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)

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

Ten patients with disequilibrium, ataxia, and cerebrovascular abnormalities were studied using computer aided eye tracking and vestibular function tests. The patients had severe abnormalities in smooth pursuit (decreased gain) and saccade tests (increased delay, decreased accuracy). Optokinetic responses were less affected. The gain of the vestibulo-oculomotor reflex was sometimes affected. Patients with eye tracking abnormalities frequently had symptoms of difficulty reading and watching television. When the lesion was asymmetrical, abnormal eye tracking tests usually pointed to the side of the lesion. Computer aided eye tracking tests are a useful adjunct to the evaluation of the patient with suspected vascular disease. They help to locate areas of central nervous system dysfunction, and produce an objective measurement of the severity of impairment. Conversely, when impairment of the smooth pursuit or saccade system is detected in patients being evaluated for disequilibrium, an assessment of the patients' cerebrovascular system should be considered.
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PMID:Eye tracking abnormalities in patients with cerebrovascular disease. 635 Jul 69

The aim of this study was to describe the gait of persons with a unilateral transfemoral amputation by means of a questionnaire, gait analysis and measurement of energy expenditure, and to find correlations among the variables studied. The study included 29 transfemoral amputees amputated for other reasons than a chronic vascular disease. The patients were assessed using the following methods: 1) A questionnaire rating the walking distance and walking difficulty in different circumstances. 2) Gait analysis measuring temporal variables and goniometry of hips and knees. 3) Measurement of energy expenditure during sitting and walking. Scores on the questionnaire showed a correlation with socket design, a negative correlation with age and energy expenditure, and a positive correlation with fast speed. The gait of transfemoral amputees was asymmetrical as far as temporal variables were concerned, and for most amputees also for the range of motion of hip and knee. The walking speed of the amputees was lower than that of non-amputees and showed a positive correlation with hip extension-flexion range of motion and a negative correlation with age and stride time. The energy expenditure of the amputees during ambulation was higher than that of non-amputees, and seemed to correlate with residual limb length and the hip abduction-adduction range of motion.
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PMID:The gait of unilateral transfemoral amputees. 787 97

Patients with vasculitic neuropathy may present with either mononeuritis multiplex, or a symmetrical or asymmetrical sensorimotor neuropathy. In those patients whose neuropathy is part of a systemic vasculitis the neuropathy can be expected to improve leaving only mild or moderate functional disability. Nevertheless, the long-term outlook for such patients is poor with a 5-year survival of around 50% with most excess deaths being due to vascular disease. The prognosis in non-systemic vasculitic neuropathy is almost certainly substantially better than this. Treatment of vasculitic neuropathy should be based on diagnosis by tissue biopsy, usually of nerve, and early use of aggressive immunosuppression.
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PMID:Vasculitic neuropathy. 792 89

Investigation of the smaller of a pair of unequal kidneys showed a band of atrophy in the inner medulla, sparing the papillary tip, which was viable and contained collecting ducts. The kidney had extensive cortical atrophy with glomerulocystic disease and multiple tiny renal cell neoplasms. These changes were considered secondary to the medullary lesion. Study of 85 other kidneys taken a autopsy and surgery showed 8 other cases with similar band-like atrophy in the medulla to various degrees. All 9 cases had severe vascular disease. This asymmetrical or band-like atrophy of the renal medulla seemed to be fairly common but previously unreported, could be differentiated from renal papillary necrosis, and was most likely due to an episode of severe ischaemia, possibly in kidneys with pre-existing vascular narrowing.
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PMID:Asymmetrical atrophy of the renal medulla: a previously unreported abnormality. 795 3

