Diabetes - Information and References:Extensive coverage of topics including diagnosis, treatment, food - cooking- and dietary aspects, research and new trends

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Diabetes - Information and References

Extensive coverage of topics including diagnosis, treatment, food - cooking- and dietary aspects, research and new trends

includes recent published research regarding angionesis (based on PubMed):

Citations:

Balamurugan, A. N., Y. Gu, et al. (2003). "Bioartificial pancreas transplantation at prevascularized intermuscular space: effect of angiogenesis induction on islet survival." Pancreas 26(3): 279-85.
INTRODUCTION Bioartificial pancreas (BAP) transplantation offers a potential treatment of diabetes mellitus. The optimal site for BAP transplantation has not yet been established.AIM To monitor the effect of induction of neovascularization at the intermuscular space on islet survival after allogenic transplantation of BAP. METHODOLOGY Angiogenesis was induced at the intermuscular space of diabetic Lewis rats by implanting a polyethylene terephthalate (PET) mesh bag, which enclosed a collagen sponge and biodegradable gelatin microspheres containing basic fibroblast growth factor. After confirmation of angiogenesis, BAP was prepared by mixing of 5% agarose with approximately 2,800 isolated rat (Sprague-Dawley) islets and transplanted into the prevascularized PET mesh bag. RESULTS Neovascularization was observed in and around the PET mesh bag within 10 days after implantation as confirmed by macroscopic and microscopic examinations. In the presence of a collagen sponge, new blood vessels penetrated into the PET mesh bag and formed a vascular bed. After transplantation, normoglycemia was achieved in the rats within 3 days and maintained for >35 days. The rats gradually gained body weight, and the results of intravenous glucose tolerance test showed normal patterns of blood glucose clearance 1 month after transplantation. CONCLUSION It can be concluded that the prevascularized PET mesh bag enabled transplanted BAP to survive and maintain function, thus indicating a potential site for BAP transplantation.(More citations towards end).

11. Publications International Ltd., 365 favorite brand name diabetic recipes. 1998, Lincolnwood, IL: Publications International. 336 p. Three hundred sixty-five favorite brand name diabetic recipes

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17. Dustan, H.P., J.E. Denman, and University of Alabama in Birmingham. Dept. of Dietetics., All new cookbook for diabetics and their families. 1988, Birmingham, Ala.: Oxmoor House. vi, 234 p. foreword by Harriet P. Dustan ; [editor, Joan Erskine Denman].

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55. Kozak, G.P., Clinical diabetes mellitus. 1982, Philadelphia: Saunders. xviii, 541 p., [15] p. of plates [edited by] George P. Kozak.

56. Podolsky, S., Clinical diabetes, modern management. 1980, New York: Appleton-Century-Crofts. xx, 633 p. edited by Stephen Podolsky.

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63. Cohen, A.M. and E. Rosenmann, The Cohen diabetic rat. 1990, Basel ; New York: Karger. xii, 206 p. editors, A.M. Cohen, E. Rosenmann.

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66. Chappell, A.C., University of Alabama at Birmingham. General Clinical Research Center., and University of Alabama Hospital. Dept. of Food and Nutrition Services., The complete step-by-step diabetic cookbook. 1995, Birmingham, Ala.: Oxmoor House. 368 p. developed by the Research Nutritionist of the General Clinical Research Center, School of Medicine, and the Registered Dietitians of the Department of Food and Nutrition Services, University Hospital, University of Alabama at Birmingham ; [editor, Anne C. Chappell].

69. Keen, H. and J. Jarrett, Complications of diabetes. 1975, London: Edward Arnold. xiii, 289 p., [6] p. of plates edited by Harry Keen and John Jarrett ; with a foreword by Sir Ronald E. Turnbridge.

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72. Jovanovic-Peterson, L., Controversies in diabetes and pregnancy. 1988, New York: Springer-Verlag. xiv, 205 p., 2 p. of plates Lois Jovanovic, editor ; with a foreword by Steven G. Gabbe.

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78. Taylor, S.I., Current review of diabetes. 1999, Philadelphia: Current Medicine. x, 170 p. edited by Simeon I. Taylor.

79. DeFronzo, R.A., Current therapy of diabetes mellitus. Current therapy series. 1998, St. Louis: Mosby. xiv, 273 p. [edited by] Ralph A. DeFronzo.

80. Time-Life Books., Cut the fat! : the new diabetic cookbook. 1996, Alexandria, Va.: Time-Life Books. 96 p. from the editors of Time-Life Books.

81. Harmel, A.P., R. Mathur, and M.B. Davidson, Davidson's diabetes mellitus : diagnosis and treatment. 5th ed. 2004, Philadelphia, Pa.: W.B. Saunders. p. Diabetes mellitus

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98. Van Son, A.R., Diabetes and patient education : a daily nursing challenge. Appleton patient education series. 1982, New York: Appleton-Century-Crofts. xi, 210 p. Allene R. Van Son, editor.

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127. Gulledge, J., S. Beard, and Health and Administration Development Group (Aspen Publishers), Diabetes management : clinical pathways, guidelines, and patient education. Aspen chronic disease management series. 1999, Gaithersburg, Md.: Aspen Publishers. xvii, 306 p. Health & Administration Development Group ; Jo Gulledge, executive director ; Shawn Beard, research editor.

128. Peterson, C.M., Diabetes management in the '80s : the role of home blood glucose monitoring and new insulin delivery systems. 1982, New York, N.Y.: Praeger. xi, 328 p. edited by C.M. Peterson.

130. LeRoith, D., S.I. Taylor, and J.M. Olefsky, Diabetes mellitus : a fundamental and clinical text. 1996, Philadelphia: Lippincott-Raven. xx, 876 p. edited by Derek LeRoith, Simeon Taylor, Jerrold M. Olefsky ; with 176 additional contributors.

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133. Brownlee, M., L.M. Sherwood, and Medical Advisory Council (Merck Sharp & Dohme International), Diabetes mellitus and its complications : pathogenesis and treatment : Merck Sharp & Dohme International, Medical Advisory Council, Copenhagen, Denmark, September 18 and 19, 1989. 1990, Philadelphia: Hanley & Belfus. xvi, 300 p. editors, Michael Brownlee, Louis M. Sherwood.

134. Brodoff, B.N. and S.J. Bleicher, Diabetes mellitus and obesity. 1982, Baltimore: Williams & Wilkins. xvii, 816 p. editors, Bernard N. Brodoff, Sheldon J. Bleicher.

135. United States. Congress. House. Select Committee on Aging., Diabetes mellitus and older African Americans : a high price to pay : a report. 1993, Washington: U.S. G.P.O. : For sale by the U.S. G.P.O., Supt. of Docs., Congressional Sales Office. v, 31 p. by the chairman of the Select Committee on Aging, House of Representatives, One Hundred Second Congress, second session.

138. Tsuji, S., Diabetes mellitus in Asia, 1970; proceedings of a symposium, Kobe, Japan, 24 May 1970. International congress series 221. 1971, [Amsterdam]: Excerpta Medica. 258 p. Editors: S. Tsuji [and] M. Wada. Co-editors: C. N. Hales, G. M. Addison [and] P. Ghosh.

140. Reece, E.A. and D.R. Coustan, Diabetes mellitus in pregnancy. 2nd ed. 1995, New York: Churchill Livingstone. xx, 455 p., [2] p. of plates [edited by] E. Albert Reece, Donald R. Coustan.

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147. Petrides, P., Diabetes mellitus. 3., neubearb. Aufl. ed. 1976, Mčunchen ; Berlin ; Wien: Urban und Schwarzenberg. xiv, 158 p., [2] leaves of plates Platon Petrides ... [et al.].

148. Schnatz, J.D., Diabetes mellitus : problems in management. Clinical practice series. 1982, Menlo Park, Calif.: Addison-Wesley Pub. Co., Medical/Nursing Division edited by J. David Schnatz.

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150. Petrides, P., Diabetes mellitus : theory and management. 1978, Baltimore: Urban & Schwarzenberg. xii, 143 p. Platon Petrides ... [et al.] ; translated by Derek H. Williamson.

151. Ellenberg, M. and H. Rifkin, Diabetes mellitus : theory and practice. 3rd ed. 1983, New Hyde Park, N.Y.: Medical Examination Pub. Co. xx, 1105 p. edited by Max Ellenberg, Harold Rifkin.

154. Katzen, H.M. and R.J. Mahler, Diabetes, obesity, and vascular disease : metabolic and molecular interrelationships. Advances in modern nutrition ; v. 2. 1978, Washington

155. Market Intelligence Research Corporation., Diabetes product markets : product penetration increases with patient awareness. 1993, Mountain View, CA: Market Intelligence. 1 v. (various pagings) 29 cm. main themes: Diabetes treatment equipment industry United States.

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168. Diabetic cook book. 1st ed. 1992, Des Moines: Better Homes and Gardens Books. 112 p. col. ill. ; 29 cm.

169. Sunset Books., Diabetic cookbook. 1996, Menlo Park, CA: Sunset Pub. 112 p. by the editors of Sunset Books.

170. Publications International Ltd., Diabetic cooking. 2003, Lincolnwood, IL: Publications International. 384 p. col. ill. ; 23 cm.

171. Publications International Ltd., Diabetic cooking : delicious, light & easy. 1996, Lincolnwood, IL: Publications International. 128 p. col. ill. ; 26 cm.

172. Publications International Ltd., Diabetic desserts. 2002, Lincolnwood, IL: Publications International. 93 p. At head of title: Favorite brand name

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175. Levin, M.E. and L.W. O'Neal, The Diabetic foot. 3rd ed. 1983, St. Louis: Mosby. xvi, 397 p. edited by Marvin E. Levin, Lawrence W. O'Neal.

176. Levin, M.E., L.W. O'Neal, and J.H. Bowker, The Diabetic foot. 5th ed. 1992, St. Louis: Mosby Year Book. xxiv, 635 p., [12] p. of plates [edited by] Marvin E. Levin, Lawrence W. O'Neal, John H. Bowker.

178. Nagano, M. and N.S. Dhalla, The Diabetic heart. 1991, New York: Raven Press. xxv, 533 p. editors, Makoto Nagano, Naranjan S. Dhalla.

179. Friedman, E.A. and C.M. Peterson, Diabetic nephropathy : strategy for therapy. Developments in nephrology ; 9. 1986, Boston

180. Volk, B.W. and E.R. Arquilla, The Diabetic pancreas. 2nd ed. 1985, New York: Plenum Medical Book Co. xxiv, 628 p. edited by Bruno W. Volk and Edward R. Arquilla.

181. Volk, B.W. and K.F. Wellmann, The Diabetic pancreas. 1977, New York: Plenum Press. xviii, 599 p. edited by Bruno W. Volk and Klaus F. Wellmann.

182. Merkatz, I.R. and P.A.J. Adam, The Diabetic pregnancy : a perinatal perspective. 1979, New York: Grune & Stratton. xviii, 267 p., [4] leaves of plates edited by Irwin R. Merkatz, Peter A. J. Adam.

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202. Morsiani, M., Epidemiology and screening of diabetes. 1989, Boca Raton, Fla.: CRC Press. 282 p. editor, Mario Morsiani.

204. Lawrence, R.C., et al., Epidemiology of the rheumatic diseases : proceedings of the fourth international conference, National Institutes of Health. Current topics in rheumatology. 1984, New York: Gower Medical Pub. xvii, 381 p. [editors] Reva C. Lawrence, Lawrence E. Shulman.

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206. Tabor, E., et al., Etiology, pathology, and treatment of hepatocellular carcinoma. Advances in applied biotechnology series ; v. 13. 1991, Woodlands, Tex.

208. Gerstein, H.C. and R.B. Haynes, Evidence-based diabetes care. 2001, Hamilton, Ont. ; London: B C Decker. x, 573 p. editors, Hertzel C. Gerstein, R. Hrian Haynes.

210. McNeill, J.H., Experimental models of diabetes. 1999, Boca Raton, Fla.: CRC Press LLC. 418 p. edited by John H. McNeill.

211. Publications International Ltd., Favorite brand name diabetic recipes. 1998, Lincolnwood, Ill.: Publications International. 93 p. Diabetic recipes

212. Peterson, C.M., L. Jovanovic-Peterson, and B. Formby, Fetal islet transplantation. The language of science. 1995, New York: Plenum Press. x, 191 p. edited by Charles M. Peterson, Lois Jovanovic-Peterson, and Bent Formby.

216. Australia. Dept. of Health and Family Services. and Australian Institute of Health and Welfare., First report on national health priority areas 1996 : cardiovascular health, cancer control, injury prevention and control, mental health, diabetes mellitus. 1997, Canberra: Australian Institute of Health and Welfare & Commonwealth Dept. of Health & Family Services. vii, 193 p. 30 cm.

218. Boulton, A.J.M., H. Connor, and P.R. Cavanagh, The foot in diabetes. 2nd ed. 1994, Chichester ; New York ;: Wiley. ix, 256 edited by Andrew J.M. Boulton, Henry Connor, Peter Cavanagh.

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602. Caron, K.L. and A. Henry, The everyday meal planner for type 2 diabetics. 2002, Chicago: Contemporary Books. xiii, 178 p. Kristen L. Caron and Aaron Henry.

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604. Carter, A.R., Between a rock and a hard place. 1995, New York: Scholastic. 213 p.Although neither fifteen-year-old Mark Severson nor his diabetic cousin Randy are looking forward to the canoe trip that is a family rite of passage, they begin to enjoy themselves as they make their way through Minnesota's lake country, until the trip becomes a fight for survival. Alden R. Carter.

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620. Chantiles, V.L., Diabetic cooking from around the world. 1st ed. 1989, New York: Harper & Row. xvii, 343 p. Vilma Liacouras Chantiles.

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652. Cooper, N., The joy of snacks. 1987, Minnetonka, Minn.: Diabetes Center. ix, 269 p. Nancy Cooper.

653. Court, J.M., Helping your diabetic child. 1975, New York: Taplinger Pub. Co. 223 p. John M. Court.

654. Court, J.M., Your child has diabetes: a guide to parents and to their children who have diabetes. 1972, Sydney,: Ure Smith. 256 p. [by] John M. Court.

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656. Covelli, P., Borrowing time : growing up with juvenile diabetes. 1st ed. 1979, New York: Crowell. 160 p. Pat Covelli.

658. Craig, J., Jenny Craig diabetes cookbook : easy homestyle recipes for healthy living. 1997, Birmingham, Ala.: Oxmoor House. 368 p. Diabetes cookbook

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664. Cross, D. and A. Williams, Real food for people with diabetes. Revised 2nd ed. 2001, Roseville, Calif.: Prima Health. xxi, 293 p. Doris Cross with Alice Williams.

