Miracle-dz/UniFAR-FTUs huggingface dataset:
Investigations of load transfer capabilities of GIS disconnectors for DC grids

The paper focuses on the role of disconnectors for load transfer duties in the operation of MTDC meshed grids. As there are no topology existing today and no standard, some switching duties are presented for which disconnectors could act instead of using circuit breaker. Based on an empirical model relying on tests performed in air, severity of the different switching duties are presented and first conclusions are proposed.
Effects of two plant growth regulators, indole-3-acetic acid and β-naphthoxyacetic acid, on genotoxicity in Drosophila SMART assay and on proliferation and viability of HEK293 cells from the perspective of carcinogenesis

In this study, the mutagenic and recombinogenic effects of indole-3-acetic acid (IAA), a plant growth regulator naturally synthesized in plants but produced synthetically, and β-naphthoxyacetic acid (BNOA), a synthetic plant growth regulator widely used in agricultural regions, were investigated using the somatic mutation and recombination test (SMART) in Drosophila wings. The effect of the same plant growth regulators against the proliferation and viability of a human immortalized embryonic kidney HEK293 cells which is at the early stage of carcinogenesis were also examined with MTT and trypan-blue exclusion assays. For the SMART assay, two different crosses were used: a standard and a high-bioactivation (HB) cross, involving the flare-3 and the multiple wing hairs markers. The HB cross involved flies characterized by an increased cytochrome P-450-dependent bioactivation capacity, which permits the more efficient biotransformation of promutagens and procarcinogens. In both crosses, the wings of the two types of progeny, inversion-free marker heterozygotes and balancer heterozygotes, were analyzed. The results show that IAA and BNOA are not mutagenic or recombinogenic in the wing cells of Drosophila. Furthermore, neither plant growth regulator affected the proliferation rate of HEK293 cells; however, both of them induced cell death at high concentrations.
Just Who Is John Galt, Anyway?: A Carnivalesque Approach to Atlas Shrugged

Based on a paper delivered at a conference devoted to carnivalesque studies, this article focuses attention on Rand’s masterwork, Atlas Shrugged. By utilizing the carnivalesque techniques of Menippean satire and the “dialogic” interplay of narrative voices, with trickster-heroes as the agents of social change, the author argues that Rand ruthlessly deconstructs the logic of command economies and models a society turned, as Bakhtin would say, “topsy turvy” in favor of pure free enterprise. In doing so, she also contests the political boundaries of a stereotypically left-wing genre whose scholars are also typically Marxian.
Modelling neutral and selective evolution of protein folding

We examine a model evolutionary space consisting of genotypes mapped to their corresponding phenotypes. This mapping is derived from a lattice model for proteins which, despite its highly idealized nature, has been shown to share general properties with real proteins. Large evolutionary networks are observed, with genotypes corresponding to non-lethal phenotypes linked by unit mutational steps. Neutral mutations are necessary for traversing the evolutionary networks, and even one neutral mutation in a genotype can change the phenotypes attainable by a unit mutational step.
Reliability study on tri-gate nanowires poly-Si TFTs under DC and AC hot-carrier stress

This work studies reliability after dc and ac hot-carrier stress of polysilicon thin-film transistors (poly-Si TFTs) with single-channel and ten-nanowire channels, respectively. For single-channel (S1) poly-Si TFT, the device characteristics degradation under ac hot-carrier stress is severer than dc stress. In addition, the Vth and SS variation increases with the frequency increasing from 1 K Hz to 1 MHz. On the contrary, for tennanowire channels (M10) tri-gate poly-Si TFT, the Vth and SS variation is much lower than the S1 TFT with different stressing frequency. These results indicate that the M10 TFT has less deep state generation after dc and ac stress. Because the M10 TFT has more effective NH3 plasma passivation than that of S1 TFT due to the ten split nanowire channels has wide NH3 plasma passivation area. Moreover, M10 TFT has robust tri-gate control can reduce the lateral electrical field and its penetration from the drain to reduce hot-carrier effect. In ac stress study, the device degradation is dependent on the pulse falling time rather than rising time. In temperature study, the device degradation is improved as the operation temperature increasing from 25degC to 75degC.
Respiration rhythm monitoring in sleep based on weight movement using hetero-core fiber optic sensors

