18 resultados para Gecko-inspired

em Scielo Saúde Pública - SP


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Redescriptions are given of the mature oocysts of Isospora ameivae Carini, 1932, from the teiid lizard Ameiva ameiva, and Isospora hemidactyli Carini,1936 from the gecko Hemidactylus mabouia, in north Brazil. The endogenous stages of the two parasites in the small intestine are described. Those of I. ameivae are intracytoplasmic, whereas those of I. hemidactyli are intranuclear.

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The ultrastructure is described of the meronts, microgamonts and young oocyst stages of Isospora hemidactyli of the gecko Hemidactylus mabouia from Belém, PA, north Brazil. The endogenous stages all develop in the nucleus of the gut epithelial cells. The nucleus remains intact up to the latest stages of the parasite's development, but degenerates by the time the oocyst appears. Merogonic division appears to be asynchronous, and some of the differentiated merozoites contained more than one nucleus. Microgamonts conform in structure with those of other eimeriids. Some of the type 2 wall-forming bodies disintegrate into smaller globules and ground substance of lower density.

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Octocrylene (2-ethylhexyl 2-cyano-3,3-diphenyl-2-propenoate) is present in several sunscreens and is known to work synergistically with UV filters. We prepared eight octocrylene-related compounds to test their photoprotective activities by measuring diffuse transmittance. The compounds had varied photoprotection profiles, with Sun Protection Factors (SPF) ranging from 1 to 5 and UVA Protection Factors (UVAPF) ranging from 1 to 8. Compounds 4, 5, and 7 showed the best protection against UVB sunrays, while compounds 5, 6, and 7 presented the best results for protection from UVA, so compound 7 had the most balanced protection overall. Results for compounds 4, 8, and 9 are reported for the first time in the literature.

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The European Union's (EU) decision to include aviation into the Emissions Trade Scheme was heatedly contested. Countries around the world, but mainly the Brazil, Russia, India, China and South Africa group (BRICS) and the US, denounced the EU's initiate as illegal and unilateral. Following a decade of frustrated negotiations at the International Civil Aviation Organization (ICAO), this paper interrogates why such measure, in principle climate-friendly, inspired so much global resentment. I argue that concerns with competitiveness and risks of legal inconsistency are important, but insufficient elements to explain the core of the conflict. The paper suggests that the EU was strongly criticized because third countries perceived this action as an imposed solution, which fostered an environment of distrust. Therefore, I claim that the problem has more to do with a normative divide than with a substantive divergence on what should be done regarding aviation emissions. My analysis is informed by the present literature on the links between trade and climate change, but gives particular weight to first-hand information through interviews with key stakeholders. The paper is divided in three parts. First, it presents the scope of the EU directive in historical perspective. Second, it explores the EU's measure through three different angles: legal, economical and political. The final part explores some possible solutions to overcome these divergences.

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After the transfer of the Portuguese administration to China, Macau kept its role as a bridge between East and West, inspired in the Portuguese settlement 500 years ago. The pragmatism of the Chinese central government, using the Lusophone specificities of this Special Administrative Region, supported the creation of the Forum for Economic and Trade Cooperation between China and the Portuguese-speaking Countries, reviving the statute of the Portuguese language and culture in its own territory.

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A description is given of Madathamugadia wanjii n. sp., a Splendidofilariinae parasite of the gecko Ptyodactylus hasselquistii, on the west bank of the River Jordan and of its life cycle in Phlebotomus duboscqi. The new species is close to M. ivaschkini (Annaev, 1976) n. comb., of Turkmenistan, wich is also transmitted by sandflies (Reznik, 1982). The genus Madathamugadia is now comprised of four species, two from Madagascar and two from the Mediterranean sub-region; it differs from the genus Thamugadia by the presence of a double row of papillae anterior to the cloaca of the male. The larval characters of Splendidofilarinae of lizards confirm the affinity of these parasites to the Splendidofilarinae of birds (Chandlerella and Splendidofilaria); the first group could have arisen from the second by "captures" wich could have occurred in several places.

