547 research outputs found
Benchmark calculations for elastic fermion-dimer scattering
We present continuum and lattice calculations for elastic scattering between
a fermion and a bound dimer in the shallow binding limit. For the continuum
calculation we use the Skorniakov-Ter-Martirosian (STM) integral equation to
determine the scattering length and effective range parameter to high
precision. For the lattice calculation we use the finite-volume method of
L\"uscher. We take into account topological finite-volume corrections to the
dimer binding energy which depend on the momentum of the dimer. After
subtracting these effects, we find from the lattice calculation kappa a_fd =
1.174(9) and kappa r_fd = -0.029(13). These results agree well with the
continuum values kappa a_fd = 1.17907(1) and kappa r_fd = -0.0383(3) obtained
from the STM equation. We discuss applications to cold atomic Fermi gases,
deuteron-neutron scattering in the spin-quartet channel, and lattice
calculations of scattering for nuclei and hadronic molecules at finite volume.Comment: 16 pages, 5 figure
Identification of novel genes expressed during metanephric induction through single-cell library screening
Identification of novel genes expressed during metanephric induction through single-cell library screening.BackgroundDevelopment of the mature kidney is dependent on a series of inductive events between a portion of the epithelial bud at the distal end of the nephric duct and a neighboring domain of committed metanephric mesenchyme. Several genes have been identified to date that are critical in the inductive process. For example, the deletion of Bmp7 from the mouse genome results in dysgenesis or agenesis of the kidney. These findings suggest that Bmp7 controls the expression of genes important for nephrogenesis, but the identity of these genes has remained largely undetermined.MethodsSingle cells were isolated from mouse metanephric mesenchyme during the time of induction (between E11.0 and E11.5) and cDNA libraries constructed from induced and uninduced tissue. Subtractive hybridization was performed to isolate genes that were expressed during E11.5 but not E11.0.ResultsUsing this approach, we identified eight previously known genes, three of which were known to be involved in metanephric induction, thus validating our approach, and nine novel genes. Eight of these genes were completely novel, whereas one was similar to a member of the yeast Anaphase Promoting Complex.ConclusionsThrough subtractive hybridization of mouse E11.0 and E11.5 metanephric mesenchyme single-cell cDNA libraries, we have identified novel genes that are candidates for involvement in nephrogenesis through their up-regulation during the inductive process
Multi-Armed Bandits for Correlated Markovian Environments with Smoothed Reward Feedback
We study a multi-armed bandit problem in a dynamic environment where arm
rewards evolve in a correlated fashion according to a Markov chain. Different
than much of the work on related problems, in our formulation a learning
algorithm does not have access to either a priori information or observations
of the state of the Markov chain and only observes smoothed reward feedback
following time intervals we refer to as epochs. We demonstrate that existing
methods such as UCB and -greedy can suffer linear regret in such
an environment. Employing mixing-time bounds on Markov chains, we develop
algorithms called EpochUCB and EpochGreedy that draw inspiration from the
aforementioned methods, yet which admit sublinear regret guarantees for the
problem formulation. Our proposed algorithms proceed in epochs in which an arm
is played repeatedly for a number of iterations that grows linearly as a
function of the number of times an arm has been played in the past. We analyze
these algorithms under two types of smoothed reward feedback at the end of each
epoch: a reward that is the discount-average of the discounted rewards within
an epoch, and a reward that is the time-average of the rewards within an epoch.Comment: Significant revision of prior version including deeper discussion of
related work, gap-independent regret bounds, and regret bounds for discounted
reward
Multiple verification in computational modeling of bone pathologies
We introduce a model checking approach to diagnose the emerging of bone
pathologies. The implementation of a new model of bone remodeling in PRISM has
led to an interesting characterization of osteoporosis as a defective bone
remodeling dynamics with respect to other bone pathologies. Our approach allows
to derive three types of model checking-based diagnostic estimators. The first
diagnostic measure focuses on the level of bone mineral density, which is
currently used in medical practice. In addition, we have introduced a novel
diagnostic estimator which uses the full patient clinical record, here
simulated using the modeling framework. This estimator detects rapid (months)
