Miracle-dz/UniFAR-FTUs huggingface dataset:
Summary Proceedings From the Neurology Group on Hypoxic-Ischemic Encephalopathy

Hypoxic-ischemic cerebral injury that occurs during the perinatal period is one of the most commonly recognized causes of severe, long-term neurologic deficits in children; it is often referred to as cerebral palsy. Despite improvements in perinatal practice during the past several decades, the incidence of cerebral palsy attributed to intrapartum asphyxia has remained essentially unchanged, primarily because management strategies were supportive and not targeted toward the processes of ongoing injury. Two processes of neuronal injury can be demonstrated after hypoxia-ischemia: neuronal necrosis and apoptosis. Because the mechanisms of these processes likely differ, strategies to minimize brain damage in an affected infant after hypoxia-ischemia likely will have to include interventions that target both processes. The goals of management of a newborn infant who has sustained a hypoxic-ischemic insult and is at risk for evolving injury should include (1) early identification of the infant at highest risk for evolving to the syndrome of hypoxic-ischemic encephalopathy, (2) supportive care to facilitate adequate perfusion and nutrients to the brain, and (3) consideration of interventions to ameliorate the processes of ongoing brain injury. Although the neurology group was unable to develop a definitive framework for the study of neuroprotective strategies for neonatal encephalopathy, it (1) listed key questions to be addressed before exploring possible study designs for managing hypoxic-ischemic encephalopathy in neonates, (2) identified important study-design issues, (3) determined general principles and key elements for neuroprotective-treatment strategies, (4) identified potential treatment strategies, (5) proposed a clinical-trial framework, and (6) identified key elements for a potential clinical-trial framework comparing hypothermia with hypothermia “plus” for moderate-to-severe encephalopathy.
Identification of WASP mutations in 14 Spanish families with Wiskott-Aldrich syndrome.

The Wiskott-Aldrich syndrome (WAS) is an X-linked immunodeficiency caused by mutations in the WASP gene. The disease is known to be associated with extensive clinical variability, and mutation studies indicate that genotypes are also highly variant among WAS patients. In this study, we performed mutation analysis of the WASP gene in 14 unrelated Spanish families by single strand conformation analysis (SSCA) and sequencing, resulting in the identification of a novel mutation and nine known mutations. No mutation was identified in one family. The ten different mutations include point mutations resulting in amino acid substitutions, stop codons, and small deletions and insertions causing frameshifts. Missense mutations were preferentially located in the amino-terminal part of the protein, exons 2 and 4, whereas stop and frameshift mutations were located in the carboxyl-terminal region, exons 10 and 11. However, in two families, two missense mutations in exon 11 were identified. Our study demonstrates that WASP genotypes have some concordance with the patients' phenotypes, although mutation 1019delC, identified in a family with several affected members, resulted in high intrafamilial clinical variability.
Stress: a modifiable factor in the etiology of adolescent depression.

Neuroimaging studies have helped us to understand neurobiology of stress and depression in the living brain in a noninvasive manner. Early life stressors are found to be associated with reduced fractional anisotropy values in the genu of the corpus callosum despite the absence of clinically significant psychiatric symptoms [5]. Fractional anisotropy, a useful measure on the Diffusion tensor Imaging (DTI) of the structural integrity of white fiber tracts, helps us to study human brain in vivo. White matter micro-structural abnormalities are reported in fronto-limbic neural pathways in adolescents with Major Depressive Disorders [6].
Improving 3D-TV view synthesis using motion compensated temporal interpolation

Nowadays, the development of three-dimension (3D) video applications such as three-dimensional television (3D-TV) and free-viewpoint television (FTV) has greatly increased human experiences. View synthesis method like depth-image-based-rendering (DIBR), plays a significant role in 3D content creation, 3D transmission, and has been integrated into video coding standards such as 3D-High efficiency video coding (3D-HEVC). However, the current DIBR method employs only the disparity correlation between views to create a so-called synthesized view; thus, unable to take full advantages of available synthesized information. In this paper, we propose a novel view synthesis method which takes advantages of not only the disparity correlation but also the temporal correlation between views. In the proposed method, an effective motion compensation based frame interpolation is employed to generate a temporal prediction view which is then combined with the DIBR rendered view to obtain the final synthesized view. Experimental results show that the proposed method can achieve the synthesized view with significantly outperforming other conventional techniques in terms of both peak signal-to noise ratio (PSNR) and subjective visual quality.
Contrast constancy: deblurring in human vision by spatial frequency channels.

