There is growing evidence that acute changes in fundamental mechanisms of impulse control contribute to the transition from social drinking to abusive drinking. One component of impulsivity concerns the ability to inhibit maladaptive behaviors (i.e., inhibitory control). Inhibitory mechanisms are reliably shown to be sensitive to the impairing effects of alcohol, and studies have begun to show that this impairment fails to recover at the same speed as other aspects of behavior. However, the degree to which inhibitory control develops tolerance to alcohol has only been examined under limited conditions. This dissertation consists of three studies examining contexts in which tolerance has been observed for a host of prototypic behaviors, and will compare the degree to which it fails to develop for inhibitory control. Study 1 examined the rate of recovery for inhibitory control compared with other behaviors as blood alcohol concentrations (BACs) declined to zero following a dose of alcohol in 24 social drinkers. Results revealed prolonged alcohol impairment of inhibitory control along the BAC curve, even as BACs approached zero. By contrast, behaviors including reaction time and motor coordination began to show recovery markedly faster, as BACs were still significantly elevated. Study 2 examined the degree to which recent drinking patterns predict acute alcohol impairment from alcohol in a group of 52 drinkers. Recent, heavy consumption predicted less impairment of motor coordination, but bore no relationship to the magnitude of impairment of inhibitory control. Study 3 examined whether increasing the stimulus strength of environmental cues signaling the need to inhibit behavior could reduce alcohol impairment of inhibitory control in 56 participants. Results showed that increasing stimuli strength reduced alcohol impairment of behavioral activation, but actually increased inhibitory failures. Taken together, the findings contribute to the growing body of evidence suggesting that inhibitory control is especially vulnerable to the impairing effects of alcohol compared with other behaviors. Indeed, these studies systematically assessed the pharmacokinetic and environmental factors that contribute to tolerance, indicating that inhibition is disrupted in circumstances under which response activation is unimpaired. The findings have important implications for understanding the behaviorally-disruptive effects of alcohol.

This article presents a study conducted on data containing drug concentrations. The data was obtained from femoral venous blood samples collected at medico legal autopsies in Sweden. Cases positive for antidepressant drugs were scrutinized and divided in to two groups for 15 antidepressant drugs: B‑cases, where the cause of death was intoxication with more than one drug detected in the blood sample. C‑cases, where the cause of death was NOT intoxication and at least one drug (the antidepressant) was detected in the blood sample. This data was then processed to find frequencies of concomitant drugs taken together with the antidepressant drugs. Frequencies of the most common concomitant drugs were then compared between B-cases and C-cases for each antidepressant drug. This revealed that the drugs dextropropoxyphene, ethanol, codeine, flunitrazepam, paracetamol, propiomazine and alimemazine were signifcantly more common as concomitant drugs in B-cases (intoxications) than in C‑cases (non‑intoxications). With regards to unknown interactions the most interesting combinations were: Propiomazine with mirtazapine, venlafaxine, citalopram or fluoxetine; Paracetamol with paroxetine; Flunitrazepam with mirtazapine, venlafaxine or citalopram; Codeine with mirtazapine or sertraline. These combinations should be further investigated.

Background: Victims of sexual assault have been reported to blame themselves for the incident. They see themselves as having somehow contributed to the situation. Self-blame associated with a sexual assault is argued to be socially constructed, influenced by culture’s perception of sexual crimes. A specific behaviour that appears to contribute to victim’s self-blame is alcohol use during the sexual assault incident. Approximately half of sexual assaults are associated with alcohol consumption by one or both parties. Victims who consume alcohol during the incident are more likely to blame themselves for the event. Self-blame has been linked to a decreased likelihood of reporting a sexual assault to authorities, as victims predict that others will disapprove their behaviour and blame them for their victimization. Limited research has been conducted on attribution of blame to the female victims who have been under the influence of alcohol during the sexual assault incident. Objective: To examine the association between a female’s level of intoxication and the level of blame attributed to her, and how this is modified by initiation and severity of the event, in a hypothetical date-rape scenario. Methods: Secondary data analyses of 1004 quantitative telephone surveys completed in Sweden by randomly selected young adults aged 16-24. Date-rape vignettes were used and male’s and female’s levels of intoxication, severity of the outcome and the person initiating the sexual contact (perpetrator or victim) were manipulated. The depended variable was the amount of blame assigned to the female in the hypothetical date-rape scenario. The attribution of blame to the female was analysed using factorial ANOVA in SAS. Results: For female respondents, the level of blame attributed to the female in the hypothetical date-rape scenario depended on a three-way interaction between the inebriation level, initiation, and severity, controlling for female respondents’ living situation in the last 12 months, their frequency of drinking five or more drinks in the past 12 months, and their expectancy that ‘alcohol makes people more sexual’. For male respondents, however, the level of blame attributed only depended on the severity of the situation, controlling for male respondents’ mean number of standard drinks to feel the effects of alcohol and their attitude that ‘alcohol lessons control’. Conclusion: The inebriation level of the female in the date-rape scenario has been illustrated to impact the amount of blame attributed to her, by female respondents. This has implications for reporting rates of sexual crimes, and thus should be addressed by future policies and programs.

