University of Costa Rica

About: University of Costa Rica is a education organization based out in San José, Costa Rica. It is known for research contribution in the topics: Population & Venom. The organization has 9817 authors who have published 16781 publications receiving 238208 citations. The organization is also known as: UCR & Universidad de Costa Rica.

Cellular pathology induced by snake venom phospholipase A2 myotoxins and neurotoxins: common aspects of their mechanisms of action

Abstract: A large variety of snake toxins evolved from PLA2 digestive enzymes through a process of ‘accelerated evolution’. These toxins have different tissue targets, membrane receptors and mechanisms of alteration of the cell plasma membrane. Two of the most commonly induced effects by venom PLA2s are neurotoxicity and myotoxicity. Here, we will discuss how these snake toxins achieve a similar cellular lesion, which is evolutionarily highly conserved, despite the differences listed above. They cause an initial plasma membrane perturbation which promotes a large increase of the cytosolic Ca2+ concentration leading to cell degeneration, following modes that we discuss in detail for muscle cells and for the neuromuscular junction. The different systemic pathophysiological consequences caused by these toxins are not due to different mechanisms of cell toxicity, but to the intrinsic anatomical and physiological properties of the targeted tissues and cells.

Consistent multi-decadal variability in global temperature reconstructions and simulations over the Common Era.

Abstract: Multi-decadal surface temperature changes may be forced by natural as well as anthropogenic factors, or arise unforced from the climate system. Distinguishing these factors is essential for estimating sensitivity to multiple climatic forcings and the amplitude of the unforced variability. Here we present 2,000-year-long global mean temperature reconstructions using seven different statistical methods that draw from a global collection of temperature-sensitive paleoclimate records. Our reconstructions display synchronous multi-decadal temperature fluctuations, which are coherent with one another and with fully forced CMIP5 millennial model simulations across the Common Era. The most significant attribution of pre-industrial (1300-1800 CE) variability at multi-decadal timescales is to volcanic aerosol forcing. Reconstructions and simulations qualitatively agree on the amplitude of the unforced global mean multi-decadal temperature variability, thereby increasing confidence in future projections of climate change on these timescales. The largest warming trends at timescales of 20 years and longer occur during the second half of the 20th century, highlighting the unusual character of the warming in recent decades.

Coffee, CYP1A2 genotype and risk of myocardial infarction.

Abstract: The association between coffee intake and risk of myocardial infarction (MI) remains controversial [1, 2]. Coffee is a major source of caffeine, which is metabolized by the polymorphic CYP1A2 enzyme. An A to C substitution at position 734 (CYP1A2*1F) in the CYP1A2 gene decreases enzyme inducibility as measured by plasma or urinary [caffeine]/[caffeine metabolite] ratio after a dose of caffeine, resulting in impaired caffeine metabolism [3]. Individuals who are homozygous for the CYP1A2*1A allele (A/A) are “rapid” caffeine metabolizers whereas carriers of the variant CYP1A2*1F are “slow” caffeine metabolizers. The objective of this study was to determine whether CYP1A2 genotype modifies the association between coffee consumption and risk of MI. Cases (n = 2,014) with a first acute non-fatal MI and population-based controls (n = 2,014) were genotyped by RFLP-PCR. A food frequency questionnaire was used to assess coffee intake. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using conditional logistic regression. For carriers of the slow *1F allele, the ORs (95% CI) for risk of MI associated with consuming <1, 1, 2–3 and 4 or more cups/day were 1.00 (reference), 0.99 (0.69–1.44), 1.36 (1.01–1.83), and 1.64 (1.14–2.34), respectively. Corresponding ORs (95% CI) for individuals with the rapid *1A/*1A genotype were 1.00, 0.75 (0.51–1.12), 0.78 (0.56–1.09), and 0.99 (0.66–1.48) (P = 0.04 for gene-diet interaction). It has previously been suggested that coffee may be associated with an increased risk of MI only among younger individuals. Thus, we examined the effects of coffee among subjects below the age of 50 years. For carriers of the *1F allele the ORs (95% CI) of MI associated with consuming <1, 1, 2–3, or ≥4 cups/day of coffee were 1.00, 2.12 (0.86–5.24), 2.43 (1.22–4.82), and 4.07 (1.89–8.74), respectively (Fig. 1). Corresponding ORs (95% CI) for those with the *1A/*1A genotype were 1.00, 0.39 (0.15–0.97), 0.35 (0.17–0.76), and 0.81 (0.32–2.05) (P < 0.001 for gene-coffee interaction). The protective effects observed among rapid metabolizers suggest that the efficient elimination of caffeine might have unmasked the protective effects of other chemicals in coffee. Compounds in coffee such as caffeic acid and chlorogenic acid have antioxidant properties that might protect against heart disease [4]. In summary, intake of coffee was associated with an increased risk of MI only among those with impaired caffeine metabolism, suggesting that caffeine plays a major role in this association.