Reshaping commensal gut microbiota in early life with amoxicillin presents with lower blood pressure
Contributors: Saroj Chakraborty
... Pediatric hypertension is recognized as an emerging global health concern. While new guidelines are developed for facilitating clinical management, the reasons for the prevalence of hypertension in children remain unknown. Genetics and environmental factors do not fully account for the growing incidence of pediatric hypertension. Because stable bacterial flora in early life are linked with health outcomes later in life, we hypothesized that reshaping of gut microbiota in early developmental stages of life affects blood pressure (BP) of pediatric subjects. To test this hypothesis, we administered amoxicillin, the most commonly prescribed pediatric antibiotic, to alter gut microbiota of young, genetically hypertensive rats (study 1) and dams during gestation and lactation to reshape microbiota of offspring (study 2). Reshaping of microbiota, with reductions in Firmicutes/Bacteriodetes ratio observed in Amoxicillin treated young rats and in dams. Amoxicillin treated rats also had lower blood pressure compared to the untreated rats. In the young rats treated with amoxicillin, the lowering effect on blood pressure persisted even after the antibiotics were discontinued. Similarly, the offspring from the dams treated with amoxicillin also showed lower systolic blood pressure compared to the control rats. Remarkably, in all cases, a decrease in BP was associated with lowering of Veillonellaceae, which are succinate-producing bacteria. Elevated plasma succinate is reported in hypertension. Accordingly, serum succinate was measured and found lower in animals treated with amoxicillin. Our results demonstrate a direct correlation between succinate-producing gut microbiota and early development of hypertension, and indicate that reshaping gut microbiota, especially by depleting succinate-producing microbiota early in life may have long-term benefits for hypertension-prone individuals.
Oxidative stress induced by the tetrahydrobenzimidazole TMQ0153 modulates crosstalk between apoptosis, autophagy and necroptosis in chronic myeloid leukemia (Part 3 - Figure 4 (b), Figure 5, 6, 7, Supplementary 1-5)
Contributors: Sungmi Song
... Aims: We demonstrate the capacity of the cytotoxic synthetic tetrahydrobenzimidazole (TMQ) hydroquinone (HQ) derivative TMQ0153 to induce reactive oxygen species (ROS) and mediate differential cell death modalities in chronic myeloid leukemia (CML). Results: Results showed that concentrations of TMQ0153 30 µM lead to ROS-mediated necrostatin-sensitive necroptosis. Moreover, TMQ0153 allowed us to elucidate the interplay of ROS-mediated cell death and cell stress/survival mechanisms as this compound triggers protective autophagy in response to metabolic stress in CML cells. Importantly, the modulation of cell stress prior to TMQ0153-induced cell death enhances the exposure of “find-me”/“eat-me” signals considered as hallmarks of immunogenic cell death (ICD), altogether providing a pro-oxidant therapeutic strategy against CML. Innovation: We suggest here a pro-oxidant anti-CML therapy leading to differential cell death modalities in both imatinib-sensitive and -resistant CML cell types. Moreover, we elucidated the interplay between apoptosis, autophagy and controlled necrosis induced by TMQ0153 leading to disruption of mitochondrial homeostasis. Conclusion: Our findings indicate that TMQ0153-induced ROS act as a rheostat determining the onset of apoptotic- or autophagy-related controlled necrotic cell death in CML.
A new method for analyzing sustainability performance of global supply chains and its application to material resources
Contributors: Livia Cabernard, Stephan Pfister, Stefanie Hellweg
... VERSION 2 Compared to version 1, version 2 runs without matlab. The file “Instructions.pdf” attached below explains how to install and use this application. The file “Explanation_method_examples.pptx” attached below illustrates the principle of the method and how to use the application with several examples. OVERALL DESCRIPTION (same as for version 1): We share here the data compiled to calculate the results presented in the study «A new method for analyzing sustainability performance of global supply chains and its application to material resources». In order to allow for the compilation of all results of interest, we provide an application. This application is based on the multi-regional-input output database EXIOBASE3 (version 3.4) and data to assess the potential environmental impacts of emissions and resource use. While the data for assessing the environmental impacts is provided here, the user must download the Exiobase data from the Exiobase website (due to copyright issues). The provided application allows to assess the cumulated upstream impacts of any sector or region on the globe without double-counting and to track these impacts upstream and downstream the global value chain. The application covers a broad set of environmental and socio-economic indicators and the timespan from 1995 to 2011. The methodology of this application is comprehensively explained in the study: «A new method for analyzing sustainability performance of global supply chains and its application to material resources» (e.g Section 2.1 gives a broad overview of the principle of the method). Link to the study: https://doi.org/10.1016/j.scitotenv.2019.04.434
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Data for: A Chink in the Armor: The Influence of Training on Generalization Learning Impairments After Viewing Traumatic Stimuli
Contributors: Einat Levy-Gigi
... Attached are the following files: 1. SPSS Data file 2. Two power-point presentations that were used to manipulate the neutral and traumatic exposure. 3. A link to an online version of the Cue-Context Reversal Task
Contributors: Ines Diaz-Laviada, Belen Sanchez, Alicia Bort, Pedro Mateos, Nieves Rodríguez-Henche
... Data used to generate figures of the paper “Combination of the natural product capsaicin and docetaxel synergistically kills human prostate cancer cells through the metabolic regulator AMP-activated kinase” Sánchez BG, Bort A, Mateos-Gómez PA, Rodríguez-Henche N, Díaz-Laviada I. Cancer Cell Int. 2019 Mar 8;19:54. doi: 10.1186/s12935-019-0769-2. eCollection 2019. In this study we demonstrate that the spicy ingredient of peepers, capsaicin, sensitizes prostate cancer cell to docetaxel. The metabolic regulator AMPK plays a pivotal role.
