954 resultados para A not B error
Resumo:
Multipotent mesenchymal stromal cells (MSCs) were first isolated from bone marrow and then from various adult tissues including placenta, cord blood, deciduous teeth, and amniotic fluid. MSCs are defined or characterized by their ability to adhere to plastic, to express specific surface antigens, and to differentiate into osteogenic, chondrogenic, adipogenic, and myogenic lineages. Although the molecular mechanisms that control MSC proliferation and differentiation are not well understood, the involvement of microRNAs has been reported. In the present study, we investigated the role of miR-125b during osteoblastic differentiation in humans. We found that miR-125b increased during osteoblastic differentiation, as well as Runx2 and ALPL genes. To study whether the gain or loss of miR-125b function influenced osteoblastic differentiation, we transfected MSCs with pre-miR-125b or anti-miR-125b and cultured the transfected cells in an osteoblastic differentiation medium. After transfection, no change was observed in osteoblastic differentiation, and Runx2, OPN, and ALPL gene expression were not changed. These results suggest that the gain or loss of miR-125b function does not influence levels of Runx2, OPN, and ALPL during osteoblastic differentiation.
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Cocaine is a widely used drug and its abuse is associated with physical, psychiatric and social problems. Abnormalities in newborns have been demonstrated to be due to the toxic effects of cocaine during fetal development. The mechanism by which cocaine causes neurological damage is complex and involves interactions of the drug with several neurotransmitter systems, such as the increase of extracellular levels of dopamine and free radicals, and modulation of transcription factors. The aim of this review was to evaluate the importance of the dopaminergic system and the participation of inflammatory signaling in cocaine neurotoxicity. Our study showed that cocaine activates the transcription factors NF-κB and CREB, which regulate genes involved in cellular death. GBR 12909 (an inhibitor of dopamine reuptake), lidocaine (a local anesthetic), and dopamine did not activate NF-κB in the same way as cocaine. However, the attenuation of NF-κB activity after the pretreatment of the cells with SCH 23390, a D1 receptor antagonist, suggests that the activation of NF-κB by cocaine is, at least partially, due to activation of D1 receptors. NF-κB seems to have a protective role in these cells because its inhibition increased cellular death caused by cocaine. The increase in BDNF (brain-derived neurotrophic factor) mRNA can also be related to the protective role of both CREB and NF-κB transcription factors. An understanding of the mechanisms by which cocaine induces cell death in the brain will contribute to the development of new therapies for drug abusers, which can help to slow down the progress of degenerative processes.
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Treatments for patients with hematologic malignancies not in remission are limited, but a few clinical studies have investigated the effects of salvaged unrelated cord blood transplantation (CBT). We retrospectively studied 19 patients with acute leukemia, 5 with myelodysplastic syndrome (MDS with refractory anemia with excess blasts [RAEB]), and 2 with non-Hodgkin's lymphoma who received 1 CBT unit ≤2 loci human leukocyte antigen (HLA)-mismatched after undergoing myeloablative conditioning regimens between July 2005 and July 2014. All of them were in non-remission before transplantation. The infused total nucleated cell (TNC) dose was 4.07 (range 2.76-6.02)×107/kg and that of CD34+ stem cells was 2.08 (range 0.99-8.65)×105/kg. All patients were engrafted with neutrophils that exceeded 0.5×109/L on median day +17 (range 14-37 days) and had platelet counts of >20×109/L on median day +35 (range 17-70 days). Sixteen patients (61.5%) experienced pre-engraftment syndrome (PES), and six (23.1%) patients progressed to acute graft-versus-host disease (GVHD). The cumulative incidence rates of II-IV acute GVHD and chronic GVHD were 50% and 26.9%, respectively. After a median follow-up of 27 months (range 5-74), 14 patients survived and 3 relapsed. The estimated 2-year overall survival (OS), disease-free survival (DFS), and non-relapse mortality (NRM) rates were 50.5%, 40.3%, and 35.2%, respectively. Salvaged CBT might be a promising modality for treating hematologic malignancies, even in patients with a high leukemia burden.
