David Mcdonagh Anesthesiology and Pain Management Correlating Angiographic Vessel Caliber with Transcranial Doppler Flow V
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Role of Estrogen Receptor Beta and the Isoflavone Genistein
WCP2018 OR28-3 Oral session White-to-brown adipose differentiation: role of estrogen receptor beta and the isoflavone genistein Alessandra Bitto, Federica Mannino, Natasha Irrera, Giovanni Pallio, Domenica Altavilla, Francesco Squadrito Clinical and experimental medicine, University of Messina, Italy The two types of fat cells in mammals brown and white have different functions. White adipose tissue (WAT) stores excess energy in the form of triglyceride and releases free fatty acids during caloric deficiency. Brown adipose tissue (BAT) on the other hand can dissipate energy through thermogenesis. Genistein can have an effect on energy expenditure UCP (uncoupling protein) expression and protect against the obesogenic effect of a high calorie diet. The effect of genistein in inducing white-to-brown transdifferentiation was investigated in 3T3-L1 cells differentiated into white adipocytes with a specific medium (DMEM 10% calf serum 1% penicillin/streptomycin 500 uM 3isobutyl1 methylxanthine 10ug/ml insulin 250 nM dexmethasone 8 ug/ml biotin and 4 ug/ml pantothenic acid). Fully differentiated white adipocytes were treated after 10 days with different genistein doses (10-50-100-200 uM) for 24-48h or left untreated. Two specific ER-beta and PPAR-gamma receptor inhibitors were also used to understand if genistein effects are mediated by the estrogen or the PPAR receptor. Also a CRISPR/Cas9 approach was used to delete either ER-beta or PPAR-gamma to clarify which receptor is involved in genistein action. Intracellular lipid accumulation was determined by oil-red-O staining after 24 and 48hours of treatment. The expression of UCP1 estrogen receptor alpha and beta PPARalpha and gamma DIO2 (Type II iodothyronine deiodinase) PRDM16 (PR domain containing 16) and CIDEA (cell death inducing DNA fragmentation factor) were evaluated by qPCR after 24 and 48hours of genistein treatment. -
Reelin Is Preferentially Expressed in Neurons Synthesizing ␥-Aminobutyric Acid in Cortex and Hippocampus of Adult Rats
Proc. Natl. Acad. Sci. USA Vol. 95, pp. 3221–3226, March 1998 Neurobiology Reelin is preferentially expressed in neurons synthesizing g-aminobutyric acid in cortex and hippocampus of adult rats C. PESOLD*†,F.IMPAGNATIELLO*, M. G. PISU*, D. P. UZUNOV*, E. COSTA*, A. GUIDOTTI*, AND H. J. CARUNCHO*‡ *Psychiatric Institute, Department of Psychiatry, College of Medicine, University of Illinois at Chicago, Chicago, IL 60612; and ‡Department of Morphological Sciences, University of Santiango de Compostela School of Medicine, 15705 Santiago de Compostela, Spain Contributed by Erminio Costa, December 24,1997 ABSTRACT During embryonic development of brain lam- sion, prevent Reelin transcription or secretion (4, 12, 14). In inated structures, the protein Reelin, secreted into the extracel- the cortex and hippocampus of rat embryos, Reelin begins to lular matrix of the cortex and hippocampus by Cajal–Retzius be synthesized in Cajal–Retzius (CR) cells from embryonic day (CR) cells located in the marginal zone, contributes to the 13 to the second postnatal week, and in the cerebellum Reelin regulation of migration and positioning of cortical and hip- is expressed first in the external granule cell layer (EGL) pocampal neurons that do not synthesize Reelin. Soon after before the granule cell migration to the internal granule cell birth, the CR cells decrease, and they virtually disappear during layer (IGL) (2, 15–17). When the CR50 antibody is added to the following 3 weeks. Despite their disappearance, we can embryonic preparations expressing normal histogenetic pat- quantify Reelin mRNA (approximately 200 amolymg of total terns of lamination, it induces typical histogenetic abnormal- RNA) and visualize it by in situ hybridization, and we detect the ities of the Relnrl phenotype (7, 9, 10, 17). -
Reelin Supplementation Into the Hippocampus Rescues Abnormal Behavior in a Mouse Model of Neurodevelopmental Disorders