Mémoire (M.Ress.Renouv.)-- Université du Québec à Chicoutimi, 1993. / Document électronique également accessible en format PDF. CaQCU

Thesis--Helsinki. / Errata slip inserted. Includes bibliographical references (p. 152-164).

Thesis--Helsinki. / Errata slip inserted. Bibliography: p. 152-164.

Submitted by Jos? Henrique Henrique (jose.neves@ufvjm.edu.br) on 2017-01-04T17:34:19Z No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) marcio_marques_silva.pdf: 2786122 bytes, checksum: 4da1fad39fb206cdf4baf5459f0e0cb3 (MD5) / Approved for entry into archive by Rodrigo Martins Cruz (rodrigo.cruz@ufvjm.edu.br) on 2017-01-06T11:52:58Z (GMT) No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) marcio_marques_silva.pdf: 2786122 bytes, checksum: 4da1fad39fb206cdf4baf5459f0e0cb3 (MD5) / Made available in DSpace on 2017-01-06T11:52:58Z (GMT). No. of bitstreams: 2 license_rdf: 0 bytes, checksum: d41d8cd98f00b204e9800998ecf8427e (MD5) marcio_marques_silva.pdf: 2786122 bytes, checksum: 4da1fad39fb206cdf4baf5459f0e0cb3 (MD5) Previous issue date: 2016 / Coordena??o de Aperfei?oamento do Pessoal de N?vel Superior (CAPES) / O clomazone ? um herbicida inibidor da s?ntese de carotenoides. Esse herbicida ? facilmente solubilizado e volatilizado e por consequ?ncia, pode causar danos ao ambiente. Em vista do problema, objetivou-se com esta pesquisa: avaliar a sensibilidade de esp?cies forrageiras e daninhas a res?duos atmosf?ricos do clomazone e determinar a campo o efeito do res?duo atmosf?rico do clomazone sobre a fisiologia de plantas forrageiras e daninhas. Foram realizados dois experimentos. O primeiro foi conduzido em c?maras experimentais de 500 dm? em ambiente monitorado, delineado inteiramente casualizado com 5 repeti??es. Os tratamentos foram arranjados em esquema fatorial 6x5, sendo, seis esp?cies vegetais: triticale, milho, sorgo, braquiar?o, beldroega e campim braquiaria e o segundo cinco doses de clomazone 0, 90, 180, 270 e 360 g ha-1 (equivalentes ?s concentra??es atmosf?ricas de 0,0; 0,05; 0,10; 0,15 e 0,20 mg L-1, considerado o volume). As esp?cies ficaram expostas ao herbicida no interior das c?maras por per?odo de 96 horas em atmosfera controlada. Ap?s esse intervalo, as c?maras foram abertas, procedendo-se ? primeira avalia??o, repetida aos 7 e 14 dias ap?s a abertura. Avaliou-se a intoxica??o e o teor de clorofila. Com exce??o do milho, todas as esp?cies testadas mostraram-se sens?veis ?s concentra??es residuais de clomazone na atmosfera, podendo ser utilizadas no monitoramento da qualidade do ar. O segundo experimento foi conduzido a campo. Delineado em blocos causalizados com quatro repeti??es, em esquema fatorial 6x4, sendo seis esp?cies vegetais [quatro plantas forrageiras: lab lab, sorgo, braqui?r?o e java, e duas plantas daninhas: beldroega e sida] e quatro solu??es de aplica??o do clomazone (0, 360, 720 e 1.080 g ha-1, equivalentes a 0; 0,05; 0,10 e 0,20 mg L-1, considerado o volume). As plantas forrageiras e daninhas ficaram expostas ao clomazone, em tuneis cobertos por filme de polietileno de baixa densidade (150 ?m) de volume de 12m?, por per?odo de 72 horas. Ap?s esse tempo, os t?neis foram abertos, procedendo-se ?s seguintes avalia??es: intoxica??o das plantas, fluoresc?ncia inicial, fluoresc?ncia m?xima, a raz?o entre a fluoresc?ncia vari?vel e fluoresc?ncia m?xima, quenching fotoqu?mico e quenching n?o-fotoqu?mico, taxa de transporte de el?trons e do teor de clorofila. Mesmo em concentra??es que n?o promovem efeito visual, o clomazone ? capaz de causar danos significativos na atividade fotossint?tica das esp?cies. As vari?veis fisiol?gicas, clorofila total, rendimento qu?ntico m?ximo do PSII e fluoresc?ncia inicial da clorofila podem ser utilizadas de forma eficiente no monitoramento de res?duos do clomazone na atmosfera. / Disserta??o (Mestrado) ? Programa de P?s-Gradua??o em Produ??o Vegetal, Universidade Federal dos Vales do