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At least 109 records · Page 6Linked to original sources
PubMed1984

Comparison of the effects of smooth and skeletal tropomyosin on skeletal actomyosin subfragment 1 ATPase.

Chicken gizzard tropomyosin, like rabbit skeletal tropomyosin, inhibits and activates skeletal actomyosin subfragment 1 ATPase at low and high [subfragment 1], respectively, showing that both smooth and skeletal tropomyosin qualitatively produce similar cooperative effects on activity. For gizzard tropomyosin, however, the extent of the inhibition was less, and the activation curve rose more sharply at lower [subfragment 1]. In terms of a two-state cooperative activity model for the actin-tropomyosin filament (Hill, T. L., Eisenberg, E., and Chalovich, J. (1981) Biophys. J. 35, 99-112), these results qualitatively suggest that, for the gizzard tropomyosin system, more units are initially in the active state (in the absence of subfragment 1) and that the switching of units to the active state is more cooperative. The greater cooperativity indicated for the gizzard system may be a consequence of the greater rigidity of gizzard tropomyosin indicated from conformational studies.

Adenosine Triphosphatases↗
PubMed2000

Binding properties of (3)H-PbTx-3 and (3)H-saxitoxin to brain membranes and to skeletal muscle membranes of puffer fish Fugu pardalis and the primary structure of a voltage-gated Na(+) channel alpha-subunit (fMNa1) from skeletal muscle of F. pardalis.

The dissociation constants for (3)H-saxitoxin to brain membranes and to skeletal muscle membranes of puffer fish Fugu pardalis have been estimated to be 190- and 460-fold, respectively, larger than those to corresponding membranes of rat, by a rapid filtration assay, while these values for (3)H-PbTx-3 have been estimated to be one-third and one-half of those to rat, respectively. We have obtained a cDNA, encoding an entire voltage-gated Na(+) channel alpha-subunit (fMNa1, 1880 residues) from skeletal muscle of F. pardalis by composition of the fragments obtained from cDNA library and RT-PCR products. In fMNa1 protein, the residues for ion-selective filter and voltage sensor and the charged residues in SS2 regions of domains I-IV were conserved, but the aromatic amino acid (Phe/Tyr), commonly located in the SS2 region of domain I of tetrodotoxin-sensitive Na(+) channels, was replaced by Asn. With this particular criterion, we propose that the fMNa1 protein is a tetrodotoxin-resistant Na(+) channel.

Amino Acid Sequence↗
PubMed2001

Physiologic characteristics of canine skeletal muscle: implications for timing skeletal muscle cardiac assist devices.

BACKGROUND: Optimal clinical stimulation for skeletal muscle cardiac assist systems (such as dynamic cardiomyoplasty) is not clearly defined. The pressure-generating capacity of canine skeletal muscle ventricles (SMVs) at a variety of preloads and stimulation frequencies was examined as was time for SMVs to develop peak pressure. METHODS: SMVs were analyzed just after construction and after 3 months of electrical conditioning. Pressure generation and time to develop peak pressure were determined using a distensible mandrel. RESULTS: Higher preloads resulted in increased pressure generation; conditioned SMVs generated significantly less pressure than unconditioned SMVs. Increasing stimulation frequency from 20 to 50 Hz increased pressure-generating capacity; increases beyond 50 Hz did not result in further increases. Time to 90% peak pressure was least at 10 HZ and 65 Hz. CONCLUSIONS: Higher stimulation frequencies and preloads result in a more quickly contracting muscle, which generates more pressure. Midrange stimulation frequencies of 30 Hz provide optimal muscle strength and minimize time to develop peak pressure. Initiation of contraction should begin before the time maximal pressure is desired.

Animals↗
PubMed1998

Glycosphingolipids of skeletal muscle: I. Subcellular distribution of neutral glycosphingolipids and gangliosides in rabbit skeletal muscle.

