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PubMed2003

Reduced muscle strength in abduction of the index finger: an important clinical sign in hand-arm vibration syndrome.

Muscle strength in extrinsic and intrinsic hand muscle was assessed in 21 patients with hand-arm vibration syndrome. Twenty-one age-matched healthy workers served as controls. Grip and pinch strength was significantly reduced in the vibration-exposed group (18%; p = 0.006 and 18% p = 0.007, respectively) as well as strength of palmar abduction of the thumb (28%; p < 0.0001) and radial abduction of the index finger (37%; p < 0.0001) while abduction strength in the little finger was not significantly reduced (7%). We postulate that the reduced manipulative skill and impaired dexterity of the hand, which often is associated with vibration syndrome, is not only of sensorineural origin but may also be an effect of reduced intrinsic muscle strength. Reduced strength in abduction of the index finger is an important indicator of intrinsic muscular dysfunction in subjects who use hand-held vibrating tools.

Analysis of Variance↗

PubMed2000

New insights into sympathetic regulation of glucose and fat metabolism.

The autonomic nervous system modulates glucose and fat metabolism through both direct neural effects and hormonal effects. This review presents recent concepts on the sympathetic regulation of glucose and fat metabolism. Focally released norepinephrine from sympathetic nerves is likely to increase glucose uptake in skeletal muscle and adipose tissues independent of insulin but norepinephrine does not contribute so much as epinephrine to hepatic glucose production. Epinephrine increases hepatic glucose production and inhibits insulin secretion and the glucose uptake by tissues that is induced by insulin. Additionally, catecholamines can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. It is likely that beta-(beta3)-adrenergic receptors mediate these responses. Alterations of central neurotransmission and environmental factors can change the relative contribution of sympathetic outflow to the pancreas, liver, adrenal medulla and adipose tissues, leading to the modulation of glucose and fat metabolism. Recent studies have proposed that leptin, an adipocyte hormone, affects the central nervous system to increase sympathetic outflow independent of feeding. The effects of leptin on glucose and fat metabolism could be in part mediated by the sympathetic nervous system. Studies using mice with a genetic disruption of serotonin 5-HT2c receptor indicate that central neural mechanisms in the regulation of sympathetic outflow and satiety could be dissociated. Abnormalities of sympathetic effects, including disturbances of leptin and beta3-adrenergic receptor signalling, are likely to cause obesity and impaired glucose tolerance in rodents and humans. These findings indicate that dysfunction of the sympathetic nervous system could predispose to obesity and Type II (non-insulin-dependent) diabetes mellitus.

Adipose Tissue↗

PubMed1988

Mitochondrial myopathy with lactic acidaemia, Fanconi-De Toni-Debré syndrome and a disturbed succinate: cytochrome c oxidoreductase activity.

A patient with severe muscular hypotonia, failure to thrive, a metabolic acidosis and a renal tubular dysfunction is presented. The disease followed a fatal course. Blood lactate and pyruvate levels as well as lactate/pyruvate ratios were strongly elevated. There were a massive excretion of lactate in urine, a generalized hyperaminoaciduria, a proteinuria and a mellituria. The carnitine concentration was diminished in blood and muscle tissue. Biochemical investigations of skeletal muscle and liver tissue revealed a defect in the respiratory chain at the level of succinate: cytochrome c oxidoreductase. The defect could not be demonstrated in cultured fibroblasts.

Acidosis, Lactic↗

PubMed2004

Eye muscle antibodies in Graves' ophthalmopathy: pathogenic or secondary epiphenomenon?