The neuropathy associated with diabetes mellitus is arguably the most common peripheral neuropathy in the developed world. It can be classified into symmetrical and asymmetrical forms. The symmetrical form is predominantly sensory and autonomic, whereas the asymmetrical form can be sensory, or motor, or both, and can affect individual cranial or peripheral nerves. Pathologic and electrophysiologic studies indicate that the symmetrical polyneuropathy is characterized by a distally accentuated loss of myelinated and unmyelinated axons. The multifocal nature of the axonal degeneration and its association with vascular disease in the same pathologic specimens strongly suggest an ischemic cause involving the endoneurial microvascular circulation. The underlying biochemical abnormality appears to be the production of advanced glycosylated end products (AGEPs), in the presence of chronic hyperglycemia, which accumulate on endothelial proteins, causing basement membrane thickening and endothelial cell change. This produces multifocal vascular disease that, in turn, reduces nerve blood flow, causing endoneurial hypoxia and generating oxygen free radicals. Multifocal ischemic neuronal damage results. Currently, there is no accepted treatment, although long-term control of hyperglycemia is beneficial. Symptomatic relief of the burning pain is the most vexing therapeutic problem; tricyclic antidepressants and anticonvulsants have been used alone and together with varying success.
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PMID:Diabetic neuropathy. 822 54

Hyperhomocyst(e)inaemia is associated with endothelial dysfunction in animals and humans. Mechanisms responsible for endothelial dysfunction in hyperhomocyst(e)inaemia are poorly understood, but may involve impaired bioavailability of endothelium-derived nitric oxide (NO). We hypothesized that acute elevation of homocyst(e)ine by oral methionine loading may stimulate the formation of asymmetrical dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, due to a transmethylation reaction during the formation of homocyst(e)ine from methionine. We studied nine healthy human subjects (five males, four females) aged 29+/-2 years. Flow-mediated vasodilation (FMD) in the brachial artery (endothelium-dependent) and vasodilation induced by nitroglycerine (endothelium-independent) were measured with high-resolution ultrasound before and 8 h after oral methionine (100 mg/kg in cranberry juice) or placebo (cranberry juice), on separate days and in random order. Plasma homocyst(e)ine and ADMA concentrations were measured by specific HPLC methods. After a methionine bolus, elevation of homocyst(e)ine (28.4+/-3.5 micromol/l) was associated with an increased plasma concentration of ADMA (2.03+/-0.18 micromol/l) and reduced FMD (1.54+/-0.92%). Placebo had no effect on these parameters. There was a significant inverse linear relationship between ADMA concentration and FMD (r=-0.49; P<0.05), which was stronger than the relationship between the homocyst(e)ine concentration and FMD (r=-0.36; not significant). We conclude that acute elevation of the homocyst(e)ine concentration impairs vascular endothelial function by a mechanism in which an elevated concentration of ADMA may be involved. This finding may have importance for understanding the mechanism(s) leading to homocyst(e)ine-associated vascular disease, and its potential treatment.
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PMID:Elevation of asymmetrical dimethylarginine may mediate endothelial dysfunction during experimental hyperhomocyst(e)inaemia in humans. 1117 Dec 84

Despite significant progress in renal replacement therapy, the mortality from cardiovascular disease (CVD) in patients with chronic renal failure (CRF) is many times higher than in the general population. The traditional risk factors are frequently present in CRF patients. However, based upon conventional risk factor analysis, these factors do not fully explain the extraordinary increase in morbidity and mortality in CVD among patients with CRF. Accumulating evidence suggests that CRF is associated with impaired endothelial cell function. In recent years, the role of endothelial dysfunction (ED) and excessive oxidative stress (OS) in the development of CVD has been highlighted. ED is an early feature of vascular disease in different diseases such diabetes, hypertension, hypercholesterolemia, and coronary heart disease. The precise mechanism which induces ED is not clear. Several factors however, including OS-related accumulation of uremic toxins, hypertension and shear stress, dyslipidemia with cytotoxic lipoprotein species such as small, dense low-density lipoprotein (LDL) particles, competitive inhibition of endothelial nitric oxide (NO) by increased production by asymmetrical dimethylarginine (ADMA) are pathogenic. In addition, it is known that excessive OS causes ED. An overproduction of reactive oxygen species (ROS) may injure the endothelial cell membrane, inactivate NO, and cause oxidation of an essential cofactor of nitric oxide synthase (NOS). Recent studies have demonstrated that an impaired endothelium-dependent vasodilation and OS are closely related to each other in patients with CRF.
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PMID:Endothelium-dependent vasodilation and oxidative stress in chronic renal failure: impact on cardiovascular disease. 1269 8

