Miracle-dz/UniFAR-FTUs huggingface dataset:
B-Lymphocyte Proliferation during Bovine Leukemia VirusInduced Persistent Lymphocytosis Is Enhanced by T-Lymphocyte-Derived Interleukin-2

ABSTRACT Bovine leukemia virus (BLV)-induced persistent lymphocytosis is characterized by a polyclonal expansion of CD5+ B lymphocytes. To examine the role of the cytokine microenvironment in this virus-induced B-lymphocyte expansion, the expression of interleukin-2 (IL-2), IL-4, IL-10, and gamma interferon (IFN-γ) mRNA, was measured in stimulated peripheral blood mononuclear cells from persistently lymphocytotic BLV-infected cows, nonlymphocytotic BLV-infected cows, and uninfected cows. IL-2 and IL-10 mRNA expression and IL-2 functional activity were significantly increased when peripheral blood mononuclear cells from persistently lymphocytotic cows were stimulated with concanavalin A (ConA). Additionally, during persistent lymphocytosis, peak IL-2 and IL-10 mRNA expression was delayed, and elevated expression was prolonged. To determine the potential biologic importance of increased IL-2 and IL-10 expression, the response of isolated B lymphocytes from persistently lymphocytotic cows to human recombinant cytokines and to cytokine-containing supernatants from isolated T lymphocytes was examined. While recombinant human IL-10 (rhIL-10) did not consistently induce detectable changes, rhIL-2 increased viral protein (p24) and IL-2 receptor expression in isolated B lymphocytes from persistently lymphocytotic cows. Additionally, rhIL-2 and supernatant from ConA-stimulated T lymphocytes enhanced B-lymphocyte proliferation. The stimulatory activity of the T-lymphocyte supernatant could be completely inhibited with a polyclonal anti-rhIL-2 antibody. Finally, polyclonal anti-rhIL-2 antibody, as well as anti-BLV antibody, inhibited spontaneous proliferation of peripheral blood mononuclear cells from persistently lymphocytotic cows, demonstrating that the spontaneous lymphoproliferation characteristic of BLV-induced persistent lymphocytosis is IL-2 dependent and antigen dependent. Collectively, these findings strongly suggest that increased T-lymphocyte expression of IL-2 in BLV-infected cows contributes to development and/or maintenance of persistent B lymphocytosis.
Provably Useful Kernel Matrix Approximation in Linear Time

We give the first algorithms for kernel matrix approximation that run in time linear in the number of data points and output an approximation which gives provable guarantees when used in many downstream learning tasks, including kernel principal component analysis, kernel $k$-means clustering, kernel ridge regression, and kernel canonical correlation analysis. Our methods require just $\tilde O(n\cdot k)$ kernel evaluations and $\tilde O(n \cdot k^2)$ additional runtime, where $n$ is the number of training data points and $k$ is a target rank or effective dimensionality parameter. These runtimes are significantly sub-linear in the size of the $n \times n$ kernel matrix and apply to any kernel matrix, without assuming regularity or incoherence conditions. The algorithms are based on a ridge leverage score Nystr\"om sampling scheme (RLS-Nystr\"om) which was recently shown to yield strong kernel approximations, but which had no efficient implementation. We address this shortcoming by introducing fast recursive sampling methods for RLS-Nystr\"om, while at the same time proving extended approximation guarantees for this promising new method.
Desflurane, Sevoflurane, and Isoflurane Affect Left Atrial Active and Passive Mechanical Properties and Impair Left Atrial–Left Ventricular Coupling In Vivo: Analysis Using Pressure–Volume Relations

