Miracle-dz/UniFAR-FTUs huggingface dataset:
Preliminary clusters analysis based on functional disability scales for chronic Low Back Pain. Kinematic and EMG differences

Chronic Low Back Pain (cLBP) can be caused by several origins with important consequences on life, which induce psychosocial consequences. cLBP is not a pathology but a symptom. Patients with cLBP constitute a heterogeneous population. Psychological subgrouping scheme based on multiple Fear-Avoidance Model has been proposed (Beneciuk et al. 2012), but no relation with life of patients and quantitative data have been analyzed. The impact of LBP on life represents a primary concern. The Quebec Back Pain Disability Scale (QBPDS) and the Dallas Pain Questionnaire (DPQ) are the more used scales. QBPDS is a functional evaluation. The DPQ is based on a cognitive and behavioral conception of chronic pain. This impact is evaluated: on a patient’s daily (part 1), work and leisure activities (part 2), on levels of anxiety, depression (part 3), and sociability (part 4). Finally, HAD is applied as a self-report instrument used to evaluate depression and anxiety. Electromyographic (EMG) and kinematic analysis are applied to evaluate patients other than such clinical scales. Median Frequency (MF) and Root Mean Square (RMS) have been used with such population to describe fatigue process and amplitude of muscular activity (Cardozo et al. 2004). Kinematic quantifies impact on movement, specifically. However, in case of cLBP, trunk is associated with the adoption of a protective movement strategy which overall decreased mobility. Deconditioning appears and induces psychosocial consequences. The aims of this study were: (1) to defined clusters on cLBP patients from clinical scales which evaluate impact of this symptom on daily life, (2) compare these clusters on muscular activity (erector spinae during hip flexion-extension) and trunk mobility index (during hip flexion-extension/bending/torsion). 2. Methods
Antidepressant Drugs Transactivate TrkB Neurotrophin Receptors in the Adult Rodent Brain Independently of BDNF and Monoamine Transporter Blockade

Background Antidepressant drugs (ADs) have been shown to activate BDNF (brain-derived neurotrophic factor) receptor TrkB in the rodent brain but the mechanism underlying this phenomenon remains unclear. ADs act as monoamine reuptake inhibitors and after prolonged treatments regulate brain bdnf mRNA levels indicating that monoamine-BDNF signaling regulate AD-induced TrkB activation in vivo. However, recent findings demonstrate that Trk receptors can be transactivated independently of their neurotrophin ligands. Methodology In this study we examined the role of BDNF, TrkB kinase activity and monoamine reuptake in the AD-induced TrkB activation in vivo and in vitro by employing several transgenic mouse models, cultured neurons and TrkB-expressing cell lines. Principal Findings Using a chemical-genetic TrkBF616A mutant and TrkB overexpressing mice, we demonstrate that ADs specifically activate both the maturely and immaturely glycosylated forms of TrkB receptors in the brain in a TrkB kinase dependent manner. However, the tricyclic AD imipramine readily induced the phosphorylation of TrkB receptors in conditional bdnf −/− knock-out mice (132.4±8.5% of control; P = 0.01), indicating that BDNF is not required for the TrkB activation. Moreover, using serotonin transporter (SERT) deficient mice and chemical lesions of monoaminergic neurons we show that neither a functional SERT nor monoamines are required for the TrkB phosphorylation response induced by the serotonin selective reuptake inhibitors fluoxetine or citalopram, or norepinephrine selective reuptake inhibitor reboxetine. However, neither ADs nor monoamine transmitters activated TrkB in cultured neurons or cell lines expressing TrkB receptors, arguing that ADs do not directly bind to TrkB. Conclusions The present findings suggest that ADs transactivate brain TrkB receptors independently of BDNF and monoamine reuptake blockade and emphasize the need of an intact tissue context for the ability of ADs to induce TrkB activity in brain.
Towards Simulator Interoperability and Model Interreplaceability in Network Simulation and Emulation Through AMINES-HLA