665. Cross, D. and A. Williams, Real food for people with diabetes. 1997, Rocklin, CA: Prima Pub. xx, 251 p. Doris Cross with Alice Williams.

666. Cross, D., Real Italian food for people with diabetes. 1999, Rocklin, CA: Prima Publishing. xv, 262 p. Doris Cross.

667. Cross, D., Real Mexican food for people with diabetes. 1998, Rocklin, CA: Prima Publishing. xiii, 270 p. Doris Cross.

668. Cull, J.G. and R.E. Hardy, Counseling and rehabilitating the diabetic. 1974, Springfield, Ill.,: Thomas. xi, 152 p. [edited by] John G. Cull [and] Richard E. Hardy.

670. Dacquino, V.T., Kiss the candy days good-bye. 1982, New York: Delacorte Press. 129 p.Seventh-grader Jimmy James needs the support of his family and friends when he learns that he has diabetes. V.T. Dacquino.

671. D'Adamo, P. and C. Whitney, Diabetes : fight it with the blood type diet. The eat right 4 your type library. 2004, New York: Putnam Peter J. D'Adamo with Catherine Whitney.

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679. Davidson, M.B., Diabetes mellitus, diagnosis and treatment. A Wiley medical publication. 1981, New York: Wiley. vii, 480 p. Mayer B. Davidson.

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688. Deutsche Diabetes-Gesellschaft., et al., Muskelstoffwechsel, kčorperliche Leistungsfčahigkeit und Diabetes mellitus : Theorie u. Praxis : 2. wissenschaftl. Arbeitstagung d. Dt. Diabetes-Ges. in Bad Neuenahr am 6. u. 7. November 1975. 1977, Stuttgart ; New York: Schattauer. xv, 336 p. hrsg. von K. Jahnke, H. Mehnert und H. E. Reis.

689. Deutsche Diabetes-Gesellschaft. Ausschuss Ernčahrung., Fett-Austausch-Tabelle fčur Diabetiker. 1970, Stuttgart,: G. Thieme. 11 p. Hrsg. vom Ausschuss Ernčahrung der Deutschen Diabetes-Gesellschaft.

690. Heidland, A., K.M. Koch, and E. Heidbreder, Diabetes and the kidney. 1989, Basel ; New York: Karger. 232 p. Dialysis-Workshop (24th : 1988 : Prien am Chiemsee, Germany)

691. Girard, M.-L., C. Laroche, and F. Rousselet, Biologie du diabáete. Probláemes actuels de biochimie appliquâee ; 7. sâer. 1974, Paris: Masson. vi, 207 p. Dimanches biologiques de Lariboisiáere (13th : 1973? : Paris, France)

694. Dolger, H. and B. Seeman, How to live with diabetes. 3d ed. 1971, New York,: Norton. 208 p. [by] Henry Dolger and Bernard Seeman.

695. Dolger, H. and B. Seeman, How to live with diabetes. [1st ed. 1958, New York,: W.W. Norton. 192 p. [by] Henry Dolger and Bernard Seeman.

696. Dolger, H. and B. Seeman, How to live with diabetes. 4th ed. 1978, New York: Schocken Books. 224 p. Henry Dolger and Bernard Seeman.

697. Dolger, H. and B. Seeman, How to live with diabetes. 4th ed. 1977, New York: Norton. 224 p. Henry Dolger and Bernard Seeman.

698. Dolger, H. and B. Seeman, How to live with diabetes. 5th ed. 1985, New York: Norton. 204 p. Henry Dolger, Bernard Seeman.

699. Dominick, A., Needles. 1998, New York: Scribner. 220 p. Andie Dominick.

702. Dorian, C.R. and M. Shifrine, I have diabetes, too! : Molly's story. 2003, North Bergen, NJ: Basic Health Pub. xi, 132 p.Information about the symptoms and treatment of Type 1 and Type 2 diabetes, along with discussion of exercise, eating plans, and more are presented from the perspective of Molly, a monkey with insujlin-dependent diabetes. Camille R. Dorian & Moshe Shifrine.

703. Douglas, L.A., Cooking for the wayward diabetic. 2nd ed. 1971, London,: Faber and Faber Ltd. 109 p. [by] Lily Macleod.

704. Dranov, P., Diabetes : a Random House personal medical handbook. 1st ed. 1990, New York: Random House. xliv, 162 p. Paula Dranov with a foreword by Lois Jovanovic-Peterson.

710. Drum, D.E. and T. Zierenberg, The type II diabetes sourcebook. 1997, Los Angeles

711. Ducat, L. and S.S. Cohen, Diabetes, a new & complete guide to healthier living for parents, children & young adults with insulin-dependent diabetes. 1st ed. 1983, New York: Harper & Row. xv, 253 p. by Lee Ducat & Sherry Suib Cohen.

712. Duncan, T.G., The diabetes fact book. 1982, New York: C. Scribner. xi, 146 p. Theodore G. Duncan.

714. Dunning, T., Care of people with diabetes : a manual of nursing practice. 1994, Oxford ; Boston: Blackwell Scientific Publications. xviii, 188 p. Trisha Dunning.

715. Eagles, D.A., Nutritional diseases. 1987, New York: F. Watts. 96 p.Explains the development, symptoms, treatment, and possible prevention of such diseases as osteoporosis, arteriosclerosis, phenylketonuria, and diabetes, as well as conditions such as anorexia and bulemia, which are the result of inadequate nutrition. Douglas A. Eagles.

716. Edelman, S.V. and R.R. Henry, Diagnosis and management of type 2 diabetes. 4th ed. 2001, [Caddo, Okla.]: Professional Communications, Inc. 256 p. Steven V. Edelman, Robert R. Henry.

717. Edelman, S.V., Taking control of your diabetes. 2000, Caddo, Okla.: Professional Communications, Inc. 272 p. Steven V. Edelman.

718. Edelwich, J. and A. Brodsky, Diabetes : caring for your emotions as well as your health. Rev. ed. 1998, Reading, Mass.: Perseus Books. xii, 317 p. Jerry Edelwich, Archie Brodsky ; foreword by Ronald A. Arky.

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959. Jones, J., The calculating cook; a gourmet cookbook for diabetics & dieters. 1972, San Francisco,: 101 Productions; [distributed by Scribner. 192 p. Drawings by Holly Zapp.

960. Jones, J., More calculated cooking. 1981, San Francisco

961. Jorgensen, C.D. and J.E. Lewis, The ABCs of diabetes. 1979, New York: Crown. xii, 305 p. by Caryl Dow Jorgensen and John E. Lewis.

962. Aznar Reig, A. and Seville. Universidad. Escuela de Endocrinologâia., Obesidad y diabetes mellitus : primeras Jornadas Endocrinolâogicas de Sevilla (29-30 de octubre de 1973). 1974, [Sevilla]: Universidad de Sevilla. 298 p. Jornadas Endocrinolâogicas de Sevilla, 1973.

963. Joslin, E.P., C.R. Kahn, and G.C. Weir, Joslin's diabetes mellitus. 13th ed. 1994, Philadelphia: Lea & Febiger. xix, 1068 p. edited by C. Ronald Kahn, Gordon C. Weir.

964. Joslin, E.P., Joslin's Diabetes mellitus. 12th ed. 1985, Philadelphia: Lea & Febiger. xvi, 1007 p. ill. ; 27 cm. main themes: Diabetes.

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968. Jovanovic-Peterson, L., C.M. Peterson, and M.B. Stone, A touch of diabetes : a guide for people who have type II, noninsulin-dependent diabetes. 1991, Minneapolis, MN: DCI Pub. viii, 126 p. Lois Jovanovic-Peterson, Charles M. Peterson & Morton B. Stone.

970. Jovanovic-Peterson, L., C.M. Peterson, and M.B. Stone, A touch of diabetes. Rev. & expanded ed. 1995, Minneapolis, MN: Chronimed Pub. viii, 144 p. Lois Jovanovic-Peterson, Charles M. Peterson, and Morton B. Stone.

972. Juliano, J. and D. Young, The diabetic's innovative cookbook : a positive approach to living with diabetes. 1st ed. 1994, New York: H. Holt. xv, 416 p. Joseph Juliano and Dianne Young.

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978. Kamoshida, K., Tĺonyĺo rettĺo : "10-nin ni hitori no yamai" no mokushiroku. 1991, Tĺokyĺo: Jĺohĺo Sentĺa Shuppankyoku. 221 p. Kamoshida Keiichi.

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982. Kaplan, D.J., The comprehensive diabetic cookbook. 1972, New York,: F. Fell. 211 p. by Dorothy J. Kaplan. With a foreword by Robert Kaye.

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990. Kelly, P., Coping with diabetes. 1st ed. Coping. 1998, New York: Rosen Pub. Group. 145 p.Discusses the types and causes of diabetes, how the disease is diagnosed and treated, and ways of managing this condition and its impact on your life. Pat Kelly.

991. Kelnar, C., Childhood and adolescent diabetes. 1994, New York, NY: Chapman & Hall Medical. p. C. Kelnar.

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993. Kendrick, J.M., et al., Diabetes in pregnancy. 2nd ed. 1998, White Plains, NY: Education Services Dept., March of Dimes Jo M. Kendrick ; editor, Lynn G. Wellman ; consulting editor, Margaret Comerford Freda.

994. Khachadurian, A.K. and S.H. Schneider, Diabetes & metabolic diseases : modern directions in therapy. 1982, Garden City, N.Y.: Medical Examination Pub. Co. vii, 157 p. Avedis K. Khachadurian, Stephen H. Schneider.

997. Kipnis, L., S. Adler, and R. Benkof, You can't catch diabetes from a friend. 1979, Gainesville, Fla.: Triad Scientific Publishers. 63 p.Relates daily experiences of four children who have diabetes. by Lynne Kipnis and Susan Adler ; photos. by Richard Benkof.

1003. Kokkonen, J., Lasten mahalaukun toiminnalliset hčairičot : tutkimus ohutsuoliperčaistča malabsorptiota, atopiaa, diabetesta ja Sjčogrenin syndroomaa sairastavien lasten mahalaukun erityistoiminnasta ja morfologiasta = Gastric function disorders in children : a study on gastric secretory function and morphology in children with malabsorption, atopy, diabetes mellitus and Sjčogren's syndrome. 1980, Oulu: Oulun yliopiston lastentautien klinikka. 49, [45] p. Jorma Kokken.

1005. Komogorëtěseva, E.G., Vliëiěanie çekologicheskikh faktorov na razvitie i techenie gestaëtěsionnogo sakharnogo diabeta. 2001, Irkutsk: RIO GIUVa. 103 p. Komogorëtěseva E.G.

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1034. Ley, B.M., Medicinal mushrooms for immune enhancement : agaricus blazei murill : discover the beta glucan secret!. [Rev. and updated 2nd ed. A health learning handbook. 2001, Detroit Lakes, MN: BL Publications. 39 p. Beth M. Ley.

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1038. Little, B. and C.J. Bellamy, Recipes for diabetics. Rev. and updated Perigee ed. 1999, New York: Perigee Book. xv, 271 p. Billie Little ; preface by Selvyn B. Bleifer ; revised by Candace J. Bellamy.

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1046. Lodewick, P.A., J. Biermann, and B. Toohey, The diabetic man : a guide to health and success in all areas of your life : with advice, empathy, and support for those who have a diabetic man in their lives. 3rd ed. 1999, Los Angeles

1047. Lodewick, P.A., J. Biermann, and B. Toohey, The diabetic man : a guide to health and success in all areas of your life : with advice, empathy, and support for those who have a diabetic man in their lives. 1992, Los Angeles

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1062. Ludi, M.A. and N.R. Hull, Balance your act : a book for adults with diabetes. 1990, Atlanta, GA: Pritchett & Hull Associates. 96 p. by Maria Alogna Ludi, Nancy Hull.

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1069. Ma, K.M. and American Dietetic Association. Diabetes Care and Education Dietetic Practice Group., Chinese American food practices, customs, and holidays. Ethnic and regional food practices--a series. 1990, Chicago, Ill.

1070. MacCracken, J., The sun, the rain, and the insulin : growing up with diabetes. 1996, Orono, Me.: Tiffin Press of Maine. xx, 250 p. Joan MacCracken.

1071. MacRae, N.M., Canning and preserving without sugar. 2nd ed. 1988, Chester, Conn.: Globe Pequot Press. 230 p. by Norma M. MacRae.

1079. Marks, B. and L.H. Schechter, The international menu diabetic cookbook. 1985, Chicago: Contemporary Books. xx, 364 p. [Betty Marks and Lucille Haley Schechter].

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1082. Marquis, K.H., J.E. Ware, and Center for Disease Control., Measures of diabetic patient knowledge, attitudes, and behavior regarding self-care : summary report. 1979, Santa Monica, CA: Rand. xi, 43 p. prepared for the Center for Disease Control, U.S. Department of Health, Education, and Welfare [by] Kent H. Marquis, John E. Ware, Jr.

1084. Martin, A.M., The truth about Stacey. 1995, Milwaukee, Wis.: Gareth Stevens Pub. 167 p. (large print).Stacey, a member of the Baby-sitters Club, struggles with her parents who refuse to believe that she has diabetes. Ann M. Martin.

1088. Mayer, A.M. and H. Henriksen, Sir Frederick Banting, doctor against diabetes. 1974, Mankato, Minn.,: Creative Education; [distributed by Childrens Press, Chicago. 36 p.Recounts the life of the Canadian doctor who discovered the means of keeping the once fatal disease of diabetes under control. Illustrated by Harold Henriksen.

1090. Maynard, K., et al., Cooking for diabetics. 1989, Nashville, Tenn.: Rutledge Hill Press. vi, 229 p., [16] p. of plates Kitty E. Maynard, Lucian Maynard, Theodore G. Duncan ; Julia M. Pitkin, editor.

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1095. McDaniel, L.V., et al., Selected medical disabilities; a programmed text for allied health service trainees. 1973, Thorofare, N.J.,: C. B. Slack. xiii, 102 p. edited by Lucy V. McDaniel. Contributors: Kay Cerny, Kathy M. McIntosh [and] Jane D. Lightfoot. Illustrated by Ursula Wolf-Rottkay.

