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The Atlantic Niño is an important source of the year‐to‐year variability of the tropical Atlantic, consisting in an irregular oscillation of the Sea Surface Temperature (SST) in the eastern tropical Atlantic. The physical mechanism underlying this oscillation is topic of debate. Some theories, known as dynamical, suggest that the Atlantic Niño is driven by internal wave dynamics. Other theories, termed thermodynamic, propose that the eastern tropical Atlantic SST variability is caused by thermodynamic processes associated with heat fluxes at the ocean surface and/or heat transport by oceanic currents. Here, we examine the SST variability from 1940 to 2022 and find that it can be described in terms of two spatial modes: one in the central and the other in eastern tropical Atlantic. However, focusing on the period from 1993 to 2022, these patterns behave differently. In 1993–2009 they concur in determining the eastern tropical Atlantic SST variability, while in 2010–2022 they act in opposite direction. Therefore, we use Sea Surface Height data and heat fluxes advected by oceanic currents to explore the relative contribution of wave dynamics and heat advection to the eastern tropical Atlantic SST fluctuation. We show that, between 1993 and 2010, the eastern tropical Atlantic SST variability is mainly determined by heat advected from the south by horizontal currents, while between 2010 and 2022 it can be explained in terms of wave dynamics. This finding suggests that the two spatial patterns determining the eastern tropical Atlantic SST variability, are two distinct physical phenomena forced by different physical mechanisms. Plain Language Summary: The Atlantic Niño/Niña is a significant pattern of interannual tropical climate variability. It is characterized by irregular oscillations of the temperature in the eastern tropical Atlantic, alternating between warm (Atlantic Niño) and cold (Atlantic Niña) phases. The physical mechanisms underlying these oscillations are still a matter of debate. Some theories, known as thermodynamic, attribute them to heat fluxes at the ocean surface and/or heat transport by oceanic currents. Other theories, referred to as dynamical, suggest that the temperature oscillations are driven by equatorial internal waves, which modify the vertical structure of the Ocean and affect the heat content of the water column. Recent research has also revealed that oscillations of the eastern Atlantic temperature are associated with two distinct spatial patterns: one in the central tropical Atlantic and the other in the eastern. We show that both wave dynamics and heat advection by oceanic currents play a role in determining changes in the temperature of the eastern tropical Atlantic. However, they act selectively, leading us to hypothesize that the two spatial modes of the eastern Atlantic temperature variability are two distinct physical phenomena driven by the alternate superposition of heat fluxes caused by oceanic currents and wave dynamics. Key Points: The variability of the sea surface temperature in the eastern tropical Atlantic can be described by two independent spatial modesThe eastern tropical Atlantic sea surfacetemperature variability is determined by Kelvin wave dynamics and heat advected by ocean currentsThe action on the sea surface temperature variability of wave dynamics and heatadvection caused by ocean currents is selective [ABSTRACT FROM AUTHOR]

Simple Summary: The cannabinoid type 1 receptor (CB1) is a primary cannabinoid receptor prominently found in the central nervous system and peripheral tissues, notably skeletal muscle. Muscle tissue CB1 is located on the cell and mitochondrial membrane. This study investigates how this receptor contributes to mitochondrial homeostasis in gastrocnemius muscle. The results indicate that CB1 absence induces a shift from fast-twitch to slow-twitch fibers, coupled with increased oxidative capacity and alterations in the antioxidant defense systems. Analysis of mitochondrial quality control (MQC) shows enhanced biogenesis, fusion, mitophagy, and UPRmt. Our study reveals the multifaceted impact of CB1 absence on the mitochondrial homeostasis of gastrocnemius muscle. This study aims to explore the complex role of cannabinoid type 1 receptor (CB1) signaling in the gastrocnemius muscle, assessing physiological processes in both CB1+/+ and CB1−/− mice. The primary focus is to enhance our understanding of how CB1 contributes to mitochondrial homeostasis. At the tissue level, CB1−/− mice exhibit a substantial miRNA-related alteration in muscle fiber composition, characterized by an enrichment of oxidative fibers. CB1 absence induces a significant increase in the oxidative capacity of muscle, supported by elevated in-gel activity of Complex I and Complex IV of the mitochondrial respiratory chain. The increased oxidative capacity is associated with elevated oxidative stress and impaired antioxidant defense systems. Analysis of mitochondrial biogenesis markers indicates an enhanced capacity for new mitochondria production in CB1−/− mice, possibly adapting to altered muscle fiber composition. Changes in mitochondrial dynamics, mitophagy response, and unfolded protein response (UPR) pathways reveal a dynamic interplay in response to CB1 absence. The interconnected mitochondrial network, influenced by increased fusion and mitochondrial UPR components, underlines the dual role of CB1 in regulating both protein quality control and the generation of new mitochondria. These findings deepen our comprehension of the CB1 impact on muscle physiology, oxidative stress, and MQC processes, highlighting cellular adaptability to CB1−/−. This study paves the way for further exploration of intricate signaling cascades and cross-talk between cellular compartments in the context of CB1 and mitochondrial homeostasis. [ABSTRACT FROM AUTHOR]

Research has been conducted on the human angiogenin. The structural basis for the altered functional properties of the human angiogenin variants has been investigated via X-ray chrystallography and the results are reported.

Research has been conducted on the bovine seminal RNase, a homodimeric enzyme with a cytotoxic activity selective for tumor cells. The relationship between its cytotoxic activity and dimeric structure and its resistance to cytosolic RNase inhibitor have been examined via site-directed mutagenesis.