Miracle-dz/UniFAR-FTUs huggingface dataset:
Mucosal Healing and Risk for Lymphoproliferative Malignancy in Celiac Disease

BACKGROUND Celiac disease (CD) is associated with an increased risk for lymphoproliferative malignancy (LPM). Whether this risk is affected by the results of follow-up intestinal biopsy, performed to document mucosal healing, is unknown. OBJECTIVE To examine the association between mucosal healing in CD and subsequent LPM. DESIGN Population-based cohort study. SETTING 28 pathology departments in Sweden. PATIENTS 7625 patients with CD who had follow-up biopsy after initial diagnosis. MEASUREMENTS The risk for LPM was compared with that of the general population by using expected rates. The rate of LPM in patients with persistent villous atrophy was compared with that of those with mucosal healing by using Cox regression. RESULTS Among 7625 patients with CD and follow-up biopsy, 3308 (43%) had persistent villous atrophy. The overall risk for LPM was higher than that in the general population (standardized incidence ratio [SIR], 2.81 [95% CI, 2.10 to 3.67]) and was greater among patients with persistent villous atrophy (SIR, 3.78 [CI, 2.71 to 5.12]) than among those with mucosal healing (SIR, 1.50 [CI, 0.77 to 2.62]). Persistent villous atrophy compared with mucosal healing was associated with an increased risk for LPM (hazard ratio [HR], 2.26 [CI, 1.18 to 4.34]). The risk for T-cell lymphoma was increased (HR, 3.51 [CI, 0.75 to 16.34]) but not for B-cell lymphoma (HR, 0.97 [CI, 0.21 to 4.49]). LIMITATION No data on dietary adherence. CONCLUSION Increased risk for LPM in CD is associated with the follow-up biopsy results, with a higher risk among patients with persistent villous atrophy. Follow-up biopsy may effectively stratify patients with CD by risk for subsequent LPM.
Signaling interactions between squamous and columnar epithelia of the Drosophila wing disc

Understanding the interactions between distinct epithelial cells would help us to understand the development of tissues. Drosophila imaginal discs, which are made up of two types of epithelial cells, provide good model systems for such studies. The disc proper or the columnar epithelial cells are apposed to a layer of squamous epithelial cells (the peripodial membrane). We have examined organization of peripodial and disc proper cells vis-à-vis their polarity since cell polarity plays an important role in the polarized transport of signaling molecules. With the help of polarity-specific cell markers, we have observed that apical surfaces of peripodial and disc proper cells face each other. This provides the cellular basis for the recently demonstrated signaling interactions between peripodial and disc proper cells during disc patterning. We also report significant similarities as well as differences between peripodial and disc proper cells in Engrailed-dependent wingdisc-patterning events, which make them an appropriate model system for studying the mechanism of diffusion of signal molecules, such as Hedgehog. Results with wild-type and two mutant forms of Hedgehog suggest that direct cell-cell contact is a requirement for the movement of wild-type Hedgehog signal and reconfirm that cholesterol-modification of Hedgehog makes it a short-range signaling molecule by restricting its movement.
Fuzzy Approximation-Based Adaptive Backstepping Control of an Exoskeleton for Human Upper Limbs

This paper presents fuzzy approximation-based adaptive backstepping control of an exoskeleton for human upper limbs to provide forearm movement assistance so that a human forearm can track any continuous desired trajectory (or constant setpoint) in the presence of parametric/functional uncertainties, unmodeled dynamics, actuator dynamics, and/or disturbances from environments. Given the desired trajectories of human forearm positions, in the developed control, adaptive fuzzy approximators are used to estimate the dynamical uncertainties of the human-robot system, and an iterative learning scheme is utilized to compensate for unknown time-varying periodic disturbances. With the synthesis of the backstepping, iterative learning, and Lyapunov function approaches, the developed controller does not require exact knowledge of the exoskeleton model, and the close-loop system can be proven to be semiglobally uniformly bounded. Three comparison experiments are conducted to illustrate the effectiveness of the proposed control scheme by tracking periodic/repeated trajectories.
Resource Abundance, Poverty and Development

