504 resultados para Dickinson, Jonathan, 1688-1747
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One aim of the Australasian Nutrition Care Day Survey (ANCDS) was to explore dietary intake and nutritional status of acute care hospital patients. Dietitians from 56 hospitals in Australia and New Zealand completed a 24-hour nutritional status and dietary intake audit of 3000 adult patients. Participants were evaluated for nutritional risk using the Malnutrition Screening Tool (MST). Those ‘at risk’ underwent nutritional assessment using Subjective Global Assessment (SGA). Dietitians observed participants’ dietary intake at each main meal and recorded mid-meal intake via participant interviews. Intakes were recorded as 0%, 25%, 50%, 75%, or 100% of that offered for each meal during the 24-hour audit. Preliminary results for 1550 participants (males = 853; females = 697), age = 64 ± 17 years and BMI = 27 ± 7 kg/m2. Fifty-five percent (n = 853) of the participants had BMI > 25 kg/m2. The MST identified 41% (n = 636) ‘at risk’ for malnutrition. Of those ‘at risk’, 70% were assessed as malnourished resulting in an overall malnutrition prevalence of 30% (25% moderately malnourished, 5% severely malnourished). One-quarter of malnourished participants (n = 118) were on standard hospital diets without additional nutritional support. Fifty percent of malnourished patients (n = 235) and 40% of all patients (n = 620) had an overall 24-hour food consumption of ≤50% during the 24-hour audit. The ANCDS found that skeletons in the hospital closet continue to exist and that acute care patients continue to have suboptimal dietary intake. The ANCDS provides valuable insight into gaps in existing nutrition care practices.
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High tumor kallikrein-related-peptidase 4 (KLK4) levels are associated with a poor outcome for women with serous epithelial ovarian cancer (EOC), for which peritoneal dissemination and chemoresistance are key events. To determine the role of KLK4 in these events, we examined KLK4-transfected SKOV-3 and endogenous KLK4 expressing OVCA432 cells in 3-dimensional (3D) suspension culture to mimic the ascites microenvironment. KLK4-SKOV-3 cells formed multicellular aggregates (MCAs) as seen in ascites, as did SKOV-3 cells treated with active KLK4. MCA formation was reduced by treatment with a KLK4 blocking antibody or the selective active site KLK4 sunflower trypsin inhibitor (SFTI-FCQR). KLK4-MCAs formed larger cancer cell foci in mesothelial cell monolayers than those formed by vector and native SKOV-3 cells, suggesting KLK4-MCAs are highly invasive in the peritoneal microenvironment. A high level of KLK4 is expressed by ascitic EOC cells compared to matched primary tumor cells, further supporting its role in the ascitic microenvironment. Interestingly, KLK4 transfected SKOV-3 cells expressed high levels of the KLK4 substrate, urokinase plasminogen activator (uPA), particularly in 3D-suspension, and high levels of both KLK4 and uPA were observed in patient cells taken from ascites. Importantly, the KLK4-MCAs were paclitaxel resistant which was reversed by SFTI-FCQR and to a lesser degree by the general serine protease inhibitor, Aprotinin, suggesting that in addition to uPA, other as yet unidentified substrates of KLK4 must be involved. Nonetheless, these data suggest that KLK4 inhibition, in conjunction with paclitaxel, may improve the outcome for women with serous epithelial ovarian cancer and high KLK4 levels in their tumors.
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This paper details the progress to date, toward developing a small autonomous helicopter. We describe system architecture, avionics, visual state estimation, custom IMU design, aircraft modelling, as well as various linear and neuro/fuzzy control algorithms. Experimental results are presented for state estimation using fused stereo vision and IMU data, heading control, and attitude control. FAM attitude and velocity controllers have been shown to be effective in simulation.
