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Journal articles on the topic 'Chronic Allograft Rejection'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Wong, John, Paul Kubes, Yikun Zhang, et al. "Role of ICAM-1 in chronic hepatic allograft rejection in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 283, no. 1 (2002): G196—G203. http://dx.doi.org/10.1152/ajpgi.00222.2001.

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The pathogenesis of hepatic allograft rejection remains unclear. We aimed to clarify the early role of intercellular adhesion molecule-1 (ICAM-1)-mediated cell recruitment in chronic hepatic rejection. Liver transplantation was performed from Lewis to Lewis rats (isograft controls) and from Lewis to Brown Norway rats (allograft rejection group). The allografted rats were treated with either ICAM-1 antisense oligonucleotides (10 mg · kg−1· day−1× 6 days ip) or a control preparation (either ICAM-1 missense oligonucleotide or normal saline). Hepatic leukocyte recruitment in vivo was studied on da

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2

Kupiec-Weglinski, Jerzy W. "Chronic allograft rejection." Current Opinion in Organ Transplantation 4, no. 1 (1999): 1. http://dx.doi.org/10.1097/00075200-199903000-00001.

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3

Wedel, Johannes, Sarah Bruneau, Nora Kochupurakkal, Leo Boneschansker, and David M. Briscoe. "Chronic allograft rejection." Current Opinion in Organ Transplantation 20, no. 1 (2015): 13–20. http://dx.doi.org/10.1097/mot.0000000000000155.

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4

Hayry, Pekka, Helena Isoniemi, Serdar Yilmaz, et al. "Chronic Allograft Rejection." Immunological Reviews 134, no. 1 (1993): 33–81. http://dx.doi.org/10.1111/j.1600-065x.1993.tb00639.x.

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5

Shirwan, Haval. "CHRONIC ALLOGRAFT REJECTION." Transplantation 68, no. 6 (1999): 715–26. http://dx.doi.org/10.1097/00007890-199909270-00001.

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6

Hancock, Wayne W., Bao Lu, Wei Gao, et al. "Requirement of the Chemokine Receptor CXCR3 for Acute Allograft Rejection." Journal of Experimental Medicine 192, no. 10 (2000): 1515–20. http://dx.doi.org/10.1084/jem.192.10.1515.

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Chemokines provide signals for activation and recruitment of effector cells into sites of inflammation, acting via specific G protein–coupled receptors. However, in vitro data demonstrating the presence of multiple ligands for a given chemokine receptor, and often multiple receptors for a given chemokine, have led to concerns of biologic redundancy. Here we show that acute cardiac allograft rejection is accompanied by progressive intragraft production of the chemokines interferon (IFN)-γ–inducible protein of 10 kD (IP-10), monokine induced by IFN-γ (Mig), and IFN-inducible T cell α chemoattrac

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7

DUIJVESTIJN, ADRIAN M., and PETER J. C. VAN BREDA VRIESMAN. "CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 52, no. 2 (1991): 195–202. http://dx.doi.org/10.1097/00007890-199108000-00003.

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8

Demetris, Anthony J., Eric C. Seaberg, Kenneth P. Batts, et al. "Chronic Liver Allograft Rejection." American Journal of Surgical Pathology 22, no. 1 (1998): 28–39. http://dx.doi.org/10.1097/00000478-199801000-00004.

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9

Glicklich, Daniel, Bharat Gupta, Gerrilinn Schurter-Frey, Stuart M. Greenstein, Richard S. Schechner, and Vivian A. Tellis. "CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 66, no. 3 (1998): 398–99. http://dx.doi.org/10.1097/00007890-199808150-00019.

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10

Jain, Dhanpat, Marie E. Robert, Victor Navarro, Amy L. Friedman, and James M. Crawford. "Total Fibrous Obliteration of Main Portal Vein and Portal Foam Cell Venopathy in Chronic Hepatic Allograft Rejection." Archives of Pathology & Laboratory Medicine 128, no. 1 (2004): 64–67. http://dx.doi.org/10.5858/2004-128-64-tfoomp.

