SOUTH AMERICAN COLLABORATION IN SCIENTIFIC PUBLICATIONS ON LEISHMANIASIS: BIBLIOMETRIC ANALYSIS IN SCOPUS (2000-2011)

Objectives: Evaluate the production and the research collaborative network on Leishmaniasis in South America. Methods: A bibliometric research was carried out using SCOPUS database. The analysis unit was original research articles published from 2000 to 2011, that dealt with leishmaniasis and that included at least one South American author. The following items were obtained for each article: journal name, language, year of publication, number of authors, institutions, countries, and others variables. Results: 3,174 articles were published, 2,272 of them were original articles. 1,160 different institutional signatures, 58 different countries and 398 scientific journals were identified. Brazil was the country with more articles (60.7%) and Oswaldo Cruz Foundation (FIOCRUZ) had 18% of Brazilian production, which is the South American nucleus of the major scientific network in Leishmaniasis. Conclusions: South American scientific production on Leishmaniasis published in journals indexed in SCOPUS is focused on Brazilian research activity. It is necessary to strengthen the collaboration networks. The first step is to identify the institutions with higher production, in order to perform collaborative research according to the priorities of each country.

Effects of chronic L-NAME treatment lung tissue mechanics, eosinophilic and extracellular matrix responses induced by chronic pulmonary inflammation

The importance of lung tissue in asthma pathophysiology has been recently recognized. Although nitric oxide mediates smooth muscle tonus control in airways, its effects on lung tissue responsiveness have not been investigated previously. We hypothesized that chronic nitric oxide synthase (NOS) inhibition by N-omega-nitro-L-arginine methyl ester (L-NAME) may modulate lung tissue mechanics and eosinophil and extracellular matrix remodeling in guinea pigs with chronic pulmonary inflammation. Animals were submitted to seven saline or ovalbumin exposures with increasing doses (1 similar to 5 mg/ml for 4 wk) and treated or not with L-NAME in drinking water. After the seventh inhalation (72 h), animals were anesthetized and exsanguinated, and oscillatory mechanics of lung tissue strips were performed in baseline condition and after ovalbumin challenge (0.1%). Using morphometry, we assessed the density of eosinophils, neuronal NOS (nNOS)- and inducible NOS (iNOS)-positive distal lung cells, smooth muscle cells, as well as collagen and elastic fibers in lung tissue. Ovalbumin-exposed animals had an increase in baseline and maximal tissue resistance and elastance, eosinophil density, nNOS- and iNOS-positive cells, the amount of collagen and elastic fibers, and isoprostane-8-PGF(2 alpha) expression in the alveolar septa compared with controls (P < 0.05). L-NAME treatment in ovalbumin-exposed animals attenuated lung tissue mechanical responses (P < 0.01), nNOS- and iNOS-positive cells, elastic fiber content (P < 0.001), and isoprostane-8-PGF(2 alpha) in the alveolar septa (P < 0.001). However, this treatment did not affect the total number of eosinophils and collagen deposition. These data suggest that NO contributes to distal lung parenchyma constriction and to elastic fiber deposition in this model. One possibility may be related to the effects of NO activating the oxidative stress pathway.

Hemodynamic responses to aortic depressor nerve stimulation in conscious L-NAME-induced hypertensive rats

Durand MT, Castania JA, Fazan R Jr, Salgado MC, Salgado HC. Hemodynamic responses to aortic depressor nerve stimulation in conscious L-NAME-induced hypertensive rats. Am J Physiol Regul Integr Comp Physiol 300: R418-R427, 2011. First published November 24, 2010; doi: 10.1152/ajpregu.00463.2010.-The present study investigated whether baroreflex control of autonomic function is impaired when there is a deficiency in NO production and the role of adrenergic and cholinergic mechanisms in mediating reflex responses. Electrical stimulation of the aortic depressor nerve in conscious normotensive and nitro-L-arginine methyl ester (L-NAME)-induced hypertensive rats was applied before and after administration of methylatropine, atenolol, and prazosin alone or in combination. The hypotensive response to progressive electrical stimulation (5 to 90 Hz) was greater in hypertensive (-27 +/- 2 to -64 +/- 3 mmHg) than in normotensive rats (-17 +/- 1 to -46 +/- 2 mmHg), whereas the bradycardic response was similar in both groups (-34 +/- 5 to -92 +/- 9 and -21 +/- 2 to -79 +/- 7 beats/min, respectively). Methylatropine and atenolol showed no effect in the hypotensive response in either group. Methylatropine blunted the bradycardic response in both groups, whereas atenolol attenuated only in hypertensive rats. Prazosin blunted the hypotensive response in both normotensive (43%) and hypertensive rats (53%) but did not affect the bradycardic response in either group. Prazosin plus angiotensin II, used to restore basal arterial pressure, provided hemodynamic responses similar to those of prazosin alone. The triple pharmacological blockade abolished the bradycardic response in both groups but displayed similar residual hypotensive response in hypertensive (-13 +/- 2 to -27 +/- 2 mmHg) and normotensive rats (-10 +/- 1 to -25 +/- 3 mmHg). In conclusion, electrical stimulation produced a well-preserved baroreflex-mediated decrease in arterial pressure and heart rate in conscious L-NAME-induced hypertensive rats. Moreover, withdrawal of the sympathetic drive played a role in the reflex bradycardia only in hypertensive rats. The residual fall in pressure after the triple pharmacological blockade suggests the involvement of a vasodilatory mechanism unrelated to NO or deactivation of alpha(1)-adrenergic receptor.

