BackgroundThe aim of this study was to assess the main factors related to maternal mortality reduction in large time series available in Chile in context of the United Nations' Millennium Development Goals (MDGs).MethodsTime series of maternal mortality ratio (MMR) from official data (National Institute of Statistics, 1957–2007) along with parallel time series of education years, income per capita, fertility rate (TFR), birth order, clean water, sanitary sewer, and delivery by skilled attendants were analysed using autoregressive models (ARIMA). Historical changes on the mortality trend including the effect of different educational and maternal health policies implemented in 1965, and legislation that prohibited abortion in 1989 were assessed utilizing segmented regression techniques.ResultsDuring the 50-year study period, the MMR decreased from 293.7 to 18.2/100,000 live births, a decrease of 93.8%. Women's education level modulated the effects of TFR, birth order, delivery by skilled attendants, clean water, and sanitary sewer access. In the fully adjusted model, for every additional year of maternal education there was a corresponding decrease in the MMR of 29.3/100,000 live births. A rapid phase of decline between 1965 and 1981 (−13.29/100,000 live births each year) and a slow phase between 1981 and 2007 (−1.59/100,000 live births each year) were identified. After abortion was prohibited, the MMR decreased from 41.3 to 12.7 per 100,000 live births (−69.2%). The slope of the MMR did not appear to be altered by the change in abortion law.ConclusionIncreasing education level appears to favourably impact the downward trend in the MMR, modulating other key factors such as access and utilization of maternal health facilities, changes in women's reproductive behaviour and improvements of the sanitary system. Consequently, different MDGs can act synergistically to improve maternal health. The reduction in the MMR is not related to the legal status of abortion.

Objective. To assess the blood pressure control and cardiovascular risk factors (CVRFs) in a population of hypertensive patients with access to care under a government-financed program, the Cardiovascular Health Program (CHP). Design. A cross-sectional and multicenter study. Setting. 52 primary care centers, metropolitan area of Santiago, Chile. Participants. 1,194 patients were selected by a systematic random sampling from a universe of 316,654 hypertensive patients. Key Measurements. Demographic information, blood pressure (BP) measurements, and CVRF were extracted from medical records of patients followed for a 12-month period. Results. 59.7% of patients reached target BP <140/90 mmHg. More women were captured in the sampling (2.1 : 1), achieving better BP control than men. Diabetic patients (26.4%) had worse BP control than nondiabetics. Antihypertensive medications were used in 91.5%, with multidrug therapy more frequent in patients with higher BP and more difficult control. Conclusions. The success in improving the BP control to values <140/90 mmHg from 45.3% to 59.7% underscores the contribution of this program in the Chilean primary care cardiovascular preventive strategies. However, fewer hypertensive men than women were captured by this program, and it is of concern the underperforming of BP control observed in diabetics.

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The transient receptor potential (TRP) ion channel family consists of a broad variety of non-selective cation channels that integrate environmental physicochemical signals for dynamic homeostatic control. Involved in a variety of cellular physiological processes, TRP channels are fundamental to the control of the cell life cycle. TRP channels from the vanilloid (TRPV) family have been directly implicated in cell death. TRPV1 is activated by pain-inducing stimuli, including inflammatory endovanilloids and pungent exovanilloids, such as capsaicin (CAP). TRPV1 activation by high doses of CAP (>10 μM) leads to necrosis, but also exhibits apoptotic characteristics. However, CAP dose–response studies are lacking in order to determine whether CAP-induced cell death occurs preferentially via necrosis or apoptosis. In addition, it is not known whether cytosolic Ca2+ and mitochondrial dysfunction participates in CAP-induced TRPV1-mediated cell death. By using TRPV1-transfected HeLa cells, we investigated the underlying mechanisms involved in CAP-induced TRPV1-mediated cell death, the dependence of CAP dose, and the participation of mitochondrial dysfunction and cytosolic Ca2+ increase. Together, our results contribute to elucidate the pathophysiological steps that follow after TRPV1 stimulation with CAP. Low concentrations of CAP (1 μM) induce cell death by a mechanism involving a TRPV1-mediated rapid and transient intracellular Ca2+ increase that stimulates plasma membrane depolarization, thereby compromising plasma membrane integrity and ultimately leading to cell death. Meanwhile, higher doses of CAP induce cell death via a TRPV1-independent mechanism, involving a slow and persistent intracellular Ca2+ increase that induces mitochondrial dysfunction, plasma membrane depolarization, plasma membrane loss of integrity, and ultimately, cell death.