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

Ischemia plays an important role in the development of neuropathies associated with various disorders, such as peripheral vascular occlusive diseases, necrotizing vasculitides, diabetes mellitus and nerve compression or trauma. Although a multiple mononeuropathy or an asymmetrical polyneuropathy is the usual clinical presentation of ischemic neuropathy, some patients present with a neuropathy that is mainly distal and symmetrical. Pathologically, nerve ischemia results in focal or multifocal central fascicular or sector fiber degeneration. These ischemic lesions tend to begin at mid-upper arm or midthigh level, which is the watershed zone of poor perfusion, and become more diffuse distally. Nerve ischemia at the level of distal small fascicles often induces sub-perineurial crescent lesion rather than central fascicular fiber degeneration. Physiologically, reduced nerve blood flow with endoneurial hypoxia has been demonstrated in experimental diabetic and galactose neuropathies. Endoneurial ischemia/hypoxia in galactose neuropathy appears to be due to increased intercapillary distances and constriction of trans-perineurial vessels resulting from endoneurial edema. Although acute ischemic neuropathy has been well investigated, little is known about functional or structural responses of peripheral nerve to chronic ischemia.
 ...
PMID:[Ischemic neuropathy]. 209 82

A patient presented with a neuropathy originally ascribed to prolonged effect of epidural anesthesia following major intraabdominal surgery. Subsequent investigation revealed the cause of the neuropathy to be an arterial thrombosis. Two percent lidocaine and 0.5% bupivicaine were used intraoperatively and epidural morphine was administered at the end of the operation. The causes of prolonged neural blockade from epidural anesthesia are reviewed. Ischemia is a well known cause of neuropathy, and when ischemic pain is masked with the use of epidural narcotics, the neurologic deficit produced can be similar to that of prolonged action of epidurally administered local anesthesia. Ischemia should be included in the differential diagnosis of prolonged neurologic deficit in this situation. If examination reveals ischemia as a possible cause of neurologic deficit (e.g., asymmetrical or absent pulses), an angiogram should be obtained quickly to provide the best opportunity for rapid surgical treatment.
 ...
PMID:Ischemic neuropathy presenting as prolonged epidural anesthesia. 217 16

We report the neuropathologic findings in a 63-year-old white male with a history of birth asphyxia, cerebral palsy, seizures and mild mental retardation in conjunction with similar brain pathologic findings in animal models of perinatal asphyxia. The human case showed a left cerebral hemispheric hemiatrophy associated with an extensive ulegyria involving all cerebral lobes on that side and a single microscopic focus of cortical atrophy in the right hemisphere. Among a large number of experimental perinatal asphyctic exposures only an occasional animal, like the human case described, showed unilateral hemispheric injury with softening and necrosis if examined early and ulegyria with hemispheric hemiatrophy if examined late. The present paper suggests that perinatal asphyxia under specific pathophysiologic conditions may cause unilateral brain injury. Our experimental studies suggest the specific condition of perinatal asphyxia potentially causing unilateral or asymmetrical brain damage is marked hypoxemia combined with substantial reductions in blood pressure but without circulatory collapse. Given these conditions, the asymmetry of the brain damage likely reflects fetal head position within the gravitational field relative to the heart. With disturbed cerebral blood flow autoregulation from asphyxia, the gravitational field likely accentuates the ischemia of those brain areas most elevated above the level of the heart. Thus, we postulate head position may play a pivotal role in defining brain regions that are damaged in hypotensive perinatal asphyxia. This interpretation may affect the intensive care of hypoxemic, hypotensive newborns aimed at minimizing the risk of brain damage.
 ...
PMID:Cerebral hemiatrophy--correlation of human with animal experimental data. 325 12