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Background Non-fatal health outcomes from diseases and injuries are a crucial consideration in the promotion and monitoring of individual and population health. The Global Burden of Disease (GBD) studies done in 1990 and 2000 have been the only studies to quantify non-fatal health outcomes across an exhaustive set of disorders at the global and regional level. Neither effort quantified uncertainty in prevalence or years lived with disability (YLDs). Methods Of the 291 diseases and injuries in the GBD cause list, 289 cause disability. For 1160 sequelae of the 289 diseases and injuries, we undertook a systematic analysis of prevalence, incidence, remission, duration, and excess mortality. Sources included published studies, case notification, population-based cancer registries, other disease registries, antenatal clinic serosurveillance, hospital discharge data, ambulatory care data, household surveys, other surveys, and cohort studies. For most sequelae, we used a Bayesian meta-regression method, DisMod-MR, designed to address key limitations in descriptive epidemiological data, including missing data, inconsistency, and large methodological variation between data sources. For some disorders, we used natural history models, geospatial models, back-calculation models (models calculating incidence from population mortality rates and case fatality), or registration completeness models (models adjusting for incomplete registration with health-system access and other covariates). Disability weights for 220 unique health states were used to capture the severity of health loss. YLDs by cause at age, sex, country, and year levels were adjusted for comorbidity with simulation methods. We included uncertainty estimates at all stages of the analysis. Findings Global prevalence for all ages combined in 2010 across the 1160 sequelae ranged from fewer than one case per 1 million people to 350 000 cases per 1 million people. Prevalence and severity of health loss were weakly correlated (correlation coefficient −0·37). In 2010, there were 777 million YLDs from all causes, up from 583 million in 1990. The main contributors to global YLDs were mental and behavioural disorders, musculoskeletal disorders, and diabetes or endocrine diseases. The leading specific causes of YLDs were much the same in 2010 as they were in 1990: low back pain, major depressive disorder, iron-deficiency anaemia, neck pain, chronic obstructive pulmonary disease, anxiety disorders, migraine, diabetes, and falls. Age-specific prevalence of YLDs increased with age in all regions and has decreased slightly from 1990 to 2010. Regional patterns of the leading causes of YLDs were more similar compared with years of life lost due to premature mortality. Neglected tropical diseases, HIV/AIDS, tuberculosis, malaria, and anaemia were important causes of YLDs in sub-Saharan Africa. Interpretation Rates of YLDs per 100 000 people have remained largely constant over time but rise steadily with age. Population growth and ageing have increased YLD numbers and crude rates over the past two decades. Prevalences of the most common causes of YLDs, such as mental and behavioural disorders and musculoskeletal disorders, have not decreased. Health systems will need to address the needs of the rising numbers of individuals with a range of disorders that largely cause disability but not mortality. Quantification of the burden of non-fatal health outcomes will be crucial to understand how well health systems are responding to these challenges. Effective and affordable strategies to deal with this rising burden are an urgent priority for health systems in most parts of the world. Funding Bill & Melinda Gates Foundation.
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The steady problem of free surface flow due to a submerged line source is revisited for the case in which the fluid depth is finite and there is a stagnation point on the free surface directly above the source. Both the strength of the source and the fluid speed in the far field are measured by a dimensionless parameter, the Froude number. By applying techniques in exponential asymptotics, it is shown that there is a train of periodic waves on the surface of the fluid with an amplitude which is exponentially small in the limit that the Froude number vanishes. This study clarifies that periodic waves do form for flows due to a source, contrary to a suggestion by Chapman & Vanden-Broeck (2006, J. Fluid Mech., 567, 299--326). The exponentially small nature of the waves means they appear beyond all orders of the original power series expansion; this result explains why attempts at describing these flows using a finite number of terms in an algebraic power series incorrectly predict a flat free surface in the far field.
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Cold water immersion (CWI) is a popular recovery modality, but actual physiological responses to CWI after exercise in the heat have not been well documented. The purpose of this study was to examine effects of 20-min CWI (14 degrees C) on neuromuscular function, rectal (T(re)) and skin temperature (T(sk)), and femoral venous diameter after exercise in the heat. Ten well-trained male cyclists completed two bouts of exercise consisting of 90-min cycling at a constant power output (216+/-12W) followed by a 16.1km time trial (TT) in the heat (32 degrees C). Twenty-five minutes post-TT, participants were assigned to either CWI or control (CON) recovery conditions in a counterbalanced order. T(re) and T(sk) were recorded continuously, and maximal voluntary isometric contraction torque of the knee extensors (MVIC), MVIC with superimposed electrical stimulation (SMVIC), and femoral venous diameters were measured prior to exercise, 0, 45, and 90min post-TT. T(re) was significantly lower in CWI beginning 50min post-TT compared with CON, and T(sk) was significantly lower in CWI beginning 25min post-TT compared with CON. Decreases in MVIC, and SMVIC torque after the TT were significantly greater for CWI compared with CON; differences persisted 90min post-TT. Femoral vein diameter was approximately 9% smaller for CWI compared with CON at 45min post-TT. These results suggest that CWI decreases T(re), but has a negative effect on neuromuscular function.
