29 research outputs found

    What is the impact of contraceptive methods and mixes of contraceptive methods on contraceptive prevalence, unmet need for family planning, and unwanted and unintended pregnancies?

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    Background - In many low-and middle-income countries, there is high maternal, infant and child mortality due in part to low contraceptive use and high unmet need for family planning. The aim of this overview of systematic reviews is to synthesise the findings of systematic reviews conducted in this area to assess the impact of various contraceptive methods and mixes of contraceptive methods on contraceptive prevalence, unwanted and unintended pregnancies, and unmet need (a desire to limit the number of children but not currently using any contraception) for family planning in developing countries/regions.Methods - Eight databases (Bioline international, The Cochrane Library, Latin American and Caribbean Health Sciences Literature - LILACS, Popline, PubMed, Turning Research Into Practice, World Health Organisation Reproductive Health Library and Zetoc) were searched from 28 October 2010 to 08 December 2010. Cochrane and non-Cochrane systematic reviews were included. Eligible reviews included studies whose participants were sexually active women or men from countries classified as ‘developing’, ‘low-income’ or ‘middle-income’. Systematic reviews of any intervention (or combination of interventions) designed to increase contraceptive prevalence, reduce fertility or both were eligible. Data were extracted and synthesised narratively. A Measurement Tool to Assess Systematic Reviews, AMSTAR, was used to evaluate the quality of the included systematic reviews, and Grading of Recommendations, Assessment, Development and Evaluation (GRADE) was used to evaluate the quality of the body of evidence for each comparison. To aid the interpretation of the findings for a variety of settings, relevant contextual information was presented where possible.Results - There were 22 systematic reviews included in this overview of reviews. The overview examined a range of contraceptive methods, including modern (terminal and spacing) and traditional methods (such as withdrawal and periodic abstinence which do not require contraceptive substances or devices and also do not require clinical procedures). However, the systematic reviews included did not address all the objectives of the overview.The results of the review are summarised below according to the objectives.Objective 1: To assess the impact of various contraceptive methods and mixes ofcontraceptive methods on contraceptive prevalence in developing countries/regions. There was no systematic review that met this objective.Objective 2: To assess the impact of various contraceptive methods and mixes ofcontraceptive methods on unwanted and unintended pregnancies in developingcountries/regions.The body of evidence for the relative efficacy or effectiveness of a variety ofcontraceptive methods to prevent pregnancy in developing countries was generally rated as of low or moderate quality. There was, however, a number of comparisons (between different derivatives of the same contraceptive methods) for which the evidence was rated as of high or moderate quality. Evidence from systematic reviews is lacking on the acceptability of contraceptive methods and their impact on prevalence and on unmet needs for family planning. The evidence for the relative effectiveness of a variety of contraceptive methods to prevent pregnancy in developing countries is generally of low quality. There is some high-quality evidence comparing different derivatives of the same contraceptive methods, although this is more often evidence of efficacy than evidence of effectiveness.Objective 3: To assess the impact of various contraceptive methods and mixes ofcontraceptive methods on unmet need for family planning in developing countries/regions.There was no systematic review that met this objective

    Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease

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    Chronic obstructive pulmonary disease (COPD) is a global health problem. The current therapies for COPD are poorly effective and the mainstays of pharmacotherapy are bronchodilators. A better understanding of the pathobiology of COPD is critical for the development of novel therapies. In the present review, we have discussed the roles of oxidative/aldehyde stress, inflammation/immunity, and chromatin remodeling in the pathogenesis of COPD. An imbalance of oxidants/antioxidants caused by cigarette smoke and other pollutants/biomass fuels plays an important role in the pathogenesis of COPD by regulating redox-sensitive transcription factors (e.g., NF-κB), autophagy and unfolded protein response leading to chronic lung inflammatory response. Cigarette smoke also activates canonical/alternative NF-κB pathways and their upstream kinases leading to sustained inflammatory response in lungs. Recently, epigenetic regulation has been shown to be critical for the development of COPD because the expression/activity of enzymes that regulate these epigenetic modifications have been reported to be abnormal in airways of COPD patients. Hence, the significant advances made in understanding the pathophysiology of COPD as described herein will identify novel therapeutic targets for intervention in COPD