Membrane vesicles were prepared from rabbit skeletal muscle, separated by sucrose density gradient centrifugation and characterized by their specific marker enzymes, ligand binding, and ion flux activities. The fractions obtained (in the order of increasing density) were sarcolemma (SL), T-tubules (TT), sarcoplasmic reticulum (SR1 and SR2) and triads/mitochondria (Tr/M). Their glycosphingolipid compositions were analyzed by biochemical and immunochemical methods with specific antibodies (TLC immunostaining) and characteristic patterns were obtained from respective membrane fractions, expressed on a protein basis. Glucosylceramide, the main neutral glycosphingolipid of rabbit muscle, was found in SL and TT fractions, whereas SR and Tr/M vesicles lack this compound. Lactosylceramide was selectively recovered in the SR1 fraction. GM3(Neu5Ac), the main ganglioside in rabbit muscle, was found to account for 64% in the SL, 13% in the TT, 7% in the SR1, 3% in the SR2 and 13% in the Tr/M fractions. IV3Neu5Ac-nLcOse4Cer was mostly abundant in SL and decreased in the order SL > TT, Tr/M > SR1, SR2. IV6Neu5Ac-nLcOse4Cer was only detected in the SL and Tr/M fractions in noteworthy quantities. Ganglioseries gangliosides GM1, GD1a, GD1b and GT1b displayed homogeneous distribution patterns in each membrane preparation. They were expressed only in small amounts but mainly in SL, TT and Tr/M vesicles and to less extent in SR1 and SR2 fractions. The presence of GM3(Neu5Ac) in the SL as well as on subcellular level was confirmed in transverse muscle cryosections by means of indirect immunofluorescence microscopy. The SL was brightly stained, but considerable intracellular fluorescence was observed as expected from the biochemical analyses. Thus, the neutral GSL and ganglioside expression of the SL and the intracellular membraneous network is different in skeletal muscle both in terms of quantitative and qualitative GSL composition as demonstrated in details by means of biochemical and immunochemical techniques. The modulatory functions of GM3 and gangliosides of the neolacto- and ganglio-series towards the voltage dependent Ca(2+)-channel, largely preponderant in the triads-containing Tr/M fraction, is the subject of the accompanying paper (J. Müthing, U. Maurer, and S. Weber-Schürholz, Carbohydr. Res., 307 (1998) 147-157).

Animals↗
PubMed2004

Biomimetic model of skeletal muscle isometric contraction: II. A phenomenological model of the skeletal muscle excitation-contraction coupling process.

This paper describes a new macroscopic, phenomenological model of the skeletal muscle excitation-contraction coupling process, as represented by four principal and consecutive compartments (biophysical, biochemical, and biomechanical phases) characteristic of isometric excitation-contraction coupling in mammalian skeletal muscle, and coupled by a system of simultaneous, first-order linear ordinary differential equations. The model is based upon biological compartmental transport kinetics and irreversible thermodynamic energy transformation, and represents a distinct improvement over other biomimetic models. The model was derived using physiological parameter data published in the literature, and validated using MATLAB R12.

Calcium↗
PubMed2002

Effect of exercise training on skeletal muscle fibre characteristics in men with chronic heart failure. Correlation between skeletal muscle alterations, cytokines and exercise capacity.

