Miracle-dz/UniFAR-FTUs huggingface dataset:
Somatosensory and visual evoked potentials in children with cerebral palsy: Correlations and discrepancies with MRI findings and clinical picture

Purpose: To determine if there is any association between the findings of visual evoked potentials (VEPs), somatosensory evoked potentials (SEPs), and magnetic resonance imaging (MRI) findings with the neurodevelopment and severity in children with cerebral palsy (CP). Methods: The present study included 15 children with spastic diplegic CP and five children with spastic hemiplegic CP and 42 healthy children as controls. The number of the controls was two-times greater than the study group to increase statistical power of this study. VEPs and SEPs were recorded in the CP children and compared with healthy controls. All MR scans were obtained using a 1.5 T MR scanner. Results: A significant difference was found in the latencies P100 (VEP) between the CP and controls. No correlations between increased P100 latencies and asphyxia, prematurity, the CP severity, MRI findings and mental retardation were noted. A significant difference in N13–N20 conductions (SEPs) between the subjects with CP and the control group was found. SEPs were positively correlated with mental retardation in CP children. The brain lesions in MRI showed a significant correlation with the CP severity scores and mental retardation. Conclusion: The differences in VEPs and SEPs were determined between CP children and healthy children. The MRI findings were positively correlated with the CP severity and mental retardation.
Umbilical and uterine artery flow velocity waveforms. Effect of the sampling site on Doppler ratios.

Pulsed Doppler duplex sonography was performed on 58 patients in order to determine whether Doppler ratios of umbilical and uterine artery flow velocity waveforms vary with the site at which measurements are taken along their respective arterial beds. Umbilical artery ratios were significantly higher at the fetal end of the cord when compared to ratios at the placental cord insertion. In the maternal circulation, ratios from arcuate artery waveforms were lower than those obtained from the uterine artery. This site‐dependent difference in ratios could be clinically important when studying ratios from the umbilical artery. Accuracy of Doppler measurements in the individual patient and in scientific investigations may be improved if uniform measurement techniques are used.
Accuracy and Perceived Expert Status in Group Decisions: When Minority Members Make Majority Members More Accurate Privately

We examined how the minority’s perceived (i.e., not real) expertise affects group discussion and performance. In two experiments, participants were randomly assigned to interacting groups in which the minority faction was perceived as either expert or not. Groups performed a decision task that involved solving a murder mystery. Both experiments showed that minorities perceived as expert (vs. not perceived as expert) made majority individuals acquire more accurate private judgments after group discussion, although the public group decision was not more accurate. In parallel, perceived expertise made minority members change their own judgments less. Experiment 1 also showed that minorities’ questioning behaviors mediated the effect of minorities’ perceived expertise on majority members’ private accuracy. Experiment 2 further showed that majority members’ deeper processing was also a mediator. Thus, minorities with perceived expertise serve as a catalyst, increasing the quality of majority members’ cognitions, but not their own.
Voluntary Breath-hold Technique for Reducing Heart Dose in Left Breast Radiotherapy

Breath-holding techniques reduce the amount of radiation received by cardiac structures during tangential-field left breast radiotherapy. With these techniques, patients hold their breath while radiotherapy is delivered, pushing the heart down and away from the radiotherapy field. Despite clear dosimetric benefits, these techniques are not yet in widespread use. One reason for this is that commercially available solutions require specialist equipment, necessitating not only significant capital investment, but often also incurring ongoing costs such as a need for daily disposable mouthpieces. The voluntary breath-hold technique described here does not require any additional specialist equipment. All breath-holding techniques require a surrogate to monitor breath-hold consistency and whether breath-hold is maintained. Voluntary breath-hold uses the distance moved by the anterior and lateral reference marks (tattoos) away from the treatment room lasers in breath-hold to monitor consistency at CT-planning and treatment setup. Light fields are then used to monitor breath-hold consistency prior to and during radiotherapy delivery.
Identification of human CYP isoforms involved in the metabolism of propranolol enantiomers--N-desisopropylation is mediated mainly by CYP1A2.

