PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-25 (101)
 

Clipboard (0)
None

Select a Filter Below

Journals
more »
Year of Publication
more »
1.  Decline in Decreased Cephalosporin Susceptibility and Increase in Azithromycin Resistance in Neisseria gonorrhoeae, Canada 
Emerging Infectious Diseases  2016;22(1):65-67.
Antimicrobial resistance profiles were determined for Neisseria gonorrhoeae strains isolated in Canada during 2010–2014. The proportion of isolates with decreased susceptibility to cephalosporins declined significantly between 2011 and 2014, whereas azithromycin resistance increased significantly during that period. Continued surveillance of antimicrobial drug susceptibilities is imperative to inform treatment guidelines.
doi:10.3201/eid2201.151247
PMCID: PMC4696705  PMID: 26689114
Neisseria gonorrhoeae; gonorrhoea; gonorrhea; antimicrobial resistance; rates; bacteria; cephalosporins; susceptibility; azithromycin; Canada
2.  The role of orbital ultrasonography in distinguishing papilledema from pseudopapilledema 
Eye  2014;28(12):1425-1430.
Purpose
To determine the sensitivity and specificity of orbital ultrasonography in distinguishing papilledema from pseudopapilledema in adult patients.
Methods
The records of all adult patients referred to the neuro-ophthalmology service who underwent orbital ultrasonography for the evaluation of suspected papilledema were reviewed. The details of history, ophthalmologic examination, and results of ancillary testing including orbital ultrasonography, MRI, and lumbar puncture were recorded. Results of orbital ultrasonography were correlated with the final diagnosis of papilledema or pseudopapilledema on the basis of the clinical impression of the neuro-ophthalmologist. Ultrasound was considered positive when the optic nerve sheath diameter was ≥3.3 mm along with a positive 30° test.
Results
The sensitivity of orbital ultrasonography for detection of papilledema was 90% (CI: 80.2–99.3%) and the specificity in detecting pseudopapilledema was 79% (CI: 67.7–90.7%).
Conclusions
Orbital ultrasonography is a rapid and noninvasive test that is highly sensitive, but less specific in differentiating papilledema from pseudopapilledema in adult patients, and can be useful in guiding further management of patients in whom the diagnosis is initially uncertain.
doi:10.1038/eye.2014.210
PMCID: PMC4268455  PMID: 25190532
3.  Characteristics of Small Intestinal Diseases on Single-Balloon Enteroscopy 
Medicine  2015;94(42):e1652.
Abstract
The small intestine has been considered inaccessible for a long term. The development of single-balloon endoscopy has greatly improved the diagnosis and treatment possibilities for small intestinal diseases.
In this study, we aimed to explore the demographic characteristics and small intestinal diseases of patients who underwent single-balloon enteroscopy between 2009 and 2014 at our endoscopy center. We determined the enteroscopic findings for each small intestinal disease and the most susceptible age groups.
In total, 186 patients were included in the study. Their mean age was 45.87 ± 15.77 years. Patients who underwent single-balloon enteroscopy were found to have neoplasms (most common age group: 14–45 years, most common lesion location: jejunum), lymphoma (46–59 and 60–74 years, ileum), protuberant lesions (45–59 years, jejunum), inflammation (14–45 and 46–59 years, ileum), benign ulcers (14–45 years, jejunum), diverticulum (14–45 years, ileum), vascular malformations (60–74 years, jejunum), polyps (14–45 years, jejunum), Crohn's disease (14–45 years, jejunum), hookworm infection (14–45 years, jejunum), lipid pigmentation (14–45 and 46–59 years, jejunum), undetermined bleeding (46–59 years, ileum), or undetermined stenosis (31 years, duodenum). Each small intestinal disease had distinct enteroscopic findings.
doi:10.1097/MD.0000000000001652
PMCID: PMC4620798  PMID: 26496270
4.  BAC transgenic mice provide evidence that p53 expression is highly regulated in vivo 
Cell Death & Disease  2015;6(9):e1878-.
p53 is an important tumor suppressor and stress response mediator. Proper control of p53 level and activity is tightly associated with its function. Posttranslational modifications and the interactions with Mdm2 and Mdm4 are major mechanisms controlling p53 activity and stability. As p53 protein is short-lived and hardly detectable in unstressed situations, less is known on its basal level expression and the corresponding controlling mechanisms in vivo. In addition, it also remains obscure how p53 expression might contribute to its functional regulation. In this study, we established bacterial artificial chromosome transgenic E.coli β-galactosidase Z gene reporter mice to monitor p53 expression in mouse tissues and identify important regulatory elements critical for the expression in vivo. We revealed preferentially high level of p53 reporter expressions in the proliferating, but not the differentiated compartments of the majority of tissues during development and tissue homeostasis. In addition, tumors as well as regenerating tissues in the p53 reporter mice also expressed high level of β-gal. Furthermore, both the enhancer box sequence (CANNTG) in the p53 promoter and the 3′ terminal untranslated region element were critical in mediating the high-level expression of the reporter. We also provided evidence that cellular myelocytomatosis oncogene was a critical player regulating p53 mRNA expression in proliferating cells and tissues. Finally, we found robust p53 activation preferentially in the proliferating compartment of mouse tissues upon DNA damage and the proliferating cells exhibited an enhanced p53 response as compared with cells in a quiescent state. Together, these results suggested a highly regulated expression pattern of p53 in the proliferating compartment controlled by both transcriptional and posttranscriptional mechanisms, and such regulated p53 expression may impose functional significance upon stress by setting up a precautionary mode in defense of cellular transformation and tumorigenesis.
doi:10.1038/cddis.2015.224
PMCID: PMC4650433  PMID: 26379189
5.  A polymorphism in the DNA repair domain of APEX1 is associated with the radiation-induced pneumonitis risk among lung cancer patients after radiotherapy 
Li, H | Liu, G | Xia, L | Zhou, Q | Xiong, J | Xian, J | Du, M | Zhang, L | Liao, L | Su, X | Li, Z | Luo, Q | Cheng, Y | Zhang, T | Wang, D | Yang, Z-Z
The British Journal of Radiology  2014;87(1040):20140093.
Objective:
To examine the association of tag single nucleotide polymorphisms (tagSNPs) (rs1130409, rs1760944, rs2307486 and rs3136817) in APEX1 with the risk of severe radiation-induced pneumonitis (RP) after radiotherapy among Han Chinese patients with lung cancer.
Methods:
A total of 168 patients with lung cancer who were receiving radiotherapy were prospectively recruited. RP was evaluated according to the Radiation Therapy Oncology Group. A case–control study was performed. The case group included patients with RP grade of ≥3, while the control group comprised patients with RP grades <3. Four tagSNPs of APEX1 were genotyped in 126 patients with complete follow-up by multi-SNaPshot® (Genesky Biotechnologies Inc., Shanghai, China) genotyping assays. Results were assessed by a logistic regression model for RP risk and Mantal–Cox log-rank test for the cumulative RP probability by the genotypes.
Results:
rs1130409 was associated with severe RP. GT genotype of rs1130409 was significantly higher in patients with RP than in those of the control group [68.8% vs 41.8%; p = 0.025; resulting odds ratio (OR), 5.98]. Patients with lung cancer bearing the G allele had a 5.83-fold higher risk of RP than those with the wild TT genotype [OR = 5.83; 95% confidence interval (CI), 1.27–26.90; p = 0.024], and this was further confirmed by the binary regression adjusted by some confounding factors, including Karnofsky performance scale, concurrent chemotherapy–radiotherapy and lung volume receiving >30 Gy (OR = 6.96; 95% CI, 1.36–35.77; p = 0.02). rs1130409 was also associated with the time to occurrence of severe RP (p = 0.04). Three-dimensional model APEX1 protein showed that rs1130409 is located in the random coil structure corresponding to the DNA repair function region.
Advances in knowledge:
rs1130409 of APEX1 can be a predictor of RP grades ≥3 among patients with lung cancer.
doi:10.1259/bjr.20140093
PMCID: PMC4112388  PMID: 24884729
6.  Shear stress regulates endothelial cell autophagy via redox regulation and Sirt1 expression 
Cell Death & Disease  2015;6(7):e1827-.
Disturbed cell autophagy is found in various cardiovascular disease conditions. Biomechanical stimuli induced by laminar blood flow have important protective actions against the development of various vascular diseases. However, the impacts and underlying mechanisms of shear stress on the autophagic process in vascular endothelial cells (ECs) are not entirely understood. Here we investigated the impacts of shear stress on autophagy in human vascular ECs. We found that shear stress induced by laminar flow, but not that by oscillatory or low-magnitude flow, promoted autophagy. Time-course analysis and flow cessation experiments confirmed that this effect was not a transient adaptive stress response but appeared to be a sustained physiological action. Flow had no effect on the mammalian target of rapamycin-ULK pathway, whereas it significantly upregulated Sirt1 expression. Inhibition of Sirt1 blunted shear stress-induced autophagy. Overexpression of wild-type Sirt1, but not the deacetylase-dead mutant, was sufficient to induce autophagy in ECs. Using both of gain- and loss-of-function experiments, we showed that Sirt1-dependent activation of FoxO1 was critical in mediating shear stress-induced autophagy. Shear stress also induced deacetylation of Atg5 and Atg7. Moreover, shear stress-induced Sirt1 expression and autophagy were redox dependent, whereas Sirt1 might act as a redox-sensitive transducer mediating reactive oxygen species-elicited autophagy. Functionally, we demonstrated that flow-conditioned cells are more resistant to oxidant-induced cell injury, and this cytoprotective effect was abolished after inhibition of autophagy. In summary, these results suggest that Sirt1-mediated autophagy in ECs may be a novel mechanism by which laminar flow produces its vascular-protective actions.
doi:10.1038/cddis.2015.193
PMCID: PMC4650738  PMID: 26181207
7.  Wnt pathway aberrations including autocrine Wnt activation occur at high frequency in human non-small-cell lung carcinoma 
Oncogene  2009;28(21):2163-2172.
