RESUMEN
Pulmonary arterial hypertension (PAH) is a devastating cardiovascular disorder characterized by the remodelling of pre-capillary pulmonary arteries. The vascular remodelling observed in PAH patients results from excessive proliferation and apoptosis resistance of pulmonary arterial smooth muscle cells (PASMCs) and pulmonary arterial endothelial cells (PAECs). We have previously demonstrated that mutations in the type II receptor for bone morphogenetic protein (BMPRII) underlie the majority of the familial and inherited forms of the disease. We have further demonstrated that BMPRII deficiency promotes excessive proliferation and attenuates apoptosis in PASMCs, but the underlying mechanisms remain unclear. The major objective of this study is to investigate how BMPRII deficiency impairs apoptosis in PAH. Using multidisciplinary approaches, we demonstrate that deficiency in the expression of BMPRII impairs apoptosis by modulating the alternative splicing of the apoptotic regulator, B-cell lymphoma X (Bcl-x) transcripts: a finding observed in circulating leukocytes and lungs of PAH subjects, hypoxia-induced PAH rat lungs as well as in PASMCs and PAECs. BMPRII deficiency elicits cell specific effects: promoting the expression of Bcl-xL transcripts in PASMCs while inhibiting it in ECs, thus exerting differential apoptotic effects in these cells. The pro-survival effect of BMPRII receptor is mediated through the activin receptor-like kinase 1 (ALK1) but not the ALK3 receptor. Finally, we show that BMPRII interacts with the ALK1 receptor and pathogenic mutations in the BMPR2 gene abolish this interaction. Taken together, dysfunctional BMPRII responsiveness impairs apoptosis via the BMPRII-ALK1-Bcl-xL pathway in PAH. We suggest Bcl-xL as a potential biomarker and druggable target.
Asunto(s)
Quinasa de Linfoma Anaplásico/genética , Apoptosis , Receptores de Proteínas Morfogenéticas Óseas de Tipo II/genética , Hipertensión Pulmonar Primaria Familiar/genética , Miocitos del Músculo Liso/metabolismo , Proteína bcl-X/metabolismo , Receptores de Activinas Tipo II/metabolismo , Quinasa de Linfoma Anaplásico/metabolismo , Animales , Receptores de Proteínas Morfogenéticas Óseas de Tipo II/metabolismo , Caspasas/metabolismo , Supervivencia Celular/genética , Células Endoteliales/metabolismo , Hipertensión Pulmonar Primaria Familiar/metabolismo , Células HEK293 , Humanos , Hipoxia/metabolismo , Leucocitos/metabolismo , Pulmón/metabolismo , Músculo Liso Vascular/metabolismo , Ratas , Transducción de Señal , Proteína bcl-X/antagonistas & inhibidoresRESUMEN
BACKGROUND: We report striking and unanticipated improvements in maladaptive behaviours in Prader-Willi syndrome (PWS) during a trial of vagus nerve stimulation (VNS) initially designed to investigate effects on the overeating behaviour. PWS is a genetically determined neurodevelopmental disorder associated with mild-moderate intellectual disability (ID) and social and behavioural difficulties, alongside a characteristic and severe hyperphagia. METHODS: Three individuals with PWS underwent surgery to implant the VNS device. VNS was switched on 3 months post-implantation, with an initial 0.25 mA output current incrementally increased to a maximum of 1.5 mA as tolerated by each individual. Participants were followed up monthly. RESULTS: Vagal nerve stimulation in these individuals with PWS, within the stimulation parameters used here, was safe and acceptable. However, changes in eating behaviour were equivocal. Intriguingly, unanticipated, although consistent, beneficial effects were reported by two participants and their carers in maladaptive behaviour, temperament and social functioning. These improvements and associated effects on food-seeking behaviour, but not weight, indicate that VNS may have potential as a novel treatment for such behaviours. CONCLUSIONS: We propose that these changes are mediated through afferent and efferent vagal projections and their effects on specific neural networks and functioning of the autonomic nervous system and provide new insights into the mechanisms that underpin what are serious and common problems affecting people with IDs more generally.