We first studied the distribution of radioactivity during continuous inhalation of C15O2 and 15O2 in traverse tomograms of the greatest diameter of legs, at rest and immediately after exercise (ankle flexions). C15O2 and 15O2 were distributed homogeneously and symmetrically in both legs of normal subjects at rest. The activity accumulated in the anterolateral region after exercise. In patients, this pattern of distribution was similar but asymmetrical, depending on the arterial pathology. No systematic distribution of either C15O2 or 15O2 was observed. In a second step, we studied quantitatively blood flow (F), oxygen uptake (R) and oxygen extraction (E) in 11 subjects: 5 normals (23 +/- 1 years) and 6 patients (60 +/- 11 years) suffering from unilateral intermittent claudication. We used the bolus inhalation technique of C15O2 and 15O2. In the normal leg at rest, ranges were 2.5 to 8.0 ml/min.hg for F, 0.9 to 21.3 mumol/min.hg for R and 3.6 to 33.4% for E. In the pathological leg at rest, ranges were 3.7 to 11.3 ml/min.hg for F, 3.8 to 10.6 mumol/min.hg for R and 7.1 to 24.5% for E. After exercise, ranges were 6.4 to 62.8 ml/min.hg for F, 66.0 to 386.3 mumol/min.hg for R and 29.2 to 89.5% for E in both legs. There was no straight difference between normal and pathological legs soon after exercise. This study allows us to expect that the demonstration of such a difference implies a longer delay of data acquisition following the slow post-ischemia recovery.
 ...
PMID:[Regional blood flow and oxygen consumption in the leg muscles of normal subjects and in those with arterial insufficiency. Study of the distribution of C15O2 and of 15O2 using positron emission tomography]. 326 Sep 34

In order to evaluate regional muscle blood flow and oxygen utilization, we study with positron emission tomography (PET) the distribution of C15O2 and 15O2 in 17 subjects: 5 normals (24 +/- 3 years) and 12 patients (63 +/- 13.5 years). C15O2 and 15O2 are inhalated with a steady-state technique. Positron tomograms are recorded in supine position at the greatest diameter of the leg. Exercise consists in simultaneous ankle flexions. In all normals, C15O2 and 15O2 are distributed homogeneously and symmetrically in both legs. At rest, they concentrate in the region of vascular pedicle. After exercise, C15O2 and 15O2 are electively distributed in the anterolateral region of the leg. In patients, this pattern of distribution is similar but asymmetrical. Moreover, the regional uptake of C15O2 and 15O2 often dissociates. In conclusion, C15O2 and 15O2 allow to study repeatedly muscle blood flow and oxygen utilization in patients with peripheral ischemia, both at rest and after exercise. The broad spectrum of pathological changes observed in this study needs further metabolic investigations.
 ...
PMID:Effect of exercise on the leg distribution of C15O2 and 15O2 in normals and in patients with peripheral ischemia: a study using positron tomography. 326 17

Thirty-nine neonates including 29 prematures had correlation studies of trans-fontanelle ultrasounds with post-mortem anatomic findings. Occipital hyper-echogenicity can be physiological when it is symmetric in the premature infant, and may indicate ischemia and/or anoxia when it is asymmetrical. No abnormal pathology went undetected by echo. Cortical gyri were never seen prior to 32 weeks gestational age.
 ...
PMID:[Transfontanelle echography: correlation with anatomopathological data. Apropos of 39 cases in newborn infants]. 356 52

We measured acute changes in monoamine metabolites in corpus striatum of immature rat pups exposed to hypoxia-ischemia, hypoxia alone, or total global ischemia. Carotid ligations and two hours of 8% oxygen environment in 7-day-old pups led to asymmetrical turning behavior, a 70% decrease in endogenous striatal dopamine levels, and a 125% increase in homovanillic acid (HVA) concentrations on the side of ligation. In contrast, hypoxia alone and total global ischemia alone were not associated with HVA level elevation. Elevation of HVA level with hypoxia-ischemia showed a threshold effect between 1 and 1.5 hours, and this time course paralleled that for production of gross morphological changes in rats raised to maturity. The data suggest that dopamine release from striatal nerve terminals is associated with events causing brain injury during perinatal hypoxia-ischemia. Tissue HVA in the animal model appears to be a quantitative marker for the effects of the insult on a population of nerve terminals.
 ...
PMID:Effects of hypoxia-ischemia on monoamine metabolism in the immature brain. 620 78

