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At least 775 records · Page 43Linked to original sources
PubMed1992

Beta-adrenergic system in myotonic dystrophy.

Myotonic dystrophy (DM) is considered an inherited membrane disorder, but the basic defect is unknown. We studied plasma catecholamines as well as lymphocyte and muscle beta-adrenergic receptor densities and functioning in 19 DM patients and 15 control subjects. Plasma adrenaline and noradrenaline concentrations were not significantly different between DM patients and controls. In isolated lymphocytes basal cAMP production was 157 +/- 26 pmol/mg protein/10 min in DM patients and 91 +/- 12 pmol/mg protein/10 min in controls (n.s.), whereas isoproterenol-stimulated cAMP production was significantly higher in DM patients (285 +/- 42 pmol/mg protein) compared with control subjects (168 +/- 21 pmol/mg protein, P less than 0.05). Lymphocyte beta-adrenoceptor densities were similar among DM patients (50 +/- 3 fmol/mg protein) and controls (47 +/- 5 fmol/mg protein). beta-Adrenoceptor densities were also similar in muscle biopsy specimens (12.9 +/- 1 in DM and 13.1 +/- fmol/mg protein in controls). The correlation between lymphocyte and skeletal muscle receptor densities was r = 0.35 in DM patients and r = 0.22 in controls. The results do not support the hypothesis of adrenergic dysfunction in DM despite its membrane involvement.

Adolescent↗
PubMed2006

The Belfast approach to managing complex lower limb vascular injuries.

INTRODUCTION: Complex lower limb vascular injuries (CLVIs) in high-energy penetrating or blunt trauma are associated with an unacceptably high incidence of complications including amputation. Traumatic ischaemia and ischaemia-reperfusion injury (IRI) of skeletal muscle often lead to limb loss, the systemic inflammatory response syndrome (SIRS) which affects remote organs and even the potentially fatal multiple organ dysfunction syndrome (MODS). Surgical care of CLVIs everywhere, including Northern Ireland until 1978, was governed by an anxiety to restore arterial flow quickly often using expedient and flawed repair techniques while a damaged major vein was frequently ligated. MATERIALS AND METHODS: A new policy centred on early intraluminal shunting of both artery and vein, restoring arterial inflow and venous outflow, respectively, was introduced at the Regional Vascular Surgery Unit of The Royal Victoria Hospital, Belfast in 1979. It imposed a disciplined one-stage comprehensive approach to treatment involving a sequence of operative manoeuvres in which all damaged anatomical elements receive meticulous and optimal attention unshackled by time constraints. RESULTS: Comparisons drawn between the pre-shunt period of unplanned treatment (1969-1978) and the post-shunt period centred on the use of shunts (1979-2000) showed that early shunting of both artery and vein in both penetrating (P) and blunt (B) injuries significantly reduced the necessity for fasciotomy (P: p=0.016, B: p=0.02) and caused a significant fall in the incidence of contracture (P: p=0.018, B: p=0.02) and of amputation (P: p=0.009, P: p=0.012). CONCLUSIONS: The policy of early shunting of artery and vein in CLVIs has proved to be of great benefit in terms of significantly improved outcomes, better operative discipline and harmonious collaboration among the specialists involved.

Blood Vessels↗
PubMed2006

Bone marrow-derived mesenchymal stem cells for regenerative medicine in craniofacial region.

The craniofacial region contains many specified tissues including bone, cartilage, muscle, blood vessels and neurons. Defect or dysfunction of the craniofacial tissue after post-cancer ablative surgery, trauma, congenital malformations and progressive deforming skeletal diseases has a huge influence on the patient's life. Therefore, functional reconstruction of damaged tissues is highly expected. Bone marrow-derived mesenchymal stem cells (BMMSCs) are one of the most well characterized postnatal stem cell populations, and considered to be utilized for cell-based clinical therapies. Here, the current understanding and the potential applications in craniofacial tissue regeneration of BMMSCs are reviewed, and the current limitations and drawbacks are also discussed.

Animals↗
PubMed1996

Assessment of the distribution of mitochondrial ribosomal RNA in melas and in thrombotic cerebral infarcts by in situ hybridization.