Lung cancer is the most common cause of cancer mortality worldwide. Non-small-cell lung carcinomas (NSCLCs), which represent around 80% of lung tumors, exhibit poor prognosis and are usually refractory to conventional chemotherapy. Elucidating the molecular and cellular mechanisms that are dysregulated in NSCLCs may lead to new possibilities for targeted therapy or enhanced efficacy of current therapies. Here we demonstrate Wnt pathway activation in around 50% of human NSCLC cell lines and primary tumors, through different mechanisms, including autocrine Wnt pathway activation involving upregulation of specific Wnt ligands. Downregulation of activated Wnt signaling inhibited NSCLC proliferation and induced a more differentiated phenotype. Together, our findings establish importance of activated Wnt signaling in human NSCLCs and offer the possibility of targeting upregulated Wnt signaling as a new therapeutic modality for this disease.
doi:10.1038/onc.2009.82
PMCID: PMC4451819  PMID: 19377513
autocrine; lung cancer; wnt
8.  Comparative pathogenicity of Coxsackievirus A16 circulating and noncirculating strains in vitro and in a neonatal mouse model 
An enterovirus 71 (EV71) vaccine for the prevention of hand, foot, and mouth disease (HMFD) is available, but it is not known whether the EV71 vaccine cross-protects against Coxsackievirus (CV) infection. Furthermore, although an inactivated circulating CVA16 Changchun 024 (CC024) strain vaccine candidate is effective in newborn mice, the CC024 strain causes severe lesions in muscle and lung tissues. Therefore, an effective CV vaccine with improved pathogenic safety is needed. The aim of this study was to evaluate the in vivo safety and in vitro replication capability of a noncirculating CVA16 SHZH05 strain. The replication capacity of circulating CVA16 strains CC024, CC045, CC090 and CC163 and the noncirculating SHZH05 strain was evaluated by cytopathic effect in different cell lines. The replication capacity and pathogenicity of the CC024 and SHZH05 strains were also evaluated in a neonatal mouse model. Histopathological and viral load analyses demonstrated that the SHZH05 strain had an in vitro replication capacity comparable to the four CC strains. The CC024, but not the SHZH05 strain, became distributed in a variety of tissues and caused severe lesions and mortality in neonatal mice. The differences in replication capacity and in vivo pathogenicity of the CC024 and SHZH05 strains may result from differences in the nucleotide and amino acid sequences of viral functional polyproteins P1, P2 and P3. Our findings suggest that the noncirculating SHZH05 strain may be a safer CV vaccine candidate than the CC024 strain.
doi:10.1590/1414-431X20144298
PMCID: PMC4445665  PMID: 25831207
Coxsackievirus A16; Pathogenicity; Circulating strain; Non-circulating strain
9.  Dexamethasone and sodium carboxymethyl cellulose prevent postoperative intraperitoneal adhesions in rats 
We aimed to evaluate the effects of the barrier agent sodium carboxymethyl cellulose (SCMC) with and without dexamethasone for the prevention of postoperative adhesion formation in a rat model of postoperative peritoneal adhesion. A total of 160 three-month old male and female Wistar rats underwent a laparotomy, and adhesions were induced by ileocecal abrasion. Rats were randomly assigned to 4 groups (n=40 each): group A, untreated; group B, treated with SCMC only; group C1, treated with SCMC + 3 mg dexamethasone, and group C2, treated with SCMC + 8 mg dexamethasone. After 12 days, adhesion formation and histopathological changes were compared. In groups A, B, C1, and C2, the mortality rates were 10, 5, 5, and 5%, respectively. In groups C1 and C2, the adhesions were filmy and easy to dissect and were milder compared with those in groups A and B. The total adhesion score in group C1 (3.38±0.49) was significantly lower than that of group B (6.01±0.57; P<0.01) or group A (8.01±0.67; P<0.05). There was no significant difference in adhesion formation between groups C1 and C2. Compared with groups A and B, groups C1 and C2 exhibited milder histopathological changes. SCMC in combination with dexamethasone can prevent adhesion formation and is a better barrier agent than SCMC alone. The safety and feasibility of SCMC in combination with dexamethasone to prevent adhesion formation after abdominal surgery warrants further clinical study.
doi:10.1590/1414-431X20144211
PMCID: PMC4418365  PMID: 25714889
Dexamethasone; Sodium carboxymethyl cellulose; Adhesions
10.  ROLE OF MITOCHONDRIAL hOGG1 AND ACONITASE IN OXIDANT-INDUCED LUNG EPITHELIAL CELL APOPTOSIS 
Free radical biology & medicine  2009;47(6):750-759.
8-oxoguanine DNA glycosylase (Oggl) repairs 8-oxo-7,8-dihydroxyguanine (8-oxoG), one of the most abundant DNA adducts caused by oxidative stress. In the mitochondria, Oggl is thought to prevent activation of the intrinsic apoptotic pathway in response to oxidative stress by augmenting DNA repair. However, the predominance of the β-Oggl isoform, which lacks 8-oxoG DNA glycosylase activity, suggests that mitochondrial Oggl functions in a role independent of DNA repair. We report here that overexpression of mitochondria-targeted human α-hOggl (mt-hOggl) in human lung adenocarcinoma cells with some alveolar epithelial cell characteristics (A549 cells) prevents oxidant-induced mitochondrial dysfunction and apoptosis by preserving mitochondrial aconitase. Importantly, mitochondrial α-hOggl mutants lacking 8-oxoG DNA repair activity were as effective as wild-type mt-hOggl in preventing oxidant-induced caspase-9 activation, reductions in mitochondrial aconitase and apoptosis suggesting that the protective effects of mt-hOgg 1 occur independent of DNA repair. Notably, wild-type and mutant mt-hOggl co-precipitate with mitochondrial aconitase. Furthermore, overexpression of mitochondrial aconitase abolishes oxidant-induced apoptosis whereas hOggl silencing using shRNA reduces mitochondrial aconitase and augments apoptosis. These findings suggest a novel mechanism that mt-hOggl acts as a mitochondrial aconitase chaperone protein to prevent oxidant-mediated mitochondrial dysfunction and apoptosis that might be important in the molecular events underlying oxidant-induced toxicity.
doi:10.1016/j.freeradbiomed.2009.06.010
PMCID: PMC4331123  PMID: 19524665
DNA repair; aconitase; Oggl; free radicals; asbestos; mitochondria
11.  Andrographolide suppresses RANKL-induced osteoclastogenesis in vitro and prevents inflammatory bone loss in vivo 
British Journal of Pharmacology  2014;171(3):663-675.
Background and Purpose
Osteoclasts play a pivotal role in diseases such as osteoporosis, rheumatoid arthritis and tumour bone metastasis. Thus, searching for natural compounds that may suppress osteoclast formation and/or function is promising for the treatment of osteoclast-related diseases. Here, we examined changes in osteoclastogenesis and LPS-induced osteolysis in response to andrographolide (AP), a diterpenoid lactone isolated from the traditional Chinese and Indian medicinal plant Andrographis paniculata.
Experimental Approach
Effects of AP on osteoclast differentiation and bone resorption were measured in vitro. Western blots and RT-PCR techniques were used to examine the underlying molecular mechanisms. The bone protective activity of AP in vivo was assessed in a mouse model of osteolysis.
Key Results
AP concentration-dependently suppressed RANKL-mediated osteoclast differentiation and bone resorption in vitro and reduced the expression of osteoclast-specific markers, including tartrate-resistant acid phosphatase, calcitonin receptors and cathepsin K. Further molecular analysis revealed that AP impaired RANKL-induced NF-κB signalling by inhibiting the phosphorylation of TGF-β-activated kinase 1, suppressing the phosphorylation and degradation of IκBα, and subsequently preventing the nuclear translocation of the NF-κB p65 subunit. AP also inhibited the ERK/MAPK signalling pathway without affecting p38 or JNK signalling.
Conclusions and Implications
AP suppressed RANKL-induced osteoclastogenesis through attenuating NF-κB and ERK/MAPK signalling pathways in vitro, thus preventing bone loss in vivo. These data indicated that AP is a promising natural compound for the treatment of osteoclast-related bone diseases.
doi:10.1111/bph.12463
PMCID: PMC3969079  PMID: 24125472
andrographolide; osteoclast; osteolysis; NF-κB; ERK
12.  Liraglutide inhibits autophagy and apoptosis induced by high glucose through GLP-1R in renal tubular epithelial cells 
ZHAO, X | LIU, G | SHEN, H | GAO, B | LI, X | FU, J | ZHOU, J | JI, Q
Tubular atrophy and dysfunction is a critical process underlying diabetic nephropathy (DN). Understanding the mechanisms underlying renal tubular epithelial cell survival is important for the prevention of kidney failure associated with glucotoxicity. Autophagy is a cellular pathway involved in protein and organelle degradation. It is associated with many types of cellular homeostasis and human diseases. To date, little is known of the association between high concentrations of glucose and autophagy in renal tubular cells. In the present study, we investigated high glucose-induced toxicity in renal tubular epithelial cells by means of several complementary assays, including cell viability, cell death assays and changes in ultrastructure in an immortalized human kidney cell line, HK-2 cells. The extent of apoptosis was significantly increased in the HK-2 cells following treatment with high levels of glucose. In addition, in in vivo experiments using diabetic rats, high glucose exerted harmful effects on the tissue structure of the kidneys in the diabetic rats. Chronic exposure of the HK-2 cells and tubular epithelial cells of nephritic rats to high levels of glucose induced autophagy. Liraglutide inhibited these effects; however, treatment witht a glucagon-like peptide-1 receptor (GLP-1R) antagonist enhanced these effects. Our results also indicated that the exposure of the renal tubular epithelial cells to high glucose concentrations in vitro led to the downregulation of GLP-1R expression. Liraglutide reversed this effect, while the GLP-1R antagonist promoted it, promoting autophagy, suggesting that liraglutide exerts a renoprotective effect in the presence of high glucose, at least in part, by inhibiting autophagy and increasing GLP-1R expression in the HK-2 cells and kidneys of diabetic rats.
