47 research outputs found

    Development of a Method to Compensate for Signal Quality Variations in Repeated Auditory Event-Related Potential Recordings

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    Reliable measurements are mandatory in clinically relevant auditory event-related potential (AERP)-based tools and applications. The comparability of the results gets worse as a result of variations in the remaining measurement error. A potential method is studied that allows optimization of the length of the recording session according to the concurrent quality of the recorded data. In this way, the sufficiency of the trials can be better guaranteed, which enables control of the remaining measurement error. The suggested method is based on monitoring the signal-to-noise ratio (SNR) and remaining measurement error which are compared to predefined threshold values. The SNR test is well defined, but the criterion for the measurement error test still requires further empirical testing in practice. According to the results, the reproducibility of average AERPs in repeated experiments is improved in comparison to a case where the number of recorded trials is constant. The test-retest reliability is not significantly changed on average but the between-subject variation in the value is reduced by 33–35%. The optimization of the number of trials also prevents excessive recordings which might be of practical interest especially in the clinical context. The efficiency of the method may be further increased by implementing online tools that improve data consistency

    Effect of slow-release FSH on embryo recovery in dairy cows

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    AETE, Bath, UK, 8-9 September, 2017201

    Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors : modeling the function of an inactivating receptor mutation

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    Follicle-stimulating hormone (FSH) is crucial in the development and regulation of reproductive functions. The actions of human FSH and its receptor (FSHR) and mutations therein have mainly been studied using in vivo models, primary cells, cancer cells and cell lines ectopically expressing the FSHR. To allow studies of endogenous FSHR function in vitro, we differentiated FSHR-expressing cells from human pluripotent stem cells. FSH stimulation of the wild-type (WT), but not the inactivating Finnish founder mutant (A189V) receptor, activated the canonical cyclic adenosine monophosphate (cAMP)-dependent signaling pathway and downstream mediators. To investigate protein-protein interaction partners of FSHR at resting state and upon FSH stimulation, we expressed FSHR in HEK293 cells followed by affinity purification mass spectrometry analyses. We found 19 specific high-confidence interacting proteins for WT FSHR and 14 for A189V FSHR, several of which have been linked to infertility. Interestingly, while only WT FSHR interacted with FSH, insulin-like growth factor 1 receptor (IGF1R), for example, interacted with both WT and A189V FSHR upon FSH stimulation. In conclusion, our protocol allows detailed studies of FSH action and disease modeling in human cells endogenously expressing FSHR.Peer reviewe

    Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors : modeling the function of an inactivating receptor mutation

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    Follicle-stimulating hormone (FSH) is crucial in the development and regulation of reproductive functions. The actions of human FSH and its receptor (FSHR) and mutations therein have mainly been studied using in vivo models, primary cells, cancer cells and cell lines ectopically expressing the FSHR. To allow studies of endogenous FSHR function in vitro, we differentiated FSHR-expressing cells from human pluripotent stem cells. FSH stimulation of the wild-type (WT), but not the inactivating Finnish founder mutant (A189V) receptor, activated the canonical cyclic adenosine monophosphate (cAMP)-dependent signaling pathway and downstream mediators. To investigate protein-protein interaction partners of FSHR at resting state and upon FSH stimulation, we expressed FSHR in HEK293 cells followed by affinity purification mass spectrometry analyses. We found 19 specific high-confidence interacting proteins for WT FSHR and 14 for A189V FSHR, several of which have been linked to infertility. Interestingly, while only WT FSHR interacted with FSH, insulin-like growth factor 1 receptor (IGF1R), for example, interacted with both WT and A189V FSHR upon FSH stimulation. In conclusion, our protocol allows detailed studies of FSH action and disease modeling in human cells endogenously expressing FSHR.Peer reviewe

    Human pluripotent stem cell-derived cells endogenously expressing follicle-stimulating hormone receptors: modeling the function of an inactivating receptor mutation

    Get PDF
    Follicle-stimulating hormone (FSH) is crucial in the development and regulation of reproductive functions. The actions of human FSH and its receptor (FSHR) and mutations therein have mainly been studied using in vivo models, primary cells, cancer cells and cell lines ectopically expressing the FSHR. To allow studies of endogenous FSHR function in vitro, we differentiated FSHR-expressing cells from human pluripotent stem cells. FSH stimulation of the wild-type (WT), but not the inactivating Finnish founder mutant (A189V) receptor, activated the canonical cyclic adenosine monophosphate (cAMP)-dependent signaling pathway and downstream mediators. To investigate protein-protein interaction partners of FSHR at resting state and upon FSH stimulation, we expressed FSHR in HEK293 cells followed by affinity purification mass spectrometry analyses. We found 19 specific high-confidence interacting proteins for WT FSHR and 14 for A189V FSHR, several of which have been linked to infertility. Interestingly, while only WT FSHR interacted with FSH, insulin-like growth factor 1 receptor (IGF1R), for example, interacted with both WT and A189V FSHR upon FSH stimulation. In conclusion, our protocol allows detailed studies of FSH action and disease modeling in human cells endogenously expressing FSHR