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Whether sleep problems of menopausal women are associated with vasomotor symptoms and/or changes in estrogen levels associated with menopause or age-related changes in sleep architecture is unclear. This study aimed to determine if poor sleep in middle-aged women is correlated with menopause. This study recruited women seeking care for the first time at the menopause outpatient department of our hospital. Inclusion criteria were an age ≥40 years, not taking any medications for menopausal symptoms, and no sleeping problems or depression. Patients were assessed with the Pittsburgh Sleep Quality Index (PSQI), modified Kupperman Index (KI), and Menopause Rating Scale (MRS). A PSQI score of <7 indicated no sleep disorder and ≥7 indicated a sleep disorder. Blood specimens were analyzed for follicle-stimulating hormone and estradiol levels. A total of 244 women were included in the study; 103 (42.2%) were identified as having a sleep disorder and 141 as not having one. In addition, 156 (64%) women were postmenopausal and 88 (36%) were not menopausal. Follicle-stimulating hormone and estradiol levels were similar between the groups. Patients with a sleep disorder had a significantly higher total modified KI score and total MRS score (both, P<0.001) compared with those without a sleep disorder. Correlations of the PSQI total score with the KI and MRS were similar in menopausal and non-menopausal women. These results do not support that menopause per se specifically contributes to sleep problems.
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Metabolic acidosis has profound effects on vascular tone. This study investigated the in vivo effects of acute metabolic acidosis (AMA) and chronic metabolic acidosis (CMA) on hemodynamic parameters and endothelial function. CMA was induced by ad libitum intake of 1% NH4Cl for 7 days, and AMA was induced by a 3-h infusion of 6 M NH4Cl (1 mL/kg, diluted 1:10). Phenylephrine (Phe) and acetylcholine (Ach) dose-response curves were performed by venous infusion with simultaneous venous and arterial blood pressure monitoring. Plasma nitrite/nitrate (NOx) was measured by chemiluminescence. The CMA group had a blood pH of 7.15±0.03, which was associated with reduced bicarbonate (13.8±0.98 mmol/L) and no change in the partial pressure of arterial carbon dioxide (PaCO2). The AMA group had a pH of 7.20±0.01, which was associated with decreases in bicarbonate (10.8±0.54 mmol/L) and PaCO2 (47.8±2.54 to 23.2±0.74 mmHg) and accompanied by hyperventilation. Phe or ACh infusion did not affect arterial or venous blood pressure in the CMA group. However, the ACh infusion decreased the arterial blood pressure (ΔBP: -28.0±2.35 mm Hg [AMA] to -4.5±2.89 mmHg [control]) in the AMA group. Plasma NOx was normal after CMA but increased after AMA (25.3±0.88 to 31.3±0.54 μM). These results indicate that AMA, but not CMA, potentiated the Ach-induced decrease in blood pressure and led to an increase in plasma NOx, reinforcing the effect of pH imbalance on vascular tone and blood pressure control.
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After a traumatic injury to the central nervous system, the distal stumps of axons undergo Wallerian degeneration (WD), an event that comprises cytoskeleton and myelin breakdown, astrocytic gliosis, and overexpression of proteins that inhibit axonal regrowth. By contrast, injured neuronal cell bodies show features characteristic of attempts to initiate the regenerative process of elongating their axons. The main molecular event that leads to WD is an increase in the intracellular calcium concentration, which activates calpains, calcium-dependent proteases that degrade cytoskeleton proteins. The aim of our study was to investigate whether preventing axonal degeneration would impact the survival of retinal ganglion cells (RGCs) after crushing the optic nerve. We observed that male Wistar rats (weighing 200-400 g; n=18) treated with an exogenous calpain inhibitor (20 mM) administered via direct application of the inhibitor embedded within the copolymer resin Evlax immediately following optic nerve crush showed a delay in the onset of WD. This delayed onset was characterized by a decrease in the number of degenerated fibers (P<0.05) and an increase in the number of preserved fibers (P<0.05) 4 days after injury. Additionally, most preserved fibers showed a normal G-ratio. These results indicated that calpain inhibition prevented the degeneration of optic nerve fibers, rescuing axons from the process of axonal degeneration. However, analysis of retinal ganglion cell survival demonstrated no difference between the calpain inhibitor- and vehicle-treated groups, suggesting that although the calpain inhibitor prevented axonal degeneration, it had no effect on RGC survival after optic nerve damage.