BackgroundThe effects of volatile anesthetics on left atrial function in vivo have not been described. The authors tested the hypothesis that desflurane, sevoflurane, and isoflurane alter left atrial mechanics evaluated with invasively derived pressure–volume relations. MethodsBarbiturate-anesthetized dogs (n = 24) were instrumented for measurement of aortic, left atrial, and left ventricular pressures (micromanometers) and left atrial volume (orthogonal sonomicrometers). Left atrial contractility and chamber stiffness were assessed with end-systolic and end-reservoir pressure–volume relations, respectively, obtained from differentially loaded diagrams. Relaxation was determined from the slope of left atrial pressure decline after contraction. Stroke work and reservoir function were assessed by A and V loop areas, respectively. Left atrial–left ventricular coupling was determined by the ratio of left atrial contractility and left ventricular elastance. Dogs received 0.6, 0.9, and 1.2 minimum alveolar concentration desflurane, sevoflurane, or isoflurane in a random manner, and left atrial function was determined after 20-min equilibration at each dose. ResultsDesflurane, sevoflurane, and isoflurane decreased heart rate, mean arterial pressure, and maximal rate of increase of left ventricular pressure and increased left atrial end-diastolic, end-systolic, and maximum volumes. All three anesthetics caused dose-related reductions in left atrial contractility, relaxation, chamber stiffness, and stroke work. Administration of 0.6 and 0.9 minimum alveolar concentration desflurane, sevoflurane, and isoflurane increased V loop area. All three anesthetics decreased the ratio of stroke work to total left atrial pressure–volume diagram area, increased the ratio of conduit to reservoir volume, and reduced left atrial contractility–left ventricular elastance to equivalent degrees. ConclusionsThe results indicate that desflurane, sevoflurane, and isoflurane depress left atrial contractility, delay relaxation, reduce chamber stiffness, preserve reservoir and conduit function, and impair left atrial–left ventricular coupling in vivo.
Th1 Disabled Function in Response to TLR4 Stimulation of Monocyte-Derived DC from Patients Chronically-Infected by Hepatitis C Virus

Background Lack of protective antibodies and inefficient cytotoxic responses are characteristics of chronic hepatitis C infection. A defect in dendritic cell (DC) function has thus been suspected, but this remains a controversial issue. Methods and Findings Here we show that monocyte-derived DC (MoDC) from chronically-infected patients can mature in response to TLR1/2, TLR2/6 or TLR3 ligands. In contrast, when stimulated with the TLR4 ligand LPS, MoDC from patients show a profound defect in inducing IFNγ secretion by allogeneic T cells. This defect is not due to defective phenotypic maturation or to the presence of HCV-RNA in DC or monocytes but is correlated to reduced IL-12 secretion by DC. Restoration of DC ability to stimulate IFNγ secretion can be obtained by blocking MEK activation in DC, indicating that MEK/ERK pathway is involved in the Th1 defect of MoDC. Monocytes from HCV patients present increased spontaneous secretion of cytokines and chemokines, especially MIP-1β. Addition of MIP-1β on healthy monocytes during differentiation results in DC that have Th1 defect characteristic of MoDC from HCV patients, suggesting that MIP-1β secretion by HCV monocytes participates in the Th1 defect of DC. Conclusions Our data indicate that monocytes from HCV patients are activated in vivo. This interferes with their differentiation into DC, leading to deficient TLR4 signaling in these cells that are enable to induce a Th1 response. This specific defect is linked to the activation of the MEK/ERK pathway.
MicroRNA-107: a novel promoter of tumor progression that targets the CPEB3/EGFR axis in human hepatocellular carcinoma

MicroRNAs (miRNAs) are dysregulated in many types of malignancies, including human hepatocellular carcinoma (HCC). MiR-107 has been implicated in several types of cancer regulation; however, relatively little is known about miR-107 in human HCC. In the present study, we showed that the overexpression of miR-107 accelerates the tumor progression of HCC in vitro and in vivo through its new target gene, CPEB3. Furthermore, our results demonstrated that CPEB3 is a newly discovered tumor suppressor that acts via the EGFR pathway. Therefore, our study demonstrates that the newly discovered miR-107/CPEB3/EGFR axis plays an important role in HCC progression and might represent a new potential therapeutic target for HCC treatment.
Quality of life in women with urinary incontinence is impaired and comparable to women with chronic diseases.