This paper describes respiration monitoring during sleep using hetero-core fiber optic pressure sensors. The hetero-core fiber optic sensor has high sensitivity to macro-bending action as a result of the core diameter difference corresponding to the sensor portion due to stable single-mode transmission. Pressure sensors employing hetero-core fiber optics were fabricated to have a wide sensitivity to small pressure changes resulting from minute body motions such as respiration in sleep and large pressure changes such as a roll-over action. The fabricated pressure sensors were installed in a conventional bed. The pressure characteristic performance of all the fabricated pressure sensors was found to show a monotonic response in the optical loss change with weight changes. The sensitivities of the hetero-core pressure sensors for a weight change of 3.0 kg were in the range of 0.55-1.80 dB. Additionally, even in the case of different body postures such as lying on one's side, a slight body movement due to respiration could be detected by the hetero-core pressure sensors.
Supplier collaboration practices: implications for focal firm innovation performance

Purpose Due to the increasing complexity in supply chains and networks, several key practices have been highlighted as beneficial for supply chain performance. However, it is less known whether adopting such practices affects the innovation performance of the focal firm. This study hypothesises that supplier collaboration practices in four specific areas (green and ethical supply management, early supplier involvement, systemic purchasing and inter-firm learning) may lead to higher focal firm innovation performance, as they require the firm to adopt new business models, processes and product features. Design/methodology/approach The hypotheses drawn from previous research are tested with a quantitative survey study of 165 Finnish firms and analysed by means of regression analysis. Findings The results show that two examined practices are positively related to focal firm innovation performance: systemic purchasing and green and ethical supply management. Interestingly, early supplier involvement and inter-firm learning did not influence innovation performance. Originality/value Little is known about whether adopting certain practices in supply management affects the innovation performance of the firm. In fact, among the performance indicators of supply management, innovation is rarely studied, and more studies using innovation as a performance indicator are called for. Thus, this study focuses on supplier collaboration practices and their relation to the focal firm’s innovation performance.
Identification and characterization of a high-affinity interaction between v-Crk and tyrosine-phosphorylated paxillin in CT10-transformed fibroblasts

The genome of avian sarcoma virus CT10 encodes a fusion protein in which viral Gag sequences are fused to cellular Crk sequences containing primarily Src homology 2 (SH2) and Src homology 3 (SH3) domains. Transformation of chicken embryo fibroblasts (CEF) with the Gag-Crk fusion protein results in the elevation of tyrosine phosphorylation on specific cellular proteins with molecular weights of 130,000, 110,000, and 70,000 (p130, p110, and p70, respectively), an event which has been correlated with cell transformation. In this study, we have identified the 70-kDa tyrosine-phosphorylated protein in CT10-transformed CEF (CT10-CEF) as paxillin, a cytoskeletal protein suggested to be important for organizing the focal adhesion. Tyrosine-phosphorylated paxillin was found to be complexed with v-Crk in vivo as evident from coimmunoprecipitation studies. Moreover, a bacterially expressed recombinant glutathione S-transferase (GST)-CrkSH2 fragment bound paxillin in vitro with a subnanomolar affinity, suggesting that the SH2 domain of v-Crk is sufficient for binding. Mapping of the sequence specificity of a GST-CrkSH2 fusion protein with a partially degenerate phosphopeptide library determined a motif consisting of pYDXP, and in competitive coprecipitation studies, an acetylated A(p)YDAPA hexapeptide was able to quantitatively inhibit the binding of GST-CrkSH2 to paxillin and p130, suggesting that it meets the minimal structural requirements necessary for the interaction of CrkSH2 with physiological targets. To investigate the mechanism by which v-Crk elevates the tyrosine phosphorylation of paxillin in vivo, we have treated normal CEF and CT10-CEF with sodium vanadate to inhibit protein tyrosine phosphatase activity. These data suggest that paxillin is involved in a highly dynamic kinase-phosphatase interplay in normal CEF and that v-Crk binding may interrupt this balance to increase the steady-state level of tyrosine phosphorylation. By contrast, the 130-kDa protein was not tyrosine phosphorylated upon vanadate treatment of normal CEF and only weakly affected in the CT10-CEF, suggesting that a different mechanism may be involved in its phosphorylation.
A modular and scalable control architecture for navigation of autonomous underwater vehicles

In the present paper, a hybrid architecture based on multi-agent systems is proposed, where it is included a module for formal evaluation. This module, allows the processes verification involved in the level/layer/environment steps. It is also developed a methodology for trajectory tracking based on the generation of a reliable virtual space, on which the navigation takes place under operative conditions (safety and effectiveness). Time processing operations reduction is expected during the inspection.
Asymptomatic carriage of Clostridium difficile and serum levels of IgG antibody against toxin A.

