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JCI table of contents, October 21, 2002

JCI Journals

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Selective parasympathetic innervation of subcutaneous and intra-abdominal fat - functional implications

Felix Kreier
Netherlands Institute for Brain Research
Meibergdreef 33, 1105 AZ
Phone: 31-20-566-5500
Fax: 31-20-696-1006

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Insights into the molecular mechanisms of bradycardia-triggered arrhythmias in long QT-3 syndrome

Robert S. Kass
Department of Pharmacology
Columbia University College of Physicians and Surgeons
630 W. 168th St.
New York, NY 10032
Phone: 212-305-7444
Fax: 212-342-2703

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Table of Contents:

Bacterial infectious disease control by vaccine development

Roy Curtiss
Dept. Of Biology
Washington University
1 Brookings Drive, Campus Box 1137
St. Louis, MO 63130-4899
Phone: 1: 314-935-6819
Fax: 314-935-7246

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Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiency

The leptin-deficient ob/ob mouse presents with a multitude of phenotypic abnormalities including severe obesity, infertility, immune system dysfunction and limited growth - all reversible following subcutaneous leptin administration. Much less is known about human leptin deficiency. I. Sadaf Farooqi and colleagues previously reported on 2 children with congenital leptin deficiency suffering from hyperphagia and severe obesity. These conditions were reduced following 1 year of subcutaneous recombinant human leptin therapy in the older subject. The authors now report (on pages 1093-1103) on the status of these two children, as well as a third, after up to 50 months of chronic r-metHuLeptin therapy. Treatment induced a decrease in caloric intake and fat mass (while lean mass increased in keeping with increased linear growth). Surprisingly, the basal metabolic rate in all subjects remained unchanged and allowed appropriately timed pubertal development. Reversal of severely impaired lymphocyte function suggests that leptin is a key molecule in both CD4+ T cell development and function and raises the possibility of leptin-replacement therapy for other immunodeficiencies.

I. Sadaf Farooqi
University Department of Medicine and Department of Clinical Biochemistry
Addenbrooke's Hospital
Phone: 44-1223-762-634
Fax: 44-1223-762-657

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CCL25 mediates the localization of recently activated CD8ab+ lymphocytes to the small-intestinal mucosa

Given the continuous exposure of the intestine to foreign antigens, it is not surprising that large numbers of T lymphocytes are recruited from the blood to the intestine. In addition to lymphocytic expression of adhesion molecules that direct lymphocyte migration from the blood into intestinal tissues, evidence is mounting that chemokines and their receptors may also be involved. On pages 1113-1121 William Agace and colleagues demonstrate that expression of the chemokine receptor CCR9 is selectively maintained on CD8+ T cells activated in murine gut-associated lymphoid tissues and that neutralization of the CCR9 ligand CCL25 with a blocking antibody inhibits the accumulation of these cells in the small intestinal epithelial compartment. These results provide direct in vivo demonstration of a functional role for a chemokine/receptor pair in lymphocyte localization to the intestinal mucosa.

William W. Agace
Immunology Section
Department of Cell and Molecular Biology
Lund University
BMC I-13, S-22184
Phone: 46-46-2220416
Fax: 46-46-2224218

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Intestinal Attraction: CCL25 functions in effector lymphocyte recruitment to the small intestine

Daniel J. Campbell
154B, 3801 Miranda Ave.
Palo Alto, California,94304
Phone: 650-493-5000 Ext. 63132
Fax: 650-858-3986

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Neutrophil-independent mechanisms of caspase-1- and IL-18-mediated ischemic acute tubular necrosis in mice

Acute tubular necrosis is the predominant pathological process in animal models of ischemic acute renal failure (ARF) and in post-transplantation ARF in humans. Caspase proteases are involved in apoptotic as well as necrotic cell death, and several lines of evidence suggest that caspases play a role in ischemic ARF in mice. Charles Edelstein and colleagues have previously shown that mice lacking proinflammatory caspase-1 are protected from ischemic ARF and that this is (at least in part) due to lack of caspase activation of IL-18. The caspase-1 knockout mice also show less neutrophil infiltration. In a new set of experiments (pages 1083-1091), the researchers tested the potential of a new caspase inhibitor to protect against ischemic ARF and further examined the role of neutrophils in damage to the kidney. The experiments demonstrated efficacy of the drug in mice and revealed a novel mechanism of IL-18-mediated renal toxicity that acts independently of neutrophils.

