Publications by authors named "Bustos G"

Cancer is the second leading cause of death worldwide. >90 % of cancer-related deaths are due to metastasis, a process that depends on the ability of cancer cells to leave the primary tumor, migrate, and colonize different tissues. Inositol 1,4,5-trisphosphate receptor (IPR)-mediated Ca signaling plays an essential role in maintaining the homeostasis of cancer cells and the sustained proliferation.

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Allergic rhinitis (AR), a condition characterized by sensitivity to allergens leading to poor quality of life, including disrupted sleep, reduced vitality, lowered mood, changes in blood pressure limited frustration tolerance, impaired focus, decreased performance in academic and professional settings, and millions of missed work and school days every year. Approximately 20–40% of individuals in the United States are affected by AR, which carries notable clinical and financial burdens. Interestingly, there is a strong link between AR and asthma to the extent that countries with a high prevalence of rhinitis have asthma rates ranging from 10% to 25%.

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Increasing evidence supports the hypothesis that cancer progression is under mitochondrial control. Mitochondrial fission plays a pivotal role in the maintenance of cancer cell homeostasis. The inhibition of DRP1, the main regulator of mitochondrial fission, with the mitochondrial division inhibitor (mdivi-1) had been associated with cancer cell sensitivity to chemotherapeutics and decrease proliferation.

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Cancer is a leading cause of death worldwide. All major tumor suppressors and oncogenes are now recognized to have fundamental connections with metabolic pathways. A hallmark feature of cancer cells is a reprogramming of their metabolism even when nutrients are available.

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In the last few years, metabolism has been shown to be controlled by cross-organelle communication. The relationship between the endoplasmic reticulum and mitochondria/lysosomes is the most studied; here, inositol 1,4,5-triphosphate (IP3) receptor (IP3R)-mediated calcium (Ca) release plays a central role. Recent evidence suggests that IP3R isoforms participate in synthesis and degradation pathways.

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy whose chemoresistance and relapse persist as a problem despite significant advances in its chemotherapeutic treatments. Mitochondrial metabolism has emerged as an interesting therapeutic target given its essential role in maintaining bioenergetic and metabolic homeostasis. T-ALL cells are characterized by high levels of mitochondrial respiration, making them suitable for this type of intervention.

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Poly (lactic acid)/lignin nanocomposites (PLA/Lig-Np) containing cinnamaldehyde (Ci) were obtained by a combination of melt extrusion and supercritical impregnation process. In this work, Ci impregnation tests were carried out in a high-pressure cell at 40 °C for 3 h using 12 MPa and 1 MPa min of depressurization rate, obtaining impregnation yields ranging from 5.7 to 10.

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Recently, it has been suggested that the liquid fraction of anaerobic digestate, derived from the treatment of wastewater and solid wastes, could be used in vermicomposting as a solution to its disposal, and even for its valorization. Nevertheless, the literature does not provide enough information about its impact on the process of vermicomposting itself and on the final quality of the end-product. In this study, the effect of different doses of digestate in the vermicomposting process treating market waste is assessed measuring earthworm population dynamics, the bacterial community succession present in the vermibeds, as well as maturation and the end-quality of the vermicompost.

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Article Synopsis
  • The study shows that calcium (Ca) signals from a specific channel in cells help mitochondria make energy (ATP) effectively.
  • When energy production is messed up, cells have a backup way to keep functioning, but it's not as good.
  • If Ca flow between the endoplasmic reticulum and mitochondria is blocked, it can lead to cell death, especially in cells with poor energy production, suggesting this Ca flow might help treat cancer.
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Mitochondria are highly dynamic organelles constantly undergoing fusion and fission. Ca regulates many aspects of mitochondrial physiology by modulating the activity of several mitochondrial proteins. We previously showed that inhibition of constitutive IP3R-mediated Ca transfer to the mitochondria leads to a metabolic cellular stress and eventually cell death.

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Staphylococcus epidermidis has emerged as the leading agent causing neonatal late-onset sepsis in preterm neonates; although the severity of the episodes caused by this species is often underestimated, it might exert relevant short- and long-term detrimental effects on neonatal outcomes. In this context, the objective of this study was to characterize a collection of S. epidermidis strains obtained from meconium and feces of preterm infants, and to assess the potential role of the enteral feeding tubes as potential reservoirs for this microorganism.

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Background: Nosocomial sepsis is the main problem that preterms have to face during their stay at neonatal intensive care units (NICU). is an emerging cause of preterm sepsis but its epidemiology is still largely unknown. Consequently, the aims of this study were to know the rate of preterms colonized by during their stay at the NICU and the characteristics and evolution of the population, including the susceptibility to clinically relevant antibiotics.

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Cytosolic calcium (Ca) entry into mitochondria is facilitated by the mitochondrial membrane potential (ΔΨm), an electrochemical gradient generated by the electron transport chain (ETC). Is has been assumed that as long as mutations that affect the ETC do not affect the ΔΨm, the mitochondrial Ca (Ca) homeostasis remains normal. We show that knockdown of NDUFAF3 and SDHB reduce ETC activity altering Ca efflux and influx rates while ΔΨm remains intact.

