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The circulating collagen in the A3 domain purchase viagra plus cheap online, and platelet integrin IIb 3 in the (now globular form allows VWF to survey the intact vasculature without termed) C4 domain discount 400mg viagra plus with mastercard. VWF monomers dimerize in the endoplasmic unnecessary binding to platelets 400 mg viagra plus. Globular VWF binds fide bonds in the Golgi apparatus cheap viagra plus 400 mg online. VWF multimers can be released constitutively the previously hidden platelet-binding sites in the A1 domains. It is from endothelial cells into the bloodstream4 or upon demand from this exposure that now confers the ability of VWF to specifically either endothelial cells or platelets in response to specific activation. Once released from the endothelium into the circulation, VWF folds into a globular conformation in which the A3 domain high-affinity The ability of VWF to fulfill this platelet-tethering function is highly collagen-binding site is exposed. These sites enable recruitment of dependent upon its multimeric size/composition. The larger VWF VWF to subendothelial extracellular matrices exposed at sites of multimers are the most hemostatically competent, not only because 292 American Society of Hematology Figure 1. Bottom: Major ligand-binding sites in VWF are highlighted. Top: Location of the ADAMTS13 cleavage site in the A2 domain is highlighted. Bottom: Highlighted functional aspects of ADAMTS13 domains. The N-terminal domains recognize/bind to unraveled VWF, whereas the C-terminal domains interact with both globular and unraveled VWF. The disintegrin-like domain is of critical because they more readily unravel in response to rheological shear. Indeed, contributes to the positioning of the scissile bond into the active site an appreciable proportion of the VWF produced by endothelial cells cleft contained within the metalloprotease domain. The VWF plasma multimeric size, and thus its platelet-tethering func- The ADAMTS13 metalloprotease domain contains a characteristic tion, is therefore further regulated after secretion into the blood by Zn2 -binding motif (HEXXHXXGXXHD) involving 3 His residues processing of UL-VWF by the plasma metalloprotease ADAMTS13. In addition to the active site Zn2 ion, Ca2 ions are also necessary for ADAMTS13 ADAMTS13 function. The ADAMTS13 metalloprotease domain contains a Intriguingly, the same shear-dependent unfolding of VWF that double Ca2 -binding site involving Glu83, Asp173, Cys281, and imparts its platelet-tethering function is also a major determinant of Asp28416 and a highly important single Ca2 -binding site involving its proteolysis by ADAMTS13 that regulates its function. ADAMTS13 residues as the target cleavage site (Tyr1605-Met1606). This interaction is of particular importance ADAMTS13 is an 180 kDa multidomain plasma metalloprotease in guiding the cleavage site over the active site. It comprises a metalloprotease, disintegrin-like, throm- 2 specific subsites on either side of the catalytic Zn specifically bospondin type 1 (TSP) repeat and cysteine-rich and spacer accommodate the P1 (Tyr1605) and P1 (Met1606) residues in domains. Thereafter, there are 7 further TSP repeats and 2 C- 18 8 VWF and dictate cleavage site specificity of ADAMTS13. The regulation of VWF multimer size by ADAMTS13 is particularly complex and requires multiple interac- Based on our understanding of the importance of distinct tions between the 2 proteins. The C-terminal domains of functional sites in ADAMTS13 and the nature of VWF unravel- ADAMTS13, involving the TSP domains 2-8 and CUB domains, 10,11 ing, a model of VWF regulation by ADAMTS13 has been appear to be important for ADAMTS13 to bind globular VWF. In this form, site for the C-terminal residues in the VWF A2 domain. This spacer the VWF A2 domain is folded and the cleavage site is hidden. When shear forces induce the VWF teine-rich domain of ADAMTS13 is essential for ADAMTS13 to adopt its string-like conformation (ie, when secreted, when function, very likely by supporting the functional conformation of tethered to the site of vessel injury by its A3 domain, or during the spacer domain. The ADAMTS13 spacer domain first recognizes VWF domain and the disintegrin-like domain is currently unclear, but is residues Glu1660-Arg1668, which appreciably increases the Hematology 2013 293 Figure 2. Locations of ADAMTS13 cleavage of VWF and its deficiency in TTP. Shown is a diagram illustrating the sites of VWF proteolysis by ADAMTS13. UL-VWF is synthesized by the endothelium and stored within Weibel-Palade bodies (WPB). VWF multimers of various sizes, including UL-VWF, can