Jequitinhonha e Mucuri, 2016. / The herbicide Clomazone is an inhibitor of carotenoids synthesis. This herbicide is easily solubilized and volatilized, and by consequence, can cause damage to environment. Due to this problem, the objective of this study was evalue the sensibility of forage and weeds species to atmospheric wastes of Clomazone and to determinate in field the effect of atmosferic waste of Clomazone in phisiology of forage and weeds plants. Two experiments were performed. The first was conducted in 500dm? experimental chambers in a monitored environment, completely randomized design design with five repetitions. The treatments was arranged in 6x5factorial scheme, being six vegetable species: triticale, corn, sorghum, braquiar?o, beldroega e capim braquiara and the second five doses of Clomazone 0, 90, 180, 270 e 360 g ha-1 (equivalent to atmospheric concentrations of 0,0; 0,05; 0,10; 0,15 e 0,20 mg L-1, volume considered). The species were exposed to the herbicide inside the chambers for 96 hours in controled atmosphere. After this interval, the chambers were open, proceeding the first evaluation, repeated at 7 and 14 days after the opening. Was rated the intoxication and the chlorophyll contente. Excepting the corn, all tested species proved to be sensitive to Clomazone residual concentration in atmosphere, and can be used in ais quality monitoring. The second experiment was conducted in field. An experiment was conducted in a randomized block design with four repetitions, in 6x4 factorial scheme, being six vegetable species [ four forage plants :lab lab, sorghum, braquiar?o and java, and two weed plants: beldroega and sida] and four Clomazone application solutions (0, 360, 720 e 1.080 g ha-1, equivalentes a 0; 0,05; 0,10 e 0,20 mg L-1, volume considered). The forage and weeds plants were exposed to Clomazone, in tunnels covered by polyethylene film of low density (150 ?m), volume of 12m?, for 72 hours. After this time, the tunnels were open, proceeding this following evaluations: plants intoxication, initial fluorescence, maximum fluorescence, ratio of the variable fluorescence and maximum fluorescence, photochemical quenching and non-photochemical quenching, el?ctron transport rate and chlorophyll contente. Even in concentrations that don?t promote visual effect, the Clomazone is able to cause significative damage in photosynthetic activity of species. The phisiologic variables, total chlorophyll, PSII maximum quantum yield and chlorophill initial fluorescence can be used efficiently in monitoring of Clomazone wastes in atmosphere.

1 The crime of habitual drunkenness under s. 360 of the Criminal C. Abstract The aim of this diploma thesis is to analyze complexly the problems associated with the legal regulation of the crime of drunkenness. The crime of habitual drunkenness or otherwise called the "Rauschdelikt" is an illustrative option of how to deal with the issue of an insane people, which act unlawfully and how to punish them. The person which commits an unlawful act in a state of insanity, committed an act of otherwise criminal, quasi-delict. Where the perpetrator has caused a state of insanity by consuming or applying an addictive substance. The above-mentioned concept of "Rauschdelikt" appears to be the best option, for the sake of consistency with the fundamental principles and principles of criminal law, the nullum crimen sine culpa principle. The thesis is organized in individual chapters, which are gradually dealing with the historical development, and this crime does not present in modern criminal law no novelty; on the contrary, the institute of drunkenness has deep historical roots. The following chapters analyzes some individual basic terms that are necessary for the definition of a crime of habitual drunkenness and include and clarify the legal institutes that are close to and closely related to this crime, such as the...

