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Biomedical subjects

M Laakso

Publications and source records attributed to M Laakso.

At least 361 records · Page 20Linked to original sources
PubMed1981

Prolonged Q-T interval and severe tachyarrhythmias, common features of sotalol intoxication.

The findings in six patients admitted to hospital 0.5-4.5 h after the ingestion of an overdose of 2.4-8 g sotalol are described. In addition to bradycardia and hypotension, all patients had a considerably prolonged corrected Q-T interval, up to 172 +/- 8% of normal. Severe ventricular tachyarrhythmias occurred in five of the six patients, the risk was greatest up to 20 h after the ingestion of sotalol. The long Q-T interval returned to normal over 3 to 4 days, which is consistent with the long half-life of sotalol. In addition to its beta-blocking action, sotalol has marked electrophysiological properties of a Class III antiarrhythmic drugs, which are likely to be able to account for its observed effects. Special attention should be paid to the risk of severe ventricular arrhythmias in sotalol intoxications.

Adolescent↗
PubMed1979

Comparison of effects of pentobarbital and ethanol on the neuronal activity in the posterior parietal association cortex.

The problem of this study was whether the effects produced by alcohol in the posterior parietal association cortex are specific to this drug or shared by other centrally acting depressant drugs such as barbiturates. The effect of graded doses of pentobarbital on multineuronal impulse activity was recorded with transdural microelectrode technique in 30 expts. in Brodmann's area 7 of five stump-tailed monkeys (Macaca speciosa). The results were compared with those from 32 expts. performed with alcohol and published separately. The dosage of the two drugs was determined on the basis of the monkeys' sensori-motor coordination which was assessed with a rating scale of reaching accuracy for food rewards. There were several recording sites where the actions of the two drugs were similar at similar behavioural levels of intoxication. However, in the distribution of effects among various functional types of recording sites a significant difference was found between pentobarbital and alcohol. Alcohol commonly diminished cellular activity related to motor behaviour (reaching, grasping) and only rarely responses to somesthetic stimuli, whereas the effects of pentobarbital were the opposite being most common on somatosensory responses and least common on activity related to motor behaviour. Also responses to visual stimuli were more sensitive to pentobarbital than to alcohol. The actions of pentobarbital and alcohol on responses evoked by sensory stimulation differed significantly (P less than 0.01). We conclude that significant differences exist in the mechanisms of action of alcohol and barbiturate on the associative systems of the brain.

Animals↗
PubMed1978

Effect of ethanol on neuronal activity in the parietal association cortex of alert monkeys.

The effect of alcohol was studied in alert monkeys on the cellular mechanisms of the posterior parietal association cortex, a region that normally participates in visuo-spatial co-ordination of hand movements. In thirty-two experiments, the effects of intracardiac administration of ethanol were monitored by the intracortical multiple-unit recording technique. Alcohol produced rhythmic groupings of the spontaneous impulse activity; the rhythm was accentuated by closing the eyes. The dominant frequency of this rhythm (3.5 to 1 Hz) correlated inversely with the blood alcohol level. Three groups of response types were studied in Brodmann's area 7. At 8 of 12 recording sites, a close correlation was observed between the monkey's reaching accuracy and the magnitude of integrate multineuronal responses to reaching with the contralateral arm under visual guidance, or to grasping an object. Half of the 10 recording sites which were activated by complex visual stimulation also showed a close correlation with the behavioural action of alcohol. Least sensitive to alcohol were somatosensory responses; only 3 of 10 of such recording sites were influenced by moderate doses of alcohol. Larger doses producing coma increased the proportion of responses blocked by alcohol, whereas no effects were observed in the adjacent primary somatosensory cortex. Our results show that the posterior parietal association cortex is very sensitive to the action of alcohol. Moreover, these findings support the theory that the action of alcohol in various parts of the central nervous system depends on the complexity of synaptic contacts to the location under study.

Action Potentials↗
PubMedDate not supplied

Reducing the burden of diabetes: managing cardiovascular disease.