doi:10.3892/ijmm.2014.2052
PMCID: PMC4314412  PMID: 25573030
high glucose; autophagy; autophagy-related gene; glucagon-like peptide-1 receptor; liraglutide
13.  In Vitro and In Vivo Imaging of Peptide-Encapsulated Polymer Nanoparticles for Cancer Biomarker Activated Drug Delivery 
Gelatin nanoparticles coated with Cathepsin D-specific peptides were developed as a vehicle for the targeted delivery of the cancer drug doxorubicin (DOX) to treat breast malignancy. Cathepsin D, a breast cancer cell secretion enzyme, triggered the release of DOX by digesting the protective peptide-coating layer of nanoparticles. Fabricated nanoparticles were successfully detected with ultrasound imaging in both in vitro conditions and in vivo mouse cancer models. Cell viability experiments were conducted to determine the efficacy of biomarker activation specific to breast cancer cell lines. These experimental results were compared with the outcome of a viability experiment conducted on noncancerous cells. Viability decreased in human MCF7 mammary adenocarcinoma and mouse 4T1 mammary carcinoma cells, while that of noncancerous 3T3 fibroblast cells remained unaffected. Next, a real-time video of nanoparticle flow in mouse models was obtained using in vivo ultrasound imaging. The fluorescent profile of DOX was used as a means to examine nanoparticle localization in vivo. Results show the distribution of nanoparticles concentrated primarily within bladder and tumor sites of subject mice bodies. These findings support the use of biomarker coated nanoparticles in target specific therapy for breast cancer treatment.
doi:10.1109/TNB.2013.2274781
PMCID: PMC3962524  PMID: 23955780
Chemotherapy; doxorubicin; gelatin nanoparticles; in vivo ultrasound imaging; targeted drug delivery
14.  Propofol pretreatment attenuates lipopolysaccharide-induced acute lung injury in rats by activating the phosphoinositide-3-kinase/Akt pathway 
The aim of this study was to investigate the effect of propofol pretreatment on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the role of the phosphoinositide-3-kinase/protein kinase B (PI3K/Akt) pathway in this procedure. Survival was determined 48 h after LPS injection. At 1 h after LPS challenge, the lung wet- to dry-weight ratio was examined, and concentrations of protein, tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) in bronchoalveolar lavage fluid (BALF) were determined using the bicinchoninic acid method or ELISA. Lung injury was assayed via lung histological examination. PI3K and p-Akt expression levels in the lung tissue were determined by Western blotting. Propofol pretreatment prolonged survival, decreased the concentrations of protein, TNF-α, and IL-6 in BALF, attenuated ALI, and increased PI3K and p-Akt expression in the lung tissue of LPS-challenged rats, whereas treatment with wortmannin, a PI3K/Akt pathway specific inhibitor, blunted this effect. Our study indicates that propofol pretreatment attenuated LPS-induced ALI, partly by activation of the PI3K/Akt pathway.
doi:10.1590/1414-431X20143949
PMCID: PMC4244672  PMID: 25387673
Acute lung injury; Propofol; Lipopolysaccharide; PI3K/Akt pathway
15.  A regulatory circuit that involves HR23B and HDAC6 governs the biological response to HDAC inhibitors 
Cell Death and Differentiation  2013;20(10):1306-1316.
Histone deacetylase (HDAC) is an emergent anticancer target, and HR23B is a biomarker for response to HDAC inhibitors. We show here that HR23B has impacts on two documented effects of HDAC inhibitors; HDAC inhibitors cause apoptosis in cells expressing high levels of HR23B, whereas in cells with low level expression, HDAC inhibitor treatment is frequently associated with autophagy. The mechanism responsible involves the interaction of HDAC6 with HR23B, which downregulates HR23B and thereby reduces the level of ubiquitinated substrates targeted to the proteasome, ultimately desensitising cells to apoptosis. Significantly, the ability of HDAC6 to downregulate HR23B occurs independently of its deacetylase activity. An analysis of the HDAC6 interactome identified HSP90 as a key effector of HDAC6 on HR23B levels. Our results define a regulatory mechanism that involves the interplay between HR23B and HDAC6 that influences the biological outcome of HDAC inhibitor treatment.
doi:10.1038/cdd.2013.47
PMCID: PMC3770323  PMID: 23703321
cancer; HDAC inhibitor; biology
16.  A novel urine peptide biomarker-based algorithm for the prognosis of necrotising enterocolitis in human infants 
Gut  2013;63(8):1284-1292.
Objective
Necrotising enterocolitis (NEC) is a major source of neonatal morbidity and mortality. The management of infants with NEC is currently complicated by our inability to accurately identify those at risk for progression of disease prior to the development of irreversible intestinal necrosis. We hypothesised that integrated analysis of clinical parameters in combination with urine peptide biomarkers would lead to improved prognostic accuracy in the NEC population.
Design
Infants under suspicion of having NEC (n=550) were prospectively enrolled from a consortium consisting of eight university-based paediatric teaching hospitals. Twenty-seven clinical parameters were used to construct a multivariate predictor of NEC progression. Liquid chromatography/mass spectrometry was used to profile the urine peptidomes from a subset of this population (n=65) to discover novel biomarkers of NEC progression. An ensemble model for the prediction of disease progression was then created using clinical and biomarker data.
Results
The use of clinical parameters alone resulted in a receiver-operator characteristic curve with an area under the curve of 0.817 and left 40.1% of all patients in an ‘indeterminate’ risk group. Three validated urine peptide biomarkers (fibrinogen peptides: FGA1826, FGA1883 and FGA2659) produced a receiver-operator characteristic area under the curve of 0.856. The integration of clinical parameters with urine biomarkers in an ensemble model resulted in the correct prediction of NEC outcomes in all cases tested.
Conclusions
Ensemble modelling combining clinical parameters with biomarker analysis dramatically improves our ability to identify the population at risk for developing progressive NEC.
doi:10.1136/gutjnl-2013-305130
PMCID: PMC4161026  PMID: 24048736
17.  Expression analysis of miRNA and target mRNAs in esophageal cancer 
We aimed to investigate miRNAs and related mRNAs through a network-based approach in order to learn the crucial role that they play in the biological processes of esophageal cancer. Esophageal squamous-cell carcinoma (ESCC) and adenocarcinoma (EAC)-related miRNA and gene expression data were downloaded from the Gene Expression Omnibus database, and differentially expressed miRNAs and genes were selected. Target genes of differentially expressed miRNAs were predicted and their regulatory networks were constructed. Differentially expressed miRNA analysis selected four miRNAs associated with EAC and ESCC, among which hsa-miR-21 and hsa-miR-202 were shared by both diseases. hsa-miR-202 was reported for the first time to be associated with esophageal cancer in the present study. Differentially expressed miRNA target genes were mainly involved in cancer-related and signal-transduction pathways. Functional categories of these target genes were related to transcriptional regulation. The results may indicate potential target miRNAs and genes for future investigations of esophageal cancer.
doi:10.1590/1414-431X20143906
PMCID: PMC4143210  PMID: 25098614
Esophageal adenocarcinoma; Esophageal squamous-cell carcinoma; miRNA expression network; Pathway; Gene ontology
18.  Usp9x- and Noxa-mediated Mcl-1 downregulation contributes to pemetrexed-induced apoptosis in human non-small-cell lung cancer cells 
Yan, J | Zhong, N | Liu, G | Chen, K | Liu, X | Su, L | Singhal, S
Cell Death & Disease  2014;5(7):e1316-.
Pemetrexed, a folate antimetabolite, combined with cisplatin is used as a first-line therapy for malignant pleural mesothelioma (MPM) and locally advanced or metastatic non-small-cell lung cancer (NSCLC). Pemetrexed arrests cell cycle by inhibiting three enzymes in purine and pyrimidine synthesis that are necessary for DNA synthesis. Pemetrexed also promotes apoptosis in target cells, but little is known about its mechanism in cancer cells. We have previously shown that pemetrexed can result in endoplasmic reticulum (ER) stress, and it can lead to downstream apoptosis. In this study, we further elucidate this mechanism. Our data show that pemetrexed increases Noxa expression through activating transcription factor 4 (ATF4) and activating transcription factor 3 (ATF3) upregulation. Furthermore, pemetrexed induces apoptosis by activating the Noxa–Usp9x–Mcl-1 pathway. Inhibition of Noxa by small interfering RNA (siRNA) promotes Usp9x (ubiquitin-specific peptidase 9, X-linked) expression. Moreover, downregulation of the deubiquitinase Usp9x by pemetrexed results in downstream reduction of myeloid cell leukemia 1 (Mcl-1) expression. Mechanistically, Noxa upregulation likely reduces the availability of Usp9x to Mcl-1, thereby promoting its ubiquitination and degradation, leading to the apoptosis of neoplastic cells. Thus, our findings demonstrate that Noxa–Usp9x-Mcl–1 axis may contribute to pemetrexed-induced apoptosis in human lung cancer cells.
