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Jan Rozman - One of the best experts on this subject based on the ideXlab platform.
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Long-term proteasomal inhibition in transgenic mice by UBB^+1 expression results in dysfunction of central Respiration Control reminiscent of brainstem neuropathology in Alzheimer patients
Acta Neuropathologica, 2012Co-Authors: Martin Irmler, Romina J.g. Gentier, Frank J. A. Dennissen, Holger Schulz, Ines Bolle, Sabine M. Hölter, Magdalena Kallnik, Jing Jun Cheng, Martin Klingenspor, Jan RozmanAbstract:Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin–proteasome system (UPS). In tauopathies and polyglutamine diseases, a mutant form of ubiquitin B (UBB^+1) accumulates in disease-specific aggregates. UBB^+1 mRNA is generated at low levels in vivo during transcription from the ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB^+1 accumulation, we used a UBB^+1 expressing transgenic mouse line that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB^+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wild-type littermate mice. Accordingly, UBB^+1 was strongly expressed in brainstem regions of transgenic mice Controlling Respiration. These regions included, e.g., the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nucleus. In addition, UBB^+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented Controls. We conclude that long-term UPS inhibition due to UBB^+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB^+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.
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long term proteasomal inhibition in transgenic mice by ubb 1 expression results in dysfunction of central Respiration Control reminiscent of brainstem neuropathology in alzheimer patients
Acta Neuropathologica, 2012Co-Authors: Martin Irmler, Romina J.g. Gentier, Frank J. A. Dennissen, Holger Schulz, Ines Bolle, Sabine M. Hölter, Magdalena Kallnik, Jing Jun Cheng, Martin Klingenspor, Jan RozmanAbstract:Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin–proteasome system (UPS). In tauopathies and polyglutamine diseases, a mutant form of ubiquitin B (UBB+1) accumulates in disease-specific aggregates. UBB+1 mRNA is generated at low levels in vivo during transcription from the ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB+1 accumulation, we used a UBB+1 expressing transgenic mouse line that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wild-type littermate mice. Accordingly, UBB+1 was strongly expressed in brainstem regions of transgenic mice Controlling Respiration. These regions included, e.g., the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nucleus. In addition, UBB+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented Controls. We conclude that long-term UPS inhibition due to UBB+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.
Yaoqin Xie - One of the best experts on this subject based on the ideXlab platform.
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Coupled Temporal Fluctuation and Global Signal Synchronization of Spontaneous Brain Activity in Hypnosis for Respiration Control: An fMRI Study
Neuroscience, 2020Co-Authors: Liu Yanjun, Li Rongmao, Yaoqin XieAbstract:Abstract Hypnosis is a psychological technology proved to be effective in respiratory motion Control, which is essential to reduce radiation dose during radiotherapy. This study explored the neural mechanisms and cognitive neuroscience of hypnosis for Respiration Control by functional magnetic resonance imaging with a within-subject design of 15 healthy volunteers in rest state (RS) and hypnosis state (HS). Temporal fluctuation and signal synchronization of brain activity were employed to investigate the altered physiological performance in hypnosis. The altered correlations between temporal fluctuation and signal synchronization were examined within large scale of intrinsic networks which were identified by seed-wise functional connectivity. As a result, hypnosis was observed with increased activity in the right calcarine, bilateral fusiform gyrus and left middle temporal gyrus, and with decreased activity in the left cerebellum posterior lobe (inferior semilunar lobule part). Compared to RS, enhanced positive correlations were observed between temporal fluctuation and signal synchronization in HS. Most importantly, coupled correlation was observed between temporal fluctuation and global signal synchronization within the identified intrinsic networks (R = 0.3843, p > 0.05 in RS; R = 0.6212, p
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su f j 139 amplitude of low frequency fluctuation alff and regional homogeneity reho study of the Respiration motion Control byhypnosis
Medical Physics, 2016Co-Authors: Yanjun Liu, Yaoqin XieAbstract:Purpose: Respiration Control by hypnosis is a method in reducing the detriment to the healthy organs or organizations for patients during radiotherapy, especially for lung and abdomen cancer (Fig.1). It's hypothesized that there exists alterations neurological brain activity during the hypnosis state of respiratory motion Control in comparison with resting state. Methods: Thirteen healthy volunteers were organized to participate in a hypnosis experiment that consisted of two sectional scans of functional magnetic resonance imaging (fMRI), rest state condition (RSC) scanning and hypnosis state condition (HSC) scanning. In addition, the coronal section of the lung was scanned during both conditions. During the hypnosis scan, the volunteers were under the hypnotists’ guidance to keep peace and stable Respiration. To evaluate the altered physiological performance of hypnosis in the respiratory Control, three conventional indicators ALFF/fALFF (0.01–0.08Hz) and ReHo, were applied to identify the difference. Results: Compared with RSC, HSC showed significant (p<0.05) higher ReHo in superior temporal gyrus, middle temporal gyrus, frontal lobe, middle occipital gyrus, parietal lobe, cerebellum anterior Lobe and lingual gyrus, and left brainstem (Fig.2). While significant lower ReHo in middle frontal gyrus, superior frontal gyrus, inferior semi-lunar lobule, sub-lobar and limbic lobe (Fig.2). As for the ALFF results, significant higher value of HSC was observed in superior temporal gyrus, middle temporal gyrus, middle occipital gyrus, middle occipital gyrus, cerebellum anterior lobe, lingual gyrus, sub-lobar, limbic lobe, and lower in cerebellum posterior lobe, inferior semi-lunar lobule, inferior parietal lobule right middle frontal gyrus, cerebellar tonsil (Fig.3). The results of fALFF were similar to ALFF (Fig.4). The above results demonstrated that most significant regions of brain were uniform between ReHo and ALFF/fALFF. Conclusion: Hypnosis is a new psychological and helpful technology for Respiration Control. This study provides new insights of neurological brain activity during hypnosis of Respiration Control. This work is supported by grants from Guangdong Innovative Research Team Program of China (Grant No. 2011S013), National 863 Programs of China (Grant Nos. 2012AA02A604 and 2015AA043203), the National High-tech R&D Program for Young Scientists by the Ministry of Science and Technology of China (Grant No. 2015AA020917)
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SU-F-J-139: Amplitude of Low Frequency Fluctuation(ALFF) and Regional Homogeneity (ReHo) Study of the Respiration Motion Control Byhypnosis
Medical Physics, 2016Co-Authors: Liu Yanjun, Li Rongmao, Yaoqin XieAbstract:Purpose: Respiration Control by hypnosis is a method in reducing the detriment to the healthy organs or organizations for patients during radiotherapy, especially for lung and abdomen cancer (Fig.1). It's hypothesized that there exists alterations neurological brain activity during the hypnosis state of respiratory motion Control in comparison with resting state. Methods: Thirteen healthy volunteers were organized to participate in a hypnosis experiment that consisted of two sectional scans of functional magnetic resonance imaging (fMRI), rest state condition (RSC) scanning and hypnosis state condition (HSC) scanning. In addition, the coronal section of the lung was scanned during both conditions. During the hypnosis scan, the volunteers were under the hypnotists’ guidance to keep peace and stable Respiration. To evaluate the altered physiological performance of hypnosis in the respiratory Control, three conventional indicators ALFF/fALFF (0.01–0.08Hz) and ReHo, were applied to identify the difference. Results: Compared with RSC, HSC showed significant (p
Johan H. Huijsing - One of the best experts on this subject based on the ideXlab platform.
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Design of integrated thermal flow sensors using thermal sigma—delta modulation
Sensors and Actuators A: Physical, 1996Co-Authors: Huibert-jan Verhoeven, Johan H. HuijsingAbstract:Abstract Large-scale use of thermal flow sensors in consumer electronics, medical and automotive applications is seriously hampered by the limited response speed and the non-standardized format of the output signal of conventional thermal flow sensors. A thermal sigma—delta-based feedback system can be used to provide an optimal interface for a wide variety of new as well as existing thermal flow sensors. Advantages of this system are an improved response time of the sensor system and an inherent analog-to-digital conversion of the measurement signal. Realized sensor implementations range from sensors for flow Control in consumer electronics, Respiration Control, to industrial mass-flow Control.
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Design Of Integrated Thermal Flow Sensors Using Thermal Sigma-delta Modulation
Proceedings of the International Solid-State Sensors and Actuators Conference - TRANSDUCERS '95, 1Co-Authors: Huibert-jan Verhoeven, Johan H. HuijsingAbstract:Large scale introduction of thermal flow sensors in consumer electronics, medical and automotive applications is seriously hampered by the limited response speed and the non-standardized format of the output signal of conventional thermal flow sensors. A thermal sigma-delta based feedback system can be used to provide an optimal interface for a wide variety of new as well as existing thermal flow sensors. Advantages of this system are an improved response time of the sensor system and an inherent analog to digital conversion of the measurement signal. Realized sensor implementations range from flow Control in consumer electronics, Respiration Control, to industrial mass flow Control.
Martin Irmler - One of the best experts on this subject based on the ideXlab platform.
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Long-term proteasomal inhibition in transgenic mice by UBB^+1 expression results in dysfunction of central Respiration Control reminiscent of brainstem neuropathology in Alzheimer patients
Acta Neuropathologica, 2012Co-Authors: Martin Irmler, Romina J.g. Gentier, Frank J. A. Dennissen, Holger Schulz, Ines Bolle, Sabine M. Hölter, Magdalena Kallnik, Jing Jun Cheng, Martin Klingenspor, Jan RozmanAbstract:Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin–proteasome system (UPS). In tauopathies and polyglutamine diseases, a mutant form of ubiquitin B (UBB^+1) accumulates in disease-specific aggregates. UBB^+1 mRNA is generated at low levels in vivo during transcription from the ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB^+1 accumulation, we used a UBB^+1 expressing transgenic mouse line that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB^+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wild-type littermate mice. Accordingly, UBB^+1 was strongly expressed in brainstem regions of transgenic mice Controlling Respiration. These regions included, e.g., the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nucleus. In addition, UBB^+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented Controls. We conclude that long-term UPS inhibition due to UBB^+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB^+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.
