Gotowe bibliografie tematyczne / Muscle rigidity

Gotowa bibliografia na temat „Muscle rigidity”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 30 lipca 2024

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Artykuły w czasopismach na temat "Muscle rigidity"

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Matsuki, Yuka. "Muscle Rigidity Associated with Pregabalin". Pain Physician 3;15, nr 3;5 (14.05.2012): E350. http://dx.doi.org/10.36076/ppj.2012/15/e350.

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Jenkins, J. G. "Masseter muscle rigidity after vecuronium". European Journal of Anaesthesiology 16, nr 2 (luty 1999): 137–39. http://dx.doi.org/10.1097/00003643-199902000-00011.

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Smith, H. L., i G. R. Park. "Muscle rigidity in meningococcal meningitis". Anaesthesia 48, nr 12 (22.02.2007): 1103–4. http://dx.doi.org/10.1111/j.1365-2044.1993.tb07544.x.

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Manners, J. M. "Muscle rigidity in miningococcal meningitis". Anaesthesia 49, nr 6 (czerwiec 1994): 544. http://dx.doi.org/10.1111/j.1365-2044.1994.tb03537.x.

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Jenkins, J. G. "Masseter muscle rigidity after vecuronium". European Journal of Anaesthesiology 16, nr 2 (luty 1999): 137–39. http://dx.doi.org/10.1046/j.1365-2346.1999.00448.x.

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Markelov, Grigory I. "To the symptomatology of trembling paralysis". Neurology Bulletin XVI, nr 2 (14.03.2022): 237–48. http://dx.doi.org/10.17816/nb101118.

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The main feature in the clinical picture of trembling paralysis must be recognized as increased rigidity of the muscles, muscle stiffness. This latter imposes on the patient that peculiar imprint, which often makes it possible to recognize this disease by appearance alone. Giving in various cases one or another fluctuation in distribution and intensity, this increased rigidity of the muscles is the most characteristic symptom of Parkinson's disease.
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Vankova, Miriana E., Matthew B. Weinger, Dong-Yi Chen, J. Brian Bronson, Valerie Motis i George F. Koob. "Role Central Mu, Delta-1, and Kappa-1 Opioid Receptors in Opioid-induced Muscle Rigidity in the Rat". Anesthesiology 85, nr 3 (1.09.1996): 574–83. http://dx.doi.org/10.1097/00000542-199609000-00017.

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Background Opioids appear to produce their physiologic effects by binding to at least three types of opioid receptors, the mu (mu), delta (delta), and kappa (kappa) receptors. Muscle rigidity occurs after administration of supra-analgesic doses of potent mu-preferring agonists like alfentanil. The role of different supraspinal opioid receptors in this rigidity has been addressed only recently. To elucidate the contribution of central mu, delta, and kappa receptors to muscle rigidity, the effects of intracerebroventricularly administered opioid receptor-selective agonists and antagonists on alfentanil-induced muscle rigidity were examined in rats. Methods Rats in which chronic intracerebroventricular cannulae had been implanted received an intracerebroventricular infusion of either saline or a mu (D-Ala2,N-Me-Phe4-Gly5-olenkephalin; DAMGO), delta(1) (D-Pen2,D-Pen5-enkephalin; DPDPE), or kappa(1) (trans-(+/-)-3,4-dichloro-N-methyl-N-(2-(1-pyrrolidinyl)- cyclohexyl)-benzene-acetamide methane sulfonate; U50,488H) opioid agonist. Ten minutes later, they received either saline or the mu-agonist alfentanil subcutaneously. Muscle rigidity was assessed using hindlimb electromyographic activity. Different groups of animals were pretreated with an intracerebroventricular infusion of either saline or a mu (D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2; CTAP), delta (naltrindole), or kappa(1) (norbinaltorphimine) opioid antagonist before administration of either saline or a selective intracerebroventricular agonist. Results The mu agonist DAMGO alone dose-dependently induced muscle rigidity. This effect was antagonized by pretreatment with the mu-selective antagonist CTAP. Neither DPDPE nor U50,488H, when administered alone, affected muscle tone. However, both the delta(1) and kappa(1) agonists dose-dependently attenuated alfentanil-induced rigidity. This antagonism of alfentanil rigidity was abolished after pretreatment with the delta (naltrindole) and kappa(1) (nor-binaltorphimine) antagonists, respectively. Conclusions The present data demonstrate that whereas systemic opiate-induced muscle rigidity is primarily due to the activation of central mu receptors, supraspinal delta(1) and kappa(1) receptors may attenuate this effect. This finding is consistent with previous demonstrations of functional interactions between different central opioid receptor populations in other opiate effects, and could have important pharmacotherapeutic implications.
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Khan, Bashir A., Mazhar U. Khan, Md Umar Majid i Md Mohib Hussain. "Masseter Muscle Rigidity Following Succinylcholine Administration". Journal of Contemporary Medicine and Dentistry 2, nr 2 (20.08.2014): 64–68. http://dx.doi.org/10.18049/jcmad/229a14.

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&NA;. "Benzodiazepines attenuate alfentanil-induced muscle rigidity". Inpharma Weekly &NA;, nr 972 (luty 1995): 13. http://dx.doi.org/10.2165/00128413-199509720-00028.

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Mayumi, Takahisa, Naoki Matsumiya, Satoshi Fujita i Shuji Dohi. "Diazepam prevents fentanyl-induced muscle rigidity". Journal of Anesthesia 4, nr 1 (styczeń 1990): 82–84. http://dx.doi.org/10.1007/s0054000040082.

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Rozprawy doktorskie na temat "Muscle rigidity"

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張劍強 i Kim-keung Cheung. "The effect of hamstring stretching technique on hamstring flexibility and isokinetic strength". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B3125715X.

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Cheung, Kim-keung. "The effect of hamstring stretching technique on hamstring flexibility and isokinetic strength /". Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23425374.