Charles L. Edelstein
Division of Renal Diseases and Hypertension
University of Colorado School of Medicine
Box C281, 4200 East 9th Ave.
Denver, Colorado 80262
Phone: 303-315-8764
Fax: 303-315-4852

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mRNA expression profiles for Escherichia coli ingested by normal and phagocyte oxidase-deficient human neutrophils

Henry Rosen
Box 356420
Department of Medicine
University of Washington
Seattle, Washington 98195
Phone: 206-543-3238
Fax: 206-543-3947

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Genome-wide responses of a pathogenic bacterium to its host

David A. Relman
Veterans Affairs
Palo Alto Healthcare System 154T
Building 101 Rm. B4-185
3801 Miranda Ave.
Palo Alto, California 94304
Phone: 650-852-3308
Fax: 650-852-3291

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Noncoding RNA danger motifs bridge innate and adaptive immunity and are potent adjuvants for vaccination

Adrian Bot
Alliance Pharmaceutical, Corp.
Department of Immunology
3040 Science Park Road
San Diego, CA 92121
Phone 1: 858-410-5259
Fax 1: 858-410-5612

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Long QT syndrome, Brugada syndrome, and conduction system disease are linked to a single sodium channel mutation

Augustus Grant
Duke University Medical Center
Division of Cardiology
Box 3504
Durham, NC 27710
Phone 1: 919-684-3901
Fax 1: 919-681-8978

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Defective cardiac ion channels: from mutations to clinical syndromes

Colleen Clancy
Columbia University
Department of Pharmacology
New York, NY
Phone 1: 212-305-8696
Fax 1: 212-305-8780

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Amiloride-blockable acid-sensing ion channels are leading acid sensors expressed in human nociceptors

Shinya Ugawa
Nagoya City University Medical School
Department of Anatomy II
1 Kawasumi, Mizuho-cho
Nagoya, 467-8601
Phone 1: 8152-853-8126
Fax 1: 8152-852-8887

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Role of matrix metalloproteinase-9 in angiogenesis caused by ocular infection with herpes simplex virus

Barry T. Rouse
University of Tennessee
M409 Walters Life Sciences Building
Department of Microbiology
Knoxville, TN 37996-0845
Phone 1: 865-974-4026
Fax 1: 865-974-4007

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EphB6 crosslinking results in costimulation of T cells

Jiangping Wu
CHUM, Notre-Dame Campus
Laboratory of Transplantation Immunology
Pavilion DeSeve, Research Center Rm Y-5616
1560 Sherbrooke St. East
Montreal, Quebec H2L 4M1,
Phone 1: 514 890-8000 ext. 25164
Fax 1: 514 412-7596

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Benzodiazepine-induced superoxide signals B cell apoptosis: mechanistic insight and potential therapeutic utility

Gary Glick
Department Of Chemistry
University Of Michigan
930 N. University Ave.
3817 Chem
Ann Arbor, MI 48109-1055
Phone 1: 734-764-4578
Fax 1: 734-615-8902

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Cholic acid mediates negative feedback regulation of bile acid synthesis in mice

David Russell
UT Southwestern
Molecular Genetics
5323 Harry Hines Blvd.
Dallas, TX 75390-9046
Phone 1: 214-648-2007
Fax 1: 214-649-6899

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Does loss of bile acid homeostasis make mice melancholy?

David D. Moore
Department of Molecular and Cellular Biology
Baylor College of Medicine
1 Baylor Plaza
Houston, Texas 77030
Phone: 713-798-3313
Fax: 713-798-3017

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Collagen deposition in HIV-1 infected lymphatic tissues and T cell homeostasis

Timothy Schacker
University of Minnesota
MMC 250
PWB 14-106
516 Delaware Street SE
Minneapolis, MN 55455
Phone 1: 612-624-9955
Fax 1: 612-625-4410

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