Asunto(s)
Agresión/fisiología , Trastornos de Alimentación y de la Ingestión de Alimentos/terapia , Síndrome de Prader-Willi/terapia , Trastorno de la Conducta Social/terapia , Estimulación del Nervio Vago/métodos , Adulto , Composición Corporal , Peso Corporal , Trastornos de Alimentación y de la Ingestión de Alimentos/etiología , Femenino , Humanos , Masculino , Síndrome de Prader-Willi/complicaciones , Trastorno de la Conducta Social/etiología , Resultado del Tratamiento , Estimulación del Nervio Vago/efectos adversos , Adulto JovenRESUMEN
Massive stars (those ≥8 solar masses at formation) have radiative envelopes that cannot sustain a dynamo, the mechanism that produces magnetic fields in lower-mass stars. Despite this, approximately 7% of massive stars have observed magnetic fields, the origin of which is debated. We used multi-epoch interferometric and spectroscopic observations to characterize HD 148937, a binary system of two massive stars. We found that only one star is magnetic and that it appears younger than its companion. The system properties and a surrounding bipolar nebula can be reproduced with a model in which two stars merged (in a previous triple system) to produce the magnetic massive star. Our results provide observational evidence that magnetic fields form in at least some massive stars through stellar mergers.
RESUMEN
Dust associated with various stellar sources in galaxies at all cosmic epochs remains a controversial topic, particularly whether supernovae play an important role in dust production. We report evidence of dust formation in the cold, dense shell behind the ejecta-circumstellar medium (CSM) interaction in the Type Ia-CSM supernova (SN) 2018evt three years after the explosion, characterized by a rise in mid-infrared emission accompanied by an accelerated decline in the optical radiation of the SN. Such a dust-formation picture is also corroborated by the concurrent evolution of the profiles of the Hα emission line. Our model suggests enhanced CSM dust concentration at increasing distances from the SN as compared to what can be expected from the density profile of the mass loss from a steady stellar wind. By the time of the last mid-infrared observations at day +1,041, a total amount of 1.2 ± 0.2 × 10-2 Mâ of new dust has been formed by SN 2018evt, making SN 2018evt one of the most prolific dust factories among supernovae with evidence of dust formation. The unprecedented witness of the intense production procedure of dust may shed light on the perceptions of dust formation in cosmic history.
RESUMEN
Pulmonary arterial hypertension (PAH) is a rare disease that can be caused by (likely) pathogenic germline genomic variants. In addition to the most prevalent disease gene, BMPR2 (bone morphogenetic protein receptor 2), several genes, some belonging to distinct functional classes, are also now known to predispose to the development of PAH. As a consequence, specialist and non-specialist clinicians and healthcare professionals are increasingly faced with a range of questions regarding the need for, approaches to and benefits/risks of genetic testing for PAH patients and/or related family members. We provide a consensus-based approach to recommendations for genetic counselling and assessment of current best practice for disease gene testing. We provide a framework and the type of information to be provided to patients and relatives through the process of genetic counselling, and describe the presently known disease causal genes to be analysed. Benefits of including molecular genetic testing within the management protocol of patients with PAH include the identification of individuals misclassified by other diagnostic approaches, the optimisation of phenotypic characterisation for aggregation of outcome data, including in clinical trials, and importantly through cascade screening, the detection of healthy causal variant carriers, to whom regular assessment should be offered.
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Hipertensión Pulmonar , Hipertensión Arterial Pulmonar , Humanos , Asesoramiento Genético/métodos , Hipertensión Arterial Pulmonar/genética , Hipertensión Pulmonar/diagnóstico , Hipertensión Pulmonar/genética , Hipertensión Pulmonar/terapia , Mutación , Hipertensión Pulmonar Primaria Familiar/diagnóstico , Hipertensión Pulmonar Primaria Familiar/genética , Pruebas Genéticas/métodos , Predisposición Genética a la EnfermedadRESUMEN
Pulmonary arterial hypertension (PAH) is a life-threatening disease characterised by vasoconstriction and remodelling of the pulmonary vasculature. The serotonin (5-hydroxytryptamine (5-HT)) pathway has been shown to play a major role in the pathogenesis of PAH, but pharmacological modulation of this pathway for treatment of PAH is, to date, at a pre-clinical level. Terguride is a 5-HT receptor (5-HTR) antagonist that is well tolerated and clinically approved for ovulation disorders. Immunohistochemistry against 5-HTR(2A/B) on human lungs revealed their localisation to the vascular smooth muscle layer and quantitative RT-PCR showed 5-HTR(2B) upregulation in pulmonary artery smooth muscle cells (PASMC) isolated from PAH patients. Proliferation and migration of cultured primary human PASMC were dose-dependently blocked by terguride. Therapeutic 5-HT signalling inhibition was 1) demonstrated in isolated, ventilated and perfused rat lungs and 2) by chronic terguride treatment of rats with monocrotaline (MCT)-induced pulmonary hypertension in a preventive or curative approach. Terguride inhibited proliferation of PASMCs and abolished 5-HT-induced pulmonary vasoconstriction. Chronic terguride treatment prevented dose-dependently the development and progression of MCT-induced PAH in rats. Thus, terguride represents a valuable novel therapeutic approach in PAH.