OBJECTIVES To evaluate the quality of life in women with urinary incontinence (categorised by urodynamic findings). DESIGN Prospective cohort study on patients. SETTING Urogynaecology unit of a university teaching hospital in Hong Kong. PATIENTS. Female patients presenting to our clinic from July 2008 to December 2009 and having their urinary incontinence categorised by urodynamic study. MAIN OUTCOME MEASURES Patient's quality of life was assessed using the Medical Outcomes Study Short Form, Urogenital Distress Inventory Short Form, and Incontinence Impact Questionnaire Short Form. Their quality of life was compared according to their urodynamic category and a subgroup analysis was performed on patients having continence surgery for urodynamic stress incontinence. RESULTS Among the 223 women studied, 46% had urodynamic stress incontinence, 18% had detrusor overactivity, 2% had both urodynamic stress incontinence and detrusor overactivity, and 34% had no urodynamic abnormality. In all, the Medical Outcomes Study Short Form scoring was lower than normal local population. The Medical Outcomes Study Short Form score in detrusor overactivity group was significantly lower than urodynamic stress incontinence group in vitality and mental health domains. Detrusor overactivity group also had higher scores in Incontinence Impact Questionnaire Short Form in travel, social and emotional health subscales and total score (46.3 vs 29.1; P<0.01). Women with urodynamic stress incontinence and required continence surgery had higher scores in Incontinence Impact Questionnaire Short Form. CONCLUSION Women with urinary incontinence had impaired quality of life and it was comparable to other chronic medical diseases. Women with detrusor overactivity have more impaired quality of life than women with urodynamic stress incontinence. Severity of urodynamic stress incontinence did not correlate with quality of life. Women who opted for continence surgery had poorer quality of life.
Application of Virtual Reality Graphics in Assessment of Concussion

Abnormal balance in individuals suffering from traumatic brain injury (TBI) has been documented in numerous recent studies. However, specific mechanisms causing balance deficits have not been systematically examined. This paper demonstrated the destabilizing effect of visual field motion, induced by virtual reality graphics in concussed individuals but not in normal controls. Fifty five student-athletes at risk for concussion participated in this study prior to injury and 10 of these subjects who suffered MTBI were tested again on day 3, day 10, and day 30 after the incident. Postural responses to visual field motion were recorded using a virtual reality (VR) environment in conjunction with balance (AMTI force plate) and motion tracking (Flock of Birds) technologies. Two experimental conditions were introduced where subjects passively viewed VR scenes or actively manipulated the visual field motion. Long-lasting destabilizing effects of visual field motion were revealed, although subjects were asymptomatic when standard balance tests were introduced. The findings demonstrate that advanced VR technology may detect residual symptoms of concussion at least 30 days post-injury.
Phospholipase D1 Mediates TNFα-Induced Inflammation in a Murine Model of TNFα-Induced Peritonitis

Background Tumor Necrosis Factor alpha (TNFα) is a pleiotropic cytokine extensively studied for its role in the pathogenesis of a variety of disease conditions, including in inflammatory diseases. We have recently shown that, in vitro, that TNFα utilizes PLD1 to mediate the activation of NFκB and ERK1/2 in human monocytes. The aim of this study was to investigate the role(s) played by phospholipase D1 (PLD1) in TNFα-mediated inflammatory responses in vivo. Methodology/Findings Studies were performed in vivo using a mouse model of TNFα-induced peritonitis. The role of PLD1 was investigated by functional genomics, utilizing a specific siRNA to silence the expression of PLD1. Administration of the siRNA against PLD1 significantly reduced PLD1 levels in vivo. TNFα triggers a rapid pyrogenic response, but the in vivo silencing of PLD1 protects mice from the TNFα-induced rise in temperature. Similarly TNFα caused an increase in the serum levels of IL-6, MIP-1α and MIP-1β: this increase in cytokine/chemokine levels was inhibited in mice where PLD1 had been silenced. We then induced acute peritonitis with TNFα. Intraperitoneal injection of TNFα triggered a rapid increase in vascular permeability, and the influx of neutrophils and monocytes into the peritoneal cavity. By contrast, in mice where PLD1 had been silenced, the TNFα-triggered increase in vascular permeability and phagocyte influx was substantially reduced. Furthermore, we also show that the TNFα-mediated upregulation of the cell adhesion molecules VCAM and ICAM1, in the vascular endothelium, were dependent on PLD1. Conclusions These novel data demonstrate a critical role for PLD1 in TNFα-induced inflammation in vivo and warrant further investigation. Indeed, our results suggest PLD1 as a novel target for treating inflammatory diseases, where TNFα play key roles: these include diseases ranging from sepsis to respiratory and autoimmune diseases; all diseases with considerable unmet medical need.
Expression of Carbonic Anhydrase V in Pancreatic Beta Cells Suggests Role for Mitochondrial Carbonic Anhydrase in Insulin Secretion*