    Pontiella desulfatans gen. Nov., sp. nov., and pontiella sulfatireligans sp. nov., two marine anaerobes of the pontiellaceae fam. nov. producing sulfated glycosaminoglycan-like exopolymers

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    Recently, we isolated two marine strains, F1T and F21T, which together with Kiritimatiella glycovorans L21-Fru-ABT are the only pure cultures of the class Kiritimatiellae within the phylum Verrucomicrobiota. Here, we present an in-depth genome-guided characterization of both isolates with emphasis on their exopolysaccharide synthesis. The strains only grew fermentatively on simple carbohydrates and sulfated polysaccharides. Strains F1T, F21T and K. glycovorans reduced elemental sulfur, ferric citrate and anthraquinone-2,6-disulfonate during anaerobic growth on sugars. Both strains produced exopolysaccharides during stationary phase, probably with intracellularly stored glycogen as energy and carbon source. Exopolysaccharides included N-sulfated polysaccharides probably containing hexosamines and thus resembling glycosaminoglycans. This implies that the isolates can both degrade and produce sulfated polysaccharides. Both strains encoded an unprecedently high number of glycoside hydrolase genes (422 and 388, respectively), including prevalent alpha-L-fucosidase genes, which may be necessary for degrading complex sulfated polysaccharides such as fucoidan. Strain F21T encoded three putative glycosaminoglycan sulfotransferases and a putative sulfate glycosaminoglycan biosynthesis gene cluster. Based on phylogenetic and chemotaxonomic analyses, we propose the taxa Pontiella desulfatans F1T gen. nov., sp. nov. and Pontiella sulfatireligans F21T sp. nov. as representatives of the Pontiellaceae fam. nov. within the class Kiritimatiellae.Environmental Fluid Mechanic

    Genome-wide meta-analysis identifies 11 new loci for anthropometric traits and provides insights into genetic architecture

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    Approaches exploiting trait distribution extremes may be used to identify loci associated with common traits, but it is unknown whether these loci are generalizable to the broader population. In a genome-wide search for loci associated with the upper versus the lower 5th percentiles of body mass index, height and waist-to-hip ratio, as well as clinical classes of obesity, including up to 263,407 individuals of European ancestry, we identified 4 new loci (IGFBP4, H6PD, RSRC1 and PPP2R2A) influencing height detected in the distribution tails and 7 new loci (HNF4G, RPTOR, GNAT2, MRPS33P4, ADCY9, HS6ST3 and ZZZ3) for clinical classes of obesity. Further, we find a large overlap in genetic structure and the distribution of variants between traits based on extremes and the general population and little etiological heterogeneity between obesity subgroups

    "Rotterdam econometrics": publications of the econometric institute 1956-2005

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    This paper contains a list of all publications over the period 1956-2005, as reported in the Rotterdam Econometric Institute Reprint series during 1957-2005.

    Assessing Alternative Financing Methods for the Canadian Health Care System in View of Population Aging

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    The cost of the Canadian health care system is approximately 10% of Gross Domestic Product (GDP). Survey-evidence suggests that Canadians do not wish to have additional funds spent on health care but believe that the system should be able to deliver better quality care. Due to low fertility rates and increasing life expectancy, the Canadian population is aging. Over the next 25 years, the dependency ratio will increase, primarily due to the aging of the “baby boom generation” 2. This will place twofold cost pressures on governments responsible for maintaining the health care system: 1) As a consequence of increased life expectancy, on average, Canadians will have a longer period of health care consumption. Although age-specific cost may not increase, with an aging population aggregate annual health care expenditures are expected to increase. 2) The dependency ratio is a proxy for the ability of the population to support itself. The increasing dependency rate may result in a slowdown in GDP growth, given constant technology. In Section I, this paper attempts to quantify these factors. A single measure combining cost and quality is developed to demonstrate the magnitude of the challenge. In Section II, this paper examines a number of different approaches to health care financing including user fees and alternative compensation methods for physicians. The paper highlights documented information from Canada and international experience on the implementation issues involved. The paper evaluates the desirability of implementing these approaches in Canada.Alternative physician reimbursement models, Capitation, DALE, Disability Adjusted Life Expectancy, QAHE, Quality-Adjusted Health Expenditures, QAHE Index, SID, Supplier-Induced Demand

