methods-to-quantify-pharmacologically-induced-alterations-motor

Methods to Quantify Pharmacologically Induced Alterations in Motor Function in Human Incomplete SCI

Spinal cord injury (SCI) is a debilitating disorder, which produces profound deficits in volitional motor control. Following medical stabilization, ...

To determine whether inhibition of either the ribosomal p70 S6 kinase or eukaryotic initiation factor (eIF) 4E pathways downstream of the mammalian target of rapamycin, mTOR, contributes to rapamycin-induced growth arrest, clones of Rh30 rhabdomyosarcoma cells were selected for rapamycin resistance. Expression of c-Myc and anchorage-independent growth were enhanced in resistant cells. Resistance was unstable in each of three clones characterized. In resistant cells, as compared with parental cells, approximately 10-fold less 4E-binding protein (4E-BP) was bound to eIF4E, and total cellular 4E-BP was markedly reduced. Levels of eIF4E were unchanged. Steady-state levels of 4E-BP transcript remained unaltered, but the rate of 4E-BP synthesis was reduced in resistant cells. In cells that reverted to rapamycin sensitivity, levels of total 4E-BP returned to those of parental cells. Compared with parental cells, resistant clones had either similar or lower levels and activity of ribosomal p70 S6 kinase, but c-Myc levels were elevated in both resistant and revertant clones. Several colon carcinoma cell lines with intrinsic rapamycin resistance were found to have low 4E-BP:eIF4E ratios. In stable clones of HCT8 carcinoma engineered to overexpress 4E-BP, rapamycin sensitivity increased markedly (>1000-fold) as 4E-BP expression increased. These results suggest that the 4E-BP:eIF4E ratio is an important determinant of rapamycin resistance and controls certain aspects of the malignant phenotype.

4E-binding proteins, the suppressors of eukaryotic initiation factor 4E, are down-regulated in cells with acquired or intrinsic resistance to rapamycin.

4E-bindende Proteine, die Suppressoren von eukaryotischen Initiationsfaktor 4E, sind herunter reguliert in Zellen mit erworbener oder intrinsischer Resistenz gegen Rapamycin.

It is thought that G(1) cyclin/CDK mediated phosphorylation of pocket proteins from mid G(1) to mitosis is reversed via dephosphorylation in mitosis. We examined the mechanisms involved in the unexpectedly rapid dephosphorylation of the pocket proteins induced via inhibition of cellular protein synthesis by cycloheximide (CHX) as well as direct inhibition of CDKs by flavopiridol. CHX and flavopiridol-induced dephosphorylation of pocket proteins is attributable to inactivation of D-type cyclin/CDKs and G(1)/S CDKs, respectively, which unmasks a phosphatase activity that targets the three pocket proteins apparently throughout the cell cycle. Treatment of cells with phosphatase inhibitors at concentrations selective for PP2A inhibition prevents CHX and flavopiridol-mediated dephosphorylation of pocket proteins in vivo. Also, ectopic expression of SV40 small t antigen, which inhibits PP2A via disruption of trimeric PP2A holoenzymes, delays CHX-induced pocket protein dephosphorylation. Moreover, dephosphorylation of p130 and p107 in cell extracts is inhibited by concentrations of okadaic acid known to inhibit PP2A, but not PP1. Finally, the PP2A catalytic subunit (PP2A/C) specifically interacts with both p130 and p107 in quiescent cells as well as cells progressing throughout the cell cycle. Together, these results demonstrate that the overall phosphorylation state of pocket proteins is determined, at least in part, by a dynamic equilibrium between CDKs and PP2A, or a closely related PP2A-like enzyme. These findings have important implications, as cell cycle or checkpoint-dependent inhibition of CDK activities counteracted by an active PP2A should have imminent effects on the phosphorylation state and activities of pocket proteins.

A dynamic equilibrium between CDKs and PP2A modulates phosphorylation of pRB, p107 and p130.

