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Biomedical subjects

I Kjellmer

Publications and source records attributed to I Kjellmer.

At least 19 recordsLinked to original sources
PubMed1997

Recording non-nutritive sucking in the neonate. Description of an automatized system for analysis.

A new method for automatic analysis of non-nutritive sucking in newborn infants is described, which uses a specially designed computer program that analyses an analogue signal obtained from a pressure transducer inside a pacifier. Validation is done with four independent methods: electromyogram, visual identification, control of the automatic treatment and comparison of inter-observer results. A high degree of correspondence is shown. The system was applied to 58 healthy full-term neonates. Infants less than 24 h old demonstrated a significantly different sucking pattern compared with the 3-day-old infant. The duration of their bursts was longer (3.7 vs 2.8 s), the frequency of their sucking was lower (1.7 vs 2.0 Hz) and the variability of their sucking pattern was greater. These results also testify to the validity of the method inasmuch as the values for the different sucking parameters are similar to corresponding values presented earlier.

Age Factors↗
PubMed1997

Long-term effects of intrauterine growth retardation.

Intrauterine growth retardation (IUGR) was studied both after experimental induction in rats and spontaneously occurring in man. The growth-retarded rat pups were compared to appropriately grown litter mates with developmental and behavioural tests at 50 and 90 days of age. Female rats exhibited no differences between growth-retarded and control rats but growth-retarded male rats had poor performance at 50 but not at 90 days compared to male controls. In the patient study 25 growth-retarded babies were compared with 21 appropriately grown controls. The growth-retarded babies had delayed latency periods of the visual evoked potentials at term and 6 weeks later, and at follow-up (18 months) demonstrated significantly more developmental and behavioural problems than the control group.

Animals↗
PubMed1997

Can paediatricians benefit from the Internet?

It is likely that many paediatricians will find the Internet useful. The main benefits are probably the ease and speed of communication and immediate access to a few databases such as MEDLINE. It is also practical to integrate the import, processing, storage, and export of data into one's own computer. It is also possible that the Internet in all its forms will become an integrated part of our daily paediatric practice as a result of the increased usage of the Internet by patients, parents, and paediatricians.

Computer Communication Networks↗
PubMed1996

Impact of reoxygenation with oxygen and air on the extent of the brain damage after hypoxia-ischaemia in neonatal rats.

Brain damage after hypoxia-ischaemia develops partly during the state of reoxygenation. The generation of free oxygen radicals is considered to be one possible mechanism. In order to evaluate the role of hyperoxygenation, a comparison was made between reoxygenation with pure oxygen and with air after hypoxia-ischaemia in a rat model of unilateral cerebral hemisphere damage. Brain damage was induced in 7-day-old rats. The animals were treated during reoxygenation with either 100% oxygen for 0.5 h or air. The extent of the brain damage was determined at 3 weeks of age by weighing the left and right hemispheres separately. No significant difference in weight deficit of the hemispheres was seen in the oxygen-treated group (15.5%, median) compared to the air-treated group (25.0%). Reoxygenation with pure oxygen after hypoxia-ischaemia in neonatal rats does not cause increased brain damage compared with reoxygenation with room air.

Air↗
PubMed1996

Posthypoxic cooling of neonatal rats provides protection against brain injury.

AIM: To determine whether moderate hypothermia, applied after a hypoxic-ischaemic insult in neonatal rats, reduces cerebral damage. METHOD: Unilateral hypoxic-ischaemic brain damage was induced in 7 day old rats by left carotid ligation, followed by 120 minutes of normothermic exposure to 8% O2, followed by random selection to three hours of hypothermia (rectal temperature, mean (SD), 32.5 (0.4) degrees C) or normothermia (38.3 (0.4) degrees C). One hundred and one animals were used for brain temperature or blood chemistry studies and 24 for survival studies (7 days) with neuropathology, including cell counting as outcome measures. RESULTS: Thirty sections from each brain were histologically examined with respect to distribution and pattern of damage and given a score from 0 to 4. Animals treated with hypothermia had significantly less damage than normothermic animals (score 0.5 (0.3) vs 1.8 (0.5)). CONCLUSIONS: Posthypoxic hypothermia reduces brain damage in awake, unrestrained 7 day old rats.

Animals↗
PubMed1995

Neuron specific enolase in asphyxiated newborns: association with encephalopathy and cerebral function monitor trace.