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Mitochondria-associated membranes (MAMs) are central microdomains that fine-tune bioenergetics by the local transfer of calcium from the endoplasmic reticulum to the mitochondrial matrix. Here, we report an unexpected function of the endoplasmic reticulum stress transducer IRE1α as a structural determinant of MAMs that controls mitochondrial calcium uptake. IRE1α deficiency resulted in marked alterations in mitochondrial physiology and energy metabolism under resting conditions.

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Background: Carbapenemase-producing Enterobacteriaceae (CPE) have taken great importance on public health at global scale, which makes it necessary to implement rapid test for its prompt detection.

Aim: To evaluate three screening methods to detect CPE in rectal swabs.

Material And Methods: Transverse study, prospective.

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Highly malignant triple-negative breast cancer (TNBC) cells rely mostly on glycolysis to maintain cellular homeostasis; however, mitochondria are still required for migration and metastasis. Taking advantage of the metabolic flexibility of TNBC MDA-MB-231 cells to generate subpopulations with glycolytic or oxidative phenotypes, we screened phenolic compounds containing an ortho-carbonyl group with mitochondrial activity and identified a bromoalkyl-ester of hydroquinone named FR58P1a, as a mitochondrial metabolism-affecting compound that uncouples OXPHOS through a protonophoric mechanism. In contrast to well-known protonophore uncoupler FCCP, FR58P1a does not depolarize the plasma membrane and its effect on the mitochondrial membrane potential and bioenergetics is moderate suggesting a mild uncoupling of OXPHOS.

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Pain is a sensory experience of a complex physiological nature in which is not only involved the nervous system. Among its many features is the development of chronic pain that is more complicated to treat because of the central somatization processes involved, becoming inefficient treatments used in other forms of pain. Among them is the role of glial cells, whose participation is such that some authors have proposed to chronic pain as a gliopathy.

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An abnormal colonization pattern of the preterm gut may affect immune maturation and exert a long-term influence on the intestinal bacterial composition and host health. However, follow-up studies assessing the evolution of the fecal microbiota of infants that were born preterm are very scarce. In this work, the bacterial compositions of fecal samples, obtained from sixteen 2-year-old infants were evaluated using a phylogenetic microarray; subsequently, the results were compared with those obtained in a previous study from samples of meconium and feces collected from the same infants while they stayed in the neonatal intensive care unit (NICU).

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Cancer is characterized by an uncontrolled cell proliferation rate even under low nutrient availability, which is sustained by a metabolic reprograming now recognized as a hallmark of cancer. Warburg was the first to establish the relationship between cancer and mitochondria; however, he interpreted enhanced aerobic glycolysis as mitochondrial dysfunction. Today it is accepted that many cancer cell types need fully functional mitochondria to maintain their homeostasis.

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Studies focused on the stomach microbiota are relatively scarce, and most of them are focused on the adult population. The aim of this work is to describe the bacterial communities inhabiting the gastric content (GC) of preterm neonates. For that purpose, GC samples were collected weekly from a total of 13 preterm neonates during their first month of life within their hospital stay.

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We present the results of a pilot project of the Spanish Ministry of Health, Social Services and Equality, envisaged to the development of a national integrated data repository of maternal-child care information. Based on health information standards and data quality assessment procedures, the developed repository is aimed to a reliable data reuse for (1) population research and (2) the monitoring of healthcare best practices. Data standardization was provided by means of two main ISO 13606 archetypes (composed of 43 sub-archetypes), the first dedicated to the delivery and birth information and the second about the infant feeding information from delivery up to two years.

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Clinical studies have suggested a survival benefit in ovarian cancer patients with type 2 diabetes mellitus taking metformin, however the mechanism by which diabetic concentrations of metformin could deliver this effect is still poorly understood. Platelets not only represent an important reservoir of growth factors and angiogenic regulators, they are also known to participate in the tumor microenvironment implicated in tumor growth and dissemination. Herein, we investigated if diabetic concentrations of metformin could impinge upon the previously reported observation that platelet induces an increase in the tube forming capacity of endothelial cells (angiogenesis) and upon ovarian cancer cell aggressiveness.

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In the absence of low-level ER-to-mitochondrial Ca(2+) transfer, ATP levels fall, and AMPK-dependent, mTOR-independent autophagy is induced as an essential survival mechanism in many cell types. Here, we demonstrate that tumorigenic cancer cell lines, transformed primary human fibroblasts, and tumors in vivo respond similarly but that autophagy is insufficient for survival, and cancer cells die while their normal counterparts are spared. Cancer cell death is due to compromised bioenergetics that can be rescued with metabolic substrates or nucleotides and caused by necrosis associated with mitotic catastrophe during their proliferation.

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