Miracle-dz/UniFAR-FTUs huggingface dataset:
Sleep problems in children with autism

Autism is a developmental disability characterized by severe deficits in social interaction and communication, and the presence of repetitive‐ritualistic behaviors. Sleep problems are frequently reported by parents of children with autism with prevalence estimates of 44–83% for sleep disorders in this population. To better understand sleep in autism, we surveyed sleep problems in 210 children with autism using a Likert‐based questionnaire for parent report. The most frequently reported sleep problems included difficulty in falling asleep, restless sleep, not falling asleep in own bed, and frequent wakenings. Least frequently reported sleep problems were sleep walking, morning headaches, crying during sleep, apnea, and nightmares. When surveys were divided into mental retardation (MR)/not MR categories, no significant differences were identified in frequencies of reported sleep problems except for waking at night which occurred much more frequently in the MR group. There was also no difference in sleep problems related to age of the child other than nocturnal enuresis. An association was noted between certain medical problems and sleep problems. Vision problems, upper respiratory problems, and runny nose were associated with decreased nighttime sleep. Vision problems, poor appetite, and poor growth were associated with increased nighttime waking. Poor appetite and poor growth were associated with decreased willingness to fall asleep. This study confirms a high prevalence of sleep problems reported by parents of children with autism and points to the need for more systematic research as an initial step in developing treatment strategies.
Influence of nearest neighbor sequence on the stability of base pair mismatches in long DNA; determination by temperature-gradient gel electrophoresis.

Temperature-gradient gel electrophoresis (TGGE) was employed to determine the thermal stabilities of 48 DNA fragments that differ by single base pair mismatches. The approach provides a rapid way for studying how specific base mismatches effect the stability of a long DNA fragment. Homologous 373 bp DNA fragments differing by single base pair substitutions in their first melting domain were employed. Heteroduplexes were formed by melting and reannealing pairs of DNAs, one of which was 32P-labeled on its 5'-end. Product DNAs were separated based on their thermal stability by parallel and perpendicular temperature-gradient gel electrophoresis. The order of stability was determined for all common base pairs and mismatched bases in four different nearest neighbor environments; d(GXT). d(AYC), d(GXG). d(CYC), d(CXA). d(TYG), and d(TXT). d(AYA) with X,Y = A, T, C, or G. DNA fragments containing a single mismatch were destabilized by 1 to 5 degrees C with respect to homologous DNAs with complete Watson-Crick base pairing. Both the bases at the mismatch site and neighboring stacking interactions influence the destabilization caused by a mismatch. G.T, G.G and G.A mismatches were always among the most stable mismatches for all nearest neighbor environments examined. Purine.purine mismatches were generally more stable than pyrimidine.pyrimidine mispairs. Our results are in very good agreement with data where available from solution studies of short DNA oligomers.
Neurotoxicity of manganese chloride in neonatal and adult CD rats following subchronic (21‐day) high‐dose oral exposure

The purpose of this study was to evaluate the relative sensitivity of neonatal and adult CD rats to manganese‐induced neurotoxicity. Identical oral manganese chloride (MnCl2) doses (0, 25, or 50 mg kg−1 body wt. day−1) were given to neonatal rats throughout lactation (i.e. from postnatal day (PND) 1 through 21) and to adult male rats for 21 consecutive days. The MnCl2 doses administered to neonates were ca. 100‐fold higher than those resulting from the consumption of an equivalent volume of rat's milk. Rats were assessed using similar behavioral and neurochemical evaluations. Several statistically significant changes occurred in Mn‐exposed rats relative to control animals. Neonates given the high dose of MnCl2 had reduced body weight gain. An increased pulse‐elicited acoustic startle response amplitude was observed in neonates from both MnCl2 treatment groups on PND 21. Increased striatal, hippocampal, hindbrain and cortical Mn concentrations were observed in all Mn‐exposed neonates on PND 21. Increased hypothalamic and cerebellar Mn concentrations were also observed on PND 21 in neonates from the high‐dose group only. Increased striatal, cerebellar and brain residue Mn concentrations were observed in adult rats from the high‐dose group. Increased striatal dopamine and 3,4‐dihydroxyphenylacetic acid levels were observed only in PND 21 neonates from the high‐dose group. No treatment‐related changes were observed in clinical signs, motor activity (assessed in neonates on PND 13, 17, 21 ± 1 and in adults), passive avoidance (assessed in neonates on PND 20 ± 1 and in adults) or neuropathology (assessed in PND 21 neonates only). The results of our experiment suggest that neonates may be at greater risk for Mn‐induced neurotoxicity when compared to adults receiving similar high oral levels of Mn. Copyright © 2000 John Wiley & Sons, Ltd.
Adaptive nonlinear compensation for asymmetrical half bridge DC-DC converters

