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Biomedical subjects

V Jäntti

Publications and source records attributed to V Jäntti.

At least 19 recordsLinked to original sources
PubMed2006

Development of permanent national register of blood component use utilizing electronic hospital information systems.

BACKGROUND AND OBJECTIVES: We wanted to establish a permanent national database system, which can be utilized to study transfusion recipients and blood use in Finland. MATERIALS AND METHODS: A regularly updated register for permanent use was developed. To study the usability of the database, years 2002 and 2003 were further analysed. Database included all transfused patients in major blood-transfusing hospitals from four university and five central hospital districts managing altogether 63% of Finnish inpatient hospital episodes. RESULTS: Audit of gathered data reveal 96.8% match in adult blood components with Finnish Red Cross, Blood Service sales figures. Model data set includes 59,535 transfused patients (44.3% men and 55.7% women) having received 529,104 blood components. Half of all blood units were transfused in connection with surgical operations. Most of the blood recipients were elderly (51.6% are over 64 years of age). Blood-component use and transfusion-related costs varied widely between hospitals. CONCLUSION: Hospital data managing systems can be useful for creating a population-based database system to monitor and compare transfusion practices. This record provides information about transfusion epidemiology for transfusion professionals, hospital management, and hospital administration.

Adolescent↗
PubMed2004

Evoked EEG patterns during burst suppression with propofol.

BACKGROUND: During EEG suppression with isoflurane or sevoflurane anaesthesia, median nerve stimulation causes cortical responses of two kinds: an N20 wave with a latency of 20 ms and an EEG burst with a latency of 200 ms. We tested the possibility that median nerve stimulation during EEG suppression with propofol would cause an EEG response that was consistent enough to be of use for neuromonitoring. METHODS: Eight patients were anaesthetized with propofol to allow burst suppression. Electrical stimulation of the median nerve was applied during general anaesthesia and the EEG was measured. RESULTS: The EEG response to a painful stimulus had four successive components: (i) N20 and P22 potentials, reflecting activation of fast somatosensory pathways; (ii) a high-amplitude negative wave, possibly reflecting activation of the somatosensory cortex SII bilaterally; (iii) a burst (i.e. a negative slow wave with superimposed 10 Hz activity, probably reflecting an arousal mechanism); and (iv) a 13-15 Hz spindle, probably originating from the thalamus, similar to sleep spindles. These could be seen separately and in different combinations. Bursts and spindles during burst suppression were also seen without stimulation. In deepening propofol anaesthesia, spindles were seen in the continuous EEG before burst suppression was achieved. In deep anaesthesia, spindles were seen when bursts had ceased, and painful stimuli evoked sharp waves without subsequent bursts. CONCLUSION: In addition to SSEP (somatosensory evoked potentials), three different evoked responses are noted that could be useful for clinical monitoring.

Adult↗
PubMed2001

Propofol anesthesia induces phase synchronization changes in EEG.

OBJECTIVE: Phase coupling between EEG channel pairs in various frequency bands was evaluated during propofol anesthetic induction and recovery periods. METHODS: Twenty-three patients participated in the study. Phase synchronization indices based on the Hilbert transform were investigated on frequency bands 0.05-1 Hz, 1-4 Hz, 4-8 Hz, 8-12 Hz and 12-16 Hz for all pairs of the 9 EEG channels covering midline and frontal areas. A straight line was used to approximate the index values as a function of time and the Sign Test statistics were applied to the slope parameters. RESULTS: Systematic phase synchronization changes were detected. Generally, phase synchronization in the sub-delta band decreased during the induction and increased during the recovery, while the directions were reversed in the alpha band. The changes were dependent on the channel pair. In the delta, theta and beta bands, the changes were aligned more irregularly than in the sub-delta or in the alpha bands. Highly asymmetric behavior between the induction and the recovery periods was also observed in these bands. CONCLUSIONS: Induction and recovery from propofol anesthesia changes the phase synchronization between the EEG channels. The passband and location-specific behavior of these changes reveals the effects of the anesthetic to the different neural mechanisms.

