Search

Objective: The objective was to study people's judgments, through the use of external indices, of their expected degree of inebriation and to characterize the cognitive processes involved in making these judgments., Method: The participants were 143 adults living in France. In accordance with N. H. Anderson's functional theory of cognition (1982, 1996), their primary task was to read 64 cards depicting drinking situations characterized by three parameters: number of glasses, type of drink, and temporal relation to eating; to associate with each situation a certain degree of personal intoxication; and to indicate this degree of expected intoxication on linear scale anchored by Not at all drunk and Extremely drunk., Results: Participants were able to judge the general direction and combination of effects. They indicated incorrectly, however, that incremental effects decrease at higher levels of consumption (4 or more glasses) and at higher concentrations of alcohol in a drink. On the other hand, they indicated correctly that eating food decreases the impact of drinking alcohol. Drinkers and nondrinkers used different rules for self-assessment from external indices. IMPICATIONS: The systematic errors in both drinkers' and nondrinkers' use of external clues could, unless corrected, result in their becoming more inebriated than intended.

Background: Most people are aware that smoking cigarettes increases the risk of ill health, in particular of lung cancer. The precise way in which they relate amount of exposure to smoke and level of health risk has not, however, been determined., Methods: A convenience sample of 155 French adolescents and adults ages 15 to 75 rated the risk of "smoker's cancer"--the popular term for lung cancer--in 24 scenarios depicting eight levels of daily cigarette consumption of three concentrations of nicotine. The data were analyzed according to functional measurement methodology to ascertain the forms of the relationship between exposure and perceived risk., Results: All subjects perceived that the risk of smoker's cancer increased as smoking increased. Yet at high levels of consumption, additional cigarettes were generally judged to result in decreasing increments of risk, regardless of the nicotine content of the cigarettes and the sex and smoking status of the participants. Adolescents, however, were more likely than adults to perceive a linear, rather than a negatively accelerated, relationship., Conclusions: The actual form of the relationship between the dose of cigarette smoke and risk of lung cancer is either linear or positively accelerated. Public health educators and physicians should be aware that, at least in France, many people, particularly adults, incorrectly perceive this relationship as negatively accelerated.

Medullary carcinoma of the thyroid (MCT) is an uncommon malignant neoplasm, which occurs sporadically and in three familial syndromes with a dominant autosomal transmission mode. We studied a family of 13 members in which four of them (two males and two females: sons, mother and niece) were involved with MCT. All of them underwent mode-B echography and colour-Doppler echography and pulsed colour Doppler, with measurement of carcinoembryonic antigen (CEA) and calcitonin, in an attempt to delineate a pattern useful to differentiate malignant from benign thyroid pathology. Colour Doppler signal was of little usefulness for histologic characterization in function of vascularization, although it was useful for delineating nodules in non-homogeneous glands.

Agmatine is an amine derived from the decarboxylation of arginine by arginine decarboxylase (ADC) and metabolized to putrescine by agmatinase. While prevalent in bacteria and plants, agmatine and its metabolic enzymes have been recently identified in mammalian tissues. In the present study we sought to determine: (a) whether macrophages (cell line RAW 264.7) express ADC and agmatinase, and (b) if the enzymes are regulated by lipopolysaccharide (LPS), and/or by the inhibitory cytokines transforming growth factor-beta (TGF-beta), interleukin-10 (IL-10) and interleukin-4 (IL-4). LPS induced a dose-dependent stimulation of agmatinase, while it decreased ADC, the effect in both cases being maximum at 20 h. As expected, LPS dose-dependently stimulated the inducible nitric oxide synthase activity (iNOS). A strong correlation was observed between the effects of LPS on the agmatine-related enzymes and iNOS. By contrast, exposure to IL-10 and TGF-beta caused a reduction in ADC and agmatinase, whereas IL-4 was ineffective on ADC, but reverted the LPS-induced increase of agmatinase. We conclude that the agmatine pathway may be an alternative metabolic route for arginine in macrophages, suggesting a regulatory role of agmatine during inflammation.