The perception of contrast was measured in humans by a technique of subjective contrast‐matching, and was compared with contrast sensitivity as defined by threshold measures. 2. Contrast‐matching between different spatial frequencies was performed correctly (especially at frequencies above 5 c/deg) despite the attenuation by optical and neural factors which cause large differences in contrast thresholds. 3. Contrast‐matching between single lines of different widths was also veridical, and was not limited by the spatial integration (Ricco's Law) present at threshold. Adaptation to gratings altered the appearance of lines, and this could be best understood in Fourier terms. 4. The generality of these results was shown by matching the contrast of pictures which had been filtered so that each contained a one octave band of spatial frequencies. 5. Within the limits imposed by threshold and resolution, contrast‐matching was largely independent of luminance and position on the retina. 6. Six out of eleven astigmatic observers showed considerable suprathreshold compensation for their orientation‐specific neural deficit in contrast sensitivity. 7. These results define a new property of vision: contrast constancy. It is argued that spatial frequency channels in the visual cortex are organized to compensate for earlier attenuation. This achieves a dramatic 'deblurring' of the image, and optimizes the clarity of vision.
Application of static synchronous series compensators in mitigating Ferranti effect

This paper discusses a novel application of the SSSC which is a VSC-based FACTS device connected in series with the transmission line. An unloaded transmission line experiences Ferranti effect, i.e. the unloaded end of the transmission line experiences a voltage rise, which increases in magnitude as the length of the line increases. The SSSC can inject a controllable voltage in quadrature with the line current. Since the transmission line current is also in quadrature with the line voltage in the unloaded condition, the SSSC can take advantage of this to reduce the line voltage magnitude by injecting a voltage in phase with it. To verify this effect, the system is implemented in PSCAD along with a two-level VSC based SSSC with slightly altered controls. Voltage reduction at the receiving end was achieved when the SSSC was put in operation.
Intratumoral genomic heterogeneity in advanced head and neck cancer detected by comparative genomic hybridization.

OBJECTIVES Little is known about the extent of intratumoral genetic heterogeneity in head and neck squamous cell carcinoma (HNSCC). MATERIAL Therefore, we examined 79 stage III and IV primary HNSCCs and matched lymph node metastases for over- and underrepresentation of specific chromosome regions by comparative genomic hybridization. RESULTS The overall ratio of gains and losses was higher in metastases (M) than in primary (P) tumors (4/1 vs. 2.5/1). Gains of 3q (78.1% P vs. 87.5% M) and 11q (78.1% P vs. 62.5% M), and deletions of 3p (43.8% P vs. 34.4% M) and 9p (31.3% P vs. 15.6% M) were most frequently detected. The highest rate of intratumoral discordance was observed for primary tumors and corresponding metastases (32.8%) compared to matched pairs of 2 metastases (26.5%), and of 2 anatomically distinct sides of 1 primary tumor (24.3%). Furthermore, the discordance rate was dependent on the primary tumor site (oral cavity 49.2%, oropharynx 31%, hypopharynx 30.3% and larynx 27.3%). In some tumors, the extent of genomic discordance argues against a monoclonal origin. CONCLUSION We demonstrate a high individual variation of intratumoral genomic heterogeneity depending on the localization and selection of matched pairs. These findings are of specific importance in view of establishing prognostic markers.
Enoxaparin versus unfractionated heparin in elective percutaneous coronary intervention.