Of the threats to health and life that beset the person with diabetes, cardiovascular disease (CVD), particularly coronary heart disease (CHD) but also cerebrovascular and peripheral vascular disease, represent the heaviest burden. The relative risk for CVD is very high for Type 1 diabetes, but the absolute risk, in terms of numbers, is much higher for Type 2. In all societies, diabetes increases cardiovascular risk twofold or more, compared with the local non-diabetic population. Some of the evidence for this diabetes-related increase in cardiovascular risk is reviewed and its relationship to recognised cardiovascular risk factors considered. The explanation of the enhanced susceptibility to atherosclerotic disease in diabetes remains a matter of contention. How much can be explained by greater prevalence in diabetes of such risk factors as hypertension and dyslipidaemia? To what extent is the impact of a given level of risk factor magnified by a co-existing diabetic state? Is the increased cardiovascular morbidity and mortality secondary to risk factors specifically related to the diabetic state itself? Does the explanation lie in altered coagulability due to changes in platelet activation and aggregability, fibrinogen levels, Factor VII, von Willebrand factor or PAI-1, in the concentration or composition of plasma lipoproteins, in defective endothelial cell function or other metabolic abnormalities of the arterial wall? To what extent is cardiovascular risk related to the degree of hyperglycaemia, protein glycation, relative hyperinsulinaemia and insulin resistance? Data from recent epidemiological, intervention and laboratory investigations bearing on causation, management and prevention of CVD in diabetes are reviewed. Evidence for the impact of correction of glycaemia, dyslipidaemia and raised arterial pressure is considered and reasons are adduced for a broad and proactive therapeutic approach with early identification and vigorous correction of key risk factors.

Cardiovascular Diseases↗
PubMedDate not supplied

Auditory brainstem latencies in type I (insulin-dependent) diabetic patients.

INTRODUCTION: This study was undertaken to compare auditory brainstem response latencies in insulin-dependent diabetics, and to compare these findings with metabolic control, microangiopathy, neuropathy, and the duration of diabetes. METHODS: Auditory brainstem latencies were studied in 53 type I diabetic patients and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years. Three different stimulus repetition rates (10, 30, and 50 Hz) were used. All subjects had normal hearing ability. RESULTS: Wave V latencies were longer in diabetic patients when compared with those of control subjects at all repetition rates. At repetition rates of 10 and 50 Hz, diabetic patients had a prolonged I-V interwave latency, and at a repetition rate of 50 Hz, diabetics had a longer III-V interwave latency than control subjects. These findings indicate a central disturbance in the auditory pathway. Microvascular complications (retinopathy, nephropathy) and the duration of diabetes were associated with the prolongation of auditory brainstem latencies. In contrast, poor metabolic control (high fasting blood glucose and glycated hemoglobin A1c) at the time of the present study was only marginally associated with prolonged auditory brainstem latencies. The changes in auditory brainstem latencies associated with diabetic neuropathy (measured with five cardiac autonomic nervous function tests) appeared simultaneously with microvascular complications and in patients with diabetes of long duration, and thus a causative role of diabetic neuropathy in the pathogenesis of prolonged auditory brainstem latencies remains unsolved. CONCLUSION: Delayed auditory brainstem latencies in type I diabetic patients are probably caused by the long duration of diabetes and the microvascular complications associated with it.

Adult↗
PubMedDate not supplied

Acoustic-reflex responses in patients with insulin-dependent diabetes mellitus.