Overexpression of AMP-activated kinase sensitizes Sorafenib-resistant Hepatocellular cancer cells and decreases stem cell markers
Contributors: Ines Diaz-Laviada
... Data used to generate figures of the paper by Bort A, Sánchez BG, Mateos-Gómez PA, Vara-Ciruelos D, Rodríguez-Henche N, Díaz-Laviada I. “Targeting AMP-activated kinase impacts hepatocellular cancer stem cells induced by long-term treatment with sorafenib” Mol Oncol. 2019 May;13(5):1311-1331. doi: 10.1002/1878-0261.12488. In this study we demonstrate that the AMP-activated kinase AMPK reverse the Cancer Stem cell features of Hepatocellular CSC.
Regional heterogeneity in gene expression, regulation and coherence in hippocampus and prefrontal cortex across development and in schizophrenia. Collado-Torres et al, Neuron, 2019.
Contributors: Leonardo Collado-Torres, Emily E Burke, Amy Peterson, Joo Heon Shin, Richard E Straub, Nina Rajpurohit, Stephen A Semick, William S Ulrich, BrainSeq Consortium, Amanda J Price
... This dataset contains the Supplementary Figures and Tables for the "Regional heterogeneity in gene expression, regulation and coherence in hippocampus and prefrontal cortex across development and in schizophrenia" article by Collado-Torres et al, Neuron, 2019. Please cite the original article as well as the data itself if appropriate. For clarifications about the figures or data, please contact us by creating an issue at https://github.com/LieberInstitute/brainseq_phase2/issues. Thank you!
The NAD-booster nicotinamide riboside potently stimulates hematopoiesis through increased mitochondrial clearance
Contributors: Olaia Naveiras
... It has been recently shown that increased oxidative phosphorylation, as reflected by increased mitochondrial activity, together with impairment of the mitochondrial stress response can severely compromise hematopoietic stem cell (HSC) regeneration. Here we show that the NAD+-boosting agent Nicotinamide Riboside (NR) reduces mitochondrial activity within HSCs through increased mitochondrial clearance, leading to increased asymmetric HSC divisions. NR dietary supplementation results in a significantly enlarged pool of progenitors, without concurrent HSC exhaustion, improves survival by 80%, and accelerates blood recovery after murine lethal irradiation and limiting-HSC transplantation. In immune-deficient mice, NR increased the production of human leucocytes from hCD34+ progenitors. Our work demonstrates for the first time a positive effect of NAD+ boosting strategies on the most primitive blood stem cells, establishes a novel link between HSC mitochondrial stress, mitophagy and stem cell fate decision, and unveils the potential of NR to improve recovery of patients suffering from hematological failure including post-chemo/radiotherapy.
Contributors: Claudio De Virgilio, Riko Hatakeyama, Marie-Pierre Peli-Gulli, Zehan Hu, Malika Jaquenoud, Guillermo Miguel Garcia Osuna, Alessandro Sardu, Jörn Dengjel
... Online on December 6th, 2018 in : Molecular Cell Print: Molecular Cell 73, 1–14, January 17, 2019 This is the original data set that contains all of the unprocessed microscopy images, gels, and blots used in this manuscript.
Raw, not cropped supporting Western blot files for: Mavrommati, I., ... Pagano, M., D'Angiolella, V.: β-TrCP- and Casein Kinase II-Mediated Degradation of Cyclin F Controls Timely Mitotic Progression. Cell Rep. (2018)
Contributors: Michele Pagano
... Raw, not cropped supporting Western blot files for: Mavrommati I, Faedda R, Galasso G, Li J, Burdova K, Fischer R, Kessler BM, Carrero ZI, Guardavaccaro D, Pagano M, D'Angiolella V. β-TrCP- and Casein Kinase II-Mediated Degradation of Cyclin F Controls Timely Mitotic Progression. Cell Rep. 2018 Sep 25;24(13):3404-3412. doi: 10.1016/j.celrep.2018.08.076. PMID: 30257202 PMCID: PMC6172692 DOI: 10.1016/j.celrep.2018.08.076