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https://www.readbyqxmd.com/read/27911406/ultrasound-guided-botulinum-toxin-a-injections-a-method-of-treating-sialorrhea
#1
Pierangelo Barbero, Marco Busso, Carlo Alberto Artusi, Stefania De Mercanti, Marco Tinivella, Andrea Veltri, Luca Durelli, Marinella Clerico
Neurological diseases can be complicated by sialorrhea, an excessive flow of saliva. Patients suffering from moderate to severe sialorrhea have an impaired quality of life, often worsened by correlated complications such as aspiration pneumonia, oral infections, dental caries, and maceration of the skin. Diverse therapeutic approaches have been proposed for the treatment of sialorrhea, including surgery and the use of anticholinergic agents, with limited results and the possible occurrence of serious adverse events...
November 9, 2016: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/27911334/matrix-metalloproteinases-and-tissue-inhibitor-of-metalloproteinases-in%C3%A2-inflammation-and-fibrosis-of-skeletal-muscles
#2
Hala S Alameddine, Jennifer E Morgan
In skeletal muscles, levels and activity of Matrix MetalloProteinases (MMPs) and Tissue Inhibitors of MetalloProteinases (TIMPs) have been involved in myoblast migration, fusion and various physiological and pathological remodeling situations including neuromuscular diseases. This has opened perspectives for the use of MMPs' overexpression to improve the efficiency of cell therapy in muscular dystrophies and resolve fibrosis. Alternatively, inhibition of individual MMPs in animal models of muscular dystrophies has provided evidence of beneficial, dual or adverse effects on muscle morphology or function...
November 29, 2016: Journal of Neuromuscular Diseases
https://www.readbyqxmd.com/read/27906078/four-week-rapamycin-treatment-improves-muscular-dystrophy-in-a-fukutin-deficient-mouse-model-of-dystroglycanopathy
#3
Steven J Foltz, Junna Luan, Jarrod A Call, Ankit Patel, Kristen B Peissig, Marisa J Fortunato, Aaron M Beedle
BACKGROUND: Secondary dystroglycanopathies are a subset of muscular dystrophy caused by abnormal glycosylation of α-dystroglycan (αDG). Loss of αDG functional glycosylation prevents it from binding to laminin and other extracellular matrix receptors, causing muscular dystrophy. Mutations in a number of genes, including FKTN (fukutin), disrupt αDG glycosylation. METHODS: We analyzed conditional Fktn knockout (Fktn KO) muscle for levels of mTOR signaling pathway proteins by Western blot...
June 2, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27906065/dystrophin-deficient-dogs-with-reduced-myostatin-have-unequal-muscle-growth-and-greater-joint-contractures
#4
Joe N Kornegay, Daniel J Bogan, Janet R Bogan, Jennifer L Dow, Jiahui Wang, Zheng Fan, Naili Liu, Leigh C Warsing, Robert W Grange, Mihye Ahn, Cynthia J Balog-Alvarez, Steven W Cotten, Monte S Willis, Candice Brinkmeyer-Langford, Hongtu Zhu, Joe Palandra, Carl A Morris, Martin A Styner, Kathryn R Wagner
BACKGROUND: Myostatin (Mstn) is a negative regulator of muscle growth whose inhibition promotes muscle growth and regeneration. Dystrophin-deficient mdx mice in which myostatin is knocked out or inhibited postnatally have a less severe phenotype with greater total mass and strength and less fibrosis and fatty replacement of muscles than mdx mice with wild-type myostatin expression. Dogs with golden retriever muscular dystrophy (GRMD) have previously been noted to have increased muscle mass and reduced fibrosis after systemic postnatal myostatin inhibition...
April 4, 2016: Skeletal Muscle
https://www.readbyqxmd.com/read/27904496/adipose-derived-stem-cells-enhance-myogenic-differentiation-in-the-mdx-mouse-model-of-muscular-dystrophy-via-paracrine-signaling
#5
Ji-Qing Cao, Ying-Yin Liang, Ya-Qin Li, Hui-Li Zhang, Yu-Ling Zhu, Jia Geng, Li-Qing Yang, Shan-Wei Feng, Juan Yang, Jie Kong, Cheng Zhang
Adipose-derived stem cells have been shown to promote peripheral nerve regeneration through the paracrine secretion of neurotrophic factors. However, it is unclear whether these cells can promote myogenic differentiation in muscular dystrophy. Adipose-derived stem cells (6 × 10(6)) were injected into the gastrocnemius muscle of mdx mice at various sites. Dystrophin expression was found in the muscle fibers. Phosphorylation levels of Akt, mammalian target of rapamycin (mTOR), eIF-4E binding protein 1 and S6 kinase 1 were increased, and the Akt/mTOR pathway was activated...
