The Utility of Genetic Risk Scores in Predicting the Onset of Stroke March 2021 6
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Research Brief March 2017 Publication #2017-16
Research Brief March 2017 Publication #2017-16 Flourishing From the Start: What Is It and How Can It Be Measured? Kristin Anderson Moore, PhD, Child Trends Christina D. Bethell, PhD, The Child and Adolescent Health Measurement Introduction Initiative, Johns Hopkins Bloomberg School of Every parent wants their child to flourish, and every community wants its Public Health children to thrive. It is not sufficient for children to avoid negative outcomes. Rather, from their earliest years, we should foster positive outcomes for David Murphey, PhD, children. Substantial evidence indicates that early investments to foster positive child development can reap large and lasting gains.1 But in order to Child Trends implement and sustain policies and programs that help children flourish, we need to accurately define, measure, and then monitor, “flourishing.”a Miranda Carver Martin, BA, Child Trends By comparing the available child development research literature with the data currently being collected by health researchers and other practitioners, Martha Beltz, BA, we have identified important gaps in our definition of flourishing.2 In formerly of Child Trends particular, the field lacks a set of brief, robust, and culturally sensitive measures of “thriving” constructs critical for young children.3 This is also true for measures of the promotive and protective factors that contribute to thriving. Even when measures do exist, there are serious concerns regarding their validity and utility. We instead recommend these high-priority measures of flourishing -
Murine MPDZ-Linked Hydrocephalus Is Caused by Hyperpermeability of the Choroid Plexus
Thomas Jefferson University Jefferson Digital Commons Cardeza Foundation for Hematologic Research Sidney Kimmel Medical College 1-1-2019 Murine MPDZ-linked hydrocephalus is caused by hyperpermeability of the choroid plexus. Junning Yang Thomas Jefferson University Claire Simonneau Thomas Jefferson University Robert Kilker Thomas Jefferson University Laura Oakley ThomasFollow this Jeff anderson additional University works at: https://jdc.jefferson.edu/cardeza_foundation Part of the Medical Pathology Commons Matthew D. Byrne ThomasLet us Jeff knowerson Univ howersity access to this document benefits ouy Recommended Citation See next page for additional authors Yang, Junning; Simonneau, Claire; Kilker, Robert; Oakley, Laura; Byrne, Matthew D.; Nichtova, Zuzana; Stefanescu, Ioana; Pardeep-Kumar, Fnu; Tripathi, Sushil; Londin, Eric; Saugier-Veber, Pascale; Willard, Belinda; Thakur, Mathew; Pickup, Stephen; Ishikawa, Hiroshi; Schroten, Horst; Smeyne, Richard; and Horowitz, Arie, "Murine MPDZ-linked hydrocephalus is caused by hyperpermeability of the choroid plexus." (2019). Cardeza Foundation for Hematologic Research. Paper 49. https://jdc.jefferson.edu/cardeza_foundation/49 This Article is brought to you for free and open access by the Jefferson Digital Commons. The Jefferson Digital Commons is a service of Thomas Jefferson University's Center for Teaching and Learning (CTL). The Commons is a showcase for Jefferson books and journals, peer-reviewed scholarly publications, unique historical collections from the University archives, and teaching tools. The Jefferson Digital Commons allows researchers and interested readers anywhere in the world to learn about and keep up to date with Jefferson scholarship. This article has been accepted for inclusion in Cardeza Foundation for Hematologic Research by an authorized administrator of the Jefferson Digital Commons. For more information, please contact: [email protected]. -
How Can We Create Environments Where Hate Cannot Flourish?