Adult↗
PubMed2001

Sevoflurane mask induction of anaesthesia is associated with epileptiform EEG in children.

BACKGROUND: Sevoflurane inhalation induction of anaesthesia is widely used in paediatric anaesthesia. We have found that this method is frequently associated with epileptiform electroencephalogram (EEG) in adults, especially if controlled hyperventilation is used. METHODS: We assessed EEG during sevoflurane inhalation induction in 31 children, aged 2-12 yr. Anaesthesia was induced with 8% sevoflurane in O2 in N2O 1:2. The patients were randomized to undergo controlled ventilation (CV group), or to breathe spontaneously (SB group) for 5 min. EEG was recorded as were noninvasive blood pressure and heart rate (HR). EEG recordings were classified by a clinical neurophysiologist. RESULTS: Three different types of interictal epileptiform discharge were detected. Suppression with spikes (SSP) was found in 25% and 0% in the CV and SB groups, rhythmic polyspikes (PSR) in 44% and 20%, and periodic epileptiform discharges (PED) in 44% and 0% (P<0.01), respectively. The incidence of all different types of interictal epileptiform discharge (SSP+PSR+PED) was 88% and 20% (P<0.001), respectively. Epileptiform EEG was associated with increased heart rate and blood pressure during anaesthetic induction. CONCLUSION: Both ventilation modes produced epileptiform EEG. With controlled ventilation, epileptiform discharges were seen in 88% of children. This warrants further studies of the suitability of this induction type in general, and especially in children with epilepsy.

Anesthetics, Inhalation↗
PubMed2001

The N-methyl-D-aspartate antagonist memantine has no neuroprotective effect during hypothermic circulatory arrest: a study in the chronic porcine model.

BACKGROUND: Glutamate excitotoxicity has an important role in the development of brain injury after prolonged hypothermic circulatory arrest. The goal of the present study was to determine the potential efficacy of memantine, an N -methyl-D -aspartate receptor antagonist, to mitigate cerebral injury after hypothermic circulatory arrest. METHODS: Twenty pigs (23-33 kg) were randomly assigned to receive memantine (5 mg/kg) or placebo in a blinded fashion before a 75-minute period of hypothermic circulatory arrest at 20 degrees C. Hemodynamic, electroencephalographic, and metabolic monitoring were carried out. The intracerebral concentrations of glucose, lactate, glutamate, and glycerol were measured by means of enzymatic methods on a microdialysis analyzer. Daily behavioral assessment was performed until the animals died or were put to death on day 7. Histologic analysis of the brain was carried out in all animals. RESULTS: In the memantine group, 5 of 10 animals survived 7 days compared with 9 of 10 in the placebo group. The median behavioral score at day 7 was 3.5 in the memantine group and 7.5 in the placebo group (P >.2). Among the surviving animals, medians were 9.0 and 8.0 on day 7 (P >.2), respectively. The medians of recovered electroencephalographic bursts were equal in both groups. The median of total histopathologic score was 16 in the memantine group and 14 in the placebo group (P >.2). There was a negative correlation between glutamate levels and electroencephalographic burst recovery (tau = -0.377, P =.043). A positive correlation was found between the highest individual glutamate value and histopathologic score (tau = 0.336, P =.045). CONCLUSIONS: The present study demonstrates that memantine has no neuroprotective effect after hypothermic circulatory arrest in the pig. In addition, we have shown the accuracy of cerebral glutamate measurements to predict histopathologic injury after hypothermic ischemia.

Animals↗
PubMed2001

Serum and salivary anti-capsular antibodies in infants and children immunized with the heptavalent pneumococcal conjugate vaccine.

