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receptor beta gene in probands of different weight extremes: Identi cation of several genetic variants. J. Clin. Endocrinol. Metab., 83, 4524 4527. Rosmond R., Bouchard C. & Bjorntorp P. (2001) Tsp5091 polymorphism in exon 2 of the glucocorticoid receptor gene in realtion to obesity and cortisol secretion: Cohort study. BMJ, 322, 652 653. Rossi, M., Kim, M.S., Morgan, D.G., Small, C.J., Edwards, C.M., Sunter, D., Abusnana, S., Goldstone, A.P., Russell, S.H., Stanley, S.A., Smith, D.M., Yagaloff, K., Ghatei, M.A. & Bloom, S.R. (1998) A C-terminal fragment of agouti-related protein increases feeding and antagonises the effect of alpha-melanocyte stimulating hormone in vivo. Endocrinology, 139, 4428 4431. Roth, H., Korn, T., Rosenkranz, K., Hinney, A., Ziegler, A., Kunz, J., Siegfried, W., Mayer, H., Hebebrand, J. & Grzeschik, K.H. (1998) Transmission disequilibrium and sequence variants at the leptin receptor gene in extremely obese German children and adolescents. Hum. Genet., 103, 540 546. Rutherford, J., McGuf n, P., Katz, R. & Murray, R. (1993) Genetic in uences on eating attitudes in a normal female twin population. Psychol. Med., 23, 425 436. Son, J.H., Baker, H., Park, D.H. & Joh, T.H. (1994) Drastic and selective hyperinnervation of central serotonergic neurons in a lethal neurodevelopmental mouse mutant, Anorexia (anx). Mol. Brain. Res., 25, 129 134. Sorbi, S., Nacmias, B., Tedde, A., Ricca, V., Mezzani, B. & Rotella, C.M. (1998) 5-HT2a promoter polymorphism in anorexia nervosa. Lancet, 351, 1785. Sorensen, T.I.A. & Echwald, S.M. (2001) Obesity genes. BMJ, 322, 639 631. Spiegelman B.M. & Flier J.S. (2001) Obesity and the regulation of energy balance. Cell, 104, 531 543. Spitz, M.R., Detry, M.A., Pillow, P. et al. (1999) Variant alleles of the D2 dopamine receptor gene and obesity. Nutr. Res., 20, 371 380. Stein, D., Lilenfeld, L.R., Plotnicov, K., Pollice, C., Rao, R., Strober, M. & Kaye, W. (1998) Familial aggregation of eating disorders: Results from a controlled family study of bulimia nervosa. Int. J. Eat. Disord., 26, 211 215. Strobel, A., Issad, T., Camoin, L., Ozata, M. & Strosberg, A.D. (1998) A leptin missense mutation associated with hypogonadism and morbid obesity. Nat. Genet., 18, 213 215. Strober, M., Freeman, R., Lampert, C., Diamond, J. & Kaye, W. (2000) Controlled family study of anorexia nervosa and bulimia nervosa: Evidence of shared liability and transmision of partial syndromes. Am. J. Psychiat., 157, 393 401. Sullivan, P.F., Bulik, C.M., & Kendler, K.S. (1998) The genetic epidemiology of binging and vomiting. Br. J. Psychiat., 173, 75 79. Sun, G., Gagnon, J., Chagnon, Y.C., Perusse, L., Despres, J.P., Leon, A.S., Wilmore, J.H., Skinner, J.S., Borecki, I., Rao, D.C. & Bouchard, C. (1999) Association and linkage between an insulin-like growth factor-1 gene polymorphism and fat free mass in the HERITAGE family study. Int. J. Obes. Relat. Metab. Disord., 23, 929 935. Sundaramurthy, D., Pieri, L.F., Gape, H., Markham, A.F. & Campbell, D.A. (2000) Analysis of the serotonin transporter gene linked polymorphism (5-HTTLPR) in anorexia nervosa. Am. J. Med. Genet., 96, 53 55. Tartaglia, L.A., Dembski, M., Weng, X., Deng, N., Culpepper, J., Devos, R., Richards, G.J., Camp eld, L.A., Clark, F.T., Deeds, J. et al. (1995) Identi cation and expression cloning of a leptin receptor, OB-R. Cell, 83, 1263 1271. Thomas, G.N., Tomlinson, B. & Critchley, J.A. (2000) Modulation of blood pressure and obesity with the dopamine D2 receptor gene Taq1 polymorphism. Hypertension, 36, 177 182. Treasure, J.L. & Collier, D. (2001) The spectrum of eating disorders in humans. In J.B. Owen, J.L. Treasure & D. Collier (Eds), Animal Models Disorders of Eating Behaviour and Body Composition (pp.19 49). Boston: Kluwer Academic Publishers. Treasure, J. & Holland, A. (1989) Genetic vulnerability to eating disorders: Evidence from twin and family studies. In H. Remschmidt & M.H. Schmidt (Eds), Child and Youth Psychiatry: European Perspectives (pp. 59 68). New York: Hogrefe & Huber. Treasure, J.L. & Owen, J.B. (1997) Intriguing links between animal behaviour and anorexia nervosa. Int. J. Eat. Disord., 21, 307 311. Vaisse, C., Clement, K., Guy-Grand, B. & Froguel, P. (1998) A frameshift mutation in human MC4R is associated with a dominant form of obesity. Nat. Genet., 20, 113 114.