Asymmetrical half-bridge dc-dc converter has favorable features, which allow the converter to operate at higher frequencies with higher power density. However, asymmetrical half bridge dc-dc converter displays nonlinear dc gain variation with input voltage and duty cycle. The conventional compensator design is based on a small-signal transfer function of power stage and worst case has to be considered in the closed-loop design. With the variation of input line, the system loop gain deviates from the nominal designed trajectory, and correspondingly, the system bandwidth, phase margin and gain margin are going to vary with input voltage line. As a result, the system steady-state and dynamic performance are affected as well. This paper proposes an adaptive nonlinear compensation approach to adjust the system loop gain dynamically and thus achieve unified system loop gain, bandwidth and performance. The adaptive digital compensation algorithm is simulated and verified based on PSIM simulation software
Partial validation of a design specification with respect to requirements

The paper presents a method for partial validation of system design specifications. In the method presented, the requirements are given as a set of views described with MSC and referred to as a set of MSC/sub R/. The design specification can be given in any formal language. Our method allows for the verification, against each MSC/sub R/, of each simulation of the design specification collected into a MSC and referred to as MSC/sub T/ in the paper. For the verification of MSC/sub T/ against MSCR, we introduce a conformance relation and an algorithm to verify this relation. Our method is illustrated with an example, the INRES protocol.
Evaluating sport club board performance: a customer perspective.

When assessing board performance, customers are often overlooked as a stakeholder group. Yet, dissatisfied customers have successfully acted to have boards removed, and we have seen this scenario occur repeatedly among professional sport organizations governed by boards. The purpose of this research was to identify the factors affecting customer perceptions of sport club board performance, and guide organizations in the management of those perceptions. After extensive qualitative research, over 20,000 season ticket holders (STHs) from 14 different professional sport clubs were surveyed. The results suggest that a combination of overt performance measures (e.g., profits) and subjective, nonfinancial measures (e.g., feelings of inclusion) are used by customers to assess sport boards. Overall perceptions of the board directly influence customer satisfaction, and are strongly correlated with on-field performance and customer inclusion, suggesting boards are perceived to have a role to play in both areas. Perc.
Mycobacterial recA is cotranscribed with a potential regulatory gene called recX

The recA gene of Mycobacterium smegmatis has been cloned and sequenced. The amino acid sequence of the RecA protein is highly homologous to other RecA proteins. Three other potential open reading frames were identified. One of these showed extensive homology to a protein, HypB, involved in the incorporation of nickel into hydrogenases. Another, found downstream of and overlapping recA, was similar to a gene, recX, which has been proposed to play a regulatory role related to recA function. The homology between the M. smegmatis sequence and that of Mycobacterium tuberculosis extended upstream of the recA coding region for 140 bp including a motif identical to the Cheo‐box consensus sequence which has been shown to bind LexA. In addition, the transcriptional start sites were found to be identical to those identified previously for M. tuberculosis. Transcriptional fusions to the reporter gene chloramphenicol acetyltransferase (CAT) revealed that recA was DNA‐damage inducible and that expression required sequences at some distance from the mapped transcriptional start sites. Although a motif with only one mismatch to the Cheo box was found in the intergenic region between orf1 and orf2 these open reading frames were not DNA‐damage inducible, nor was this motif required for regulation of recA expression. Gel retardation assays revealed that the reason for this was that LexA did not bind to this sequence containing a mismatch. Reverse transcription/polymerase chain reaction analysis of M. smegmatis RNA demonstrated that recA and orf3 (recX ) are within the same trancriptional unit.
Boswellic acids reduce Th17 differentiation via blockade of IL‐1β‐mediated IRAK1 signaling

