Miracle-dz/UniFAR-FTUs huggingface dataset:
The Role of Driver Education in the Licensing Process in Quebec

Problem. In many jurisdictions, driver education (DE) graduates, compared to non-graduates, are granted a time-discount that allows them to drive unsupervised several months earlier, despite little evidence of a safety benefit and consistent evidence of increased crash risk. Confounding factors may be threatening the validity of DE evaluations. A theoretical framework called the “licensing process” (LP) is proposed to identify and explore potential confounding factors in DE evaluations. Method. Prospective study data on a cohort of 1804 novice drivers 16 to 19 years of age of both sexes are analyzed in relation to the LP framework. These data derive from two sources that were linked together: an extensive questionnaire on learning methods, risk-taking, and lifestyles, and government records on exam performance, violations, and crashes. Results. Violation and crash records are not associated with DE attendance. DE attendance is associated with younger ages, greater financial support from family, and fewer hours of supervised driving practice with a learner's permit. For both sexes, more hours of supervised driving practice with a learner's permit is associated with increased crash risk. Most participants, particularly males under 19 years of age, attended DE partly or entirely to save time or money; these motivations are associated with higher violation and crash rates. Discussion. DE evaluations need to identify and control for potential confounding factors. Research is needed to understand the associations between increased crash risk and potential confounding factors like motivation to attend DE and hours of supervised driving practice.
Despite Transcriptional and Functional Coordination, Cyclooxygenase-2 and Microsomal Prostaglandin E Synthase-1 Largely Reside in Distinct Lipid Microdomains in WISH Epithelial Cells

Cytokine-induced prostaglandin (PG)E2 synthesis requires increased expression of cyclooxygenase-2 (COX-2) in human WISH epithelial cells. Recently, an inducible downstream PGE synthase (microsomal PGE synthase-1, mPGES-1) has been implicated in this inflammatory pathway. We evaluated cooperation between COX-2 and mPGES-1 as a potential mechanism for induced PGE2 production in WISH cells. Cytokine stimulation led to increased expression of both enzymes. Selective pharmacological inhibition of these enzymes demonstrated that induced PGE2 release occurred through a dominant COX-2/mPGES-1 pathway. Unexpectedly, immunofluorescent microscopy revealed that the expression of these enzymes was not tightly coordinated among cells after cytokine challenge. Within cells expressing high levels of both mPGES-1 and COX-2, immunolabeling of high-resolution semithin cryosections revealed that COX-2 and mPGES-1 were largely segregated to distinct regions within continuous intracellular membranes. Using biochemical means, it was further revealed that the majority of mPGES-1 resided within detergent-insoluble membrane fractions, whereas COX-2 was found only in detergent-soluble fractions. We conclude that although mPGES-1 and COX-2 show transcriptional and functional coordination in cytokine-induced PGE2 synthesis, complementary morphological and biochemical data suggest that a majority of intracellular mPGES-1 and COX-2 are segregated to discrete lipid microdomains in WISH epithelial cells.
Coagulation Factor IXa Binding to Activated Platelets and Platelet-Derived Microparticles: A Flow Cytometric Study

Summary Factor IX plays a central role in blood coagulation, since it can be activated by either XIa (intrinsic pathway) or tissue factor-VIIa (extrinsic pathway). Activated factor IX (IXa), in a surface-bound complex with factor Villa, then activates factor X. Platelets provide the catalytic surface upon which this Xase complex is assembled in vivo. We have used flow cytometry to examine binding of factor IXa to thrombin-activated platelets in the absence of added Villa. Platelet-bound IXa and platelet protein GPIb were detected by indirect immunofluorescence staining followed by two-color flow cytometric analysis. Microparticles were identified by their light scattering characteristics. Two binding sites for factor IXa were detected. The high affinity binding site saturated at about 10 nM, with a K d of 1.6 nM. A second binding curve, with a K d of about 100 nM, was observed at higher concentrations of IXa. The high affinity factor IXa binding sites comprise about 7% of the total factor IXa binding. Binding to both sites was dependent on the presence of calcium. Thus, we conclude that factor IXa, in addition to its high affinity binding, has a calcium-dependent low affinity association with activated platelets and microparticles. Sims et al. have shown that binding sites for a different coagulation factor, factor Va, are concentrated on microparticles relative to platelet membrane proteins, such as GPIb. GPIb is distributed on platelets and microparticle in proportion to plasma membrane surface. At 100 nM factor IXa, 1–3% of the total bound factor IXa was associated with microparticles, as was a similar proportion of the total GPIb. However, at 10 nM IXa, factor IXa binding to microparticles was concentrated about 2-fold relative to GPIb staining. Thus, the high affinity factor IXa binding site is concentrated on microparticles to a small degree, while the low affinity binding site is not.
Histopathological studies on the local reactions induced by complete fReund's adjuvant (CFA), bacterial lipopolysaccharide (LPS), and synthetic lipopeptide (P3C) conjugates

