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Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled M eanAge:45 discount 5mg singulair with amex. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed M eanscoreforPatientSatisfaction(onscaleof 0-10 generic singulair 10 mg online,with 10 G an being m ostsatisfied) 2004 A:10(range:8-10) 2/0/75 N R SingleCenter B:8. C Patientsatisfaction(score:0-10"m ostsatisfied") J okela A:9(range:0-10) 2002 21/N R /179 B:9(range:0--10) N R M ulticenter C:10(range:0-10),p = 0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting Studygroup:IV dex am ethasone 8m g in2m L volum eafter successfulintubation,andIV ondansetron4m g within15m in beforetrachealex tubationatthe endof anesthesia,thenO D T of ASA I-II patientsundergoing ondansetron8m g atthetim eof outpatientlaparoscopic dischargefrom PACU andonthe gynecologicalsurgerieswith Pan m orning of postoperativeday1 generalanesthesia;aged 2008 and2athom e. R CT,D B L aparoscopic gynecologicalsurgeries >18years;having allthree TwoSites patientspecific em etic risk U S Controlgroup:IV placeboof 2m L factors;abilitytofollow study norm alsalineaftersuccessful protocolinstructions;andwilling intubation,andIV ondansetron tocom pletethedailydiary 4m g within15m inbeforetracheal ex tubationatendof anesthesia, thenplaceboO D T atdischarge andonthem orning of postoperativeday1and2at hom e. A:30% ox ygeninnitrogenand ASA I-III fem alesaged18-75 Purhonen saline2m li. Antiemetics Page 392 of 492 Final Report Update 1 Drug Effectiveness Review Project Evidence Table 11. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled Preoperativem edicationconsisted Pan of 0-2m g ivm idaz olam andoral M eanage:34. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed Studygroup vsControlgroup Patientsreporting nauseaaffecting Q O L :33% vs60% (p<0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting A:O nd8m g iv R eihner Breastsurgery 1999 R CT,ACT N on-pregnant,non-obeseASA B:droperidol(drop)1. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled M eanage:54y Historyof PO N V:43. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed R eihner 1999 9/N R /207 N R StayinPACU (m in):120vs120vs120,N S SingleCenter Sweden Sandhu O verallsatisfactionscore(0-10"satisfied"): M eantim etodischarge(m in):189vs199vs205,N S 1999 N R /N R /87 PACU :9vs9vs9;N S N R Hom e:8vs8vs8,N S Steinbrook 1996 15/N R /200 N R D ischargetim e(m in):293vs288,N S SingleCenter U S Antiemetics Page 397 of 492 Final Report Update 1 Drug Effectiveness Review Project Evidence Table 11. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting A dults:Placebo- controlled trials Dolasetron Ptsundergoing surgerywith general A:D ol12. B:D ol25po orII ptswith noalcoholordrug 1997 R CT,PCT C:D ol50po addictionandnorm alserum N a m ulticenter D B G yn. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled A dults:Placebo- controlled trials Dolasetron M eanAge:40. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed A dults:Placebo- controlled trials Dolasetron Patientsatisfaction(VAS score:0= notatallsatisfiedto100= D iem unsch com pletesatisfaction) 1997 N R /0/337 N R m ulticenter VAS scoresnotgiven;theonlything saidwasthatD ol-treated E urope ptswerem oresatisfiedwith treatm entthanplacebopts (p<0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting A:O nd4m g iv Han B:placebo 2004 electivesurgeryundergen. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled M eanage:67. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed Han Ptsatisfactionforanalgesiatherapy,A vs. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting Scuderi 1999 Single-center R CT,PCT O utpatientsurgerywith general A:O nd4m g iv ASA I,II,orIII outpatients U S D B anesthesia B:placebo A:O nd4m g ivbeforeinductionof am bulatoryotolaryngologic procedures anest. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled M eanage:38. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed Scuderi 1999 Tim etodischargefrom PACU todayhospital(m in):59 Single-center Satisfactionwith controlof PO N V:#yes/#no,A vsB: vs58,N S, U S 230/7(97%)vs212/16(93%),p = 0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting A:30% inspiredox ygeninairplus intravenousadm inistrationof saline Trescha B:80% inspiredox ygeninairplus 2005 ASA I orII ptsscheduledto R CT,D B Strabism us intravenousadm inistrationof SingleCenter undergostrabism ussurgery saline G erm any C:30% inspiredox ygeninairplus 75µg/kg ondansetron intravenously during induction Palonosetron A:Palonosetron0. D :Placebo R S-25259 Antiemetics Page 407 of 492 Final Report Update 1 Drug Effectiveness Review Project Evidence Table 11. