Decker, M.W.; Brioni, J.D.; Sullivan, J.P.; Buckley, M.J.; Radek, R.J.; Raskiewicz, J.L.; Kang, C.H.; Kim, D.J.B.; Giardina, W.J.; Wasicak, J.T.; Garvey, D.S.; Williams, M.; Arneric, S.P. J. Pharmacol. Exp. Ther., 1994, 270, 319. Decker, M.W.; Curzon, P.; Brioni, J.D.; Arneric, S.P. Eur. J. Pharmacol., 1994, 261, 217. Kem, W.R. Behav. Brain Res., 2000, 113, 169. Lin, N.-H.; Gunn, D.E.; Ryther, K.B.; Garvey, D.S.; Donnelly-Roberts, D.L.; Decker, M.W.; Brioni, J.D.; Buckey, M.J.; Rodrigues, A.D.; Marsh, K.G.; Anderson, D.J.; Buccafusco, J.J.; Prendergast, M.A.; Sullivan, J.P.; Williams, M.; Arneric, S.P.; Holladay, M.W. J. Med. Chem., 1997, 40 , 385. Vernier, J.-M.; El-Abdellaoui, H.; Holsenback, H.; Cosford, N.D.P.; Bleicher, L.; Barker, G.; Bontempi, B.; Chavez-Noriega, L.; Menzaghi, F.; Rao, T.S.; Reid, R.; Sacaan, A.I.; Suto, C.; Washburn, M.; Lloyd, G.K.; McDonald, I.A. J. Med. Chem., 1999, 42 , 1684. Decker, M.W.; Bannon, A.W.; Curzon, P.; Gunther, K.L.; Brioni, J.D.; Holladay, M.W.; Lin, N.-H.; Li, Y.; Daanen, J.F.; Buccafusco, J.J.; Prendergast, M.A.; Jackson, W.J.; Arneric, S.P. J. Pharmacol. Exp. Ther., 1997, 283, 247. Lloyd, G.K.; Menzaghi, F.; Bontempi, B.; Suto, C.; Siegel, R.; Akong, M.; Stauderman, K.; Velicelebi, G.; Johnson, E.; Harpold, M.M.; Rao, T.S.; Sacaan, A.I.; Chavez-Noriega, L.E.; Washburn, M.S.; Vernier, J.M.; Cosford, N.D.P.; McDonald, L.A. Life Sci., 1998, 62 , 1601. Rylett, R.J.; Ball, J.M.; Colhoun, E.H. Brain Res., 1983, 289, 169. Ricciardi, S.; Bisiani, C.; Camisasca, C.; Fusi, R.; Ornaghi, F.; Pastoris, R.; Scatturin, M.; Masotto, C. J. Drug Dev., 1994, 6, 159. Chaki, H.; Yamabe, H.; Sugano, M.; Morita, S.; Bessho, T.; Tabata, R.; Saito, K.-I.; Egawa, M.; Tobe, A.; Morinaka, Y. Bioorg. Med. Chem. Lett., 1995, 5, 1495. Schneider, L.S. Curr. Opin. CPNS Invest. Drugs, 2000, 2, 427. Giacobini, E. Neurochem. Int., 1998, 32 , 413. Brufani, M.; Filocamo, L.; Lappa, S.; Maggi, A. Drugs Future, 1997, 22 , 397. Imbimbo, B.P. CNS Drugs, 2001, 15 , 375. Imbimbo, B.P.; Martelli, P.; Troetel, W.M.; Lucchelli, F.; Lucca, U.; Thal, L.J. Neurology, 1999, 52 , 700. Snape, M.F.; Misra, A.; Murray, T.K.; De Souza, R.J.; Williams, J.L.; Cross, A.J.; Green, A.R. Neuropharmacology, 1999, 38 , 181. Miguel-Hidalgo, J.J. Curr. Opin. CPNS Invest. Drugs, 2000, 2, 438. Greig, N.H.; De Micheli, E.; Holloway, H.W.; Yu, Q.-S.; Utsuki, T.; Perry, T.A.; Brossi, A.; Ingram, D.K.
