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)

Six experiments were carried out to compare go/no-go and choice paradigms for studying the effects of intradimensional discrimination training on subsequent measures of stimulus generalization in human subjects. Specifically, the purpose was to compare the two paradigms as means of investigating generalization gradient forms and frame of reference effects. In Experiment 1, the stimulus dimension was visual intensity (brightness); in Experiment 2, it was line orientation (line-angle stimuli). After learning to respond (or to respond "right") to stimulus value (SV) 4 and not to respond (or to respond "left") to SV2 (in Experiment 1) or SV1 (in Experiment 2), the subjects were tested for generalization (recognition) with an asymmetrical set of values ranging from SV1 to SV11. Go/no-go training produced peaked gradients, whereas choice training produced sigmoid gradients. The asymmetrical testing resulted in a gradual shift of the peak of responding (go/no-go group) or in the point of subjective indifference (PSI; choice group) toward the central value of the test series; thus, both paradigms revealed a frame of reference effect. The results were comparable for the quantitative (intensity) and the qualitative (line-angle) stimulus dimensions. Experiment 3 compared the go/no-go procedure with a yes/no procedure in which subjects responded "right" to SV4 and "left" to all other intensities and found no differences between these procedures. Thus the difference in gradient forms in go/no as opposed to (traditional) choice paradigms depends on whether one or two target stimuli are used in training. In Experiment 4, in which visual intensity was used, the shift in the PSI following choice training varied positively with the range of asymmetrical test stimuli employed. In Experiment 5, also with visual intensity, the magnitude of the peak shift following go/no-go training varied as a function of overrepresenting a high or a low stimulus value during generalization testing. Experiment 6, with line angles, showed that the PSI following choice training varies in a similar way. The frame of reference effects obtained in these experiments are consistent with an adaptation-level model.
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PMID:A comparison of generalization functions and frame of reference effects in different training paradigms. 162 May 65

Frontotemporal dementia is a progressive dementing illness characterized clinically by personality change, disinhibition, and apathy. Neuropathologically, neuronal cell loss, astrogliosis, and microvacuolation are present in the superficial frontotemporal cortical layers, with variable involvement of subcortical and limbic structures. The clinical picture and anatomical distribution of the degenerative changes, as well as motor neuron involvement, differentiate four neuropathological groups: 1) frontal lobe type, 2) thalamostriatal type, 3) motor neuron type, and 4) asymmetrical type. The authors review the results of four large postmortem studies with a special emphasis on cliniconeuropathological correlation.
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PMID:Frontotemporal dementia: a clinicopathological review of four postmortem studies. 884 92

Benznidazole (N-benzyl-2-nitro-1-imidazoleacetamide) is an antiprotozoan agent of the nitroimidazole group used extensively in South America to treat Chagas' disease. In humans, its most important side effect is peripheral polyneuropathy, the frequency of which is dose related. To evaluate this effect, we administered benznidazole to adult, male, mongrel dogs at doses ranging from 5 to 40 mg/kg/day (0.5 to 4 times the dose used to treat chagasic patients). Subsequent neurological examination revealed apathy, ataxia, spastic tetraplegia with hyperreflexia of stretching reflexes, balance disorders and asymmetrical gait. These alterations appeared earlier and were more intense at the higher doses. Drug withdrawal also left dose- and time-dependent sequelae like ataxia, hypertonia, hyperreflexia and alterations of balance. No peripheral neuropathy was detected. The present findings suggest that a careful reevaluation of the side effects of benznidazole in humans is necessary.
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PMID:Experimental benznidazole encephalopathy: I. Clinical-neurological alterations. 926 Aug 52

Emotional reactions are sometimes observed during the intracarotid sodium amobarbital test. For instance, euphoric/indifference reactions can be seen during right hemisphere inactivation and catastrophic reactions may accompany left hemisphere inactivation. Less dramatic changes can also be detected in affective self-report during left and right hemisphere amobarbital tests, with more negative affect reported during left hemisphere inactivation and either neutral or mildly positive affective states reported during right hemisphere inactivation. The current study not only replicated this effect, but in addition, found significant group differences. The first group (right way) showed a pattern of affective self-report during left and right amobarbital tests entirely consistent with prior findings, while a second group (wrong way) showed results that behaved in a diametrically opposite fashion. A third group (no change) showed little, if any, difference in affective self-report during left and right amobarbital tests. The major factor distinguishing the wrong way group from the other two appeared to be an asymmetrical distribution of left and right temporal lobe lesions in the former group. In contrast, the factor differentiating the right way group from the no change group appeared to be the relative degree of left hemisphere inactivation during the left hemisphere amobarbital test. The results are discussed not only in terms of their impact on theories of cerebral lateralization for emotion, but also in terms of methodological issues in this field.
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PMID:Affective self-report during the intracarotid sodium amobarbital test: group differences. 1101 12