doi:10.1038/cddis.2014.281
PMCID: PMC4123075  PMID: 24991768
19.  Measurement of charged particle multiplicities and densities in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$pp$$\end{document}pp collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}=7\;$$\end{document}s=7TeV in the forward region 
Aaij, R. | Adeva, B. | Adinolfi, M. | Affolder, A. | Ajaltouni, Z. | Albrecht, J. | Alessio, F. | Alexander, M. | Ali, S. | Alkhazov, G. | Alvarez Cartelle, P. | Alves, A. A. | Amato, S. | Amerio, S. | Amhis, Y. | Anderlini, L. | Anderson, J. | Andreassen, R. | Andreotti, M. | Andrews, J. E. | Appleby, R. B. | Aquines Gutierrez, O. | Archilli, F. | Artamonov, A. | Artuso, M. | Aslanides, E. | Auriemma, G. | Baalouch, M. | Bachmann, S. | Back, J. J. | Badalov, A. | Balagura, V. | Baldini, W. | Barlow, R. J. | Barschel, C. | Barsuk, S. | Barter, W. | Batozskaya, V. | Bauer, Th. | Bay, A. | Beddow, J. | Bedeschi, F. | Bediaga, I. | Belogurov, S. | Belous, K. | Belyaev, I. | Ben-Haim, E. | Bencivenni, G. | Benson, S. | Benton, J. | Berezhnoy, A. | Bernet, R. | Bettler, M.-O. | van Beuzekom, M. | Bien, A. | Bifani, S. | Bird, T. | Bizzeti, A. | Bjørnstad, P. M. | Blake, T. | Blanc, F. | Blouw, J. | Blusk, S. | Bocci, V. | Bondar, A. | Bondar, N. | Bonivento, W. | Borghi, S. | Borgia, A. | Borsato, M. | Bowcock, T. J. V. | Bowen, E. | Bozzi, C. | Brambach, T. | vanden Brand, J. | Bressieux, J. | Brett, D. | Britsch, M. | Britton, T. | Brook, N. H. | Brown, H. | Bursche, A. | Busetto, G. | Buytaert, J. | Cadeddu, S. | Calabrese, R. | Callot, O. | Calvi, M. | Calvo Gomez, M. | Camboni, A. | Campana, P. | Campora Perez, D. | Carbone, A. | Carboni, G. | Cardinale, R. | Cardini, A. | Carranza-Mejia, H. | Carson, L. | Carvalho Akiba, K. | Casse, G. | Cassina, L. | Castillo Garcia, L. | Cattaneo, M. | Cauet, Ch. | Cenci, R. | Charles, M. | Charpentier, Ph. | Cheung, S.-F. | Chiapolini, N. | Chrzaszcz, M. | Ciba, K. | Cid Vidal, X. | Ciezarek, G. | Clarke, P. E. L. | Clemencic, M. | Cliff, H. V. | Closier, J. | Coca, C. | Coco, V. | Cogan, J. | Cogneras, E. | Collins, P. | Comerma-Montells, A. | Contu, A. | Cook, A. | Coombes, M. | Coquereau, S. | Corti, G. | Counts, I. | Couturier, B. | Cowan, G. A. | Craik, D. C. | Cruz Torres, M. | Cunliffe, S. | Currie, R. | D’Ambrosio, C. | Dalseno, J. | David, P. | David, P. N. Y. | Davis, A. | De Bonis, I. | De Bruyn, K. | De Capua, S. | De Cian, M. | De Miranda, J. M. | De Paula, L. | De Silva, W. | De Simone, P. | Decamp, D. | Deckenhoff, M. | Del Buono, L. | Déléage, N. | Derkach, D. | Deschamps, O. | Dettori, F. | Di Canto, A. | Dijkstra, H. | Donleavy, S. | Dordei, F. | Dorigo, M. | Dorosz, P. | Dosil Suárez, A. | Dossett, D. | Dovbnya, A. | Dupertuis, F. | Durante, P. | Dzhelyadin, R. | Dziurda, A. | Dzyuba, A. | Easo, S. | Egede, U. | Egorychev, V. | Eidelman, S. | Eisenhardt, S. | Eitschberger, U. | Ekelhof, R. | Eklund, L. | El Rifai, I. | Elsasser, Ch. | Esen, S. | Falabella, A. | Färber, C. | Farinelli, C. | Farry, S. | Ferguson, D. | Fernandez Albor, V. | Ferreira Rodrigues, F. | Ferro-Luzzi, M. | Filippov, S. | Fiore, M. | Fiorini, M. | Fitzpatrick, C. | Fontana, M. | Fontanelli, F. | Forty, R. | Francisco, O. | Frank, M. | Frei, C. | Frosini, M. | Fu, J. | Furfaro, E. | Gallas Torreira, A. | Galli, D. | Gandelman, M. | Gandini, P. | Gao, Y. | Garofoli, J. | Garra Tico, J. | Garrido, L. | Gaspar, C. | Gauld, R. | Gavardi, L. | Gersabeck, E. | Gersabeck, M. | Gershon, T. | Ghez, Ph. | Gianelle, A. | Giani, S. | Gibson, V. | Giubega, L. | Gligorov, V. V. | Göbel, C. | Golubkov, D. | Golutvin, A. | Gomes, A. | Gordon, H. | Grabalosa Gándara, M. | Graciani Diaz, R. | Granado Cardoso, L. A. | Graugés, E. | Graziani, G. | Grecu, A. | Greening, E. | Gregson, S. | Griffith, P. | Grillo, L. | Grünberg, O. | Gui, B. | Gushchin, E. | Guz, Yu. | Gys, T. | Hadjivasiliou, C. | Haefeli, G. | Haen, C. | Hafkenscheid, T. W. | Haines, S. C. | Hall, S. | Hamilton, B. | Hampson, T. | Hansmann-Menzemer, S. | Harnew, N. | Harnew, S. T. | Harrison, J. | Hartmann, T. | He, J. | Head, T. | Heijne, V. | Hennessy, K. | Henrard, P. | Henry, L. | Hernando Morata, J. A. | van Herwijnen, E. | Heß, M. | Hicheur, A. | Hill, D. | Hoballah, M. | Hombach, C. | Hulsbergen, W. | Hunt, P. | Hussain, N. | Hutchcroft, D. | Hynds, D. | Iakovenko, V. | Idzik, M. | Ilten, P. | Jacobsson, R. | Jaeger, A. | Jans, E. | Jaton, P. | Jawahery, A. | Jing, F. | John, M. | Johnson, D. | Jones, C. R. | Joram, C. | Jost, B. | Jurik, N. | Kaballo, M. | Kandybei, S. | Kanso, W. | Karacson, M. | Karbach, T. M. | Kelsey, M. | Kenyon, I. R. | Ketel, T. | Khanji, B. | Khurewathanakul, C. | Klaver, S. | Kochebina, O. | Komarov, I. | Koopman, R. F. | Koppenburg, P. | Korolev, M. | Kozlinskiy, A. | Kravchuk, L. | Kreplin, K. | Kreps, M. | Krocker, G. | Krokovny, P. | Kruse, F. | Kucharczyk, M. | Kudryavtsev, V. | Kurek, K. | Kvaratskheliya, T. | La Thi, V. N. | Lacarrere, D. | Lafferty, G. | Lai, A. | Lambert, D. | Lambert, R. W. | Lanciotti, E. | Lanfranchi, G. | Langenbruch, C. | Latham, T. | Lazzeroni, C. | Le Gac, R. | van Leerdam, J. | Lees, J.-P. | Lefèvre, R. | Leflat, A. | Lefrançois, J. | Leo, S. | Leroy, O. | Lesiak, T. | Leverington, B. | Li, Y. | Liles, M. | Lindner, R. | Linn, C. | Lionetto, F. | Liu, B. | Liu, G. | Lohn, S. | Longstaff, I. | Lopes, J. H. | Lopez-March, N. | Lowdon, P. | Lu, H. | Lucchesi, D. | Luisier, J. | Luo, H. | Luppi, E. | Lupton, O. | Machefert, F. | Machikhiliyan, I. V. | Maciuc, F. | Maev, O. | Malde, S. | Manca, G. | Mancinelli, G. | Manzali, M. | Maratas, J. | Marconi, U. | Marino, P. | Märki, R. | Marks, J. | Martellotti, G. | Martens, A. | Martín Sánchez, A. | Martinelli, M. | Martinez Santos, D. | Martinez Vidal, F. | Martins Tostes, D. | Massafferri, A. | Matev, R. | Mathe, Z. | Matteuzzi, C. | Mazurov, A. | McCann, M. | McCarthy, J. | McNab, A. | McNulty, R. | McSkelly, B. | Meadows, B. | Meier, F. | Meissner, M. | Merk, M. | Milanes, D. A. | Minard, M.-N. | Molina Rodriguez, J. | Monteil, S. | Moran, D. | Morandin, M. | Morawski, P. | Mordà, A. | Morello, M. J. | Mountain, R. | Muheim, F. | Müller, K. | Muresan, R. | Muryn, B. | Muster, B. | Naik, P. | Nakada, T. | Nandakumar, R. | Nasteva, I. | Needham, M. | Neri, N. | Neubert, S. | Neufeld, N. | Nguyen, A. D. | Nguyen, T. D. | Nguyen-Mau, C. | Nicol, M. | Niess, V. | Niet, R. | Nikitin, N. | Nikodem, T. | Novoselov, A. | Oblakowska-Mucha, A. | Obraztsov, V. | Oggero, S. | Ogilvy, S. | Okhrimenko, O. | Oldeman, R. | Onderwater, G. | Orlandea, M. | Otalora Goicochea, J. M. | Owen, P. | Oyanguren, A. | Pal, B. K. | Palano, A. | Palombo, F. | Palutan, M. | Panman, J. | Papanestis, A. | Pappagallo, M. | Pappalardo, L. | Parkes, C. | Parkinson, C. J. | Passaleva, G. | Patel, G. D. | Patel, M. | Patrignani, C. | Pavel-Nicorescu, C. | Pazos Alvarez, A. | Pearce, A. | Pellegrino, A. | Penso, G. | Pepe Altarelli, M. | Perazzini, S. | Perez Trigo, E. | Perret, P. | Perrin-Terrin, M. | Pescatore, L. | Pesen, E. | Pessina, G. | Petridis, K. | Petrolini, A. | Picatoste Olloqui, E. | Pietrzyk, B. | Pilař, T. | Pinci, D. | Pistone, A. | Playfer, S. | Plo Casasus, M. | Polci, F. | Polok, G. | Poluektov, A. | Polycarpo, E. | Popov, A. | Popov, D. | Popovici, B. | Potterat, C. | Powell, A. | Prisciandaro, J. | Pritchard, A. | Prouve, C. | Pugatch, V. | Puig Navarro, A. | Punzi, G. | Qian, W. | Rachwal, B. | Rademacker, J. H. | Rakotomiaramanana, B. | Rama, M. | Rangel, M. S. | Raniuk, I. | Rauschmayr, N. | Raven, G. | Redford, S. | Reichert, S. | Reid, M. M. | dos Reis, A. C. | Ricciardi, S. | Richards, A. | Rinnert, K. | Rives Molina, V. | Roa Romero, D. A. | Robbe, P. | Roberts, D. A. | Rodrigues, A. B. | Rodrigues, E. | Rodriguez Perez, P. | Roiser, S. | Romanovsky, V. | Romero Vidal, A. | Rotondo, M. | Rouvinet, J. | Ruf, T. | Ruffini, F. | Ruiz, H. | Ruiz Valls, P. | Sabatino, G. | Saborido Silva, J. J. | Sagidova, N. | Sail, P. | Saitta, B. | Salustino Guimaraes, V. | Sanmartin Sedes, B. | Santacesaria, R. | Santamarina Rios, C. | Santovetti, E. | Sapunov, M. | Sarti, A. | Satriano, C. | Satta, A. | Savrie, M. | Savrina, D. | Schiller, M. | Schindler, H. | Schlupp, M. | Schmelling, M. | Schmidt, B. | Schneider, O. | Schopper, A. | Schune, M.