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9. Kunkler RB, Osborn DE, Abbott RJ. Retroperitoneal fibrosis caused by treatment with pergolide in a patient with Parkinson's disease [case report]. Br J Urol. 1998; 82: 147. Balachandran KP, Stewart D, Berg GA, Oldroyd KG. Chronic pericardial constriction linked to the antiparkinsonian dopamine agonist pergolide. Postgrad Med J. 2002; 78: 49-50. Tolar M, Gorelick R, Feldman R. Constrictive pericarditis in Parkinson's disease patients treated with pergolide [abstract]. Ann Neurol. 2001; 50: S32. 12. Pergolide: serosal fibrotic complications. Mersey ADR Newsletter. 2000 2001: 2. Kuwabara T. Pergolide-induced pleural effusion in a patient with juvenile parkinsonism [in Japanese]. Rinsho Shinkeigaku. 2002; 42: 757-760. Pritchett AM, Morrison JF, Edwards WD, Schaff HV, Connolly HM, Espinosa RE. Valvular heart disease in patients taking pergolide. Mayo Clin Proc. 2002; 77: 1280-1286. Van Camp G, Flamez A, Cosyns B, Goldstein J, Perdaens C, Schoors D. Heart valvular disease in patients with Parkinson's disease treated with high-dose pergolide. Neurology. 2003; 61: 859-861. Bhatt MH, Keenan SP, Fleetham JA, Calne DB. Pleuropulmonary disease associated with dopamine agonist therapy. Ann Neurol. 1991; 30: 613-616. Pleuropulmonary changes during long-term bromocriptine treatment for Parkinson's disease [letter]. Lancet. 1981; 1: 44-45. Ling LH, Ahlskog JE, Munger TM, Limper AH, Oh JK. Constrictive pericarditis and pleuropulmonary disease linked to ergot dopamine agonist therapy cabergoline ; for Parkinson's disease. Mayo Clin Proc. 1999; 74: 371-375. Geminiani G, Fetoni V, Genitrini S, Giovannini P, Tamma F, Caraceni T. Cabergolihe in Parkinson's disease complicated by motor fluctuations. Mov Disord. 1996; 11: 495-500. Oechsner M, Groenke L, Mueller D. Pleural fibrosis associated with dihydroergocryptine treatment. Acta Neurol Scand. 2000; 101: 283-285. Silberstein SD. Methysergide. Cephalalgia. 1998; 18: 421-435. Robiolio P, Rigolin V, Wilson J. Carcinoid heart disease: correlation of high serotonin levels with valvular abnormalities detected by cardiac catheterization and echocardiography. Circulation. 1995; 92: 790-795. Misch K. Development of heart valve lesions during methysergide therapy. BMJ. 1974; 2: 365-366. Redfield M, Nicholson W, Edwards W, Tajik A. Valve disease associated with ergot alkaloid use: echocardiographic and pathological relations. Ann Intern Med. 1992; 117: 50-52. Connolly H, Crary J, McGoon M. Valvular heart disease associated with fenfluramine-phentermine. N Engl J Med. 1997; 337: 581-588 and levodopa.

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Usa; b department of obstetrics and gynecology a, lis maternity hospital, tel aviv medical center, sakler school of medicine, tel aviv university, tel aviv, israel address of corresponding author gynecologic and obstetric investigation 1999; -32 doi: 1 1159 000010129 ; key words polyhydramnios risk factors congenital malformations abstract objective: to evaluate maternal and fetal factors associated with congenital malformations in patients with polyhydramnios and cilostazol.
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Contributors: VVK and JRN carried out the clinical workup. A VK reviewed the literature and drafted the manuscript. VVK supervised drafting of the paper and will act as guarantor for the paper. Funding : HCJMRI, Jehangir Hospital, Pune. Competing interests: None stated. REFERENCES 1. Cannavo S, Bartolone L, Blandino A, Spinella S, Galatioto S, Trimarchi F. Shrinkage of a PRL-secreting pituitary macroadenoma resistant to cabergoline. J Endocrinol lnvest 1999, 22: 306-309. Pinheiro MM, Liberman B, Salgado LR, Goldman J, Nery M, Cukiert A. Identical twins discordant for Cushing's disease: Case report. Arq Neuropsiquiatr 1999, 57: 686-688. Forest MG. Adrenal steroid excess. In: Clinical Pediatric Endocrinology, 3rd edn. Ed. Brook CGD, London, Blackwell Science, 1995; pp 499-533. Levy SR, Wynne CV, Lorenz BW. Cushing's syndrome in infancy secondary to Pituitary Adenoma. J Dis Child 1982, 136: 605-607. Powell M, Thompson D. The Neuro-physiological approach to hypothalamo-hypophyseal tumors. In: Clinical Pediatric Endocrinology, 3rd edn. Ed. Brook CGD, London, Blackwell Science, 1995; pp 353. Niemann LK. Therapy of Cushing's disease. Pituitary 2002; 5: 77-82.
