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A licitação é o meio utilizado por entidades públicas para que sejam efetuadas as aquisições e contratações; porém, há casos específicos em que é dispensável a sua realização. Nessas ocasiões, aplica-se a sua inexigibilidade ou a sua dispensa. A dispensa de licitação, objeto da presente pesquisa, pode ser realizada por dois procedimentos diferentes: o primeiro é o método tradicional, que fora adotado desde a implementação da Lei 8.666/1993 e, o segundo, é a cotação eletrônica, que foi regulamentada através da Portaria no 306/2001 como uma forma de buscar maior transparência, redução de custos e agilidade nos processos de aquisição. Neste contexto, o trabalho objetivou avaliar comparativamente, em relação à tempestividade, economicidade e competitividade, como ocorre o processo de aquisição de bens em situações de dispensa de licitação na Empresa Brasileira de Pesquisa Agropecuária (EMBRAPA/CNPMF), situada na cidade de Cruz das Almas - BA. Para alcançar esse objetivo, realizou-se uma pesquisa descritiva, de caráter quali-quantitativo, através de um estudo de caso. Os dados analizados provem do levantamento e análise dos processos de dispensa tradicional e por cotação eletrônica, realizados na EMBRAPA durante os anos de 2009 a 2016. Os dados foram coletados de processos constantes no sitio de compras governamentais e de processos físicos arquivados na unidade. Os resultados encontrados demonstraram que a cotação eletrônica, no período de estudo, se mostrou mais vantajosa para a EMBRAPA do que a dispensa tradicional, visto que obteve uma maior tempestividade, prazos menores de realização e números maiores de fornecedores participantes, demonstrando elevada competitividade; e também obteve mais economicidade, pois a média de valores dos anos foi menor que o método tradicional.

A incontinência urinária é uma afecção multifatorial entre as causas de perda de força e funcionalidade do assoalho pélvico. Para iní­cio do diagnóstico, prognóstico e tratamento, o assoalho pélvico pode ser avaliado por meio da eletromiografia, que é um dos métodos de maior especificidade. A prevalência de incontinência urinária em adultas jovens vem crescendo afetando aspectos fí­sicos, sociais, ocupacionais e/ou sexuais destas mulheres. Por isso, o objetivo deste estudo foi avaliar a atividade eletromiográfica dos músculos do assoalho pélvico e do reto abdominal, bem como os dados obtidos por meio do King"™s Health Questionnaire em adultas jovens incontinentes. Para isso, foram avaliadas 14 mulheres com idade de 21 a 29 anos, que responderam a ficha de anamnese e King"™s Health Questionnaire e realizaram o protocolo de eletromiografia por meio de dois testes (um para fibra fásica e outro para fibra tônica) em cada uma das duas posições propostas (decúbito dorsal e ortostatismo). O estudo apontou pouca interferência na qualidade de vida, obtendo-se escores baixos no King"™s Health Questionnaire. Na eletromiografia, percebeu-se uma maior efetividade nas amplitudes de contração de fibras fásicas em ortostatismo e de fibras tônicas em decúbito dorsal.Palavras-chave: incontinência urinária, eletromiografia, diafragma da pelve, qualidade de vida.

We have interpreted the two-photon absorption spectrum of water-soluble copper indium sulfide (CIS) QDs with stoichiometry 0.18 (Cu), 0.42 (In), and 2 (S) and an average diameter of approximately 2.6 nm. For that, we employed the wavelength-tunable femtosecond Z-scan technique and the parabolic effective-mass approximation model, in which the excitonic transition energies were phenomenologically corrected due to the stoichiometry of the nanocrystal. This model considers a conduction band and three valence sub-bands allowing excitonic transitions via centrosymmetric (Δl = ±1, where l is the angular momentum of the absorbing state) and non-centrosymmetric (Δl = 0) channels. In such case, this became relevant because the CIS QDs with chalcopyrite crystalline structure is a non-centrosymmetric semiconductor. Thus, our experimental results pointed out two 2 PA allowed bands located at 715 nm (2hv = 3.47 eV) and 625 nm (2hv = 3.97 eV) with cross sections of (6.3 ± 1.0) x 102 GM and (4.5 ± 0.7) x 102 GM, respectively. According to the theoretical model, these 2 PA bands can be ascribed to the 1P1/2(h3) → 1S3/2(e) (lower energy band) and 1P1/2(hheavy) → 1S3/2(e) (90%)/(10%)1P1/2(hsplit-off) → 1P3/2(e) (higher energy band) excitonic transitions. A good agreement (magnitude and spectral position) between the experimental and theoretical data were obtained. However, our experimental data suggest that the higher-energy 2 PA band may have other contributions due to the mixing between the heavy- and the light-hole bands, which the effective mass model does not take into consideration.