Simulation interoperability and model interreplaceability still remain as goals to be attained in network simulation. We have previously developed a high level architecture for network simulators, named AMINES-HLA. In this paper, we discuss AMINES-HLA with respect to IEEE HLA standard, DEVS, and the architectures of OMNeT++ and NS-2. We describe two scenarios which demonstrate how simulation interoperability and model interreplacement can be realized through AMINES-HEA. In the first scenario, we show how a virtualized program and protocol stack can be used to replace a specific model in a simulator built on AMEMES-HLA. In the context of the second scenario, we discuss how two simulators can be interoperated
Non‐IgE‐mediated gastrointestinal food allergies in children

Non‐IgE‐mediated gastrointestinal food allergic disorders (non‐IgE‐GI‐FA) including food protein‐induced enterocolitis syndrome (FPIES), food protein‐induced enteropathy (FPE), and food protein‐induced allergic proctocolitis (FPIAP) are relatively uncommon in infants and young children, but are likely under‐diagnosed. Non‐IgE‐GI‐FA have a favorable prognosis, with majority resolving by age 3–5 years. Diagnosis relies on the recognition of symptoms pattern in FPIAP and FPIES and biopsy in FPE. Further studies are needed for a better understanding of the pathomechanism, which will lead eventually to the development of diagnostic tests and treatments. Limited evidence supports the role of food allergens in subsets of constipation, gastroesophageal reflux disease, irritable bowel syndrome, and colic. The immunologic pathomechanism is not fully understood and empiric prolonged avoidance of food allergens should be limited to minimize nutrient deficiency and feeding disorders/food aversions in infants.
Spasticity and Its Contribution to Hypertonia in Cerebral Palsy

Spasticity is considered an important neural contributor to muscle hypertonia in children with cerebral palsy (CP). It is most often treated with antispasticity medication, such as Botulinum Toxin-A. However, treatment response is highly variable. Part of this variability may be due to the inability of clinical tests to differentiate between the neural (e.g., spasticity) and nonneural (e.g., soft tissue properties) contributions to hypertonia, leading to the terms “spasticity” and “hypertonia” often being used interchangeably. Recent advancements in instrumented spasticity assessments offer objective measurement methods for distinction and quantification of hypertonia components. These methods can be applied in clinical settings and their results used to fine-tune and improve treatment. We reviewed current advancements and new insights with respect to quantifying spasticity and its contribution to muscle hypertonia in children with CP. First, we revisit what is known about spasticity in children with CP, including the various definitions and its pathophysiology. Second, we summarize the state of the art on instrumented spasticity assessment in CP and review the parameters developed to quantify the neural and nonneural components of hypertonia. Lastly, the impact these quantitative parameters have on clinical decision-making is considered and recommendations for future clinical and research investigations are discussed.
Enrichment of Gene-Coding Sequences in Maize by Genome Filtration

Approximately 80% of the maize genome comprises highly repetitive sequences interspersed with single-copy, gene-rich sequences, and standard genome sequencing strategies are not readily adaptable to this type of genome. Methodologies that enrich for genic sequences might more rapidly generate useful results from complex genomes. Equivalent numbers of clones from maize selected by techniques called methylation filtering and High C0t selection were sequenced to generate ∼200,000 reads (approximately 132 megabases), which were assembled into contigs. Combination of the two techniques resulted in a sixfold reduction in the effective genome size and a fourfold increase in the gene identification rate in comparison to a nonenriched library.
Polycythemia vera in young patients: a study on the long-term risk of thrombosis, myelofibrosis and leukemia.

BACKGROUND AND OBJECTIVES Polycythemia vera (PV) is unusual in young patients, so that little information is available on long-term clinical evolution in this particular group. The aim of this study was to define the long-term risk of thrombosis, acute leukemia (AL) and myelofibrosis with myeloid metaplasia (MMM) in young PV patients. DESIGN AND METHODS From 1975 to 2000, 70 PV patients aged less than 50 years were followed for a median time of 14 years (range 2-26). About three quarters were treated with pipobroman. The Kaplan-Meier method and Cox regression were used for survival analysis. The standardized mortality ratio (SMR) was calculated using Italian age/sex specific mortality rates. RESULTS The risk of thrombosis increased during the observation period, reaching a plateau of 14% at 10 years and was markedly higher in individuals with a previous history of thrombosis (p=0.0023). No patient had progression into AL or MMM before the 9th year of follow-up. Subsequently, five patients (7%) developed AL and five (7%) MMM, with a 20-year cumulative risk of 15% and 10%, respectively. Overall survival at 20 years was 62%, with nine patients dying of progression into AL or MMM, four of vascular events, one of lung cancer, and four of non-PV-related causes. The SMR was 5.3, indicating a mortality significantly higher than that of the general population (p<0.000). INTERPRETATION AND CONCLUSIONS This long-term retrospective cohort study shows that although the median survival of young patients with PV exceeds 23 years, their life expectancy is markedly lower than that of the general population because of disease evolution into AL or MMM.
On-the-Fly Algorithms for Bisimulation Metrics