The extra ocular (eye) muscles are one of the principal tissues involved in the autoimmune-mediated inflammation of Graves' ophthalmopathy (GO). Several eye muscle proteins are targeted by autoantibodies or sensitized T lymphocytes, or both, and include: G2s, which is now identified as the terminal 141 amino acids of the winged-helix transcription factor FOXP1, the flavoprotein (Fp) subunit of the mitochondrial enzyme succinate dehydrogenase, the so-called "64kDa protein", a non-tissue specific membrane protein called 1D and the calcium binding protein calsequestrin. Of these, antibodies against G2s and Fp are the most sensitive markers of eye muscle damage in patients with thyroid autoimmunity even though neither antigen is specific to eye muscle and neither antibody is specific to GO. However, the recent finding that the calsequestrin gene is 4.7 times more expressed in eye muscles than other skeletal muscles suggests that we should reconsider the possible role of anti-calsequestrin autoantibodies in ophthalmopathy. GO may comprise two main subtypes with different pathogenetic mechanisms, namely ocular myopathy in which eye muscle inflammation predominates and congestive ophthalmopathy where inflammatory changes occur in the periorbital connective tissues in the absence of eye muscle dysfunction. Anti-G2s and anti-Fp antibodies are closely associated with the ocular myopathy subtype of GO while antibodies targeting type XIII collagen, the only member of the collagen family to have a transmembrane domain, are closely linked to congestive ophthalmopathy. Since both G2s and Fp are intracellular antigens it is unlikely that either antibody causes eye muscle fiber damage in GO, although a role in the later stages of the disease when the fiber has released its cellular contents has not been excluded. Eye muscle antibodies that are cytotoxic to eye muscle cells in antibody-dependent cell-mediated cytotoxicity (ADCC) are more likely to play a role in eye muscle fiber damage since they target a putative eye muscle cell membrane antigen, the identity of which is currently being investigated. While anti-G2s and anti-Fp antibodies are probably secondary to an underlying reaction, such as cytotoxic T lymphocyte targeting of an eye muscle membrane antigen that has yet to be identified, they are reliable markers of immunologically mediated eye muscle fiber damage in patients with Graves' hyperthyroidism. In conclusion, while a pathogenic role for eye muscle antibodies has not been excluded, they are most likely secondary to cytotoxic T cell reactions in GO and, as such, good markers of this autoimmune disease.

Animals↗

PubMed1982

Myopathy with pathological features of both centronuclear myopathy and multicore disease.

Two adult patients are described with long-standing primary myopathy characterised on light microscopy of skeletal muscle biopsy by central nuclei within muscle fibres, and on electron microscopy by multiple minicores causing sarcomere disruption. The total pathological picture is not typical of either "centro-nuclear myopathy" or "multicore disease". The apparently benign long-term prognosis of the myopathy in these patients contrasts with the severe respiratory dysfunction described in two recently reported infants affected by a pathologically similar myopathy, and justifies extensive respiratory support measures in such cases. In both cases electrophoresis of native myosin revealed only the "slow" isoenzymic forms. This finding is consistent with the overwhelming predominance of Type I fibres in the muscle biopsy. No foetal myosins, which characterize developing or regenerating muscle, were detected.

Adult↗

PubMed2003

Beneficial effects of L-carnitine in myoblastic C2C12 cells. Interaction with zidovudine.

L-Carnitine is a key molecule in the transfer of fatty acid across mitochondrial membranes. Bioavailable L-carnitine is either provided by an endogeneous biosynthesis or after intestinal absorption of dietary items containing L-carnitine. After intestinal absorption or hepatic biosynthesis, L-carnitine is transferred to organs whose metabolism is dependent upon fatty acid oxidation, such as skeletal muscle. To cross the muscle plasma membrane, there are several transporters involved. Among those transporters, OCTN2 is actually the only one to have been clearly characterized. Zidovudine is a commonly used inhibitor of human immunodeficiency virus (HIV) replication. Zidovudine has many side effects, including induction of myopathy characterized by a metabolic mitochondria dysfunction and a diminution of the muscle L-carnitine content. In this study, we described the characteristics of L-carnitine transport in C2C12 cells. We also demonstrated that zidovudine inhibited the L-carnitine transporter. This inhibition led to a significant reduction of the muscle cell growth. In C2C12 cells, the supplementation of L-carnitine prevented the effects of zidovudine and restored the normal cell growth.

Animals↗

PubMed2000

Nonsurgical and nonextraction treatment of skeletal Class III open bite: its long-term stability.

