29 research outputs found
Ratliff–Rush filtrations associated with ideals and modules over a Noetherian ring
No full textAbstractLet R be a commutative Noetherian ring, M a finitely generated R-module and I a proper ideal of R. In this paper we introduce and analyze some properties of r(I,M)=⋃k⩾1(Ik+1M:IkM), the Ratliff–Rush ideal associated with I and M. When M=R (or more generally when M is projective) then r(I,M)=I˜, the usual Ratliff–Rush ideal associated with I. If I is a regular ideal and annM=0 we show that {r(In,M)}n⩾0 is a stable I-filtration. If Mp is free for all p∈SpecR∖m-SpecR, then under mild condition on R we show that for a regular ideal I, ℓ(r(I,M)/I˜) is finite. Further r(I,M)=I˜ if A∗(I)∩m-SpecR=∅ (here A∗(I) is the stable value of the sequence Ass(R/In)). Our generalization also helps to better understand the usual Ratliff–Rush filtration. When I is a regular m-primary ideal our techniques yield an easily computable bound for k such that In˜=(In+k:Ik) for all n⩾1. For any ideal I we show that InM˜=InM+HI0(M) for all n≫0. This yields that R˜(I,M)=⊕n⩾0InM˜ is Noetherian if and only if depthM>0. Surprisingly if dimM=1 then G˜I(M)=⊕n⩾0InM˜/In+1M˜ is always a Noetherian and a Cohen–Macaulay GI(R)-module. Application to Hilbert coefficients is also discussed
The Lebanese allele at the LDLR in normocholesterolemic people merits reconsideration of genotype phenotype correlations in familial hypercholesterolemia
No full text[No abstract available]Abifadel M, 2009, HUM MUTAT, V30, pE682, DOI 10.1002-humu.21002; Bodamer OA, 2002, CLIN CHEM, V48, P1913; Brusgaard K, 2010, J CLIN LIPIDOL, V4, P181, DOI 10.1016-j.jacl.2010.02.009; DAVIS CG, 1986, CELL, V45, P15, DOI 10.1016-0092-8674(86)90533-7; Day INM, 1997, HUM MUTAT, V10, P116; Deiana L, 2000, ARTERIOSCL THROM VAS, V20, P236; Fahed AC, 2011, MOL GENET METAB, V102, P181, DOI 10.1016-j.ymgme.2010.11.006; Fahed AC, 2011, NUTR METAB, V8, DOI 10.1186-1743-7075-8-23; FIGUEIREDO MS, 1992, J MED GENET, V29, P813, DOI 10.1136-jmg.29.11.813; HOBBS HH, 1986, J BIOL CHEM, V261, P3114; HOBBS HH, 1989, J CLIN INVEST, V84, P656, DOI 10.1172-JCI114212; Huijgen R, 2012, HUM MUTAT, V33, P448, DOI 10.1002-humu.21660; KHACHADURIAN AK, 1964, AM J MED, V37, P402, DOI 10.1016-0002-9343(64)90196-2; LEHRMAN MA, 1987, J BIOL CHEM, V262, P401; LEHRMAN MA, 1985, CELL, V41, P735, DOI 10.1016-S0092-8674(85)80054-4; LEHRMAN MA, 1985, SCIENCE, V227, P140, DOI 10.1126-science.3155573; NORA JJ, 1985, AM J MED GENET, V22, P585, DOI 10.1002-ajmg.1320220317; OPPENHEIM A, 1991, HUM GENET, V88, P75, DOI 10.1007-BF00204933; SUDHOF TC, 1985, SCIENCE, V228, P815, DOI 10.1126-science.2988123; Tarugi P, 2011, ADV CLIN CHEM, V54, P81, DOI 10.1016-B978-0-12-387025-4.00004-2; Teslovich TM, 2010, NATURE, V466, P707, DOI 10.1038-nature09270; YAMAMOTO T, 1984, CELL, V39, P27, DOI 10.1016-0092-8674(84)90188-0; YAMAMOTO T, 1986, SCIENCE, V232, P1230, DOI 10.1126-science.301046611
Matrix representations of linear transformations on bicomplex space
No full textAn algebraic investigation on bicomplex numbers is carried out here.