    Clinical assessment of Renal Ischaemic Injury and the Role of Cryopreservation; Peritoneal Cooling an Non-Heart-Beating Donation and Topical Cooling for Laparoscopic Surgery

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    Abstract The project aims focussed on three main areas of study; ischaemic injury assessment, laparoscopic renal cryopreservation and peritoneal cooling for non-heart-beating organ donation. The effects of renal ischaemia represent significant challenges for transplantation and urological surgery in that with sufficient unchecked ischaemic duration, permanent loss of function is inevitable. Prior to consideration of novel approaches to ischaemic protection, aimed at producing improved graft quality for transplantation and an increased safe operating times for partial renal resections, deficiencies in the literature regarding the efficacy of viability testing were targeted. Techniques of ischaemic injury assessment are intended to allow identification of retrieved kidneys which are likely to have lost the potential for adequate function if transplanted. Such organs can then be discarded, thus improving outcomes and decreasing rates of primary non-function. Results pertaining to ischaemic injury assessment provided support for protocols of viability assessment based on hypothermic machine perfusion. The effect of warm ischaemia on renal viability criteria has been successfully demonstrated in a large animal model, and novel approaches to the use of such assessments have been explored in order to maximise organ resource opportunities and utilisation. The project has made an important contribution in the technical approach to laparoscopic partial nephrectomy and laparoscopic renal hypothermia. The studies involving the ‘Newcastle Laparoscopic Renal Cooling Device’ succeeded in achieving ‘proof of concept’ with demonstration of effective renal cooling and preservation.. Studies relating to preservation interventions in the porcine model of the uncontrolled NHBD have produced striking results. These results strongly suggest that uncontrolled NHBD centres employing cold in-situ perfusion approaches to preservation would be wise to consider supplementary techniques of organ cooling

    On the Development and Management of Adaptive Business Collaborations.

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    Today’s business climate demands a high rate of change with which Information Technology (IT)-minded organizations are required to cope. Organizations face rapidly changing market conditions, new competitive pressures, new regulatory fiats that demand compliance, and new competitive threats. All of these situations and more drive the need for the IT infrastructure of an organization to respond quickly in support of new business models and requirements. This dissertation studies the adaptive development and management of such dynamic business models and requirements. A rule based environment is developed in which the people who develop and manage business collaborations in organizations can do so in a way that is as independent of specific implementation technologies as possible; and where they can take business requirements into consideration, and in which they can respond to changes as effectively as possible.

    On the antioxidant mechanisms of Bcl-2: A retrospective of NF-κB signaling and oxidative stress