The inflammatory reactions following subcutaneous application of adjuvants revealed characteristic pathological patterns. The injection of complete Freund's adjuvant (CFA) resulted in the formation of large lipid deposits encircled by an inflammatory reaction and concentrically arranged collagen bundles. Bacterial lipopolysaccharide (LPS) caused granulomatous aggregations of mononuclear cells with thrombotic vessel occlusions. Inoculation of the lipopeptide adjuvants induced accumulation of mononculear cells with only minimal fibrotic changes which were resolved after day 28. Lipopeptide conjugates based on the head group tripalmitoyl‐S‐glyceryl‐cysteinyl‐serin (P3CS) can thus be used as effective immunogens and adjuvants without long‐term tissue damage.
Toll‐like receptor 3 signaling attenuates liver regeneration

The current model for liver regeneration suggests that cell damage triggers Toll‐like receptor (TLR) signaling via MyD88, leading to the induction of nuclear factor κB (NF‐κB) and secretion of inflammatory cytokines that in turn prime liver regeneration. TLR3 is unique among TLRs in that it signals through TRIF (TIR domain‐containing adaptor‐inducing interferon‐β), not through MyD88, and may lead to activation of either the inflammatory or apoptotic pathway. The inflammatory pathway leads to NF‐κB activation, whereas the apoptotic pathway, believed to be mediated by Rip3, leads to caspase‐8 activation. In this study, we explored the role of TLR3 in liver regeneration by comparing the response to 70% partial hepatectomy of TLR3wt and TLR3−/− mice. We found that following partial hepatectomy, TLR3−/− mice demonstrated earlier hepatocyte proliferation. Furthermore, within the first hours, we observed a dramatic TLR3‐dependent NF‐κB activation and an increase in Rip3 levels in hepatocytes, accompanied by caspase‐8 activation but without an apoptotic outcome. Conclusion: TLR3 plays an inhibitory role in the priming of liver regeneration, thus reinforcing the role of the innate immune system in balancing tissue regeneration. (HEPATOLOGY 2009.)
Safe-Play Knowledge, Aggression, and Head-Impact Biomechanics in Adolescent Ice Hockey Players.

CONTEXT Addressing safe-play knowledge and player aggression could potentially improve ice hockey sport safety. OBJECTIVES To compare (1) safe-play knowledge and aggression between male and female adolescent ice hockey players and (2) head-impact frequency and severity between players with high and low levels of safe-play knowledge and aggression during practices and games. DESIGN Cohort study. SETTING On field. PATIENTS OR OTHER PARTICIPANTS Forty-one male (n = 29) and female (n = 12) adolescent ice hockey players. INTERVENTION(S) Players completed the Safe Play Questionnaire (0 = less knowledge, 7 = most knowledge) and Competitive Aggressiveness and Anger Scale (12 = less aggressive, 60 = most aggressive) at midseason. Aggressive penalty minutes were recorded throughout the season. The Head Impact Telemetry System was used to capture head-impact frequency and severity (linear acceleration [g], rotational acceleration [rad/s(2)], Head Impact Technology severity profile) at practices and games. MAIN OUTCOME MEASURE(S) One-way analyses of variance were used to compare safe play knowledge and aggression between sexes. Players were categorized as having high or low safe-play knowledge and aggression using a median split. A 2 × 2 mixed-model analysis of variance was used to compare head-impact frequency, and random-intercept general linear models were used to compare head-impact severity between groups (high, low) and event types (practice, game). RESULTS Boys (5.8 of 7 total; 95% confidence interval [CI] = 5.3, 6.3) had a trend toward better safe-play knowledge compared with girls (4.9 of 7 total; 95% CI = 3.9, 5.9; F1,36 = 3.40, P = .073). Less aggressive male players sustained significantly lower head rotational accelerations during practices (1512.8 rad/s (2) , 95% CI = 1397.3, 1637.6 rad/s(2)) versus games (1754.8 rad/s (2) , 95% CI = 1623.9, 1896.2 rad/s(2)) and versus high-aggression players during practices (1773.5 rad/s (2) , 95% CI = 1607.9, 1956.3 rad/s (2) ; F1,26 = 6.04, P = . 021). CONCLUSIONS Coaches and sports medicine professionals should ensure that athletes of all levels, ages, and sexes have full knowledge of safe play and should consider aggression interventions for reducing head-impact severity among aggressive players during practice.
A Review on Hybrid Controller Using Soft Computing Algorithms