Carbonic anhydrase V (CA-V) is a mitochondrial enzyme that provides bicarbonate for pyruvate carboxylase in liver and kidney. In the course of a survey of the tissue distribution of CA-V, we detected intense immunostaining in pancreatic islets when sections from rat and mouse pancreases were reacted with a polyclonal antibody to recombinant mouse CA-V. The distribution and large number of CA-V-positive cells in each islet suggested that they represented beta cells. Double immunofluorescence staining of tissue sections and isolated islet cells showed cellular colocalization of CA-V and insulin, confirming that beta cells contain CA-V. Western blotting of rat islets of Langerhans and primary beta cells showed 33- and 30-kDa polypeptides of precursor and mature CA-V, respectively. The CA-V expression was beta cell-specific since no CA-V immunoreaction was detected in the primary alpha cells. Immunohistochemical staining for CA-I, CA-II, CA-IV, CA-VI, and CA-IX was negative in beta cells, and Western blotting of beta cells also failed to identify any CA in beta cells except CA-V. The specific localization of CA-V in beta cells led us to hypothesize that CA-V may be functionally linked to the regulation of insulin secretion. Consistent with this hypothesis, the CA inhibitor acetazolamide was found to be a strong inhibitor of glucose-stimulated insulin secretion by isolated rat pancreatic islets.
CRY2 Is Associated with Depression

Background Abnormalities in the circadian clockwork often characterize patients with major depressive and bipolar disorders. Circadian clock genes are targets of interest in these patients. CRY2 is a circadian gene that participates in regulation of the evening oscillator. This is of interest in mood disorders where a lack of switch from evening to morning oscillators has been postulated. Principal Findings We observed a marked diurnal variation in human CRY2 mRNA levels from peripheral blood mononuclear cells and a significant up-regulation (P = 0.020) following one-night total sleep deprivation, a known antidepressant. In depressed bipolar patients, levels of CRY2 mRNA were decreased (P = 0.029) and a complete lack of increase was observed following sleep deprivation. To investigate a possible genetic contribution, we undertook SNP genotyping of the CRY2 gene in two independent population-based samples from Sweden (118 cases and 1011 controls) and Finland (86 cases and 1096 controls). The CRY2 gene was significantly associated with winter depression in both samples (haplotype analysis in Swedish and Finnish samples: OR = 1.8, P = 0.0059 and OR = 1.8, P = 0.00044, respectively). Conclusions We propose that a CRY2 locus is associated with vulnerability for depression, and that mechanisms of action involve dysregulation of CRY2 expression.
The Size of a Hypergraph and its Matching Number

More than forty years ago, Erdős conjectured that for any $t \leq \frac{n}{k}$, every k-uniform hypergraph on n vertices without t disjoint edges has at most max${\binom{kt-1}{k}, \binom{n}{k}-\binom{n-t+1}{k}\}$ edges. Although this appears to be a basic instance of the hypergraph Turán problem (with a t-edge matching as the excluded hypergraph), progress on this question has remained elusive. In this paper, we verify this conjecture for all $t < \frac{n}{3k^2}$. This improves upon the best previously known range $t = O\bigl(\frac{n}{k^3}\bigr)$, which dates back to the 1970s.
Molecular Determinants of Species-Specific Activation or Blockade of TRPA1 Channels

TRPA1 is an excitatory, nonselective cation channel implicated in somatosensory function, pain, and neurogenic inflammation. Through covalent modification of cysteine and lysine residues, TRPA1 can be activated by electrophilic compounds, including active ingredients of pungent natural products (e.g., allyl isothiocyanate), environmental irritants (e.g., acrolein), and endogenous ligands (4-hydroxynonenal). However, how covalent modification leads to channel opening is not understood. Here, we report that electrophilic, thioaminal-containing compounds [e.g., CMP1 (4-methyl-N-[2,2,2-trichloro-1-(4-nitro-phenylsulfanyl)-ethyl]-benzamide)] covalently modify cysteine residues but produce striking species-specific effects [i.e., activation of rat TRPA1 (rTRPA1) and blockade of human TRPA1 (hTRPA1) activation by reactive and nonreactive agonists]. Through characterizing rTRPA1 and hTRPA1 chimeric channels and point mutations, we identified several residues in the upper portion of the S6 transmembrane domains as critical determinants of the opposite channel gating: Ala-946 and Met-949 of rTRPA1 determine channel activation, whereas equivalent residues of hTRPA1 (Ser-943 and Ile-946) determine channel block. Furthermore, side-chain replacements at these critical residues profoundly affect channel function. Therefore, our findings reveal a molecular basis of species-specific channel gating and provide novel insights into how TRPA1 respond to stimuli.
Self-construal and cultural orientation as predictors for developmental goals: A comparison between Brazilian and German caregivers

