Advances in understanding of air-sea exchange and cycling of greenhouse gases in the upper ocean

\ua9 2024 University of California Press. All rights reserved. The air–sea exchange and oceanic cycling of greenhouse gases (GHG), including carbon dioxide (CO2), nitrous oxide (N2O), methane (CH4), carbon monoxide (CO), and nitrogen oxides (NOx \ubc NO \ufe NO2), are fundamental in controlling the evolution of the Earth’s atmospheric chemistry and climate. Significant advances have been made over the last 10 years in understanding, instrumentation and methods, as well as deciphering the production and consumption pathways of GHG in the upper ocean (including the surface and subsurface ocean down to approximately 1000 m). The global ocean under current conditions is now well established as a major sink for CO2, a major source for N2O and a minor source for both CH4 and CO. The importance of the ocean as a sink or source of NOx is largely unknown so far. There are still considerable uncertainties about the processes and their major drivers controlling the distributions of N2O, CH4, CO, and NOx in the upper ocean. Without having a fundamental understanding of oceanic GHG production and consumption pathways, our knowledge about the effects of ongoing major oceanic changes—warming, acidification, deoxygenation, and eutrophication—on the oceanic cycling and air–sea exchange of GHG remains rudimentary at best. We suggest that only through a comprehensive, coordinated, and interdisciplinary approach that includes data collection by global observation networks as well as joint process studies can the necessary data be generated to (1) identify the relevant microbial and phytoplankton communities, (2) quantify the rates of ocean GHG production and consumption pathways, (3) comprehend their major drivers, and (4) decipher economic and cultural implications of mitigation solutions

Antiepileptic drugs’ tolerability and safety – a systematic review and meta-analysis of adverse effects in dogs

<p>Various anti-epileptic drugs (AEDs) are used for the management of idiopathic epilepsy (IE) in dogs. Their safety profile is an important consideration for regulatory bodies, owners and prescribing clinicians. However, information on their adverse effects still remains limited with most of it derived from non-blinded non-randomized uncontrolled trials and case reports.</p><p><span>This poster won third place, which was presented at the Veterinary Evidence Today conference, Edinburgh November 1-3, 2016. </span></p><br /> <img src="https://www.veterinaryevidence.org/rcvskmod/icons/oa-icon.jpg" alt="Open Access" /

Mapping the Spatio-Temporal Pattern of the Mammalian Target of Rapamycin (mTOR) Activation in Temporal Lobe Epilepsy

Growing evidence from rodent models of temporal lobe epilepsy (TLE) indicates that dysregulation of the mammalian target of rapamycin (mTOR) pathway is involved in seizures and epileptogenesis. However, the role of the mTOR pathway in the epileptogenic process remains poorly understood. Here, we used an animal model of TLE and sclerotic hippocampus from patients with refractory TLE to determine whether cell-type specific activation of mTOR signaling occurs during each stage of epileptogenesis. In the TLE mouse model, we found that hyperactivation of the mTOR pathway is present in distinct hippocampal subfields at three different stages after kainate-induced seizures, and occurs in neurons of the granular and pyramidal cell layers, in reactive astrocytes, and in dispersed granule cells, respectively. In agreement with the findings in TLE mice, upregulated mTOR was observed in the sclerotic hippocampus of TLE patients. All sclerotic hippocampus (n = 13) exhibited widespread reactive astrocytes with overactivated mTOR, some of which invaded the dispersed granular layer. Moreover, two sclerotic hippocampus exhibited mTOR activation in some of the granule cells, which was accompanied by cell body hypertrophy. Taken together, our results indicate that mTOR activation is most prominent in reactive astrocytes in both an animal model of TLE and the sclerotic hippocampus from patients with drug resistant TLE

Two Prp19-Like U-Box Proteins in the MOS4-Associated Complex Play Redundant Roles in Plant Innate Immunity

Plant Resistance (R) proteins play an integral role in defense against pathogen infection. A unique gain-of-function mutation in the R gene SNC1, snc1, results in constitutive activation of plant immune pathways and enhanced resistance against pathogen infection. We previously found that mutations in MOS4 suppress the autoimmune phenotypes of snc1, and that MOS4 is part of a nuclear complex called the MOS4-Associated Complex (MAC) along with the transcription factor AtCDC5 and the WD-40 protein PRL1. Here we report the immuno-affinity purification of the MAC using HA-tagged MOS4 followed by protein sequence analysis by mass spectrometry. A total of 24 MAC proteins were identified, 19 of which have predicted roles in RNA processing based on their homology to proteins in the Prp19-Complex, an evolutionarily conserved spliceosome-associated complex containing homologs of MOS4, AtCDC5, and PRL1. Among these were two highly similar U-box proteins with homology to the yeast and human E3 ubiquitin ligase Prp19, which we named MAC3A and MAC3B. MAC3B was recently shown to exhibit E3 ligase activity in vitro. Through reverse genetics analysis we show that MAC3A and MAC3B are functionally redundant and are required for basal and R protein–mediated resistance in Arabidopsis. Like mos4-1 and Atcdc5-1, mac3a mac3b suppresses snc1-mediated autoimmunity. MAC3 localizes to the nucleus and interacts with AtCDC5 in planta. Our results suggest that MAC3A and MAC3B are members of the MAC that function redundantly in the regulation of plant innate immunity