AIM: To study the ability of seven-valent experimental pneumococcal polysaccharide CRM197 protein conjugate vaccine (PncCRM) to induce antibodies in serum and saliva of infants. METHODS: Sixty Finnish infants received Pnc-CRM vaccine at 2, 4 and 6 months of age and were boosted with PncCRM (n = 30) or pneumococcal polysaccharide (PncPS) (n = 29) vaccine at the age of 15 months. Serum IgG antibody concentrations to vaccine serotypes 4, 6B, 9V, 14, 18C, 19F and 23F were measured by enzyme immunoassay at 2, 4, 6, 7, 15, 16 and 24 months of age. Salivary IgA, IgG and secretory Ig antibody titers at 7 and 16 months of ages were analyzed by enzyme immunoassay against the same serotypes, except 23F. RESULTS: PncCRM induced systemic immune responses and immunologic memory. At 7 months of age 69 to 100% of children, depending on the serotype, had serum IgG antibody concentrations exceeding the value of 1.0 microg/ml. At 15 months the titers were still higher than before the vaccinations. Booster doses of either PncPS or PncCRM induced an increase in antibody concentrations. The titers were still elevated at 24 months of age. Salivary IgA and IgG antibodies were found rarely at 7 months of age, but in up to 80% of samples taken at 16 months of age, depending on the serotype and nature of the booster vaccine. Salivary IgG correlated with IgG in serum, supporting the theory that salivary IgG is derived from serum. Salivary IgA and secretory Ig correlated positively, which indicates that IgA was locally produced. CONCLUSIONS: PncCRM induces both systemic and mucosal immune responses in infants.

Antibodies, Bacterial↗
PubMed2001

Peripheral nerve function is increasingly impaired during puberty in adolescents with type 1 diabetes.

OBJECTIVE: To evaluate the impact of puberty on peripheral nerve function in adolescents with type 1 diabetes. RESEARCH DESIGN AND METHODS: Of 138 eligible patients with type 1 diabetes, 100 patients (age >9 years and diabetes duration >2 years) attending an outpatient diabetes clinic and 100 age- and sex-matched healthy control subjects took part in this cross-sectional study. Peripheral motor and sensory nerve conduction tests, cardiovascular reflex tests on the autonomic nervous system, and measurements of vibration-perception threshold (VPT) were performed. RESULTS: Nerve conduction velocity (NCV) in the distal motor and sensory nerves, the motor nerve distal latency, and the sensory nerve action potential (SNAP) amplitude were impaired in the adolescent patients with type 1 diabetes. The deterioration in motor NCV, H-reflex latency, and SNAP amplitude became more conspicuous in late puberty and postpuberty and was related to poor metabolic control. A total of 10 patients had distal diabetic polyneuropathy (DP) neurophysiologically, and these patients had significantly lower heart-rate variation in the deep breathing test than the other patients. Three of the patients with DP had peripheral neurological signs or symptoms. A slight difference in the VPT between the patients and control subjects was observed after puberty. CONCLUSIONS: Increasing subclinical motor nerve impairment can be detected during late puberty and after puberty, and sensory NCV and SNAP amplitude are reduced in adolescents with type 1 diabetes. Poor metabolic control during puberty appears to induce deteriorating peripheral neural function in young patients with type 1 diabetes.

Action Potentials↗
PubMed2000

Salivary antibody response to vaccination with meningococcal A/C polysaccharide vaccine in previously vaccinated and unvaccinated Gambian children.

Development of salivary antibodies at the age of 4 or 5 years to group A and C meningococcal polysaccharides (MenA/C PS) was studied among Gambian children, who had received MenA/C conjugate or PS vaccine in infancy. There was also a control group of 64 age matched children. IgG, IgA, and secretory Ig concentrations were measured by enzyme immuno assay. MenA/C PS vaccine induced antibodies both in previously vaccinated and unvaccinated children. The previous vaccination had not induced long lasting IgA-mediated memory. IgA antibodies were secretory, and most of IgG was serum derived. The IgG salivary response seen was similar to the serum response.