Interferon‐gamma producing CD4+ T (Th1) cells and IL‐17‐producing CD4+ T (Th17) cells are involved in the pathogenesis of several autoimmune diseases including multiple sclerosis. Therefore, the development of treatment strategies controlling the generation and expansion of these effector cells is of high interest. Frankincense, the resin from trees of the genus Boswellia, and particularly its prominent bioactive compound acetyl‐11‐keto‐β‐boswellic acid (AKBA), have potent anti‐inflammatory properties. Here, we demonstrate that AKBA is able to reduce the differentiation of human CD4+ T cells to Th17 cells, while slightly increasing Th2‐ and Treg‐cell differentiation. Furthermore, AKBA reduces the IL‐1β‐triggered IL‐17A release of memory Th17 cells. AKBA may affect IL‐1β signaling by preventing IL‐1 receptor‐associated kinase 1 phosphorylation and subsequently decreasing STAT3 phosphorylation at Ser727, which is required for Th17‐cell differentiation. The effects of AKBA on Th17 differentiation and IL‐17A release make the compound a good candidate for potential treatment of Th17‐driven diseases.
Project Joy: Faith Based Cardiovascular Health Promotion for African American Women

Objective. The authors tested the impact on cardiovascular risk profiles of African American women ages 40 years and older after one year of participation in one of three church-based nutrition and physical activity strategies: a standard behavioral group intervention, the standard intervention supplemented with spiritual strategies, or self-help strategies. Methods. Women were screened at baseline and after one year of participation. The authors analyzed intention-to-treat within group and between groups using a generalized estimating equations adjustment for intra-church clustering. Because spiritual strategies were added to the standard intervention by participants themselves, the results from both active groups were similar and, thus, combined for comparisons with the self-help group. Results. A total of 529 women from 16 churches enrolled. Intervention participants exhibited significant improvements in body weight (−1.1 lbs), waist circumference (−0.66 inches), systolic blood pressure (−1.6 mmHg), dietary energy (−117 kcal), dietary total fat (−8 g), and sodium intake (−145 mg). The self-help group did not. In the active intervention group, women in the top decile for weight loss at one year had even larger, clinically meaningful changes in risk outcomes (−19.8 lbs). Conclusions. Intervention participants achieved clinically important improvements in cardiovascular disease risk profiles one year after program initiation, which did not occur in the self-help group. Church-based interventions can significantly benefit the cardiovascular health of African American women.
Modulation of White Adipose Tissue Lipolysis by Nitric Oxide*

In isolated adipocytes, the nitrosothiolsS-nitroso-N-acetyl-penicillamine (SNAP) andS-nitrosoglutathione stimulate basal lipolysis, whereas the nitric oxide (NO ⋅ ) donor 1-propamine, 3-(2-hydroxy-2-nitroso-1-propylhydrazine) (PAPA-NONOate) or NO gas have no effect. The increase in basal lipolysis due to nitrosothiols was prevented by dithiothreitol but not by a guanylate cyclase inhibitor. In addition the cyclic GMP-inhibited low K m , cyclic AMP phosphodiesterase activity was inhibited by SNAP suggesting that SNAP acting as NO+ donor increases basal lipolysis through a S-nitrosylation mediated inhibition of phosphodiesterase. Contrasting with these findings, SNAP reduced both isoproterenol-stimulated lipolysis and cyclic AMP production, whereas it failed to modify forskolin-, dibutyryl cyclic AMP-, or isobutylmethylxanthine-stimulated lipolysis, suggesting that SNAP interferes with the β-adrenergic signal transduction pathway upstream the adenylate cyclase. In contrast with SNAP, PAPA-NONOate or NO gas inhibited stimulated lipolysis whatever the stimulating agents used without altering cyclic AMP production. Moreover PAPA-NONOate slightly reduces (30%) the hormone-sensitive lipase (HSL) activity indicating that stimulated lipolysis inhibition by NO ⋅ is linked to both inhibition of the HSL activity and the cyclic AMP-dependent activation of HSL. These data suggest that NO ⋅ or related redox species like NO+/NO− are potential regulators of lipolysis through distinct mechanisms.
An ultra low-power front-end IC for wearable health monitoring system

