Gyriosomus granulipennis Pizarro-Araya & Flores 2004 (Coleoptera: Tenebrionidae): An extreme case to preserve

El archipiélago de Los Choros, conformado por las islas Choros, Damas y Gaviota forma parte de la Reserva Nacional Pingüino de Humboldt y está situado dentro del desierto costero transicional de Chile (25º-32º S). Estudios recientes realizados en el archipiélago dan cuenta de una especie endémica de Tenebrionidae (Coleoptera) de la isla Choros (29º15’ S, 71º32’ O) descripta como Gyriosomus granulipennis Pizarro-Araya & Flores. El objetivo del presente trabajo es evaluar la prioridad de conservación de esta especie en el archipiélago mediante el análisis del Índice de Prioridad de Conservación (CPI), clasifi cación del Ministerio de Medio Ambiente (MMA) de Chile y lista roja de la IUCN. Nuestros resultados sostienen que esta especie puede ser catalogada en categoría En peligro por el índice CPI y Vulnerable según el MMA. Según criterios IUCN esta especie debería ser categorizada con Datos Defi cientes (DD), ya que muchos de los datos necesarios para la clasifi cación son difíciles de obtener para insectos o pueden sobrestimar o subestimar el riesgo de extinción de esta especie. Consideramos importante monitorear la continuidad de esta especie y conservarla a través del hábitat, para lo cual proponemos evitar el acceso a turistas y erradicar el conejo silvestre europeo.The Choros Archipelago includes three islands: Choros, Damas and Gaviota and it is part of The Pingüino de Humboldt National Reserve. These insular ecosystems are within the Chilean transitional coastal (25º-32º S). Prior researches in the archipelago reported a species of Tenebrionidae (Coleoptera) endemic to Choros island (29º15’ S, 71º32’ W) described as Gyriosomus granulipennis Pizarro-Araya & Flores. The objective of this paper is to evaluate the vulnerability of this species in the archipelago through Conservation Priority Index (CPI), Environmental Ministery of Chile (MMA) and Red List of IUCN. We concluded that G. granulipennis is Endangered by CPI index, and Vulnerable by MMA of Chile. Additionally, this species can be classiffi ed with Defi cient Data (DD) by IUCN because many of data are impossible or diffi cult to obtain for insects and can overestimate or underestimate the risk of extinction of this species. We consider important to monitoring the continuity of this species and the protection of habitat, for which we propose not allow access the tourists and eradication of European rabbit.Fil: Pizarro Ayala, Jaime. Universidad de La Serena; ChileFil: Flores, Gustavo Ernesto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto Argentino de Investigaciones de las Zonas Áridas. Provincia de Mendoza. Instituto Argentino de Investigaciones de las Zonas Áridas. Universidad Nacional de Cuyo. Instituto Argentino de Investigaciones de las Zonas Áridas; ArgentinaFil: Vergara, Olivia E.. Universidad de Concepción; Chil

Noninvasive monitoring of serial changes in pulmonary vascular resistance and acute vasodilator testing using cardiac magnetic resonance

Objectives The study sought to evaluate the ability of cardiac magnetic resonance (CMR) to monitor acute and long-term changes in pulmonary vascular resistance (PVR) noninvasively. Background PVR monitoring during the follow-up of patients with pulmonary hypertension (PH) and the response to vasodilator testing require invasive right heart catheterization. Methods An experimental study in pigs was designed to evaluate the ability of CMR to monitor: 1) an acute increase in PVR generated by acute pulmonary embolization (n = 10); 2) serial changes in PVR in chronic PH (n = 22); and 3) changes in PVR during vasodilator testing in chronic PH (n = 10). CMR studies were performed with simultaneous hemodynamic assessment using a CMR-compatible Swan-Ganz catheter. Average flow velocity in the main pulmonary artery (PA) was quantified with phase contrast imaging. Pearson correlation and mixed model analysis were used to correlate changes in PVR with changes in CMR-quantified PA velocity. Additionally, PVR was estimated from CMR data (PA velocity and right ventricular ejection fraction) using a formula previously validated. Results Changes in PA velocity strongly and inversely correlated with acute increases in PVR induced by pulmonary embolization (r = –0.92), serial PVR fluctuations in chronic PH (r = –0.89), and acute reductions during vasodilator testing (r = –0.89, p ≤ 0.01 for all). CMR-estimated PVR showed adequate agreement with invasive PVR (mean bias –1.1 Wood units,; 95% confidence interval: –5.9 to 3.7) and changes in both indices correlated strongly (r = 0.86, p < 0.01). Conclusions CMR allows for noninvasive monitoring of acute and chronic changes in PVR in PH. This capability may be valuable in the evaluation and follow-up of patients with PH

Triatoma infestans Calreticulin: Gene cloning and expression of a main domain that interacts with the host complement system