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Arthropod-borne diseases caused by a variety of microorganisms such as dengue virus and malaria parasites afflict billions of people worldwide imposing major economic and social burdens. Despite many efforts, vaccines against diseases transmitted by mosquitoes, with the exception of yellow fever, are not available. Control of such infectious pathogens is mainly performed by vector management and treatment of affected individuals with drugs. However, the numbers of insecticide-resistant insects and drug-resistant parasites are increasing. Therefore, inspired in recent years by a lot of new data produced by genomics and post-genomics research, several scientific groups have been working on different strategies to control infectious arthropod-borne diseases. This review focuses on recent advances and perspectives towards construction of transgenic mosquitoes refractory to malaria parasites and dengue virus transmission.

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Inspired by the structure and biological activities of resorcinolic lipids and, particularly cytosporone A- a potent inhibitor of plantule germination and growth, we have performed the synthesis of the analogs 3-heptyl-3-hydroxy-5,7-dimethoxy-2-benzofuran-1(3H)-one (1) and 3-heptyl-3-hydroxy-4,6-dimethoxy-2-benzofuran-1(3H)-one (2). The intermediates and products were submitted to allelopathic test using Lactuca sativa L. seeds. Target compound 1 showed an inhibitory effect on germination and growth of hypocotyl and radicle in milimolar range.

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The article discusses how Nietzsche understands the institution of law and morals in distinction to Kant and the Christian tradition. It argues that Nietzsche to a large extent is inspired by the paradigm-shift toward a evolutionary biological thinking introduced by several of his peers in the late 19th century, among else F. A. Lange, who sees this shift as a sobering scientific-materialistic alternative to Kant. In Nietzsche, the Kantian moral imperative is replaced with a notion of a morality emerging thanks to historical, or pre-historical, civilizational processes, imposed on a feebleminded human without any inherent rational dispositions to obey Law. It is also a process, which rather than universalizing the human, splits it in a duality where one part obeys old immediate self-interests and another part obeys new 'commands,' having been shouted 'into the ear' by a so-called 'commander.' The compliance with law takes two radically different forms in Nietzsche: servile and mediocre individuals need to be exposed to discipline and punishment in order to adopt Law; while so-called 'sovereign' individuals are able to impose law upon themselves. The figure of the 'sovereign' has consequently been an issue for vigorous debate in especially the Anglo-Saxon tradition of Nietzsche research, since his apparent 'respect for law' and 'sense of duty' reiterate typical Kantian qualities. Relating to these discussions, I suggest that Nietzsche's 'sovereign' (in one context) is identical his 'commander' (in other contexts). When the 'sovereign' as such imposes law upon himself and others, his act is conventional and arbitrary (like language in Saussure), and is rather irrational than rational as in Kant. His will is not a good will, nor a rational will with a vision of human autonomy. His command of himself and others is a performative, thus without truth-value (like illocutionary speech-acts in Austin and Searle).

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The objective of the present study was to determine the effects of hypoxia and temperature on the cardiovascular and respiratory systems and plasma glucose levels of the winter bullfrog Rana catesbeiana. Body temperature was maintained at 10, 15, 25 and 35oC for measurements of breathing frequency, heart rate, arterial blood pressure, metabolic rate, plasma glucose levels, blood gases and acid-base status. Reducing body temperature from 35 to 10oC decreased (P<0.001) heart rate (bpm) from 64.0 ± 3.1 (N = 5) to 12.5 ± 2.5 (N = 6) and blood pressure (mmHg) (P<0.05) from 41.9 ± 2.1 (N = 5) to 33.1 ± 2.1 (N = 6), whereas no significant changes were observed under hypoxia. Hypoxia-induced changes in breathing frequency and acid-base status were proportional to body temperature, being pronounced at 25oC, less so at 15oC, and absent at 10oC. Hypoxia at 35oC was lethal. Under normoxia, plasma glucose concentration (mg/dl) decreased (P<0.01) from 53.0 ± 3.4 (N = 6) to 35.9 ± 1.7 (N = 6) at body temperatures of 35 and 10oC, respectively. Hypoxia had no significant effect on plasma glucose concentration at 10 and 15oC, but at 25oC there was a significant increase under conditions of 3% inspired O2. The arterial PO2 and pH values were similar to those reported in previous studies on non-estivating Rana catesbeiana, but PaCO2 (37.5 ± 1.9 mmHg, N = 5) was 3-fold higher, indicating increased plasma bicarbonate levels. The estivating bullfrog may be exposed not only to low temperatures but also to hypoxia. These animals show temperature-dependent responses that may be beneficial since during low body temperatures the sensitivity of most physiological systems to hypoxia is reduced