The aim of this study was to investigate caregivers' developmental goals in Brazil and Germany and to explain inter- and intracultural variations in these goals by taking their respective subjective cultural values into account. The main question was whether caregivers' preferences of developmental goals depend on their perception of prevailing norms in the culture or on their personal value preferences. German and Brazilian kindergarten teachers and mothers of 5-year-old children (N = 128) participated in the study. They were asked to select and rank the developmental goals based on importance out of a given list of goals. Furthermore, the caregivers' self-construal (SCS) and their normative and evaluative cultural orientation (COS) were assessed. Results yielded culture-specific differences for self-construal, cultural orientation, and preferences of developmental goals. The caregivers' perception of prevailing cultural norms was the best predictor for goal preferences.
On cosets of the generalized first-order reed-muller code with low PMEPR

Golay sequences are well suited for use as codewords in orthogonal frequency-division multiplexing (OFDM), since their peak-to-mean envelope power ratio (PMEPR) in q-ary phase-shift keying (PSK) modulation is at most 2. It is known that a family of polyphase Golay sequences of length 2m organizes in m! /2 cosets of a q-ary generalization of the first-order Reed-Muller code, RMq(1,m). In this paper, a more general construction technique for cosets of RM q(1,m) with low PMEPR is established. These cosets contain so-called near-complementary sequences. The application of this theory is then illustrated by providing some construction examples. First, it is shown that the m! /2 cosets of RMq(1,m) comprised of Golay sequences just arise as a special case. Second, further families of cosets of RMq(1,m) with maximum PMEPR between 2 and 4 are presented, showing that some previously unexplained phenomena can now be understood within a unified framework. A lower bound on the PMEPR of cosets of RMq(1,m) is proved as well, and it is demonstrated that the upper bound on the PMEPR is tight in many cases. Finally, it is shown that all upper bounds on the PMEPR of cosets of RMq(1,m) also hold for the peak-to-average power ratio (PAPR) under the Walsh-Hadamard transform (WHT)
Direct Bandgap Transition in Many‐Layer MoS2 by Plasma‐Induced Layer Decoupling

We report a robust method for engineering the optoelectronic properties of many‐layer MoS2 using low‐energy oxygen plasma treatment. Gas phase treatment of MoS2 with oxygen radicals generated in an upstream N2–O2 plasma is shown to enhance the photoluminescence (PL) of many‐layer, mechanically exfoliated MoS2 flakes by up to 20 times, without reducing the layer thickness of the material. A blueshift in the PL spectra and narrowing of linewidth are consistent with a transition of MoS2 from indirect to direct bandgap material. Atomic force microscopy and Raman spectra reveal that the flake thickness actually increases as a result of the plasma treatment, indicating an increase in the interlayer separation in MoS2. Ab initio calculations reveal that the increased interlayer separation is sufficient to decouple the electronic states in individual layers, leading to a transition from an indirect to direct gap semiconductor. With optimized plasma treatment parameters, we observed enhanced PL signals for 32 out of 35 many‐layer MoS2 flakes (2–15 layers) tested, indicating that this method is robust and scalable. Monolayer MoS2, while direct bandgap, has a small optical density, which limits its potential use in practical devices. The results presented here provide a material with the direct bandgap of monolayer MoS2, without reducing sample thickness, and hence optical density.
Bridging the gap between I/O research and HR practice: Improving team composition, team training, and team task design

This article identifies a series of critical gaps between the scientific body of knowledge on team functioning and actual HR practice regarding teams. These gaps span across the areas of team composition, training, and task design. The article then discusses specific theoretical and methodological advancements from recent team research that address each knowledge gap. In other words, what does the scientific literature suggest about team composition, training, and task design, and how does the scientific knowledge compare to actual HR practice? The applied implications and implementation issues associated with each of these knowledge gaps are also discussed, using the scientific literature as a foundation for developing specific recommendations. © 2004 Wiley Periodicals, Inc.