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long term proteasomal inhibition in transgenic mice by ubb 1 expression results in dysfunction of central Respiration Control reminiscent of brainstem neuropathology in alzheimer patients
Acta Neuropathologica, 2012Co-Authors: Martin Irmler, Romina J.g. Gentier, Frank J. A. Dennissen, Holger Schulz, Ines Bolle, Sabine M. Hölter, Magdalena Kallnik, Jing Jun Cheng, Martin Klingenspor, Jan RozmanAbstract:Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin–proteasome system (UPS). In tauopathies and polyglutamine diseases, a mutant form of ubiquitin B (UBB+1) accumulates in disease-specific aggregates. UBB+1 mRNA is generated at low levels in vivo during transcription from the ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB+1 accumulation, we used a UBB+1 expressing transgenic mouse line that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wild-type littermate mice. Accordingly, UBB+1 was strongly expressed in brainstem regions of transgenic mice Controlling Respiration. These regions included, e.g., the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nucleus. In addition, UBB+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented Controls. We conclude that long-term UPS inhibition due to UBB+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.
Martin Klingenspor - One of the best experts on this subject based on the ideXlab platform.
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Long-term proteasomal inhibition in transgenic mice by UBB^+1 expression results in dysfunction of central Respiration Control reminiscent of brainstem neuropathology in Alzheimer patients
Acta Neuropathologica, 2012Co-Authors: Martin Irmler, Romina J.g. Gentier, Frank J. A. Dennissen, Holger Schulz, Ines Bolle, Sabine M. Hölter, Magdalena Kallnik, Jing Jun Cheng, Martin Klingenspor, Jan RozmanAbstract:Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin–proteasome system (UPS). In tauopathies and polyglutamine diseases, a mutant form of ubiquitin B (UBB^+1) accumulates in disease-specific aggregates. UBB^+1 mRNA is generated at low levels in vivo during transcription from the ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB^+1 accumulation, we used a UBB^+1 expressing transgenic mouse line that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB^+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wild-type littermate mice. Accordingly, UBB^+1 was strongly expressed in brainstem regions of transgenic mice Controlling Respiration. These regions included, e.g., the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nucleus. In addition, UBB^+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented Controls. We conclude that long-term UPS inhibition due to UBB^+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB^+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.
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long term proteasomal inhibition in transgenic mice by ubb 1 expression results in dysfunction of central Respiration Control reminiscent of brainstem neuropathology in alzheimer patients
Acta Neuropathologica, 2012Co-Authors: Martin Irmler, Romina J.g. Gentier, Frank J. A. Dennissen, Holger Schulz, Ines Bolle, Sabine M. Hölter, Magdalena Kallnik, Jing Jun Cheng, Martin Klingenspor, Jan RozmanAbstract:Aging and neurodegeneration are often accompanied by a functionally impaired ubiquitin–proteasome system (UPS). In tauopathies and polyglutamine diseases, a mutant form of ubiquitin B (UBB+1) accumulates in disease-specific aggregates. UBB+1 mRNA is generated at low levels in vivo during transcription from the ubiquitin B locus by molecular misreading. The resulting mutant protein has been shown to inhibit proteasome function. To elucidate causative effects and neuropathological consequences of UBB+1 accumulation, we used a UBB+1 expressing transgenic mouse line that models UPS inhibition in neurons and exhibits behavioral phenotypes reminiscent of Alzheimer’s disease (AD). In order to reveal affected organs and functions, young and aged UBB+1 transgenic mice were comprehensively phenotyped for more than 240 parameters. This revealed unexpected changes in spontaneous breathing patterns and an altered response to hypoxic conditions. Our findings point to a central dysfunction of respiratory regulation in transgenic mice in comparison to wild-type littermate mice. Accordingly, UBB+1 was strongly expressed in brainstem regions of transgenic mice Controlling Respiration. These regions included, e.g., the medial part of the nucleus of the tractus solitarius and the lateral subdivisions of the parabrachial nucleus. In addition, UBB+1 was also strongly expressed in these anatomical structures of AD patients (Braak stage #6) and was not expressed in non-demented Controls. We conclude that long-term UPS inhibition due to UBB+1 expression causes central breathing dysfunction in a transgenic mouse model of AD. The UBB+1 expression pattern in humans is consistent with the contribution of bronchopneumonia as a cause of death in AD patients.