be secreted directly into the circulation. Under these circumstances, the VWF A2 domain unfolds to enable ADAMTS13 (scissors) to cleave VWF and release the VWF string. However, during passage through the microvasculature, globular UL-VWF in the free circulation may partially/transiently unravel. At sites of vessel damage, endothelial damage results in exposure of subendothelial collagen; plasma VWF binds to this, unravels, and recruits platelets. The presence of collagen and thrombin induce rapid platelet activation, which, along with fibrin, consolidates the platelet plug. ADAMTS13 deficiency either through anti-ADAMTS13 antibodies or through inherited deficiency in the ADAMTS13 gene results in the loss of VWF processing. Under these circumstances, platelets (Pl) can bind unraveled VWF, leading to the accumulation of VWF-platelet aggregates that occlude the microvasculature, as seen in patients presenting with TTP. The ADAMTS13 disintegrin- It is unlikely that all of the VWF that is secreted by the endothelium like domain exosite (Arg349/Leu350) then forms a low-affinity is proteolytically processed in this way. Therefore, despite this interaction with Asp1614 in VWF. Thereafter, essential binding mechanism, some UL-VWF still gets released into the circulation. This so VWF species by ADAMTS13 in the free circulation. In this way, called “molecular zipper” model is rather unique, and this just the UL-VWF is processed into multimer sizes that are less multistep process goes some way to explaining the unprec- susceptible to spontaneous unraveling in the absence of collagen edented specificity of ADAMTS13 for nothing other than binding. Proteolysis of VWF by ADAMTS13 in these first 2 unfolded VWF. There seem to be 3 distinct situations when ADAMTS13-mediated VWF proteolysis occurs: (1) during secretion of VWF from endothe- The third location of ADAMTS13 function is at sites of vessel lial cells, (2) in free circulation, and (3) during unraveling of VWF damage. It is perhaps paradoxical that the unfolding that is at sites of vessel damage (Figure 2). Although proteolysis in each necessary to enable platelet tethering is also the very process that location probably fulfills a different role, all rely on shear-dependent renders VWF susceptible to ADAMTS13 proteolysis, which re- unfolding of VWF. Therefore, there is a balance between pro- and anti-platelet-tethering mechanisms. Vascular Endothelial VWF is synthesized in various sizes, but an appreciable damage exposes collagen, to which circulating VWF binds and proportion of this is in UL-VWF forms that are hyperreactive and, if undergoes its structural transition in response to shear forces, which left unprocessed, potentially pathogenic. However, as VWF is secreted from the endothelium, the Weibel-Palade bodies contain- allows circulating platelets to bind. The binding of platelet GPIb to ing VWF fuse with the plasma membrane to release the stored VWF occurs rapidly at a rate that likely exceeds that of VWF proteolysis by ADAMTS13. During this release, it seems that VWF unravels through a small aperture, resulting in its transient tethering to the endothelial the presence of both collagen and thrombin can act as potent local surface. This process enables the shear forces of the blood to unravel activators of recruited platelets that prompt further VWF- VWF into the string-like form that is permissive to proteolysis. These platelets can thus become resistant is released from the endothelial surface and adopts a globular, to the consequences of ADAMTS13-mediated VWF proteolysis. However, as a platelet plug extends beyond the site of injury (and 294 American Society of Hematology therefore has little/no exposure to collagen and thrombin), VWF- mutations) in the ADAMTS13 gene. Heterozygous carriers of an ADAMTS13 mutation formation to the site of vessel damage. A large number of mutations, single nucleotide polymor- The importance of the modulation of VWF multimeric size is phisms, and sequence variations have been reported in the exemplified clinically by disorders associated with an imbalance in ADAMTS13 gene. Patients with type 2A VWD been analyzed cause severe deficiency due to disruption of classically harbor mutations in the VWF A2 domain that promote ADAMTS13 folding during synthesis, leading to severe intracellu- the destabilization and unfolding of the domain in circulation. Congenital TTP patients, therefore, generally exhibit Therefore, excessive proteolysis of VWF in plasma occurs that markedly reduced ADAMTS13 antigen levels in plasma in combi- transforms much of the plasma VWF pool into hemostatically nation with the consequent reduction in activity levels.

