Miracle-dz/UniFAR-FTUs huggingface dataset:
A Multilevel Analysis of U.S. Hospital Patient Safety Culture Relationships With Perceptions of Voluntary Event Reporting

Objectives Patient safety events offer opportunities to improve patient care, but, unfortunately, events often go unreported. Although some barriers to event reporting can be reduced with electronic reporting systems, insight on organizational and cultural factors that influence reporting frequency may help hospitals increase reporting rates and improve patient safety. The purpose of this study was to evaluate the associations between dimensions of patient safety culture and perceived reporting practices of safety events of varying severity. Methods We conducted a cross-sectional survey study using previously collected data from The Agency for Healthcare Research and Quality Hospital Survey of Patient Safety Culture as predictors and outcome variables. The dataset included health-care professionals in U.S. hospitals, and data were analyzed using multilevel modeling techniques. Results Data from 223,412 individuals, 7816 work areas/units, and 967 hospitals were analyzed. Whether examining near miss, no harm, or potential for harm safety events, the dimension feedback about error accounted for the most unique predictive variance in the outcome frequency of events reported. Other significantly associated variables included organizational learning, nonpunitive response to error, and teamwork within units (all P < 0.001). As the perceived severity of the safety event increased, more culture dimensions became significantly associated with voluntary reporting. Conclusions To increase the likelihood that a patient safety event will be voluntarily reported, our study suggests placing priority on improving event feedback mechanisms and communication of event-related improvements. Focusing efforts on these aspects may be more efficient than other forms of culture change.
Delta-Sigma based bit-stream controller for a D.C. motor

The present paper proposes a Delta Sigma (ΔΣ) modulator based control to control linear systems. This control method processes bit stream signals to control physical systems and offers various advantages compared to traditional methods of controller implementation, which uses multi-bit processing. To evaluate the performance of the bit-stream controller in real-life control applications, a digital controller based on a delta operator is used as a benchmark to which the controller utilizing bit-stream technique is compared. The effectiveness of the proposed bit-stream controller is experimentally validated considering an example of a DC motor. The results of the experiment show that the technique utilizing bit-stream signals are more attractive as an alternative to processing of multi-bit digital signal. Although both controllers display a comparable performance in simulation and experiment, the controller utilizing bit-stream uses approximately 400 logic elements (LE) on an Altera Cyclone FPGA comparing to the conventional controller which costs 600 (LE) and 17 9-bit multipliers.
Induction of the Escherichia coli aidB gene under oxygen-limiting conditions requires a functional rpoS (katF) gene

The Escherichia coli aidB gene is regulated by two different mechanisms, an ada-dependent pathway triggered by methyl damage to DNA and an ada-independent pathway triggered when cells are grown without aeration. In this report we describe our search for mutations affecting the ada-independent aidB induction pathway. The mutant strain identified carries two mutations affecting aidB expression. These mutations are named abrB (aidB regulator) and abrD. The abrB mutation is presently poorly characterized because of instability of the phenotype it imparts. The second mutation, abrD1, reduces the expression of aidB observed when aeration is ceased and oxygen becomes limiting. Genetic and phenotypic analysis of the abrD1 mutation demonstrates that it is an allele of rpoS. Thus, aidB is a member of the family of genes that are transcribed by a sigma S-directed RNA polymerase holoenzyme. Examination of aidB expression in an rpoS insertion mutant strain indicates that both rpoS13::Tn10 and abrD1 mutations reduce aidB expression under oxygen-limiting conditions that prevail in unaerated cultures, reduce aidB induction by acetate at a low pH, but have little or no effect on the ada-dependent alkylation induction of aidB.
Efficacy and safety of adalimumab in Canadian patients with moderate to severe Crohn's disease: results of the Adalimumab in Canadian SubjeCts with ModErate to Severe Crohn's DiseaSe (ACCESS) trial.