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Saidi, Azadeh. "Robotic Evaluation Of Rigidity In Parkinson's As A Function Of Speed-Comparison To Clinical Scales". VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd_retro/147.

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Rigidity is one of the cardinal symptoms in Parkinson's disease, along with Bradykinesia, tremor and postural instability. Rigidity in PD has been understudied, but its pathophysiological basis remains unclear. Various types of neurophysiological and biomechanical approach have been developed in order to investigate the neural control of muscle tone. A common approach is to observe the sensitivity of muscle resistance in response to stretch velocity or displacement [Kamper, Rea, He]. A recent study on elbow flexors in patients with spasticity and rigidity showed a velocity dependent increase in reactive torque in both groups [Lee H, et al). Even though this Study shows a correlation between elbow flexors and velocity, it doesn't discuss the role of elbow extensors. We studied the rigidity response in the elbow of both arms to different speed movements in 12 patients suffering from Parkinson's disease ON or OFF medication. The purpose of this study was to look at both elbow flexion and extension and show that quantitative measures of rigidity and movement disorders in subjects with Parkinson's disease correlate with the currently used clinical evaluations and also find the correlation between velocity and both elbow extension and flexion at the same time. Elbow was flexed and extended by means of a robotic arm,under four different speeds. The resistance to movement was recorded with a torque sensor and EMG of two elbow muscles; Biceps and Triceps; was recorded while the subjects were attempting to relax. The patients were also examined by physicians and their elbow rigidity and muscle tone and Parkinson's disease stage was evaluated and a Universal score in the categories of UPDRS, MMSE, and CAPIT was assigned for each arm of each individual. In the end we will argue that there is a very strong correlation between speed and elbow Extension and Flexion, muscle activity and the rigidity presented in each arm. We will also present the correlation between the robotic torque measurement and the clinical scores given to each subject.
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Dowler, Elizabeth Safety Science Faculty of Science UNSW. "Effects of neutral posture on muscle tension, pain and performance for computer users". Awarded by:University of New South Wales, 1998. http://handle.unsw.edu.au/1959.4/37113.

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This study focuses on developing a new approach to seated work positions. It was conducted on 67 office workers who use the Video Display Terminal (VDT) as a major function of their working day. Muscle tension was measured by surface electromyography when subjects were asked to adopt four selected working postures. Pain was measured before and after ergonomic intervention on the Nordic scale, which was modified for this study. Performance was measured on timed typing tests. A psychosocial questionnaire was used to determine influences of job demands, and a diagnostic assessment was performed to determine symptoms and pre-existing musculoskeletal conditions. Furniture was used to place subjects in desired positions during the clinical testing sessions and the extended intervention period. The chair seat pan was adjusted to a forward tilt to promote a lordotic curve of the low back, resulting in an erect upper body and upright head position. The desk and keyboard were adjusted to the proper height for each worker. A neutral wrist position was obtained by lowering and tilting the keyboard away from the user. Results revealed muscle tension scores in the upper trapezius and forearm extensors were significantly reduced when the workers were placed with the head in a midline position, with forward-tilting seating and with use of a negative sloping keyboard tray. Subjects reported low pain scores at pretest so no changes were noted after intervention. Loss of control over job elements, lack of job satisfaction, and fear of job loss were related to an increase in muscle tension. Only fear of job loss correlated to increased pain levels. There was no relationship between any of the job demand factors and performance.
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Graham, Daniel Joseph. "The Long Term Effects of Short-Wave Diathermy and Long-Duration Static Stretch on Hamstring Flexibility". Diss., CLICK HERE for online access, 2004. http://contentdm.lib.byu.edu/ETD/image/etd624.pdf.

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Stecco, Antonio. "Ialuronidasi per la rigidità muscolare nella spasticità Hyaluronidase for muscle stiffness in spasticity". Doctoral thesis, Università degli studi di Padova, 2016. http://hdl.handle.net/11577/3424238.

