Searching for molecular outflows in Hyper-Luminous Infrared Galaxies

We present constraints on the molecular outflows in a sample of five Hyper-Luminous Infrared Galaxies using Herschel observations of the OH doublet at 119 {\mu}m. We have detected the OH doublet in three cases: one purely in emission and two purely in absorption. The observed emission profile has a significant blueshifted wing suggesting the possibility of tracing an outflow. Out of the two absorption profiles, one seems to be consistent with the systemic velocity while the other clearly indicates the presence of a molecular outflow whose maximum velocity is about ~1500 km/s. Our analysis shows that this system is in general agreement with previous results on Ultra-luminous Infrared Galaxies and QSOs, whose outflow velocities do not seem to correlate with stellar masses or starburst luminosities (star formation rates). Instead the galaxy outflow likely arises from an embedded AGN.Comment: Accepted for publication in MNRAS. 13 pages, 11 figures, 4 table

An infrared study of the double nucleus in NGC3256

We present new resolved near and mid-IR imaging and N-band spectroscopy of the two nuclei in the merger system NGCA3256, the most IR luminous galaxy in the nearby universe. The results from the SED fit to the data are consistent with previous estimates of the amount of obscuration towards the nuclei and the nuclear star formation rates. However, we also find substantial differences in the infrared emission from the two nuclei which cannot be explained by obscuration alone. We conclude that the northern nucleus requires an additional component of warm dust in order to explain its properties. This suggests that local starforming conditions can vary significantly within the environment of a single system.Comment: Accepted for publication (MNRAS

Caracterização de germoplasma de jaqueira em Pernambuco por meio de descritos agronômicos.

Anais do 1° Simpósio da Rede de Recursos Genéticos Vegetais do Nordeste (I RGVNE), Cruz das Almas, nov. 2013

Evolução da salinidade do solo por aplicação de fertilizantes em cultivo de beterraba fertirrigado.

A salinização dos solos pode ter origem natural ou ser induzida pelo homem, sendo a segunda maneira geralmente associada ao manejo inadequado da irrigação ou fertirrigação. O objetivo desse estudo foi verificar a evolução da salinidade provocada pela fertirrigação em um cultivo de beterraba. Um experimento foi realizado na FCA UNESP campus de Botucatu, em vasos de 15L, para a obtenção de curvas de salinização artificial do solo. O solo foi salinizado artificialmente pela fertirrigação excessiva. Os tratamentos foram formados da combinação de dois fatores: salinidade inicial do solo com 5 níveis (S1=1,0; S3=3,0;S6 =6,0; S9=9,0; S12=12,0 dS m-1) e dois manejos de fertirrigação (M1= tradicional e M2 = com controle da concentração iônica da solução do solo). O delineamento adotado foi o de blocos casualizados, com 4 repetições, e os fatores arranjados em esquema fatorial 5 x 2. A obtenção da condutividade elétrica do solo com a correção da umidade do solo proporcionou valores com maiores precisões para a manutenção da salinidade na solução do solo. Os maiores níveis da salinidade do solo ocorreram nas camadas mais profundas do perfil do solo no manejo tradicional da fertirrigação, devido aos altos valores de condutividade elétrica observados neste tratamento

Dissimilaridade entre acessos de jaqueira (Artocarpus heterophyllus Lam.) com base em características de fruto.

Anais do 1º Simpósio da Rede de Recursos Genéticos Vegetais do Nordeste (I RGVNE), Cruz das Almas, nov. 2013

Comportamento de linhagens e cultivares de algodoeiro no Cerrado do Mato Grosso: resultados da safra 2003/2004.

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Restoring the infected powerhouse:Mitochondrial quality control in sepsis

Sepsis is a dysregulated host response to an infection, characterized by organ failure. The pathophysiology is complex and incompletely understood, but mitochondria appear to play a key role in the cascade of events that culminate in multiple organ failure and potentially death. In shaping immune responses, mitochondria fulfil dual roles: they not only supply energy and metabolic intermediates crucial for immune cell activation and function but also influence inflammatory and cell death pathways. Importantly, mitochondrial dysfunction has a dual impact, compromising both immune system efficiency and the metabolic stability of end organs. Dysfunctional mitochondria contribute to the development of a hyperinflammatory state and loss of cellular homeostasis, resulting in poor clinical outcomes. Already in early sepsis, signs of mitochondrial dysfunction are apparent and consequently, strategies to optimize mitochondrial function in sepsis should not only prevent the occurrence of mitochondrial dysfunction, but also cover the repair of the sustained mitochondrial damage. Here, we discuss mitochondrial quality control (mtQC) in the pathogenesis of sepsis and exemplify how mtQC could serve as therapeutic target to overcome mitochondrial dysfunction. Hence, replacing or repairing dysfunctional mitochondria may contribute to the recovery of organ function in sepsis. Mitochondrial biogenesis is a process that results in the formation of new mitochondria and is critical for maintaining a pool of healthy mitochondria. However, exacerbated biogenesis during early sepsis can result in accumulation of structurally aberrant mitochondria that fail to restore bioenergetics, produce excess reactive oxygen species (ROS) and exacerbate the disease course. Conversely, enhancing mitophagy can protect against organ damage by limiting the release of mitochondrial-derived damage-associated molecules (DAMPs). Furthermore, promoting mitophagy may facilitate the growth of healthy mitochondria by blocking the replication of damaged mitochondria and allow for post sepsis organ recovery through enabling mitophagy-coupled biogenesis. The remaining healthy mitochondria may provide an undamaged scaffold to reproduce functional mitochondria. However, the kinetics of mtQC in sepsis, specifically mitophagy, and the optimal timing for intervention remain poorly understood. This review emphasizes the importance of integrating mitophagy induction with mtQC mechanisms to prevent undesired effects associated with solely the induction of mitochondrial biogenesis.</p