OBJECTIVE To evaluate open-label adalimumab therapy for clinical effectiveness, fistula healing, patient-reported outcomes and safety in Canadian patients with moderate to severe Crohn's disease (CD) who were either naive to or previously exposed to antitumour necrosis factor (anti-TNF) therapy. METHODS Patients with moderate to severe CD (CD activity index [CDAI] score of greater than 220, or Harvey-Bradshaw index [HBI] of 7 or greater) were eligible. Patients received open-label adalimumab as induction (160 mg and 80 mg subcutaneously [sc]) at weeks 0 and 2, respectively and maintenance (40 mg sc every other week) therapy. At or after eight weeks, patients with flare or nonresponse could have their dosage increased to 40 mg sc weekly. Patients were followed for a minimum of six months or until adalimumab was commercially available in Canada. RESULTS Of the 304 patients enrolled, 160 were infliximab experienced, while 144 were anti-TNF naive. HBI remission (HBI score of 4 or lower) at week 24 was achieved by 53% of anti-TNF-naive and 36% of infliximab-experienced patients (P<0.01; P<0.001 for both groups for all visits versus baseline). Fistula healing rates at week 12 were 48% for anti-TNF-naive patients, and 26% for infliximab-experienced patients. At week 24, fistula healing rates were significantly greater for the anti-TNF-naive group (60% versus 28%; P<0.01). Improvements in quality of life and work productivity were sustained from week 4 to week 24 for all patients. Serious infections occurred in 2% of patients. CONCLUSIONS Adalimumab therapy induced and sustained steroidfree remission in both infliximab-experienced and anti-TNF-naive patients with moderate to severe CD. Clinically meaningful rates of fistula healing were also observed. Improvements in patient-reported outcomes were sustained throughout the 24-week study period.
Percutaneous Endoscopic Debridement and Drainage with Four Different Approach Methods for the Treatment of Spinal Infection.

BACKGROUND The incidence of spinal infection seems to be increasing in recent years. Percutaneous endoscopic debridement and drainage (PEDD) has become an effective alternative to extensive open surgery. OBJECTIVE This study reviewed the charter of patients who received PEDD using 4 different approach methods to evaluate the clinical results. STUDY DESIGN An Institutional Review Board (IRB)-approved retrospective chart review. SETTING University hospital inpatient referred to our pain clinic. METHODS A retrospective patient chart analysis of PEDD procedures in spinal infections over a 7-year period was done for the evaluation of structural location, symptoms and signs, etiologic agents, and outcomes. RESULTS Seventeen patients (11 men and 6 women, mean age 70.4 ± 11.1 years) with spinal infections received PEDD. According to the structural localization of the spinal infections, 6 cases of spondylodiscitis alone, 5 cases of spondylodiscitis with a psoas abscess, one case of spondylodiscitis with an epidural abscess, 4 cases of spondylodiscitis with epidural and psoas abscesses, and one case of spondylodiscitis with a facet joint abscess were found. All patients had preoperative symptoms of unremitting backache and febrile sensation, and signs of paravertebral muscle tenderness and limitation of spine motion. The most common etiologic bacteria were Staphylococcus aureus. Most patients (14/17) improved; the 2 failed patients received a second PEDD after recurrence, and the other received open surgery without re-PEDD. Both the numeric rating scale and Oswestry disability index scores were significantly reduced after PEDD. No complications related to PEDD were found. LIMITATION This study is limited by its retrospective design. CONCLUSIONS PEDD using 4 different routes brought immediate pain relief and reduced disability in treating spinal infections, especially in elderly patients with comorbid underlying disorders.Key words: Percutaneous discectomy, psoas abscess, spinal epidural abscess, spondylodiscitis, surgical endoscopy.
Concordance of coronary artery calcium estimates between MDCT and electron beam tomography.

OBJECTIVE The objective of our study was to compare MDCT with electron beam tomography (EBT) for the quantification of coronary artery calcification (CAC). MATERIALS AND METHODS Sixty-eight patients underwent both MDCT and EBT within 2 months for the quantification of CAC. The images were scored in a blinded fashion and independently by two observers with a minimum of 7 days between the interpretations of images obtained from one scanner type to the other. RESULTS Presence versus absence of CAC was discordant by EBT versus MDCT in 6% (n = 4) of the cases by observer 1, with one of these cases also discordant by observer 2. All cases except one (aortic calcium misidentified as CAC) were among those with a mean Agatston score of less than 5 present on EBT but absent on MDCT. EBT and MDCT scores correlated well (r = 0.98-0.99). The relative median variability between EBT and MDCT for the Agatston score was 24% for observer 1 and 27% for observer 2 and was 18% and 14%, respectively, for volume score (average for both observers: 27% for Agatston score and 16% for volume score). Scores were higher for EBT than MDCT in approximately half of the cases, with little systematic difference between the two (median EBT-MDCT difference: Agatston score, -0.55; volume score, 3.4 mm3). The absolute median difference averaged for the two observers was 28.75 for the Agatston score and 15.4 mm3 for the volume score. CONCLUSION Differences in CAC measurements using EBT and MDCT are similar to interscan differences in CAC measurements previously reported for EBT or for other MDCT scanners individually.
Experimentally induced ischaemic pain in healthy humans is attenuated by the adenosine receptor antagonist theophylline.