Ein dynamisches Gleichgewicht zwischen CDKs und PP2A moduliert Phosphorylierung von pRb, p107 und p130.

(1), Skelettmuskulatur Gr&ouml;&szlig;e in der unteren Extremit&auml;t Muskeln des Menschen nach unvollst&auml;ndigen R&uuml;ckenmarkverletzung (SCI), zu quantifizieren, (2) zur Bewertung der Unterschiede in der Muskelmasse zwischen beteiligten unteren Gliedma&szlig;en, (3) die Auswirkungen der ambulanten Status (mit Rollstuhl f&uuml;r Gemeinschaft Mobilit&auml;t Vs nicht durch einen Rollstuhl f&uuml;r die Gemeinschaft Mobilit&auml;t) auf Muskelgr&ouml;&szlig;e nach unvollst&auml;ndigen SCI ermitteln und (4) um festzustellen, ob die differenzielle Atrophie zwischen den einzelnen Muskeln nach unvollst&auml;ndigen Sci auftritt

Untere Extremit&auml;t Muskel Querschnittsfl&auml;che nach unvollst&auml;ndigen R&uuml;ckenmarkverletzung.

(1) To quantify skeletal muscle size in lower-extremity muscles of people after incomplete spinal cord injury (SCI), (2) to assess differences in muscle size between involved lower limbs, (3) to determine the impact of ambulatory status (using wheelchair for community mobility vs not using a wheelchair for community mobility) on muscle size after incomplete SCI, and (4) to determine if differential atrophy occurs among individual muscles after incomplete SCI.

Lower-extremity muscle cross-sectional area after incomplete spinal cord injury.

Muscle atrophy is clearly related to a loss of muscle torque, but the reduction in muscle size cannot entirely account for the decrease in muscle torque. Reduced neural input to muscle has been proposed to account for much of the remaining torque deficits after disuse or immobilization. The purpose of this investigation was to assess the relative contributions of voluntary muscle activation failure and muscle atrophy to loss of plantarflexor muscle torque after immobilization. Nine subjects (ages 19-23) years with unilateral ankle malleolar fractures were treated by open reduction-internal fixation and 7 weeks of cast immobilization. Subjects participated in 10 weeks of rehabilitation that focused on both strength and endurance of the plantarflexors. Magnetic resonance imaging, isometric plantarflexor muscle torque and activation (interpolated twitch technique) measurements were performed at 0, 5, and 10 weeks of rehabilitation. Following immobilization, voluntary muscle activation (56.8 +/- 16.3%), maximal cross-sectional area (CSA) (35.3 +/- 7.6 cm(2)), and peak torque (26.2 +/- 12.7 N-m) were all significantly decreased ( p < 0.0056) compared to the uninvolved limb (98.0 +/- 2.3%, 48.0 +/- 6.8 cm(2), and 105.2 +/- 27.0 N-m, respectively). During 10 weeks of rehabilitation, muscle activation alone accounted for 56.1% of the variance in torque ( p < 0.01) and muscle CSA alone accounted for 35.5% of the variance in torque ( p < 0.01). Together, CSA and muscle activation accounted for 61.5% of the variance in torque ( p < 0.01). The greatest gains in muscle activation were made during the first 5 weeks of rehabilitation. Both increases in voluntary muscle activation and muscle hypertrophy contributed to the recovery in muscle strength following immobilization, with large gains in activation during the first 5 weeks of rehabilitation. In contrast, muscle CSA showed fairly comparable gains throughout both the early and later phase of rehabilitation.

Relative contributions of muscle activation and muscle size to plantarflexor torque during rehabilitation after immobilization.