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Abstract Context.—Chronic hepatic allograft rejection is characterized by arteriopathy and bile duct loss. Pathology of the portal vein or its branches is not considered to play a major role in chronic rejection. Objective.—A recent case of chronic rejection with total fibrous obliteration of the portal vein at the hilum and graft loss prompted us to retrospectively analyze cases of failed allografts for portal vein changes. Design.—Six cases of failed hepatic allograft recorded in our files from 1994 to 1998 were selected for the study. For comparison, 4 cases of hepatitis C cirrhosis were in

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11

Kaufman, Christina L., Jean Kanitakis, Annemarie Weissenbacher, et al. "Defining chronic rejection in vascularized composite allotransplantation—The American Society of Reconstructive Transplantation and International Society of Vascularized Composite Allotransplantation chronic rejection working group: 2018 American Society of Reconstructive Transplantation meeting report and white paper Research goals in defining chronic rejection in vascularized composite allotransplantation." SAGE Open Medicine 8 (January 2020): 205031212094042. http://dx.doi.org/10.1177/2050312120940421.

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Objectives: This report summarizes a collaborative effort between the American Society of Reconstructive Transplantation and the International Society of Vascularized Composite Allotransplantation to establish what is known about chronic rejection in recipients of vascularized composite allografts, with an emphasis on upper extremity and face transplants. As a picture of chronic rejection in hand and face vascularized composite allografts emerges, the results will be applied to other types of vascularized composite allografts, such as uterine transplantation. Methods: The overall goal is to de

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12

Womer, Karl L., Richard S. Lee, Joren C. Madsen, and Mohamed H. Sayegh. "Tolerance and chronic rejection." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1409 (2001): 727–38. http://dx.doi.org/10.1098/rstb.2001.0852.

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The most common cause of chronic allograft loss is an incompletely understood clinicopathological entity called chronic rejection (CR). Recent reports suggest an improvement in long–term renal allograft survival, although it is not clear from these data whether a true reduction of biopsy–proven CR has occurred. Although newer immunosuppressive medications have greatly reduced the incidence of acute rejection (AR) in the early post–transplantation period, the ideal therapy for both AR and CR would be to achieve a state of tolerance. By definition, such a state should allow for indefinite allogr

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13

Tufveson, Gunnar, and Cecilia Johnsson. "CHRONIC ALLOGRAFT DYSFUNCTION???CHRONIC REJECTION REVISITED." Transplantation 70, no. 3 (2000): 411–12. http://dx.doi.org/10.1097/00007890-200008150-00002.

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14

Higuchi, Haruka, Daisuke Kamimura, Jing-Jing Jiang, et al. "Orosomucoid 1 is involved in the development of chronic allograft rejection after kidney transplantation." International Immunology 32, no. 5 (2020): 335–46. http://dx.doi.org/10.1093/intimm/dxaa003.

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Abstract Chronic allograft rejection is the most common cause of long-term allograft failure. One reason is that current diagnostics and therapeutics for chronic allograft rejection are very limited. We here show that enhanced NFκB signaling in kidney grafts contributes to chronic active antibody-mediated rejection (CAAMR), which is a major pathology of chronic kidney allograft rejections. Moreover, we found that urinary orosomucoid 1 (ORM1) is a candidate marker molecule and therapeutic target for CAAMR. Indeed, urinary ORM1 concentration was significantly higher in kidney transplant recipien

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15

Joosten, Simone A., Cees Kooten, and Leendert C. Paul. "Pathogenesis of chronic allograft rejection." Transplant International 16, no. 3 (2003): 137–45. http://dx.doi.org/10.1111/j.1432-2277.2003.tb00277.x.

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16

Verleden, Geert M. "Chronic Allograft Rejection (Obliterative Bronchiolitis)." Seminars in Respiratory and Critical Care Medicine 22, no. 05 (2001): 551–58. http://dx.doi.org/10.1055/s-2001-18427.

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17

Scharf, Rüdiger E. "In Vitro Thromboxane Synthesis of Depleted Blood Platelets Following Renal Transplantation." Thrombosis and Haemostasis 64, no. 01 (1990): 161–64. http://dx.doi.org/10.1055/s-0038-1647274.