-H. | Schwemmer, R. | Sciascia, B. | Sciubba, A. | Seco, M. | Semennikov, A. | Senderowska, K. | Sepp, I. | Serra, N. | Serrano, J. | Seyfert, P. | Shapkin, M. | Shapoval, I. | Shcheglov, Y. | Shears, T. | Shekhtman, L. | Shevchenko, O. | Shevchenko, V. | Shires, A. | Silva Coutinho, R. | Simi, G. | Sirendi, M. | Skidmore, N. | Skwarnicki, T. | Smith, N. A. | Smith, E. | Smith, E. | Smith, J. | Smith, M. | Snoek, H. | Sokoloff, M. D. | Soler, F. J. P. | Soomro, F. | Souza, D. | De Paula, B. Souza | Spaan, B. | Sparkes, A. | Spinella, F. | Spradlin, P. | Stagni, F. | Stahl, S. | Steinkamp, O. | Stevenson, S. | Stoica, S. | Stone, S. | Storaci, B. | Stracka, S. | Straticiuc, M. | Straumann, U. | Stroili, R. | Subbiah, V. K. | Sun, L. | Sutcliffe, W. | Swientek, S. | Syropoulos, V. | Szczekowski, M. | Szczypka, P. | Szilard, D. | Szumlak, T. | T’Jampens, S. | Teklishyn, M. | Tellarini, G. | Teodorescu, E. | Teubert, F. | Thomas, C. | Thomas, E. | van Tilburg, J. | Tisserand, V. | Tobin, M. | Tolk, S. | Tomassetti, L. | Tonelli, D. | Topp-Joergensen, S. | Torr, N. | Tournefier, E. | Tourneur, S. | Tran, M. T. | Tresch, M. | Tsaregorodtsev, A. | Tsopelas, P. | Tuning, N. | Ubeda Garcia, M. | Ukleja, A. | Ustyuzhanin, A. | Uwer, U. | Vagnoni, V. | Valenti, G. | Vallier, A. | Vazquez Gomez, R. | Vazquez Regueiro, P. | Vázquez Sierra, C. | Vecchi, S. | Velthuis, J. J. | Veltri, M. | Veneziano, G. | Vesterinen, M. | Viaud, B. | Vieira, D. | Vilasis-Cardona, X. | Vollhardt, A. | Volyanskyy, D. | Voong, D. | Vorobyev, A. | Vorobyev, V. | Voß, C. | Voss, H. | de Vries, J. A. | Waldi, R. | Wallace, C. | Wallace, R. | Wandernoth, S. | Wang, J. | Ward, D. R. | Watson, N. K. | Webber, A. D. | Websdale, D. | Whitehead, M. | Wicht, J. | Wiechczynski, J. | Wiedner, D. | Wiggers, L. | Wilkinson, G. | Williams, M. P. | Williams, M. | Wilson, F. F. | Wimberley, J. | Wishahi, J. | Wislicki, W. | Witek, M. | Wormser, G. | Wotton, S. A. | Wright, S. | Wu, S. | Wyllie, K. | Xie, Y. | Xing, Z. | Yang, Z. | Yuan, X. | Yushchenko, O. | Zangoli, M. | Zavertyaev, M. | Zhang, F. | Zhang, L. | Zhang, W. C. | Zhang, Y. | Zhelezov, A. | Zhokhov, A. | Zhong, L. | Zvyagin, A.
Charged particle multiplicities are studied in proton–proton collisions in the forward region at a centre-of-mass energy of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s} = 7\;$$\end{document}s=7TeV with data collected by the LHCb detector. The forward spectrometer allows access to a kinematic range of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$2.0<\eta <4.8$$\end{document}2.0<η<4.8 in pseudorapidity, momenta greater than \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$2\;\text{ GeV/ }c$$\end{document}2GeV/c and transverse momenta greater than \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$0.2\;\text{ GeV/ }c$$\end{document}0.2GeV/c. The measurements are performed using events with at least one charged particle in the kinematic acceptance. The results are presented as functions of pseudorapidity and transverse momentum and are compared to predictions from several Monte Carlo event generators.
doi:10.1140/epjc/s10052-014-2888-1
PMCID: PMC4371048  PMID: 25814891
20.  Measurement of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\psi {(2S)} $$\end{document}ψ(2S) polarisation in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$pp$$\end{document}pp collisions at \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\sqrt{s}$$\end{document}s = 7 TeV 
Aaij, R. | Adeva, B. | Adinolfi, M. | Affolder, A. | Ajaltouni, Z. | Albrecht, J. | Alessio, F. | Alexander, M. | Ali, S. | Alkhazov, G. | Alvarez Cartelle, P. | Alves, A. A. | Amato, S. | Amerio, S. | Amhis, Y. | An, L. | Anderlini, L. | Anderson, J. | Andreassen, R. | Andreotti, M. | Andrews, J. E. | Appleby, R. B. | Aquines Gutierrez, O. | Archilli, F. | Artamonov, A. | Artuso, M. | Aslanides, E. | Auriemma, G. | Baalouch, M. | Bachmann, S. | Back, J. J. | Badalov, A. | Balagura, V. | Baldini, W. | Barlow, R. J. | Barschel, C. | Barsuk, S. | Barter, W. | Batozskaya, V. | Bauer, Th. | Bay, A. | Beddow, J. | Bedeschi, F. | Bediaga, I. | Belogurov, S. | Belous, K. | Belyaev, I. | Ben-Haim, E. | Bencivenni, G. | Benson, S. | Benton, J. | Berezhnoy, A. | Bernet, R. | Bettler, M.-O. | van Beuzekom, M. | Bien, A. | Bifani, S. | Bird, T. | Bizzeti, A. | Bjørnstad, P. M. | Blake, T. | Blanc, F. | Blouw, J. | Blusk, S. | Bocci, V. | Bondar, A. | Bondar, N. | Bonivento, W. | Borghi, S. | Borgia, A. | Borsato, M. | Bowcock, T. J. V. | Bowen, E. | Bozzi, C. | Brambach, T. | van den Brand, J. | Bressieux, J. | Brett, D. | Britsch, M. | Britton, T. | Brook, N. H. | Brown, H. | Bursche, A. | Busetto, G. | Buytaert, J. | Cadeddu, S. | Calabrese, R. | Callot, O. | Calvi, M. | Calvo Gomez, M. | Camboni, A. | Campana, P. | Campora Perez, D. | Carbone, A. | Carboni, G. | Cardinale, R. | Cardini, A. | Carranza-Mejia, H. | Carson, L. | Carvalho Akiba, K. | Casse, G. | Cassina, L. | Castillo Garcia, L. | Cattaneo, M. | Cauet, Ch. | Cenci, R. | Charles, M. | Charpentier, Ph. | Cheung, S.-F. | Chiapolini, N. | Chrzaszcz, M. | Ciba, K. | Cid Vidal, X. | Ciezarek, G. | Clarke, P. E. L. | Clemencic, M. | Cliff, H. V. | Closier, J. | Coca, C. | Coco, V. | Cogan, J. | Cogneras, E. | Collins, P. | Comerma-Montells, A. | Contu, A. | Cook, A. | Coombes, M. | Coquereau, S. | Corti, G. | Corvo, M. | Counts, I. | Couturier, B. | Cowan, G. A. | Craik, D. C. | Cruz Torres, M. | Cunliffe, S. | Currie, R. | D’Ambrosio, C. | Dalseno, J. | David, P. | David, P. N. Y. | Davis, A. | De Bruyn, K. | De Capua, S. | De Cian, M. | De Miranda, J. M. | De Paula, L. | De Silva, W. | De Simone, P. | Decamp, D. | Deckenhoff, M. | Del Buono, L. | Déléage, N. | Derkach, D. | Deschamps, O. | Dettori, F. | Di Canto, A. | Dijkstra, H. | Donleavy, S. | Dordei, F. | Dorigo, M. | Dosil Suárez, A. | Dossett, D. | Dovbnya, A. | Dupertuis, F. | Durante, P. | Dzhelyadin, R. | Dziurda, A. | Dzyuba, A. | Easo, S. | Egede, U. | Egorychev, V. | Eidelman, S. | Eisenhardt, S. | Eitschberger, U. | Ekelhof, R. | Eklund, L. | El Rifai, I. | Elsasser, Ch. | Esen, S. | Evans, T. | Falabella, A. | Färber, C. | Farinelli, C. | Farry, S. | Ferguson, D. | Fernandez Albor, V. | Ferreira Rodrigues, F. | Ferro-Luzzi, M. | Filippov, S. | Fiore, M. | Fiorini, M. | Firlej, M. | Fitzpatrick, C. | Fiutowski, T. | Fontana, M. | Fontanelli, F. | Forty, R. | Francisco, O. | Frank, M. | Frei, C. | Frosini, M. | Fu, J. | Furfaro, E. | Gallas