This paper presents a low-power front-end IC for wearable health monitoring systems. The IC, designed in a standard 0. 13μm CMOS technology, fully integrates a low-noise analog front-end (AFE) to process the weak bio-signals, followed by an analog-to-digital converter (ADC) to digitize the extracted signals. An AC-coupled driving buffer, that interfaces between the AFE and the ADC is introduced to scale down the power supply of the ADC. The power consumption decreases by 50% compared to the case without power supply scaling. The AFE passes signals from 0.5Hz to 280Hz and from 0.7Hz to 160Hz with a simulated input referred noise of 1. 6μVrms and achieves a maximum gain of 35dB/41dB respectively, with a noise-efficiency factor (NEF) of the AFE is 1. The 8-bit ADC achieves a simulated 7.96-bit resolution at 10KS/s sampling rate under 0.5V supply voltage. The overall system consumes only 0. 86μW at dual supply voltages of 1V (AFE) and 0.5 V (ADC).
Generation of MHC class I diversity in primary tumors and selection of the malignant phenotype

Intratumor heterogeneity among cancer cells is promoted by reversible or irreversible genetic alterations and by different microenvironmental factors. There is considerable experimental evidence of the presence of a variety of malignant cell clones with a wide diversity of major histocompatibility class I (MHC‐I) expression during early stages of tumor development. This variety of MHC‐I phenotypes may define the evolution of a particular tumor. Loss of MHC‐I molecules frequently results in immune escape of MHC‐negative or ‐deficient tumor cells from the host T cell‐mediated immune response. We review here the results obtained by our group and other researchers in animal models and humans, showing how MHC‐I intratumor heterogeneity may affect local oncogenicity and metastatic progression. In particular, we summarize the data obtained in an experimental mouse cancer model of a methylcholanthrene‐induced fibrosarcoma (GR9), in which isolated clones with different MHC‐I expression patterns demonstrated distinct local tumor growth rates and metastatic capacities. The observed “explosion of diversity” of MHC‐I phenotypes in primary tumor clones and the molecular mechanism (“hard”/irreversible or “soft”/reversible) responsible for a given MHC‐I alteration might determine not only the metastatic capacity of the cells but also their response to immunotherapy. We also illustrate the generation of further MHC heterogeneity during metastatic colonization and discuss different strategies to favor tumor rejection by counteracting MHC‐I loss. Finally, we highlight the role of MHC‐I genes in tumor dormancy and cell cycle control.
Melanocortin receptor agonists in the treatment of male and female sexual dysfunctions: results from basic research and clinical studies

Introduction: Over the last 20 years, basic and clinical research activities studying the male and female sexual responses have led to several pharmacological options to treat male erectile dysfunction (ED) and female arousal and orgasmic disorders. While some strategies exclusively focus on peripheral mechanisms – such as nitric oxide/cyclic GMP signaling, which is known to play a role in the control of genital vascular and nonvascular smooth muscle – others have considered the central pathways involved in mediating arousal and orgasmic functions in females as well as the induction of penile erection in males. Aside from dopaminergic agonists, drugs known to target the central melanocortin system have also been assumed to have a promising potential in the treatment of female and male sexual dysfunctions. Areas covered: The present review summarizes the achievements that have been made in the clinical development of melanocortin receptor (MCR) agonists (melanotan I, melanotan II, bremelanotide) for the treatment of symptoms of sexual arousal and orgasmic disorders in adult females and ED in males. Expert opinion: The data available at present have facilitated our understanding of how the melanocortin pathway regulates both the male and female sexual functions. Indeed the data warrant further investigation to demonstrate the impact of the activation of MCRs by specific agonists on penile erection and female arousal and orgasm function.
Histomorphometry of the porcine scleral lamina cribrosa surface.

