945 research outputs found
Limit on the mass of a long-lived or stable gluino
We reinterpret the generic CDF charged massive particle limit to obtain a
limit on the mass of a stable or long-lived gluino. Various sources of
uncertainty are examined. The -hadron spectrum and scattering cross sections
are modeled based on known low-energy hadron physics and the resultant
uncertainties are quantified and found to be small compared to uncertainties
from the scale dependence of the NLO pQCD production cross sections. The
largest uncertainty in the limit comes from the unknown squark mass: when the
squark -- gluino mass splitting is small, we obtain a gluino mass limit of 407
GeV, while in the limit of heavy squarks the gluino mass limit is 397 GeV. For
arbitrary (degenerate) squark masses, we obtain a lower limit of 322 GeV on the
gluino mass. These limits apply for any gluino lifetime longer than
ns, and are the most stringent limits for such a long-lived or stable gluino.Comment: 15 pages, 5 figures, accepted for publication in JHE
Gauge links for transverse momentum dependent correlators at tree-level
In this paper we discuss the incorporation of gauge links in hadronic matrix
elements that describe the soft hadronic physics in high energy scattering
processes. In this description the matrix elements appear in soft correlators
and they contain non-local combinations of quark and gluon fields. In our
description we go beyond the collinear approach in which case also the
dependence on transverse momenta of partons is taken into consideration. The
non-locality in the transverse direction leads to a complex gauge link
structure for the full process, in which color is entangled, even at
tree-level. We show that at tree-level in a 1-parton unintegrated (1PU)
situation, in which only the transverse momentum of one of the initial state
hadrons is relevant, one can get a factorized expression involving transverse
momentum dependent (TMD) distribution functions. We point out problems at the
level of two initial state hadrons, even for relatively simple processes such
as Drell-Yan scattering.Comment: 25 pages, corrected typos and updated reference
Social interaction, noise and antibiotic-mediated switches in the intestinal microbiota
The intestinal microbiota plays important roles in digestion and resistance
against entero-pathogens. As with other ecosystems, its species composition is
resilient against small disturbances but strong perturbations such as
antibiotics can affect the consortium dramatically. Antibiotic cessation does
not necessarily restore pre-treatment conditions and disturbed microbiota are
often susceptible to pathogen invasion. Here we propose a mathematical model to
explain how antibiotic-mediated switches in the microbiota composition can
result from simple social interactions between antibiotic-tolerant and
antibiotic-sensitive bacterial groups. We build a two-species (e.g. two
functional-groups) model and identify regions of domination by
antibiotic-sensitive or antibiotic-tolerant bacteria, as well as a region of
multistability where domination by either group is possible. Using a new
framework that we derived from statistical physics, we calculate the duration
of each microbiota composition state. This is shown to depend on the balance
between random fluctuations in the bacterial densities and the strength of
microbial interactions. The singular value decomposition of recent metagenomic
data confirms our assumption of grouping microbes as antibiotic-tolerant or
antibiotic-sensitive in response to a single antibiotic. Our methodology can be
extended to multiple bacterial groups and thus it provides an ecological
formalism to help interpret the present surge in microbiome data.Comment: 20 pages, 5 figures accepted for publication in Plos Comp Bio.
