Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From two different, compatible staphylococcal plasmids that determine streptomycin and chloramphenicol resistance, respectively, a recombinant plasmid was obtained. This plasmid can be transduced with a rather high frequency (10(-4)/plaque-forming unit) to plasmid-negative strains, the linkage of the two markers being 100%. The maintenance of the recombinant plasmid in the host cell seems to be controlled by the chloramphenicol resistance plasmid. The recombinant plasmid proved to be incompatible with both parental plasmids, which are unrelated. The relationship between the chloramphenicol resistance plasmid and the recombinant plasmid was the same as the between genetically marked derivatives of the recombinant plasmid, whereas the relationship of the streptomycin resistance plasmid to the recombinant plasmid was of a different, asymmetrical type.
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PMID:Recombinant plasmid obtained from two different, compatible staphylococcal plasmids. 118 73

The luminal surface of mammalian urothelium is covered with numerous plaques (also known as the asymmetric unit membrane or AUM) composed of semi-crystalline, hexagonal arrays of 12-nm protein particles. Despite the presumed importance of these plaques in stabilizing the urothelial surface during bladder distention, relatively little is known about their protein composition. Using a mouse mAb, AE31, we have identified a 27-kD protein that is urothelium-specific and is differentially expressed in superficial umbrella cells. This protein (pI approximately 5.8) partitions into the detergent phase during Triton X-114 phase separation. Pulse-chase experiments using cultured bovine urothelial cells showed that this protein is synthesized as a 32-kD precursor that is processed through a 30-kD intermediate, to the mature 27-kD form. In cytoplasmic vesicles containing immature AUM, the AE31 epitope is detected in patches on the cytoplasmic side, but in mature, apical AUM it is detected exclusively on the luminal side. This suggests an unusual translocation of the AE31 epitope during AUM maturation; more data are required, however, to substantiate this interpretation. Immunoaffinity purification of the 27-kD protein results in the copurification in approximately molar ratio of a 15-kD protein, as well as a small and variable amount of a 47-kD protein. Immunoblotting data indicate that these three proteins are immunologically distinguishable. This copurified 15-kD protein is relative basic (pI approximately 8.0). Like the 27-kD protein, it is urothelium-specific and is present mainly in the umbrella cells. Together, our data indicate that a 27-kD protein is urothelial plaque-associated (uroplakin I). Based on complex formation data, we provisionally name the 15-kD protein uroplakin II; additional data will be required to determine whether this and the 47-kD protein are integral parts of AUM. The identification of these AUM-associated and -related proteins, plus the availability of a culture system capable of synthesizing and processing some of these molecules, offer new opportunities for studying the detailed structure, assembly, and function of asymmetrical unit membrane.
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PMID:Uroplakin I: a 27-kD protein associated with the asymmetric unit membrane of mammalian urothelium. 169 95

Thirty patients (26 men, 4 women) aged from 32 to 73 years (mean 54 years) who developed anterior (14 cases) or posterior (16 cases) myocardial infarction received intravenous streptokinase in doses of 1,500,000 units 2 to 10 hours (mean 4 hours) after the onset of infarction. Coronary angiography, performed 18.6 days on average after thrombolysis, showed a distinct predominance of asymmetrical stenosis with irregular walls and a narrow neck (10 cases, 33 p. 100) or of complete occlusion (12 cases, 40 p. 100) in the artery responsible for the infarction. Complete occlusion probably was the ultimate stage of stenosis. In contrast, the various angiographic images observed in arteries unrelated to the infarction were evenly distributed. The radiological morphology of coronary arterial lesions after a recent infarction is suggestive of ruptured atheromatous plaque, sometimes complicated by thrombosis in situ. Identical images are seen in unstable angina. These findings indicate that one single therapeutic approach should be applied to the most severe types of coronary disease due to atherosclerosis.
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PMID:[Angiographic morphology of the coronary arteries after a recent myocardial infarction treated by intravenous thrombolysis]. 249 70

In plaque psoriasis it is likely that biochemical and ultrastructural changes precede the appearance of the typical plaque that is recognizable clinically. Currently, no technique exists by which the very early changes in psoriasis can be investigated. We report a method in which plaques of psoriasis are serially traced to identify their advancing edge. Eight-two untreated plaques from 15 patients and 38 treated plaques from 6 patients were traced over a three-week period; 65% of untreated and 57% of treated plaques showed consistent asymmetrical movement, allowing identification of an active and an inactive edge of each plaque. Using this technique, the active edge of two or more plaques was identified in each of ten patients. Blood flow measured by laser Doppler flowmetry indicated a 2.5-to-4.5-fold increase in cutaneous blood flow at the active edge compared with the inactive edge of each plaque. Punch biopsies from the sites investigated by laser Doppler flowmetry were examined by routine histology and monoclonal antibody immunohistology, but revealed no epidermal change and no T lymphocytic excess when the two areas were compared. We infer from these findings that the earliest change in a developing plaque is an increased blood flow, probably associated with a diffusable, and possibly humoral, initiating factor that accumulates at the active edge, stimulating transformation of normal skin to psoriatic plaque.
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PMID:Active and inactive edges of psoriatic plaques: identification by tracing and investigation by laser--Doppler flowmetry and immunocytochemical techniques. 265 71