We examine the relationship between resource abundance and several indicators of human welfare. Consistent with the existing literature on the relationship between resource abundance and economic growth, we find that resource-abundant countries tend to suffer low levels of human development. While we find no support for a direct link between resources and welfare, there is an indirect link that operates through institutional quality. There are also significant differences in the effects that resources have on different measures of institutional quality. These results imply that the “resource curse” is a more encompassing phenomenon than previously considered, and that key differences exist between the effects of different resource types on various aspects of governance and human welfare.
A Near-Optimal Exploration-Exploitation Approach for Assortment Selection

We consider an online assortment optimization problem, where in every round, the retailer offers a K-cardinality subset (assortment) of N substitutable products to a consumer, and observes the response. We model consumer choice behavior using the widely used multinomial logit (MNL) model, and consider the retailer's problem of dynamically learning the model parameters, while optimizing cumulative revenues over the selling horizon T. Formulating this as a variant of a multi-armed bandit problem, we present an algorithm based on the principle of "optimism in the face of uncertainty. " A naive MAB formulation would treat each of the N choose K possible assortments as a distinct "arm", leading to regret bounds that are exponential in K. We show that by exploiting the specific characteristics of the MNL model it is possible to design an algorithm with Õ(√NT) regret, under a mild assumption. We demonstrate that this performance is nearly optimal, by providing a (randomized) instance of this problem on which any online algorithm would incur at least ΩOmega(√NT/K) regret.
Multilamellar packing of myelin modeled by lipid‐bound MBP

Membrane compaction and adhesion at the major dense line (cytoplasmic apposition) of myelin, particularly in the central nervous system (CNS), is typically attributed to myelin basic protein (MBP). To explore the role of MBP in myelin membrane adhesion, we attempted to reconstitute the major dense line of myelin from purified lipid‐bound MBP, which is a detergent‐soluble form of MBP that retains the binding of all the myelin lipids. Removal of detergent by long‐term dialysis yielded a precipitate, which, when analyzed by sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS‐PAGE) and thin‐layer chromatography, contained MBP that was still associated with myelin lipids, but in different proportions than in the native membrane. Comparison of lipid composition among isolated myelin, MBP‐free myelin lipids, and lipid‐bound MBP aggregates showed that the lipid‐bound form of the protein was specifically enriched in phosphatidylethanolamine, phosphatidylcholine, sphingomyelin, phosphatidylinositol, and phosphatidylserine. Electron microscopy and x‐ray diffraction demonstrated that the lipid‐MBP complexes formed multilayers having periods of 70–85 Å, which correspond in width to individual myelin membranes. By contrast, the lipids alone assembled as multilayers having a period of ∼40 Å. Thus, the detergent‐soluble form of MBP, which is bound to lipids, might serve as a simple model for the cytoplasmic apposition of myelin. J. Neurosci. Res. 59:513–521, 2000 © 2000 Wiley‐Liss, Inc.
Hippocampal Neurogenesis, Cognitive Deficits and Affective Disorder in Huntington's Disease

Huntington's disease (HD) is a neurodegenerative disorder caused by a tandem repeat expansion encoding a polyglutamine tract in the huntingtin protein. HD involves progressive psychiatric, cognitive, and motor symptoms, the selective pathogenesis of which remains to be mechanistically elucidated. There are a range of different brain regions, including the cerebral cortex and striatum, known to be affected in HD, with evidence for hippocampal dysfunction accumulating in recent years. In this review we will focus on hippocampal abnormalities, in particular, deficits of adult neurogenesis. We will discuss potential molecular mechanisms mediating disrupted hippocampal neurogenesis, and how this deficit of cellular plasticity may in turn contribute to specific cognitive and affective symptoms that are prominent in HD. The generation of transgenic animal models of HD has greatly facilitated our understanding of disease mechanisms at molecular, cellular, and systems levels. Transgenic HD mice have been found to show progressive behavioral changes, including affective, cognitive, and motor abnormalities. The discovery, in multiple transgenic lines of HD mice, that adult hippocampal neurogenesis and synaptic plasticity is disrupted, may help explain specific aspects of cognitive and affective dysfunction. Furthermore, these mouse models have provided insight into potential molecular mediators of adult neurogenesis deficits, such as disrupted serotonergic and neurotrophin signaling. Finally, a number of environmental and pharmacological interventions which are known to enhance adult hippocampal neurogenesis have been found to have beneficial affective and cognitive effects in mouse models, suggesting common molecular targets which may have therapeutic utility for HD and related diseases.
Network analysis of cortical visual pathways mapped with PET

