Pulmonary rehabilitation (PR) improves physical capacity and health quality in patients with chronic obstructive pulmonary disease (COPD). However, the effect of exercise on oxidative stress markers in COPD patients is only partially known. This study was designed to evaluate the oxidative stress response to long-term exercise in patients with COPD enrolled in a PR program. Fifteen COPD patients (FEV1 < 60%), age between 50 and 60 years, ex-smokers, were separated in two groups: exercise-trained (n=8) and sedentary group (n=7). Exercise consisted of an 8-week conditioning program using a cycle ergometer (three times a week, 1h session). An endurance test (60% of maximal load in an incremental cycle test) was performed before and after PR. Blood samples were obtained at baseline and immediately after each endurance test. We measured the index of lipid peroxidation, thiobarbituric acid reactive species (TBARS), total radical-trapping antioxidant parameter (TRAP) and xanthine oxidase (XO) activity. TRAP was significantly different between the exercise-trained group and sedentary group of COPD patients. Baseline TBARS values were increased after the exercise training program but decreased after the endurance test. XO decrease after effort in the trained and untrained groups. The results suggest that patients with COPD are characterized by increased systemic and pulmonary oxidative stress markers both at rest as well as induced by cardiopulmonary exercise test and that PR program was associated with decreased systemic exercise-induced oxidative damage.

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Patients with acute panic disorder (PD) use a more maladaptive pattern of defense mechanisms. This study investigated the use of defense mechanisms by patients with acute symptomatic PD and those in complete remission. Thirty-three patients and 33 controls were evaluated by the Mini International Neuropsychiatric Interview. The defense mechanisms were evaluated by the Defense Style Questionnaire at the beginning of the study and after 16 weeks of sertraline treatment. Panic disordered patients used more neurotic (4.6 vs. 3.6; p = 0.003) and immature (3.6 vs. 3.0; p = 0.024) defenses at baseline. Patients who achieved complete remission (N=25) differed from the control group in the use of neurotic defenses at the baseline (4.4 vs. 3.6; p = 0.033). After treatment, they showed a reduction in the use of neurotic (4.4 vs. 3.7; p=0.014) and immature (3.4 vs. 3.1; p = 0.019) defenses. Defense mechanisms in PD are influenced by the presence of symptoms, severity, and outcome of the disease.

This study aims to evaluate the defense mechanisms most frequently used by Brazilian patients with panic disorder when compared with a control group. The study also examines the association between severity of disease and comorbidity and the use of specific defense mechanisms. Sixty panic-disordered patients and 31 controls participated in the study. The Mini International Neuropsychiatric Interview was used to confirm the panic disorder diagnosis and to establish the comorbid diagnosis. The Clinical Global Impression (CGI) was used to assess severity and the Defensive Style Questionnaire (DSQ-40) was used to evaluate the defense mechanisms. Panic patients used more neurotic (mean = 4.9 versus 3.6; p < 0.001) and immature (mean = 3.9 versus 2.8; p < 0.001) defenses as compared with controls. Panic patients with severe disease (n = 37; CGI>4) had more depression comorbidity and used more immature defenses than patients with CGI