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    Antioxidant and prooxidant signaling pathways are emanating as major players in, and regulators of, cell death and apoptosis. Redox conception of the critical role of oxidative stress in determining cell fate is being established-a foundation that craves deeper than the basic understanding of physiochemical interactions to extend beyond that into the realms of deciphering the molecular codes implicated with apoptosis. The proto-oncogene Bcl-2 is no stranger being a major player and decoder in controlling apoptosis, ostensibly via the regulation of redox equilibrium and disequilibrium. One of those potential mechanisms exhibited by Bcl-2 is its ability to counteract the detrimental effects of cell damage caused by free radicals, thereby gaining its well-known property of being an antioxidant. But the question is: what are the molecular mechanisms involved with the antioxidant role of Bcl-2 in the face of cell damage and apoptosis? Currently, a stance is being upheld in that the Bcl-2 antioxidant efficacy should be weighed against its ability to manipulate transcriptional control, through the regulation of specific transcription factors. NF-κB is no doubt one of the best candidates when it comes to the arena of oxidative stress, inflammation, and apoptosis. Therein, current themes in the burgeoning antioxidant role of Bcl-2 are exposed within the context of transcriptional control of NF-κB, thereby holding potential avenues for alleviating therapeutic approaches in the regulation of apoptosis. © 2004 Published by Elsevier Inc.Abraham MC, 2004, TRENDS CELL BIOL, V14, P184, DOI 10.1016-j.tcb.2004.03.002; Adachi-Yamada T, 2004, J BIOCHEM, V136, P13, DOI 10.1093-jb-mvh099; Adams JM, 2002, CURR OPIN CELL BIOL, V14, P715, DOI 10.1016-S0955-0674(02)00381-2; Agostini M, 2002, INT J IMMUNOPATH PH, V15, P157; Aoki M, 2001, HYPERTENSION, V38, P48; Beckman KB, 1998, PHYSIOL REV, V78, P547; Bergamini CM, 2004, CURR PHARM DESIGN, V10, P1611, DOI 10.2174-1381612043384664; Bian X, 2001, J BIOL CHEM, V276, P48921, DOI 10.1074-jbc.M108674200; Bian X, 2002, J BIOL CHEM, V277, P42144, DOI 10.1074-jbc.M203891200; Block G, 2004, J AM COLL NUTR, V23, P141; Brunelle JK, 2002, APOPTOSIS, V7, P475, DOI 10.1023-A:1020668923852; Cardoso SM, 2003, FREE RADICAL RES, V37, P967, DOI 10.1080-10715760310001595757; Cardoso SM, 2003, FREE RADICAL RES, V37, P241, DOI 10.1080-1071576021000041023; Chang H, 2003, FREE RADICAL RES, V37, P655, DOI 10.1080-1071576031000094907; Chen Q, 2003, LEUKEMIA LYMPHOMA, V44, P1209, DOI 10.1080-1042819031000068052; Chung KC, 2000, J NEUROSCI RES, V59, P117, DOI 10.1002-(SICI)1097-4547(20000101)59:1117::AID-JNR143.0.CO;2-Q; Clement MV, 1999, FREE RADICAL RES, V30, P247, DOI 10.1080-10715769900300271; CORY S, 1994, PHILOS T ROY SOC B, V345, P289, DOI 10.1098-rstb.1994.0108; Cross CE, 2003, PEDIATR RES, V53, P365, DOI 10.1203-01.PDR.0000049510.15555.30; Cross CE, 2004, CRIT CARE MED, V32, P892, DOI 10.1097-01.CCM.0000115259.05303.91; Cui ZG, 2004, FREE RADICAL RES, V38, P363, DOI 10.1080-1071576042000191754; Danial NN, 2004, CELL, V116, P205, DOI 