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Risk for relapse among those who continued their maintenance treatment, it was only 22 percent, so a fourfold reduction in risk with maintenance treatment. LC: And Adele, in terms of the time to relapse, how far out did patients really get before they started to get sick, because that looks like a pretty steep drop in the survival curve? [GRAPHIC DISPLAYED] AV: It is a very steep drop and very similar to the unipolar population. We found that most of the relapses occurring within the first nine weeks, so early on in the first trimester. And another observation was that most of the relapses were into depression and not mania. So it's interesting, we talked about depression, your experience in bipolar disorder, and just historically the data on panic disorder, OCD, there's essentially consistent findings across all of these disorders that pregnancy is not protective with respect to risk for relapse. So that's pretty convincing in terms of, Zach, a lot of rigorous analysis in multiple conditions that this is not a time of protection, so the stage is set in terms of if you're going to treat, or if you're going to decide how you're going to treat, how do you weigh the priorities? Well, I think, Bob, that first you've got to approach it as we approach all medical illnesses, and that is that it's a balancing of risking the impact of the untreated illness versus the risk of treatment. And certainly, it seems like the bulk of individuals seem to feel far more anxious about the risk of treatment, which is unfortunate because I don't think people are quite as aware as they need to be about the risk of illness. When you look at the impact of maternal depression on obstetrical outcome, the impact of maternal anxiety on later infant outcome, you're really talking about probably over 6, 000 patients who've been included in these studies, and you're not talking about an insignificant risk. The untreated illness certainly poses a significant risk. Now then, you have to balance that against what we know about our medicines, and in which case I think as we're going to be discussing, I think most of our category systems and news coverage is quite misleading with respect to the amount of information we actually have. So Adele, let's take Zach's lead and start moving on to discussing specific medications that we prescribed. What do we know about these medications in terms of prescribing psychotropic medications to women during their pregnancy? Well, I think we're very fortunate now to be living in the 21st century, because in the last two decades we've collected an amazing amount of data on the reproductive safety of many of the psychotropics, so we do have information to inform patients, at least to share with them what the risks and benefits are. I think it's very important, though, when we talk about the risk of these medications, the teratogenic risk, meaning their ability to potentially cause a birth defect, that we bear in mind that spontaneously in and
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Echocardiographic predictors of poor outcome following AMI, and are superior to indexes of global LV performance. Both parameters should be taken into consideration when deciding about the management of these patients. 478. Hemostatic Alterations in Patients with Obstructive Sleep Apnea and the Implications for Cardiovascular Disease - Von K nel R. and Dimsdale J.E. [Dr. R. Von K nel, Institute for Behava a ioral Sciences, Swiss Fed. Institute of Technology, Turnerstrasse 1, CH-8092 Z rich, Switzerland] - CHEST 2003 124 5 ; u summ in ENGL Study objectives: Patients with obstructive sleep apnea OSA ; are at increased risk for coronary artery and cerebrovascular diseases. Numerous studies suggest that a hypercoagulable state is prospectively related to atherothrombotic events. This review explores whether changes in hemostasis may constitute one biological link between OSA and vascular disease. Design: Ten studies on hemostatic variables in OSA were located by electronic library search and descriptively reviewed. Work on hemostatic function with physiologic conditions similar to those found in OSA hypoxemia and hyperactivity of the sympathetic nervous system ; was considered to discuss potential molecular mechanisms of procoagulant disturbances in OSA. Measurements and results: The reviewed data suggest that, as compared to non-OSA control subjects, patients with OSA have elevated plasma fibrinogen levels, exaggerated platelet activity, and reduced fibrinolytic capacity. Although not consistently shown, severity of OSA ie, apneahypopnea index ; and plasma epinephrine were independent predictors of platelet activity, and average minimal oxygen saturation was an independent predictor of fibrinogen. In some studies, treatment with continuous positive airway pressure decreased platelet activity, plasma fibrinogen levels, and activity of clotting factor VII. Conclusions: There is some evidence for a hypercoagulable state in OSA, which might help explain the increased prevalence of vascular diseases in this population. To further confirm such a notion, future studies need to be performed on sufficiently large samples to be able to control for confounders of hemostatic activity. Prospective studies are needed to examine the association between hemostasis molecules and strong vascular end points. 479. Biopolymeric delivery matrices for angiogenic growth factors - Zisch A.H., Lutolf M.P. and Hubbell J.A. [A.H. Zisch, Institute for Biomedical Engineering, Swiss Fed. Inst. of Technol. Zurich, Moussonstrasse 18, 8044 Zurich, Switzerland] - CARDIOVASC. PATHOL. 2003 12 6 ; - summ in ENGL The development of new therapeutic approaches that aim to help the body exert its natural mechanisms for vascularized tissue growth therapeutic angiogenesis ; has become one of the most active areas of tissue engineering. Through basic research, several growth factor families and cytokines that are capable to induce physiological blood vessel formation have been identified. Indeed, preclinical and clinical investigations have indicated that therapeutic administration of angiogenic factors, such as the prototypic vascular endothelial growth factor VEGF ; or basic fibroblast growth factor bFGF ; , to sites of ischemia in the heart or the limb can improve regional blood flow. For new and lasting tissue vascularization, prolonged tissue exposure to these factors could be critical. Furthermore, as shown for VEGF, dosage must be tightly controlled, as excess amounts of VEGF can cause severe vascular leakage and hypotension. This review emphasizes natural and synthetic polymer matrices with respect to their development as vehicles for local and controlled delivery of angiogenic proteins, such as VEGF and bFGF, and their clinical applicability. In the dawn of experimental vascular engineering, new biomaterial schemes for clinical growth factor administration that take better account of biological principles of angiogenic growth factor function and the cell biological basis necessary to produce functional vasculature are evolving. Alongside their base function as protective embedment for angiogenic growth factors, these new classes of bioactive polymers are engineered with additional functionalities that better preserve growth factor activity and more closely mimic the in vivo release mechanisms and profiles of angiogenic growth factors from the extracellular matrix ECM ; . Consequently, the preparation of both natural or completely synthetic materials with biological characteristics of the ECM has become central to many tissue engineering approaches that aim to 96.
Values of 24-hour BP are shown in Table 1. Subjects with IHA had higher not only systolic but also diastolic BP than the control group [ systolic diastolic BP ; P 0.005 0.03]. As shown in Table 2, the nighttime systolic BP decline in the APA group was significantly lower than that of diastolic BP in comparison with the control group absolute decline: P 0.02 0.13, relative decline: P 0.01 0.06 ; . The incidence of dipping status in the APA group did not differ significantly from the control group in either criterion A: nighttime BP decline 10 %; B: night-to-day ratio 100 % ; , but the difference according the criterion A was borderline P 0.06 ; . Subjects with IHA had a significantly lower and
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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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