Particularly matrices and linear maps defined on them are discussed. A new kind
of cartesian product, referred to as an idempotent product, is introduced and
studied. The elements of this space are linear maps of a special form. These
linear maps are examined with respect to usual notions like kernel, range, and
singularity. Their matrix representation is also discussed
Impact of AREDS in a developing country 5 years after publication of the study
No full textPURPOSE. The Age-Related Eye Disease Study (AREDS) is the only large-scale study to demonstrate a reduction in the risk of progression to end-stage age-related macular degeneration (AMD) when vitamin supplementation was given to patients with advanced forms of the disease. Our study assesses the impact of this study on vitamin supplementation in patients with advanced AMD from 5 years before publication of the AREDS results until 5 years after. METHODS. Medical records of patients with AMD presenting between September 1996 and October 2006 were reviewed. Patients were subclassified according to AREDS categories. The proportion of advanced cases on vitamin replacement before October 2001 was compared to that after October 2001. Since October 2001, the different reasons for abstinence were investigated and analyzed. RESULTS. Only 2403 patients of the 40,000 medical records reviewed met the AREDS AMD criteria. Of these, 137 patients verifying categories 3 and 4 were diagnosed prior to October 2001. Fourteen were on supplements then. Fifty-three patients complied with the represcribed vitamins during subsequent visits after October 2001, raising the percentage significantly to 48.9percent (p0.001). Also, from October 2001 until October 2006, an additional 76 patients verified categories 3 and 4. Fifty-three (69.7percent) of them were on vitamins (p=0.001). Financial burden was the principal reason for abstinence in 67.7percent of patients prescribed vitamins after October 2001. CONCLUSION. The results of AREDS had an impressive impact on prescribing supplements in AREDS category 3 and 4 patients in Lebanon. The main reason for noncompliance is financial. © 2010 Wichtig Editore.Age-Related Eye Disease Study Research Group, 2001, ARCH OPHTHALMOL, V119, P1417; [Anonymous], 1999, CONTROL CLIN TRIALS, V20, P573; Chen SJ, 2008, INVEST OPHTH VIS SCI, V49, P3126, DOI 10.1167-iovs.08-1803; Chen Wen, 2003, J Huazhong Univ Sci Technolog Med Sci, V23, P414; Evans J. R., 2006, COCHRANE DB SYST REV, V19; Everitt AV, 2006, CLIN INTERV AGING, V1, P11, DOI 10.2147-ciia.2006.1.1.11; Fraser-Bell S, 2008, AM J OPHTHALMOL, V145, P308, DOI 10.1016-j.ajo.2007.10.007; Gupta SK, 2007, INVEST OPHTH VIS SCI, V48, P1007, DOI 10.1167-iovs.06-0712; Hirakawa M, 2008, BRIT J OPHTHALMOL, V92, P630, DOI 10.1136-bjo.2007.130575; Hogg RE, 2008, OPHTHALMOLOGY, V115, P1046, DOI 10.1016-j.ophtha.2007.07.031; Iyengar SK, 2004, AM J HUM GENET, V74, P20, DOI 10.1086-380912; Kawasaki R, 2008, OPHTHALMOLOGY, V115, P1735, DOI 10.1016-j.ophtha.2008.02.012; Kawasaki R, 2008, OPHTHALMOLOGY, V115, P1376, DOI 