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Agonistas de Dopamina/uso terapéutico , Hipertensión Pulmonar/tratamiento farmacológico , Lisurida/análogos & derivados , Pulmón/efectos de los fármacos , Antagonistas del Receptor de Serotonina 5-HT2/farmacología , Adulto , Animales , Proliferación Celular/efectos de los fármacos , Células Cultivadas , Femenino , Humanos , Hipertensión Pulmonar/inducido químicamente , Hipertensión Pulmonar/patología , Lisurida/uso terapéutico , Pulmón/patología , Pulmón/fisiopatología , Trasplante de Pulmón , Masculino , Monocrotalina/farmacología , Músculo Liso Vascular/efectos de los fármacos , Músculo Liso Vascular/patología , Músculo Liso Vascular/fisiopatología , Arteria Pulmonar/efectos de los fármacos , Arteria Pulmonar/patología , Arteria Pulmonar/fisiopatología , RatasRESUMEN
A unique subpopulation of peripheral blood mononuclear cells that exhibit a parallel expression of haematopoietic and mesenchymal markers has been described as "circulating fibrocytes". These cells were demonstrated to obtain a fibroblastic phenotype in tissues or cell culture and contribute to pulmonary fibrotic disorders and tissue remodelling processes. The aim of our study was to characterise the recruitment of circulating fibrocytes in vivo in the model of chronic hypoxic pulmonary hypertension in mice and to analyse the therapeutic effect of the stable prostacyclin analogue trepostinil with respect to this cell population. To track circulating fibrocytes in vivo, we transplanted wild-type mice with bone marrow from ubiquitously eGFP expressing mice and subjected them to chronic hypoxia. We observed significantly increased recruitment of circulating fibrocytes to the remodelled pulmonary resistance arteries in response to hypoxia. Treatment with treprostinil significantly reduced the recruitment of these cells compared to normoxic mice. Treprostinil also reduced right ventricular systolic pressure and slightly reduced the vascular remodelling but failed to reverse the right ventricular hypertrophy. In summary, we show that circulating fibrocytes contribute to hypoxic pulmonary vascular remodelling and may be specifically targeted by a prostacyclin analogue. Further investigations of cellular and paracrine mechanisms are warranted to decipher their role in pulmonary hypertension.
Asunto(s)
Antihipertensivos/farmacología , Antihipertensivos/farmacocinética , Antihipertensivos/uso terapéutico , Epoprostenol/análogos & derivados , Fibroblastos/efectos de los fármacos , Hipertensión Pulmonar/tratamiento farmacológico , Leucocitos Mononucleares/efectos de los fármacos , Animales , Circulación Sanguínea , Vasos Sanguíneos/efectos de los fármacos , Vasos Sanguíneos/fisiopatología , Células de la Médula Ósea/efectos de los fármacos , Quimerismo , Enfermedad Crónica , Epoprostenol/farmacología , Epoprostenol/uso terapéutico , Femenino , Humanos , Hipertensión Pulmonar/sangre , Hipertensión Pulmonar/fisiopatología , Hipertrofia Ventricular Derecha/tratamiento farmacológico , Hipertrofia Ventricular Derecha/fisiopatología , Hipoxia/fisiopatología , Pulmón/irrigación sanguínea , Pulmón/efectos de los fármacos , Pulmón/fisiopatología , Masculino , Ratones , Ratones Endogámicos C57BL , Ratones Transgénicos , Músculo Liso Vascular/efectos de los fármacos , Músculo Liso Vascular/fisiopatología , Arteria Pulmonar/efectos de los fármacos , Arteria Pulmonar/fisiopatologíaRESUMEN
Pulmonary hypertension is an orphan disease that until recently has received limited attention within the wider medical community. This has changed distinctly in the last 10 years with the advent of new classes of therapy and a renewed interest in mechanisms of pathogenesis. This review utilized information gathered from recent conferences, and a review of the literature was conducted using MedLine and Pubmed. Accepted mechanisms of pathogenesis and currently available treatments are presented. We will discuss interesting new concepts in pathogenesis, including the importance of genetic forms of the disease and in particular the transforming growth factor receptor superfamily and the evolving evidence of the contribution of dysregulated immunity. Areas of research may yield therapeutic benefits in the not-too-distant future, including anti-proliferative therapies and stem cell therapy.
