Autonomy and work in medicine

We discuss autonomy in medical work as resulting from two basic moments: as social work consuming and producing goods and services, reproducing the dominant mode of production and its ethical foundations; and as a service in which autonomy, limited as social work, expresses some attributes acquired by medical work (technical independence and self-regulation) as a result of the monopoly in the use of science to deal with individually perceived health-related needs. These moments are expressed in the doctor-patient relationship, which makes uncertainties surrounding that relationship more evident. From this understanding about medical work and its autonomous condition, we discuss some theoretical concepts related to the study of labor and/or services in contemporary society and which provide us with an epistemological basis for more adequate approaches to scientific research concerning that object.     

Time trends in death rates from homicides in the city of Sao Paulo, Brazil, 1979-1994

To study homicide trends by gender and age, 1979-1994, S?o Paulo, Brazil, cubic polynomials were used to determine the best model for adjusting to time trends in homicide mortality rates by age and gender in the city of S?o Paulo, Brazil, 1979-1994. The model best adjusted to each group was selected considering the regression coefficient (Beta) , R2 value, residual analysis, and model's simplicity. The results show linear growth for total rates and rates by gender due to behavior of rates in the 20-29 and 30-39 year age groups. The reciprocal model adjusted best to rates for the 40-49 and 50-59 year age groups, while rates for adolescents followed the multiplicative model. There was no significant relationship between homicide rates and time for the remaining groups (under 10 and over 59 years). Rates for males were considerably higher in all age groups. The remarkably steady growth in homicide rates among adolescents and young adults is consistent with trends observed in other urban areas in developing and developed countries and denotes deteriorating living conditions and increased poverty.     

Discriminating the ecotoxicity due to metals and to low pH in acid mine drainage

Several techniques have been developed to assess the ecotoxicity of contaminated watercourses. Most of these techniques involve chemical alterations of water samples, by diluting it or by adding chelating agents. These changes become particularly severe when assessing the toxicity of samples with very low pH and with high quantities of contaminants. Trying to overcome this problem, a novel toxicity test, specific for acid waters, was previously developed and field validated. The toxicity of acid samples is assessed using the survival time of Ceriodaphnia dubia. During this study, the novel test was applied to a field situation, where an aquatic system is seriously impacted with acid mine drainage. Its efficiency was tested and compared with two classical toxicity tests: the Microtox and the median lethal dilution with C. dubia. The survival time test was performed without adjusting pH and after adjusting pH to a fixed value (pH 2, 3, and 4). At pH 2 and 4 no acceptable results were obtained; at pH 3 it was possible to distinguish the toxicity due to pH from the toxicity due to other toxicants. The test conducted at local pH was able to discriminate toxicity sources only for highly contaminated samples. The toxicity evaluation of acid mine drainage samples was possible neither with the median lethal dilution test nor with Microtox.     

Novel bioassay based on acetylcholinesterase and lactate dehydrogenase activities to evaluate the toxicity of chemicals to soil isopods

This study developed a bioassay with the isopod Porcellio dilatatus based on the activity of the enzymes acetylcholinesterase (AChE) and lactate dehydrogenase (LDH). The in vivo effects of the insecticides parathion-ethyl and endosulfan-sulfate on AChE and LDH activities of P. dilatatus under laboratory conditions were investigated. The route of uptake of the pesticides was through the food (alder leaves). Isopods were exposed to a wide range of concentrations of parathion or endosulfan (0.1, 1, 10, 25, 50, 100, 250, and 500 microg/g of food) for 21 days. After this period, the activity of AChE and LDH was determined. Parathion induced significant depression of both AChE and LDH activities. Animals fed with endosulfan-contaminated food exhibited lower LDH activities than control animals, while AChE activity was similar in all treatments. The results of the present investigation suggest that the isopod. P. dilatatus is a suitable species for use in toxicity tests and indicate that the enzymes AChE and LDH could be used as effect criteria both in laboratory and in field studies with this species.     

Clonal karyotypic abnormalities in gynecomastia

Gynecomastia is a benign condition that frequently occurs in the male breast gland; however, the cytogenetic data on this entity are very limited. To our knowledge, three cases have been reported in the literature, and the only one with an abnormal karyotype had a concomitant breast carcinoma. In this study we report clonal chromosomal alterations in a gynecomastia sample without any signs of adjacent malignant tissue. The nonrandom abnormalities observed were a deletion of 12p, monosomies of chromosomes 9, 17, 19, and 20, and the presence of a marker chromosome. Most of these alterations have been previously described in the literature in other breast lesions, including benign and malignant (male and female) tumors, indicating their recurrence and nonrandomness in abnormal processes of the mammary gland.     