Sympathetic activity is not increased in L-NAME hypertensive rats

Santos FM, Dias DPM, Silva CAA, Fazan Jr R, Salgado HC. Sympathetic activity is not increased in L-NAME hypertensive rats. Am J Physiol Regul Integr Comp Physiol 298: R89-R95, 2010. First published November 4, 2009; doi:10.1152/ajpregu.00449.2009.-The role played by the sympathetic drive in the development of N(G)-nitro-L-arginine methyl ester (L-NAME)-induced hypertension is not firmly established. Therefore, the present study was undertaken in conscious rats in which hypertension was induced by treatment with L-NAME over the course of either 2 or 14 days. Mean arterial pressure (MAP) was measured via a catheter placed in the femoral artery, drugs were administered via a cannula placed in the femoral vein, and renal sympathetic nerve activity (RSNA) was monitored using an implanted electrode. Despite the remarkable increase in arterial pressure, heart rate did not change after treatment with L-NAME. RSNA was similar in L-NAME-induced hypertensive rats treated over the course of 2 or 14 days, as well as in normotensive rats. It was also demonstrated that L-NAME-induced hypertensive rats displayed a resetting of the baroreflex control of RSNA to hypertensive levels, with decreased sensitivity over the course of 2 or 14 days. Furthermore, the sympathetic-vagal balance examined in the time and frequency domain and the renal and plasma norepinephrine content did not differ between groups. In conclusion, the evaluation of the sympathetic drive in conscious rats demonstrated that the arterial hypertension induced by L-NAME treatment over the course of 2 and 14 days does not show sympathetic overactivity.

Jules Cotard (1840-1889) - His life and the unique syndrome which bears his name

Dr. Jules Cotard (1840-1889) was a Parisian neurologist who first described the delire des negations. Cotard's syndrome or Cotard's delusion comprises any one of a series of delusions ranging from the fixed and unshakable belief that one has lost organs, blood, or body parts to believing that one has lost one's soul or is dead. In its most profound form, the delusion takes the form of a professed belief that one does not exist. Encountered primarily in psychoses such as schizophrenia and bipolar disorder, Cotard's syndrome has also been described in organic lesions of the nondominant temporoparietal cortex as well as in migraine. Cotard's delusion is the only self-certifiable syndrome of delusional psychosis. Jules Cotard, a Parisian neurologist and psychiatrist and former military surgeon, was one of the first to induce cerebral atrophy by the experimental embolization of cerebral arteries in animals and a pioneer in studies of the clinicopathologic correlates of cerebral atrophy secondary to perinatal and postnatal pathologic changes. He was the first to record that unilateral cerebral atrophy in infancy does not necessarily lead to aphasia and was also the pioneer of studies of altered conscious states in diabetic hyperglycemia.

Vanamea GEN. NOV. FOR Livoneca symmetricaVAN NAME,1925, (CRUSTACEA, ISOPODA, CYMOTHOIDAE) AND A REDESCRIPTION OF THE SPECIES BASED ON SPECIMENS FROM BRAZILIAN PIRANHAS

Studies of the cymothoid isopod Livoneca symmetricaVan Name, 1925, showed that this species has characters that preclude its inclusion in LivonecaLeach, 1818, or in any other known genus. The species is redescribed on the basis of male and female specimens from the mouth cavities of Amazonian piranhas (Serrasalmus spilopleura(Kner) and S. elongatusKner) and Vanameagen. nov. is proposed for it. The new genus is defined as having: a cephalon that is not immersed in pereonite 1; mandibles that are "foot-shaped" and without incisors, pereopods that are long and unequal in size and shape; a pleon that is not immersed in the pereon; and a pleotelson that is inflated anteriorly and medially.

Treinamento resistido controla a pressão arterial de ratos hipertensos induzidos por l-NAME

FUNDAMENTO: A hipertensão arterial é uma síndrome multifatorial, crônica, causada tanto por fatores congênitos ou adquiridos. OBJETIVO: Avaliar os efeitos do treinamento físico resistido (TR) sobre pressão arterial, reatividade e morfologia vascular de ratos hipertensos induzidos por L-NAME. MÉTODOS: Ratos Wistar machos (200-250 g) foram divididos em 3 grupos: normotenso sedentário (NS), hipertenso sedentário (HS) e hipertenso treinado (HT). A hipertensão foi induzida pela administração de L-NAME (40 mg/kg) na água de beber por 4 semanas. A pressão arterial foi avaliada antes e após o TR. O TR foi realizado utilizando 50% de 1RM, em 3 séries de 10 repetições, 3 vezes por semana, durante quatro semanas. A reatividade vascular foi mensurada em artéria mesentérica superior por curvas concentração resposta ao nitroprussiato de sódio (NPS) e fenilefrina (FEN). Além disso, foram realizadas análises histológicas e estereológicas. RESULTADOS: O TR inibiu o aumento das pressões arteriais média e diastólica. Foi observada uma redução significativa na resposta máxima e na potência da FEN entre os grupos HS e HT. A análise histológica evidenciou aspecto normal para as túnicas íntima, média e adventícia em todos os grupos. Não houve diferença significativa nas áreas do lúmen, da túnica média e total das artérias dos grupos HS e HT em relação ao NS. A razão parede/lúmen arterial do grupo HS apresentou diferença significativa em relação ao NS (p < 0,05), mas esta não foi diferente do HT. CONCLUSÕES: O TR foi capaz de prevenir a elevação da pressão arterial sob as condições deste estudo. Este controle parece envolver a regulação de mecanismo vasoconstritor e a manutenção do diâmetro luminal de ratos hipertensos induzidos por L-NAME.