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- Alamdari, Nima, et al.
(author)
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Loss of muscle strength during sepsis is in part regulated by glucocorticoids and is associated with reduced muscle fiber stiffness
- 2012
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In: American Journal of Physiology. Regulatory Integrative and Comparative Physiology. - : American Physiological Society. - 0363-6119 .- 1522-1490. ; 303:10, s. R1090-R1099
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Journal article (peer-reviewed)abstract
- Sepsis is associated with impaired muscle function but the role of glucocorticoids in sepsis-induced muscle weakness is not known. We tested the role of glucocorticoids in sepsis-induced muscle weakness by treating septic rats with the glucocorticoid receptor antagonist RU38486. In addition, normal rats were treated with dexamethasone to further examine the role of glucocorticoids in the regulation of muscle strength. Sepsis was induced in rats by cecal ligation and puncture and muscle force generation (peak twitch and tetanic tension) was determined in lower extremity muscles. In other experiments, absolute and specific force as well as stiffness (reflecting the function of actomyosin cross-bridges) were determined in isolated skinned muscle fibers from control and septic rats. Sepsis and treatment with dexamethasone resulted in reduced maximal twitch and tetanic force in intact isolated extensor digitorum longus muscles. The absolute and specific maximal force in isolated muscle fibers was reduced during sepsis together with decreased fiber stiffness. These effects of sepsis were blunted (but not abolished) by RU38486. The results suggest that muscle weakness during sepsis is at least in part regulated by glucocorticoids and reflects loss of contractility at the cellular (individual muscle fiber) level. In addition, the results suggest that reduced function of the cross-bridges between actin and myosin (documented as reduced muscle fiber stiffness) may be involved in sepsis-induced muscle weakness. An increased understanding of mechanisms involved in loss of muscle strength will be important for the development of new treatment strategies in patients with this debilitating consequence of sepsis.
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- Cristea, Alexander, et al.
(author)
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Effects of aging and gender on the spatial organization of nuclei in single human skeletal muscle cells
- 2010
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In: Aging Cell. - : Wiley. - 1474-9718 .- 1474-9726. ; 9:5, s. 685-697
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Journal article (peer-reviewed)abstract
- The skeletal muscle fibre is a syncitium where each myonucleus regulates the gene products in a finite volume of the cytoplasm, i.e., the myonuclear domain (MND). We analysed aging- and gender-related effects on myonuclei organization and the MND size in single muscle fibres from six young (21–31 years) and nine old men (72–96 years), and from six young (24–32 years) and nine old women (65–96 years), using a novel image analysis algorithm applied to confocal images. Muscle fibres were classified according to myosin heavy chain (MyHC) isoform expression. Our image analysis algorithm was effective in determining the spatial organization of myonuclei and the distribution of individual MNDs along the single fibre segments. Significant linear relations were observed between MND size and fibre size, irrespective age, gender and MyHC isoform expression. The spatial organization of individual myonuclei, calculated as the distribution of nearest neighbour distances in 3D, and MND size were affected in old age, but changes were dependent on MyHC isoform expression. In type I muscle fibres, average NN-values were lower and showed an increased variability in old age, reflecting an aggregation of myonuclei in old age. Average MND size did not change in old age, but there was an increased MND size variability. In type IIa fibres, average NN-values and MND sizes were lower in old age, reflecting the smaller size of these muscle fibres in old age. It is suggested that these changes have a significant impact on protein synthesis and degradation during the aging process.
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4. |
- Khan, Rizwan, et al.
(author)
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A High Dynamic Range Imaging Method for Short Exposure Multiview Images
- 2023
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In: Pattern Recognition. - : Elsevier BV. - 0031-3203 .- 1873-5142. ; 137
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Journal article (peer-reviewed)abstract
- The restoration and enhancement of multiview low dynamic range (MVLDR) images captured in low lighting conditions is a great challenge. The disparity maps are hardly reliable in practical, real-world scenarios and suffers from holes and artifacts due to large baseline and angle deviation among multi-ple cameras in low lighting conditions. Furthermore, multiple images with some additional information (e.g., ISO/exposure time, etc.) are required for the radiance map and poses the additional challenges of deghosting to encounter motion artifacts. In this paper, we proposed a method to reconstruct multiview high dynamic range (MVHDR) images from MVLDR images without relying on disparity maps. We de-tect and accurately match the feature points among the involved input views and gather the brightness information from the neighboring viewpoints to optimize an image restoration function based on input exposure gain to finally generate MVHDR images. Our method is very reliable and suitable for a wide baseline among sparse cameras. The proposed method requires only one image per viewpoint without any additional information and outperforms others.
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5. |
- Khan, Rizwan, et al.
(author)
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Dental image enhancement network for early diagnosis of oral dental disease
- 2023
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In: Scientific Reports. - : Springer Nature. - 2045-2322. ; 13:1
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Journal article (peer-reviewed)abstract
- Intelligent robotics and expert system applications in dentistry suffer from identification and detection problems due to the non-uniform brightness and low contrast in the captured images. Moreover, during the diagnostic process, exposure of sensitive facial parts to ionizing radiations (e.g., X-Rays) has several disadvantages and provides a limited angle for the view of vision. Capturing high-quality medical images with advanced digital devices is challenging, and processing these images distorts the contrast and visual quality. It curtails the performance of potential intelligent and expert systems and disincentives the early diagnosis of oral and dental diseases. The traditional enhancement methods are designed for specific conditions, and network-based methods rely on large-scale datasets with limited adaptability towards varying conditions. This paper proposed a novel and adaptive dental image enhancement strategy based on a small dataset and proposed a paired branch Denticle-Edification network (Ded-Net). The input dental images are decomposed into reflection and illumination in a multilayer Denticle network (De-Net). The subsequent enhancement operations are performed to remove the hidden degradation of reflection and illumination. The adaptive illumination consistency is maintained through the Edification network (Ed-Net). The network is regularized following the decomposition congruity of the input data and provides user-specific freedom of adaptability towards desired contrast levels. The experimental results demonstrate that the proposed method improves visibility and contrast and preserves the edges and boundaries of the low-contrast input images. It proves that the proposed method is suitable for intelligent and expert system applications for future dental imaging.
