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A idade da populacao vem aumentando de forma relevante no mundo e no Brasil. Com o aumento da idade da populacao, aumentam tambem as preocupacoes e cuidados com relacao aos riscos de suicidio, associados a fatores biopsicossociais envolvidos no avanco da idade. Este estudo teve como objetivo avaliar a prevalencia do risco de suicidio em uma populacao entre 60 e 79 anos. Metodo: Estudo transversal com base de dados populacionais, que avaliou 1.021 idosos. Foram realizadas entrevistas domiciliares com a versao em portugues do Mini International Neropsychiatric Interview (MINI), bem como coleta de dados sociodemograficos e clinicos. O risco foi classificado em ausente ou presente, e ainda em leve, moderado ou grave. Resultados: O risco de suicidio foi classificado como presente em 26 individuos (2,5% da amostra), 22 tinham risco leve e 4 foram classificados como risco moderado. A media de idade dos pacientes que apresentavam risco de suicidio foi superior ao dos que nao apresentavam. Os fatores de risco encontrados foram nao ter companheiro, transtorno de humor, ex-tabagista, comparado com quem nunca fumou, sendo que o tabagismo atual nao foi fator de risco. Nao tiveram associacao com risco de suicidio: genero, escolaridade, hipertensao arterial sistemica e infarto agudo do miocardio, colesterol total e transtorno de ansiedade. Conclusoes: Os dados demonstram que o risco de suicidio em idosos da comunidade e expressivo e esta em consonância com resultados de outras pesquisas no Brasil e sul do Brasil. O risco aumenta com a idade, ausencia de companheiro e transtorno de humor, corroborando dados da literatura cientifica nacional e internacional.

Pneumococcal meningitis is a life-threatening infection of the central nervous system (CNS) with a high mortality rate. In addition to causing severe neurological sequelae infectious diseases of the CNS can play a significant role in the pathogenesis of neuropsychiatric disorders. In this study infant Wistar rats, postnatal day 11, received intracerebroventricular (i.c.v.) either artificial cerebrospinal fluid (CSF) or a Streptococcus pneumoniae suspension to a concentration of 1 × 106 colony-forming units (CFU). 18 h later animals received antibiotic treatment as usual during 7 days. On postnatal day 46, the animals received imipramine intraperitoneal (i.p.) or sterile NaCl during 14 days (postnatal days 46-60). Then, on postnatal days 59-60 we evaluated the consumption of sweet food (an index of anhedonia). On postnatal day 60 the animals were submitted to the forced swimming task. 60 min after this task the animals were decapitated and the blood was collected to evaluate adrenocorticotropic hormone (ACTH) and corticosterone. Immediately after blood collection the hippocampus was removed to evaluate brain-derived neurotropic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). The meningitis group exhibited depressive-like behavior as evidenced by decreased sucrose intake and increased immobility time in the forced swimming task, and BDNF and GDNF decrease in the hippocampus. ACTH levels were increased in the blood. Imipramine treatment reversed depressive-like behaviors, re-established hippocampal BDNF and GDNF expression, and normalized ACTH levels in the blood. Here we demonstrate that meningitis during early life period can trigger depressive-like behavior in adult life of rats.

Objective The present study assessed the prevalence of depressive disorders and associated factors in a sample of elderly persons in the south of Santa Catarina. Methods A cross-sectional study based on population data was performed, evaluating 1021 elderly individuals aged between 60 and 79 years. Home interviews were carried out using the Portuguese version of the Mini International Neuropsychiatric Interview (MINI), in order to collect demographic data, information on hypertension and reports of acute myocardial infarction. The disorders studied were current depressive episode, dysthymia and a comorbidity of a depressive episode and dysthymia, representing double depression. The comparison of mean age and prevalence was made with the t-test and other associations were analyzed using the Chi-squared test. Results The prevalence of depression was 26.2%, while 5.5% of the sample suffered from dysthymia and 2.7% experienced double depression. Risk factors for depression were: nine or more years of schooling [PR = 1.44 (1.17 to 1.77); p