Dopamine transporter BetaCIT ; binding in a healthy normal individual and patients with early, moderate and severe Parkinson's disease. Note the asymmetric loss particularly in the putamen in the early case and the progressive loss bilaterally in both putamen and caudate with disease progression. Picture courtesy of Dr Ken Marek and with permission from JAMA and clindamycin.

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51. Jorgenson C, Bressot N, Bologna C, Sany J. Dysregulation of the hypothalamo-pituitary axis in rheumatoid arthritis. J Rheumatol 1995; 22: 1829-33. Halko G, Urrows S, Affleck G, Waterman J. Serum prolactin levels and disease activity in rheumatoid arthritis. Arthritis Rheum 1995; 38: S289. 53. Ram S, Blumberg D, Newton P, Anderson N, Gama R. Raised serum prolactin in rheumatoid arthritis: genuine or laboratory artefact? Rheumatology 2004; 43: 1272-74. Dougados M, Duchesne L, Amor B. Bromocriptine and cyclosporin A combination therapy in rheumatoid arthritis. Arthritis Rheum 1988; 31: 1333-34. Marguerie C, David J, So A, Walport M. A pilot study comparing bromocriptine with D-penicillamine in the treatment of rheumatoid arthritis. Br J Rheumatol 1990; 29 suppl 2: 3. 56. Mader R. Bromocriptine for refractory rheumatoid arthritis. Harefuah 1997; 133: 527-29. Figueroa F, Carrion F, Martinez M, Rivero S, Mamani I. Bromocriptine induces immunological changes related to disease parameters in rheumatoid arthritis. Br J Rheumatol 1997; 36: 1022-27. Eijsbouts A, van den Joogen F, Laan R, Hermus A, Sweep F, van de Putte L. Treatment of rheumatoid arthritis with the dopamine agonist quinagolide. J Rheumatol 1999; 26: 2284-85. Erb N, Pace A, Delamere J, Kitas G. Control of unremitting rheumatoid arthritis by the prolactin antagonist cabergoline. Rheumatology 2001; 40: 237-39. Bravo G, Zazueta B, Lavalle C. An acute remission of Reiter's syndrome in male patients treated with bromocriptine. Journal of Rheumatology 1992; 19: 747-50. Sanchez Regana M, Millet P. Psoriasis in association with prolactinoma: three cases. Br J Dermatol 2000; 143: 864-67. Weber G, Frey H. Treatment of psoriasis arthropathica with bromocriptine. Z Hautkr 1986; 61: 1456-66. Eulry F, Bauduceau B, Mayaudon H, Lechevalier D, Ducorps M, Magnin J. Therapeutic efficacy of bromocriptine in psoriatic arthritis two case-reports ; . Rev Rheum Engl Ed 1995; 62: 607-8. Buskila D, Sukenik S, Holcberg G, Horowitz J. Improvement of psoriatic arthritis in a patient treated with bromocriptine for hyperprolactinemia. J Rheumatol 1991; 18: 6112. Eulry F, Mayaudon H, Bauduceau B, et al. Blood prolactin under the effect of protirelin in spondylarthropathies. Treatment trial of 4 cases of reactive arthritis and 2 cases of psoriatic arthritis with bromocriptine. Ann Med Interne Paris ; 1996; 147: 15-9. Eulry F, Mayaudon H, Lechevalier D, et al. Treatment of rheumatoid psoriasis with bromocriptine. Presse Med 1995; 24: 1642-4. Weber G, Frey H. Treatment of psoriatic arthritis with bromocriptine. J Acad Dermatol 1987; 16: 388-89. Zierhut M, Thiel HJ, Pleyer U, Waetjen R, Weidle EG. Bromocriptine in therapy of chronic recurrent anterior uveitis. Fortschr Ophthalmol 1991; 88: 161-4. Regurgitation. Of the 31, six were taking pergolide and six cabergoline; the remaining 19 had no current or recent exposure within 12 months of the index date ; to any dopamine agonist. 663 controls were matched to the case patients. Compared to controls, the rate of heart valve regurgitation was raised in patients currently taking pergolide adjusted incidence-rate ratio 7.1; [95% CI 2.3 to 22.3] ; and xabergoline 4.9; [1.5 to 15.6] ; , but not in those taking other dopamine agonists. The authors conclude that cabergoine and pergolide taken for more than six months, especially at higher doses, are associated with an increased risk of VHD; other dopamine agonists, including those derived from ergot, do not appear to increase the risk. There was an indication of a possible association with use of amantadine, which they suggest should be studied further. The second paper2 describes an echocardiographic study carried out on patients from a PD clinic. All eligible patients attending the clinic over a sixmonth period were asked to have an echocardiograph to identify VHD prevalence. 155 patients 64 taking pergolide, 49 cabergoline and 42 non-ergot dopamine agonists ; and 90 controls who had never had treatment with a dopamine agonist ; had satisfactory echocardiography. Heart valve regurgitation was observed in patients in both the pergolide 23.4% ; and cabergoline 28.6% ; groups. There were no instances in the non-ergot group, and 5.6% in the control group. Relative risk for moderate or severe regurgitation was between 4.2 and 6.3 in the pergolide group and 4.6 and 7.3 in the cabergoline group. The authors conclude that treatment with pergolide or cabergoline is associated with an increased risk of clinically significant heart valve regurgitation, and suggest that this should be added to the risk-benefit equation for these drugs. An accompanying article3 discusses the two studies. The author suggests that the common factor appears to be agonistic activity at the 5-HT2b receptor, which induces inappropriate mitogenic stimulation of normally quiescent valve cells. He notes that lisuride, an antagonist at 5-HT2a and 5HT2c but not 5-HT2b receptors, has not been associated with heart valve abnormalities, and suggests that in future, drugs and their major metabolites should be screened for activity at this receptor before entering clinical trials.

