Cytosporin-related compounds from the marine-derived fungus Eutypella scoparia

[EN] Chemical investigation of the culture broth of the fungus Eutypella scoparia ICB-OBX, isolated from the marine pulmonate mollusc Onchidium sp., led to the finding of novel compounds 1 and 2, structurally related to angiotensin II binding inhibitors cytosporins, along with unrelated known nitrogen metabolites (compounds 3¿5). The structure and the relative stereochemistry of the novel metabolites were assigned mainly by a detailed analysis of two-dimensional NMR techniques whereas the absolute stereochemistry was proposed by modified Mosher's method. Compound 2 contains an unusual cyclic carbonate functionality that is rare among natural products.Ciavatta, ML.; López-Gresa, MP.; Gavagnin, M.; Nicoletti, R.; Manzo, E.; Mollo, E.; Guo, Y.... (2008). Cytosporin-related compounds from the marine-derived fungus Eutypella scoparia. Tetrahedron. 64(22):5365-5369. https://doi.org/10.1016/j.tet.2008.03.016S53655369642

Impact of the adherence to medical treatment on the main urinary metabolic disorders in patients with kidney stones

To assess the effect of the adherence to medical treatment on urinary parameters in the 24-h metabolic study of patients with kidney stones. A retrospective, longitudinal, descriptive, and observational study was carried out by reviewing the hospital electronic medical record from 2014 to 2018. The adherence to drug treatment was measured 6 months after its initiation, and the numerical values of the metabolic studies were compared. Wilcoxon tests were performed to compare the difference before and after treatment. Ninety patients were evaluated, with 73.3% of adherence. The 180-day overall adherence rate was 61.2% in patients treated with a single drug and 85.4% in patients treated with multiple drugs. There is a statistically significant increase in citrate levels in patients with good adherence in comparison with non-adherent patients (p =0.031 vs. p =0.528). Medical treatment and dietary measures in patients with kidney stones have an initial impact at 6 months on the values of the main urinary metabolic alterations that predispose to calculi formation; the most significant is seen in those patients with adherence to medical treatment for hypocitraturia

Kiwi : manejo del suelo, riego y fertilización

Esta publicación, producto del accionar de la Estación Experimental Agropecuaria Balcarce de INTA, junto con la Cámara de Productores de Kiwi de Mar del Plata, el Proyecto Regional con Enfoque Territorial del Sudeste Bonaerense y el Grupo de Cambio Rural (Ministerio de Agroindustria de Ia Nación - INTA), busca integrar los conocimientos generados por el Proyecto Específico “Superación de Brechas Tecnológicas que Limitan la Calidad en las Cadenas Frutícolas” del Programa Nacional de Frutales, en lo referente al manejo del suelo, riego y fertilización, prácticas que influyen en la productividad del kiwi, la calidad de su fruto a cosecha y su conservación poscosecha. Asimismo, se informa como fue la evolución de los sistemas de riego y los factores que llevaron a su elección.EEA BalcarceFil: Yommi, Alejandra Karina. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Balcarce; ArgentinaFil: Sanchez, Enrique Eduardo. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Balcarce; ArgentinaFil: Manzo, Enrique: Asesor Privado; ArgentinaFil: Benés, Gisela. Consultora Privada; ArgentinaFil: Murray, Ricardo Ernesto. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Oliveros; ArgentinaFil: Rosenstein, Susana. Universidad Nacional de Rosario. Facultad de Ciencias Agrarias; ArgentinaFil: Viteri, Maria Laura. Instituto Nacional de Tecnología Agropecuaria (INTA). Estación Experimental Agropecuaria Balcarce; Argentin

Glycolysis Upregulation Is Neuroprotective As A Compensatory Mechanism In Als

Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodegenerative disorder, with TDP-43 inclusions as a major pathological hallmark. Using a Drosophila model of TDP-43 proteinopathy we found significant alterations in glucose metabolism including increased pyruvate, suggesting that modulating glycolysis may be neuroprotective. Indeed, a high sugar diet improves locomotor and lifespan defects caused by TDP-43 proteinopathy in motor neurons or glia, but not muscle, suggesting that metabolic dysregulation occurs in the nervous system. Overexpressing human glucose transporter GLUT-3 in motor neurons mitigates TDP-43 dependent defects in synaptic vesicle recycling and improves locomotion. Furthermore, PFK mRNA, a key indicator of glycolysis, is upregulated in flies and patient derived iPSC motor neurons with TDP-43 pathology. Surprisingly, PFK overexpression rescues TDP-43 induced locomotor deficits. These findings from multiple ALS models show that mechanistically, glycolysis is upregulated in degenerating motor neurons as a compensatory mechanism and suggest that increased glucose availability is protective

