As políticas de saúde no Brasil: reconstrução histórica e perspectivas atuais

A partir de revisão bibliográfica, as autoras discorrem sobre a questão das políticas públicas de saúde no Brasil, procedendo a uma re-leitura do processo. Apontam para a importância da discussão sobre a questão nos cursos de graduação em Enfermagem.

Pela reconstrução dos mitos da enfermagem a partir da qualidade emancipatória do cuidado

Esse estudo teórico se debruça sobre a influencia dos mitos e tradições históricas da enfermagem na prática profissional, presentes em muitos dos seus agentes, à luz triedro emancipatório do cuidar, expresso pelo conhecer para cuidar melhor, cuidar para confrontar, cuidar para emancipar. Remete-se ao estudo da fragilidade política do enfermeiro para desvelar aspectos conservadores e positivistas recorrentes na profissão, fruto da historicidade que a constrói. Objetiva-se refletir teoricamente sobre os discursos conservadores da enfermagem e indicar, com base na perspectiva emancipatória do cuidar, possibilidades para reconstrução do fazer histórico da categoria, ampliando as dimensões da prática social. Propõe-se que a enfermagem assuma os mitos e ritos como ricas contradições da realidade, desmitificando-os reflexivamente por meio da politicidade do cuidado (mediação entre ajuda e poder capaz de forjar autonomias).

Influência dos parâmetros de reconstrução analíticos e iterativos na cintigrafia de perfusão do miocárdio

As guidelines de cardiologia nuclear europeia e americanas não são específicas na escolha dos melhores parâmetros de reconstrução de imagem a utilizar na Cintigrafia de Perfusão do Miocárdio (CPM). Assim, o presente estudo teve como objectivo estabelecer e comparar o efeito dos parâmetros quantitativos dos métodos de reconstrução: Retroprojecção Filtrada (FBP) e Ordered ‑Sub‑set Expectation Maximization (OSEM). Métodos: Foi utilizado um fantoma cardíaco, cujos valores do volume telediastólico (VTD), volume telesistólico (VTS) e fracção de ejecção ventricular esquerda (FEVE) eram conhecidos. O software Quantitative Gated SPECT/Quantitative Perfusion SPECT foi utilizado em modo semi‑automático, a fim de obter esses parâmetros quantitativos. O filtro Butterworth foi usado no FBP com as frequências de corte entre 0,2 e 0,8 ciclos/pixel combinadas com as ordens de 5, 10, 15 e 20. Na reconstrução OSEM, foram utilizados os subconjuntos 2, 4, 6, 8, 10, 12 e 16, combinados com os números de iterações de 2, 4, 6, 8, 10, 12, 16, 32 e 64. Durante a reconstrução OSEM efectuou‑se uma outra reconstrução baseada no número de iterações equivalentes - Expectation‑Maximization (EM) 12, 14, 16, 18, 20, 22, 26, 28, 30 e 32. Resultados: Após a reconstrução com FBP verificou‑se que os valores de VTD e VTS aumentavam com o aumento da frequência de corte, enquanto o valor da FEVE diminui. Esse mesmo padrão é verificado na reconstrução OSEM. No entanto, com OSEM há uma estimativa mais precisa dos parâmetros quantitativos, especialmente com as combinações 2I × 10S e 12S × 2I. Conclusão: A reconstrução OSEM apresenta uma melhor estimativa dos parâmetros quantitativos e uma melhor qualidade de imagem do que a reconstrução com FBP. Este estudo recomenda o uso de 2 iterações com 10 ou 12 subconjuntos para a reconstrução OSEM e uma frequência de corte de 0,5 ciclos/pixel com as ordens 5, 10 ou 15 para a reconstrução com FBP como a melhor estimativa para a quantificação da FEVE através da CPM.

Alveolar epithelial CNGA1 channels mediate cGMP-stimulated, amiloride-insensitive, lung liquid absorption.

Impairment of lung liquid absorption can lead to severe respiratory symptoms, such as those observed in pulmonary oedema. In the adult lung, liquid absorption is driven by cation transport through two pathways: a well-established amiloride-sensitive Na(+) channel (ENaC) and, more controversially, an amiloride-insensitive channel that may belong to the cyclic nucleotide-gated (CNG) channel family. Here, we show robust CNGA1 (but not CNGA2 or CNGA3) channel expression principally in rat alveolar type I cells; CNGA3 was expressed in ciliated airway epithelial cells. Using a rat in situ lung liquid clearance assay, CNG channel activation with 1 mM 8Br-cGMP resulted in an approximate 1.8-fold stimulation of lung liquid absorption. There was no stimulation by 8Br-cGMP when applied in the presence of either 100 μM L: -cis-diltiazem or 100 nM pseudechetoxin (PsTx), a specific inhibitor of CNGA1 channels. Channel specificity of PsTx and amiloride was confirmed by patch clamp experiments showing that CNGA1 channels in HEK 293 cells were not inhibited by 100 μM amiloride and that recombinant αβγ-ENaC were not inhibited by 100 nM PsTx. Importantly, 8Br-cGMP stimulated lung liquid absorption in situ, even in the presence of 50 μM amiloride. Furthermore, neither L: -cis-diltiazem nor PsTx affected the β(2)-adrenoceptor agonist-stimulated lung liquid absorption, but, as expected, amiloride completely ablated it. Thus, transport through alveolar CNGA1 channels, located in type I cells, underlies the amiloride-insensitive component of lung liquid reabsorption. Furthermore, our in situ data highlight the potential of CNGA1 as a novel therapeutic target for the treatment of diseases characterised by lung liquid overload.

