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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiomyopathy was diagnosed in several members of two families. This familial cardiomyopathy showed symmetrical or asymmetrical hypertrophy of the ventricular walls with or without obstruction to the left ventricular outflow tract. Certain forms were asymptomatic and were revealed by the family history and echocardiography. Myocardial and intercostal muscle biopsy was performed for a biochemical and ultrastructural analysis. Different myocardial features were observed in the two families: a large increase in the glycogen deposits in the one, without clinical signs of a glycogen storage disease, and intracellular deposits of a filamentous protein substance in the other.
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PMID:[Familial cardiomyopathy: a study of two families with myocardial and skeletal muscle biopsies]. 11 77

The electromyographic (EMG) responses from soleus and tibialis anterior muscles and the monosynaptic H- and T-reflex responses from soleus muscles were recorded bilaterally from conscious baboon while unexpectedly dropping it with unrestricted vision. These responses were recorded either after unilateral vestibular neurectomy (U.N. Baboons) or after bilateral neurectomy performed in one stage (B.N. 1 baboons) and in two stages (B.N. 2 baboons). A positive correlation was found between modifications and development of EMG responses and reflex data. In the U.N. baboons, some differences were observed when comparing data from the H- and T-reflex methods, suggesting that recovery of normal responses to fall is achieved both by means of direct influences on alpha-motoneurons and via the gamma-loop. In the U.N. baboons postural reactions to fall developed in three distinct periods. The first or critical stage showed asymmetrical EMG and reflex responses with increased responses from contralateral soleus muscle and decreased responses from ipsilateral soleus. Opposite effects were recorded from tibialis anterior flexor muscles. The second or acute stage which began around 4 to 7 days after surgery exhibited symmetrical, but very reduced, responses when compared to the control in soleus muscles, and symmetrical, but increased, responses from tibialis anterior muscles. This stage lasted until about the end of the second postoperative week and was followed by the third or compensatory stage during which EMG as well as reflex responses developed towards the control pattern in all tested muscles. Almost normal responses were recorded on both sides 3 weeks after surgery. Only a partial recovery was found in the B.N. 1 baboons, indicating that the contralateral remaining labyrinthine afferences constitute a necessary condition for the full compensation of postural reactions to fall in the case of unilateral vestibular neurectomy. The Bechterew's compensation was obtained in the B.N. 2 baboons. These results are discussed in relation with the general organization of the vestibulospinal pathways and with those concerning development of the postoperative activity at the vestibular nuclei level. A model of vestibular compensation achieved by means of a multisensory substitution process is suggested.
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PMID:Compensation of postural reactions to fall in the vestibular neurectomized monkey. Role of the reamining labyrinthine afferences. 11 46

In layer IV of the visual cortex of two primate species three small neurons were found that gave rise to short presynaptic somatic protrusions. The protrusions contained a cluster of predominantly round vesicles and established asymmetrical synaptic contacts with the characteristics of Gray's type 1 terminals.
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PMID:Neurons with presynaptic somatic protrusions in the visual cortex of monkeys. 11 85

The effects of acute severe aortic regurgitation on the left ventricle were investigated in conscious, chronically instrumented dogs. Left ventricular dimensions and volumes were measured from biplane cineradiographs of beads positioned near the endocardium. Data were collected before and after the production of aortic regurgitation by a catheter technique. The aortic regurgitation resulted in increases in mean aortic pulse pressure from 44 to 73 mmHg (P smaller than 0.001), heart rate from 87 to 122 beats/min (P smaller than 0.02), and left ventricular end-diastolic pressure from 11 to 25 mmHg (P smaller than 0.05). Mean end-diastolic volume rose from 61 to 69 cc (P smaller than 0.001), while end-systolic volume remained unchanged at 37 cc. The end-diastolic dilatation following regurgitation was asymmetrical in that the increase in size was due principally to an increase in the septal-lateral axis. The acute volume load of aortic regurgitation was accomplished by an increase in end-diastolic volume, i.e., the Frank-Starling mechanism. The tachycardia probably reflects augmented cardiac sympathetic activity, but the constant end-systolic volume at a similar mean systolic pressure suggests that the net contractile state was unchanged.
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PMID:Dimensional analysis of the left ventricle: effects of acute aortic regurgitation. 12 19

Subjects with asymmetrical hypertrophy of the heart are prone to sudden death. Neither the pathogenesis of the eccentric hypertrophy nor the mechanism of sudden death is fully understood. In this report we describe certain postmortem findings in the hearts of 22 subjects who died suddenly, silently and unexpectedly, and in whom the only significant abnormality at autopsy was asymmetrical hypertrophy of the heart. Deep clefts were present in the septum in seven hearts, the small coronary arteries were abnormally narrowed in ten, the sinus node was sclerosed by fibrosis in 12, there was variable narrowing of the atrioventricular (A-V) node artery in many and the His bundle was too thin in three. There were multiple cysts or channels in the central fibrous body and of the adjacent A-V node and His bundle in four hearts. Most of the hearts displayed a fetal dispersion of the A-V node and His bundle throughout the central fibrous body, but this was particularly conspicuous in 13 hearts. These abnormalities in all parts of the conduction system suggest a variety of possible mechanisms by which the heart could become electrically unstable but do not indicate that one single mechanism is at fault in all. They offer some explanation for the reported high incidence of atrial fibrillation in such patients, and why they fare so badly with this arrhythmia. While the pathogenesis of asymmetrical hypertrophy may in some part be attributable to narrowed small coronary arteries or to an abnormal sequence or speed of septal and ventricular activation or to mechanical deficiency caused by deep septal clefts, none of these features was universally present in our series. Both asymmetrical hypertrophy of the heart and the sudden death which so frequently accompanies it probably develop by a variety of pathogenetic mechanisms.
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PMID:De subitaneis mortibus. XII. Asymmetrical hypertrophy of the heart. 12 34