We study the problem of determining approximate equivalences in Markov Decision Processes with rewards using bisimulation metrics. We provide an extension of the framework previously introduced in Ferns et al. (2004), which computes iteratively improving approximations to bisimulation metrics using exhaustive pairwise state comparisons. The similarity between states is determined using the Earth Mover's Distance, as extensively studied in optimization and machine learning. We address two computational limitations of the above framework: first, all pairs of states have to be compared at every iteration, and second, convergence is proven only under exact computations. We extend their work to incorporate "on-the-fly" methods, which allow computational effort to focus first on pairs of states where the impact is expected to be greater. We prove that a method similar to asynchronous dynamic programming converges to the correct value of the bisimulation metric. The second relaxation is based on applying heuristics to obtain approximate state comparisons, building on recent work on improved algorithms for computing Earth Mover's Distance. Finally, we show how this approach can be used to generate new algorithmic strategies, based on existing prioritized sweeping algorithms used for prediction and control in MDPs.
Localization of the mobile agent using indirect Kalman filter in distributed sensor networks

This paper proposes a localization algorithm for mobile agents in sensor networks using the data fusion method based on indirect Kalman filter. The fusion method of an inertial navigation sensor and sensor nodes data is used to acquire the correct position information. Since indirect Kalman filter is used for estimation of the mobile agent position, the position of the mobile agent can be estimated even when the sensor node cannot work or data acquired from the network are not reliable. Because measurement errors are used for estimation, its implementation is easy. Finally, a sequence of simulations is carried out to confirm the performance of the proposed localization algorithm.
ETTM: A Scalable Fault Tolerant Network Manager

In this paper, we design, implement, and evaluate a new scalable and fault tolerant network manager, called ETTM, for securely and efficiently managing network resources at a packet granularity. Our aim is to provide network administrators a greater degree of control over network behavior at lower cost, and network users a greater degree of performance, reliability, and flexibility, than existing solutions. In our system, network resources are managed via software running in trusted execution environments on participating end-hosts. Although the software is physically running on end-hosts, it is logically controlled centrally by the network administrator. Our approach leverages the trend to open management interfaces on network switches as well as trusted computing hardware and multicores at end-hosts. We show that functionality that seemingly must be implemented inside the network, such as network address translation and priority allocation of access link bandwidth, can be simply and efficiently implemented in our system.
[About the 350th anniversary of the foundation of the chair of anatomy of the faculty of medicine at Strasbourg (1652-2002)].

Some historical and bibliographical elements are given at the occasion of the 350th anniversary of the foundation of the chair of anatomy at Strasbourg. Strasbourg played an important role in the dissemination of the anatomical knowledge in the end of the 15th and the first half of the 16th century. In 1517, the first official human dissection organized in Strasbourg was performed. In 1652, a specific chair of anatomy founded, and the first holder was J. A. Sebiz (1614-1685). In 1670, an anatomical lecture theatre was created. Strasbourg became a French town in 1681 with no modification of the university and of the chair of anatomy. In 1872, after the annexation of Alsace, a new German university was founded ; normal anatomy and pathology were separated and each chair attached to a particular institute. In 1919, when the Faculty of Medicine was reorganized after Alsace was restored to France, specific chairs and institutes were founded for histology and embryology. Among the famous morphologists and scientists who worked in Strasbourg were in anatomy : H. Brunschwig (? -1534), W. H. Ryff (c. 1505-1548), J. Winter von Andernach (1497-1574), T. Lauth (1758-1826), F. D. Reisseissen (1773-1828), J. F. Lobstein (1777-1835), E. A. Lauth (1803-1837), E. Koeberlé (1828-1915), E. Beaunis (1830-1921), H. D. Bouchard (1833-1899), J. G. Joessel (1838-1892), W. Waldeyer (1836-1921), G. Schwalbe (1844-1916), W. Pfitzner (1853-1903), F. Keibel (1861-1929), A. Forster (1878-1957), and P. Bellocq (1888-1962) ; in pathology : F. D. von Rechlinghausen (1833-1910), H. Chiari (1851-1916), J. G. Mönckeberg (1877-1925), P. Masson (1880-1959), and L. Géry (1883-1957) ; in histology : P. Bouin (1870-1962), M. Aron (1892-1974), R. Courrier (1895-1986), and M. Klein (1905-1975) ; in embryology : P. Ancel (1873-1961), P. Vintemberger (1891-1983), J. Benoit (1896-1982), E. Wolff (1904-1996), and J. Clavert (1912-1994).
Clustering and lexical information support for the recovery of design pattern in source code

