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Biomedical subjects

M Björkman

Publications and source records attributed to M Björkman.

At least 19 recordsLinked to original sources
PubMed1999

A novel subtype of prostacyclin receptor in the central nervous system.

Recently, in the course of our search for the prostacyclin receptor in the brain, we found a novel subtype, designated as IP2, which was finely discriminated by use of the specific ligand (15R)-16-m-tolyl-17,18,19,20-tetranorisocarbacyclin (15R-TIC) and specifically localized in the rostral part of the brain. In the present study, the tritiated compound 15R-[15-(3)H]TIC was synthesized and utilized for more specific research on IP2. The specificity of binding to rat brain regions was confirmed by use of several prostacyclin derivatives including 15S-TIC. Mapping of 15R- and 15S-[3H]TIC binding in adjacent pairs of frozen sections of rat brain demonstrated a quite similar pattern of distribution in almost all rostral brain regions, indicating that the regions may contain only the IP2 subtype. On the other hand, 15R-[3H]TIC binding was very faint as compared with 15S-[3H]TIC binding in the caudal medullary region. High densities of 15R-[3H]TIC binding sites were shown in the dorsal part of the lateral septal nucleus, thalamic nuclei, limbic structures, and some of the cortical regions. Scatchard plot analysis showed two components of high-affinity 15R-[3H]TIC binding in the rostral regions, one with a K(D) value at approximately 1 nM and the other with approximately 30 nM. These results strengthen our previous finding that a different subtype of prostacyclin receptor is expressed in the CNS, and the map with 15R-[3H]TIC obtained here could guide further studies on the molecular and functional properties of the IP2.

Animals↗
PubMed1999

Compounds labelled with short-lived beta(+)-emitting radionuclides and some applications in life sciences. The importance of time as a parameter.

Some examples of recent development of the synthesis of compounds labelled with short-lived beta(+)-emitting radionuclides will be discussed with an emphasis on the importance of time in selecting a synthetic strategy. Furthermore the use of such labelled compounds to monitor certain processes in areas within the field of analytical chemistry and in various applications in drug development will be presented.

Animals↗
PubMed1998

Synthesis of 11C/13C-labelled prostacyclins.

A one-pot synthesis of (15R)-16-(3-[11C]methylphenyl)-17,18,19, 20-tetranoriso-carbacyclin methyl ester was performed using a palladium-promoted reaction of [11C]methyl iodide with (15R)-16-(3-tri-n-butylstannylphenyl)-17,18,19, 20-tetranorisocarbacyclin methyl ester. The C-15 epimer (15S)-16-(3-[11C]methylphenyl)-17,18,19,20-tetranorisocarbacyclin methyl ester was synthesised in the same way starting from (15S)-16-(3-tributylstannylphenyl)-17,18,19,20-tetranorisocarba cyclin methyl ester. The decay-corrected radiochemical yields were 33-45% based on [11C]methyl iodide produced, and the radiochemical purity of the product was > 95%. The total synthesis time was 35 min, counted from end of radionuclide production to product ready for administration. The 11C-labelled prostacyclin methyl esters were easily hydrolysed using sodium hydroxide affording the 11C-labelled prostacyclin acids in quantitative yields. The stereoisomers (15R)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin [11C]methyl ester and (15S)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin [11C]methyl ester were synthesised by esterification using [11C]methyl iodide and the tetrabutylammonium salts of (15R)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin acid and (15S)-16-(3-methylphenyl)-17,18,19,20-tetranorisocarbacyclin acid, respectively. The decay-corrected radiochemical yields were in the range of 55% counting from [11C]methyl iodide produced, and the radiochemical purity of the product was > 95%. The total synthesis time was 35 min, counting from end of radionuclide production to product ready for administration. Both of these labelling methods can be used for labelling with 13C when (13C)methyl iodide is used. The methods described herein have already proved important since they enable the in vivo use of PET to study the action of prostacyclins in the brain.

Carbon Isotopes↗
PubMed1993

Realism of confidence in sensory discrimination: the underconfidence phenomenon.

This paper documents a very pervasive underconfidence bias in the area of sensory discrimination. In order to account for this phenomenon, a subjective distance theory of confidence in sensory discrimination is proposed. This theory, based on the law of comparative judgment and the assumption of confidence as an increasing function of the perceived distance between stimuli, predicts underconfidence--that is, that people should perform better than they express in their confidence assessments. Due to the fixed sensitivity of the sensory system, this underconfidence bias is practically impossible to avoid. The results of Experiment 1 confirmed the prediction of underconfidence with the help of present-day calibration methods and indicated a good quantitative fit of the theory. The results of Experiment 2 showed that prolonged experience of outcome feedback (160 trials) had no effect on underconfidence. It is concluded that the subjective distance theory provides a better explanation of the underconfidence phenomenon than do previous accounts in terms of subconscious processes.

Adult↗
PubMed1988

Noise annoyance with regard to neurophysiological sensitivity, subjective noise sensitivity and personality variables.

