Figure 2: Adjusted treatment difference difference in mean change between an active treatment group and the placebo group adjusted for the baseline value ; for the activities of daily living part II ; and motor part III ; UPDRS scores at week 11 in the phase II trial of rotigotine monotherapy in early-stage Parkinson's disease. Data from the Parkinson Study Group, 2003.24 Figure reproduced with permission from SCHWARZ PHARMA!
Great strides have been made in identifying and managing the organ-based complications of systemic sclerosis SSc ; . There is no room for the nihilism towards treating this disease that used to be so prevalent. However, there is still relatively little hard evidence on which to base treatment decisions. Previous trials have been constrained by the low disease prevalence and the difficulty in recruiting sufficient patients especially with disease of recent onset. The results of past trials have often been confounded by the failure to recognize the marked heterogeneity of SSc and the inclusion of patient subsets with widely varying disease expression, course and outcome. It is recognized that progress will only be made in this area with coordinated multicentre studies. As a result, national and international networks of clinicians with expertise in the management of SSc have been formed. In the UK, the Systemic Sclerosis Study Group has established a national scleroderma register and, together with the Scleroderma Special Interest Group of the British Society for Rheumatology BSR ; , a multicentre base for therapeutic studies. As a result of developments in our understanding of the pathogenesis of scleroderma and our ability to subset patients more effectively, a number of rather more rational approaches to treating the disease and its complications are being tested. In parallel with this, considerable progress is being made in developing universally agreed measures of disease activity and severity and in identifying surrogate laboratory markers of disease activity that are relevant to therapeutic studies. These multicentre trials need substantial funding and often do not attract support from the pharmaceutical industry. It was because of the difficulty in financing long-term, multicentre studies in uncommon conditions that the ARCuBSR Clinical Trials Programme was established. The QUINS trial, which is funded by this Programme, is described here as an example of one of several therapeutic protocols being developed by the UK Systemic Sclerosis Study Group that are currently being tested in multicentre trials. Contact details are provided in the appendix for clinicians who are interested in registering patients on the UK Scleroderma Register or participating in this or in the other therapeutic studies. KEY WORDS: Scleroderma, ACE inhibition, Disease activity, Autoantibodies, for instance, ocuflox eye drops.
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Atosiban is a synthetic peptide, an oxytocin analogue, designed to inhibit uterine contractions before the normal term of pregnancy by acting on oxytocin receptors. Pharmacodynamics In vitro studies Receptor binding: Arginine-vasopressin AVP ; and oxytocin OT ; receptors are distinct, though structurally related, gene products belonging to the family of G protein-coupled receptors. They are classified as follows on the basis of their order of potency AVP OT for AVP receptors and OT VP for OT receptors ; : AVP-V vasopressin receptors, coupled to Gq 11 protein, mediate the contractile effects of AVP on vascular smooth muscle and its glycogenolytic response in the liver. V receptor mediates the vasopressor effect. AVP-V2 vasopressin receptors, coupled to Gs protein, mediate the antidiuretic effect. OT, oxytocin receptor, coupled to Gq 11 protein, mediate uterine contractions and contractions of myoepithelial cells surrounding mammary alveoli which lead to milk ejection.
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There were no significant differences in liver tests or hematocrit at the onset of treatment Table 2 ; . Results of liver tests at the 1-mo follow-up period are shown in Table 3. No significant changes were noted during the.
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ITEM 1B. Unresolved Staff Comments. None. ITEM 2. Properties. On March 14, 2007 we announced our plans to close our operations in Salt Lake City, Utah and Toronto, Ontario. We will continue to maintain our corporate headquarters in Parsippany, New Jersey. In Parsippany, we lease approximately 76, 500 square feet of administrative space. The Parsippany lease will expire in October 2007. We expect to secure new office space in New Jersey upon expiration of the Parsippany lease for space sufficient for approximately 35 employees. In connection with our 2006 restructuring initiative, we closed our technical operations facility in Mississauga, Ontario in October 2006. Our building in Mississauga, which consists of 90, 000 square feet of laboratory, support and administrative space is currently being offered for sale. In December 2005, we closed a transaction for the sale and leaseback of our 93, 000 square foot laboratory and office building in Salt Lake City. As part of the transaction, we entered into a lease agreement for all of the laboratory and office space in the building. The lease will expire