How can we create environments where hate cannot flourish? Saturday, February 1 9:30 a.m. – 10:00 a.m. Check-In and Registration Location: Field Museum West Entrance 10:00 a.m. – 10:30 a.m. Introductions and Program Kick-Off JoAnna Wasserman, USHMM Education Initiatives Manager Location: Lecture Hall 1 10:30 a.m. – 11:30 a.m. Watch “The Path to Nazi Genocide” and Reflections JoAnna Wasserman, USHMM Education Initiatives Manager Location: Lecture Hall 1 11:30 a.m. – 11:45 a.m. Break and walk to State of Deception 11:45 a.m. – 12:30 p.m. Visit State of Deception Interpretation by Holocaust Survivor Volunteers from the Illinois Holocaust Museum Location: Upper level 12:30 p.m. – 1:00 p.m. Breakout Session: Reflections on Exhibit Tim Kaiser, USHMM Director, Education Initiatives David Klevan, USHMM Digital Learning Strategist JoAnna Wasserman, USHMM Education Initiatives Manager Location: Lecture Hall 1, Classrooms A and B Saturday, February 2 (continued) 1:00 p.m. – 1:45 p.m. Lunch 1:45 p.m. – 2:45 p.m. A Survivor’s Personal Story Bob Behr, USHMM Survivor Volunteer Interviewed by: Ann Weber, USHMM Program Coordinator Location: Lecture Hall 1 2:45 p.m. – 3:00 p.m. Break 3:00 p.m. – 3:45 p.m. Student Panel: Beyond Indifference Location: Lecture Hall 1 Moderator: Emma Pettit, Sustained Dialogue Campus Network Student/Alumni Panelists: Jazzy Johnson, Northwestern University Mary Giardina, The Ohio State University Nory Kaplan-Kelly, University of Chicago 3:45 p.m. – 4:30 p.m. Breakout Session: Sharing Personal Reflections Tim Kaiser, USHMM Director, Education Initiatives David Klevan, USHMM Digital Learning Strategist JoAnna Wasserman, USHMM Education Initiatives Manager Location: Lecture Hall 1, Classrooms A and B 4:30 p.m. -
Identify Distinct Prognostic Impact of ALDH1 Family Members by TCGA Database in Acute Myeloid Leukemia
Open Access Annals of Hematology & Oncology Research Article Identify Distinct Prognostic Impact of ALDH1 Family Members by TCGA Database in Acute Myeloid Leukemia Yi H, Deng R, Fan F, Sun H, He G, Lai S and Su Y* Department of Hematology, General Hospital of Chengdu Abstract Military Region, China Background: Acute myeloid leukemia is a heterogeneous disease. Identify *Corresponding author: Su Y, Department of the prognostic biomarker is important to guide stratification and therapeutic Hematology, General Hospital of Chengdu Military strategies. Region, Chengdu, 610083, China Method: We detected the expression level and the prognostic impact of Received: November 25, 2017; Accepted: January 18, each ALDH1 family members in AML by The Cancer Genome Atlas (TCGA) 2018; Published: February 06, 2018 database. Results: Upon 168 patients whose expression level of ALDH1 family members were available. We found that the level of ALDH1A1correlated to the prognosis of AML by the National Comprehensive Cancer Network (NCCN) stratification but not in other ALDH1 members. Moreover, we got survival data from 160 AML patients in TCGA database. We found that high ALDH1A1 expression correlated to poor Overall Survival (OS), mostly in Fms-like Tyrosine Kinase-3 (FLT3) mutated group. HighALDH1A2 expression significantly correlated to poor OS in FLT3 wild type population but not in FLT3 mutated group. High ALDH1A3 expression significantly correlated to poor OS in FLT3 mutated group but not in FLT3 wild type group. There was no relationship between the OS of AML with the level of ALDH1B1, ALDH1L1 and ALDH1L2. Conclusion: The prognostic impacts were different in each ALDH1 family members, which needs further investigation. -
M.'S Story Jay and Tava Musial, Who Were Living in Michigan at the Time