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SummaryRenal transplant rejection is associated with platelet activation in vivo which may lead to partially α- and γ-granule-depleted platelets that continue to circulate. These “exhausted” platelets are hemostatically defective. Tb quantitate the extent of platelet granule depletion following kidney transplantation, we determined intraplatelet levels of β-thromboglobulin (βTG), platelet factor 4 (PF4), and serotonin (5-hydroxytryptamine, 5-HT) ex vivo in Tiiton X-1O0-treated platelet lysates. To explore biochemical alterations of partially depleted platelets, we studied platelet thromboxane

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18

Troxell, Megan L., John P. Higgins, and Neeraja Kambham. "Evaluation of C4d Staining in Liver and Small Intestine Allografts." Archives of Pathology & Laboratory Medicine 130, no. 10 (2006): 1489–96. http://dx.doi.org/10.5858/2006-130-1489-eocsil.

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Abstract Context.—Antibody-mediated humoral rejection in kidney and heart allografts is well recognized and is often associated with poor outcome. C4d deposition in allograft biopsy specimens occurs at sites of antibody-mediated complement activation and has become one of the histopathologic criteria for diagnosis of humoral rejection in the kidney and the heart. Objective.—To study immunohistochemical C4d staining as a potential diagnostic marker in liver and small intestine allograft biopsy specimens. Design.—Thirty-six small intestine and 71 liver specimens, including native specimens, allo

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19

Zhu, Peng, Carl Atkinson, Suraj Dixit, et al. "Organ preservation with targeted rapamycin nanoparticles: a pre-treatment strategy preventing chronic rejection in vivo." RSC Advances 8, no. 46 (2018): 25909–19. http://dx.doi.org/10.1039/c8ra01555d.

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(a) Rapamycin nanotherapeutic pre-treatment improves tracheal allograft outcome after transplantation. (b) Nanotherapy reduces aortic allograft vasculopathy. (c) Dose dependency of the nanotherapy in aortic interposition allografts.

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20

Zakrzewicz, Anna, Srebrena Atanasova, Winfried Padberg, and Veronika Grau. "Monocytic Tissue Transglutaminase in a Rat Model for Reversible Acute Rejection and Chronic Renal Allograft Injury." Mediators of Inflammation 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/429653.

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Acute rejection is a major risk factor for chronic allograft injury (CAI). Blood leukocytes interacting with allograft endothelial cells during acute rejection were suggested to contribute to the still enigmatic pathogenesis of CAI. We hypothesize that tissue transglutaminase (Tgm2), a multifunctional protein and established marker of M2 macrophages, is involved in acute and chronic graft rejection. We focus on leukocytes accumulating in blood vessels of rat renal allografts (Fischer-344 to Lewis), an established model for reversible acute rejection and CAI. Monocytes in graft blood vessels ov

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21

Minamoto, Kanji, and David J. Pinsky. "Recipient iNOS but Not eNOS Deficiency Reduces Luminal Narrowing in Tracheal Allografts." Journal of Experimental Medicine 196, no. 10 (2002): 1321–33. http://dx.doi.org/10.1084/jem.20012135.

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Chronic airway rejection is characterized by prolonged inflammation, epithelial damage, and eventual luminal obliterative bronchiolitis (OB). In cardiac allografts, the inducible nitric oxide synthase (iNOS) promotes acute rejection but paradoxically reduces neointimal formation, the hallmark of chronic rejection. The specific roles of NOS isoforms in modulating lymphocyte traffic and airway rejection are not known. Using a double lumen mouse tracheal transplant model, tracheal grafts from B10.A (allo) or C57BL/6J (iso) mice were transplanted into cyclosporine-treated wild-type (WT) iNOS−/− or

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22

Arjuna, Ashwini, Michael T. Olson, Sofya Tokman, et al. "Antibody-Mediated Rejection and Sponge Effect in a Redo Lung Transplant Recipient." Case Reports in Transplantation 2021 (June 10, 2021): 1–4. http://dx.doi.org/10.1155/2021/6637154.