We propose an approach that leverages lexical information and fuzzy clustering to reduce the number of the design pattern instances that existing approaches based on structural information (i.e., navigating the dependencies among software elements) erroneously recover in source code. To assess the effectiveness of the techniques, we present the results of a case study conducted on four open source software systems implemented in java. The data analysis indicates that the use of lexical information and fuzzy clustering improves the correctness of the results achieved by existing design pattern recovery approaches based on structural information, while preserving the number of design pattern instances correctly identified.
Developmental Changes in Expression of Genes Involved in Regulation of Apoptosis in the Bovine Preimplantation Embryo1

The early bovine preimplantation embryo is resistant to proapoptotic signals until around the 8- to 16-cell stage. We hypothesized that 2-cell embryos have higher amounts of antiapoptotic proteins and lower amounts of proapoptotic proteins when compared to embryos ≥16 cells. Steady-state concentrations of mRNA for the antiapoptotic genes BCL2 and HSPA1A were higher for MII oocytes, 2-cell embryos, and 2-cell embryos treated with alpha-amanitin as compared to ≥16-cell embryos. Steady-state concentrations of mRNA for the proapoptotic gene BAD increased in embryos ≥16 cells. There was no significant effect of stage of development on steady-state mRNA concentrations of BCL2L1, DFFA, or BAX. Using immunohistochemistry, it was found that BCL2 was present in greater relative concentrations for 2-cell embryos than for embryos ≥16 cells. These results were confirmed by Western blotting. Relative amounts of immunoreactive BAX detected by immunofluorescence were lower for 2-cell embryos than for embryos ≥16 cells. Using Western blotting, a high molecular weight (46 kDa) form of BAX was highest in ≥16-cell embryos, intermediate in 2-cell embryos, and lowest in MII oocytes. There were no effects of stage of development on relative amounts of immunoreactive BCL2L1, HSPA1A, or BAD, as determined by immunofluorescence. Treatment of embryos with alpha-amanitin from Day 0 to Day 5 or Day 4 to Day 5 after insemination reduced activation of group II caspases and terminal deoxynucleotidyl transferase dUTP nick end labeling after treatment with the proapoptotic signal C2 ceramide at Day 5 after fertilization. Thus, transcription of BAX or other proteins is required for acquisition of the capacity for apoptosis. Results support the idea that changes in amounts of BCL2 family members are important for the inhibition of apoptosis in the 2-cell embryo and in the establishment of the capacity for apoptosis later in development.
Building reconstruction from a single DEM

We present a new approach for building reconstruction from a single Digital Elevation Model (DEM). It treats buildings as an assemblage of simple urban structures extracted from a library of 3D parametric blocks (like a LEGOreg set). This method works on various data resolutions such as 0.7 m satellite and 0.1 m aerial DEMs and allows us to obtain 3D representations with various levels of detail. First, the 2D supports of the urban structures are extracted either interactively or automatically. Then, 3D blocks are placed on the 2D supports using a Gibbs model. A Bayesian decision finds the optimal configuration of 3D blocks using a RJMCMC sampler. Experimental results on complex buildings and dense urban areas are presented using data at various resolutions.
Protumor Activities of the Immune Response: Insights in the Mechanisms of Immunological Shift, Oncotraining, and Oncopromotion