negative changes in bone mineral density. Independently of the actual bone
mineral density, when the decrease occurs rapidly it is important to alarm the
patient and monitor him/her more closely to detect insurgence of other bone
co-morbidities. A third estimator takes into account the variance of the bone
density, which could address the investigation of metabolic syndromes, diabetes
and cancer. Our implementation could make use of different logical combinations
of these statistical estimators and could incorporate other biomarkers for
other systemic co-morbidities (for example diabetes and thalassemia). We are
delighted to report that the combination of stochastic modeling with formal
methods motivate new diagnostic framework for complex pathologies. In
particular our approach takes into consideration important properties of
biosystems such as multiscale and self-adaptiveness. The multi-diagnosis could
be further expanded, inching towards the complexity of human diseases. Finally,
we briefly introduce self-adaptiveness in formal methods which is a key
property in the regulative mechanisms of biological systems and well known in
other mathematical and engineering areas.Comment: In Proceedings CompMod 2011, arXiv:1109.104
GSK-3ÎČ Function in Bone Regulates Skeletal Development, Whole-Body Metabolism, and Male Life Span
Glycogen synthase kinase 3 ÎČ (GSK-3ÎČ) is an essential negative regulator or âbrakeâ on many anabolic-signaling pathways including Wnt and insulin. Global deletion of GSK-3ÎČ results in perinatal lethality and various skeletal defects. The goal of our research was to determine GSK-3ÎČ cell-autonomous effects and postnatal roles in the skeleton. We used the 3.6-kb Col1a1 promoter to inactivate the Gsk3b gene (Col1a1-Gsk3b knockout) in skeletal cells. Mutant mice exhibit decreased body fat and postnatal bone growth, as well as delayed development of several skeletal elements. Surprisingly, the mutant mice display decreased circulating glucose and insulin levels despite normal expression of GSK-3ÎČ in metabolic tissues. We showed that these effects are due to an increase in global insulin sensitivity. Most of the male mutant mice died after weaning. Prior to death, blood glucose changed from low to high, suggesting a possible switch from insulin sensitivity to resistance. These male mice die with extremely large bladders that are preceded by damage to the urogenital tract, defects that are also seen type 2 diabetes. Our data suggest that skeletal-specific deletion of GSK-3ÎČ affects global metabolism and sensitizes male mice to developing type 2 diabetes. (Endocrinology 154: 3702â3718, 2013
Osteoblast-specific deficiency of ectonucleotide pyrophosphatase or phosphodiesterase-1 engenders insulin resistance in high-fat diet fed mice
Supraphysiological levels of the osteoblastâenriched mineralization regulator ectonucleotide pyrophosphatase or phosphodiesteraseâ1 (NPP1) is associated with type 2 diabetes mellitus. We determined the impact of osteoblastâspecific Enpp1 ablation on skeletal structure and metabolic phenotype in mice. Female, but not male, 6âweekâold mice lacking osteoblast NPP1 expression (osteoblastâspecific knockout [KO]) exhibited increased femoral bone volume or total volume (17.50% vs. 11.67%; pâ<â.01), and reduced trabecular spacing (0.187 vs. 0.157âmm; pâ<â.01) compared with floxed (control) mice. Furthermore, an enhanced ability of isolated osteoblasts from the osteoblastâspecific KO to calcify their matrix in vitro compared to fl/fl osteoblasts was observed (pâ<â.05). Male osteoblastâspecific KO and fl/fl mice showed comparable glucose and insulin tolerance despite increased levels of insulinâsensitizing underâcarboxylated osteocalcin (195% increase; pâ<â.05). However, following highâfatâdiet challenge, osteoblastâspecific KO mice showed impaired glucose and insulin tolerance compared with fl/fl mice. These data highlight a crucial local role for osteoblast NPP1 in skeletal development and a secondary metabolic impact that predominantly maintains insulin sensitivity
Heterogeneity in reporting on urinary outcome and cure after surgical interventions for stress urinary incontinence in adult neuro-urological patients: A systematic review
Aims: To describe all outcome parameters and definitions of cure used to report on outcome of surgical interventions for stress urinary incontinence (SUI) in neuro-urological (NU) patients. Methods: This systematic review was performed and reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. The study protocol was registered and published (CRD42016033303; http://www.crd.york.ac.uk/PROSPERO). Medline, Embase, Cochrane controlled trials databases, and clinicaltrial.gov were systematically searched for relevant publications until February 2017. Result
Reference intervals for serum osteocalcin concentrations in adult men and women from the study of health in Pomerania
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