Made available in DSpace on 2014-06-11T19:23:47Z (GMT). No. of bitstreams: 0 Previous issue date: 2006Bitstream added on 2014-06-13T18:48:26Z : No. of bitstreams: 1 camplesi_ac_me_botfmvz.pdf: 654743 bytes, checksum: 9569fad0ddea3a3238a78ce94669d913 (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Fundação para o Desenvolvimento da UNESP (FUNDUNESP) / O presente trabalho teve por objetivo avaliar os aspectos clínico, laboratorial, eletrocardiográfico de cães intoxicados por veneno de sapo, além de verificar a resposta ao tratamento com propranolol. Para tanto, foram utilizados 20 cães sem raça definida, machos e fêmeas, sadios, divididos em 2 grupos: controle (n=5) e intoxicados com veneno de sapo (n=15). Os cães foram submetidos à indução anestésica com tiopental sódico IV e mantidos em anestesia volátil com isoflurano a 3% durante o período de avaliação e registro de dados (duas horas e meia). Neste período, os animais do grupo controle receberam somente placebo (solução fisiológica) e os do grupo Intoxicado receberam uma alíquota do veneno de sapo por sonda orogástrica. Os animais que apresentaram taquicardia ventricular foram tratados com propranolol a 0,5 mg/kg IV. Durante a avaliação foram observadas as alterações dos sinais clínicos, tais como: freqüência e ritmo cardíacos, sialorréia, irritação da mucosa oral, evacuação e micção, alterações respiratórias, coloração das mucosas, temperatura corpórea e freqüência de pulso. Também foi mensurada a pressão arterial (sistólica, diastólica e média) e colhido material para dosagem de marcadores cardíacos (CK-MB e TnIc), além de dosagem de eletrólitos plasmáticos (Na, K e Ca iônico) e os animais foram monitorados com eletrocardiógrafo para verificação de arritmias. Os resultados mostraram que a intoxicação por bufotoxina causa alterações cardiovasculares, como hipertensão e arritmias ventriculares (VPCs e TV); alterações neurológicas com sinais variáveis; alterações gastrointestinais com vômito, sialorréia, hiperemia da mucosa e diarréia. Além disso, os animais intoxicados apresentaram elevação de CK-MB e TnIc, mostrando lesão miocárdica aguda... / The purpose of this study was to evaluate the clinical, laboratorial and eletrocardiographic aspects of the dogs intoxicated with toad venom, besides to check the answer to therapeutic with the use of propranolol. For this, were used 20 dogs without definitive breed, males and females, healthy, divided in two groups: Control (n=5) and Intoxicated with toad venom (n=15). These dogs were submitted to anesthesic induction with sodic thiopental IV and maintained in volatile anaesthesia with isoflurane 3% during the period of evaluation and value records (two and half hours). In this period, the Control group received only phisiologic solution and the Intoxicated group animals received a fraction of the toad venom through oro-gastric catheter. The animals that showed ventricular taquicardiac were treated with 0,5 mg/Kg Iv of propranolol. During the evaluation, was observed the present or not of these clinical signs: cardiac frequence and rhythm, profuse salivation, oral mucoses irritation, evacuation, urine, respiratory changes, color mucous, body temperature and pulse frequency. Also was mensured the arterial pressure (systolic, diastolic and medium) and was collected material by dosing cardiac markers (CK-MB and TnIc), besides dosing of eletrolyte plasmatics (Na, K and Ca ionic) and these animals were monitored with eletrocardiographic by cheking arrhythmias. The results showed that the intoxication by bufotoxin causes cardiovasculars alterations as hypertension and ventriculars arrhythmias (VPCs e TV), neurologics alterations with signs variables, digestive tract alterations as vomits, profuse salivation, hyperemic mucous membranes and diarrhoea. Besides, the intoxicated animals showed elevation of CK-MB and TnIc, showing sharp lesion of miocardic. Propranolol, in the dose utilized showed to be a medicine enough sufficient by treatment of ventryculars arrhythmias affronted by toad venom... (Complete abstract click eletronic address below)