Objective: The aim of the present study was to investigate the depressive symptoms and changes in neurotrophins (BDNF, NGF, NT-3), and cortisol levels in serum of peripheral blood from ostomy patients compared to healthy control group. Methods: We evaluated ostomy (n = 29) and healthy control (n = 30) patients. The neurotrophin (BDNF, NGF, NT-3), and cortisol levels were assessed by ELISA in serum of peripheral blood. Depressive symptoms were defined based on the Hamilton Depression Rating Scale (HDRS), and major depression disorder was based on clinical interviews and was confirmed with the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I). Results: The results showed a significant decrease in BDNF levels and, a significant increase in NT-3 levels in serum of peripheral blood from ostomy patients when compared to healthy controls. The levels of NGF and cortisol showed no significant differences between groups. The depressive symptom evaluations by HDRS demonstrated a significant increase in ostomy patients when compared to healthy controls. The major depression disorder diagnosis by SCID-I showed no significant difference between groups. Conclusion: Our results suggest ostomy triggers significant depressive symptoms and alterations in neurotrophins levels in serum of peripheral blood samples collected from these patients.

Streptococcus pneumoniae is a common cause of bacterial meningitis, with a high mortality rate and neurological sequelae. In contrast, folic acid plays an important role in neuroplasticity and the preservation of neuronal integrity. In the present study, we evaluated the influence of folic acid on memory, oxidative damage, enzymatic defence, and brain-derived neurotrophic factor (BDNF) expression in experimental pneumococcal meningitis. In animals that received folic acid at a dose of 10 or 50 mg, there was a reduction in both crossing and rearing during an open-field task compared with the training session, demonstrating habituation memory. During a step-down inhibitory avoidance task, there was a difference between the training and the test sessions, demonstrating aversive memory. In the hippocampus, BDNF expression decreased in the meningitis group; however, adjuvant treatment with 10 mg of folic acid increased BDNF expression, decreased lipid peroxidation, protein carbonylation, nitrate/nitrite levels, and myeloperoxidase activity and increased superoxide dismutase activity. In frontal cortex adjuvant treatment with 10 mg of folic acid decreased lipid peroxidation and protein carbonylation. There is substantial interest in the role of folic acid and related pathways in nervous system function and in folic acid's potential therapeutic effects. Here, adjuvant treatment with vitamin B9 prevented memory impairment in experimental pneumococcal meningitis.

Several studies have suggested that alterations in brain-derived neurotrophic factor (BDNF) and increased oxidative stress have a central role in bipolar disorder (BD). Intracerebroventricular (ICV) injection of ouabain (OUA) in rats alters oxidative stress parameters and decreases BDNF levels in the brain. In this context, the present study aims to investigate the effects of BDNF ICV administration on BDNF levels and oxidative stress parameters in brains of rats submitted to animal model of mania induced by OUA. Wistar rats received an ICV injection of OUA, artificial cerebrospinal fluid (ACSF), OUA plus BDNF, or ACSF plus BDNF. Locomotor activity and risk-taking behavior in the rats were measured using the open-field test. In addition, we analyzed the BDNF levels and oxidative stress parameters (TBARS, Carbonyl, CAT, SOD, GR, and GPx) in the frontal cortex and hippocampus of rats. The BDNF was unable to reverse the ouabain-induced hyperactivity and risk-taking behavior. Nevertheless, BDNF treatment increased BDNF levels, modulated the antioxidant enzymes, and protected the OUA-induced oxidative damage in the brain of rats. These results suggest that BDNF alteration observed in BD patients may be associated with oxidative damage, both seen in this disorder.

The present study aimed to investigate the effects of mood stabilizers, specifically lithium (Li) and valproate (VPA), on the PI3K/Akt signaling pathway in the brains of rats subjected to the ouabain (OUA)-induced animal model of mania. In addition, the effects of AR-A014418, a GSK-3β inhibitor, on manic-like behavior induced by OUA were evaluated. In the first experimental protocol Wistar rats received a single ICV injection of OUA or artificial cerebrospinal fluid (aCSF). From the day following ICV injection, the rats were treated for 6 days with intraperitoneal injections of saline, Li or VPA twice a day. In the second experimental protocol, rats received OUA, aCSF, OUA plus AR-A014418, or aCSF plus AR-A014418. On the 7th day after OUA injection, locomotor activity was measured using the open-field test. In addition, we analyzed the levels of p-PI3K, p-MAPK, p-Akt, and p-GSK-3β in the brain of rats by immunoblot. Li and VPA reversed OUA-related hyperactivity. OUA decreased p-PI3K, p-Akt and p-GSK-3β levels. Li and VPA improved these OUA-induced cellular dysfunctions; however, the effects of the mood stabilizers were dependent on the protein and brain region analyzed. In addition, AR-A014418 reversed the manic-like behavior induced by OUA. These findings suggest that the manic-like effects of ouabain are associated with the activation of GSK-3β, and that Li and VPA exert protective effects against OUA-induced inhibition of the GSK-3β pathway.

