
March 2003 From Journal of Clinical Investigation JCI Table of Contents, March 14, 2003 Journal of Clinical Investigation is the source of these articles ONLINE FIRST ARTICLESWNK kinases regulate thiazide-sensitive Na-Cl cotransport CONTACT: David H. Ellison Oregon Health Sciences University Nephrology/Suite 262 3314 SW US Veterans Hospital Rd Portland, OR 97201 USA Phone 1-503-494-8490 Fax 1-503-494-5330 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/17443.pdf Bone marrow transplantation reveals an essential synergy between neuronal and hemopoietic cell neurokinin production in pulmonary inflammation CONTACT: J. Julio Perez Fontan Washington University School of Medicine St. Louis Children's Hospital Department of Pediatrics One Children's Place St. Louis, MO 63110 USA Phone 1-314-454-2527 Fax 1-314 361 0733 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/17458.pdf TABLE OF CONTENTS Immune suppression by measles virus Measles virus infection is often associated with a generalized state of immunosuppression that facilitates health- and life-threatening secondary infections. To understand the mechanisms of immunosuppression, Michael Oldstone and colleagues studied mice that were genetically engineered to be susceptible to measles virus infection. These mice were infected with measles virus five days before challenge with Listeria monocytogenes and compared with age-matched naive and L. monocytogenes�infected mice that did not receive measles virus. The results (pages 805�810) demonstrated that concurrent measles virus infection suppresses innate as well as adaptive immune responses, which prevents effective clearance of the bacterial infection. Future studies are needed to determine how the virus exerts its effects, and it is hoped that these will aid in the development of improved treatment strategies. CONTACT: Michael B.A. Oldstone Dept. Of Neuropharmacology The Scripps Research Inst. 10550 N. Torrey Pines Road (IMM-6) La Jolla, CA 92037 USA Phone 1-858-784-8798 Fax 1-858-784-9981 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/13603.pdf Proinsulin, diabetes, and the NOD mouse Accumulating evidence supports a role for proinsulin as a key autoantigen in type I diabetes. In contrast to humans, who have one proinsulin gene, mice express two proinsulin isoforms, which are encoded by different genes. To study the role of proinsulin 2, the predominant isoform in the thymus, Christian Boitard and colleagues have introduced a null mutation for the gene into mice of the NOD genetic background, which spontaneously develop diabetes at a high frequency. As they report (pages 851�857), the absence of proinsulin 2 in these animals was associated with accelerated insulitis and diabetes, increased capacity to transfer diabetes, and elevated levels of anti-insulin autoantibodies. These results demonstrate the importance of proinsulin as an autoantigen in the NOD mouse and suggest that future studies in this system could shed light on the pathogenic or regulatory role of insulin-directed autoimmunity. CONTACT: Christian Boitard Contact: Boitard, Christian INSERM U561 Hopital St. Vincent de Paul 82 Bd Denfert Rochereau 75014 Paris, FRANCE Phone 1-331-4048-8249 Fax 1-331-4048-8352 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/16584.pdf Cathepsin S promotes atherosclerosis Remodeling of the ECM contributes to atherosclerosis at multiple stages, and several lines of evidence have implicated the elastolytic cathepsins S (Cat S) and K. Seeking direct evidence for a role of Cat S, Guo-Ping Shi and colleagues crossed mice lacking Cat S with atherosclerosis-prone LDL receptor�deficient mice. They found (pages 897�906) that the double mutants -- when fed a high-cholesterol diet -- had an attenuated response: atherosclerosis was reduced by more than 50% after 12 weeks on an atherogenic diet, and by 30% after 26 weeks. While this study does not reveal the mechanism by which Cat S contributes to atherogenesis, it does suggest several possible modes of action and underscores the possibility that Cat S may serve as a therapeutic target in arterial diseases. CONTACT: Guo-Ping Shi University of California, San Francisco Surge 203, Box 0911 90 Medical Center Way San Francisco, CA 94143 USA Phone 1-415-514-1208 Fax 1-415-476-9749 E-mail: [email protected]
