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Biomedical subjects

U Strömbom

Publications and source records attributed to U Strömbom.

At least 19 recordsLinked to original sources
PubMed2006

Steroid-free immunosuppression in kidney transplant recipients and prograf monotherapy: an interim analysis of a prospective multicenter trial.

This report described an interim analysis of a investigator-driven multicenter trial in renal transplant recipients: the Prospective Quality of life Renal Transplantation Switch Study; Tacrolimus-based immunosuppression ("PQRST study"). Patients included in the trial initially treated with cyclosporine-based immunosuppression after renal transplantation who experienced side effects, such as hypertension, hyperlipidemia, hypertrichosis, or other adverse reactions, were converted to a tacrolimus-based immunosuppressive regimen (n = 31). Steroids were subsequently discontinued between 3 and 6 months after the conversion. As of today 19/31 (50%) patients have been successfully weaned off steroids with the remaining patients in this process. In this interim analysis, with a follow-up ranging from 1 to 18 months both patient and graft survivals were 100%. No patient experienced an acute rejection episode; none of the grafts were lost. Blood pressure decreased in 22/31 (71%) of the patients. No patient developed de novo diabetes or other serious side effect related to the conversion. Three patients were withdrawn from the trial because of side effects: bleeding, depression, and proteinuria. However, none of these adverse events were felt to be directly related to the change of the immunosuppressive regimen to tacrolimus monotherapy. In conclusion, conversion from cyclosporine to tacrolimus-based therapy was safe and well tolerated; it may improve the cardiovascular risk profile after kidney transplantation.

Adult↗
PubMed1997

Improvement of ED prediction of cardiac mortality among patients with symptoms suggestive of acute myocardial infarction.

A study was undertaken to evaluate the 1-year risk of cardiac death for patients with chest pain/suspected acute myocardial infarction in the emergency department (ED) and express the prognosis in a statistical model. Clinical variables and electrocardiogram were correlated to cardiac death during 1 year. Cox regression model was used to estimate the risk of death as a continuous function of a risk score and the time interval. From these, the prognosis for each patient can be calculated. There were 6,794 visits by 5,303 patients followed for 1 year, during which 604 patients died. The absolute risk of cardiac death can be calculated from the independent predictors for cardiac death: age; sex; histories of diabetes mellitus, hypertension, and congestive heart failure; and symptoms, electrocardiographic pattern, and degree of suspicion of acute myocardial infarction on admission. This model allows estimation of the prognosis for every patient with chest pain/suspected acute myocardial infarction from data easily available in the ED.

Adolescent↗
PubMed1996

The concentrations of monoamine metabolites and neuropeptides in the cerebrospinal fluid of obese women with different body fat distribution.

DESIGN AND SUBJECTS: Several studies suggest neuroendocrine abnormalities in, particularly, abdominal, central obesity in humans, a condition with high morbidity and mortality. Therefore the concentrations of neuropeptides and catecholamines in cerebrospinal fluid (CSF) were analysed in 48 obese women, subdivided into groups with central, abdominal and gluteo-femoral distribution of body fat, utilising the waist-to-hip circumference ratio (WHR) for division. RESULTS: In comparisons with non-obese control women concentration of 5-hydroxyindol acetic acid (5-HIAA), methoxyhydroxyphenylglycol (MHPG), corticotropin releasing hormone (CRH), beta-endorphins (END) and neuropeptide Y (NPY) were lower, while homovanillic acid (HVA) was not different in obese women, HIAA, HVA and END correlated negatively with the WHR only in abdominally obese women, suggesting a threshold effect. HIAA vs HVA as well as CRF vs END correlated strongly in the total and both subgroups. An interrelationship between all these four substances was found in abdominal but not in gluteo-femoral obesity, suggesting a tighter functional coupling in the former group. Several correlations were found between CSF substance levels and appetite registrations, including END vs voracious eating, and for carbohydrate craving vs HIAA and vs HVA (negatively). This was also found only in abdominally obese women. CONCLUSION: Although the concentrations of monoamine metabolites and neuropeptides in the CSF sampled at the level of the lumber spine might not be representative for those at regulatory centers in the brain, the findings suggest that low 5-HIAA is characteristic of human obesity, and coupled to CRH as well as eating abnormalities, particularly in abdominal obesity. Since CRH is regulating the balance between the autonomic nervous systems, insulin secretion and thermogenesis in animals, corresponding anomalies in abdominal obesity in humans may have a central origin.

Adipose Tissue↗
PubMed1993

One-year prognosis in patients hospitalized with a history of unstable angina pectoris.

