| 1. |
- Georgsson, Fredrik, et al.
(författare)
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Development of an Autonomous Path Tracking Forest Machine : a status report
- 2005
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- In many respects traditional automation in the forest-machine industry has reached an up- per limit, since the driver already has to deal with an excess of information and take too many decisions at a very high pace. To further automation still, introduction of semi-autonomous and autonomous functions are expected and considered necessary. This paper describes an ongoing project along these ideas. We describe the development of the hardware and software of an unmanned shuttle that shifts timber from the area of felling to the main roads for fur- ther transportation. A new path-tracking algorithm is introduced, and demonstrated as being superior to standard techniques, such as Follow-the-Carrot and Pure-Pursuit. To facilitate the research and development, a comprehensive software architecture for sensor and actuator interfacing is developed. Obstacle avoidance is accomplished by a new kind of radar, developed for and by the automotive industry. Localization is accomplished by a Kalman filter combining data from a Real-Time Kinematic Differential GPS/GLONASS and a gyro/compass. Tests conducted on a simulator and a small-scale robot show promising results. Tests on the real forest machine are ongoing, and will be completed before the end of 2005.
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| 2. |
- Andersen, Grethe Neumann, et al.
(författare)
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Bronchoalveolar matrix metalloproteinase 9 relates to restrictive lung function impairment in systemic sclerosis.
- 2007
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Ingår i: Respiratory Medicine. - : Elsevier BV. - 0954-6111 .- 1532-3064. ; 101:10, s. 2199-2206
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Tidskriftsartikel (refereegranskat)abstract
- Systemic sclerosis (SSc) is frequently associated with interstitial lung disease (ILD) often leading to lung fibrosis. In this study we investigated whether matrix metalloproteinase 9 (MMP-9) and its natural inhibitor; the tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), would be associated with remodelling in ILD in SSc. Levels of total MMP-9, pro-MMP-9 and TIMP-1 were measured in bronchoalveolar lavage (BAL) fluid from nine SSc patients with ILD, seven SSc patients without ILD and 16 age- and sex-matched healthy controls. Total MMP-9 and pro-MMP-9 levels were significantly elevated in SSc patients with ILD, compared to levels in SSc patients without ILD and healthy controls. In SSc patients with ILD calculated active MMP-9 levels were significantly higher than in SSc patients without ILD and tended to be higher than in healthy controls. TIMP-1 levels were elevated in both patient groups compared to healthy controls. Total-, pro- and active MMP-9 levels as well as pro-MMP-TIMP-1 and active MMP-9/TIMP-1 ratios were inversely associated with total lung capacity. The present study suggests that MMP-9 plays a pathophysiological role in the remodelling in ILD and lung fibrosis associated with SSc, and may represent a new therapeutic target in this condition.
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| 4. |
- Axenrot, Thomas, et al.
(författare)
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Multifrequency discrimination of fish and mysids
- 2009
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Ingår i: ICES Journal of Marine Science. - : Oxford University Press (OUP). - 1054-3139 .- 1095-9289. ; 66:6, s. 1106-1110
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Tidskriftsartikel (refereegranskat)abstract
- The opossumshrimp (Mysis relicta) is common in many lakes in the northernparts of Eurasia and North America. The shrimp is often an importantlink in the foodweb for fish, either throughout life or in earlylife stages. Generally, quantitative measurements of mysidsin large volumes of water are difficult to obtain with traditionalsampling methods. In this pilot study, measurements of volume-backscatteringstrength (Sv) at 38, 120, and 200 kHz were used to separatebackscattering from fish and mysids. Mysids were sampled withtrawls. Where mysids were caught, the correlations between mysidbiomass (dry weight) and mean Sv at 120 and 200 kHz were positive(r2 = 0.89 and 0.81, respectively). Where mysids were abundant,the Sv exhibited a characteristic frequency response. This wasnot found where mysids were scarce or absent. Therefore, areaswith great abundances of mysids can be identified, and theirbiomasses estimated from data collected during ecosystem monitoring.
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| 5. |
- Behndig, Annelie, et al.
(författare)
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Airway antioxidant and inflammatory responses to diesel exhaust exposure in healthy humans.