PURPOSE: Patients with insulin-dependent diabetes mellitus (IDDM) are especially susceptible to microangiopathic complications such as nephropathy, retinopathy, and neuropathy. Microangiopathic changes are also the most important findings in histopathologic studies of the inner ear and central nervous systems in diabetic subjects. No previous studies have measured acoustic-reflex latencies (ARL) or amplitudes (ARA) in patients with IDDM. ARL and ARA reflect the function of the acoustic-reflex arch. Furthermore, possible changes in the tympanic membrane, ossicular chain, and stapedius muscle may affect the shape of acoustic-reflex. SUBJECTS AND METHODS: Acoustic-reflex thresholds, latencies, and amplitudes were studied in 53 patients with IDDM and 42 randomly selected nondiabetic control subjects, aged between 20 and 40 years, using the Madsen Model ZO 73 Impedance Bridge (Madsen Electronics, Copenhagen, Denmark). Subjects with an abnormal tympanic membrane, conductive hearing loss, and known cause for hearing impairment eg, noise damage, were excluded from the study. RESULTS: There were no differences between control and diabetic subjects in the contralateral acoustic-reflex thresholds. In contrast, patients with IDDM had longer ARLs and decreased ARAs compared with those of control subjects. ARA amplitude had linear correlation with the amplitude of tympanogram, whereas ARL had no linear correlation with auditory brainstem latencies in the same study subjects. Acoustic-reflex responses in insulin-dependent diabetic patients were not associated with the duration of diabetes, metabolic control, microangiopathy, or neuropathy. CONCLUSIONS: Prolonged ARLs and decreased ARAs in patients with insulin-dependent diabetes are probably caused more by the stiff middle ear system than disturbances in the brainstem.

Acoustic Impedance Tests↗
PubMedDate not supplied

Improvement of metabolic control does not normalize auditory brainstem latencies in subjects with insulin-dependent diabetes mellitus.

INTRODUCTION: In our previous study (Am J Otolaryngol 14:413-418, 1993), we reported that prolonged auditory brainstem response latencies are associated with microvascular complications and the duration of diabetes in patients with insulin-dependent diabetes mellitus (IDDM). To investigate whether short-term improvement in metabolic control also affects ABR-responses, we compared ABR-latencies in subjects with IDDM before and after intensified insulin and diet therapy. MATERIALS AND METHODS: Auditory brainstem latencies were measured in 13 subjects with IDDM (mean age: 25 years) before and after intensified insulin and diet therapy. The acoustic stimulus was a half sine wave with a duration of 0.250 millisecond and a frequency of 2,000 Hz. The stimulus was presented monaurally with fixed polarity through shielded headphones TDH-39 at repetition rate of 10 Hz and at 90 dB hearing level. All subjects had normal hearing ability. Glycated hemoglobin A1C (GHbA1C), blood glucose immediately before ABR-measurements, and mean blood glucose during 24 hours before auditory studies were measured before and after intensified therapy. RESULTS: During intensified insulin therapy, GHbA1C improved significantly (P < .05) in study subjects. However, no changes were observed in ABR-latencies. We also studied those 10 patients whose blood glucose improved during intensified insulin therapy. Although blood glucose was significantly lower (P < .01) after intensified insulin therapy compared with that at baseline, no changes were observed between ABR-latencies at baseline and follow-up. CONCLUSION: ABR-latencies were not affected by improvement in metabolic control in patients with IDDM. Our finding suggests that delayed ABR-latencies found in patients with IDDM are not caused by poor metabolic control of diabetes but rather by other mechanisms, for example, microvascular complications.

Adult↗
PubMedDate not supplied

Diabetes mellitus and brain atrophy: a computed tomography study in an elderly population.

Previous studies have suggested that noninsulin dependent diabetes mellitus (NIDDM) could lead to learning and memory deficits. We studied cognitive performance and computed tomography (CT) findings of the brain in elderly subjects with drug treated NIDDM (n = 12), with diet treated NIDDM (n = 13), and in nondiabetic individuals (ND, n = 59). The cognitive performance (orientation and up-to-date knowledge, praxic functions, understanding of speech, expressive speech, memory, general reasoning) did not differ between the groups. The drug treated diabetics had more pronounced central temporal atrophy compared to that in the ND subjects as evidenced by wider right temporal horn (ANCOVA adjusted for age, p = 0.011). The drug treated diabetics (all women) also had wider frontal horns than did the ND women. The CT measures of diet treated diabetics were comparable with those of the ND group. The fasting glucose level was positively correlated with the width of the right temporal horn but not with other CT measures in diabetic subjects. The results suggest that NIDDM and poor glucose control may carry a risk for accelerated brain atrophy in the elderly.