BACKGROUND: In patients with congestive heart failure (CHF) there is a shift from aerobic type I muscle fibres to less aerobic type II fibres. Exercise training has been shown to have beneficial effects on exercise performance, peripheral pathology and the neurohumoral profile in stable patients with CHF. This study evaluated the effect of a 3 month exercise training program on skeletal muscle characteristics and the correlation of these to cytokines and exercise capacity in CHF patients. METHODS: Skeletal muscle biopsies for enzyme-histochemical analysis were performed in 15 CHF patients in New York Heart Association classes II-III, with a mean ejection fraction of 33+/-5% before and after a 12 week training period. The patients were trained for 30 min, five times a week at 80% of the peak heart rate achieved at baseline ergometer cycle test. Fifteen healthy men were used as controls. Plasma samples were examined by enzyme immunoassays for levels of pro-inflammatory cytokines. RESULTS: (a) At baseline we found muscle atrophy in five of the patients. The percent area of type I fibres (40.7+/-12.0 vs. 56.4+/-11.0%, P<0.05) and the thickness of type IIA (56.10+/-7.8 vs. 71.6+/-11.9 microm, P<0.001) and B-fibres (49.0+/-8.9 vs. 63.9+/-10.6 microm, P<0.001) were reduced, whereas the percent area of type IIA fibres (52.1+/-13.3 vs. 36.4+/-9.9%, P<0.05) was increased in heart failure patients compared to healthy controls. There was a modest correlation between fibre thickness and the level of interleukin 6 (r=-0.657, P=0.008). (b) After exercise training there was a reduction in muscle area examined by light-microscopy, measured as a percentage of field (-2.7, P=0.003) with an concomitant increase in interstitium. This reduction correlated to the increase in the 6-min walk test (r=-0.558, P=0.031). The thickness of type IIB fibres increased (+5.6 microm, P=0.068) and the area of type I fibres decreased (-6.1%, P=0.062). CONCLUSIONS: Patients with CHF have a relatively increased area of type IIA fibres and a relatively decreased area of type I fibres compared to healthy individuals. The thickness of type IIA and type IIB fibres is decreased compared to normal individuals. A modest negative correlation between the level of interleukin 6 and fibre thickness at baseline, suggests that inflammatory cytokines may be involved in the pathogenesis of the CHF related myopathy. A significant correlation between the reduction of muscle area, with increased interstitum, and the increase in the 6-min walk test may indicate that the improvement is due to increased capillary density permitting better flow reserve to exercising muscles.

Aged↗
PubMed1994

Bioelectrical impedance can predict skeletal muscle and fat-free skeletal muscle of beef cows and their carcasses.

Multiple linear regression equations predicting total skeletal muscle (TM) and total skeletal fat-free muscle (TFFM) weight were developed from data of 33 beef cows. Animals varied in weight (385 to 749 kg), age (3 to 10 yr), and fatness (.13 to 2.54 cm). A four-terminal impedance meter/plethysmograph measured resistance and reactance on the live animals, exsanguinated (bled) animals, and on the subsequent hot and cold carcasses. Stainless steel, sterile needles (20-gauge) were used as electrodes. They were inserted to depths of 12.7 mm for measurements made before and after exsanguination and to 25.4 mm for carcass measurements. Cold carcass resistance and reactance were measured a second time using 13-gauge needles inserted to depth of 76.2 mm. Distance between detector electrodes was measured. Carcass sides were physically separated into muscle, fat, and bone. Chemical composition (moisture, protein, and fat) was determined on the muscle portion. Equations predicting TM weight from live, bled, hot carcass, and cold carcass data had adjusted R2 values of .90, .96, .94, and .92, respectively. Analogous adjusted R2 values for TFFM weight were .87, .93, .90, and .87. Resistance was a predictor variable in all equations. The use of larger needles resulted in higher adjusted R2 values and inclusion of reactance as a predictor variable. Mallows Cp values were close to the ideal value of the number of independent variables in the prediction equations plus one (1).(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1994

Bioelectrical impedance can predict skeletal muscle and fat-free skeletal muscle of beef cow primal cuts.

