New method to determine motor point and electrical activity of muscle (IEMG) during effort.
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Adult↗
Biomedical subjects
U Nousiainen
Publications and source records attributed to U Nousiainen.
Lipids and apolipoproteins A-I, B and C-II and different rapid weight loss programs (weight lifters, wrestlers, boxers and judokas).
Apolipoproteins A-I, B, C-II and lipids were studied before and after rapid weight loss schedules. The compared groups were all athletic. Apolipoproteins were determined by electroimmunoassay methods using apoproteins purified by chromatofocusing column method. Dextran T10 was shown to increase rocket height in ApoB assay. Over 1% Dextran concentrations gave poor response. The linearity during calibration was from 0.3 to 3.0 g ApoB/l. Baseline values of ApoA-I in wrestlers, weightlifters, boxers and judokas were slightly higher as compared to "normal" population; ApoB was clearly reduced (mean value of 690 mg/l). Weight-loss was significant in each experimental group; mean value of 4.1% in active exercise, sauna and diuretic groups together. Compared as the whole sportsmen group in passive weight loss (or sauna) and diuretic groups the most pronounced changes were seen to be elevated apoprotein concentrations, whereas weight-loss by active rapid exercise resulted no apoprotein changes, but instead an increment in HDL cholesterol and decrement in triglycerides, respectively. The present study was the first to evaluate baseline values of apoproteins A-I, B and C-II in first class athletes and also the possible changes in these and lipid values in rapid weight-loss practices.
Adolescent↗
Effects of phenobarbital and p,p'-DDT on carboxylesterase activity and hydrolysis of propanidid in rat liver.
Time-dependent responses of microsomal and cytosolic carboxylesterases (EC 3.1.1.1) to administration of phenobarbital or p,p'-DDT were studied in rat liver using p-nitrophenylacetate and propanidid as substrates. In vitro and in vivo studies indicate that the hepatic carboxylesterases are induced by phenobarbital and p,p'-DDT. The induced metabolism of propanidid does not appear to be due to the microsomal polysubstrate monooxygenase system of the liver.
Animals↗
Differential induction of various carboxylesterases by certain polycyclic aromatic hydrocarbons in the rat.
Hepatic and extrahepatic carboxylesterase (EC 3.1.1.1) activities were studied after the exposure of rats to polycyclic aromatic hydrocarbons. In dose- and time-dependent studies, the carcinogens benz[a]anthracene, benzo[a]pyrene and 3-methylcholanthrene moderately induced the hepatic cytosolic and kidney microsomal carboxylesterase activities, while the non-carcinogenic compounds anthracene, phenanthrene and chrysene had no effects on these enzyme activities. The hepatic microsomal and kidney cytosolic enzyme activities were not altered by the polycyclic aromatic hydrocarbons tested. Carboxylesterase activity in the postmitochondrial fraction of the intestinal mucosa decreased the serum enzyme activity slightly increased after the administration of the carcinogenic compounds. Although the in vitro hydrolysis of propanidid by hepatic cytosolic and kidney microsomal preparations was increased, the biological half-life of propanidid in vivo was not changed by 3-methylcholanthrene treatment.
Animals↗
High-performance liquid chromatography of propanidid in rat plasma.
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Animals↗
The effects of phenobarbital, bis-p-nitrophenyl phosphate and disulfiram on the hydrolysis of propanidid in Wistar rats.
The short-acting anesthetic propanidid was used in vivo as a model substrate in studies of phenobarbital-inducible carboxylesterases in Wistar rats. Phenobarbital shortened the duration of anesthesia produced by intravenous (25 mg/kg) or intraperitoneal (750 mg/kg) administration of propanidid which was in good agreement with the lowered plasma concentration and the shortened half-life of propanidid in phenobarbital-pretreated rats. The treatment of rats with bis-p-nitrophenyl phosphate or disulfiram with or without phenobarbital-pretreatment prolonged the sleeping time and the half-life of propanidid in plasma.
Animals↗
Serum lipids and hepatic microsomal enzymes with special reference to serum cholinesterase in Wistar rats.
Serum pseudocholinesterase in accordance with indicators revealing the lipid metabolism and liver function was studied in rats exposed to phenobarbital, bis-p-nitrophenylphosphate and disulfiram in vivo. Phenobarbital markedly induced the hepatic microsomal drug-metabolizing enzymes and tended to decrease the triglyceride content in serum. Serum lipids remained almost unaffected after the treatment of bis-p-nitrophenylphosphate. However, serum gamma-glutamyltransferase activity showed a marked decrease to this organophosphorus compound. Disulfiram activated the microsomal UDP-glucuronosyltransferase (p-nitrophenol) activity, and caused an enhancement of serum total cholesterol, which suggests that this drug might be atherogenic.