The alpha2A- and alpha2C-adrenoceptor subtypes were evaluated in postmortem brains from suicides with depression (n = 22), suicides with other diagnoses (n = 12), and controls (n = 26). Membrane assays with the antagonist [3H]RX821002 (2-[3H]methoxyidazoxan) suggested the presence of alpha2A-adrenoceptors in the frontal cortex and both alpha2C-adrenoceptors and alpha2A-adrenoceptors in the caudate. The proportions in caudate were similar in controls (alpha2A, 86%; alpha2C, 14%), depressed suicides (alpha2A, 91%; alpha2C, 9%), and suicides with other diagnoses (alpha2A, 88%; alpha2C, 12%). Autoradiography of [3H]RX821002 binding under alpha(2B/C)-adrenoceptor-masking conditions confirmed the similar densities of alpha2A-adrenoceptors in the cortex, hippocampus, and striatum from controls and suicides. In the frontal cortex of depressed suicides, competition of [3H]RX821002 binding by (-)-adrenaline revealed a greater proportion (61 +/- 9%) of alpha2A-adrenoceptors in the high-affinity conformation for agonists than in controls (39 +/- 5%). Simultaneous analysis with the agonists [3H]clonidine and [3H]UK14304 and the antagonist [3H]RX821002 in the same depressed suicides confirmed the enhanced alpha2A-adrenoceptor density when evaluated by agonist, but not by antagonist, radioligands. The results indicate that depression is associated with a selective increase in the high-affinity conformation of the brain alpha2A-adrenoceptors.

Agmatine (decarboxylated arginine), an endogenous ligand for imidazoline receptors, has been identified in brain where it is synthesized from arginine by arginine decarboxylase. Here we report a mechanism for the transport of agmatine into rat brain synaptosomes. The uptake of agmatine was energy- and temperature-dependent and saturable with a Km of 18.83 +/- 3.31 mM and a Vmax of 4.78 +/- 0.67 nmol/mg of protein/min. Treatment with ouabain (Na+,K+-ATPase inhibitor) or removal of extracellular Na+ did not attenuate the uptake rate. Agmatine transport was not inhibited by amino acids, polyamines, or monoamines, indicating that the uptake is not mediated by any amino acid, polyamine, or monoamine carriers. When we examined the effects of some ion-channel agents on agmatine uptake, only Ca2+-channel blockers inhibited the uptake, whereas a reduction in extracellular Ca2+ increased it. In addition, some imidazoline drugs, such as idazoxan and phentolamine, were strong noncompetitive inhibitors of agmatine uptake. Thus, a selective, Na+-independent uptake system for agmatine exists in brain and may be important in regulating the extracellular concentration of agmatine.

Introduction: The hepatic oxidative metabolism is essential for the biotransformation of a large number substances, among which are found many drugs which are commonly used in clinical practice. The nutritional status of individuals has been shown to be of influence on this function. Aging produces a deterioration of the hepatic oxidative metabolism, without the cause for this situation having been clarified. Also, aging modifies the body composition of the individuals. The objective of this study is to evaluate whether the modifications which arise in the nutritive status due to age, can alter the hepatic oxidative capacity., Material and Methods: 165 elderly people of both sexes were studied, with an average age of 82 years, and 24 young people, with an average age of 29 years. All participants were subjected to a clinical questionnaire, along with an evaluation of anthropometric, biochemical, and immunological nutritive parameters. The study of the oxidative metabolism was conducted by evaluating the kinetics of antipyrine., Results: The elderly people showed a decrease in the antipyrine clearance rate (Ap Cl) (P < 0.001), and a lengthening of their life-span (P < 0.05) with respect to the younger people. There was a significant correlation in the elderly people, between the Ap Cl and age, weight, size, the distribution volume, and the muscular area of the arm. A multiple regression analysis showed a predictive value which was independent for age, the AST, the lymphocytes, and size., Conclusion: Elderly people have a marked depression of the hepatic oxidative metabolism. The factors which participate in their nutritional situation, are of influence on this function. It is necessary to keep all the above in mind when it comes to prescribing drugs which require this type of biotransformation, in order to avoid adverse effects or drug interactions.