Aged↗
PubMedDate not supplied

Dopaminergic system and monoamine oxidase-B activity in Alzheimer's disease.

The possible involvement of dopaminergic neurons in dementia of Alzheimer type (AD/SDAT) was studied in autopsied brains from 20 patients with AD/SDAT. Dopamine (DA) concentrations were decreased significantly in the temporal cortex, hippocampal cortex and hippocampus in AD/SDAT patients. Levels of homovanillic acid (HVA) were not altered compared to controls. The HVA/DA ratio was significantly higher in the hippocampus of AD/SDAT patients, suggesting overactivity of the remaining DA neurons. Histological findings of substantia nigra suggesting coexistent pathology of Parkinson's disease (PD) found in 25% of cases were associated with lowered levels of DA in striatum and with reduced HVA in CSF. The activity of monoamine oxidase-B was significantly increased in the cortical areas and in the hippocampus, obviously reflecting the underlying cell loss and substantial gliosis in these areas of the brain. In general, DA neurons seemed to be only mildly involved in AD/SDAT. Coexistent PD pathology can explain the loss of DA in the striatum and the presence of clinical PD symptoms in some patients with AD/SDAT. Otherwise the clinical relevance of these dopaminergic alterations is unclear.

Aged↗
PubMedDate not supplied

Dyslipidemia, morbidity, and mortality in non-insulin-dependent diabetes mellitus. Lipoproteins and coronary heart disease in non-insulin-dependent diabetes mellitus.

Lipid and lipoprotein abnormalities in non-insulin-dependent diabetes mellitus (NIDDM) include particularly elevated levels of total and very-low-density lipoprotein (VLDL) triglycerides and reduced levels of high-density lipoprotein (HDL) cholesterol. Total and low-density lipoprotein (LDL) cholesterol levels are usually normal if glycemic control is adequate. The worsening of glycemic control deteriorates lipid and lipoprotein abnormalities and particularly total and LDL cholesterol levels are often elevated in patients with poor glycemic control. According to prospective population-based studies total cholesterol is a powerful risk factor for coronary heart disease (CHD) in NIDDM patients as in nondiabetic subjects. In contrast, high total triglycerides and low HDL cholesterol may be even stronger risk factors for CHD in NIDDM patients than in nondiabetic individuals, but more prospective studies are needed to substantiate this view. Compositional changes in LDL and VLDL particles may further increase the risk for CHD but epidemiologic data are missing to support this notion. Preliminary data from the Scandinavian Simvastatin Survival Study including 202 diabetic patients seem to indicate that diabetic patients benefit from simvastatin treatment equally to nondiabetic subjects.

Clinical Trials as Topic↗
PubMedDate not supplied

Astrogliosis and the ApoE genotype. an immunohistochemical study of postmortem human brain tissue.

Significantly increased glial fibrillary acidic protein (GFAP) expression was seen in postmortem brain tissue from demented patients with Alzheimer's disease (AD) (73 cases, 61 females/12 males, mean age 84 +/- 9 years) compared to controls (22 cases, 10 females/12 males, mean age 78 +/- 9 years). In demented patients, the GFAP expression, counts of AD lesions, senile/neuritic plaques (SP/NP) and neurofibrillary tangles (NFT) were higher in patients carrying the apolipoprotein E (ApoE) epsilon4 allele compared to those without the ApoE epsilon4 allele. The astrogliosis correlated significantly with the counts of NFT in demented patients both with and without the ApoE epsilon4 allele. Furthermore, the astrogliosis correlated significantly with the counts of SP/NP, but this correlation, however, was influenced by the ApoE epsilon4 allele, being significant only in those cases without the ApoE epsilon4 allele. Our results demonstrate that not only the extent of AD lesions and GFAP expression, but also the relationship between AD lesions and the GFAP expression is influenced by the ApoE epsilon4 allele.

Aged↗