Nitrogen compounds at Mexican and USA coasts on the Gulf of Mexico.

In recent decades, anthropogenic emissions in the Gulf of Mexico have caused a deterioration in air quality in surrounding areas, mainly due to particulate matter, sulfur dioxide and nitrogen dioxide. Over this period, interest in reactive nitrogen compounds has increased due to their relationships to air quality and ecosystem impacts associated with atmospheric deposition. In this study we summarize air concentrations of nitrogen dioxide in ambient air and wet atmospheric deposition of nitrate and ammonium along the southern coast of the United States of America and eastern Mexico over the period 2017 to 2020.

Further Probing the Properties of a Unique Sponge-derived Alkaloid Through the Isolation of a New (-)-(5)-(8)-(14)-Mycothiazole Analogue.

Scale-up isolation of (+)-(5)-(8)-(14)-mycothiazole () from Vanuatu specimens of to semisynthesize (+)-(5)-(8)-8--acetyl-(14)-mycothiazole () revealed a new diastereomer, (-)-(5)-(8)-(14)-mycothiazole (). The structure of was determined using HRMS, NMR, and comparing optical rotation to (-)-(5)-(8)-(14)-mycothiazole () and . The maximum tolerated dose of in mice was 0.

The extracellular matrix integrates mitochondrial homeostasis.

Cellular homeostasis is intricately influenced by stimuli from the microenvironment, including signaling molecules, metabolites, and pathogens. Functioning as a signaling hub within the cell, mitochondria integrate information from various intracellular compartments to regulate cellular signaling and metabolism. Multiple studies have shown that mitochondria may respond to various extracellular signaling events.

Distinct mechanisms of non-autonomous UPR mediated by GABAergic, glutamatergic, and octopaminergic neurons.

The capacity to deal with stress declines during the aging process, and preservation of cellular stress responses is critical to healthy aging. The unfolded protein response of the endoplasmic reticulum (UPR) is one such conserved mechanism, which is critical for the maintenance of several major functions of the ER during stress, including protein folding and lipid metabolism. Hyperactivation of the UPR by overexpression of the major transcription factor, , solely in neurons drives lifespan extension as neurons send a neurotransmitter-based signal to other tissue to activate UPR in a non-autonomous fashion.

A metabolic atlas of mouse aging.

Humans are living longer, but this is accompanied by an increased incidence of age-related chronic diseases. Many of these diseases are influenced by age-associated metabolic dysregulation, but how metabolism changes in multiple organs during aging in males and females is not known. Answering this could reveal new mechanisms of aging and age-targeted therapeutics.

Mechanical stress through growth on stiffer substrates impacts animal health and longevity in .

Mechanical stress is a measure of internal resistance exhibited by a body or material when external forces, such as compression, tension, bending, etc. are applied. The study of mechanical stress on health and aging is a continuously growing field, as major changes to the extracellular matrix and cell-to-cell adhesions can result in dramatic changes to tissue stiffness during aging and diseased conditions.

Investigating impacts of the mycothiazole chemotype as a chemical probe for the study of mitochondrial function and aging.

Small molecule inhibitors of the mitochondrial electron transport chain (ETC) hold significant promise to provide valuable insights to the field of mitochondrial research and aging biology. In this study, we investigated two molecules: mycothiazole (MTZ) - from the marine sponge C. mycofijiensis and its more stable semisynthetic analog 8-O-acetylmycothiazole (8-OAc) as potent and selective chemical probes based on their high efficiency to inhibit ETC complex I function.

Glial-derived mitochondrial signals affect neuronal proteostasis and aging.

The nervous system plays a critical role in maintaining whole-organism homeostasis; neurons experiencing mitochondrial stress can coordinate the induction of protective cellular pathways, such as the mitochondrial unfolded protein response (UPR), between tissues. However, these studies largely ignored nonneuronal cells of the nervous system. Here, we found that UPR activation in four astrocyte-like glial cells in the nematode, , can promote protein homeostasis by alleviating protein aggregation in neurons.

Glial-derived mitochondrial signals impact neuronal proteostasis and aging.

The nervous system plays a critical role in maintaining whole-organism homeostasis; neurons experiencing mitochondrial stress can coordinate the induction of protective cellular pathways, such as the mitochondrial unfolded protein response (UPR), between tissues. However, these studies largely ignored non-neuronal cells of the nervous system. Here, we found that UPR activation in four, astrocyte-like glial cells in the nematode, , can promote protein homeostasis by alleviating protein aggregation in neurons.

Lipid homeostasis is essential for a maximal ER stress response.

Changes in lipid metabolism are associated with aging and age-related diseases, including proteopathies. The endoplasmic reticulum (ER) is uniquely a major hub for protein and lipid synthesis, making its function essential for both protein and lipid homeostasis. However, it is less clear how lipid metabolism and protein quality may impact each other.

Iron associated lipid peroxidation in Alzheimers disease is increased in lipid rafts with decreased ferroptosis suppressors, tested by chelation in mice.