M.’s Story Jay and Tava Musial, who were living in Michigan at the time, had planned a family trip for Memorial Day weekend, but not before stopping by their daughter’s pediatrician’s office. Tava had noticed her daughter M. Rhapsody frequently had to go to the bathroom. Assuming she had a urinary tract infection, they hoped to get antibiotics and be on their way. M.’s lab work revealed no signs of bacteria but indicated her blood sugar was extremely high. Five days after her eighth birthday, M. was diagnosed with Type 1 diabetes. The Musials’ weekend getaway quickly rerouted to St. John’s Hospital in Detroit where M. spent a full week learning how to manage diabetes. Shortly after M’s diagnosis, the Musial family relocated to Sheppard Air Force Base in Wichita Falls, Texas. Relocating also meant finding a new endocrinologist for M. It was at that first appointment that Dr. John Caras recommended Diabetes Education at United Regional. Diabetes is a disease that affects the whole family, especially when a child is diagnosed. Diabetes Education also provides a support group for kids and their families. “M. comes to every appointment with a smile on her face and has never let her diabetes hold her back on anything,” said Nicole Benz, Diabetes Nurse Educator at United Regional. Children’s Miracle Network at United Regional provides scholarships for kids with Type 1 Diabetes to go to Camp Sweeney. This three-week camp’s goal is that every child who attends camp will not only learn about his or her condition but will find the inner strength each day to do what it takes to live a healthy lifestyle. -
R-Codox-M / R-Ivac Indication
Lymphoma group R-CODOX-M / R-IVAC INDICATION Burkitt lymphoma, ‘double hit’ lymphoma or high IPI diffuse large B-cell lymphoma. TREATMENT INTENT Curative. PRE-ASSESSMENT 1. Ensure histology is confirmed prior to administration of chemotherapy and document in notes. 2. Record stage of disease - MRI scan of brain (+/- spinal cord) with Gadolinium enhancement, CT scan (neck, chest, abdomen and pelvis) +/- PET, presence or absence of B symptoms, clinical extent of disease, consider bone marrow aspirate and trephine (with cytogenetics/FISH as indicated). 3. Blood tests - FBC, DAT, U&Es, LDH, ESR, urate, calcium, magnesium, creatinine, LFTs, glucose, Igs, β2 microglobulin, hepatitis B core antibody and hepatitis BsAg, hepatitis C antibody, EBV, CMV, VZV, HIV 1+2 after consent, group and save. 4. A number of drugs can interfere with tubular secretion of methotrexate. These include penicillins, aspirin and NSAIDs. Tazocin should NOT be used during high dose methotrexate administration or rescue. Consider using meropenem or other alternative. Review indications for aspirin and NSAIDs and consider stopping during methotrexate treatment. 5. Patients MUST NOT receive co-trimoxazole, starting from the week before the first methotrexate infusion. Consider pentamidine treatment if considered at risk from Pneumocystis infection. 6. CSF examination • cell count +/- immunophenotype, protein and glucose: can be done as part of 1st intrathecal. 7. Ophthalmic examination - if clinically indicated. 8. Urine pregnancy test • before cycle 1 of each new chemotherapy for women of child-bearing age unless they are post-menopausal, have been sterilised or undergone a hysterectomy. 9. ECG +/- Echo - if clinically indicated. 10. Record performance status (WHO/ECOG), height and weight. -
CM4L9 Assessment 1) the Specific Heat of Aluminum Is 0.900 J/G Oc
CM4L9 Assessment 1) The specific heat of aluminum is 0.900 J/g oC. How much heat is required to raise the temperature of a 30.0g block of aluminum from 25.0oC to 75.0oC? a. 0.540 J (Incorrect) b. 1.50 J (Incorrect) Show work regardless if student got answer c. 1350 J (Correct) correct or incorrect d. 1670 J (Incorrect) q = mC∆T q = (30.0g)(0.900J/goC)(50oC) q = 1350 J 2) Given the balanced equation representing a reaction at 101.3 kPa and 298K: N2(g) + 3H2(g) 2NH3(g) + 91.8kJ a. It is exothermic and ∆H equals -91.8 kJ (Correct; exothermic reactions have energy as a product and a negative ∆H) b. It is exothermic and ∆H equals +91.8 kJ (Incorrect; exothermic reactions have a negative ∆H) c. It is endothermic and ∆H equals -91.8 kJ (Incorrect; endothermic reactions have a positive ∆H and have energy as a reactant) d. It is endothermic and ∆H equals +91.8 kJ (Incorrect; endothermic reactions have energy as a reactant) 3) The table below shows the specific heat capacity of four substances. Substance Specific Heat J / g oC Water 4.18 Copper 0.39 Gold 0.13 Silver 0.24 For an equal mass of each substance, which one will require the least amount of heat to raise its temperature from 40oC to 50oC? a. water (Incorrect; water would require the most amount of heat (energy) to raise it’s temperature) b. copper (Incorrect; it would take 0.39 J for each degree change in copper. -
