner.

Txndc9 (thioredoxin domain containing protein 9) has been shown to be involved in mammalian mitosis; however, its function in mammalian oocyte meiosis remains unclear. In this study, we initially found that Txndc9 is expressed during meiotic maturation of mouse oocytes and higher expression of Txndc9 mRNA and protein occurred in germinal vesicle (GV) stage. By using confocal scanning, we observed that Txndc9 localized at both nucleus and cytoplasm, especially at spindle microtubules. Specific depletion of Txndc9 by siRNA in mouse oocyte resulted in decreasing the rate of first polar body extrusion and increasing abnormal spindle assemble. Moreover, knockdown of Txndc9 in germinal vesicle (GV) stage oocytes led to higher level of reactive oxygen species (ROS) and lower level of antioxidant glutathione (GSH) as compared with control oocytes, which indicated that Txndc9 may be involved in mediating the redox balance. In summary, our results demonstrated that Txndc9 is crucial for mouse oocyte maturation by regulating spindle assembly, polar body extrusion, and redox status.

Low cloning efficiency is considered to be caused by the incomplete or aberrant epigenetic reprogramming of differentiated donor cells in somatic cell nuclear transfer (SCNT) embryos. Oxamflatin, a novel class of histone deacetylase inhibitor (HDACi), has been found to improve the in vitro and full-term developmental potential of SCNT embryos. In the present study, we studied the effects of oxamflatin treatment on in vitro porcine SCNT embryos. Our results indicated that the rate of in vitro blastocyst formation of SCNT embryos treated with 1 μM oxamflatin for 15 h postactivation was significantly higher than all other treatments. Treatment of oxamflatin decreased the relative histone deacetylase (HDAC) activity in cloned embryos and resulted in hyperacetylation levels of histone H3 at lysine 9 (AcH3K9) and histone H4 at lysine 5 (AcH4K5) at pronuclear, two-cell, and four-cell stages partly through downregulating HDAC1. The suppression of HDAC6 through oxamflatin increased the nonhistone acetylation level of α-tubulin during the mitotic cell cycle of early SCNT embryos. In addition, we demonstrated that oxamflatin downregulated DNA methyltransferase 1 (DNMT1) expression and global DNA methylation level (5-methylcytosine) in two-cell-stage porcine SCNT embryos. The pluripotency-related gene POU5F1 was found to be upregulated in the oxamflatin-treated group with a decreased DNA methylation tendency in its promoter regions. Treatment of oxamflatin did not change the locus-specific DNA methylation levels of Sus scrofa heterochromatic satellite DNA sequences at the blastocyst stage. Meanwhile, our findings suggest that treatment with HDACi may contribute to maintaining the stable status of cytoskeleton-associated elements, such as acetylated α-tubulin, which may be the crucial determinants of donor nuclear reprogramming in early SCNT embryos. In summary, oxamflatin treatment improves the developmental potential of porcine SCNT embryos in vitro.

Objectives This study sought to evaluate the long-term safety and efficacy of everolimus-eluting stents (EES) and paclitaxel-eluting stents (PES) in patients with obstructive coronary artery disease. Background The use of EES compared to PES has been shown to result in improved clinical outcomes in patients undergoing PCI. However, there have been concerns regarding the durability of these benefits over longer-term follow-up. Methods SPIRIT III was a prospective, multicenter trial in which 1,002 patients were randomized 2:1 to EES versus PES. Endpoints included ischemia-driven target vessel failure (TVF) (death, myocardial infarction (MI), or ischemia-driven target vessel revascularization [TVR]), the pre-specified primary endpoint), target lesion failure (TLF) (cardiac death, target-vessel MI, or ischemia-driven target lesion revascularization [TLR]), major adverse cardiac events (MACE) (cardiac death, MI, or ischemia-driven TLR), their individual components and stent thrombosis. Results Five-year follow-up was available in 91.9% of patients. Treatment with EES versus PES resulted in lower 5-year Kaplan-Meier rates of TVF (19.3% vs. 24.5%, p = 0.05), TLF (12.7% vs. 19.0%, p = 0.008), and MACE (13.2% vs. 20.7%, p = 0.007). EES also resulted in reduced rates of all-cause death (5.9% vs. 10.1%, p = 0.02), with nonsignificantly different rates of MI, stent thrombosis, and TLR, and no evidence of late catch-up of TLR over time. Conclusions At 5 years after treatment, EES compared to PES resulted in durable benefits in composite safety and efficacy measures as well as all-cause mortality. Additionally, the absolute difference in TLR between devices remained stable over time without deterioration of effect during late follow-up.

Oxidative stress and amyloid-β (Aβ) formation are important processes that occur in Alzheimer's disease (AD). Amyloid formation is associated with the aggregation and precipitation of the Aβ peptide, while oxidative stress results from an imbalance in pro-oxidant/antioxidant homeostasis that produces harmful reactive oxygen species. The methionine-35 (Met35) residue of the Aβ peptide plays an important role in AD oxidative stress events and the associated neurotoxicity. We and other research groups previously demonstrated that in vitro oxidation of the Met35 side-chain to the sulfoxide (Met35red → Met35ox) impedes assembly and aggregation of monomeric Aβ peptide into protofibrils, the latter being the immediate precursors of amyloid plaques. Here, we report that Met35 oxidation state affects the stability of preexisting amyloid fibrils and plaques, where the Met35red → Met35ox process leads to changes in the morphology of filaments, protofibrils, mature fibrils, and loss of Congo red birefringence in senile plaques isolated from the brains of AD patients. The most notable differences were in fibril flexibility, as evidenced by changes from straight fibrils to irregularly shaped, rope-like fibrils. These findings suggest that the Met35 oxidation state and amyloid plaque formation may be intimately linked.

The aim of this study was to determine whether patients from the Clinical Evaluation of the XIENCE V Everolimus Eluting Coronary Stent System in the Treatment of Patients With de Novo Native Coronary Artery Lesions (SPIRIT) IV trial who underwent percutaneous coronary intervention, who had target lesions with jailed side branches, had improved clinical outcomes when treated with the XIENCE V versus Taxus Express 2 drug-eluting stent. In the SPIRIT III randomized trial, patients with target lesions with jailed side branches after XIENCE V compared with Taxus Express 2 implantation had lower 2-year rates of major adverse cardiac events. The SPIRIT IV trial represents a larger more diverse patient population compared with SPIRIT III. In the large-scale, prospective, multicenter, randomized SPIRIT IV trial, 3,687 patients who underwent coronary stenting with up to 3 de novo native coronary artery lesions were randomized 2:1 to receive XIENCE V versus Taxus Express 2 stents. Two-year clinical outcomes of patients with or without jailed side branches after stenting were compared. A jailed side branch was defined as any side branch >1.0 mm in diameter within the target segment being stented, excluding bifurcations deemed to require treatment. Of the 3,687 patients in SPIRIT IV, a total of 1,426 had side branches that were jailed during angioplasty of the target lesion. Patients with jailed side branches after XIENCE V compared with Taxus Express 2 implantation had significantly lower 2-year rates of target lesion failure (6.5% vs 11.9%, p = 0.001), major adverse cardiac events (6.6% vs 12.2%, p = 0.0008), ischemia-driven target vessel revascularization (4.1% vs 7.9%, p = 0.004), and stent thrombosis (0.6% vs 2.8%, p = 0.001). In conclusion, patients with jailed side branches after stenting with XIENCE V compared to Taxus Express 2 devices had superior clinical outcomes at 2 years in the large-scale randomized SPIRIT IV trial.