Significant knowledge gaps exist regarding the fate and transport of persistent organic pollutants like dichlorodiphenyltrichloroethane (DDT) in tropical environments. In Brazil, indoor residual spraying with DDT to combat malaria and leishmaniasis began in the 1950s and was banned in 1998. Nonetheless, high concentrations of DDT and its metabolites were recently detected in human breast milk in the community of Lake Puruzinho in the Brazilian Amazon. In this work, we couple analysis of soils and sediments from 2005 to 2014 at Puruzinho with a novel dynamic floodplain model to investigate the movement and distribution of DDT and its transformation products (dichlorodiphenyldichloroethylene (DDE) and dichlorodiphenyldichloroethane (DDD)) and implications for human exposure. The model results are in good agreement with the accumulation pattern observed in the measurements, in which DDT, DDE, and DDD (collectively, DDX) accumulate primarily in upland soils and sediments. However, a significant increase was observed in DDX concentrations in soil samples from 2005 to 2014, coupled with a decrease of DDT/DDE ratios, which do not agree with model results assuming a post-ban regime. These observations strongly suggest recent use. We used the model to investigate possible re-emissions after the ban through two scenarios: one assuming DDT use for IRS and the other assuming use against termites and leishmaniasis. Median DDX concentrations and p,p'-DDT/p,p'-DDE ratios from both of these scenarios agreed with measurements in soils, suggesting that the soil parameterization in our model was appropriate. Measured DDX concentrations in sediments were between the two re-emission scenarios. Therefore, both soil and sediment comparisons suggest re-emissions indeed occurred between 2005 and 2014, but additional measurements would be needed to better understand the actual re-emission patterns. Monte Carlo analysis revealed model predictions for sediments were very sensitive to highly uncertain parameters associated with DDT degradation and partitioning. With this model as a tool for understanding inter-media cycling, additional research to refine these parameters would improve our understanding of DDX fate and transport in tropical sediments.

Cyclosporine (CsA) blocks in vitro polyclonal activation of primary murine T-cells in a complex manner. This cannot be completely reversed by exogenous IL2, and leads to a partial blockade in expression of the IL2 receptor (p55 chain) and, more intensely, in CD69. In proliferation assays, T-cells recovered from CsA-treated cultures and washed free from CsA were markedly refractory to restimulation in the presence of fresh accessory cells. In cell titration restimulation assays, CsA-treated, but not control T-cells, were also markedly unresponsive to accessory cell-independent stimuli provided by immobilized anti-CD3 antibody or rIL2, combined to phorbol ester. CsA-treated, but not control activated T-cells, undergo progressive cell death after drug removal and reculturing. In contrast, primary T-cells activated by a CsA-resistant pathway (rIL2 plus phorbol ester) and treated with CsA, did not develop unresponsiveness, compared to controls. When primary T-cells were stimulated with rIL2 plus phorbol ester in the presence of the calcium ionophore ionomycin, treatment with CsA resulted in marked unresponsiveness of the T-cells, compared to untreated controls. The data indicate that primary activation of T-cells in vitro in the presence of CsA induces an unresponsive state which lasts independent of the presence of CsA, and results in progressive cell death. We suggest that these effects could characterize one additional mechanism of CsA action in vivo.

Resting murine T cell activation induced by either CD3 complexes or Thy1 molecules was investigated in vitro, using surface-bound anti-CD3 mAb as the stimulus. One mitogenic anti-Thy 1 mAb (G7) lost mitogenicity when presented to T cells immobilized on a plastic surface, even in the presence of phorbol ester. Moreover, T cell activation induced by immobilized anti-CD3 was potently blocked by coimmobilized anti-Thy 1 mAb. Nonmitogenic anti-Thy 1 mAb also blocked CD3-induced activation when coimmobilized with anti-CD3. Control experiments showed that anti-Thy 1 specifically blocked T cell activation, even in the presence of measurable and functional concentrations of plastic-bound anti-CD3. Coimmobilized anti-Thy 1 potently blocked IL2 secretion stimulated by anti-CD3. Addition of exogenous rIL2 completely prevented anti-Thy 1-mediated blockade. On the other hand, while completely blocking T cell proliferation, immobilized anti-Thy 1 only partially blocked secretion of IL3-like activity by the T cells. One IgM anti-Thy 1 mAb (2A3) induced secretion of IL3-like activity by T cells when immobilized in the absence of bound anti-CD3. These results indicate that extensive aggregation of Thy 1 molecules delivers a potent negative signal which antagonizes CD3-mediated T cell activation and growth.

The roles of potassium and calcium in the slow hyperpolarizations of membranes of activated macrophages are investigated using standard intracellular electrical recording techniques. The amplitude of spontaneous slow hyperpolarizations decreases as a logarithmic function of the external potassium concentration in the culture medium. Similar dependence on the potassium gradient is observed when different levels of membrane potentials are imposed by constant current injection. The reversal potential for electrically evoked slow hyperpolarizations is −90 mV. A 10-fold increase in external potassium concentration causes a 60 mV shift of the reversal potential towards zero. Divalent cation ionophores (A23187 and X537A) can induce slow hyperpolarization responses in quiescent cells or permanent hyperpolarization in spontaneously active cells. The amplitude of the ionophore-induced hyperpolarizations is reduced by an increase in external potassium concentration in a manner consistent with data on slow hyperpolarization responses in the absence of ionophore. The calcium antagonist, verapamil, depresses the slow hyperpolarization responses at the concentration of 10−5 M. It is suggested that the development of the hyperpolarizing response is due to a calcium-dependent potassium channel. The data support the assumption that spontaneous and artificially elicited slow hyperpolarization responses share a common calcium-dependent mechanism.