Should possible recurrence of disease contraindicate liver transplantation in patients with end-stage alveolar echinococcosis? A 20-year follow-up study.

Liver transplantation (LT) is currently contraindicated in patients with residual or metastatic alveolar echinococcosis (AE) lesions. We evaluated the long-term course of such patients who underwent LT and were subsequently treated with benzimidazoles. Clinical, imaging, serological, and therapeutic data were collected from 5 patients with residual/recurrent AE lesions who survived for more than 15 years. Since 2004, [(18) F]-2-fluoro-2-deoxyglucose (FDG)-positron emission tomography (PET) images were available, and the levels of serum antibodies (Abs) against Echinococcus multilocularis-recombinant antigens were evaluated. Median survival time after LT was 21 years. These patients were from a prospective cohort of 23 patients with AE who underwent LT: 5 of 8 patients with residual/recurrent AE and 4 of 9 patients without residual/recurrent AE were alive in September 2009. High doses of immunosuppressive drugs, the late introduction of therapy with benzimidazoles, its withdrawal due to side effects, and nonadherence to this therapy adversely affected the prognosis. Anti-Em2(plus) and anti-rEm18 Ab levels and standard FDG-PET enabled the efficacy of therapy on the growth of EA lesions to be assessed. However, meaningful variations in Ab levels were observed below diagnostic cutoff values; and in monitoring AE lesions, images of FDG uptake taken 3 hours after its injection were more sensitive than images obtained 1 hour after its injection. In conclusion, benzimidazoles can control residual/recurrent AE lesions after LT. Using anti-rEm18 or anti-Em2(plus) Ab levels and the delayed acquisition of FDG-PET images can improve the functional assessment of disease activity. The potential recurrence of disease, especially in patients with residual or metastatic AE lesions, should not be regarded as a contraindication to LT when AE is considered to be lethal in the short term.

A new infectious mammary tumor virus in the milk of mice implanted with C4 hyperplastic alveolar nodules.

We have previously characterized an infectious mouse mammary tumor virus [(MMTV(SW)] which induces a strong superantigen response in vivo. Here we describe the isolation and characterization of MMTV(C4) which was derived from milk of mice implanted with hyperplastic alveolar nodules. MMTV(C4) stimulates V beta 2 expressing T cells after local injection in vivo. Comparison with known open reading frame (orf) sequences revealed high homology to Mtv-6, an endogenous virus interacting with V beta 3-expressing T cells. The carboxyl-terminal amino acids were, however, altered. High homology including the carboxyl-terminal orf amino acids were found with MMTV(C3H-K). We show here that MMTV(C3H-K) has lost its superantigen function. Sequence comparisons permitted the characterization of few key amino acids which could be important for T cell receptor interaction and superantigen processing.

Thrombin-induced contraction in alveolar epithelial cells probed by traction microscopy

Contractile tension of alveolar epithelial cells plays a major role in the force balance that regulates the structural integrity of the alveolar barrier. The aim of this work was to study thrombin-induced contractile forces of alveolar epithelial cells. A549 alveolar epithelial cells were challenged with thrombin, and time course of contractile forces was measured by traction microscopy. The cells exhibited basal contraction with total force magnitude 55.0 ± 12.0 nN (mean ± SE, n = 12). Traction forces were exerted predominantly at the cell periphery and pointed to the cell center. Thrombin (1 U/ml) induced a fast and sustained 2.5-fold increase in traction forces, which maintained peripheral and centripetal distribution. Actin fluorescent staining revealed F-actin polymerization and enhancement of peripheral actin rim. Disruption of actin cytoskeleton with cytochalasin D (5 µM, 30 min) and inhibition of myosin light chain kinase with ML-7 (10 µM, 30 min) and Rho kinase with Y-27632 (10 µM, 30 min) markedly depressed basal contractile tone and abolished thrombin-induced cell contraction. Therefore, the contractile response of alveolar epithelial cells to the inflammatory agonist thrombin was mediated by actin cytoskeleton remodeling and actomyosin activation through myosin light chain kinase and Rho kinase signaling pathways. Thrombin-induced contractile tension might further impair alveolar epithelial barrier integrity in the injured lung.