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled Pediatric patients(aged<15years): Pre-m edicatedwith m idaz olam 31. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed 30O 2vs80O 2vsO N D U seof rescuetherapy0-24h aftersurgery:15% vs12% Trescha vs7% 2005 N R /N R /210 N odifferenceinpatientsatisfaction(num bersN R ) U seof rescuetherapy0-6h aftersurgery:10% vs9% vs SingleCenter 6% G erm any U seof rescuetherapy6-24h aftersurgery:10% vs4% vs1% Palonosetron Palonosetron0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting A:R S-252590. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled N R /N ouseof antagonists, Tang M eanweight(kg):72. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or W ith drawn/ Y ear L ostto fu/ R esults -Satisfaction R esults -R esource utiliz ation Setting A nalyz ed A vsBvsC vsD vsE vsF U seof rescuem edication0-2h aftersurgery:22% vs 22% vs23% vs20% vs23% vs31% U seof rescuem edication0-12h aftersurgery:63% vs 56% vs43% vs43% vs46% vs72% (p<0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or Y ear Design Surgery type Inclusioncriteria Intervention Setting C h ildren:A ctive- controlled trials O ndansetron Bach-Styles 1997 A:O ndansetron(O nd)0. A:O nd75m cg/kg E lectivestrabism usrepairsurgeryw/o 1995 R CT,ACT ASA I orII pediatric andadult B:O nd150m cg/kg gastric suctioning SingleCenter D B pts C:D roperidol75m cg/kg M eansurgerytim e:87m in SaudiArabia D avis,P. A:O nd100m cg/kg iv 1995 R CT D entalsurgery(with stom ach B:D roperidol(drop)75m cg/kg iv ASA I andII pediatric pts SingleCenter D B suctioning atend) C:placebo U S L itm an Strabism usrepair healthyASA I andII children 1995 R CT,ACT A:O nd0. Preventionofpostoperative nauseaand vom iting:A ctive-controland placebo-controlled trials A uth or A ge/ Screened/ R un-in/ Y ear A llow oth erm edication G ender/ O th erpopulationch aracteristics Eligible/ W ash out Setting Eth nicity Enrolled C h ildren:A ctive- controlled trials O ndansetron Bach-Styles "AN O VA showednosignificant M eanAge:N R 1997 differencebetweenthe3studygroups R ange:1-17y SingleCenter with regardtoAge,height,weight,ASA U S N R N R /N R status,historyof vom iting,no. Allptsprem edicatedwith either R ange:2-8yrs 1995 m idaz olam intranasally(0.

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Increased activity of coagulation The contact pathway has seen a resurgence in interest because of the factor XII (Hageman factor) causes hereditary angioedema type III 10mg singulair with mastercard. Bork K order 4mg singulair with mastercard, Wulff K, Meinke P, Wagner N, Hardt J, Witzke G. A novel of the contact proteins are protected against thrombosis. These mutation in the coagulation factor 12 gene in subjects with hereditary observations led to the development of several compounds targeting angioedema and normal C1-inhibitor. Missense mutations in the coagulation factor XII approach to target (one of the) contact proteins would constitute an (Hageman factor) gene in hereditary angioedema with normal C1 effective and safe strategy for antithrombotic treatment. In addition, it will be essential to identify the deficiency. Effects of factor IX or factor XI deficiency on ferric chloride-induced carotid artery occlusion in mice. Effects of factor XI deficiency on Conflict-of-interest disclosures: J. FXI is essential for thrombus formation following FeCl3-induced injury of the carotid artery in the Correspondence mouse. Meijers, PhD, Department of Plasma Proteins, Sanquin factor XI prolongs APTT without increased bleeding risk in cynomolgus Research, Plesmanlaan 126, 1066 CX Amsterdam, the Netherlands; monkeys. Phone: 31-20-5123151; Fax: 31-20-5123310; e-mail: j. Inhibition of the intrinsic coagulation pathway factor XI by antisense oligonucleotides: a novel References antithrombotic strategy with lowered bleeding risk. A role for factor XIIa-mediated 2010:104(5):867-874. The procoagulant and proinflammatory plasma contact 3981-3989. The coagulation system and its function in anti-human factor XI antibodies prevent cessation of blood flow in a early immune defense. Thrombosis as an intravascular effector of antisense factor XI oligonucleotide treatment in primates. Prevention of vascular graft 64 American Society of Hematology occlusion and thrombus-associated thrombin generation by inhibition of 39. Factor XI Regulates generation through direct interaction with fibrin. Girolami A, Candeo N, De Marinis GB, Bonamigo E, Girolami B. Defective thrombus formation deficiency on haemostasis and thrombosis in mice: murine ortholog of in mice lacking coagulation factor XII. Factor