fncel-14-00285 August 31, 2020 Time: 14:32 # 1 ORIGINAL RESEARCH published: 02 September 2020 doi: 10.3389/fncel.2020.00285 Reelin Supplementation Into the Hippocampus Rescues Abnormal Behavior in a Mouse Model of Neurodevelopmental Disorders Daisuke Ibi1*†, Genki Nakasai1†, Nayu Koide1†, Masahito Sawahata2, Takao Kohno3, Rika Takaba1, Taku Nagai2,4, Mitsuharu Hattori3, Toshitaka Nabeshima5, Kiyofumi Yamada2* and Masayuki Hiramatsu1 1 Department of Chemical Pharmacology, Faculty of Pharmacy, Meijo University, Nagoya, Japan, 2 Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya, Japan, 3 Department of Biomedical Science, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan, 4 Project Office for Neuropsychological Research Center, Fujita Health University, Toyoake, Japan, 5 Advanced Diagnostic System Research Laboratory, Fujita Health University, Graduate School of Health Sciences, Toyoake, Japan Edited by: Marie-Eve Tremblay, In the majority of schizophrenia patients, chronic atypical antipsychotic administration University of Victoria, Canada produces a significant reduction in or even complete remission of psychotic symptoms Reviewed by: such as hallucinations and delusions. However, these drugs are not effective in Dilja Krueger-Burg, improving cognitive and emotional deficits in patients with schizophrenia. Atypical University Medical Center Göttingen, Germany antipsychotic drugs have a high affinity for the dopamine D2 receptor, and a José M. Delgado-García, -
Letters to the Editor
LETTERS TO THE EDITOR The closely related rare and severe acute myeloid leukemias carrying EVI1 or PRDM16 rearrangements share singular biological features In a recent issue of Haematologica , Matsuo et al .1 pinpoint the pejorative effect of EVI1 overexpression in 18 acute myeloid leukemias (AML) with MLL rearrangements. However, EVI1 overexpression has also been reported in patients with translocations involving chromosome 3 and the EVI1 gene. 2,3 Because of the poor prognosis associated to these anomalies, it is important to investigate them at an early stage in order to adapt patient management. Indeed, previous reports 4-6 and the 2008 WHO classification 7 indi - cate that EVI1-rearranged (EVI1-r) AML display typical fea - tures, such as absence of thrombopenia, atypical megakary - Figure 1. Algorithm for the suspicion of EVI1 and PRDM16 AMLs. ocytes and multilineage dysplasia 2-4 which can be detected by current diagnostic reference methods. In this line, we compared a cohort of 17 EVI1-r AML, aged between 8 and 79-years old (median 54 years) to 1822 other cases of AML months. diagnosed in the same laboratory over 14 years. At diagno - This study consolidates the unusual base-line character - sis, there were similar hemoglobin levels or white blood istics and clinical features of EVI1-r AML cases. Moreover, cell counts in both groups. Median platelet counts were it indicates a very low rate of MPO expression in EVI1-r 9 9 123x10 /L, higher than 100x10 /L in 53% of EVI1-r AML AML patients. It is interesting to note that relationships patients, compared to 25% in the control AML population have been reported between EVI1 expression and MPO (P=0.02). -
Clinical Study High Complement Factor I Activity in the Plasma of Children with Autism Spectrum Disorders
Hindawi Publishing Corporation Autism Research and Treatment Volume 2012, Article ID 868576, 6 pages doi:10.1155/2012/868576 Clinical Study High Complement Factor I Activity in the Plasma of Children with Autism Spectrum Disorders Naghi Momeni,1 Lars Brudin,2 Fatemeh Behnia,3 Berit Nordstrom,¨ 4 Ali Yosefi-Oudarji,5 Bengt Sivberg,4 Mohammad T. Joghataei,5 and Bengt L. Persson1 1 School of Natural Sciences, Linnaeus University, 39182 Kalmar, Sweden 2 Department of Clinical Physiology, Kalmar County Hospital, 39185 Kalmar, Sweden 3 Department of Occupational Therapy, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran 4 Department of Health Sciences, Autism Research, Faculty of Medicine, Lund University, Box 157, 22100 Lund, Sweden 5 Cellular and Molecular Research Centre, Tehran University of Medical Sciences (TUMS), Tehran, Iran Correspondence