1. Studies using human liver microsomes and six recombinant human CYP isoforms (i.e. CYP1A2, 2A6, 2B6, 2D6, 2E1 and 3A4) were performed to identify the cytochrome P450 (CYP) isoform(s) involved in the ring 4-hydroxylation and side-chain N-desisopropylation of propranolol enantiomers in humans. 2. alpha-Naphthoflavone and 7-ethoxyresorufin (selective inhibitors of CYP1A1/2) inhibited the N-desisopropylation of R- and S-propranolol by human liver microsomes by 20 and 40%, respectively, while quinidine (a selective inhibitor of CYP2D6) abolished the 4-hydroxylation of both propranolol enantiomers almost completely. In contrast, sulphaphenazole (CYP2C8/9 inhibitor), S-mephenytoin (CYP2C19 inhibitor), troleandomycin (CYP3A3/4 inhibitor) and diethyldithiocarbamate (CYP2E1 inhibitor) elicited only weak inhibitory effects on propranolol metabolism via the two measured metabolic pathways. 3. Significant (P < 0.01) correlations were observed between the microsomal N-desisopropylation of both propranolol enantiomers and that for the O-deethylation of phenacetin among the 11 different human liver microsome samples (r = 0.98 and 0.77 for R- and S-propranolol, respectively). A marginally significant (r = 0.60, P congruent to 0.05) correlation was also observed between N-desisopropylation of S-, but not of R-propranolol and the 4'-hydroxylation of S-mephenytoin. No significant correlations were observed between the N-desisopropylation of propranolol enantiomers and the 2-hydroxylation of desipramine, the hydroxylation of tolbutamide or the 6 beta-hydroxylation of testosterone. 4. Significant (P < 0.01) correlations were observed between the microsomal 4-hydroxylation of R- and S-propranolol and the 2-hydroxylation of desipramine (r = 0.85 and 0.98, respectively). A weak (r = 0.66), albeit significant (P < 0.05) correlation was observed between the 4-hydroxylation of R-, but not of S-propranolol and the hydroxylation of tolbutamide. No significant correlations were observed between the 4-hydroxylation of propranolol enantiomers and the oxidation of other substrates for CYP1A2, 2C19, and 3A3/4. 5. Recombinant human CYP1A2 and CYP2D6 exhibited comparable catalytic activity with respect to the N-desisopropylation of both propranolol enantiomers; only expressed CYP2D6 exhibited a marked catalytic activity with respect to the 4-hydroxylation of both propranolol enantiomers. (ABSTRACT TRUNCATED AT 400 WORDS)
A requirement of FancL and FancD2 monoubiquitination in DNA repair

The rare hereditary disorder Fanconi anemia (FA) can be caused by mutations in components of the FA core complex (FancA/B/C/E/F/G/L/M), a key regulator FancD2, the breast cancer susceptibility protein BRCA2/FancD1, or the newly identified FancJ/BRIP1 helicase. By performing yeast two‐hybrid (Y2H) screens using N‐terminal chicken (ch) FancD2 as a bait, we have identified chFancL, the likely ubiquitin E3 ligase subunit of the FA core complex. We also found that ectopically expressed FancD2 and FancL co‐immunoprecipitated in 293T cells, and this interaction was dependent on the PHD domain of FancL. FANCL‐disrupted chicken DT40 cells displayed defects in both FancD2 monoubiquitination and focus formation. Importantly, cell lines lacking the FANCL or FANCD2 genes, or carrying a “knock‐in” mutation of the FancD2 monoubiquitination site (where the Lys 563 residue is changed to Arg), displayed quantitatively identical defects in the repair of I‐SceI‐induced chromosomal breaks by homologous recombination (HR). These data establish the role of FANCL and FancD2 monoubiquitination in HR repair.
Physical Fitness and Functional Ability of Children with Intellectual Disability: Effects of a Short-Term Daily Treadmill Intervention