10.1016-j.ophtha.2007.11.015; KLEIN R, 1992, OPHTHALMOLOGY, V99, P933; Klein R, 2006, OPHTHALMOLOGY, V113, P373, DOI 10.1016-j.ophtha.2005.12.013; Leske MC, 2006, OPHTHALMOLOGY, V113, P29, DOI 10.1016-j.ophtha.2005.08.012; Nowak JZ, 2006, PHARMACOL REP, V58, P353; Plestina-Borjan I, 2007, COLLEGIUM ANTROPOL, V31, P33; Robman L, 2007, CAN J OPHTHALMOL, V42, P720, DOI 10.3129-canjophthahnol.i07-116; SanGiovanni JP, 2008, ARCH OPHTHALMOL-CHIC, V126, P1274, DOI 10.1001-archopht.126.9.1274; Santos Laura Patrícia Ferreira, 2005, Arq Bras Oftalmol, V68, P229, DOI 10.1590-S0004-27492005000200014; Schaumberg DA, 2001, ARCH OPHTHALMOL-CHIC, V119, P1259; Seddon JM, 2003, ARCH OPHTHALMOL-CHIC, V121, P1728, DOI 10.1001-archopht.121.12.1728; Seddon JM, 2006, ARCH OPHTHALMOL-CHIC, V124, P995, DOI 10.1001-archopht.124.7.995; SOMMER A, 1991, NEW ENGL J MED, V325, P1412, DOI 10.1056-NEJM199111143252004; Sommerburg O, 1998, BRIT J OPHTHALMOL, V82, P907, DOI 10.1136-bjo.82.8.907; Sparrow J M, 1997, Ophthalmic Epidemiol, V4, P49; van Leeuwen R, 2003, BRIT MED J, V326, P255, DOI 10.1136-bmj.326.7383.255; Wilson HL, 2004, AM J OPHTHALMOL, V137, P615, DOI 10.1016-j.ajo.2003.10.02522
Low-density lipoprotein levels and not mutation status predict Intima-media thickness in familial hypercholesterolemia
No full textBackground Intima-media thickness (IMT) is a well-described marker of cardiovascular disease. In this study we aim to determine whether low-density lipoprotein (LDL) levels and disease-related mutation status can predict IMT in patients with severe familial hypercholesterolemia (FH) referred for or on LDL apheresis. Methods Genetic screening, lipid profile testing, and IMT measurements were performed on a series of 33 severe FH patients (19 homozygous) on LDL apheresis treatments (LDL 447 ± 151 mg-dL, age range 6-60 years). Data were then compared with literature IMT-LDL data for normal subjects, mild FH patients, and severe FH patients (18, 41, and 6 studies, respectively). Results Age-adjusted IMT was linearly related to LDL levels over a wide range of values (500 mg-dL), except for the severe FH no-apheresis cohort. Alternatively, our severe FH population (mostly on apheresis) did follow the mild FH-control age-adjusted IMT-LDL relation. Conclusions In severe FH, measuring LDL levels is more predictive of increased IMT than genetic screening. © 2014 Elsevier Inc. All rights reserved.Descamps OS, 2001, EUR J CLIN INVEST, V31, P958, DOI 10.1046-j.1365-2362.2001.00915.x; Fahed AC, 2011, MOL GENET METAB, V102, P181, DOI 10.1016-j.ymgme.2010.11.006; Fahed AC, 2011, NUTR METAB, V8, DOI 10.1186-1743-7075-8-23; Feinstein SB, 2002, AM J CARDIOL, V89, p31C; Guardamagna O, 2009, J PEDIATR, V155, P199, DOI 10.1016-j.jpeds.2009.02.022; Kastelein JJP, 2008, NEW ENGL J MED, V358, P1431, DOI 10.1056-NEJMoa0800742; Kastelein JJP, 2007, NEW ENGL J MED, V356, P1620, DOI 10.1056-NEJMoa071359; Koga N, 1999, J INTERN MED, V246, P35, DOI 10.1046-j.1365-2796.1999.00466.x; Nolting PRWD, 2003, ARCH INTERN MED, V163, P18370
Familial Hypercholesterolemia: The Lipids or the Genes?