should be addressed to Bengt Sivberg, [email protected] Received 17 June 2011; Revised 22 August 2011; Accepted 22 August 2011 Academic Editor: Judy Van de Water Copyright © 2012 Naghi Momeni et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Autism spectrum disorders (ASDs) are neurodevelopmental and behavioural syndromes affecting social orientation, behaviour, and communication that can be classified as developmental disorders. ASD is also associated with immune system abnormality. Im- mune system abnormalities may be caused partly by complement system factor I deficiency. Complement factor I is a serine pro- tease present in human plasma that is involved in the degradation of complement protein C3b, which is a major opsonin of the complement system. -
Supplementary Table 1. Pain and PTSS Associated Genes (N = 604
Supplementary Table 1. Pain and PTSS associated genes (n = 604) compiled from three established pain gene databases (PainNetworks,[61] Algynomics,[52] and PainGenes[42]) and one PTSS gene database (PTSDgene[88]). These genes were used in in silico analyses aimed at identifying miRNA that are predicted to preferentially target this list genes vs. a random set of genes (of the same length). ABCC4 ACE2 ACHE ACPP ACSL1 ADAM11 ADAMTS5 ADCY5 ADCYAP1 ADCYAP1R1 ADM ADORA2A ADORA2B ADRA1A ADRA1B ADRA1D ADRA2A ADRA2C ADRB1 ADRB2 ADRB3 ADRBK1 ADRBK2 AGTR2 ALOX12 ANO1 ANO3 APOE APP AQP1 AQP4 ARL5B ARRB1 ARRB2 ASIC1 ASIC2 ATF1 ATF3 ATF6B ATP1A1 ATP1B3 ATP2B1 ATP6V1A ATP6V1B2 ATP6V1G2 AVPR1A AVPR2 BACE1 BAMBI BDKRB2 BDNF BHLHE22 BTG2 CA8 CACNA1A CACNA1B CACNA1C CACNA1E CACNA1G CACNA1H CACNA2D1 CACNA2D2 CACNA2D3 CACNB3 CACNG2 CALB1 CALCRL CALM2 CAMK2A CAMK2B CAMK4 CAT CCK CCKAR CCKBR CCL2 CCL3 CCL4 CCR1 CCR7 CD274 CD38 CD4 CD40 CDH11 CDK5 CDK5R1 CDKN1A CHRM1 CHRM2 CHRM3 CHRM5 CHRNA5 CHRNA7 CHRNB2 CHRNB4 CHUK CLCN6 CLOCK CNGA3 CNR1 COL11A2 COL9A1 COMT COQ10A CPN1 CPS1 CREB1 CRH CRHBP CRHR1 CRHR2 CRIP2 CRYAA CSF2 CSF2RB CSK CSMD1 CSNK1A1 CSNK1E CTSB CTSS CX3CL1 CXCL5 CXCR3 CXCR4 CYBB CYP19A1 CYP2D6 CYP3A4 DAB1 DAO DBH DBI DICER1 DISC1 DLG2 DLG4 DPCR1 DPP4 DRD1 DRD2 DRD3 DRD4 DRGX DTNBP1 DUSP6 ECE2 EDN1 EDNRA EDNRB EFNB1 EFNB2 EGF EGFR EGR1 EGR3 ENPP2 EPB41L2 EPHB1 EPHB2 EPHB3 EPHB4 EPHB6 EPHX2 ERBB2 ERBB4 EREG ESR1 ESR2 ETV1 EZR F2R F2RL1 F2RL2 FAAH FAM19A4 FGF2 FKBP5 FLOT1 FMR1 FOS FOSB FOSL2 FOXN1 FRMPD4 FSTL1 FYN GABARAPL1 GABBR1 GABBR2 GABRA2 GABRA4 -
ETV6 Mutations in Early Immature Human T Cell Leukemias
Published December 12, 2011 Brief Definitive Report ETV6 mutations in early immature human T cell leukemias Pieter Van Vlierberghe,1 Alberto Ambesi-Impiombato,1 Arianne Perez-Garcia,1 J. Erika Haydu,1 Isaura Rigo,1 Michael Hadler,1 Valeria Tosello,1 Giusy Della Gatta,1 Elisabeth Paietta,4 Janis Racevskis,4 Peter H. Wiernik,4 Selina M. Luger,5 Jacob M. Rowe,6 Montserrat Rue,7 and Adolfo A. Ferrando1,2,3 1Institute for Cancer Genetics, 2Department of Pediatrics, and 3Department of Pathology, Columbia University Medical Center, New York, NY 10032 4Montefiore Medical Center North, Bronx, New York, NY 10467 5Hematologic Malignancies and Stem Cell Transplant Program, Hematology-Oncology Division, University of Pennsylvania Medical Center, Philadelphia, PA 19104 6 Rambam Medical Center, Haifa 31096, Israel Downloaded from 7Department of Basic Medical Sciences, University of Lleida, Lleida 25003, Spain Early immature T cell acute lymphoblastic leukemias (T-ALLs) account for 5–10% of pediatric T-ALLs and are associated with poor prognosis. However, the genetic defects that drive the biology of these tumors remain largely unknown. In this study, analysis of micro- array gene expression signatures in adult T-ALL demonstrated a high prevalence of early immature leukemias and revealed a close relationship between these tumors and myeloid jem.rupress.org leukemias. Many adult immature T-ALLs harbored mutations in myeloid-specific oncogenes and tumor suppressors including IDH1, IDH2, DNMT3A, FLT3, and NRAS. Moreover, we identifiedETV6 mutations as a novel genetic lesion uniquely present in immature adult T-ALL. Our results demonstrate that early immature adult T-ALL represents a heterogeneous category of leukemias characterized by the presence of overlapping myeloid and T-ALL on May 30, 2015 characteristics, and highlight the potential role of ETV6 mutations in these tumors. -