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Prediction of ventricular arrhythmia in phospholamban p.Arg14del mutation carriers–reaching the frontiers of individual risk prediction
Aims: This study aims to improve risk stratification for primary prevention implantable cardioverter defibrillator (ICD) implantation by developing a new mutation-specific prediction model for malignant ventricular arrhythmia (VA) in phospholamban (PLN) p.Arg14del mutation carriers. The proposed model is compared to an existing PLN risk model. / Methods and results: Data were collected from PLN p.Arg14del mutation carriers with no history of malignant VA at baseline, identified between 2009 and 2020. Malignant VA was defined as sustained VA, appropriate ICD intervention, or (aborted) sudden cardiac death. A prediction model was developed using Cox regression. The study cohort consisted of 679 PLN p.Arg14del mutation carriers, with a minority of index patients (17%) and male sex (43%), and a median age of 42 years [interquartile range (IQR) 27-55]. During a median follow-up of 4.3 years (IQR 1.7-7.4), 72 (10.6%) carriers experienced malignant VA. Significant predictors were left ventricular ejection fraction, premature ventricular contraction count/24 h, amount of negative T waves, and presence of low-voltage electrocardiogram. The multivariable model had an excellent discriminative ability {C-statistic 0.83 [95% confidence interval (CI) 0.78-0.88]}. Applying the existing PLN risk model to the complete cohort yielded a C-statistic of 0.68 (95% CI 0.61-0.75). / Conclusion: This new mutation-specific prediction model for individual VA risk in PLN p.Arg14del mutation carriers is superior to the existing PLN risk model, suggesting that risk prediction using mutation-specific phenotypic features can improve accuracy compared to a more generic approach
Expression and subcellular localization of cyclin D1 protein in epithelial ovarian tumour cells
The expression of cyclin D1 protein in tumour sections from 81 patients with epithelial ovarian cancer was analysed using immunohistochemistry. The tumours that overexpressed cyclin D1 in more than 10% of neoplastic cells were considered positive. Thus overexpression of cyclin D1 was observed in 72/81 (89%) of the cases examined. Protein was detected in both the nucleus and the cytoplasm in 24/81 (30%) and localized exclusively in the cytoplasm in 48/81 (59%) of the tumours. Cyclin D1 was overexpressed in both borderline and invasive tumours. There was no association between protein overexpression and tumour stage and differentiation. Furthermore, no correlation between cyclin D1 expression and clinical outcome was observed. However, in tumours overexpressing cyclin D1 (n = 72), the proportion displaying exclusively cytoplasmic localization of protein was higher in those with serous compared with non-serous histology (P = 0.004, odds ratio 4.8, 95% confidence interval 1.4–19.1). Western analysis using a monoclonal antibody to cyclin D1 identified a 36 kDa protein in homogenates from seven tumours displaying cytoplasmic only and one tumour demonstrating both nuclear and cytoplasmic immunostaining. Using restriction fragment length polymorphism polymerase chain reaction and PCR-multiplex analysis, amplification of the cyclin D1 gene (CCNDI) was detected in 1/29 of the tumours demonstrating overexpression of cyclin D1 protein. We conclude that deregulation of CCND1 expression leading to both cytoplasmic and nuclear protein localization is a frequent event in ovarian cancer and occurs mainly in the absence of gene amplification. © 1999 Cancer Research Campaig
Role of urothelial cells in BCG immunotherapy for superficial bladder cancer
Intravesical instillation of Bacillus Calmette-Guérin (BCG) is used for the treatment of superficial bladder cancer, both to reduce the recurrence rate of bladder tumour and to diminish the risk of progression. Since its first therapeutic application in 1976, major research efforts have been directed to decipher the exact mechanism of action of the BCG-associated antitumour effect. Bacillus Calmette-Guérin causes an extensive local inflammatory reaction in the bladder wall. Of this, the massive appearance of cytokines in the urine of BCG-treated patients stands out. Activated lymphocytes and macrophages are the most likely sources of these cytokines, but at present other cellular sources such as urothelial tumour cells cannot be ruled out. Bacillus Calmette-Guérin is internalised and processed both by professional antigen-presenting cells and urothelial tumour cells, resulting in an altered gene expression of these cells that accumulates in the presentation of BCG antigens and secretion of particular cytokine
Decorin and TGF-β(1 )polymorphisms and development of COPD in a general population
BACKGROUND: Decorin, an extracellular matrix (ECM) proteoglycan, and TGF-β(1 )are both involved in lung ECM turnover. Decorin and TGF-β(1 )expression are decreased respectively increased in COPD lung tissue. Interestingly, they act as each other's feedback regulator. We investigated whether single nucleotide polymorphisms (SNPs) in decorin and TGF-β(1 )underlie accelerated decline in FEV(1 )and development of COPD in the general population. METHODS: We genotyped 1390 subjects from the Vlagtwedde/Vlaardingen cohort. Lung function was measured every 3 years for a period of 25 years. We tested whether five SNPs in decorin (3'UTR and four intron SNPs) and three SNPs in TGF-β(1 )(3'UTR rs6957, C-509T rs1800469 and Leu10Pro rs1982073), and their haplotypes, were associated with COPD (last survey GOLD stage = II). Linear mixed effects models were used to analyze genotype associations with FEV(1 )decline. RESULTS: We found a significantly higher prevalence of carriers of the minor allele of the TGF-β(1 )rs6957 SNP (p = 0.001) in subjects with COPD. Additionally, we found a significantly lower prevalence of the haplotype with the major allele of rs6957 and minor alleles for rs1800469 and rs1982073 SNPs in TGF-β(1 )in subjects with COPD (p = 0.030), indicating that this association is due to the rs6957 SNP. TGF-β(1 )SNPs were not associated with FEV(1 )decline. SNPs in decorin, and haplotypes constructed of both TGF-β(1 )and decorin SNPs were not associated with development of COPD or with FEV(1 )decline. CONCLUSION: Our study shows for the first time that SNPs in decorin on its own or in interaction with SNPs in TGF-β(1 )do not underlie the disturbed balance in expression between these genes in COPD. TGF-β(1 )SNPs are associated with COPD, yet not with accelerated FEV(1 )decline in the general population
Soft-Gluon-Pole Contribution in Single Transverse-Spin Asymmetries of Drell-Yan Processes
We use multi-parton states to examine the leading order collinear
factorization of single transverse-spin asymmetries in Drell-Yan processes.