1096. McFarland, K.F. and E.D. Bransome, Self-assessment of current knowledge in clinical endocrinology, metabolism, and diabetes : 1,004 multiple choice questions and referenced answers. 1975, Flushing, N.Y.: Medical Examination Pub. Co. 137 p. by Kay F. McFarland, Edwin D. Bransome, Jr.

1098. McIntosh, C.S., Coming to terms with diabetes. 1986, Poole ; New York

1099. Meggs, W.J. and C. Svec, The inflammation cure : how to combat the hidden factor behind heart disease, arthritis, asthma, diabetes, Alzheimer's disease, osteoporosis, and other diseases of aging. 2004, Chicago: Contemporary Books. xvi, 238 p. William Joel Meggs with Carol Svec.

1100. Mehnert, H., Diabetes : eine lebenslange Herausforderung. Ecomed Biographien. 2000, Landsberg: Ecomed. 352 p. Hellmut Mehnert.

1102. Meirelles, J., Diabetes is not a piece of cake : prescribed for family, friends & co-workers of folks with diabetes. Rev. 3rd ed. 1997, Lake Oswego, Or.: Lincoln Pub. vi, 282 p. by Janet Meirelles ; foreword by Andrew J. Ahmann ; illustrated by Lee Wright.

1104. Miall, L., M. Rudolf, and M.I. Levene, Paediatrics at a glance. 2002, Malden, Mass.: Blackwell Science. p. Lawrence Miall, Mary Rudolf, Malcolm Levene.

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1106. Klachko, D.M. and University of Missouri--Columbia. College of Agriculture., The endocrine pancreas and juvenile diabetes. Advances in experimental medicine and biology ; v. 124. 1979, New York: Plenum Press. xiv, 205 p. Midwest Conference on Endocrinology and Metabolism, University of Missouri--Columbia, 1977.

1107. Milchovich, S.K. and B. Dunn-Long, Diabetes mellitus : a practical handbook. 5th ed. 1990, Palo Alto, CA

1108. Milchovich, S.K. and B. Dunn-Long, Diabetes mellitus : a practical handbook. 7th ed. 1999, Palo Alto, Calif.

1109. Milchovich, S.K. and B. Dunn-Long, Diabetes mellitus : a practical handbook. 6th ed. 1995, Palo Alto, Calif.

1110. Milchovich, S.K. and B. Dunn-Long, Diabetes mellitus : practical handbook. 8th ed. 2003, Boulder, CO: Bull Pub. Sue K. Milchovich, and Barbara Dunn-Long. main themes: Diabetes Handbooks, manuals, etc.

1113. Mirsky, S. and J.R. Heilman, Diabetes--controlling it the easy way. 1st ed. 1982, New York: Random House. 244 p. Stanley Mirsky and Joan Rattner Heilman.

1114. Mitchell, D.R., Natural medicine for diabetes. The Dell natural medicine library. 1997, New York, N.Y.: Dell. xiv, 273 p. Deborah R. Mitchell ; foreward by Gabriel Cousens.

1115. Moe, B.A., Coping with chronic illness. Coping. 1992, New York: Rosen Pub. Group. 177 p.Discusses chronic illness and its problems, with specific chapters on asthma, diabetes, epilepsy, cancer, cystic fibrosis, sickle cell anemia, and stress. Barbara Moe.

1118. Monk, A., Convenience food facts : help for planning quick, healthy, and convenient meals. Rev. & expanded, 3rd ed. Wellness & nutrition library. 1991, Minneapolis, Minn.: DCI/Chronimed Pub. 457 p. Arlene Monk with INTRODUCTION by Marion J. Franz.

1122. Montoro Marâin Pedro., La diabetes y su control. 1973, Murcia: [Tip. San Francisco]. 227 p. illus. main themes:

1124. Moser, M. and J.R. Sowers, Clinical management of cardiovascular risk factors in diabetes. 1st ed. 2002, Caddo, OK: Professional Communications. 240 p. Marvin Moser and James R. Sowers.

1128. Muhammad, K.A., Obesity, diabetes & how to eat to live. 2nd ed. 2002, Newark, DE: TechDoc. p. Kevin A. Muhammad.

1129. Mukherjee, S.K., et al., Progress of diabetes research in India during 20th century. 1st ed. 2002, New Delhi: National Institute of Science Communication. vi, 105 p. S.K. Mukherjee, A.M. Saxena, G. Shukla ; editors, Gian Singh, T.K. Mukherjee.

1133. Murray, M.T. and M.R. Lyon, How to prevent and treat diabetes with natural medicine. 2004, New York: Riverhead Books by Michael T. Murray, Michael R. Lyon. main themes: Diabetes Alternative treatment.

1134. Nagy, J. and L. Somogyi, A cukorbetegsâeg diâetâas âetrendjei âes az âetelek elkâeszâitâesi mâodjai. 5. kiad. ed. 1977, Budapest: Medicina. 221 p. Nagy Jâozsefnâe, Somogyi Lâaszlâonâe.

1135. Nala, N., Usada kencing manis. Cet. 1. ed. 1996, Denpasar: Upada Sastra. ix, 104 p.Selected medicinal plants as remedy against diabetes mellitus according to Balinese Hinduism. [Ngurah Nala].

1138. Connor, H., A.J.M. Boulton, and J.D. Ward, The foot in diabetes : proceedings of the 1st National Conference on the Diabetic Foot, Malvern, May 1986. A Wiley medical publication. 1987, Chichester ; New York: Wiley. xiii, 168 p. National Conference on the Diabetic Foot (1st : 1986 : Malvern, Worcestershire)

1140. Natow, A.B. and J.-A. Heslin, The diabetes carbohydrate & calorie counter. 1991, New York: Pocket Books. xvi, 265 p. Annette B. Natow and Jo-Ann Heslin.

1142. Nelson, B.L., M. Hippen, and J. Ewan, A diabetic party cookbook. 1979, Sarasota, FL: Booklore Publishers. xiii, 220 p. by the 3 aunts, Betty Lou Nelson, Margaret Hippen, Jane Ewan.

1143. Nemanic, A., et al., Diabetes care made easy : a simple step-by-step guide for controlling your diabetes. 1992, Minneapolis: Chronimed Pub. 155 p.Describes how diabetics can care for themselves, discussing how to take insulin, what foods to eat or avoid, and what exercises to do. Allison Nemanic, Gretchen Kauth, Marion J. Franz ; illustrated by Jan Westberg.

1145. Baynes, J.W. and V.M. Monnier, The Maillard reaction in aging, diabetes, and nutrition : proceedings of an NIH Conference on the Maillard Reaction in Aging, Diabetes, and Nutrition, held in Bethesda, Maryland, September 22-23, 1988. Progress in clinical and biological research ; v. 304. 1989, New York: A.R. Liss. xxii, 410 p. NIH Conference on the Maillard Reaction in Aging, Diabetes, and Nutrition (1988 : Bethesda, Md.)

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1151. Oakley, W.G., D.A. Pyke, and K.W. Taylor, Diabetes and its management. 2nd ed. 1975, Oxford: Blackwell Scientific. viii, 203 p., [4] p. of plates [by] W. G. Oakley, D. A. Pyke, K. W. Taylor.

1152. O'Brien, C.J., A joyful diabetic for thirty five years. 1st ed. 1983, Great Neck, N.Y.: Todd & Honeywell. 62 p. Charles J. O'Brien.

1153. Oexmann, M.J., TAG : a diabetic food system. 1st ed. 1989, New York: W. Morrow. 190 p. Mary Joan Oexmann.

1156. Olson, M. and S. Olson, How I feel : a book about diabetes. 2002, New York: Lantern Books.The author describes his younger brother's experiences finding out that he had diabetes and learning to live with this condition. written and illustrated by Michael Olson, as told by Steven Olson. main themes: Olson, Steven Health

1158. Olson, O.C., Diagnosis and management of diabetes mellitus. 2nd ed. 1988, New York: Raven Press. xviii, 333 p. O. Charles Olson.

1159. O'Neill, L., Having diabetes. 2001, Vero Beach, FL: Rourke Press. 32 p.Discusses the causes and effects of diabetes and ways to control the disease. Linda O'Neill.

1160. O'Reilly, E. and British Diabetic Association., Measure for measure; calorie and carbohydrate controlled recipes. 1973, London,: Heinemann. xiv, 127 p. compiled by Elizabeth O'Reilly [for the British Diabetic Association]

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1162. Otto, H. and L. Niklas, Die Betreuung des Diabetikers in der Praxis. 1. Aufl. ed. 1976, Stuttgart: Fischer. x, 147 p. von Hellmut Otto u. Lothar Niklas.

1164. Owens, D.R., Human insulin : clinical pharmacological studies in normal man. 1986, Lancaster ; Boston: MTP Press. x, 297 p. D.R. Owens.

1166. Palumbo, P.J. and J.D. Margie, The all-in-one diabetic cookbook. 1987, New York: Plume. x, 357 p. P.J. Palumbo and Joyce Daly Margie ; with recipes for young cooks by Paul Margie.

1167. Palumbo, P.J. and J.D. Margie, The complete diabetic cookbook. 1987, New York, N.Y.: New American Library by P.J. Palumbo and Joyce Daly Margie.

1168. Paul, S. and D.P. Orchanian, PocketGuide to assessment in occupational therapy. 2003, Clifton Park, NY: Delmar Learning. ix, 238 p. Stanley Paul, David P. Orchanian.

1169. Pavy, F.W., Researches on the nature and treatment of diabetes. 1977, Oceanside, N.Y.: Dabor Science Publications. [6], ix, 210 p. F.W. Pavy ; with an introd. by Lawrence A. May.

1170. Peacock, C.A., et al., Sugar was my best food : diabetes and me. 1998, Morton Grove, Ill.: Whitman. 55 p.An eleven-year-old boy describes how he learned that he had diabetes, the effect of this disease on his life, and how he learned to cope with the changes in his life. Carol Antoinette Peacock, Adair Gregory, and Kyle Carney Gregory ; illustrated by Mary Jones.

1172. Pedersen, J.r., The pregnant diabetic and her newborn : problems and management. 2d ed. 1977, Copenhagen

1173. Pelican, S., K. Bachman-Carter, and American Dietetic Association. Diabetes Care and Education Dietetic Practice Group., Navajo food practices, customs, and holidays. Ethnic and regional food practices--a series. 1991, Chicago, Ill.

1174. Perikos, G., The Chios gum mastic : a unique worldwide natural product aids diabetes, ulcers, cholesterol, high blood pressure, has anticancer properties, strengthens the immunisation system. 1993, Greece: J. Perikos. 95 p. John Perikos.

1176. Peterson, C.M. and L. Jovanovic-Peterson, The diabetes self-care method : the breakthrough program of self-management that will help you lead a better, freer, more normal life. 1990, Los Angeles

1177. Peterson, C.M. and L. Jovanovic-Peterson, The diabetes self-care method : the breakthrough program of self-management that will help you lead a healthier life. 3rd ed. 1998, Los Angeles: Lowell House. x, 166 p. Charles M. Peterson and Lois Jovanovic.

1181. Philpott, W.H. and D.K. Kalita, Victory over diabetes : a bio-ecologic triumph. 1983, New Canaan, Conn.: Keats Pub. 294 p. William H. Philpott and Dwight K. Kalita ; INTRODUCTION by W.D. Currier.

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1196. Power, L., D.L. Bakker, and M.I. Cooper, Diabetes outpatient care through physician assistants; a model for health maintenance organizations. 1973, Springfield,: C. C. Thomas. xi, 101 p. by Lawrence Power, Doris L. Bakker [and] Marilyn I. Cooper.

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1200. Prince, F. and Gourmet recipes for diabetics., Francine Prince's Gourmet recipes for diabetics. 1983, New York: Cornerstone Library. 189 p. with a foreword by Martin Feldman.

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1207. Rapetti, A., Crescere con il diabete : il vissuto di cronicitáa in etáa evolutiva. 1989, Roma: Bulzoni. 222 p. Alessandra Rapetti ; con la collaborazione di G. Aurisicchio e G. Spagna ; presentazione di Adriano Ossicini.

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1234. Rubin, A.L., F. Stach, and D.C. Sharf, Diabetes cookbook for dummies. 2000, Foster City, CA: IDG Books Worldwide. 375 p. by Alan L. Rubin, with Fran Stach and Denise C. Sharf.

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1394. Zosel, R.J., Diabetes: an emotional journey. 2004, Covington, WA: Zay Pub. p. Renea Jo Zosel.

Brem, H., T. Jacobs, et al. (2003). "Wound-healing protocols for diabetic foot and pressure ulcers." Surg Technol Int 11: 85-92.
Diabetic foot and pressure ulcers are chronic wounds by definition. They share similar pathogeneses; i.e., a combination of increased pressure and decreased angiogenic response. Neuropathy, trauma, and deformity also often contribute to development of both types of ulcers. Early intervention and proper treatment should result in complete healing of non-ischemic diabetic foot and pressure ulcers, as defined by 100% epithelialization and no drainage (if no osteomyelitis is present). The authors developed the following paradigm, which has proved to be highly effective for complete healing of these wounds: 1) recognition that all patients with limited mobility are at risk for a sacral, ischial, trochanteric, or heel pressure ulcer; 2) daily self-examination of the sacral, ischium, buttocks hips, and heels of all bed-bound patients and the feet of patients with diabetes with risk factors (e.g., neuropathy); 3) initiation of a treatment protocol immediately upon recognition of a break in the skin (i.e., emergence of a new wound); 4) objective measurement by planimetry of every wound (at a minimum, weekly) and documentation of its progress; 5) establishment of a moist wound-healing environment; 6) relief of pressure from the wound; 7) debridement of all non-viable tissue in the wound; 8) elimination of all drainage and cellulitis; 9) cellular therapy or growth factors for patients with wounds that do not heal rapidly after initial treatment; and 10) continuous physical and psychosocial support for all patients. If this paradigm is followed, most diabetic foot and pressure ulcers are expected to heal.

Brigstock, D. R. (2003). "The CCN family: a new stimulus package." J Endocrinol 178(2): 169-75.
The CCN family comprises cysteine-rich 61 (CYR61/CCN1), connective tIssue growth factor (CTGF/CCN2), nephroblastoma overexpressed (NOV/CCN3), and Wnt-induced secreted proteins-1 (WISP-1/CCN4), -2 (WISP-2/CCN5) and -3 (WISP-3/CCN6). These proteins stimulate mitosis, adhesion, apoptosis, extracellular matrix production, growth arrest and migration of multiple cell types. Many of these activities probably occur through the ability of CCN proteins to bind and activate cell surface integrins. Accumulating evidence supports a role for these factors in endocrine pathways and endocrine-related processes. To illustrate the broad role played by the CCN family in basic and clinical endocrinology, this Article highlights the relationship between CCN proteins and hormone action, skeletal growth, placental angiogenesis, IGF-binding proteins and diabetes-induced fibrosis.