Human alveolar macrophages infected by virulent bacteria expressing SipB are a major source of active interleukin-18.

Recent publications have demonstrated that the protease caspase-1 is responsible for the processing of pro-interleukin 18 (IL-18) into the active form. Studies on cell lines and murine macrophages have shown that the bacterial invasion factor SipB activates caspase-1, triggering cell death. Thus, we investigated the role of SipB in the activation and release of IL-18 in human alveolar macrophages (AM), which are the first line of defense against inhaled pathogens. Under steady-state conditions, AM are a more important source of IL-18 than are dendritic cells (DC) and monocytes. Cytokine production by AM and DC was compared after both types of cells had been infected with a virulent strain of Salmonella enterica serovar Typhimurium and an isogenic sipB mutant, which were used as an infection model. Infection with virulent Salmonella led to marked cell death with features of apoptosis while both intracellular activation and release of IL-18 were demonstrated. In contrast, the sipB mutant did not induce such cell death or the release of active IL-18. The specific caspase-1 inhibitor Ac-YVAD-CMK blocked the early IL-18 release in AM infected with the virulent strain. However, the type of Salmonella infection did not differentially regulate IL-18 gene expression. We concluded that the bacterial virulence factor SipB plays an essential posttranslational role in the intracellular activation of IL-18 and the release of the cytokine in human AM.

Importance of ENaC-mediated sodium transport in alveolar fluid clearance using genetically-engineered mice.

The lung possesses specific transport systems that intra- and extracellularly maintain salt and fluid balance necessary for its function. At birth, the lungs rapidly transform into a fluid (Na(+))-absorbing organ to enable efficient gas exchange. Alveolar fluid clearance, which mainly depends on sodium transport in alveolar epithelial cells, is an important mechanism by which excess water in the alveoli is reabsorbed during the resolution of pulmonary edema. In this review, we will focus and summarize on the role of ENaC in alveolar lung liquid clearance and discuss recent data from mouse models with altered activity of epithelial sodium channel function in the lung, and more specifically in alveolar fluid clearance. Recent data studying mice with hyperactivity of ENaC or mice with reduced ENaC activity clearly illustrate the impaired lung fluid clearance in these adult mice. Further understanding of the physiological role of ENaC and its regulatory proteins implicated in salt and water balance in the alveolar cells may therefore help to develop new therapeutic strategies to improve gas exchange in pulmonary edema.

Professores e dificuldades do ofício: preservação e reconstrução da dignidade profissional

Os professores enfrentam dificuldades geralmente agrupadas sob a denominação vaga de "mal-estar docente". O artigo descreve e analisa, à luz de uma sociologia pragmática, como eles procedem diante da introdução de novas normas de trabalho. Utilizando a resistência, ajustes, astúcias e diversas estratégias, tentam construir o sentido do ofício e sua própria dignidade e, ao mesmo tempo, "salvar a pele". A pesquisa etnográfica, suporte do artigo, mostra que a gestão das dificuldades está na essência do ofício.

ENaC-mediated alveolar fluid clearance and lung fluid balance depend on the channel-activating protease 1.

Sodium transport via epithelial sodium channels (ENaC) expressed in alveolar epithelial cells (AEC) provides the driving force for removal of fluid from the alveolar space. The membrane-bound channel-activating protease 1 (CAP1/Prss8) activates ENaC in vitro in various expression systems. To study the role of CAP1/Prss8 in alveolar sodium transport and lung fluid balance in vivo, we generated mice lacking CAP1/Prss8 in the alveolar epithelium using conditional Cre-loxP-mediated recombination. Deficiency of CAP1/Prss8 in AEC induced in vitro a 40% decrease in ENaC-mediated sodium currents. Sodium-driven alveolar fluid clearance (AFC) was reduced in CAP1/Prss8-deficient mice, due to a 48% decrease in amiloride-sensitive clearance, and was less sensitive to beta(2)-agonist treatment. Intra-alveolar treatment with neutrophil elastase, a soluble serine protease activating ENaC at the cell surface, fully restored basal AFC and the stimulation by beta(2)-agonists. Finally, acute volume-overload increased alveolar lining fluid volume in CAP1/Prss8-deficient mice. This study reveals that CAP1 plays a crucial role in the regulation of ENaC-mediated alveolar sodium and water transport and in mouse lung fluid balance.

La cresta alveolar atrófica en implantología oral

Los implantes dentales endoóseos constituyen una alternativa terapéutica ideal en pacienfes parcial o totalmente edéntulos; sin embargo, en ocasiones, la atrofia ósea generalizada o localizada contraindica el tratamiento, siendo necesario realizar un aumento de cresta alveolar que permita, bien simultáneamente o deforma diferida, la adecuada rehabilitación implantológica. En el presente trabajo, hacemos una revisión de las distintas técnicas y materiales utilizados actualmente en implantología, para mejorar las condiciones de recepción de los implantes, en presencia de defectos óseos.