BACKGROUND Despite its limitations, unfractionated heparin has been the standard anticoagulant used during percutaneous coronary intervention (PCI). Several small studies have suggested that intravenous enoxaparin may be a safe and effective alternative. Our primary aim was to assess the safety of enoxaparin as compared with that of unfractionated heparin in elective PCI. METHODS In this prospective, open-label, multicenter, randomized trial, we randomly assigned 3528 patients with PCI to receive enoxaparin (0.5 or 0.75 mg per kilogram of body weight) or unfractionated heparin adjusted for activated clotting time, stratified according to the use or nonuse of glycoprotein IIb/IIIa inhibitors. The primary end point was the incidence of major or minor bleeding that was not related to coronary-artery bypass grafting. The main secondary end point was the percentage of patients in whom the target anticoagulation levels were reached. RESULTS Enoxaparin at a dose of 0.5 mg per kilogram was associated with a significant reduction in the rate of non-CABG-related bleeding in the first 48 hours, as compared with unfractionated heparin (5.9% vs. 8.5%; absolute difference, -2.6; 95% confidence interval [CI], -4.7 to -0.6; P=0.01), but the higher enoxaparin dose was not (6.5% vs. 8.5%; absolute difference, -2.0; 95% CI, -4.0 to 0.0; P=0.051). The incidence of major bleeding was significantly reduced in both enoxaparin groups, as compared with the unfractionated heparin group. Target anticoagulation levels were reached in significantly more patients who received enoxaparin (0.5-mg-per-kilogram dose, 79%; 0.75-mg-per-kilogram dose, 92%) than who received unfractionated heparin (20%, P<0.001). CONCLUSIONS In elective PCI, a single intravenous bolus of 0.5 mg of enoxaparin per kilogram is associated with reduced rates of bleeding, and a dose of 0.75 mg per kilogram yields rates similar to those for unfractionated heparin, with more predictable anticoagulation levels. The trial was not large enough to provide a definitive comparison of efficacy in the prevention of ischemic events. (ClinicalTrials.gov number, NCT00077844 [ClinicalTrials.gov].).
Animal models in myopia research

Our current understanding of the development of refractive errors, in particular myopia, would be substantially limited had Wiesel and Raviola not discovered by accident that monkeys develop axial myopia as a result of deprivation of form vision. Similarly, if Josh Wallman and colleagues had not found that simple plastic goggles attached to the chicken eye generate large amounts of myopia, the chicken model would perhaps not have become such an important animal model. Contrary to previous assumptions about the mechanisms of myopia, these animal models suggested that eye growth is visually controlled locally by the retina, that an afferent connection to the brain is not essential and that emmetropisation uses more sophisticated cues than just the magnitude of retinal blur. While animal models have shown that the retina can determine the sign of defocus, the underlying mechanism is still not entirely clear. Animal models have also provided knowledge about the biochemical nature of the signal cascade converting the output of retinal image processing to changes in choroidal thickness and scleral growth; however, a critical question was, and still is, can the results from animal models be applied to myopia in children? While the basic findings from chickens appear applicable to monkeys, some fundamental questions remain. If eye growth is guided by visual feedback, why is myopic development not self‐limiting? Why does undercorrection not arrest myopic progression even though positive lenses induce myopic defocus, which leads to the development of hyperopia in emmetropic animals? Why do some spectacle or contact lens designs reduce myopic progression and others not? It appears that some major differences exist between animals reared with imposed defocus and children treated with various optical corrections, although without the basic knowledge obtained from animal models, we would be lost in an abundance of untestable hypotheses concerning human myopia.
Region 2.5 of the Escherichia coli RNA polymerase σ70 subunit is responsible for the recognition of the ‘extended −10’ motif at promoters

At some bacterial promoters, a 5′‐TG‐3′ sequence element, located one base upstream of the −10 hexamer element, provides an essential motif necessary for transcription initiation. We have identified a mutant of the Escherichia coli RNA polymerase σ70 subunit that has an altered preference for base sequences in this ‘extended −10’ region. We show that this mutant σ70 subunit substantially increases transcription from promoters bearing 5′‐TC‐3′ or 5′‐TT‐3′ instead of a 5′‐TG‐3′ motif, located one base upstream of the −10 hexamer. The mutant results from a single base pair substitution in the rpoD gene that causes a Glu to Gly change at position 458 of σ70. This substitution identifies a functional region in σ70 that is immediately adjacent to the well‐characterized region 2.4 (positions 434–453, previously shown to contact the −10 hexamer). From these results, we conclude that this region (which we name region 2.5) is involved in contacting the 5′‐TG‐3′ motif found at some bacterial promoters: thus, extended −10 regions are recognized by an extended region 2 of the RNA polymerase σ70 subunit.
Abnormal excitatory neurotransmitter metabolism in schizophrenic brains.