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Background: Spasticity is a common neurological impairment after injury to the central nervous system, but the neural and biomechanical contributions to it are still poorly understood. Histopathological studies have demonstrated a generalized increase in extracellular connective tissue in spastic muscles, which can decrease its compliance, and reduce the threshold for stimulation of the spindle receptors. Here we propose and provide preliminary evidence for a novel hypothesis for exacerbation of spasticity in an immobilized limb - the hyaluronan hypothesis. We hypothesize that the extracellular connective tissue, which is composed chiefly of hyaluronan, becomes hyper-viscous and stiff in an immobilized limb due to its non-Newtonian properties. Methods: In this case series, we assessed the safety, tolerability, and efficacy of human recombinant hyaluronidase, which hydrolyzes hyaluronan, in combination with saline in restoring tissue compliance. Twenty-one individuals, with moderate-severe upper limb spasticity affecting more than one joint, received multiple intramuscular injections of hyaluronidase-saline. Adverse effects were monitored over 15 weeks. The Modified Ashworth Scale (MAS) assessed reduction in spasticity while active and passive range of motion was assessed using quantitative video analysis of upper limb movement. Findings: 21 participants were included. The procedure was well tolerated. Extensive safety monitoring in all patients revealed no clinically significant adverse events at 15 weeks. Treatment seemed to be effective at reducing spasticity in all twenty-one participants who received the injections (p<0.05 in 16 evaluation over 24 in passive ROM and 17 over 24 in active ROM). The measures of motor function (MAS) showed still improvement at 15 months (p=.000). Interpretations: Subcutaneous administration of hyaluronidase-saline in a multiple sites was fairly safe and well tolerated in adult patients with spasticity; however, these results must be viewed as preliminary until data from blinded, controlled clinical trials are available.
Introduzione: La spasticità è un danno neurologico comune conseguente ad una lesione al sistema nervoso centrale, ma i contributi neurali e biomeccanici ad esso correlati sono ancora poco conosciuta. Studi istopatologici hanno dimostrato un aumento generalizzato nel tessuto connettivo extracellulare nei muscoli spastici, che può diminuire la sua funzionalità e ridurre la soglia per la stimolazione dei fusi neuromuscolari. Con questo lavoro proponiamo e forniamo le prove preliminari per una nuova ipotesi per l'esacerbazione della spasticità in un arto immobilizzato: l'ipotesi ialuronato. Si Ipotizza che il tessuto connettivo extracellulare, che è composto principalmente da ialuronato, diventi iper-viscoso e rigido in un arto immobilizzato grazie alle sue proprietà non-Newtoniane. Metodi: In questo case series, è stata valutata la sicurezza, tollerabilità e efficacia della ialuronidasi ricombinante umana, che idrolizza lo ialuronato, in combinazione con una soluzione salina per ripristinare la funzionalità dei tessuti. Ventuno persone fisiche, con moderata-grave spasticità degli arti superiori in più di una articolazione, hanno ricevuto multiple iniezioni intramuscolari di ialuronidasi-salina. Gli effetti avversi sono stati monitorati per 15 settimane. La Modified Ashworth Scale (MAS) ha valutato la riduzione della spasticità mentre la l’escursione articolare di movimento attiva e passiva è stata valutata mediante analisi quantitativa del movimento dell'arto (ROM) superiore tramite video. Risultati: 21 partecipanti sono stati inclusi. La procedura è stata ben tollerata. Il monitoraggio estensivo sulla sicurezza dei pazienti non ha rivelato eventi avversi clinicamente significativi a 15 settimane. Il trattamento è risultato efficace nel ridurre la spasticità in tutti i ventuno partecipanti che hanno ricevuto le iniezioni (p <0.05 di 16 valutazione su 24 nella ROM passivo e 17 su 24 nel ROM attivo). Le misure di funzione motoria (MAS) hanno mostrato un mantenimento del miglioramento a 15 mesi (p = 0,000). Conclusioni: La somministrazione di ialuronidasi-salina in più siti è risultata sicura e ben tollerata in pazienti adulti con spasticità; tuttavia, questi risultati devono essere visti come preliminari fino a quando ulteriori studi clinici controllati in cieco non saranno disponibili.
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Rouleau, André-Jean. "Influence de la rigidité du microenvironnement sur les cellules progénitrices myogéniques du muscle squelettique". Mémoire, Université de Sherbrooke, 2016. http://hdl.handle.net/11143/9491.

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La matrice extracellulaire (MEC) subit plusieurs modifications au cours du vieillissement, ce qui altère ses propriétés biomécaniques. Les cellules responsables de la régénération de la portion myogénique du muscle sont les cellules satellites, qui, une fois activées, sont appelées les cellules progénitrices myogéniques (CPM). La rigidité du muscle, influence le devenir des CPM. La capacité régénérative du muscle squelettique diminue lors du vieillissement. Nous avons posé l’hypothèse selon laquelle la rigidité observée dans le tissu âgé pourrait nuire à la capacité régénérative des CPM. Nous avons tout d’abord validé les modifications subies par la MEC suite au vieillissement en les comparant au tissu adulte. Les résultats montrent une augmentation de la quantité de collagènes et de réticulation non enzymatique. En plus, une augmentation de la rigidité du muscle et des fibres individualisées a été observée par microscopie à force atomique (AFM). L’équipe s’est ensuite intéressée à leur activité myogénique dans un modèle de fibres musculaires en culture (ex vivo). Nous avons observé une diminution du nombre de cellules myogéniques sur les fibres de tissus âgés, comparativement aux tissus adultes. Nous avons montré que les proportions de cellules quiescentes sont plus élevées sur des fibres adultes suite à l’isolement et que les proportions de cellules prolifératives et en voie de différenciation sont plus élevées sur les fibres âgées. De plus, sur des fibres endommagées gardées en culture six jours, nous avons observé que les proportions de cellules prolifératives sont plus élevées sur les fibres adultes et que celles des cellules en voie de différenciation sont plus élevées sur les fibres âgées. Enfin, nous avons observé l’activité myogénique des CPM ainsi que l’impact de la rigidité en culture (in vitro). Nous n’avons observé aucune différence des capacités de prolifération et de différenciation des myoblastes adultes et âgés. En terminant, nos recherches ont montré qu’une rigidité de 2.0 kPa favorise un état prolifératif tandis qu’une rigidité de 18 kPa stimule plutôt l’engagement vers la différenciation. Ces résultats suggèrent que la rigidité peut être une cause de la diminution du potentiel régénératif du muscle vieillissant. En résumé, ces travaux soulignent l’importance de l’augmentation de la rigidité du microenvironnement sur les CPM comme cause de la diminution du potentiel de régénération du muscle vieillissant.
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Belozertseva, Ekaterina. "Effets du récepteur minéralocorticoïde, de l’intégrine αv et de vimentine sur les fonctions des cellules musculaires lisses vasculaires et la rigidité artérielle". Thesis, Université de Lorraine, 2016. http://www.theses.fr/2016LORR0165/document.