RESUMO Objetivo Avaliar a prevalência de transtornos ansiosos e fatores associados em uma amostra populacional de idosos do Sul de Santa Catarina. Métodos Estudo transversal com base em dados populacionais, que avaliou 1.021 indivíduos idosos entre 60 e 79 anos. Foram realizadas entrevistas domiciliares para aferição de variáveis sobre transtornos ansiosos, por meio do questionário MINI, dados sociodemográficos, hipertensão arterial sistêmica (HAS), infarto agudo do miocárdio (IAM) e dosagem de colesterol. Resultados As prevalências entre os transtornos ansiosos foram de 22,0% para o transtorno de ansiedade generalizada (TAG); 14,8% para fobia social (FS); 10,5% para transtorno do pânico (TP); e 8,5% para o transtorno obsessivo-compulsivo (TOC). Além disso, 40,5% dos indivíduos apresentaram pelo menos um transtorno de ansiedade. A distribuição dos transtornos foi semelhante nos dois gêneros; TAG foi mais prevalente nos indivíduos de menor escolaridade; TOC foi mais presente em indivíduos casados ou em união estável. Em relação às variáveis clínicas, HAS foi associada à presença de TOC; FS foi associada com IAM; TOC e FS foram associados com HDL > 40 mg/dL. Conclusão Os dados demonstram que os quadros de ansiedade são muito frequentes em idosos da comunidade, se sobrepõem de forma significativa e estão associados a algumas variáveis clínicas cardiovasculares. ABSTRACT Objective This study evaluated the prevalence of anxiety disorders and associated factors in a population sample of elderly from South of Santa Catarina. Methods Cross-sectional study based on population data, which evaluated 1,021 elderly individuals, between 60 and 79 years. Home interviews were conducted to measure the variables of anxiety disorders, through of the MINI questionnaire, sociodemographic data, systemic arterial hypertension (SAH), acute myocardial infarction (AMI) and serum cholesterol measurements. Results The prevalence among anxiety disorders were 22.0% for generalized anxiety disorder (GAD), 14.8% for social phobia (FS); 10.5% for panic disorder (PD); 8.5% for obsessive-compulsive disorder (OCD), and with only, at least one disorder 40.5%. The distribution of the disorders were similar in both genders, GAD was more prevalent among those with lower education; OCD was more prevalent in individuals who were married or in union stable. In relation to clinical variables, SAH was associated with the presence of OCD; FS was associated with AMI; FS and OCD were associated with HDL > 40 mg/dL. Conclusion The data demonstrate that anxiety conditions are very common in older adults, significantly overlap and are associated with cardiovascular clinical variables.

OBJETIVO: O presente estudo tem como objetivo investigar os efeitos da injecao intracerebroventricular de ouabaina sobre os niveis de BDNF na amigdala e no hipocampo de ratos Wistar. METODOS: Os animais receberam uma unica injecao intracerebroventricular de ouabaina (10-3 and 10-2 M) ou fluido cerebroespinhal artificial e, imediatamente, 3h, 24h ou sete dias apos a injecao, os niveis de BDNF foram mensurados na amigdala e hipocampo dos ratos por ELISA sandwich (n = 8 animais por grupo). RESULTADOS: Quando avaliados imediatamente apos a injecao, 3h ou 24h, ouabaina nas doses 10-2 e 10-3 M nao alterou os niveis de BDNF em ambas as estruturas avaliadas. Entretanto, quando avaliados sete dias apos a injecao, ouabaina nas doses 10-2 e 10-3 M mostrou uma significante reducao nos niveis de BDNF em amigdala e hipocampo. CONCLUSAO: Em conclusao, propoe-se que a administracao de ouabaina diminuiu os niveis de BDNF em amigdala e hipocampo quando avaliados sete dias apos a injecao, suportando a hipotese da participacao da Na/K ATPase no transtorno bipolar.