in December 2020. The building is located on land in the Research Park of the University of Utah and is subject to 40-year ground lease. In March 2005, we entered into a lease agreement with the MaRS Discovery District in Toronto for an approximately 60, 000 square foot laboratory and office building. In September 2005, we completed construction of leasehold improvements on this facility and relocated certain personnel from our Mississauga facility to the MaRS facility. The lease will expire in March 2015. In connection with our March 2007 restructuring, we plan to close our Salt Lake City and Toronto facilities. ITEM 3. Legal Proceedings. Securities Class Action. A consolidated shareholders' securities class action lawsuit is currently pending against us and certain of our present and former officers and directors in the United States District Court for the District of Utah, Central Division, as Case No. 2: 06cv00570 PGC. By order dated September 14, 2006, the court consolidated four separately filed lawsuits into this action. By order dated November 17, 2006, the court appointed lead plaintiff and counsel for the proposed class. On January 16, 2007, the lead plaintiff and its counsel filed a consolidated amended complaint asserting two federal securities claims on behalf of lead plaintiff and all other shareholders of NPS who purchased publicly traded shares of NPS between August 7, 2001, and May 2, 2006, which period of time is referred to in this paragraph as the "class period." The consolidated complaint asserts two claims: a claim founded upon Section 10 b ; of the Securities Exchange Act of 1934, or the 1934 Act, and SEC Rule 10b-5 promulgated thereunder, which is asserted against all defendants, and a claim founded upon Section 20 a ; of the 1934 Act, which is asserted against the individual defendants. Both claims are based on the allegations that, during the class period, NPS and the individual defendants made false and misleading statements to the investing public concerning PREOS. The consolidated complaint alleges that false and misleading statements were made during the class period concerning the efficacy of PREOS as a treatment for postmenopausal osteoporosis, the potential market for PREOS, the dangers of hypercalcemic toxicity as a side effect of injectable PREOS, and the prospects of FDA approval of NPS's New Drug Application for injectable PREOS. The complaint also alleges claims of option backdating and insider trading of NPS stock during the class period. The consolidated complaint seeks compensatory damages in an unspecified amount, unspecified equitable or injunctive relief, and an award of an unspecified amount for plaintiff's costs and attorneys fees. We intend to vigorously defend our self and the related defendants in this action. We believe the claims are without merit and intend to file a motion to dismiss the consolidated complaint. That motion will be filed on or about March 19, 2007, in accordance with the court's scheduling order. Although we are optimistic about the motion being granted, no assurances can be given in this regard. We maintain insurance for actions of this nature, which we believe is adequate. 36.
NORDITROPIN.33 norelgestromin EE.31 norethindrone. 31 norethindrone acetate. 32 norethindrone acetate EE 1.5 30. norethindrone acetate EE 1 20 norethindrone acetate EE iron.30 norethindrone acetate EE iron 1.5 30 . 30 norethindrone acetate EE iron 1 20. 30 norethindrone EE.30, 31 norethindrone EE 0.4 35 .30 norethindrone EE 0.5 35. 30 norethindrone EE 1 35 norethindrone EE 1 50 .30 norethindrone ME 1 50. 30 norgestimate EE. 31 norgestimate EE 0.25 35 . 30 norgestrel .31 norgestrel EE 0.3 30 . 30 norgestrel EE 0.5 50 . 30 NORINYL 1 + 35.30 NORINYL 1 + 50.30 NORPACE .16 NORPACE CR.16 NORPRAMIN .22 NOR-QD .31 nortriptyline . 14, 22 NORVASC.17, 18 NORVIR .9 NOVAHISTINE DH.37 NOVOLIN 70 30 .29 NOVOLIN N.29 NOVOLIN R .28 NOVOLOG.28 NOVOSEVEN .15 NOXAFIL .10 NULYTELY.28 NUTROPIN NUTROPIN AQ.33 NUVARING.31 nystatin . 10, 34 nystatin triamcinolone. 34 NYTOL.23 OCUFEN .25 OCUFLOX .24 OCUPRESS .25 ofloxacin . 8, 11, 24 ofloxacin otic.26 OGEN .31 olanzapine.22 olanzapine fluoxetine.22 olmesartan.18 olmesartan hydrochlorothiazide.18 olopatadine .25 olsalazine sodium.28 OMACOR .19 omalizumab.37 omega-3 acid ethyl esters .19 omeprazole .27 omeprazole delayed-rel. 27 OMNICEF.7, 10, 11 ondansetron . 27 ONETOUCH BASIC .29 and theo-dur.
Address requests for reprints to: Richard L. Prince, M.D., FRACP, University Department of Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia 6009, Australia.
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References AMIN, D., CORNELL, S. A., GUSTAFSON, S. K., NEEDLE, S. N., BILDER, G. E., ULLRICH, J. W. AND PERRONE, M. H.: Bisphosphonates used for the treatment of bone disorders inhibit squalene synthase and cholesterol biosynthesis. J. Lipid Res. 33: 16571663, 1992. AMIN, D., GUSTAFSON, S. K., WEINACHT, J. M., CORNELL, S. A., NEUENSCHWANDER, K., KOSMIDER, B., SCOTESE, A., REGAN, J. R. AND PERRONE, M. H.: RG 12561 Dalvastatin ; : A novel synthetic inhibitor of HMG-CoA reductase and cholesterol-lowering agent. Pharmacology 46: 1322, 1993. AMIN, D., NEEDLE, S., RUTLEDGE, R., GALCZENSKI, H., BUSH, R., HELE, D., MAGU, because dexamethasone.
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