| 1. |
- Brolin, Karin, et al.
(author)
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Work-related traumatic brain injury in the construction industry in Sweden and Germany
- 2021
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In: Safety Science. - : ELSEVIER. - 0925-7535 .- 1879-1042. ; 136
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Journal article (peer-reviewed)abstract
- Work-related traumatic brain injuries (wrTBIs) in the construction industry have been studied in North America but, to the best of our knowledge, not in Europe. This study analyzed sets of public data on head injuries occurring in the construction industry from the workers' compensation systems in Sweden and Germany, 2014 - 2018. The ratio of wrTBI varied from 11% to 61% of all head injuries, with higher ratios for more severe injuries. The average yearly incidence (per 100,000 FTE) of wrTBI resulting in more than four days absence from work was nine in Sweden and 117 in Germany, as compared to 22-212 in North American studies. A limitation of studies based on workers' compensation claims is that they underestimate the true burden of wrTBI. The most frequent events leading to wrTBI were falls, followed by loss of control, failure of material agents, and body movements without stress. Falls from a height caused 35% of all wrTBI with more than 14 days off work in Sweden and 57% of all new injury pensions granted in Germany. In North American studies, 52-78% of the wrTBI were caused by falls. This highlights the relevance of fall safety measures to reduce wrTBI in the construction industry, such as avoiding work at heights, use of safety nets, education, and etcetera. The energy absorption of safety helmets mainly protects the head excluding face of which 49-62% were wrTBI, indicating that helmet testing standards should evaluate protection against TBI as well as skull fractures.
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| 2. |
- Cheng, Arthur J., et al.
(author)
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Intact single muscle fibres from SOD1(G93A) amyotrophic lateral sclerosis mice display preserved specific force, fatigue resistance and training-like adaptations
- 2019
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In: Journal of Physiology. - : Cambridge University Press. - 0022-3751 .- 1469-7793. ; 597:12, s. 3133-3146
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Journal article (peer-reviewed)abstract
- Key points:How defects in muscle contractile function contribute to weakness in amyotrophic lateral sclerosis (ALS) were systematically investigated.Weakness in whole muscles from late stage SOD1G93A mice was explained by muscle atrophy as seen by reduced mass and maximal force.On the other hand, surviving single muscle fibres in late stage SOD1G93A have preserved intracellular Ca2+ handling, normal force-generating capacity and increased fatigue resistance.These intriguing findings provide a substrate for therapeutic interventions to potentiate muscular capacity and delay the progression of the ALS phenotype.Amyotrophic lateral sclerosis (ALS) is a motor neuron disease characterized by degeneration and loss of motor neurons, leading to severe muscle weakness and paralysis. The SOD1G93A mouse model of ALS displays motor neuron degeneration and a phenotype consistent with human ALS. The purpose of this study was to determine whether muscle weakness in ALS can be attributed to impaired intrinsic force generation in skeletal muscles. In the current study, motor neuron loss and decreased force were evident in whole flexor digitorum brevis (FDB) muscles of mice in the late stage of disease (125–150 days of age). However, in intact single muscle fibres, specific force, tetanic myoplasmic free [Ca2+] ([Ca2+]i), and resting [Ca2+]i remained unchanged with disease. Fibre-type distribution was maintained in late-stage SOD1G93A FDB muscles, but remaining muscle fibres displayed greater fatigue resistance compared to control and showed increased expression of myoglobin and mitochondrial respiratory chain proteins that are important determinants of fatigue resistance. Expression of genes central to both mitochondrial biogenesis and muscle atrophy where increased, suggesting that atrophic and compensatory adaptive signalling occurs simultaneously within the muscle tissue. These results support the hypothesis that muscle weakness in SOD1G93A is primarily attributed to neuromuscular degeneration and not intrinsic muscle fibre defects. In fact, surviving muscle fibres displayed maintained adaptive capacity with an exercise training-like phenotype, which suggests that compensatory mechanisms are activated that can function to delay disease progression.