OBJETIVO: Avaliar o nível de conhecimento dos pais sobre segurança no transporte de crianças em veículos automotores e motocicletas. MÉTODOS: Estudo transversal, realizado por meio de questionário autoaplicável em pais e responsáveis que acompanhavam crianças na sala de espera de ambulatórios público e privado. Para avaliar os conhecimentos sobre segurança no transporte de crianças, foram utilizadas as recomendações da Associação Brasileira de Medicina do Tráfego. A análise dos dados foi realizada por meio do teste do qui-quadrado e as variáveis quantitativas testadas por Mann-Whitney, sendo significante p

There is a body of evidence suggesting that BDNF is involved in bipolar disorder (BD) pathogenesis. Intracerebroventricular (ICV) injection of ouabain (OUA), a specific Na + /K + ATPase inhibitor, induces hyperlocomotion in rats, and has been used as an animal model of mania. The present study aims to investigate the effects of the lithium (Li) and valproate (VPT) in an animal model of mania induced by ouabain. In the reversal model, animals received a single ICV injection of OUA or cerebrospinal fluid (aCSF). From the day following the ICV injection, the rats were treated for 6 days with intraperitoneal (IP) injections of saline (SAL), Li or VPT twice a day. In the maintenance treatment (prevention model), the rats received IP injections of Li, VPT, or SAL twice a day for 12 days. In the 7th day of treatment the animals received a single ICV injection of either OUA or aCSF. After the ICV injection, the treatment with the mood stabilizers continued for more 6 days. Locomotor activity was measured using the open-field test and BDNF levels were measured in rat hippocampus and amygdala by sandwich-ELISA. Li and VPT reversed OUA-related hyperactive behavior in the open-field test in both experiments. OUA decreased BDNF levels in first and second experiments in hippocampus and amygdala and Li treatment, but not VPT reversed and prevented the impairment in BDNF expression after OUA administration in these cerebral areas. Our results suggest that the present model fulfills adequate face, construct and predictive validity as an animal model of mania.

Although electroconvulsive therapy (ECT) has been used as a treatment for mental disorder since 1930s, little progress has been made in the mechanisms underlying its therapeutic or adverse effects. The aim of this work was to analyze the expression of DARPP-32 (a protein with a central role in dopaminergic signaling) in striatum, cortex, hippocampus and cerebellum of Wistar rats subjected to acute or chronic electroconvulsive stimulation (ECS). Rats were submitted to a single stimulation (acute) or to a series of eight stimulations, applied one every 48 h (chronic). Animals were killed for collection of tissue samples at time zero, 0.5, 3, 12, 24 and 48 h after stimulation in the acute model and at the same time intervals after the last stimulation in the chronic model. Our results indicated that acute ECS produces smaller changes in the expression of DARPP-32 but, interestingly, chronic ECS increased transient expression of DARPP-32 in several time frames, in striatum and hippocampus, after the last stimulation. Results on the expression of proteins involved in signaling pathways are relevant for neuropsychiatric disorders and treatment, in particular ECT, and can contribute to shed light on the mechanisms related to therapeutic and adverse effects.

Decreased antioxidant activity is considered as one of the causes of tardive dyskinesia in schizophrenic patients in a prolonged neuroleptic treatment course. Haloperidol (HAL) has been hypothesized to increase oxidative stress, while clozapine (CLO) would produce less oxidative damage. The objective was to determine whether CLO for 28 days could reverse or attenuate HAL-induced oxidative damage in animals previously treated with HAL for 28 days. HAL significantly increased thiobarbituric acid reactive substances levels in the cortex (CX) and striatum and increased protein carbonyls in hippocampus (HP) and CX and this was not attenuated by CLO treatment. In the total radical trapping antioxidant parameter assay there was a decrease in the HP total antioxidant potential induced by HAL and by treatment with HAL + CLO. Our findings demonstrated that the atypical antipsychotic CLO could not revert oxidative damage caused by HAL.

Although electroconvulsive therapy (ECT) has been used as a treatment for mental disorder since 1930s, little progress has been made towards understanding the mechanisms underlying its therapeutic and adverse effects. The aim of this work was to analyze the expression of NCS-1 (neuronal calcium sensor 1, a protein that was found to be altered in post-mortem prefrontal cortex of schizophrenic patients) in striatum, cortex, hippocampus and cerebellum of Wistar rats after acute or chronic electroconvulsive stimulation (ECS). Rats were submitted to a single stimulation (acute) or to a series of eight stimulations, applied one every 48 h (chronic). Animals were killed for collection of tissue samples at time zero, 30 min, 3, 12, 24 and 48 h after stimulation in the acute model and at the same time intervals after the last stimulation in the chronic model. Our results indicated that chronic ECS increased the expression of NCS-1 only in cerebellum. Such results on the expression of proteins involved in signaling pathways that are relevant for neuropsychiatric disorders and treatment, in particular ECT, can contribute to shed light on the mechanisms related to therapeutic and adverse effects.

