Kinematic and electromyographic analyses of a karate punch

The aims of this study were: (i) to present the kinematic and electromyographic patterns of the choku-zuki punch performed by 18 experienced karatekas from the Portuguese team, and (ii) to compare it with the execution of 19 participants without any karate experience. The kinematic and electromyographic data were collected from the arm and forearm during the execution of the specific punch. A two-way analysis of variance (ANOVA) was used with significant level set at p ? 0.05. We found that the kinematic and neuromuscular activity in this punch occurs within 400 ms. Muscle activities and kinematic analysis presented a sequence of activation bracing a near-distal end, with the arm muscles showing greater intensity of activation than muscles in the forearm. In the skill performance, the arm, flexion and internal rotation, and the forearm extension and pronation movements were executed with smaller amplitude in the karate group. Based on the results of this study, the two groups’ presented distinct kinematic and electromyographic patterns during the performance of the choku-zuki punch.     

Pathogenic LRRK2 mutations do not alter gene expression in cell model systems or human brain tissue

Point mutations in LRRK2 cause autosomal dominant Parkinson's disease. Despite extensive efforts to determine the mechanism of cell death in patients with LRRK2 mutations, the aetiology of LRRK2 PD is not well understood. To examine possible alterations in gene expression linked to the presence of LRRK2 mutations, we carried out a case versus control analysis of global gene expression in three systems: fibroblasts isolated from LRRK2 mutation carriers and healthy, non-mutation carrying controls; brain tissue from G2019S mutation carriers and controls; and HEK293 inducible LRRK2 wild type and mutant cell lines. No significant alteration in gene expression was found in these systems following correction for multiple testing. These data suggest that any alterations in basal gene expression in fibroblasts or cell lines containing mutations in LRRK2 are likely to be quantitatively small. This work suggests that LRRK2 is unlikely to play a direct role in modulation of gene expression, although it remains possible that this protein can influence mRNA expression under pathogenic cicumstances.     

Quantification of Superoxide Radical in the Brain of Rats with Experimentally Induced Obstructive Jaundice

The study aimed to directly measure in vivo superoxide radical (O₂⁻) a direct indicator of oxidative stress, in the brain of rats with experimentally induced obstructive jaundice by employing a new quantitative ultrasensitive fluorescent assay requiring minimum sample. O₂⁻ anion is specific for dihydroethidine (DHE) and upon reaction gives a characteristic product, namely 2-OH-ethidium. Ten male rats underwent laparotomy and were divided into two groups: I, sham operated and II bile duct ligation. Ten days later, following injection with DHE (a O₂⁻ trap), all animals were killed and samples from cerebral cortex, midbrain and cerebellum were removed for analysis. It was shown that compared to group I, in group II the O₂⁻ was increased by 67% in the cerebral cortex and by 37% in the midbrain as a consequence of experimental obstructive jaundice, while its levels were unaffected in the cerebellum. The data in this experimental obstructive jaundice model imply a region-specific increase of O₂⁻ formation rate, being higher in cerebral cortex, less so in the midbrain and not at all in cerebellum.     

Mutations in LRRK2 linked to Parkinson disease sequester Rab8a to damaged lysosomes and regulate transferrin-mediated iron uptake in microglia

Mutations in leucine-rich repeat kinase 2 (LRRK2) cause autosomal dominant Parkinson disease (PD), while polymorphic LRRK2 variants are associated with sporadic PD. PD-linked mutations increase LRRK2 kinase activity and induce neurotoxicity in vitro and in vivo. The small GTPase Rab8a is a LRRK2 kinase substrate and is involved in receptor-mediated recycling and endocytic trafficking of transferrin, but the effect of PD-linked LRRK2 mutations on the function of Rab8a is poorly understood. Here, we show that gain-of-function mutations in LRRK2 induce sequestration of endogenous Rab8a to lysosomes in overexpression cell models, while pharmacological inhibition of LRRK2 kinase activity reverses this phenotype. Furthermore, we show that LRRK2 mutations drive association of endocytosed transferrin with Rab8a-positive lysosomes. LRRK2 has been nominated as an integral part of cellular responses downstream of proinflammatory signals and is activated in microglia in postmortem PD tissue. Here, we show that iPSC-derived microglia from patients carrying the most common LRRK2 mutation, G2019S, mistraffic transferrin to lysosomes proximal to the nucleus in proinflammatory conditions. Furthermore, G2019S knock-in mice show a significant increase in iron deposition in microglia following intrastriatal LPS injection compared to wild-type mice, accompanied by striatal accumulation of ferritin. Our data support a role of LRRK2 in modulating iron uptake and storage in response to proinflammatory stimuli in microglia.

Brain iron deposition is a feature of Parkinson’s disease pathology, but how this contributes to neurodegeneration is unclear. This study show that Parkinson’s disease-linked mutations in LRRK2 cause aberrant brain iron accumulation in vivo and iron dyshomeostasis in vitro, supporting a role of LRRK2 in modulating iron uptake and storage in response to proinflammatory stimuli in microglia.     

Does methocarbamol affect fatigue markers in the low-back electromyogram?