Muskelschwund ist deutlich im Zusammenhang mit einem Verlust von Muskel-Drehmoment, aber der R&uuml;ckgang der Muskelmasse kann nicht g&auml;nzlich entfallen, der R&uuml;ckgang der Muskel Drehmoment. Reduzierten neuronalen Input f&uuml;r Muskel ist vorgeschlagen worden, um f&uuml;r einen Gro&szlig;teil der verbleibenden Drehmoment Defizite nach Nichtnutzung oder Immobilisierung zu ber&uuml;cksichtigen. Der Zweck dieser Untersuchung war, die relative Beitr&auml;ge von Freiwilligen Aktivierung Scheitern und Muskel Muskelschwund zu Verlust von Plantarflexor Muskel Drehmoment nach Immobilisierung. Neun Themen (Alter 19-23) Jahre mit einseitigen Kn&ouml;chel Malleolar Frakturen wurden offene Reduktion-Osteosynthese und 7 Wochen nach der Besetzung Immobilisierung behandelt. Themen nahm an 10 Wochen Rehabilitation, die sich auf sowohl St&auml;rke und Ausdauer von der Plantarflektoren. Kernspintomographie, isometrische Plantarflexor Muskel Drehmoment- und Aktivierung (interpolierte zucken Technik) Messungen wurden durchgef&uuml;hrt, bei 0, 5 und 10 Wochen Rehabilitation. Nach Immobilisation freiwillige Muskelaktivierung (56,8 +/-16,3 %), maximale Querschnittsfl&auml;che (CSA) (35,3 +/-7.6 cm(2)) und Max. Drehmoment (26,2 +/-12,7 nm) wurden alle deutlich verminderte (p &lt; 0.0056) im Vergleich zu den unbeteiligt Gliedma&szlig;en (98,0 +/-2,3 % 48,0 +/-6.8 cm(2) und 105,2 +/-27.0 N-m, beziehungsweise). W&auml;hrend 10 Wochen Rehabilitation Muskelaktivierung allein entfielen 56,1 % der Varianz im Drehmoment (p &lt; 0,01) und Muskel CSA allein entfielen 35,5 % der Varianz im Drehmoment (p &lt; 0,01). CSA und Muskel-Aktivierung entfielen zusammen 61,5 % der Varianz im Drehmoment (p &lt; 0,01). Die gr&ouml;&szlig;ten Zuw&auml;chse in Muskelaktivierung wurden in den ersten 5 Wochen Rehabilitation. Sowohl steigende freiwillige Muskelaktivierung und Muskelhypertrophie beigetragen zur Erholung in Muskelkraft nach Immobilisation, mit gro&szlig;en Gewinne Aktivierung w&auml;hrend der ersten 5 Wochen Rehabilitation. Im Gegensatz dazu erh&auml;lt Muskel CSA ziemlich vergleichbare zeigte w&auml;hrend der fr&uuml;hen und sp&auml;teren Phase der Rehabilitation.

Relative Beitr&auml;ge von Muskelaktivierung und Muskelmasse zu Plantarflexor Drehmoment w&auml;hrend der Rehabilitation nach Immobilisierung.

Metabolic factors have been proposed to explain strength deficits observed in skeletal muscle with immobilization that are not completely accounted for by changes in muscle cross-sectional area (CSA) and neural adaptations. The aim of this study was to quantify changes in the resting inorganic phosphate (Pi) concentration from the medial gastrocnemius muscle during immobilization, reloading and rehabilitation. Additionally, we assessed the contributions of CSA, muscle activation and Pi concentration to plantar flexor torque during rehabilitation following immobilization. Eight persons with a surgically stabilized ankle fracture participated. Subjects were immobilized for 6-8 weeks and subsequently participated in 10 weeks of rehabilitation. Localized (31)P-Magnetic resonance spectroscopy, magnetic resonance imaging, isometric torque and activation testing were performed on the immobilized and uninvolved limbs. At 6 weeks of immobilization, significant differences were noted between the immobilized and uninvolved limbs for the Pi concentration and the Pi/PCr ratio (P < 0.05). From 6 weeks of immobilization to 3-5 days of reloading, the increase in Pi concentration (15%, P = 0.26) and Pi/PCr (20%, P = 0.29) was not significant. During rehabilitation, the relative contributions of CSA, muscle activation and Pi concentration to plantarflexor torque were 32, 44 and 40%, respectively. Together, CSA, muscle activation and Pi concentration accounted for 76% of the variance in torque (P < 0.01). In summary, our findings suggest that immobilization, independent of reloading, leads to a significant increase in the resting Pi concentration of human skeletal muscle. Additionally, alterations in resting Pi concentration may contribute to strength deficits with immobilization not accounted for by changes in muscle CSA or neural adaptations.

