Automatic discrimination of myoelectric signals via parallel cascade identification

It has recently been shown that it is possible to discriminate accurately among myoelectric signals underlying different muscle contraction types, specifically elbow flexion and extension and forearm pronation and supination. It was reported that once a number of distinctive features had been extracted from the myoelectric signals, a neural network could be trained to distinguish the contraction types with an impressively high accuracy. In the present paper, we show that a technique known as parallel cascade identification can be used to construct classifiers that can also accurately, differentiate the contraction types. The use of parallel cascades has the benefit of dispensing with the need for feature extraction, so that raw myoelectric signal data can be used directly. In addition, very little data are required to train the parallel cascades to distinguish accurately novel incoming myoelectric signals. Results of using parallel cascades to distinguish foream pronation, supination, and elbow flexion are presented.     

Effects of Ethanol on the Contractile Function of the Heart: A Review

Chronic ethanol consumption leads to a number of alterations in the contractile function of the heart and is a leading cause of cardiomyopathy. Ethanol also has an acute negative inotropic effect mediated by direct interaction with cardiac muscle cells, although this action is often masked by indirect actions resulting from enhanced release of catecholamines in vivo. This article reviews the effects of ethanol on the contractile function of the heart. The specific targets affected by ethanol in cardiac muscle cells are discussed in terms of potential mechanisms underlying the depressions of contractility resulting from both acute and chronic actions of ethanol.     

Change in urethral pressure during voluntary pelvic floor muscle contraction and vaginal electrical stimulation

The purpose of the study was to compare the effect of voluntary pelvic floor muscle (PFM) contraction and vaginal electrical stimulation on urethral pressure. Twelve women with genuine stress incontinence, mean age 49.4 years (range 33–66) participated in the study. The urethral and bladder pressures were recorded simultaneously through a double-lumen 8 Ch catheter. The patients first performed three voluntary PFM contractions. Then two electrical stimulators, Conmax and Medicon MS 105, 50 Hz, were used in random order. A visual analog scale was used to measure pain and discomfort. Pain was reported to mean 6.8, SEM 0.64 (range 0.7–9.9) and mean 6.1, SEM 0.81 (range 0–9.1) with Conmax and Medicon MS 105, respectively. The mean paired difference in favor of voluntary contraction with Conmax was ?8.0, SD 6.7,P=0.0067, and with Medicon MS 105 it was ?12.2, SD 5.9,P=0.0022. The results demonstrated that voluntary PFM contraction increased urethral pressure significantly more than did vaginal electrical stimulation.     

Expression of smooth muscle actin in osteoblasts in human bone.

It is well known that certain connective tissue cells (viz., dermal fibroblasts) can express the gene for a muscle actin--alpha-smooth muscle actin--and can contract. This process contributes to skin wound closure and is responsible for Dupuytren's contracture. The objective of this study was to determine if human osteoblasts can also express the gene for alpha-smooth muscle actin. Immunohistochemistry using a monoclonal antibody for alpha-smooth muscle actin was performed on human cancellous bone samples obtained from 20 individuals at the time of total joint arthroplasty. The percentages of resting and active osteoblasts on the bone surfaces containing this muscle actin isoform were evaluated. Explants of human bone were also studied for the expression of alpha-smooth muscle actin in the tissue and in the outgrowing cells with time in culture. Western blot analysis was performed to quantify the alpha-smooth muscle actin content of the outgrowing cells relative to smooth muscle cell controls. Nine +/- 2% (mean +/- SEM; n = 20) of the cells classified as inactive osteoblasts and 69 +/- 3% (n = 19) of the cells identified as active osteoblasts on the bone surface contained alpha-smooth muscle actin. This difference was highly statistically significant (Student's t test, p < 0.0001). Similar profiles of alpha-smooth muscle actin-expressing cells were found in explants cultured for up to 12 weeks. Cells forming a layer on the surface of the explants and growing out from them in monolayer also contained alpha-smooth muscle actin by immunohistochemistry and Western blot analysis. Human osteoblasts can express the gene for alpha-smooth muscle actin. This expression should be considered a phenotypic characteristic of this cell type, conferred by its progenitor cells: bone marrow stromal-derived stem cells, and perhaps pericytes and smooth muscle cells.     

