Flicker perimetry using a luminance threshold strategy at frequencies from 5–25 Hz in glaucoma, ocular hypertension and normal controls

1994 ◽  
Vol 13 (10) ◽  
pp. 717-723 ◽  
Author(s):  
Michael W. Austin ◽  
Colm J. O'brien ◽  
Peter K. Wishart
Keyword(s):  
Ocular Hypertension ◽  
Threshold Strategy ◽  
Luminance Threshold ◽  
Normal Controls

scholarly journals Psychophysical assessment of magno- and parvocellular function in schizophrenia

2006 ◽  
Vol 23 (3-4) ◽  
pp. 645-650 ◽  
Author(s):  
SANDRINE DELORD ◽  
MARIA GIOVANNA DUCATO ◽  
DELPHINE PINS ◽  
FRÉDÉRIC DEVINCK ◽  
PIERRE THOMAS ◽  
...  
Keyword(s):  
Forced Choice ◽  
Target Luminance ◽  
Luminance Threshold ◽  
Schizophrenic Patients ◽  
Luminance Discrimination ◽  
Normal Controls ◽  
Integrated Processes

Recently developed psychophysical techniques permit the biasing of the processing of the stimulus by early visual channels so that responses reflect characteristics of either magno- or parvocellular pathways (Pokorny & Smith, 1997). We used such techniques to test psychophysically whether the global magnocellular dysfunction reported in schizophrenia also affects early processes. Seven schizophrenic patients and 19 normal controls participated. The task was a four-alternative forced-choice luminance discrimination, using a 2 × 2 configuration of four 1-deg squares. Target luminance threshold was determined in three conditions: the stimulus, including the target, was pulsed for 17 ms (pulse paradigm); the target was presented on a steady background of four squares (steady paradigm), or the target was presented alone (no background paradigm). We replicated previous results demonstrating magnocellular and parvocellular signatures in control participants. No evidence for an early magnocellular deficit could be detected as the thresholds of all schizophrenic observers were higher both in the steady paradigm (presumed magnocellular mediation) and in the pulse paradigm (presumed parvocellular mediation). Magnocellular dysfunction, if present in schizophrenia, must concern more integrated processes, possibly at levels at which parvocellular and magnocellular paths interact.

The self and schizophrenia: a cognitive approach

2003 ◽  
Vol 62 (1) ◽  
pp. 45-51 ◽  
Author(s):  
Marek Nieznanski
Keyword(s):  
Normal Subjects ◽  
Control Group ◽  
Cognitive Approach ◽  
Schizophrenic Patients ◽  
Self Schema ◽  
Persons With Schizophrenia ◽  
Basic Features ◽  
Trait Words ◽  
Patients Experience ◽  
Normal Controls

The aim of the study was to explore the basic features of self-schema in persons with schizophrenia. Thirty two schizophrenic patients and 32 normal controls were asked to select personality trait words from a check-list that described themselves, themselves as they were five years ago, and what most people are like. Compared with the control group, participants from the experimental group chose significantly more adjectives that were common to descriptions of self and others, and significantly less that were common to self and past-self descriptions. These results suggest that schizophrenic patients experience their personality as changing over time much more than do healthy subjects. Moreover, their self-representation seems to be less differentiated from others-representation and less clearly defined than in normal subjects.

Parallel Reduction of Plasma Levels of High and Low Molecular Weight Kininogen in Patients with Cirrhosis

1999 ◽  
Vol 82 (11) ◽  
pp. 1428-1432 ◽  
Author(s):  
Cheryl Scott ◽  
Francesco Salerno ◽  
Elettra Lorenzano ◽  
Werner Müller-Esterl ◽  
Angelo Agostoni ◽  
...  
Keyword(s):  
Molecular Weight ◽  
Liver Disease ◽  
Liver Function ◽  
Plasma Levels ◽  
Plasma Concentrations ◽  
Normal Subjects ◽  
Low Molecular Weight ◽  
Major Band ◽  
Sds Page ◽  
Normal Controls

