Biomedical subjects

A Chalkiadaki

Publications and source records attributed to A Chalkiadaki.

8 recordsLinked to original sources

PubMed2006

Evaluation of a risk score for interhospital transport of critically ill patients.

BACKGROUND: Interhospital transfer imposes essential risk for critically ill patients. The Risk Score for Transport Patients (RSTP) scale can be used as a triage tool for patient severity. METHODS: In total, 128 transfers of critically ill patients were classified in two groups of severity according to the RSTP. Statistical analysis was performed using the receiver operating characteristic (ROC) curve and goodness of fit statistics. RESULTS: In total, 66 patients (51.5%) were classified as group I and 62 (48.4%) as group II. Major en route complications were more common in group II patients (19.3% v 3%, p<0.001). Haemodynamic instability was the most common complication. There were significant differences in the mean risk scores between group I and II patients (mean (SD) 4.48 (1.01) v 11.04 (3.47), p<0.001). Discrimination power of RSTP was acceptable (area under the ROC curve 0.743; cutoff value > or =8). Goodness of fit was adequate (p = 0.390). CONCLUSION: The RSTP had acceptable discrimination and adequate goodness of fit and could be considered as a triage tool. Haemodynamic instability is the most common problem encountered during transfer.

Adolescent↗

PubMed2001

[Early pain reduction in the treatment of spasticity after a single injection of botulinum A toxin].

UNLABELLED: HISTORY, ADMISSION FINDINGS AND DIAGNOSIS: After stem-cell transplantation a 45-year-old woman (case 1) had an attack of general hypoxia requiring resuscitation. She then developed a quadriplegia and spasticity of all limbs notably of the right arm and a severe pain syndrome which had to be treated by oral and intravenous analgesics. Immobilisation and secondary complications aggravated the already difficult situation. In the 2nd case a 66-year-old woman was admitted to our outpatient clinic with long-standing left-sided spastic hemiparesis after territorial infarction of the right middle cerebral artery. Beside the spasticity she also suffered from a distinct pain syndrome which did not respond to any oral analgesics. TREATMENT AND COURSE: For the treatment of the main symptoms, both patients received intramuscular injections of 1000 MU botulinum toxin A (Dysport(R) Ipsen Pharma). Astonishingly, both patients experienced pain relief the next day, whereas spasticity started to respond only 5-6 days later. CONCLUSIONS: In our experience pain relief after botulinum toxin A injections occurs not only due to reduced muscle hyperactivity, especially when such a temporal dissociation between pain relief and muscle relaxation appears as in the two cases reported above. Rather, we believe that botulinum toxin A interferes with the release of other neurotransmitters e. g. substance P (SP) and calcitonine-gene-related-peptide (CGRP) having a key function in the nociceptive cascade.

Aged↗

PubMed2001

[Reduction of pain and muscle spasms by botulinum toxin A].

Botulinum toxin A (BoNT-A) develops its muscle-relaxing effect by the inhibition of acetylcholine (ACh) release. This toxin is also known to relieve muscular pain in different disorders. Conspicuously, pain in some patients responds earlier and sometimes even better than muscle tension, indicating that the effect of BoNT-A on pain is not only due to inhibition of ACh release. A questionnaire was distributed to 88 patients suffering from cervical dystonia (CD). Thirty-five completed questionnaires could be used for data analysis. After intramuscular injections of BoNT-A, patients with CD experience significant reductions in pain which sometimes occur significantly earlier than the improvements in head posture. In the iris sphincter muscle of the rabbit and in dorsal root ganglion cells (DRG) of the rat, inhibition of the release of substance P by BoNT-A has been shown experimentally, and BoNT-C has been proven to develop endopeptidase activity toward substance P (SP) in vitro. Findings in the current literature and our observations allow the conclusion that alleviation of muscle pain by BoNT-A may also be due to an effect on the release of nociceptive neuropeptides, among which SP seems to have a key function.

Aged↗

PubMed2000

Spatially restricted factors cooperate with notch in the regulation of Enhancer of split genes.

Expression of the Drosophila Enhancer of split [E(spl)] genes, and their homologues in other species, is dependent on Notch activation. The seven E(spl) genes are clustered in a single complex and their functions overlap significantly; however, the individual genes have distinct patterns of expression. To investigate how this regulation is achieved and to find out whether there is shared or cross regulation between E(spl) genes, we have analysed the enhancer activity of sequences from the adjacent E(spl)mbeta, E(spl)mgamma and E(spl)mdelta genes and made comparisons to E(spl)m8. We find that although regulatory elements can be shared, most aspects of the expression of each individual gene are recapitulated by small (400-500 bp) evolutionarily conserved enhancers. Activated Notch or a Suppressor of Hairless-VP16 fusion are only sufficient to elicit transcription from the E(spl) enhancers in a subset of locations, indicating a requirement for other factors. In tissue culture cells, proneural proteins synergise with Suppressor of Hairless and Notch to promote expression from E(spl)mgamma and E(spl)m8, but this synergy is only observed in vivo with E(spl)m8. We conclude that additional factors besides the proneural proteins limit the response of E(spl)mgamma in vivo. In contrast to the other genes, E(spl)mbeta exhibits little response to proneural proteins and its high level of activity in the wing imaginal disc suggests that wing-specific factors cooperate with Notch to activate the E(spl)mbeta enhancer. These results demonstrate that Notch activity must be integrated with other transcriptional regulators and, since the activation of target genes is critical in determining the developmental consequences of Notch activity, provide a framework for understanding Notch function in different developmental contexts.