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Bovine colostrum has been shown to influence the cytokine production of bovine leukocytes. However, it remains unknown whether processed bovine colostrum, a supplement popular among athletes to enhance immune function, is able to modulate cytokine secretion of human lymphocytes and monocytes. The aim of this investigation was to determine the influence of a commercially available bovine colostrum protein concentrate (CPC) to stimulate cytokine production by human peripheral blood mononuclear cells (PBMCs). Blood was sampled from four healthy male endurance athletes who had abstained from exercise for 48 h. PBMCs were separated and cultured with bovine CPC concentrations of 0 (control), 1.25, 2.5, and 5% with and without lipopolysaccharide (LPS) (3 microg/mL) and phytohemagglutinin (PHA) (2.5 microg/mL). Cell supernatants were collected at 6 and 24 h of culture for the determination of tumor necrosis factor (TNF), interferon (IFN)-gamma, interleukin (IL)-10, IL-6, IL-4, and IL-2 concentrations. Bovine CPC significantly stimulated the release of IFN-gamma, IL-10, and IL-2 (p < 0.03). The addition of LPS to PBMCs cocultured with bovine CPC significantly stimulated the release of IL-2 and inhibited the early release of TNF, IL-6, and IL-4 (p < 0.02). Phytohemagglutinin stimulation in combination with bovine CPC significantly increased the secretion of IL-10 and IL-2 at 6 h of culture and inhibited IFN-gamma and TNF (p < 0.05). This data show that a commercial bovine CPC is able to modulate in vitro cytokine production of human PBMCs. Alterations in cytokine secretion may be a potential mechanism for reported benefits associated with supplementation.
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CC-chemokine receptor 2 (CCR2) and its ligand, monocyte chemotactic protein-1 (MCP-1, also known as CCL2), are crucial for the recruitment of monocytes/macrophages to sites of inflammation. We conducted a series of experiments to investigate the relationship between stress, monocyte CCR2 expression and migration activity. First, we collected peripheral blood mononuclear cells (PBMC) from untrained subjects (n=8) and measured CCR2 expression on CD14(+) monocytes cultured with cortisol, epinephrine and norepinephrine. Second, we collected PBMC from the subjects before and after they cycled for 60 min at 70% peak O(2) uptake (VO2(peak)), and measured alterations in CCR2 expression on monocytes following exercise. Third, we cultured PBMC with serum obtained before and after exercise and the glucocorticoid antagonist RU-486 to determine the effect of cortisol on CCR2 expression in vitro. Last, we measured the ability of PBMC treated with serum or cortisol to migrate through membrane filters in response to CCL2. Cortisol (but not epinephrine or norepinephrine) increased CCR2 expression on monocytes in a dose- and time-dependent manner. Exercise did not influence CCR2 expression on PBMC, whereas incubation of PBMC with post-exercise serum significantly increased CCR2 expression. Both cortisol and post-exercise serum increased the migration of PBMC toward CCL2. The increase in CCR2 expression on PBMC following stimulation with cortisol and serum was blocked by the glucocorticoid receptor antagonist RU-486. In conclusion, cortisol released during exercise increased monocyte CCR2 expression and migration activity in vitro. These alterations may influence inflammation and regeneration of damaged tissue after acute stress.