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Hipertensión Pulmonar/etiología , Hipertensión Pulmonar/terapia , Autoanticuerpos/metabolismo , Receptores de Proteínas Morfogenéticas Óseas de Tipo II/genética , Factores de Crecimiento Endotelial/antagonistas & inhibidores , Humanos , Inflamación/inmunología , Mutación , Trasplante de Células Madre , Vasodilatadores/uso terapéuticoRESUMEN
There is mounting interest in the concept of endothelial progenitor cell (EPC) therapy for the treatment of pulmonary arterial hypertension (PAH). Recent successful pilot studies in idiopathic PAH have raised questions about the contribution of progenitor cells circulating in the peripheral blood to pulmonary vascular homeostasis and to the process of vascular remodelling. This review will summarise the work performed to date in animal and human therapeutic trials and clarify what is known about the potential contribution of EPCs to the pathophysiology of PAH.
Asunto(s)
Células Endoteliales/citología , Endotelio Vascular/citología , Hipertensión Pulmonar/terapia , Trasplante de Células Madre/métodos , Células Madre/citología , Animales , Ensayos Clínicos como Asunto , Células Endoteliales/trasplante , Humanos , Proyectos PilotoRESUMEN
Approximately 10% of patients who have a spontaneous pneumothorax have a positive family history. In 1977, Birt, Hogg and Dube (BHD) described a genodermatosis characterised by benign tumours of the hair follicle that has been associated with renal neoplasms and spontaneous pneumothorax. The BHD locus is located on chromosome 17p11.2 and is now known to be due to heterozygous germline mutations in the Folliculin gene. We report three generations of an English family who suffered spontaneous pneumothoraces in the absence of other features of the BHD syndrome and were found to have lung cysts. In addition, we report an antenatal diagnosis (34 weeks gestation) of lung cysts in one affected family member. Genetic analysis in the family has revealed a unique deletion mutation (c. 1537 del-C) involving exon 10. To our knowledge, this mutation has not been previously described and there is no previous report of antenatal detection of the pulmonary abnormality in BHD syndrome.
Asunto(s)
Quistes/genética , Enfermedades Pulmonares/genética , Neumotórax/genética , Proteínas Proto-Oncogénicas/genética , Proteínas Supresoras de Tumor/genética , Adolescente , Adulto , Anciano , Cromosomas Humanos Par 17 , Medios de Contraste , Quistes/diagnóstico , Inglaterra , Exones , Femenino , Mutación de Línea Germinal , Humanos , Enfermedades Pulmonares/diagnóstico , Masculino , Linaje , Embarazo , Pruebas de Función Respiratoria , Tomografía Computarizada por Rayos X , Ultrasonografía PrenatalRESUMEN
Research on the molecular basis of PAH caused by BMPR-II mutations is beginning to yield novel approaches to therapy, for example, small molecule inhibitors of ALK-5. Enhancement of BMP signalling may be possible with BMP-derived ligands or rescue of BMPR-II cell surface expression for some mutations. For mutations leading to nonsense mediated mRNA decay, approaches aimed at transcript stabilisation provide another possible intervention. To further our genetic understanding of this rare disease, large international collaborative studies are needed to generate the numbers of patients necessary to undertake meaningful genome wide association studies for novel susceptibility genes or disease modifying genes. In addition, to provide accurate information to families, longitudinal cohort studies, coupled with biomarker studies, are required of affected and unaffected individuals in families segregating BMPR-II mutations.