Two female patients, aged 14 years 5 months and 17 years 3 months with skeletal Class III open bite and temporomandibular dysfunction are presented. They had previously been classified as orthognathic surgical cases, involving first premolar removal. The primary treatment objective was to eliminate those skeletal and neuromuscular factors that were dominant in establishing their malocclusions. These included abnormal behavior of the tongue with short labial and lingual frenula, bilateral imbalance of chewing muscles, a partially blocked nasopharyngeal airway causing extrusion of the molars, with rotation of the mandible and narrowing of the maxillary arch. Resultant occlusal interference caused the mandible to shift to one side, which in turn produced the abnormal occlusal plane and curve of Spee. As a result, the form and function of the joints were adversely affected by the structural and functional asymmetry. These cases were treated by expanding the maxillary arch, which brought the maxilla downward and forward. The mandible moved downward and backward, with a slight increase in anterior facial height. Intruding and uprighting the posterior teeth, combined with a maxillary protraction, reconstructed the occlusal plane. A favorable perioral environment was created with widened tongue space in order to produce an adequate airway. Myofunctional therapy after lingual and labial frenectomy was assisted by vigorous gum chewing during and after treatment, together with a tooth positioner. Normal nasal breathing was achieved.

Adolescent↗

PubMed1999

Influence of FR 167653, an inhibitor of TNF-alpha and IL-1, on the cardiovascular responses to chronic infusion of lipopolysaccharide in conscious rats.

Conscious, male Long Evans rats (350-450 g) chronically instrumented for the measurement of regional haemodynamics, were infused with FR 167653, a dual inhibitor of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) synthesis (0.32 mg/kg/h) for 24 h, beginning 1 h before coinfusion of saline, or with saline for 24 h beginning 1 h before coinfusion of lipopolysaccharide (150 microg/kg/h), or with FR 167653 beginning 1 h before coinfusion of lipopolysaccharide. Animals infused with FR 167653 and saline showed progressive hindquarters vasoconstriction over the 24-h period, but this was not different from the change seen in animals (n = 3) infused with saline alone. However, plasma analysis at the end of the coinfusion of FR 167653 and saline showed substantial elevation in levels of creatine kinase, lactate dehydrogenase, and potassium, consistent with some tissue damage (heart, liver, or skeletal muscle, or a combination of these). Animals coinfused with saline and lipopolysaccharide showed biphasic decreases in mean arterial blood pressure accompanied by renal hyperaemic vasodilatation, and decreases followed by increases in mesenteric and hindquarters flows and vascular conductances. At the end of the infusion period, plasma analysis showed signs of renal dysfunction (elevated creatinine) and hepatic dysfunction (elevated alkaline phosphatase, gamma-glutamyl transferase, and alanine aminotransferase). In the presence of FR 167653, the hypotensive effects of lipopolysaccharide were abolished, but regional haemodynamics were unchanged, as were signs of organ dysfunction. One explanation of these observations is that FR 167653 causes a relative improvement in cardiac function during infusion of lipopolysaccharide, and this opposes the hypotensive effects of the latter, in spite of its persistent vasodilator effects.

Animals↗

PubMed2001

Disseminated eosinophilic disease resembling idiopathic hypereosinophilic syndrome in a dog.

True idiopathic hypereosinophilic syndrome has been described in human beings and cats, but not in dogs. The syndrome is characterised by prolonged unexplained peripheral mature eosinophilia, the infiltration of many organs by eosinophils, organ dysfunction and a fatal outcome. This paper describes an idiopathic disseminated eosinophilic disease in a dog involving various organs, manly the heart and the lungs, accompanied by a leukemoid eosinophilic response, and a fatal outcome. The histopathological findings included the infiltration of the myocardium, lung parenchyma, liver, spleen, lymph nodes and skeletal muscles with eosiniphils.

Animals↗

PubMed1996

Chloride transport across kidney epithelia through CLC chloride channels.