The Suppressive Effects of 1,25-Dihydroxyvitamin D3 and Vitamin D Receptor on Brown Adipocyte Differentiation and Mitochondrial Respiration
University of Tennessee, Knoxville TRACE: Tennessee Research and Creative Exchange Masters Theses Graduate School 8-2014 The Suppressive Effects of 1,25-dihydroxyvitamin D3 and Vitamin D Receptor on Brown Adipocyte Differentiation and Mitochondrial Respiration Carolyn Jeanne Ricciardi University of Tennessee - Knoxville, [email protected] Follow this and additional works at: https://trace.tennessee.edu/utk_gradthes Part of the Molecular, Genetic, and Biochemical Nutrition Commons Recommended Citation Ricciardi, Carolyn Jeanne, "The Suppressive Effects of 1,25-dihydroxyvitamin D3 and Vitamin D Receptor on Brown Adipocyte Differentiation and Mitochondrial Respiration. " Master's Thesis, University of Tennessee, 2014. https://trace.tennessee.edu/utk_gradthes/2876 This Thesis is brought to you for free and open access by the Graduate School at TRACE: Tennessee Research and Creative Exchange. It has been accepted for inclusion in Masters Theses by an authorized administrator of TRACE: Tennessee Research and Creative Exchange. For more information, please contact [email protected]. To the Graduate Council: I am submitting herewith a thesis written by Carolyn Jeanne Ricciardi entitled "The Suppressive Effects of 1,25-dihydroxyvitamin D3 and Vitamin D Receptor on Brown Adipocyte Differentiation and Mitochondrial Respiration." I have examined the final electronic copy of this thesis for form and content and recommend that it be accepted in partial fulfillment of the equirr ements for the degree of Master of Science, with a major in Nutrition. -
Timing of Novel Drug 1A-116 to Circadian Rhythms Improves Therapeutic Effects Against Glioblastoma
pharmaceutics Article Timing of Novel Drug 1A-116 to Circadian Rhythms Improves Therapeutic Effects against Glioblastoma Laura Lucía Trebucq 1, Georgina Alexandra Cardama 2, Pablo Lorenzano Menna 2, Diego Andrés Golombek 1 , Juan José Chiesa 1,*,† and Luciano Marpegan 3,*,† 1 Laboratorio de Cronobiología, Universidad Nacional de Quilmes-CONICET, Bernal 1876, Buenos Aires, Argentina; [email protected] (L.L.T.); [email protected] (D.A.G.) 2 Laboratorio de Oncología Molecular, Universidad Nacional de Quilmes-CONICET, Bernal 1876, Buenos Aires, Argentina; [email protected] (G.A.C.); [email protected] (P.L.M.) 3 Departamento de Física Médica, Comisión Nacional de Energía Atómica, Bariloche 8400, Río Negro, Argentina * Correspondence: [email protected] (J.J.C.); [email protected] (L.M.) † These authors contributed equally to this work. Abstract: The Ras homologous family of small guanosine triphosphate-binding enzymes (GTPases) is critical for cell migration and proliferation. The novel drug 1A-116 blocks the interaction site of the Ras-related C3 botulinum toxin substrate 1 (RAC1) GTPase with some of its guanine exchange factors (GEFs), such as T-cell lymphoma invasion and metastasis 1 (TIAM1), inhibiting cell motility and proliferation. Knowledge of circadian regulation of targets can improve chemotherapy in glioblastoma. Thus, circadian regulation in the efficacy of 1A-116 was studied in LN229 human Citation: Trebucq, L.L.; glioblastoma cells and tumor-bearing nude mice. Methods. Wild-type LN229 and BMAL1-deficient Cardama, G.A.; Lorenzano Menna, P.; (i.e., lacking a functional circadian clock) LN229E1 cells were assessed for rhythms in TIAM1, BMAL1, Golombek, D.A.; Chiesa, J.J.; and period circadian protein homolog 1 (PER1), as well as Tiam1, Bmal1, and Rac1 mRNA levels. -
Single Cell Regulatory Landscape of the Mouse Kidney Highlights Cellular Differentiation Programs and Disease Targets
