Miracle-dz/UniFAR-FTUs huggingface dataset:
Postural stability and vehicle kinematics during an evasive lane change manoeuvre: A driver training study

The purpose of this study was to investigate the effect of a 2-day driver-training course that emphasised postural stability maintenance during critical driving situations on postural stability and vehicle kinematics during an evasive lane change manoeuvre. Following training, the trainee group experienced enhanced postural stability during specific phases of the task. In terms of vehicle kinematics, the main adaptation to training was that trained drivers reduced the extent to which they experienced vehicle decelerations during rapid turning compared to controls. Such a strategy may confer a safety benefit due to the increased risks associated with simultaneous braking while turning during an evasive manoeuvre. The newly learned strategy was consistent with the strategy used by a group of highly skilled drivers (driving instructors). Taken together, the results of the study suggest postural stability may be a useful variable to consider in relation to the skill-based component of hierarchical driver training programmes. The findings of this study provide some preliminary evidence to suggest that postural stability may be an important consideration when instructing individuals on how to safely negotiate obstacles during driving.
C-KIT mutation cooperates with full-length AML1-ETO to induce acute myeloid leukemia in mice

The full-length AML1-ETO (AE) fusion gene resulting from t(8;21)(q22;q22) in human acute myeloid leukemia (AML) is not sufficient to induce leukemia in animals, suggesting that additional mutations are required for leukemogenesis. We and others have identified activating mutations of C-KIT in nearly half of patients with t(8;21) AML. To test the hypothesis that activating C-KIT mutations cooperate with AE to cause overt AML, we generated a murine transduction and transplantation model with both mutated C-KIT and AE. To overcome the intracellular transport block of human C-KIT in murine cells, we engineered hybrid C-KIT (HyC-KIT) by fusing the extracellular and transmembrane domains of the murine c-Kit in-frame to the intracellular signaling domain of human C-KIT. We showed that tyrosine kinase domain mutants HyC-KIT N822K and D816V, as well as juxtamembrane mutants HyC-KIT 571+14 and 557-558Del, could transform murine 32D cells to cytokine-independent growth. The protein tyrosine kinase inhibitor dasatinib inhibited the proliferation of 32D cells expressing these C-KIT mutants, with potency in the low nanomolar range. In mice, HyC-KIT N822K induced a myeloproliferative disease, whereas HyC-KIT 571+14 induces both myeloproliferative disease and lymphocytic leukemia. Interestingly, coexpression of AE and HyC-KIT N822K led to fatal AML. Our data have further enriched the two-hit model that abnormalities of both transcription factor and membrane/cytosolic signaling molecule are required in AML pathogenesis. Furthermore, dasatinib prolonged lifespan of mice bearing AE and HyC-KIT N822K-coexpressing leukemic cells and exerted synergic effects while combined with cytarabine, thus providing a potential therapeutic for t(8;21) leukemia.
Mutations induced by (−)‐anti‐11R,12S‐dihydrodiol 13S,14R‐epoxide of dibenzo[a,l]pyrene in the coding region of the hypoxanthine phosphoribosyltransferase (Hprt) gene in Chinese hamster V79 cells

The polycyclic aromatic hydrocarbon dibenzo[a,l]pyrene (DB[a,l]P) is an exceptionally potent carcinogen. Its direct DNA‐reactive metabolite, the fjord region (−)‐anti‐11R,12S‐dihydrodiol 13S,14R‐epoxide [(−)‐anti‐DB[a,l]PDE], was used to investigate induction of mutations in the coding region of the hypoxanthine phosphoribosyltransferase (Hprt) gene in Chinese hamster V79 cells. Cells exposed to 1–10 nM (−)‐anti‐DB[a,l]PDE exhibited a close dose‐responsive increase in the frequency of mutant clones resistant to 6‐thioguanine. RNA was isolated from mutant clones and cDNAs were prepared by reverse transcription. The coding region of the cDNA of the Hprt gene was amplified by polymerase chain reaction and sequenced. Analysis of the DNA base sequence changes induced by (−)‐anti‐DB[a,l]PDE indicated that base substitutions were the most prevalent mutations, followed by exon deletions. Among the groups of V79 cells treated with low concentrations of (−)‐anti‐DB[a,l]PDE, most displayed high selectivity for both A:T→T:A transversions and A:T→G:C transitions, while cells exposed to a higher dose (10 nM) formed predominantly G:C→T:A transversions. Also, the number of base substitutions per mutant clone increased with dose. In general, the mutation profiles induced by (−)‐anti‐DB[a,l]PDE exhibited a wide spectrum; in addition to base substitutions, deletions, insertions, frameshift mutations, as well as tandem mutations were detected. Analysis of the DNA adduct levels induced by (−)‐anti‐DB[a,l]PDE revealed that a concentration‐dependent increase in the level of adduct formation preceded the concentration‐dependent increase in mutational events in these cells and that an increasing proportion of DNA adducts at deoxyadenosine were formed with dose. The results of this study demonstrate a correspondence between the concentration and types of DNA adducts and the frequency and types of mutations induced by (−)‐anti‐DB[a,l]PDE in V79 cells. Environ. Mol. Mutagen. 41:131–139, 2003. © 2003 Wiley‐Liss, Inc.
Molecular mechanisms of fibrinolysis