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| 3. |
- Halldin, Peter, et al.
(author)
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Evaluation of blunt impact protection in a military helmet designed to offer blunt & ballistic impact protection.
- 2013
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In: Proceedings of the 1<sup>st</sup> International Conference on Helmet Performance and Design.
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Conference paper (peer-reviewed)abstract
- This paper describes both a numerical and an experimental approach to measuring the ballistic and blunt impact protection offered by military helmets. The primary purpose of military helmets is to protect users from ballistic impact but modern military helmets protect users from blunt force as well. Altering ballistic shell stiffness, lining the shell with material of different density, even separating the liner from the shell so that they can move independently all affect the transfer of stress to the head and the resulting strain experienced by the brain. The results of this study suggest that there is potential for a helmet that protects the user from both blunt and ballistic impact and can be further improved by implementing an energy absorbing sliding layer, such as the MIPS system, between the shell and the liner to mitigate the effect of oblique impacts.
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| 4. |
- Lanner, Daniel, et al.
(author)
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Evaluation of finite element human body models in lateral padded pendulum impacts to the shoulder
- 2010
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In: International Journal of Crashworthiness. - : Informa UK Limited. - 1358-8265 .- 1754-2111. ; 15:2, s. 125-142
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Journal article (peer-reviewed)abstract
- Lateral impacts are of great concern for occupant safety. In order to design side protective systems, it is of importance that the timing of the body and the head should be well predicted. Today, experimental and numerical Anthropometric Test Devices (ATDs) are used as human substitutes to predict the human kinematics. As a complement to the ATDs, numerical Human Body Models (HBMs) are used as research tools. The objective of this study is to compare the loading and kinematics of the shoulder complex in three different HBMs with published biological experiments. This study also compares the models with each other and with two numerical ATDs. The results indicate that no HBM can be used for detailed prediction of the kinematics of the human shoulder complex. However, in the presented statistical analysis, all HBMs show a better overall correlation to experiments compared to the numerical ATDs.
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| 6. |
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| 7. |
- Liu, Zhengye, et al.
(author)
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Mitochondrial NDUFA4L2 is a novel regulator of skeletal muscle mass and force
- 2021
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In: The FASEB Journal. - : John Wiley & Sons. - 0892-6638 .- 1530-6860. ; 35:12
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Journal article (peer-reviewed)abstract
- The hypoxia-inducible nuclear-encoded mitochondrial protein NADH dehydrogenase (ubiquinone) 1 alpha subcomplex, 4-like 2 (NDUFA4L2) has been demonstrated to decrease oxidative phosphorylation and production of reactive oxygen species in neonatal cardiomyocytes, brain tissue and hypoxic domains of cancer cells. Prolonged local hypoxia can negatively affect skeletal muscle size and tissue oxidative capacity. Although skeletal muscle is a mitochondrial rich, oxygen sensitive tissue, the role of NDUFA4L2 in skeletal muscle has not previously been investigated. Here we ectopically expressed NDUFA4L2 in mouse skeletal muscles using adenovirus-mediated expression and in vivo electroporation. Moreover, femoral artery ligation (FAL) was used as a model of peripheral vascular disease to induce hind limb ischemia and muscle damage. Ectopic NDUFA4L2 expression resulted in reduced mitochondrial respiration and reactive oxygen species followed by lowered AMP, ADP, ATP, and NAD(+) levels without affecting the overall protein content of the mitochondrial electron transport chain. Furthermore, ec-topically expressed NDUFA4L2 caused a similar to 20% reduction in muscle mass that resulted in weaker muscles. The loss of muscle mass was associated with increased gene expression of atrogenes MurF1 and Mul1, and apoptotic genes caspase 3 and Bax. Finally, we showed that NDUFA4L2 was induced by FAL and that the Ndufa4l2 mRNA expression correlated with the reduced capacity of the muscle to generate force after the ischemic insult. These results show, for the first time, that mitochondrial NDUFA4L2 is a novel regulator of skeletal muscle mass and force. Specifically, induced NDUFA4L2 reduces mitochondrial activity leading to lower levels of important intramuscular metabolites, including adenine nucleotides and NAD(+), which are hallmarks of mitochondrial dysfunction and hence shows that dysfunctional mitochondrial activity may drive muscle wasting.