SummaryLittle is known about the regulation of high-molecular-weight-kininogen (HK) and low-molecular-weight-kininogen (LK) or the relationship of each to the degree of liver function impairment in patients with cirrhosis. In this study, we evaluated HK and LK quantitatively by a recently described particle concentration fluorescence immunoassay (PCFIA) and qualitatively by SDS PAGE and immunoblotting analyses in plasma from 33 patients with cirrhosis presenting various degrees of impairment of liver function. Thirty-three healthy subjects served as normal controls. Patients with cirrhosis had significantly lower plasma levels of HK (median 49 μg/ml [range 22-99 μg/ml]) and LK (58 μg/ml [15-100 μg/ml]) than normal subjects (HK 83 μg/ml [65-115 μg/ml]; LK 80 μg/ml [45-120 μg/ml]) (p < 0.0001). The plasma concentrations of HK and LK were directly related to plasma levels of cholinesterase (P < 0.0001) and albumin (P < 0.0001 and P < 0.001) and inversely to the Child-Pugh score (P < 0.0001) and to prothrombin time ratio (P < 0.0001) (reflecting the clinical and laboratory abnormalities in liver disease). Similar to normal individuals, in patients with cirrhosis, plasma HK and LK levels paralleled one another, suggesting that a coordinate regulation of those proteins persists in liver disease. SDS PAGE and immunoblotting analyses of kininogens in cirrhotic plasma showed a pattern similar to that observed in normal controls for LK (a single band at 66 kDa) with some lower molecular weight forms noted in cirrhotic plasma. A slight increase of cleavage of HK (a major band at 130 kDa and a faint but increased band at 107 kDa) was evident. The increased cleavage of HK was confirmed by the lower cleaved kininogen index (CKI), as compared to normal controls. These data suggest a defect in hepatic synthesis as well as increased destructive cleavage of both kininogens in plasma from patients with cirrhosis. The decrease of important regulatory proteins like kininogens may contribute to the imbalance in coagulation and fibrinolytic systems, which frequently occurs in cirrhotic patients.

The Clinical Usefulness of the Platelet Aggregation Test for the Diagnosis of Heparin-Induced Thrombocytopenia

1993 ◽  
Vol 69 (04) ◽  
pp. 344-350 ◽  
Author(s):  
B H Chong ◽  
J Burgess ◽  
F Ismail
Keyword(s):  
Platelet Aggregation ◽  
Heparin Therapy ◽  
Serotonin Release ◽  
Point System ◽  
Control Groups ◽  
Heparin Induced Thrombocytopenia ◽  
Heparin Concentration ◽  
Release Test ◽  
The Mean ◽  
Normal Controls

SummaryThe platelet aggregation test is widely used for the diagnosis of heparin-induced thrombocytopenia (HIT), a potentially serious complication of heparin therapy. We have evaluated its sensitivity and specificity in comparison with those of the 14C-serotonin release test. The sensitivity of the platelet aggregation test was found to vary with the heparin concentration and the donor of the platelets used in the test. The optimal heparin concentrations were between 0.1 and 1.0 U/ml. Using these heparin concentrations, the mean sensitivity varied from 39% (with the least reactive platelets) to 81% (with the most reactive platelets). In comparison, the sensitivity of the release test ranged from 65% to 94%. The specificities of the platelet aggregation test were 82%, 90% and 100% for the following control groups: (1) non-thrombocytopenic patients given heparin, (2) patients with thrombocytopenia due to other causes, and (3) normal controls not given heparin, respectively. The corresponding specificities for the release test was 94%, 90% and 100%. The specificities can be further increased to 100% for all controls with the adoption of a two-point system which defines a positive result as one in which platelet aggregation occurs with a low heparin concentration (0.5 U/ml) but not with 100 U heparin/ml. For optimal results, a two-point platelet aggregation test should be performed with heparin concentrations of 0.5 and 100 U/ml and using platelets of more reactive donors.

Heparin Response and Clearance in Acute and Chronic Liver Disease

1985 ◽  
Vol 54 (03) ◽  
pp. 591-594 ◽  
Author(s):  
H Sette ◽  
R D Hughes ◽  
P G Langley ◽  
A E S Gimson ◽  
R Williams
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Peak Level ◽  
Chronic Liver ◽  
Clotting System ◽  
Activated Clotting Time ◽  
At Iii ◽  
Increased Sensitivity ◽  
Low Levels ◽  
Normal Controls