The molecular mechanisms that finely co‐ordinate fibrin formation and fibrinolysis are now well defined. The structure and function of all major fibrinolytic proteins, which include serine proteases, their inhibitors, activators and receptors, have been characterized. Measurements of real time, dynamic molecular interactions during fibrinolysis of whole blood clots can now be carried out in vitro. The development of gene‐targeted mice deficient in one or more fibrinolytic protein(s) has demonstrated expected and unexpected roles for these proteins in both intravascular and extravascular settings. In addition, genetic analysis of human deficiency syndromes has revealed specific mutations that result in human disorders that are reflective of either fibrinolytic deficiency or excess. Elucidation of the fine control of fibrinolysis under different physiological and pathological haemostatic states will undoubtedly lead to novel therapeutic interventions. Here, we review the fundamental features of intravascular plasmin generation, and consider the major clinical syndromes resulting from abnormalities in fibrinolysis.
Analysis and design of active antenna arrays

In this paper, the FDTD method is extended successfully to analyze active antennas using Z-transform method for small signal model and by a stable scheme for large signal model. The two approaches are validated by comparison with analytical impedance expression in frequency domain. Through these approaches, we analyze active antennas and antenna arrays containing tunnel diodes. Effects of various device parameters are investigated in order to find desired oscillations. Single and array active antennas are designed and tested. Experimental and simulated results are given and compared.
Mechanisms of Diastolic Dysfunction in Cardiovascular Disease Afterload-induced diastolic dysfunction contributes to high filling pressures in experimental heart failure with preserved ejection fraction

Sara Leite,* Sara Rodrigues,* Marta Tavares-Silva, José Oliveira-Pinto, Mohamed Alaa, Mahmoud Abdellatif, Dulce Fontoura, X Inês Falcão-Pires, Thierry C. Gillebert, Adelino F. Leite-Moreira, and X André P. Lourenço Department of Physiology and Cardiothoracic Surgery, Faculty of Medicine, University of Porto, Porto, Portugal; Cardiovascular Research Centre, Faculty of Medicine, University of Porto, Porto, Portugal; Department of Cardiology, Hospital São João, Porto, Portugal; Department of Vascular Surgery, Hospital São João, Porto, Portugal; Department of Cardiothoracic Surgery, Suez Canal University, Ismaileya, Egypt; Department of Cardiology, Ghent University, Ghent, Belgium; Department of Cardiothoracic Surgery, Hospital São João, Porto, Portugal; and Department of Anesthesiology, Hospital São João, Porto, Portugal
Unusual Anchor of a Motor Complex (MyoD–MLC2) to the Plasma Membrane of Toxoplasma gondii

Toxoplasma gondii possesses 11 rather atypical myosin heavy chains. The only myosin light chain described to date is MLC1, associated with myosin A, and contributing to gliding motility. In this study, we examined the repertoire of calmodulin‐like proteins in Apicomplexans, identified six putative myosin light chains and determined their subcellular localization in T. gondii and Plasmodium falciparum. MLC2, only found in coccidians, is associated with myosin D via its calmodulin (CaM)‐like domain and anchored to the plasma membrane of T. gondii via its N‐terminal extension. Molecular modeling suggests that the MyoD–MLC2 complex is more compact than the reported structure of Plasmodium MyoA–myosin A tail‐interacting protein (MTIP) complex. Anchorage of this MLC2 to the plasma membrane is likely governed by palmitoylation.
Quantifying the auditory saltation illusion: an objective psychophysical methodology.