The electrical field application technique has revealed that the electrotonic length of the distal apical dendrites of hippocampal CA1 pyramidal neurones is long compared to the rest of the cell. This difference may be due to an asymmetrical distribution of channels responsible for the leak conductance in distal and proximal membrane segments. One such conductance, the hyperpolarization-activated cation current, I(h), is reported to display an increasing density with distance from the soma along the apical dendrite. Such asymmetry of I(h) could be a major cause of the increased electrotonic length of the distal apical dendrite. In the present study we found that blockade of I(h), by bath application of Cs(+) (3 mM) or ZD7288 (20 microM), reduced the electrical field-induced transmembrane polarization (TMP) in the distal apical dendrites. In some neurones the polarization reversed polarity, reflecting a movement of the indifference point (site of zero polarization) from the distal dendrites, across the recording site to a more proximal position. These effects were more pronounced when Cs(+) and ZD7288 were applied locally to the distal apical dendrites. Bath application of another antagonist of leak conductance, Ba(2+) (1 mM), also decreased the average field-induced polarization. This latter effect, however, did not reach statistical significance. These data suggest that I(h) is partly responsible for the distal location of the indifference point, and indicate that an elevated activity of I(h) contributes to the relatively increased electrotonic length of the most distal part of the apical dendrites.
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PMID:Influence of the hyperpolarization-activated cation current, I(h), on the electrotonic properties of the distal apical dendrites of hippocampal CA1 pyramidal neurones. 1187 94

In this article the value orientations of justice and of the good are analysed in their concrete meanings for nursing proceeding. Firstly, the usual interpretation of justice in the practice field which reduces it to economical justice of distribution, is criticized. A stronger orientation of justice to the criterion of adequacy is proposed as an alternative. This would make possible a synthesis between the two demands of a just care and of a good care and would permit the mediation of two value orientations that often seem to be irreconcilable in nursing practice. The definition of the contents of good care attributes high importance to the aspect of relation. Because the nursing relation is in its essence an asymmetrical relation, the dimension of power has a decisive importance in this context. This leads to the question which kind of conditions must be created to give nurses the opportunity to use the power that they get from their function in a responsible way and to cultivate an attitude of non-indifference toward those who need their help.
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PMID:[Justice and good nursing care]. 1246 61

Highly variable bisection performance in neglect patients has been attributed to an increased 'zone of indifference'. The indifference zone indicates the discrepancy between two line lengths which are judged as equal in length. Following this argumentation, the central area of a line should be expanded in neglect patients. The present two experiments investigated for the first time the expansion of the central area using a modified version of the Landmark Task. The location of a central or asymmetrical bisection mark on a horizontal line had to be judged (centre/left/right). In both experiments neglect patients, unlike healthy and patient controls, showed clear deficits in judging the location of the mark correctly and tended to judge asymmetrical marks of up to 4 cm as centrally positioned. The results are in agreement with and provide the first clear evidence of an enlarged perceptual zone of indifference in patients with hemispatial visual neglect.
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PMID:The effect of hemispatial neglect on the perception of centre. 1517 15

Mutations in the progranulin gene (GRN) are a major cause of frontotemporal lobar degeneration with ubiquitin-positive, tau-negative inclusions (FTLD-U) but the distinguishing clinical and anatomical features of this subgroup remain unclear. In a large UK cohort we found five different frameshift and premature termination mutations likely to be causative of FTLD in 25 affected family members. A previously described 4-bp insertion mutation in GRN exon 2 comprised the majority of cases in our cohort (20/25), with four novel mutations being identified in the other five affected members. Additional novel missense changes were discovered, of uncertain pathogenicity, but deletion of the entire gene was not detected. The patient collection was investigated by a single tertiary referral centre and is enriched for familial early onset FTLD with a high proportion of patients undergoing neuropsychological testing, MRI and eventual neuropathological diagnosis. Age at onset was variable, but four mutation carriers presented in their 40s and when analysed as a group, the mean age at onset of disease in GRN mutation carriers was later than tau gene (MAPT) mutation carriers and duration of disease was shorter when compared with both MAPT and FTLD-U without mutation. The most common clinical presentation seen in GRN mutation carriers was behavioural variant FTLD with apathy as the dominant feature. However, many patients had language output impairment that was either a progressive non-fluent aphasia or decreased speech output consistent with a dynamic aphasia. Neurological and neuropsychological examination also suggests that parietal lobe dysfunction is a characteristic feature of GRN mutation and differentiates this group from other patients with FTLD. MR imaging showed evidence of strikingly asymmetrical atrophy with the frontal, temporal and parietal lobes all affected. Both right- and left-sided predominant atrophy was seen even within the same family. As a group, the GRN carriers showed more asymmetry than in other FTLD groups. All pathologically investigated cases showed extensive type 3 TDP-43-positive pathology, including frequent neuronal cytoplasmic inclusions, dystrophic neurites in both grey and white matter and also neuronal intranuclear inclusions. Finally, we confirmed a modifying effect of APOE-E4 genotype on clinical phenotype with a later onset in the GRN carriers suggesting that this gene has distinct phenotypic effects in different neurodegenerative diseases.
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PMID:A distinct clinical, neuropsychological and radiological phenotype is associated with progranulin gene mutations in a large UK series. 1823 97

