| 1. |
- Niu, Xiaorui, et al.
(författare)
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On the sensitivity of seasonal and diurnal precipitation to cumulus parameterization over CORDEX-EA-II
- 2020
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Ingår i: Climate Dynamics. - : Springer Science and Business Media LLC. - 0930-7575 .- 1432-0894. ; 54, s. 373-393
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Tidskriftsartikel (refereegranskat)abstract
- The ability of the Weather Research and Forecasting (WRF) model in simulating the seasonal and diurnal cycles of rainfall over the Coordinated Regional Climate Downscaling Experiment East Asia Phase II (CORDEX-EA-II) domain is validated against the Tropical Rainfall Measuring Mission (TRMM) datasets. A focus is placed on the role of convective parameterization (CP) schemes. A set of numerical experiments at a 25km resolution for 1998–2009, using six different CPs, is performed to evaluate the physics-dependency of simulation results. All CPs simulate realistic summer mean precipitation and its northward propagation, with the best performance in the Simplified Arakawa-Schubert (SAS). The biases in the seasonal evolution of rainfall are related to the deficiency in simulated low-level winds and the northward propagation of the cyclonic vorticity. The simulated earlier peak time in other CPs is delayed by about 1–2h by the Kain-Fritsch with a modified trigger function (KFMT), although this scheme shows a disadvantage in the magnitude. The performance of different CPs in simulating diurnal rainfall cycles is dependent on regions, and none of them performs better than the others for all the sub-regions. The initiation of simulated convection is weakly physics-dependent. However, the timing and magnitude of stratiform precipitation differ among the six experiments. A furtheranalysisshows that the dry biases over the lower Yangtze River basin are a result of the weakened southwesterly water vapor transport, while the excessive afternoon rainfall in the Kain-Fritsch (KF) simulation is attributed to the largest positive perturbation in the lower level atmosphere, especially the enhanced vertical transport of humidity.
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| 2. |
- Niu, Xiaorui, et al.
(författare)
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The performance of CORDEX-EA-II simulations in simulating seasonal temperature and elevation-dependent warming over the Tibetan Plateau
- 2021
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Ingår i: Climate Dynamics. - : Springer Science and Business Media LLC. - 0930-7575 .- 1432-0894. ; 57, s. 1135-1153
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Tidskriftsartikel (refereegranskat)abstract
- To explore the driving mechanisms of elevation-dependent warming (EDW) over the Tibetan Plateau (TP), the output from a suite of numerical experiments with different cumulus parameterization schemes (CPs) under the Coordinated Regional Climate Downscaling Experiments-East Asia (CORDEX-EA-II) project is examined. Results show that all experiments can broadly capture the observed temperature distributions over the TP with consistent cold biases, and the spread in temperature simulations commonly increases with elevation with the maximum located around 4000-5000 m. Such disagreements among the temperature simulations could to a large extent be explained by their spreads in the surface albedo feedback (SAF). All the experiments reproduce the observed EDW below 5000 m in winter but fail to capture the observed EDW above 4500 m in spring. Further analysis suggests that the simulated EDW during winter is mainly caused by the SAF, and the clear-sky downward longwave radiation (LWclr) plays a secondary role in shaping EDW. The models' inability in simulating EDW during spring is closely related to the SAF and the surface cloud radiative forcing (CRFs). Furthermore, the magnitude and structure of the simulated EDW are sensitive to the choice of CPs. Different CPs generate diverse snow cover fractions, which can modulate the simulated SAF and its effect on EDW. Also, the CPs show great influence on the LWclr via altering the low-level air temperature. Additionally, the mechanism for different temperature changes among the experiments varies with altitudes during summer and autumn, as the diverse temperature changes appear to be caused by the LWclr for the low altitudes while by the SAF for the middle-high altitudes.
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| 3. |
- Nordquist, Jenny, et al.
(författare)
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Transcription factors in muscle atrophy caused by blocked neuromuscular transmission and muscle unloading in rats
- 2007
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Ingår i: Molecular Medicine. - 1076-1551 .- 1528-3658. ; 13:9-10, s. 461-470
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Tidskriftsartikel (refereegranskat)abstract
- The muscle wasting associated with long-term intensive care unit (ICU) treatment has a negative effect on muscle function resulting in prolonged periods of rehabilitation and a decreased quality of life. To identify mechanisms behind this form of muscle wasting, we have used a rat model designed to mimic the conditions in an ICU. Rats were pharmacologically paralyzed with a postsynaptic blocker of neuromuscular transmission, and mechanically ventilated for one to two weeks, thereby unloading the limb muscles. Transcription factors were analyzed for cellular localization and nuclear concentration in the fast-twitch muscle extensor digitorum longus (EDL) and in the slow-twitch soleus. Significant muscle wasting and upregulation of mRNA for the ubiquitin ligases MAFbx and MuRF1 followed the treatment. The IκB family–member Bcl-3 displayed a concomitant decrease in concentration, suggesting altered κB controlled gene expression, although NFκB p65 was not significantly affected. The nuclear levels of the glucocorticoid receptor (GR) and the thyroid receptor α1 (TRα1) were altered and also suggested as potential mediators of the MAFbx- and MuRF1-induction in the absence of induced Foxo1. We believe that this model, and the strategy of quantifying nuclear proteins, will provide a valuable tool for further, more detailed, analyses of the muscle wasting occurring in patients kept on a mechanical ventilator.