Multiple linear regression equations predicting total skeletal muscle (TM) and total skeletal fat-free muscle (TFFM) of chuck, rib, loin, and round were developed from data of 33 beef cows. Primal cuts were obtained in accordance with NAMP specifications. A four-terminal impedance meter/plethysmograph measured resistance and reactance on each cut using 20- and 13-gauge needles as electrodes. Weight, internal temperature, and distance between detector electrodes were recorded. Each cut was physically separated into muscle, fat, and bone. Chemical composition (moisture, protein, and fat) was obtained on the muscle portion of each cut so that TFFM could be obtained by multiplying TM x 1 minus the percentage of fat from the proximate analysis. The predictor variables for all combinations of cuts and electrode sizes were weight, distance between detector electrodes, temperature, and resistance, except for the round for which reactance was a fifth predictor. The P value for the resistance coefficient was < .001 for all 16 prediction equations. Adjusted R2 values of the prediction equations ranged from an average of .91 for the rib to an average of .96 for the round. Mallows Cp values were close to the ideal value of the number of independent variables in the prediction equations plus one (1). Prediction equations for the different size electrodes were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Sarcoplasmic reticulum calcium pump in cardiac and slow twitch skeletal muscle but not fast twitch skeletal muscle undergoes phosphorylation by endogenous and exogenous Ca2+/calmodulin-dependent protein kinase. Characterization of optimal conditions for calcium pump phosphorylation.

We have demonstrated recently that in cardiac sarcoplasmic reticulum (SR), a membrane-associated Ca2+/calmodulin-dependent protein kinase (CaM kinase) phosphorylates and activates the Ca(2+)-pumping ATPase (Ca(2+)-ATPase) in addition to phosphorylating the previously characterized substrates, phospholamban, and Ca2+ release channel (ryanodine receptor) (Xu, A., Hawkins, C., and Narayanan, N. (1993) J. Biol. Chem. 268, 8394-8397). The present study shows that a CaM kinase regulatory system capable of modulating SR Ca2+ pump activity through direct phosphorylation of the Ca(2+)-ATPase is functional in slow twitch but not fast twitch skeletal muscle. Incubation of SR vesicles isolated from rabbit slow twitch (soleus) and fast twitch (adductor magnus) skeletal muscles in the presence of Ca2+ and calmodulin resulted in phosphorylation of the Ca(2+)-ATPase in slow twitch muscle SR but not in fast twitch muscle SR. Exogenous CaM kinase II, which stimulated phosphorylation of the cardiac and slow twitch muscle SR Ca(2+)-ATPase, failed to phosphorylate fast twitch muscle SR Ca(2+)-ATPase. These observations demonstrate that CaM kinase-catalyzed phosphorylation of the Ca2+ pump is isoform-specific since heart and slow twitch muscle express the same Ca(2+)-ATPase isoform (SERCA2a), which is distinct from that of fast twitch muscle (SERCA1). As in the case of cardiac SR Ca(2+)-ATPase, phosphorylation of the slow twitch muscle SR Ca(2+)-ATPase (occurring at a serine residue) resulted in a 2-fold increase in catalytic activity of the enzyme without alteration in its Ca2+ sensitivity. In addition, Ca2+/calmodulin-dependent prephosphorylation of slow twitch muscle SR resulted in a greater than 2-fold increase in its Ca2+ transport activity. In both cardiac and slow twitch muscle SR, phosphorylation of the Ca(2+)-ATPase by the endogenous CaM kinase occurred rapidly (maximum within 2 min at 37 degrees C), had similar pH optimum (8.5-9.0), temperature optimum (30 degrees C), and calmodulin concentration-dependence (k0.5 50-60 nM). cAMP-dependent protein kinase did not phosphorylate the Ca(2+)-ATPase appreciably in either cardiac or slow twitch muscle SR. These findings suggest a muscle-specific role for the membrane-associated CaM kinase in the modulation of Ca2+ uptake and release functions of the SR. In cardiac and slow twitch muscle, phosphorylation of the SR Ca(2+)-ATPase by CaM kinase might provide a novel mechanism for the modulation of the enzymatic and Ca2+ transport functions of this enzyme.

Animals↗
PubMed1983

Skeletal lesions following meningococcemia and disseminated intravascular coagulation. A recognizable skeletal dystrophy.