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La rigidité artérielle et la fibrose ont une valeur prédictive dans le développement des maladies cardiovasculaires (CV). Ces 2 phénotypes impliquent les cellules musculaires lisses vasculaires (CMLVs) notamment des récepteurs membranaires et les protéines du cytosquelette. Les objectifs ont été d’étudier : (i) l’influence du récepteur minéralocorticoïde (MR) sur la réactivité vasculaire, (ii) le rôle de l’intégrine αvβ3 dans le développement de la rigidité artérielle et la fibrose vasculaire, et (iii) l’impact de la vimentine et la synémine sur la structure et la fonction artérielle. Ces trois études ont utilisées des souris avec invalidation génétiques des protéines d’intérêt. Résultats : l’absence du MR diminue la réactivité vasculaire en altérant le couplage contraction/relaxation des CMLVs via des mécanismes Ca2+- et NO-dépendants (une diminution de la vasoconstriction en réponse au Ca2+ extracellulaire et une altération de la vasorelaxation endothélium-dépendante en réponse à l’acétylcholine). L’invalidation de la sous-unité αv prévient la fibrose en réponse à l’administration d’angiotensine II. L’absence de la vimentine et non celle de la synémine augmente la rigidité artérielle via des changements des adhésions focales des CMLVs mais aussi des cellules endothéliales. En conclusion, les récepteurs membranaires et protéines intracellulaires étudiées influencent la fonction et la structure des artères grâce à des actions spécifiques sur le tonus musculaire, la mécanotransduction et l’organisation ultra-structurale des CMLVs. Ces études montrent au niveau cellulaire et moléculaire le déterminisme plurifactoriel des phénotypes de rigidité-fibrose de la paroi artérielle. Ces résultats nécessitent des travaux plus mécanistiques pour affirmer l’implication de ces protéines dans les maladies CV liées au vieillissement
Arterial stiffness and fibrosis have a predictive value in the development of cardiovascular diseases (CV). These two phenotypes involve vascular smooth muscle cells (VSMCs) including membrane receptors and cytoskeletal proteins. The objectives were to examine: (i) the influence of the mineralocorticoid receptor (MR) on vascular reactivity, (ii) the role of avb3 integrin in the development of arterial stiffness and vascular fibrosis, and (iii) the impact of vimentin and synemin on arterial structure and function. The mice with genetic invalidation of the proteins of interest were used in these three studies. Results: the absence of MR decreased vascular reactivity by altering the contraction/relaxation coupling of VSMC through Ca2+- and NO-dependent mechanisms (a decrease of vasoconstriction in response to extracellular Ca2+ and impaired endothelium-dependent vasorelaxation in response to acetylcholine). The invalidation of the αv subunit prevented fibrosis in response to the administration of angiotensin II. The absence of vimentin, and not that of the synemin, increased arterial stiffness via changes in focal adhesions of VSMCs as well as endothelial cells. In conclusion, the studied membrane receptors and intracellular proteins that influenced the structure and function of arteries through specific actions on muscle tone, the mechanotransduction and the ultra-structural organization of VSMCs. These studies show the multifactorial dependency of the stiffness-fibrosis phenotypes of the arterial wall at the cellular and molecular levels. These results require more mechanistic work to determine the role of these proteins in CV diseases related to aging
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Stuyvers, Bruno. "Modélisation et description du comportement instantané de la rigidité du muscle cardiaque : application à l'hypertrophie ventriculaire gauche expérimentale consécutive à une hypertension rénovasculaire chez le rat (modèle 2K-1C R.H.R)". Bordeaux 2, 1991. http://www.theses.fr/1991BOR28154.

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La methodologie developpee au cours de ce travail permet la modelisation du comportement de la rigidite face a la contrainte d'un muscle papillaire (isole de cur de rat) a un moment determine de son activation. Appliquee a differents instants de l'activite du muscle stimule, cette methodologie rend compte de l'evolution de la relation rigidite-contrainte en fonction du degre d'activation. La meme procedure est appliquee au muscle papillaire de cur hypertrophie (hypertrophie induite par hypertension renovasculaire: modele 2k-1c rhr). Les resultats obtenus montrent que dans certaines conditions de fonctionnement, la resistance opposee par le muscle a une augmentation de la contrainte fait intervenir a la fois une resistance elastique et une resistance visqueuse. L'expression de la resistance visqueuse depend de la vitesse de variation de la contrainte et semble en outre controlee par les phenomenes activateurs de la force musculaire au niveau cellulaire. La rigidite apparait donc comme un phenomene viscoelastique dont l'intensite est modulable par les processus actifs de la contraction au travers de proprietes encore peu connues de la viscosite musculaire. La resistance a la contrainte determinee en relaxation subit un accroissement significatif au cours de l'hypertrophie. Cette anomalie semble etre liee directement aux perturbations des mouvements du calcium dans le myocyte pathologique. Ainsi, dans le cur, tout agent pharmacologique ou tout mecanisme pathologique ayant une incidence sur le metabolisme du calcium pourrait avoir des consequences notables sur la rigidite par modification de la resistance visqueuse
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Hovhannisyan, Yeranuhi. "Modélisation cardiaque des myopathies myofibrillaires à l'aide de cellules souches pluripotentes induites pour explorer la pathogenèse cardiaque Polyacrylamide Hydrogels with Rigidity-Independent Surface Chemistry Show Limited Long-Term Maintenance of Pluripotency of Human Induced Pluripotent Stem Cells on Soft Substrates Modéliser la myopathie myofibrillaire pour élucider la pathogenèse cardiaque Synemin-related skeletal and cardiac myopathies: an overview of pathogenic variants Desmin prevents muscle wasting, exaggerated weakness and fragility, and fatigue in dystrophic mdx mouse Effects of the selective inhibition of proteasome caspase-like activity by CLi a derivative of nor-cerpegin in dystrophic mdx mice". Thesis, Sorbonne université, 2020. http://www.theses.fr/2020SORUS095.

