Miracle-dz/UniFAR-FTUs huggingface dataset:
Developmental and hormonal regulation of cumulus expansion and secretion of cumulus expansion‐enabling factor (CEEF) in goat follicles

The objective of this article was to study the developmental and hormonal regulation of cumulus expansion and secretion of cumulus expansion‐enabling factor (CEEF) in goat follicles. M‐199 medium was conditioned for 24 hr with cumulus‐denuded oocytes (DOs), oocytectomized complexes (OOXs), or mural granulosa cells (MGCs) from goat follicles of different sizes. Mouse OOXs and eCG were added to culture drops of the conditioned medium and cumulus expansion was scored at 18 hr of culture to assess CEEF production. While mouse OOXs did not expand, goat OOXs underwent full cumulus expansion when cultured in nonconditioned eCG‐supplemented M‐199 medium. When cultured in nonconditioned medium containing 10% follicular fluid (FF) from goat medium (2–4 mm) and small (0.8–1.5 mm) follicles, 71–83% mouse OOXs expanded; but expansion rates decreased (P < 0.05) at either lower or higher FF concentrations. FF from large (5–6 mm) follicles did not support mouse OOX expansion at any concentrations. While medium conditioned with DOs from follicles of all the three sizes supported expansion of 80–90% mouse OOXs, medium conditioned with mature DOs had no effect. While cumulus cells from follicles of all the three sizes secreted CEEF in the absence of gonadotropins, MGCs from large follicles became gonadotropin dependent for CEEF production. Both FSH and LH stimulated CEEF production by large follicle MGCs, but FSH had a shorter half‐life than LH to expand mouse OOXs. Few meiosis‐incompetent goat oocytes from small follicles underwent cumulus expansion when cultured in medium conditioned with goat DOs or cocultured with goat COCs from medium follicles. It is concluded that (1) goat cumulus expansion is independent of the oocyte; (2) the limited CEEF activity in FF from large follicles was due mainly to the inability of MGCs in these follicles to secret the factor in absence or short supply of gonadotropins; (3) the cumulus expansion inability of the meiosis incompetent goat oocytes was due to the inability of their cumulus cells to respond to rather than to produce CEEF. Mol. Reprod. Dev. 75: 1387–1395, 2008. © 2008 Wiley‐Liss, Inc.
Time-Motion Analysis of Italian Elite Women's Basketball Games: Individual and Team Analyses

Abstract Conte, D, Favero, TG, Lupo, C, Francioni, FM, Capranica, L, and Tessitore, A. Time-motion analysis of Italian elite women's basketball games: Individual and team analyses. J Strength Cond Res 29(1): 144–150, 2015—The aim of this study was to assess elite women's basketball game performance. Five elite women's games (3 Italian first division and 2 Euroleague) were analyzed for individual and team time-motion analyses. The individual analysis evaluated the players' movement patterns with particular focus on high-intensity activity (HIA), sprint activity, and repeated sprint events (RSEs). Team analysis included live time (LT), stoppage time (ST), and their ratio, transfer (TR) phases, and half court and full court actions. The frequency of occurrence of changes of activities was n = 576 ± 110, one every 2.56 seconds of LT. Total HIA was 8.5 ± 1.8% of LT and no significant differences between quarter periods were observed. In general, players performed linear sprints (48.3 ± 2.9%) over 1–5 m distance (56.8 ± 5.6%). The occurrence of RSE was 4.4 ± 1.7, with 58.6 ± 18.5% passive recovery between sprints. Team analysis showed no significant difference between games for LT and ST phases (ratio = 1.18 ± 0.25). For game analysis, LT and ST were 43.4 ± 7.8% and 51.1 ± 8.4%, respectively. A difference between games was found for half court actions (p < 0.01) and TR phases (p ⩽ 0.05). Moreover, 1 TR and 2 TR were the most performed (45.3 and 23.9%) actions. These results encourage coaches to include repeated sprint ability with mainly linear and short sprints into a comprehensive training program.
Automated registration of diagnostic to prediagnostic x-ray mammograms: evaluation and comparison to radiologists' accuracy.