In situ hybridization to mitochondrial ribosomal RNA (rRNA) has been used to study the distribution of mitochondria in paraffin-embedded autopsy brain tissue from two patients with MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes) and other organs from one of the patients. Comparison of in situ hybridization and electron microscopic findings in an antemortem biopsy specimen of pylorus from the latter patient showed a close correspondence between the distribution of hybridization signal on light microscopy and of mitochondria in ultrathin sections. Strong hybridization signal was present over smooth muscle fibres of the muscularis externa, which contained abnormal accumulations of mitochondria on electron microscopy. Hybridization to sections of skeletal muscle confirmed previous reports of 'ragged-red' fibres in this disorder and of mitochondrial accumulations in the walls of intramuscular blood vessels. To try to elucidate the role of vessel wall accumulation of mitochondria in the genesis of the stroke-like lesions, the distribution of mitochondrial rRNA was assessed in sections of brain from both of the cases of MFLAS and several cases of atherothrombotic cerebrovascular disease. Blood vessels in and adjacent to the cerebral lesions of MELAS showed strong hybridization signal with the mitochondrial probes, as was also seen in infarcts of various ages in the control brains. Only weak signal was present in the walls of blood vessels distant from the lesions, in both MELAS and control brains. These findings suggest that mitochondria accumulate in vascular endothelium and tunica media as a normal response to cerebral infarction or ischaemia. The accumulation of mitochondria in the cerebral lesions of MELAS may, at least in part, be a reaction to the destructive effects of the underlying metabolic dysfunction.

Brain↗
PubMed2002

The A8344G mutation in mitochondrial DNA associated with stroke-like episodes and gastrointestinal dysfunction.

We report an unusual case of encephalo-entero-myopathy associated with the A8344G mutation in the tRNA(Lys) gene of mitochondrial DNA (mtDNA). This patient had mitochondrial myopathy, multiple lipomatosis, mild hearing loss, stroke-like episodes, and paralytic ileus, but she lacked the canonical clinical features of MERRF, myoclonus, epilepsy, or ataxia. We conducted genetic, biochemical, histochemical, and immunohistochemical studies in skeletal muscle, brain, intestine, and lipoma tissue. The mutation was abundant in all tissues, and cytochrome c oxidase (COX) activity was selectively decreased in brain and small intestine. COX deficiency was also documented histochemically and immunohistochemically in the small intestine, suggesting that mitochondrial dysfunction played a role in the pathogenesis of paralytic ileus. This case illustrates an unusual and dramatic clinical phenotype of the A8344G mutation, characterized by stroke-like episodes and acute ileus.

Adult↗
PubMed1992

Skeletal muscle function, morphology, and metabolism in patients with congestive heart failure.

Work by a number of laboratories over the last decade has revealed that skeletal muscle in patients with congestive heart failure (CHF) exhibits altered metabolism, biochemistry, and histology. These alterations appear to be at least in part independent of systemic hemodynamic abnormalities and they lead to abnormal muscle function. Furthermore, muscle dysfunction may play a role in limiting exercise capacity. While blood flow to exercising muscle may be impaired in CHF, both the functional and metabolic changes are, to some degree, independent of the changes in blood flow. Deconditioning and muscle atrophy may be responsible for some of these functional metabolic alterations in muscle, but other factors appear to be operating as well. Finally, the finding that many of the changes in skeletal muscle associated with CHF can be reversed by exercise training suggests that activity should be encouraged in patients with CHF.

Exercise↗
PubMed2004

Myofascial dysfunction in the pelvis.

Chronic pelvic pain is a potentially devastating condition that affects many women with severe consequences. A multifaceted condition, chronic pelvic pain enjoys a diverse etiology, a myriad of treatments, and a correspondingly irregular response to therapy. The condition can be associated with severe physical dysfunction in relation to voiding, defecation, and sexual function. Although emphasis has been placed on surgical approaches to therapy, there is increasing interest in alternative therapies, particularly using the principles of the treatment of myofascial dysfunction.

Adult↗
PubMed2001

Movement and stability dysfunction--contemporary developments.