Brain metabolic mapping techniques, such as positron emission tomography (PET), can provide information about the functional interactions within entire neural systems. With the large quantity of data that can accumulate from a mapping study, a network analysis, which makes sense of the complex interactions among neural elements, is necessary. A network analysis was performed on data obtained from a PET study that examined both the changes in regional cerebral blood flow (rCBF) and interregional correlations among human cortical areas during performance of an object vision (face matching) and spatial vision (dot- location matching) task. Brain areas for the network were selected based on regions showing significant rCBF or interregional correlations between tasks. Anterior temporal and frontal lobe regions were added to the network using a principal components analysis. Interactions among selected regions were quantified with structural equation modeling. In the structural equation models, connections between brain areas were based on known neuroanatomy and the interregional correlations were used to calculate path coefficients representing the magnitude of the influence of each directional path. The combination of the anatomical network and interregional correlations created a functional network for each task. The functional network for the right hemisphere showed that in the object vision task, dominant path influences were among occipitotemporal areas, while in the spatial vision task, occipitoparietal interactions were stronger. The network for the spatial vision task also had a strong feedback path from area 46 to occipital cortex, an effect that was absent in the object vision task. There were strong interactions between dorsal and ventral pathways in both networks. Functional networks for the left hemisphere did not differ between tasks. Networks for the interhemispheric interactions showed that the dominant pathway in the right hemisphere also had stronger effects on homologous left hemisphere areas and are consistent with a hypothesis that intrahemispheric interactions were greater in the right hemisphere in both tasks, and that these influences were transmitted callosally to the left hemisphere.
Ultrastructural Pathology of Rat Lung Injury Induced by Ischemic Acute Kidney Injury

Abstract Ischemic acute kidney injury (AKI) is a common complication during inpatient hospitalization, and often induces acute lung injury (ALI). A lot of studies have concentrated on the relevance between AKI and ALI, but the underlying mechanisms of AKI- associated ALI have remained unclear until now. One reason is that evidence of the ultrastructural pathology of AKI-associated ALI has been scarce and needed to be accumulated. The aims of present study are to observe ultrastructural changes, and to reveal leukocyte trafficking of ALI induced by ischemic AKI in rats. For this purpose light microscopy (LM) and electron microscopy (EM), as well as morphometric analysis, were employed in present study. LM observations revealed distinct regions of collapsed alveoli, hemorrhage in alveoli, and interstitial edema in AKI-induced ALI. EM examinations provided facts that alveolar epithelial cells, including type I and type II cells, were necrotic, and endothelia cells undergoing apoptosis as well as interstitial cells undergoing necroptosis were noted in AKI lungs. In addition, shrinkage and decreased or disappeared lamellar bodies were evident in alveolar type II cell of AKI rat lungs. Leukocyte numerical density on area (NA) in AKI lungs was significantly more than that in sham lungs. Based on the morphological criteria from EM examinations and morphometric analysis, a conclusion was that necrosis, including necroptosis, and apoptosis were involved in damaged lung induced by AKI. And inflammation also contributed to acute lung injury of rats with AKI.
Diversity and plasticity of mononuclear phagocytes