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Long-term survival after lung transplant remains severely limited by chronic lung allograft dysfunction. Antibody-mediated rejection of lung transplant allografts is usually caused by donor-specific antibodies (DSAs) directed toward donor human leukocyte antigens (HLAs). Typically, patients with antibody-mediated rejection have significantly higher circulating DSAs and increased mean fluorescence intensity than those without antibody-mediated rejection. However, some patients with antibody-mediated rejection have low mean fluorescence intensities, partly due to the “sponge effect” related to D

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23

ISONIEMI, HELENA, EERO TASKINEN, and PEKKA HAYRY. "HISTOLOGICAL CHRONIC ALLOGRAFT DAMAGE INDEX ACCURATELY PREDICTS CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 58, no. 12 (1994): 1195–97. http://dx.doi.org/10.1097/00007890-199412000-00010.

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24

Isoniemi, Helena, Eero Taskinen, and Pekka Häyry. "HISTOLOGICAL CHRONIC ALLOGRAFT DAMAGE INDEX ACCURATELY PREDICTS CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 58, no. 11 (1994): 1195–98. http://dx.doi.org/10.1097/00007890-199412150-00010.

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25

ISONIEMI, HELENA, EERO TASKINEN, and PEKKA HAYRY. "HISTOLOGICAL CHRONIC ALLOGRAFT DAMAGE INDEX ACCURATELY PREDICTS CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 58, no. 12 (1994): 1195–97. http://dx.doi.org/10.1097/00007890-199412270-00010.

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26

WOMER, KARL L., JAMES R. STONE, BARBARA MURPHY, ANIL CHANDRAKER, and MOHAMED H. SAYEGH. "Indirect Allorecognition of Donor Class I and II Major Histocompatibility Complex Peptides Promotes the Development of Transplant Vasculopathy." Journal of the American Society of Nephrology 12, no. 11 (2001): 2500–2506. http://dx.doi.org/10.1681/asn.v12112500.

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Abstract. Recent clinical and experimental evidence suggests that indirect allorecognition may promote the development of chronic rejection, but definitive experimental studies are lacking. To study the contribution of indirect allorecognition to chronic rejection, naïve Lewis (RT11) rats were immunized with synthetic Wistar Furth (WF) class II-RT1u.D (HLA-DR—like) or -RT1u.B (HLA-DQ—like) or class I-RT1u.A (HLA-A—like) peptides emulsified in complete Freund's adjuvant 7 d before transplantation (n = 5 to 7/group). Experimental and control animals then acted as recipients of fully mismatched W

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27

Govindaraj, Satish, Elena Fedorova, Eric M. Genden, et al. "Reepithelialization of Orthotopic Tracheal Allografts Prevents Rejection after Withdrawal of Immunosuppression." Annals of Otology, Rhinology & Laryngology 114, no. 4 (2005): 279–88. http://dx.doi.org/10.1177/000348940511400406.

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Prior work has demonstrated that immunosuppressed orthotopic tracheal allografts undergo progressive reepithelialization over a 48-day period with recipient-derived tracheal epithelium. We hypothesized that reepithelialization of tracheal allografts would prevent rejection after withdrawal of immunosuppression. BALB/c murine tracheal grafts were transplanted orthotopically into either syngeneic or allogeneic C57/BL6 recipients. The recipients were either not immunosuppressed, immunosuppressed with cyclosporine A (10 mg/kg per day) continuously, or immunosuppressed for 48 days and then withdraw

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28

Valantine-von Kaeppler, H. A. "Prevention of chronic heart allograft rejection." Transplantation Proceedings 31, no. 1-2 (1999): 1288–89. http://dx.doi.org/10.1016/s0041-1345(98)02000-4.

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29

Paul, L. C. "Pathophysiology of chronic renal allograft rejection." Transplantation Proceedings 31, no. 7 (1999): 2715–16. http://dx.doi.org/10.1016/s0041-1345(99)00537-0.

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30

Yilmaz, Serdar, Eero Taskinen, Timo Paavonen, Ari Mennander, and Pekka Häyry. "Chronic rejection of rat renal allograft." Transplant International 5, no. 2 (1992): 85–95. http://dx.doi.org/10.1111/j.1432-2277.1992.tb01761.x.

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31

Kreis, Henri. "Chronic allograft rejection: concept and diagnosis." Revue Française des Laboratoires 2003, no. 349 (2003): 24–26. http://dx.doi.org/10.1016/s0338-9898(03)80048-3.

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32

Tullius, Stefan G., Wayne W. Hancock, Uwe Heemann, Haruhito Azuma, and Nicholas L. Tilney. "REVERSIBILITY OF CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 58, no. 1 (1994): 93–98. http://dx.doi.org/10.1097/00007890-199407000-00016.