View the PDF of this article at: https://www.the-jci.org/press/14915.pdf Stem cells mobilized by crisis Sickle cell disease affects 150 million people worldwide. The only curative therapy is hematopoietic stem cell transplantation. Because of the limited number of matched donors and the toxicity associated with allogeneic transplants, various gene therapy approaches in autologous stem cells are under development. Encouraged by the observation that sickle cell patients have increased numbers of cells expressing stem cell markers in the peripheral blood, Catherine Verfaillie and colleagues tested peripheral blood from patients during acute crisis and chronic stages of disease for the presence of primitive hematopoietic progenitors (pages 811�819). They found that during acute crisis, patients spontaneously mobilize significant numbers of progenitors with multiple-lineage and repopulation potential into the peripheral blood, suggesting that collection of these progenitors could yield a source of autologous cells suitable for genetic manipulation and subsequent transplantation. CONTACT: Catherine M. Verfaillie University of Minnesota MMC 716 420 Delaware Street SE Minneapolis, MN 55455 USA Phone 1-612-624-3921 Fax 1: 612-624-2436 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/15956.pdf Mismatch repair awry in lung cancer Mutations in DNA mismatch repair genes cause inherited colon cancer syndromes, and somatic mutations and promoter methylation of these genes have been found in a variety of human cancers characterized by microsatellite instability (MSI). Having previously shown that MSI and loss of hMLH1 protein expression is common in lung cancer patients from Taiwan, Yi-Ching Wang and colleagues now report (pages 887�895) results from a comprehensive genetic and epigenetic analysis of 77 resected primary non-small cell lung tumors. Of these tumors, 70% had lost expression of either hMLH1 or hMSH2, and promoter methylation seemed to be the predominant cause. Moreover, promoter methylation of hMLH1 (whose expression is lost in over 50% of the samples) appears to be an early event in tumorigenesis and can be detected in sputum samples. Thus it might serve as a potential diagnostic marker. CONTACT: Yi-Ching Wang National Taiwan Normal University Department of Biology No. 88, Sec. 4 Tingchou Road Taipei 116, TAIWAN Phone 1-8862-2933-6876 Fax 1-8862-293-12904 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/15475.pdf Immunization with Neuronal Nicotinic Acetylcholine Receptor Induces Neurological Autoimmune Disease CONTACT: Vanda A. Lennon Neuroimmunology Lab., 828 Guggenheim Mayo Medical School 200 First Street S.W. Rochester, MN 55905 USA Phone 1-507-284-8727 Fax 1-507-284-1814 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/17429.pdf ACCOMPANYING COMMENTARY: Autonomic "Myasthenia": The case for an autoimmune pathogenesis CONTACT: Daniel B. Drachman Neurology/Neuromuscular Unit Johns Hopkins School Of Medicine 600 N. Wolfe St., 5-119 Meyer Bldg. Baltimore, MD 21205 USA Phone 1-410-955-5406 Fax 1: 410-955-1961 E-mail: [email protected]
View the PDF of this commentary at: https://www.the-jci.org/press/18180.pdf Suppressor of cytokine signaling-1 regulates acute inflammatory arthritis and T cell activation CONTACT: Ian P. Wicks The Walter & Eliza Hall Institute of Medical Res. Reid Rheumatology Laboratory Division of Autoimmunity & Transplantation Post Office, The Royal Melbourne Hospital Victoria 3050, AUSTRALIA Phone 1-61-3-9345-2466 Fax 1-61-3-9347-0852 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/16156.pdf ACCOMPANYING COMMENTARY: Can SOCS make arthritis better? CONTACT: Lionel B. Ivashkiv Hospital for Special Surgery Department of Medicine 535 East 70th Street New York, NY 10021 USA Phone 1-212-606-1653 Fax 1-212-774-2337 E-mail: [email protected] View the PDF of this commentary at: https://www.the-jci.org/press/18113.pdf Mechanisms of TNF-alpha and RANKL mediated osteoclastogenesis and bone resorption in psoriatic arthritis CONTACT: Christopher Ritchlin University of Rochester 601 Elmwood Ave Box 695 Rochester, NY 14642 USA Phone 1-585-273-2125 Fax 1-585-506-1979 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/16069.pdf The Role of the Grb2-p38 MAPK Signaling Pathway in Cardiac Hypertrophy and Fibrosis CONTACT: Anthony J. Muslin Washington University School of Medicine Departments of Medicine, Cell Biology, & Physiol Center for Cardiovascular Res. Campus Box 8086 660 S. Euclid Ave St. Louis, MO 63110 USA Phone 1-314-747-3525 Fax 1-314-362-0186 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/16290.pdf DNA damage is a novel response to sublytic complement C5b-9�induced injury in podocytes CONTACT: Stuart J. Shankland University of Washington Medical Center Division of Nephrology Box 356521 1959 NE Pacific Avenue, BB1269 Seattle, WA 98195-6521 USA Phone 1-206-543-3792 Fax 1-206-685-8661 E-mail: [email protected] View the PDF of this article at: https://www.the-jci.org/press/15645.pdf |