Twist-3 operators are involved in the factorization. We find that the so-called
soft-gluon-pole contribution in the factorization must exist in order to make
the factorization correct. This contribution comes from the corresponding
cross-section at one-loop, while the hard-pole contribution in the
factorization comes from the cross-section at tree-level. Although the two
contributions come from results at different orders, their perturbative
coefficient functions in the factorization are at the same order. This is in
contrast to factorizations only involving twist-2 operators. The
soft-gluon-pole contribution found in this work is in agreement with that
derived in a different way. For the hard-pole contributions we find an extra
contribution from an extra parton process contributing to the asymmetries. We
also solve a part of discrepancy in evolutions of the twist-3 operator. The
method presented here for analyzing the factorization can be generalized to
other processes and can be easily used for studying factorizations at higher
orders, because the involved calculations are of standard scattering
amplitudes.Comment: typos eliminated. Published in JHEP 1104:062,201
Bessel-Weighted Asymmetries in Semi Inclusive Deep Inelastic Scattering
The concept of weighted asymmetries is revisited for semi-inclusive deep
inelastic scattering. We consider the cross section in Fourier space, conjugate
to the outgoing hadron's transverse momentum, where convolutions of transverse
momentum dependent parton distribution functions and fragmentation functions
become simple products. Individual asymmetric terms in the cross section can be
projected out by means of a generalized set of weights involving Bessel
functions. Advantages of employing these Bessel weights are that they suppress
(divergent) contributions from high transverse momentum and that soft factors
cancel in (Bessel-) weighted asymmetries. Also, the resulting compact
expressions immediately connect to previous work on evolution equations for
transverse momentum dependent parton distribution and fragmentation functions
and to quantities accessible in lattice QCD. Bessel weighted asymmetries are
thus model independent observables that augment the description and our
understanding of correlations of spin and momentum in nucleon structure.Comment: Matches published version, JHEP style, 36 pages and 2 figures, minor
correction
Pharmacological Inhibition of Caspase and Calpain Proteases: A Novel Strategy to Enhance the Homing Responses of Cord Blood HSPCs during Expansion
Background: Expansion of hematopoietic stem/progenitor cells (HSPCs) is a well-known strategy employed to facilitate the transplantation outcome. We have previously shown that the prevention of apoptosis by the inhibition of cysteine proteases, caspase and calpain played an important role in the expansion and engraftment of cord blood (CB) derived HSPCs. We hypothesize that these protease inhibitors might have maneuvered the adhesive and migratory properties of the cells rendering them to be retained in the bone marrow for sustained engraftment. The current study was aimed to investigate the mechanism of the homing responses of CB cells during expansion. Methodology/Principal Findings: CB derived CD34 + cells were expanded using a combination of growth factors with and without Caspase inhibitor-zVADfmk or Calpain 1 inhibitor- zLLYfmk. The cells were analyzed for the expression of homingrelated molecules. In vitro adhesive/migratory interactions and actin polymerization dynamics of HSPCs were assessed. In vivo homing assays were carried out in NOD/SCID mice to corroborate these observations. We observed that the presence of zVADfmk or zLLYfmk (inhibitors) caused the functional up regulation of CXCR4, integrins, and adhesion molecules, reflecting in a higher migration and adhesive interactions in vitro. The enhanced actin polymerization and the RhoGTPase protein expression complemented these observations. Furthermore, in vivo experiments showed a significantly enhanced homing to the bone marrow of NOD/SCID mice
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