Under conditions of rapid presentation, brief acoustic stimuli repeatedly delivered first at one location, then at another, are systematically mislocalized, with stimuli perceived as traveling smoothly between the two locations. This robust illusory motion percept is termed "auditory saltation. " Currently, the characteristics and mechanisms of auditory saltation are not well understood. The lack of objective methods capable of quantifying the illusion on an individual basis seems a limiting factor for this area of research. In this study, we outline an objective psychophysical task that estimates the interstimulus interval at which the saltation illusion is reliably distinguishable from simulated motion. Experiment 1 examined the psychophysical function relating task performance to ISI and addressed the suitability of the task for use with adaptive psychophysical procedures. Experiment 2 directly compared performance on the task with that of another quantification method. The results suggested that this objective approach to the study of auditory saltation overcomes difficulties associated with more subjective methods, and provides a reliable paradigm within which to quantify the temporal parameters of saltation on an individual basis.
Attentional control in patients with temporal lobe epilepsy.

Across different studies, patients with temporal lobe epilepsy (TLE) demonstrate impairments on numerous measures of attentional control that are classically associated with frontal lobe functioning. One aspect of attentional control that has not been examined in TLE is the ability to execute two modality-specific tasks concurrently. We sought to examine the status of dual-task coordination in TLE. We further examined the cohorts' performance on a range of traditional measures of attentional control. Eighteen TLE patients and 22 healthy controls participated in the study. Dual-task performance involved comparing the capacity to execute a tracking and a digit recall task simultaneously with the capacity to execute the tasks separately. We also administered measures of: set shifting (odd-man-out test), sustained attention (elevator counting), selective attention (elevator counting with distraction), and divided attention (trail making test). We found that the proportional decrement in dual-task performance relative to single-task performance did not vary between the groups (TLE = 92.48%; controls = 93.70%), nor was there a significant difference in sustained attention (p > .10). Patients with TLE did demonstrate marked deficits in selective attention (p < .0001), divided attention (p < .01), and set shifting (p < .01). These findings add to the knowledge about cognitive dysfunction in TLE, indicating that impairments in attentional control in TLE tend to be selective. The greatest deficits appear to be on tasks that invoke a high level of processing resources. In contrast, sustained attention is less compromised and the capacity to allocate cognitive resources appears to be normal in patients with TLE.
Employment Generation among Women in NREGS: A Synthesis on the basis of Micro Level Field Investigation

Government of India has initiated the Mahatma Gandhi National Rural Employment Guarantee Scheme (MGNREGS) or N REGS in 2006 where the basic objective is to provide 100 full man-days of employment to each willing rural household. The adjoining act (NREG Act of 2005) that guarantees employment of every rural household for 100 days has different provisions to incentivize participation of women in the programme. The programme indeed has both direct and indirect aspects towards favoring the participation of women in order to fulfill a larger objective of women empowerment. Thus it becomes imperative to focus on the extent to which the programme is inclusive of women. Official data suggest that 47% of all NREGS workers are women. However, in this regard, there is substantial variation not only across states but also across different regions within a state. The present paper based on a primary survey made in Birbhum district of West Bengal, attempts to investigate whether expansion of NREGS has been able to help the female job-card holders to get employment through NREGS where we have considered ratio of female man days to total man days of a household as the outcome variable. It is observed that the heterogeneity in the value of the stated outcome variable is significantly caused by nature of works the female job card holders have to carry out under NREGS and family parameters faced by them which somehow emanate from socio-cultural factor(s) in general and binding in particular. Apart from this, although there is inevitability of the influence of total number of NREGS man- days received in the entire reference period by the household to which the female member(s) belongs, yet, there seems no one to one correspondence between the outcome variable and the same.
Hinged Ilizarov external fixation for correction of antebrachial deformities.