Aadaptability and self-organization of a system is two key factors, when it comes to how well the system is surviving for the changes to the environment and how these work within the plant. Different tuning methods and soft computing techniques improve these two factors in controllers. Considering the increasing complexity of dynamic systems along with their need for feedback controls, using more complicated controls has become necessary and these techniques can be a suitable response to this necessity. This paper briefly describes a review on different techniques used for PID tuning as well as soft computing algorithm for hybrid controllers. This paper provides a comprehensive reference source for people working with hybrid controllers.
Peeing barbed wire. Symptom experiences in women with lower urinary tract infection.

OBJECTIVE To explore the contents and presentation of symptoms experienced by female patients with lower urinary tract infections. DESIGN Qualitative study based on written answers to open-ended questions on symptom experiences, analysis with Giorgi's phenomenological approach, explanatory model as frame of reference. SETTING Twelve general practices in the Bergen area of Norway. SUBJECTS Ninety-four women aged 19-97 years who consulted because they suspected to have an acute cystitis and who had leucocyturia and growth of 10(5) or more uropathogens/ml in the urine. MAIN OUTCOME MEASURES Descriptions and nuances considered mainstream for cystitis or as a supplement to the traditional medical symptom descriptions. RESULTS We found a great diversity of symptoms. Typical symptom descriptions were a terrible scorch when the bladder is nearly empty, frequent need to void followed by only a few drops, sometimes so suddenly that it may go wrong, or a constant ache in the low back and belly. Subjects also described constant aching or pressure in the genital area, or they felt miserable and no good in the whole body. Specific symptoms were also localized elsewhere in the body. CONCLUSION Diverse symptom descriptions complementing previous knowledge were revealed, as well as symptoms not usually mentioned in textbooks or reviews.
Streamlined models of dementia care mapping

Dementia Care Mapping (DCM) is an observational tool that provides rich data about the quality of life and quality of care of persons with dementia in group care settings. The method is time-consuming and thus costly to implement in practice. This paper presents an attempt to ‘streamline’ DCM for the sake of simplifying it and reducing the financial resources required to implement it. Data were collected for 166 persons with dementia in three types of care settings. Seven streamlined time-sampling models were tested against the original DCM model. In general, results support the use of certain models for specific purposes. The strengths and limitations of these streamlined models are discussed and recommendations are made.
Determination of proton metabolite concentrations and relaxation parameters in normal human brain and intracranial tumours

Quantitative proton spectroscopic studies were performed on 39 volunteers and 16 patients with intracranial tumours. Estimates of T2 were obtained in white matter, grey matter, cerebellum, astrocytomas and meningiomas; T1 was determined in white matter only. White matter values of T2 for trimethylamines, creatine and N‐acetyl aspartate (NAA) were 309±84, 195±41 and 369±124ms, respectively (mean±SD, n = 20). Metabolite concentrations in white matter were 2.0±0.4 m̈mol/g wet weight for trimethylamines, 7.3±1.1 for creatine and 11.4±1.4 for NAA. The mean concentrations of creatine and NAA in grey matter and all of three metabolites in cerebellum were greater than those in white matter. Tumour spectra were characterized by increased trimethylamines, reduced creatine and NAA and occasionally the presence of lactate. Meningiomas were further characterized by the presence of alanine. The mean T2 and concentration of trimethylamines in tumours was significantly greater than in normal brain. Creatine and NAA concentrations were decreased in all tumours. The longer T2 of trimethylamines and presence of alanine in meningiomas indicate that important differences exist in membrane and glucose metabolism within these tumours when compared to either astrocytomas or normal brain tissue.
Molecular physiology of aluminum toxicity and tolerance in plants