XIIa inhibitor dase depletion induces vascular dysfunction with hypertension and recombinant human albumin Infestin-4 abolishes occlusive arterial faster arterial thrombosis. Factor XII regulates brain barrier damage, and inflammation. Factor XII inhibition knockout mice are protected from thrombosis by increased nitric oxide reduces thrombus formation in a primate thrombosis model. A factor XIIa inhibitory decrease thrombosis in Bdkrb2 / mice by increasing NO and antibody provides thromboprotection in extracorporeal circulation with- prostacyclin to reduce platelet spreading and glycoprotein VI activation. Meijers1,2 1Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands; and 2Department of Plasma Proteins, Sanquin Research, Amsterdam, the Netherlands The contact pathway of coagulation consists of the proteins factor XI, factor XII, prekallikrein, and high-molecular- weight kininogen. Activation of the contact system leads to procoagulant and proinflammatory reactions. The contact system is essential for surface-initiated coagulation, as exemplified by aPTT, but there is probably no role for the contact system in initiating physiologic in vivo coagulation. However, over the last few years, there has been renewed interest, especially because of experimental evidence suggesting that the contact system contributes to thrombosis. Knockout mice deficient in one of the contact proteins were protected against artificially induced thrombosis. Furthermore, inhibiting agents such as monoclonal antibodies, antisense oligonucleotides, and small molecules were found to prevent thrombosis in rodents and primates in both venous and arterial vascular beds. Although it remains to be established whether targeting the contact system will be effective in humans and which of the contact factors is the best target for anticoagulation, it would constitute a promising approach for future effective and safe antithrombotic therapy. The contact system has a remarkable resemblance to the innate Learning Objectives 3 immune system based on the recognition molecules. Indeed, the ● To understand that the contact system consists of 4 proteins: contact system recognizes an increasing number of bacterial patho- factor XI, factor XII, PK, and HK gens and other types of microorganisms. Therefore, the contact system is part of the new method to prevent thrombosis in mice research field referred to as “immunothrombosis.

The phosphoino- are tolerable and highly active in patients with relapsed or sitide 3 -kinase delta inhibitor purchase singulair 4mg amex, CAL-101 discount 5 mg singulair otc, inhibits B-cell recep- refractory chronic lymphocytic leukemia (CLL): results from a tor signaling and chemokine networks in chronic lymphocytic phase I study [abstract]. B-cell receptor a phase 1 study of CAL-101, An isoform-selective inhibitor of triggers drug sensitivity of primary CLL cells by controlling phosphatidylinositol 3-kinase P110, in patients with glucosylation of ceramides. Oncogenically active (ASH Annual Meeting Abstracts). Exploiting synthetic demonstrates clinical activity and pharmacodynamic effects in lethality for the therapy of ABC diffuse large B cell lymphoma. Bruton’s tyrosine kinase (BTK) inhibitor PCI-32765 with 35. Chemokines and chemokine receptors in chronic bendamustine (B)/rituximab (R) (BR) in patients (pts) with lymphocytic leukemia (CLL): from understanding the basics relapsed/refractory (R/R) chronic lymphocytic leukemia (CLL): towards therapeutic targeting. A phase I trial of the tic strategy for chronic lymphocytic leukemia by combining Bruton’s tyrosine kinase (BTK) inhibitor, ibrutinib (PCI- GS-1101, a PI3 kinase delta (PI3K) inhibitor and a novel 32765), in combination with rituximab (R) and bendamustine in highly selective spleen tyrosine kinase (Syk) inhibitor, GS- patients with relapsed/refractory non-Hodgkin’s lymphoma 9973 [abstract]. A phase I/II study of evaluating activity and tolerability of BTK inhibitor PCI-32765 the selective phosphatidylinositol 3-kinase-delta (PI3K) and ofatumumab in patients with chronic lymphocytic leukemia/ inhibitor, GS-1101 (CAL-101), with ofatumumab in patients with small lymphocytic lymphoma (CLL/SLL) and related diseases. Younes A, Flinn I, Berdeja J, Friedberg J, Alberti S. Phase 1b plasma levels and the risk for disease progression in chronic study combining ibrutinib with rituximab, cyclophosphamide, lymphocytic leukemia. Paraffin-based 6-gene with CD20-positive B-cell non-Hodgkin lymphoma (NHL). Beyond JAK2 V617F, a more detailed picture of the pathobiologic basis for activated JAK-STAT signaling has emerged. In some patients