Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the generalized chronic idiopathic inflammatory myopathies, inclusion body myositis (IBM) has emerged as a clinico-pathologic variant during the past two decades. It occurs primarily in elderly persons (in approximately the sixth decade of life), but young adults (in approximately the second decade of life) may also be affected. Slowly progressive weakness of distal as well as proximal muscle groups in IBM is usually not associated with skin rash, malignancy or collagen-vascular disease, and is refractory to treatment with steroids or other immunosuppressants. Exceptions to each of these general rules have been found. Muscle biopsy and electromyography may suggest a neurogenic process mixed with myopathic features. Rimmed vacuoles with basophilic granules in cryostat sections stained with hematoxylin-eosin are strongly suggestive of IBM if accompanied by the histopathologic triad of polymyositis. The presence of eosinophilic intranuclear or cytoplasmic inclusions in affected myofibers is further suggestive of IBM. The ultimate diagnosis, however, depends on ultrastructural demonstration of characteristic microtubular filaments resembling the nucleocapsids of the paramyxovirus group. Recent reports of immunostaining of the inclusions for mumps virus antigen strongly suggest a chronic persistent mumps virus infection as the cause of IBM. IBM is considered to be pathologically related to both distal myopathy (DM) and oculopharyngeal muscular dystrophy (OPMD).
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PMID:Inclusion body myositis: a chronic persistent mumps myositis? 301 64

A 12-year-old diabetic girl is reported who developed faintly violaceous nodules on the back of the right thigh. These spread to the posterior aspect of the left thigh and to both legs. She complained of some muscular weakness. A diagnosis of cutaneous polyarteritis nodosa was considered. No blood eosinophilia was detected. Skin biopsy disclosed scattered dermal foci of eosinophilic and granular degeneration of collagen with a palisade of histiocytes and eosinophils in a flame configuration. The lesions did not correspond to the sites of insulin injections. Eight childhood cases of eosinophilic cellulitis were found in the literature, all of them in males. The specificity and meaning of the flame configuration are discussed.
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PMID:[Childhood Wells syndrome]. 305 92

Vitamin A toxicity has been associated with alterations in mineral metabolism and may result in osteopenia, fractures, deformities, and growth arrest. The pathogenesis of the bone lesions that occur in vitamin A toxicity is, however, ill defined and was examined in the present study. The administration of pharmacological doses of vitamin A to growing male rats resulted in weakness and spontaneous fractures. Undecalcified bone histology of vitamin A toxic animals was characterized by increased bone resorption, osteoclastosis, a paucity of trabecular surfaces covered with osteoid, and lesions which appear to be pathognomonic of hypervitaminosis A. The serum calcium and magnesium levels of vitamin A-toxic animals were unremarkable, but serum phosphate levels were significantly higher than control values. Urinary hydroxyproline excretion reflected bone histology and was significantly increased in experimental rats. Circulating levels of the potent bone resorbers, PTH, 1,25-dihydroxyvitamin D, and 25-hydroxyvitamin D, were, however, comparable in vitamin A-toxic and control animals, suggesting a possible direct effect of vitamin A on bone. Subsequently, the effects of vitamin A (retinol) on in vitro collagen synthesis (incorporation of [3H]proline into collagen) and bone resorption (45Ca release from bone) were examined using a fetal rat calvarial culture. Retinol added to the culture medium for 20-24 h in concentrations ranging from 0.5-10 micrograms/ml selectively inhibited collagen synthesis in a dose-dependent fashion. Higher concentrations of retinol were toxic and resulted in a general inhibition of protein synthesis. Bone resorption was stimulated by 0.5 and 2.5 micrograms/ml retinol. We conclude that vitamin A toxicity in rats causes bone lesions, the genesis of which can be explained, at least in part, by a direct effect of the vitamin on skeletal tissue.
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PMID:Effects of hypervitaminosis A on the bone and mineral metabolism of the rat. 337 Dec 68