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Predisposición Genética a la Enfermedad , Hipertensión Pulmonar/genética , Receptores de Activinas Tipo II/genética , Receptores de Proteínas Morfogenéticas Óseas de Tipo II/genética , Proteínas Morfogenéticas Óseas/fisiología , Pruebas Genéticas/métodos , Humanos , Mutación , Transducción de Señal/fisiologíaRESUMEN
Although chronic thromboembolic pulmonary hypertension (CTEPH) is characterised by the persistence of organised thrombus, few pro-thrombotic risk factors have been identified in subjects with the disease. The aim of the present study was to compare the prevalence of eight functionally relevant haemostatic polymorphisms between CTEPH subjects and healthy controls. Genomic DNA was isolated from 214 CTEPH subjects and 200 healthy controls, and analysed for Factor V Leiden, prothrombin guanine (G) to adenine (A) substitution at nucleotide 20210 (20210G>A), plasminogen activator inhibitor-1 4G/5G, tissue plasminogen activator 7351 cytosine (C)>thymidine (T), Factor XIII 100G>T, fibrinogen Aalpha substitution of threonine with alanine at position 312 (Thr312Ala), fibrinogen Bbeta substitution of arginine with lysine at position 448 (Arg448Lys) and fibrinogen Bbeta 455G>A polymorphisms. A significant difference was demonstrated in fibrinogen Aalpha Thr312Ala genotype and allele frequencies between CTEPH subjects and controls. The presence of the alanine allele significantly increased the risk of CTEPH. The fibrinogen Aalpha alanine 312 allele alters fibrinogen alpha-alpha chain cross-linkage and has previously been associated with both increased risk of embolisation and increased resistance to thrombolysis. An association between this polymorphism and chronic thromboembolic pulmonary hypertension, therefore, supports an embolic aetiology for this disease, and may provide a mechanism by which thrombus persists following an acute event.
Asunto(s)
Fibrinógeno/genética , Predisposición Genética a la Enfermedad/genética , Hipertensión Pulmonar/genética , Polimorfismo de Nucleótido Simple/genética , Tromboembolia/genética , Adulto , Anciano , Estudios de Cohortes , Factor V/genética , Femenino , Humanos , Hipertensión Pulmonar/complicaciones , Masculino , Persona de Mediana Edad , Tromboembolia/complicacionesRESUMEN
Pulmonary endarterectomy (PEA) surgery is the treatment of choice in surgically accessible chronic thromboembolic pulmonary hypertension and is potentially curative. The UK is served by seven specialist pulmonary hypertension centres and, consequently, there are regions which do not have a specialist unit. Since 2000, Papworth Hospital (Papworth Everard, UK) has been the sole PEA provider for the UK, offering the opportunity to study the national incidence of operable disease and give potential insight into factors that might affect geographical distribution within the UK. All 262 UK residents who underwent PEA surgery between April 2000 and May 2006 were included in the present study. The age-adjusted cumulative referral rates were compared between regions to test for uniformity. Overall, observed rates differed significantly from expected, with evidence of significant nonuniformity across the UK. The highest rates were observed in proximity to the nationally designated specialist centres and in particular in East Anglia and the West Midlands, nearest Papworth. These two regions differed by >2 x SD from the national mean rate. The present study demonstrates wide geographical variation in the number of patients referred for pulmonary endarterectomy surgery. This suggests that there may be patients who are not presently being offered this potentially curative option.