OBJECTIVE To evaluate hinged circular external fixation for correction of antebrachial deformities in dogs. STUDY DESIGN Uncontrolled clinical trial. ANIMAL POPULATION Seven client-owned dogs. METHODS Six dogs had one radius corrected and one dog had both radii corrected. Preoperative planning included measurement of the craniocaudal and mediolateral angular deformities, rotational deformity, length deficit, origin of deformity, graphical or mathematical determination of the amplitude and direction of the actual limb deformity, and frame assembly. RESULTS Preoperatively, function and cosmesis were assessed to be fair to poor in all dogs. Deformity correction started 48 to 60 hours postoperatively and ranged from 0.46 mm to 1.36 mm twice daily. Hospitalization time ranged from 4 to 6 days. Corrections were mostly made by the owners, at home. Lengthening and angular correction ranged from 3 to 38 mm and 18 degrees to 48 degrees. Mean residual deformities were 2.7% of radial length and 2.7 degrees. The time duration with the circular external fixators in place ranged from 29 to 71 days. Two additional surgeries were necessary in one dog because of wire breakage. Mean follow-up was 40 months. Long-term function and cosmesis were good to excellent in all dogs. CONCLUSION Although complications were present in six of seven dogs, the outcome of hinged Ilizarov external fixation was successful in all dogs treated for deformities of the antebrachium. CLINICAL RELEVANCE Despite complex preoperative planning, the placement of hinged circular external fixators is straightforward, and allows precise correction of complex antebrachial deformities with minimal tissue trauma.
The Carboxyl Termini of KATP Channels Bind Nucleotides*

ATP-sensitive potassium (KATP) channels are expressed in many excitable, as well as epithelial, cells and couple metabolic changes to modulation of cell activity. ATP regulation of KATP channel activity may involve direct binding of this nucleotide to the pore-forming inward rectifier (Kir) subunit despite the lack of known nucleotide-binding motifs. To examine this possibility, we assessed the binding of the fluorescent ATP analogue, 2′,3′-O-(2,4,6-trinitrophenylcyclo-hexadienylidene)adenosine 5′-triphosphate (TNP-ATP) to maltose-binding fusion proteins of the NH2- and COOH-terminal cytosolic regions of the three known KATP channels (Kir1.1, Kir6.1, and Kir6.2) as well as to the COOH-terminal region of an ATP-insensitive inward rectifier K+ channel (Kir2.1). We show direct binding of TNP-ATP to the COOH termini of all three known KATP channels but not to the COOH terminus of the ATP-insensitive channel, Kir2.1. TNP-ATP binding was specific for the COOH termini of KATP channels because this nucleotide did not bind to the NH2 termini of Kir1.1 or Kir6.1. The affinities for TNP-ATP binding to KATP COOH termini of Kir1.1, Kir6.1, and Kir6.2 were similar. Binding was abolished by denaturing with 4 m urea or SDS and enhanced by reduction in pH. TNP-ATP to protein stoichiometries were similar for all KATP COOH-terminal proteins with 1 mol of TNP-ATP binding/mole of protein. Competition of TNP-ATP binding to the Kir1.1 COOH terminus by MgATP was complex with both Mg2+ and MgATP effects. Glutaraldehyde cross-linking demonstrated the multimerization potential of these COOH termini, suggesting that these cytosolic segments may directly interact in intact tetrameric channels. Thus, the COOH termini of KATPtetrameric channels contain the nucleotide-binding pockets of these metabolically regulated channels with four potential nucleotide-binding sites/channel tetramer.
A systematic review of meta-analyses of the efficacy of oral atypical antipsychotics for the treatment of adult patients with schizophrenia

Introduction: Meta-analyses are a convenient way for clinicians and researchers to review data regarding different interventions. Meta-analyses can overcome many of the limitations of individual studies, namely the power to detect differences, and help resolve the results of inconsistent studies. Areas covered: This paper is a review of meta-analyses of oral atypical antipsychotics for the treatment of schizophrenia, located through PubMed and the Cochrane Database of Systematic Reviews. A total of 91 meta-analyses were identified that included efficacy outcome data for the 10 atypical antipsychotics available in the USA (11 focused on clozapine, 17 for risperidone, 8 for olanzapine, 5 for quetiapine, 3 for ziprasidone, 10 for aripiprazole, 5 for paliperidone, 1 for iloperidone, 0 for asenapine or lurasidone, and 31 others that were classified more broadly). These include Cochrane Reviews and other similarly executed reports, as well as pooled analyses meta-tagged in PubMed as a meta-analysis. Expert opinion: In general, there is heterogeneity among the atypical antipsychotics in terms of efficacy, with clozapine evidencing consistent superiority over typical antipsychotics, trailed behind by olanzapine and risperidone. Meta-analyses generally do not support efficacy differences between the other atypical antipsychotics compared with the older typical agents. Although this review is focused on efficacy, other considerations are also important, including the large tolerability differences among all the agents and the need to individualize medication choice based on past history of therapeutic response, past history of tolerability issues and the individual's personal values and preferences.
Co-expression of Transforming Growth Factor-β1 and Glial Cell Line–Derived Neurotrophic Factor in Vestibular Schwannoma

