Nurses\u27 Alumnae Association Bulletin - Volume 17 Number 1

Alumnae Notes Committee Reports Digest of Alumnae Association Meetings Greetings from Miss Childs Greetings from the Educational Director Greetings from the President Graduation Awards - 1951 Jefferson\u27s New Hospital Addition Marriages Necrology Neurosurgery Department New Arrivals New Drugs Notes on the Cause of Leukemia Nursing Staff Saul Among the Prophets Staff Activities, 1951-1952 Students\u27 Corner The Hospital Pharmacy The Student Nurse Association of Pennsylvania White Haven and Barton Memorial Division

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Exploring links between NHS leadership and improvement

While the need for leadership in health care is well recognised, there is still the need to better understand how leadership contributes to improving healthcare services. The body of knowledge concerning improvement has grown significantly in recent years, but evidence about links between leadership and health services improvement remains poor, especially within the UK National Health Service. It remains unclear how and why leadership is important to service improvement, and how leadership development can optimise service improvement.This paper describes a study commissioned by The Health Foundation, exploring the links between leadership behaviours reported by clinicians and managers in NHS organisations and their service improvement work. The study highlights leadership behaviours that appear to be positively associated with NHS improvement work. This paper provides insights into which aspects of leadership are used for different types of improvement work and considers lessons for leadership development

“Osteogenesis Imperfecta Patients Wish Orthopedic Surgeons Had Better Strategies to Help with…”—Results of a Patient and Parent-Oriented Survey

Osteogenesis Imperfecta (OI) is a rare genetic disorder in Type I collagen characterized by bone fractures, fragility, and deformity. Current treatments are focused on decreasing fracture rates, improving bone strength, and improving overall global function. Recent research has focused primarily on fracture fixation and outcomes of intramedullary rodding of long bones. While surgical techniques continue to evolve, recent trends in OI research are focusing on patient quality of life and patient-reported outcomes. We created a 12-question survey seeking information regarding aspects of orthopedic care that OI patients and families feel are the most pressing to improve. The survey was electronically administered, and 341 individuals participated. A total of 75% of respondents who answered the age question (254/335) were adults. Regarding surgical intervention for long bones, only 16% of respondents recall being told they could not have surgery because they were too young. Of the 16%, 37.8% were told that <5 years was too young, 13.4% <4 years was too young, and 48.8% <3 years of age was too young for surgical intervention for fractures or deformities. Nearly 22% of respondents were told that their bones were too small for intramedullary fixation. The patient and family responses help elucidate the topics requiring focus for the improvement of OI orthopedic care. Patient concerns and insights should drive the research questions we ask to advance the orthopedic care of OI patients

Laminin-411 Is a Vascular Ligand for MCAM and Facilitates TH17 Cell Entry into the CNS

<div><p>TH17 cells enter tissues to facilitate pathogenic autoimmune responses, including multiple sclerosis (MS). However, the adhesion molecules involved in the unique migratory capacity of TH17 cells, into both inflamed and uninflamed tissues remain unclear. Herein, we characterize MCAM (CD146) as an adhesion molecule that defines human TH17 cells in the circulation; following in vitro restimulation of human memory T cells, nearly all of the capacity to secrete IL-17 is contained within the population of cells expressing MCAM. Furthermore, we identify the MCAM ligand as laminin 411, an isoform of laminin expressed within the vascular endothelial basement membranes under inflammatory as well as homeotstatic conditions. Purified MCAM-Fc binds to laminin 411 with an affinity of 27 nM, and recognizes vascular basement membranes in mouse and human tissue. MCAM-Fc binding was undetectable in tissue from mice with targeted deletion of laminin 411, indicating that laminin 411 is a major tissue ligand for MCAM. An anti-MCAM monoclonal antibody, selected for inhibition of laminin binding, as well as soluble MCAM-Fc, inhibited T cell adhesion to laminin 411 <em>in vitro</em>. When administered in vivo, the antibody reduced TH17 cell infiltration into the CNS and ameliorated disease in an animal model of MS. Our data suggest that MCAM and laminin 411 interact to facilitate TH17 cell entry into tissues and promote inflammation.</p> </div

hMCAM binds to a ligand in the ECM with identical staining to laminin α4.

<p>Calcein labeled, hMCAM expressing MOLT 4 cells were preincubated with either isotype control (A) or anti-hMCAM (clone 17) (B) followed by incubation on tissue sections from healthy mice. After gentle washing of unbound cells, and mounting with DAPI, bound cells were visualized by fluorescent microscopy. Healthy mouse brain sections containing choroid plexus were stained with fluorescently labeled mMCAM-Fc protein and pan-laminin antibody. Staining of mMCAM-Fc was detected on choroid plexus (C) as well as the vasculature throughout the tissues (D). Fluorescently labeled mMCAM-Fc protein was preincubated with either isotype control (E) or anti-mMCAM (clone 15) (F) before addition to tissue sections of healthy mouse brain. Healthy mouse tissues were stained with fluorescently labeled mMCAM-Fc and CD31 (G) anti-mMCAM and pan laminin (H) or anti-mMCAM alone (I). Tissues from mice with active EAE were stained with fluorescently labeled mMCAM-Fc and pan-laminin (J) or mMCAM-Fc and an antibody specific to the α4 chain of laminin (K).</p

mMCAM colocalizes with laminin 411 on the choroid plexus, and shows no specific binding to tissues from LAMA4−/− mice.

<p><i>(A)</i> Staining of healthy mouse choroid plexus with anti-laminin, anti-laminin α4 and mMCAM-Fc (B) Staining of healthy brain tissues from LAMA4−/− mice with anti-laminin and mMCAM-Fc.</p