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PURPOSE: Heat stress might attenuate the effects of carbohydrate on immunoendocrine responses to exercise by increasing endogenous glucose production and reducing the rate of exogenous carbohydrate oxidation. The authors compared the efficacy of carbohydrate consumption on immune responses to exercise in temperate vs. hot conditions. METHODS: Ten male cyclists exercised on 2 separate occasions in temperate (18.1 +/- 0.4 degrees C, 58% +/- 8% relative humidity) and on another 2 occasions in hot conditions (32.2 +/- 0.7 degrees C, 55% +/- 2% relative humidity). On each occasion, the cyclists exercised in a fed state for 90 min at approximately 60% VO2max and then completed a 16.1-km time trial. Every 15 min during the first 90 min of exercise, they consumed 0.24 g/kg body mass of a carbohydrate or placebo gel. RESULTS: Neutrophil counts increased during exercise in all trials (p < .05) and were significantly lower (40%, p = .006) after the carbohydrate than after the placebo trial in 32 degrees C. The concentrations of serum interleukin (IL)-6, IL-8, and IL-10 and plasma granulocyte-colony-stimulating factor, myeloperoxidase, and calprotectin also increased during exercise in all trials but did not differ significantly between the carbohydrate and placebo trials. Plasma norepinephrine concentration increased during exercise in all trials and was significantly higher (50%, p = .01) after the carbohydrate vs. the placebo trial in 32 degrees C. CONCLUSION: Carbohydrate ingestion attenuated neutrophil counts during exercise in hot conditions, whereas it had no effect on any other immune variables in either temperate or hot conditions.
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The aim of the present study was to determine the effect of carbohydrate (CHO; sucrose) ingestion and environmental heat on the development of fatigue and the distribution of power output during a 16.1-km cycling time trial. Ten male cyclists (Vo(2max) = 61.7 +/- 5.0 ml.kg(-1).min(-1), mean +/- SD) performed four 90-min constant-pace cycling trials at 80% of second ventilatory threshold (220 +/- 12 W). Trials were conducted in temperate (18.1 +/- 0.4 degrees C) or hot (32.2 +/- 0.7 degrees C) conditions during which subjects ingested either CHO (0.96 g.kg(-1).h(-1)) or placebo (PLA) gels. All trials were followed by a 16.1-km time trial. Before and immediately after exercise, percent muscle activation was determined using superimposed electrical stimulation. Power output, integrated electromyography (iEMG) of vastus lateralis, rectal temperature, and skin temperature were recorded throughout the trial. Percent muscle activation significantly declined during the CHO and PLA trials in hot (6.0 and 6.9%, respectively) but not temperate conditions (1.9 and 2.2%, respectively). The decline in power output during the first 6 km was significantly greater during exercise in the heat. iEMG correlated significantly with power output during the CHO trials in hot and temperate conditions (r = 0.93 and 0.73; P < 0.05) but not during either PLA trial. In conclusion, cyclists tended to self-select an aggressive pacing strategy (initial high intensity) in the heat.
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Confusion exists as to the age of the Abor Volcanics of NE India. Some consider the unit to have been emplaced in the Early Permian, others the Early Eocene, a difference of ∼230 million years. The divergence in opinion is significant because fundamentally different models explaining the geotectonic evolution of India depend on the age designation of the unit. Paleomagnetic data reported here from several exposures in the type locality of the formation in the lower Siang Valley indicate that steep dipping primary magnetizations (mean = 72.7 ± 6.2°, equating to a paleo-latitude of 58.1°) are recorded in the formation. These are only consistent with the unit being of Permian age, possibly Artinskian based on a magnetostratigraphic argument. Plate tectonic models for this time consistently show the NE corner of the sub-continent >50°S; in the Early Eocene it was just north of the equator, which would have resulted in the unit recording shallow directions. The mean declination is counter-clockwise rotated by ∼94°, around half of which can be related to the motion of the Indian block; the remainder is likely due local Himalayan-age thrusting in the Eastern Syntaxis. Several workers have correlated the Abor Volcanics with broadly coeval mafic volcanic suites in Oman, NE Pakistan–NW India and southern Tibet–Nepal, which developed in response to the Cimmerian block peeling-off eastern Gondwana in the Early-Middle Permian, but we believe there are problems with this model. Instead, we suggest that the Abor basalts relate to India–Antarctica/India–Australia extension that was happening at about the same time. Such an explanation best accommodates the relevant stratigraphical and structural data (present-day position within the Himalayan thrust stack), as well as the plate tectonic model for Permian eastern Gondwana.