No full textAbstract Familial Hypercholesterolemia (FH) is a common cause of premature cardiovascular disease and is often undiagnosed in young people. Although the disease is diagnosed clinically by high LDL cholesterol levels and family history, to date there are no single internationally accepted criteria for the diagnosis of FH. Several genes have been shown to be involved in FH; yet determining the implications of the different mutations on the phenotype remains a hard task. The polygenetic nature of FH is being enhanced by the discovery of new genes that serve as modifiers. Nevertheless, the picture is still unclear and many unknown genes contributing to the phenotype are most likely involved. Because of this evolving polygenetic nature, the diagnosis of FH by genetic testing is hampered by its cost and effectiveness. In this review, we reconsider the clinical versus genetic nomenclature of FH in the literature. After we describe each of the genetic causes of FH, we summarize the known correlation with phenotypic measures so far for each genetic defect. We then discuss studies from different populations on the genetic and clinical diagnoses of FH to draw helpful conclusions on cost-effectiveness and suggestions for diagnosis.</p
Editional critic of Köprülüzâde Nûman Pasha's manuscript titled "Kayfiyyatu'l-Qira'ah bi'l-jam'"
No full textKıraat ilmi ile ilgili telif edilen eserlerin sayısı fazla olduğundan bunların tek tek sayılması zordur. Özellikle kıraat ilmi doğru nakle dayandığından bu literatürün çoğunun tashih ve tespit edilmesine ihtiyaç duyulmaktadır. Köprülüzâde Nûman Paşa'nın "Keyfiyyetu'l-Kırâe bi'l-Cem'" adlı risâlesi, Şatıbiyye adlı manzumede derlenen yedi kıraati esas alan eserlerden birisidir. Eserin tahkiki ve içinde bulunan birtakım müşkil meselelerin izahı gereksinimi bulunmaktaydı. Araştırmada yedi kıraatin usulleri açıklanmış, müellifin hayatına da değinilmiştir. Ayrıca eserin içeriği üzerinde durulmuş ve müellifin kullandığı kaynaklar incelenerek eserin tahkikli metnine yer verilmiştir. Tahkik esnasında doğru ifadeler teyit edilirken, hatalar düzeltilmiştir. Buna göre araştırma üç bölüme ayrılmaktadır. Birinci bölüm Kıraat ilminin tanımını, imamların hayatlarını, usullerini, birtakım kıraat terimlerini ve kıraatlerin nasıl cem edildiğini içermektedir. İkinci bölümde müellifin hayatına ayrıntılı bir biçimde yer verilmiştir. Üçüncü bölümde ise müellifin kaynaklarına atıf yapılması ve belirsizliklerin giderilmesi suretiyle oluşturulan tahkikli metne yer verilmiştir. Son olarak müellifin ulaştığı sonuçlar ve gayreti değerlendirilmiştir.It is difficult to count the works written about the science of Qira'at one by one since the number of these works is high. Especially the science of Qira'at is based on authenticity of transmission and for this reason, most of this literature need to be corrected and examined. Köprülüzâde Nûman Pasha's epistle named "Kayfiyyatu'l-Qira'at bi'l-Jam'" is one of the works based on seven qira'at (recitation) compiled in the poem named Shatibiyyah. There was a need for the verification of the work and the