Iron-mediated cell death (ferroptosis) is a proposed mechanism of Alzheimers disease (AD) pathology. While iron is essential for basic biological functions, its reactivity generates oxidants which contribute to cell damage and death. To further resolve mechanisms of iron-mediated toxicity in AD, we analyzed postmortem human brain and ApoEFAD mice.

Historical view of medical Spanish instruction in a medical school at the US-Mexico border region.

With a growing speaking Spanish population in the USA, it is necessary to help meet their healthcare needs. The Paul L. Foster School of Medicine is located in El Paso at the US-Mexico border.

Large-scale genetic screens identify BET-1 as a cytoskeleton regulator promoting actin function and life span.

The actin cytoskeleton is a three-dimensional scaffold of proteins that is a regulatory, energyconsuming network with dynamic properties to shape the structure and function of the cell. Proper actin function is required for many cellular pathways, including cell division, autophagy, chaperone function, endocytosis, and exocytosis. Deterioration of these processes manifests during aging and exposure to stress, which is in part due to the breakdown of the actin cytoskeleton.

Hijacking Cellular Stress Responses to Promote Lifespan.

Organisms are constantly exposed to stress both from the external environment and internally within the cell. To maintain cellular homeostasis under different environmental and physiological conditions, cell have adapted various stress response signaling pathways, such as the heat shock response (HSR), unfolded protein responses of the mitochondria (UPR), and the unfolded protein response of the endoplasmic reticulum (UPR). As cells grow older, all cellular stress responses have been shown to deteriorate, which is a major cause for the physiological consequences of aging and the development of numerous age-associated diseases.

Surveying Low-Cost Methods to Measure Lifespan and Healthspan in Caenorhabditis elegans.

The discovery and development of Caenorhabditis elegans as a model organism was influential in biology, particularly in the field of aging. Many historical and contemporary studies have identified thousands of lifespan-altering paradigms, including genetic mutations, transgenic gene expression, and hormesis, a beneficial, low-grade exposure to stress. With its many advantages, including a short lifespan, easy and low-cost maintenance, and fully sequenced genome with homology to almost two-thirds of all human genes, C.

Cross-species screening platforms identify EPS-8 as a critical link for mitochondrial stress and actin stabilization.

The dysfunction of mitochondria is associated with the physiological consequences of aging and many age-related diseases. Therefore, critical quality control mechanisms exist to protect mitochondrial functions, including the unfolded protein response of the mitochondria (UPR). However, it is still unclear how UPR is regulated in mammals with mechanistic discrepancies between previous studies.

Imaging of Actin Cytoskeletal Integrity During Aging in C. elegans.

The actin cytoskeleton plays a fundamental role in the regulation of multiple cellular pathways, including trafficking and locomotion. The functional integrity of the cytoskeleton is important during aging, as the decline of cytoskeletal integrity contributes to the physiological consequence of aging. Moreover, improving cytoskeletal form and function throughout aging is sufficient to drive life span extension and promote organismal health in multiple model systems.

Divergent Nodes of Non-autonomous UPR Signaling through Serotonergic and Dopaminergic Neurons.

In multicellular organisms, neurons integrate a diverse array of external cues to affect downstream changes in organismal health. Specifically, activation of the endoplasmic reticulum (ER) unfolded protein response (UPR) in neurons increases lifespan by preventing age-onset loss of ER proteostasis and driving lipid depletion in a cell non-autonomous manner. The mechanism of this communication is dependent on the release of small clear vesicles from neurons.

UPR promotes lipophagy independent of chaperones to extend life span.

Longevity is dictated by a combination of environmental and genetic factors. One of the key mechanisms to regulate life-span extension is the induction of protein chaperones for protein homeostasis. Ectopic activation of the unfolded protein response of the endoplasmic reticulum (UPR) specifically in neurons is sufficient to enhance organismal stress resistance and extend life span.

Spatial regulation of the actin cytoskeleton by HSF-1 during aging.

There are many studies suggesting an age-associated decline in the actin cytoskeleton, and this has been adopted as common knowledge in the field of aging biology. However, a direct identification of this phenomenon in aging multicellular organisms has not been performed. Here, we express LifeAct::mRuby in a tissue-specific manner to interrogate cytoskeletal organization as a function of age.

Spatial and temporal variability of atmospheric mercury concentrations emitted from a coal-fired power plant in Mexico.

Unlabelled: Atmospheric mercury in the environment as a result of the consumption of fossil fuels, such as coal used in electricity generation, has gained increased attention worldwide because of its toxicity, atmospheric persistence, and bioaccumulation. Determining or predicting the concentration of this pollutant in ambient air is essential for determining sensitive areas requiring health protection. This study investigated the spatiotemporal variability of gaseous elemental mercury (GEM) concentrations and its dry deposition surrounding the Presidente Plutarco Elías Calles (CETEPEC) coal-fired power plant, located on Mexico's Pacific coast.