Deficit in human muscle strength with cast immobilization: contribution of inorganic phosphate.

Metabolische Faktoren sind vorgeschlagen worden, St&auml;rke Defizite beobachtet in der Skelettmuskulatur mit Immobilisierung zu erkl&auml;ren, die komplett nicht von Ver&auml;nderungen im Muskel-Querschnitt (CSA) und neuronale Anpassungen ber&uuml;cksichtigt werden. Ziel dieser Studie war es, &Auml;nderungen in der ruhelosigkeit anorganischen Phosphat (Pi)-Konzentration von der medialen Musculus gastrocnemius w&auml;hrend Immobilisation, Nachladen und Rehabilitation zu quantifizieren. Dar&uuml;ber hinaus beurteilen wir die Beitr&auml;ge der CSA, Muskelaktivierung und Pi-Konzentration zu plantar Musculus Flexor Drehmoment w&auml;hrend der Rehabilitation nach Immobilisierung. Acht Personen mit einem operativ stabilisierten Sprunggelenk Fraktur teilgenommen. Themen waren f&uuml;r 6-8 Wochen immobilisiert und daraufhin wirkte in 10 Wochen Rehabilitation. Lokalisierte (31) P-magnetische Resonanzspektroskopie, Kernspintomographie, isometrische Drehmoment und Aktivierung Tests wurden an den Gliedma&szlig;en immobilisierten und unbeteiligten durchgef&uuml;hrt. 6 Wochen der Immobilisation, signifikante Unterschiede zwischen den immobilisierten und unbeteiligten Gliedma&szlig;en f&uuml;r die Pi-Konzentration und das Verh&auml;ltnis von Pi/PCr festgestellt wurden (P &lt; 0,05). Von 6 Wochen der Immobilisation zu 3-5 Tage Nachladen, den Anstieg der Konzentration von Pi (15 %, P = 0,26) und Pi/PCr (20 %, P = 0,29) war nicht signifikant. W&auml;hrend der Rehabilitation wurden die relativen Beitr&auml;ge der CSA, Muskelaktivierung und Pi-Konzentration auf Plantarflexor Drehmoment 32, 44 und 40 %. Zusammen, CSA, Muskelaktivierung und Pi-Konzentration entfallen 76 % der Varianz im Drehmoment (P &lt; 0,01). Zusammenfassend l&auml;sst sich sagen empfehlen unsere Ergebnisse die Immobilisierung, unabh&auml;ngig von Nachladen, zu einem signifikanten Anstieg der ruhelosigkeit Pi-Konzentration von menschlichen Skelettmuskulatur f&uuml;hrt. Dar&uuml;ber hinaus k&ouml;nnen Ver&auml;nderungen in Ruhe Pi Konzentration zu St&auml;rke Defizite mit Immobilisierung nicht durch Ver&auml;nderungen im Muskel CSA oder neuronale Anpassungen entfielen beitragen.

Defizit in menschliche Muskelkraft mit Besetzung Immobilisation: Beitrag der anorganischen Phosphat.

To determine whether 9 weeks of locomotor training (LT) results in changes in muscle strength and alterations in muscle size and activation after chronic incomplete spinal cord injury (SCI).

Locomotor training and muscle function after incomplete spinal cord injury: case series.

Um zu bestimmen, ob 9 Wochen lokomotorische Training (LT) f&uuml;hrt zu &Auml;nderungen in Muskelkraft und Ver&auml;nderungen im Muskelgr&ouml;&szlig;e und Aktivierung nach chronischer unvollst&auml;ndige R&uuml;ckenmarkverletzung (SCI).