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La myopathie myofibrillaire est une maladie neuromusculaire à évolution lente caractérisée par de graves troubles musculaires causés par des mutations dans le gène codant pour des protéines du cytosquelette. L'un des gènes affectés en relation avec le développement de la MFM est DES. Des mutations dans le gène de la desmine entraînent des myopathies des muscles squelettiques et cardiaques. Cependant, les évènements qu'elles entraînent et qui sont à l’origine des phénotypes pathologiques cardiaques restent mal connus. Mon objectif est de créer un modèle in vitro de MFM basé sur des cellules souches pluripotentes humaines afin d'étudier le rôle des mutations spécifiques dans la desmine sur le développement et la fonction des cellules cardiaques. Pour atteindre cet objectif, en collaboration avec les docteurs A. Behin, K. Wahbi et la société Phenocell, nous avons généré des iPSC à partir des cellules sanguines périphériques de patients souffrant d'une forme de cardiomyopathie induite par une mutation de la desmine. Les lignées iPSC générées contenant les mutations du gène codant la desmine ont permis d’étudier le rôle d’une mutation dans la spécification et la fonction des cardiomyocytes. La bioénergétique mitochondriale, la structure cellulaire et la fonction contractiles ont été évaluées au niveau cellulaire. En conclusion, il convient de noter que les mutations de la desmine conduisent à une désorganisation des structures des sarcomères dans les cardiomyocytes et à une perturbation de l'expression des protéines mitochondriales. Ce qui conduit à une altération des fonctions de la mitochondrie. Ces données permettent d’améliorer notre compréhension des mécanismes moléculaire qui sous-tendent le développement de la MFM
Myofibrillar Myopathy is a slowly progressive neuromuscular disease characterized by severe muscular disorders caused by mutations in the gene encoded cytoskeletal proteins. One of the genes described in connection with the development of MFM is DES. Mutations in the desmin gene lead to skeletal and cardiac muscles myopathies. However, the cardiac pathological consequences caused by them remain poorly understood. My objective is to create an in vitro human stem cell model of MFM to specifically investigate the role of patient-specific mutations in desmin on cardiac lineage development and function. To achieve that objective, in collaboration with Drs. Behin and K. Wahbi and Phenocell, we generate patient-specific iPSC from peripheral blood cells of the patient suffering severel form of desmin-deficient cardiomyopathy. The generated iPSC lines carrying DES gene mutations enable a powerful examination of the role of desmin mutation on cardiomyocyte specification and function. Bioenergetic, structural, and contractile function will be assessed in a single cell. In conclusion, it should be noted that desmin mutations lead to a disorganization of sarcomere structures in cardiomyocytes and to a perturbation of mitochondrial protein expression. This leads to a distortion of functions in the mitochondria. These data facilitate the understanding of the molecular pathway underlying the development of desmin-related myopathy. And the system we have created could also allow us to better evaluate the correlation between the desmin genotype and phenotype in terms of effect on the heart
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Książki na temat "Muscle rigidity"

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Avela, Janne. Stretch-reflex adaptation in man. Jyväskylä: University of Jyväskylä, 1998.

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Gelb, Harold. Killing painwithout prescription: A new and simple way to free yourself from headache, backache and other sources of chronic pain. Wellingborough: Thorsons, 1987.

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Dreaver, Jim. Somatic therapy: A neuromuscular approach to chronic pain and stiffness. Wyd. 2. Sebastopol, Calif. (7724 Healdsburg Ave., Sebastopol 95472): Wild Goose Press, 1991.

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Fujimoto, Yasushi. He ji rou suan tong shuo bai bai! man hua tu jie jian, jing, yao, bei man xing teng tong quan xiao chu. Xinbei Shi Xindian Qu: Ren lei zhi ku shu wei ke ji wen hua you xian gong si, 2016.

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Muscles, Masses and Motion: The Physiology of Normality, Hypotonicity, Spasticity and Rigidity (Clinics in Developmental Medicine (Mac Keith Press)). Cambridge University Press, 1993.

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Stafstrom, Carl E. Disorders Caused by Botulinum Toxin and Tetanus Toxin. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199937837.003.0156.

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Anaerobic organisms of the genus Clostridia (C) can cause significant human disease. Exotoxins secreted by C botulinum and C tetani cause botulism and tetanus, respectively (summarized in Table 156.1). Botulinum neurotoxin causes neuromuscular blockade by interfering with vesicular acetylcholine release, leading to cholinergic blockade at the neuromuscular junctions of skeletal muscle, and consequently, symmetric flaccid paralysis. Tetanus toxin prevents release of inhibitory neurotransmitters at central synapses, leading to overactivity of motor neurons and muscle rigidity and spasms. This chapter reviews clinical features of botulism and tetanus and discusses their pathophysiological basis.
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Cohen, Jeffrey A., Justin J. Mowchun, Victoria H. Lawson i Nathaniel M. Robbins. A 30-Year-Old Male with Severe Cramps. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190491901.003.0029.

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Muscle cramps are a common complaint. When not associated with weakness, the course is usually benign but can still be frustrating to patients. Diffuse cramping may be indicative of a neuromuscular disorder. Cramps can be associated with a metabolic or endocrine disorder or medications. Normal nerve conduction studies and electromyography are reassuring for a benign cause of cramps. In motor neuron disease cramps are common. There are rare spontaneous activity syndromes associated with cramping. Stiff person syndrome is rare and usually has severe axial rigidity. It can be treated with immune modulating medications. McArdles disease has a prominent symptom of diffuse muscle cramping associated with activity. Unfortunately not always will a specific cause for cramps be discovered. Various treatment modalities are presented.
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Suzzen, Marrinaz Ton. Serotonin Syndrome Symptoms: Hyperthermia,Agitation and Restlessness,Ocular Clonus,Muscle Rigidity,Headaches,Tremor,Nausea, Vomiting, and Diarrhea,Heavy Sweating,Shivering and Goose Bumps,High Blood Pressure and Rapid Heart Rate. Independently Published, 2021.

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Muscles, Masses and Motion:The Physiology of Normality, Hypotonicity, Spasticity and Rigidity (Classics in Developmental Medicine). MacKeith Press, 1992.

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Części książek na temat "Muscle rigidity"

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Struppler, A., i C. Jakob. "Measurement of Muscle Tone — Demarcation Between Spasticity and Rigidity". W Instrumental Methods and Scoring in Extrapyramidal Disorders, 56–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-78914-4_6.

