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H J Ulenkate

Publications and source records attributed to H J Ulenkate.

7 recordsLinked to original sources
PubMed2000

Evaluation of LabRespond, a new automated validation system for clinical laboratory test results.

BACKGROUND: Manual validation of laboratory test results is time-consuming, creating a demand for expert systems to automate this process. We have started to set up the program "LabRespond", which covers five validation levels: administrative, technical, sample, patient, and clinical validation. We present the evaluation of a prototype of an automated patient validation system based on statistical methods, in contrast to the commercially available program "VALAB", a rule-based automated validation system. METHODS: In the present study, 163 willfully altered, erroneous test results out of 5421 were submitted for validation to LabRespond, VALAB, and to a group of clinical chemists (n = 9) who validated these test results manually. The test results rejected by three or more clinical chemists (n = 281) served as a secondary reference standard. RESULTS: The error recovery rates of clinical chemists ranged from 23.9% to 71.2%. The recovery rates of LabRespond and VALAB were 77.9% and 71.8%, respectively (difference not significant). The false-positive rates were 82.7% for LabRespond, 83.6% for VALAB, and 27.8-86.7% for clinical chemists. Using the consensus of three or more clinical chemists as the secondary reference standard, we found error recovery rates of 64.8% for LabRespond and 72.2% for VALAB (P = 0.06). Compared with VALAB, LabRespond detected more (P = 0.003) erroneous test results of the type that were changed from abnormal to normal. CONCLUSIONS: The statistical plausibility check used by LabRespond offers a promising automated validation method with a higher error recovery rate than the clinical chemists participating in this study, and a performance comparable to VALAB.

Clinical Laboratory Techniques↗
PubMed1998

A re-appraisal of the tri-axial chart for monitoring arterial acid-base values.

OBJECTIVE: To demonstrate the practicability of a tri-axial chart for the graphical and quantitative monitoring of arterial pH, arterial carbon dioxide partial pressure (PaCO2) and actual arterial bicarbonate-ion concentration (a[HCO3-]) in intensive care patients. DESIGN: Case report. SETTING: A general intensive care unit (ICU). METHODS: Using a standard mathematical transformation, a data set of pH, log PaCO2 and log a[HCO3-] values can be transformed in such a way that a graphical display of all three variables is possible while being faithful to their linear relationship. Remarkably, the graphical display closely resembles the tri-axial chart that Hastings and Steinhaus described in 1931 for studying displacements of the acid-base balance. Two new monitoring parameters based on the chart and the transformation are described. One monitors the abnormality of the acid-base status while the other monitors the rate of acid-base changes. CONCLUSIONS: With the tri-axial acid-base chart, the complete acid-base status can be faithfully monitored. Moreover, the proposed monitoring parameters provide extra information about the arterial acid-base status that, otherwise, would remain hidden.

Acid-Base Imbalance↗
PubMed1996

Effects of ciliary neurotrophic factor on retrograde cell reaction after facial nerve crush in young adult rats.

Locally applied ciliary neurotrophic factor (CNTF) has a powerful effect on retrograde axonal reaction following facial nerve crush in neonatal rats. We examined whether it also exerts a strong effect on retrograde axonal reaction in young adult rats when administered subcutaneously. The dose was 1 mg/kg body weight, three times a week, similar to that used in a previous experiment in which CNTF was reported to have an effect. We studied changes in the morphology of the motor nerve cell bodies, in the number of perineuronal microglial cells and in the expression of five proteins. It appeared that CNTF prevented swelling of the facial motoneuron cell bodies but it did not influence the swelling of the nucleus nor the shift of the nucleus towards the periphery. In saline-treated rats, facial nerve crush resulted from day two to day six in a marked increase in the number of perineuronal glial cells. This increase was neither diminished nor augmented by CNTF. Following facial nerve crush, the immunoreactivity of the proteins C3bi, GFAP, B-50 and CGRP increased in the glial cells and motoneuron cell bodies, whilst the immunoreactivity of synaptophysin at the membrane of the motoneuron cell bodies decreased. CNTF had no obvious effect on these changes. It was concluded that in young adult rats under the present conditions, CNTF had only a small effect on a specific aspect of the retrograde cell reaction. The small effects might be explained by the minor availability of CNTF to the motoneuron cell bodies. The gain in body weight of rats treated with CNTF was less than that of saline-treated rats.

Age Factors↗
PubMed1994

Ciliary neurotrophic factor improves muscle fibre reinnervation after facial nerve crush in young rats.

