Social inequalities in the association between partner/marital status and health among workers in Spain

The objectives of this study are to examine the association between partner/marital status and several health outcomes among workers and to assess whether it depends on gender and occupational social class. The sample was composed of all workers aged 21-64 years interviewed in the 2006 Spanish National Health Survey (8563 men and 5881 women). Partner/marital status had seven categories: married and living with the spouse (reference category), married and not living with the spouse, cohabiting, single and living with parents, single and not living with parents, separated/divorced and widowed. Four health outcomes were analysed: self-perceived health status, mental health, psychiatric drugs consumption and hypertension. Multiple logistic regression models stratified by sex and social class were fitted. Female manual workers who were cohabiting were more likely to report poor self-perceived health status, poor mental health status, psychiatric medication consumption and hypertension than their married and living with the spouse counterparts. In that group the prevalence of poor health outcomes was even higher when compared with single people. Among male non-manual workers, being married and not living with the spouse was associated with poor self-perceived health status, poor mental health status and hypertension. There were almost no differences in health between being married and the rest of partner/marital status categories for different combinations of gender and social class and, even, some groups of single people reported better health outcomes than people who were married. Our results show no evidence that being married and living with the spouse is unequivocally linked to better health status among Spanish workers. They emphasize the importance of not only considering marital status, but also partner status, as well as the role of gender, social class and the sociocultural context in the analysis of the association between family characteristics and health.     

Mortalidad por complicaciones médicas y quirúrgicas,impacto de la crisis y gasto sanitario en España, 2002-2013

ObjectiveTo describe the evolution of mortality risks for complications due to medical care or surgery between the periods prior to (2002-2007) and after (2008-2013) the beginning of the economic crisis for Spain and by autonomous region, and to analyse the relationship between the changes in the risks of death and the socioeconomic impact of the crisis and the variation in health spending.MethodEcological study based on age-standardized mortality rates, synthetic index of vulnerability as a socioeconomic indicator and variation in health expenditure as an indicator of health expenditure. The relative risk of death between periods was estimated with Poisson regression models.ResultsThe number of deaths increased for Spain in the period studied. Although the relationship between the increase in public investment in health and the decrease in mortality due to this cause has not been clearly demonstrated, it was possible to determine that the autonomous regions with the lowest increase in health expenditure had rates higher than the rest throughout the period, and that the most vulnerable to the crisis and with the lowest increase in spending presented the greatest increase in the risk of death between the periods.ConclusionsGiven the increase in these deaths, due to avoidable failures of the system, it is necessary to continue investigating this cause of mortality.     

Diagnosis of laryngeal tuberculosis in a high TB burden area

European Archives of Oto-Rhino-Laryngology - The larynx is the second most commonly affected site in the head and neck region in patients with extrapulmonary tuberculosis (TB). Despite this, the...     

Impaired aquaporins expression in the gastrointestinal tract of rat after mercury exposure

The main route of exposure to mercury in humans is through the diet. Consequently, the gastrointestinal mucosa is exposed to the mercurial forms, where they cause intestinal fluid accumulation, mucosal injuries and diarrhea. The relationship between inorganic mercury (HgCl₂) and methylmercury (CH₃HgCl) exposure and water movement in the gastrointestinal tract is still unexplored. The leading role of aquaporins (AQPs) in the rapid bidirectional movement of fluid in the gastrointestinal tract of mammals is well established. The present study evaluates the effect of HgCl₂ and CH₃HgCl exposure on AQP expression in different portions of the gastrointestinal tract of rats treated by gavage (5 mg kg^–1 of mercury species, single dose, 4 days). The results show that mercury species reduce mRNA and protein levels of AQPs in different parts of the gastrointestinal tract. In the stomach, treated rats show a significant reduction of expression of AQP3 (80–90% for mRNA and 50% for protein) and AQP4 (95–99% for mRNA and 20–40% for protein). In the small and large intestine, treated rats experience a significant reduction of AQP3 and AQP7 expression. Protein contents of both AQPs are reduced in similar proportions in jejunum (AQP3: 40–50%; AQP7: 45–50%) and colon (AQP3: 35–40%; AQP7: 45–60%), regardless of the treatment. Our results indicate that some AQPs are downregulated in the rat gastrointestinal tract by mercury exposure, suggesting a possible role of AQPs in the development of mercury gastrointestinal symptoms. Copyright © 2015 John Wiley & Sons, Ltd.     

