Gender and the Production of Health Care Services: Issues for Women's Roles in Health Development

Summary Female health workers often make up to 75 per cent or more of the health sector workforce in developing countries, and yet they remain underpaid and relatively powerless. This article looks at the role of women in the production of health care services at different levels within the health sector, discussing primary health care and the effect of the economic crises. The article discusses how professions, which insulate the power and status of doctors, also insulate and rigidify the status and power of nurses. It looks at how this contributes to the limitation of the crucial role of nurses in primary health care. It also looks at the informal sector workers and auxiliaries, the bulk of the female health workers, who are inadequately resourced and vulnerable in their work. The article addresses a research agenda for the subject. Resumé Le genre, les soins de santé primaires et la prestation des services de soins de santé: questions relatives aux rôles des femmes dans le développement des soins de santé durant la décennie à venir Les femmes qui travaillent dans les services de soins de santé constituent souvent 75%, et parfois même plus, de la force ouvrière du secteur des soins de santé au sein des pays en voie de développement; or souvent elles restent sous?rémunérées et relativement écartées du pouvoir. Le présent article examine le rôle des femmes dans la prestation des soins de santé à divers niveaux dans ce secteur; l'auteur y discute les soins de santé primaires ainsi que l'effet des crises économiques. L'article décrit aussi comment les professions qui isolent le pouvoir et le rang socio?économique des médecins sont également responsables pour l'isolement et l'inflexibilité de la situation des infirmières. L'auteur examine aussi la manière dans laquelle ce phénomène peut limiter le rôle crucial des infirmières dans les soins de santé primaires. L'article d'adresse également aux travailleurs et assistants ancillaires dans le secteur général de la santé, principalement des femmes, qui ne possèdent que de faibles ressources et qui sont vulnérables dans leur travail. L'article tente de dresser un calendrier de recherche dans ce domaine. Resumen El Género, la Atención Sanitaria Pública y la Producción de Servicios de Salud: temas para el papel de la mujer en el desarrollo de la salud en la próxima década Las mujeres constituyen el 75% o más del personal de trabajadores de salud en los países en desarrollo, y sin embargo, permanecen relativamente sin ningún control y muy mal pagadas. Este artículo se concentra en el papel de la mujer en la producción de servicios de salud a diferentes niveles dentro del sector sanitario, examinando la atención sanitaria básica y el efecto de las crisis económicas. Expone cómo las profesiones, que aíslan el poder y la posición de los médicos, también rigidizan y aíslan la posición y las atribuciones de las enfermeras. Esto contribuye a la limitación del papel crucial de las enfermeras en el cuidado básico de los pacientes. También se observa al sector de los trabajadores informales y auxiliares, que constituyen la inmensa mayoría de mujeres en el área de la salud, y que sufren de carencia de recursos y vulnerabilidad en su trabajo. El artículo plantea la preparación de una agenda de investigación para este tema

Concise Review: Mesenchymal Stem Cells for Acute Lung Injury: Role of Paracrine Soluble Factor

Morbidity and mortality have declined only modestly in patients with clinical acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), despite extensive research into the pathophysiology. Current treatment remains primarily supportive with lung-protective ventilation and a fluid conservative strategy. Pharmacologic therapies that reduce the severity of lung injury in preclinical models have not yet been translated to effective clinical treatment options. Consequently, further research in translational therapies is needed. Cell-based therapy with mesenchymal stem cells (MSCs) is one attractive new therapeutic approach. MSCs have the capacity to secrete multiple paracrine factors that can regulate endothelial and epithelial permeability, decrease inflammation, enhance tissue repair, and inhibit bacterial growth. This review will focus on recent studies, which support the potential therapeutic use of MSCs in ALI/ARDS, with an emphasis on the role of paracrine soluble factors

Opposing Effects of the Angiopoietins on the Thrombin-Induced Permeability of Human Pulmonary Microvascular Endothelial Cells

