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Ferroptosis is a unique form of cell death that was first described in 2012 and plays a significant role in various diseases, including neurodegenerative conditions. It depends on a dysregulation of cellular iron metabolism, which increases free, redox‐active, iron that can trigger Fenton reactions, generating hydroxyl radicals that damage cells through oxidative stress and lipid peroxidation. Lipid peroxides, resulting mainly from unsaturated fatty acids, damage cells by disrupting membrane integrity and propagating cell death signals. Moreover, lipid peroxide degradation products can further affect cellular components such as DNA, proteins, and amines. In ischemic stroke, where blood flow to the brain is restricted, there is increased iron absorption, oxidative stress, and compromised blood–brain barrier integrity. Imbalances in iron‐transport and ‐storage proteins increase lipid oxidation and contribute to neuronal damage, thus pointing to the possibility of brain cells, especially neurons, dying from ferroptosis. Here, we review the evidence showing a role of ferroptosis in ischemic stroke, both in recent studies directly assessing this type of cell death, as well as in previous studies showing evidence that can now be revisited with our new knowledge on ferroptosis mechanisms. We also review the efforts made to target ferroptosis in ischemic stroke as a possible treatment to mitigate cellular damage and death. [ABSTRACT FROM AUTHOR]

Objective: To estimate the surface water balance in the Chapingo River microbasin in the years 2014, 2016, 2017, and 2018, based on information collected on rainfall and runoff, the use of interception simulation models, and the estimation of the of infiltration as a remainder of the balance. Design/Methodology/Approach: During the 2014, 2016, 2017, and 2018 wet seasons, the water balance in water depth was estimated based on rainfall and runoff data, mathematical interception simulation models, and estimation of infiltration as a remainder of the balance. Results: The highest interception rate was recorded in 2014, with a shorter range and lower dispersion of rainfall, while the lowest interception occurred in 2018 with opposite rainfall characteristics. A linear relationship was found, in two years, between rainfall and surface runoff with R² greater than 0.81. The interception rate was lower in the oyamel fir forest (7.7-9.3%), while the variation in interception between grasslands, pine forests, oak forests, and agricultural areas ranged from 20% to 23%. The remaining infiltration water represented between 85.5% and 88.2% of the rainfall. Study Limitations/Implications: Determining the temporal evolution of the interception and humidity in the soil is necessary to specify the potential recharge to the aquifer. Findings/Conclusions: Interception is the main vehicle by which water reaches the ground in areas covered by vegetation. Rainfall intensity has a negative impact on interception and infiltration. The basin under study offers a high recharge potential to the Texcoco aquifer. [ABSTRACT FROM AUTHOR]

Ras are a family of small GTPases that function as signal transduction mediators and are involved in cell proliferation, migration, differentiation and survival. The significance of Ras is further evidenced by the fact that Ras genes are among the most mutated oncogenes in different types of cancers. After translation, Ras proteins can be targets of post-translational modifications (PTM), which can alter the intracellular dynamics of the protein. In this review, we will focus on how S-nitrosylation of Ras affects the way these proteins interact with membranes, its cellular localization, and its activity. S-Nitrosylation occurs when a nitrosyl moiety of nitric oxide (NO) is covalently attached to a thiol group of a cysteine residue in a target protein. In Ras, the conserved Cys118 is the most surface-exposed Cys and the preferable residue for NO action, leading to the initiation of transduction events. Ras transduces the mitogen-activated protein kinases (MAPK), the phosphoinositide-3 kinase (PI3K) and the RalGEF cellular pathways. S-Nitrosylation of elements of the RalGEF cascade remains to be identified. On the contrary, it is well established that several components of the MAPK and PI3K pathways, as well as different proteins associated with these cascades, can be modified by S-nitrosylation. Overall, this review presents a better understanding of Ras S-nitrosylation, increasing the knowledge on the dynamics of these proteins in the presence of NO and the underlying implications in cellular signaling. [ABSTRACT FROM AUTHOR]