explanation of some complicated issues inside it. In the research, the methods of seven qira'at is explained and the life of the author is also mentioned. Moreover, the content of the work is discussed and the verified text of the work is included by examining the sources used by the author. While the correct statements are reiterated during the verification, the existing errors are corrected. In this context, the study consists of three parts. The first chapter includes the definition of the science of qira'at, the lives of imams, their methods, some terms of qira'at and how to combine recitations (qira'at). In the second part, the life of the author is given in detail. In the third part, the verified text is given by referring to the sources of the author and eliminating the ambiguities. Finally, the results achieved by the author and his efforts have been evaluated
Connecting the lines between hypogonadism and atherosclerosis
No full textEpidemiological studies show that atherosclerotic cardiovascular disease is a leading cause of morbidity and mortality worldwide and point to gender differences with ageing males being at highest risk. Atherosclerosis is a complex process that has several risk factors and mediators. Hypogonadism is a commonly undiagnosed disease that has been associated with many of the events, and risk factors leading to atherosclerosis. The mechanistic relations between testosterone levels, atherosclerotic events, and risk factors are poorly understood in many instances, but the links are clear. In this paper, we summarize the research journey that explains the link between hypogonadism, each of the atherosclerotic events, and risk factors. We look into the different areas from which lessons could be learned, including epidemiological studies, animal and laboratory experiments, studies on androgen deprivation therapy patients, and studies on testosterone-treated patients. We finish by providing recommendations for the clinician and needs for future research. Copyright © 2012 Akl C. Fahed et al.Adiels M, 2008, ARTERIOSCL THROM VAS, V28, P1225, DOI 10.1161-ATVBAHA.107.160192; Akishita M, 2007, HYPERTENS RES, V30, P1029, DOI 10.1291-hypres.30.1029; Alexandersen P, 1999, CIRC RES, V84, P813; Ariyo AA, 2003, NEW ENGL J MED, V349, P2108, DOI 10.1056-NEJMoa001066; Aversa A, 2010, J SEX MED, V7, P3495, DOI 10.1111-j.1743-6109.2010.01931.x; BARRETTCONNOR E, 1992, ANN INTERN MED, V117, P807; Basaria S, 2010, J CLIN ENDOCR METAB, V95, P1533, DOI 10.1210-jc.2009-1579; Bhatia V, 2006, DIABETES CARE, V29, P2289, DOI 10.2337-dc06-0637; Bolla M, 1997, NEW ENGL J MED, V337, P295, DOI 10.1056-NEJM199707313370502; Bourghardt J, 2010, ENDOCRINOLOGY, V151, P5428, DOI 10.1210-en.2010-0663; Boyanov M A, 2003, Aging Male, V6, P1; Brown-Sequard C., 1889, LANCET, V134, P105; Cakir E, 2005, J CLIN ENDOCR METAB, V90, P1651, DOI 10.1210-jc.2004-2045; Calof OM, 2005, J GERONTOL A-BIOL, V60, P1451; Caminiti G, 2009, J AM COLL CARDIOL, V54, P919, DOI 10.1016-j.jacc.2009.04.078; Choong K, 2010, AGING MALE, V13, P1, DOI 10.3109-13685530903410625; Cornoldi A, 2010, INT J