Inclination Measurement of Human Movement Using a 3-D Accelerometer With Autocalibration

In the medical field, accelerometers are often used for measuring inclination of body segments and activity of daily living (ADL) because they are small and require little power. A drawback of using accelerometers is the poor quality of inclination estimate for movements with large accelerations. This paper describes the design and performance of a Kalman filter to estimate inclination from the signals of a triaxial accelerometer. This design is based on assumptions concerning the frequency content of the acceleration of the movement that is measured, the knowledge that the magnitude of the gravity is 1 g and taking into account a fluctuating sensor offset. It is shown that for measuring trunk and pelvis inclination during the functional three-dimensional activity of stacking crates, the inclination error that is made is approximately 2/spl deg/ root-mean square. This is nearly twice as accurate as compared to current methods based on low-pass filtering of accelerometer signals

Inertial and magnetic sensing of human movement near ferromagnetic materials

This paper describes a Kalman filter design to estimate orientation of human body segments by fusing gyroscope, accelerometer and magnetometer signals. Ferromagnetic materials near the sensor disturb the local magnetic field and therefore the orientation estimation. The magnetic disturbance can be detected by looking at the total magnetic density and a magnetic disturbance vector can be calculated. Results show the capability of this filter to correct for magnetic disturbances

Compensation of Magnetic Disturbances Improves Inertial and Magnetic Sensing of Human Body Segment Orientation

This paper describes a complementary Kalman filter design to estimate orientation of human body segments by fusing gyroscope, accelerometer, and magnetometer signals from miniature sensors. Ferromagnetic materials or other magnetic fields near the sensor module disturb the local earth magnetic field and, therefore, the orientation estimation, which impedes many (ambulatory) applications. In the filter, the gyroscope bias error, orientation error, and magnetic disturbance error are estimated. The filter was tested under quasi-static and dynamic conditions with ferromagnetic materials close to the sensor module. The quasi-static experiments implied static positions and rotations around the three axes. In the dynamic experiments, three-dimensional rotations were performed near a metal tool case. The orientation estimated by the filter was compared with the orientation obtained with an optical reference system Vicon. Results show accurate and drift-free orientation estimates. The compensation results in a significant difference (p<0.01) between the orientation estimates with compensation of magnetic disturbances in comparison to no compensation or only gyroscopes. The average static error was 1.4/spl deg/ (standard deviation 0.4) in the magnetically disturbed experiments. The dynamic error was 2.6/spl deg/ root means square

Prenatal smoke exposure induces persistent Cyp2a5 methylation and increases nicotine metabolism in the liver of neonatal and adult male offspring

Prenatal smoke exposure (PSE) is a risk factor for nicotine dependence. One susceptibility gene for nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine and nicotine clearance in the liver. Higher activity of the CYP2A6 enzyme is associated with nicotine dependence, but no research has addressed the PSE effects on the CYP2A6 gene or its mouse homologue Cyp2a5. We hypothesized that PSE affects Cyp2a5 promoter methylation, Cyp2a5 mRNA levels, and nicotine metabolism in offspring. We used a smoke-exposed pregnant mouse model. RNA, DNA, and microsomal protein were isolated from liver tissue of foetal, neonatal, and adult offspring. Enzyme activity, Cyp2a5 mRNA levels, and Cyp2a5 methylation status of six CpG sites within the promoter region were analysed via HPLC, RT-PCR, and bisulphite pyrosequencing. Our data show that PSE induced higher cotinine levels in livers of male neonatal and adult offspring compared to controls. PSE-induced cotinine levels in neonates correlated with Cyp2a5 mRNA expression and promoter methylation at CpG-7 and CpG+45. PSE increased methylation in almost all CpG sites in foetal offspring, and this effect persisted at CpG-74 in male neonatal and adult offspring. Our results indicate that male offspring of mothers which were exposed to cigarette smoke during pregnancy have a higher hepatic nicotine metabolism, which could be regulated by DNA methylation. Given the detected persistence into adulthood, extrapolation to the human situation suggests that sons born from smoking mothers could be more susceptible to nicotine dependence later in life

Postnatal Smoke Exposure Further Increases the Hepatic Nicotine Metabolism in Prenatally Smoke Exposed Male Offspring and Is Linked with Aberrant Cyp2a5 Methylation