Facilitation by arachidonic acid of acetylcholine release from the rat hippocampus

We investigated the effect of arachidonic acid (AA) on the release of [3H]acetylcholine ([3H]ACh) from the rat hippocampus. AA (3-30 microM) increased the basal tritium outflow and the field-electrically evoked release of [3H]ACh from hippocampal slices in a concentration-dependent manner. AA (30 microM) produced a 69+/-7% facilitation of the evoked and a 36+/-3% facilitation of basal tritium outflow. The effect of AA (30 microM) on the evoked tritium release was prevented by bovine serum albumin (BSA, 1%), which quenches AA, and was unaffected by the cyclooxygenase inhibitor, indomethacin (100 microM), and the lipooxygenase inhibitor, nordihydroguaiaretic acid (50 microM). Phospholipase A2 (PLA2, 2 U/ml), an enzyme that releases AA from the sn-2 position of phospholipids, mimicked the facilitatory effect of AA on the evoked tritium release (86+/-14% facilitation), an effect prevented by BSA (1%). The PLA2 activator, melittin (1 microM), enhanced the evoked tritium release by 98+/-11%, an effect prevented by the PLA2 inhibitor, arachidonyl trifluromethylketone (AACOCF3, 20 microM), and by BSA (1%). AA (30 microM), but not arachidic acid (30 microM), also facilitated (72+/-9%) the veratridine (10 microM)-evoked [3H]ACh release from superfused hippocampal synaptosomes, whereas PLA2 (2 U/ml) and melittin (1 microM) caused a lower facilitation (46+/-1% and 38+/-5%, respectively). The present results show that both exogenously added and endogenously produced AA increase the evoked release of [3H]ACh from rat hippocampal nerve terminals. Since muscarinic activation triggers AA production and we now observed that AA enhances ACh release, it is proposed that AA may act as a facilitatory retrograde messenger in hippocampal cholinergic muscarinic transmission as it has been proposed to act in glutamatergic transmission.     

Tachykinin NK(3)receptor involvement in anxiety

This study investigates the effects of intracerebroventricular injection of selective agonists and antagonists of tachykinin NK(3)receptor on performance of mice in the elevated plus-maze test. Mice were treated with either vehicle or 1, 10, 100 or 500 pmol of neurokinin B or senktide ([succinil-Asp(6), MePhe(8)]substance P(6-11), a natural and synthetic selective NK(3)receptor agonists, respectively. Other mice received similar doses of [Trp(7)beta-Ala(8)]NKA(4-10)or SR 142801 ((S)-N-(1-(3-(1-benzoyl-3-(3, 4-dichlorophenyl)-piperidin-3-yl)propyl)-4-phenyl-piperidin- 4-yl)-N-m ethylacetamide) tachykinin NK(3)receptor selective peptide and non-peptide antagonists, respectively. Senktide significantly increased the frequency of entries and the time spent in the open arms, which is compatible with an anxiolytic action. Neurokinin B treatment did not alter the plus-maze parameters in a significant way. Conversely, the NK(3)peptide antagonist [Trp(7)beta-Ala(8)]NKA(4-10), but not SR142801 non-peptide antagonist, showed a reverse effect, i.e. an anxiogenic profile of action, reducing the frequency and the time spent in the open arms. Co-injection of either senktide plus [Trp(7)beta-Ala(8)]NKA((4-10)), or senktide plus SR 142801, blocked the effects promoted by senktide, indicating that centrally-administered NK(3)receptor agonists and antagonists can modulate experimental anxiety.     

Adenosine modulates synaptic plasticity in hippocampal slices from aged rats

Adenosine is known to modulate synaptic plasticity in the hippocampus of young animals through activation of adenosine A1 receptors. The objective of the present study is to investigate whether the modulatory role of adenosine on phenomena of synaptic plasticity is maintained or modified in the hippocampus of aged animals. We compared the effects of the selective adenosine A1 receptor antagonist, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 50 nM), on paired-pulse facilitation (PPF), long-term depression (LTD), long-term potentiation (LTP) and depotentiation elicited in hippocampal slices taken from young adult (5-6 weeks) and old (2 years old) male Wistar rats. DPCPX attenuated PPF both in young (1.64 +/- 0.05 vs. 1.76 +/- 0.05%, n = 6) and in old rats (1.33 +/- 0.05 vs. 1.55 +/- 0.1%, n = 6). LTD was only observed in the presence of DPCPX in both young (21.3 +/- 0.6%, n = 4) and old rats (14.4 +/- 0.9%, n = 6). LTP induced by high-frequency stimulation (HFS) was not significantly different in young and old animals, in the presence or in the absence of DPCPX. A larger depotentiation was observed in the presence of DPCPX in young rats (27.6 +/- 4.4% vs. 16.8 +/- 4.7%, n = 7) as well as in old rats (41.3 +/- 5.1% vs. 16.1 +/- 2.7%, n = 6). LTP induced by theta-burst stimulation was observed only in the presence of DPCPX (53.9 +/- 4.9%, n = 5) in young rats, but could be obtained either in the control solution (81.8 +/- 17.9%, n = 7) or in the presence of DPCPX (98.5 +/- 24.2%, n = 7) in old rats. The modulatory role of endogenous adenosine on synaptic plasticity is generally maintained in aged animals. Drugs interfering with adenosine A1 receptor effects could then be used in old animals to modify synaptic plasticity with relevant behavioural consequences.     

Slow sharp waves.

Slow sharp waves (SSHW) are of longer duration (around 200 msec and longer) than typical sharp wave discharges (70 to 200 msec). This pattern is not merely of academic interest, as the electroclinical correlation showed that SSHW were found in 23 patients, mostly above age 50 years, with serious illnesses of various etiologies. Epileptic seizures occurred in a minority of the cases. The electrophysiological basis remains unclear and there is no answer to the question, "what causes the relatively long duration of these discharges?"