In the present study we examined the effect of recombinant human ciliary neurotrophic factor (rH-CNTF) on muscle fibre reinnervation. After facial nerve crush, rats were treated systemically with either rH-CNTF (1 mg/kg per 48 h) or saline and were killed on days 10-13 after nerve crush when muscle fibre reinnervation becomes apparent. Blind counting of the number of reinnervated motor endplates and the length of the synaptophysin-positive staining was used to assess the effect of CNTF treatment on muscle fibre reinnervation in the whisker muscle. On day 10, both treatment groups showed a limited number of reinnervated motor endplates. Both the saline- and CNTF-treated rats showed a significant increase in the percentage of reinnervated motor endplates and in the length of the synaptophysin-positive staining with time. On days 10 and 11, there was no difference in muscle fibre reinnervation between the treated groups. On days 12 and 13, the CNTF-treated rats showed an increased muscle fibre reinnervation which was significant compared to the saline-treated rats. These results suggest that after facial nerve crush in young rats, CNTF enhances muscle fibre reinnervation, most probably by stimulating the intramuscular branching. There is no support for an effect of CNTF on nerve sprouting in the proximal axonal part or on axonal elongation; the CNTF effect on intramuscular branching might be mediated by the muscle fibres.

Animals↗
PubMed1993

The neurotrophic analogue of ACTH(4-9) reduces the perineuronal microglial reaction after rat facial nerve crush.

Following peripheral nerve crush, microglial cells proliferate and migrate to motoneuron cell bodies of the injured nerves. Newly formed glial processes displace nerve terminals from the cell bodies. This process is known as synaptic stripping. In animal models of peripheral nerve diseases, the ACTH(4-9) analogue, ORG2766, was shown to facilitate axonal regeneration and to protect against experimental neuropathy. In the present study we examined the effect of ORG2766 on the microglial reaction. After facial nerve crush, rats were treated with either ORG2766 (75 micrograms/kg/48 h) or saline and were killed on day 2-6 after operation. Blind counting of the number of perineuronal glial cells in the facial nucleus was used to assess the effect of ORG2766 treatment on the microglial reaction. In the saline-treated animals the number of perineuronal glial cells per motoneuron cell body on the crushed side increased significantly. This number increased up to day 5 after operation and decreased significantly from day 5 to 6. After an initial increase in the peptide-treated animals, however, the number of perineuronal glial cells remained constant from day 3 onwards. Hence, on post-operation days 4 and 5, this number was significantly less than that seen in saline-treated animals. Microglial cells proliferate, presumably through signalling by injured motoneurons. It is suggested that the decrease in the number of perineuronal glial cells in the ORG2766-treated animals is the result of a peptide-induced reduction in the release of mediating signals/cytokines or, alternatively, increased protection of motoneurons by stress proteins. Further research should address the mechanism of action of ORG2766 in animal models of motoneuron disease.

Adrenocorticotropic Hormone↗
PubMed1987

Basal and electrically stimulated release of [3H]noradrenaline and [3H]dopamine from rat amygdala slices in vitro: effects of 4 beta-phorbol 12,13-dibutyrate, 4 alpha-phorbol 12,13-didecanoate and polymyxin B.

The protein kinase C activator 4 beta-phorbol 12,13-dibutyrate (PDB) enhanced in a concentration-dependent manner the electrically stimulated release of [3H]noradrenaline ([3H]NA) and [3H]dopamine ([3H]DA) from rat amygdala slices in vitro. PDB enhanced the basal release of [3H]NA and [3H]DA as well. 4 alpha-Phorbol 12,13-didecanoate, which lacks the capacity to activate protein kinase C, was without effect on either basal or electrically stimulated release of [3H]NA and [3H]DA. Polymyxin B, which is a relatively selective protein kinase C inhibitor, decreased in a concentration-dependent manner the electrically stimulated release of both [3H]NA and [3H]DA from amygdala slices, whereas it enhanced the basal release of both neuromessengers. In the presence of 1.5 X 10(-7) M PDB, a concentration which when added to the superfusion medium alone doubled the electrically stimulated release of both [3H]NA and [3H]DA, polymyxin B again decreased in a concentration-dependent manner the release of both neuromessengers. At all polymyxin B concentrations used, the effect of the PKC inhibitor, expressed as percent inhibition, in the presence of PDB was approximately the same as that observed in the absence of PDB. This suggests that the antagonism between PDB and polymyxin B at the level of protein kinase C is not a competitive one. The effects of PDB and polymyxin B on basal release were additive. Taken together, these data suggest that in the amygdala presynaptically localized protein kinase C plays a role in signal transduction processes related to the exocytotic secretion of NA and DA from their nerve terminals.

Amygdala↗