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| 8. |
- Pipkorn, Bengt, 1963, et al.
(author)
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Mathematical human body models in side impacts- A validation study with particular emphasis on the torso and shoulder and their influence on head and neck motion
- 2008
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In: Int. Res. Counc. Biomech. Inj. - Int. IRCOBI Conf. Biomech. Inj., Proc.. - 9783033015807 ; , s. 99-114, s. 99-114
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Conference paper (peer-reviewed)abstract
- The ability of three mathematical human body models to predict previously published human responses in two different side impact loading configurations was evaluated using an objective rating method. In particular the kinematics of the shoulder, T1 and head were evaluated. The human body models evaluated were THUMS, HUMOS 2 and the GM model. The impact loading configurations used were pendulum impact tests and sled tests. In the pendulum configurations, the closest correlation to the published responses was shown by THUMS followed by the GM model. In the sled configuration, closest correlation to the published responses was shown by HUMOS 2 followed by THUMS. According to the objective rating method the published responses in the pendulum configuration were predicted by all human body models. The published responses in the sled configuration were predicted by HUMOS 2 and THUMS.
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| 9. |
- von Holst, Hans, et al.
(author)
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White Shark Protein Metabolism may be a Model to Improve the Outcome of Cytotoxic Brain Tissue Edema and Cognitive Deficiency after Traumatic Brain Injury and Stroke
- 2018
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In: Journal of Neurology and Neurobiology. - : Sci Forschen, Inc.. - 2379-7150. ; 4:2
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Journal article (peer-reviewed)abstract
- Increased intracellular water content defined as cytotoxic brain tissue edema is a serious secondary clinical complication to traumatic brain injury (TBI) and stroke and without knowledge to the etiology. Recently a hypothesis to the nervous tissue edema was presented suggesting that external dynamic and internal mechanical static impact forces caused protein unfolding resulting in an increased brain tissue water content. The hypothesis was confirmed by computer simulation tests. In this laboratory study we further evaluated the hypothesis by using the mature protein laminin LN521 upon the effects of both dynamic as well as static impact forces, respectively. Laminin was chosen as a representative protein due to it´s general and abundance presence in the cells. The treated laminin solutions were then analyzed with denatured electrophoresis and Electron Microscopy showing aggregation and fragmentation of the laminin structures. The present results confirm earlier hypothesis and computer simulation suggesting for the first time that dynamic impact force in an accident and increased mechanical static force in stroke unfold mature proteins having the potential to increase the intracellular water content defined as cytotoxic brain tissue edema. The clinical condition resembles the phenomenon when elasmobranchs including white sharks prevent their cells from too high hydrostatic pressure in the deep sea. Thus, the present laboratory study results and knowledge from marine physics may be considered to improve the clinical treatment and outcome of TBI and stroke patients.
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| 10. |
- Yamada, Takashi, et al.
(author)
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Nitrosative modifications of the Ca2+ release complex and actin underlie arthritis-induced muscle weakness.
- 2015
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In: Annals of the Rheumatic Diseases. - : BMJ. - 1468-2060 .- 0003-4967. ; 74:10, s. 1907-1914
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Journal article (peer-reviewed)abstract
- Skeletal muscle weakness is a prominent clinical feature in patients with rheumatoid arthritis (RA), but the underlying mechanism(s) is unknown. Here we investigate the mechanisms behind arthritis-induced skeletal muscle weakness with special focus on the role of nitrosative stress on intracellular Ca(2+) handling and specific force production.
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