A good understanding of the control processes used to maintain stability in functional movements is essential for clinicians who attempt to treat or manage musculoskeletal pain problems. There is evidence of muscle dysfunction related to the control of the movement system. There is a clear link between reduced proprioceptive input, altered slow motor unit recruitment and the development of chronic pain states. Dysfunction in the global and local muscle systems is presented to support the development of a system of classification of muscle function and development of dysfunction related to musculoskeletal pain. The global muscles control range of movement and alignment, and evidence of dysfunction is presented in terms of imbalance in recruitment and length between the global stability muscles and the global mobility muscles. Direction related restriction and compensation to maintain function is identified and related to pathology. The local stability muscles demonstrate evidence of failure of adequate segmental control in terms of allowing excessive uncontrolled translation or specific loss of cross-sectional area at the site of pathology. Motor recruitment deficits present as altered timing and patterns of recruitment. The evidence of local and global dysfunction allows the development of an integrated model of movement dysfunction.

Chronic Disease↗
PubMed2002

Clinical considerations in the use of surface electromyography: three experimental studies.

BACKGROUND: The validity and applicability of erector spinae electromyogram (EMG) use in clinical practice is questionable. Differences in the amplitude of the EMG signal between populations with low back pain (LBP) and controls have been hypothesized but not sufficiently documented. OBJECTIVE: To examine issues of EMG asymmetry and repeatability in populations with LBP and populations without LBPin 3 separate studies. STUDY DESIGN: Three separate experimental research studies. METHODS: Study 1 examined the intraclass correlation of the EMG signal of the paraspinal musculature at L3 on 3 separate days during quiet stance with use of 3 different normalization techniques: percent maximum voluntary contraction, percent submaximal voluntary contraction, and percent averaged submaximal contractions. Study 2 used a population with chronic LBP to compare the bilateral asymmetry of paraspinal musculature in segments exhibiting pain with segments not exhibiting pain during quiet stance. A 1-way analysis of variance was used to compare differences between asymmetry scores in the pain and nonpain groups. In study 3, persons with LBP and persons in the control group had the dynamic asymmetry of paraspinal musculature compared during forward bending. A cross-correlation coefficient assessing bilateral muscle activity was calculated for each subject and differences between groups were evaluated using a 1-way analysis of variance. RESULTS: Study 1: Subjects showed excellent repeatability (ICC > 0.75) regardless of the normalization technique. Study 2: During quiet stance no differences were found in bilateral asymmetry between painful and nonpainful motion segments. Study 3: No differences existed in bilateral dynamic symmetry for the upper erector spinae; however, differences between groups did exist for the lower erector spinae. CONCLUSION: Repeatability of the EMG signal during quiet stance is acceptable; however, bilateral asymmetry may not be a definitive indicator of dysfunction.

Adult↗
PubMed1988

Vitamin E deficiency and neurologic disease.

During the recent resurgence of interest in the clinical uses of vitamin E, one of the major foci of attention has been the neurologic role of vitamin E in humans. Studies in patients with secondary vitamin E deficiency, caused by fat malabsorption disorders and total parenteral nutrition lacking an adequate supply of vitamin E, have elucidated a clinical disorder and histologic lesions of the nervous system and muscle that closely resemble those of experimental vitamin-E-deficient animal models. Investigations of the primary form of human vitamin E deficiency, the isolated vitamin E deficiency syndrome, have further substantiated the relationship between neurologic dysfunction and human vitamin E deficiency. It is now clear that vitamin E is an essential nutrient necessary for the optimal development and maintenance of the integrity and function of the human nervous system and skeletal muscle. The task for future study is to determine the mechanism by which vitamin E deficiency causes degeneration of selective regions of the nervous system and to investigate possible benefits of vitamin E supplementation in other neurologic disorders. In addition, further study of the isolated vitamin E deficiency syndrome promises to teach us more about normal physiologic mechanisms of vitamin E absorption and transport in humans.

Female↗
PubMed1999

Vascular reactivity.

Endothelial dysfunction appears to be an integral aspect of the insulin resistance syndrome, independently of hyperglycemia. The ability of insulin to cause endothelium-derived nitric oxide (NO)-dependent vasodilation amplifies its overall effect of stimulating skeletal muscle glucose uptake and modulating vascular tone. The dose-dependent physiologic increase in skeletal muscle blood flow in response to insulin, which is highly associated with the rate of glucose metabolism, is impaired in insulin-resistant states. Insulin appears to mediate vasodilation by direct stimulation of release of NO from endothelium. Studies of the response to the endothelium-dependent vasodilator methacholine chloride in lean and obese nondiabetic subjects and obese subjects with type 2 diabetes mellitus indicate that there may be marked endothelial dysfunction very early in insulin resistance. The potent vasoprotective effects of NO mitigate various atherogenic processes, including vascular smooth muscle cell proliferation, platelet adhesion and thrombogenesis, lipid peroxidation, and monocyte adhesion to endothelial cells. The interaction between insulin and NO may contribute to the prominent outcomes of insulin resistance syndrome (viz., hypertension, thrombosis, and atherosclerosis).