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Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened generic 400 mg viagra plus with mastercard, Eligible purchase viagra plus visa, Enrolled purchase viagra plus 400 mg visa, Author Esophagitis Grade (Grading Withdrawn order viagra plus mastercard, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Pace et al, 2005 549 patients, multi center Grade 0: 1% Screened NR, Eligible rabeprazole 20 mg: PP 91. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Pace et al, 2005 rabeprazole 20 mg: PP 97. Patients w/ complete heartburn relief (day and nighttime) in each day of first week of treatment (ITT patients) Rabeprazole n=245 32. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Pace et al, 2005 Healing rates of oesophagitis grade at endpoint (4 or No significant difference Fair. Lack of ITT analysis, exclusion of people Janssen-Cilag, Italy 8 weeks), rabeprazole vs omeprazole: grade I: 99. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened, Eligible, Enrolled, Author Esophagitis Grade (Grading Withdrawn, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Mee 604 patients at multiple Grade 1: 39% 604 enrolled, 565 lansoprazole 30 mg: 62% 1996 centers, UK and Ireland, Grade 2: 44% eligible, 537 evaluable omeprazole 20 mg: 56. Grade 4: 2% (Savary-Miller) Proton pump inhibitors Page 54 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Mee lansoprazole 30 mg: 75. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Mee Healing of esophagitis by baseline grade, Not reported Good/Fair: Allocation concealment method not 1 of 2 authors from 1996 lansoprazole vs omeprazole: given. Lederle Laboratories, Week 4: funding info not Grade I: 79% vs 68% given. Grade II: 72% vs 62% Grade III: 45% vs 57% Grade IV: 43% vs 60% Week 8 (cumulative): Grade I: 92% vs 87% Grade II: 88% vs 81% Grade III: 73% vs 72% Grade IV: 50% vs 50% Esophagitis grade and treatment were included in a logistic regression model. Odds ratio of healing on lansoprazole compared with omeprazole was 1. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened, Eligible, Enrolled, Author Esophagitis Grade (Grading Withdrawn, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Mulder 211 patients at multiple Grade 1: 0. Grade 4A: 8% withdrew for lack of PP (Savary-Miller) efficacy, 1 withdrawn for 86. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Mulder lansoprazole 30 mg lansoprazole 30 mg "Because of the low number of patients not healed at 4 weeks, analysis of 1996 ITT: No symptoms: symptoms was not performed at 8 weeks. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Mulder Healing of esophagitis by baseline grade, None Fair: randomization and allocation concealment Supported by 1996 lansoprazole vs omeprazole: not reported, Hoechst Marion Week 4: Roussel BV and Grade II: 90. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened, Eligible, Enrolled, Author Esophagitis Grade (Grading Withdrawn, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Mulder et al. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Mulder et al. NR (omeprazole vs lansoprazole vs (omeprazole vs lansoprazole vs pantoprazole) 2002 pantoprazole) Heartburn relief : 87% vs. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Mulder et al. Symptom relief at 4 and 8 weeks was similar for No difference in AEs Fair: randomization and allocation methods not Supported by 2002 each grade of esophagitis. AstraZeneca Maintenance phase (with omeprazole 20 mg or 40 considered treatment mg only, N=391): symptom relief with omeprazole 20 related. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened, Eligible, Enrolled, Author Esophagitis Grade (Grading Withdrawn, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Richter et al, 2425 patients at 163 US Grade A: esomeprazole 40 mg 4798 screened, 2425 esomeprazole 40 mg vs 2001a centers; mean age 47 (sd 35%; omeprazole 20 mg 32% randomized; 109 did not omeprazole 20 mg 12); 61% male; ethnicity Grade B: esomeprazole 40 mg complete: 24 for cumulative life table rate: 93. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Richter et al, esomeprazole 40 mg vs esomeprazole 40 mg "Cumulative analysis at week 8 not done because pts could complete the 2001a omeprazole 20 mg resolution of heartburn: study at week 4 with healed reflux esophagitis, even if symptoms were cumulative life table rate: 68. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Richter et al, Greater efficacy of esomeprazole 40 mg vs 1% in each group Good Supported by Astra 2001a omeprazole 20 mg at 4 weeks was consistent when Zeneca, one or more adjusting for baseline esophagitis grade. Week 4 healing rates by baseline esophagitis grade (approximate, estimated from figure): esomeprazole 40 mg vs omeprazole 20 mg: Grade A: 88% vs 82% Grade B: 79% vs 66% Grade C: 71% vs 53% Grade D: 55% vs 35% Week 8 healing rates by baseline esophagitis grade (approximate, estimated from figure): esomeprazole 40 mg vs omeprazole 20 mg: Grade A: 93% vs 91% Grade B: 90% vs 82% Grade C: 88% vs 70% Grade D: 80% vs 62% (p=0. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened, Eligible, Enrolled, Author Esophagitis Grade (Grading Withdrawn, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Richter et al. Grade 3: 25% Grade 4: 7% (See Appendix F for scale) Proton pump inhibitors Page 66 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Richter et al. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Richter et al. Pharmaceuticals Proton pump inhibitors Page 68 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Number Screened, Eligible, Enrolled, Author Esophagitis Grade (Grading Withdrawn, Lost to Year Population, Setting Criteria), Other Characteristics Followup Healing Rate at 4 Weeks Scholten et al. Proton pump inhibitors Page 69 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 1. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Year Healing Rate at 8 Weeks Symptoms at 4 Weeks Symptoms at 8 Weeks Scholten et al. Erosive gastroesophageal reflux disease short-term trials of proton pump inhibitor compared with proton pump inhibitor Author Withdrawals Due to Year Results by Baseline Severity Adverse Events Quality rating Funding source Scholten et al. Proton pump inhibitors Page 71 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Quality assessment of included trials Internal Validity Author, Allocation Eligibility Outcome Year Randomization concealment criteria assessors Care provider Country adequate? Adachi 2003 Method not reported Yes Yes Yes No- open No Ando 2005 Method not reported Not reported Some Yes Yes Yes Armstrong et al Method not reported Not reported Yes Yes Described as double-Described as double- 2004 blind, not specified blind, not specified Bardhan 2001 Method not reported Not reported More smokers in Yes No- open No pantoprazole group (31% vs 22%), more males in omeprazole group (64% vs 52%) Bardhan 2007 Yes Yes Yes Yes NR Unclear, used identical appearance in shape and color medications Proton pump inhibitors Page 72 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Quality assessment of included trials Author, Reporting of attrition, Post- Year crossovers, adherence, and Loss to follow-up: Intention-to-treat (ITT) randomization Country Patient masked? Ando 2005 Yes attrition yes, adherence no, No No Yes crossovers no, contamination no Armstrong et al Described as No Not reported Unable to determine (defined Unable to 2004 double-blind, not as all randomized patients determine specified who took at least one dose of study medication and had post-randomization data, but number withdrawn not reported) Bardhan 2001 No Attrition and adherence yes No Yes No Bardhan 2007 Yes Attrition yes, others no Somewhat, 29% Yes Yes, post pantoprazole and 27% randomization esomeprazole withdrew exclusions for protocol violation, but these people were included in ITT analysis Proton pump inhibitors Page 73 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Quality assessment of included trials Author, Year Country Quality Rating Adachi 2003 Fair-poor Ando 2005 Fair Armstrong et al Fair 2004 Bardhan 2001 Fair Bardhan 2007 Fair Proton pump inhibitors Page 74 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Quality assessment of included trials Internal Validity Author, Allocation Eligibility Outcome Year Randomization concealment criteria assessors Care provider Country adequate? Bate 1995 Method not reported Method not reported Yes Yes Not reported Not reported Boccia 2007 Yes Yes Yes Yes Yes Yes Bour 2005 Randomization, method No - open label Mostly, except for on-demand Yes No - open label No - open label not described