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Sleep is important for the recovery of a critically ill patient, as lack of sleep is known to influence negatively a person’s cardiovascular system, mood, orientation, and metabolic and immune function and thus, it may prolong patients’ intensive care unit (ICU) and hospital stay. Intubated and mechanically ventilated patients suffer from fragmented and light sleep. However, it is not known well how non-intubated patients sleep. The evaluation of the patients’ sleep may be compromised by their fatigue and still position with no indication if they are asleep or not. The purpose of this study was to evaluate ICU patients’ sleep evaluation methods, the quality of non-intubated patients’ sleep, and the sleep evaluations performed by ICU nurses. The aims were to develop recommendations of patients’ sleep evaluation for ICU nurses and to provide a description of the quality of non-intubated patients’ sleep. The literature review of ICU patients’ sleep evaluation methods was extended to the end of 2014. The evaluation of the quality of patients’ sleep was conducted with four data: A) the nurses’ narrative documentations of the quality of patients’ sleep (n=114), B) the nurses’ sleep evaluations (n=21) with a structured observation instrument C) the patients’ self-evaluations (n=114) with the Richards-Campbell Sleep Questionnaire, and D) polysomnographic evaluations of the quality of patients’ sleep (n=21). The correspondence of data A with data C (collected 4–8/2011), and data B with data D (collected 5–8/2009) were analysed. Content analysis was used for the nurses’ documentations and statistical analyses for all the other data. The quality of non-intubated patients’ sleep varied between individuals. In many patients, sleep was light, awakenings were frequent, and the amount of sleep was insufficient as compared to sleep in healthy people. However, some patients were able to sleep well. The patients evaluated the quality of their sleep on average neither high nor low. Sleep depth was evaluated to be the worst and the speed of falling asleep the best aspect of sleep, on a scale 0 (poor sleep) to 100 (good sleep). Nursing care was mostly performed while the patients were awake, and thus the disturbing effect was low. The instruments available for nurses to evaluate the quality of patients’ sleep were limited and measured mainly the quantity of sleep. Nurses’ structured observatory evaluations of the quality of patients’ sleep were correct for approximately two thirds of the cases, and only regarding total sleep time. Nurses’ narrative documentations of the patients’ sleep corresponded with patients’ self-evaluations in just over half of the cases. However, nurses documented several dimensions of sleep that are not included in the present sleep evaluation instruments. They could be classified according to the components of the nursing process: needs assessment, sleep assessment, intervention, and effect of intervention. Valid, more comprehensive sleep evaluation methods for nurses are needed to evaluate, document, improve and study patients’ quality of sleep.
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In the present study, the efficacy of ozone inactivation of B. subtilis spores and E. coli in cassava starch was evaluated. Cassava starch with 18 and 30% moisture content was processed with ozone at concentrations of 40-118 ppm and exposure times of 15-120 minutes. The processing at 113 ppm/120 minutes (maximum exposure level to ozone evaluated) at 18% of moisture content did not cause significant reduction of B. subtilis spores and caused the reduction of only 2 decimal of E. coli. On the other hand, when the ozonation process was carried out for 120 minutes at 30% of moisture content, 3.6 decimal reduction of B. subtilis was achieved at 40 ppm of ozone and total B. subtilis load reduction (>5 log cycles) was observed at 118 ppm of ozone. Similarly, total E. coli load reduction (>7 log cycles) was achieved at 40 ppm of ozone exposure for 60 minutes. Therefore, the results indicate that the ozone efficacy against microorganisms in cassava starch was mainly dependent on the sample moisture content and to ozone concentration and exposure time. Moreover, it was observed that ozone is a promising technology to reduce microbial counts in dried food.
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In this study, a neuro-fuzzy estimator was developed for the estimation of biomass concentration of the microalgae Synechococcus nidulans from initial batch concentrations, aiming to predict daily productivity. Nine replica experiments were performed. The growth was monitored daily through the culture medium optic density and kept constant up to the end of the exponential phase. The network training followed a full 3³ factorial design, in which the factors were the number of days in the entry vector (3,5 and 7 days), number of clusters (10, 30 and 50 clusters) and internal weight softening parameter (Sigma) (0.30, 0.45 and 0.60). These factors were confronted with the sum of the quadratic error in the validations. The validations had 24 (A) and 18 (B) days of culture growth. The validations demonstrated that in long-term experiments (Validation A) the use of a few clusters and high Sigma is necessary. However, in short-term experiments (Validation B), Sigma did not influence the result. The optimum point occurred within 3 days in the entry vector, 10 clusters and 0.60 Sigma and the mean determination coefficient was 0.95. The neuro-fuzzy estimator proved a credible alternative to predict the microalgae growth.