BACKGROUND Schizophrenia has been hypothesized to be caused by a hypofunction of glutamatergic neurons. Findings of reduced concentrations of glutamate in the cerebrospinal fluid of patients with schizophrenia and the ability of glutamate-receptor antagonists to cause psychotic symptoms lend support to this hypothesis. N-acetylaspartylglutamate (NAAG), a neuropeptide that is highly concentrated in glutamatergic neurons, antagonizes the effects of glutamate at N-methyl-D-aspartate receptors. Moreover, NAAG is cleaved to glutamate and N-acetylaspartate by a specific peptidase, N-acetyl-alpha-linked acidic dipeptidase (NAALADase). To test the glutamatergic hypothesis of schizophrenia, we studied the NAAG-related glutamatergic variables in postmortem brains from patients with schizophrenia, neuroleptic-treated controls, and normal individuals, with particular emphasis on the prefrontal cortex and hippocampus. METHOD Different regions of frozen brain tissue from three different groups (patients with schizophrenia, neuroleptic-treated controls, and normal controls) were assayed to determine levels of NAAG, N-acetylaspartate, NAALADase, and several amino acids, including aspartate and glutamate. RESULTS Our study demonstrates alterations in brain levels of aspartate, glutamate, and NAAG and in NAALADase activity. Levels of NAAG were increased and NAALADase activity and glutamate levels were decreased in the schizophrenic brains. Notably, the changes in NAAG level and NAALADase activity in schizophrenic brains were more selective than those for aspartate and glutamate. In neuroleptic-treated control brains, levels of aspartate, glutamate, and glycine were found to be increased. CONCLUSIONS The changes in levels of aspartate, glutamate, NAAG, and NAALADase are prominent in the prefrontal and hippocampal regions, where previous neuropathological studies of schizophrenic brains demonstrate consistent changes. These findings support the hypothesis that schizophrenia results from a hypofunction of certain glutamatergic neuronal systems. They also suggest that the therapeutic efficacy of neuroleptics may be related to increased glutamatergic activity.
Concentration‐dependent mechanisms of cell penetration and killing by the de novo designed antifungal hexapeptide PAF26

Recent evidence indicates that antimicrobial peptides can kill microbes in more complex ways than just by membrane permeabilization. In this study, the mechanism of internalization of the de novo designed cationic hexapeptide PAF26 has been characterized in detail using Neurospora crassa. Live‐cell imaging of fluorescently labelled PAF26, organelle probes and mutants indicate that the peptide is endocytically internalized at low fungicidal concentrations (2.0–5 µM). At these concentrations, PAF26 initially accumulated in vacuoles that expanded, and then was actively transported into the cytoplasm, which coincided with cell death. Deletion mutants of the endocytic proteins RVS‐161, RVS‐167 and RAB‐5 exhibited reduced rates of PAF26 internalization and fungicidal activity. Pharmacological experiments with live‐cell probes showed that PAF26 internalization and antifungal action at low fungicidal concentrations was energy‐dependent, primarily actin‐mediated, and disrupted intracellular calcium homeostasis. PAF26 antifungal activity at low concentrations was shown to rely on its endocytic internalization. PAF26 also induced plasma membrane depolarization which, however, was independent of peptide internalization and killing of fungal cells. At high fungicidal concentrations (20 µM), PAF26 internalization was energy‐independent, suggesting the involvement of passive peptide translocation. Our results provide new mechanistic insights into the mode‐of‐action of small cationic antimicrobial peptides that should facilitate improvements in their design.
Hygienemaßnahmen auf der Intensivstation