© 2017 by The American Society of Tropical Medicine and Hygiene.Triatoma infestans is an important hematophagous vector of Chagas disease, a neglected chronic illness affecting approximately 6 million people in Latin America. Hematophagous insects possess several molecules in their saliva that counteract host defensive responses. Calreticulin (CRT), a multifunctional protein secreted in saliva, contributes to the feeding process in some insects. Human CRT (HuCRT) and Trypanosoma cruzi CRT (TcCRT) inhibit the classical pathway of complement activation, mainly by interacting through their central S domain with complement component C1. In previous studies, we have detected CRT in salivary gland extracts from T. infestans. We have called this molecule TiCRT. Given that the S domain is responsible for C1 binding, we have tested its role in the classical pathway of complement activation in vertebrate blood. We have cloned and characterized the complete nucleotide sequence of CRT from T. inf

Beta-3 adrenergic agonists reduce pulmonary vascular resistance and improve right ventricular performance in a porcine model of chronic pulmonary hypertension

Beta-3 adrenergic receptor (beta 3AR) agonists have been shown to produce vasodilation and prevention of ventricular remodeling in different conditions. Given that these biological functions are critical in pulmonary hypertension (PH), we aimed to demonstrate a beneficial effect of beta 3AR agonists in PH. An experimental study in pigs (n = 34) with chronic PH created by pulmonary vein banding was designed to evaluate the acute hemodynamic effect and the long-term effect of beta 3AR agonists on hemodynamics, vascular remodeling and RV performance in chronic PH. Ex vivo human experiments were performed to explore the expression of beta 3AR mRNA and the vasodilator response of beta 3AR agonists in pulmonary arteries. Single intravenous administration of the beta 3AR agonist BRL37344 produced a significant acute reduction in PVR, and two-weeks treatment with two different beta 3AR selective agonists, intravenous BRL37344 or oral mirabegron, resulted in a significant reduction in PVR (median of -2.0 Wood units/m(2) for BRL37344 vs. + 1.5 for vehicle, p = 0.04; and -1.8 Wood units/m(2) for mirabegron vs. + 1.6 for vehicle, p = 0.002) associated with a significant improvement in magnetic resonance-measured RV performance. Histological markers of pulmonary vascular proliferation (p27 and Ki67) were significantly attenuated in beta 3AR agonists-treated pigs. beta 3AR was expressed in human pulmonary arteries and beta 3AR agonists produced vasodilatation. beta 3AR agonists produced a significant reduction in PVR and improved RV performance in experimental PH, emerging as a potential novel approach for treating patients with chronic PH.This work was supported by Fonde Europeo de Desarrollo Regional (FEDER) Instituto de Salud Carlos III-Fondo de Investigacion Sanitaria PI13/02339 (to A. G-A), and the competitive grant ``CNIC-Translational 01-2009´´ (to BI). R F-J is recipient of a ``Rio Hortega´´ fellowship granted by the ISCIII. R F-J is recipient of the ``FICNIC´´ fellowship granted by the ``Fundacio Jesus Serra´´, ``Fundacion Interhospitalaria de Investigacion Cardiovascular (FIC)´´ and CNIC. A. G-A, B. I, L. F-F, R. F-J, M. S and JM. G-R are members of ``Red de Investigacion Cardiovascular´´ (RIC RD12/0042/0006 and RD12/0042/0054) from the Ministerio de Economia y Competitividad, ISCIII´´. The CNIC is supported by the Spanish Ministry of Economy and Competitiveness (MINECO) and the Pro-CNIC Foundation, and is a Severo Ochoa Center of Excellence (MINECO award SEV-2015-0505).S

Impact of Left Ventricular Hypertrophy on Troponin Release During Acute Myocardial Infarction: New Insights From a Comprehensive Translational Study

Background-Biomarkers are frequently used to estimate infarct size (IS) as an endpoint in experimental and clinical studies. Here, we prospectively studied the impact of left ventricular (LV) hypertrophy (LVH) on biomarker release in clinical and experimental myocardial infarction (MI). Methods and Results-ST-segment elevation myocardial infarction (STEMI) patients (n=140) were monitored for total creatine kinase (CK) and cardiac troponin I (cTnI) over 72 hours postinfarction and were examined by cardiac magnetic resonance (CMR) at 1 week and 6 months postinfarction. MI was generated in pigs with induced LVH (n=10) and in sham-operated pigs (n=8), and serial total CK and cTnI measurements were performed and CMR scans conducted at 7 days postinfarction. Regression analysis was used to study the influence of LVH on total CK and cTnI release and IS estimated by CMR (gold standard). Receiver operating characteristic (ROC) curve analysis was performed to study the discriminatory capacity of the area under the curve (AUC) of cTnI and total CK in predicting LV dysfunction. Cardiomyocyte cTnI expression was quantified in myocardial sections from LVH and sham-operated pigs. In both the clinical and experimental studies, LVH was associated with significantly higher peak and AUC of cTnI, but not with differences in total CK. ROC curves showed that the discriminatory capacity of AUC of cTnI to predict LV dysfunction was significantly worse for patients with LVH. LVH did not affect the capacity of total CK to estimate IS or LV dysfunction. Immunofluorescence analysis revealed significantly higher cTnI content in hypertrophic cardiomyocytes. Conclusions-Peak and AUC of cTnI both significantly overestimate IS in the presence of LVH, owing to the higher troponin content per cardiomyocyte. In the setting of LVH, cTnI release during STEMI poorly predicts postinfarction LV dysfunction. LV mass should be taken into consideration when IS or LV function are estimated by troponin release.This work was supported by an award from the Fondo de Investigacion Sanitaria (FIS 10/02268) and by the competitive grant ``CNIC translational 01/2009.´´ Fernandez-Jimenez is the recipient of a Rio Hortega fellowship. The ``Red de Investigacion Cardiovascular (RIC)´´ of the Spanish Ministry of Health supports Ibanez (RD 12/0042/0054) and Redondo (RD 12/0042/0022). The ``Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC)´´ is supported by the Spanish Ministry of Economy and Competitiveness and the Pro-CNIC Foundation.S