A patient is presented in whom coexisting bicuspid valvular aortic stenosis and asymmetrical septal hypertrophy were suggested by echocardiography. A focal area of hypertrophy noted at operation was excised. Subsequent histological examination did not reveal evidence to support the echographic and surgical observations. The necessity for careful intraoperative assessment of the degree and nature of subvalvular muscular hypertrophy is stressed. The absence of classic echographic findings in these patients is noted.
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PMID:Apparent coexistent valvular and subvalvular left ventricular outflow tract obstruction. 12 48

An echocardiographic and electrocardiographic evaluation of left ventricular hypertrophy (LVH) was carried out in 50 patients with chronic pressure or volume overload of the left ventricle, and in 16 patients with cardiomyopathy. In contrast to the ECG, echocardiography permitted good differentiation of ventricular dilatation, symmetrical and asymmetrical wall thickening. Positive voltage criteria (SOKOLOFF) were found in 76% of cases with abnormal muscle mass, but the height of QRS amplitude showed no close correlation with the degree of LVH. The presence of absence of ST/T changes was an unreliable index in predicting wall thickness. The practical value of echocardiagraphy in the differential diagnosis of left ventricular disorders is discussed.
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PMID:[Proceedings: Echocardiography for the diagnosis of left ventricular hypertrophy]. 12 54

Echocardiographic patterns in 15 patients with hypertrophic cardiomyopathy were compared with those in 30 healthy persons. Correlations with angiocardiographic data indicated that most of the anatomical abnormalities in hypertrophic cardiomyopathy can be assessed reliably by echocardiography. These include abnormal mitral valve motion, a reduction of the anteroposterior dimension of the left ventricular outflow tract and of the left and right ventricular cavities, increased thickness of the interventricular septum and the posterior left ventricular wall. Comparision of the haemodynamic and echocardiographic data showed that some degree of abnormal mitral valve motion during systole may occur in the absence of left ventricular outflow tract obstruction. On the other hand, it need not always be present with left ventricular outflow tract obstruction. Other, hitherto unrecognized, abnormalities in hypertrophic cardiomyopathy detected by this technique were: (1) Aortic valve regurgitation in three out of nine patients with evidence of left ventricular cutflow tract obstruction at cardiac catheterization. (2) Left ventricular inflow tract obstruction at the mitral valve level associated with gross septal hypertrophy (five cases). (3) Abnormal forward displacement of the posterior mitral valve leaflet and of the chordae tendineae during systole in 10 patients, in seven of whom there was confirmatory angiocardiographic evidence. Seven patients with miscellaneous cardiac disorders are described in whom asymmetric septal hypertrophy was revealed by echocardiography. In one of these patients coexisting hypertrophic cardiomyopathy was excluded histologically; thus asymmetrical septal hypertrophy is not confined to patients with hypertrophic cardiomyopathy.
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PMID:Echocardiographic spectrum of hypertrophic cardiomyopathy. 13 64

The morphology and distribution of sensory endings in snake (Elaphe quadrivirgata) muscle spindles was studied in silver preparations. The sensory axon supplying long-capsule spindles often bifurcates before or after penetrating the capsule and runs for some distance along the intrafusal fibre. The sensory axon supplying short-capsule spindles penetrates the capsule at a sharp angle, and, without ramification, terminates abruptly on the intrafusal fibre. The sensory terminal is composed of terminal bulbs and small links. In long-capsule spindles the sensory ending is arranged longitudinally in one or two rows. The sensory ending in short-capsule spindles ramifies extensively, covering densely the intrafusal fibre. The area occupied by sensory bulbs was estimated to be slightly higher in short-capsule (15-17?) THAN IN LONG-CAPSULE SPINDLES (12-13). The functional significance of these findings is discussed. Motor innervation of muscle spindles in the snake Elaphe quadrivirgata was studied using AchE staining for light microscopy in conjection with electron microscopy. In the polar region of either type of spindle, the majority of the motor endings are of grape type. In long-capsule spindles plate endings may occur in the spindle pole as well as in the capsular region. Motor endings in the capsular region are mostly of plate type. Plate endings rarely occur in short-capsule spindles. Identified single motor endings were studied by electron microscopy. Intrafusal grape endings are characterized by a smooth post-synaptic membrane. Intrafusal plate endings in the polar region are characterized by junctional folds or gutterings; plate endings in the capsular region show less developed gutterings or indentations. The distribution of intrafusal motor endings was examined along the length of single intrafusal fibres. The long-capsule spindle often receives asymmetrical motor innervation around the capsular region, whereas motor endings in the short-capsule spindle distribute more symmetrically.
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PMID:The innervation of muscle spindles in the snake, Elaphe quadrivirgata. 13 49

Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).
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PMID:Giant T wave inversion as a manifestation of asymmetrical apical hypertrophy (AAH) of the left ventricle. Echocardiographic and ultrasono-cardiotomographic study. 13 32


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