Animals↗

PubMed2000

Leukocytoclastic vasculitis: is propranolol implicated?

Drugs frequently cause cutaneous adverse reactions. The suspected agent is sometimes difficult to identify, especially in patients receiving multidrug treatment and with underlying illnesses that may contribute to the clinical picture. In our patient, propranolol-induced leukocytoclastic vasculitis was diagnosed by exclusion.

Adrenergic beta-Antagonists↗

PubMed1999

Cerebrovascular mechanisms in neurocardiogenic syncope with and without postural tachycardia syndrome.

BACKGROUND AND PURPOSE: Recent transcranial Doppler studies in patients with neurocardiogenic syncopes (NCS) have demonstrated that the cerebrovascular response to sudden systemic hypotension is vasoconstriction instead of compensatory vasodilation (autoregulation). We tried to characterize the conditions leading to this unexpected response in NCS patients further by continuously monitoring autoregulation and autonomic parameters during a standardized tilt-table test (TTT). METHODS: Sixteen patients below the age of 50 years with a history of at least three syncopes of undetermined cause and tilt-table verified NCS and 20 normal controls were studied. Arterial blood pressure (ABP) and heart rate (HR) were monitored by Finapres and cerebral blood flow velocity (CBFV) of the left middle cerebral artery by transcranial Doppler. Baroreflex sensitivity and autoregulation parameters were measured continuously, using cross-spectral analysis of Mayer waves (3-9 cycles per minute oscillations) in ABP, HR and CBFV, respectively. Pulsatility indices (PI) of CBFV and ABP were determined continuously. Measurements were taken during 5 min in supine and during 5 min in tilted position. In patients, tilting was continued for a maximum of 45 min until the onset of syncope or presyncope. RESULTS: According to the maximum increase in heart rate (deltaHR) during the first 5 min of standing, heart rate responses were classified as postural tachycardia syndrome (POTS) (deltaHR > 35/min) or as normal. Only one out of 20 control subjects showed a POTS (5%) in contrast to seven patients (44%). Patients with a POTS had significantly lower PI values in ABP and higher ratios between the PI of CBFV and the PI of ABP both in supine and in tilted positions. Baroreflex sensitivity during standing decreased significantly in POTS patients when compared to controls. Although autoregulation remained intact during standing, mean CBFV decreased significantly and continuously. The nine patients without a POTS showed almost the same cardiovascular and cerebrovascular responses as the control subjects. All 16 patients showed similar circulatory responses during syncope (sudden hypotension, relative or absolute bradycardia, reduced CBFV and increased PI in CBFV). CONCLUSIONS: The development of a POTS during tilting indicates a high risk for fainting. The characteristic hemodynamic features in the initial phase of standing in these patients can be interpreted in terms of central hypovolemia (low PI of ABP) with sufficient ABP regulation and increased cerebrovascular resistance (defined as the ratio between PI of CBFV and ABP). Cerebral autoregulation seems not to be affected in patients suffering from NCS.

Adult↗

PubMed1999

Overexpression of the m4 and malpha genes of the E(spl)-complex antagonizes notch mediated lateral inhibition.

Intercellular signalling mediated by Notch proteins is crucial to many cell fate decisions in metazoans. Its profound effects on cell fate and proliferation require that a complex set of responses involving positive and negative signal transducers be orchestrated around each instance of signalling. In Drosophila the basic-helix-loop-helix (bHLH) repressor encoding genes of the E(spl) locus are induced by Notch signalling and mediate some of its effects, such as suppression of neural fate. Here we report on a novel family of Notch responsive genes, whose products appear to act as antagonists of the Notch signal in the process of adult sensory organ precursor singularization. They, too, reside in the E(spl) locus and comprise transcription units E(spl) m4 and E(spl) malpha. Overexpression of these genes causes downregulation of E(spl) bHLH expression accompanied by cell autonomous overcommitment of sensory organ precursors and tufting of bristles. Interestingly, negative regulation of the Notch pathway by overexpression of E(spl) m4 and malpha is specific to the process of sensory organ precursor singularization and does not impinge on other instances of Notch signalling.

Amino Acid Sequence↗

PubMed1996

Transcranial Doppler during neurocardiogenic syncope.

The purpose of the present study was to investigate changes in cerebral circulation during neurocardiogenic syncope (NCS). Twenty patients with a history of unexplained syncopes were studied over a 45 min period in a tilted position. Heart rate and arterial blood pressure were recorded non-invasively using Finapres. Cerebral blood flow velocity of both middle cerebral arteries was measured with transcranial Doppler (TCD). Ten patients (50%) developed a NCS during the tilt test, with a strong reduction in blood pressure (mean, 48/34 mmHg) and heart rate (mean, 54 beats/min). Simultaneously, diastolic blood flow velocities dropped to values close to zero. However, systolic blood flow velocities did not decrease. In consequence, the pulsatility index (PI) increased considerably from 0.93 to 2.01. The increase in PI suggests that there is a constriction of cerebral resistance vessels during NCS. Despite the drop in blood pressure and the putative increase in cerebrovascular resistance, systolic blood flow velocities remained unchanged in the TCD records. This fact can be explained by a lumen narrowing of the middle cerebral artery at the site of insonation. In conclusion, the typical changes in cerebral blood flow velocity during NCS are probably due to a strong constriction of both the proximal and the peripheral segments of cerebral arteries. It is clear that, in addition to vasodepression and cardiac inhibition, cerebral vasoconstriction is a further mechanism in the pathogenesis of a NCS.

Adult↗