This work was performed in order to determine the level of oxidative damage and antioxidant enzymes activities late after acute and chronic electroconvulsive shock (ECS) in rats. We measured oxidative parameters in hippocampus, cortex, and striatum, at 45, 60, 90 and 120 days after a single or multiple ECS. We demonstrated an increase in lipid peroxidation after multiple ECS in the hippocampus and striatum. This was also the case for protein carbonyls in the single or multiple protocols. In this way, we demonstrated an increase in catalase in cortex in contrast to striatum and hippocampus, were there were decreases sometimes in chronic ECS. The superoxide dismutase activities decrease in different times after single and multiple ECS in the hippocampus. Our findings demonstrated that there is a delayed increase after ECS in oxidative damage and decrease in antioxidant enzymes activities in hippocampus and striatum.

Streptococcus pneumoniae is the relevant cause of bacterial meningitis, with a high-mortality rate and long-term neurological sequelae, affecting up to 50% of survivors. Pneumococcal compounds are pro-inflammatory mediators that induce an innate immune response and tryptophan degradation through the kynurenine pathway. Vitamin B6 acts as a cofactor at the active sites of enzymes that catalyze a great number of reactions involved in the metabolism of tryptophan, preventing the accumulation of neurotoxic intermediates. In the present study, we evaluated the effects of vitamin B6 on memory and on brain-derived neurotrophic factor (BDNF) expression in the brain of adult Wistar rats subjected to pneumococcal meningitis. The animals received either 10 µL of artificial cerebral spinal fluid (CSF) or an equivalent volume of S. pneumoniae suspension. The animals were divided into four groups: control, control treated with vitamin B6, meningitis, and meningitis treated with vitamin B6. Ten days after induction, the animals were subjected to behavioral tests: open-field task and step-down inhibitory avoidance task. In the open-field task, there was a significant reduction in both crossing and rearing in the control group, control/B6 group, and meningitis/B6 group compared with the training session, demonstrating habituation memory. However, the meningitis group showed no difference in motor and exploratory activity between training and test sessions, demonstrating memory impairment. In the step-down inhibitory avoidance task, there was a difference between training and test sessions in the control group, control/B6 group, and meningitis/B6 group, demonstrating aversive memory. In the meningitis group, there was no difference between training and test sessions, demonstrating impairment of aversive memory. In the hippocampus, BDNF expression decreased in the meningitis group when compared to the control group; however, adjuvant treatment with vitamin B6 increased BDNF expression in the meningitis group. Thus, vitamin B6 attenuated the memory impairment in animals subjected to pneumococcal meningitis.

Objective: To assess the presence of anxiety disorders and quality of life in patients with insulin-dependent type 2 diabetes. Methods: Case-control study of 996 patients with type 2 diabetes and 2,145 individuals without diabetes. The sole inclusion criterion for the case group was insulin-dependent type 2 diabetes. We compared the case and control groups for sociodemographic variables, laboratory and clinical data, and presence of anxiety disorders. Quality of life was evaluated using the WHOQOL-BREF instrument, and the prevalence of anxiety disorder was evaluated by the Mini International Neuropsychiatric Interview (MINI). Results: Patients with diabetes had a higher prevalence of generalized anxiety disorder, panic disorder, and obsessive-compulsive disorder. The presence of these disorders in combination with type 2 diabetes was associated with worse quality of life in the physical, social, psychological, and environmental domains. Conclusions: This study demonstrates the importance of diagnosing and treating anxiety disorders in patients with diabetes, so as to prevent more serious complications associated with these comorbidities.

Neonatal Escherichia coli meningitis continues to be an important cause of mortality and morbidity in newborns worldwide. The aim of this study was to investigate the cytokines/chemokines, brain-derived neurotrophic factor (BDNF) levels, blood–brain barrier integrity in neonatal rats following E. coli K1 experimental meningitis infection and subsequent behavioural parameters in adulthood. In the hippocampus, interleukin increased at 96 h, IL-6 at 12, 48 and 96 h, IL-10 at 96 h, cytokine-induced neutrophil chemoattractant-1 at 6, 12, 24, 48 and 96 h, and BDNF at 48 and 96 h. In the cerebrospinal fluid, tumour necrosis factor alpha levels increased at 6, 12, 24, 48 and 96 h. The BBB breakdown occurred at 12 h in the hippocampus, and at 6 h in the cortex. We evaluated behavioural parameters in adulthood: habituation to the open-field, step-down inhibitory avoidance, object recognition, continuous multiple-trials step-down inhibitory avoidance and forced swimming tasks. In adulthood, the animals showed habituation and aversive memory impairment. The animals needed a significant increase in the number of training periods to learn and not had depressive-like symptoms.