Nonpigmenting fixed drug eruption is a distinctive, clinically recognizable entity. Characteristically, the lesions are large, symmetrical, well-circumscribed tender erythematous plaques that suddenly appear and reappear in exactly the same sites. They fade without pigmentation or any other trace over a 2- to 3-week period. Management requires recognition and avoidance of the responsible drug. Acute attacks may call for short-term systemic steroid therapy. Three examples of this overlooked reaction pattern are presented. The first case was associated with Night-Time cold formula and was proved by specific component challenge to be due to d-pseudoephedrine hydrochloride. The second case was due to PediaCare 3 Children's Cough Syrup, also containing d-pseudoephedrine hydrochloride. The third case was due to Visine eye drops, which contain an imidazole derivative, tetrahydrozoline. There is a need to increase our awareness that fixed drug eruptions come in two very different clinical forms: the classic pigmenting asymmetrical form, and the nonpigmenting symmetrical erythematous plaque form, in both of which the patient will give a history of the eruption being recurrent in the same area.
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PMID:Nonpigmenting fixed drug eruption as a distinctive reaction pattern: examples caused by sensitivity to pseudoephedrine hydrochloride and tetrahydrozoline. 1221 20

Cutis marmorata telangiectatica congenita (CMTC) is characterized by a persistent vascular mottling of the skin, usually on the limbs. Four cases (2 males and 2 females) followed up for varying lengths of time are reported. In the first patient, whose vascular lesions were mild, careful re-examination after 10 years revealed some scars. In the second patient the lesions were located on the right side of the body, notably on the leg; 6 years later atrophic scars and a brownish plaque were visible on that leg. In the third patient the lesions occupied almost the entire body, although one side was more affected than the other and hypotrophic; the child's face was asymmetrical because of hypoplasia of the jaw and curvature of the nose; after 1 year the patient's general condition was satisfactory and the skin lesions were less evident but still present. In the fourth patient hypoplasia of a lumbar vertebra was discovered; the skin lesions were similar to those observed in the third patient. Examination of the deep vessels, performed whenever possible, did not show any abnormality, but the possibility of future vascular defects, such as varicosities, must be considered. While some authors emphasize the functional character of the disease, in our opinion the high frequency of multiple associated congenital abnormalities makes CMTC not only a vascular disorder but also a syndrome including other neuroectodermal and mesodermal defects. Therefore, any patient presenting with the cutaneous changes typical of CMTC should be examined with this in mind.
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PMID:[Cutis marmorata telangiectatica congenita. 4 new cases and review of the literature]. 332 46

Growth characteristics of a wide range of influenza A viruses from different mammals and bird species were examined in an established line of canine kidney (MDCK) cells at an ordinary (37 degrees C) and a high temperature (42 degrees C). Although all viruses employed in the present study possessed a capability of replicating at 37 degrees C, virus growth at 42 degrees C showed considerable variation and reflected differences in the natural hosts of the isolates. All reference strains and isolates from bird species grew well in the MDCK cells maintained at 42 degrees C, but human viruses did not, showing an asymmetrical growth behavior. In contrast to this, growth of swine and equine viruses showed growth characteristics intermediate between human and avian viruses. Of the two swine viruses examined, replication of one strain occurred equally well at both temperatures and another failed to grow at 42 degrees C. Similarly, two of the three equine viruses tested belonging to H3N8 antigenic subtypes grew at 42 degrees C. However, the results obtained from comparison of plaque sizes and growth curves indicated that the replication of the above swine and equine viruses was restricted under a stringent temperature when compared to avian viruses. The detailed analysis of cloned viruses revealed that some of the swine and equine viruses contained two variants which are readily distinguished by growth behavior at 42 degrees C. Genome analysis of parental and virus clones by oligonucleotide mapping and migration profiles of RNA segments did not detect any differences among the above variants exhibiting the asymmetrical growth characteristics at 42 degrees C.
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PMID:Difference in growth behavior of human, swine, equine, and avian influenza viruses at a high temperature. 340 Nov 17

