Until recently,3, has been considered an inactive by-product of triiodothyronine (T3) deiodination. However, studies from several laboratories have shown that 3,5-T2 has specific, nongenomic effects on mitochondrial oxidative capacity and respiration rate that are distinct from those due to T3. Nevertheless, little is known about the putative genomic effects of 3,5-T2. We have previously shown that hyperthyroidism induced by supraphysiological doses of 3,5-T2 inhibits hepatic iodothyronine deiodinase type 2 (D2) activity and lowers mRNA levels in the killifish in the same manner as T3 and T4, suggesting a pretranslational effect of 3,5-T2 (Garcia-G C, Jeziorski MC, Valverde-R C, Orozco A. Gen Comp Endocrinol 135: 201-209, 2004). The question remains as to whether 3,5-T2 would have effects under conditions similar to those that are physiological for T3. To this end, intact killifish were rendered hypothyroid by administering methimazole. Groups of hypothyroid animals simultaneously received 30 nM of either T3, reverse T3, or 3,5-T2. Under these conditions, we expected that, if it were bioactive, 3,5-T2 would mimic T3 and thus reverse the compensatory upregulation of D2 and tyroid receptor 1 and downregulation of growth hormone that characterize hypothyroidism. Our results demonstrate that 3,5-T2 is indeed bioactive, reversing both hepatic D2 and growth hormone responses during a hypothyroidal state. Furthermore, we observed that 3,5-T2 and T3 recruit two distinct populations of transcription factors to typical palindromic and DR4 thyroid hormone response elements. Taken together, these results add further evidence to support the notion that 3,5-T 2 is a bioactive iodothyronine. deiodinase type 2; thyroid hormone receptor 1; thyroid hormone response element; killifish IODOTHYRONINES OR THYROID hormones (TH) are essential in regulating energy expenditure and development. Triiodothyronine (T 3 ) is the bioactive TH, which modulates gene expression in virtually every vertebrate tissue through ligand-dependent transcription factors, the TH receptors (TR). Sequential deiodination of thyroxine (T 4 ) generates T 3 as well as other iodothyronines that have been considered inactive by-products, but, recently, interest has grown in identifying bioactive iodothyronines in addition to T 4 and T 3 . Studies from several laboratories have suggested that 3,5-diiodothyronine (3,5-T 2 ), a putative product of the deiodination pathway involved in T 3 metabolism, could be a peripheral mediator of some effects of TH on mitochondrial oxidative capacity and respiration rate. To date, results in mammals suggest that 3,5-T 2 has specific actions on oxygen consumption that are distinct from those of T 3 : they are not attenuated by inhibition of protein synthesis and are more rapid than those due to T 3 (for review, see Ref. 12). Genomic effects of 3,5-T 2 have been analyzed in only a few classic iodothyronine-dependent genes, such as thyroid stimulating hormone (TSH), thyroid receptor 2 (TR2), iodothyronine deiodinase type 1 (D1)...
Objectives. To evaluate the impact of the April 2016 7.8-magnitude earthquake in Ecuador on the incidence of Zika virus (ZIKV) cases.Methods. We used the national public health surveillance system for reportable transmissible conditions and included suspected and laboratory-confirmed ZIKV cases. We compared the number of cases before and after the earthquake in areas closer to and farther from the epicenter.Results. From January to July 2016, 2234 patients suspected of having ZIKV infection were reported in both affected and control areas. A total of 1110 patients had a reverse transcription-polymerase chain reaction assay, and 159 were positive for ZIKV. The cumulative incidence of ZIKV in the affected area was 11.1 per 100 000 after the earthquake. The odds ratio of having ZIKV infection in those living in the affected area was 8.0 (95% CI = 4.4, 14.6; P < .01) compared with the control area and adjusted for age, gender, province population, and number of government health care facilities. METHODSWe included all confirmed ZIKV cases in areas affected by the earthquake and in control areas that are similar in elevation, average temperature, proximity to the coast, and population size. We also included suspected ZIKV cases to evaluate the geographic relationship between these cases and those confirmed by laboratory.The epicenter of the 2016 earthquake was 17 miles south-southeast of Muisne, Esmeraldas, in the northeastern part of the country. The Manabí and Esmeraldas provinces had the most earthquake-related damage, with 705 and 420 destroyed buildings, respectively.7 Before the earthquake, Manabí had 199 health centers and 15 hospitals. After the earthquake, 7 hospitals had major damage and were inoperative. 8,9Almost all earthquake-related deaths in Ecuador were reported in Manabí; the earthquake affected larger urban centers in Manabí than in Esmeraldas, Guayas, and Los Ríos. Definitions of EarthquakeAffected AreasWe defined the earthquake-affected area as the province of Manabí, which is 30 miles south of the epicenter. The rationale for using only this province was that the roads to Esmeraldas province and the health care facilities most proximal to the epicenter were completely destroyed, 10,11 preventing the collection of any confirmatory samples, whereas several facilities in nearby Manabí remained partially operational and accessible by car. Manabí has larger urban areas and more health care facilities and transportation infrastructure than Esmeraldas. To better evaluate the relationship between earthquake-related damage and ZIKV incidence, we also collected data at the county Correspondence should be sent to Denisse C. Pareja, MD, MSPH, Department of Veterans Affairs, Bruce W. Carter VA Medical Center, 1201 NW 16th Street, 207G, Miami, FL 33125-1693 (denpareja@gmail.com). Reprints can be ordered at http://www. ajph.org by clicking the "Reprints" link.
Epidemiological vigilance in Navarre (601,874 inhabitants) in 2006 included 34 diseases whose notification is compulsory and epidemic outbreaks. Notification is carried out on a weekly basis by the doctors from paediatrics, primary care and specialised care facing any suspicion of these processes, and is completed with microbiological diagnoses. In 2006 the incidence of influenza reached 16.8 cases per 1,000 inhabitants (Epidemic Index, EI: 0.46), showing a late seasonal peak (March) of low dimensions. The incidence of respiratory tuberculosis was 11.3 cases per 100,000 inhabitants, and that of non-respiratory tuberculosis was 2.3; both at similar levels to recent years. Seven cases of tuberculosis occurred in three aggregates amongst cohabitants, and another 7 in non-cohabiting persons resident in the same municipality. Six percent of the cases were coinfected with HIV, and 37% occurred in immigrants. The incidence of meningococcal disease rose to 19 cases (3.2 cases per 100,000 inhabitants; EI 1.46), all of them sporadic. Neisseria meningitidis serogroup B was isolated in 16 cases. There was one case of serogroup C, in a child who had received 3 doses of combined vaccine. In two cases (11%) death occurred. The incidence of legionnaire's disease rose to 28 cases per 100,000 inhabitants (EI:4.88), due to a community outbreak that affected 146 people. Excluding this outbreak, incidence was similar to previous years (3.3 per 100,000 inhabitants). In August an outbreak of parotitis began, and 911 cases had been counted until the end of 2006; and it has continued during 2007. Eleven cases of malaria were registered, all imported. Notifications of toxic food infections has continued to fall (IE:0.48).
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