Brodsky, S. V., M. Smith, et al. (2003). "A model for ex vivo renal angiogenesis." Nephron Exp Nephrol 93(1): e46-52.
Attempts to study renal angiogenesis have been hampered by the lack of an appropriate model. Here we present data on a successful ex vivo culture of renal medullary explants in three-dimensional collagen 1 or Matrigel lattices and characterize the dynamics of capillary formation by sprouting endothelial cells. Initially, endothelial cells represented 71 +/- 3% among the sprouting cells, but within a week growing capillaries were comprised exclusively of endothelial cells. The quantitative analysis showed that the number of sprouting capillaries progressively increased until 12 days in culture, after which capillaries underwent involution. Occasional formation of glomeruloid bodies was noted. Capillaries were characterized by a well-defined lumen, whereas glomeruloid bodies showed cellular debris occupying the luminal space. In view of the existing controversy regarding angiogenic competence in diabetic nephropathy, we applied this ex vivo culture system to Zucker diabetic rat model of diabetes mellitus. Comparative analysis of capillary sprouting in Zucker diabetic fat and lean nondiabetic control rats showed no differences in angiogenic properties of renal explants obtained at the age of 11 weeks. However, when kidneys were obtained from rats at age of 21 weeks, the capillary sprouting was significantly reduced in Zucker diabetic rats compared to age-matched lean rats. The rate of capillary involution was unaffected in Zucker diabetic rats. In CONCLUSION , the data presented herein delineate the first successful ex vivo model of angiogenesis initiated from the renal medullary explants of adult rats and provide evidence of impaired angiogenesis in Zucker diabetic rats with the established, but not with incipient diabetes mellitus.

Cai, J., S. Ahmad, et al. (2003). "Activation of Vascular Endothelial Growth Factor Receptor-1 Sustains Angiogenesis and Bcl-2 Expression Via the Phosphatidylinositol 3-Kinase Pathway in Endothelial Cells." Diabetes 52(12): 2959-2968.
Vascular insufficiency and retinal ischemia precede many proliferative retinopathies and stimulate secretion of various vasoactive growth factors, including vascular endothelial growth factor (VEGF) and placenta growth factor (PlGF). It is unclear, however, how PlGF, which is elevated in proliferative diabetic retinopathy and is a VEGF homolog that binds only to VEGF receptor (VEGFR)-1, promotes pathological angiogenesis. When primary microvascular endothelial cells were grown on collagen gels, PlGF-containing ligands upregulated Bcl-2 expression and stimulated the formation of capillary-like tube networks that were retained for up to 14 days in culture. The inhibition of VEGFR-1 RESULTS in a dramatic decrease in the number of capillary connections, indicating that VEGFR-1 ligands promote branching angiogenesis. In contrast, VEGF-induced tube formations and Bcl-2 expression were significantly decreased at the end of this period. Flow cytometry analysis of annexin-V/propidium iodide-stained cells revealed that PlGF and PlGF/VEGF heterodimer inhibited apoptosis in serum-deprived endothelial cells. These two growth factors stimulated a survival signaling pathway phosphatidylinositol 3-kinase (PI3K), as identified by increased Akt phosphorylation and because blocking PI3K signalling by adenovirus-mediated overexpression of wild-type phosphatase and tensin homolog on chromosome 10 (PTEN) disrupted angiogenesis and decreased Bcl-2 expression by PlGF and PlGF/VEGF heterodimer, whereas a dominant-negative PTEN mutant enhanced endothelial sprout formation and Bcl-2 expression. Together, these findings indicate that PlGF-containing ligands contribute to pathological angiogenesis by prolonging cell survival signals and maintaining vascular networks.

Dandona, P., A. Aljada, et al. (2003). "Insulin suppresses plasma concentration of vascular endothelial growth factor and matrix metalloproteinase-9." Diabetes Care 26(12): 3310-4.
OBJECTIVE: We recently demonstrated a potent anti-inflammatory and thus a potential antiatherogenic effect of insulin in human aortic endothelial cells and mononuclear cells at physiologically relevant concentrations. We have now further investigated the anti-inflammatory suppressive action of insulin on vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-9. VEGF and MMP-9 play a central regulatory role in angiogenesis, contribute to the pathogenesis of proliferative retinopathy, and have also been found to accelerate atherosclerosis. RESEARCH DESIGN AND METHODS: Insulin was infused (2 IU/h) in 5% dextrose (100 ml/h) and KCl (8 mmol/h) into 10 fasting, obese, nondiabetic subjects for 4 h. Subjects were also infused with 5% dextrose without insulin and with saline on two separate occasions. Blood samples were obtained at 0, 2, 4, and 6 h. RESULTS : Plasma insulin concentrations increased from a basal level of 12.5 +/- 2.2 to 28.2 +/- 3.3 micro U/ml at 2 h and 24.4 +/- 3.7 micro U/ml at 4 h after insulin infusion. VEGF concentration decreased from 307.2 +/- 163.8 pg/ml (100%) at 0 h to 73.5 +/- 20.9% of the basal level at 2 h and 67.1 +/- 23.2% at 4h. Plasma MMP-9 concentrations decreased from 375 +/- 196.3 ng/ml (100%) at 0 h to 83 +/- 22% of the basal level at 2 h and to 82 +/- 21% of the basal level at 4 h (P < 0.05). Dextrose infusion alone did not change plasma VEGF concentration. However, plasma MMP-9 concentration increased significantly at 4 h following dextrose infusion alone (P < 0.05). Saline infusions without insulin caused no alteration in glucose, insulin, VEGF, or MMP-9. CONCLUSION S: These observations may have implications for a potential antiretinopathic and antiatherosclerotic effect of insulin in the long term.

Dzau, V. J. (2003). "Predicting the future of human gene therapy for cardiovascular diseases: what will the management of coronary artery disease be like in 2005 and 2010?" Am J Cardiol 92(9B): 32N-35N.
Gene therapy is the use of gene delivery as a means to achieve high levels of the therapeutic gene product (ie, "drug" delivery) to treat acquired cardiovascular diseases. Human gene therapy for cardiovascular disease is expected to provide important advances in therapeutic angiogenesis, myocardial protection, myocardial regeneration and repair, restenosis, prevention of bypass graft failure, and risk-factor management. The data from ongoing phase 2 and future phase 3 studies will provide evidence to show whether therapeutic angiogenesis is effective, and these studies will identify the types of patients who may benefit. An important therapeutic target is the cell cycle. Data from the Project in Ex-Vivo Vein Graft Engineering via Transfection (PREVENT) I and II studies suggest that a synthetic DNA decoy can sequester the E2F family of transcription factors and arrest cells at the gap period (G1) checkpoint. This mechanism prevents intimal hyperplasia, which is associated with atherosclerosis and coronary graft failure. Administration of a myocardial protective gene (eg, heme oxygenase) via a recombinant adeno-associated virus vector reduces infarct size in animal models of ischemia and reperfusion. Other studies have shown that fractionated bone marrow stem cells promote myocardial repair and regeneration in myocardial infarction. If applied in humans, it will be possible to use a single administration of gene therapy to provide long-term prophylaxis against secondary coronary events and to promote myocardial repair in patients who have experienced an infarct, as well as in those at high risk of myocardial injury. In the future, new technology using stable gene integration may lead to the development of more effective and lifelong therapy for diabetes, familial homozygous hypercholesterolemia, and other acquired diseases.

Emanuelia, C. and P. Madeddu (2003). "Human tissue kallikrein: a new bullet for the treatment of ischemia." Curr Pharm Des 9(7): 589-97.
Recently, therapeutic angiogenesis has been proposed as an alternative for the treatment of ischemic diseases unresponsive to conventional therapy. This strategy is based on the concept that a supply-side approach with growth factors would overcome the endogenous deficit and result in more robust collateralization. We have developed a strategy based on local delivery of human tissue kallikrein gene for potentiation of microcirculation and rescue of peripheral ischemia. Following successful application in otherwise healthy animals, the approach resulted to be of therapeutic value in rats with endothelial dysfunction caused by arterial hypertension. In addition, human tissue kallikrein prevents or rescues microvascular rarefaction caused by diabetes mellitus. In this model, human tissue kallikrein was able to stimulate vascular growth and contrast apoptosis. The strategy displays interesting pharmacological features because is devoid of obvious side effects and is effective even at low infecting doses. In addition, the neovascularization promoted by human tissue kallikrein is well organized and durable. It is reasonable to anticipate that the new approach will have a great impact in the treatment of cardiovascular ischemic complications.

Favot, L., T. Keravis, et al. (2003). "VEGF-induced HUVEC migration and proliferation are decreased by PDE2 and PDE4 inhibitors." Thromb Haemost 90(2): 334-43.
Migration and proliferation of endothelial cells in response to VEGF play an important role in angiogenesis associated to pathologies such as atherosclerosis, diabetes and tumor development. Elevation of cAMP in endothelial cells has been shown to inhibit growth factor-induced proliferation. Our hypothesis was that inactivation of cAMP-specific phosphodiesterases (PDEs) would inhibit angiogenesis. The purpose of this study was to evaluate the effect of PDE inhibitors on in vitro and in vivo angiogenesis, using human umbilical vein endothelial cell (HUVEC) and chick chorioallantoic membrane (CAM) models respectively. Here, we report that: 1) PDE2, PDE3, PDE4 and PDE5 are expressed in HUVEC; 2) EHNA (20 microM), PDE2 selective inhibitor, and RP73401 (10 microM), PDE4 selective inhibitor, are able to increase the intracellular cAMP level in HUVEC; 3) EHNA and RP73401 are able to inhibit proliferation, cell cycle progression and migration of HUVEC stimulated by VEGF; 4) these in vitro effects can be mimic by treating HUVEC with the cAMP analogue, 8-Br-cAMP (600 microM); 5) only the association of EHNA and RP73401 inhibits in vivo angiogenesis, indicating that both migration and proliferation must be inhibited. These data strongly suggest that PDE2 and PDE4 represent new potential therapeutic targets in pathological angiogenesis.

Felmeden, D. C., C. G. Spencer, et al. (2003). "Relation of thrombogenesis in systemic hypertension to angiogenesis and endothelial damage/dysfunction (a substudy of the Anglo-Scandinavian Cardiac Outcomes Trial [ASCOT])." Am J Cardiol 92(4): 400-5.
Increasing evidence points toward a prothrombotic state in hypertension and atherosclerosis, conditions associated with thrombosis-related complications, such as myocardial infarction and stroke. We hypothesized that this increased risk of thrombogenesis may be related to endothelial damage/dysfunction and abnormal angiogenesis, and thus, an increased risk of future cardiovascular disease. Thrombogenesis, endothelial damage/dysfunction, and angiogenesis can be assessed by measurement of tissue factor (TF), von Willebrand Factor (vWF), flow-mediated dilatation (FMD), and vascular endothelial growth factor (VEGF), respectively. To test this hypothesis, we measured TF, vWF, FMD, and VEGF in 76 patients with systemic hypertension (71 men; mean age 64; mean blood pressure 167/72 mm Hg), considered additional risk factors such as diabetes, and related them to the patient's 10-year cardiovascular and cerebrovascular risk score using the Framingham equation. Patients were compared with 48 healthy normotensive controls. In these patients, the effects of 6 months of intensified blood pressure and (where appropriate) lipid-lowering treatment were investigated. In our patients, TF, VEGF, and vWF levels were higher, but FMD was lower (all p <0.001) compared with the controls. All markers correlated with each other and with both cardiovascular and cerebrovascular risk scores (all p <0.001). After intensified blood pressure and hypercholesterolemia treatment, total cholesterol, blood pressure, TF, VEGF, and vWF levels all decreased, whereas FMD increased (all p <0.001). Thus, in subjects with hypertension and other risk factors, endothelial damage/dysfunction (and thus, atherogenesis), thrombogenesis, and angiogenesis are abnormal, correlate with overall cardiovascular risk, and importantly, can be related to each other in a "Birmingham Vascular Triangle." Furthermore, these processes are beneficially affected by intensive blood pressure and lipid treatment.

Galeano, M., B. Deodato, et al. (2003). "Adeno-associated viral vector-mediated human vascular endothelial growth factor gene transfer stimulates angiogenesis and wound healing in the genetically diabetic mouse." Diabetologia 46(4): 546-55.
AIM S/HYPOTHESIS: We studied the gene therapy efficacy of diabetes-associated wound healing disorder with an adeno-associated virus (AAV) vector expressing the 165-amino acid isoform of human vascular endothelial growth factor-A (VEGF-A) by using an incisional skin-wound model produced on the back of female diabetic C57BL/KsJ db+/db+ mice and their normal littermates ( db+/+m). METHODS: Animals were randomized to receive intradermally into the wound edges either rAAV-LacZ (a control gene), or rAAV-VEGF165. Animals were killed on different days (7 and 14 days after skin injury) and wounded skin tissues were used for gene marker studies, histological evaluation and immunohistochemistry, and wound breaking strength analysis. Furthermore we studied the VEGF mature protein in the wounds. RESULTS : We found that AAV vectors are highly efficient for gene transfer to the mouse skin, displaying an exquisite tropism for the panniculus carnosus by using the beta-galactosidase activity assay. We confirmed the increased expression of the angiogenic factor at day 7 by measuring the wound content of the mature protein. Delivery of VEGF165 to incisional skin wounds of diabetic mice resulted in a remarkable induction of new vessel formation with consequent improvement in the wound healing process. The rAAV-VEGF165 gene improved wound healing in diabetic mice through the stimulation of angiogenesis, reepithelization, synthesis and maturation of extracellular matrix. Moreover the recombinant AAV encoding the human VEGF165 increased the breaking strength of the wound and enhanced the wound content of VEGF. CONCLUSION /INTERPRETATION: Our study suggests that VEGF gene transfer might represent a new approach to treat wound healing disorders associated with diabetes.