This review summarizes recent progress in elucidating the chloride-transporting mechanisms in kidney epithelia, focusing particularly on those which act through the newly identified chloride channels. A family of chloride channel proteins (ClC chloride channels) consisting of at least 9 members (ClC-1, 2, 3, 4, 5, 6, 7, K1 and K2) has recently been identified in mammals. Although all of these ClC channels, except for skeletal muscle-specific ClC-1, are expressed in the kidney, only ClC-K1 and K2 are kidney-specific ClC chloride channels, suggesting that they play an important role in the kidney. The functional properties and intrarenal localization of these chloride channels are summarized, and their involvement in certain tubular dysfunctions and physiological roles are discussed in this report.

Biological Transport↗

PubMed1996

Vulnerability to dysfunction and muscle injury after unloading.

OBJECTIVE: To test whether unloading increases vulnerability to eccentric exercise-induced dysfunction and muscle injury. DESIGN: Before-after trial. SETTING: General community. PATIENTS OR OTHER PARTICIPANTS: Two women and 5 men (73 +/- 3kg [mean +/- SE]) who were active college students but were not trained in lower body resistance exercise volunteered. INTERVENTION: Five weeks of unilateral lower limb suspension (ULLS), which has been shown to decrease strength and size of the unloaded, left, but not load-bearing, right quadriceps femoris muscle group (QF) by 20% and 14%, respectively; performance of 10 sets of ten eccentric actions with each QF immediately after the ULLS strength tests with a load equivalent to 65% of the post-ULLS eccentric 1-repetition maximum. MAIN OUTCOME MEASURE(S): Concentric and eccentric 1-repetition maximum for the left, unloaded and the right, load-bearing QF measured immediately after ULLS and 1,4,7,9, and 11 days later; cross-sectional area and spin-spin relaxation time (T2) of each QF as determined by magnetic resonance imaging and measured the last day of ULLS and 3 days later. RESULTS: The mean load used for eccentric exercise was 23 +/- 2 and 30 +/- 3kg for the left, unloaded and right, load-bearing QF, respectively. The concentric and eccentric 1-repetition maximum for the unloaded and already weakened left QF was further decreased by 18% (p = .000) and 27% (p = .000), respectively, 1 day after eccentric exercise. Strength did not return to post-ULLS levels until 7 days of recovery. The right, load-bearing QF showed a 4% decrease (p = .002) in the eccentric 1-repetition maximum 1 day after eccentric exercise. The left, unloaded QF showed an increase in T2 (p = .002) in 18% of its cross-sectional area 3 days after the eccentric exercise, thus indicating muscle injury. The right, load-bearing QF showed no elevation in T2 (p = .280). CONCLUSION: Unloading increases vulnerability to eccentric exercise-induced dysfunction and muscle injury, even at relatively light loads.

Adult↗

PubMed1995

Insulin stimulation of mitogen-activated protein kinase, p90rsk, and p70 S6 kinase in skeletal muscle of normal and insulin-resistant mice. Implications for the regulation of glycogen synthase.

UNLABELLED: Skeletal muscles from mice stimulated with insulin in vivo were used to evaluate relationships between the insulin receptor tyrosine kinase, mitogen-activated protein (MAP) kinase, p90rsk, p70 S6 kinase (p70S6k), and glycogen synthase. Two models of insulin resistance were also evaluated: (a) transgenic mice with a severe insulin receptor defect and (b) gold thioglucose (GTG) mice (obesity with minimal insulin receptor dysfunction). In normal mice, insulin stimulated MAP kinase (6-fold), p90rsk (RSK2, 5-fold), p70S6k (10-fold), and glycogen synthase (30-50% increase in fractional velocity). In transgenic mice, stimulation of MAP kinase and RSK2 were not detectable, whereas activation of p70S6k and glycogen synthase were preserved. In GTG mice, activation of MAP kinase, RSK2, p70S6k, and glycogen synthase were impaired. Since p70S6k and glycogen synthase were correlated, rapamycin was used to block p70S6k, and glycogen synthase activation was unaffected in normal mice; however, it was partially impaired in transgenic mice. CONCLUSIONS: (a) stimulation of p70S6k and glycogen synthase are selectively preserved in muscles with a severe insulin receptor kinase defect, indicating signal amplification in pathways leading to these effects; (b) MAP kinase-RSK2 and p70S6k activation are impaired in obese mice, suggesting multiple loci for postreceptor insulin resistance; (c) glycogen synthase was dissociated from MAP kinase and RSK2, indicating that they are not required for this effect of insulin; and (d) p70S6k is not essential for glycogen synthase activation, but it may participate in redundant signaling pathways leading to this effect of insulin.