Aluminum being the third most abundant metal in the earth’s crust poses a serious threat to crop productivity in acid soils, which comprise almost half of the arable land. This review travels across time and updates research done on aluminum stress in plants. In its phytotoxic forms, aluminum affects root growth by acting in the root apical zone, resulting in growth inhibition in a very short time at micromolar concentrations. The mechanisms of aluminum toxicity in plants may proceed by growth inhibition, callose accumulation, cytoskeletal distortion, disturbance of plasma membrane surface charge, and H+-ATPase activity, lipid peroxidation of membranes, production of reactive oxygen species in cytosol and mitochondria, respiratory dysfunction, opening of mitochondrial permeability transition pores, collapsing of inner mitochondrial membrane potential, activation of mitochondrial protease, and induction of nuclear apoptosis, resulting ultimately in programmed cell death. In contrast, the mechanism of tolerance involves the exudation of organic acid anions, complexation of aluminum with organic acids, and subsequent detoxification. Many oxidative stress genes and other metabolically important genes have also been found to be induced under aluminum stress and overexpression analyses have also shown some plants to develop some degree of tolerance. In the future, researchers in the area of aluminum research should investigate more basic mechanisms of aluminum toxicity and discover and study more aluminum-responsive genes that confer resistance against this toxic metal, to ensure food security for ever-increasing human populations in the future.
Emodin protects rat liver from CCl(4)-induced fibrogenesis via inhibition of hepatic stellate cells activation.

AIM To investigate the role of emodin in protecting the liver against fibrogenesis caused by carbon tetrachloride (CCl(4)) in rats and to further explore the underlying mechanisms. METHODS Rat models of experimental hepatic fibrosis were established by injection with CCl(4); the treated rats received emodin via oral administration at a dosage of 20 mg/kg twice a week at the same time. Rats injected with olive oil served as a normal group. Histopathological changes were observed by hematoxylin and eosin staining. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and hepatic hydroxyproline content were assayed by biochemical analyses. The mRNA and protein relevant to hepatic stellate cell (HSC) activation in the liver were assessed using real-time reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, western blotting and enzyme-linked immunosorbent assay. RESULTS The degree of hepatic fibrosis increased markedly in the CCl(4) group compared to the normal group (P < 0.01), and decreased markedly in the emodin group compared to the CCl(4) group according to METAVIR scale (P < 0.01) compared with those in the normal control group (51.02 +/- 10.64 IU/L and 132.28 +/- 18.14 IU/L). The activities of serum ALT and AST were significantly higher in rats injected with CCl(4) (289.25 +/- 68.84 IU/L and 423.89 +/- 35.67 IU/L, both P < 0.05). The activities of serum ALT and AST were significantly reduced by administration of emodin (176.34 +/- 47.29 IU/L and 226.1 +/- 44.52 IU/L, both P < 0.05). Compared with the normal controls (54.53 +/- 13.46 mg/g), hepatic hydroxyproline content was significantly higher in rats injected with CCl(4) (120.27 +/- 28.47 mg/g, P < 0.05). Hepatic hydroxyproline content was significantly reduced in the rats treated with emodin at 20 mg/kg (71.25 +/- 17.02 mg/g, P < 0.05). Emodin significantly protected the liver from injury by reducing serum AST and ALT activities and reducing hepatic hydroxyproline content. The mRNA levels of transforming growth factor-beta1 (TGF-beta1), Smad4 and alpha-SMA in liver tissues were significantly down-regulated in SD rats that received emodin treatment. Furthermore, significant down-regulation of serum TGF-beta1 protein levels and protein expression of Smad4 and alpha-SMA in liver tissues was also observed in the rats. Emodin inhibited HSC activation by reducing the abundance of TGF-beta1 and Smad4. CONCLUSION Emodin protects the rat liver from CCl(4)-induced fibrogenesis by inhibiting HSC activation. Emodin might be a therapeutic antifibrotic agent for the treatment of hepatic fibrosis.
Induction of micronucleated erythrocytes by recombinant human erythropoietin.