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Wetting pattern geometry is useful in determining the spacing between emitters and the irrigation time in drip irrigation systems. This research aimed to generate an empirical model to estimate the width and depth of the wetting front in surface drip irrigation based on experimental tests in a cube-shaped container with transparent walls in soils with a sandy clay loam texture, with hydraulic conductivities from 2.316 to 3.945 cm h−1, and organic matter contents from 1.7 to 2.8%, and different irrigation conditions: discharge rates of 1.44, 2.90, 3.00, 3.75, and 4.00 L h−1, initial moisture levels between permanent wilting point and field capacity, and irrigation times from 0.58 to 9.50 h. The experimental conditions and the strategy for measuring the wetting front and soil moisture are detailed so the experiment is verifiable. The proposed model performed better than five other empirical models, with average values of 3 cm for the root mean square error and 0.88 for the Nash and Sutcliffe efficiency coefficient. The generated model is efficient and simple and can be a very useful tool for the design and operation of surface drip irrigation systems in soils with conditions similar to those of this study. [ABSTRACT FROM AUTHOR]

E3 ubiquitin ligases mediate the last step of the ubiquitination pathway in the ubiquitin-proteasome system (UPS). By targeting transcriptional regulators for their turnover, E3s play a crucial role in every aspect of plant biology. In plants, SKP1/CULLIN1/F-BOX PROTEIN (SCF)-type E3 ubiquitin ligases are essential for the perception and signaling of several key hormones including auxins and jasmonates (JAs). F-box proteins, TRANSPORT INHIBITOR RESPONSE 1 (TIR1) and CORONATINE INSENSITIVE 1 (COI1), bind directly transcriptional repressors AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) and JASMONATE ZIM-DOMAIN (JAZ) in auxin- and JAs-depending manner, respectively, which permits the perception of the hormones and transcriptional activation of signaling pathways. Redox modification of proteins mainly by S-nitrosation of cysteines (Cys) residues via nitric oxide (NO) has emerged as a valued regulatory mechanism in physiological processes requiring its rapid and versatile integration. Previously, we demonstrated that TIR1 and Arabidopsis thaliana SKP1 (ASK1) are targets of S-nitrosation, and these NO-dependent posttranslational modifications enhance protein-protein interactions and positively regulate SCFTIR1 complex assembly and expression of auxin response genes. In this work, we confirmed S-nitrosation of Cys140 in TIR1, which was associated in planta to auxin-dependent developmental and stress-associated responses. In addition, we provide evidence on the modulation of the SCFCOI1 complex by different S-nitrosation events. We demonstrated that S-nitrosation of ASK1 Cys118 enhanced ASK1-COI1 protein-protein interaction. Overexpression of non-nitrosable ask1 mutant protein impaired the activation of JA-responsive genes mediated by SCFCOI1 illustrating the functional relevance of this redox-mediated regulation in planta. In silico analysis positions COI1 as a promising S-nitrosation target, and demonstrated that plants treated with methyl JA (MeJA) or S-nitrosocysteine (NO-Cys, S-nitrosation agent) develop shared responses at a genome-wide level. The regulation of SCF components involved in hormonal perception by S-nitrosation may represent a key strategy to determine the precise time and site-dependent activation of each hormonal signaling pathway and highlights NO as a pivotal molecular player in these scenarios. [ABSTRACT FROM AUTHOR]

Neutrophils destroy invading microorganisms by phagocytosis by bringing them into contact with bactericidal substances, among which ROS are the most important. However, ROS also function as important physiological regulators of cellular signaling pathways. Here, we addressed the involvement of oxygen derivatives in the regulation of human neutrophil rolling, an essential component of the inflammatory response. Flow experiments using dihydroethidium‐preloaded human neutrophils showed that these cells initiate an early production of intracellular ROS during the rolling phase of the adhesion cascade, a phenomenon that required cell rolling, and the interaction of the chemokine receptor CXCR2 with their ligand CXCL8. Flow cytometry experiments demonstrated that L‐selectin shedding in neutrophils is triggered by ROS through an autocrine–paracrine mechanism. Preincubation of neutrophils with the NADPH oxidase complex inhibitor diphenyleniodonium chloride significantly increased the number of rolling neutrophils on endothelial cells. Interestingly, the same effect was observed when CXCL8 signaling was interfered using either a blocking monoclonal antibody or an inhibitor of its receptor. These findings indicate that, in response to CXCL8, neutrophils initiate ROS production during the rolling phase of the inflammatory response. This very early ROS production might participate in the modulation of the inflammatory response by inducing L‐selectin shedding in neutrophils. We propose that activation of the NADPH oxidase complex by CXCL8 releases superoxide anions to the extracellular milieu. This superoxide generates an oxidative attack on the prodomain thiol group of ADAM‐17, which is activated and process the extracellular domain of L‐selectin, causing its release from the cell membrane. [ABSTRACT FROM AUTHOR]