Animals↗

PubMed2003

Insulin signalling pathways in aorta and muscle from two animal models of insulin resistance--the obese middle-aged and the spontaneously hypertensive rats.

AIMS/HYPOTHESIS: The aim of this study was to investigate insulin signalling pathways directly in vivo in skeletal muscle and thoracic aorta from obese middle-aged (12-month-old) rats, which have insulin resistance but not cardiovascular disease, and from spontaneously hypertensive rats (SHR), an experimental model of insulin resistance and cardiovascular disease. METHODS: We have used in vivo insulin infusion, followed by tissue extraction, immunoprecipitation and immunoblotting. RESULTS: Obese middle-aged rats and the SHR showed marked insulin resistance, which parallels the reduced effects of this hormone in the insulin signalling cascade in muscle. In aortae from obese middle-aged rats, the PI 3-kinase/Akt pathway is preserved, leading to a normal activation of endothelial nitric oxide synthase. In SHR this pathway is severely blunted, with reductions in eNOS protein concentration and activation. Both animals, however, showed higher concentrations and higher tyrosine phosphorylation of mitogen-activated protein (MAP) kinase isoforms in aortae. CONCLUSIONS/INTERPRETATION: Alterations in the IRS/PI 3-K/Akt pathway in muscle of 12-month-old rats and SHR could be involved in the insulin resistance of these animals. The preservation of this pathway in aorta of 12-month-old rats, apart from increases in MAP kinase protein concentration and activation, could be a factor that contributes to explaining the absence of cardiovascular disease in this animal model. However, in aortae of SHR, the reduced insulin signalling through IRS/PI 3-kinase/Akt/eNOS pathway could contribute to the endothelial dysfunction of this animal.

Age Factors↗

PubMed2001

Autologous primary muscle-derived cells transfer into the lower urinary tract.

The goal of these experiments was to establish the basic methodology for future clinical applications of muscle-derived cells (MDC) tissue engineering and gene transfer for the treatment of urological dysfunction. Primary MDC isolated via preplating techniques from adult female SD rats were transduced with retrovirus encoding the expression of beta-galactosidase reporter gene. The MDC were injected into the right and left lateral walls of the bladder and proximal urethra of the autologous animals (n = 6) with a 10 microl Hamilton micro syringe. The amount of injected MDC ranged from 1 to 2 x 10(6) cells. The injected tissue was harvested after 7, 14, and 28 days, sectioned and examined histologically for beta-galactosidase and immunohistochemically for fast myosin heavy chain specific to skeletal muscle. The tissues were also stained for anti-CD4 and anti-CD8 antibodies to assess for cellular immune reaction. We have detected a large number of autologous MDC expressing beta-galactosidase and positively stained for fast myosin heavy chain in the bladder and urethral wall. Many injected myoblasts and myotubes were also seen in the bladder and urethral wall at each time point. Staining of lymphocytes with anti-CD4 and anti-CD8 antibodies was negative after MDC injection at each time point. We have demonstrated the long-term survival of autologous MDC and MDC mediated gene transfer into the bladder and urethral wall. Autologous MDC and MDC mediated gene transfer may be a promising treatment to augment bladder and urethral sphincter function.

Animals↗

PubMed1997

Cardiac sarcoplasmic reticular function in rats with chronic heart failure following myocardial infarction.