BACKGROUND Clostridium difficile infection can result in asymptomatic carriage, mild diarrhea, or fulminant pseudomembranous colitis. We studied whether antibody responses to C. difficile toxins affect the risks of colonization, diarrhea, and asymptomatic carriage. METHODS We prospectively studied C. difficile infections in hospitalized patients who were receiving antibiotics. Serial stool samples were tested for C. difficile colonization by cytotoxin assay and culture. Serum antibody (IgA, IgG, and IgM) levels and fecal antibody (IgA and IgG) levels against C. difficile toxin A, toxin B, and nontoxin antigens were measured by an enzyme-linked immunosorbent assay (ELISA). RESULTS Of 271 patients, 37 (14 percent) were colonized with C. difficile at the time of admission, 18 of whom were asymptomatic carriers. An additional 47 patients (17 percent) became infected in the hospital, 19 of whom remained asymptomatic. The baseline antibody levels were similar in the patients who later became colonized and those who did not. After colonization, those who became asymptomatic carriers had significantly greater increases in serum levels of IgG antibody against toxin A than did the patients in whom C. difficile diarrhea developed (P<0.001). The adjusted odds ratio for diarrhea was 48.0 (95 percent confidence interval, 3.4 to 678) among patients with colonization who had a serum level of IgG antibody against toxin A of 3.00 ELISA units or less, as compared with patients with colonization who had a level of more than 3.00 ELISA units. CONCLUSIONS We find no evidence of immune protection against colonization by C. difficile. However, after colonization there is an association between a systemic anamnestic response to toxin A, as evidenced by increased serum levels of IgG antibody against toxin A, and asymptomatic carriage of C. difficile.
24R,25-dihydroxyvitamin D3 increases cyclic GMP contents, leading to an enhancement of osteocalcin synthesis by 1,25-dihydroxyvitamin D3 in cultured human osteoblastic cells.

The effect of the physiological vitamin D metabolite 24R, 25-dihydroxyvitamin D3 [24R,25(OH)2D3] on human osteoblastic cells was assessed. Physiological concentrations (10(-9)-10(-8) M) of 24R, 25(OH)2D3 significantly increased the cyclic guanosine 5'-monophosphate (cGMP) content in the human osteoblastic cells by approximately 200% in 5 to 15 min. In contrast, 24S, 25-dihydroxyvitamin D3 had only a weak effect on the cGMP content, and 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] did not affect the content. The production of osteocalcin was not induced by 10(-9)-10(-8) M of 24R,25(OH)2D3 in the absence of 1,25(OH)2D3. However, the same concentration of 24R,25(OH)2D3 showed stimulatory effects on osteocalcin synthesis in the presence of 10(-9) M 1, 25(OH)2D3. Rp-8Br-cyclic GMP, a specific inhibitor of cyclic GMP-dependent protein kinase, significantly inhibited the cooperative effect of 24R,25(OH)2D3 with 1,25(OH)2D3 on the osteocalcin synthesis, although Rp-8Br-cyclic AMP, a specific inhibitor of cyclic AMP-dependent protein kinase, did not affect the cooperative effect. In addition, okadaic acid enhanced the osteocalcin synthesis induced by 1,25(OH)2D3. These observations suggest that 24R,25(OH)2D3 has a unique activity of increasing cGMP contents in osteoblastic cells, and that the increase in cGMP contents may lead to the cooperative effect of 24R,25(OH)2D3 with 1, 25(OH)2D3 on osteocalcin synthesis. These data support the hypothesis that 24R,25(OH)2D3 has a physiological role in human bone and mineral metabolism.
The STOP-Bang equivalent model and prediction of severity of obstructive sleep apnea: relation to polysomnographic measurements of the apnea/hypopnea index.