Lokomotorische Ausbildung und Muskel-Funktion nach unvollst&auml;ndigen R&uuml;ckenmarkverletzung: RS Serie.

The objective of this study was to determine the impact of treadmill locomotor training on the expression of insulin-like growth factor I (IGF1) and changes in myogenic regulatory factors (MRFs) in rat soleus muscle following spinal cord injury (SCI). Moderate, midthoracic (T(8)) contusion SCIs were produced using a NYU (New York University) impactor. Animals were randomly assigned to treadmill training or untrained groups. Rats in the training group were trained starting at 1 week after SCI, for either 3 bouts of 20 min over 1.5 days or 10 bouts over 5 days. Five days of treadmill training completely prevented the decrease in soleus fiber size resulting from SCI. In addition, treadmill training triggered increases in IGF1, MGF and IGFBP4 mRNA expression, and a concurrent reduction of IGFBP5 mRNA in skeletal muscle. Locomotor training also caused an increase in markers of muscle regeneration, including small muscle fibers expressing embryonic myosin and Pax7 positive nuclei and increased expression of the MRFs, myogenin and MyoD. We concluded that treadmill locomotor training ameliorated muscle atrophy in moderate contusion SCI rats. Training-induced muscle regeneration and fiber hypertrophy following SCI was associated with an increase in IGF1, an increase in Pax7 positive nuclei, and upregulation of MRFs.

Impact of treadmill locomotor training on skeletal muscle IGF1 and myogenic regulatory factors in spinal cord injured rats.

Ziel dieser Studie war es, die Auswirkung des Laufband lokomotorische Ausbildung &uuml;ber die Expression des Insulin-Like Growth Factor I (IGF1) und &Auml;nderungen in Myogener regulatorische Faktoren (MRFs) in Ratte Soleus Muskel nach Verletzung des R&uuml;ckenmarks (SCI) bestimmen. Moderat, Midthoracic (T(8)) Kontusion SCIs wurden hergestellt unter Verwendung eines Sto&szlig;k&ouml;rper NYU (New York University). Tiere wurden nach dem Zufallsprinzip zugewiesen Laufbandtraining oder unge&uuml;bt Gruppen. Ratten in der Trainingsgruppe wurden ausgebildet, ab 1 Woche nach SCI, f&uuml;r 3 Anf&auml;lle von 20 min &uuml;ber 1,5 Tage oder 10 Anf&auml;lle &uuml;ber 5 Tage. F&uuml;nf Tage von Laufbandtraining verhindert vollst&auml;ndig den R&uuml;ckgang der Schollenmuskel Faser Gr&ouml;&szlig;e aus Sci. Dar&uuml;ber hinaus erh&ouml;ht Laufbandtraining ausgel&ouml;st in IGF1, MGF und IGFBP4 mRNA Ausdruck und eine gleichzeitige Reduktion der IGFBP5 mRNA in der Skelettmuskulatur. Lokomotorische Training verursachte auch eine Erh&ouml;hung in Marker der Muskel-Regeneration, einschlie&szlig;lich kleine Muskelfasern, die embryonale Myosin und Pax7 positive Kerne und erh&ouml;hte Expression des MRFs, Myogenin und MyoD auszudr&uuml;cken. Wir festgestellt, dass die lokomotorische Laufbandtraining Muskelschwund bei moderaten Kontusion SCI Ratten einged&auml;mmt. Ausbildung-induzierte Regeneration und Faser Muskelhypertrophie nach SCI war eine Zunahme der IGF1, eine Zunahme Pax7 positive Kerne und Hochregulation des MRFs zugeordnet.

Auswirkungen der lokomotorischen Laufbandtraining Skelettmuskulatur IGF1 und myogener regulatorische Faktoren im R&uuml;ckenmark verletzt Ratten.