Animals↗
Differentiation of microsomal and cytosolic carboxylesterases in the rat liver by in vivo and in vitro inhibition.
We studied inhibition of rat tissue esterases by organophosphates and disulfiram, with special reference to hepatic microsomal and cytosolic carboxylesterases in vivo and in vitro. Hepatic microsomal carboxylesterase was strongly inhibited by disulfiram and bis-p-nitrophenyl-phosphate both in vivo and in vitro and by diisopropyl fluorophosphate in vitro, while cytosolic esterase was only slightly impaired. Pretreatment with phenobarbital did not affect the inhibition profiles of hepatic esterases in vitro. Based on these results, we conclude that hepatic cytosol of Wistar rats contains a soluble carboxylesterase that does not originate in the endoplasmic reticulum.
Animals↗
Differential effects of sauna-, diuretic-, and exercise-induced hypohydration.
The physiological effects on submaximal and maximal exercise of three methods commonly used by athletes for achieving rapid weight loss were determined by measuring cardiorespiratory variables in 62 nonendurance athletes. A mean weight loss of 4.1% was achieved by those who followed either a sauna (SAU), diuretic (DIU), or exercise (ACT) protocol, compared with the average weight loss of 1.2% in the control group. At maximal exercise O2 consumption, O2 pulse, blood lactate concentration, and work load decreased in SAU and DIU groups relative to the ACT group, whereas only a few differences were observed at the aerobic threshold. Weight loss achieved over a 48-h period was less detrimental to an athlete than was a more rapid (24-h) weight reduction achieved through sauna bathing or the use of diuretics. We conclude that not only the quantity of weight loss but also the method itself may limit physical performance.
Adult↗
Changes in serum lipids and lecithin: cholesterol acyltransferase enzyme during 1 week weight reduction of women on a low-calorie diet.
In 32 women of normal body weight who volunteered to participate in the study, the effect of rapid weight reduction by a low-calorie liquid diet on serum lipids and lecithin:cholesterol acyltransferase (LCAT) enzyme activity was studied. Women were on this 400 kJ/day diet for 7 days and fasting blood samples were drawn before and immediately after the diet. Serum cholesterol decreased from 5.7 +/- 1.0 to 5.2 +/- 1.1 mmol/l and high density lipoprotein cholesterol from 1.77 +/- 0.43 to 1.50 +/- 0.35 mmol/l. The serum LCAT activity decreased significantly during the weight reduction period. When serum LCAT activity was correlated to lipid parameters, a positive correlation was found with total cholesterol and triglyceride concentrations before weight reduction and also between changes in LCAT activity and total cholesterol concentration. The data suggest that serum LCAT activity might have a prominent role in the regulation of serum lipid levels.
Acyltransferases↗
End-plate spikes in electromyography are fusimotor unit potentials.
Spontaneous negative-positive potentials (NPPs) in electromyography were often activated by movement of the needle electrode or by tetanic stimulation. Coactivation of NPPs was sometimes observed in voluntary effort. Circulatory arrest or hyperventilation had no consistent effect. These facts and the differences of firing of NPPs from usual ectopic firing patterns indicate that NPPs are not driven by ectopic activity of motor axons. Instead, the firing of NPPs is similar to activity of muscle spindle afferents during fusimotor drive. We believe that NPPs are action potentials of intrafusal muscle fibers driven by gamma motor neurons.
Action Potentials↗
Induction of aldehyde dehydrogenase by polycyclic aromatic hydrocarbons in rats.
Short-term intragastric administration of selected polycyclic aromatic hydrocarbons (100 mg/kg daily for 4 days) to male Wistar rats resulted in marked changes in liver cytosolic aldehyde dehydrogenase activity. Non-carcinogenic anthracene, phenanthrene and chrysene produced a 2.5--3-fold increase in the activity assayed with propionaldehyde as substrate and NAD as coenzyme. Weakly carcinogenic 1,2-benzanthracene enhanced aldehyde dehydrogenase activity 9-fold and the potent carcinogens 3,4-benzpyrene and 3-methylcholanthrene 30-fold. With benzaldehyde as substrate and NADP as coenzyme the differences between the groups were even more pronounced. Somewhat similar but less manifest effects on aldehyde dehydrogenase activity were detected also in the liver microsomes and in the postmitochondrial fractions of the small intestinal mucosa. On the basis of their ability to induce aldehyde dehydrogenase activity the compounds could be divided into three groups. This classification was found to correlate well with the carcinogenic potency of the compounds. It appeared that the exposure to polycyclic aromatic hydrocarbons, especially the carcinogenic ones, was followed by synthesis of a new aldehyde dehydrogenase form. This new form was differentiated from the normally existing cytosolic aldehyde dehydrogenase by its ability to oxidize benzaldehyde in the presence of NADP.