CARDIOL, V142, P50, DOI 10.1016-j.ijcard.2008.12.107; Ding EL, 2009, NEW ENGL J MED, V361, P1152, DOI 10.1056-NEJMoa0804381; Ding EL, 2006, JAMA-J AM MED ASSOC, V295, P1288, DOI 10.1001-jama.295.11.1288; Ezaki K, 2010, CIRC J, V74, P2448, DOI 10.1253-circj.CJ-10-0221; Fernandez-Balsells MM, 2010, J CLIN ENDOCR METAB, V95, P2560, DOI 10.1210-jc.2009-2575; Foresta C, 2006, J CLIN ENDOCR METAB, V91, P4599, DOI 10.1210-jc.2006-0763; Foresta C, 2008, CLIN ENDOCRINOL, V68, P284, DOI 10.1111-j.1365-2265.2007.03036.x; Freeman ER, 2001, J UROLOGY, V165, P371, DOI 10.1097-00005392-200102000-00004; Fu L, 2008, ASIAN J ANDROL, V10, P214, DOI 10.1111-j.1745-7262.2008.00335.x; Gustafson B, 2007, ARTERIOSCL THROM VAS, V27, P2276, DOI 10.1161-ATVBAHA.107.147835; Haddad RM, 2007, MAYO CLIN PROC, V82, P29; HAFFNER SM, 1993, J CLIN ENDOCR METAB, V77, P1610, DOI 10.1210-jc.77.6.1610; Haidar A, 2007, AGING MALE, V10, P189, DOI 10.1080-13685530701653538; Hak AE, 2002, J CLIN ENDOCR METAB, V87, P3632, DOI 10.1210-jc.87.8.3632; Hanke H, 2001, CIRCULATION, V103, P1382; Hatakeyama H, 2002, FEBS LETT, V530, P129, DOI 10.1016-S0014-5793(02)03440-3; Heitzer T, 2001, CIRCULATION, V104, P2673, DOI 10.1161-hc4601.099485; Heufelder AE, 2009, J ANDROL, V30, P726, DOI 10.2164-jandrol.108.007005; Hougaku H, 2006, AM J PHYSIOL-ENDOC M, V290, pE234, DOI 10.1152-ajpendo.00059.2005; Isidori AM, 2005, CLIN ENDOCRINOL, V63, P280, DOI 10.1111-j.1365-2265.2005.02339.x; JAFFE MD, 1977, BRIT HEART J, V39, P1217; Johnsen SH, 2005, CIRCULATION, V112, P498, DOI 10.1161-CIRCULATIONAHA.104.522706; Jones TH, 2011, DIABETES CARE, V34, P828, DOI 10.2337-dc10-1233; Jones TH, 2009, ATHEROSCLEROSIS, V207, P318, DOI 10.1016-j.atherosclerosis.2009.04.016; Kalinchenko SY, 2010, CLIN ENDOCRINOL, V73, P602, DOI 10.1111-j.1365-2265.2010.03845.x; Kang SM, 2002, AM J CARDIOL, V89, P862, DOI 10.1016-S0002-9149(02)02202-6; Kaplan SA, 2010, AGING MALE, V13, P40, DOI 10.3109-13685530903536676; Kapoor D, 2007, EUR J ENDOCRINOL, V156, P595, DOI 10.1530-EJE-06-0737; Kapoor D, 2006, EUR J ENDOCRINOL, V154, P899, DOI 10.1530-eje.1.02166; Keating NL, 2006, J CLIN ONCOL, V24, P4448, DOI 10.1200-JCO.2006.06.2497; Kenny AM, 2002, J GERONTOL A-BIOL, V57, pM460; Keymel S, 2008, BASIC RES CARDIOL, V103, P582, DOI 10.1007-s00395-008-0742-z; Kumanov P, 2007, INT J ANDROL, V30, P41, DOI 10.1111-j.1365-2605.2006.00706.x; Kumanov P, 2002, ANDROLOGIA, V34, P29, DOI 10.1046-j.1439-0272.2002.00468.x; Laaksonen DE, 2005, J CLIN ENDOCR METAB, V90, P712, DOI 10.1210-jc.2004-0970; Laaksonen DE, 2003, EUR J ENDOCRINOL, V149, P601, DOI 10.1530-eje.0.1490601; Laaksonen DE, 2004, DIABETES CARE, V27, P1036, DOI 10.2337-diacare.27.5.1036; Leifke E, 2008, HORM METAB RES, V40, P56, DOI 10.1055-s-2007-1004529; LERNER DJ, 1986, AM HEART J, V111, P383, DOI 10.1016-0002-8703(86)90155-9; Lesser MA, 1942, NEW ENGL J MED, V226, P51, DOI 10.1056-NEJM194201082260203; LESSER MA, 1946, J CLIN ENDOCR METAB, V6, P549; Ling SH, 2002, ENDOCRINOLOGY, V143, P1119, DOI 10.1210-en.143.3.1119; Liva SM, 2001, J IMMUNOL, V167, P2060; Ly LP, 2001, J CLIN ENDOCR METAB, V86, P4078, DOI 