Muskelschw&auml;che entwickelt sich schneller nach Schlaganfall, motor Leistung beeintr&auml;chtigen und zu eingeschr&auml;nkter Funktionsf&auml;higkeit beitragen. W&auml;hrend die Beitr&auml;ge der strukturellen und funktionellen Ver&auml;nderungen in der Skelettmuskulatur zu Schw&auml;che post-stroke gut wurden beschrieben, die Beziehung zwischen motor Weg Integrit&auml;t, gemessen mit sowohl radiologische als auch elektrophysiologische Techniken, und Hirninfarkt Muskelschw&auml;che ist nicht klar. Diese Studie versucht, die Rolle des kortikospinalen Trakts (CST) Integrit&auml;t auf Knie Streckmuskel Schw&auml;che in der chronischen Schlaganfall &Uuml;berlebenden zu bestimmen.

Kortikospinalen Trakts Integrit&auml;t korreliert mit Knie Streckmuskel Schw&auml;che in der chronischen Schlaganfall-&Uuml;berlebenden.

Muscle weakness develops rapidly after stroke, adversely affecting motor performance, and contributing to reduced functional ability. While the contributions of structural and functional alterations in skeletal muscle to post-stroke weakness have been well described, the relationship between motor pathway integrity, measured using both radiological and electrophysiological techniques, and post-stroke muscle weakness is not clear. This study sought to determine the role of corticospinal tract (CST) integrity on knee extensor weakness in chronic stroke survivors.

Corticospinal tract integrity correlates with knee extensor weakness in chronic stroke survivors.

Despite greater muscle fatigue in individuals with spinal cord injury (SCI) when compared to neurologically intact subjects using neuromuscular electrical stimulation (NMES)protocols, few studies have investigated the extent of volitional fatigue in motor incomplete SCI. Using an established protocol of 20 repeated, intermittent, maximal volitional effort (MVE) contractions, we previously demonstrated that subjects with incomplete SCI unexpectedly demonstrated a 15% increase in peak knee extensor torques within the first five MVEs with minimal evidence of fatigue after 20 contraction. In the present study, we investigated potential segmental mechanisms underlying this supramaximal torque generation. Changes in twitch properties and maximum compound muscle action potentials (M-waves) were assessed prior to and following one, three and five MVEs, revealing a significant 17% increase only in maximum twitch torques after a single MVE. Despite this post-activation potentiation of the muscle, use of conventional NMES protocols to elicit repeated muscular contractions resulted in a significant decrease in evoked torque generation, suggesting limited the muscular contributions to the observed phenomenon. To evaluate potential central mechanisms underlying the augmented torques, non-linear responses to wide-pulse width (1 ms), low-intensity, variable-frequency (25â€“100 Hz) NMES were also tested prior to and following repeated MVEs.When variable-frequency NMES was applied following the repeated MVEs, augmented and prolonged torques were observed and accompanied by sustained quadriceps electromyographic activity often lasting > 2s after stimulus termination. Such data suggest a potential contribution of elevated spinal excitability to the reserve in volitional force generation in incomplete SCI.

Central excitability contributes to supramaximal volitional contractions in human incomplete spinal cord injury.