Antibodies, Bacterial↗
PubMed2000

Natural development of antibodies to pneumococcal surface protein A, pneumococcal surface adhesin A, and pneumolysin in relation to pneumococcal carriage and acute otitis media.

Pneumococcal surface protein A (PspA), pneumococcal surface adhesin A (PsaA), and pneumolysin (Ply) are common to virtually all Streptococcus pneumoniae isolates. They are immunogenic and protective against pneumococcal challenge in animals and are the major candidates for a protein-based pneumococcal vaccine for humans. However, little is known of the natural development of antibodies to these proteins in humans. The objective of this study was to evaluate the natural development of antibodies to PspA, PsaA, and Ply in relation to pneumococcal infection and carriage in young children. Serum antibodies to these proteins were measured by EIA in children at ages 6, 12, 18, and 24 months and in their mothers. All age groups were capable of producing antibodies to the 3 proteins. The antibody concentrations increased with age and were strongly associated with pneumococcal exposure, whether by carriage or infection (acute otitis media).

Adhesins, Bacterial↗
PubMed2000

Histamine in the control of porcine and human sphincter of Oddi activity.

Histamine decreases sphincter of Oddi (SO) contractility in vivo in opossum, but increases contractility in vitro in guinea-pig. In resistor-like SO, such as in pig and man, the histamine effect is poorly known. We investigated the effect of histamine on pig SO in vivo and in vitro and on human SO in vitro. Perfusion manometry catheter and two silver electrodes for simultaneous pressure and electromyography registration were inserted into the SO transduodenally by laparotomy in six anaesthetized pigs weighing for 25-28 kg. Histamine (5-10 microgram kg-1) was infused intra-arterially (i.a.) into the pancreaticoduodenal artery with and without diphenhydramine (75 microgram kg-1) i.a. premedication. Acetylcholine (4 microgram kg-1) i.a., a potent SO stimulator, was used as positive control. After these experiments, the SO was removed and, together with seven human SO from Whipple specimens, were cut into 1.0-1.5 mm thick transverse sections (rings). The rings were placed between two hooks in oxygenated organ bath solution at 37 degrees C. The SO contraction force was measured with isometric force-displacement transducers and registered on a polygraph. SO rings were incubated with histamine (10-100 micromol L-1) and acetylcholine (100 micromol L-1) with or without diphenhydramine (10 micromol L-1), cimetidine (10 micromol L-1), or atropine (1 micromol L-1). Acetylcholine induced huge electrical bursts, and basal SO pressure increased by 20 +/- 10 mmHg. Histamine (10 microgram kg-1) induced strong SO contraction and the SO remained oedematous for over 10 min. Histamine (5 microgram kg-1) resulted in electromyographic burst activity with phasic SO contractions and increase in basal SO pressure by 34 +/- 19 mmHg for over 15 min. Diphenhydramine did not alter acetylcholine-induced SO motility, but significantly decreased histamine-induced contractions and almost abolished electrical activity. In vitro, acetylcholine induced SO contractions in pig (335 +/- 111 mg) and in man (323 +/- 54 mg). Histamine did not change SO tone in man, but in pig it induced dose-dependent contractions in the same way as acetylcholine. These contractions could be inhibited by diphenhydramine, but not by cimetidine or atropine. We conclude that histamine has a stimulatory effect, mediated by H1-receptor, on the pig SO motility. The SO response to histamine is different in adult humans from that observed in young pigs.

Acetylcholine↗
PubMed2000

Lamotrigine improves cerebral outcome after hypothermic circulatory arrest: a study in a chronic porcine model.