In the frontal cortex of suicide victims, the density of I2-imidazoline receptors labeled by [3H]idazoxan was lower (40%) than that in healthy subjects. In the same brains, the immunoreactivity of a 29/30 kDa imidazoline receptor protein was also found to be significantly decreased (19%) and it showed a positive correlation with the density of I2-imidazoline receptors. Also in the same brains, the density of alpha 2-adrenoceptor antagonist binding sites labeled by [3H]RX821002 (2-methoxy idazoxan) was found to be unchanged. The density of brain I2-imidazoline receptors, correlated with aging in control subjects but not in suicides. The density of brain MAO-B sites labeled by [3H]Ro 19-6327 (lazabemide) in suicides was no different to that in age-matched controls. As expected the density of brain MAO-B sites in suicides showed a positive correlation with age, but it did not correlate with the density of I2-imidazoline receptors in the same brains. The data indicate that the I2-imidazoline receptors labeled by [3H]idazoxan in the brain of suicides is related to a 29/30 kDa imidazoline receptor protein identified by immunoblot analysis. The data also indicate that the brain I2-imidazoline receptor cannot be identified with the MAO-B isoenzyme. The decreased density of I2-imidazoline receptors in the brain of suicide victims might play a role in the pathogenesis of major depression.

Agmatinase, the enzyme that hydrolyzes agmatine to form putrescine and urea in lower organisms, was found in rat brain. Agmatinase activity was maximal at pH 8-8.5 and had an apparent K(m) of 5.3 +/- 0.99 mM and a Vmax of 530 +/- 116 nmol/mg of protein/h. After subcellular fractionation, most of the enzyme activity was localized in the mitochondrial matrix (333 +/- 5 nmol/mg of protein/h), where it was enriched compared with the whole-brain homogenate (7.6-11.8 nmol/mg of protein/ h). Within the CNS, the highest activity was found in hypothalamus, a region rich in imidazoline receptors, and the lowest in striatum and cortex. It is interesting that other agmatine-related molecules such as arginine decarboxylase, which synthesizes agmatine, and I2 imidazoline receptors, for which agmatine is an endogenous ligand, are also located in mitochondria. The results show the existence of rat brain agmatinase, mainly located in mitochondria, indicating possible degradation of agmatine by hydrolysis at its sites of action.

Background: Imidazoline receptors are a newly discovered family of receptors, some of which, like alpha 2-adrenoceptors, have a presynaptic inhibitory effect on the release of norepinephrine. The aim of this study was to identify by immunodetection imidazoline receptor proteins in human platelets and the brain to assess their status in depression and suicide., Methods: Platelets were collected from 26 drug-free depressed patients and 26 controls. Specimens of frontal cortex (Brodmann area 9) were collected from 13 suicide victims and 11 controls. Levels of imidazoline receptor proteins were assessed by immunoblotting techniques. Solubilized imidazoline receptors were separated by gel electrophoresis, transferred to nitrocellulose membranes, labeled with a specific anti-imidazoline receptor antiserum, and quantitated by image analysis., Results: Platelet and brain membranes expressed similar 45-kd imidazoline receptor proteins, and their mean +/- SEM immunoreactivities were found to be increased in depressed patients (platelets, 40% +/- 5%) and suicide victims (brain, 51% +/- 14%). Platelets also expressed a 35-kd imidazoline receptor protein that was also found to be up-regulated in depressed patients (21% +/- 4%). In contrast, brain membranes did not express this 35-kd protein but revealed a 29/30-kd imidazoline receptor protein that was found to be down-regulated in suicide victims (19% +/- 3%). In a subset of depressed patients who underwent antidepressant treatment, a change in the immunoreactivity of the up-regulated 45-kd platelet imidazoline receptor protein (-35% +/- 5%), but not of the 35-kd protein, was observed., Conclusion: The results support a role for the newly discovered imidazoline receptors (mainly the 45-kd receptor expressed in the brain and platelets) in the pathogenesis of depression.