The cerebral distribution of peripheral-type benzodiazepine binding sites (PBBS) in human brain has been investigated by positron emission tomography (PET) with the specific radioligand [11C]PK11195 in diverse neuropathological conditions. However, little is known about the pattern of PK11195 binding sites in healthy brain. Therefore, we used quantitative autoradiography to measure the saturation binding parameters for [3H]PK11195 in cryostat sections from young Landrace pigs. Specific binding was lowest in the cerebellar white matter (85 fmol mg(-1)) and highest in the caudate nucleus (370 fmol mg(-1)), superior colliculus (400 fmol mg(-1)), and anterior thalamic nucleus (588 fmol mg(-1)). The apparent affinity was in the range of 2-6 nM in vitro, predicting high specific binding in PET studies of living brain. However, the distribution volume (V(d), ml g(-1)) of high specific activity [11C]PK11195 was nearly homogeneous (3 ml g(-1)) throughout brain of healthy Landrace pigs, and was nearly identical in studies with lower specific activity, suggesting that factors in vivo disfavor the detection of PBBS in Landrace pigs with this radioligand. In young, adult Göttingen minipig brain, the magnitude of V(d) for [11C]PK11195 was in the range 5-10 ml g(-1), and had a heterogeneous distribution resembling the in vitro findings in Landrace pigs. There was a trend toward globally increased V(d) in a group of minipigs with acute MPTP-induced parkinsonism, but no increase in V(d) was evident in the same pigs rescanned at 2 weeks after grafting of fetal mesencephalon to the partially denervated striatum. Thus, [11C]PK11195 binding was not highly sensitive to constituitively expressed PBBS in brain of young Landrace pigs, and did not clearly demonstrate the expected microglial activation in the MPTP/xenograft model of minipigs.

Our data are in accordance to the literature and corroborates the theory of an anxiety diathesis, suggesting that a history of anxiety disorders in childhood is associated with an anxiety disorder diagnosis, mainly social anxiety disorder, in adulthood.

-Based on a previous study showing that panic disorder patients had increased expression of naïve phenotype lymphocytes (CD45RA+ and CD62L+), increased plasma cortisol, as well as decreased interleukin-2 (IL-2) producion, we hypothesized that changes in the percentage of expression of these lymphocyte surface molecules could be related to the substances released by the hypothalamic-pituitary-adrenal (HPA) axis and possibly associated to panic disorder (cortisol, IL-2, serotonin and epinephrine). In order to study the altered expression, blood mononuclear cells of normal volunteers were stimulated with mitogen, in the presence of dexamethasone, IL-2, serotonin and epinephrin. CD62L is decreased by IL-2 in vitro. Serotonin and epinephrine did not promote changes in the expression of these surface molecules. The results of the ex vivo study are in agreement with a previous clinical study with panic patients. It could be suggested that stress is responsible for certain immunologic dysfunctions and new studies should be conducted.KEY WORDS: corticosteroids, interleukin-2, lymphocyte migration, adhesion molecules, panic disorder.Regulação do receptor de alojamento linfocitário CD62L (L Regulação do receptor de alojamento linfocitário CD62L (L Regulação do receptor de alojamento linfocitário CD62L (L Regulação do receptor de alojamento linfocitário CD62L (L Regulação do receptor de alojamento linfocitário CD62L (L-selectina) pelo estresse -selectina) pelo estresse -selectina) pelo estresse -selectina) pelo estresse -selectina) pelo estresse RESUMO -Baseado em estudo prévio que demonstrou que os pacientes com transtorno do pânico apresentavam aumento na porcentagem de expressão de linfócitos com fenótipo virgem (CD45RA+ e CD62L+), aumento no cortisol plasmático, assim como diminuição na produção de interleucinas, foi sugerido que as alterações na porcentagem de expressão dessas moléculas de superfície dos linfócitos poderia estar relacionada com a liberação de substâncias pelo eixo hipotálamo-hipófise-adrenal (HHA) e possivelmente associada ao transtorno do pânico (cortisol, IL-2, serotonina e epinefrina). Com o objetivo de estudar essas alterações, células mononucleares do sangue periférico de voluntários normais foram estimuladas com mitógeno, na presença de dexametasona, IL-2, serotonina e epinefrina. A expressão de CD62L "in vitro" é diminuida com IL-2. Serotonina e epinefrina não promovem alterações na expressão dessas moléculas de superfície. Os resultados desse estudo "in vitro" estão de acordo com o estudo clínico prévio com pacientes com transtorno do pânico. Podese sugerir que o estresse é responsável por algumas disfunções imunológicas e novos estudos devem ser delineados para testar essa hipótese.PALAVRAS-CHAVE: corticosteróides, interleucina-2, migração linfocitária, moléculas de adesão, transtorno do pânico.

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