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33

Tullius, Stefan G., Wayne W. Hancock, Uwe Heemann, Haruhito Azuma, and Nicholas L. Tilney. "REVERSIBILITY OF CHRONIC RENAL ALLOGRAFT REJECTION." Transplantation 58, no. 1 (1994): 93–98. http://dx.doi.org/10.1097/00007890-199407150-00016.

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34

Lin, D., Cohen G. Freue, A. Bergman, et al. "BIOMARKERS OF CHRONIC HEART ALLOGRAFT REJECTION." Transplantation Journal 90 (July 2010): 303. http://dx.doi.org/10.1097/00007890-201007272-00572.

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35

Smith, R. Neal, Takuya Ueno, Toshiro Ito, Katsunori Tanaka, Susan P. Shea, and Reza Abdi. "Chemokines and Chronic Heart Allograft Rejection." Transplantation 84, no. 3 (2007): 442–44. http://dx.doi.org/10.1097/01.tp.0000277535.02541.30.

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36

Abu-Elmagd, Kareem M., Anthony J. Demetris, George V. Mazariegos, et al. "CHRONIC REJECTION OF THE INTESTINAL ALLOGRAFT." Transplantation 69, Supplement (2000): S166. http://dx.doi.org/10.1097/00007890-200004271-00203.

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37

Joosten, Simone A., YVO W. J. Sijpkens, Cees van Kooten, and Leendert C. Paul. "Chronic renal allograft rejection: Pathophysiologic considerations." Kidney International 68, no. 1 (2005): 1–13. http://dx.doi.org/10.1111/j.1523-1755.2005.00376.x.

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38

Paul, Leendert C. "New insights in chronic allograft rejection." Current Opinion in Urology 12, no. 2 (2002): 89–93. http://dx.doi.org/10.1097/00042307-200203000-00002.

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39

Rotman, Samuel, Nathalie Koch, Lucie Wiesner, et al. "Nonvascularized human skin chronic allograft rejection." American Journal of Transplantation 19, no. 11 (2019): 3191–96. http://dx.doi.org/10.1111/ajt.15542.

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40

Qun, Yan, Zhang Peng, and Yang Chuanyong. "Chronic kidney isograft and allograft rejection." Journal of Huazhong University of Science and Technology [Medical Sciences] 22, no. 3 (2002): 253–54. http://dx.doi.org/10.1007/bf02828195.

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41

Mennander, Ari, Sinikka Tiisala, Timo Paavonen, Jorma Halttumen, and Pekka H�yry. "Chronic rejection of rat aortic allograft." Transplant International 4, no. 3 (1991): 173–79. http://dx.doi.org/10.1007/bf00335340.

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42

Yilmaz, Serdar, Eero Taskinen, Timo Paavonen, Ari Mennander, and Pekka H�yry. "Chronic rejection of rat renal allograft." Transplant International 5, no. 2 (1992): 85–95. http://dx.doi.org/10.1007/bf00339222.

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43

Lowes, John R., Stefan G. Hubscher, and James M. Neuberger. "CHRONIC REJECTION OF THE LIVER ALLOGRAFT." Gastroenterology Clinics of North America 22, no. 2 (1993): 401–20. http://dx.doi.org/10.1016/s0889-8553(21)00075-3.

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44

Noguchi, Shin-ichi, Jorge Reyes, George V. Mazariegos, Maria Parizhskaya, and Ronald Jaffe. "Pediatric Intestinal Transplantation: The Resected Allograft." Pediatric and Developmental Pathology 5, no. 1 (2002): 3–21. http://dx.doi.org/10.1007/s10024-001-0140-0.

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We reviewed the clinical and pathologic finding of 22 resected allografts from 19 of the 83 children who underwent a variety of small intestinal transplant procedures in the years 1990–2000 at the Children's Hospital of Pittsburgh. Resections were compared with prior mucosal biopsies because resections allow for evaluation of the entire bowel thickness, including the feeding vessels, and obviate the problems of limited sampling. Partial resections that were done soon after the transplant, or soon after additional surgery, were for surgical problems such as leaks, adhesions, and volvulus. None

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45

Roden, Anja C., Dara L. Aisner, Timothy Craig Allen, et al. "Diagnosis of Acute Cellular Rejection and Antibody-Mediated Rejection on Lung Transplant Biopsies: A Perspective From Members of the Pulmonary Pathology Society." Archives of Pathology & Laboratory Medicine 141, no. 3 (2016): 437–44. http://dx.doi.org/10.5858/arpa.2016-0459-sa.