Cell Movement↗
PubMedDate not supplied

A clinical and pharmacologic review of skeletal muscle relaxants for musculoskeletal conditions.

Muscle strains and other musculoskeletal disorders (MSDs) are a leading cause of work absenteeism. Muscle pain, spasm, swelling, and inflammation are symptomatic of strains. The precise relationship between musculoskeletal pain and spasm is not well understood. The dictum that pain induces spasm, which causes more pain, is not substantiated by critical analysis. The painful muscle may not show EMG activity, and when there is, the timing and intensity often do not correlate with the pain. Clinical and physiologic studies show that pain tends to inhibit rather than facilitate reflex contractile activity. The decision to treat and choice of therapy are largely dictated by the duration, severity of symptoms, and degree of dysfunction. Trigger point injections are sometimes used with excellent results in the treatment of muscle spasm in myofacial pain and low-back pain. NSAIDs are used with much greater frequency than oral skeletal muscle relaxants (SMRs) or opioids in the treatment of acute MSDs. Unfortunately, remarkably little sound science guides the choice of drug for the treatment of acute, uncomplicated MSDs, and the evaluation of efficacy of one agent over another is complicated by numerous factors. Only a limited number of high-quality, randomized, controlled trials (RCTs) provide evidence of the effectiveness of NSAIDs or SMRs in the treatment of acute, uncomplicated MSDs. The quality of design, execution, and reporting of trials for the treatment of MSDs needs to be improved. The combination of an SMR and an NSAID or COX-2 inhibitor or the combination of SMR and tramadol/acetaminophen is superior to single agents alone.

Acute Disease↗
PubMed1997

Clinical and brain bioenergetics improvement with idebenone in a patient with Leber's hereditary optic neuropathy: a clinical and 31P-MRS study.

We used phosphorus magnetic resonance spectroscopy (31P-MRS) to study in vivo brain and muscle bioenergetics in a male patient with Leber's hereditary optic neuropathy (LHON) and mtDNA mutation at 11,778 bp who developed spastic paraparesis with white matter lesions on brain MR imaging. The study was performed before and during treatment with idebenone (135 mg t.i.d.) and after withdrawal. Clinical amelioration and worsening were associated with parallel changes in brain and skeletal muscle bioenergetics following the administration or withdrawal of idebenone. Reversal of paraparesis by idebenone was paralleled by normalization of 31P-MRS, serum lactate and central motor conduction. Extra-ocular neurological dysfunction in LHON may be amenable to treatment by appropriate quinones.

Adult↗
PubMed2005

Creatine has no beneficial effect on skeletal muscle energy metabolism in patients with single mitochondrial DNA deletions: a placebo-controlled, double-blind 31P-MRS crossover study.

The purpose of our randomized, double-blind, placebo-controlled crossover study in 15 patients with chronic progressive external ophthalmoplegia (CPEO) or Kearns-Sayre syndrome (KSS) because of single large-scale mitochondrial (mt) DNA deletions was to determine whether oral creatine (Cr) monohydrate can improve skeletal muscle energy metabolism in vivo. Each treatment phase with Cr in a dosage of 150 mg/kg body weight/day or placebo lasted 6 weeks. The effect of Cr was estimated by phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS), clinical and laboratory tests. (31)P-MRS analysis prior to treatment showed clear evidence of severe mitochondrial dysfunction. However, there were no relevant changes in (31)P-MRS parameters under Cr. In particular, phosphocreatine (PCr)/ATP at rest did not increase, and there was no facilitation of post-exercise PCr recovery. Clinical scores and laboratory tests did not alter significantly under Cr, which was tolerated without major side-effects in all patients. Cr supplementation did not improve skeletal muscle oxidative phosphorylation in our series of patients. However, one explanation for our negative findings may be the short study duration or the limited number of patients included.

