Miracle-dz/UniFAR-FTUs huggingface dataset:
Hungarian Word-Sense Disambiguated Corpus

To create the first Hungarian WSD corpus, 39 suitable word form samples were selected for the purpose of word sense disambiguation. Among others, selection criteria required the given word form to be frequent in Hungarian language usage, and to have more than one sense considered frequent in usage. HNC and its Heti Világgazdaság subcorpus provided the basis for corpus text selection. This way, each sample has a relevant context (whole article), and information on the lemma, POS-tagging and automatic tokenization is also available. When planning the corpus, 300-500 samples of each word form were to be annotated. This size makes it possible that the subcorpora prepared for the individual word forms can be compared to data available for other languages. However, the finalized database also contains unannotated samples and samples with single annotation, which were annotated only by one of the linguists. The corpus follows the ACLs SensEval/SemEval WSD tasks format. The first version of the corpus was developed within the scope of the project titled The construction Hungarian WordNet Ontology and its application in Information Extraction Systems (Hatvani et al., 2007). The corpus  for research and educational purposes is available and can be downloaded free of charge.
High-level simulation of substrate noise in high-ohmic substrates with interconnect and supply effects

Substrate noise is a major obstacle for mixed-signal integration. In this paper we propose a fast and accurate high-level methodology to simulate substrate noise generated by large digital circuits. The methodology can handle any substrate type, e.g. bulk-type or EPI-type, and takes into account the effects of interconnect and supply. For each standard cell a substrate macromodel is used in order to efficiently simulate the total system, which consists of a network of such macromodels. For a 40K gates telecom circuit fabricated in a 0.18 mm CMOS process, measurements indicate that substrate noise is simulated by using our methodology within 20% error but several orders of magnitude faster in CPU time than a full SPICE simulation.
Mechanisms of heteroresistance in methicillin-resistant Staphylococcus aureus

Characteristic for methicillin-resistant (Mcr) staphylococci is the heterogeneous expression of the intrinsic methicillin resistance. The majority of the cells express resistance to low concentrations of methicillin, and a minority of the cells express resistance to much higher concentrations. We show here (i) that the presence of the mecA encoding region on plasmid pBBB79 was sufficient to render a methicillin-susceptible (Mcs) Staphylococcus aureus strain heteroresistant and (ii) that this Mcr strain segregated highly resistant subclones which retained the high-resistance phenotype under nonselective growth conditions. The Mcr strain with only mecA on plasmid pBBB79 thus behaved identically to a Mcr strain carrying the complete mec determinant integrated at its proper chromosomal site. (iii) Curing a such highly resistant subclone from plasmid pBBB79 yielded an Mcs strain that was as susceptible as the original Mcs parent strain. (iv) Comparisons were made between the original parent and the cured Mcs strain by backcrossing pBBB79 into them and looking at their progeny. Transductants derived from the formerly highly resistant cured strain became resistant to high concentrations of methicillin, whereas transductants derived from the original parent strain were resistant to lower concentrations of methicillin and showed the typical heterogeneous resistance. We deduced therefrom that the high-level resistance expressed by the minority of the population of Mcr S. aureus was due to a chromosomal mutation(s) (chr*) involving neither mecA nor the additional 30 kb of mec-associated DNA. Moreover, we could show that this postulated mutation chr* was not linked to the femAB operon, which is known to affect methicillin resistance levels.
Emerging Link between Alzheimer's Disease and Homeostatic Synaptic Plasticity