Muscle and joint pains and/or weakness are not usually stressed as central symptoms in hypothyroidism. Two cases of long-standing hypothyroidism presenting with prominent myopathic symptoms are described. The first patient presented with a 12-year history of proximal myopathy, arthropathy and skin abnormalities, and florid primary myxedema was diagnosed. No evidence for a systemic autoimmune process was found. The second patient had been treated with irradiation to the neck 23 years before admission and presented with clinical and laboratory signs of both proximal myopathy and hypothyroidism. Thyroid hormone replacement resulted in a complete recovery of all the musculoskeletal symptoms, with reversion to normal of the very high muscle enzyme levels in both patients. The cases presented illustrate that hypothyroidism can lead to the development of a variety of muscular, rheumatic and dermatologic syndromes easily confused with dermatomyositis or other collagen diseases.
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PMID:Musculoskeletal symptoms as a presenting sign of long-standing hypothyroidism. 343 93

Inheritance of vertical fiber hide defect (VFHD), a structural defect in collagen fiber orientation that causes weakness and reduced value of leather, was examined using histological data on hide biopsies obtained from 465 Hereford cattle by 65 sires. The data set included 44 offspring-dam pairs, for which VFHD phenotypes had been diagnosed on both the offspring and dam. Examination of offspring and parental frequency distributions indicated that inheritance of the condition was likely to be due to an autosomal recessive. In a subsequent experiment, a Hereford bull with a known VFHD phenotype was mated to Hereford cows with known VFHD phenotypes and to Angus cows not showing the defect. Angus were chosen because the defect has never been observed in the breed. All offspring (5) resulting from VFHD X VFHD matings expressed the defect, while no offspring (12) out of VFHD X non-VFHD matings (Angus cows) expressed the defect. It was concluded that VFHD is inherited as an autosomal recessive. The role that selection and alternative crossbreeding systems can play reducing phenotypic frequency of the defect is discussed.
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PMID:Inheritance of vertical fiber hide defect in cattle. 357 45

Cardiac rupture accounts for 8% to 10% of patient deaths after acute myocardial infarction, suggesting that myocyte necrosis weakens the ventricular wall in the initial days after occlusion. To test this theory, permanent occlusion of the left anterior descending coronary artery was performed in dogs. Twenty-four hours after occlusion, the tensile strength, strain at rupture, and stiffness of necrotic epicardium, midmyocardium, endocardium, subepicardium, and the visceral pericardium (VP) were quantified and compared with those of noninfarcted cardiac tissue. The relationship between tensile strength, stiffness, and collagen content was also examined. These material properties did not differ between necrotic and normal myocardium in any of the layers, indicating that myocyte necrosis, per se, does not weaken the myocardium. In both necrotic and normal tissue, marked transmural heterogeneity was observed; tensile strength of the endo- and epicardium (21.3 +/- 3.3 and 21.3 +/- 3.2 gm/mm2) was significantly greater (p less than 0.01) than that of the midmyocardium (4.0 +/- 0.3 gm/mm2) and subepicardium (5.0 +/- 0.5 gm/mm2), whereas the VP was substantially stronger (greater than 100 gm/mm2) than any myocardial layer. Similar results were obtained for stiffness. In contrast, strain at rupture did not vary significantly among myocardial layers and ranged from 0.40 +/- 0.03 (VP) to 0.53 +/- 0.03 (endocardium). Both tensile strength and stiffness of the myocardial layers were found to correlate directly with their collagen content: the higher the hydroxyproline concentration, the greater the tensile strength (r = 0.83). These results support the concept that the collagen fibroskeleton is an important determinant of the material properties of the myocardium. As myocyte necrosis, per se, did not affect tensile strength, we tentatively conclude that cardiac rupture may be a consequence of a defect or weakness in the collagenous framework of the heart.
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PMID:Effect of myocyte necrosis on strength, strain, and stiffness of isolated myocardial strips. 368 88