To evaluate the relation between annoyance to environmental noise, general neurophysiological sensitivity, subjective noise sensitivity and other individual characteristics, experiments were undertaken in which 93 subjects assessed their subjective annoyance after exposure to noise under laboratory conditions. Evaluations were made of the discomfort threshold for pulsating sound, the light discomfort, and heat and cold discomfort. The heart rate and discomfort after exposure to a series of impulse noises was also determined. Subjective noise sensitivity, attitudes to noise, mood and personality characteristics of the subjects were evaluated using questionnaires. The results show that the annoyance after exposure to noise was not closely related to the general neurophysiological sensitivity, measured as discomfort threshold for noise, heat, cold and light; or to the heart rate reaction or discomfort after exposure to impulse noise. The annoyance was highly correlated with subjectively reported noise sensitivity and with the attitude to noise. There was also a relationship with neuroticism, measured with the EPI scale. It is suggested that the subjective noise sensitivity, attitude and neuroticism for the definition of noise sensitivity be defined in future studies of long term effects of noise exposure.

Adolescent↗
PubMed1983

Sleep disturbance before and after traffic noise attenuation in an apartment building.

A study on traffic noise sleep disturbance was made in an apartment building before and after the installation of noise insulating windows. Three tenants completed a questionnaire each morning one week before and one week after the insulation of windows, and body movements during sleep were recorded during these periods. All persons demonstrated a decrease in the number of body movements after the windows had been insulated and two reported improved sleep quality. The results suggest that subjectively judged sleep quality as well as recordings of bed movements are useful tools for evaluating actions to reduce noise.

Adult↗
PubMed1982

Effect of noise on blood pressure and 'stress' hormones.

1. Noise stimulation (95 dBA) for 20 min caused a significant increase in diastolic (12%, P less than 0.001) and mean arterial pressure (7%, P less than 0.001) in 15 healthy normotensive male subjects. 2. There was no significant change in systolic blood pressure or heart rate during exposure to noise. 3. Adrenaline, noradrenaline, prolactin, cortisol and growth hormone concentration in venous plasma were not affected during noise stimulation.

Adult↗
PubMed1981

Haemodynamic effects of noise exposure before and after beta 1-selective and non-selective beta-adrenoceptor blockade in patients with essential hypertension.

1. Noise stimulation (100 dBA) for 10 min caused a significant increase in diastolic (7.0%, P less than 0.001) and mean arterial blood pressure (4.3%, P less than 0.01) in patients with essential hypertension. 2. The blood pressure response to noise was due to an increase in total peripheral resistance (4.8%, P less than 0.02); heart rate, stroke volume and cardiac output were unchanged. 3. beta 1-selective adrenoceptor blockade (metoprolol) did not change the haemodynamic reaction pattern induced by noise. 4. Noise exposure during non-selective beta-adrenoceptor blockade (propranolol) caused an accentuated blood pressure response with increments of both systolic and diastolic blood pressure as well as a more pronounced rise in total peripheral resistance. 5. The haemodynamic changes induced by noise stimulation at 100 dBA totally disappeared after 5 min of quiet rest at 40 dBA.

Adult↗
PubMed1980

Noise as a contributory factor in the development of elevated arterial pressure. A study of the mechanisms by which noise may raise blood pressure in man.

Arterial pressure and other hemodynamic variables (stroke volume (SV), cardiac output and total peripheral resistance) were studied in 18 healthy males before and during exposure to recorded industrial noise. All measurements took place under strictly standardized conditions in a noise laboratory. the frequency distribution and level of noise used for stimulation were continuously monitored and kept constant within close limits throughout the experiments. SV was measured with impedance cardiography. Indirect blood pressure (BP) in the brachial artery was measured with an automatic device and the derived parameters, cardiac output and total peripheral resistance, were calculated from these measurements. Compared with resting conditions at 40 dBA, stimulation with industrial noise at 95 dBA caused significant increases in diastolic BP, mean arterial pressure and total peripheral resistance. Minor but statistically significant reductions of SV and cardiac output were seen. Heart rate and systolic BP did not change. These alterations of the hemodynamic variables persisted throughout 20 min of noise stimulation and were maintained for 5 min following cessation of noise stimulation. All variables had returned to their initial levels 10 min after discontinuation of noise stimulation. This study suggests that exposure to industrial noise at levels prevailing during several industrial processes may cause acute elevations of arterial BP and peripheral vascular resistance. In animal studies, repeated elevations of BP due to exposure to noise have been shown to cause a permanent elevation of BP. Therefore, we suggest that noise may be one of several external stimuli contributing to the development of arterial hypertension in man.

Adult↗
PubMed1979

Hemodynamic and hormonal changes induced by noise.

Eighteen healthy male volunteers with normal hearing were exposed to industrial noise at different sound levels (75, 85 and 95 dB A) in a noise laboratory. Blood pressure, heart rate, stroke volume and cardiac output were recorded with noninvasive techniques. Adrenaline and noradrenaline concentration in venous plasma were analyzed before and during noise exposure. The mean resting blood pressure of the whole group was 120/70 mm Hg. During noise stimulation diastolic blood pressure increased (12.2%, p less than 0.001) as did mean arterial pressure (6.6%, p less than 0.001) and total peripheral resistance (12.7%, p less than 0.001). Stroke volume (7.3%, p less than 0.001) and cardiac output (5.0%, p less than 0.01) were both reduced at 95 dB A. Heart rate and systolic blood pressure did not change significantly. At 75 and 85 dB A there were similar but smaller changes in the hemodynamic parameters. There were no changes in adrenaline and noradrenaline in plasma during maximal noise exposure. The noise induced hemodynamic changes remained 5 minutes after the noise stimulation was stopped but had disappeared after 10 minutes of rest.

Adult↗