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Aim This cross-sectional study explores associations between migrant Indian mothers’ use of controlling feeding practices (pressure to eat, restriction and monitoring) and their concerns and perceptions regarding their children’s weight and picky eating behaviour. Methods Two hundred and thirty mothers with children aged 1-5 years, residing in Australia for 1-8 years, participated by completing a self-reported questionnaire. Results Perceptions and concerns regarding children’s weight were not associated with any of the controlling feeding practices. A positive association was noted between pressure feeding and perceptions of pickiness after adjusting for covariates: children’s age, gender and weight-for-age Z-score. Girls, older children, and children with higher weight-for-age z scores were pressure fed to a greater extent. Conclusions This study supports the generalisation of findings from Caucasian literature that pressure feeding and perceptions of pickiness are positively related.
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Background: Ureaplasma species in amniotic fluid at the time of second-trimester amniocentesis increases the risk of preterm birth, but most affected pregnancies continue to term (Gerber et al. J Infect Dis 2003). We aimed to model intra-amniotic (IA) ureaplasma infection in spiny mice, a species with a relatively long gestation (39 days) that allows investigation of the disposition and possible clearance of ureaplasmas in the feto-placental compartment. Method: Pregnant spiny mice received IA injections of U. parvum serovar 6 (10µL, 1x104 colony-forming-units in PBS) or 10B media (10µL; control) at 20 days (d) of gestation (term=39d). At 37d fetuses (n=3 ureaplasma, n=4 control) were surgically delivered and tissues were collected for; bacterial culture, ureaplasma mba and urease gene expression by PCR, tissue WBC counts and indirect fluorescent antibody (IFA) staining using anti-ureaplasma serovar 6 (rabbit) antiserum. Maternal and fetal plasma IgG was measured by Western blot. Results: Ureaplasmas were not detected by culture or PCR in fetal or maternal tissues but were visualized by IFA within placental and fetal lung tissues, in association with inflammatory changes and elevated WBC counts (p<0.0001). Anti-ureaplasma IgG was detected in maternal (2/2 tested) and fetal (1/2 tested) plasma but not in controls (0/3). Conclusions: IA injection of ureaplasmas in mid-gestation spiny mice caused persistent fetal lung and placental infection even though ureaplasmas were undetectable using standard culture or PCR techniques. This is consistent with resolution of IA infection, which may occur in human pregnancies that continue to term despite detection of ureaplasmas in mid-gestation.
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Bus Rapid Transit (BRT) station is the interface between passenger and service. The station is crucial to line operation as it is typically the only location where buses can pass each other. Congestion may occur here when buses maneuvering into and out of the platform lane interfere with bus flow, or when a queue of buses forms upstream of the platform lane blocking the passing lane. However, some systems include operation where express buses pass the critical station, resulting in a proportion of non stopping buses. It is important to understand the operation of the critical busway station under this type of operation, as it affects busway line capacity. This study uses micro simulation to treat the BRT station operation and to analyze the relationship between station Limit state bus capacity (B_ls), Total Bus Capacity (B_ttl). First, the simulation model is developed for Limit state scenario and then a mathematical model is defined, calibrated for a specified range of controlled scenarios of mean and coefficient of variation of dwell time. Thereafter, the proposed B_ls model is extended to consider non stopping buses and B_ttlmodel is defined. The proposed models provides better understanding to the BRT line capacity and is useful for transit authorities for designing better BRT operation.
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Between 1995 and 2003, 129 cemented primary THRs were performed using full acetabular impaction grafting to reconstruct acetabular deficiencies. These were classified as cavitary in 74 and segmental in 55 hips. Eighty-one patients were reviewed at mean 9.1 (6.2-14.3) years post-operatively. There were seven acetabular component revisions due to aseptic loosening, and a further 11 cases that had migrated >5mm or tilted >5° on radiological review - ten of which reported no symptoms. Kaplan-Meier analysis of revisions for aseptic loosening demonstrates 100% survival at nine years for cavitary defects compared to 82.6% for segmental defects. Our results suggest that the medium-term survival of this technique is excellent when used for purely cavitary defects but less predictable when used with large rim meshes in segmental defects.