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5. If outputjh > 0 and outputj,h+1 = 0, then outputj,h+k = 0 for all k dtj 6. If outputjh = 0 and outputj,h+1 > 0, then outputj,h+k > 0 for all k utj 7. a. uj,0 = 0. If outputj,h 1 = 0 and outputjh > 0, then ujh = uj,h 1 + 1; otherwise, ujh = uj,h 1 b. dj,0 = 0. If outputjh = 0 and outputj,h 1 > 0, then djh = dj,h 1 + 1; otherwise, djh = dj,h 1 8. 9. a.
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although it appeared at this point that I could assist them effectively, a contract for ongoing therapy would not be made with them until the end of the third session when a thorough assessment had been accomplished. Findings Upon briefly scanning the inventory, I noted discrepancies of 3 or more points on the CPCI (on a scale of 5) between Indira s and Jos s respective ratings on 4 out of 11 general sections: General and Specific Happiness, Communication, Sexual Adjustment, and Division of Home, Child Care, and Work Responsibilities. Because the theme of their initial comments focused on communication, I inquired further and found that the couple had never developed a method for discussing major issues (positive or negative) between them. During the early years of their relationship, they were head-over-heels in love with each other; they had few responsibilities and lots of time; and things went well for them. As they devoted more time to their careers and had children, they drifted into a routine that became increasingly difficult to manage. The discrepancies on their Happiness, Communication, Sexual Adjustment, and Home and Work Sections responses clearly reflected these difficulties. The computerized report and my analysis of the overall information provided by the couple confirmed these four aspects as major targets for treatment. Individual interviews were conducted back-to-back during an extended second session, and I focused on briefly assessing Jos and Indira as individuals. Developmental, family, and health history were discussed in an attempt to evaluate individual strengths and deficits and to screen for major disorders. Primary emphasis was placed on determining each partner s acceptance of the other and commitment to the relationship a major component added to CBCT by Jones et al. (2000). Both partners indicated that they were committed to their relationship and to working on their current difficulties. They had grown to accept each other s differences and truly liked each other, although humor and light moments had become infrequent in recent years. Jos stated that family was first and foremost for him, and he was uncomfortable knowing that Indira placed equal priority on her career. Neither had any major secrets relating to outside relationships, finances, past history, or any disorder that could interfere with improving their relationship. At the end of the third session, I presented the following to Indira and Jos : Developmentally, their relationship began with excitement and intensity and progressed well during times of low stress. As their lives became busier and they took on more responsibilities, their basic affection and commitment to each other allowed them to function effectively for the most part, but as stresses and responsibilities increased, problems often remained unsolved, and their vitality and communication as a couple decreased.
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