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Hemsley, Kim M., i Ann D. Crocker. "Antipsychotic Drug-Induced Muscle Rigidity and D2 Receptor Occupancy in the Basal Ganglia of the Rat". W Advances in Behavioral Biology, 519–25. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0179-4_52.

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Goldberg, Joshua A., Thomas Boraud, Sharon Maraton, Eilon Vaadia i Hagai Bergman. "Enhanced Synchrony in the Primary Motor Cortex of Mptp Primates May Underlie Muscle Co-Contraction and Rigidity". W Advances in Behavioral Biology, 97–106. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0715-4_11.

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Lorenc-Koci, E., G. Schulze, M. Śmiałowska, A. Kamińska, M. Bajkowska, K. Ossowska i S. Wolfarth. "Chronic Treatment with 1,2,3,4-Tetrahydroiso-Quinoline (TIQ), an Environmental and Endogenous Substance, Induces Parkinsonian like Muscle Rigidity in Young and Old Rats". W Neurotoxic Factors in Parkinson’s Disease and Related Disorders, 320. Boston, MA: Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-1269-1_40.

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"Fever, muscle rigidity, mental confusion". W 100 Cases in Psychiatry, 115–16. CRC Press, 2010. http://dx.doi.org/10.1201/b13316-44.

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Baliga, Narayan, i Theodore J. Sanford. "Difficult Airway: Opiate-Induced Muscle Rigidity". W Complications in Anesthesia, 174–75. Elsevier, 2007. http://dx.doi.org/10.1016/b978-1-4160-2215-2.50046-6.

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Vargas-Patron, Luis A., i Jessica A. Lovich-Sapola. "Malignant Hyperthermia and Masseter Muscle Rigidity". W Anesthesia Oral Board Review, 333–36. Wyd. 2. Cambridge University Press, 2023. http://dx.doi.org/10.1017/9781316181492.081.

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Miller, Aaron E., Tracy M. DeAngelis, Michelle Fabian i Ilana Katz Sand. "Gad-Awful Spasms". W Neuroimmunology, 103–8. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190693190.003.0019.

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Stiff person syndrome (SPS) is a rare autoimmune neurological disease that causes progressive, fluctuating, painful muscle rigidity and spasms, generally beginning in the axial muscles, truncal region, and progressing to proximal musculature. A hyperlordotic posture is considered an early clinical hallmark of the condition. The most common pathological correlate is with anti-glutamic acid decarboxylase (GAD) 65 antibodies, but several other associated antibodies have been identified There is a clinical spectrum of disease with variants including stiff leg syndrome, progressive encephalomyelitis with rigidity and myoclonus (PERM), and a paraneoplastic variant, often associated with anti-amphiphysin antibodies. Electromyographic findings reveal continuous motor activity. Treatment modalities for SPS focus primarily on symptomatic relief to improve quality of life. Gamma amino butyric acid (GABA)ergic agonists, including benzodiazepines, such as diazepam and baclofen, are first-line therapies for muscle rigidity and spasms. Immunotherapies such as corticosteroids, intravenous immunoglobulin (IVIg), plasmapheresis, and rituximab have demonstrated benefit, As symptoms can be provoked by anxiety and emotional stressors, psychological support with cognitive behavioral therapy should be considered.
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Shibasaki, Hiroshi, Mark Hallett, Kailash P. Bhatia, Stephen G. Reich i Bettina Balint. "Disorders of Increased Muscle Stiffness or Overactivity". W Involuntary Movements, 175–80. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190865047.003.0009.

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Increased muscle stiffness or overactivity (which differs from parkinsonian rigidity or dystonia) can be caused by a variety of disorders of central or peripheral nervous system origin and genetic, autoimmune, or infectious etiology. Increased muscle stiffness may be the cause of some joint movements, particularly when such stiffness is associated with stimulus sensitivity that causes involuntary movements. The conditions discussed in this chapter include stiff person syndrome, progressive encephalomyelitis with rigidity and myoclonus (PERM), acquired neuromyotonia (Isaacs syndrome), hereditary neuromyotonia, tetanus (which has an infectious etiology), Satoyoshi disease, neuromyotonia, and rippling muscle disease. Many of these cases are caused by decreased synaptic inhibition through an autoimmune mechanism.
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Mergens, Pamela A. "Perioperative Narcotic Problems: Muscle Rigidity and Biliary Colic". W Anesthesiology Review, 130–31. Elsevier, 2002. http://dx.doi.org/10.1016/b978-0-443-06601-6.50060-8.

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Streszczenia konferencji na temat "Muscle rigidity"

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Ueda, Shodai, i Atsushi Sakuma. "Finite Element Analysis of Dynamics of Human Muscle Compressed by Fabric Sleeve". W ASME 2018 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/imece2018-87304.

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Recently, compression wear has become the preferred performance material for many athletes, where it has the effect of reducing the burden on the body by suppressing muscle vibrations and improves athletic performance by providing the body with suitable moderate pressure. This study concerns thigh sleeves formed of compression wear. The optimal level of compression is studied in order to improve athletic performance and reduce muscular strain. Subsequently, the mechanics of the thigh compression sleeve are discussed. Here, the optimal tensile rigidity of the sleeve, which is calculated using the Young’s modulus of the sleeve in the circumferential direction, is discussed with the aim of reducing muscular strain. The finite element method model is adopted to represent the thigh, which commonly experiences muscle strain during running. The model is constructed using a semi-circular shape, which represents the thigh cut in the transverse plane. The model consists of two solid components, which reflect the muscle (outer) and femur (inner), as well as a shell that covers the thigh. The model generates sinusoidal vibrations, which reflect human behavior when running in a uniaxial direction. The maximum shear strain is approximately half of the tensile rigidity of the sleeve. Indeed, the muscle is sufficiently soft that the tensile rigidity of the sleeve is generally smaller when there is little shear strain on the muscle. From these results, it is concluded that the maximum shear strain of the muscle decreases by almost half when covered by the thigh compression sleeve compared to when no thigh compression sleeve is worn. Furthermore, the shear strain of the muscle can be reduced by varying the tensile rigidity of the sleeve when the human is running. Finally, the tensile rigidity of the sleeve can be decreased to reduce the shear strain of the muscle as it softens.
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Ayuni, C. Z. Noor, Takashi Komeda, Cheng Yee Low i Kaoru Inoue. "Emulation of muscle tone of upper limb spasticity and rigidity". W 2013 6th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2013. http://dx.doi.org/10.1109/ner.2013.6696252.