10.1210-jc.86.9.4078; Malkin CJ, 2010, CURR OPIN ENDOCRINOL, V17, P262, DOI 10.1097-MED.0b013e328339543e; Malkin CJ, 2004, J CLIN ENDOCR METAB, V89, P3313, DOI 10.1210-jc.2003-031069; Maravelias C, 2005, TOXICOL LETT, V158, P167, DOI 10.1016-j.toxlet.2005.06.005; Mårin P, 1993, Obes Res, V1, P245; Marin R, 1999, BIOL REPROD, V61, P1012, DOI 10.1095-biolreprod61.4.1012; Mathur A, 2009, EUR J ENDOCRINOL, V161, P443, DOI 10.1530-EJE-09-0092; Mattace-Raso FUS, 2006, CIRCULATION, V113, P657, DOI 10.1161-CIRCULATIONAHA.105.555235; McCrohon JA, 2000, CIRCULATION, V101, P224; Mercuro G, 2010, J CARDIOVASC MED, V11, P207, DOI 10.2459-JCM.0b013e32833178ed; Morimoto S, 2005, J ENDOCRINOL, V187, P217, DOI 10.1677-joe.1.06357; Muller M, 2005, J CLIN ENDOCR METAB, V90, P2618, DOI 10.1210-jc.2004-1158; Muller M, 2004, CIRCULATION, V109, P2074, DOI 10.1161-01.CIR.0000125854.51637.06; Naharci Mehmet Ilkin, 2007, Endocr Pract, V13, P629; Nettleship JE, 2007, CIRCULATION, V116, P2427, DOI 10.1161-CIRCULATIONAHA.107.708768; Ng MKC, 2002, ARTERIOSCL THROM VAS, V22, P1136, DOI 10.1161-01.ATV.0000022167.80130.A6; Niskanen L, 2004, DIABETES OBES METAB, V6, P208, DOI 10.1111-j.1462-8902.2004.00335.x; Pearson LJ, 2008, PEPTIDES, V29, P1057, DOI 10.1016-j.peptides.2008.02.003; Pritchard J, 1998, J CLIN ENDOCR METAB, V83, P3277, DOI 10.1210-jc.83.9.3277; Qiu Y, 2010, ENDOCRINOLOGY, V151, P3307, DOI 10.1210-en.2009-1268; Rajala Ulla M, 2007, Diabetes Care, V30, pe13, DOI 10.2337-dc06-1979; Saad F, 2011, J OBES; Schroeder ET, 2004, J CLIN ENDOCR METAB, V89, P4863, DOI 10.1210-jc.2004-0784; Schwartz BG, 2009, INT J IMPOT RES, V21, P327, DOI 10.1038-ijir.2009.38; Selvin E, 2007, DIABETES CARE, V30, P234, DOI 10.2337-dc06-1579; Shabsigh R, 2009, INT J IMPOT RES, V21, P9, DOI 10.1038-ijir.2008.31; Shahinian VB, 2005, CANCER-AM CANCER SOC, V103, P1615, DOI 10.1002-cncr.20955; Simon D, 1997, J CLIN ENDOCR METAB, V82, P682, DOI 10.1210-jc.82.2.682; Smith Matthew R, 2007, Curr Opin Endocrinol Diabetes Obes, V14, P247, DOI 10.1097-MED.0b013e32814db88c; Svartberg J, 2004, EUR J ENDOCRINOL, V150, P65, DOI 10.1530-eje.0.1500065; WU SZ, 1993, CHINESE MED J-PEKING, V106, P415; TENOVER JS, 1992, J CLIN ENDOCR METAB, V75, P1092, DOI 10.1210-jc.75.4.1092; Tharp DL, 2009, CARDIOVASC RES, V82, P152, DOI 10.1093-cvr-cvp038; THOMPSON PD, 1989, JAMA-J AM MED ASSOC, V261, P1165, DOI 10.1001-jama.261.8.1165; Tomaszewski M, 2009, ATHEROSCLEROSIS, V203, P257, DOI 10.1016-j.atherosclerosis.2008.06.002; Traish AM, 2009, VASC PHARMACOL, V51, P303, DOI 10.1016-j.vph.2009.09.003; Traish AM, 2009, FEBS J, V276, P5755, DOI 10.1111-j.1742-4658.2009.07305.x; Traish AM, 2009, J ANDROL, V30, P23, DOI 10.2164-jandrol.108.005751; Uyanik BS, 1997, JPN HEART J, V38, P73; Van Pottelbergh I, 2003, ATHEROSCLEROSIS, V166, P95, DOI 10.1016-S0021-9150(02)00308-8; Vignozzi L, 2007, J SEX MED, V4, P620, DOI 10.1111-j.1743-6109.2007.00440.x; Walker TC, 1942, J CLIN ENDOCRINOL, V2, P560; WHO, 2011, GLOB STAT REP NONC D; Yeap BB, 2010, CURR OPIN ENDOCRINOL, V17, P269, DOI 10.1097-MED.0b013e3283383031; Zgliczynski S, 1996, ATHEROSCLEROSIS, V121, P35, DOI 10.1016-0021-9150(95)05673-4; Zitzmann M, 2007, J CLIN ENDOCR METAB, V92, P3844, DOI 10.1210-jc.2007-0620; Zitzmann M, 2008, J ANDROL, P54; Zitzmann M, 2002, J CLIN ENDOCR METAB, V87, P5030, DOI 10.1210-jc.2002-020504; Zumoff B, 2003, METABOLISM, V52, P1126, DOI 10.1016-S0026-0495(03)00186-078