The prognosis during 1 year of follow-up in 715 patients admitted to one single hospital due to suspected acute myocardial infarction (AMI) with a history of unstable angina pectoris immediately preceding hospitalization is described. AMI developed in 192 patients (27%) during the first three days and in 255 patients (38%) during the first year. The mortality during hospitalization was 7% (50 patients) and during 1 year 19% (130 patients). Of the nonsurvivors, 54% died of AMI, 28% of congestive heart failure, and 20% of cardiogenic shock. Based on simple clinical parameters on admission to the emergency room, risk indicators for death during the following year could be identified as follows, in the order of significance: high age (p < 0.001), ST-segment depression on admission (p < 0.001), and a history of diabetes mellitus (p < 0.05). At admission to the emergency room, risk indicators for development of AMI during the following year were as follows: initial degree of suspicion of AMI (p < 0.001), electrocardiographic signs of acute ischemia on admission (p < 0.001), ST-segment elevation on admission (p < 0.01), age (p < 0.05), and lack of a previous history of chronic stable angina pectoris (p < 0.05). We conclude that, among patients admitted to hospital due to suspected AMI with a history of unstable angina pectoris immediately preceding hospitalization, 38% developed a confirmed infarction and 19% died during the following year.

Age Factors↗
PubMed1993

Prognosis in diabetics in whom the initial suspicion of acute myocardial infarction was not confirmed.

For 2,058 consecutive patients hospitalized for suspected acute myocardial infarction (AMI) but in whom AMI was later ruled out, we describe the prognosis with particular emphasis on diabetics. In all, a previous history of diabetes mellitus occurred in 290 (14%) of the patients. Compared with nondiabetics, they had a longer delay time between onset of symptoms and arrival in hospital. During 1 year of follow-up, their mortality rate was 28% compared with 14% for nondiabetics (p < 0.001), and their reinfarction rate was 20% compared with 10% for nondiabetics. More diabetics died in association with a fatal myocardial infarction and more frequently had ventricular fibrillation preceding death. With the exception of reinfarction, no clear difference in terms of morbidity was observed between the two groups. We conclude that the prognosis in diabetics in whom AMI is ruled out is poor, with between one-quarter and one-third not surviving 1 year.

Aged↗
PubMed1992

Prognosis for patients with initially suspected acute myocardial infarction in relation to presence of chest pain.

In all 4,232 patients admitted to a single hospital during a 21-month period due to initially suspected acute myocardial infarction (AMI), the prognosis and risk factor pattern were related to whether patients had chest pain or not. Symptoms other than chest pain that raised a suspicion of AMI were mainly acute heart failure, arrhythmia, and loss of consciousness. In 377 patients (9%) symptoms other than chest pain raised an initial suspicion of AMI. These patients developed a confirmed infarction during the first three days in hospital with a similar frequency (22%) as compared with patients having chest pain (22%). However, patients with "other symptoms" had a one-year mortality of 28% versus 15% for chest pain patients (p less than 0.001). Patients with "other symptoms" more often died in association with ventricular fibrillation and less often in association with cardiogenic shock as compared with chest pain patients. Among the 921 patients who developed early AMI, 64 (7%) had symptoms other than chest pain. They had a one-year mortality of 48% versus 27% for chest pain patients (p less than 0.001). We conclude that in a nonselected group of patients hospitalized due to suspected AMI, those with symptoms other than chest pain have a one-year mortality, which is nearly twice that of patients with chest pain.

Aged↗
PubMed1992

Early identification of acute myocardial infarction and prognosis in relation to mode of transport to hospital.

Of 2,840 consecutive patients who were admitted to the emergency department of a Swedish university hospital due to suspected acute myocardial infarction (AMI), only 25% were reached by the mobile coronary care unit (MCCU), and only 4% simultaneously fulfilled traditional criteria for prehospital thrombolysis (ie, had ST-segment elevation on admission electrocardiogram and a delay time of less than 6 hours). In the subset of patients who fulfilled criteria for a confirmed AMI, 31% were reached by an MCCU and 11% fulfilled criteria for prehospital thrombolysis. Among patients with confirmed AMI, the hospital mortality rate was highest in patients transported by standard ambulance (19%) versus 15% in those transported by an MCCU and 8% in those transported by other means. The authors conclude that AMI patients transported by ambulance are high-risk patients for early death. Prehospital thrombolysis might reduce their rate of mortality. However, according to the authors' experience only a minor fraction of patients are available for prehospital thrombolysis.

Aged↗
PubMed1991

Prognosis in suspected acute myocardial infarction in relation to delay time between onset of symptoms and arrival in hospital.