group had fewer years with reflux Bytzer 2004 Yes Yes Yes Not reported Yes Bytzer 2006 Yes Yes Yes Yes NR NR Bytzer et al. Method not reported Not reported Yes Yes Yes Yes 2004 Proton pump inhibitors Page 75 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Quality assessment of included trials Author, Reporting of attrition, Post- Year crossovers, adherence, and Loss to follow-up: Intention-to-treat (ITT) randomization Country Patient masked? Yes Attrition yes, others no No No (analyzed patients who No 2004 had data on at least 1 postrandomization visit; number not specified) Proton pump inhibitors Page 76 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Fair 2004 Proton pump inhibitors Page 77 of 304 Final Report Update 5 Drug Effectiveness Review Project Evidence Table 2. Quality assessment of included trials Internal Validity Author, Allocation Eligibility Outcome Year Randomization concealment criteria assessors Care provider Country adequate? Caos 2000 Method not reported Method not reported No - placebo had higher Yes Not reported Not reported baseline GERDheartburn frequency. Caos 2005 Yes Method not reported Yes Yes Not reported Not reported Caos et al. Quality assessment of included trials Author, Reporting of attrition, Post- Year crossovers, adherence, and Loss to follow-up: Intention-to-treat (ITT) randomization Country Patient masked? They only discuss analysis, but unable to parse parse out, others no who withdrew because of out AEs. Devault 2006 Yes Attrition yes, others no No, 2% from esomeprazole Stated, but when you look at Yes, they excluded and 3% from lansoprazole the number of peoeple on the 3% from withdrew table is the PP not the ITT esomeprazole and population 3. Quality assessment of included trials Author, Year Country Quality Rating Caos 2000 Fair Caos 2005 Fair Caos et al. Quality assessment of included trials Internal Validity Author, Allocation Eligibility Outcome Year Randomization concealment criteria assessors Care provider Country adequate? Fennerty 2005 Yes Yes Yes Yes Yes Yes Festen 1999 Yes Method not reported Yes Yes Not reported Not reported Florent 1994 Method not reported Not reported More patients with previous Yes Unclear Unclear hemorrhage in O group Fock et al. Quality assessment of included trials Author, Reporting of attrition, Post- Year crossovers, adherence, and Loss to follow-up: Intention-to-treat (ITT) randomization Country Patient masked? Quality assessment of included trials Author, Year Country Quality Rating Fennerty 2005 Good Festen 1999 Fair Florent 1994 Poor Fock et al.

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Journal of the American Academy of Child & Adolescent Psychiatry. Long-term atomoxetine treatment in adolescents with attention-deficit/hyperactivity disorder. A randomized, single-blind, substitution study of OROS methylphenidate (Concerta) in ADHD adults receiving immediate release methylphenidate. Comparing guanfacine and dextroamphetamine for the treatment of adult attention-deficit/hyperactivity disorder. Efficacy of modafinil compared to dextroamphetamine for the treatment of attention deficit hyperactivity disorder in adults. Attention deficit hyperactivity disorder 136 of 200 Final Update 4 Report Drug Effectiveness Review Project 189. Functional outcomes in the treatment of adults with ADHD. A pilot study of the effects of atomoxetine on driving performance in adults with ADHD. Atomoxetine in adults with ADHD: two randomized, placebo-controlled studies. Effectiveness and tolerability of tomoxetine in adults with attention deficit hyperactivity disorder. Simulated driving changes in young adults with ADHD receiving mixed amphetamine salts extended release and atomoxetine. Once-daily atomoxetine for adult attention- deficit/hyperactivity disorder: a 6-month, double-blind trial. Once-daily treatment with atomoxetine in adults with attention-deficit/hyperactivity disorder: A 24-week, randomized, double- blind, placebo-controlled trial. Atomoxetine treatment in adults with attention-deficit/hyperactivity disorder and comorbid social anxiety disorder. McRae-Clark AL, Carter RE, Killeen TK, Carpenter MJ, White KG, Brady KT. A placebo-controlled trial of atomoxetine in marijuana-dependent individuals with attention deficit hyperactivity disorder. A randomized double-blind trial