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Song, Seung Yun, Yinan Pei, Jiahui Liang i Elizabeth T. Hsiao-Wecksler. "Design of a Portable Position, Velocity, and Resistance Meter (PVRM) for Convenient Clinical Evaluation of Spasticity or Rigidity". W 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3503.

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Spasticity is a common consequence of the upper motor neuron syndrome and usually associated with brain lesion, stroke, cerebral palsy, spinal cord injury, and etc. On the other hand, rigidity is a neuromuscular disorder often found in Parkinson’s disease patients. Both of spasticity and rigidity are characterized by abnormal hypertonic muscle behaviors that will cause discomfort and hinder daily activities. Worldwide, the estimated affected population of spasticity is around 12 million [1], and rigidity affects more than 10 million people [2]. Clinical evaluation of spasticity or rigidity involves personal assessment using qualitative scales, such as the Modified Ashworth Scale (MAS) or Modified Tardieu Scale (MTS) for spasticity and Unified Parkinson’s Disease Rating Scale (UPDRS) for rigidity. However, this evaluation method heavily relies on the rater’s personal experience/interpretation and usually results in poor consistency and low reliability. The goal of this design was to develop a quantitative measurement device that can be used to assist clinical evaluation of spasticity or rigidity. This portable device, the Position, Velocity, and Resistance Meter (PVRM), can be strapped around a patient’s limb to measure angular position, angular velocity and muscle resistance of a given joint while the patient’s limb is passively stretched by the clinician. Acquiring this quantitative data from patients will not only allow clinicians to make more reliable assessments but also help researchers gain additional insights into the quantification of spasticity and rigidity.
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He, Maxine, Mahshid Mansouri, Yinan Pei, Isaac Pedroza, Christopher M. Zallek i Elizabeth T. Hsiao-Wecksler. "Clinical Validation Testing Of An Upper Limb Robotic Medical Education Training Simulator For Rigidity Assessment". W 2022 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/dmd2022-1073.

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Abstract An upper limb robotic training simulator was developed to replicate the haptic feeling of lead-pipe rigidity of the biceps. Rigidity is the increased muscle tone observed during passive movement of a joint. To validate the realism of our training simulator, a clinical validation study was conducted with 11 experienced clinicians. Testing involved two parts: Blinded Assessment followed by Disclosed Assessment. There were 12 randomized trials (4 levels of rigidity with 3 repetitions each) in the Blind Assessment. The participants were asked to rate the rigidity level using the Unified Parkinson’s Disease Rating Scale (UPDRS) in each trial without knowing the selected UPDRS level. During the Disclosed Assessment, participants were informed about the selected level and were asked to closely evaluate the fidelity of each UPDRS level. Participants completed a post-test evaluation questionnaire to rate the simulator’s accuracy in replicating rigidity and its potential as a medical education tool for healthcare students. Results from the first six participants indicated that the simulated muscle resistance magnitude was too high compared to their clinical experience. Therefore, the resistance magnitude was reduced for all 4 UPDRS levels. The second set of five participants reported that the training simulator closely replicated the UPDRS levels of rigidity compared to their clinical experience.
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Garavaglia, Lorenzo, Elena Beretta, Sandra Strazzer, Felice Sala, Morena Delle Fave, Fabio Brunati, Francesca Passaretti i Simone Pittaccio. "Dynamic Splints, Functionally-Customized With Nitinol, Can Reduce Joint Rigidity in Pediatric Subjects With Spasticity". W ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14246.

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Neuromuscular diseases as a consequence of brain damage are complex phenomena involving disuse, immobility, brain tissue remodeling and cortical function remapping. They may have various causes and strike any part of the population. The vicious circle leading to a worsening of the patients’ conditions proceeds through muscle shortening by contractures, disruption of the normal reflex behavior and sensory problems, development of spasticity [1]. Physical rehabilitation alone or in association with surgery or pharmacological treatments can be useful in limiting those degenerations. Besides manual rehabilitation, splints and braces are prescribed to control the limb posture and obtain stretching of the muscles. The role of those orthoses is to maintain the paretic limb in a set ‘physiological’ position and let it relax into that posture, in an attempt to reduce muscle rigidity and contractures. However applying a fixed constraint to the limb and waiting for relaxation to take place, may cause discomfort, pain, skin rash, and sundry different complications [2]. Also, any residual voluntary movement is prevented by a fixed-angle splinting. In addition, all these negative characteristics limit tolerability and daily application times. This work presents a different way to promote limb repositioning, based on the application of NiTi-alloy-based dynamic splints, which favor mobility and any residual use of the affected limb. Furthermore it suggests that application of mild contact forces prolonged in time has the advantage of feeling less painful and uncomfortable for the patients, improving overall treatment tolerability.
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Song, Seung Yun, Yinan Pei, Steven R. Tippett, Dronacharya Lamichhane, Christopher M. Zallek i Elizabeth T. Hsiao-Wecksler. "Validation of a Wearable Position, Velocity, and Resistance Meter for Assessing Spasticity and Rigidity". W 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6906.