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Abstract In the postharvest stage, taste and flavor are the key components of the marketability of tomato. Therefore, greater emphasis is now being placed on improving traits such as sugar content. In this study postharvest ultraviolet-B (UV-B) treatments on sugar, total soluble solids, and color of tomatoes harvested at different stages were investigated. Tomatoes harvested at turning, pink, and red stages were treated with two different doses of UV-B irradiation: UVB4 and UVB8. Color L* and hue angle values of tomatoes treated with UV-B were found to be high, which means the red color of tomatoes was improved. UVB4 treatments increased the color a* and saturation index values of tomatoes at pink and red harvest stage, although it did not affect at the turning stage. Additionally, UV-B irradiation treatments had no effect on sucrose content of the tomatoes. Fructose, glucose, and TSS content of tomatoes treated with UVB8 at red harvest stage were found to be high. Hence, the results obtained from this study are of great importance in terms of providing an increase in the amount of sugar without the need for breeding, and also consumer satisfaction.
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Arabic cookery book, dated tentatively to 12th or 13th century by the editors (Öhrnberg & Mroueh) on the basis of the script. Aro suggests (grounds not made explicit) that the manuscript came to the library from the collections of G. A. Wallin, but Öhrnberg & Mroueh simply describe it as being of unknown provenance.
Resumo:
Tämän kandidaatintutkielman tarkoituksena oli tutkia rahoituksellisen velkaantuneisuuden vaikutusta yritysten B/P-lukuihin ja keskimääräisiin tuottoihin Suomen osakemarkkinoilla vuosina 1996–2012. Tutkielman perustana oleva ilmiö on B/P-anomalia, jonka mukaan korkean B/P:n osakkeet eli arvo-osakkeet menestyvät osakemarkkinoilla paremmin kuin matalan B/P:n osakkeet eli kasvuosakkeet. Useiden tutkijoiden mielestä arvoanomalioiden syynä on korkeampi systemaattinen riski, jonka yksi komponenteista on rahoituksellinen velkaantuneisuus. Näiden tutkimusten perusteella korkean B/P:n yrityksillä pitäisi olla korkeampi systemaattinen riski ja siten todennäköisesti myös korkeampi rahoituksellinen velkaantuneisuus. Aineistona tutkimuksessa toimi Helsingin pörssin yritykset vuosilta 1996–2012 pois lukien rahoitus- ja vakuutusalan yritykset sekä kiinteistösijoitusyhtiöt. Tulosten perusteella B/P:n sekä rahoituksellisen velkaantuneisuuden välillä oli positiivinen, monotoninen ja tilastollisesti merkitsevä suhde, kun aineiston yritykset olivat jaettu kolmeen portfolioon niiden B/P-lukujen perusteella, mutta yhteyttä ei ollut löydettävissä kuuden portfolion tapauksessa. B/P-anomaliasta oli viitteitä, kun portfolioina käytettiin kolmea B/P-luvun pohjalta muodostettua portfoliota, mutta erot eivät olleet tilastollisesti merkitseviä. Rahoituksellisen velkaantuneisuuden sekä keskimääräisten vuosituottojen väliltä ei ollut löydettävissä tilastollisesti merkitsevää yhteyttä tästä aineistosta.