Gunga, H. C., D. Fries, et al. (2003). "Austrian Moderate Altitude Study (AMAS 2000) - fluid shifts, erythropoiesis, and angiogenesis in patients with metabolic syndrome at moderate altitude (congruent with 1700 m)." Eur J Appl Physiol 88(6): 497-505.
It was hypothesized that subjects with metabolic syndrome (hypertension, obesity, hyperlipidemia, diabetes mellitus): (1) develop measurable peripheral edema at moderate altitude and (2) might show differences on erythropoiesis, iron status and vascular endothelial growth factor (VEGF) in comparison to healthy subjects during and after a long-term stay (3-week exposure) at moderate altitude (congruent with 1700 m). Twenty-two male subjects with metabolic syndrome were selected. Baseline investigations (t1) were performed in Innsbruck (500 m). All participants were transferred by bus to 1700 m (Alps) and remained there for 3 weeks with examinations on day 1 (after the first night at altitude, t2), day 4 (t3), day 9 (t4) and day 19 (t5). After returning to Innsbruck, post-altitude examinations were conducted after 7-10 days (t6) and 6-7 weeks (t7), respectively. Body mass was decreased from t1 to t7 (P<0.01). Total body water was decreased at t2 (P<0.01), returned to control level (t3, t4), and was found elevated at t7 (P<0.01). Lean body mass did not change, but body fat decreased during the study (P<0.01). Tissue thickness at the forehead decreased during and after altitude exposure (P<0.01), whereas tissue thickness at the tibia did not alter. Erythropoietin (EPO) was elevated as early as t2 and remained increased until t5. Reticulocyte count was increased at t3 and remained above pre-altitude values. VEGF levels were unchanged. After a 3-week exposure to moderate altitude, patients with metabolic syndrome had reduced their body mass, mainly because of a reduction in body fat. The moderate altitude was found to stimulate erythropoiesis in these patients but this was not sufficient to increase serum VEGF concentration.

Guschmann, M. (2003). "[Solitary and multiple chorangiomas--clinical consequences, expression of growth factors and differences in the growth rate]." Z Geburtshilfe Neonatol 207(1): 6-11.
BACKGROUND: Chorangiomas are regarded as hamartous lesions of the placenta which may complicate a pregnancy if they grow large. The etiology of these lesion is still unclear. We suspected a link between the development of chorangiomas and an increase of the expression of the angiogenic growth factor bfgf and angiopoietin-1 within the tumour. MATERIAL AND METHODS: We examined 20 placentas without tumour, 19 placentas with solitary chorangiomas and 10 placentas with multiple chorangiomas (chorangiomatosis) with respect of the difference in clinical complications, regarding the expression of bfgf and angiopoietin-1 and with regard to the proliferation rate. RESULTS : The expression of the growth factors in solitary chorangiomas did not differ from that in the normal placental tissue. Both groups showed moderate expression of growth factors. In placentas with multiple chorangiomas all cases were associated with a strong expression of bfgf and angiopoietin-1. Proliferating cells and fibroblasts were seen more often in placentas with chorangiomatosis. There were clinical differences with regard to the maternal age. The mean age in case of normal placentas was 24 years, in placentas with solitary chorangiomas 32 years and for placentas with multiple chorangiomas 28 years. There were more complications such as HELLP-syndrome, diabetes, preterm birth and additional maturational arrest of the placenta in case of chorangiomas. CONCLUSION : There is a link between the development of multiple chorangiomas and an increase of the expression of bfgf and angiopoietin-1 in the placenta. In our study there is no correlation between multiple tumours and complications of pregnancy.

Harsch, I. A., T. Brzozowski, et al. (2003). "Impaired gastric ulcer healing in diabetic rats: role of heat shock protein, growth factors, prostaglandins and proinflammatory cytokines." Eur J Pharmacol 481(2-3): 249-60.
Gastric mucosa of diabetic rats is highly vulnerable to acute injury, but little is known about the influence of diabetic conditions on the healing of gastric ulcers. In this study, streptozotocin (70 mg/kg injected intraperitoneally) was used to induce diabetes mellitus in rats. Four weeks after streptozotocin injection, gastric ulcers were induced using the acetic acid method, and 10 days later, the healing rate and the gastric blood flow (GBF) were measured by planimetry and hydrogen (H(2))-gas clearance method, respectively. Six major groups of rats with gastric ulcers were used: (1) vehicle (saline); (2) streptozotocin alone; (3) insulin (4 IU/day intraperitoneally); (4) streptozotocin plus insulin; (5) pentoxifylline, an inhibitor of synthesis and release of tumor necrosis factor-alpha (TNFalpha); and (6) aspirin, a non-selective inhibitor of cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2), and rofecoxib, the highly selective COX-2. In the diabetic rats, a significant delay in ulcer healing ( approximately by 300%), accompanied by a decrease in the gastric mucosal blood flow was observed. The prolongation of the healing in diabetic animals was associated with an increase in gastric mucosal expression and release of TNFalpha, interleukin-1beta (IL-1beta), suppression of the vascular endothelial growth factor (VEGF), platelet endothelial cell adhesion molecule-1 (PECAM-1) and the mucosal overexpression of heat shock protein 70 (HSP 70). Administration of insulin reversed the delay in ulcer healing and significantly decreased the expression of IL-1beta and TNF-alpha, while producing the rise in the expression of VEGF and PECAM. Pentoxifylline, an inhibitor of TNF-alpha, which by itself accelerated ulcer healing in non-diabetic rats, counteracted the increase in the area of gastric ulcer induced by streptozotocin, raised significantly gastric blood flow and suppressed the plasma TNF-alpha levels. Aspirin and rofecoxib, that significantly suppressed the mucosal prostaglandin E(2) generation in ulcer area, delayed significantly the rate of ulcer healing and decreased the GBF at ulcer margin in non-diabetic rats, and these changes were significantly augmented in diabetic animals. We conclude that: (1) Experimental diabetes dramatically impairs ulcer healing, depending upon the increased release of proinflammatory cytokines and the attenuation of angiogenesis that can limit the ulcer healing effects of locally produced HSP 70 and TNF-alpha. (2) Insulin reversed this impairment of ulcer healing in diabetic rats, mainly due to the enhancement of angiogenesis and reduction in expression of cytokines in the ulcer area. (3) Classic non-steroidal anti-inflammatory drugs such as aspirin prolonged ulcer healing under diabetic conditions due to suppression of endogenous prostaglandins and the fall in the microcirculation at the ulcer margin and these effects were mimicked by selective, so called "safe" COX-2 inhibitor, rofecoxib, suggesting that both COX isoforms are important sources of prostaglandins that are essential in the ulcer healing in diabetes.

Hirata, K., T. S. Li, et al. (2003). "Autologous bone marrow cell implantation as therapeutic angiogenesis for ischemic hindlimb in diabetic rat model." Am J Physiol Heart Circ Physiol 284(1): H66-70.
The angiogenic effect induced by autologous bone marrow cell implantation (BMCI) was examined in the ischemic hindlimbs of diabetic and nondiabetic rats. Diabetes mellitus was induced by the systemic administration of streptozotocin. We investigated the production of angiogenic factors and endothelial differentiation from bone marrow cells and the native recovery of blood flow in the ischemic hindlimbs. To observe the angiogenic effect induced by BMCI treatment, 6 x 10(7) bone marrow cells were injected intramuscularly at six points into the ischemic limbs, and regional perfusion recovery was evaluated with colored microspheres 2 wk later. No difference was found between diabetic and nondiabetic rats in the release of angiogenic factors or endothelial differentiation from bone marrow cells in vitro. The levels of nitric oxide in plasma were significantly lower, and native perfusion recovery in the ischemic hindlimbs was significantly slower in the diabetic rats than in the nondiabetic rats. However, although perfusion recovery was achieved in the ischemic hindlimbs, there was no significant increase in systemic VEGF after BMCI treatment in either the diabetic or nondiabetic rats. Therefore, therapeutic angiogenesis induced by BMCI could be a safe and effective treatment for ischemic limb disease in diabetic patients.

Jiang, Z. Y., Z. He, et al. (2003). "Characterization of multiple signaling pathways of insulin in the regulation of vascular endothelial growth factor expression in vascular cells and angiogenesis." J Biol Chem 278(34): 31964-71.
The effects of insulin on vascular endothelial growth factor (VEGF) expression in cultured vascular cells and in angiogenesis were characterized. Insulin increased VEGF mRNA levels in mouse aortic smooth muscle cells from 10(-9) to 10(-7) m with an initial peak of 3.7-fold increases at 1 h and a second peak of 2.8-fold after 12 h. The first peak of VEGF expression was inhibited by LY294002, an inhibitor of phosphatidylinositol (PI) 3-kinase, and by the overexpression of dominant negative forms of p85 subunit of PI 3-kinase or Akt. Inhibitors of MEK kinase, PD98059, or overexpression of dominant negative forms of Ras was ineffective. In contrast, the chronic effect of insulin on VEGF expression was partially inhibited by both LY294002 or PD98059 as well as by the overexpression of dominant negatives of PI 3-kinase or Ras. The importance of PI 3-kinase-Akt pathway on VEGF expression was confirmed in mouse aortic smooth muscle cells isolated from insulin receptor substrate -1 knockout (IRS-1-/-) mice that showed parallel reductions of 46-49% in insulin-stimulated VEGF expression and PI 3-kinase-Akt activation. Insulin-induced activation of PI 3-kinase-Akt on hypoxia-induced VEGF expression and neovascularization was reduced by 40% in the retina of neonatal hypoxia model using IRS-1-/- mice. Thus, unlike other cells, insulin can regulate VEGF expression by both IRS-1/PI 3-kinase-Akt cascade and Ras-MAPK pathways in aortic smooth muscle cells. The in vivo RESULTS provide direct evidence that insulin can modulate hypoxia-induced angiogenesis via reduction in VEGF expression in vivo.

Jin, X., N. Fukuda, et al. (2003). "Effects of leptin on endothelial function with OB-Rb gene transfer in Zucker fatty rats." Atherosclerosis 169(2): 225-33.
The metabolic syndrome in association with obesity is a major clinical problem inducing hypertension, diabetes mellitus, and atherosclerosis. Leptin induces angiogenesis by its proliferative effects on endothelial cells (ECs) via OB receptor (OB-Rb) gene. We evaluated the growth of ECs and intracellular signalings in response to leptin in vitro and the angiogenic effects of leptin in the cornea in vivo with and without adenovirus-mediated transfer of the OB-Rb gene in Zucker fatty (ZF) rats as a model for the metabolic syndrome. Recombinant adenovirus vector encoding rat OB-Rb (Ad.OB-Rb) or Escherichia coli. LacZ (Ad.LacZ) was transfected into cultured ECs from Zucker lean (ZL) rats and ZF rats. Leptin increased DNA synthesis dose-dependently in ECs from ZL rats but not ZF rats. Infection with Ad.OB-Rb, but not with Ad.LacZ, improved the growth effects of leptin in ECs from ZF rats. Leptin induced phosphorylation of Janus kinase (JAK)2, signal transducer and activator of transcription (STAT)3, and extracellular signal-regulated kinase (ERK) in ECs from ZL rats but not ZF rats. Infection with Ad.OB-Rb restored phosphorylation of JAK2 and STAT3 in ECs from ZF rats. Leptin induced angiogenesis in cornea from ZL rats, but not from ZF rats. Coadministration of leptin and Ad.OB-Rb induced angiogenesis in cornea from ZF rats. Ad.LacZ did not influence the angiogenic effects of leptin. The impaired endothelial function with the leptin resistance may be one of causes of the atherosclerosis in the metabolic syndrome.

Kang, D. H. and R. J. Johnson (2003). "Vascular endothelial growth factor: a new player in the pathogenesis of renal fibrosis." Curr Opin Nephrol Hypertens 12(1): 43-9.
PURPOSE OF REVIEW: There is new and emerging evidence that renal vascular changes contribute to progressive renal disease and that alteration of vascular endothelial growth factor might play an important role in modulating microvascular loss or macrovascular remodeling in the kidney. RECENT FINDINGS: Microvascular endothelial loss both in glomerular and peritubular capillaries of progressive renal disease is directly linked to impaired blood flow, the development of renal ischemia and scarring. Vascular endothelial growth factor is a proliferative survival factor for endothelial cells, which could preserve stressed endothelium or stimulate angiogenesis, stabilize renal function and slow histologic progression as shown in different animal models of progressive renal disease. However, there has been some evidence for the mitogen playing a role in the development and progression of atherosclerosis via a mechanism that amplifies the inflammatory reaction. Whether vascular endothelial growth factor is detrimental in early stages of diabetic nephropathy or other renal conditions is not yet clearly answered. SUMMARY: Despite dramatic progress in current knowledge of vascular biology in progressive renal disease, there are still controversies about the mechanism by which vascular endothelial growth factor works in the kidney in different conditions and at different time points. We suggest it is now time to think of integral effects of this angiogenic factor as a new player in renal fibrosis with its potential therapeutic implication.

Kelkar, B. R. (2003). "Induced angiogenesis for limb ischemia." Clin Orthop(412): 234-40.
Between May 1990 and April 2000, 61 patients with severe occlusive arterial disease (44 with thromboangiitis obliterans, 13 with atherosclerosis, and four with diabetes mellitus), who had not responded to previous nonsurgical and surgical treatment and had chronic critical ischemia in the lower limbs, had corticotomy near major neurovascular bundles and periosteal elevation along the whole length of the bone. This corticotomy consisted of elevation of a longitudinal window in the lateral cortex of the tibia to induce formation of neovascularity. The neovascularity is a part of the inflammatory response to fracture and periosteal elevation. The longest followup was 10 years and the shortest was 6 months. In 50 of 61 patients there was complete relief from pain at rest and indefinite postponement of amputation. Digital subtraction angiography studies before and after surgery showed the presence of a new vascular collateral network across the affected arteries, a process that improved the circulatory status of the ischemic limbs. The induced neovascularity acted as endogenous biologic bypass conduits and seemed to provide relief for patients with small and diffuse artery disease, when vascular reconstruction otherwise was impossible.

Khan, Z. A. and S. Chakrabarti (2003). "Growth factors in proliferative diabetic retinopathy." Int J Exp Diabesity Res 4(4): 287-301.
Many growth factors are implicated in the pathogenesis of proliferative diabetic retinopathy. Alteration of growth factors and their receptors in diabetes has been shown in both experimental and clinical studies. Sustained hyperglycemia resulting from long-standing diabetes leads to several biochemical abnormalities that consequently result in retinal hypoxia. Retinal oxygenation state regulates various growth factors that promote angiogenesis in order to meet the oxygen demands of the tissue. However, unregulated expression of these growth factors and induction of complex cascades leading to augmentation of other proangiogenic factors, which may not be regulated by tissue oxygenation, leads to uncontrolled retinal neovascularization and blindness in diabetic patients.