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Endarterectomía/estadística & datos numéricos , Hipertensión Pulmonar/cirugía , Embolia Pulmonar/cirugía , Derivación y Consulta/estadística & datos numéricos , Adulto , Anciano , Femenino , Humanos , Masculino , Área sin Atención Médica , Persona de Mediana Edad , Reino Unido/epidemiologíaRESUMEN
Previous studies suggest that while lung angiotensin converting enzyme (ACE) activity is reduced during chronic hypoxia, inhibitors of ACE attenuate hypoxic pulmonary hypertension. In an attempt to explain this paradox we investigated the possibility that whole lung ACE activity may not reflect local pulmonary vascular ACE expression. The experimental approach combined in vivo hemodynamic studies in control and chronically hypoxic rats, measurement of whole lung ACE activity, and evaluation of local pulmonary vascular ACE expression by in situ hybridization and immunohistochemistry. Total lung ACE activity was reduced to 50% of control activity by 5 d of hypoxia and remained low for the duration of the study. Immunohistochemistry showed a marked reduction of ACE staining in alveolar capillary endothelium. However, an increase in ACE staining was observed in the walls of small newly muscularized pulmonary arteries at the level of alveolar ducts and walls. In situ hybridization studies showed increased signal for ACE mRNA in the same vessels. Inhibition of ACE by captopril during chronic hypoxia attenuated pulmonary hypertension and markedly reduced distal muscularization of small pulmonary arteries. In addition, we demonstrated marked longitudinal variation in ACE expression along the normal pulmonary vasculature with the highest levels found in small muscular arteries associated with terminal and respiratory bronchioles. We conclude that local ACE expression is increased in the walls of small pulmonary arteries during the development of hypoxic pulmonary hypertension, despite a generalized reduction in alveolar capillary ACE expression, and we speculate that local arteriolar ACE may play a role in the vascular remodeling associated with pulmonary hypertension.
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Hipertensión Pulmonar/enzimología , Hipoxia/complicaciones , Peptidil-Dipeptidasa A/biosíntesis , Arteria Pulmonar/enzimología , Inhibidores de la Enzima Convertidora de Angiotensina/uso terapéutico , Animales , Hipertensión Pulmonar/tratamiento farmacológico , Hipertensión Pulmonar/etiología , Inmunohistoquímica , Hibridación in Situ , Riñón/enzimología , Masculino , Peptidil-Dipeptidasa A/genética , ARN Mensajero/análisis , Ratas , Ratas Sprague-DawleyAsunto(s)
Antihipertensivos/farmacología , Antihipertensivos/farmacocinética , Antihipertensivos/uso terapéutico , Epoprostenol/análogos & derivados , Fibroblastos/citología , Fibroblastos/efectos de los fármacos , Fibroblastos/patología , Hipertensión Pulmonar/sangre , Hipertensión Pulmonar/tratamiento farmacológico , Hipertensión Pulmonar/patología , Leucocitos Mononucleares/efectos de los fármacos , Mesodermo/citología , Fagocitos/citología , Animales , Femenino , Humanos , MasculinoRESUMEN
Nebulised iloprost is established therapy of severe pulmonary hypertension; however, the effects on the bronchoalveolar compartment have not been investigated so far. We studied the short- and long-term effects of nebulised iloprost on pulmonary function tests and gas exchange in 63 patients with severe pulmonary hypertension (idiopathic n=17, chronic thromboembolism n=15, connective tissue disease n=12, congenital heart disease n=11, respiratory diseases n=8). Patients received iloprost in increasing dose up to 140 micro g iloprost/24h via an ultrasonic nebuliser. Short-term effects were assessed before and after every nebulisation: peak expiration flow decreased in mean by 1.9% (423+/-98 to 415+/-98) and percutaneous oxygen saturation increased in mean by 0.7% (90+/-6 to 91+/-5) post-nebulisation. There were no significant differences concerning underlying diagnosis or dose of nebulised iloprost. Within 3 months, 9 patients stopped treatment due to non-compliance with frequent nebulisations (n=3), or severe side effects (n=4); 2 patients with additional obstructive lung disease developed bronchoconstriction. Long-term effects were assessed by pulmonary function tests and gas exchange parameters at baseline and after 3 months treatment. There were no significant differences after 3 months therapy neither in FEV(1), FVC, TLC, residual volume nor in diffusions capacity, SO(2) at rest and during 6 min walking test, also in respect of the underlying diseases. However, there was a significant increase in 6 min walking distance (6 MWD) after 3 months (246+/-113 to 294+/-115 m, P<0.05). In conclusion, treatment with nebulised iloprost leads to functional improvement in severe pulmonary hypertension without systematic adverse short- and long-term effects on pulmonary function test or gas exchange. Patients with additional obstructive lung disease might develop bronchoconstriction. Severe side effects leading to discontinuation of treatment occurred in 9% of patients.