ARTICLE https://doi.org/10.1038/s41467-021-22266-1 OPEN Single cell regulatory landscape of the mouse kidney highlights cellular differentiation programs and disease targets Zhen Miao 1,2,3,8, Michael S. Balzer 1,2,8, Ziyuan Ma 1,2,8, Hongbo Liu1,2, Junnan Wu 1,2, Rojesh Shrestha 1,2, Tamas Aranyi1,2, Amy Kwan4, Ayano Kondo 4, Marco Pontoglio 5, Junhyong Kim6, ✉ Mingyao Li 7, Klaus H. Kaestner2,4 & Katalin Susztak 1,2,4 1234567890():,; Determining the epigenetic program that generates unique cell types in the kidney is critical for understanding cell-type heterogeneity during tissue homeostasis and injury response. Here, we profile open chromatin and gene expression in developing and adult mouse kidneys at single cell resolution. We show critical reliance of gene expression on distal regulatory elements (enhancers). We reveal key cell type-specific transcription factors and major gene- regulatory circuits for kidney cells. Dynamic chromatin and expression changes during nephron progenitor differentiation demonstrates that podocyte commitment occurs early and is associated with sustained Foxl1 expression. Renal tubule cells follow a more complex differentiation, where Hfn4a is associated with proximal and Tfap2b with distal fate. Mapping single nucleotide variants associated with human kidney disease implicates critical cell types, developmental stages, genes, and regulatory mechanisms. The single cell multi-omics atlas reveals key chromatin remodeling events and gene expression dynamics associated with kidney development. 1 Renal, Electrolyte, and Hypertension Division, Department of Medicine, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, USA. 2 Institute for Diabetes, Obesity, and Metabolism, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA, USA. -
Thymic Epithelial Cell Support of Thymopoiesis Does Not Require Klotho Yan Xing, Michelle J
Thymic Epithelial Cell Support of Thymopoiesis Does Not Require Klotho Yan Xing, Michelle J. Smith, Christine A. Goetz, Ron T. McElmurry, Sarah L. Parker, Dullei Min, Georg A. This information is current as Hollander, Kenneth I. Weinberg, Jakub Tolar, Heather E. of September 28, 2021. Stefanski and Bruce R. Blazar J Immunol published online 29 October 2018 http://www.jimmunol.org/content/early/2018/10/28/jimmun ol.1800670 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 28, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2018 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published October 29, 2018, doi:10.4049/jimmunol.1800670 The Journal of Immunology Thymic Epithelial Cell Support of Thymopoiesis Does Not Require Klotho Yan Xing,*,1 Michelle J. Smith,*,†,1 Christine A. Goetz,*,† Ron T. McElmurry,* Sarah L. Parker,* Dullei Min,‡ Georg A. Hollander,x,{ Kenneth I. Weinberg,‡ Jakub Tolar,* Heather E. Stefanski,*,2 and Bruce R. -
(Foxn1-/-) Mice Affects the Skin Wound Healing Process Sylwia Ma
bioRxiv preprint doi: https://doi.org/10.1101/2020.08.04.237388; this version posted August 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. Impairment of the Hif-1α regulatory pathway in Foxn1-deficient (Foxn1-/-) mice affects the skin wound healing process Sylwia Machcinska, Marta Kopcewicz, Joanna Bukowska, Katarzyna Walendzik and Barbara Gawronska-Kozak* Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland * Correspondence: Barbara Gawronska-Kozak Institute of Animal Reproduction and Food Research, Polish Academy of Sciences, Olsztyn, Poland; Tuwima 10; 10-748, Olsztyn, Poland; Tel: (4889) 5234634; Fax: (4889) 5240124. E-mail: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.08.04.237388; this version posted August 11, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. ABSTRACT Hypoxia and hypoxia-regulated factors [e. g., hypoxia-inducible factor-1α (Hif-1α), factor inhibiting Hif-1α (Fih-1), thioredoxin-1 (Trx-1), aryl hydrocarbon receptor nuclear translocator 2 (Arnt-2)] have essential roles in skin wound healing. Using Foxn1-/- mice that can heal skin injuries in a unique scarless manner, we investigated the interaction between Foxn1 and hypoxia-regulated factors. The Foxn1-/- mice displayed impairments in the regulation of Hif-1α, Trx-1 and Fih-1 but not Arnt-2 during the healing process. An analysis of wounded skin showed that the skin of the Foxn1-/- mice healed in a scarless manner, displaying rapid re-epithelialization and an increase in transforming growth factor β (Tgfβ-3) and collagen III expression.