The quantitative VCG criteria (VCGer) for left ventricular hypertrophy (LVH) and their diagnostic power were determined in 165 hypertensive men and 86 women over 40 years of age without congestive cardiac failure in comparison with 91 normal men and 108 normal women. The patients were grouped according to the presence or absence of LVH determined by X-ray (men: 96 without and 69 with LVH, women: 41 without and 45 with LVH). The proper statistical methods were used taking into account whether their distributions were symmetrical or asymmetrical. We found some sex differences of VCG criteria. The most striking results were the lack of increased voltage, and the great sensitivity of the orientation of Q vectors to the left (Q left). Q left may be induced by: 1. a septal hypertrophy, alone or accompanied by a hypertrophy of the anterior and posterior paraseptal regions of LV wall, 2. by a subendocardial ischemia at these levels induced by the increase of intraventricular pressure, 3. by possible spatial change of the septum, 4. by all these factors acting synchronously, 5. by other, unknown factors. These VCGcr for LVH found by us are different from those in the literature, but they are valid in Romania.
 ...
PMID:Absence of increased cardiac voltage and the importance of Q vectors for the diagnosis of left ventricular hypertrophy in early stages of hypertension in patients over 40 years of age. 623 49

A mother and son suffer from hemiplegic migraine with onset in childhood. Both have nystagmus which has not changed for many years, but the date of onset is uncertain. They have an asymmetrical tremor, clinically indistinguishable from essential tremor. Neuroophthalmological examination revealed inability to produce smooth pursuit, gaze-paretic nystagmus, rebound nystagmus, failure of fixation suppression of the vestibuloocular reflex both horizontally and vertically, and low gain of the optokinetic system. These abnormalities, confirmed by electrooculography, are commonly seen in disease of the cerebellum and brainstem. Treatment with propranolol and pizotyline lessened the number of episodes of hemiplegia and improved the tremor. Hemiplegic migraine has been reported in association with nystagmus, retinal degeneration, deafness, and ataxia in varying combinations in three other families with autosomal dominant inheritance. These associated neurological manifestations likely represent system degenerations rather than the effect of repeated ischemia imputable to the migraine itself. The syndrome of hemiplegic migraine, tremor, and ocular smooth pursuit system disorder seen in this family appears to be inherited as a single autosomal dominant trait, although more than one autosomal dominant gene may be involved.
 ...
PMID:An autosomal dominant syndrome of hemiplegic migraine, nystagmus, and tremor. 743 78

ATP-sensitive K+ (KATP) channels are thought only to open during conditions of metabolic impairment (e.g., myocardial ischemia). However, the regulation of KATP channel opening during ischemia remains poorly understood. We tested whether thiol (SH) group oxidation, which is known to occur during ischemia, may be involved in KATP channel regulation. Inside-out membrane patches were voltage clamped at a constant potential (O mV) in asymmetrical K+ solutions. The effects of compounds that specifically modify SH groups [p-chloromercuri-phenylsulfonic acid (pCMPS), 5-5'-dithio-bis(2-nitrobenzoic acid) [DTNB], and thimerosal] were tested. The membrane-impermeable compound, pCMPS (> or = 5 microM), caused a quick and irreversible inhibition of KATP channel activity. The reducing agent, dl-dithiothreitol (DTT) (3 mM) was able to reverse this inhibition. DTNB (500 microM) caused a rapid, but spontaneously reversible, block of KATP channel activity. After DTNB, no change was observed in single channel conductance. Oxidized glutathione (GSSG, 3 mM) did not block KATP channel activity. Thimerosal (100-500 microM) induced a DTT-reversible block of partially rundown KATP channels, or channels that underwent complete rundown; these channels were reactivated with trypsin (1 mg/ml). Thimerosal did not block KATP channels that had a high degree of activity. However, the ATP sensitivity was decreased; the concentration of ATP needed to half-maximally inhibit the channel (Ki) was increased from 47 +/- 12 to 221 +/- 35 microM (n = 6, P < 0.05). This was not due to a spontaneous change with time.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of thiol-modifying agents on KATP channels in guinea pig ventricular cells. 750 58


1 2 3 4 Next >>