October 2016: Neural Regeneration Research
https://www.readbyqxmd.com/read/27882347/ml372-blocks-smn-ubiquitination-and-improves-spinal-muscular-atrophy-pathology-in-mice
#6
Mahlet B Abera, Jingbo Xiao, Jonathan Nofziger, Steve Titus, Noel Southall, Wei Zheng, Kasey E Moritz, Marc Ferrer, Jonathan J Cherry, Elliot J Androphy, Amy Wang, Xin Xu, Christopher Austin, Kenneth H Fischbeck, Juan J Marugan, Barrington G Burnett
Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease and one of the leading inherited causes of infant mortality. SMA results from insufficient levels of the survival motor neuron (SMN) protein, and studies in animal models of the disease have shown that increasing SMN protein levels ameliorates the disease phenotype. Our group previously identified and optimized a new series of small molecules, with good potency and toxicity profiles and reasonable pharmacokinetics, that were able to increase SMN protein levels in SMA patient-derived cells...
November 17, 2016: JCI Insight
https://www.readbyqxmd.com/read/27881412/renin-angiotensin-aldosterone-system-inhibitors-improve-membrane-stability-and-change-gene-expression-profiles-in-dystrophic-skeletal-muscles
#7
Jessica A Chadwick, Sayak Bhattacharya, Jeovanna Lowe, Noah Weisleder, Jill A Rafael-Fortney
Angiotensin-converting enzyme inhibitors and mineralocorticoid receptor (MR) antagonists are FDA approved drugs that inhibit the renin-angiotensin-aldosterone system (RAAS) and are used to treat heart failure. Combined treatment with the angiotensin-converting enzyme inhibitor lisinopril and the non-specific MR antagonist spironolactone surprisingly improves skeletal muscle, in addition to heart function and pathology in a Duchenne muscular dystrophy mouse model. We recently demonstrated that MR is present in all limb and respiratory muscles and functions as a steroid hormone receptor in differentiated normal human skeletal muscle fibers...
November 23, 2016: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/27874066/cl316-243-a-%C3%AE-3-adrenergic-receptor-agonist-induces-muscle-hypertrophy-and-increased-strength
#8
Daniela Puzzo, Roberto Raiteri, Clotilde Castaldo, Raffaele Capasso, Ester Pagano, Mariateresa Tedesco, Walter Gulisano, Lisaveta Drozd, Pellegrino Lippiello, Agostino Palmeri, Pietro Scotto, Maria Concetta Miniaci
Studies in vitro have demonstrated that β3-adrenergic receptors (β3-ARs) regulate protein metabolism in skeletal muscle by promoting protein synthesis and inhibiting protein degradation. In this study, we evaluated whether activation of β3-ARs by the selective agonist CL316,243 modifies the functional and structural properties of skeletal muscles of healthy mice. Daily injections of CL316,243 for 15 days resulted in a significant improvement in muscle force production, assessed by grip strength and weight tests, and an increased myofiber cross-sectional area, indicative of muscle hypertrophy...
November 22, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27873355/isoquercitrin-protects-against-pulmonary-hypertension-via-inhibiting-pasmcs-proliferation
#9
Yongtao Zhang, Yuqian Cui, Wei Deng, Hao Wang, Weidong Qin, Chengmin Huang, Chen Li, Jianning Zhang, Yuan Guo, Dawei Wu, Haipeng Guo
Pulmonary vascular remodeling is a common feature among the heterogeneous disorders that cause pulmonary arterial hypertension (PAH), and pulmonary arterial smooth muscle cells (PASMCs) proliferation impact the long-term prognosis of the patient. Isoquercitrin (IQC) is a flavonoid with anti-oxidative, anti-inflammatory and anti-proliferative activations. This study aimed to investigate whether IQC could prevent PASMCs proliferation and vascular remodeling in monocrotaline (MCT) induced PAH. Male Wistar rats were administered with vehicle or 0...
November 22, 2016: Clinical and Experimental Pharmacology & Physiology
https://www.readbyqxmd.com/read/27872157/exendin-4-increases-oxygen-consumption-and-thermogenic-gene-expression-in-muscle-cells
#10
Jin-Seung Choung, Young-Sun Lee, Hee-Sook Jun
Glucagon-like peptide-1 (GLP1) has many anti-diabetic actions and also increases energy expenditure in vivo. Since skeletal muscle is a major organ controlling energy metabolism, we investigated whether GLP1 can affect energy metabolism in muscle. We found that treatment of differentiated C2C12 cells with Exendin-4 (Ex-4), a GLP1 receptor agonist, reduced oleate:palmitate-induced lipid accumulation and triglyceride content compared with cells without Ex-4 treatment. When we examined the oxygen consumption rate (OCR), not only the basal OCR but also the OCR induced by oleate:palmitate addition was significantly increased in Ex-4-treated differentiated C2C12 cells, and this was inhibited by Exendin-9, a GLP1 receptor antagonist...