Cell interaction mechanisms play a crucial role in almost all biological processes. This volume covers many of the areas in which the study of direct cell-to-cell communication has been used as a tool to probe the nature of several phenomena. Immunology deals with a complex of cellular and humoral factors that allow an organism not only to recognize its own cells but also to react to foreign cells and detect the deviation from self to nonself due to cell transformation.

Effects of four known blockers of T-lymphocyte potassium channels [verapamil, quinine, 4-aminopyridine (4-AP) and tetraethylammonium (TEA)], were studied on polyclonal T-cell activation induced by two plant mitogens (phytohemmaglutinin; PHA and concanavalin A; ConA), a mitogenic anti-Thy 1.2 monoclonal antibody (mAb G7) and phorbol ester (phorbol myristate acetate; PMA). Potassium channel blockers blocked all four modes of T-cell activation in a dose-dependent fashion with the same rank order of potency (verapamil greater than quinine greater than 4-AP greater than TEA). Kinetic studies of the timing of potassium channel blocker effect, indicated that, while 4-AP and TEA interfere only with early events of T-cell activation, verapamil and quinine can also interfere with later steps of T-cell mitogenesis. This notion was confirmed by studies of interleukin 2(IL-2)-directed activated T-cell growth. Verapamil and quinine blocked this late step in different types of activated T-cells with the same potency they blocked induction of resting T-cell mitogenesis. On the other hand, 4-AP and TEA, at maximal inhibitory doses for resting T-cells, showed little or no effect at IL-2-directed growth. Kinetic studies of the timing of quinine effect showed that the target of quinine action on activated T-cells is critically involved in IL-2 signalling within the first 2-4 h of IL-2 addition. These studies suggest that, besides the voltage-gated potassium channel previously described, a second target for verapamil and quinine action controls IL-2-derived signals to activated T-cells.

Electrophysiological properties of activated mouse macrophages cultured in vitro were studied using microelectrode techniques. In a high percentage of the individual cells analysed a slow hyperpolarization (SH) was observed with a concomitant decrease (2–4 times) of the input resistance. Increasing doses of tetraethyl ammonium progressively reduce the amplitude of the SH and at a concentration of 15 mM complete blockade of the phenomena is observed. Valinomycin, at a concentration of 10−7 M produces rapid and permanent hyperpolarization, with a shift in the membrane potential to about −50 mV. These data strongly support the previously proposed hypothesis that the development of SH is due to an increase in the membrane permeability to potassium ions.

We have recently demonstrated that polyclonal T-cell activation induced by PHA defines an activation pathway which is resistant to blockade by barium (Ba2+) ions. Other modes of T-cell activation, including ConA-induced responses, are completely blocked by Ba2+, which seems to affect an early Ca2+-dependent step of T-cell activation, as determined by kinetic and competition experiments. In the present study, we have analysed the lymphokine requirements of Ba2+-resistant pathway of PHA-induced T-cell activation by means of functional blocking experiments with monoclonal antibodies (mAbs) directed against mouse IL-2 (mAb S4B6) and against mouse IL-4 (mAb 11B11). We found that Ba2+-resistant T-cell activation can be blocked by either S4B6 or 11B11. Thus, both IL-2 and IL-4 participate in Ba2+-resistant T-cell growth induced by PHA. In addition, we found that cyclosporin A (CsA) completely blocks T-cell activation induced by either ConA or by PHA plus Ba2+, but not T-cell activation induced by PHA in the absence of Ba2+, which is reduced by less than 50% in most experiments. This CsA-resistant proliferative component of the PHA response is, thus, distinct from the Ba2+-resistant response, and is carried out by proliferating T-cells. Although mAbs S4B6 and 11B11 are potent blockers of ConA-induced responses, they failed to block CsA-resistant T-cell growth induced by PHA. At the doses of CsA employed, no IL-2 and/or IL-4 activity could be detected in the supernatants of CsA-treated, PHA-stimulated T-cell cultures. The data indicate that this CsA-resistant pathway is both IL-2 and IL-4-independent. The lymphokine involved in this T-cell activation pathway remains to be identified.

The role of Ia antigens expressed at the level of the antigen-presenting cell (APC) or macrophage has been firmly established as essential to the process of antigen recognition by T cells (1, 2). The observation that only responder but not nonresponder parental macrophages can present the relevant immune response (Ir) gene controlled antigen to (responder x nonresponder)F1 T lymphocytes suggested that the Ir gene products are functionally expressed at the level of the APC (3). Further studies on the Ir gene control of T cell responses to native and synthetic insulin polypeptides (4, 5) were consistent with the view that the ability to select and display a specific antigen epitope to the immune T cell is an Ir gene function expressed by the APC-the “determinant selection model.”