Phagocytes are the founding pillars of innate immunity [1] and, as such, have been the object of intense scrutiny in the past few years. Mononuclear phagocytes constitute a system characterised by considerable diversity. Indeed, two major themes have emerged in recent macrophage investigations: their heterogeneity in different tissue environments and phenotypic plasticity in various physiologic and pathologic states [2–5]. Macrophages contribute to tissue homeostasis by the clearance of effete and injured host components and to defence against infection by phagocytosis and microbial killing. Their secretory activities are central to inflammation and its resolution;and it has been widely recognised that they are prominent in modified forms of inflammation such as atherosclerosis and cancer. Yet, many questions remain regarding the molecular basis of their role in pathogenesis and the identification of potential targets for therapeutic manipulation. The Viewpoints in this issue of the journal provide an overview of some of the central themes in macrophage research.
Signaling through the Phosphatidylinositol 3-Kinase (PI3K)/Mammalian Target of Rapamycin (mTOR) Axis Is Responsible for Aerobic Glycolysis mediated by Glucose Transporter in Epidermal Growth Factor Receptor (EGFR)-mutated Lung Adenocarcinoma

Background: EGFR signaling maintains aerobic glycolysis, but the molecular mechanism is still undefined. Results: Drug inhibition studies reveal that downstream signaling via the PI3K pathway is critical for glucose transport and metabolism. Conclusion: The PI3K signaling regulates key metabolic activities in EGFR-mutant lung adenocarcinoma. Significance: These data may guide the development of chemotherapeutic options, including targeting of the PI3K pathway and glucose transporter machinery. Oncogenic epidermal growth factor receptor (EGFR) signaling plays an important role in regulating global metabolic pathways, including aerobic glycolysis, the pentose phosphate pathway (PPP), and pyrimidine biosynthesis. However, the molecular mechanism by which EGFR signaling regulates cancer cell metabolism is still unclear. To elucidate how EGFR signaling is linked to metabolic activity, we investigated the involvement of the RAS/MEK/ERK and PI3K/AKT/mammalian target of rapamycin (mTOR) pathways on metabolic alteration in lung adenocarcinoma (LAD) cell lines with activating EGFR mutations. Although MEK inhibition did not alter lactate production and the extracellular acidification rate, PI3K/mTOR inhibitors significantly suppressed glycolysis in EGFR-mutant LAD cells. Moreover, a comprehensive metabolomics analysis revealed that the levels of glucose 6-phosphate and 6-phosphogluconate as early metabolites in glycolysis and PPP were decreased after inhibition of the PI3K/AKT/mTOR pathway, suggesting a link between PI3K signaling and the proper function of glucose transporters or hexokinases in glycolysis. Indeed, PI3K/mTOR inhibition effectively suppressed membrane localization of facilitative glucose transporter 1 (GLUT1), which, instead, accumulated in the cytoplasm. Finally, aerobic glycolysis and cell proliferation were down-regulated when GLUT1 gene expression was suppressed by RNAi. Taken together, these results suggest that PI3K/AKT/mTOR signaling is indispensable for the regulation of aerobic glycolysis in EGFR-mutated LAD cells.
Nucleotide sequence of the L genome segment of Hantaan virus.

Hantaan virus, strain 76-118, is the prototype virus of the Hantavirus genus of the Bunyaviridae family and is the etiologic agent ofKorean hemorrhagic fever. Hantaan virus has a tripartite, single-stranded, negative sense RNA genome with segments designated as large (L), medium (M), and small (S). Molecular cloning, sequence analysis, and expression studies revealed that the S and M segments of Hantaan virus, respectively, encode the nucleocapsid and envelope glycoproteins (1, 2, 3, 4, 5). The L genome segment is presumed to encode the virion-associated transcriptase. To complete the characterization of the Hantaan virus genome, the nucleotide sequence of the L segment of Hantaan virus was determined. A 3' terminal to prime on virion templates. RNAse H digestion and cDNA synthesis with Klenow were used for second-strand Double-stranded cDNA was into Bluescript (Strategene), either The blot hybridization cDNA to Hantaan virion L chain 5' virion chain
A Novel Modification of PSO Algorithm for SML Estimation of DOA