Persons with intellectual disability (ID) and associated multiple disabilities have been found by many researchers to be a population with deficient physical fitness measures, which can be explained by an inactive lifestyle, a result of lack of awareness of the positive physical effects of physical exercise, or lack of motivation for any motor activity. Various plans for physical exercise have been put forward, but many are found impractical in nonresearch-based intervention. In this study, 15 children with ID on a motor functioning level of 7—14 months used a treadmill daily for 2 months. Our findings indicated a most significant improvement in the level of physical fitness of the participants (p < 0.005), as measured by pulse at rest and during effort. The improvement in physical fitness modestly (r = 0.5), but significantly (p < 0.05), correlated with a significant (p < 0.0007) improvement in functional ability of the participating children. Further examination a year after intervention terminated showed a return to preintervention pulse-at-rest values. The research examined the treadmill training method and found that it can be operated with the support of an unskilled staff person under the supervision of a physiotherapist. The research was performed under real-life conditions, enabling relatively easy implementation in the existing conditions of special education centers. This method is a type of exercise that is easy to operate without entailing long-term budgetary expenses and might improve the health status of children with ID, who are a population at risk for developing heart-related diseases at a young age.
The Oscillatory Behavior of Pancreatic Islets from Mice with Mitochondrial Glycerol-3-phosphate Dehydrogenase Knockout*

Glucose stimulation of pancreatic β cells induces oscillations of the membrane potential, cytosolic Ca2+ ([Ca2+] i ), and insulin secretion. Each of these events depends on glucose metabolism. Both intrinsic oscillations of metabolism and repetitive activation of mitochondrial dehydrogenases by Ca2+ have been suggested to be decisive for this oscillatory behavior. Among these dehydrogenases, mitochondrial glycerol-3-phosphate dehydrogenase (mGPDH), the key enzyme of the glycerol phosphate NADH shuttle, is activated by cytosolic [Ca2+] i . In the present study, we compared different types of oscillations in β cells from wild-type and mGPDH−/− mice. In clusters of 5–30 islet cells and in intact islets, 15 mm glucose induced an initial drop of [Ca2+] i , followed by an increase in three phases: a marked initial rise, a partial decrease with rapid oscillations and eventually large and slow oscillations. These changes, in particular the frequency of the oscillations and the magnitude of the [Ca2+] rise, were similar in wild-type and mGPDH−/− mice. Glucose-induced electrical activity (oscillations of the membrane potential with bursts of action potentials) was not altered in mGPDH−/− β cells. In single islets from either type of mouse, insulin secretion strictly followed the changes in [Ca2+] i during imposed oscillations induced by pulses of high K+ or glucose and during the biphasic elevation induced by sustained stimulation with glucose. An imposed and controlled rise of [Ca2+] i in β cells similarly increased NAD(P)H fluorescence in control and mGDPH−/− islets. Inhibition of the malate-aspartate NADH shuttle with aminooxyacetate only had minor effects in control islets but abolished the electrical, [Ca2+] i and secretory responses in mGPDH−/− islets. The results show that the two distinct NADH shuttles play an important but at least partially redundant role in glucose-induced insulin secretion. The oscillatory behavior of β cells does not depend on the functioning of mGPDH and on metabolic oscillations that would be generated by cyclic activation of this enzyme by Ca2+.
Getting Close to Rwandans since the Genocide: Studying Everyday Life in Highly Politicized Research Settings

Abstract: Research with people in highly politicized research settings illuminates the gap between the images that most African governments strive to represent and the sociopolitical realities of everyday life. This article discusses the opportunities and challenges of doing research in postgenocide Rwanda and is a useful resource for researchers contemplating their own projects under such conditions, whether in Rwanda or elsewhere. It discusses the importance of creating personal relationships and meeting people on their terms, as well as such topics as the identification of the research site, building rapport and trust with respondents, safeguarding anonymity and confidentiality, and working with local research assistants and partners.
Dung beetles and fecal helminth transmission: patterns, mechanisms and questions