Trotz gr&ouml;&szlig;erer Muskelerm&uuml;dung bei Patienten mit Querschnittsl&auml;hmung (SCI) im Vergleich zu neurologisch intakten Themen &uuml;ber neuromuskul&auml;re Elektrostimulation (NMES) Protokolle, nur wenige Studien haben untersucht das Ausma&szlig; der volitional M&uuml;digkeit in Motor unvollst&auml;ndig Sci Using ein erstelltes Protokoll von 20 Kontraktionen der wiederholten, intermittierende, Max. volitional Aufwand (MVE), wir zuvor gezeigt, dass Probanden mit unvollst&auml;ndigen SCI unerwarteterweise eine 15 % Zunahme der Spitze Knie Streckmuskel Drehmomente innerhalb der ersten f&uuml;nf MVEs mit minimalen Beweis von M&uuml;digkeit nach 20 R&uuml;ckgang bewiesen. In der vorliegenden Studie untersuchten wir potenzielle segmentale Mechanismen dieser Supramaximal Drehmoment-Generation. Ver&auml;nderten sich zucken Eigenschaften und maximale zusammengesetzte Muskel Aktionspotentiale (M-Wellen) beurteilten vor und nach einem, drei und f&uuml;nf MVEs, offenbart einen deutlichen 17 % Anstieg nur maximale zucken Drehmomente nach einem einzigen MVE. Trotz dieser post-activation Potenzierung des Muskels wiederholte Verwendung von konventionellen NMES-Protokollen zu entlocken Muskelkontraktionen eine signifikante Abnahme in evozierte Drehmoment Generation schl&auml;gt begrenzte die muskul&auml;re Beitr&auml;ge auf das beobachtete Ph&auml;nomen gef&uuml;hrt. M&ouml;gliche zentrale Mechanismen der augmented auswerten Drehmomente, nichtlineare Antworten zu weiten-Pulsbreite (1 ms), niedriger Intensit&auml;t, Variable Frequenz (25&ndash;100 Hz) Wirkstoffe wurden auch getestet vor und folgen wiederholter MVEs.When Variable Frequenz NMES wurde angewendet, nach dem wiederholten MVEs, erg&auml;nzt und verl&auml;ngerte Drehmomente wurden beobachtet und begleitet von anhaltenden Quadrizeps elektromyographische Aktivit&auml;t oft dauerhafte &gt; 2s nach Beendigung der Reiz. Solche Daten zeigen einen m&ouml;glichen Beitrag der erh&ouml;hten spinalen Erregbarkeit der Reserve in volitional Kraft Generation unvollst&auml;ndig Sci.

Zentrale Erregbarkeit tr&auml;gt zur Supramaximal volitional Kontraktionen in menschlichen unvollst&auml;ndige R&uuml;ckenmarkverletzung.

. Neural plasticity may contribute to motor recovery following spinal cord injury (SCI). In rat models of SCI with respiratory impairment, acute intermittent hypoxia (AIH) strengthens synaptic inputs to phrenic motor neurons, thereby improving respiratory function by a mechanism known as respiratory long-term facilitation. Similar intermittent hypoxia-induced facilitation may be feasible in somatic motor pathways in humans.

Article	Year
4E-binding proteins, the suppressors of eukaryotic initiation factor 4E, are down-regulated in cells with acquired or intrinsic resistance to rapamycin. The Journal of biological chemistry\| PubMed ID: 11847216	2002
A dynamic equilibrium between CDKs and PP2A modulates phosphorylation of pRB, p107 and p130. Cell cycle (Georgetown, Tex.)\| PubMed ID: 15467457	2004
Lower-extremity muscle cross-sectional area after incomplete spinal cord injury. Archives of physical medicine and rehabilitation\| PubMed ID: 16731211	2006
Relative contributions of muscle activation and muscle size to plantarflexor torque during rehabilitation after immobilization. Journal of orthopaedic research : official publication of the Orthopaedic Research Society\| PubMed ID: 16779833	2006
Deficit in human muscle strength with cast immobilization: contribution of inorganic phosphate. European journal of applied physiology\| PubMed ID: 16841201	2006
Locomotor training and muscle function after incomplete spinal cord injury: case series. The journal of spinal cord medicine\| PubMed ID: 18581666	2008
Impact of treadmill locomotor training on skeletal muscle IGF1 and myogenic regulatory factors in spinal cord injured rats. European journal of applied physiology\| PubMed ID: 20213470	2010
Corticospinal tract integrity correlates with knee extensor weakness in chronic stroke survivors. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology\| PubMed ID: 21333591	2011
Central excitability contributes to supramaximal volitional contractions in human incomplete spinal cord injury. The Journal of physiology\| PubMed ID: 21610138	2011
Exposure to acute intermittent hypoxia augments somatic motor function in humans with incomplete spinal cord injury. Neurorehabilitation and neural repair\| PubMed ID: 21821826	2012

Arun Jayaraman

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