During a 21-month period, the prognosis in all patients admitted to a hospital ward from the emergency room with suspected acute myocardial infarction (AMI) was prospectively recorded and related to the time between onset of symptoms and arrival in hospital. They were classified as early arrivers (less than or equal to 2 h), intermediate arrivers (2-8 h) and late arrivers (greater than 8 h). Among patients developing a confirmed AMI (n = 909) the 1-year mortality rate was 26.0% in early arrivers, 28.1% in intermediate arrivers and 32.6% in late arrivers. The corresponding figures for patients in whom AMI was ruled out (n = 2,035) were 15.2, 15.1 and 17.6%, respectively. In AMI patients, various morbidity aspects during hospitalization and 1 year of follow-up appeared mainly independent of delay time, whereas among those in whom AMI was ruled out congestive heart failure during hospitalization was most common in early arrivers. We conclude that patients with suspected AMI who do not arrive early in hospital have a high 1-year mortality rate regardless of whether they develop AMI or not. Whether their prognosis can be improved by shortening of delay time remains to be clarified.

Aged↗
PubMed1988

Elevated plasma concentration of neuropeptide Y and low level of circulating adrenaline in elderly asthmatics during rest and acute severe asthma.

Twenty-five elderly asthmatic patients attending the internal medicine emergency ward because of an acute exacerbation of asthma were sampled, prior to acute treatment, for determination of systemic venous plasma levels of noradrenaline (NA), adrenaline (A) and neuropeptide Y-like immunoreactivity (NPY-LI). Whereas NA and NPY-LI were about two-fold higher than control values, plasma A levels were not significantly increased. Twelve of the asthmatic patients were also tested at resting stable conditions and were essentially asymptomatic. All values were then similar to those of control subjects (n = 28) except for a significantly higher NPY-LI plasma level in asthmatics. In seven of these patients a near maximal physical exercise test caused significantly increased NA, A and NPY-LI plasma levels. It is concluded that the acute asthma attack is associated with elevated NA and NPY-LI plasma levels, but an impaired A response. Furthermore, that circulating NPY under these conditions has a nervous rather than adrenal origin.

Acute Disease↗
PubMed1980

Clonidine: attenuation of sedative action by facilitated central noradrenergic neurotransmission.

Administration of clonidine, 0.05 mg/kg i.p. to mice 30 min before trial significantly depressed the exploration of a Y-maze. This effect was completely antagonized by 1-amphetamine, 0.75 mg/kg i.p., given 10 min before trial, which by itself did not change the behaviour studied. The clonidine-induced behavioural depression also appeared reduced after pretreatment with desipramine (10 mg/kg i.p., 30 min before clonidine) which, like l-amphetamine, by itself was inactive. The above treatment with clonidine significantly reduced the accumulation of dopa after inhibition of central aromatic L-amino acid decarboxylase both in the noradrenaline (NA) rich neocortex and the dopamine-rich neocortex and the dopamine-rich corpus striatum, whereas the dopa accumulation in the limbic brain regions was not significantly affected. l-Amphetamine, 0.75 mg/kg i.p., did not by itself significantly affect the dopa accumulation, but reduced the clonidine-induced effects. The results are compatible with the notion that the depression of exploratory behaviour by clonidine is related to impaired central NA-neurotransmission and rule out the possibility that it is due to activation of central post-synaptic NA-(alpha-)-receptors.

Amphetamine↗
PubMed1979

Qualitative aspects on motility changes in mice induced by low doses of apomorphine and clonidine.

Single mice were treated with apomorphine (0.05, 0.2 or 0.8 mg/kg) or clonidine (0.025 or 0.05 mg/kg), and were placed in a new kind of motility meter, allowing classification of movements in terms of size, and also charting the motility with the help of an X/Y pen recorder. All treatments induced reduction of motility in this model. Apomorphine, 0.8 mg/kg, considerably changed the motility type, whereas the lower doses did not. This finding is consistent with earlier studies on gross lobomotor activity and suggests that the higher dose alone evokes a significant direct net stimulation of postsynaptic dopamine receptors, whereas the lower doses merely reduce the physiological stimulation of these receptors by inhibiting dopamine neurotransmission. Clonidine, 0.025 mg/kg, depressed motility at least as much as did 0.05 mg/kg, in agreement with previous behavioural studies.

Animals↗
PubMed1979

Regulation of the state of phosphorylation of specific neuronal proteins in mouse brain by in vivo administration of anesthetic and convulsant agents.

The effect of drug treatment in vivo on the state of phosphorylation of two specific neuronal proteins, proteins Ia and Ib, has been studied in mouse brain. For this purpose, animals were killed by immersion into liquid nitrogen, and proteins Ia and Ib were extracted by a procedure designed to prevent alterations in their state of phosphorylation. Several anesthetic agents (pentobarbital, chloral hydrate, and urethane) each caused a decrease in the state of phosphorylation of these proteins. Conversely, the convulsant agents pentylenetetrazol and picrotoxin each caused an increase in the state of phosphorylation of these proteins. Neither the anesthetic nor the convulsant agents affected the total amount of these proteins. The results are compatible with a role for proteins Ia and Ib in neuronal function.