PURPOSE To compare and evaluate intensity-based registration methods for computation of serial x-ray mammogram correspondence. METHODS X-ray mammograms were simulated from MRIs of 20 women using finite element methods for modeling breast compressions and employing a MRI/x-ray appearance change model. The parameter configurations of three registration methods, affine, fluid, and free-form deformation (FFD), were optimized for registering x-ray mammograms on these simulated images. Five mammography film readers independently identified landmarks (tumor, nipple, and usually two other normal features) on pairs of diagnostic and corresponding prediagnostic digitized images from 52 breast cancer cases. Landmarks were independently reidentified by each reader. Target registration errors were calculated to compare the three registration methods using the reader landmarks as a gold standard. Data were analyzed using multilevel methods. RESULTS Between-reader variability varied with landmark (p < 0.01) and screen (p = 0.03), with between-reader mean distance (mm) in point location on the diagnostic/prediagnostic images of 2.50 (95% CI 1.95, 3.15)/2.84 (2.24, 3.55) for nipples and 4.26 (3.43, 5.24)/4.76 (3.85, 5.84) for tumors. Registration accuracy was sensitive to the type of landmark and the amount of breast density. For dense breasts (> or = 40%), the affine and fluid methods outperformed FFD. For breasts with lower density, the affine registration surpassed both fluid and FFD. Mean accuracy (mm) of the affine registration varied between 3.16 (95% CI 2.56, 3.90) for nipple points in breasts with density 20%-39% and 5.73 (4.80, 6.84) for tumor points in breasts with density < 20%. CONCLUSIONS Affine registration accuracy was comparable to that between independent film readers. More advanced two-dimensional nonrigid registration algorithms were incapable of increasing the accuracy of image alignment when compared to affine registration.
Structured large margin learning

This paper presents a new large margin learning approach, namely structured large margin machine (SLMM), which incorporates both merits of "structured" learning models and advantages of large margin learning schemes. The promising features of this model, such as enhanced generalization ability, scalability, extensibility, and noise tolerance, are demonstrated theoretically and empirically. SLMM is of theoretical importance because it is a generalization of learning models like SVM, MPM, LDA, and M4 etc. Moreover, it provides a novel insight into the study of learning methods and forms a foundation for conceiving other "structured" classifiers.
Recognizability for sequences of morphisms

We investigate different notions of recognizability for a free monoid morphism $\unicode[STIX]{x1D70E}:{\mathcal{A}}^{\ast }\rightarrow {\mathcal{B}}^{\ast }$ . Full recognizability occurs when each (aperiodic) point in ${\mathcal{B}}^{\mathbb{Z}}$ admits at most one tiling with words $\unicode[STIX]{x1D70E}(a)$ , $a\in {\mathcal{A}}$ . This is stronger than the classical notion of recognizability of a substitution $\unicode[STIX]{x1D70E}:{\mathcal{A}}^{\ast }\rightarrow {\mathcal{A}}^{\ast }$ , where the tiling must be compatible with the language of the substitution. We show that if $|{\mathcal{A}}|=2$ , or if $\unicode[STIX]{x1D70E}$ ’s incidence matrix has rank $|{\mathcal{A}}|$ , or if $\unicode[STIX]{x1D70E}$ is permutative, then $\unicode[STIX]{x1D70E}$ is fully recognizable. Next we investigate the classical notion of recognizability and improve earlier results of Mossé [Puissances de mots et reconnaissabilité des points fixes d’une substitution. Theoret. Comput. Sci. 99(2) (1992), 327–334] and Bezuglyi et al [Aperiodic substitution systems and their Bratteli diagrams. Ergod. Th. & Dynam. Sys. 29(1) (2009), 37–72], by showing that any substitution is recognizable for aperiodic points in its substitutive shift. Finally we define recognizability and also eventual recognizability for sequences of morphisms which define an $S$ -adic shift. We prove that a sequence of morphisms on alphabets of bounded size, such that compositions of consecutive morphisms are growing on all letters, is eventually recognizable for aperiodic points. We provide examples of eventually recognizable, but not recognizable, sequences of morphisms, and sequences of morphisms which are not eventually recognizable. As an application, for a recognizable sequence of morphisms, we obtain an almost everywhere bijective correspondence between the $S$ -adic shift it generates, and the measurable Bratteli–Vershik dynamical system that it defines.
Interleukin-12 p40- and Fas Ligand-Dependent Apoptotic Pathways Involving STAT-1 Phosphorylation Are Triggered during Infection with a Virulent Strain of Toxoplasma gondii