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Employees Stock Option Scheme and Compensation Commitee At the Extraordinary General Meeting of the Company held on 28th February, 2004, the shareholders had approved an Employee Stock Option Scheme s ; thereunder for the benefit of its present and future eligible employees and eligible Directors of the Company. As per the approval received from the shareholders, the same is also applicable and extended to the eligible employees and eligible directors of Subsidiary Companies of the Company. At the board meeting held on 20th May, 2004, a Compensation Committee comprising three independent directors was constituted in order to implement the Employees Stock Option Scheme. Mr. Prafull Sheth will act as Chairman and Mr. Ramdas Gandhi and Mr. Prafull Anubhai will act as other members of the Committee. 4. AUDIT COMMITTEE The Audit Committee comprised three Non-executive and Independent Directors Mr. Prafull Anubhai Chairman ; , Mr. B. C. Modi and Mr. Ramdas Gandhi who are eminent professionals knowledgeable in project finance, accounts and corporate laws. Mr. B. C. Modi ceased to be a Director of the Company w.e.f. 22nd September, 2003 and consequently, he ceased to be a member of the Audit Committee. Hence, Mr. Nasser Munjee was appointed as a member of the Audit Committee in the Board meeting held on 22nd September, 2003. Mr. Nasser Munjee is a Non-executive Independent Director. Mr. K. Subharaman, Company Secretary acts as the Secretary to the Audit Committee. Audit Committee met four times during the year: June 14, 2003; July 28, 2003; October 16, 2003 and January 23, 2004. The following Table gives attendance record of Audit Committee members. Name of Director Mr. Prafull Anubhai Mr. Ramdas Gandhi Mr. Nasser Munjee Mr. B. C. Modi No. of Meetings held 4 Meetings attended 4 0 Appointed as a member w.e.f. September 22, 2003 Ceased to be a director on September 22, 2003 The terms of reference of the committee are wide enough covering the matters specified below: Remarks and cafergot.

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Graph Bipartization is the following problem: Given a graph G, remove as few vertices or edges ; as possible from it so that it becomes bipartite1 . Bipartization by either vertexor edge-deletion is NP-complete [Yann81]. However, making use of the fact that in our applications--those presented in Chapter 7--the graphs that we are to bipartize will most likely be rather small and "almost" bipartite, we develop an exact algorithm for solving Graph Bipartization on these graphs. An implementation of this algorithm is presented in Section 6.4. In this section, we also test the algorithm on random graphs, seeing that the Graph Bipartization problem is already intractable for moderately sized random graphs. However, as will be shown in Section 7.4 of the next chapter, the developed algorithms generally allow the bipartization of graphs obtained during SNP analysis even if they contain a few hundred vertices. References: 1. Drossman. Aliment Pharmacol Ther. 1999; 13 suppl 2 ; : 3-14. 2. Drug Facts and Comparisons. 1999: 298-298c. Akinesia upon waking and nocturnal akinesia are considered to be an expression of end-stage deterioration. In the case of nocturnal akinesia, it may be useful to: - add a slow-release formulation of L-dopa before going to bed; - combine this formulation with entacapone; - add a DA-agonist with a long half-life, such as cabergoline or pergolide, in the late evening. In this phase of the disease, the above therapeutic options may also allow better control of akinesia upon waking. If no improvement upon waking is observed, a more rapidly absorbed formulation of L-dopa levodopa-methyl or a liquid or dispersible formulation ; can be used for the first administration of the day in order to obtain an earlier motor response. On-off phenomena The majority of parkinsonian patients with a fluctuating motor response can present episodes of an unpredictable motor block off ; that is unrelated to L-dopa administration Fig. 7 ; . The patient may pass from a state of good mobility on ; to one of marked akinesia off ; in the space of a few seconds minutes. In this advanced stage of the disease, the on phase is often accompanied by dyskinesias. The pathogenesis of this phenomenon has not yet been defined. Some of the sudden off periods may have a pharmacokinetic cause insofar as even minimal fluctuations in the availability of L-dopa can lead to a transition from an on phase with dyskinesia to a suddenonset off phase. However, there is also a lot of evidence suggesting that pharmacodynamic factors play an important role, and so the pathogenesis may be more complex. 8. Why can't I just have pain killers so that I can use affected the limb? Painkillers pain meds ; are a part of the whole treatment regimen. This condition has "neuropathic pain" and traditional painkillers alone will not control the pain. 9. What medications are helpful for treatment?, for instance, cabergoline use. 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