BACKGROUND Various models and questionnaires have been developed for screening specific populations for obstructive sleep apnea (OSA) as defined by the apnea/hypopnea index (AHI); however, almost every method is based upon dichotomizing a population, and none function ideally. We evaluated the possibility of using the STOP-Bang model (SBM) to classify severity of OSA into 4 categories ranging from none to severe. METHODS Anthropomorphic data and the presence of snoring, tiredness/sleepiness, observed apneas, and hypertension were collected from 1426 patients who underwent diagnostic polysomnography. Questionnaire data for each patient was converted to the STOP-Bang equivalent with an ordinal rating of 0 to 8. Proportional odds logistic regression analysis was conducted to predict severity of sleep apnea based upon the AHI: none (AHI < 5/h), mild (AHI ≥ 5 to < 15/h), moderate (≥ 15 to < 30/h), and severe (AHI ≥ 30/h). RESULTS Linear, curvilinear, and weighted models (R(2) = 0.245, 0.251, and 0.269, respectively) were developed that predicted AHI severity. The linear model showed a progressive increase in the probability of severe (4.4% to 81.9%) and progressive decrease in the probability of none (52.5% to 1.1%). The probability of mild or moderate OSA initially increased from 32.9% and 10.3% respectively (SBM score 0) to 39.3% (SBM score 2) and 31.8% (SBM score 4), after which there was a progressive decrease in probabilities as more patients fell into the severe category. CONCLUSIONS The STOP-Bang model may be useful to categorize OSA severity, triage patients for diagnostic evaluation or exclude from harm.
Characterization of Fusion Determinants Points to the Involvement of Three Discrete Regions of Both E1 and E2 Glycoproteins in the Membrane Fusion Process of Hepatitis C Virus

ABSTRACT Infection of eukaryotic cells by enveloped viruses requires the merging of viral and cellular membranes. Highly specific viral surface glycoproteins, named fusion proteins, catalyze this reaction by overcoming inherent energy barriers. Hepatitis C virus (HCV) is an enveloped virus that belongs to the genus Hepacivirus of the family Flaviviridae. Little is known about the molecular events that mediate cell entry and membrane fusion for HCV, although significant progress has been made due to recent developments in infection assays. Here, using infectious HCV pseudoparticles (HCVpp), we investigated the molecular basis of HCV membrane fusion. By searching for classical features of fusion peptides through the alignment of sequences from various HCV genotypes, we identified six regions of HCV E1 and E2 glycoproteins that present such characteristics. We introduced conserved and nonconserved amino acid substitutions in these regions and analyzed the phenotype of HCVpp generated with mutant E1E2 glycoproteins. This was achieved by (i) quantifying the infectivity of the pseudoparticles, (ii) studying the incorporation of E1E2 and their capacity to mediate receptor binding, and (iii) determining their fusion capacity in cell-cell and liposome/HCVpp fusion assays. We propose that at least three of these regions (i.e., at positions 270 to 284, 416 to 430, and 600 to 620) play a role in the membrane fusion process. These regions may contribute to the merging of viral and cellular membranes either by interacting directly with lipid membranes or by assisting the fusion process through their involvement in the conformational changes of the E1E2 complex at low pH.
The outcome and role of drugs in patients with unexplained gastrointestinal bleeding

Abstract Objective. Studies on unexplained gastrointestinal bleeding (GIB) are lacking. We aimed to study the clinical outcomes of patients with unexplained GIB and to determine the incidence of obscure GIB. Material and methods. A population-based study on all patients undergoing endoscopy at the National University Hospital of Iceland in 2010. Indications, results of endoscopies and drug history were prospectively registered with a follow-up of 3 years. A national pharmaceutical database containing prescription data was utilized. Patients were categorized into unexplained overt and occult GIB and obscure GIB. Patients undergoing endoscopy and without GIB acted as controls. Results. Of 2471 patients undergoing endoscopy, 11% had unexplained GIB. Of those, 46% had unexplained overt GIB, 44% had unexplained occult GIB and 11% had obscure GIB. Multivariate analysis showed that patients with unexplained GIB and unexplained overt GIB had greater odds of NSAID use than controls, OR 1.8 (CI 1.03–3.03) and OR 2.0 (CI 1.01–3.77), respectively. Warfarin was strongly associated with all bleeder groups, OR 4–4.8. The incidence of obscure GIB was 10/100,000 inhabitants annually. Two (0.8%) patients were diagnosed with colon cancer 16 and 30 months after the index colonoscopy. Of patients with unexplained overt, unexplained occult GIB and controls, 5%, 6% and 3.5% (NS) had another overt bleeding episode, during the study period. Conclusions.NSAIDs and warfarin seem to play an important role in unexplained GIB. The incidence of obscure GIB is low and missed cancers are very rare. The probability of a repeat bleeding episode is similar to that of controls.
Protection against acetaminophen hepatotoxicity by clofibrate pretreatment: Role of catalase induction