Epidemiological associations are now well-established between insulin resistance, the metabolic syndrome and worsened cardiovascular outcomes. A direct role of insulin in vascular biology is also now broadly recognized. Specifically, insulin can directly stimulate the action of nitric oxide synthase, an effect that can be demonstrated both in vitro and in vivo. Insulin resistance, whether present endogenously or produced experimentally through exposure to fatty acids, glucosamine or tumour necrosis factor alpha, is associated with impaired endothelium-dependent vasodilation and, specifically, with impaired insulin-stimulated vasodilation. A number of potential molecular explanations for these observations are being pursued, with evidence to support a number of concurrent pathogenic mechanisms. These include insulin resistance-associated reductions in nitric oxide availability due to increases in oxidative stress (not requiring the presence of hyperglycemia), reduced availability of tetrahydrobiopterin and excess levels of asymmetrical dimethylarginine. A strong body of evidence also supports an excess of the vasoconstrictor endothelin, which may result directly from hyperinsulinemia and/or indirectly due to a loss of the suppressive effects of nitric oxide on endothelin production and action. The current leading edge of investigations into the association between insulin-resistant states and vascular dysfunction involves the expanding repertoire of adipocyte-derived hormones. Of these, particular interest has been focused on adiponectin, which has both vascular and metabolic actions, and may contribute importantly to the connection between metabolism and vascular function. Progress along these novel lines of investigation will continue to expand the understanding of the mechanisms linking insulin resistance, the metabolic syndrome and vascular disease.
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PMID:Insulin resistance, metabolic syndrome and vascular diseases: update on mechanistic linkages. 1530 8

The objective of this study is to better define the pathological characteristics of pathologically proven progressive supranuclear palsy (PSP) presenting with the corticobasal syndrome (CBS). PSP is characterized by early falls, vertical supranuclear ophthalmoplegia, and axial rigidity, whereas asymmetric limb features, including rigidity, bradykinesia, apraxia, alien limb phenomena, and cortical sensory loss are characteristic of CBS. We investigated clinicopathological characteristics of 5 cases of PSP that presented with CBS (CBS-PSP). Comprehensive pathological analysis was undertaken to determine the presence of concomitant pathological processes as well as quantitative tau burden in cortical regions of CBS-PSP, compared with 8 typical PSP cases (Typ-PSP). The clinical features in the CBS-PSP cases included asymmetrical features, apraxia, alien limb phenomena, and progressive aphasia. All cases had Parkinsonism, and vertical supranuclear ophthalmoplegia was noted in all but 1 case of CBS-PSP. Secondary neuropathological diagnoses included argyrophilic grain disease (AGD) in 1 of the 8 cases of Typ-PSP, whereas Alzheimer's disease (AD), Lewy body disease, AGD, and vascular disease was found in 3 cases of CBS-PSP. Image analysis of cortical tau burden performed in 8 Typ-PSP and 3 CBS-PSP cases revealed a significant increased tau burden in mid-frontal and inferior-parietal cortices in the CBS-PSP cases. This study demonstrates that when PSP presents as CBS, it is most likely due to either a concurrent cortical pathology from a secondary process such as AD or from the primary pathology of PSP extending into cortical areas that are primarily and commonly affected in CBD.
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PMID:Increased tau burden in the cortices of progressive supranuclear palsy presenting with corticobasal syndrome. 1583 57


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