Anesthetics↗
PubMed1978

Antagonism of morphine-induced central stimulation in mice by small doses of catecholamine-receptor agonists.

The morphine (75 mg/kg i.p.) induced stimulation of motor activity in mice was significantly suppressed by small doses of central catecholamine (CA) receptor agonists, apomorphine (0.2 mg/kg) and clonidine (0.05 mg/kg). In the same dose, and at the same time interval as the behavioural stimulation was obtained, morphine did not significantly affect the in vivo rate of tyrosine hydroxylation in two dopamine (DA)-rich mouse brain regions, the corpus striatum and in the limbic system, or in the noradrenaline (NA)-rich, but DA-poor hemispheres, measured as the Dopa-accumulation during 30 min after inhibition of aromatic amino-acid decarboxylase by 3-hydroxybenzylhydrazine (NSD 1015) 150 mg/kg. The apomorphine induced reduction in Dopa accumulation in the DA-rich brain regions was not significantly affected by morphine. The disappearance rate of brain NA after inhibition of tyrosine hydroxylase by alpha-methyltyrosine methylester (250 mg/kg), the utilization of NA, was accelerated by morphine, whereas that of DA was not affected. Clonidine (0.05 mg/kg) retarded selectively brain NA utilization, and also suppressed the morphine-induced increase in NA utilization. In conclusion, morphine's stimulation of motor activity in mice, an effect which previously has been found to be correlated with its dependence producing action, could be inhibited by apomorphine or clonidine in small doses which inhibit brain DA- and NA-neurons, respectively. Thus, we have now shown the psychomtor stimulation by two euphoriant and dependence-producing drugs, ethanol and morphine, to be suppressed by CA "autoreceptor" activation.

Animals↗
PubMed1977

Locomotor stimulation by L-dopa: relative importance of noradrenaline receptor activation.

The importance of brain noradrenaline synthesis and receptor activation for the hyperkinesia induced by carbidopa plus L-Dopa in reserpine-treated or normal mice was analyzed in four different models. After pretreatment with reserpine and the monoamine oxidase inhibitor nialamide, the hyperkinesia induced by L-Dopa (25 mg/kg i.p.) was partly mediated via stimulation of noradrenaline receptors since it was significantly antagonized by the noradrenaline receptor-blocking agent phenoxybenzamine. Treatment with reserpine plus L-Dopa (125 mg/kg i.p.) produced an increase in motor activity probably due to stimulation of dopamine receptors since it was not accompanied by an accumulation of noradrenaline and it was not inhibited by phenoxybenzamine. The hyperkinesia following treatment with reserpine and a higher dose of L-Dopa (250 mg/kg i.p.) was probably due to stimulation of both dopamine and noradrenaline receptors since the dopamine-beta-hydroxylase inhibitor FLA-63 partly reduced the effect of L-Dopa. Phenoxybenzamine potentiated the motor stimulation by L-Dopa (125 mg/kg i.p.) in mice not pretreated with reserpine, perhaps depending on a slight enhancement of the net accumulation of brain dopamine. Thus, noradrenaline receptor activation is of importance for the L-Dopa-induced hyperkinesia, at least after high doses or after monoamine oxidase inhibition.

Animals↗
PubMed1977

Antagonism of ethanol's central stimulation in mice by small doses of catecholamine-receptor agonists.

Small doses of apomorphine (0.03-0.25 mg/kg i.p.) caused a dose-dependent suppression of the ethanol-induced (2.36 g/kg, 15% v/v, i.p.) locomotor stimulation in mice and higher doses (0.5--2 mg/kg i.p.) caused a delayed suppression. The delay increased with increased doses. Very small doses of clonidine (0.025 or 0.05 mg/kg i.p.), which per se did not or only slightly affect the activity of control mice, also markedly suppressed the ethanol-induced motor stimulation. Ethanol alone (2.36 g/kg i.p.) did not significantly affect the amount of Dopa accumulating in various mouse brain regions (limbic system, corpus striatum, hemispheres and brain stem) during 30 min following administration of 3-hydroxybenzylhydrazine (NSD 1015), an inhibitor of aromatic amino-acid decarboxylase. Both the hypothermia and the locomotor stimulation by ethanol were antagonized by NSD 1015. The reduction in Dopa accumulation induced by a small dose of apomorphine (0.25 mg/kg i.p.) in the dopamine-rich regions in the mouse brain was slightly enhanced by ethanol, whereas the clonidine-induced decrease in Dopa accumulation was, if anything, reduced. In conclusion, ethanol's behavioural stimulant action in mice can be largely suppressed by apomorphine or clonidine, drugs which in the small doses used probably inhibit central catecholamine (CA) neurons.

Animals↗