of paroxetine and/or dextroamphetamine and problem-focused therapy for attention- deficit/hyperactivity disorder in adults. Paterson R, Douglas C, Hallmayer J, Hagan M, Krupenia Z. A randomised, double-blind, placebo-controlled trial of dexamphetamine in adults with attention deficit hyperactivity disorder. Efficacy and safety of dexmethylphenidate extended-release capsules in adults with attention-deficit/hyperactivity disorder. Double-blind, placebo-controlled study of the efficacy and safety of lisdexamfetamine dimesylate in adults with attention- deficit/hyperactivity disorder. Randomized, double-blind, placebo-controlled, crossover study of the efficacy and safety of lisdexamfetamine dimesylate in adults with attention-deficit/hyperactivity disorder: novel findings using a simulated adult workplace environment design. Effect size of lisdexamfetamine dimesylate in adults with attention-deficit/hyperactivity disorder. Attention deficit hyperactivity disorder 137 of 200 Final Update 4 Report Drug Effectiveness Review Project 204. Efficacy of a mixed amphetamine salts compound in adults with attention-deficit/hyperactivity disorder. Mixed amphetamine salts extended-release in the treatment of adult ADHD: a randomized, controlled trial. Effects of two doses of methylphenidate on simulator driving performance in adults with attention deficit hyperactivity disorder. The efficacy of 2 different dosages of methylphenidate in treating adults with attention-deficit hyperactivity disorder. Canadian Journal of Psychiatry - Revue Canadienne de Psychiatrie. Carpentier PJ, de Jong CA, Dijkstra BA, Verbrugge CA, Krabbe PF. A controlled trial of methylphenidate in adults with attention deficit/hyperactivity disorder and substance use disorders. Effect of stimulant medication on driving performance of young adults with attention-deficit hyperactivity disorder: a preliminary double-blind placebo controlled trial. Kooij JJ, Burger H, Boonstra AM, Van der Linden PD, Kalma LE, Buitelaar JK. Efficacy and safety of methylphenidate in 45 adults with attention-deficit/hyperactivity disorder. A randomized placebo-controlled double-blind cross-over trial. Methylphenidate effects on symptoms of attention deficit disorder in adults. Double-blind placebo-controlled trial of methylphenidate in the treatment of adult ADHD patients with comorbid cocaine dependence. A large, double-blind, randomized clinical trial of methylphenidate in the treatment of adults with attention-deficit/hyperactivity disorder. Spencer T, Wilens T, Biederman J, Faraone SV, Ablon JS, Lapey K. A double-blind, crossover comparison of methylphenidate and placebo in adults with childhood-onset attention-deficit hyperactivity disorder. Tenenbaum S, Paull JC, Sparrow EP, Dodd DK, Green L. An experimental comparison of Pycnogenol and methylphenidate in adults with Attention-Deficit/Hyperactivity Disorder (ADHD). Attention deficit hyperactivity disorder 138 of 200 Final Update 4 Report Drug Effectiveness Review Project 219. Turner DC, Blackwell AD, Dowson JH, McLean A, Sahakian BJ. Neurocognitive effects of methylphenidate in adult attention-deficit/hyperactivity disorder. Methylphenidate significantly improves driving performance of adults with attention-deficit hyperactivity disorder: a randomized crossover trial. A controlled study of methylphenidate in the treatment of attention deficit disorder, residual type, in adults. Diagnosis and treatment of minimal brain dysfunction in adults: a preliminary report. A randomised, placebo-controlled, 24- week, study of low-dose extended-release methylphenidate in adults with attention- deficit/hyperactivity disorder. European Archives of Psychiatry and Clinical Neuroscience. A randomized, placebo-controlled trial of OROS methylphenidate in adults with attention-deficit/hyperactivity disorder. Efficacy of osmotic-release oral system (OROS) methylphenidate for mothers with attention-deficit/hyperactivity disorder (ADHD): preliminary report of effects on ADHD symptoms and parenting. A randomized, placebo-controlled trial of three fixed dosages of prolonged-release OROS methylphenidate in adults with attention- deficit/hyperactivity disorder. Efficacy and safety of OROS methylphenidate in adults with attention deficit/hyperactivity disorder.

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