Adult↗
PubMed2004

Mitochondrial DNA abnormalities and autistic spectrum disorders.

OBJECTIVES: To further characterize mtDNA defects associated with autistic features, especially the A3243G mtDNA mutation and mtDNA depletion.Study design Five patients with autistic spectrum disorders and family histories of mitochondrial DNA diseases were studied. We performed mtDNA analysis in all patients and magnetic resonance spectroscopy in three. RESULTS: Three patients manifested isolated autistic spectrum features and two had additional neurologic symptoms. Two patients harbored the A3243G mutation. In two others, the A3243G mutation was not found in accessible tissues but was present in tissues from their mothers. The fifth patient had 72% mtDNA depletion in skeletal muscle. CONCLUSIONS: Autistic spectrum disorders with or without additional neurologic features can be early presentations of the A3243G mtDNA mutation and can be a prominent clinical manifestation of mtDNA depletion. Mitochondrial dysfunction should be considered in patients who have autistic features and associated neurologic findings or who have evidence of maternal inheritance.

Adolescent↗
PubMed2006

The effects of atorvastatin on coronary endothelial function in patients with recent myocardial infarction.

BACKGROUND: Endothelial dysfunction is a key early event in atherosclerosis that occurs in acute coronary syndrome. It was reported that atorvastatin improves the endothelial function of skeletal muscle vessels, but the effect on the coronary artery is unknown. HYPOTHESIS: The purpose of this study is to determine the effects of atorvastatin on coronary endothelial function in humans. METHODS: Non-infarct-related coronary arteries of 48 patients with acute myocardial infarction who had undergone successful percutaneous transluminal coronary angioplasty were examined. Three groups were studied: hyperlipidemia with use of atorvastatin (Group 1, n=17), hyperlipidemia without statin use (Group 2, n=18), and normal cholesterol level controls (Group 3, n=13). Statin treatment was started at discharge. Acetylcholine (Ach) was infused into the coronary artery and the diameter was assessed by quantitative angiography at baseline and after 6 months. RESULTS: Acetylcholine given in doses of 1, 3, 10, and 30 mg/min increased the coronary artery diameter change in a dose-dependent manner. In the initial study, patients in the three groups had similar responses to Ach. The mean diameter change after 6 months was significantly improved in Group 1 compared with Groups 2 and 3 (-11 +/- 3% vs. -20 +/- 7% and -21 +/- 6%, respectively; p < 0.01 in each case). Multivariate regression analysis showed that atorvastatin (p < 0.01) was the significant determinant for improvement of endothelial function. CONCLUSIONS: These findings suggest that atorvastatin improves endothelial function of the coronary artery in patients with myocardial infarction.

Acetylcholine↗
PubMed1990

Biochemical alterations in skeletal muscle induced by 2,4-dichlorophenoxyacetic butyl ester during chick embryonic development.

2,4-Dichlorophenoxyacetic butyl ester (2,4-D b.e.) (3.1 mg/egg) was applied on fertile hen eggs before starting the incubation. Chicks hatched from treated eggs showed motor dysfunctions, postural troubles and edematous muscles. The electromyography revealed muscular weakness, prolonged motor distal latency, and myotonia. The biochemical composition of leg and complexus muscles from 1-day-old chicks was determined. A significant diminution (24%) in the glycogen level of leg muscles was produced by the treatment. There was a small increase (15%) in sarcoplasmic proteins from leg muscles and an increase of a 20 kD protein in the myofibrillar proteins from complexus muscles. Even though total lipid content was not changed, 2,4-D b.e. treatment produced a diminution of sterol esters (20%) and phosphatidylcholine (11%) and an increase of phosphatidylserine (61%), triglycerides (37%) and free fatty acids (FFA) (448%) in leg muscles. Increases of phosphatidylethanolamine (16%), sterols (58%) and FFA (267%) were detected in complexus muscles. A remarkable increase (700-1500%) of unsaturated FFA, e.g. oleic, linoleic and arachidonic acids, was observed. Considering the avian embryo lipid metabolism, it is proposed that FFA and triglycerides were accumulated because they could not be metabolized in the mitochondria. Since FFA are potent cytotoxic compounds, their increase may be a key factor in the 2,4-D b.e. toxic action in muscle and other tissues during embryonic development.

2,4-Dichlorophenoxyacetic Acid↗