This study evaluated the association of mood disorders, suicidal ideation and the quality of life in patients with type 2 diabetes. We used a case–control study employing 996 patients suffering with type 2 diabetes (using insulin for over 1 year), and 2.145 individuals without diabetes. The groups were then used to evaluate the presence of different mood disorders and suicidal ideation, beyond quality of life. In addition to this, fasting glucose and glycosylated hemoglobin (Hb1C) were also evaluated. The data were analyzed using the Pearson chi-squared test, logistic regression, ANCOVA and Student’s t-tests. We showed an association between type 2 diabetes and depressive episodes (adjusted OR = 1.8, CI 95 % 1.7–2.0, p < 0.001), recurrent depressive episodes (adjusted OR = 2.4, CI 95 % 2.2–2.6, p < 0.001), dysthymia (adjusted OR = 5.2, CI 95 % 4.9–5.5, p < 0.001), mood disorder with psychotic symptoms (adjusted OR = 2.5, CI 95 % 1.5–3.4, p < 0.001) and suicidal ideation (adjusted OR = 3.6, CI 95 % 2.5–4.8, p < 0.001, light; adjusted OR = 4.6, CI 95 % 1.5–7.7, p < 0.01, moderate and severe). The recurrent depression (OR = 1.3, CI 95 % 1.1–1.7, p < 0.05) and psychotic symptoms (OR = 4.1, CI 95 % 1.1–15.1, p < 0.05) were associated with higher levels of Hb1C. Dysthymia was associated with high blood glucose (OR = 1.6, CI 95 % 1.1–2.5, p < 0.05). Patients had lower mean scores in the following domains: physical [36.5 (13.6) × 56.0 (4.9), p < 0.001)], psychological [42.6 (8.6) × 47.9 (8.6), p < 0.001] and environmental [40.0 (8.6) × 49.3 (8.3), p < 0.001], but had higher scores in the area of social relations [50.2 (16.9) × 35.7 (27.9), p < 0.001]. The data demonstrated a worse quality of life, a high comorbidity of type 2 DM with depressive disorders and suicidal ideation. In addition, the poor control of DM is associated with the severity of mood disorders.

OBJECTIVES: To analyze eating disorders among female university students and to assess the frequency of bulimia nervosa, anorexia nervosa, and inappropriate weight loss strategies in this population. METHODS: The sample comprised 214 female university students attending different health science programs at a university in southern Brazil, aged over 18 years, assessed using self-administered questionnaires. The 26-item version of the Eating Attitudes Test (EAT-26), the Bulimic Investigatory Test, Edinburgh (BITE), and a supplementary questionnaire covering data on weight status and inappropriate weight loss strategies were used to assess dietary abnormalities. RESULTS: Mean age (± standard deviation) was 21±9.93 years, and mean body mass index (BMI) was 21.1±2.59. Among the respondents, 72.9% said they would like to weigh less, 29% reported the use of different weight loss methods (diuretics were the most common, followed by laxatives, amphetamine-derived drugs, and self-induced vomiting). With regard to EAT-26 scores, 22.4% (95%CI 17.7-27.1) revealed abnormal feeding patterns; BITE indicated that 9.8% (95%CI 6.5-13.1) were at risk for developing bulimia and 36.9% (95%CI 31.5-42.3) required clinical evaluation. Mean BMI was lower among students with normal scores on both tests, but no association was found between BMI and satisfaction with own weight. CONCLUSION: There was a strong trend toward eating disorders in the health science students assessed, as demonstrated by EAT-26 and BITE scores; inadequate weight loss strategies are frequently used as well. OBJETIVOS: Analisar a presença de transtornos alimentares em universitárias e avaliar a frequência dos quadros de bulimia, anorexia nervosa e estratégias inadequadas para emagrecimento na amostra estudada. MÉTODOS: Foram estudadas 214 universitárias matriculadas em diferentes cursos da área da saúde em uma universidade do sul do Brasil, com idade igual ou superior a 18 anos; a avaliação se deu por meio de questionários autoaplicáveis. A frequência de padrões alimentares anormais foi avaliada de acordo com os escores das versões em português do Eating Attitudes Test, versão de 26 itens (EAT-26), do Bulimic Investigatory Test, Edinburgh (BITE), e um questionário complementar com itens sobre a situação ponderal e estratégias inadequadas utilizadas para emagrecer. RESULTADOS: As estudantes tinham média (± desvio padrão) de idade de 21±9,93 anos e índice de massa corporal (IMC) médio de 21,1±2,59. Entre as participantes, 72,9% afirmaram que gostariam de pesar menos e 29% relataram o uso de estratégias inadequadas para emagrecer (o uso de diurético foi o mais frequente, seguido de laxantes, derivados de anfetaminas e vômitos induzidos). De acordo com a pontuação do EAT-26, 22,4% das estudantes (IC95% 17,7-27,1) apresentaram padrão alimentar anormal. Já o BITE indicou que 9,8% (IC95% 6,5-13,1) se encontravam no grupo com grande possibilidade de bulimia e 36,9 (IC95% 31,5-42,3) apresentavam necessidade de avaliação clínica. A média do IMC foi menor entre as universitárias com escores normais nos dois testes, porém não foi encontrada associação entre IMC e satisfação com o próprio peso. CONCLUSÕES: Nas futuras profissionais da saúde avaliadas, houve uma alta taxa de tendência a transtornos alimentares, conforme evidenciado pelos escores do EAT-26 e do BITE; o uso frequente de técnicas inadequadas de emagrecimento também foi constatado.