November 21, 2016: Journal of Molecular Endocrinology
https://www.readbyqxmd.com/read/27871005/nickel-affects-gill-and-muscle-development-in-oriental-fire-bellied-toad-bombina-orientalis-embryos
#11
Chan Jin Park, Sang Ha Song, Dae Han Kim, Myung Chan Gye
The developmental toxicity of nickel was examined in the embryos of Bombina orientalis, a common amphibian in Korea. Based on a standard frog embryo teratogenesis assay, the LC50 and EC50 for malformation of nickel after 168h of treatment were 33.8μM and 5.4μM, respectively. At a lethal concentration (100μM), nickel treatment decreased the space between gill filaments and caused epithelial swelling and abnormal fusion of gill filaments. These findings suggest that nickel affects the functional development of gills, leading to embryonic death...
November 15, 2016: Aquatic Toxicology
https://www.readbyqxmd.com/read/27870893/activin-receptor-type-iib-inhibition-improves-muscle-phenotype-and-function-in-a-mouse-model-of-spinal-muscular-atrophy
#12
Min Liu, David W Hammers, Elisabeth R Barton, H Lee Sweeney
Spinal muscular atrophy (SMA) is a devastating neurodegenerative disorder that causes progressive muscle atrophy and weakness. Using adeno-associated virus-mediated gene transfer, we evaluated the potential to improve skeletal muscle weakness via systemic, postnatal inhibition of either myostatin or all signaling via the activin receptor type IIB (ActRIIB). After demonstrating elevated p-SMAD3 content and differential content of ActRIIB ligands, 4-week-old male C/C SMA model mice were treated intraperitoneally with 1x1012 genome copies of pseudotype 2/8 virus encoding a soluble form of the ActRIIB extracellular domain (sActRIIB) or protease-resistant myostatin propeptide (dnMstn) driven by a liver specific promoter...
2016: PloS One
https://www.readbyqxmd.com/read/27867023/the-role-of-white-matter-microstructure-in-inhibitory-deficits-in-patients-with-schizophrenia
#13
Xiaoming Du, Peter Kochunov, Ann Summerfelt, Joshua Chiappelli, Fow-Sen Choa, L Elliot Hong
BACKGROUND: Inhibitory-excitatory (I-E) imbalance has increasingly been proposed as a fundamental mechanism giving rise to many schizophrenia-related pathophysiology. The integrity of I-E functions should require precise and rapid electrical signal transmission. OBJECTIVE/HYPOTHESIS: We hypothesized that part of the I-E abnormality in schizophrenia may originate from their known abnormal white matter connectivity that may interfere the I-E functions. METHODS: We test this using short-interval intracortical inhibition (SICI) vs...
November 12, 2016: Brain Stimulation
https://www.readbyqxmd.com/read/27861881/testosterone-rescues-the-de-differentiation-of-smooth-muscle-cells-through-serum-response-factor-myocardin
#14
Carolina Leimgruber, Amado A Quintar, Nahuel Peinetti, María V Scalerandi, Juan P Nicola, Joseph M Miano, Cristina A Maldonado
Prostatic smooth muscle cells (pSMCs) differentiation is a key factor for prostatic homeostasis, with androgens exerting multiple effects on these cells. Here, we demonstrated that the myodifferentiator complex Srf/Myocd is up-regulated by testosterone in a dose-dependent manner in primary cultures of rat pSMCs, which was associated to the increase in Acta2, Cnn1, and Lmod1 expressions. Blocking Srf or Myocd by siRNAs inhibited the myodifferentiator effect of testosterone. While LPS led to a dedifferentiated phenotype in pSMCs, characterized by down-regulation of Srf/Myocd and smooth muscle cell (SMC)-restricted genes, endotoxin treatment on Myocd-overexpressing cells did not result in phenotypic alterations...