The lamina cribrosa surface of the pig was examined using trypsin digestion, scanning electron microscopy, and computerized image analysis. Six normal eyes from healthy pigs were studied. The total intralaminar scan area, total number of laminar pores, median individual laminar pore areas, median individual pore form factors, and mean pore density were determined for the dorsal, ventral, nasal and temporal hemicircles, the dorsal-nasal, dorsal-temporal, ventral-nasal, and ventral-temporal quadrants, and their central and peripheral subdivisions. The mean (+/- SD) total intralaminar scan area was 8.29 +/- 1.54 mm2. The mean (+/- SD) total laminar pore count was 517 +/- 73 pores. The mean pore count was significantly larger in the ventral than the dorsal hemicircle (292 +/- 39 vs. 225 +/- 38 pores, respectively; P = 0.001), and significantly greater in the periphery compared to the center (388 +/- 58 vs. 129 +/- 27 pores, respectively; P = 0.0001). The overall mean (+/- SD) pore density was 67 +/- 7 pores mm-2. Mean pore density was significantly greater in the ventral than the dorsal hemicircle (70 +/- 8 vs. 64 +/- 6 pores mm-2, respectively; P = 0.019), and significantly greater in the center compared to the periphery (75 +/- 9 vs. 60 +/- 8 pores mm-2, respectively; P = 0.020). The mean (+/- SD) median individual pore area was 3752 +/- 572 &mgr;m2. The mean (+/- SD) median pore form factor was 0.680 +/- 0.035. No significant regional differences were found in mean median pore form factor or mean median individual pore areas. The intralaminar optic nerve of pigs is 55.1% non-neural connective and vascular tissue. A pigmented ventral fascial groove in the scleral lamina cribrosa appears unique to the porcine lamina cribrosa, and may be a vestige of the embryonic optic fissure.
Genetic Variation in C-Reactive Protein (CRP) Gene May Be Associated with Risk of Systemic Lupus Erythematosus and CRP Concentrations

Objective The gene coding for C-reactive protein (CRP) is located on chromosome 1q23.2, which falls within a linkage region thought to harbor a systemic lupus erythematosus (SLE) susceptibility gene. Recently, 2 single-nucleotide polymorphisms (SNP) in the CRP gene (+838, +2043) have been shown to be associated with CRP concentrations and/or SLE risk in a British family-based cohort. Our study was done to confirm the reported association in an independent population-based case-control cohort, and also to investigate the influence of 3 additional CRP tagSNP (−861, −390, +90) on SLE risk and serum CRP concentrations. Methods DNA from 337 Caucasian women who met the American College of Rheumatology criteria for definite (n = 324) or probable (n = 13) SLE and 448 Caucasian healthy female controls was genotyped for 5 CRP tagSNP (−861, −390, +90, +838, +2043). Genotyping was performed using restriction fragment length polymorphism-polymerase chain reaction, pyrosequencing, or TaqMan assays. Serum CRP levels were measured using ELISA. Association studies were performed using the chi-squared distribution, Z-test, Fisher’s exact test, and analysis of variance. Haplotype analysis was performed using EH software and the haplo.stats package in R 2.1. 2. Results While none of the SNP were found to be associated with SLE risk individually, there was an association with the 5 SNP haplotypes (p < 0.001). Three SNP (−861, −390, +90) were found to significantly influence serum CRP level in SLE cases, both independently and as haplotypes. Conclusion Our data suggest that unique haplotype combinations in the CRP gene may modify the risk of developing SLE and influence circulating CRP levels.
Multi-objective V2G energy storage system for grid support with cost and emission reduction

Power grid operates in real time without any significant storage system. Due to this, all decisions must be made with accuracy of seconds. The present operating condition needs to get some reformation with minimum cost and least affect on environment. The energy storage system(ESS) provides a solution with capability to solve the problem. One form of ESS is V2G concept which utilizes electric vehicles(EVs) storage for grid support. In developing countries emergency storage backups(IBKs) are used to supply in power failure situations. In this paper authors analysed the effect of operating IBKs on principle of V2G for grid support. Further more the EVs capability of reducing end users operating cost and emission reduction was demonstrated. Authors formulated this problem as a multi-objective optimization problem and solved it using non dominated sorting genetic algorithm (NSGA-II). The results were also compared with other multi-objective optimization techniques such as multi objective particle swarm optimization(MOPSO), strength pareto evolutionary algorithm(SPEA).