SUMMARY Dung beetles are detrivorous insects that feed on and reproduce in the fecal material of vertebrates. This dependency on vertebrate feces implies frequent contact between dung beetles and parasitic helminths with a fecal component to their life-cycle. Interactions between dung beetles and helminths carry both positive and negative consequences for successful parasite transmission, however to date there has been no systematic review of dung beetle-helminth interactions, their epidemiological importance, or their underlying mechanisms. Here we review the observational evidence of beetle biodiversity–helminth transmission relationships, propose five mechanisms by which dung beetles influence helminth survival and transmission, and highlight areas for future research. Efforts to understand how anthropogenic impacts on biodiversity may influence parasite transmission must include the development of detailed, mechanistic understanding of the multiple interactions between free-living and parasitic species within ecological communities. The dung beetle–helminth system may be a promising future model system with which to understand these complex relationships.
Functional role of dendritic spines.

A number of speculations have been made on the functional role of dendritic spines. Some emphasize that a spine modulates the effect of a chemical synapse on the spine head. Others propose that spines isolate neighboring synapses from each others' effects. Still others suggest that spines play a role in short- or long-term plasticity, while others deny any functional role for spines at all. This paper brings some quantitative calculations to bear on these questions. In contrast to previous studies of the steady-state voltage attenuation in dendrites having spines, our calculations predict the voltage transient throughout a dendrite due to activation of a chemical synapse on a spine-head, causing a time-dependent postsynaptic conductance change associated with a depolarizing reversal potential. We assume passive membrane in the spine and the dendrite. Computations were performed using a compartmental model of a long dendrite and a single spine, having parameters described by Jack et al. (1975). Voltage-divider approximations to the spine-neck were compared with direct compartmental models and with eigenfunction expansions to check the validity of the numerical integrations. In the spine-head, a pronounced transient depolarization is produced, more than twice that predicted by Jack et al. (1975) for steady-state current injection. The EPSP amplitude at the base of the spine was much smaller, and was slightly reduced by placing the synapse on the head of the spine rather than on the dendritic shaft. (ABSTRACT TRUNCATED AT 250 WORDS)
EFFECTS OF MICROWAVE RADIATION ON ENZYMES *

The increasing use of microwave power during the last two decades in a variety of applications has spawned much research and discussion about the safety of microwave power as an energy source, especially with respect to damage to living organisms, notably humans. Western research in the 1950s had apparently defined safe threshold levels based on the human body's ability to dissipate the additional thermal input due to absorption of microwave power. However, Soviet bloc work reported in the last 10 years seemingly deduced statistically significant neurologic and other effects that arise from microwave exposure levels well below the thermally safe threshold. A question still remains about thermal dosimetry, which thus produces the controversy over the existence of so-called nonthermal microwave effects. At least a portion of the confusion originates from the extreme difficulty in performing reproducible experiments. The variables involved in attempting to accurately measure dosage, to provide a reproducible microwave field, to deal with biologic variables, and to deal with the many psychologic effects in laboratory animals have resulted in a wide variety of unreproducible experiments. Another approach to this same problem would be to identify some factor that significantly affects life processes and to investigate the sensitivity of this factor to microwave energy, which would thus hopefully yield some insight as to what the microwave effects on the entire organism might be. Enzymes provide a particularly convenient subject for such an investigation. They are essential for many life processes; they can be conveniently procured in easy-to-handle forms. Because they are usually present in small quantities in living organisms, damage to a particular enzyme by microwave radiation can cause large-scale perturbations in life processes. In addition, for many enzymes, the biologic assay procedures are quite straightforward, which thus facilitates the data collection process. It is for these reasons, then, that the experiment described below was performed.
Genetic Myopathies Initially Diagnosed and Treated as Inflammatory Myopathy