ABSTRACT Toxoplasma gondii is an opportunistic intracellular parasite. Infection with the high-virulence T. gondii strain RH induces inflammatory cytokine overproduction and uncontrolled apoptosis in lymphoid organs. Here, we show by fluorescent terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and binding of fluorescein isothiocyanate-conjugated VAD-FMK, an irreversible pan-caspase inhibitor, that parasite-triggered apoptosis occurs among CD4+, CD8+, B220+, Gr-1+, and NK1.1+ splenic populations. Caspases 8 and 9 were activated during infection, implicating cell surface death receptors and mitochondria in apoptosis. Induction of apoptosis was absent among all cell populations in both interleukin-12 (IL-12) p40- and Fas ligand (FasL)-negative mice. STAT-1 phosphorylation correlated with onset of apoptosis during infection, but in the absence of IL-12 p40 and functional FasL, activation of this transcription factor failed to occur. The results demonstrate T. gondii-induced activation of multiple apoptotic pathways, dependent upon both IL-12 p40 and FasL, that may play a role in the lethal pathology of infection.
The Pain and Opioids IN Treatment study: characteristics of a cohort using opioids to manage chronic non-cancer pain

Abstract There has been a recent increase in public and professional concern about the prescription of strong prescription opioids for pain. Despite this concern, research to date has been limited because of a number of factors such as small sample sizes, exclusion of people with complex comorbidities, and studies of short duration. The Pain and Opioids IN Treatment is a 2-year prospective cohort study of 1500 people prescribed with pharmaceutical opioids for their chronic pain. This article provides an overview of the demographic and clinical characteristics of the cohort using the baseline data of 1514 community-based people across Australia. Participants had been in pain for a period of 10 years and had been on prescription opioids for approximately 4 years. One in 10 was on a daily morphine equivalent dose of ≥200 mg. Employment and income levels were low, and two-thirds of the sample reported that their pain had impacted on their employment status. Approximately 50% screened positive for current moderate-to-severe depression, and 1 in 5 had made a lifetime suicide attempt. There were a number of age-related differences. The younger groups experienced higher levels of pain and pain interference, more mental health and substance use issues, and barriers to treatment, compared with the older group. This study found that the people who have been prescribed strong opioids for chronic pain have very complex demographic and clinical profiles. Major age-related differences in the experiences of pain, coping, mental health, and substance use suggest the necessity of differential approaches to treatment.
The desmosome: cell science lessons from human diseases

Human skin diseases have revealed fundamental mechanisms by which cytoskeletal proteins contribute to tissue architecture and function. In particular, the analysis of epidermal blistering disorders and the role of keratin gene mutations in these diseases has led to significant increases in our understanding of intermediate filament biology. The major cell-surface attachment site for intermediate filament networks is the desmosome, an adhesive intercellular junction prominent in the epidermis and the heart. During the past decade, substantial progress has been made in understanding the molecular basis of a variety of epidermal autoimmune diseases, skin fragility syndromes, and disorders that involve a combination of heart and skin defects caused by perturbations in desmosome structure and function. These human diseases reveal key roles for desmosomes in maintaining tissue integrity, but also suggest functions for desmosomal components in signal transduction pathways and epidermal organization.
The Acidic Domain of GPIHBP1 Is Important for the Binding of Lipoprotein Lipase and Chylomicrons*

GPIHBP1, a glycosylphosphatidylinositol-anchored endothelial cell protein of the lymphocyte antigen 6 (Ly6) family, plays a key role in the lipolysis of triglyceride-rich lipoproteins (e.g. chylomicrons). GPIHBP1 is expressed along the luminal surface of endothelial cells of heart, skeletal muscle, and adipose tissue, and GPIHBP1-expressing cells bind lipoprotein lipase (LPL) and chylomicrons avidly. GPIHBP1 contains an amino-terminal acidic domain (amino acids 24-48) that is enriched in aspartate and glutamate residues, and we previously speculated that this domain might be important in binding ligands. To explore the functional importance of the acidic domain, we tested the ability of polyaspartate or polyglutamate peptides to block the binding of ligands to pgsA-745 Chinese hamster ovary cells that overexpress GPIHBP1. Both polyaspartate and polyglutamate blocked LPL and chylomicron binding to GPIHBP1. Also, a rabbit antiserum against the acidic domain of GPIHBP1 blocked LPL and chylomicron binding to GPIHBP1-expressing cells. Replacing the acidic amino acids within GPIHBP1 residues 38-48 with alanine eliminated the ability of GPIHBP1 to bind LPL and chylomicrons. Finally, mutation of the positively charged heparin-binding domains within LPL and apolipoprotein AV abolished the ability of these proteins to bind to GPIHBP1. These studies indicate that the acidic domain of GPIHBP1 is important and that electrostatic interactions play a key role in ligand binding.
The RL neurovirulence locus in herpes simplex virus type 2 strain HG52 plays no role in latency.