AIMS Endogenous adenosine is considered a prominent pain mediator in ischaemia. In contrast, it has been shown that exogenous adenosine can reduce tourniquet induced ischaemic pain in healthy volunteers. The aim of this study was to investigate if pharmacological antagonism of endogenous adenosine actions with an intravenous infusion of theophylline could attenuate experimentally induced ischaemic pain. METHODS Nineteen healthy volunteers, 11 males, eight female, received theophylline 7 mg kg-1 or placebo intravenously, in a randomized, double blind and crossover fashion, prior to a sub-maximum effort forearm tourniquet test. Experiments were carried out with 1-week intervals to avoid pre-conditioning. Pain scores [visual analogue scale (VAS), 0-100] were assessed every minute up to a maximum of 30 min. RESULTS The sum of pain scores (accumulation of VAS scores) was attenuated by theophylline, 691 [200-1550 (median and 25-75% percentiles)], compared with placebo, 1231 (545-1675), P < 0.001. Also, peak VAS pain was lower during theophylline treatment, 48 +/- 38 (mean +/- SD), compared with placebo, 74 +/- 27, P < 0.001. Blood pressure increased during the experiment with no difference between treatments. Heart rate was not affected by tourniquet or drug treatment. CONCLUSIONS It is concluded that the adenosine receptor antagonist theophylline is able to attenuate the development of ischaemia pain during experimental ischaemia in humans. This implies a role for adenosine as both facilitatory mediator and a modulator of ischaemia skeletal muscle pain.
Efficient de novo assembly of highly heterozygous genomes from whole-genome shotgun short reads

Although many de novo genome assembly projects have recently been conducted using high-throughput sequencers, assembling highly heterozygous diploid genomes is a substantial challenge due to the increased complexity of the de Bruijn graph structure predominantly used. To address the increasing demand for sequencing of nonmodel and/or wild-type samples, in most cases inbred lines or fosmid-based hierarchical sequencing methods are used to overcome such problems. However, these methods are costly and time consuming, forfeiting the advantages of massive parallel sequencing. Here, we describe a novel de novo assembler, Platanus, that can effectively manage high-throughput data from heterozygous samples. Platanus assembles DNA fragments (reads) into contigs by constructing de Bruijn graphs with automatically optimized k-mer sizes followed by the scaffolding of contigs based on paired-end information. The complicated graph structures that result from the heterozygosity are simplified during not only the contig assembly step but also the scaffolding step. We evaluated the assembly results on eukaryotic samples with various levels of heterozygosity. Compared with other assemblers, Platanus yields assembly results that have a larger scaffold NG50 length without any accompanying loss of accuracy in both simulated and real data. In addition, Platanus recorded the largest scaffold NG50 values for two of the three low-heterozygosity species used in the de novo assembly contest, Assemblathon 2. Platanus therefore provides a novel and efficient approach for the assembly of gigabase-sized highly heterozygous genomes and is an attractive alternative to the existing assemblers designed for genomes of lower heterozygosity.
Fate of grafted embryonic purkinje cells in the cerebellum of the adult “purkinje cell degeneration” mutant mouse. I. Development of reciprocal graft‐host interactions