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Hypoxia elicits hyperventilation and hypothermia, but the mechanisms involved are not well understood. The nitric oxide (NO) pathway is involved in hypoxia-induced hypothermia and hyperventilation, and works as a neuromodulator in the central nervous system, including the locus coeruleus (LC), which is a noradrenergic nucleus in the pons. The LC plays a role in a number of stress-induced responses, but its participation in the control of breathing and thermoregulation is unclear. Thus, in the present study, we tested the hypothesis that LC plays a role in the hypoxia-induced hypothermia and hyperventilation, and that NO is involved in these responses. Electrolytic lesions were performed bilaterally within the LC in awake unrestrained adult male Wistar rats weighing 250-350 g. Body temperature and pulmonary ventilation (VE) were measured. The rats were divided into 3 groups: control (N = 16), sham operated (N = 7) and LC lesioned (N = 19), and each group received a saline or an NG-nitro-L-arginine methyl ester (L-NAME, 250 µg/µl) intracerebroventricular (icv) injection. No significant difference was observed between control and sham-operated rats. Hypoxia (7% inspired O2) caused hyperventilation and hypothermia in both control (from 541.62 ± 35.02 to 1816.18 ± 170.7 and 36.3 ± 0.12 to 34.4 ± 0.09, respectively) and LC-lesioned rats (LCLR) (from 694.65 ± 63.17 to 2670.29 ± 471.33 and 36 ± 0.12 to 35.3 ± 0.12, respectively), but the increase in VE was higher (P<0.05) and hypothermia was reduced (P<0.05) in LCLR. L-NAME caused no significant change in VE or in body temperature under normoxia, but abolished both the hypoxia-induced hyperventilation and hypothermia. Hypoxia-induced hyperventilation was reduced in LCLR treated with L-NAME. L-NAME also abolished the hypoxia-induced hypothermia in LCLR. The present data indicate that hypoxia-induced hyperventilation and hypothermia may be related to the LC, and that NO is involved in these responses.

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The carotid bodies of rats made chronically hypoxic by breathing 12% O2 in a normobaric chamber (inspired PO2 91 mmHg) were compared with those of controls. Serial 5-µm sections of the organs were examined using an interactive image analysis system. The total volume of the carotid bodies was increased by 64%. The total vascular volume rose by 103% and was likely due to an increase in size of the large vessels (>12 µm lumen diameter) because the small vessel (5-12 µm lumen diameter) volume did not increase significantly while the small vessel density tended to decrease. The extravascular volume was increased by 57%. Expressed as a percentage of the total volume of the organ, the total vascular volume did not change, but the small vessel volume was significantly decreased from 7.83 to 6.06%. The large vessel volume must therefore have been increased. The proportion occupied by the extravascular volume was virtually unchanged (84 vs 82%). In accordance with these findings, the small vessel endothelial surface area per unit carotid body volume was diminished from 95.2 to 76.5 mm-1, while the extravascular area per small vessel was increased from 493 to 641 µm2 or by 30%. In conclusion, the enlargement of the carotid body in chronic hypoxia is most likely due to an increase in total vascular volume, mainly involving the "large" vessels, and to an increase in extravascular volume. This is in contrast to our previously published findings indicating that in the spontaneous insulin-dependent diabetic rat the enlargement of the carotid body is due solely to an increase in extravascular volume.