A Missense Mutation in ALDH1A3 Causes Isolated Microphthalmia/Anophthalmia in Nine Individuals from an Inbred Muslim Kindred
European Journal of Human Genetics (2014) 22, 419–422 & 2014 Macmillan Publishers Limited All rights reserved 1018-4813/14 www.nature.com/ejhg SHORT REPORT A missense mutation in ALDH1A3 causes isolated microphthalmia/anophthalmia in nine individuals from an inbred Muslim kindred Adi Mory1,2, Francesc X Ruiz3, Efrat Dagan2,4, Evgenia A Yakovtseva3, Alina Kurolap1, Xavier Pare´s3, Jaume Farre´s3 and Ruth Gershoni-Baruch*,1,2 Nine affected individuals with isolated anophthalmia/microphthalmia from a large Muslim-inbred kindred were investigated. Assuming autosomal-recessive mode of inheritance, whole-genome linkage analysis, on DNA samples from four affected individuals, was undertaken. Homozygosity mapping techniques were employed and a 1.5-Mbp region, homozygous in all affected individuals, was delineated. The region contained nine genes, one of which, aldehyde dehydrogenase 1 (ALDH1A3), was a clear candidate. This gene seems to encode a key enzyme in the formation of a retinoic-acid gradient along the dorsoventral axis during an early eye development and the development of the olfactory system. Sanger sequence analysis revealed a missense mutation, causing a substitution of valine (Val) to methionine (Met) at position 71. Analyzing the p.Val71Met missense mutation using standard open access software (MutationTaster online, PolyPhen, SIFT/PROVEAN) predicts this variant to be damaging. Enzymatic activity, studied in vitro, showed no changes between the mutated and the wild-type ALDH1A3 protein. European Journal of Human Genetics (2014) 22, 419–422; doi:10.1038/ejhg.2013.157; published online 24 July 2013 Keywords: ALDH1A3 gene; anophthalmia/microphthalmia; homozogosity mapping INTRODUCTION METHODS Anophthalmia and microphthalmia (A/M) are rare developmental Patients and families anomalies resulting in absent or small ocular globes, respectively. -
Supplementary Table 1: Adhesion Genes Data Set
Supplementary Table 1: Adhesion genes data set PROBE Entrez Gene ID Celera Gene ID Gene_Symbol Gene_Name 160832 1 hCG201364.3 A1BG alpha-1-B glycoprotein 223658 1 hCG201364.3 A1BG alpha-1-B glycoprotein 212988 102 hCG40040.3 ADAM10 ADAM metallopeptidase domain 10 133411 4185 hCG28232.2 ADAM11 ADAM metallopeptidase domain 11 110695 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 195222 8038 hCG40937.4 ADAM12 ADAM metallopeptidase domain 12 (meltrin alpha) 165344 8751 hCG20021.3 ADAM15 ADAM metallopeptidase domain 15 (metargidin) 189065 6868 null ADAM17 ADAM metallopeptidase domain 17 (tumor necrosis factor, alpha, converting enzyme) 108119 8728 hCG15398.4 ADAM19 ADAM metallopeptidase domain 19 (meltrin beta) 117763 8748 hCG20675.3 ADAM20 ADAM metallopeptidase domain 20 126448 8747 hCG1785634.2 ADAM21 ADAM metallopeptidase domain 21 208981 8747 hCG1785634.2|hCG2042897 ADAM21 ADAM metallopeptidase domain 21 180903 53616 hCG17212.4 ADAM22 ADAM metallopeptidase domain 22 177272 8745 hCG1811623.1 ADAM23 ADAM metallopeptidase domain 23 102384 10863 hCG1818505.1 ADAM28 ADAM metallopeptidase domain 28 119968 11086 hCG1786734.2 ADAM29 ADAM metallopeptidase domain 29 205542 11085 hCG1997196.1 ADAM30 ADAM metallopeptidase domain 30 148417 80332 hCG39255.4 ADAM33 ADAM metallopeptidase domain 33 140492 8756 hCG1789002.2 ADAM7 ADAM metallopeptidase domain 7 122603 101 hCG1816947.1 ADAM8 ADAM metallopeptidase domain 8 183965 8754 hCG1996391 ADAM9 ADAM metallopeptidase domain 9 (meltrin gamma) 129974 27299 hCG15447.3 ADAMDEC1 ADAM-like, -