The fluorescent dye dichlorotriazinyl aminofluorescein will bind to amino groups of proteins covalently under physiological conditions. It has been used to dye the connective tissue around an ulcer or nonpenetrating, linear incision in the rabbit cornea and sclera, and the healing of the tissue has been examined up to 1 yr later. Sagittal sections were stained for light microscopy, and adjacent unstained sections were examined in the fluorescence microscope. The stained sections showed the reestablishment of the lamellar organization of the stromal collagen across the site of the incision; the fluorescence showed where the connective tissue that was present when the wound was made persisted, and thereby defined the limits of remodeling in the healing process. In Bowman's layer and the adjacent stroma, there was often an abrupt transition from fluorescent to new, undyed connective tissue. Deeper in the scar, and particularly around the ulcer, dark streaks were observed between the fluorescent lamellae, showing apparently new (non-fluorescent) tissue interdigitating with the old. These observations are discussed in relation to the mechanism of healing and the residual mechanical weakness that persists across scars in the cornea and sclera.
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PMID:Connective tissue remodeling in corneal and scleral wounds. 375 66

The accepted view that varicose veins are primarily due to valvular incompetence is challenged and the alternative theory of weakness of the vein wall is supported by the correlation of clinical, operative and histological findings. It is shown that there appears to be a basic abnormality of the muscle cell associated with abnormal collagen infiltration. The morphological changes in the vein wall are demonstrated by light microscopy and transmission electron microscopy. It is thought that the cause of these changes are to be sought in an investigation of the enzyme systems involved in maintaining tissue equilibrium in the vein wall.
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PMID:Some thoughts on the aetiology of varicose veins. 376 14

A 52-year-old woman presented with increasing pain, weakness, and paraesthesiae of four months' duration in the lower limbs. She suffered from chronic obstructive airways disease and hypertension. Neurological examination revealed wasting of the quadriceps muscles, weakness of the lower limbs, and absent ankle jerks. The sensory examination was normal. Full blood count, ESR, biochemical, immunological, and viral studies, urinary heavy metal assays, and cerebrospinal fluid examination were normal. Nerve conduction studies were consistent with a sensorimotor neuropathy, and electromyographic sampling was consistent with acute denervation. A sural nerve biopsy showed axonal degeneration and segmental demyelination. One month after admission, she developed carbon dioxide retention. Her weakness spread to affect the upper limbs, and she could not be resuscitated after a cardiac arrest three months after admission. General autopsy examination revealed bronchopneumonia. Neuropathological examination showed a lymphocytic infiltrate in the nerve roots of the cauda equina, the lumbosacral plexus, and the sural and vagal nerves. Increased cellularity and collagen were evident in these nerves. A diagnosis of chronic inflammatory polyneuropathy was made. The neuropathology of this entity is discussed.
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PMID:Neuropathological findings in a case of chronic inflammatory polyneuropathy. 384 15

Healing process of operative cardiac wounds was studied histopathologically in 14 patients who died 28 hours to 5 years after the operation of cardiac valve replacement. Repair of wounds in aorta and free wall of atrium was characterized by production of neointima and proliferation of collagen fiber at adventitia of aorta or epicardium of heart. Adhesion with granulation tissue at left ventricular venting wounds was observed in the case of 18th post-operative day. Reticulofibrosis of surrounding intracardiac muscle played an important role in development of granulation tissue. Cicatrix with collagen fiber was appeared from one month after the operation. In spite of attenuation of ventricular scar, aneurysmal bulging could not be observed. The basic healing pattern of wound in atrial septum was production and thickening of neointima. Granulation tissue rarely developed at the septum. Adhesion between sutured edges of atrial septal endocardium could not be observed and the dead space there remained over a period of 7 months after the operation. These findings indicated the continuous presence of unexpected weakness of the sutured septum until sufficient thickening of neointima had developed.
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PMID:[Healing of operative cardiac wounds]. 400 Jan 3


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