with myelofibrosis (MF), next-generation sequencing technologies have revealed a complex clonal architecture affecting both genetic and epigenetic regulators of cell growth and differentiation. Although these bench-top findings have informed the clinical development of JAK inhibitors in MF, they have also provided scientific context for some of their limitations. The JAK1/JAK2 inhibitor ruxolitinib is approved for treatment of MF in North America and Europe and other lead JAK inhibitors discussed herein (fedratinib [SAR302503], momelotinib [CYT387], and pacritinib [SB1518]), have entered advanced phases of trial investigation. Uniformly, these agents share the ability to reduce spleen size and symptom burden. A major challenge for practitioners is how to optimize dosing of these agents to secure clinically relevant and durable benefits while minimizing myelosuppression. Suboptimal responses have spurred a “return to the bench” to characterize the basis for disease persistence and to inform new avenues of drug therapy. Lessons from the bench mutations in LNK or CBL ( 5% frequency)15,16 or abrogation of Normal hematopoiesis relies on the cytoplasmic tyrosine kinase suppressor of cytokine signaling (SOCS) activity (due to SOCS gene JAK2, which associates with the type I cytokine receptors for hypermethylation or increased protein phosphorylation) provide alter- erythropoietin, thrombopoietin, and G-CSF. Initial models predicted that logic pathways is common in MPN (Table 1)6,22 and contributes to the mutation relieves inhibition of the kinase (JH1) domain by the disease initiation and progression. Such modeling information is critical to the development chronic myeloid leukemia (CML), BCR-ABL1 is sufficient as a of next-generation mutant-specific inhibitors, which may exhibit genetic driver and has served as a paradigmatic target of better targeting of the malignant clone with less suppression of successful therapy with ABL tyrosine kinase inhibitors. Abnormalities in ment for cytokine receptor binding by ligand. Although activation of epigenetic pathways that control DNA methylation and modifica- the JAK-STAT pathway is common in myeloproliferative neoplasms tion of chromatin (detailed by Abdel-Wahab24) and mutations in (MPNs), it cannot be solely explained by the V617F or exon 12 JAK2 spliceosome factors have also emerged as important aspects of mutations that are found in 1% to 3% of PV patients. For example, transmembrane domain mutations (eg, W515 L/K) in MPL,13,14 the receptor for thrombopoietin, are found Among the MPNs, MF is notoriously characterized by a patho- in 1% to 5% of patients with ET and in 5% to 10% of PMF patients and logic milieu of proinflammatory and profibrotic cytokines (eg, lead to cytokine-independent growth and constitutive JAK-STAT IL-6, basic FGF, TGF- , TNF- , hepatocyte growth factor, signaling. Impaired negative regulation of JAK-STAT signaling due to VEGF, and others). Mutation frequency in chronic-phase and post-MPN AML cades and V617F-bearing neoplastic cells is a rational applica- tion of these drugs. In this regard, cytokine down-modulation by ruxolitinib25 and fedratinib27 has been demonstrated. It has also been shown that cytokines secreted by BM stromal cells protect MPN clones from JAK2 inhibitor treatment,28 highlighting the need to target both the BM microenvironment and malignant clone. Lessons from the bedside In MF, the decision regarding when and what type of therapy to initiate depends on a nexus of factors related to the patient, disease stage,29 primary clinical manifestations, drug-specific consider- ations, and treatment goals (Figure 1). Similarly, after treatment is initiated, a nuanced understanding of the relationship among drug dose, hematologic and nonhematologic adverse events, and efficacy outcomes is critical to optimizing patient care. The experience with JAK inhibitors highlights many of these interacting issues. The extramedullary hematopoiesis associated with MF-related constitutional symptoms and disease-related ca- splenomegaly is a cardinal feature of MF and is linked to abdominal chexia. Increased cytokine blood levels have been correlated pain and impairment of quality of life (QOL). A 35% reduction in with transfusion dependence, increased splenomegaly, thrombo- spleen volume by CT/MRI has been validated as a radiographic cytopenia, and shortened survival. Pre- and on-treatment considerations with use of JAK inhibitors in MF. Studies of lead JAK inhibitors in patients with MF the primary end point of a 35% reduction in spleen volume at vassed the unique spectrum of symptoms afflicting MF patients.