A technique has been developed for isolating cells from the intimal and medial layers of the human aorta by enzymatic dispersion. After mechanical separation of intima, media and adventitia the intima and the media were dispersed by collagenase and elastase. Enzyme-isolated cells seeded in the culture with at a frequency of 30 to 50%. In the primary culture differentiated aortic cells were morphologically heterogenous. It was possible to define four main types of cells according to their shape: polygonal, elongated, asymmetrical and stellate. Polygonal and stellate cells are found only in cultures of grossly normal intima, whereas elongated and asymmetric cells are found in practically all cultures. The ratio of elongated to asymmetric cells in cultures obtained from healthy aorta and atherosclerotic plaque is more or less the same at approximately 3:1. In cultures of fatty streaks the proportion of asymmetric cells exceeds 50%. Using immunofluorescence, all four types of cell were identified as smooth muscle cells. The possible reasons for the cellular polymorphism in primary culture and the prospects of utilizing this culture for the study of cellular aspects of atherosclerosis' pathogenesis are discussed.
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PMID:Primary cultures of enzyme-isolated cells from normal and atherosclerotic human aorta. 651 17

This study aims to evaluate and compare the current pathological criteria for the diagnosis of hypertrophic cardiomyopathy (HOCM). The following criteria were applied to 39 autopsy patients whose hearts showed myofibre disarray: (i) disarray involving more than 5% of ventricular septal myofibres, (ii) asymmetrical septal hypertrophy (ASH), (iii) mirror-image subaortic plaque, and (iv) a positive histologic HOCM index (HHI). Group 1 (27 patients) with greater than 5% ventricular septal myofibre disarray were diagnosed as HCM, whereas group 2 (12 patients) had less than 5% disarray. The mean disarray value in group 1 was 52% compared to 1.2% in group 2. The two groups showed significant differences regarding ASH and in the amounts of myofibre disarray in the free walls of both ventricles. A new finding was that the histologic HOCM index was significantly higher in patients who died suddenly. The HHI was the commonest positive criterion in group 1, followed by ASH and a mirror-image endocardial plaque. None of the current imperfect pathological criteria for the diagnosis of HCM can be used as the 'gold standard'.
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PMID:Evaluation of pathological criteria for diagnosis of hypertrophic cardiomyopathy. 653 46

The cerebral cortices of macaques (ranging in age from 10 to 37 years; n = 17) were analyzed by immunocytochemistry and electron microscopy to determine the cellular and subcellular localizations of the amyloid precursor protein and beta-amyloid protein, the cellular participants in the formation of senile plaques and parenchymal deposits of the beta-amyloid protein, and the temporal/spatial development of these lesions. Amyloid precursor protein was enriched within the cytoplasm of pyramidal and nonpyramidal neuronal cell bodies in young and old monkeys. In the neuropil, amyloid precursor protein was most abundant within dendrites and dendritic spines; few axons, axonal terminals, and resting astrocytes and microglia contained the amyloid precursor protein. At synapses, amyloid precursor protein was found predominantly within postsynaptic elements and was enriched at postsynaptic densities of asymmetrical synapses. The earliest morphological change related to senile plaque formation was an age-related abnormality in the cortical neuropil characterized by the formation of dense bodies within presynaptic terminals and dendrites and an augmented localization of the amyloid precursor protein to astrocytes and microglia. In most monkeys > 26 years of age, the neocortical parenchyma exhibited neuritic pathology and plaques characterized by swollen cytoplasmic processes, interspersed somata of neurons, and reactive glia within or at the periphery of senile plaques. Neurites and reactive astrocytes and microglia within these plaques were enriched with the amyloid precursor protein. In diffuse plaques, nonfibrillar beta-amyloid protein immunoreactivity was visualized within cytoplasmic lysosomes of neuronal perikarya and dendrites and the cell bodies and processes of activated astrocytes and microglia. In mature plaques, beta-amyloid protein immunoreactivity was associated with extracellular fibrils within the parenchyma; some cytoplasmic membranes of degenerating dendrites and somata as well as processes of activated glia showed diffuse intracellular beta-amyloid protein immunoreactivity. We conclude that morphological abnormalities at synapses (including changes in both pre- and postsynaptic elements) precede the accumulation of the amyloid precursor protein within neurites and activated astrocytes and microglia as well as the deposition of extracellular fibrillar beta-amyloid protein; neuronal perikarya/dendrites and reactive glia containing the amyloid precursor protein are primary sources of the beta-amyloid protein within senile plaques; and nonfibrillar beta-amyloid protein exists intracellularly within neurons and nonneuronal cells prior to the appearance of extracellular deposits of the beta-amyloid protein and the formation of beta-pleated fibrils.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synaptic pathology and glial responses to neuronal injury precede the formation of senile plaques and amyloid deposits in the aging cerebral cortex. 799 40


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