Abstract Objectives: Differentiating genetic myopathies from inflammatory myopathies can be challenging because of multiple overlapping clinical features. Examples are presented to highlight important clinical features that assist in the differentiation between the two. Methods: Clinical features including age at onset, history, pattern of weakness, serum creatine kinase activity, electromyography findings, and muscle biopsies are reported in six patients initially thought to have an inflammatory myopathy in whom the final diagnosis was a genetic myopathy. Results: All six patients met Bohan and Peter criteria for at least probable idiopathic polymyositis and were subsequently found to have a genetic myopathy (4 DYSF, RYR1, and GNE). The key distinguishing clinical were minimal to no response to immunosuppression and atypical involvement of distal muscles in the majority of cases. Conclusions: Patients diagnosed with inflammatory myopathies should be reevaluated for the possibility of a genetic myopathy if they fail to respond to a course of disease-modifying agents and/or there is atypical distal muscle involvement. RÉSUMÉ Cas de myopathies d’origine génétique diagnostiqués initialement et traités comme des cas de myopathies inflammatoires. Objectifs: Établir une distinction entre des cas de myopathies d’origine génétique et des cas de myopathies inflammatoires peut s’avérer difficile étant donné la multiplicité des aspects cliniques qui se chevauchent. Des exemples sont ici présentés afin de mettre en relief les aspects les plus susceptibles de permettre une distinction entre ces deux myopathies. Méthode: Les aspects cliniques incluent l’âge du patient au moment de l’apparition de la pathologie, l’histoire de cas, une tendance à la faiblesse musculaire, une activité sérique de la créatine kinase, ainsi que des résultats spécifiques à la suite d’un électromyogramme et de biopsies musculaires. Ces aspects ont été signalés chez six patients qu’on croyait au départ affectés par une myopathie inflammatoire et auxquels on a finalement transmis un diagnostic définitif de myopathie d’origine génétique. Résultats: Tous les six patients ont satisfait aux critères de Bohan et Peter, ce qui pourrait, à tout le moins, révéler la probabilité d’une polymyosite idiopathique. On a découvert par la suite qu’ils étaient atteints d’une myopathie d’origine génétique (gènes 4 DYSF, RYR1 et GNE). Dans la majorité des cas, les principaux signes cliniques se sont révélés être une faible, voire une absence, de réponse à l’immunosuppression et une atteinte atypique des muscles distaux. Conclusions: Les patients chez qui on a diagnostiqué des myopathies inflammatoires devraient être réévalués. Si ces derniers ne réagissent pas à un traitement immunomodulateur et/ou si l’on note chez eux une atteinte atypique des muscles distaux, il est en effet possible qu’ils soient atteints d’une myopathie d’origine génétique.
NFATc1 Induction in Peripheral T and B Lymphocytes

NFAT transcription factors control the proliferation and survival of peripheral lymphocytes. We have reported previously that the short isoform NFATc1/αA whose generation is induced by immune receptor stimulation supports the proliferation and inhibits the activation-induced cell death of peripheral T and B cells. We will show in this study that in novel bacterial artificial chromosome transgenic mice that express EGFP under the control of entire Nfatc1 locus the Nfatc1/Egfp transgene is expressed as early as in double-negative thymocytes and in nonstimulated peripheral T and B cells. Upon immune receptor stimulation, Nfatc1/Egfp expression is elevated in B, Th1, and Th2 cells, but only weakly in T regulatory, Th9, and Th17 cells in vitro whose generation is affected by TGFβ. In naive lymphocytes, persistent immune receptor signals led to a 3–5 increase in NFATc1/αA RNA levels during primary and secondary stimulation, but a much stronger induction was observed at the protein level. Whereas anti-CD3+CD28 stimulation of primary T cells induces both NFATc1/αA and their proliferation and survival, anti-IgM stimulation of B cells induces NFATc1/αA and proliferation, but activation-induced cell death after 3-d incubation in vitro. The anti-IgM–mediated activation-induced cell death induction of B cells in vitro is suppressed by anti-CD40–, LPS-, and CpG-mediated signals. In addition to inducing NF-κB factors, together with anti-IgM, these signals also support the generation of NFATc1/αA. According to these data and the architecture of its promoter region, the Nfatc1 gene resembles a primary response gene whose induction is affected at the posttranscriptional level.