Partial destruction of the right humeral and right femoral head were discovered in a 30-month-old girl, two years after her recovery from meningococcal septicemia and disseminated intravascular coagulation (DIC). Additional findings were symmetrical epiphyseal-metaphyseal lesions of the lower femora and upper and lower tibiae. The combined skeletal lesions seem to be characteristic sequelae of infantile meningococcemia complicated by DIC. Since this condition is no longer uniformly fatal, the characteristic skeletal dystrophy will be encountered more frequently and should be recognized by radiologists, pediatricians, and orthopedists. The features shared by our patient and the seven previously published cases are presented.

Bone Diseases↗
PubMed1995

Paradoxical effects of phosphate to directly regulate the level of skeletal alkaline phosphatase activity in human osteosarcoma (SaOS-2) cells and inversely regulate the level of skeletal alkaline phosphatase mRNA.

Recent studies indicate that the amount of alkaline phosphatase (ALP) activity in human osteoblast-line cells is proportional to the concentration of phosphate in the culture medium. The current studies were intended to extend those observations and to determine whether the effects of phosphate (and phosphate esters and analogs) to alter the cellular level of ALP activity, in human osteosarcoma SaOS-2 cells, reflected regulation at the level of transcription. Consistent with previous findings, we found direct, time- and dose-dependent correlations between the concentration of phosphate and the amount of ALP activity/mg cell protein (P < 0.05). Surprisingly, we also found a negative correlation between the phosphate concentration in the medium and the level of skeletal ALP mRNA (e.g., r = -0.98, P < 0.01 at 24 hours). As the highest cellular levels of skeletal ALP activity were associated with the lowest levels of ALP mRNA, these data indicated that the phosphate-dependent increase in ALP activity was not mediated by an increase in transcription and, conversely, that the effect of phosphate withdrawal to decrease ALP activity was not mediated by a decrease in transcription.(ABSTRACT TRUNCATED AT 250 WORDS)

Alkaline Phosphatase↗
PubMed1992

Progressive predominance of 'skeletal' versus 'cardiac' types of excitation-contraction coupling during in vitro skeletal myogenesis.

Simultaneous recordings, in the presence or absence of cadmium, of current and contraction of skeletal muscle cells in primary culture (myoballs) showed that the relative part of contraction depending on calcium current progressively decreases with the age of cells whereas the cadmium-insensitive component becomes predominant. The coexistence of "cardiac" and "skeletal" excitation-contraction coupling mechanisms in developing muscle and its developmental regulation are consistent with recent molecular data showing the expression, in newborn animals, of an abbreviated isoform of the alpha 1 subunit of the DHP-receptor of muscle cells.

Animals↗
PubMed1977

The value of enzyme histochemical techniques in the classification of fibre types of human skeletal muscle. 2. The histochemical demonstration of myosin adenosine triphosphatase in skeletal muscles from adult patients with or with no diseases of the neuromuscular system. A comparison between results obtained by calcium salt and lead salt techniques.

In the present investigation the results of a lead salt technique and two calcium salt techniques for the deomonstration of the activity of myosin adenosine triphosphatase in sections of both normal and pathological human skeletal muscle specimens are compared. It was seen that the histochemical results obtained by the different techniques are similar, especially with regard to the identification of fibre-types. It can be clearly stated, that the alkaline phosphatase activity present in muscle fibers of diseased skeletal msucles revealed only a very slight activity with the substrate ATP, so the alkaline phosphatase activity in general did not disturb the reliability of the different myosin ATPase techniques. Moreover it was found that the presence of the mitochondrial Ca2+ -ion activated ATPase with a high pH-optimum in muscle fibers did not give rise to faulty results. From studies with dinitrophenol it can be concluded that this substance activates the myosin ATPase present in type I fibres especially.

Adenosine Triphosphatases↗
PubMed1984

Quinidine-induced changes in serum and skeletal muscle digoxin concentration; evidence of saturable binding of digoxin to skeletal muscle.