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Mechanical ventilation with high tidal volumes (V T) has been shown to induce lung injury. We examined the hypothesis that this procedure induces lung injury with inflammatory features. Anesthetized male Wistar rats were randomized into three groups: group 1 (N = 12): V T = 7 ml/kg, respiratory rate (RR) = 50 breaths/min; group 2 (N = 10): V T = 21 ml/kg, RR = 16 breaths/min; group 3 (N = 11): V T = 42 ml/kg, RR = 8 breaths/min. The animals were ventilated with fraction of inspired oxygen of 1 and positive end-expiratory pressure of 2 cmH2O. After 4 h of ventilation, group 3, compared to groups 1 and 2, had lower PaO2 [280 (range 73-458) vs 517 (range 307-596), and 547 mmHg (range 330-662), respectively, P<0.05], higher wet lung weight [3.62 ± 0.91 vs 1.69 ± 0.48 and 1.44 ± 0.20 g, respectively, P<0.05], and higher wet lung weight/dry lung weight ratio [18.14 (range 11.55-26.31) vs 7.80 (range 4.79-12.18), and 6.34 (range 5.92-7.04), respectively, P<0.05]. Total cell and neutrophil counts were higher in group 3 compared to groups 1 and 2 (P<0.05), as were baseline TNF-alpha concentrations [134 (range <10-386) vs 16 (range <10-24), and 17 pg/ml (range <10-23), respectively, P<0.05]. Serum TNF-alpha concentrations reached a higher level in group 3, but without statistical significance. These results suggest that mechanical ventilation with high V T induces lung injury with inflammatory characteristics. This ventilatory strategy can affect the release of TNF-alpha in the lungs and can reach the systemic circulation, a finding that may have relevance for the development of a systemic inflammatory response.

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Tumor necrosis factor-alpha (TNF-alpha) is one of the most important proinflammatory cytokines which plays a central role in host defense and in the acute inflammatory response related to tissue injury. The major source of TNF-alpha are immune cells such as neutrophils and macrophages. We tested the hypothesis that pentoxifylline, a methylxanthine derivative, down-regulates proinflammatory cytokine expression during acute lung injury in rats. Male Wistar rats weighing 250 to 450 g were anesthetized ip with 50 mg/kg sodium thiopental and randomly divided into three groups: group 1 (N = 7): tidal volume (V T) = 7 ml/kg, respiratory rate (RR) = 50 breaths/min and normal saline infusion; group 2 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and normal saline infusion; group 3 (N = 7): V T = 42 ml/kg, RR = 9 breaths/min and pentoxifylline infusion. The animals were ventilated with an inspired oxygen fraction of 1.0, a positive end-expiratory pressure of 3 cmH2O, and normal saline or pentoxifylline injected into the left femoral vein. The mRNA of TNF-alpha rapidly increased in the lung tissue within 180 min of ventilation with a higher V T with normal saline infusion. The concentrations of inflammatory mediators were decreased in plasma and bronchoalveolar lavage (BAL) in the presence of higher V T with pentoxifylline infusion (TNF-alpha: plasma, 102.2 ± 90.9 and BAL, 118.2 ± 82.1; IL-1ß: plasma, 45.2 ± 42.7 and BAL, 50.2 ± 34.9, P < 0.05). We conclude that TNF-alpha produced by neutrophil influx may function as an alert signal in host defense to induce production of other inflammatory mediators.

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The interaction between pulmonary ventilation (V E) and body temperature (Tb) is essential for O2 delivery to match metabolic rate under varying states of metabolic demand. Hypoxia causes hyperventilation and anapyrexia (a regulated drop in Tb), but the neurotransmitters responsible for this interaction are not well known. Since L-glutamate is released centrally in response to peripheral chemoreceptor stimulation and glutamatergic receptors are spread in the central nervous system we tested the hypothesis that central L-glutamate mediates the ventilatory and thermal responses to hypoxia. We measured V E and Tb in 40 adult male Wistar rats (270 to 300 g) before and after intracerebroventricular injection of kynurenic acid (KYN, an ionotropic glutamatergic receptor antagonist), alpha-methyl-4-carboxyphenylglycine (MCPG, a metabotropic glutamatergic receptor antagonist) or vehicle (saline), followed by a 1-h period of hypoxia (7% inspired O2) or normoxia (humidified room air). Under normoxia, KYN (N = 5) or MCPG (N = 8) treatment did not affect V E or Tb compared to saline (N = 6). KYN and MCPG injection caused a decrease in hypoxia-induced hyperventilation (595 ± 49 for KYN, N = 7 and 525 ± 84 ml kg-1 min-1 for MCPG, N = 6; P < 0.05) but did not affect anapyrexia (35.3 ± 0.2 for KYN and 34.7 ± 0.4ºC for MCPG) compared to saline (912 ± 110 ml kg-1 min-1 and 34.8 ± 0.2ºC, N = 8). We conclude that glutamatergic receptors are involved in hypoxic hyperventilation but do not affect anapyrexia, indicating that L-glutamate is not a common mediator of this interaction.