Alzheimer's disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory. Although intracellular neurofibrillary tangles and extracellular senile plaques, composed of insoluble amyloid-β (Aβ) peptides, have been the hallmarks of postmortem AD brains, memory impairment in early AD correlates better with pathological accumulation of soluble Aβ oligomers and persistent weakening of excitatory synaptic strength, which is demonstrated by inhibition of long-term potentiation, enhancement of long-term depression, and loss of synapses. However, current, approved interventions aiming to reduce Aβ levels have failed to retard disease progression; this has led to a pressing need to identify and target alternative pathogenic mechanisms of AD. Recently, it has been suggested that the disruption of Hebbian synaptic plasticity in AD is due to aberrant metaplasticity, which is a form of homeostatic plasticity that tunes the magnitude and direction of future synaptic plasticity based on previous neuronal or synaptic activity. This review examines emerging evidence for aberrant metaplasticity in AD. Putative mechanisms underlying aberrant metaplasticity in AD will also be discussed. We hope this review inspires future studies to test the extent to which these mechanisms contribute to the etiology of AD and offer therapeutic targets.
A comparative study of thermal performance in two VCSEL structures for high bit rate digital optical links

Two Vertical Cavity Surface Emitting Laser (VCSEL) diode structures based on InGaAs-GaAs and GaAs-AlGaAs are considered for thermal analysis and their impact on 850 nm digital optical link are investigated. The effect of Multi Mode Fiber (MMF) link length and VCSEL temperature on the overall link performance is compared for both the cases under 1.25 Gb/s transmissions. Bit Error Rate (BER) of 2.02 × 10<sup>−5</sup>, 1.48 × 10<sup>−5</sup> and 2.15 × 10<sup>−5</sup>, 1.55 × 10<sup>−5</sup> for InGaAs-GaAs based VCSEL and GaAs-AlGaAs based VCSEL at 25°C and 40°C are predicted at a fiber length of 1 km. Optimum biasing conditions pertaining to maximum 3 dB bandwidth for both the structures are also determined.
Approximation Algorithms for Computing Capacity of Wireless Networks with SINR Constraints

A fundamental problem in wireless networks is to estimate its throughput capacity - given a set of wireless nodes, and a set of connections, what is the maximum rate at which data can be sent on these connections. Most of the research in this direction has focused on either random distributions of points, or has assumed simple graph-based models for wireless interference. In this paper, we study capacity estimation problem using the more general Signal to Interference Plus Noise Ratio (SINR) model for interference, on arbitrary wireless networks. The problem becomes much harder in this setting, because of the non-locality of the SINR model. Recent work by Moscibroda et al. (2006) has shown that the throughput in this model can differ from graph based models significantly. We develop polynomial time algorithms to provably approximate the total throughput in this setting.
H-NS Mediates the Silencing of Laterally Acquired Genes in Bacteria

Histone-like nucleoid structuring protein (H-NS) is a modular protein that is associated with the bacterial nucleoid. We used chromatin immunoprecipitation to determine the binding sites of H-NS and RNA polymerase on the Salmonella enterica serovar Typhimurium chromosome. We found that H-NS does not bind to actively transcribed genes and does not co-localize with RNA polymerase. This shows that H-NS principally silences gene expression by restricting the access of RNA polymerase to the DNA. H-NS had previously been shown to preferentially bind to curved DNA in vitro. In fact, at the genomic level we discovered that the level of H-NS binding correlates better with the AT-content of DNA. This is likely to have evolutionary consequences because we show that H-NS binds to many Salmonella genes acquired by lateral gene transfer, and functions as a gene silencer. The removal of H-NS from the cell causes un-controlled expression of several Salmonella pathogenicity islands, and we demonstrate that this has deleterious consequences for bacterial fitness. Our discovery of this novel role for H-NS may have implications for the acquisition of foreign genes by enteric bacteria.
Metabolic and toxicological considerations for sepsis drug treatments