改变在体兔左心室后负荷对其电生理参数的影响

目的：探讨改变在体兔左心室后负荷对室性心律失常发生情况及左心室电生理参数的影响。方法：改变左心室后负荷，观察室性心律失常发生情况，并测定左心室舒张阈值（ＶＤＴ），相对不应期（ＲＲＰ），有效不应期（ＥＲＰ）及其不应期离散和心室纤颤阈（ＶＦＴ）。结果：逐级增加左心室后负荷（ＡＢ级）可使左室空间ＲＲＰ，ＥＲＰ离散增加（Ｂ级，Ｐ＜００５），ＶＦＴ降低（Ｂ级，Ｐ＜００１）；各实验动物均出现室性心律失常（Ｂ级）；而逐级减小左室后负荷（ＣＤ级），心室电生理参数无变化（Ｐ＞００５），各实验动物亦无室性心律失常发生。结论：增加左心室后负荷诱发室性心律失常，与左室空间不应期离散增加有关。     

Cell-volume-dependent vascular smooth muscle contraction: role of Na+, K+, 2Cl− cotransport, intracellular Cl− and L-type Ca2+ channels

This study elucidates the role of cell volume in contractions of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat aorta. We observed that hyposmotic swelling as well as hyper- and isosmotic shrinkage led to VSMR contractions. Swelling-induced contractions were accompanied by activation of Ca²⁺ influx and were abolished by nifedipine and verapamil. In contrast, contractions of shrunken cells were insensitive to the presence of L-type channel inhibitors and occurred in the absence of Ca²⁺_o. Thirty minutes preincubation with bumetanide, a potent Na⁺,K⁺,Cl^– cotransport (NKCC) inhibitor, decreased Cl^–_i content, nifedipine-sensitive ⁴⁵Ca uptake and contractions triggered by modest depolarization ([K⁺]_o=36 mM). Elevation of [K⁺]_o to 66 mM completely abolished the effect of bumetanide on these parameters. Bumetanide almost completely abrogated phenylephrine-induced contraction, partially suppressed contractions triggered by hyperosmotic shrinkage, but potentiated contractions of isosmotically shrunken VSMR. Our results suggest that bumetanide suppresses contraction of modestly depolarized cells via NKCC inhibition and Cl^–_i-mediated membrane hyperpolarization, whereas augmented contraction of isosmotically shrunken VSMR by bumetanide is a consequence of suppression of NKCC-mediated regulatory volume increase. The mechanism of bumetanide inhibition of contraction of phenylephrine-treated and hyperosmotically shrunken VSMR should be examined further.     

The source and action of histamine in the isolated guinea-pig gallbladder

We have investigated the effects of histamine on motility of the gallbladder and characterized the receptor types involved. Histamine and the histamine H₁-receptor agonist, 2-thiazolylethylamine (2-TEA) contracted the isolated guinea-pig gallbladder strip in a dose dependent manner. The contractile response to histamine was shifted to the right by the H₁-receptor antagonist, mepyramine. In pre-contracted gallbladder strips, the H₂-receptor agonist dimaprit reduced the tension generated in a dose dependent fashion. The histamine H₂-receptor antagonist, ranitidine shifted the histamine concentration effect curve to the left and attenuated the dose dependent relaxations elicited at high concentrations. The histamine H₃-receptor agonist, (R)--methylhistamine (RMHA) elicited dose dependent contraction of the tissue which was significantly inhibited in the presence of mepyramine. The effects of electrical field stimulation (EFS) on the strips were not significantly altered by the presence of RMHA (10^–10–10^–7 M) indicating little pre-synaptic H₃ activity in this tissue. Histamine immunoreactivity (IR) was detected in gallbladder whole mount preparations of the mucosa and the muscularis/serosa. The histamine IR appeared cell bound in cells of varying morphological characteristics but no IR was detected in nerve fibres or cell bodies (ganglia). Alcian blue staining was consistent with the distribution of histamine IR cells as mast cells. The results indicate that histamine is distributed in the guinea-pig gallbladder and it can regulate contractile activity via activation of H₁ and H₂ but not H₃ receptors.     