Resumo:
In studies of cognitive processing, the allocation of attention has been consistently linked to subtle, phasic adjustments in autonomic control. Both autonomic control of heart rate and control of the allocation of attention are known to decline with age. It is not known, however, whether characteristic individual differences in autonomic control and the ability to control attention are closely linked. To test this, a measure of parasympathetic function, vagal tone (VT) was computed from cardiac recordings from older and younger adults taken before and during performance of two attentiondemanding tasks - the Eriksen visual flanker task and the source memory task. Both tasks elicited event-related potentials (ERPs) that accompany errors, i.e., error-related negativities (ERNs) and error positivities (Pe's). The ERN is a negative deflection in the ERP signal, time-locked to responses made on incorrect trials, likely generated in the anterior cingulate. It is followed immediately by the Pe, a broad, positive deflection which may reflect conscious awareness of having committed an error. Age-attenuation ofERN amplitude has previously been found in paradigms with simple stimulus-response mappings, such as the flanker task, but has rarely been examined in more complex, conceptual tasks. Until now, there have been no reports of its being investigated in a source monitoring task. Age-attenuation of the ERN component was observed in both tasks. Results also indicated that the ERNs generated in these two tasks were generally comparable for young adults. For older adults, however, the ERN from the source monitoring task was not only shallower, but incorporated more frontal processing, apparently reflecting task demands. The error positivities elicited by 3 the two tasks were not comparable, however, and age-attenuation of the Pe was seen only in the more perceptual flanker task. For younger adults, it was Pe scalp topography that seemed to reflect task demands, being maximal over central parietal areas in the flanker task, but over very frontal areas in the source monitoring task. With respect to vagal tone, in the flanker task, neither the number of errors nor ERP amplitudes were predicted by baseline or on-task vagal tone measures. However, in the more difficult source memory task, lower VT was marginally associated with greater numbers of source memory errors in the older group. Thus, for older adults, relatively low levels of parasympathetic control over cardiac response coincided with poorer source memory discrimination. In both groups, lower levels of baseline VT were associated with larger amplitude ERNs, and smaller amplitude Pe's. Thus, low VT was associated in a conceptual task with a greater "emergency response" to errors, and at the same time, reduced awareness of having made them. The efficiency of an individual's complex cognitive processing was therefore associated with the flexibility of parasympathetic control of heart rate, in response to a cognitively challenging task.
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Aggressive behaviours within the sport of hockey appear to be increasing in both prevalence and consequence (Biasca, Wirth, & Tegner, 2002). Accordingly, this area of inquiry is currently garnering a considerable amount of attention from society and academics alike. The problem however, is that our current understanding of these behaviours has been deemed both incomplete and unreliable. The inconsistencies inherent within this body of knowledge have been traced back to a variety of methodological shortcomings. The purpose of this investigation was to assess hostile aggression using a more ecologically valid and comprehensive research design. Ten Junior B hockey games were tapped and subsequently coded by three independent observers, using a validated operational list. Two hundred and fifty-nine behaviours were extrapolated and examined according to the score differential, period, position of the aggressor, status of the aggressor's team, and whether the aggressor was a member of the home or visiting team. It was concluded that the frequency of aggressive behaviours significantly differed according to the score differential, and status of the aggressor's team (p < .01). However, these hostile acts did not differ according the aggressor's position, period, and the home versus away status of the aggressor's team (p > .01). It was also determined that the majority of aggressive acts (69.1 1%) across these ten games went unsanctioned. This highlights the profound influence that "positive misses" have on penalty measures of aggression, while concurrently highlighting the ecological validity present with observational designs. Consequently, by assessing aggressive behaviour in a more inclusive and ecologically valid manner, a more accurate picture of the frequency and distribution of hostile aggression may be provided.
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Event-related potentials were recorded from 10-year-old children and young adults in order to examine the developmental dififerences in two frontal lobe functions: detection of novel stimuli during an auditory novelty oddball task, and error detection during a visual flanker task. All participants showed a parietally-maximal P3 in response to auditory stimuli. In children, novel stimuli generated higher P3 amplitudes at the frontal site compared with target stimuli, whereas target stimuli generated higher P3 amplitudes at the parietal site compared with novel stimuli. Adults, however, had higher P3 amplitude to novel tones compared with target tones at each site. Children also had greater P3 amplitude at more parietal sites than adults during the novelty oddball and flanker tasks. Furthermore, children and adults did not show a significant reduction in P3 amplitude from the first to second novel stimulus presentation. No age differences were found with respect to P3 latency to novel and target stimuli. These findings suggest that the detection of novel and target stimuli is mature in 10-year-olds. Error trials typically elicit a negative ERP deflection (the ERN) with a frontal-central scalp distribution that may reflect response monitoring. There is also evidence of a positive ERP peak (the Pe) with a posterior scalp distribution which may reflect subjective recognition of a response. Both children and adults showed an ERN and Pe maximal at frontal-central sites. Children committed more errors, had smaller ERN across sites, and had a larger Pe at the parietal site than adults. This suggests that response monitoring is still immature in 10-year-olds whereas recognition of and emotional responses to errors may be similar in children and adults.