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- Liu, Jing-Xia, et al.
(author)
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Myonuclear domain size and myosin isoform expression in muscle fibres from mammals representing a 100 000-fold difference in body size
- 2009
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In: Experimental Physiology. - : Wiley. - 0958-0670 .- 1469-445X. ; 94:1, s. 117-129
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Journal article (peer-reviewed)abstract
- This comparative study of myonuclear domain (MND) size in mammalian species representing a 100 000-fold difference in body mass, ranging from 25 g to 2500 kg, was undertaken to improve our understanding of myonuclear organization in skeletal muscle fibres. Myonuclear domain size was calculated from three-dimensional reconstructions in a total of 235 single muscle fibre segments at a fixed sarcomere length. Irrespective of species, the largest MND size was observed in muscle fibres expressing fast myosin heavy chain (MyHC) isoforms, but in the two smallest mammalian species studied (mouse and rat), MND size was not larger in the fast-twitch fibres expressing the IIA MyHC isofom than in the slow-twitch type I fibres. In the larger mammals, the type I fibres always had the smallest average MND size, but contrary to mouse and rat muscles, type IIA fibres had lower mitochondrial enzyme activities than type I fibres. Myonuclear domain size was highly dependent on body mass in the two muscle fibre types expressed in all species, i.e. types I and IIA. Myonuclear domain size increased in muscle fibres expressing both the β/slow (type I; r= 0.84, P < 0.001) and the fast IIA MyHC isoform (r= 0.90; P < 0.001). Thus, MND size scales with body size and is highly dependent on muscle fibre type, independent of species. However, myosin isoform expression is not the sole protein determining MND size, and other protein systems, such as mitochondrial proteins, may be equally or more important determinants of MND size.
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- Naseer, Amtul, et al.
(author)
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The robust catalysts (Ni1-x-Mo-x/doped ceria and Zn1-x-Mo-x/doped ceria, x=0.1 and 0.3) for efficient natural gas reforming in solid oxide fuel cells
- 2020
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In: Electrochimica Acta. - : Elsevier BV. - 0013-4686. ; 361
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Journal article (peer-reviewed)abstract
- Nickel is a promising catalyst in Solid Oxide fuel cell (SOFC) due to its electrocatalytic performance, however, the practical utilization of Ni-based materials is hindered by the undesirable carbon deposition during methane decomposition. Herein, molybdenum is incorporated into the Ni- and Zn-based cermets (Ni1-x-Mo-x/GDC and Zn1-x-Mo-x/GDC, x = 0.1 and 0.3) to enhance electrocatalytic properties and avoid the carbon deposition during cell operation. The desired composites are synthesized by the impregnation method and adopted as anode in SOFCs. The catalytic activity for methane oxidation has been significantly improved due to the introduction on Mo, which hindered the carbon deposition due to higher graphitization and abundant active sites accessible to fuel. The detailed Raman spectroscopy and conductivity analysis revealed that addition of Mo reduced the amount of deposited carbon and enhanced the electrical conductivity. By using natural gas, as a fuel, the as-prepared Mo-doped Ni-GDC rendered a maximum power density of 690 mW cm(-2) at 600 degrees C. It is worth mentioning that the achieved stable power density is one of the best in existing literature. The current study presents a novel strategy to improve the catalytic behavior of electrode materials and demonstrate the optimal performance at low operating temperature. (C) 2020 Elsevier Ltd. All rights reserved.
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8. |
- Ochala, Julien, et al.
(author)
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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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In: Journal of Physiology. - : Wiley. - 0022-3751 .- 1469-7793. ; 589:8, s. 2007-2026
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Journal article (peer-reviewed)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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10. |
- Qaisar, Rizwan, 1982-, et al.
(author)
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Contractile function and myonuclear organization in single fibers from monozygotic female twins discordant for hormone replacement therapy
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Other publication (other academic/artistic)abstract
- Ageing is associated with a decline in muscle mass and strength leading to increased physical dependency in old age. Post-menopausal women experience a greater decline than men of similar age due to a dramatic decrease in sex hormones production. We recruited six monozygous female twin pairs (55 – 59 years old) discordant for postmenopausal hormone replacement therapy (HRT use = 7.8 ± 4.3 years) to investigate the association of HRT with the cytoplasmic domain supported by individual myonuclei (myonuclear domain size, MND) together with specific force at the single fiber level. MyHC isoform content of the fibers was determined using silver-stained SDS-PAGE. HRT use was associated with a significantly smaller (~27%; p < 0.05) mean MND size in muscle fibers expressing the type I but not the IIa MyHC isoform. An increase in specific force was recorded in the HRT user group both in muscle fibers expressing type I (~27%; p < 0.05) and type IIa (~23%; p < 0.05) MyHC isoforms. These positive effects on specific force were fiber-type dependent, i.e., in fast-twitch muscle fibers the increased specific force was primarily caused by an increased force per cross-bridge while slow-twitch fibers relied on both an increase in both number and force per cross-bridge. HRT use had no effect on fiber cross-sectional area (CSA), velocity of unloaded shortening (V0) and relative proportion of MyHC isoforms. In conclusion, HRT has significant positive effects on both regulation of muscle contraction and myonuclei organization in menopausal women, but the response is fiber-type specific.
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