Neuron specific enolase (NSE) in serum and cerebrospinal fluid (CSF) and glutamate in CSF were investigated in the immediate postasphyctic period in 22 term newborn infants. The cerebral function monitor (CFM) pattern was also assessed and hypoxic-ischaemic encephalopathy (HIE) was graded. NSE was significantly increased in the CSF of infants with HIE (median value 25.4 micrograms/l) compared with control infants (10.0 micrograms/l). Infants with the highest concentrations died. NSE in CSF correlated with the degree of asphyxial damage. Glutamate and NSE in CSF did not correlate, presumably due to the different time factors of the release after the insult. NSE in CSF corresponded well with the type of CFM pattern, which was also highly predictive of outcome.

Asphyxia Neonatorum↗
PubMed1993

Excitatory amino acids in the cerebrospinal fluid of asphyxiated infants: relationship to hypoxic-ischemic encephalopathy.

Asphyxiated (n = 27) and control infants (n = 25) were subjected to spinal taps. Amino acids were measured with liquid chromatography and the degree of hypoxic-ischemic encephalopathy was determined in each case. In asphyxiated infants, the concentrations of aspartate and glutamate were 286% and 387% (p < or = 0.01 and p < or = 0.05) of the control values, respectively. The cerebrospinal fluid aspartate levels were significantly (p < or = 0.05) higher in the group with severe (3.4 mumol/l) compared with the group with mild hypoxic-ischemic encephalopathy (1.0 mumol/l). Glutamate was also higher in the group with severe (12.3 mumol/l) than in the groups with mild (2.7 mumol/l) or moderate (3.2 mumol/l) hypoxic-ischemic encephalopathy (p < or = 0.05). High concentrations of excitatory amino acids were present in the CSF of asphyxiated infants which may exert excitotoxic effects.

Amino Acids↗
PubMed1993

Scavengers of free oxygen radicals in combination with magnesium ameliorate perinatal hypoxic-ischemic brain damage in the rat.

The effect of oxygen radical scavengers in combination with magnesium administered after a hypoxic-ischemic insult was evaluated in a model of perinatal brain damage. A mixture of scavengers of oxygen-derived free radicals (L-methionine, 0.2 g; mannitol, 0.5 g) and magnesium sulfate (0.3 g) per kg body weight was given to 34 1-wk-old rat pups immediately after a session of unilateral carotid artery ligation and 2 h of hypoxia (8% O2 in N2). Thirty-four littermates served as controls; they received a placebo. At 3 wk of age, there was a significantly smaller reduction of hemisphere weight ipsilateral to the ligation in the treated animals compared with the controls (0.7 versus 8.8% of contralateral hemisphere weight median values, p < 0.01). The difference was especially marked for the most severe degrees of brain damage. Only one of the 34 treated animals, compared with 13 of 34 control animals, had a reduction of ipsilateral hemisphere weight > 25%. The protection offered by the mixture used was larger than in previously published studies using this model and treatment after the hypoxic exposure with only one protective agent. It is concluded that a combination of oxygen radical scavengers and magnesium administered in the phase of resuscitation mitigates perinatal postasphyxial brain damage in the rat. An additive protective effect of different therapeutic strategies on the brain damage may be present in this situation.

Animals↗
PubMed1992

Cerebral function in the growth-retarded fetus and neonate.

Intrauterine growth retardation is associated with increased risks for permanent neurological disabilities. A series of studies was undertaken to elucidate whether fetal growth retardation causes a primary perturbation of brain function and development and whether an increased vulnerability for periods of oxygen lack exists. In two groups of neonates who were small for gestational age (SGA) evoked potentials were investigated. A high frequency of abnormal recordings were obtained in SGA babies. SGA babies had significantly longer latency periods for the primary evoked potentials than appropriately grown controls. In guinea pigs and rats growth retardation was induced by reducing the placental blood flow during late gestation. Growth retarded guinea pups demonstrated a considerable reduction of the ability to retain normal somatosensory evoked response during hypoxia compared to appropriately grown littermates. Growth retarded rat fetuses exhibited marked changes of the monoamine metabolism in the brain inasmuch as basal levels of serotonin and its main metabolite were low while an inappropriate acceleration of the serotonin synthesis rate took place during hypoxia. The tissue concentrations of aspartate were also significantly lower in growth retarded fetuses than normally grown littermates. Finally, lipid peroxidation was assessed. During adequate oxygenation no difference was observed when lipid peroxidation was assessed. During adequate oxygenation no difference was observed when lipid peroxidation in brain tissue of growth retarded and appropriately grown fetuses was compared but during mild-moderate hypoxia lipid peroxidation was significantly more intense in the growth retarded group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Linear growth in children with cystic fibrosis. I. Birth to 8 years of age.