We have demonstrated that the variant JH2604 of the herpes simplex virus type 2 (HSV-2) strain HG52 is completely avirulent in BALB/c mice following intracranial inoculation, with an LD50 of greater than 10(7) p.f. u. /mouse compared to the wild-type LD50 of less than 10(2) p.f. u. /mouse. In JH2604, a 1.5 kbp deletion extends from the DR1/Ub junction of the 'a' sequence to 511 bp upstream of the 5' end of IE1 in both long repeats. We have since constructed a second variant (2701) in which only 850 bp are removed from the RL. This deletion lies entirely within the sequences deleted in JH2604 and leaves intact most of a short 189 bp open reading frame (ORF) highly conserved between HSV-1 and HSV-2. Like JH2604, 2701 shows wild-type growth characteristics and is neither host range- nor temperature-restricted. This was most noteworthy in the case of mouse 3T6 cells. 2701 has an LD50 of 5 x 10(5) p.f. u. /mouse on intracranial inoculation, a value intermediate between those of HG52 and JH2604. In assays for intracranial replication, JH2604 exhibits no detectable growth with a rapid decline in virus titre, 2701 shows limited growth over the first 24 to 36 h post-inoculation before the titre again declines and HG52 grows rapidly, reaching a high titre until the mice die. Taken together these results suggest that a region of the genome upstream of IE1 encodes a gene product essential for HSV replication in neurons of the central nervous system. It is highly likely that the conserved ORF is in an important region of a polypeptide essential for neurovirulence, although the upstream sequences present in 2701 but absent from JH2604 must also play a role. Although JH2604 and 2701 are avirulent, they both establish latent infection in the dorsal root ganglia of BALB/c mice and reactivate in vitro in a manner indistinguishable from HG52. This suggests a distinct separation of the factors involved in neurovirulence and the establishment of/reactivation from latency.
Caractérisation biochimique du complexe AFL et identification des partenaires de LEC2 lors du développement de la graine

Les spermaphytes majoritairement representes par les angiospermes ou plantes a fleur, ont le trait fondamental de pouvoir se multiplier par la formation de graine. Les graines representent un caractere essentiel pour la survie des plantes, leur dissemination et un usage important pour l’industrie, notamment agro-alimentaire. Lors de la formation de la graine, des transitions cruciales ont lieu, en particulier pour le developpement, l’etablissement des reserves, la maturation, l’acquisition de la tolerance a la dessiccation et la dormance. Ces etapes sont regulees par des facteurs de transcription et notamment les LAFL (LEC1, ABI3, FUS3, LEC2). Les LAFL sont composes de deux familles, les facteurs de transcription a domaine B3 (ABI3, FUS3, LEC2) et les NF-Y (LEC1), qui sont impliques dans la regulation genique dans differentes etapes du developpement de la graine. Des etudes suggerent la possibilite de la formation d’un complexe compose de ABI3, LEC1 et LEC2 sur le promoteur de l’OLEOSINE1 permettant d’activer plus fortement la transcription du gene. Neanmoins la caracterisation des proteines, leur action, regulation et leur capacite a interagir entre elles et former un complexe, restent encore meconnues. Dans un premier temps, je me suis attachee a caracteriser la formation du complexe proteique compose d’ABI3, LEC1 et LEC2, plus particulierement, l’interaction entre LEC1 et LEC2. La localisation subcellulaire des deux proteines par etiquetage in planta, ou grâce a des anticorps specifiques, leur interaction dans un systeme double hybride et la mesure de l’effet de LEC1 sur LEC2 par thermophorese ont permis de montrer que LEC2 et LEC1 peuvent former un dimere sur le promoteur de l’OLEOSINE1 et que cette association change l’affinite de LEC2 pour son ADN cible. Dans une deuxieme approche, j’ai cherche a identifier des partenaires avec (donnees bibliographiques) et sans (approche de TAP-tag) a priori pour completer l’etude.
Spectrometric evidence for the flavin-1-phenylcyclopropylamine inactivator adduct with monoamine oxidase N.