Induction of micronucleated erythrocytes by a recombinant human erythropoietin (rhEPO) was examined using both in vitro and in vivo test systems. A small, significant and dose-related increase in the frequency of micronucleated polychromatic erythrocytes (MNPCE) in bone marrow of mice administered i.p. with 12,500-50,000 IU/kg rhEPO was induced at 48 h sampling time. A clear positive dose--response relationship and significant increase in the frequency of micronucleated reticulocytes (MNRET) in peripheral blood of mice administered i.p. with 400-50,000 IU/kg rhEPO was noted at 48, 72 and 96 h sampling times. Conversely, in bacterial reverse mutation tests, no noticeable increase of auxotrophic revertants was observed in Salmonella typhimurium, TA100, TA98, TA1535, TA1537, or Escherichia coli, WP2 uvrA-, by treatment with 188-6000 IU/plate of rhEPO, with or without S9 mix. Furthermore, rhEPO at 750-6000 IU/ml did not induce chromosomal aberrations in vitro in CHL cells or human peripheral blood lymphocytes in a direct method nor in a metabolic activation method. Moreover, chromosomal aberrations were not detected in bone marrow cells of CD-1 male mice, even at high rhEPO concentrations (100,000 IU/kg) in vivo. Consequently, it was concluded that errors in the process of enucleation or differentiation of the erythrocytes should be equally considered as possible mechanisms for the increased frequencies of MNPCE and MNRET alongside induction of DNA damage or errors in the process of DNA repair.
Detection of recurrent colorectal cancer by 18F-FDG PET/CT comparison with contrast enhanced CT scan.

OBJECTIVE To evaluate diagnostic performance of 18F-FDG PET/CT in assessment of recurrence colorectal cancer after treatment in Siriraj Hospital. MATERIAL AND METHOD The authors retrospectively studied 48 treated colorectal cancer patients with suspected recurrence who underwent 18F-FDG PET/CT and contrast-enhanced CT (CECT). Clinical information, image follow-up for at least one year, and pathological reports of the patients were reviewed for gold standard RESULTS Recurrent or metastatic disease was found in 36 of 48 patients. Calculated sensitivity, specificity and accuracy of 18F-FDG PET/CT were 94.4%, 66.7%, and 87.5%. 18F-FDG PET/CT can reduce false positive results of CECT in six patients, thus specificity of 18F-FDG PET/CT was statistically significantly better than that of CECT. Using lesion-based analysis with 65 recurrent sites and 26 non-recurrent lesion, 18F-FDG PET/CT showed better sensitivity 87.7%, specificity 61.5%, and accuracy 80.2 than CECT without statistical significance. CONCLUSION 18F-FDG PET/CT overall showed higher sensitivity, specificity, and accuracy than CECT.
Engraftment syndrome after allogeneic hematopoietic cell transplantation in adults

We performed a retrospective study of the engraftment syndrome (ES) as defined by the Spitzer Criteria in adult patients undergoing allogeneic hematopoietic cell transplantation (HCT) for various hematological malignancies at a single institution, over a decade, and analyzed its relationship to acute GVHD; 217 patients underwent either myeloablative (38.7%) or reduced intensity (61.3%) HCT; 22.1% met the criteria for ES. Acute GVHD prophylaxis (P = 0.006) and transplants prior to 2006 (P < 0.0001) were significantly associated with a risk of ES in univariable analysis. Early aGVHD within 4 weeks of engraftment was significantly more common in the ES compared to the non ES cohort (21 vs. 8.3% respectively, P = 0.02). ES did not predict for future GVHD, as at day +180, the cumulative incidences of grades II–IV aGVHD (31 vs. 23%, P = 0.19) and of chronic GVHD at 2 years of engraftment (42 vs. 36%, P = 0.28) were not significantly different between the ES and non ES groups, respectively. No significant differences in NRM, overall survival and progression‐free survival were observed between the two groups. Although predictive of early aGVHD, ES occurred independently of GVHD in 79% of the patients. Survival outcomes should be evaluated in a larger randomized study to investigate if there is a correlation with ES. Am. J. Hematol. 89:698–705, 2014. © 2014 Wiley Periodicals, Inc.