Ruthenium red affects the contractile apparatus but not sarcoplasmic reticulum Ca2+ release of skinned papillary muscle

Ruthenium red has been shown to have a positive inotropic effect on isolated perfused hearts. The cellular mechanism of this action is not clear. Ruthenium red is able to block the Ca²⁺ release channel in isolated sarcoplasmic reticulum (SR) vesicle and reconstituted channel preparations. However, the effect of ruthenium red on SR Ca²⁺ release has not been studied in skinned cardiac muscle preparations. In the present study we investigated the actions of ruthenium red on both the characteristics of force generation by the contractile apparatus and Ca²⁺ release from the SR in chemically skinned rat papillary muscle. Ruthenium red (2 and 10 M) significantly increased the Ca²⁺ sensitivity of the contractile apparatus (decreasing Ca²⁺ required for the half-maximal response from 1.56±0.04 M to 1.46±0.05 M) but had no effect on the maximal Ca²⁺-activated force in triton X-100 treated fibers. This result may suggest one explanation for the positive inotropic effect of ruthenium red on the heart. On the other hand, ruthenium red had no significant effect on either caffeine-induced Ca²⁺ release or Ca²⁺-induced Ca²⁺ release from the SR in saponin-skinned muscle fibers. Lack of a blocking effect on SR Ca²⁺ release by ruthenium red in skinned fibers suggests that the SR Ca²⁺ channels in intact preparations have characteristics that are different from those of either vesicular or reconstituted channel preparations.     

Changes of tension and [Ca2+]i during β-adrenoceptor activation of single,intact fibres from mouse skeletal muscle

-Adrenergic agonists increase tension production in fast-twitch skeletal muscle, but the underlying mechanism is unknown. In the present study we have exposed intact, single fibres from a mouse muscle to the ₂-adrenergic agonist terbutaline. Fibres were stimulated to produce 350-ms tetani at 20–100 Hz while measuring the myoplasmic Ca²⁺ concentration ([Ca²⁺]_i) and tension. The fluorescent indicator Indo-1 was used to measure [Ca²⁺]_i. Application of terbutaline resulted in marked increases of both tetanic [Ca²⁺]_i and tension. Terbutaline had no significant effect on myofibrillar function as judged from normal Ca²⁺ sensitivity and tension production at saturating [Ca²⁺]_i. The rate of [Ca²⁺]_i and tension decline during relaxation was not affected by terbutaline, thus indicating a normal function of the sarcoplasmic reticulum (SR) Ca²⁺ pumps. The effect of terbutaline developed gradually over 5–10 min when fibres were stimulated each minute; the full effect of terbutaline was also obtained after a 10-min rest period in terbutaline. The [Ca²⁺]_i at rest was not affected by terbutaline. In conclusion, -adrenergic stimulation increases tetanic tension by enhancing SR Ca²⁺ release.     

The response to ether anesthesia and to electric stimulation of glycolytic metabolites in a red and a white muscle of the rat

Summary Since ether anesthesia lowered ATP by 25% in red, but not in white muscle, and only when the spinal neurones were intact, we suggested that small or intermediate muscle units were activated under ether anesthesia [8].In order to prove this postulate, some glycolytic metabolites, known to rise under muscular activation, are studied in the white musculus adductor magnus and in the red musculus pyramidalis of the rat: glucose-1-phosphate, glucose-6-phosphate, fructose-6-phosphate, fructose-1-6-diphosphate, -glycerophosphate, lactate, pyruvate, and dihydroxyacetone phosphate.The conditions compared are: Inactin (5-ethyl-5(methyl-propyl)-2-thiobarbituric acid)-anesthesia, diethyl ether anesthesia, and tetanic contraction under Inactin anesthesia.The histological assay with Sudan-black B staining shows 34.2±7.3% dark fibers in m. pyramidalis and 0.2±4.8% dark fibers in m. adductor magnus.Glucose-1-phosphate, fructose-1-6-diphosphate, and -glycerophosphate are elevated under ether anesthesia in both muscles versus Inactin anesthesia by 100–200%.Lactate in both muscles and pyruvate in the red muscle are slightly elevated under ether (by 40%) versus Inactin anesthesia.Under tetanic contraction the metabolites studied rise considerably in both muscles.As glycogen is lowered in rat muscle under ether [9], the present results suggest an activation of glycogen phosphorylase and of phosphofructokinase in both the red and the white muscle under ether anesthesia, which results in augmented glycolysis.The comparatively small increment of pyruvate and lactate in the presence of a high increment of -glycerophosphate under ether anesthesia is considered to indicate an asynchronous activation of fibers with unimpaired circulation and oxidative metabolism.