Experimental and clinical studies indicate that cells of the innate and adaptive immune system have both anti- and pro-tumor activities. This dual role of the immune system has led to a conceptual shift in the role of the immune system's regulation of cancer, in which immune-tumor cell interactions are understood as a dynamic process that comprises at least five phases: immunosurveillance, immunoselection, immunoescape, oncotraining, and oncopromotion. The tumor microenvironment shifts immune cells to perform functions more in tune with the tumor needs (oncotraining); these functions are related to chronic inflammation and tissue remodeling activities. Among them are increased proliferation and survival, increased angiogenesis and vessel permeability, protease secretion, acquisition of migratory mesenchymal characteristics, and self-renewal properties that altogether promote tumor growth and metastasis (oncopromotion). Important populations in all these pro-tumor processes are M2 macrophages, N2 neutrophils, regulatory T cells, and myeloid derived suppressor cells; the main effectors molecules are CSF-1, IL-6, metalloproteases, VEGF, PGE-2, TGF-β, and IL-10. Cancer prognosis correlates with densities and concentrations of protumoral populations and molecules, providing ideal targets for the intelligent design of directed preventive or anticancer therapies.
Simultaneous Calibration and Nonresponse Adjustment

Single and joint inclusion probabilities are generally known for complex survey designs up to the point where survey weights are modified due to nonresponse and population controls. Best practice by sophisticated survey practitioners generally includes weight modifications, first by calibration, ratio adjustment or raking to correct for nonresponse, next by further steps to impose population survey controls; and often, by final steps involving weight truncation or cell-collapsing to constrain the modified weights, usually so that the largest and smallest weights do not dier by more than a designated multiplicative factor. These adjustments are sometimes made in successive stages, the order of which may dier from one survey to another. In this article, generalized-raking calibration methodology is adapted to allow all of these adjustments to be accomplished in a single stage, after which linearization-based large-sample variance formulas are available.
Robust variance estimation in meta‐regression with dependent effect size estimates

Conventional meta‐analytic techniques rely on the assumption that effect size estimates from different studies are independent and have sampling distributions with known conditional variances. The independence assumption is violated when studies produce several estimates based on the same individuals or there are clusters of studies that are not independent (such as those carried out by the same investigator or laboratory). This paper provides an estimator of the covariance matrix of meta‐regression coefficients that are applicable when there are clusters of internally correlated estimates. It makes no assumptions about the specific form of the sampling distributions of the effect sizes, nor does it require knowledge of the covariance structure of the dependent estimates. Moreover, this paper demonstrates that the meta‐regression coefficients are consistent and asymptotically normally distributed and that the robust variance estimator is valid even when the covariates are random. The theory is asymptotic in the number of studies, but simulations suggest that the theory may yield accurate results with as few as 20–40 studies. Copyright © 2010 John Wiley & Sons, Ltd.
Development of Gonadotropes May Involve Cyclic Transdifferentiation of Growth Hormone Cells

The cyclic rise in expression of anterior pituitary gonadotropins coincides with the appearance of cells sharing gonadotropic and somatotropic phenotypes. To learn more about possible factors that regulate the origin of this cell type, we studied the time of appearance of cells that co-expressed growth hormone (GH) and gonadotropins and estrogen receptors during the estrous cycle and compared this timing with known changes in regulatory hormones or their receptors. The first event in this cell population is an increase in expression of estrogen receptor (ER)β by GH cells from estrus to metestrus suggesting that estrogen may mediate this early change. Expression of GH mRNA rises rapidly from metestrus to mid-cycle. The rise is seen first in GH cells and then in cells with luteinizing hormone (LH) antigens. These data suggest that, early in the cycle, cells bearing GH and growth hormone releasing hormone (GHRH) receptors begin to produce LH and gonadotropin releasing hormone (GnRH) receptors. Early in proestrus, there is an increase in cells with GH and follicle-stimulating hormone (FSH) suggesting that this set of multipotential cells develops later than GH-LH cells. This fits with earlier studies showing the later rise in expression of FSH mRNA. Collectively these data suggest that the anterior pituitary contains a subset of GH cells that have the capacity to respond to multiple releasing hormones and support more than one system.