The Multiplanet System TOI-421: A Warm Neptune and a Super Puffy Mini-Neptune Transiting a G9 V Star in a Visual Binary

We report the discovery of a warm Neptune and a hot sub-Neptune transiting TOI-421 (BD-14 1137, TIC 94986319), a bright (V = 9.9) G9 dwarf star in a visual binary system observed by the Transiting Exoplanet Survey Satellite (TESS) space mission in Sectors 5 and 6. We performed ground-based follow-up observations—comprised of Las Cumbres Observatory Global Telescope transit photometry, NIRC2 adaptive optics imaging, and FIbre-fed Echellé Spectrograph, CORALIE, High Accuracy Radial velocity Planet Searcher, High Resolution Échelle Spectrometer, and Planet Finder Spectrograph high-precision Doppler measurements—and confirmed the planetary nature of the 16 day transiting candidate announced by the TESS team. We discovered an additional radial velocity signal with a period of five days induced by the presence of a second planet in the system, which we also found to transit its host star. We found that the inner mini-Neptune, TOI-421 b, has an orbital period of P_b = 5.19672 ± 0.00049 days, a mass of M_b = 7.17 ± 0.66 M⊕, and a radius of R_b = 2.68^(+0.19)_(-0.18) R⊕, whereas the outer warm Neptune, TOI-421 c, has a period of Pc = 16.06819 ± 0.00035 days, a mass of M_c = 16.42^(+1.06)_(-1.04) M⊕, a radius of R_c = 5.09^(+0.16)_(-0.15) R⊕ and a density of ρ_c = 0.685^(+0.080)_(-0.072) g cm⁻³. With its characteristics, the outer planet (ρ_c = 0.685^(+0.080)_(-0.072) g cm⁻³) is placed in the intriguing class of the super-puffy mini-Neptunes. TOI-421 b and TOI-421 c are found to be well-suited for atmospheric characterization. Our atmospheric simulations predict significant Lyα transit absorption, due to strong hydrogen escape in both planets, as well as the presence of detectable CH4 in the atmosphere of TOI-421 c if equilibrium chemistry is assumed

Síndrome hepatorenal: patogénesis y tratamiento

El Síndrome Hepatorenal (SHR) es una insuficiencia renal aguda funcional y reversible, que se desarrolla en pacientes con cirrosis hepática descompensada o en insuficiencia hepática aguda severa. La característica principal del SHR es la intensa vasoconstricción renal causada por la interacción entre alteraciones hemodinámicas a nivel sistémico y portal. El aumento del volumen intravascular y un prolongado tratamiento con fármacos vasoconstrictores pueden revertir la falla renal en un porcentaje significativo de pacientes. El SHR Tipo 2, el más frecuente, generalmente presenta una evolución lenta y un mejor pronóstico que el SHR Tipo 1. La terapia vasoconstrictora con terlipresina asociado a albúmina es el tratamiento de elección en pacientes con SHR. A pesar del avance en las diferentes estrategias terapéuticas, el pronóstico a largo plazo es aún pobre y depende generalmente del grado de reversibilidad de la enfermedad hepática asociada o del acceso al trasplante hepático. En la presente revisión se discutirán los avances más recientes en el diagnóstico, patogénesis y tratamiento del SHR

Polimorfismos cercanos al gen IL28B y su relación con la infección con el virus hepatitis B

Three top single-nucleotide polymorphisms (rs12979860, rs12980275 and rs8099917) near to IL28B gene have been associated to spontaneous or relate to treatment-induced hepatitis C virus clearence. The role of this polymorphism is less known in hepatitis B virus (HBV) infection. S ome studies have been focused to relate IL28B variants and clinical course of HBV infection, found discordant results. In relation to treatment for HBV, it has been shown an association between IL28B polymorphisms and response to therapy with Peginterferon

Interferones lambdas (ifnsλ) en infección con virus hepatitis C

The current standard therapy for patients chronically infected with hepatitis C virus (HCV) is the administration of pegylated interferon-α (PEG-IFN) plus ribavirin (RBV), eliminating the virus in only about half of patients infected with the genotype most common in Chile and the world (genotype 1), being higher for genotypes 2 and 3. Genotyping of the HCV is a strong predictor of treatment response, and it defines the treatment duration (48 weeks for genotype 1 and 24 weeks for genotypes 2 and 3). Genome studies revealed the association of polymorphisms (SNPs) close to IL28B gene with increased spontaneous and treatment-inducing clearance for HCV, which are now evaluated as a strong predictor of treatment response. These SNPs are close to genes coding for type III IFNs family, known as IFNs lambda (IFNsλ), composed by IFNλ1 (IL29), IFNλ2 (IL28A) and IFNλ3 (IL28B). It has been shown that these cytokines are highly involved in antiviral immune responses, including HCV, playing IFNλ1 a central role. Today, there is an ongoing study where pegylated IFNα1 was administrated in chronic HCV patients as alternative to IFNλ therapy, seeking for a more specific response to infected hepatocytes and with fewer adverse effects

Asociación entre polimorfismos en los genes PNPLA3 y TM6SF2 y presencia de fibrosis en pacientes con infección crónica por virus hepatitis C

Hepatitis C virus (HCV) is a globally prevalent pathogen and a leading cause of death and morbidity. The most recent estimates of disease burden show an increase in seroprevalence over the last 15 years to 2.8%, equating to >185 million infections worldwide. Persistent hepatitis C infection is associated with the development of liver cirrhosis, hepatocellular cancer, liver failure and death. The magnitude of disease progression in chronic infection varies significantly among individuals. Several factors have been recognized as being associated with the progression of HCV-related liver fibrosis and with clinical outcomes. As liver fibrosis progression remains variable between individuals with similar environmental or virological risks, host genetic predispositions have been suggested as another critical determinant. The single nucleotide polymorphisms in Patatin-like phospholipase domain-containing 3 (PNPLA3) and Transmembrane 6 Superfamily Member 2 (TM6SF2) genes are genetic determinants of nonalcoholic fatty liver disease, in terms of inflammation and fibrosis. The possible action of the PNPLA3 and TM6SF2 polymorphisms on fibrosis development in chronic hepatis C is being studied, with controversial results