Impact of the timing of metoprolol administration during STEMI on infarct size and ventricular function

Pre-reperfusion administration of intravenous (IV) metoprolol reduces infarct size in ST-segment elevation myocardial infarction (STEMI). This study sought to determine how this cardioprotective effect is influenced by the timing of metoprolol therapy having either a long or short metoprolol bolus-to-reperfusion interval. We performed a post hoc analysis of the METOCARD-CNIC (effect of METOprolol of CARDioproteCtioN during an acute myocardial InfarCtion) trial, which randomized anterior STEMI patients to IV metoprolol or control before mechanical reperfusion. Treated patients were divided into short- and long-interval groups, split by the median time from 15 mg metoprolol bolus to reperfusion. We also performed a controlled validation study in 51 pigs subjected to 45 min ischemia/reperfusion. Pigs were allocated to IV metoprolol with a long (−25 min) or short (−5 min) pre-perfusion interval, IV metoprolol post-reperfusion (+60 min), or IV vehicle. Cardiac magnetic resonance (CMR) was performed in the acute and chronic phases in both clinical and experimental settings. For 218 patients (105 receiving IV metoprolol), the median time from 15 mg metoprolol bolus to reperfusion was 53 min. Compared with patients in the short-interval group, those with longer metoprolol exposure had smaller infarcts (22.9 g vs. 28.1 g; p = 0.06) and higher left ventricular ejection fraction (LVEF) (48.3% vs. 43.9%; p = 0.019) on day 5 CMR. These differences occurred despite total ischemic time being significantly longer in the long-interval group (214 min vs. 160 min; p < 0.001). There was no between-group difference in the time from symptom onset to metoprolol bolus. In the animal study, the long-interval group (IV metoprolol 25 min before reperfusion) had the smallest infarcts (day 7 CMR) and highest long-term LVEF (day 45 CMR). In anterior STEMI patients undergoing primary angioplasty, the sooner IV metoprolol is administered in the course of infarction, the smaller the infarct and the higher the LVEF. These hypothesis-generating clinical data are supported by a dedicated experimental large animal study.Sin financiación19.896 JCR (2016) Q1, 2/126 Cardiac and Cardiovascular SystemsUE

β3 adrenergic receptor selective stimulation during ischemia/reperfusion improves cardiac function in translational models through inhibition of mPTP opening in cardiomyocytes

Selective stimulation of β3 adrenergic-receptor (β3AR) has been shown to reduce infarct size in a mouse model of myocardial ischemia/reperfusion. However, its functional long-term effect and the cardioprotective mechanisms at the level of cardiomyocytes have not been elucidated, and the impact of β3AR stimulation has not been evaluated in a more translational large animal model. This study aimed at evaluating pre-perfusion administration of BRL37344 both in small and large animal models of myocardial ischemia/reperfusion. Pre-reperfusion administration of the β3AR agonist BRL37344 (5 μg/kg) reduced infarct size at 2-and 24-h reperfusion in wild-type mice. Long-term (12-weeks) left ventricular (LV) function assessed by echocardiography and cardiac magnetic resonance (CMR) was significantly improved in β3AR agonist-treated mice. Incubation with β3AR agonist (BRL37344, 7 μmol/L) significantly reduced cell death in isolated adult mouse cardiomyocytes during hypoxia/reoxygenation and decreased susceptibility to deleterious opening of the mitochondrial permeability transition pore (mPTP), via a mechanism dependent on the Akt-NO signaling pathway. Pre-reperfusion BRL37344 administration had no effect on infarct size in cyclophilin-D KO mice, further implicating mPTP in the mechanism of protection. Large-white pigs underwent percutaneous coronary ischemia/reperfusion and 3-T CMR at 7 and 45 days post-infarction. Pre-perfusion administration of BRL37344 (5 μg/kg) decreased infarct size and improved long-term LV contractile function. A single-dose administration of β3AR agonist before reperfusion decreased infarct size and resulted in a consistent and long-term improvement in cardiac function, both in small and large animal models of myocardial ischemia/reperfusion. This protection appears to be executed through inhibition of mPTP opening in cardiomyocytes.S