10.1016-S0092-8674(04)00046-7; Das DK, 2003, ARCH BIOCHEM BIOPHYS, V420, P305, DOI 10.1016-j.abb.2003.09.023; Delhalle S, 2002, ONCOGENE, V21, P3917, DOI 10.1038-sj.onc.1205489; DeLuca C, 1998, VIROLOGY, V244, P27, DOI 10.1006-viro.1998.9085; Dhanalakshmi S, 2004, CARCINOGENESIS, V25, P99, DOI 10.1093-carcin-bgg188; DIETRICH M, 2004, NUTR CANC, V45, P176; DJOURDHEUIL Z, 1997, J CLIN GASTROENTEROL, V1, pS61; Droge W, 2002, PHYSIOL REV, V82, P47; Duchen MR, 2004, DIABETES, V53, pS96, DOI 10.2337-diabetes.53.2007.S96; Earnshaw WC, 1999, ANNU REV BIOCHEM, V68, P383, DOI 10.1146-annurev.biochem.68.1.383; Esposito F, 2004, NEUROCHEM RES, V29, P617, DOI 10.1023-B:NERE.0000014832.78725.1a; Fadeel B, 1999, LEUKEMIA, V13, P719, DOI 10.1038-sj.leu.2401411; Fadeel B, 1999, FASEB J, V13, P1647; GALTER D, 1994, EUR J BIOCHEM, V221, P639, DOI 10.1111-j.1432-1033.1994.tb18776.x; Garcia-Bermejo L, 1998, J CELL SCI, V111, P637; Garg A, 2002, LEUKEMIA, V16, P1053, DOI 10.1038-sj-leu-2402482; Gartner Anton, 2004, Methods Mol Biol, V280, P257; Gohil K, 2003, FREE RADICAL BIO MED, V35, P1343, DOI 10.1016-S0891-5849(03)00509-4; Grunenfelder J, 2002, J HEART LUNG TRANSPL, V21, P244, DOI 10.1016-S1053-2498(01)00377-1; Haddad JJ, 2004, INT IMMUNOPHARMACOL, V4, P475, DOI 10.1016-j.intimp.2004.02.002; Haddad JJ, 2003, CRIT CARE, V7, P47, DOI 10.1186-cc1840; Haddad JJ, 2002, CRIT CARE, V6, P481, DOI 10.1186-cc1839; Haddad JJ, 2004, BIOCHEM BIOPH RES CO, V316, P969, DOI 10.1016-j.bbrc.2004.02.162; Haddad JJ, 2002, CELL SIGNAL, V14, P879, DOI 10.1016-S0898-6568(02)00053-0; Haddad JJE, 2000, BIOCHEM BIOPH RES CO, V271, P257, DOI 10.1006-bbrc.2000.2607; Han SW, 2003, J CLIN ENDOCR METAB, V88, P713, DOI 10.1210-jc.2002-020876; Hancock JT, 2003, ANN NY ACAD SCI, V1010, P446, DOI 10.1196-annals.1299.081; Herrmann JL, 1997, EXP CELL RES, V237, P101, DOI 10.1006-excr.1997.3737; Higuchi Y, 2003, BIOCHEM PHARMACOL, V66, P1527, DOI 10.1016-S0006-2952(03)00508-2; Hour TC, 1999, TOXICOL LETT, V110, P191, DOI 10.1016-S0378-4274(99)00158-7; Hughes SE, 2003, J PATHOL, V201, P181, DOI 10.1002-path.1447; Igaki T, 2004, BBA-MOL CELL RES, V1644, P73, DOI 10.1016-j.bbamcr.2003.09.007; Jacob AK, 1997, SURGERY, V122, P243, DOI 10.1016-S0039-6060(97)90015-5; Jang JH, 2003, BIOCHEM PHARMACOL, V66, P1371, DOI 10.1016-S0006-2952(03)00487-8; Jang JH, 2003, FREE RADICAL BIO MED, V34, P1100, DOI 10.1016-S0891-5849(03)00062-5; KANG BP, 2003, AM J PHYSIOL-RENAL, V1, pF455; Kang HS, 2001, CELL IMMUNOL, V213, P34, DOI 10.1006-cimm.2001.1861; Kanno T, 2004, FREE RADICAL RES, V38, P27, DOI 10.1080-10715760310001626266; Kutuk O, 2003, FREE RADICAL RES, V37, P1267, DOI 10.1080-10715760310001616005; LAUBER K, 2004, CELL, V14, P277; Laybutt DR, 2002, DIABETES, V51, P413; Lee DHS, 1999, J PHARMACOL EXP THER, V289, P1465; Li HL, 2002, WORLD J GASTROENTERO, V8, P431; LIN KI, 1995, J CELL BIOL, V131, P1149, DOI 10.1083-jcb.131.5.1149; Liu GY, 1998, MOL CARCINOGEN, V22, P235, DOI 10.1002-(SICI)1098-2744(199808)22:4235::AID-MC53.0.CO;2-I; Macho A, 2003, FREE RADICAL RES, V37, P611, DOI 10.1080-1071576031000083215; MAJNO G, 1995, AM J PATHOL, V146, P3; Mantell LL, 