Introduction: Sepsis, a complex interaction between pathogen and host response, presents a difficult challenge for clinicians and researchers alike. With an increasing understanding of the pathophysiology of the disease, new treatment paradigms are evolving. Areas covered: This article reviews the metabolic and toxicological considerations in sepsis, including the unique issues involved in neonatal and pediatric populations that differentiate it from adult sepsis. The authors cover metabolic issues, such as perfusion, renal and hepatic dysfunction and fluid retention in conjunction with their impact on therapy. Furthermore, the authors examine toxicological considerations of nephrotoxicity, ototoxicity and adverse drug reactions. The authors also present novel biomarkers of sepsis and current clinical tests utilized for the diagnosis of sepsis, as well as the limitations in animal models of sepsis and newer therapies. An extensive literature search including relevant formulae, publications and textbooks serves as the basis for this review. Expert opinion: Improving understanding of the metabolic and toxicological issues in sepsis will allow the development of more effective multifaceted treatments and reduction of risks. Clinical research will need to more heavily involve neonatal and pediatric patients given the number of individuals who die from sepsis within these special populations. Development of a sepsis-specific inflammatory biomarker would allow more rapid detection as well as a method to determine the effectiveness of novel therapies.
Experiences, coping and well-being of unemployed people in the North-West Province

The objective of this study was to investigate the expen ences, coping mechanisms and the well-being of unemployed people in the Potchefstroom area of the North West Province. A survey design was used and samples (N 381) were taken ,from unemployed people in the Potchefstroom area. The Experiences of Unemployment Questionnaire was developed and administered. Descriptive statistics were used to analyse the data. The results showed that most participants experienced unemployment negatively. Being unemployed was described as very unpleasant, and it was associated with boredom and loneliness. Work seemed to be the most important factor, and it was experienced as meaningful. The participants also indicated that they had asked somebody else for a job because they w~re unemployed. OPSOMMING Die doel van die studie was om die ervarings, coping en weIst and van werklose persone die Potchefstroom-area van die Noordwes Provinsie te ondersoek. 'n Dwarsdeursnee opname-ontwerp is gebruik en steekproewe (N = 381) van werklose mense in die Potchefstroom-area is geneem. Die Vraelys oor die Ervaring van Werkloosheid is gebruik. Beskrywende statistiek is gebruik om die data te ontleed. Die resultate het bevestig dat werkloosheid baie negatief deur die meeste van die deeInemers ervaar word. Rulle het werkloosheid as uiters onaangenaam ervaar, en dit het hulle verveeld en eensaam laat voel. Werk het geblyk die belangrikste faktor te wees en is as sinvol ervaar. Die deeInemers het ook aangedui dat hulle iemand anders vir werk gevra het omdat hulle werkloos was.
GABAergic terminals in nucleus maznocellularis and laminaris originate from the superior olivary nucleus

The auditory brainstem nuclei, angularis (NA), magnocellularis (NM), and laminaris (NL) of the chicken, Gallus, contain terminals that stain for antibodies against the inhibitory neurotransmitter, gamma‐aminobutyric acid (GABA). Some of these terminals originate from cells surrounding nucleus Magnocellularis. Results from this study indicate that the majority of the GABAergic terminals found in NA, NM and NL originate from the superior olivary nucleus (SON). Injections of cholera toxin and horseradish peroxidase show that superior olivary nucleus (SON) neurons, which respond to pure tones, project bilaterally to NA, NM and NL. NA and NL are reciprocally connected with the SON. More NA cells project to the SON than NL cells. While SON neurons project to NM, NM neurons do not project axons back to the SON. The configuration of SON terminals in NA, NM and NL matches the pattern of GABAimmunoreactive puncta seen in these three nuclei: they surround individual NM cells, congregate in the dendritcneuropil of NL, and blanket the NA. The data indicate that NA, NM and NL may be affected by two different inhibitory cell types: local interneurons and SON neurons. Patterns of connectivity described in this report suggest that the activity of NA cells could influence NM and NL cell physiology, Specifically, increases in NA cell activity could augment the effects of GABAergic SON neurons on NM and NL. Hence, binaural perception in the chicken may be more dependent upon changes in intensity cues than previously believed. © 1994 Wiley‐Liss, Inc.
Correlation between a loss of auxin signaling and a loss of proliferation in maize antipodal cells