Bipedal locomotion and fine motility of hand and larynx of humans introduced musculoskeletal adaptations, new pyramidal, corticostriatal, corticobulbar, nigrostriatal, and cerebellar pathways and expansions of prefrontal, cingular, parieto-temporal and occipital cortices with derived new brain capabilities. All selectively degenerate in aged homo sapiens following 16 syndromic presentations: (1) Parkinsonism: nigrostriatal control for fast automatic movements of hand, larynx, bipedal posture and gait ("simian gait and hand"). (2) Frontal (highest level) gait disorders (lower body parkinsonism, gait apraxia, retropulsion): prefrontostriatal executive control of bipedal locomotion. (3) ataxia: new synergistic coordination of bipedal gait and fine motility. (4) Dyskinesias (chorea, dystonia, tremor...): intrusions of simian basal ganglia motor subroutines. (5) motoneuron diseases: new proximo-distal and bulbar motoneurones, preserving older ones (oculomotor, abdominal...). (6) Archaic reflexes: prefrontal disinhibition of old mother/tree-climbing-oriented reflexes (sucking, grasping, Babinski/triple retraction, gegenhalten), group alarms (laughter, crying, yawning, grunting...) or grooming (tremor=scratching). (7) Dysautonomia: contextual regulation (orthostatism...). (8) REM sleep disorders of new cortical functions. (9) Corticobasal syndrome: melokinetic control of hand prehension-manipulation and language (retrocession to simian patterns). (10) Frontal/temporal lobe degeneration: medial-orbitofrontal behavioural variant: self monitoring of internal needs and social context: apathy, loss of personal hygiene, stereotypia, disinhibition, loss of concern for consequences of acts, social rules, danger and empathy; dorsolateral executive variant: inadequacy to the context of action (goal, environmental changes...); progressive non-fluent aphasia: executive and praxic processing of speech; temporal variant: abstract concepts for speech, gestures and vision (semantic dementia, progressive nonfluent aphasia) (11) Temporomesial-limbic-paralimbic-associative cortical dementias (Alzheimer's disease, Lewy body, progressive amnesia): processing of explicit cognition: amnesic syndrome, processing of hand, larynx and eye: disorientation, ideomotor apraxia, agnosia, visuospatial processing, transcortical aphasia. (12) Focal posterior atrophy (Benson, progressive apraxia): visuomotor processing of what and where. (13) Macular degeneration: retinal "spot" for explicit symbols. (14) "Psychiatric syndromes": metacognition, self monitoring and regulation of hierarchical processing of metacognition: hallucinations, delusions, magic and mystic logic, delusions, confabulations; drive: impulsivity, obsessive-compulsive disorders, mental automatisms; social interactions: theory of mind, autism, Asperger. (15) Mood disorders: control on emotions: anxio-depressive and bipolar disorders, moria, emotional lability. (16) Musculoskeletal: inclusion body myositis: muscles for bipedal gait and fine motility. Paget's disease: bones for bipedal gait and cranium. Understanding of the genetic mechanisms underlying the evolution of these recent human brain regions and paleoneurology my be the key to the focal, asymmetrical or systemic character of neurodegeneration, the pathologic heterogeneity/overlap of syndromic presentations associating gait, hand, language, cognition, mood and behaviour disorders.
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PMID:Paleoneurology: neurodegenerative diseases are age-related diseases of specific brain regions recently developed by Homo sapiens. 1870 90

In this grounded theory analysis I sought to understand dignity violation in health care and to explore the context in which such violations take place. I found that dignity violation in health care occurs through processes of rudeness, indifference, condescension, dismissal, disregard, dependence, intrusion, objectification, restriction, labeling, contempt, discrimination, revulsion, deprivation, assault, and abjection. The conditions that promote these processes reside in the positions of the actors involved; in the asymmetrical relationships between the actors; in the health care setting itself, which is characterized by multiple tensions-including those between needs and resources, crisis and routine, experience and expertise, and rhetoric and reality; and in the embeddedness of health care in a broader social order of inequality. These findings suggest several interventions that might mitigate dignity violation in health care.
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PMID:Dignity violation in health care. 1979 55


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