2000, MOL GENET METAB, V71, P359, DOI 10.1006-mgme.2000.3046; Maulik N, 1999, ANN NY ACAD SCI, V874, P401, DOI 10.1111-j.1749-6632.1999.tb09254.x; McConkey David J., 1994, Trends in Cell Biology, V4, P370, DOI 10.1016-0962-8924(94)90087-6; Mogi M, 2000, LIFE SCI, V67, P1197, DOI 10.1016-S0024-3205(00)00705-0; Nesnow S, 2002, CHEM RES TOXICOL, V15, P1627, DOI 10.1021-tx025598y; Neuzil J, 2001, BIOCHEMISTRY-US, V40, P4686, DOI 10.1021-bi002498n; Oikawa S, 2003, FREE RADICAL RES, V37, P881, DOI 10.1080-1071576031000150751; Orrenius S, 2004, TOXICOL LETT, V149, P19, DOI 10.1016-j.toxlet.2003.12.017; Osawa Y, 2001, J CELL PHYSIOL, V187, P374, DOI 10.1002-jcp.1088; Otsuki Y, 2003, PROG HISTOCHEM CYTO, V38, P275, DOI 10.1016-S0079-6336(03)80002-5; Pagano A, 2003, ANN NY ACAD SCI, V1010, P405, DOI 10.1196-annals.1299.074; Pagliari LJ, 2000, MOL CELL BIOL, V20, P8855, DOI 10.1128-MCB.20.23.8855-8865.2000; Perkins ND, 1997, INT J BIOCHEM CELL B, V29, P1433, DOI 10.1016-S1357-2725(97)00088-5; Petros AM, 2004, BBA-MOL CELL RES, V1644, P83, DOI 10.1016-j.bbamcr.2003.08.012; PEZZELLA F, 1992, BRIT J CANCER, V65, P87, DOI 10.1038-bjc.1992.16; Putcha G, 2004, CELL DEATH DIFFER, V11, P38, DOI 10.1038-sj.cdd.4401352; Ricca A, 2001, BRIT J CANCER, V85, P1914, DOI 10.1054-bjoc.2001.2174; RILEY PA, 1994, INT J RADIAT BIOL, V65, P27, DOI 10.1080-09553009414550041; Robertson JD, 2002, TOXICOLOGY, V181, P491, DOI 10.1016-S0300-483X(02)00464-X; Robertson JD, 2004, EMBO REP, V5, P643, DOI 10.1038-sj.embor.7400153; Robertson JD, 2003, CELL DEATH DIFFER, V10, P485, DOI 10.1038-sj.cdd.4401218; Robertson JD, 2000, CRIT REV TOXICOL, V30, P609, DOI 10.1080-10408440008951122; SARAFIAN TA, 1994, FREE RADICAL RES, V21, P1, DOI 10.3109-10715769409056549; SCHULTZ DR, 2003, SEMIN ARTHRITIS RHEU, V1, P345; Stergiou L, 2004, CELL DEATH DIFFER, V11, P21, DOI 10.1038-sj.cdd.4401340; Tamm C, 2004, EUR J NEUROSCI, V19, P2613, DOI 10.1111-j.1460-9568.2004.03391.x; Tanaka S, 2002, J NEUROCHEM, V82, P305, DOI 10.1046-j.1471-4159.2002.00958.x; Cuzzorcrea S, 2004, CURR MED CHEM, V11, P1147; Torres M, 2003, BIOFACTORS, V17, P287; Trump BF, 1997, TOXICOL PATHOL, V25, P82; UCHIYAMA Y, 1995, ARCH HISTOL CYTOL, V58, P127, DOI 10.1679-aohc.58.127; Valacchi G, 2004, FREE RADICAL BIO MED, V36, P673, DOI 10.1016-j.freeradbiomed.2003.12.005; Vander Heiden MG, 1999, NAT CELL BIOL, V1, P209; van der Vliet A, 2001, BIOFACTORS, V15, P83; ALBRECHT H, 1994, FEBS LETT, V351, P45, DOI 10.1016-0014-5793(94)00817-5; Voehringer DW, 2000, ANTIOXID REDOX SIGN, V2, P537, DOI 10.1089-15230860050192314; Voorhees PM, 2004, ARCH PATHOL LAB MED, V128, P210; Wagner BA, 2004, FREE RADICAL RES, V38, P167, DOI 10.1080-10715760310001643302; Wang TH, 1999, J FORMOS MED ASSOC, V98, P381; Yang J, 2003, MOL THER, V7, P341, DOI 10.1016-S1525-0016(02)00061-8; Yoo HY, 2004, INT J MOL MED, V13, P81; Zhai QW, 2000, J CELL PHYSIOL, V184, P161, DOI 10.1002-1097-4652(200008)184:2161::AID-JCP33.0.CO;2-N; Zhivotovsky B, 2004, CELL CYCLE, V3, P64; Zimmermann KC, 2001, PHARMACOL THERAPEUT, V92, P57, DOI 10.1016-S0163-7258(01)00159-021211
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