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Patients with neuromuscular disorders such as Parkinson’s disease (PD), traumatic brain or spinal cord injury, or multiple sclerosis (MS) can develop different levels of abnormal muscle behavior (hypertonia) such as rigidity and spasticity [1], [2]. Hypertonia can affect different parts of the body such as upper or lower extremities. Symptoms include pain, increased muscle tone, spasms, and decreased functional abilities. Hypertonia can interfere with many activities of daily living, greatly affecting the quality of life in patients and causing anxiety, depression, and social isolation [2].
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Nyugen, Joey, Shenbagaraj Kannapiran, Subhrajyoti Chaudhuri, Valerie Lane Gentz i Panagiotis Polygerinos. "Design of a Soft Ankle Joint Device for Correction of Inversion/Eversion Angle During Aquatic Therapy". W 2019 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2019. http://dx.doi.org/10.1115/dmd2019-3206.

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According to statistical data, approximately 800,000 individuals across the United States have strokes each year [2]. A stroke event causes neurological and orthopedic deficits, such as weak muscles, decreased proprioception, and spasticity [6]. To regain function, increase motor skills, and retrain muscles, many stoke survivors utilize aquatic therapy as a form of rehabilitation [14]. Typically inside water, the lower body part of a person has to carry 75% less weight, This decreases the effect of gravity allowing increased joint range of motion [6], [13]. This also helps increase muscle strength as water offers about 600 more resistance than air [13]. The water temperature also helps decrease pain, spasticity, and rigidity [13]. The uniform pressure along with buoyancy contributes to an improved balance of the body [13].
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Oppold, Julia, Alexander Grimm, Philipp Klocke, Mohammad Hormozi, Maria-Sophie Breu, Daniel Weiß, Del Nicholas A. Grosso i Justus Marquetand. "Muscle ultrasound in idiopathic Parkinson's disease with deep brain stimulation: Rigidity can be quantified by shear wave elastography." W Interdisziplinärer Kongress | Ultraschall 2022. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0042-1749497.

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Oliveira Júnior, Rocymar Rebouças, Ana Carolina Soares de Lira, Nilson Batista Lemos, Lucas Sávio Fernandes Carvalho, Maria Júlia Plech Guimarães, Marialice Pinto Viana Correia i Luciana Karla Viana Barroso. "The Non-motor Effects of Deep Brain Stimulation of the Subthalamic Nucleus in Patients with Motor Disorders Caused by Parkinson’s Disease". W XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.655.

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Introduction: Parkinson’s disease is a disease caused by the degeneration of dopaminergic neurons in the substantia nigra, and is characterized by a triad of symptoms: bradykinesia, muscle rigidity and rest tremors; which worsen progressively, leading the patient to resort to surgical treatment to ensure a better drug response. However, surgical intervention has proven to be efficient not only to alleviate Movement Disorders, but also to control the nonmotor symptoms of the disease. Objective: To evaluate the non-motor effects of Deep Brain Stimulation (DBS) in patients who do not respond adequately to drug treatment. Methods: This is a literature review conducted by searching the electronic databases Lilacs, Scielo, Medline and Pubmed from 2011 to 2021, using the descriptors “parkinsonism”, “deep brain stimulation”, “non-motor” and “depression”. Articles and specimens from the American and Brazilian literature on the topic were considered relevant. Results: The studies showed that patients who underwent the surgical procedure showed evolution of neurophysiological and psychosocial aspects, such as improved sleep quality, reduced risk of dementia, improved mood and minimized anxiety. In this sense, it is necessary to pay attention to the stage of Parkinson’s Disease evolution that the patient is in, in order to start the surgical treatment before it no longer has the expected expressive effects. Conclusion: It is expected, therefore, a significant improvement in the quality of life of patients undergoing PCT, which is not restricted to motor gains.
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Maynard, Jacqueline A., Ahmad S. Arabiyat, Anna Elefante, Lucas Shearer, Eoin King i Andrea Kwaczala. "Using Acoustic Waves to Modulate Stem Cell Growth and Differentiation". W ASME 2017 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/imece2017-71341.

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During spaceflight, the loss of mechanical loads due to microgravity leads to rapid bone loss, where bone deteriorates at a rate of 1–2% per month, where some astronauts can lose as much as 20% of their skeletal mass in a single expedition [NASA, 2001]. In order to prevent muscle and bone loss, long-term space flight exercise regimes are strictly implemented [Shackleford, 2004]. Current research has demonstrated that mechanical vibrations can help to maintain or improve bone mass [Chan, 2013] and reduce adiposity [Chen, 2015, Sen, 2011] when signals are applied at the appropriate frequency and amplitude. We have developed an acoustic sound chamber that can apply sound waves to stem cells grown in vitro. Characterization of the culture conditions inside the vibration chamber showed considerable variance across the culture plates where an applied acceleration of 0.6g varied at different spots in a 12-well tissue culture plate from as low as 0.47g to 0.78g. We believe the variance is caused by differences in the rigidity of the culture plates that makes the waves transmit inconsistently through the plastic. We hypothesized acoustic waves would induce osteogenic differentiation when applied to stem cells. We utilized pre-osteoblastic stem cells (MC3T3-E1-Subclone 4) to observe the effects of acoustic waves when applied at 0.3g and 0.6g, compared to non-vibrated controls. Cells were vibrated for 30 minutes a day for either 6 days (n = 24/group) or 12 days (n = 12/group). Cellular changes were characterized by assessing well-by-well cell number by a manual cell count and mineral content by Alizarin Red S staining. Differences between groups were determined using One-Way ANOVA with a post hoc test: Student’s t-test. To assess the effects of the variance across the culture plates, correlative analysis was conducted for well-by-well variation using Regression Analysis. Acoustically vibrated wells had 10x more cells after 6 days and showed more mineralization than non-vibrated wells at both 6 and 12 days. Acoustic waves have the ability to increase cell proliferation and can drive stem cell differentiation towards an osteoblastic lineage, this could lead to therapies that prevent bone loss during spaceflight.
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