Torreira, A. | Galli, D. | Gandelman, M. | Gandini, P. | Gao, Y. | Garofoli, J. | Garra Tico, J. | Garrido, L. | Gaspar, C. | Gauld, R. | Gavardi, L. | Gersabeck, E. | Gersabeck, M. | Gershon, T. | Ghez, Ph. | Gianelle, A. | Giani, S. | Gibson, V. | Giubega, L. | Gligorov, V. V. | Göbel, C. | Golubkov, D. | Golutvin, A. | Gomes, A. | Gordon, H. | Gotti, C. | Grabalosa Gándara, M. | Graciani Diaz, R. | Granado Cardoso, L. A. | Graugés, E. | Graziani, G. | Grecu, A. | Greening, E. | Gregson, S. | Griffith, P. | Grillo, L. | Grünberg, O. | Gui, B. | Gushchin, E. | Guz, Yu. | Gys, T. | Hadjivasiliou, C. | Haefeli, G. | Haen, C. | Haines, S. C. | Hall, S. | Hamilton, B. | Hampson, T. | Han, X. | Hansmann-Menzemer, S. | Harnew, N. | Harnew, S. T. | Harrison, J. | Hartmann, T. | He, J. | Head, T. | Heijne, V. | Hennessy, K. | Henrard, P. | Henry, L. | Hernando Morata, J. A. | van Herwijnen, E. | Heß, M. | Hicheur, A. | Hill, D. | Hoballah, M. | Hombach, C. | Hulsbergen, W. | Hunt, P. | Hussain, N. | Hutchcroft, D. | Hynds, D. | Iakovenko, V. | Idzik, M. | Ilten, P. | Jacobsson, R. | Jaeger, A. | Jalocha, J. | Jans, E. | Jaton, P. | Jawahery, A. | Jezabek, M. | Jing, F. | John, M. | Johnson, D. | Jones, C. R. | Joram, C. | Jost, B. | Jurik, N. | Kaballo, M. | Kandybei, S. | Kanso, W. | Karacson, M. | Karbach, T. M. | Kelsey, M. | Kenyon, I. R. | Ketel, T. | Khanji, B. | Khurewathanakul, C. | Klaver, S. | Kochebina, O. | Kolpin, M. | Komarov, I. | Koopman, R. F. | Koppenburg, P. | Korolev, M. | Kozlinskiy, A. | Kravchuk, L. | Kreplin, K. | Kreps, M. | Krocker, G. | Krokovny, P. | Kruse, F. | Kucharczyk, M. | Kudryavtsev, V. | Kurek, K. | Kvaratskheliya, T. | La Thi, V. N. | Lacarrere, D. | Lafferty, G. | Lai, A. | Lambert, D. | Lambert, R. W. | Lanciotti, E. | Lanfranchi, G. | Langenbruch, C. | Latham, T. | Lazzeroni, C. | Le Gac, R. | van Leerdam, J. | Lees, J.-P. | Lefèvre, R. | Leflat, A. | Lefrançois, J. | Leo, S. | Leroy, O. | Lesiak, T. | Leverington, B. | Li, Y. | Liles, M. | Lindner, R. | Linn, C. | Lionetto, F. | Liu, B. | Liu, G. | Lohn, S. | Longstaff, I. | Longstaff, I. | Lopes, J. H. | Lopez-March, N. | Lowdon, P. | Lu, H. | Lucchesi, D. | Luisier, J. | Luo, H. | Lupato, A. | Luppi, E. | Lupton, O. | Machefert, F. | Machikhiliyan, I. V. | Maciuc, F. | Maev, O. | Malde, S. | Manca, G. | Mancinelli, G. | Manzali, M. | Maratas, J. | Marchand, J. F. | Marconi, U. | Marino, P. | Märki, R. | Marks, J. | Martellotti, G. | Martens, A. | Martín Sánchez, A. | Martinelli, M. | Martinez Santos, D. | Martinez Vidal, F. | Martins Tostes, D. | Massafferri, A. | Matev, R. | Mathe, Z. | Matteuzzi, C. | Mazurov, A. | McCann, M. | McCarthy, J. | McNab, A. | McNulty, R. | McSkelly, B. | Meadows, B. | Meier, F. | Meissner, M. | Merk, M. | Milanes, D. A. | Minard, M.-N. | Molina Rodriguez, J. | Monteil, S. | Moran, D. | Morandin, M. | Morawski, P. | Mordà, A. | Morello, M. J. | Moron, J. | Mountain, R. | Muheim, F. | Müller, K. | Muresan, R. | Muster, B. | Naik, P. | Nakada, T. | Nandakumar, R. | Nasteva, I. | Needham, M. | Neri, N. | Neubert, S. | Neufeld, N. | Neuner, M. | Nguyen, A. D. | Nguyen, T. D. | Nguyen-Mau, C. | Nicol, M. | Niess, V. | Niet, R. | Nikitin, N. | Nikodem, T. | Novoselov, A. | Oblakowska-Mucha, A. | Obraztsov, V. | Oggero, S. | Ogilvy, S. | Okhrimenko, O. | Oldeman, R. | Onderwater, G. | Orlandea, M. | Otalora Goicochea, J. M. | Owen, P. | Oyanguren, A. | Pal, B. K. | Palano, A. | Palombo, F. | Palutan, M. | Panman, J. | Papanestis, A. | Pappagallo, M. | Parkes, C. | Parkinson, C. J. | Passaleva, G. | Patel, G. D. | Patel, M. | Patrignani, C. | Pazos Alvarez, A. | Pearce, A. | Pellegrino, A. | Penso, G. | Pepe Altarelli, M. | Perazzini, S. | Perez Trigo, E. | Perret, P. | Perrin-Terrin, M. | Pescatore, L. | Pesen, E. | Petridis, K. | Petrolini, A. | Picatoste Olloqui, E. | Pietrzyk, B. | Pilař, T. | Pinci, D. | Pistone, A. | Playfer, S. | Plo Casasus, M. | Polci, F. | Polok, G. | Poluektov, A. | Polycarpo, E. | Popov, A. | Popov, D. | Popovici, B. | Potterat, C. | Powell, A. | Prisciandaro, J. | Pritchard, A. | Prouve, C. | Pugatch, V. | Puig Navarro, A. | Punzi, G. | Qian, W. | Rachwal, B. | Rademacker, J. H. | Rakotomiaramanana, B. | Rama, M. | Rangel, M. S. | Raniuk, I. | Rauschmayr, N. | Raven, G. | Redford, S. | Reichert, S. | Reid, M. M. | dos Reis, A. C. | Ricciardi, S. | Richards, A. | Rinnert, K. | Rives Molina, V. | Roa Romero, D. A. | Robbe, P. | Rodrigues, A. B. | Rodrigues, E. | Rodriguez Perez, P. | Roiser, S. | Romanovsky, V. | Romero Vidal, A. | Rotondo, M. | Rouvinet, J. | Ruf, T. | Ruffini, F. | Ruiz, H. | Ruiz Valls, P. | Sabatino, G. | Saborido Silva, J. J. | Sagidova, N. | Sail, P. | Saitta, B. | Salustino Guimaraes, V. | Sanchez Mayordomo, C. | Sanmartin Sedes, B. | Santacesaria, R. | Santamarina Rios, C. | Santovetti, E. | Sapunov, M. | Sarti, A. | Satriano, C. | Satta, A. | Savrie, M. | Savrina, D. | Schiller, M. | Schindler, H. | Schlupp, M. | Schmelling, M. | Schmidt, B. | Schneider, O. | Schopper, A. | Schune, M.-H. | Schwemmer, R. | Sciascia, B. | Sciubba, A. | Seco, M. | Semennikov, A. | Senderowska, K. | Sepp, I. | Serra, N. | Serrano, J. | Sestini, L. | Seyfert, P. | Shapkin, M. | Shapoval, I. | Shcheglov, Y. | Shears, T. | Shekhtman, L. | Shevchenko, V. | Shires, A. | Silva Coutinho, R. | Simi, G. | Sirendi, M. | Skidmore, N. | Skwarnicki, T. | Smith, N. A. | Smith, E. | Smith, E. | Smith, J. | Smith, M. | Snoek, H. | Sokoloff, M. D. | Soler, F. J. P. | Soomro, F. | Souza, D. | Souza De Paula, B. | Spaan, B. | Sparkes, A. | Spinella, F. | Spradlin, P. | Stagni, F. | Stahl, S. | Steinkamp, O. | Stenyakin, O. | Stevenson, S. | Stoica, S. | Stone, S. | Storaci, B. | Stracka, S. | Straticiuc, M. | Straumann, U. | Stroili, R. | Subbiah, V. K. | Sun, L. | Sutcliffe, W. | Swientek, K. | Swientek, S. | Syropoulos, V. | Szczekowski, M. | Szczypka, P. | Szilard, D. | Szumlak, T. | T’Jampens, S. | Teklishyn, M. | Tellarini, G. | Teodorescu, E. | Teubert, F. | Thomas, C. | Thomas, E. | van Tilburg, J. | Tisserand, V. | Tobin, M. | Tolk, S. | Tomassetti, L. | Tonelli, D. | Topp-Joergensen, S. | Torr, N. | Tournefier, E. | Tourneur, S. | Tran, M. T. | Tresch, M. | Tsaregorodtsev, A. | Tsopelas, P. | Tuning, N. | Ubeda Garcia, M. | Ukleja, A. | Ustyuzhanin, A. | Uwer, U. | Vagnoni, V. | Valenti, G. | Vallier, A. | Vazquez Gomez, R. | Vazquez Regueiro, P. | Vázquez Sierra, C. | Vecchi, S. | Velthuis, J. J. | Veltri, M. | Veneziano, G. | Vesterinen, M. | Viaud, B. | Vieira, D. | Vieites Diaz, M. | Vilasis-Cardona, X. | Vollhardt, A. | Volyanskyy, D. | Voong, D. | Vorobyev, A. | Vorobyev, V. | Voß, C. | Voss, H. | de Vries, J. A. | Waldi, R. | Wallace, C. | Wallace, R. | Walsh, J. | Wandernoth, S. | Wang, J. | Ward, D. R. | Watson, N. K. | Webber, A. D. | Websdale, D. | Whitehead, M. | Wicht, J. | Wiedner, D. | Wiggers, L. | Wilkinson, G. | Williams, M. P. | Williams, M. | Wilson, F. F. | Wimberley, J. | Wishahi, J. | Wislicki, W. | Witek, M. | Wormser, G. | Wotton, S. A. | Wright, S. | Wu, S. | Wyllie, K. | Xie, Y. | Xing, Z. | Xu, Z. | Yang, Z. | Yuan, X. | Yushchenko, O. | Zangoli, M. | Zavertyaev, M. | Zhang, F. | Zhang, L. | Zhang, W. C. | Zhang, Y. | Zhelezov, A. | Zhokhov, A. | Zhong, L. | Zvyagin, A.