Aldehyde Dehydrogenase↗
On the inducibility of cytosolic and microsomal carboxylesterase by phenobarbital in rat tissues.
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Animals↗
Enhancement of cytosolic carboxylesterase by phenobarbital in the rat.
Previously suggested identity of soluble hepatic carboxylesterase and cytosolic aldehyde dehydrogenase was studied in the liver of the rr and RR rat substrains after phenobarbital administration. Results showed over 30% increase of carboxylesterase activity in all animals treated with phenobarbital. The total aldehyde dehydrogenase activity was increased only in RR substrain. These animals had no similar enhancement in the activity of carboxylesterase. The results indicate that the two enzymes are not identical.
Aldehyde Oxidoreductases↗
Inducible aldehyde dehydrogenases in the hepatic cytosol of the rat.
Rats of the Wistar/Af/Han/Mol/(Han 67) strain have previously been shown to respond in a variable way to phenobarbital treatment, as far as the induction of aldehyde dehydrogenase activity is concerned (Marselos 1976). This biochemical property is genetically determined and concerns the high-Km aldehyde dehydrogenase of the hepatic cytosol. In this study, administration of phenobarbital (1 mg/mo of drinking water, for 1 week) produces a uniform induction of aldehyde dehydrogenase in all rats, when measured with micromolar substrate concentration. The inducible low-Km enzyme of the cytosol is not genetically determined like the high-Km enzyme, and shows a wide specificity for aliphatic as well as for aromatic aldehydes. Despite the inducibility of the cytosolic enzymes, no alterations are found in the mitochondrial aldehyde dehydrogenase activities after phenobarbital treatment. The oxidation of D-glucuronolactone takes place only in the cytosol, and seems to be dependent on the low-Km aldehyde dehydrogenase. This is consistent with NMR studies, which showed that a very minimal amount of D-glucuronolactone is in aldehyde form under the measurement conditions usually applied. Further, the oxidation of D-glucuronolactone is also enhanced by phenobarbital in all rats without a genetic predisposition, and its dose-response curve is very similar to that of the low-Km aldehyde dehydrogenase.
Aldehyde Oxidoreductases↗
Pre- and postoperative auditory event-related potentials in temporal lobe epilepsy.
We studied auditory event-related potentials (ERPs) in 11 surgically treated patients with intractable temporal lobe epilepsy (TLE) pre- and postoperatively. ERPs through sphenoidal electrodes (Sp1-T3, Sp2-T4) provided clinically relevant and correctly lateralizing electrophysiologic evidence of temporal lobe dysfunction in 9 of 11 patients, confirmed by EEGs, electrocorticograms, neuroradiologic, and neuropsychological results, and clinical follow-up. Lateralizing asymmetries were noted in P300 amplitude, but latencies were prolonged bilaterally. Sphenoidal ERPs might serve as a new functional indicator of temporal lobe dysfunction in patients evaluated for epilepsy surgery.
Adolescent↗
Vigabatrin (gamma-vinyl-GABA): neuropathologic evaluation in five patients.
We performed neuropathologic examination of cerebral cortex specimens from 4 patients who underwent epilepsy surgery and the brain of 1 patient who died suddenly. All had severe epilepsy and had received gamma-vinyl-GABA (GVG, vigabatrin) for 3-5.5 years. Neither the surgically resected temporal lobe specimens nor the frontal and temporal lobes autopsy specimens showed abnormal white matter vacuolation.
Adult↗
Postoperative EEG and electrocorticography: relation to clinical outcome in patients with temporal lobe surgery.
To evaluate the role of different EEG methods with respect to postoperative clinical follow-up, 32 non-lesionary epilepsy patients who had undergone temporal lobectomy were studied preoperatively and at 2-week, 3-month, and 1-year postoperative follow-up. Routine, sleep, and sphenoidal EEG recordings as well as intraoperative electrocorticography (ECoG) were made for all patients. At 1-year follow-up, the EEGs with sphenoidal electrodes and with sleep deprivation procedure provided important prognostic information; the appearance of seizures was associated with the presence of interictal epileptiform abnormalities in EEG. In the postresection ECoG, however, epileptiform abnormalities were not associated with clinical outcome or with postoperative epileptiform EEG at 1 year. Routine EEG reliably reflects clinical outcome after temporal lobectomy; with sphenoidal electrodes as well as with sleep deprivation procedure, the diagnostic yield can be further improved.
Adolescent↗