1. The densities of various imidazoline receptor proteins (with apparent molecular masses of approximately 29/30-45- and 66-kDa) were quantitated by immunoblotting in the rat cerebral cortex after various drug treatments. The modulation of these imidazoline receptor proteins was then compared with the changes in the density of non-adrenoceptor [3H]-idazoxan binding sites (I2-sites) induced by the same drug treatments. 2. Chronic treatment (7 days) with the I2-selective imidazol(in)e drugs idazoxan (10 mg kg-1), cirazoline (1 mg kg-1) and LSL 60101 (10 mg kg-1) differentially increased the immunoreactivity of imidazoline receptor proteins. The levels of the 29/30-kDa protein were increased by idazoxan and LSL 60101 (23%), the levels of the 45-kDa protein only by cirazoline (44%) and those of the 66-kDa protein only by idazoxan (50%). These drug treatments also increased the density of I2-sites (32-42%). 3. Chronic treatment (7 days) with efaroxan (10 mg kg-1), RX821002 (10 mg kg-1) and yohimbine (10 mg kg-1), which possess very low affinity for I2-imidazoline receptors, did not alter either the immunoreactivity of imidazoline receptor proteins or the density of I2-sites. 4. Chronic treatment (7 days) with the monoamine oxidase (MAO) inhibitors clorgyline (10 mg kg-1) and phenelzine (10 mg kg-1) decreased the immunoreactivity of the 29/30-kDa (17-24%), 45-kDa (19%) and 66-kDa (23-31%) imidazoline receptor proteins. The alkylating agent N-ethoxycarbonyl-2-ethoxy-1, 2-dihydroquinoline (1.6 mg kg-1, 6 h) also decreased the levels of the three imidazoline receptor proteins (20-47%). These drug treatments consistently decreased the density of I2-sites (31-57%). 5. Significant correlations were found when the mean percentage changes in immunoreactivity of imidazoline receptor proteins were related to the mean percentage changes in the density of I2-sites after the various drug treatments (r = 0.92 for the 29/30-kDa protein, r = 0.69 for the 45-kDa protein and r = 0.75 for the 66-kDa protein). 6. In the rat cerebral cortex the I2-imidazoline receptor labelled by [3H]-idazoxan is heterogeneous in nature and the related imidazoline receptor proteins (29/30-, 45- and 66-kDa) detected by immunoblotting contribute differentially to the modulation of I2-sites after drug treatment.

In the postmortem human brain (20 specimens of frontal cortex, Brodmann area 9) the abundance of immunoreactive protein kinase C (PKC-alpha beta) and the activity of PKC (calcium, phosphatidylserine, and phorbol ester-dependent enzymes) were determined to study the effect of aging (range 1 month to 89 years) on this regulatory enzyme. Also, the abundance of immunoreactive G protein subunits (G alpha i1/2, G alpha i3, G alpha o, G alpha s and G beta) were assessed in parallel to investigate possible relationships with PKC-alpha beta. The abundance of PKC-alpha beta was positively correlated with aging (r = 0.62, n = 20, P < 0.005). Moreover, PKC activity also showed a significant positive correlation with the age of the subject at death (r = 0.55, n = 14, P < 0.05). Because of the known in vitro modulatory role of PKC-alpha beta on G(i) proteins, the existence of an in vivo effect of brain PKC-alpha beta on various G proteins was assessed through correlation analyses. In the brain of the same subjects, there were significant negative correlations between the immunoreactivity of PKC-alpha beta and the immunoreactivities of G alpha i1/2 (r = -0.78, n = 13, P < 0.005) and G alpha i3 (r = -0.58, n = 15, P < 0.005). In the same brains, similar negative, although non-significant, correlations were found between the levels of PKC-alpha beta and those of G alpha o, G alpha s and G beta. The results demonstrate an up-regulation of brain PKC-alpha beta with aging and suggest the existence of a relevant in vivo modulatory role of this regulatory enzyme on inhibitory Gi proteins in the human brain during the process of aging.

The aim of this study was to quantitate imidazoline receptors in postmortem brains of heroin addicts who died of an opiate overdose. The density of I2-imidazoline receptors ([3H]idazoxan binding in the presence of adrenaline) and the immunoreactivity of the related 29/30 kDa imidazoline receptor protein were decreased (39% and 28%, respectively) in the frontal cortex. The density of brain I2-imidazoline receptors was also decreased in heroin-dependent rats (27%). This novel finding indicates that opiate addiction induces down-regulation of I2-imidazoline receptors in astrocytes, and presumably down-regulation of the functions associated with these receptors.