The plant life cycle alternates between two genetically active generations: the diploid sporophyte and the haploid gametophyte. In angiosperms the gametophytes are sexually dimorphic and consist of only a few cells. The female gametophyte, or embryo sac, is comprised of four cell types: two synergids, an egg cell, a central cell, and a variable number of antipodal cells. In some species the antipodal cells are indistinct and fail to proliferate, so many aspects of antipodal cell function and development have been unclear. In maize and many other grasses, the antipodal cells proliferate to produce a highly distinct cluster at the chalazal end of the embryo sac that persists at the apex of the endosperm after fertilization. The antipodal cells are a site of auxin accumulation in the maize embryo sac. Analysis of different families of genes involved in auxin biosynthesis, distribution, and signaling for expression in the embryo sac demonstrates that all steps are expressed within the embryo sac. In contrast to auxin signaling, cytokinin signaling is absent in the embryo sac and instead occurs adjacent to but outside of the antipodal cells. Mutant analysis shows a correlation between a loss of auxin signaling and a loss of proliferation of the antipodal cells. The leaf polarity mutant Laxmidrib1 causes a lack of antipodal cell proliferation coupled with a loss of DR5 and PIN1a expression in the antipodal cells.
Characterization of the Essential Transport Function of the AIDA-I Autotransporter and Evidence Supporting Structural Predictions

ABSTRACT The current model for autodisplay suggests a mechanism that allows a passenger protein to be translocated across the outer membrane by coordinate action of a C-terminal β-barrel and its preceding linking region. The passenger protein, linker, and β-barrel are together termed the autotransporter, while the linker and β-barrel are here referred to as the translocation unit (TU). We characterized the minimal TU necessary for autodisplay with the adhesin-involved-in-diffuse-adherence (AIDA-I) autotransporter. The assumed β-barrel structure at the C terminus of the AIDA-I autotransporter was studied by constructing a set of seven AIDA-I–cholera toxin B subunit fusion proteins containing various portions of AIDA-I. Surface exposure of the cholera toxin B moiety was assessed by dot blot experiments and trypsin accessibility of the chimeric proteins expressed in Escherichia coli JK321 or UT5600. Export of cholera toxin B strictly depended on a complete predicted β-barrel region. The absolute necessity for export of a linking region and its influence on expression as an integral part of the TU was also demonstrated. The different electrophoretic mobilities of native and denatured chimeras indicated that the proposed β-barrel resides within the C-terminal 312 amino acids of AIDA-I. Together these data provide evidence for the predicted β-barrel structure and support our formerly proposed model of membrane topology of the AIDA-I autotransporter.
Breaking the Gingival Epithelial Barrier: Role of the Aggregatibacter actinomycetemcomitans Cytolethal Distending Toxin in Oral Infectious Disease

The Gram-negative bacterium Aggregatibacter actinomycetemcomitans is part of the HACEK group that causes infective endocarditis, a constituent of the oral flora that promotes some forms of periodontal disease and a member of the family of species that secrete a cytolethal distending toxin (Cdt). The family of bacteria that express the cdt genes participate in diseases that involve the disruption of a mucosal or epithelial layer. In vitro studies have shown that human gingival epithelial cells (HGEC) are native targets of the Cdt that typically induces DNA damage that signals growth arrest at the G2/M interphase of the cell cycle. The gingival epithelium is an early line of defense in the oral cavity against microbial assault. When damaged, bacteria collectively gain entry into the underlying connective tissue where microbial products can affect processes and pathways in infiltrating inflammatory cells culminating in the destruction of the attachment apparatus of the tooth. One approach has been the use of an ex vivo gingival explant model to assess the effects of the Cdt on the morphology and integrity of the tissue. The goal of this review is to provide an overview of these studies and to critically examine the potential contribution of the Cdt to the breakdown of the protective gingival barrier.
Teacher-Set Pre-Reading Purposes and Comprehension

Because some basal reader teachers’ guides recommend written pre-reading purposes while others suggest only oral ones, the major purpose of this study was to compare the comprehension of stories in the basal reader using three pre-reading purpose treatments: (1) written, (2) oral, and (3) no purpose (control). TEACHER-SET PRE-READING PURPOSES AND COMPREHENSION
Fathers’ Involvement: Correlates and Consequences for Child Socioemotional Behavior in the United Kingdom

