Cognitive sequelae of methanol poisoning involve executive dysfunction and memory impairment in cross-sectional and long-term perspective.

Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13 years), 3-8 months after methanol poisoning, and 57 control subjects (CS; age 49 ± 13 years) were administered a neuropsychological battery. Forty-six patients were followed in 2 years' perspective. Patients additionally underwent 1.5T magnetic resonance imaging (MRI). Three biochemical and toxicological metabolic markers and a questionnaire regarding alcohol abuse facilitated the classification of 24 patients with methanol poisoning without alcohol abuse (METHna) and 22 patients with methanol poisoning and alcohol abuse (METHa). All groups were compared to a control group of similar size, and matched for age, education, premorbid intelligence level, global cognitive performance, and level of depressive symptoms. Using hierarchical multiple regression we found significant differences between METH and CS, especially in executive and memory domains. METHa showed a similar pattern of cognitive impairment with generally more severe executive dysfunction. Moreover, all METH patients with extensive involvement on brain MRI (lesions in ≥2 anatomical regions) had a more severe cognitive impairment. From a longitudinal perspective, we did not find any changes in their cognitive functioning after 2 years' follow-up. Our findings suggest that methanol poisoning is associated with executive dysfunction and explicit memory impairment, supposedly due to basal ganglia dysfunction and disruption of frontostriatal circuitry proportional to the number of brain lesions, and that these changes are persistent after 2 years' follow-up.

The effect of chronic nicotine administration on bone mineral content and bone strength in normal and castrated male rats.

Tobacco, containing nicotine as the principal pharmacologically active chemical, has been identified as being a risk factor for the development of osteoporosis. Thirty-two male Wistar rats of two months of age were castrated or sham operated to evaluate the effects of long-term administration (four months) of nicotine in drinking water (9.0 mg/kg/day). The presence of cotinine in urine confirmed successful delivery of nicotine. The bones were tested mechanically by a three point bending test in a Mini Bionix (MTA) testing system. The bones from castrated rats were characterized by a reduction in bone density as well as ash, calcium and phosphate content. Castration significantly altered mechanical properties of bone (9%) and femoral cortical thickness. When intact rats were treated with a high dose of nicotine, nicotine had negative effect on tibial bone density as well as ash, calcium, phosphate content and significantly altered the mechanical properties of bone (12%) and femoral cortical thickness compared to intact animals. Nicotine itself does not exert any anti-androgenic effect and does not produce changes in the weight of seminal vesicles. Nicotine-induced bone loss is associated with high bone turnover in the male rats as expressed by increased TrACP and B-ALP. When castrated rats were treated with the high dose of nicotine the changes in bone density resulting from castration were not further potentiated. These results document the efficacy of nicotine at high doses to cause bone loss and loss of bone mechanical strength in intact rats. The results of the present study may be interpreted as supporting the hypothesis of nicotine as a risk factor for osteoporosis.

[Detection of ethanol using an enzyme method]. / Stanovení etanolu enzymatickou metodou.

In conjunction with the necessary modernization of the operation of toxicological laboratories the authors tested the dehydrogenase method for assessment of ethanol on an automatic analyzer ACA of DuPont Co. They revealed a satisfactory correlation of results as compared with gas chromatography (correlation coefficient c = 0.992, regression coefficient BO = 0.107) and an excellent correlation with Widmarks test (c = 0.994, BO = -0.001). The sensitivity of the enzyme method is 0.025 g/l and the accuracy is also satisfactory (variation coefficient for intraassay and extraassay does not exceed 3%). The method is not quite specific, high isopropanol concentrations interfere with assessment. This rapid automated method can suitable supplement the spectrum of statim toxicological analyses in clinical suspicion of ethanol intoxication or prove helpful in forensic medical practice as an alternative to Widmarks test.

Enzyme immunoassay to determine serum myoglobin in patients with acute myocardial infarction.

A method of "sandwich" enzyme immunoassay was developed for determination of human serum myoglobin with the use of myoglobin isolated from human myocardium and gammaglobulin fraction of a specific sheep antiserum labelled with horseradish peroxidase. The linear part of the calibration curve within the range of 0.08-2.2 nmol/l is suitable for accurate quantitative reading of myoglobin concentration. Intra- and interassay variation coefficients are 7% and 11.2%, respectively. A comparison of 100 serum samples assessed by means of commercially available RIA kit and by the given method revealed a correlation coefficient of 0.86.

[Differential diagnosis of elevated myoglobinemia]. / Diferenciální diagnostika zvýsené myoglobinemie.

The authors evaluate the value of examinations of myoglobinaemia as a biochemical indicator of some diseases. Clinically most significant is the transient rise of serum myoglobin levels in acute myocardial infarction. From the aspect of early diagnosis, investigation of the course of the disease and for evaluation of thrombolytic treatment the assessment of myoglobin is much more sensitive than hitherto used "cardiospecific enzymes". The authors mention other pathological conditions with damage of the cardiac tissue where elevated myoglobinaemia may be anticipated. In addition to cardiac affections the following conditions are associated with elevated serum myoglobin concentrations: a) conditions with increased myoglobin release from skeletal muscles, b) conditions with a reduced myoglobin excretion from the organism and markedly reduced glomerular filtration, c) diseases and conditions where both mentioned mechanisms participate in the rise of myoglobinaemia. The use of assessment of myoglobin concentrations for the differential diagnosis depends on the introduction of suitable locally produced kits for rapid and simple estimation.