Mice pretreated with the peroxisome proliferator clofibrate (CFB) are highly resistant to acetaminophen (APAP)‐induced hepatotoxicity. The objective of the present study was to investigate whether the increase in hepatic catalase activity following CFB pretreatment plays a role in this hepatoprotection. An irreversible inhibitor, 3‐amino‐1,2,4‐triazole (3‐AT), was used to modulate catalase activity. Hepatic catalase activity in mice pretreated with CFB (500 mg/kg, i.p., for 10 days) was significantly inhibited by 3‐AT (100 or 500 mg/kg, i.p.). In addition, the lower dose of 3‐AT (100 mg/kg) had minimal effect on biliary and urinary excretion of APAP metabolites generated from a nontoxic dose, suggesting that APAP metabolism was not modulated by this dose of 3‐AT. The mortality rate of corn‐oil‐pretreated mice challenged with APAP (800 mg/kg, p.o.) was significantly increased by 3‐AT (100 mg/kg, i.p.) given 1 h before APAP. As expected, CFB pretreatment conferred full protection against APAP‐induced hepatotoxicity. The same 3‐AT treatment, however, did not abolish hepatoprotection in CFB‐pretreated mice, despite the marked inhibition of hepatic catalase activity. In conclusion, these results indicate that elevated catalase activity in mice exposed to CFB does not appear to mediate the hepatoprotection, suggesting that other cellular defense mechanisms are involved. © 2002 Wiley Periodicals, Inc. J Biochem Mol Toxicol 16:227–234, 2002; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10043
Der p 1‐pulsed myeloid and plasmacytoid dendritic cells from house dust mite‐sensitized allergic patients dysregulate the T cell response

Although reports suggest that dendritic cells (DC) are involved in the allergic reaction characterized by a T helper cell type 2 (Th2) profile, the role of myeloid (M‐DC) and plasmacytoid DC (P‐DC), controlling the balance Th1/Th2, remains unknown. Here, we showed that in Dermatophagoides pteronyssinus (Dpt)‐sensitized allergic patients and in healthy donors, M‐DC displayed a higher capacity to capture Der p 1, a major allergen of Dpt, than did P‐DC. However, Der p 1‐pulsed M‐DC from healthy subjects overexpressed CD80 and secreted interleukin (IL)‐10, whereas M‐DC from allergic patients did not. In contrast, with Der p 1‐pulsed P‐DC from both groups, no increase in human leukocyte antigen‐DR, CD80, and CD86 and no IL‐10 secretion were detected. When cocultured with allogeneic naive CD4+ T cells from healthy donors, Der p 1‐pulsed M‐DC from allergic patients favored a Th1 profile [interferon (IFN)‐γhigh/IL‐4low] and Der p 1‐pulsed P‐DC, a Th2 profile (IFN‐γlow/IL‐4high). In healthy donors, no T cell polarization (IFN‐γlow/IL‐4low) was induced by Der p 1‐pulsed M‐DC or P‐DC, but in response to Der p 1‐pulsed M‐DC, T cells secreted IL‐10. The neutralization of IL‐10 produced by Der p 1‐pulsed M‐DC from healthy donors led to an inhibition of IL‐10 production by T cells and a polarization toward a type 1. Thus, IL‐10 produced by M‐DC might be an essential mediator controlling the balance between tolerance and allergic status. In addition, P‐DC could contribute to the steady state in healthy donors or to the development of a Th2 response in allergic donors.
Genetics of the corneal endothelial dystrophies: an evidence‐based review

The aim of this review was to provide an evidenced‐based review of the genetic basis of the corneal endothelial dystrophies. A review of the English language peer‐reviewed literature describing the molecular genetic basis of posterior polymorphous corneal dystrophy (PPCD), congenital hereditary endothelial dystrophy (CHED), Fuchs endothelial corneal dystrophy (FECD) and X‐linked endothelial corneal dystrophy (XECD) was performed. Mutations in several genes have been implicated as playing a pathogenic role in the corneal endothelial dystrophies: VSX1 mutations in PPCD1; COL8A2 mutations in PPCD2 and FECD; ZEB1 mutations in PPCD3 and FECD; and SLC4A11 mutations in CHED2 and FECD. However, linkage, association and familial segregation analyses support a role of only one gene in each corneal endothelial dystrophy: ZEB1 in PPCD3, SLC4A11 in CHED2 and COL8A2 in FECD (early onset). In addition, insufficient evidence exists to consider the autosomal dominant form of CHED (CHED1) as distinct from PPCD. An accurate classification of the corneal endothelial dystrophies requires a critical review of the evidence to support the role of each suggested chromosomal locus, gene and genetic mutation associated with a corneal endothelial dystrophy. Only after the separation of evidence from opinion is performed can a critical examination of the molecular pathways that lead to endothelial dysfunction in each of these disorders be accurately performed.