The polarisation of prompt \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\psi {(2S)} $$\end{document}ψ(2S) mesons is measured by performing an angular analysis of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\psi {(2S)} \!\rightarrow \mu ^+\mu ^- $$\end{document}ψ(2S)→μ+μ- decays using proton-proton collision data, corresponding to an integrated luminosity of 1.0\documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\,\text{ fb }^{-1} $$\end{document}fb-1, collected by the LHCb detector at a centre-of-mass energy of 7 TeV. The polarisation is measured in bins of transverse momentum \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$p_\mathrm{T} $$\end{document}pT and rapidity \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$y$$\end{document}y in the kinematic region \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$3.5< p_\mathrm{T} <15{\mathrm {\,GeV\!/}c} $$\end{document}3.5
doi:10.1140/epjc/s10052-014-2872-9
PMCID: PMC4370868  PMID: 25814889
Aaij, R. | Adeva, B. | Adinolfi, M. | Affolder, A. | Ajaltouni, Z. | Albrecht, J. | Alessio, F. | Alexander, M. | Ali, S. | Alkhazov, G. | Cartelle, P. Alvarez | Alves, A. A. | Amato, S. | Amerio, S. | Amhis, Y. | Anderlini, L. | Anderson, J. | Andreassen, R. | Andreotti, M. | Andrews, J. E. | Appleby, R. B. | Gutierrez, O. Aquines | Archilli, F. | Artamonov, A. | Artuso, M. | Aslanides, E. | Auriemma, G. | Baalouch, M. | Bachmann, S. | Back, J. J. | Badalov, A. | Balagura, V. | Baldini, W. | Barlow, R. J. | Barschel, C. | Barsuk, S. | Barter, W. | Batozskaya, V. | Bauer, Th. | Bay, A. | Beddow, J. | Bedeschi, F. | Bediaga, I. | Belogurov, S. | Belous, K. | Belyaev, I. | Ben-Haim, E. | Bencivenni, G. | Benson, S. | Benton, J. | Berezhnoy, A. | Bernet, R. | Bettler, M.-O. | van Beuzekom, M. | Bien, A. | Bifani, S. | Bird, T. | Bizzeti, A. | Bjørnstad, P. M. | Blake, T. | Blanc, F. | Blouw, J. | Blusk, S. | Bocci, V. | Bondar, A. | Bondar, N. | Bonivento, W. | Borghi, S. | Borgia, A. | Borsato, M. | Bowcock, T. J. V. | Bowen, E. | Bozzi, C. | Brambach, T. | van den Brand, J. | Bressieux, J. | Brett, D. | Britsch, M. | Britton, T. | Brook, N. H. | Brown, H. | Bursche, A. | Busetto, G. | Buytaert, J. | Cadeddu, S. | Calabrese, R. | Callot, O. | Calvi, M. | Calvo Gomez, M. | Camboni, A. | Campana, P. | Campora Perez, D. | Carbone, A. | Carboni, G. | Cardinale, R. | Cardini, A. | Carranza-Mejia, H. | Carson, L. | Carvalho Akiba, K. | Casse, G. | Castillo Garcia, L. | Cattaneo, M. | Cauet, Ch. | Cenci, R. | Charles, M. | Charpentier, Ph. | Cheung, S.-F. | Chiapolini, N. | Chrzaszcz, M. | Ciba, K. | Cid Vidal, X. | Ciezarek, G. | Clarke, P. E. L. | Clemencic, M. | Cliff, H. V. | Closier, J. | Coca, C. | Coco, V. | Cogan, J. | Cogneras, E. | Collins, P. | Comerma-Montells, A. | Contu, A. | Cook, A. | Coombes, M. | Coquereau, S. | Corti, G. | Counts, I. | Couturier, B. | Cowan, G. A. | Craik, D. C. | Cruz Torres, M. | Cunliffe, S. | Currie, R. | D’Ambrosio, C. | Dalseno, J. | David, P. | David, P. N. Y. | Davis, A. | De Bonis, I. | De Bruyn, K. | De Capua, S. | De Cian, M. | De Miranda, J. M. | De Paula, L. | De Silva, W. | De Simone, P. | Decamp, D. | Deckenhoff, M. | Del Buono, L. | Déléage, N. | Derkach, D. | Deschamps, O. | Dettori, F. | Di Canto, A. | Dijkstra, H. | Donleavy, S. | Dordei, F. | Dorigo, M. | Dorosz, P. | Dosil Suárez, A. | Dossett, D. | Dovbnya, A. | Dupertuis, F. | Durante, P. | Dzhelyadin, R. | Dziurda, A. | Dzyuba, A. | Easo, S. | Egede, U. | Egorychev, V. | Eidelman, S. | Eisenhardt, S. | Eitschberger, U. | Ekelhof, R. | Eklund, L. | El Rifai, I. | Elsasser, Ch. | Falabella, A. | Färber, C. | Farinelli, C. | Farry, S. | Ferguson, D. | Fernandez Albor, V. | Ferreira Rodrigues, F. | Ferro-Luzzi, M. | Filippov, S. | Fiore, M. | Fiorini, M. | Fitzpatrick, C. | Fontana, M. | Fontanelli, F. | Forty, R. | Francisco, O. | Frank, M. | Frei, C. | Frosini, M. | Furfaro, E. | Gallas Torreira, A. | Galli, D. | Gandelman, M. | Gandini, P. | Gao, Y. | Garofoli, J. | Garra Tico, J. | Garrido, L. | Gaspar, C. | Gauld, R. | Gersabeck, E. | Gersabeck, M. | Gershon, T. | Ghez, Ph. | Gianelle, A. | Gibson, V. | Giubega, L. | Gligorov, V. V. | Göbel, C. | Golubkov, D. | Golutvin, A. | Gomes, A. | Gordon, H. | Grabalosa Gándara, M. | Graciani Diaz, R. | Granado Cardoso, L. A. | Graugés, E. | Graziani, G. | Grecu, A. | Greening, E. | Gregson, S. | Griffith, P. | Grillo, L. | Grünberg, O. | Gui, B. | Gushchin, E. | Guz, Yu. | Gys, T. | Hadjivasiliou, C. | Haefeli, G. | Haen, C. | Hafkenscheid, T. W. | Haines, S. C. | Hall, S. | Hamilton, B. | Hampson, T. | Hansmann-Menzemer, S. | Harnew, N. | Harnew, S. T. | Harrison, J. | Hartmann, T. | He, J. | Head, T. | Heijne, V. | Hennessy, K. | Henrard, P. | Hernando Morata, J. A. | van Herwijnen, E. | Heß, M. | Hicheur, A. | Hill, D. | Hoballah, M. | Hombach, C. | Hulsbergen, W. | Hunt, P. | Huse, T. | Hussain, N. | Hutchcroft, D. | Hynds, D. | Iakovenko, V. | Idzik, M. | Ilten, P. | Jacobsson, R. | Jaeger, A. | Jans, E. | Jaton, P. | Jawahery, A. | Jing, F. | John, M. | Johnson, D. | Jones, C. R. | Joram, C. | Jost, B. | Jurik, N. | Kaballo, M. | Kandybei, S. | Kanso, W. | Karacson, M. | Karbach, T. M. | Kenyon, I. R. | Ketel, T. | Khanji, B. | Khurewathanakul, C. | Klaver, S. | Kochebina, O. | Komarov, I. | Koopman, R. F. | Koppenburg, P. | Korolev, M. | Kozlinskiy, A. | Kravchuk, L. | Kreplin, K. | Kreps, M. | Krocker, G. | Krokovny, P. | Kruse, F. | Kucharczyk, M. | Kudryavtsev, V. | Kurek, K. | Kvaratskheliya, T. | La Thi, V. N. | Lacarrere, D. | Lafferty, G. | Lai, A. | Lambert, D. | Lambert, R. W. | Lanciotti, E. | Lanfranchi, G. | Langenbruch, C. | Latham, T. | Lazzeroni, C. | Le Gac, R. | van Leerdam, J. | Lees, J.-P. | Lefèvre, R. | Leflat, A. | Lefrançois, J. | Leo, S. | Leroy, O. | Lesiak, T. | Leverington, B. | Li, Y. | Liles, M. | Lindner, R. | Linn, C. | Lionetto, F. | Liu, B. | Liu, G. | Lohn, S. | Longstaff, I. | Lopes, J. H. | Lopez-March, N. | Lowdon, P. | Lu, H. | Lucchesi, D. | Luisier, J. | Luo, H. | Luppi, E. | Lupton, O. | Machefert, F. | Machikhiliyan, I. V. | Maciuc, F. | Maev, O. | Malde, S. | Manca, G. | Mancinelli, G. | Manzali, M. | Maratas, J. | Marconi, U. | Marino, P. | Märki, R. | Marks, J. | Martellotti, G. | Martens, A. | Martín Sánchez, A. | Martinelli, M. | Martinez Santos, D. | Martins Tostes, D. | Massafferri, A. | Matev, R. | Mathe, Z. | Matteuzzi, C. | Mazurov, A. | McCann, M. | McCarthy, J. | McNab, A. | McNulty, R. | McSkelly, B. | Meadows, B. | Meier, F. | Meissner, M. | Merk, M. | Milanes, D. A. | Minard, M.-N. | Molina Rodriguez, J. | Monteil, S. | Moran, D. | Morandin, M. | Morawski, P. | Mordà, A. | Morello, M. J. | Mountain, R. | Mous, I. | Muheim, F. | Müller, K. | Muresan, R. | Muryn, B. | Muster, B. | Naik, P. | Nakada, T. | Nandakumar, R. | Nasteva, I. | Needham, M. | Neubert, S. | Neufeld, N. | Nguyen, A. D. | Nguyen, T. D. | Nguyen-Mau, C. | Nicol, M. | Niess, V. | Niet, R. | Nikitin, N. | Nikodem, T. | Novoselov, A. | Oblakowska-Mucha, A. | Obraztsov, V. | Oggero, S. | Ogilvy, S. | Okhrimenko, O. | Oldeman, R. | Onderwater, G. | Orlandea, M. | Otalora Goicochea, J. M. | Owen, P. | Oyanguren, A. | Pal, B. K. | Palano, A. | Palutan, M. | Panman, J. | Papanestis, A. | Pappagallo, M. | Pappalardo, L. | Parkes, C. | Parkinson, C. J. | Passaleva, G. | Patel, G. D. | Patel, M. | Patrignani, C. | Pavel-Nicorescu, C. | Pazos Alvarez, A. | Pearce, A. | Pellegrino, A. | Penso, G. | Pepe Altarelli, M. | Perazzini, S. | Perez Trigo, E. | Perret, P. | Perrin-Terrin, M. | Pescatore, L. | Pesen, E. | Pessina, G. | Petridis, K. | Petrolini, A. | Picatoste Olloqui, E. | Pietrzyk, B. | Pilař, T. | Pinci, D. | Pistone, A. | Playfer, S. | Plo Casasus, M. | Polci, F. | Polok, G. | Poluektov, A. | Polycarpo, E. | Popov, A. | Popov, D. | Popovici, B. | Potterat, C. | Powell, A. | Prisciandaro, J. | Pritchard, A. | Prouve, C. | Pugatch, V. | Puig Navarro, A. | Punzi, G. | Qian, W. | Rachwal, B. | Rademacker, J. H. | Rakotomiaramanana, B. | Rama, M. | Rangel, M. S. | Raniuk, I. | Rauschmayr, N. | Raven, G. | Redford, S. | Reichert, S. | Reid, M. M. | dos Reis, A. C. | Ricciardi, S. | Richards, A. | Rinnert, K. | Rives Molina, V. | Roa Romero, D. A. | Robbe, P. | Roberts, D. A. | Rodrigues, A. B. | Rodrigues, E. | Rodriguez Perez, P. | Roiser, S. | Romanovsky, V. | Romero Vidal, A. | Rotondo, M. | Rouvinet, J. | Ruf, T. | Ruffini, F. | Ruiz, H. | Ruiz Valls, P. | Sabatino, G. | Saborido Silva, J. J. | Sagidova, N. | Sail, P. | Saitta, B. | Salustino Guimaraes, V. | Sanmartin Sedes, B. | Santacesaria, R. | Santamarina Rios, C. | Santovetti, E. | Sapunov, M. | Sarti, A. | Satriano, C. | Satta, A. | Savrie, M. | Savrina, D. | Schiller, M. | Schindler, H. | Schlupp, M. | Schmelling, M. | Schmidt, B. | Schneider, O. | Schopper, A. | Schune, M.