The linear growth of Swedish children with cystic fibrosis (CF), is described using the infancy-childhood-puberty (ICP) growth model. Length/height was studied in 51 patients during their first 8 years of life. The median age at diagnosis was 0.4 years (range 0.0-6.1 years). At birth, their mean length was close to normal, but the gain in length over the first 0.25 years of life was significantly below normal, resulting in a mean length SDS of -1.3. Length remained subnormal up to 1.0 year of age. Thereafter, catch-up growth occurred, resulting in almost normal height (mean SDS-0.3) at 5.0 years of age. Between 5.0 and 8.0 years of age growth was normal. The mean age at onset of the childhood component was not significantly different from the controls. Hence, the catch-up growth did not occur until after the onset of the childhood component. This study shows that the postnatal linear growth rate is retarded in children with CF during the first months of life. This is almost completely compensated for by a supranormal growth rate that starts at the end of the first year of life.

Age Factors↗
PubMed1991

Pregnancy complications and short-term follow-up of infants born after in vitro fertilization and embryo transfer (IVF/ET).

Two hundred and six pregnancies occurring after in vitro fertilization (IVF) and embryo transfer (ET) during a 7-year period in Göteborg were analysed with respect to pregnancy outcome. The clinical abortion rate was 26%, the rate of ectopic pregnancy was 10%, the rate of ongoing pregnancies beyond 24 weeks was 15%, and the rate of deliveries was 49% (n = 100). The hospital records of 98 women with the 100 deliveries resulting in 131 infants were studied. Multiple pregnancy occurred in 27%, including one quadruplet and two triplet pregnancies. Preterm birth occurred in 30% of all pregnancies and in 20% of singleton pregnancies. Thirty-four percent of the infants had a birth weight of less than 2500 g. The perinatal mortality was 46/1000, as estimated from the 24th week of pregnancy. The incidence of major malformation, 2.3%, was similar to that reported from studies in the general population. The first 100 infants born were followed up for 18 months to 8 years. Long-term sequelae were associated with immaturity and low birth weight. No problems during follow-up were disclosed in children who had had an uneventful neonatal period. It is concluded that IVF pregnancies are an obstetric risk group requiring special attention.

Adult↗
PubMed1991

Mechanisms of perinatal brain damage.

Although the perinatal brain is more resistant towards hypoxia-ischemia than at any later stage of development, perinatal asphyxia still contributes to permanent brain damage in survivors. This short review focuses on the discussion of mechanisms of late neuronal death, i.e. cerebral damage related to lack of oxygen but caused by mechanisms during the stage of reoxygenation. Evidence is presented to indicate that the transient, dense glutamatergic innervation of basal structures of the perinatal brain may induce brain damage via overflow of excitatory amino acids during oxygen lack, causing a longstanding overstimulation of excitatory neurons. Oxygen derived free radicals may be generated during reoxygenation by several mechanisms, including the oxidation of hypoxanthine and arachidonic acid accumulated in the cerebral insterstitium during hypoxia. The increase of the intracellular concentration of free Ca-ions contributes to these events. Possible avenues for prevention of post-asphyxial brain damage include glutamate receptor antagonists, calcium antagonists, antioxidants, free radical scavengers, inhibitors of libid peroxidation and blockers of arachidonic acid metabolism.

Amino Acids↗
PubMed1991

Zinc therapy in children with cystic fibrosis.

The effect of oral zinc supplementation in patients with cystic fibrosis (CF) was investigated in a placebo-controlled, double-blind, crossover study with each treatment period covering 6 months. CF patients (n = 13, aged 2 years, 3 months to 19 years, 1 month) started with placebo and after 6 months, they received zinc therapy. Another 13 patients (aged 3 years, 5 months to 16 years, 10 months) started in the reverse order. Before zinc supplementation, all CF patients had low plasma levels of zinc which normalized during treatment. This effect was, however, transient. CF patients also had low concentrations of plasma selenium. A small decrease in the number of leukocytes was also noted during zinc therapy. In response to zinc treatment, no changes in the clinical status of the patients were observed either by the investigators or by the patients. Growth velocity was the same during the placebo and zinc treatment periods. No significant changes in lung function occurred in response to either placebo or zinc. It appears that the observed low plasma zinc concentration in CF patients was due to an impaired zinc absorption from the gut which was counteracted by an increased supply of oral zinc. No beneficial effect from zinc supplementation on clinical status, growth velocity, or lung function was found in this study.

Adolescent↗