In the postmortem human brain (15 specimens of frontal cortex), the immunodetection and quantification of imidazoline receptor (IR) proteins (29/30 and 47 kDa) and the specific binding of [3H]idazoxan to I2-IR were determined in parallel to study the effect of aging (range 3-89 years) on these proteins and its possible association. The immunoreactivity of the 29/30 kDa IR protein, similar to the I2-IR, showed a significant positive correlation with the age of the subjects at death (r = 0.54; P = 0.04). Moreover, the levels of this IR protein also correlated significantly with the density of I2-IR in the brain of the same subjects (r = 0.67; P = 0.01). It is suggested that the I2-IR labeled by [3H]idazoxan in the human brain is related to the 29/30 kDa IR protein identified by immunoblot analysis.

The biochemical status of human brain protein kinase C (PKC)-alpha beta during opiate dependence was studied by means of immunoblotting techniques in postmortem brain of heroin addicts who had died by opiate overdose. In the frontal cortex, a marked decrease (53%, p < 0.05) in the immunoreactivity of PKC-alpha beta was found in heroin addicts compared with matched controls. The loss of PKC-alpha beta in the brain of human addicts paralleled that observed in the frontal cortex of rats after chronic treatment with morphine (10-100 mg/kg i.p. for 5 days) (PKC-alpha beta decreased by 34%, p < 0.05). Chronic treatment with naloxone (1 mg/kg i.p. every 12 h for 5 days) did not alter PKC-alpha beta immunoreactivity in the rat brain. However, in morphine-dependent rats, naloxone-precipitated withdrawal induced a rapid and strong behavioral reaction with a concomitant up-regulation of PKC-alpha beta immunoreactivity to control values. These results indicated that the decrease of brain PKC-alpha beta induced by heroin/morphine is a mu-opioid receptor-mediated effect. The chronic administration of opiates has been associated with a marked sensitization of the adenylyl cyclase/cyclic AMP system, although this phenomenon is not exclusive of the opioid system but the general cellular adaptation to chronic inhibition of adenylyl cyclase. In this context, chronic treatment of rats with other inhibitory agonists (e.g., clonidine, 1 mg/kg i.p. every 12 h for 14 days) acting through receptors (e.g., alpha 2-adrenoceptors) also coupled to adenylyl cyclase did not alter brain PKC-alpha beta immunoreactivity.(ABSTRACT TRUNCATED AT 250 WORDS)

Background: Antipyrine clearance (CLAP) constitutes a sensitive indicator of hepatic microsomal enzyme activity providing specific information on hepatic function. The purpose of this study was to evaluate the influence of hypocaloric peripheral parenteral nutrition on CLAP in patients receiving nutrition support after elective surgery., Methods: CLAP was measured in 15 patients before elective gastrointestinal surgery and 6 days after the surgery. Antipyrine (1 g) was administered orally, and CLAP was determined by the one-sample method. Subjects received a postoperative 786 kcal/d regimen providing 66 g of amino acid per day and 133 g of glucose per day for 5 days. Nutritional status was evaluated by anthropometric parameters. A control group of 15 patients received no postoperative hypocaloric peripheral parenteral nutrition but received conventional fluid therapy., Results: Mean CLAP was increased by 61% (0.66 +/- 0.06 mL/min.kg-1 body wt vs 0.41 +/- 0.05 mL/min.kg-1 body wt in the preoperative period; p < .001), and antipyrine half-life was reduced by 42% (10.9 +/- 1.0 hours vs 18.9 +/- 2.0 hours; p < .001) after 5 days of hypocaloric peripheral parenteral nutrition. No significant modification was shown among control patients in CLAP (0.54 +/- 0.07 mL/min.kg-1 body wt vs 0.46 +/- 0.05 mL/min.kg-1 body wt in the preoperative period) or in antipyrine half-life (14.0 +/- 1.4 hours vs 16.5 +/- 1.8 hours). No significant correlation was observed between CLAP changes and those for the nutritional status of the patients., Conclusions: The results of our study indicate that oxidative drug-metabolizing capacity is increased in surgical patients maintained on hypocaloric peripheral parenteral nutrition. Clinicians should be conscious of the potential of this effect for altering the efficacy or toxicity of many therapeutic agents.