- 2006
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Ingår i: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 27:2, s. 359-365
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Tidskriftsartikel (refereegranskat)abstract
- Pulmonary cells exposed to diesel exhaust (DE) particles in vitro respond in a hierarchical fashion with protective antioxidant responses predominating at low doses and inflammation and injury only occurring at higher concentrations. In the present study, the authors examined whether similar responses occurred in vivo, specifically whether antioxidants were upregulated following a low-dose DE challenge and investigated how these responses related to the development of airway inflammation at different levels of the respiratory tract where particle dose varies markedly. A total of 15 volunteers were exposed to DE (100 microg x m(-3) airborne particulate matter with a diameter of <10 microm for 2 h) and air in a double-blinded, randomised fashion. At 18 h post-exposure, bronchoscopy was performed with lavage and mucosal biopsies taken to assess airway redox and inflammatory status. Following DE exposure, the current authors observed an increase in bronchial mucosa neutrophil and mast cell numbers, as well as increased neutrophil numbers, interleukin-8 and myeloperoxidase concentrations in bronchial lavage. No inflammatory responses were seen in the alveolar compartment, but both reduced glutathione and urate concentrations were increased following diesel exposure. In conclusion, the lung inflammatory response to diesel exhaust is compartmentalised, related to differing antioxidant responses in the conducting airway and alveolar regions.
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| 8. |
- Bjerg Bäcklund, Anders, 1982-
(författare)
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Epidemiology of asthma in primary school children
- 2008
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Background: Childhood asthma has increased worldwide, although recent studies report a prevalence plateau in some western countries.Aims: To investigate the prevalence of asthma and the associated risk factor patterns from ages 7-8 to 11-12 with special emphasis on the hereditary component, and further to study prevalence trends at age 7-8 from 1996 to 2006 and the possible determinants of these trends.Methods: The studies involved two cohorts from Kiruna, Luleå and Piteå: one previously identified cohort of 3430 children age 7-8 followed by yearly questionnaires until age 11-12 with 97% yearly participation. Skin-prick tests for allergic sensitisation were performed at ages 7-8 and 11-12 in subsets of 2148 and 2155 children respectively (88% of invited). In 2006 a new cohort of 7-8-year-olds was identified and examined identically. 2585 (96% of invited) and 1700 (90% of invited) participated in the questionnaire and skin-prick tests, respectively. The questionnaire included questions about symptoms of asthma, allergic rhinitis and eczema, and possible risk factors.Results: In the 1996 cohort, from age 7-8 to 11-12 the prevalence of physician-diagnosed asthma increased (5.7%-7.7%, P<0.01) while current wheeze decreased (11.7%-9.4%, P<0.01), and 34.7% reported ever wheee at ≥one occasion. Remission was 10% of which half relapsed during the study. Remission was significantly lower among sensitised children. The strongest risk factors for current asthma at ages 7-8 and 11-12 were allergic sensitisation (OR 5) and family history of asthma (OR 3). Several other significant risk factors, e.g. respiratory infections, damp house and low birth weight, had lost importance at age 11-12. At age 7-8, parental asthma was a stronger risk factor (OR 3-4) than parental rhinitis or eczema (OR 1.5-2). Sibling asthma had no independent effect. Biparental asthma had a multiplicative effect (OR 10). Maternal and paternal asthma was equally important, regardless of the child’s sex and sensitisation status.From 1996 to 2006 the prevalence of current wheeze and asthma at age 7-8 did not increase (P=0.13, P=0.18), while lifetime prevalence of ever wheeze and physician-diagnosed asthma increased (P<0.01, P=0.01). Symptoms of rhinitis and eczema were unchanged, despite 45% increase (P<0.01) in allergic sensitisation. For current asthma the adjusted population attributable fractions of sensitisation and parental asthma increased (35%-41%, 27%-45%). This was however balanced by decreased exposure to infections, maternal smoking and home dampness, resulting in stable asthma prevalence. Stratification by sex revealed that current wheeze increased in boys (P<0.01) but tended to decrease in girls (P=0.37), seemingly due to symptom persistence in males. Several asthma indices followed this pattern. The boy-to-girl ratio in exposure to all studied risk factors increased, which may explain the sex-specific prevalence trends in wheeze.Conclusions: The prevalence of current asthma and wheeze did not increase statistically significantly. However, the risk factor pattern has changed considerably since 1996, which will presumably affect the clinical features of childhood wheeze in this region. Sex-specific trends in wheeze can be explained by changes in exposure, and trends in risk factors should be explored parallel to prevalence trends.
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