BACKGROUND: Glutamate excitotoxicity has an important role in the development of brain injury after prolonged hypothermic circulatory arrest. The goal of the present studies was to determine the potential efficacy of lamotrigine, an Na(+) channel blocker, to mitigate cerebral injury after hypothermic circulatory arrest. METHODS: Sixteen pigs (21-27 kg) were randomly assigned to receive lamotrigine (20 mg/kg) or placebo in a blinded fashion before a 75-minute period of hypothermic circulatory arrest (20 degrees C). Hemodynamic, electroencephalographic, and metabolic monitoring were carried out. S-100beta protein was determined up to the first postoperative morning. Daily behavioral assessment was performed until the animal died or was put to death on day 7. Histologic analysis of the brain was carried out in all animals. RESULTS: Complete behavioral recovery was seen in 5 of 8 (63%) animals after lamotrigine administration, compared with 1 of 8 (13%) in the placebo group (P =.02). Among the animals that survived for 7 days, the median behavioral score was higher in the lamotrigine group (8 vs 7, P =.02). The medians of recovered electroencephalographic bursts in the lamotrigine group were higher than those in the placebo group 4 1/2 hours after the start of rewarming (P =.01). The median S-100beta level was lower in the lamotrigine group (0.01 microg/L) than in placebo controls (0.1 microg/L) 20 hours after the start of rewarming (P =.01). The median of total histopathologic score was 5.5 in the lamotrigine group and 7.5 in the placebo group (P =.06). CONCLUSIONS: The present data suggest that lamotrigine improves neurologic outcome after a prolonged period of hypothermic circulatory arrest.

Analysis of Variance↗
PubMed2000

Neurophysiology of anaesthesia.

Methods of clinical neurophysiology are important in studying basic problems of anaesthesia such as the problem of the depth of anaesthesia, Some of the problems of clinical neurophysiology in awake subjects, such as the generators of somatosensory evoked potentials or cognitive evoked potentials, may be resolved by recording during EEG suppression. Finally, the mechanisms by which some anaesthetics produce epileptic phenomena (others or even the same agents may suppress epileptic activity) can only be resolved by EEG and EP recordings in human subjects, and by simultaneous recordings of intracellular and extracellular potentials in animals.

Anesthesia↗
PubMed1999

Cold retrograde cerebral perfusion improves cerebral protection during moderate hypothermic circulatory arrest: A long-term study in a porcine model.

BACKGROUND: Deep hypothermic circulatory arrest is an effective method of cerebral protection, but it is associated with long cardiopulmonary bypass times and coagulation disturbances. Previous studies have shown that retrograde cerebral perfusion can improve neurologic outcomes after prolonged hypothermic circulatory arrest. We tested the hypothesis that deep hypothermic retrograde cerebral perfusion could improve cerebral outcome during moderate hypothermic circulatory arrest. METHODS: Twelve pigs (23-29 kg) were randomly assigned to undergo either retrograde cerebral perfusion (15 degrees C) at 25 degrees C or hypothermic circulatory arrest with the head packed in ice at 25 degrees C for 45 minutes. Flow was adjusted to maintain superior vena cava pressure at 20 mm Hg throughout retrograde cerebral perfusion. Hemodynamic, electrophysiologic, metabolic, and temperature monitoring were carried out until 4 hours after the start of rewarming. Daily behavioral assessment was performed until elective death on day 7. A postmortem histologic analysis of the brain was carried out on all animals. RESULTS: In the retrograde cerebral perfusion group, 5 (83%) of 6 animals survived 7 days compared with 2 (33%) of 6 in the hypothermic circulatory arrest group. Complete behavioral recovery was seen in 4 (67%) animals after retrograde cerebral perfusion but only in 1 (17%) animal after hypothermic circulatory arrest. Postoperative levels of serum lactate were higher, and blood pH was lower in the hypothermic circulatory arrest group. There were no significant hemodynamic differences between the study groups. CONCLUSIONS: Cold hypothermic retrograde cerebral perfusion during moderate hypothermic circulatory arrest seems to improve neurologic outcome compared with moderate hypothermic circulatory arrest with the head packed in ice.

Animals↗