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Were the findings of the relevant studies combined appropriately relative to the primary question the overview addresses? For Question 8 generic 4 mg singulair otc, if not attempt has been made to combine findings purchase singulair 10mg on-line, and no statement is made regarding the inappropriateness of combining findings, check “No”. Diabetes Page 91 of 99 Final Report Drug Effectiveness Review Project 9. Were the conclusions supported by the reported data? Were the conclusions made by the author(s) supported by the data and/or analysis reported in the overview? For an overview to be scored as “Yes” in Question 9, data (not just citations) must be reported that support the main conclusions regarding the primary question(s) that the overview addresses. What was the overall scientific quality of the overview? How would you rate the scientific quality of this overview? The score for Question 10, the overall scientific quality, should be based on your answers to the first nine questions. The following guidelines can be used to assist with deriving a summary score: If the “Can’t tell” option is used one or more times on the preceding questions, a review is likely to have minor flaws at best and it is difficult to rule out major flaws (i. If the “No” option is used on Question 2, 4, 6 or 8, the review is likely to have major flaws (i. Controlled Trials Assessment of Internal Validity 1. Was assignment to the treatment groups really random? Adequate approaches to sequence generation: Computer-generated random numbers Random numbers tables Inferior approaches to sequence generation: Use of alternation, case record number, birth date, or day of the week Not reported 2. Adequate approaches to concealment of randomization: Centralized or pharmacy-controlled randomization Serially-numbered identical containers On-site computer-based system with a randomization sequence that is not readable until allocation Other approaches that conceal the sequence to clinicians and patients until treatment allocation Inferior approaches to concealment of randomization: Use of alternation, case record number, birth date, or day of the week Open random-numbers lists Serially numbered envelopes (even sealed opaque envelopes can be subject to manipulation) Not reported 3. Were the groups similar at baseline in terms of prognostic factors? Diabetes Page 92 of 99 Final Report Drug Effectiveness Review Project 5. Were outcome assessors blinded to the treatment allocation? Was the patient kept unaware of the treatment received? Did the article include an intention-to-treat analysis or provide the data needed to calculate it (that is, number assigned to each group, number of subjects who finished in each group, and results for those subjects)? Did the article report attrition, crossovers, adherence, and contamination? Is there important differential loss to follow-up or overall high loss to follow-up (report numbers in each group)? Assessment of External Validity (Generalizability) 1. How similar is the population to the population to whom the intervention would be applied? What was the funding source and role of the funder in the study? Was the selection of patients for inclusion non-biased? Is there important differential loss to follow-up or overall high loss to follow-up? Was there a clear description of the techniques used to identify the events? Diabetes Page 93 of 99 Final Report Drug Effectiveness Review Project 5. Was there non-biased and accurate ascertainment of events (independent ascertainers, validation of ascertainment technique)? Were potential confounding variables and risk factors identified and examined using acceptable statistical techniques? Did the duration of follow-up correlate to reasonable timing for investigated events? How similar is the population to the population to whom the intervention would be applied? What was the funding source and role of the funder in the study? Current methods of the US Preventive Services Task Force: a review of the process. Validation of an index of the quality of review articles. Diabetes Page 94 of 99 Final Report Drug Effectiveness Review Project Appendix C.

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