    Site fertility drives temporal turnover of vegetation at high latitudes

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    Experimental evidence shows that site fertility is a key modulator underlying plant community changes under climate change. Communities on fertile sites, with species having fast dynamics, have been found to react more strongly to climate change than communities on infertile sites with slow dynamics. However, it is still unclear whether this generally applies to high-latitude plant communities in natural environments at broad spatial scales. We tested a hypothesis that vegetation of fertile sites experiences greater changes over several decades and thus would be more responsive under contemporary climate change compared to infertile sites that are expected to show more resistance. We resurveyed understorey communities (vascular plants, bryophytes, and lichens) of four infertile and four fertile forest sites along a latitudinal bioclimatic gradient. Sites had remained outside direct human disturbance. We analyzed the magnitude of temporal community turnover, changes in the abundances of plant morphological groups and strategy classes, and changes in species diversity. In agreement with our hypothesis, temporal turnover of communities was consistently greater on fertile sites compared to infertile sites. However, our results suggest that the larger turnover of fertile communities is not primarily related to the direct effects of climatic warming. Furthermore, community changes in both fertile and infertile sites showed remarkable variation in terms of shares of plant functional groups and strategy classes and measures of species diversity. This further emphasizes the essential role of baseline environmental conditions and nonclimatic drivers underlying vegetation changes. Our results show that site fertility is a key determinant of the overall rate of high-latitude vegetation changes but the composition of plant communities in different ecological contexts is variously impacted by nonclimatic drivers over time.Peer reviewe

    Clinical patterns in asthma based on proximal and distal airway nitric oxide categories

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    <p>Abstract</p> <p>Background</p> <p>The exhaled nitric oxide (eNO) signal is a marker of inflammation, and can be partitioned into proximal [J'aw<sub>NO </sub>(nl/s), maximum airway flux] and distal contributions [CA<sub>NO </sub>(ppb), distal airway/alveolar NO concentration]. We hypothesized that J'aw<sub>NO </sub>and CA<sub>NO </sub>are selectively elevated in asthmatics, permitting identification of four inflammatory categories with distinct clinical features.</p> <p>Methods</p> <p>In 200 consecutive children with asthma, and 21 non-asthmatic, non-atopic controls, we measured baseline spirometry, bronchodilator response, asthma control and morbidity, atopic status, use of inhaled corticosteroids, and eNO at multiple flows (50, 100, and 200 ml/s) in a cross-sectional study design. A trumpet-shaped axial diffusion model of NO exchange was used to characterize J'aw<sub>NO </sub>and CA<sub>NO</sub>.</p> <p>Results</p> <p>J'aw<sub>NO </sub>was not correlated with CA<sub>NO</sub>, and thus asthmatic subjects were grouped into four eNO categories based on upper limit thresholds of non-asthmatics for J'aw<sub>NO </sub>(≄ 1.5 nl/s) and CA<sub>NO </sub>(≄ 2.3 ppb): Type I (normal J'aw<sub>NO </sub>and CA<sub>NO</sub>), Type II (elevated J'aw<sub>NO </sub>and normal CA<sub>NO</sub>), Type III (elevated J'aw<sub>NO </sub>and CA<sub>NO</sub>) and Type IV (normal J'aw<sub>NO </sub>and elevated CA<sub>NO</sub>). The rate of inhaled corticosteroid use (lowest in Type III) and atopy (highest in Type II) varied significantly amongst the categories influencing J'aw<sub>NO</sub>, but was not related to CA<sub>NO</sub>, asthma control or morbidity. All categories demonstrated normal to near-normal baseline spirometry; however, only eNO categories with increased CA<sub>NO </sub>(III and IV) had significantly worse asthma control and morbidity when compared to categories I and II.</p> <p>Conclusions</p> <p>J'aw<sub>NO </sub>and CA<sub>NO </sub>reveal inflammatory categories in children with asthma that have distinct clinical features including sensitivity to inhaled corticosteroids and atopy. Only categories with increase CA<sub>NO </sub>were related to poor asthma control and morbidity independent of baseline spirometry, bronchodilator response, atopic status, or use of inhaled corticosteroids.</p
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