Asunto(s)
Hipertensión Pulmonar/tratamiento farmacológico , Iloprost/administración & dosificación , Pulmón/fisiopatología , Vasodilatadores/administración & dosificación , Adolescente , Adulto , Anciano , Anciano de 80 o más Años , Enfermedades del Tejido Conjuntivo/complicaciones , Enfermedades del Tejido Conjuntivo/fisiopatología , Femenino , Flujo Espiratorio Forzado/fisiología , Cardiopatías/congénito , Humanos , Hipertensión Pulmonar/etiología , Hipertensión Pulmonar/fisiopatología , Iloprost/efectos adversos , Masculino , Persona de Mediana Edad , Nebulizadores y Vaporizadores , Ápice del Flujo Espiratorio/fisiología , Embolia Pulmonar/complicaciones , Embolia Pulmonar/fisiopatología , Pruebas de Función Respiratoria/métodos , Dióxido de Azufre/metabolismo , Resultado del Tratamiento , Vasodilatadores/efectos adversos , Capacidad Vital/fisiologíaRESUMEN
Eleven hours after the detection of gravitational wave source GW170817 by the Laser Interferometer Gravitational-Wave Observatory and Virgo Interferometers, an associated optical transient, SSS17a, was identified in the galaxy NGC 4993. Although the gravitational wave data indicate that GW170817 is consistent with the merger of two compact objects, the electromagnetic observations provide independent constraints on the nature of that system. We synthesize the optical to near-infrared photometry and spectroscopy of SSS17a collected by the One-Meter Two-Hemisphere collaboration, finding that SSS17a is unlike other known transients. The source is best described by theoretical models of a kilonova consisting of radioactive elements produced by rapid neutron capture (the r-process). We conclude that SSS17a was the result of a binary neutron star merger, reinforcing the gravitational wave result.
RESUMEN
On 17 August 2017, Swope Supernova Survey 2017a (SSS17a) was discovered as the optical counterpart of the binary neutron star gravitational wave event GW170817. We report time-series spectroscopy of SSS17a from 11.75 hours until 8.5 days after the merger. Over the first hour of observations, the ejecta rapidly expanded and cooled. Applying blackbody fits to the spectra, we measured the photosphere cooling from [Formula: see text] to [Formula: see text] kelvin, and determined a photospheric velocity of roughly 30% of the speed of light. The spectra of SSS17a began displaying broad features after 1.46 days and evolved qualitatively over each subsequent day, with distinct blue (early-time) and red (late-time) components. The late-time component is consistent with theoretical models of r-process-enriched neutron star ejecta, whereas the blue component requires high-velocity, lanthanide-free material.
RESUMEN
On 17 August 2017, gravitational waves (GWs) were detected from a binary neutron star merger, GW170817, along with a coincident short gamma-ray burst, GRB 170817A. An optical transient source, Swope Supernova Survey 17a (SSS17a), was subsequently identified as the counterpart of this event. We present ultraviolet, optical, and infrared light curves of SSS17a extending from 10.9 hours to 18 days postmerger. We constrain the radioactively powered transient resulting from the ejection of neutron-rich material. The fast rise of the light curves, subsequent decay, and rapid color evolution are consistent with multiple ejecta components of differing lanthanide abundance. The late-time light curve indicates that SSS17a produced at least ~0.05 solar masses of heavy elements, demonstrating that neutron star mergers play a role in rapid neutron capture (r-process) nucleosynthesis in the universe.
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We report the discovery of ASASSN-15lh (SN 2015L), which we interpret as the most luminous supernova yet found. At redshift z = 0.2326, ASASSN-15lh reached an absolute magnitude of Mu ,AB = -23.5 ± 0.1 and bolometric luminosity Lbol = (2.2 ± 0.2) × 10(45) ergs s(-1), which is more than twice as luminous as any previously known supernova. It has several major features characteristic of the hydrogen-poor super-luminous supernovae (SLSNe-I), whose energy sources and progenitors are currently poorly understood. In contrast to most previously known SLSNe-I that reside in star-forming dwarf galaxies, ASASSN-15lh appears to be hosted by a luminous galaxy (MK ≈ -25.5) with little star formation. In the 4 months since first detection, ASASSN-15lh radiated (1.1 ± 0.2) × 10(52) ergs, challenging the magnetar model for its engine.