Purkinje cell replacement, with subsequent synaptic integration into the cortex of host deficient “Purkinje cell degeneration” mutant cerebella, can be obtained by cerebellar grafting (Sotelo and Alvarado‐Mallart: Proc. Natl. Acad. Sci. USA 83:1135–1139, 1986; Neuroscience 20:1–22, 1987). In this paper, we have morphologically studied the developmental events underlying the neuronal replacement, 3–21 days after grafting. Despite their abnormal environment, Purkinje cell progenitors proceed with their proliferation in the grafted neuroepithelium, with a time window similar to that characterizing proliferation of this neuronal class in control mouse embryos. Only postmitotic Purkinje cells leave the grafts and migrate to the host molecular layer following stereotyped pathways. These neurons invade the host molecular layer, either through a tangential migration under the pial basal lamina from the graft/host interface or breaking locally the latter, and passing directly from the lateral swellings of the graft lying on the surface of the host folia. Whatever the pathway for host invasion, the migrating Purkinje cells penetrate radially and/or obliquely into the host molecular layer until their inward‐oriented processes attain the molecular/granular layer interface, which occurs about 7 days after grafting. At the end of their migration, the grafted Purkinje cells with bipolar shapes and long and smooth processes begin to build up their ultimate dendritic trees. This dendritogenesis proceeds with constructive and regressive processes, passing through the same three developmental phases described by Ramón y Cajal (Trab. Lab. Invest. Biol. Univ. Madrid 24:215–251, 1926) for control Purkinje cells (phase of the fusiform cell, phase of the stellate cell with disoriented dendrons, and phase of orientation and flattening of the dendrites). In the grafted cerebella, the duration of the second and third phases is somewhat shorter than during normal cerebellar ontogenesis. Synaptogenesis between adult host axons and grafted Purkinje cells starts when the latter attain their second phase of dendritic development. Somatic filopodia emerging from grafted Purkinje cells begin, 10–11 days after grafting, to be synaptically contacted by axonal sprouts of the host climbing fibers resulting, 2 days later, in the formation of pericellular nests. Synaptogenesis between slender dendritic spines and host parallel fibers, together with that of axon terminals from host molecular layer interneurons and the smooth surface of the grafted Purkinje cells somata, begin earlier than in control mouse development, being almost simultaneous with climbing fiber/Purkinje cell synaptogenesis. Fourteen days after grafting, the climbing fibers have begun the translocation from their somatic to their dendritic location. By 21 days after grafting, the synaptic investment of the grafted Purkinje cells is qualitatively similar to that observed after long‐term survivals.
Shank–cortactin interactions control actin dynamics to maintain flexibility of neuronal spines and synapses

The family of Shank scaffolding molecules (comprising Shank1, 2 and 3) are core components of the postsynaptic density (PSD) in neuronal synapses. Shanks link surface receptors to other scaffolding molecules within the PSD, as well as to the actin cytoskeleton. However, determining the function of Shank proteins in neurons has been complicated because the different Shank isoforms share a very high degree of sequence and domain homology. Therefore, to control Shank content while minimizing potential compensatory effects, a miRNA‐based knockdown strategy was developed to reduce the expression of all synaptically targeted Shank isoforms simultaneously in rat hippocampal neurons. Using this approach, a strong (>75%) reduction in total Shank protein levels was achieved at individual dendritic spines, prompting an approximately 40% decrease in mushroom spine density. Furthermore, Shank knockdown reduced spine actin levels and increased sensitivity to the actin depolymerizing agent Latrunculin A. A SHANK2 mutant lacking the proline‐rich cortactin‐binding motif (SHANK2‐ΔPRO) was unable to rescue these defects. Furthermore, Shank knockdown reduced cortactin levels in spines and increased the mobility of spine cortactin as measured by single‐molecule tracking photoactivated localization microscopy, suggesting that Shank proteins recruit and stabilize cortactin at the synapse. Furthermore, it was found that Shank knockdown significantly reduced spontaneous remodelling of synapse morphology that could not be rescued by the SHANK2‐ΔPRO mutant. It was concluded that Shank proteins are key intermediates between the synapse and the spine interior that, via cortactin, permit the actin cytoskeleton to dynamically regulate synapse morphology and function.
Step length and width variability while walking on a motion simulator mounted treadmill