Kirchner, L. M., S. O. Meerbaum, et al. (2003). "Effects of vascular endothelial growth factor on wound closure rates in the genetically diabetic mouse model." Wound Repair Regen 11(2): 127-31.
Impaired wound healing is characteristic of diabetic patients. Potential reasons include poor inflammatory response, granulation tissue formation, and abnormal patterns of cytokine release and response. Vascular endothelial growth factor, abnormally regulated during healing in diabetics, is the major factor stimulating angiogenesis during normal wound healing. We tested our hypothesis that topically applied vascular endothelial growth factor would improve wound closure rates in diabetic animals in a full-thickness wound model in genetically diabetic mice (C57 BL/KsJ db/db). Animals received either 1.0 micro g of vascular endothelial growth factor165 or polyethylene glycol alone topically to wounds daily between days 0 and 4 post-wounding. Wound area was measured at days 0, 5, 10, 15, and 21. Data were analyzed using probit analysis and expressed as length-of-time (LT) to 50, 90, and 95% wound closure. Among untreated animals, nondiabetics had an LT50 of 8.5 days (fiducial limits 8.3-8.7), while diabetics had an LT50 of 15.8 days (15.6-16.1). Vascular endothelial growth factor-treated animals had LT50 values of 7.8 (7.6-8.1) and 11.8 days (11.6-12.0) for nondiabetics and diabetics, respectively, representing a 25% improvement in time to 50% closure in treated diabetics. We conclude that topically applied vascular endothelial growth factor improves time to wound closure in the genetically diabetic mouse model.

Kohli, M., V. Kaushal, et al. (2003). "Prospective study of circulating angiogenic markers in prostate-specific antigen (PSA)-stable and PSA-progressive hormone-sensitive advanced prostate cancer." Urology 61(4): 765-9.
OBJECTIVES: To prospectively describe and compare circulating vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in two groups of advanced prostate cancer patients undergoing androgen deprivation. The first patient group (n = 21) consisted of patients with stable serum prostate-specific antigen (PSA) and the second group (n = 20) consisted of patients with a rising serum PSA during androgen deprivation. METHODS: Patients with diabetes or active heart disease or those receiving anticoagulants were excluded. Circulating VEGF and bFGF were measured in platelet-poor plasma. bFGF was also measured in urine. Platelet factor 4 protein (PF4) assays were performed to evaluate platelet activity in platelet-poor plasma samples. Commercially available enzyme-linked immunosorbent assay kits were used for all assays, and all tests were performed in duplicate. RESULTS : The median age of this study population was 75 years (range 58 to 85). Median plasma VEGF measured in the PSA-stable group was 801.5 pg/mL and in the PSA-rising group was 655.5 pg/mL (P = 0.464). Circulating bFGF was undetectable in plasma, but 4 patients in the PSA-stable group had measurable urine levels. Platelet-poor plasma PF4 assays in all patients were less than 3 IU/mL (normal range 0 to 10). CONCLUSIONS: Our pilot study suggests elevated plasma VEGF levels in advanced prostate cancer do not increase during failure of androgen deprivation therapy. Most of the advanced cancer patients in this study expressed plasma VEGF. This suggests its potential role as a surrogate marker for response assessment during antiangiogenic therapy in this stage.

Koike, H., R. Morishita, et al. (2003). "Enhanced angiogenesis and improvement of neuropathy by cotransfection of human hepatocyte growth factor and prostacyclin synthase gene." Faseb J 17(6): 779-81.
The current therapeutic angiogenesis strategy to treat ischemic disease by using angiogenic growth factors has been limited to use of a single gene. However, as vasodilator substances such as prostacyclin are widely used for the treatment of peripheral arterial disease, it might be useful to combine angiogenesis with vasodilation of new vessels. In a mouse hind limb ischemia model, cotransfection of the hepatocyte growth factor (HGF) gene with the prostacyclin synthase gene demonstrated a further increase in blood flow and capillary density compared with a single gene. Even in the rabbit ischemia model, cotransfection of HGF plasmid with the prostacyclin synthase gene demonstrated a further increase in angiogenic activity compared with HGF alone. Because peripheral neuropathy due to diabetes is common for significant morbidity, we examined the hypothesis that experimental diabetic neuropathy can be reversed by HGF and prostacyclin synthase genes. Severe peripheral neuropathy, characterized by significant slowing of nerve conduction velocity compared with nondiabetic control animals, was ameliorated. Overall, cotransfection of the prostacyclin synthase and HGF genes is more effective than single-gene transfection to stimulate angiogenesis, and it significantly improved neuropathy. These data provide important information relating to the clinical application of therapeutic angiogenesis to treat peripheral arterial disease.

Korc, M. (2003). "Pathways for aberrant angiogenesis in pancreatic cancer." Mol Cancer 2(1): 8.
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease. Although the specific mechanisms that dictate its biological aggressiveness are not clearly established, it is characterized by a variety of molecular alterations as well as by the overexpression of mitogenic and angiogenic growth factors and their receptors. PDACs also express high levels of vascular endothelial growth factor (VEGF). Recent studies indicate that suppression of VEGF expression attenuates pancreatic cancer cell tumorigenicity in a nude mouse model, and that VEGF can exert direct mitogenic effects on some pancreatic cancer cells. These findings suggest that cancer cell derived VEGF promotes pancreatic cancer growth in vivo via a paracrine angiogenic pathway and an autocrine mitogenic pathway, and provide novel opportunities for therapeutic intervention in this deadly disease.

Kornowski, R. (2003). "Collateral formation and clinical variables in obstructive coronary artery disease: the influence of hypercholesterolemia and diabetes mellitus." Coron Artery Dis 14(1): 61-4.
BACKGROUND: Collateral circulation is severely compromised in patients who have a limited degree of spontaneous myocardial angiogenesis and arteriogenesis. METHOD: To determine the clinical characteristics associated with angiographic apparent collaterals (AAC) and myocardial blush score (MBS), this study compared the clinical variables in various AAC and MBS grades (0 = no, 1 = minimal, 2 = moderate and 3 = maximal collaterals defined by the two variables) among a consecutive group of 112 patients (aged 62 +/- 12 years, 76% men) with a native artery chronic total coronary occlusion studied by selective coronary angiograms. RESULTS : By univariate analysis, including variables such as age, sex, diabetes, hypertension, hypercholesterolemia, smoking and ejection fraction, the only variable that was found more frequently in patients with greater AAC grade was hypercholesterolemia (59%, 63%, 71% and 78% in patients with AAC grade 0, 1, 2 and 3, P = 0.003). Ejection fraction tended to be more preserved in patients with greater AAC score (46%, 48%, 51% and 54% in patients with AAC grade 0, 1, 2 and 3, respectively, P = 0.052). Diabetes mellitus was the only factor that was negatively associated with MBS (23%, 22%, 18% and 16% in patients with MBS grade 0, 1, 2 and 3, P = 0.01). Using a multivariate logistic regression analysis to predict maximal AAC grade, the only independent predictor found was hypercholesterolemia (odds ratio = 1.3, confidence limits = 1.05-1.9, P = 0.048). Diabetes mellitus was the only predictor found to be negatively associated with MBS (odds ratio = 0.72, confidence limits = 0.46-0.98, P = 0.04). It is concluded that collateral grade is associated with hypercholesterolemia and myocardial blush is negatively associated with diabetes mellitus. These findings may reflect a conflicting impact of hypercolesterolemia and diabetes mellitus upon collateral formation, leading to enhanced or depressed angiogenesis in response to obstructive coronary artery disease.

Larger, E. (2003). "[Hyperglycemia and angiogenesis]." Med Sci (Paris) 19(8-9): 840-6.
Vascular complications of chronic hyperglycemia cause most of diabetes-associated morbidity and mortality. Main targets of chronic hyperglycemia are vascular endothelial cells. Ischemia is the late consequence of vascular damage in patients with diabetes and triggers an angiogenic response. In patients with diabetes, the angiogenic response to chronic ischemia can be excessive in some of the target organs and insufficient in others, in the same individual. The direct effects of hyperglycemia on the expression level of vascular growth factors have been variably appreciated and depend on the studied organ and model. Beyond the described effects of hyperglycemia on the expression level of vascular growth factors, direct and indirect effects of hyperglycemia on endothelial cell proliferation, extra-cellular matrix and metalloproteases might be involved in the pathology of angiogenesis in diabetes.

Lerman, O. Z., R. D. Galiano, et al. (2003). "Cellular dysfunction in the diabetic fibroblast: impairment in migration, vascular endothelial growth factor production, and response to hypoxia." Am J Pathol 162(1): 303-12.
Although it is known that systemic diseases such as diabetes result in impaired wound healing, the mechanism for this impairment is not understood. Because fibroblasts are essential for wound repair, we compared the in vitro behavior of fibroblasts cultured from diabetic, leptin receptor-deficient (db/db) mice with wild-type fibroblasts from mice of the same genetic background in processes important during tissue repair. Adult diabetic mouse fibroblast migration exhibited a 75% reduction in migration compared to normal fibroblasts (P < 0.001) and was not significantly stimulated by hypoxia (1% O(2)), whereas wild-type fibroblast migration was up-regulated nearly twofold in hypoxic conditions (P < 0.05). Diabetic fibroblasts produced twice the amount of pro-matrix metalloproteinase-9 as normal fibroblasts, as measured by both gelatin zymography and enzyme-linked immunosorbent assay (P < 0.05). Adult diabetic fibroblasts exhibited a sevenfold impairment in vascular endothelial growth factor (VEGF) production (4.5 +/- 1.3 pg/ml versus 34.8 +/- 3.3 pg/ml, P < 0.001) compared to wild-type fibroblasts. Moreover, wild-type fibroblast production of VEGF increased threefold in response to hypoxia, whereas diabetic fibroblast production of VEGF was not up-regulated in hypoxic conditions (P < 0.001). To address the question whether these differences resulted from chronic hyperglycemia or absence of the leptin receptor, fibroblasts were harvested from newborn db/db mice before the onset of diabetes (4 to 5 weeks old). These fibroblasts showed no impairments in VEGF production under basal or hypoxic conditions, confirming that the RESULTS from db/db fibroblasts in mature mice resulted from the diabetic state and were not because of alterations in the leptin-leptin receptor axis. Markers of cellular viability including proliferation and senescence were not significantly different between diabetic and wild-type fibroblasts. We conclude that, in vitro, diabetic fibroblasts show selective impairments in discrete cellular processes critical for tissue repair including cellular migration, VEGF production, and the response to hypoxia. The VEGF abnormalities developed concurrently with the onset of hyperglycemia and were not seen in normoglycemic, leptin receptor-deficient db/db mice. These observations support a role for fibroblast dysfunction in the impaired wound healing observed in human diabetics, and also suggest a mechanism for the poor clinical outcomes that occur after ischemic injury in diabetic patients.

Lin, W. D., S. L. Lu, et al. (2003). "[Proliferation-inhibiting effect of advanced glycation end products modified human serum albumin to vascular endothelial cell ECV304]." Zhonghua Yi Xue Za Zhi 83(7): 572-6.
OBJECTIVE: To study the proliferation-inhibiting and apoptosis-inducing effects of advanced glycation end products (AGE) modified human serum albumin (AGE-HSA) on human vein endothelial cells. METHODS: Human umbilical vein endothelial cells ECV304 were cultured in vitro with AGE-HSA of the concentrations of 12.5, 25, 50, 100, and 200 micro g/ml for 6, 12, 24, or 48 hour, then 20 micro l of 5 mg/ml MTT were added and the optical density (OD) at each time point was determined. Another ECV304 cells were cultured with AGE-HAS for 2, 4, or 8 days and then were stained with trypan blue to calculate the number of dead cells so as to calculate the proliferation-inhibiting rate. Another ECV304 cells were cultured with AGE-HAS for 6, 12, 24, or 48 hours and then stained with annexin V Fitc and propidium iodide (PI). Flow cytometry was used to calculate the annexin V Fitc positive cells (early and middle stage apoptotic cells) and Annexin V Fitc/PL positive cells (late apoptotic cells). Inverted microscope, transmission electron microscope, and fluorescence microscope were used to observe the histological changes of apoptotic cells. FCV304 cells incubated with HSA of the above-mentioned and without addition of the other agents concentrations were used as controls. RESULTS : The OD values of ECV304 cells cultured for 48 h with low concentrations (12.5, 25, and 50 micro g/ml) of AGE-HSA were not significantly different from those of the control (1.104 +/- 0.080, 1.098 +/- 0.097 and 1.059 +/- 0.122 VS. 1.159 +/- 0.088, all P > 0.05). The OD values of ECV304 cells cultured with low concentrations of AGE-HSA for 4 days and 6 days were significantly lower than those in the control group. The OD values of ECV304 cells cultured with high concentrations (100 and 200 micro g/ml) of AGE-HSA for 6 - 48 hours decreased to 0.117 +/- 0.033 and 0.081 +/- 0.020 in comparison with that of the control group (P < 0.01). Flow cytometry and fluorescence microscopy showed higher proportions of apoptotic cells among the ECV304 cells cultured with high concentrations of AGE-HAS than among the control cells at each time point (P < 0.01). The numbers of cells in the control group exponentially increased after culture for 2, 4, and 6 days. The number of cells cultured with low concentrations of AGE-HAS for 2 days was not significantly different from that of the control group (P > 0.05), however, the numbers of cells cultured with low concentrations of AGE-HAS for 4 and 6 days were significantly lower than those of the control group (both P < 0.01). The numbers of cells cultured with 100 or 200 micro g/ml AGE-HAS for 2 days were significantly lower than those of the control group (both P < 0.01) with a proliferation-inhibiting rate of 39.56% +/- 2.82% and 60.32% +/- 4.51% respectively. The apoptotic rates in cells cultured with low concentrations of AGE-HAS for 48 hours were not significantly different from those in the control group. The apoptotic rates in cells cultured with 100 or 200 micro g/ml AGE-HAS for 6, 12, 24, or 48 hours were significantly higher than those in the control group (all P < 0.01). The apoptotic rates in 200 micro g/ml group at different time points were significantly higher than those in the 100 micro g/ml group (P < 0.05 or 0.01). The apoptotic rate and number of apoptotic cells increased along with the increase of culture time and concentration of AGE-HAS. Microscopy showed morphological changes among the cells cultured with 100 micro g/ml AGE-HAS for 6, 12, 24, and 48 hours and the numbers of apoptotic cells, mainly late apoptotic cells, and dead cells increased remarkably since the cells were cultured for 48 hours. CONCLUSION : AGE-HSA inhibits the proliferation of vascular endothelial cells and induces apoptosis in dose and time dependent manner. AGE modification-induced pathobiological cascade may be involved in the pathogenesis of impaired wound healing in diabetes by the mechanism of angiogenesis retardation.