Made available in DSpace on 2014-06-11T19:24:00Z (GMT). No. of bitstreams: 0 Previous issue date: 2004Bitstream added on 2014-06-13T19:51:03Z : No. of bitstreams: 1 andrade_sf_dr_botfmvz.pdf: 2228707 bytes, checksum: 4915d934794c6f04008560ac6b01322e (MD5) / Este trabalho teve por objetivo estudar a intoxicação experimental por amitraz em gatos e comparar a eficácia do tratamento entre dois antagonistas a2-adrenérgicos, ioimbina e atipamezole. Para tanto, foram avaliados os efeitos clínicos e toxicológicos do amitraz por via intravenosa (IV) em gatos, incluindo a medida de pressão arterial sistólica, eletrocardiograma, níveis séricos de glicose, insulina e cortisol, eritrograma, leucograma, além da avaliação das funções renal e hepática. Foram utilizados 32 gatos, divididos aleatoriamente em 4 grupos iguais (n=8), sendo que ao grupo C (controle) não foi administrado nenhum fármaco, porém realizaram-se todas as aferições e exames nos mesmos intervalos de tempos, dos grupos intoxicados. Aos do grupo A foi administrado amitraz na dose 1 mg/kg, IV, a 1,5%; aos do grupo AI amitraz nas mesmas dose e concentração do grupo A e 60 minutos após, ioimbina na dose 0,1 mg/kg, IV, a 2 mg/mL; e aos do grupo AA, amitraz nas mesmas dose e concentração do grupo A e 60 minutos após, atipamezole na dose de 0,2 mg/kg, IV, a 5 mg/mL. Foram aferidos os seguintes parâmetros nos intervalos de tempo 0, 30, 60,120, 180, 240 e 360 min após a administração do amitraz: temperatura (T), freqüência respiratória (FR), freqüência cardíaca (FC), pressão arterial sistólica (PAS), eletrocardiograma (ECG), diâmetro pupilar (DP), grau de sedação (GS) e tempo médio de recuperação da sedação (TMRS) considerado como o tempo gasto, em minutos, pelo animal para se levantar após a administração do amitraz e após a administração do antagonista a2- adrenérgico, ioimbina ou atipamezole. Foram coletadas amostras de sangue por venopuncão da jugular ou cefálica 24 horas antes e depois da intoxicação para realização de eritrograma, leucograma, uréia, creatinina, alanina aminotransferase... / This work studied the experimental intoxication for amitraz in cats and compared the effectiveness of the treatment between two a2-adrenergics antagonists, yohimbine and atipamezole. For so much, they were appraised the clinical and toxicological effects of the amitraz by intravenous route (IV), including the measure of systolic arterial pressure, electrocardiogram, serum glucose, insulin and cortisol levels, red and white blood cell counts, besides the evaluation of the renal and hepatic functions. Thirty two cats were used, aleatory divided in 4 groups (n=8). The group C (control) wasn't receive any drug, however all the exams (physical and laboratorial) were made respecting the same intervals used for the intoxicated groups. Amitraz was administered at the dose 1 mg/kg (1,5%), IV, on group A; on group AI, amitraz in the same dose and concentration of the group A and 60 minutes after, yohimbine at the dose 0,1 mg/kg (2 mg/mL), IV; and on group AA, amitraz in the same dose and concentration of the group A and 60 minutes after, atipamezole at the dose 0,2 mg/kg (5 mg/mL), IV. The following parameters were checked in the intervals of time 0, 30, 60,120, 180, 240 and 360 min after the administration of the amitraz: temperature (T), respiratory rate (RR), heart rate (HR), systolic arterial pressure (SAP), electrocardiogram (ECG), diameter pupilar (DP), degree of sedation (DS) and medium interval for sedation return (MISR) considered as the time, in minutes, for the animal to get up after the administration of the amitraz and after the a2-adrenergic antagonists administration, yohimbine or atipamezole. Blood samples were collected by jugular or cephalic puncture 24 hours before and after the intoxication for red blood cell (RBC) count, white blood cell (WBC) count, urea, creatinine, alananine aminotransferase (ALT) and aspartate aminotransferase... (Complete abstract click electronic address below)