Physiological responses to chronic hypoxia include polycythemia, pulmonary arterial remodeling, and vasoconstriction. Chronic hypoxia causes pulmonary arterial hypertension leading to right ventricular hypertrophy and heart failure. During pulmonary hypertension, pulmonary arteries exhibit increased expression of smooth muscle-α-actin and -myosin heavy chain. NFATc3 (nuclear factor of activated T cells isoform c3), which is aCa²⁺-dependent transcription factor, has been recently linked to smooth muscle phenotypic maintenance through the regulation of the expression of α-actin. The aim of this study was to determine if: (a) NFATc3 is expressed in murine pulmonary arteries, (b) hypoxia induces NFAT activation, (c) NFATc3 mediates the up-regulation of α-actin during chronic hypoxia, and (d) NFATc3 is involved in chronic hypoxia-induced pulmonary vascular remodeling. NFATc3 transcript and protein were found in pulmonary arteries. NFAT-luciferase reporter mice were exposed to normoxia (630 torr) or hypoxia (380 torr) for 2, 7, or 21 days. Exposure to hypoxia elicited a significant increase in luciferase activity and pulmonary arterial smooth muscle nuclear NFATc3 localization, demonstrating NFAT activation. Hypoxia induced up-regulation of α-actin and was prevented by the calcineurin/NFAT inhibitor, cyclosporin A (25 mg/kg/day s.c.). In addition, NFATc3 knock-out mice did not showed increased α-actin levels and arterial wall thickness after hypoxia. These results strongly suggest that NFATc3 plays a role in the chronic hypoxia-induced vascular changes that underlie pulmonary hypertension.

Successful recovery and sustainability of threatened and exploited species depends in part on retention and maintenance of genetic diversity. Theory indicates that genetic diversity is lost at a rate inversely proportional to the genetically effective population size (N_e), which is roughly equal to one-half the adult census size (N) in many organisms. However,N_ehas been reported to be up to five orders of magnitude lower thanNin species with life histories that result in type III survivorship (high fecundity, but heavy mortality in early life stages, e.g. bony fishes), prompting speculation that low values ofN_emay be a general feature of such organisms despite sometimes vast abundances. Here, we comparedN_eand the ratioN_e/Nacross three ecologically similar fish species from the arid southwestern United States, all with type III life histories but with differing expectations of egg and larval survivorship that correlate with the degree of human-imposed habitat fragmentation. Our study indicates that type III life history may be necessary, but this alone is insufficient to account for extraordinarily low values ofN_e/N. Rather, life history interacts with environmentally imposed mortality to determine the rate and magnitude of change in genetic diversity in these desert fish species.

Sleep apnea, defined as intermittent respiratory arrest during sleep, is associated with increased incidence of hypertension and peripheral vascular disease. Exposure of rodents to brief periods of intermittent hypercarbia/hypoxia (H-IH) during sleep mimics the cyclical hypoxia-normoxia of sleep apnea. Endothelin-1, an upstream activator of nuclear factor of activated T cells (NFAT), is increased during H-IH. Therefore, we hypothesized that NFATc3 is activated by H-IH and is required for H-IH-induced hypertension. Consistent with this hypothesis, we found that H-IH (20 brief exposures per hour to 5% O₂-5% CO₂for 7 h/day) induces systemic hypertension in mice [mean arterial pressure (MAP) = 97 ± 2 vs. 124 ± 2 mmHg, P < 0.05, n = 5] and increases NFATc3 transcriptional activity in aorta and mesenteric arteries. Cyclosporin A, an NFAT inhibitor, and genetic ablation of NFATc3 [NFATc3 knockout (KO)] prevented NFAT activation. More importantly, H-IH-induced hypertension was attenuated in cyclosporin A-treated mice and prevented in NFATc3 KO mice. MAP was significantly elevated in wild-type mice (Δ = 23.5 ± 6.1 mmHg), but not in KO mice (Δ = −3.9 ± 5.7). These results indicate that H-IH-induced increases in MAP require NFATc3 and that NFATc3 may contribute to the vascular changes associated with H-IH-induced hypertension.

Reform to the Chilean educational system seeks to improve public education, adapting the school curriculum to new technologies and the information revolution. Our study focused on highlighting potential issues with environmental and technological education, offering opportunities to complement the current Chilean curriculum with an interdisciplinary approach. During a five-week period interspersed through the school semester, 115 underprivileged children in seventh grade from five public schools of southern Chile participated in workshops based on Arduino technology to address current environmental problems caused by global change and anthropization. Surveys were conducted to participating students and included both open and closed-ended questions, which measured attitudes and perceptions towards science and the use of technology in classrooms and daily lives. Surveys were analysed quantitatively with basic statistics and qualitatively by building semantic networks of the relationships between different concepts expressed by the students. Results did not show significant changes in attitudes towards science or technology before and after the workshops but students reported mixed feelings about science. Indifference and fear emerged, coupled with the need for more interactive experiences. Curiosity and enthusiasm also surfaced when students were using new technologies. Since the school curriculum is generally focused exclusively towards the completion of specific curricular aims, highly vulnerable schools in Chile have few opportunities to access interactive, hands-on activities. Low-cost, emergent technologies, such Arduinos, have a high potential for improving student's attitude towards science and technology and their use should be considered when tailoring school curriculum in Chile and elsewhere.