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| 4. |
- Norman, Holly, et al.
(författare)
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Impact of post-synaptic block of neuromuscular transmission, muscle unloading and mechanical ventilation on skeletal muscle protein and mRNA expression
- 2006
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Ingår i: Pflügers Archiv. - : Springer Science and Business Media LLC. - 0031-6768 .- 1432-2013. ; 453:1, s. 53-66
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Tidskriftsartikel (refereegranskat)abstract
- To analyse mechanisms of muscle wasting in intensive care unit patients, we developed an experimental model where rats were pharmacologically paralysed by post-synaptic block of neuromuscular transmission (NMB) and mechanically ventilated for 9 2 days. Specific interest was focused on the effects on protein and mRNA expression of sarcomeric proteins, i.e., myosin heavy chain (MyHC), actin, myosin-binding protein C (MyBP-C) and myosin-binding protein H (MyBP-H) in fast- and slow-twitch limb, respiratory and masticatory muscles. Muscle-specific differences were observed in response to NMB at both the protein and mRNA levels. At the protein level, a decreased MyHC-to-actin ratio was observed in all muscles excluding the diaphragm, whereas at the mRNA level a decreased expression of the dominating MyHC isoform(s) was observed in the hind limb and intercostal muscles, but not in the diaphragm and masseter muscles. MyBP-C mRNA expression was decreased in the limb muscles, but it otherwise remained unaffected. MyBP-H conversely increased in all muscles. Furthermore, we found myofibrillar protein and mRNA expression to be affected differently when comparing NMB; animals with peripherally denervated (DEN) ambulatory rats. We report that NMB; has both a larger and different impact on muscle, at the protein and mRNA levels, than DEN has.
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| 5. |
- Ochala, Julien, et al.
(författare)
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Preferential skeletal muscle myosin loss in response to mechanical silencing in a novel rat intensive care unit model : underlying mechanisms
- 2011
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Ingår i: Journal of Physiology. - : Wiley. - 0022-3751 .- 1469-7793. ; 589:8, s. 2007-2026
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Tidskriftsartikel (refereegranskat)abstract
- Non-technical summary Wasting and severely impaired function of skeletal muscle is frequently observed in critically ill intensive care unit (ICU) patients, with negative consequences for recovery and quality of life. An experimental rat ICU model has been used to study the mechanisms underlying this unique wasting condition in neuromuscularly blocked and mechanically ventilated animals at durations varying between 6 h and 2 weeks. The complete 'mechanical silencing' of skeletal muscle (removal of both weight bearing and activation) resulted in a specific myopathy frequently observed in ICU patients and characterized by a preferential loss of the motor protein myosin. A highly complex and coordinated protein synthesis and degradation system was observed in the time-resolved analyses. It is suggested the 'mechanical silencing' of skeletal muscle is a dominating factor triggering the specific myopathy associated with the ICU intervention, and strongly supporting the importance of interventions counteracting the complete unloading in ICU patients.The muscle wasting and impaired muscle function in critically ill intensive care unit (ICU) patients delay recovery from the primary disease, and have debilitating consequences that can persist for years after hospital discharge. It is likely that, in addition to pernicious effects of the primary disease, the basic life support procedures of long-term ICU treatment contribute directly to the progressive impairment of muscle function. This study aims at improving our understanding of the mechanisms underlying muscle wasting in ICU patients by using a unique experimental rat ICU model where animals are mechanically ventilated, sedated and pharmacologically paralysed for duration varying between 6 h and 14 days. Results show that the ICU intervention induces a phenotype resembling the severe muscle wasting and paralysis associated with the acute quadriplegic myopathy (AQM) observed in ICU patients, i.e. a preferential loss of myosin, transcriptional down-regulation of myosin synthesis, muscle atrophy and a dramatic decrease in muscle fibre force generation capacity. Detailed analyses of protein degradation pathways show that the ubiquitin proteasome pathway is highly involved in this process. A sequential change in localisation of muscle-specific RING finger proteins 1/2 (MuRF1/2) observed during the experimental period is suggested to play an instrumental role in both transcriptional regulation and protein degradation. We propose that, for those critically ill patients who develop AQM, complete mechanical silencing, due to pharmacological paralysis or sedation, is a critical factor underlying the preferential loss of the molecular motor protein myosin that leads to impaired muscle function or persisting paralysis.
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