Sarcoplasmic reticular function of rats with chronic heart failure (CHF) following coronary artery ligation was examined. The coronary artery ligation produced 43% infarction of the left ventricle and increased left ventricular end-diastolic pressure 8 weeks after the operation, suggesting the development of CHF by this period. The developed force transients of the skinned fiber of coronary artery-ligated rats were decreased when the skinned fiber was preloaded for 0.25-0.5 min with 10(-5)M Ca2+ (53-70%) and when preloaded with 10(-6)M Ca2+ and then exposed to 0.1-1 mM caffeine (39-87%). The results suggest that the rate of Ca2+ uptake by the sarcoplasmic reticulum (SR) and its ability to release Ca2+ were reduced in the failing heart. [3H]Ryanodine binding activities in homogenates and SR-enriched fractions were significantly reduced in the coronary artery-ligated group (32% and 21%, respectively). The results suggest that the amount of Ca2+ released from SR decreased due to decreased Ca2+ uptake rate of SR and down-regulation of the SR Ca(2+)-release channel, which contributes to cardiac dysfunction in failing hearts following acute myocardial infarction.

Animals↗

PubMed2000

Peripheral muscle dysfunction in chronic obstructive pulmonary disease.

Peripheral muscle dysfunction is a common systemic complication of moderate to severe COPD and may contribute to disability, handicap, and premature mortality. In contrast to the lung impairment, which is largely irreversible, peripheral muscle dysfunction is potentially remediable with exercise training, nutritional intervention, oxygen, and anabolic drugs. Therapeutic success is often incomplete, however, and a better understanding of the mechanisms involved in the development of peripheral muscle dysfunction in COPD is needed to help develop innovative and more effective therapeutic strategies.

Aging↗

PubMed2000

Increased activities of antioxidant enzymes and decreased ATP concentration in cultured myoblasts with the 3243A-->G mutation in mitochondrial DNA.

The MELAS syndrome (mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes) is most commonly caused by the 3243A-->G mutation in mitochondrial DNA, resulting in impaired mitochondrial protein synthesis and decreased activities of the respiratory chain complexes. These defects may cause a reduced capacity for ATP synthesis and an increased rate of production of reactive oxygen species. Myoblasts cultured from controls and patients carrying the 3243A-->G mutation were used to measure ATP, ADP, catalase and superoxide dismutase, which was also measured from blood samples. ATP and ADP concentrations were decreased in myoblasts with the 3243A-->G mutation, but the ATP/ADP ratio remained constant, suggesting a decrease in the adenylate pool. The superoxide dismutase and catalase activities were higher than in control cells, and superoxide dismutase activity was slightly, but not significantly higher in the blood of patients with the mutation than in controls. We conclude that impairment of mitochondrial ATP production in myoblasts carrying the 3243A-->G mutation results in adenylate catabolism, causing a decrease in the total adenylate pool. The increase in superoxide dismutase and catalase activities could be an adaptive response to increased production of reactive oxygen species due to dysfunction of the mitochondrial respiratory chain.

Adenosine Diphosphate↗

PubMed2000

Neurophysiological evaluation of cortical function in the early diagnosis of ALS.

The corticomotoneuronal system is selectively vulnerable in amyotrophic lateral sclerosis (ALS). In the past it has been difficult to evaluate the upper motor neuron component of this system. Recent studies using functional imaging and neurophysiological methods are now available as potential surrogate markers in the early diagnosis of ALS. We have used peristimulus time histograms (PSTHs) to evaluate the integrity of the motor cortex in ALS and in particular the cortical colonies that synapse with single anterior horn cells. The motor cortex in ALS becomes hyperexcitable early in the course of the disease and this may persist for some time. This is reflected in the PSTH by a desynchronized, complex response. Evidence indicates that this prime abnormality in ALS is supraspinal in origin and probably due to increased repetitive firing of the corticomotoneuron. The hyperexcitability is likely to be due to a combination of increased excitation at the level of the motor cortex and decreased inhibition due to dysfunction of the cortical inhibitory interneurones that modulate the output of the corticomotoneurone.

Anterior Horn Cells↗