1-Phenylcyclopropylamine (1-PCPA) is shown to be an inactivator of the fungal flavoenzyme monoamine oxidase (MAO) N. Inactivation results in an increase in absorbance at 410 nm and is accompanied by the concomitant loss of the flavin absorption band at 458 nm. The spectral properties of the covalent adduct formed between the flavin cofactor of MAO N and 1-PCPA are similar to those reported for the irreversible inactivation product formed with 1-PCPA and mammalian mitochondrial monoamine oxidase B [Silverman, R. B. , and Zieske, P. A. (1985) Biochemistry 24, 2128-2138]. There is a hypsochromic shift of the 410 nm band upon lowering the pH to 2, indicating that an N(5)-flavin adduct formed upon inactivation. Use of the fungal enzyme, MAO N, which lacks the covalent attachment to the flavin adenine dinucleotide (FAD) cofactor present in the mammalian forms MAO A and MAO B, has allowed for the isolation and further structural identification of the flavin-inactivator adduct. The incorporation of two (13)C labels into the inactivator, [2,3-(13)C(2)]-1-PCPA, followed by analysis using on-line liquid chromatography/electrospray ionization mass spectrometry and nuclear magnetic resonance spectroscopy, provided a means to explore the structure of the flavin-inactivator adduct of MAO N. The spectral evidence supports covalent attachment of the 1-PCPA inactivator to the cofactor as N(5)-3-oxo-3-phenylpropyl-FAD.
Life in extreme environments: hydrothermal vents.

Eruption of volcanic rocks at the midocean ridges is the major mechanism by which heat is lost from the interior of the Earth. Approximately one-third of the heat is removed from the spreading centers by convective circulation of seawater (1). The magnitude of this heat loss requires that the entire volume of the oceans circulates through the midocean ridges in approximately 10 million years. Seawater interaction with volcanic rocks at near 400°C results in substantial chemical flux and makes an important contribution to buffering the composition of some elements in seawater. Cations from seawater (Mg+2, Ca+2, and Na+) form hydroxyl-bearing alteration minerals in the volcanic rocks, releasing hydrogen ion to solution. The hot, acidic altered-seawater releases metals (Fe, Mn, Zn, and Cu) and reduced sulfur (H2S) from the volcanic rock; these are transported by hydrothermal solutions to the seafloor and form metallic mineral deposits.
Antimicrobial Resistance of Escherichia coli O157 Isolated from Humans, Cattle, Swine, and Food

ABSTRACT A total of 361 Escherichia coli O157 isolates, recovered from humans, cattle, swine, and food during the years 1985 to 2000, were examined to better understand the prevalence of antimicrobial resistance among these organisms. Based on broth microdilution results, 220 (61%) of the isolates were susceptible to all 13 antimicrobials tested. Ninety-nine (27%) of the isolates, however, were resistant to tetracycline, 93 (26%) were resistant to sulfamethoxazole, 61 (17%) were resistant to cephalothin, and 48 (13%) were resistant to ampicillin. Highest frequencies of resistance occurred among swine isolates (n = 70), where 52 (74%) were resistant to sulfamethoxazole, 50 (71%) were resistant to tetracycline, 38 (54%) were resistant to cephalothin, and 17 (24%) were resistant to ampicillin. Based on the presence of Shiga toxin genes as determined by PCR, 210 (58%) of the isolates were identified as Shiga toxin-producing E. coli (STEC). Among these, resistance was generally low, yet 21 (10%) were resistant to sulfamethoxazole and 19 (9%) were resistant to tetracycline. Based on latex agglutination, 189 (52%) of the isolates were identified as E. coli O157:H7, among which 19 (10%) were resistant to sulfamethoxazole and 16 (8%) were resistant to tetracycline. The data suggest that selection pressure imposed by the use of tetracycline derivatives, sulfa drugs, cephalosporins, and penicillins, whether therapeutically in human and veterinary medicine or as prophylaxis in the animal production environment, is a key driving force in the selection of antimicrobial resistance in STEC and non-STEC O157.
Ventilatory management of acute respiratory distress syndrome: A consensus of two

ObjectiveTo synthesize the emerging body of experimental, observational, and clinical trial data into a practical guideline for safe and effective ventilatory management of acute respiratory distress syndrome. Data SourcesRelevant, peer-reviewed, scientific literature and personal observations from clinical practice. Study SelectionRelevant experimental studies and high-impact observational and clinical trials of acute respiratory distress syndrome management. Data ExtractionDetailed review of information contained in published scientific work. Data SynthesisInteractive discussions between the authors that culminated in our consensus view of appropriate management. ConclusionsPrevention of ventilator-induced lung injury while accomplishing the essential life-supporting roles of mechanical ventilation is a complex undertaking that requires application of principles founded on a broad experimental and clinical database and on the results of well-executed clinical trials. At the bedside, execution of an effective lung-protective ventilation strategy remains an empirical process best guided by integrated physiology and a readiness to revise the management approach depending on the individual’s response.