Martin, A., M. R. Komada, et al. (2003). "Abnormal angiogenesis in diabetes mellitus." Med Res Rev 23(2): 117-45.
The adverse long-term effects of diabetes mellitus have been well described and involve many organ systems. While diabetes management has largely focused on control of hyperglycemia, the presence of abnormalities of angiogenesis may cause or contribute to many of the clinical manifestations of diabetes. When compared with non-diabetic subjects, diabetics demonstrate vascular abnormalities of the retina, kidneys, and fetus. Diabetics have impaired wound healing, increased risk of rejection of transplanted organs, and impaired formation of coronary collaterals. In each of these conditions, and possibly in diabetic neuropathy as well, abnormalities of angiogenesis can be implicated in the pathogenesis. A perplexing feature of the aberrant angiogenesis is that excessive and insufficient angiogenesis can occur in different organs in the same individual. In this review, the clinical features, molecular mechanisms, and potential therapeutic options of abnormal angiogenesis in diabetes will be reviewed.

Neid, M., K. Datta, et al. (2003). "Role of insulin receptor substrates (IRS) and protein kinase C-zeta (PKC-zeta ) in vascular permeability factor/vascular endothelial growth factor (VPF/VEGF) expression in pancreatic cancer cells." J Biol Chem.
Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF), the critical molecule in tumor angiogenesis, is regulated by different stimuli such as hypoxia, oncogenes and also by growth factors. Previously we have shown that in AsPC-1 pancreatic adenocarcinoma cells, insulin like growth factor receptor (IGF-IR) regulates VPF/VEGF expression. Insulin receptor substrate-1 and -2 (IRS-1 and IRS-2) are two major downstream molecules of IGF-1R and known to be important in the genesis of diabetes. In this study, we have defined a new role of IRS in angiogenesis. Both of the IRS proteins modulate VPF/VEGF expression in pancreatic cancer cells by different mechanistic pathways. The Sp1 dependant VPF/VEGF transcription is mainly regulated by IRS-2. PKC-z plays a central role in VPF/VEGF expression and acts as a switching element. Furthermore, we have also demonstrated that the PI3K pathway, but not the Ras pathway, is a downstream event of IRS proteins for VPF/VEGF expression in AsPC-1 cells. Interestingly, like renal cancer cells, in AsPC-1 cells, PKC-z leads to direct Sp1-dependent VPF/VEGF transcription; in addition, it also promotes a negative feedback loop to IRS-2 that decreases the association of IRS-2/IGF-1R and IRS-2/p85. Taken together, our RESULTS show that in AsPC-1 pancreatic carcinoma cells, Sp1-dependent VPF/VEGF transcription is controlled by IGF-1R signalling through IRS-2 proteins and modulated by a negative feedback loop of PKC z to IRS 2. Our data also suggest that IRS proteins, which are known to play crucial roles in IGF-1R signalling are also important mediators for tumor angiogenesis.

Norata, G. D., F. Pellegatta, et al. (2003). "[Peroxisome proliferator activated receptors and cardiovascular disorders]." Ital Heart J 4(1 Suppl): 8-18.
Peroxisome proliferator activated receptors (PPARs) are transcription factors only recently discovered. Nevertheless, the interest surrounding their study has involved and involves a continuously growing number of researchers. This is due to the role that PPARs play in the understanding of the pathophysiology of clinical conditions such as obesity, diabetes, atherosclerosis, and angiogenesis. Lipid and glucidic metabolism, synthesis of cytokines, adhesion molecules, coagulation factors, fibrinolysis, are only few of the several processes controlled by PPARs. In this review the more recent acquisitions on PPAR mechanisms of action will be described. The clinical implications that their activation/deactivation induce will be also evaluate. Particular emphasis will be placed on their role in the control of the physiology of lipid and glucidic metabolism, as well as in the pathophysiology of inflammatory and atherosclerotic processes.

Oak, J. H., K. Nakagawa, et al. (2003). "Amadori-glycated phosphatidylethanolamine induces angiogenic differentiations in cultured human umbilical vein endothelial cells." FEBS Lett 555(2): 419-23.
Glycation has been implicated in the endothelial dysfunction that contributes to both diabetes- and aging-associated vascular complications. The AIM of the present study was to determine whether Amadori-glycated phosphatidylethanolamine (Amadori-PE), a lipid-linked glycation compound that is formed at an increased rate in hyperglycemic states, affected proliferation, migration and tube formation of cultured human umbilical vein endothelial cells (HUVEC). Amadori-PE at a low concentration of less than 5 microM significantly enhanced these three factors involved in angiogenesis. Furthermore, stimulation of HUVEC with Amadori-PE resulted in secretion of matrix metalloproteinase 2 (MMP-2), a pivotal enzyme in the initial step of angiogenesis. Our RESULTS demonstrated for the first time that Amadori-PE may be an important compound that promotes vascular disease as a result of its angiogenic activity on endothelial cells. We also demonstrated that MMP-2 is a primary mediator of Amadori-PE-driven angiogenesis.

Obrosova, I. G., A. G. Minchenko, et al. (2003). "Aldose reductase inhibitor fidarestat prevents retinal oxidative stress and vascular endothelial growth factor overexpression in streptozotocin-diabetic rats." Diabetes 52(3): 864-71.
The study addressed the role for aldose reductase (AR) in 1) retinal oxidative stress and vascular endothelial growth factor (VEGF) overexpression in early diabetes, and 2) high glucose-induced oxidative stress in retinal endothelial cells. In vivo experiments were performed on control rats and diabetic rats treated with or without low or high dose of the AR inhibitor (ARI) fidarestat (2 or 16 mg. kg(-1). day(-1)). In vitro studies were performed on bovine retinal endothelial cells (BREC) cultured in either 5 or 30 mmol/l glucose with or without 1 micro mol/l fidarestat. Intracellular reactive oxygen species were assessed using the 5-(and-6)-chloromethyl-2',7'-dichlorodihydrofluorescein diacetate (H(2)DCFDA) probe and flow cytometry. Both low and high doses of fidarestat (i.e., the doses that partially and completely inhibited sorbitol pathway hyperactivity) arrested diabetes-induced retinal lipid peroxidation. This was achieved due to upregulation of the key antioxidative defense enzyme activities rather than changes in reduced glutathione, oxidized glutathione, ascorbate and dehydroascorbate concentrations, and the glutathione and ascorbate redox states. Diabetes-associated 2.1-fold VEGF protein overexpression (enzyme-linked immunosorbent assay; ELISA) was dose-dependently prevented by fidarestat, whereas total VEGF mRNA and VEGF-164 mRNA (RT-PCR) abundance were not affected by either diabetes or the ARI. In BREC, fidarestat corrected hyperglycemia-induced increase in H(2)DCFDA fluorescence but not oxidative stress caused by three different pro-oxidants in normoglycemic conditions. In conclusion, increased AR activity contributes to retinal oxidative stress and VEGF protein overexpression in early diabetes. The findings justify the rationale for evaluation of fidarestat on diabetic retinopathy.

Panigrahy, D., L. Q. Shen, et al. (2003). "Therapeutic potential of thiazolidinediones as anticancer agents." Expert Opin Investig Drugs 12(12): 1925-37.
Thiazolidinediones (TZDs) are synthetic ligands that activate the nuclear receptor peroxisome proliferator-activated receptor-gamma (PPAR-gamma). These compounds are widely used in the treatment of Type 2 diabetes. TZDs have antitumour activity in a wide variety of experimental cancer models, in vitro and in vivo, by affecting the cell cycle, induction of cell differentiation and apoptosis as well as by inhibiting tumour angiogenesis. These effects are mediated through both PPAR-gamma-dependent and -independent pathways depending on concentration and tumour cell type. Angiogenesis inhibition mechanisms of TZDs include directly inhibiting endothelial cell proliferation and migration as well as decreasing tumour cell vascular endothelial growth factor production. Further studies suggest that TZDs may be effective in prevention of certain cancers and in the treatment of cancer as adjuvant therapy.

Pathak, R. D., K. Jayaraj, et al. (2003). "Thalidomide-associated hyperglycemia and diabetes: case report and review of literature." Diabetes Care 26(4): 1322-3.

Peppa, M., H. Brem, et al. (2003). "Adverse effects of dietary glycotoxins on wound healing in genetically diabetic mice." Diabetes 52(11): 2805-13.
Advanced glycoxidation end products (AGEs) are implicated in delayed diabetic wound healing. To test the role of diet-derived AGE on the rate of wound healing, we placed female db/db (+/+) (n = 55, 12 weeks old) and age-matched control db/db (+/-) mice (n = 45) on two diets that differed only in AGE content (high [H-AGE] versus low [L-AGE] ratio, 5:1) for 3 months. Full-thickness skin wounds (1 cm) were examined histologically and for wound closure. Serum 24-h urine and skin samples were monitored for N(epsilon)-carboxymethyl-lysine and methylglyoxal derivatives by enzyme-linked immunosorbent assays. L-AGE-fed mice displayed more rapid wound closure at days 7 and 14 (P < 0.005) and were closed completely by day 21 compared with H-AGE nonhealed wounds. Serum AGE levels increased by 53% in H-AGE mice and decreased by 7.8% in L-AGE mice (P < 0.04) from baseline. L-AGE mice wounds exhibited lower skin AGE deposits, increased epithelialization, angiogenesis, inflammation, granulation tissue deposition, and enhanced collagen organization up to day 21, compared with H-AGE mice. Reepithelialization was the dominant mode of wound closure in H-AGE mice compared with wound contraction that prevailed in L-AGE mice. Thus, increased diet-derived AGE intake may be a significant retardant of wound closure in diabetic mice; dietary AGE restriction may improve impaired diabetic wound healing.

Rajagopalan, S., E. Mohler, 3rd, et al. (2003). "Regional Angiogenesis with Vascular Endothelial Growth Factor (VEGF) in peripheral arterial disease: Design of the RAVE trial." Am Heart J 145(6): 1114-8.
BACKGROUND: Patients with intermittent claudication caused by infrainguinal atherosclerosis have limited pharmacologic options "Therapeutic angiogenesis" is a novel treatment approach that seeks to improve perfusion of ischemic limbs by the induction of collateral vessel formation. This trial is a phase 2 randomized double-blind placebo-controlled proof of concept trial that will use an intramuscular adenoviral gene transfer approach of vascular endothelial growth factor, 121 isoform (Ad(GV)VEGF(121.10)) to patients with severe IC caused by infrainguinal disease. METHODS: This is a phase 2, double-blind, randomized, placebo-controlled, dose-finding, multicenter study. Patients with severe intermittent claudication caused by infrainguinal atherosclerosis predominantly involving the superficial femoral artery confirmed with imaging studies that meet inclusion criteria will be stratified on the basis of the presence or absence of diabetes mellitus and randomized in a 1:1:1 fashion to low dose (4 x 10(9) particle units), high dose (4 x 10(10) particle units), or placebo arms (35-36 patients per group). Subjects are required to have exercise-limiting IC in the index extremity during 2 qualifying exercise treadmill tests, with peak walking times between 1 and 10 minutes. A single dose of Ad(GV)VEGF(121.10) will be administered as 20 intramuscular injections throughout the area of the lower limb requiring collateralization. RESULTS : The primary efficacy parameter for the Regional Angiogenesis With Vascular Endothelial Growth Factor (RAVE) trial is the change in peak walking time at 12 weeks compared with baseline. The sample size is expected to provide an 80% power to detect a difference of 1.5 minutes between any of the 2 treatment groups and the placebo group. Secondary efficacy parameters include claudication onset time, hemodynamic effects of therapy assessed with ankle-brachial index, assessment of physical impairment, and health-related quality of life as measured with the Walking Impairment Questionnaire and SF-36 Health Survey. All randomized patients will also be evaluated for safety.

Rodrigues, S., E. Van Aken, et al. (2003). "Trefoil peptides as proangiogenic factors in vivo and in vitro: implication of cyclooxygenase-2 and EGF receptor signaling." Faseb J 17(1): 7-16.
We previously established that the trefoil peptides (TFFs) pS2, spasmolytic polypeptide, and intestinal trefoil factor are involved in cellular scattering and invasion in kidney and colonic cancer cells. Using the chorioallantoic membrane (CAM) assay and the formation of tube-like structures by human umbilical vein endothelial cells (HUVEC) plated on the Matrigel matrix substratum, we report here that TFFs are proangiogenic factors. Angiogenic activity of TFFs is comparable to that induced by vascular endothelial growth factor, leptin, and transforming growth factor-alpha. Stimulation of angiogenesis by pS2 in the CAM assay is blocked by pharmacological inhibitors of cyclooxygenase COX-2 (NS-398) and epidermal growth factor receptor (EGF-R) tyrosine kinase (ZD1839), but is independent of KDR/Flk-1 and thromboxane A2 receptors. In contrast, the morphogenic switch induced by pS2 in HUVEC cells could be inhibited by the specific KDR heptapeptide antagonist ATWLPPR and by inhibitors of COX-2 and EGF-R signaling. These RESULTS implicate TFFs in the formation of new blood vessels during normal and pathophysiological processes linked to wound healing, inflammation, and cancer progression in the digestive mucosa and other human solid tumors associated with aberrant expression of TFFs.

Rubinstein, A. L. (2003). "Zebrafish: from disease modeling to drug discovery." Curr Opin Drug Discov Devel 6(2): 218-23.
The study of zebrafish, a leading model organism for developmental biology, is rapidly expanding to include human disease. Zebrafish models based on known disease mechanisms have been developed in several therapeutic areas, including blood diseases, diabetes, muscular dystrophy, neurodegenerative disease, angiogenesis and lipid metabolism. This review summarizes recent progress in disease model development, and outlines the potential of zebrafish to contribute to drug discovery through the identification of novel drug targets, validation of those targets and screening for new therapeutic compounds.