Hypothesis: Transforming growth factor-β1, glial cell line–derived neurotrophic factor, and their receptors are expressed in vestibular schwannoma, and the expression data correlate with the proliferation activity (Ki-67 labeling index) and the clinical growth rate of vestibular schwannoma tissue. Background: Glial cell line–derived neurotrophic factor is a potent growth factor for the central and peripheral nervous system. Recent results demonstrate that glial cell line–derived neurotrophic factor requires transforming growth factor-β to exert its trophic effect on neural tissue. A functional role, including that in Schwann cell proliferation, is discussed for both transforming growth factor-β1 and glial cell line–derived neurotrophic factor. Methods: Immunohistochemical analysis for transforming growth factor-β1 and glial cell line–derived neurotrophic factor and their receptors TβR II, GFR&agr;-1, and Ret was performed on formalin-fixed, paraffin-embedded archival surgical specimens. The Ki-67 labeling index (mean Ki-67 labeling index and highest Ki-67 labeling index for Antoni Type A and Type B regions) and the clinical growth rate of vestibular schwannoma were determined and correlated with the expression patterns of the examined neurotrophic factors and their receptors. Results: Results demonstrate co-expression of transforming growth factor-β1 and glial cell line–derived neurotrophic factor with higher levels in Antoni Type A than in Antoni Type B regions. Ninety-five percent of vestibular schwannomas exhibited transforming growth factor-β1 immunoreactivity, and glial cell line–derived neurotrophic factor expression was found in 100% of vestibular schwannoma specimens. Fifty percent of vestibular schwannoma displayed TβR II immunostaining, 100% showed positive reactions for GFR&agr;-1, and 86% showed positive reactions for Ret. Statistical analysis revealed no significant correlation in neurotrophin expression related to sex, age, tumor size, clinical growth rate, or Ki-67-labeling indices. Conclusions: Expression of transforming growth factor-β1 and glial cell line–derived neurotrophic factor may suggest a biological role for both growth factors in vestibular schwannomas. Trophic transforming growth factor-β/glial cell line-derived neurotrophic factor synergism seems possible and is underscored by co-expression of both neurotrophic factors and their receptors.
COMPLEMENT-MEDIATED KILLING OF BORRELIA BURGDORFERI BY NONIMMUNE SERA FROM SIKA DEER

Various species of cervid deer are the preferred hosts for adult, black-legged ticks (Ixodes scapularis and Ixodes pacificus) in the United States. Although frequently exposed to the agent of Lyme disease (Borrelia burgdorferi), these animals, for the most part, are incompetent as transmission reservoirs. We examined the borreliacidal activity of normal and B. burgdorferi-immune sera from sika deer (Cervus nippon) maintained in a laboratory setting and compared it to that of similar sera from reservoir-competent mice and rabbits. All normal deer sera (NDS) tested killed >90% of B. burgdorferi cells. In contrast, normal mouse and rabbit sera killed ≤22% of the Borrelia. Anti-B. burgdorferi antibodies could not be detected in any normal sera by indirect fluorescent antibody assay (IFA). Sera collected from deer 6 wk after exposure to B. burgdorferi by tick feeding exhibited IFA titers of 1:256, whereas sera from mice and rabbits similarly exposed had titers of >1:1,024. Heat treatment (56 C, 30 min) of NDS reduced borreliacidal activity, with <20% of the B. burgdorferi cells killed, suggesting complement-mediated killing. The chelators EGTA and EDTA were used to block the classical or both the classical and alternative complement pathways, respectively. Addition of 10 mM EGTA to NDS had a negligible effect on borreliacidal activity, with >90% of the cells killed. Addition of 10 mM EDTA reduced the killing to ∼30%, whereas the addition of Mg2+ (10 mM) restored borreliacidal activity to NDS. The addition of zymosan A, an activator of the alternative pathway, increased the survival of B. burgdorferi cells to ∼80% in NDS. These data suggest that the alternative complement activation pathway plays a major role in the borreliacidal activity of NDS. Additionally, 10 mM EGTA had almost no effect on the killing activity of B. burgdorferi-exposed deer sera, suggesting that the classical pathway is not involved in Borrelia killing, even in sera from B. burgdorferi-exposed deer.