New caulerpenyne-derived metabolites of an Elysia sacoglossan from the south indian coast

[EN] Chemical analysis of the secondary metabolite pattern of the sacoglossan mollusc Elysia cf. expansa, collected along South Indian coasts, showed the presence of the typical Caulerpa-derived sesquiterpene caulerpenyne (1) and two new minor co-occurring metabolites, the compounds dihydrocaulerpenyne (4) and expansinol (5). The chemical characterization of these molecules, structurally related to 1, is reported.We thank ICB Mass Service and ICB NMR Service Centre (Mrs. D. Melck is kindly acknowledged), Mr. C. Iodice for spectrophotometric measurements and Mr. R. Turco for graphical work. This work was partially supported by a bilateral CNR-CSIR project.Ciavatta, ML.; López-Gresa, MP.; Gavagnin, M.; Manzo, E.; Mollo, E.; D Souza, L.; Cimino, G. (2006). New caulerpenyne-derived metabolites of an Elysia sacoglossan from the south indian coast. Molecules. 11(10):808-816. doi:10.3390/11100808S808816111

Glycolysis upregulation is neuroprotective as a compensatory mechanism in ALS

Amyotrophic Lateral Sclerosis (ALS), is a fatal neurodegenerative disorder, with TDP-43 inclusions as a major pathological hallmark. Using a Drosophila model of TDP-43 proteinopathy we found significant alterations in glucose metabolism including increased pyruvate, suggesting that modulating glycolysis may be neuroprotective. Indeed, a high sugar diet improves locomotor and lifespan defects caused by TDP-43 proteinopathy in motor neurons or glia, but not muscle, suggesting that metabolic dysregulation occurs in the nervous system. Overexpressing human glucose transporter GLUT-3 in motor neurons mitigates TDP-43 dependent defects in synaptic vesicle recycling and improves locomotion. Furthermore, PFK mRNA, a key indicator of glycolysis, is upregulated in flies and patient derived iPSC motor neurons with TDP-43 pathology. Surprisingly, PFK overexpression rescues TDP-43 induced locomotor deficits. These findings from multiple ALS models show that mechanistically, glycolysis is upregulated in degenerating motor neurons as a compensatory mechanism and suggest that increased glucose availability is protective.National Institutes of Health [T32GM008659, NS091299]; Howard Hughes Medical Institute; University of Arizona; Arnold and Mabel Beckman Foundation; Association pour la Recherche sur la Sclerose Laterale Amyotrophique et autres Maladies du Motoneurone; Target ALS; Barrow Neurological Foundation; Muscular Dystrophy Association [418515]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

Ciencias de la Biología y Agronomía

Este volumen I contiene 17 capítulos arbitrados que se ocupan de estos asuntos en Tópicos Selectos de Ciencias de la Biología y Agronomía, elegidos de entre las contribuciones, reunimos algunos investigadores y estudiantes. Se presenta un Estudio Comparativo de los Recursos Hidrológico-Forestales de la Microcuenca de la Laguna de Epatlan, Pue. (1993 a 2014); la Situación Actual de la Mancha de Asfalto en Maíz (Zea mays L.) en los Municipios de Jiquipilas y Ocozocoautla, Chiapas, México; las poblaciones sobresalientes de maíz de la raza Zapalote Chico, en la Región Istmeña de Oaxaca; Se indica el índice de área foliar de cultivo de Chile Poblano mediante dos métodos en condiciones protegidas; Esquivel, Urzúa y Ramírez exploran el efecto de la biofertilización con Azospirillum en el crecimiento y producción de Jitomate; esbozan su artículo sobre la determinación del nivel de Heterosis en híbridos de Maíz para la Comarca Lagunera; una investigación sobre la estabilización de semilla de Solanum lycopersicum durante el almacenamiento y estimulación de la germinación; acotan sobre el CTAB como una nueva opción para la detección de Huanglongbing en cítricos, plantean su evaluación sobre el aluminio y cómo afecta la vida de florero de Heliconia psittacorum; indican sobre el impacto del H-564C, como un híbrido de maíz con alta calidad de proteina para el trópico húmedo de México; presetan su investigación sobre la producción de Piña Cayena Lisa y MD2 (Ananas comosus L.) en condiciones de Loma Bonita, en Oaxaca; acotan sobre el efecto de coberteras como control biológico por conservación contra áfidos en Nogal Pecanero; esbozan sobre la caracterización de cuatro genotipos de Frijol Negro en Martínez de la Torre, Veracruz, México; presentan una caracterización hidroecológica de la microcuenca de Arroyo Prieto, Yuriría, Gto., y alternativas para su restauración ambiental; presentan su investigación sobre el efecto del hongo Beauveria bassiana sobre solubilización de fosfatos y la disponibilidad de fósforo en el suelo; plantean su investigación sobre la Germinación y regeneración in vitro de Epidendrum falcatum LINDL; esbozan su artículo sobre genotipos de frijol negro y su tolerancia a sequía terminal en Veracruz, México