November 9, 2016: Journal of Cellular Physiology
https://www.readbyqxmd.com/read/27852769/tracking-the-time-course-of-top-down-contextual-effects-on-motor-responses-during-action-comprehension
#15
Lucia Amoruso, Alessandra Finisguerra, Cosimo Urgesi
: Context plays a key role in coding high-level components of others' behavior, including the goal and the intention of an observed action. However, little is known about its possible role in shaping lower levels of action processing, such as simulating action kinematics and muscular activity. Furthermore, there is no evidence regarding the time course and the neural mechanisms subserving this modulation. To address these issues, we combined single-pulse transcranial magnetic stimulation and motor-evoked potentials while healthy humans watched videos of everyday actions embedded in congruent, incongruent, or ambiguous contexts...
November 16, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27835923/ros-no-mediated-inter-organ-communication-in-skeletal-muscle-wasting-diseases
#16
Lucia Maria Leitner, Rebecca June Wilson, Zhen Yan, Axel Gödecke
SIGNIFICANCE: Cachexia is defined as a complex metabolic syndrome associated with underlying illness and a loss of muscle with or without loss of fat mass. This disease is associated with high incidence with chronic diseases such as heart failure, cancer, chronic obstructive pulmonary disease, AIDS, among others. Since there is currently no effective treatment available, cachectic patients have a poor prognosis. Elucidation of the underlying mechanisms is therefore an important medical task...
November 11, 2016: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/27832594/high-frequency-neuromuscular-electrical-stimulation-modulates-interhemispheric-inhibition-in-healthy-humans
#17
Nicolas Gueugneau, Sidney Grosprêtre, Paul J Stapley, Romuald Lepers
High frequency neuromuscular electrical stimulation (HF NMES) induces muscular contractions through neural mechanisms that partially match physiological motor control. Indeed, a portion of the contraction arises from central mechanisms, whereby spinal motoneurons are recruited through the evoked sensory volley. However, the involvement of supraspinal centers of motor control during such a stimulation remained poorly understood. Therefore, we tested whether a single HF NMES session applied to the upper limb influences interhemispheric inhibition (IHI) from left to right motor cortex (M1)...
November 9, 2016: Journal of Neurophysiology
https://www.readbyqxmd.com/read/27816329/a-complex-interplay-of-genetic-and-epigenetic-events-leads-to-abnormal-expression-of-the-dux4-gene-in-facioscapulohumeral-muscular-dystrophy
#18
REVIEW
Laura Virginia Gatica, Alberto Luis Rosa
Facioscapulohumeral muscular dystrophy (FSHD), a prevalent inherited human myopathy, develops following a complex interplay of genetic and epigenetic events. FSHD1, the more frequent genetic form, is associated with: (1) deletion of an integral number of 3.3 Kb (D4Z4) repeated elements at the chromosomal region 4q35, (2) a specific 4q35 subtelomeric haplotype denominated 4qA, and (3) decreased methylation of cytosines at the 4q35-linked D4Z4 units. FSHD2 is most often caused by mutations at the SMCHD1 (Structural Maintenance of Chromosomes Hinge Domain 1) gene, on chromosome 18p11...
September 19, 2016: Neuromuscular Disorders: NMD
https://www.readbyqxmd.com/read/27813347/early-high-intensity-versus-low-intensity-rehabilitation-after-total-knee-arthroplasty-a-randomized-controlled-trial
#19
Michael Bade, Tamara Struessel, Michael Dayton, Jared Foran, Raymond Kim, Todd Miner, Pamela Wolfe, Wendy Kohrt, Douglas Dennis, Jennifer Stevens-Lapsley
OBJECTIVE: The purpose of this study was to examine the safety and efficacy of a high-intensity progressive rehabilitation protocol (HI) beginning 4 days after total knee arthroplasty (TKA) compared to a low-intensity (LI) rehabilitation protocol. METHODS: One hundred sixty-two participants (aged 63±7 years; 89 females) were randomized to either the HI group or LI group after TKA. Key components of the HI intervention were the utilization of progressive resistance exercises and a rapid progression to weight-bearing exercises and activities...
November 3, 2016: Arthritis Care & Research
https://www.readbyqxmd.com/read/27799722/prone-positioning-reduces-severe-pushing-behavior-three-case-studies
#20
Yuji Fujino, Kazu Amimoto, Satoshi Sugimoto, Kazuhiro Fukata, Masahide Inoue, Hidetoshi Takahashi, Shigeru Makita
[Purpose] Pushing behavior is classically described as a disorder of body orientation in the coronal plane. Most interventions for pushing behavior have focused on correcting the deviation in vertical perception. However, pushing behavior seems to involve erroneous movements associated with excessive motor output by the non-paretic limbs and trunk. The present study aimed to inhibit muscular hyper-activity by placing the non-paretic limbs and trunk in the prone position. [Subjects and Methods] The subjects of the present study were 3 acute stroke patients with severe pushing behavior...
September 2016: Journal of Physical Therapy Science
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