Many low-back patients undergo electromyography (EMG)-based evaluations of muscle performance but present to the clinic after being prescribed muscle relaxants. The question that needed to be addressed was, do centrally acting muscle relaxants (methocarbamol; Robaxin®) affect the EMG spectral indices of muscle fatigue that are often used to assess muscle performance. Participants performed an isometric spine extension protocol involving a 30 s fatigue exertion trial, then 1 min rest, and finally a 10 s long repeat exertion trial, at a 60% maximum voluntary contraction (MVC) level of exertion. Seven men were tested on two separate days (approximately 3–7 days apart), one day while medicated (six doses) with Robaxin and on another while not medicated. Specifically, the following parameters were studied in the bilateral multifidus (L5), lower erector spinae (L3) and upper erector spinae (T9): the slope of median power frequencies (MPFs) over the duration of the trial and the initial y-intercept of the MPF. The results generally suggest that methocarbamol (Robaxin) does not have any significant affect on the EMG median power frequency of the extensors during a fatiguing contraction followed by a repeat exertion, at least in normal people (one exception was observed—one side of multifidus at L5). However, given that this appears to be the first study of its kind, and that a relatively small number of subjects were used in this study, further investigation is needed to make a definitive conclusion about the effects of this drug on the several features of the electromyogram, over a broad spectrum of the clinical population performing a wider variety of tasks.     

Age-Associated Alterations of the Mitochondrial Genome

Age-associated alterations of the mitochondrial genome occur in several different species; however, their physiological relevance remains unclear. The age-associated changes of mitochondrial DNA (mtDNA) include nucleotide point mutations and modifications, as well as deletions. In this review, we summarize the current literature on age-associated mtDNA mutations and deletions and comment on their abundance. A clear need exists for a more thorough evaluation of the total damage to the mitochondrial genome that accumulates in aged tissues. © 1997 Elsevier Science Inc.     

Volume conduction models for surface EMG; confrontation with measurements

Volume conduction models are used to describe and explain recorded motor unit potentials (MUPs). So far it has remained unclear which factors have to be taken into account in a volume conduction model. In the present study, five different models are confronted with measured MUP distributions over the skin surface above the m. biceps brachii generated by MUs at different depths and recorded by small surface electrodes. All model simulations include fibres of finite length. The models differ in the size of the volume conductor (finite/infinite), the number of different layers (1, 2 or 3) and the conductivities of these layers (representing muscle, subcutaneous fat and skin). All measured and simulated MUPs contain a mainly negative propagating wave followed by a positive wave simultaneously present at all electrode positions. The magnitude of the different MUP components relative to each other and as a function of motor unit (MU) and electrode position differ between the models studied and the measurements. All simulated MUPs changed faster with observation distance than the measured MUPs. The three-layer model, in which muscle tissue was surrounded by a subcutaneous fat layer and by a layer of skin resulted in MUPs closest to the measured MUPs.     

Effect of severity of knee osteoarthritis on the variability of gait parameters

Gait analysis has provided important information concerning gait patterns and variability of gait in patients with knee osteoarthritis (OA) of varying severity. The objective of this study was to clarify how the variability of gait parameters is influenced by the severity of knee OA. Gait analysis was performed at three different controlled walking speeds in three groups of subjects with varying degrees of knee OA (20 healthy subjects with no OA and 90 patients with moderate or severe OA). The variability of gait parameters was characterized by the coefficient of variance (CV) of spatial-temporal parameters, as well as by the mean coefficient variance (MeanCV) of angular parameters. Based on our results, we conclude that the complexity of gait decreases if the walking speed differs from the self-selected speed. In patients with knee OA, the decreased variability of angular parameters on the affected side represents decreased joint flexibility. This leads to decreased consistency in movements of the lower limbs from stride-to-stride, as shown by increased variability of spatial-temporal parameters. Decreased joint flexibility and consistency of movement can be associated with decreased complexity of movement. Other joints of the kinetic chain, such as joints of the non-affected side and the pelvis, play an important role in compensation and adaptation of step-by step motion and in the ability of secure gait. Results suggest that the variability of gait associated with knee osteoarthritis is gender-dependent. During rehabilitation, particular attention must be paid to improving gait stability and proprioception and gender differences should be taken into account.     

In vivo motion transmission in the inactive gastrocnemius medialis muscle-tendon unit during ankle and knee joint rotation.

The purposes of this study were: (a) to quantify the influence of passive ankle and knee joint angular displacement on the estimated mechanical and architectural properties of the gastrocnemius medialis (GM) muscle-tendon unit, and (b) to determine the strain distribution of separate structures (tendon, aponeurosis and fascicle) during passive lengthening of the GM muscle-tendon unit at rest. Ten male subjects participated in the study. The passive ankle and knee joint movements were performed on an isokinetic dynamometer. The kinematics of the left leg were recorded using the Vicon 624 system with 8 cameras. Two ultrasound probes were used to examine the elongation of the tendon, the aponeurosis, the fascicles and the angle of pennation of the GM. To calculate the elongation of the GM muscle-tendon unit the Achilles tendon path was reconstructed using a series of small reflective markers. The results show that the passive ankle joint angular displacement has a considerable influence on the elongation of the tendinous and architectural structures of the GM muscle-tendon unit. In contrast, the influence of knee joint angular displacement on the GM fascicle length and pennation angle becomes relevant only at knee angles greater than 144 degrees . The contribution of the tendon to the elongation of the GM muscle-tendon unit at rest is relevant because of its greater resting length in comparison to the resting length of the GM fascicles. The results indicate the existence of slackness in the inactive GM muscle-tendon unit between 121 degrees and 107 degrees ankle angle and between 65 degrees and 144 degrees knee angle.