-H. | Schwemmer, R. | Sciascia, B. | Sciubba, A. | Seco, M. | Semennikov, A. | Senderowska, K. | Sepp, I. | Serra, N. | Serrano, J. | Seyfert, P. | Shapkin, M. | Shapoval, I. | Shcheglov, Y. | Shears, T. | Shekhtman, L. | Shevchenko, O. | Shevchenko, V. | Shires, A. | Silva Coutinho, R. | Simi, G. | Sirendi, M. | Skidmore, N. | Skwarnicki, T. | Smith, N. A. | Smith, E. | Smith, E. | Smith, J. | Smith, M. | Snoek, H. | Sokoloff, M. D. | Soler, F. J. P. | Soomro, F. | Souza, D. | Souza De Paula, B. | Spaan, B. | Sparkes, A. | Spinella, F. | Spradlin, P. | Stagni, F. | Stahl, S. | Steinkamp, O. | Stevenson, S. | Stoica, S. | Stone, S. | Storaci, B. | Stracka, S. | Straticiuc, M. | Straumann, U. | Stroili, R. | Subbiah, V. K. | Sun, L. | Sutcliffe, W. | Swientek, S. | Syropoulos, V. | Szczekowski, M. | Szczypka, P. | Szilard, D. | Szumlak, T. | T’Jampens, S. | Teklishyn, M. | Tellarini, G. | Teodorescu, E. | Teubert, F. | Thomas, C. | Thomas, E. | van Tilburg, J. | Tisserand, V. | Tobin, M. | Tolk, S. | Tomassetti, L. | Tonelli, D. | Topp-Joergensen, S. | Torr, N. | Tournefier, E. | Tourneur, S. | Tran, M. T. | Tresch, M. | Tsaregorodtsev, A. | Tsopelas, P. | Tuning, N. | Ubeda Garcia, M. | Ukleja, A. | Ustyuzhanin, A. | Uwer, U. | Vagnoni, V. | Valenti, G. | Vallier, A. | Vazquez Gomez, R. | Vazquez Regueiro, P. | Vázquez Sierra, C. | Vecchi, S. | Velthuis, J. J. | Veltri, M. | Veneziano, G. | Vesterinen, M. | Viaud, B. | Vieira, D. | Vilasis-Cardona, X. | Vollhardt, A. | Volyanskyy, D. | Voong, D. | Vorobyev, A. | Vorobyev, V. | Voß, C. | Voss, H. | de Vries, J. A. | Waldi, R. | Wallace, C. | Wallace, R. | Wandernoth, S. | Wang, J. | Ward, D. R. | Watson, N. K. | Webber, A. D. | Websdale, D. | Whitehead, M. | Wicht, J. | Wiechczynski, J. | Wiedner, D. | Wiggers, L. | Wilkinson, G. | Williams, M. P. | Williams, M. | Wilson, F. F. | Wimberley, J. | Wishahi, J. | Wislicki, W. | Witek, M. | Wormser, G. | Wotton, S. A. | Wright, S. | Wu, S. | Wyllie, K. | Xie, Y. | Xing, Z. | Yang, Z. | Yuan, X. | Yushchenko, O. | Zangoli, M. | Zavertyaev, M. | Zhang, F. | Zhang, L. | Zhang, W. C. | Zhang, Y. | Zhelezov, A. | Zhokhov, A. | Zhong, L. | Zvyagin, A.
The lifetime of the \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$${B} _{c} ^+$$\end{document}Bc+ meson is measured using semileptonic decays having a \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$J/\psi $$\end{document}J/ψ meson and a muon in the final state. The data, corresponding to an integrated luminosity of \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$2 \text{ fb }^{-1} $$\end{document}2fb-1, are collected by the LHCb detector in \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$pp$$\end{document}pp collisions at a centre-of-mass energy of 8 TeV. The measured lifetime is \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\begin{aligned} \tau = 509\pm 8\pm 12\mathrm {~fs}, \end{aligned}$$\end{document}τ=509±8±12fs,where the first uncertainty is statistical and the second is systematic.
doi:10.1140/epjc/s10052-014-2839-x
PMCID: PMC4370795  PMID: 25814888
To investigate signal regulation models of gastric cancer, databases and literature were used to construct the signaling network in humans. Topological characteristics of the network were analyzed by CytoScape. After marking gastric cancer-related genes extracted from the CancerResource, GeneRIF, and COSMIC databases, the FANMOD software was used for the mining of gastric cancer-related motifs in a network with three vertices. The significant motif difference method was adopted to identify significantly different motifs in the normal and cancer states. Finally, we conducted a series of analyses of the significantly different motifs, including gene ontology, function annotation of genes, and model classification. A human signaling network was constructed, with 1643 nodes and 5089 regulating interactions. The network was configured to have the characteristics of other biological networks. There were 57,942 motifs marked with gastric cancer-related genes out of a total of 69,492 motifs, and 264 motifs were selected as significantly different motifs by calculating the significant motif difference (SMD) scores. Genes in significantly different motifs were mainly enriched in functions associated with cancer genesis, such as regulation of cell death, amino acid phosphorylation of proteins, and intracellular signaling cascades. The top five significantly different motifs were mainly cascade and positive feedback types. Almost all genes in the five motifs were cancer related, including EPOR, MAPK14, BCL2L1, KRT18, PTPN6, CASP3, TGFBR2, AR, and CASP7. The development of cancer might be curbed by inhibiting signal transductions upstream and downstream of the selected motifs.
doi:10.1590/1414-431X20143527
PMCID: PMC4075304  PMID: 24838641
Significantly different motifs; Human signaling network; Gastric cancer
Scientific Reports  2014;4:4205.
The selection and design of modern high-performance structural engineering materials such as nanostructured metallic multilayers (NMMs) is driven by optimizing combinations of mechanical properties and requirements for predictable and noncatastrophic failure in service. Here, the Cu/X (X = Zr, Cr) nanolayered micropillars with equal layer thickness (h) spanning from 5–125 nm are uniaxially compressed and it is found that these NMMs exhibit a maximum strain hardening capability and simultaneously display a transition from bulk-like to small-volume materials behavior associated with the strength at a critical intrinsic size h ~ 20 nm. We develop a deformation mode-map to bridge the gap between the interface characteristics of NMMs and their failure phenomena, which, as shrinking the intrinsic size, transit from localized interface debonding/extrusion to interface shearing. Our findings demonstrate that the optimum robust performance can be achieved in NMMs and provide guidance for their microstructure sensitive design for performance optimization.
doi:10.1038/srep04205
PMCID: PMC3966053  PMID: 24667702
Scientific Reports  2014;4:4167.
As two important mechanical properties, strength and ductility generally tend to be muturally exclusive in conventional engineering materials. The breakthrough of such a trade-off has been potentiated by the recently developed CuZr-based bulk metallic glass (BMG) composites ductilized by a shape memory CuZr(B2) phase. Here the microstructural dependences of tensile properties for the CuZr-based BMG composites were elucidated qualitatively and modeled quantitatively, and the underlying mechanisms were unraveled. Through the microstructural percolation induced by matching the length scales of particle size and interparticle spacing, a notable breakthrough was achieved in the composites that the general conflicts between strength and ductility can be defeated. This study is expected to greatly aid in the microstructural design and tailoring for improved properties of BMG composites. It also has implications for the development of strong and ductile materials in the future.
doi:10.1038/srep04167
PMCID: PMC3933912  PMID: 24566737

Results 1-25 (101)