Eleven patients with atrial fibrillation on maintenance digoxin therapy were investigated by analysis of serum (SDC) and skeletal muscle (SMDC) digoxin concentrations before and 24 h and 2 weeks after starting quinidine treatment. After cardioversion the maintenance dose of digoxin was reduced in order to obtain the same steady-state SDC after 2 weeks, as before quinidine. SDC was increased by quinidine therapy from 1.56 to 2.40 nmol/l after 24 h. With the reduced digoxin dose SDC was 1.68 nmol/l after 2 weeks. The ratio SMDC/SDC decreased after 24 h of quinidine treatment from 35.4 to 29.0 (p less than 0.01). After 2 weeks of quinidine treatment with the reduced digoxin dose, the ratio had risen to 38.1, which did not differ significantly from the initial ratio. The present data suggest that the reduced skeletal muscle binding of digoxin during quinidine therapy is due to saturation of digoxin binding sites secondary to the increase in the total body load of digoxin at steady-state, and not to direct interference by quinidine with digoxin binding sites.

Aged↗
PubMed1990

Distribution of skeletal metastases in prostatic and lung cancer. Mechanisms of skeletal metastases.

The distribution of skeletal metastases in prostatic and lung cancer was examined to test the hypothesis that prostatic carcinoma spreads by a unique hematogenous route. Abnormal technetium-99m methylene diphosphonate bone scans were retrospectively reviewed in 71 patients with prostatic carcinoma and 41 patients with lung cancer comparing patterns of osseous involvement. Differences in the distribution of lesions were not significant. It is concluded that prostatic carcinoma does not metastasize to specific skeletal sites by a singular hematogenous pathway.

Bone Neoplasms↗
PubMed1985

Interaction with troponin T from white skeletal muscle restores in white skeletal muscle AMP deaminase those allosteric properties removed by limited proteolysis.

Limited proteolysis of rabbit skeletal muscle AMP deaminase (AMP aminohydrolase, EC 3.5.4.6) with trypsin results in conversion of the enzyme to a form which is no longer inhibited by ATP and exhibits hyperbolic kinetics even at low K+ concentration and in the absence of ADP. The interaction with troponin T from white skeletal muscle or with the phosphorylated 42-residue N-terminal peptide of troponin T restores in the trypsin-treated AMP deaminase the sensitivity to adenine nucleotides and increases the KA for K+ activation of the enzyme from 1 mM to 12 mM, this effect being diametrically opposite to that exerted by limited proteolysis on the native enzyme. Treatment of the N-terminal peptide of troponin T with alkaline phosphatase abolishes the modulating properties of the peptide, suggesting that phosphorylation-dephosphorylation processes may be involved in the regulation of the enzyme.

AMP Deaminase↗
PubMed1991

Immunochemical analysis of the peroxisomal beta-oxidation enzymes in rat and human heart and skeletal muscle and in skeletal muscle of Zellweger patients.

Immunoblot analyses with antibodies against the peroxisomal beta-oxidation enzymes from rat liver showed the presence of these enzymes in rat and human liver and kidney and rat adrenal gland. The bifunctional protein could not be detected in muscle tissues or cultured muscle cells. Acyl-CoA oxidase was detected in rat heart and cultured human muscle cells. 3-Ketoacyl-CoA thiolase was also detected in human and rat heart and skeletal muscle; however, this enzyme was not detectable in skeletal muscle of Zellweger patients, in agreement with the absence of peroxisomal fatty acid oxidation.

Acetyl-CoA C-Acyltransferase↗
PubMed2003

Skeletal dysplasias caused by a disruption of skeletal patterning and endochondral ossification.

Identification of a number of the genes that cause skeletal dysplasias has helped clinicians to provide accurate diagnoses, genetic counseling, and pre-natal diagnosis for this complex group of disorders. This review considers how some of the recent advances in human and murine genetics have led to an increased understanding of normal bone development and, in particular, the processes of skeletal patterning and endochondral ossification.

Animals↗