This paper addresses the issue of reducing the computational complexity of Stochastic Maximum Likelihood (SML) estimation of Direction-of-Arrival (DOA). The SML algorithm is well-known for its high accuracy of DOA estimation in sensor array signal processing. However, its computational complexity is very high because the estimation of SML criteria is a multi-dimensional non-linear optimization problem. As a result, it is hard to apply the SML algorithm to real systems. The Particle Swarm Optimization (PSO) algorithm is considered as a rather efficient method for multi-dimensional non-linear optimization problems in DOA estimation. However, the conventional PSO algorithm suffers two defects, namely, too many particles and too many iteration times. Therefore, the computational complexity of SML estimation using conventional PSO algorithm is still a little high. To overcome these two defects and to reduce computational complexity further, this paper proposes a novel modification of the conventional PSO algorithm for SML estimation and we call it Joint-PSO algorithm. The core idea of the modification lies in that it uses the solution of Estimation of Signal Parameters via Rotational Invariance Techniques (ESPRIT) and stochastic Cramer-Rao bound (CRB) to determine a novel initialization space. Since this initialization space is already close to the solution of SML, fewer particles and fewer iteration times are needed. As a result, the computational complexity can be greatly reduced. In simulation, we compare the proposed algorithm with the conventional PSO algorithm, the classic Altering Minimization (AM) algorithm and Genetic algorithm (GA). Simulation results show that our proposed algorithm is one of the most efficient solving algorithms and it shows great potential for the application of SML in real systems.
Therapeutic and cosmeceutical potential of ethosomes: An overview

The main disadvantage of transdermal drug delivery is the poor penetration of most compounds into the human skin. The main barrier of the skin is located within its uppermost layer, the stratum corneum (SC). Several approaches have been developed to weaken this skin barrier. One of the approaches for increasing the skin penetration of drugs and many cosmetic chemicals is the use of vesicular systems, such as, liposomes and ethosomes. Ethosomes are phospholipid-based elastic nanovesicles containing a high content of ethanol (20–45%). Ethanol is known as an efficient permeation enhancer and has been added in the vesicular systems to prepare elastic nanovesicles. It can interact with the polar head group region of the lipid molecules, resulting in the reduction of the melting point of the stratum corneum lipid, thereby increasing lipid fluidity and cell membrane permeability. The high flexibility of vesicular membranes from the added ethanol permits the elastic vesicles to squeeze themselves through the pores, which are much smaller than their diameters. Ethosomal systems are much more efficient in delivering substances to the skin in the terms of quantity and depth, than either conventional liposomes or hydroalcoholic solutions. The scope of this small review is to introduce the novel concept of ethosomes and to describe some approaches and mechanisms of stimulating topical and transdermal products with ethosomes.
A Reconfigurable Multi-Transform VLSI Architecture Supporting Video Codec Design

This brief presents a reconfigurable VLSI architecture which is designed for multi-transform codec in several video coding standards of MPEG-2/4, VC-1, H.264/AVC and AVS. The reconfigurable multiple constant multiplication algorithm with two fusing strategies is provided to generate constant multipliers in the matrix calculation blocks. Additionally, adder-sharing strategy is adopted in the unified preprocessing/postprocessing block to save circuit areas. The proposed architecture can support different standards through static reconfiguration and forward/inverse transform functions through dynamic reconfiguration. It is suitable for the real-time processing of 1080P HD video codec with six video standards transforms.
Areas for use of PEEK material in dentistry

Polyetheretherketone (PEEK) material is a polycyclic, aromatic, thermoplastic polymer that is semi-crystalline and has a linear structure. PEEK has good mechanical and electrical properties such as resistance to high temperature and resistance to hydrolysis. In addition, because of the property of high biocompatibility, use of PEEK has increased in orthopaedic and trauma cases. The most characteristic property of PEEK material is that it has a low elasticity modulus, close to that of bone. It has been suggested that stress-based problems could be reduced with this material due to the low elasticity modulus. In the light of this information, PEEK material could be considered as an alternative to conventional materials in the field of dentistry.
Towards Formal but Flexible Scenarios

We argue that the evident utility of scenario-based modeling can be greatly enhanced when enriched with a mathematically precise notion of conditionality and partiality, such as that found in Triggered Message Sequence Charts (TMSCs). Unlike traditional Message Sequence Charts, the TMSC formalism allows scenarios to be conditional and partial, supports logical as well as behavioral operators for scenario composition, and is equipped with a refinement notion drawn from traditional process theory that provides a rigorous basis for stepwise development of specifications. This paper illustrates these points via the Center TRACON Automation System for flight control.