BACKGROUND: Angiopoietin-2 (Ang-2) is associated with lung injury in ALI/ARDS. As endothelial activation by thrombin plays a role in the permeability of acute lung injury and Ang-2 may modulate the kinetics of thrombin-induced permeability by impairing the organization of vascular endothelial (VE-)cadherin, and affecting small Rho GTPases in human pulmonary microvascular endothelial cells (HPMVECs), we hypothesized that Ang-2 acts as a sensitizer of thrombin-induced hyperpermeability of HPMVECs, opposed by Ang-1. METHODOLOGY/PRINCIPAL FINDINGS: Permeability was assessed by measuring macromolecule passage and transendothelial electrical resistance (TEER). Angiopoietins did not affect basal permeability. Nevertheless, they had opposing effects on the thrombin-induced permeability, in particular in the initial phase. Ang-2 enhanced the initial permeability increase (passage, P = 0.010; TEER, P = 0.021) in parallel with impairment of VE-cadherin organization without affecting VE-cadherin Tyr685 phosphorylation or increasing RhoA activity. Ang-2 also increased intercellular gap formation. Ang-1 preincubation increased Rac1 activity, enforced the VE-cadherin organization, reduced the initial thrombin-induced permeability (TEER, P = 0.027), while Rac1 activity simultaneously normalized, and reduced RhoA activity at 15 min thrombin exposure (P = 0.039), but not at earlier time points. The simultaneous presence of Ang-2 largely prevented the effect of Ang-1 on TEER and macromolecule passage. CONCLUSIONS/SIGNIFICANCE: Ang-1 attenuated thrombin-induced permeability, which involved initial Rac1 activation-enforced cell-cell junctions, and later RhoA inhibition. In addition to antagonizing Ang-1, Ang-2 had also a direct effect itself. Ang-2 sensitized the initial thrombin-induced permeability accompanied by destabilization of VE-cadherin junctions and increased gap formation, in the absence of increased RhoA activity

Mitochondrial dysfunction and biogenesis: do ICU patients die from mitochondrial failure?

Mitochondrial functions include production of energy, activation of programmed cell death, and a number of cell specific tasks, e.g., cell signaling, control of Ca2+ metabolism, and synthesis of a number of important biomolecules. As proper mitochondrial function is critical for normal performance and survival of cells, mitochondrial dysfunction often leads to pathological conditions resulting in various human diseases. Recently mitochondrial dysfunction has been linked to multiple organ failure (MOF) often leading to the death of critical care patients. However, there are two main reasons why this insight did not generate an adequate resonance in clinical settings. First, most data regarding mitochondrial dysfunction in organs susceptible to failure in critical care diseases (liver, kidney, heart, lung, intestine, brain) were collected using animal models. Second, there is no clear therapeutic strategy how acquired mitochondrial dysfunction can be improved. Only the benefit of such therapies will confirm the critical role of mitochondrial dysfunction in clinical settings. Here we summarized data on mitochondrial dysfunction obtained in diverse experimental systems, which are related to conditions seen in intensive care unit (ICU) patients. Particular attention is given to mechanisms that cause cell death and organ dysfunction and to prospective therapeutic strategies, directed to recover mitochondrial function. Collectively the data discussed in this review suggest that appropriate diagnosis and specific treatment of mitochondrial dysfunction in ICU patients may significantly improve the clinical outcome

Cystic Fibrosis Transmembrane Conductance Regulator Does Not Affect Neutrophil Migration across Cystic Fibrosis Airway Epithelial Monolayers

Recent studies have shown that airway inflammation dominated by neutrophils, ie, polymorphonuclear cells (PMN) was observed in infants and children with cystic fibrosis (CF) even in the absence of detectable infection. To assess whether there is a CF-related anomaly of PMN migration across airway epithelial cells, we developed an in vitro model of chemotactic migration across tight and polarized CF15 cells, a CF human nasal epithelial cell line, seeded on porous filters. To compare PMN migration across a pair of CF and control monolayers in the physiological direction, inverted CF15 cells were infected with increasing concentrations of recombinant adenoviruses containing either the normal cystic fibrosis transmembrane conductance regulator (CFTR) cDNA, the ΔF508 CFTR cDNA, or the β-galactosidase gene. The number of PMN migrating in response to N-formyl-Met-Leu-Phe across inverted CF15 monolayers expressing β-galactosidase was similar to that seen across CF15 monolayers rescued with CFTR, whatever the proportion of cells expressing the transgene. Moreover, PMN migration across monolayers expressing various amounts of mutated CFTR was not different from that observed across matched counterparts expressing normal CFTR. Finally, PMN migration in response to adherent or Pseudomonas aeruginosa was equivalent across CF and corrected monolayers. The possibility that mutated CFTR may exert indirect effects on PMN recruitment, via an abnormal production of the chemotactic cytokine interleukin-8, was also explored. Apical and basolateral production of interleukin-8 by polarized CF cells expressing mutated CFTR was not different from that observed with rescued cells, either in baseline or stimulated conditions. CF15 cells displayed a CF phenotype that could be corrected by CFTR-containing adenoviruses, because two known CF defects, Cl− secretion and increased P. aeruginosa adherence, were normalized after infection with those viruses. Thus, we conclude that the presence of a mutated CFTR does not per se lead to an exaggerated inflammatory response of CF surface epithelial cells in the absence or presence of a bacterial infection