Genetic Variant in 3' Untranslated Region of the Mouse Pycard Gene
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.26.437184; this version posted March 26, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 2 3 Title: 4 Genetic Variant in 3’ Untranslated Region of the Mouse Pycard Gene Regulates Inflammasome 5 Activity 6 Running Title: 7 3’UTR SNP in Pycard regulates inflammasome activity 8 Authors: 9 Brian Ritchey1*, Qimin Hai1*, Juying Han1, John Barnard2, Jonathan D. Smith1,3 10 1Department of Cardiovascular & Metabolic Sciences, Lerner Research Institute, Cleveland Clinic, 11 Cleveland, OH 44195 12 2Department of Quantitative Health Sciences, Lerner Research Institute, Cleveland Clinic, Cleveland, OH 13 44195 14 3Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western 15 Reserve University, Cleveland, OH 44195 16 *, These authors contributed equally to this study. 17 Address correspondence to Jonathan D. Smith: email [email protected]; ORCID ID 0000-0002-0415-386X; 18 mailing address: Cleveland Clinic, Box NC-10, 9500 Euclid Avenue, Cleveland, OH 44195, USA. 19 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.26.437184; this version posted March 26, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 20 Abstract 21 Quantitative trait locus mapping for interleukin-1 release after inflammasome priming and activation 22 was performed on bone marrow-derived macrophages (BMDM) from an AKRxDBA/2 strain intercross. -
Acquire a High Level of Retinoic Acid− Producing Capacity in Response to Vitamin D 3 This Information Is Current As of September 28, 2021
Human CD1c+ Myeloid Dendritic Cells Acquire a High Level of Retinoic Acid− Producing Capacity in Response to Vitamin D 3 This information is current as of September 28, 2021. Takayuki Sato, Toshio Kitawaki, Haruyuki Fujita, Makoto Iwata, Tomonori Iyoda, Kayo Inaba, Toshiaki Ohteki, Suguru Hasegawa, Kenji Kawada, Yoshiharu Sakai, Hiroki Ikeuchi, Hiroshi Nakase, Akira Niwa, Akifumi Takaori-Kondo and Norimitsu Kadowaki Downloaded from J Immunol 2013; 191:3152-3160; Prepublished online 21 August 2013; doi: 10.4049/jimmunol.1203517 http://www.jimmunol.org/content/191/6/3152 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2013/08/21/jimmunol.120351 Material 7.DC1 References This article cites 41 articles, 22 of which you can access for free at: http://www.jimmunol.org/content/191/6/3152.full#ref-list-1 by guest on September 28, 2021 Why The JI? Submit online. • 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 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 © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. -
The Dot Product
The Dot Product In this section, we will now concentrate on the vector operation called the dot product. The dot product of two vectors will produce a scalar instead of a vector as in the other operations that we examined in the previous section. The dot product is equal to the sum of the product of the horizontal components and the product of the vertical components. If v = a1 i + b1 j and w = a2 i + b2 j are vectors then their dot product is given by: v · w = a1 a2 + b1 b2 Properties of the Dot Product If u, v, and w are vectors and c is a scalar then: u · v = v · u u · (v + w) = u · v + u · w 0 · v = 0 v · v = || v || 2 (cu) · v = c(u · v) = u · (cv) Example 1: If v = 5i + 2j and w = 3i – 7j then find v · w. Solution: v · w = a1 a2 + b1 b2 v · w = (5)(3) + (2)(-7) v · w = 15 – 14 v · w = 1 Example 2: If u = –i + 3j, v = 7i – 4j and w = 2i + j then find (3u) · (v + w). Solution: Find 3u 3u = 3(–i + 3j) 3u = –3i + 9j Find v + w v + w = (7i – 4j) + (2i + j) v + w = (7 + 2) i + (–4 + 1) j v + w = 9i – 3j Example 2 (Continued): Find the dot product between (3u) and (v + w) (3u) · (v + w) = (–3i + 9j) · (9i – 3j) (3u) · (v + w) = (–3)(9) + (9)(-3) (3u) · (v + w) = –27 – 27 (3u) · (v + w) = –54 An alternate formula for the dot product is available by using the angle between the two vectors.