SummaryPatients with liver disease are at risk of bleeding due to abnormalities of the clotting system although they must be anticoagulated if they require haemodialysis or haemoperfusion. The anticoagulant of choice is heparin.In this study we have investigated heparin kinetics in patients with fulminant hepatic failure (FHF) after a single intravenous dose of heparin (2,500 units) and found there was an increased clearance of heparin whether measured by its anti-Xa effect (t1/2 = 27.8 ± 2.9 min compared to t1/2 = 50.2 ± 2.7 min in normal controls p <0.001) or by the whole blood activated clotting time (t1/2 = 23.7 ± 2.2 min compared to t1/2 = 37.0 ± 2.0 min p <0.001). There was a decreased peak level of heparin measured by anti-Xa effect (peak level in FHF = 0.48 ± 0.05 u/ml and in controls = 0.69 ± 0.04 u/ml, p <0.02), but an increased sensitivity to heparin (sensitivity in FHF = 0.072 ± 0.011 sec/unit, in controls 0.033 ± 0.003 sec/unit, p <0.001). Patients with FHF had very low levels of antithrombin III (AT III), but there was no correlation between this and any parameters of heparin effect or clearance. In a group of patients with chronic liver disease heparin kinetics did not differ from controls despite low levels of AT III.The changes in heparin kinetics in FHF are likely to be complex with the balance between the proteins that act as cofactors, (e.g. AT III) and the proteins that have heparin neutralising activity, controlling the response of added heparin.

QUANTITATIVE STUDIES OF IODINE METABOLISM IN SPORADIC, NON-TOXIC GOITRE

1974 ◽  
Vol 76 (1) ◽  
pp. 67-73 ◽  
Author(s):  
H. Agerbæk ◽  
S. E. Jensen
Keyword(s):  
Iodine Deficiency ◽  
Iodine Uptake ◽  
Quantitative Studies ◽  
Euthyroid State ◽  
Iodine Metabolism ◽  
Dynamic Patterns ◽  
Perchlorate Discharge Test ◽  
Normal Controls ◽  
Discharge Test

ABSTRACT In 129 patients with non-toxic goitre and 27 normal controls, thyroid dynamic patterns were estimated in an attempt to elucidate pathogenesis. The clinically euthyroid state was confirmed by measurement of PBI, T3-sephadex uptake and BMR. Thyroid clearance (th. cl.), plasma iodide (PII), and absolute iodine uptake (AIU) were determined and a perchlorate discharge test performed. Twenty patients (16%) had a high AIU and were thus suspected of having dyshormonogenesis; nine were thoroughly investigated and in six dyshormonogenesis was found. Both normals and non-toxic goitre patients had a low PII, but in the goitrous patients values were lowest. The thyroid clearance of iodide was significantly higher in the goitre patients, suggesting iodine deficiency to be a major aetiologic factor for goitre formation. AIU was higher in the goitre patients than in normals, suggesting a larger iodine leakage from the thyroid in these patients.

THE DEPENDENCE OF URINARY CALCIUM AND OTHER ELECTROLYTES ON ADRENAL FUNCTION DURING ACUTE SODIUM DEPLETION AND LOADING

1970 ◽  
Vol 64 (1) ◽  
pp. 65-74 ◽  
Author(s):  
Lars Runeberg ◽  
B.-A. Lamberg ◽  
P. Reissell ◽  
H. Adlercreutz
Keyword(s):  
Sodium Excretion ◽  
Extracellular Volume ◽  
Normal Subjects ◽  
Urinary Calcium ◽  
Calcium Excretion ◽  
Minor Importance ◽  
Sodium Depletion ◽  
Sodium Loading ◽  
Urinary Potassium ◽  
Normal Controls

ABSTRACT The time course of the renal excretion of calcium, magnesium, sodium, and potassium during sodium depletion and the rapid correction of the extracellular volume deficit was studied in normal subjects and in patients with Addison's disease (AD). The decrease in body weight was similar in the two groups, but the haematocrit value increased more in the patients with AD. Sodium depletion suppressed sodium excretion much more efficiently in normal controls than in the AD patients. Calcium excretion was roughly equally depressed in two groups. During sodium loading there was an immediate increase in renal sodium excretion in the patients with AD, whereas the sodium-retaining state generally continued for about one day in the normal controls. Urinary potassium decreased gradually during the first day of sodium loading in the normal controls but not in the AD patients. In the normal subjects calcium excretion remained low during the first day and increased on the second day of sodium loading. In the AD patients there was a gradual increase in urinary calcium during the first day of sodium loading, which did not, however, parallel the changes in urinary sodium content in individual urine samples. Urinary magnesium did not change significantly. It is concluded that the effect of adrenal steroids on renal calcium excretion is of minor importance. They may, however, to some extent induce calcium retention.

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