In this study, we assessed the oxidative stress parameters in rats submitted to an animal model of mania induced by ouabain (OUA), which included the use of lithium (Li) and valproate (VPA). Li and VPA treatment reversed and prevented the OUA-induced damage in these structures, however, this effect varies depending on the brain region and treatment regimen. Moreover, the activity of the antioxidant enzymes, namely, superoxide dismutase (SOD) and catalase (CAT) was found to be increased and decreased, respectively, in the brain of OUA-administered rats. Li and VPA modulated SOD and CAT activities in OUA-subjected rats in both experimental models. Our results support the notion that Li and VPA exert antioxidant-like properties in the brain of rats submitted to animal model of mania induced by ouabain.

There is an emerging body of data suggesting that bipolar disorder is associated with DNA damage. Intracerebroventricular (i.c.v.) administration of ouabain in rats results in manic-like alterations. We evaluated DNA damage of peripheral blood, cerebrospinal fluid and hippocampus of rats after i.c.v. ouabain injection. Ouabain-induced hyperlocomotion was examined in an open field. Additionally, we used single cell gel electrophoresis (comet assay) to measure early transient damage in cerebrospinal fluid (CSF), hippocampus and blood; and the micronucleus test to measure persistent damage in total blood samples of rats after ouabain administration. Our findings demonstrated that ouabain induced hyperlocomotion in rats, and this response remained up to 7 days following a single i.c.v. injection. In addition, we observed that the persistent increase in the rat spontaneous locomotion is associated with increased hippocampal and peripheral index of early DNA damage in rats. No significant alterations were observed in the micronucleus frequency in total blood samples of the rats after the ouabain i.c.v. injection. These results suggest that ouabain may induce peripheral and central early DNA damage, but this early damage may be repaired.

Although several advances have occurred over the past 20 years concerning refining the use and administration of electroconvulsive therapy to minimize side effects of this treatment, little progress has been made in understanding the mechanisms underlying its therapeutic or adverse effects. This work was performed in order to determine the level of oxidative damage at different times after the maintenance electroconvulsive shock (ECS). Male Wistar rats (250–300 g) received a protocol mimicking therapeutic of maintenance or simulated ECS (Sham) and were subsequently sacrificed immediately after, 48 h and 7 days after the last maintenance electroconvulsive shock. We measured oxidative damage parameters (thiobarbituric acid reactive species for lipid peroxidation and protein carbonyls for protein damage, respectively) in hippocampus, cortex, cerebellum and striatum. We demonstrated no alteration in the lipid peroxidation and protein damage in the four structures studied immediately after, 48 h and 7 days after a last maintenance electroconvulsive shock. Our findings, for the first time, demonstrated that after ECS maintenance we did protocol minimal oxidative damage in the brain regions, predominating absence of damage on the findings.