The HortSyst model is a new discrete time model for describing the dynamics of photo-thermal time (PTI), total dry matter production (DMP), N uptake (Nup), leaf area index (LAI), and evapotranspiration (ETc) for greenhouse crops. The first three variables are considered as state variables and the latter two are conceptualized as output variables. This model was developed as a tool for decision support systems in Mexican greenhouses for the application of N and water in tomato (Solanum lycopersicum L.) production. The HortSyst has 13 parameters. It was used to calibrate the model and estimate the correct parameter values for the crop season. An experiment was carried out to test model predictions in a greenhouse during the autumn-winter season in Chapingo, Mexico. Tomato 'CID F1' was grown in a hydroponic system and plants were distributed with a density of 3.5 plants m-2. The tomato crop was transplanted on 21 August 2015. A weather station was installed inside the greenhouse to measure temperature, relative humidity, and global radiation. The HortSyst model provides an excellent predictive quality for DMP, Nup, LAI, and ETc according to the statistics. Values for bias (BIAS) were DMP (-3.897), Nup (-0.071), LAI (0.026), and ETc (3.647), values for root mean square error (RMSE) were DMP (14.543), Nup (0.500), LAI (0.100), and ETc (39.330), and values for modeling efficiency (EF)were DMP (0.996), Nup (0.991), LAI (0.998), and ETc (0.815). The model proposed and described in this paper can be integrated as a decision support tool for N supply and irrigation management in greenhouse production systems. [ABSTRACT FROM AUTHOR]

Upon antigen recognition within peripheral lymphoid organs, B cells interact with T cells and other immune cells to transiently form morphological structures called germinal centers (GCs), which are required for B cell clonal expansion, immunoglobulin class switching, and affinity maturation. This process, known as the GC response, is an energetically demanding process that requires the metabolic reprogramming of B cells. We showed that the Ras-related guanosine triphosphate hydrolase (GTPase) R-Ras2 (also known as TC21) plays an essential, nonredundant, and B cell-intrinsic role in the GC response. Both the conversion of B cells into GC B cells and their expansion were impaired in mice lacking R-Ras2, but not in those lacking a highly related R-Ras subfamily member or both the classic H-Ras and N-Ras GTPases. In the absence of R-Ras2, activated B cells did not exhibit increased oxidative phosphorylation or aerobic glycolysis. We showed that R-Ras2 was an effector of both the B cell receptor (BCR) and CD40 and that, in its absence, B cells exhibited impaired activation of the PI3K-Akt-mTORC1 pathway, reduced mitochondrial DNA replication, and decreased expression of genes involved in glucose metabolism. Because most human B cell lymphomas originate from GC B cells or B cells that have undergone the GC response, our data suggest that R-Ras2 may also regulate metabolism in B cell malignancies. [ABSTRACT FROM AUTHOR]

Abstract: Growing evidence suggests a close relationship between Alzheimer′s Disease (AD) and cerebral hypoxia. Astrocytes play a key role in brain homeostasis and disease states, while some of the earliest changes in AD occur in astrocytes. We have therefore investigated whether mutations associated with AD increase astrocyte vulnerability to ischemia. Two astroglioma cell lines derived from APPSWE/PS1A246E (APP, amyloid precursor protein; PS1, presenilin 1) transgenic mice and controls from normal mice were subjected to oxygen and glucose deprivation (OGD), an in vitro model of ischemia. Cell death was increased in the APPSWE/PS1A246E line compared to the control. Increasing extracellular calcium concentration ([Ca2+]) exacerbated cell death in the mutant but not in the control cells. In order to explore cellular Ca2+ homeostasis, the cells were challenged with ATP or thapsigargin and [Ca2+] was measured by fluorescence microscopy. Changes in cytosolic Ca2+ concentration ([Ca2+]c) were potentiated in the APPSWE/PS1A246E transgenic line. Mitochondrial function was also altered in the APPSWE/PS1A246E astroglioma cells; mitochondrial membrane potential and production of reactive oxygen species were increased, while mitochondrial basal respiratory rate and ATP production were decreased compared to control astroglioma cells. These results suggest that AD mutations in astrocytes make them more sensitive to ischemia; Ca2+ dysregulation and mitochondrial dysfunction may contribute to this increased vulnerability. Our results also highlight the role of astrocyte dyshomeostasis in the pathophysiology of neurodegenerative brain disorders. [ABSTRACT FROM AUTHOR]