Antithesis among Past and Contemporary Scholars
No full textيتناول الباحث في هذه الدراسة موضوع الطباق بين القدماء والمعاصرين، معتمدًا على عدد من المراجع البلاغية القديمة والحديثة، وهو يبدأ بتعريف الطباق مبرزًا نقطة أساسية جدًا لم تُشر إليها المراجع القديمة قطّ، وهي وجوب كون المتضادّيْن دائما من مجال دلالي واحد، وكون الاختلاف بينهما اختلافًا دلاليًا فرعيًا داخل ذلك المجال.
ثمّ ينتقل إلى التقسيمات العديدة التي نجدها للطباق في الكتب البلاغية المتأخرة، أي التي كتبت في أواخر القرن السادس الهجري وما بعده، مشيرًا إلى اختلافها عن الكتب البلاغية القديمة، أي التي كتبت قبل القرن المذكور، ذاكرًا أن الكتب القديمة تكاد تخلو من التقسيمات.
ويلاحظ الباحث أن معظم الدراسات البلاغية المعاصرة سارت في أعقاب كتب البلاغة المتأخرة، معتمدة تقسيماتها كلها، ومضيفة إليها تقسيمات أخرى.
بعد هذا يتحدّث بالتفصيل عن أربعة أقسام وردت في الكتب البلاغية المتأخرة، وهي: الطباق اللفظي، الطباق المعنوي، الملحق بالطباق، إيهام الطباق.In this study, the author addresses the antithesis among past and contemporary scholars using a number of past and contemporary rhetoric references. The author starts defining Antithesis while highlighting a very basic aspect that the past references did not relate to: the Antithesis has to be in one semantic field, within which the two opposites differ semantically.
The author then relates to the various Antithesis categories that are found in the late sixth Hijri century and afterwards, indicating that these rhetoric books differ from the old books that were written before. He mentions that the old books were almost devoid of these categories.
The researcher notes that most contemporary rhetorical studies followed the late rhetoric books, using the same categories and adding new ones.
Then, the researcher elaborates on four categories that were mentioned in the late rhetoric books: verbal Antithesis, moral Antithesis, Supplement Antithesis, and deluding Antithesis.
This is followed by a detailed description of two new categories added by contemporary scholars: semantic-based categories and linguistic-based categories. The semantic-based categories have the following sub-categories: contradiction, contrast, addition, difference. The linguistic-based categories have five subcategories: sharp contrast, gradient contrast, reverse contrast, directional contrast and vertical contrast.
The researcher proposes four categories and argues that they are clear and sufficient: affirmative Antithesis, negative Antithesis, moral Antithesis and deluding Antithesis.
To conclude, the researcher reviews a few evaluative approaches that relate to Antithesis as a rhetorical type. He then sums up and argues that giving general evaluations regarding any rhetorical type is not acceptable. Each type should be evaluated within the context it occurs, while analyzing it's moral and artistic function