Metabolic Alterations and Targeted Therapies in a Drosophila Model of ALS

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease characterized by the loss of upper and lower motor neurons. Despite one hundred and fifty years since the first characterization of the disease, an effective treatment for patients has remained elusive. ALS patients often present with systemic metabolic defects that correlate with disease progression. Exactly how metabolic alterations contribute to disease pathogenesis is poorly understood. Our laboratory has developed a Drosophila model of ALS based on the genetic overexpression of TAR DNA binding protein 43 (TDP-43), a protein that is found in pathological aggregates in over 97% of all ALS patients. Using this model, we find metabolic alterations in long chain fatty acids and glycolysis end-products - suggesting altered mitochondrial function and altered glucose metabolism. Dietary supplementation with either medium chained fatty acids, ketone precursors, or glucose improves the locomotor function of TDP-43 expressing flies. Indeed, increased glucose availability through genetic expression of human glucose transporter 3 in motor neurons improves TDP-43 induced locomotor defects, improves synaptic vesicle function, and increases the number of boutons at the neuromuscular junction. Moreover, Pfk mRNA, an indicator of glycolytic flux, is upregulated in flies, patient derived motor neurons differentiated from induced pluripotent stem cells and ALS spinal cords. Interestingly, Pfk overexpression rescues TDP-43 induced locomotor defects – suggesting that increasing the rate of glycolysis in motor neurons is neuroprotective. Together, these findings show that there are clear metabolic alterations in the central nervous system of a Drosophila model of ALS that can be mitigated by either increasing the availability of medium-chained fatty acids, or increasing the rate of glycolysis

Medium-Chain Fatty Acids, Beta-Hydroxybutyric Acid and Genetic Modulation of the Carnitine Shuttle Are Protective in a Drosophila Model of ALS Based on TDP-43

ALS patients exhibit dyslipidemia, hypermetabolism and weight loss; in addition, cellular energetics deficits have been detected prior to denervation. Although evidence that metabolism is altered in ALS is compelling, the mechanisms underlying metabolic dysregulation and the contribution of altered metabolic pathways to disease remain poorly understood. Here we use a Drosophila model of ALS based on TDP-43 that recapitulates hallmark features of the disease including locomotor dysfunction and reduced lifespan. We performed a global, unbiased metabolomic profiling of larvae expressing TDP-43 (wild-type, TDPWT or disease -associated mutant, TDPG298S) and identified several lipid metabolism associated alterations. Among these, we found a significant increase in carnitine conjugated long-chain fatty acids and a significant decrease in carnitine, acetyl carnitine and beta-hydroxybutyrate, a ketone precursor. Taken together these data suggest a deficit in the function of the carnitine shuttle and reduced lipid beta oxidation. To test this possibility we used a combined genetic and dietary approach in Drosophila. Our findings indicate that components of the carnitine shuttle are misexpressed in the context of TDP-43 proteinopathy and that genetic modulation of CPT1 or CPT2 expression, two core components of the carnitine shuttle, mitigates TDP-43 dependent locomotor dysfunction, in a variant dependent manner. In addition, feeding medium-chain fatty acids or beta-hydroxybutyrate improves locomotor function, consistent with the notion that bypassing the carnitine shuttle deficit is neuroprotective. Taken together, our findings highlight the potential contribution of the carnitine shuttle and lipid beta oxidation in ALS and suggest strategies for therapeutic intervention based on restoring lipid metabolism in motor neurons.NIH [T32GM008659, NS091299, MDA 418515]; HHMI Gilliam Fellowship for Advanced Studies; Undergraduate Biology Research Program; Beckman Foundation scholarshipOpen access journal.This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]