While devices which allow scientists to perturb normal walking are becoming increasingly common, postural adaptations to these perturbations have not been fully quantified. One way to quantify postural responses to perturbations are through the assessment of variability of step length and width. In the present study we determined variability of both step length and width while subjects walked under perturbations of varying amplitude in roll, pitch, yaw, anteroposterior, lateral, and combined roll, pitch, yaw directions. Step kinematics were quantified using motion analysis. The majority of changes in step length variability occurred in Pitch (p<;0.01), mediolateral (p<;0.05) and anteroposterior (p<;0.01) directions. Changes in step width variability were most apparent in combined Roll-Pitch-Yaw (p<;0.01) as well as Roll (p<;0.05), and Yaw (p<;0.05) directions. These data demonstrate that sinusoidal perturbations while walking on a treadmill are sufficient to disrupt normal postural control. These conditions therefore may be useful in constructing rehabilitation programs to improve dynamic balance.
Cardiac Microstructure: Implications for Electrical Propagation and Defibrillation in the Heart

Abstract— Our understanding of the electrophysiological properties of the heart is incomplete. We have investigated two issues that are fundamental to advancing that understanding. First, there has been widespread debate over the mechanisms by which an externally applied shock can influence a sufficient volume of heart tissue to terminate cardiac fibrillation. Second, it has been uncertain whether cardiac tissue should be viewed as an electrically orthotropic structure, or whether its electrical properties are, in fact, isotropic in the plane orthogonal to myofiber direction. In the present study, a computer model that incorporates a detailed three-dimensional representation of cardiac muscular architecture is used to investigate these issues. We describe a bidomain model of electrical propagation solved in a discontinuous domain that accurately represents the microstructure of a transmural block of rat left ventricle. From analysis of the model results, we conclude that (1) the laminar organization of myocytes determines unique electrical properties in three microstructurally defined directions at any point in the ventricular wall of the heart, and (2) interlaminar clefts between layers of cardiomyocytes provide a substrate for bulk activation of the ventricles during defibrillation.
Evidence for phosphatidylinositol hydrolysis in pancreatic islets stimulated with carbamoylcholine. Kinetic analysis of inositol polyphosphate metabolism.

Anion-exchange h.p.l.c. was used initially to analyse the products formed after addition of either [3H]Ins(1,3,4,5)P4 or [3H]Ins(1,4,5)P3 to homogenates of pancreatic islets. Metabolic routes similar to those of other tissues were established: dephosphorylation of Ins(1,4,5)P3 to Ins(1,4)P2 and then Ins4P; and sequential degradation of Ins(1,3,4,5)P4 to Ins(1,3,4)P3, Ins(3,4)P2 and Ins(3 or 1)P. In addition, there was a limited conversion of Ins(1,3,4)P3 into Ins(1,3)P2. After stimulation of [3H]inositol-prelabelled islets with the muscarinic-receptor agonist carbamoylcholine (carbachol), there was a rapid (10 s) increase in Ins(1,4,5)P3, Ins(1,3,4)P3, Ins(1,4)P2 and Ins4P. In the presence of 10 mM-LiCl, Ins1P was also significantly increased (P less than 0.05) by 5 s, before any increase in Ins4P (10 s), Ins(1,3)P2 (60 s) or Ins(3,4)P2. When carbachol was displaced with atropine, after 1 h pre-stimulation, the maximal decreases in Ins(1,4,5)P3 and Ins1P from the stimulated steady state (5 s) clearly preceded those of the other metabolites. These declines were used to calculate the turnover times and rate of metabolic flux through the various inositol phosphates. These experiments confirmed the relatively minor importance of the Ins(1,3)P2 pathway (less than 10% of the total flux) and demonstrated that Ins(1,4,5)P3 removal was evenly distributed through the Ins(1,4)P2 and Ins(1,3,4,5)P4 routes. They also established that flux through Ins1P was 8-fold greater than that through Ins(1,4,5)P3, indicating that the former could not have been derived from PtdInsP2 hydrolysis. Similarly, in islets pretreated with neomycin, which binds to PtdInsP2 with greater affinity than to PtdIns, the increase in Ins1P caused by 1 min stimulation with carbachol was not affected, despite virtual abolition of the increase in Ins4P, and an overall inhibition of PtdInsP2 hydrolysis by 67%. The results indicate that, in addition to PtdInsP2 breakdown, carbachol also promotes a rapid PtdIns hydrolysis which becomes increasingly predominant with prolonged stimulation.