Die meisten im Krankenhaus erworbenen, nosokomialen Infektionen werden durch die patienteneigene endogene Keimflora verursacht. Bei Einhaltung evidenzbasierter krankenhaushygienischer Masnahmen konnen nosokomiale Infektionen teilweise verhindert werden. In internationalen und nationalen Studien konnte durch Implementierung eines modernen Infektions-Surveillance-Systems mit schriftlicher Einfuhrung nachweislich praventiver Masnahmen eine Reduktion nosokomialer Infektionen um ca. 30% erzielt werden (Haley et al. 1985, Zuschneid et al. 2003). Im Folgenden werden Masnahmen, welche von den entsprechenden Fachgesellschaften nachdrucklich empfohlen werden, dargestellt; diese stutzen sich auf gut geplante experimentelle, klinische oder epidemiologische Untersuchungen und haben fur jedes Krankenhaus aktuelle Gultigkeit. Diese werden in der Fachliteratur mit dem Evidenzgrad 1 A bewertet (Mangram et al. 1999, Exner et al. 1999). Surveillance nosokomialer Infektionen
Regulation of Gut Function Varies with Life‐History Traits in Chuckwallas (Sauromalus obesus: Iguanidae)

We examined the effects of hibernation and fasting on intestinal glucose and proline uptake rates of chuckwallas (Sauromalus obesus) and on the size of organs directly or indirectly related to digestion. These lizards show geographic variation in body size and growth rate that parallels an elevational gradient in our study area. At low elevation, food is available only for a short time during the spring; at high elevation, food may also be available during summer and autumn, depending on rainfall conditions in a given year. We hypothesized that low‐elevation lizards with a short season of food availability would show more pronounced regulation of gut size and function than high‐elevation lizards with prolonged or bimodal food availability. Hibernating lizards from both elevations had significantly lower uptake rates per milligram intestine for both nutrients, and lower small intestine mass, than active lizards. The combination of these two effects resulted in significantly lower total nutrient uptake in hibernating animals compared to active ones. The stomach, large intestine, and cecum showed lower masses in hibernators, but these results were not statistically significant. The heart, kidney, and liver showed no difference in mass between hibernating and nonhibernating animals. Lizards from low elevations with a short growing season also showed a greater increase in both uptake rates and small intestine mass from the hibernating to the active state, compared to those from high elevations with longer growing seasons. Thus, compared to those from long growing season areas, lizards from short growing season areas have equal uptake capacity during hibernation but much higher uptake capacity while active and feeding. This pattern of regulation of gut function may or may not be an adaptive response, but it is consistent with variation in life‐history characteristics among populations. In areas with a short season, those lizards that can extract nutrients quickly and then reduce the gut will be favored; in areas where food may be available later in the year, those lizards that maintain an active gut would be favored. While other researchers have found much greater magnitudes of gut regulation when making comparisons among species, we find the different patterns of change in gut function between different populations of chuckwallas particularly intriguing because they occur within a single species.
MidGov : middleware para governo eletrônico baseado em gradee computacionais

Agencias governamentais ao redor do mundo estao realizando grandes investimentos na utilizacao de Tecnologia da Informacao e Comunicacao em suas atividades. Essa tendencia, conhecida como Governo eletronico, impulsiona grande demanda por pesquisas cujo foco principal e o desenvolvimento de aplicacoes destinadas a um governo mais transparente e colaborativo. Aplicacoes para esse tipo de cenario introduzem uma serie de desafios que precisam ser enfrentados, incluindo maior interoperabilidade entre sistemas, escalabilidade, questoes de seguranca, entre outros. Nesse sentido, o paradigma de Arquitetura Orientada a Servicos (SOA) apresenta-se como uma interessante proposta para mitigar a heterogeneidade dos servicos prestados pelas diversas entidades envolvidas. Alem disso, computacao em grade pode ser considerada uma solucao promissora para aplicacoes de middleware em Governo eletronico, gracas a sua alta capacidade de armazenamento e processamento, alem de sua recente orientacao a servicos, tornando-a uma poderosa ferramenta para aplicacoes intra-dominio. Considerando esses desafios, este trabalho propoe uma plataforma para aplicacoes de Governo eletronico em sistemas em grades utilizando servicos de suporte fornecidos pelo Globus Toolkit 4 (GT4) no contexto da Web Semântica. O trabalho inclui a implementacao de um prototipo do middleware e sua validacao atraves de um cenario de aplicacao. Abstract