This study investigated longitudinal relationships between fathers’ involvement, as measured by reading, and child socioemotional behavior between infancy and age 7 in 9,238 intact two-parent families from the U.K. Millennium Cohort Study, a national cohort of British children born between 2000 and 2002. Once a variety of covariates and the potential bidirectional nature of relationships were taken into account, a path model showed that fathers’ involvement with their children in infancy significantly predicted better socioemotional behavior at age 3, although the relationship was not strong. Fathers’ reading with their children between ages 3 and 7 was not significantly associated with child socioemotional behavior, but mothers’ reading with their children at age 3 was significantly associated with improved child socioemotional behavior at ages 3 and 5. Results also suggested that parenting in the 21st-century British context remains fairly gendered. Both mothers and fathers were more likely to engage in physical activities with their sons and artistic activities with their daughters. Fathers’ reading was socially patterned in predicted directions.
KRAS and BRAF somatic mutations in colonic polyps and the risk of metachronous neoplasia

Background & aims High-risk features of colonic polyps are based on size, number, and pathologic characteristics. Surveillance colonoscopy is often recommended according to these findings. This study aimed to determine whether the molecular characteristics of polyps might provide information about the risk of metachronous advanced neoplasia. Methodology We retrospectively included 308 patients with colonic polyps. A total of 995 polyps were collected and tested for somatic BRAF and KRAS mutations. Patients were classified into 3 subgroups, based on the polyp mutational profile at baseline, as follows: non-mutated polyps (Wild-type), at least one BRAF-mutated polyp, or at least one KRAS-mutated polyp. At surveillance, advanced adenomas were defined as adenomas ≥ 10 mm and/or with high grade dysplasia or a villous component. In contrast, advanced serrated polyps were defined as serrated polyps ≥ 10 mm in any location, located proximal to the splenic flexure with any size or with dysplasia. Results At baseline, 289 patients could be classified as wild-type (62.3%), BRAF mutated (14.9%), or KRAS mutated (22.8%). In the univariate analysis, KRAS mutations were associated with the development of metachronous advanced polyps (OR: 2.36, 95% CI: 1.22–4.58; P = 0.011), and specifically, advanced adenomas (OR: 2.42, 95% CI: 1.13–5.21; P = 0.023). The multivariate analysis, adjusted for age and sex, also showed associations with the development of metachronous advanced polyps (OR: 2.27, 95% CI: 1.15–4.46) and advanced adenomas (OR: 2.23, 95% CI: 1.02–4.85). Conclusions Our results suggested that somatic KRAS mutations in polyps represent a potential molecular marker for the risk of developing advanced neoplasia.
Physical exercise stimulates autophagy in normal skeletal muscles but is detrimental for collagen VI-deficient muscles

Autophagy is a catabolic process that provides the degradation of altered/damaged organelles through the fusion between autophagosomes and lysosomes. Proper regulation of the autophagic flux is fundamental for the homeostasis of skeletal muscles in physiological conditions and in response to stress. Defective as well as excessive autophagy is detrimental for muscle health and has a pathogenic role in several forms of muscle diseases. Recently, we found that defective activation of the autophagic machinery plays a key role in the pathogenesis of muscular dystrophies linked to collagen VI. Impairment of the autophagic flux in collagen VI null (Col6a1–/–) mice causes accumulation of dysfunctional mitochondria and altered sarcoplasmic reticulum, leading to apoptosis and degeneration of muscle fibers. Here we show that physical exercise activates autophagy in skeletal muscles. Notably, physical training exacerbated the dystrophic phenotype of Col6a1–/– mice, where autophagy flux is compromised. Autophagy was not induced in Col6a1–/– muscles after either acute or prolonged exercise, and this led to a marked increase of muscle wasting and apoptosis. These findings indicate that proper activation of autophagy is important for muscle homeostasis during physical activity.