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Context.— The diagnosis and grading of acute cellular and antibody-mediated rejection (AMR) in lung allograft biopsies is important because rejection can lead to acute graft dysfunction and/or failure and may contribute to chronic graft failure. While acute cellular rejection is well defined histologically, no reproducible specific features of AMR are currently identified. Therefore, a combination of clinical features, serology, histopathology, and immunologic findings is suggested for the diagnosis of AMR. Objective.— To describe the perspective of members of the Pulmonary Pathology Society (

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46

Güven, Göksel, Şeref Rahmi Yılmaz, Tolga Yıldırım, Fazıl Tuncay Akı, and Yunus Erdem. "Underlying Causes and Risk Factors of Chronic Renal Allograft Dysfunction Among Renal Transplant Recipients." Acta Medica 52, no. 2 (2021): 152–61. http://dx.doi.org/10.32552/2021.actamedica.572.

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Objective: Dialysis or renal transplantation are the two treatment options for end-stage renal disease patients. Renal transplantation from an appropriate donor increases survival and quality of life compared to treatment with dialysis. Recent advances in immunosuppressive therapy have significantly improved the success in 1-year graft survival. However, the long-term graft survival remains the same. Therefore, we aimed to determine the underlying causes and risk factors of chronic allograft dysfunction in renal transplant recipients. Materials and Methods: From 2000 to 2012, all consecu

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47

Shelest, V. V., and R. O. Zograbian. "TREATMENTOFRENAL ALLOGRAFTCHRONIC REJECTION." Ukrainian Journal of Nephrology and Dialysis, no. 1(57) (February 28, 2018): 57–62. http://dx.doi.org/10.31450/ukrjnd.1(57).2018.06.

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48

Rice, J. C., J. J. Curtis, D. A. Laskow, and M. Botero-Velez. "Preferential rejection of the kidney in a simultaneous kidney-pancreas transplant." Journal of the American Society of Nephrology 4, no. 11 (1994): 1841–46. http://dx.doi.org/10.1681/asn.v4111841.

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A case of selective kidney allograft rejection with stable pancreas function in a patient who received simultaneous kidney-pancreas allograft from the same donor is reported. Pancreas function was shown to be normal within the first month posttransplant by both a glucose tolerance test (despite a high corticosteroid dose) and stable urinary amylase values during biopsy-proven acute renal allograft rejection. This patient subsequently rejected his kidney allograft as documented by histopathologic evidence of severe chronic vascular rejection and acute tubulointerstitial rejection, yet his pancr

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49

Schmidbauer, Martina, Song Rong, Marcel Gutberlet, et al. "Diffusion-Weighted Imaging and Mapping of T1 and T2 Relaxation Time for Evaluation of Chronic Renal Allograft Rejection in a Translational Mouse Model." Journal of Clinical Medicine 10, no. 19 (2021): 4318. http://dx.doi.org/10.3390/jcm10194318.

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We hypothesized that multiparametric MRI is able to non-invasively assess, characterize and monitor renal allograft pathology in a translational mouse model of chronic allograft rejection. Chronic rejection was induced by allogenic kidney transplantation (ktx) of BALB/c-kidneys into C57BL/6-mice (n = 23). Animals after isogenic ktx (n = 18) and non-transplanted healthy animals (n = 22) served as controls. MRI sequences (7T) were acquired 3 and 6 weeks after ktx and quantitative T1, T2 and apparent diffusion coefficient (ADC) maps were calculated. In addition, in a subset of animals, histologic

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50

Yamaguchi, Keiichiro, Emiko Furuta, and Hiroaki Nakamura. "Chronic Skin Allograft Rejection in Terrestrial Slugs." Zoological Science 16, no. 3 (1999): 485–95. http://dx.doi.org/10.2108/zsj.16.485.

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