Prenatal smoke exposure (PreSE) is a risk factor for nicotine dependence, which is further enhanced by postnatal smoke exposure (PostSE). One susceptibility gene to nicotine dependence is Cytochrome P450 (CYP) 2A6, an enzyme responsible for the conversion of nicotine to cotinine in the liver. Higher CYP2A6 activity is associated with nicotine dependence and could be regulated through DNA methylation. In this study we investigated whether PostSE further impaired PreSE-induced effects on nicotine metabolism, along with Cyp2a5, orthologue of CYP2A6, mRNA expression and DNA methylation. Using a mouse model where prenatally smoke-exposed adult offspring were exposed to cigarette smoke for 3 months, enzyme activity, mRNA levels, and promoter methylation of hepatic Cyp2a5 were evaluated. We found that in male offspring, PostSE increased PreSE-induced cotinine levels and Cyp2a5 mRNA expression. In addition, both PostSE and PreSE changed Cyp2a5 DNA methylation in male groups. PreSE however decreased cotinine levels whereas it had no effect on Cyp2a5 mRNA expression or methylation. These adverse outcomes of PreSE and PostSE were most prominent in males. When considered in the context of the human health aspects, the combined effect of prenatal and adolescent smoke exposure could lead to an accelerated risk for nicotine dependence later in life.</p

Mouse Protocadherin-1 gene expression is regulated by cigarette smoke exposure in vivo

Protocadherin-1 (PCDH1) is a novel susceptibility gene for airway hyperresponsiveness, first identified in families exposed to cigarette smoke and is expressed in bronchial epithelial cells. Here, we asked how mouse Pcdh1 expression is regulated in lung structural cells in vivo under physiological conditions, and in both short-term cigarette smoke exposure models characterized by airway inflammation and hyperresponsiveness and chronic cigarette smoke exposure models. Pcdh1 gene-structure was investigated by Rapid Amplification of cDNA Ends. Pcdh1 mRNA and protein expression was investigated by qRT-PCR, western blotting using isoform-specific antibodies. We observed 87% conservation of the Pcdh1 nucleotide sequence, and 96% conservation of the Pcdh1 protein sequence between men and mice. We identified a novel Pcdh1 isoform encoding only the intracellular signalling motifs. Cigarette smoke exposure for 4 consecutive days markedly reduced Pcdh1 mRNA expression in lung tissue (3 to 4-fold), while neutrophilia and airway hyperresponsiveness was induced. Moreover, Pcdh1 mRNA expression in lung tissue was reduced already 6 hours after an acute cigarette-smoke exposure in mice. Chronic exposure to cigarette smoke induced loss of Pcdh1 protein in lung tissue after 2 months, while Pcdh1 protein levels were no longer reduced after 9 months of cigarette smoke exposure. We conclude that Pcdh1 is highly homologous to human PCDH1, encodes two transmembrane proteins and one intracellular protein, and is regulated by cigarette smoke exposure in vivo

Susceptibility to chronic mucus hypersecretion, a genome wide association study

Background: Chronic mucus hypersecretion (CMH) is associated with an increased frequency of respiratory infections, excess lung function decline, and increased hospitalisation and mortality rates in the general population. It is associated with smoking, but it is unknown why only a minority of smokers develops CMH. A plausible explanation for this phenomenon is a predisposing genetic constitution. Therefore, we performed a genome wide association (GWA) study of CMH in Caucasian populations. Methods: GWA analysis was performed in the NELSON-study using the Illumina 610 array, followed by replication and meta-analysis in 11 additional cohorts. In total 2,704 subjects with, and 7,624 subjects without CMH were included, all current or former heavy smokers (≥20 pack-years). Additional studies were performed to test the functional relevance of the most significant single nucleotide polymorphism (SNP). Results: A strong association with CMH, consistent across all cohorts, was observed with rs6577641 (p = 4.25x10-6, OR = 1.17), located in intron 9 of the special AT-rich sequence-binding protein 1 locus (SATB1) on chromosome 3. The risk allele (G) was associated with higher mRNA expression of SATB1 (4.3x10 -9) in lung tissue. Presence of CMH was associated with increased SATB1 mRNA expression in bronchial biopsies from COPD patients. SATB1 expression was induced during differentiation of primary human bronchial epithelial cells in culture. Conclusions: Our findings, that SNP rs6577641 is associated with CMH in multiple cohorts and is a cis-eQTL for SATB1, together with our additional observation that SATB1 expression increases during epithelial differentiation provide suggestive evidence that SATB1 is a gene that affects CMH

Inertial and magnetic sensing of human movement near ferromagnetic materials

Abstrac

Robust Real-Time Tracking by Fusing Measurements from Inertial and Vision Sensors

The problem of estimating and predicting position and orientation (pose) of a camera is approached by fusing measurements from inertial sensors (accelerometers and rate gyroscopes) and vision. The sensor fusion approach described in this contribution is based on non-linear filtering of these complementary sensors. This way, accurate and robust pose estimates are available for the primary purpose of augmented reality applications, but with the secondary effect of reducing computation time and improving the performance in vision processing. A real-time implementation of a multi-rate extended Kalman filter is described, using a dynamic model with 22 states, where 12.5 Hz correspondences from vision and 100 Hz inertial measurements are processed. An example where an industrial robot is used to move the sensor unit is presented. The advantage with this configuration is that it provides ground truth for the pose, allowing for objective performance evaluation. The results show that we obtain an absolute accuracy of 2 cm in position and 1° in orientation