Competition [3H]RX821002 ([3H]2-methoxyidazoxan) binding experiments with alpha 2-adrenoceptor subtype-specific antagonists--BRL 44408 (alpha 2A selectively), ARC 239 (alpha 2B selective), and others--were performed to delineate through rigorous computer modeling receptor subtypes in the postmortem human brain. In the hippocampus, hypothalamus, cerebellum, and brainstem the whole population of alpha 2-adrenoceptors appears to belong to the alpha 2A subtype (100%; Bmax = 34-90 fmol/mg of protein). In the frontal cortex, the predominant receptor was the alpha 2A subtype (87%; Bmax = 53 fmol/mg of protein), although a small population of the alpha 2B/C subtype (13%; Bmax = 8 fmol/mg of protein) was also detected. In the caudate nucleus, a mixed population of alpha 2A (64%; Bmax = 9 fmol/mg of protein) and alpha 2B/C (36%; Bmax = 5 fmol/mg of protein) subtypes was detected. In the cortex and caudate and in the presence of ARC 239 (to mask the alpha 2B/C-adrenoceptors), competition experiments with the agonist guanoxabenz clearly modeled the high- and low-affinity states of the alpha 2A subtype. In the presence of ARC 239 and the GTP analogue guanylyl-5'-imidodiphosphate together with NaCl and EDTA (to eliminate the high-affinity alpha 2A-adrenoceptor) guanoxabenz only recognized the low-affinity alpha 2A-adrenoceptor. The results indicate that in the human brain the predominant alpha 2-adrenoceptor is of the alpha 2A subtype and that this functionally relevant receptor subtypes is not heterogeneous in nature.

Objective: To directly evaluate the guanine nucleotide-binding (G) protein subunits alpha, beta, and gamma, which are involved in the signal transduction of opioid receptors, in the postmortem brains of heroin addicts who had died of an opiate overdose., Methods: Specimens of the frontal cortex (Brodmann's area 9) were collected from 11 heroin addicts and 10 control subjects without a history of drug abuse. The biochemical status of human brain G protein subunits during opiate dependence was studied by means of immunoblotting techniques. Solubilized G proteins were separated by gel electrophoresis, transferred to pyroxylin membranes (western blotting) labeled with specific antiserum samples, and quantitated by image analysis after enhanced chemoluminescence., Results: In the frontal cortex, relevant increases in the immunoreactivities of G alpha i 1/2 (19% +/- 4%, P < .005), G alpha o (29% +/- 7%, P < .005), and G alpha s (26% +/- 5%, P < .005) but not of G alpha i3 were found in heroin addicts compared with age- and sex-matched controls. Moreover, the amount of G protein beta-subunit immunoreactivity was also consistently increased (27% +/- 8%, P < .01) compared with controls in the same brain region. These G protein changes in the brains of human opiate addicts paralleled (with the exception of G alpha s) those obtained in the brains of morphine hydrochloride-dependent rats. The increase in G alpha s immunoreactivity that was observed in the rat brain only after the short-term morphine administration (24% +/- 3%, P < .005) suggests that the increase in G alpha s immunoreactivity in the brains of human addicts could be the cellular response to a deadly overdose of heroin., Conclusions: Alterations in the density of specific Gi and Go protein subunits that are coupled to mu-opioid and other opioid receptors may be of clinical relevance in opiate tolerance, dependence, and abstinence syndrome.

The biochemical status of human brain mu-opioid receptors and alpha 2-adrenoceptors during opiate dependence was studied by means of the binding of [3H] [D-Ala2, MePhe4, Gly-ol5] enkephalin (DAGO) and [3H]clonidine, respectively, in postmortem brains of heroin addicts who had died by opiate overdose or other causes. In the frontal cortex, thalamus and caudate of heroin addicts the density (Bmax) and affinity (KD) of mu-opioid receptors were similar to those in controls. In contrast, the density of alpha 2-adrenoceptors in heroin addicts was found to be significantly decreased in frontal cortex (Bmax 31% lower), hypothalamus (Bmax 40% lower) and caudate (Bmax 32% lower) without changes in KD values. When heroin addicts were divided into two subgroups according to the presence or absence of morphine in body fluids, only the group with positive screening for morphine showed relevant decreases in brain alpha 2-adrenoceptor density (Bmax 36-48% lower), whereas the decreases in receptor density observed in the subgroup with negative screening for morphine did not reach statistical significance. The results suggest that desensitization of brain alpha 2A-adrenceptors is a relevant adaptative receptor mechanism during opiate addiction in humans.