Satchell, S. C. and P. W. Mathieson (2003). "Angiopoietins: microvascular modulators with potential roles in glomerular pathophysiology." J Nephrol 16(2): 168-78.
Angiopoietins are a recently discovered family of growth factors which act on endothelial cells via Tie receptors. They are widely expressed and have essential roles in regulating vascular growth, development, maturation and permeability. Disturbances in microvascular regulation play an important part in a number of diseases prominent in the developed world including diabetes, ischemic heart disease and cancer. It is the interplay between angiopoietins and other factors including vascular endothelial growth factor (VEGF) which determines endothelial behavior both in health and in these diseases. Angiopoietin-1 is unique in its ability to reduce endothelial permeability and it antagonises the effects of VEGF in its permeability and angiogenesis-inducing actions. The renal glomerulus constitutes a highly specialized microcirculation in which the permeability characteristics of the capillary wall allow its unique filtration function. Disturbance of this function may cause a reduction in glomerular filtration rate or proteinuria. Understanding of the regulation of the filtration barrier is incomplete but the expression of angiopoietins in the glomerulus suggests a mechanism for maintenance of the glomerular endothelium and modulation of the actions of glomerular VEGF. As has been clearly shown for VEGF, angiopoietins are likely to be involved in glomerular disease and recovery from it. Manipulation of angiopoietins has a wide range of potential therapeutic applications from inhibition of diabetic retinal neovascularisation to promotion of glomerular repair.

Sennlaub, F., F. Valamanesh, et al. (2003). "Cyclooxygenase-2 in human and experimental ischemic proliferative retinopathy." Circulation 108(2): 198-204.
BACKGROUND: Intravitreal neovascular diseases, as in ischemic retinopathies, are a major cause of blindness. Because inflammatory mechanisms influence vitreal neovascularization and cyclooxygenase (COX)-2 promotes tumor angiogenesis, we investigated the role of COX-2 in ischemic proliferative retinopathy. METHODS AND RESULTS : We describe here that COX-2 is induced in retinal astrocytes in human diabetic retinopathy, in the murine and rat model of ischemic proliferative retinopathy in vivo, and in hypoxic astrocytes in vitro. Specific COX-2 but not COX-1 inhibitors prevented intravitreal neovascularization, whereas prostaglandin E2, mainly via its prostaglandin E receptor 3 (EP3), exacerbated neovascularization. COX-2 inhibition induced an upregulation of thrombospondin-1 and its CD36 receptor, consistent with the observed antiangiogenic effects of COX-2 inhibition; EP3 stimulation reversed effects of COX-2 inhibitors on thrombospondin-1 and CD36. CONCLUSION S: These findings point to an important role for COX-2 in ischemic proliferative retinopathy, as in diabetes.

Shibuya, M. (2003). "VEGF-receptor inhibitors for anti-angiogenesis." Nippon Yakurigaku Zasshi 122(6): 498-503.
Angiogenesis is deeply involved in the progression of major diseases such as cancer, diabetes, and rheumatoid arthritis. Molecular mechanism on angiogenesis was extensively studied, and several signaling systems including VEGF (VEGF-A), angiopoietin, PDGF, and ephrin were shown to be crucial for physiological angiogenesis. Interestingly, among these factors, VEGF appears to play key roles in most of the pathological angiogenesis, and other factors are considered to have additional effects on its development depending on the situation. VEGF binds and activates two tyrosine kinase receptors, VEGFR-1 (Flt-1) and VEGFR-2 (KDR/Flk-1), and stimulates endothelial cell growth, survival, and vascular permeability. VEGF induces not only tumor angiogenesis but also blood-vessel-dependent metastasis. Based on the importance of VEGF in diseases, many companies and institutes are now trying to generate appropriate small molecules as well as proteins that strongly antagonize the VEGF-VEGFR system. Several molecules quite effective for suppression of tumorigenesis and pathological angiogenesis in animal models are under clinical trials.

Sigrist, S., A. Mechine-Neuville, et al. (2003). "Induction of angiogenesis in omentum with vascular endothelial growth factor: influence on the viability of encapsulated rat pancreatic islets during transplantation." J Vasc Res 40(4): 359-67.
Transplantation of pancreatic islets is proposed as a treatment for type 1 diabetes, but insufficient blood supply can cause the loss of viable grafted islets. In the present study, we investigated the influence of vascular endothelial growth factor (VEGF) on the angiogenesis of omentum during encapsulated islet allotransplantation and consequently on islet survival. Fifty rat islets, cultured for 24 h, were encapsulated in the presence or absence of human VEGF and implanted in the peritoneal cavity of rats (n = 6). After 7, 14 and 28 days of implantation, encapsulation devices with surrounding omentum were removed. Histological analysis of this tissue was performed. Cellular adhesion at the membrane surface was characterized by a phagocytosis test. The morphological aspect of the islets was analyzed and their functionality was evaluated by measuring insulin secretion. At each step of the study, there was a two-fold increase in the number of vessels in the presence of VEGF. In addition, VEGF increased the vessel diameter and the surface area of the angiogenic pedicle. Moreover, the presence of VEGF significantly decreased the distance between the devices and vessels (16.2 +/- 5.6 vs. 51.6 +/- 10.1 microm, p < 0.001). Membrane surface analysis showed a decrease in macrophage adhesion in the presence of VEGF. Furthermore, islet structure and functionality was preserved in the presence of VEGF. Stimulation of angiogenesis of omentum induced by VEGF is associated with preservation of islet viability. Local delivery of VEGF proved to be a relevant approach to ameliorate the outcome of islet transplantation.

Sivan-Loukianova, E., O. A. Awad, et al. (2003). "CD34+ blood cells accelerate vascularization and healing of diabetic mouse skin wounds." J Vasc Res 40(4): 368-77.
Diabetes is characterized by poor circulation and impaired angiogenesis, which appear to contribute to the frequent skin lesions and poor wound healing common in diabetic patients. Therapies to improve circulation commonly improve wound healing in diabetic patients. Administration of circulating CD34+ cells, cells that can function as endothelial cell progenitors, accelerates blood flow restoration to ischemic limbs of diabetic mice. We have investigated the potential of these cells to accelerate revascularization and healing in full-thickness skin wounds of hypoinsulinemic (streptozotocin-treated) diabetic mice. Wounds were injected with human CD34+ or CD34- peripheral blood mononuclear cells or no cells, and analyzed for vascularity and healing at various times thereafter. Treatment with CD34+ enriched cells decreased wound size by 4 days after treatment, accelerated epidermal healing, and rapidly and dramatically accelerated revascularization of the wounds compared to controls. Initially increased vascularization was mediated principally by an increase in vessel diameter, but later, both an increase in vascular size and number were observed. These findings indicate that blood-derived progenitors may have therapeutic potential in the treatment of skin lesions in the setting of diabetes, and give insights into how bone marrow cells exert their effects on neovascularization.

Soini, Y., T. Salo, et al. (2003). "Angiogenesis is involved in the pathogenesis of nonrheumatic aortic valve stenosis." Hum Pathol 34(8): 756-63.
Angiogenesis is an essential biological process not only in embryogenesis, but also in the progression of several major diseases, including cancer, diabetes, and inflammation. Excessive vascularization can also contribute to some cardiovascular pathologies, such as atherosclerosis, but contradictory reports still prevail regarding its impact on aortic stenosis. Using immunohistochemical techniques, we assessed the vascular density and distribution of angiogenesis (FVIII) and vascular endothelial growth factor (VEGF) expression as well as the expression of 2 VEGF receptors, Flt-1 and Flk-1, in 55 nonrheumatic and 6 control aortic valves. In the light of the fact that the angiogenic effect of VEGF is mediated by sustained formation of nitric oxide, the samples were also immunostained with 3 nitric oxide synthase (eNOS, iNOS, and nNOS) antibodies. The immunohistochemical findings of VEGF and its receptors were verified by immunoblotting techniques. Vascular density was highest in the cases with moderate valve stenosis, and the mean number of FVIII-positive blood vessels was 1.7 +/- 1.9 vessels/mm(2) in the diseased valves, whereas the normal valves contained no blood vessels. Vascular density was significantly higher in the cases showing chronic inflammation (P = 0.007). Interestingly, the patients receiving statin therapy had significantly lower vascular densities than those not receiving such therapy (P = 0.001). Diseased valves showed distinct VEGF, Flt-1, Flk-1, and eNOS positivity of activated endothelial, stromal fusiform myofibroblastic, and histocytic cells. In contrast, immunoreactivity for iNOS and nNOS was seen only in nonendothelial stromal cells, and their expression was weaker. Enhanced vascular density was significantly associated with increased expression of Flk-1 (P = 0.028 for endothelial and P = 0.009 for stromal cells) and with endothelial eNOS expression (P = 0.024). A similar tendency was also observed for VEGF, but not for Flt-1. Our RESULTS show a distinct angiogenic response and the presence of angiogenic factors in nonrheumatic aortic valve stenosis, suggesting that angiogenesis may influence on the evolution of this disease.

Sugawara, T., S. Fujii, et al. (2003). "Coronary capillary network remodeling and hypofibrinolysis in aged obese diabetic rats: implications for increased myocardial vulnerability to ischemia." Mol Cell Biochem 248(1-2): 165-70.
Despite the known abnormalities of cardiac function in patients with overt non-insulin dependent diabetes mellitus (NIDDM) the temporal changes of coronary capillary network remodeling leading to potential microcirculatory dysfunction have not been elucidated. To this end, left ventricular subendocardial capillary network of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, characterized by hypertension, obesity, hyperglycemia, hyperinsulinemia and mild NIDDM, and control Long-Evans Tokushima (LETO) rats were investigated. Total capillary density in OLETF was significantly higher than that in LETO at 20 weeks, suggesting compensatory improvement of O2 transport at early stages of NIDDM. The increase in capillary density in OLETF was lost at 40 and 60 weeks due to the decreases of intermediate capillary portions and venular capillary portions. Although capillary domain area (area innervated by single capillary) in OLETF was lower than that in LETO at 20 weeks, the values were similar between OLETF and LETO at 40 and 60 weeks, suggesting that adaptive improvement in the capacity for 02 transport with a high perfusion was lost in late stages of NIDDM. Activity of plasma plasminogen activator inhibitor-1 (PAI-1), the major physiologic inhibitor of proteo(fibrino)lysis, in OLETF was higher than that in LETO at 40 and 60 weeks, suggesting that increase of PAI-1 may downregulate compensatory adaptive capillary network remodeling by inhibiting proteolysis and angiogenesis in the cardiac interstitium. Loss of adaptive myocardial microcirculation may therefore contribute to increased vulnerability in ischemic injury and to cardiac dysfunction in NIDDM.

Tamarat, R., J. S. Silvestre, et al. (2003). "Blockade of advanced glycation end-product formation restores ischemia-induced angiogenesis in diabetic mice." Proc Natl Acad Sci U S A 100(14): 8555-60.
We hypothesized that formation of advanced glycation end products (AGEs) associated with diabetes reduces matrix degradation by metalloproteinases (MMPs) and contributes to the impairment of ischemia-induced angiogenesis. Mice were treated or not with streptozotocin (40 mg/kg) and streptozotocin plus aminoguanidine (AGEs formation blocker, 50 mg/kg). After 8 weeks of treatment, hindlimb ischemia was induced by right femoral artery ligature. Plasma AGE levels were strongly elevated in diabetic mice when compared with control mice (579 +/- 21 versus 47 +/- 4 pmol/ml, respectively; P < 0.01). Treatment with aminoguanidine reduced AGE plasma levels when compared with untreated diabetic mice (P < 0.001). After 28 days of ischemia, ischemic/nonischemic leg angiographic score, capillary density, and laser Doppler skin-perfusion ratios were 1.4-, 1.5-, and 1.4-fold decreased in diabetic mice in reference to controls (P < 0.01). Treatment with aminoguanidine completely normalized ischemia-induced angiogenesis in diabetic mice. We next analyzed the role of proteolysis in AGE formation-induced hampered neovascularization process. After 3 days of ischemia, MMP-2 activity and MMP-3 and MMP-13 protein levels were increased in untreated and aminoguanidine-treated diabetic mice when compared with controls (P < 0.05). Despite this activation of the MMP pathway, collagenolysis was decreased in untreated diabetic mice. Conversely, treatment of diabetic mice with aminoguanidine restored collagenolysis toward levels found in control mice. In conclusion, blockade of AGE formation by aminoguanidine normalizes impaired ischemia-induced angiogenesis in diabetic mice. This effect is probably mediated by restoration of matrix degradation processes that are disturbed as a result of AGE accumulation.

Unlu, F., P. G. Guneri, et al. (2003). "Expression of vascular endothelial growth factor in human periodontal tissues: comparison of healthy and diabetic patients." J Periodontol 74(2): 181-7.
BACKGROUND: Vascular endothelial growth factor (VEGF) induces proliferation of endothelial cells, stimulates angiogenesis, and increases vascular permeability, but information about its role in periodontal lesions is limited. The AIM of this study is to determine the association between VEGF expression in healthy and periodontally diseased tissues of healthy and diabetic patients. METHODS: Ten systemically healthy and 10 Type 2 diabetic patients (DM) all diagnosed with periodontitis were enrolled into the study. Gingival samples were collected from both periodontal and healthy sites in all patients. Each patient served as his/her own control. Additionally, 10 people without any systemic or periodontal diseases were enrolled as a negative control group. RESULTS : In the negative control group tissue samples, no VEGF expression was observed. Among the 10 systemically healthy people, no evidence of VEGF was observed in healthy gingival samples, but was found in diseased tissues in 2 cases. In the diabetic patients, VEGF was observed in 4 healthy gingival tissues and in 6 periodontal sites. VEGF was intensely present in monocytes and macrophages. CONCLUSION : The RESULTS of this study show that VEGF is increased in gingival tissues of diabetic patients, especially those with periodontal disease.

Yamashiro, K., A. Tsujikawa, et al. (2003). "Platelets accumulate in the diabetic retinal vasculature following endothelial death and suppress blood-retinal barrier breakdown." Am J Pathol 163(1): 253-9.
Platelet microthrombi are present in the diabetic retinal vasculature of humans and rodents; however, the mechanisms and consequences of their presence have not been defined. The current study demonstrates that platelet containing microthrombi accumulate in the retinal vasculature of the rat within 2 weeks of experimental diabetes, a timepoint at which leukocyte-mediated endothelial cell injury and death are known to occur. Platelet accumulation increased with the duration of diabetes, and crossover experiments revealed that maximal platelet accumulation required both diabetic platelets and a diabetic endothelium. Platelet accumulation also coincided with the expression of Fas and FasL in the diabetic retina. When endothelial cell apoptosis was inhibited with an anti-FasL neutralizing antibody, platelet accumulation was effectively suppressed. When platelets were depleted from the systemic circulation with an anti-platelet antibody, blood-retinal barrier breakdown worsened in the diabetic animals. These findings suggest that platelet accumulation in the diabetic retinal vasculature is secondary to endothelial cell death and serves, in part, to suppress blood-retinal barrier breakdown.