Single versus multi‐drug antimicrobial surgical infection prophylaxis for left ventricular assist devices: A systematic review and meta‐analysis

Infection remains the Achilles heel of left ventricular assist device (LVAD) therapy. However, an optimal antimicrobial surgical infection prophylaxis (SIP) regimen has not been established. This study evaluated the efficacy of a single‐drug SIP compared to a multi‐drug SIP on clinical outcomes in patients undergoing continuous‐flow LVAD (CF‐LVAD) and pulsatile LVAD (P‐LVAD) implantation. An electronic search was performed to identify studies in the English literature on SIP regimens in patients undergoing LVAD implantation. Identified articles were assessed for inclusion and exclusion criteria. Fourteen articles with 1,311 (CF‐LVAD: 888; P‐LVAD: 423) patients were analyzed. Overall, 501 (38.0%) patients received single‐drug SIP, whereas 810 (62.0%) received multi‐drug SIP. Time to infection was comparable between groups. There was no significant difference in overall incidence of LVAD‐specific infections [single‐drug: 18.7% vs. multi‐drug: 24.8%, P = 0.49] including driveline infections [single‐drug: 14.1% vs. multi‐drug: 20.8%, P = 0.37]. Compared to single‐drug SIP, patients who received multi‐drug SIP had a significantly lower survival rate [single‐drug: 90.0% vs. multi‐drug: 76.0%, P = 0.01] and infection‐free survival rate [single‐drug: 88.4% vs. multi‐drug: 77.3%, P = 0.04] at 90 days. However, there were no significant differences in 1‐year survival and 1‐year infection‐free survival between groups. No survival differences were observed in the CF‐LVAD subset as well. This study demonstrated no additional advantage of a multi‐drug compared to a single‐drug regimen for SIP. Although there was a modest advantage in early survival among CF‐LVAD and P‐LVAD patients who received single‐drug SIP, there were no significant differences in the 1‐year survival and 1‐year infection‐free survival.     

Circulating markers of angiogenesis,inflammation, and coagulation in patients with glioblastoma

Inflammation, angiogenesis, and coagulation are linked to the development of cancer. In glioblastoma, microvascular proliferation is a hallmark, and lymphocytic infiltration is a common finding. Thromboses are frequent in patients with glioblastoma. The objective of this study was to assess presurgical levels of circulating markers of inflammation, angiogenesis, and coagulation in a prospective series of patients with glioblastoma, and to explore their correlations and possible associations with clinical findings. Angiogenesis markers included were vascular endothelial growth factor (VEGF), soluble vascular endothelial growth factor-receptor 1 (sVEGFR-1), and thrombospondin-1 (TSP-1). Inflammatory markers included were C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα), and sialic acid (SA). Coagulation markers included were fibrinogen (Fg), endogen thrombin generation (ETG), prothrombin fragments 1 + 2 (F1 + 2), and tissue factor (TF). Forty-seven patients and 60 healthy subjects were included in the study. Signs of tumor necrosis in presurgical MRI were associated with shorter survival (P < 0.01). All inflammation markers, F1 + 2, ETG, VEGF and sVEGFR-1, were significantly elevated in glioblastoma patients. Correlations were found between ETG and Fg (r = 0.44, P < 0.01). Sialic acid correlated with Fg (r = 0.63, P < 0,001); CPR correlated with SA (r = 0.60, P < 0.001), Fg (r = 0.76, P < 0.001), TNFα (r = 0.56, P < 0.001), and IL-6 (r = 0.65, P < 0.001); and IL-6 also correlated positively with TNFα (r = 0.40, P < 0.02) and Fg (r = 0.45, P < 0.01). Vascular endothelial growth factor inversely correlated with sVEGFR-1 (r = −0.35, P < 0.02). No associations were found between marker levels and survival or progression-free survival.     

Hypoxia exacerbates Ca-handling disturbances induced by very low density lipoproteins (VLDL) in neonatal rat cardiomyocytes

It is known that myocardium suffers serious alterations under ischemic conditions such as lipid overloading and electrophysiological alterations. However, it is unknown whether intracellular lipid accumulation and calcium dysfunction share common pathophysiological mechanisms under ischemia. The aims of this study were 1) to analyze the effect of normal and high doses of very low density lipoproteins (VLDL) on lipid content and calcium handling; 2) to investigate whether hypoxia modulates the effect of high VLDL doses; and 3) to identify potentially underlying mechanisms in cardiomyocytes. For this purpose, neonatal rat ventricular myocytes cultures were prepared from hearts of 3-4-day-old rats. High doses of VLDL that induced cholesteryl ester (CE) and triglyceride (TG) accumulation strongly reduced sarco(endo)plasmic reticulum Ca ATPase-2 (SERCA-2) expression, calcium transient amplitude and sarcoplasmic reticulum (SR) calcium loading. Interestingly, hypoxia, by upregulating VLDL-receptor expression (4.5-fold at 16 h) increased CE (1.5-fold) and TG (3-fold) cardiomyocyte content and exacerbated the negative effect of VLDL on SERCA-2 expression. Functionally, the hypoxic exacerbation of VLDL-mediated SERCA-2 downregulation was translated into a stronger decrease in calcium transient amplitude and SR calcium loading in myocytes exposed simultaneously to hypoxia and high VLDL. In conclusion, high VLDL doses alter calcium handling in cardiomyocytes and SERCA-2 play a pivotal role in the hypoxic exacerbation of VLDL-mediated effects on cardiac calcium handling. Potentiation of VLDL's effects under hypoxia is explained, at least in part, by hypoxic upregulation of the expression of VLDL-receptor.