In the postmortem human brain (27 specimens of frontal cortex, Brodmann area 9), the specific binding of the antagonists [3H]RX 821002 (2-methoxyidazoxan) to alpha 2A-adrenoceptors and that of [3H]idazoxan to I2-imidazoline sites (a nonadrenoceptor mitochondrial site) were determined in parallel to study the effect of aging (range, 4-89 years) on both brain proteins. The density of alpha 2A-adrenoceptors and age were negatively correlated (r = -0.71; p < 0.001). In contrast, the density of I2-imidazoline sites was positively correlated with aging (r = 0.59; p < 0.005). The ratio of receptor densities (alpha 2A/I2) also showed a marked negative correlation with age (r = -0.76; p < 0.001). In an age-selected group (range, 10-89 years), the density of monoamine oxidase (MAO)-B sites labeled by [3H]Ro 19-6327 (lazabemide) also showed a positive correlation with age (r = 0.80; p < 0.005). In these subjects, the density of I2-imidazoline sites correlated well with the density of MAO-B sites (r = 0.70; p < 0.005). The ratio of the density of these sites (MAO-B/I2) did not correlate with the age of the subject at death (r = -0.15). In the human frontal cortex, idazoxan displayed very low affinity (Ki = 89 microM) against the binding of [3H]Ro 19-6327 to MAO-B, which discounted a direct interaction of [3H]idazoxan with the active center of the enzyme and indicated that the I2-imidazoline site cannot be identified with MAO-B.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of this work, has been focus an the study of an specific aspect of the memory. To verify (establish) the influence of the age in the mnesic efficiency of the auditory verbal memory in the presence of non numerical stimulus structured and non structured. After the study of the upper functions in 162 persons, 69 persons of both sexes, who didn't show any objectable sign of the cognitive deterioration were selected and that in the moment of the neuropsychologist exploration weren't diagnosed of any Kind of pathology. The selected persons were divided in two groups depending of the age. A first group of bess than 65 years persons, and a second group of people over years. We found significant differences in the total efficiency of the Audio Verbal King evidence, the same as in the efficiency of the Babcock History between the two groups that were studied, being the second group (elder one) which showed a warse efficiency in the total number of evoked words, the same as in the information unites remembered of History.

A case of Hodgkin's disease associated with long-standing Gaucher's disease is presented and compared with the only previously reported case. The two diseases coexisted in lymph nodes both above and below the diaphragm, liver, bone marrow, and pancreas. The question of a possible relationship of the two diseases is discussed.

In the present double-blind clinical trial an isoergolenyl derivative with periphal antiserotonin, central dopaminergic activity and alpha-increasing effect on the human EEG, lisuride hydrogen maleate, was tested against placebo in a six-month trial involving 240 patients. Lisuride in long-term administration significantly reduces the frequency of migraine attacks in comparison to placebo. Its advantages are good tolerance and minimal side-effects. It is therefore concluded that lisuride is a suitable and effective drug for the prevention of migraine.

Two premature female infants with a new variant of pulmonary hyaline membrane disease had both received assisted ventilation with high oxygen concentrations. Postmortem examination showed straw-yellow hyaline membranes lining the terminal bronchioles and alveoli. Pneumonocytes and macrophages also contained straw-yellow pigments in the cytoplasm. These yellow membranes and pigments in pneumonocytes and in macrophages stained positively for bile and negatively for iron. Both infants had severe intrahepatic cholestasis. Cholestasis and pulmonary changes due to oxygen toxicity are believed to be the main features leading to this curious entity.

A very rare case of cloacal exstrophy associated with other multiple congenital anomalies is presented.Other congenital anomalies included exomphalos; myelomeningocele; microcolon with blind end and rectal agenesis; absence of external genitalia, appendix, pubic arch with separation of rami, left kidney, and ureter; duplication of the uterus and vagina; lacunar defect of cranial bones; Arnold-Chiari malformations; and hydrocephalus.The literature on this subject is reviewed.