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The purpose of this study is to examine the problem of research quality in social sciences at higher education. Quality of research produced at higher education started to be questioned more often as research became the major factor determining academics' promotion and fund allocation to universities. In the study, we aimed to reveal how academics perceive research quality and what they identify as the main problems that make it difficult to achieve quality in research. Data were collected through interviews with 25 academics from 7 disciplines (educational sciences, sociology, communicational sciences, law, history, management and political science) in 7 universities. Six of the academics interviewed were professors, 7 were associate professors, 10 were assistant professors and 2 were doctors. Interviews were carried out in 2006-2007 and 2007-2008 academic years, and each lasted about one hour on average. Data collected were analyzed through content analysis. Study findings revealed that academics referred most often to methodological issues as the most important quality criterion of research, followed by issues of theoretical background and originality. Academics definitions of sub-criteria related to these were tackled in more detail in the study. As the most important hindrances that make it difficult to achieve quality in research academics mentioned lack of a long-established research culture, problems of research resources and the pressure caused by academic promotion criteria. Some recommendations related to the problems were made to develop research quality in the light of the study findings.

The aim of this study was to determine the role of polymorphic variants of apolipoprotein E ( APOE) and peroxisome proliferator-activated receptor delta ( PPARD) genes in the development of coronary heart disease (CHD), and the PPARD and APOE gene-gene interaction in a Turkish population. This study was carried out using a sample of 223 patients with CHD (103 with diabetes and 120 without diabetes) and 101 controls. PPARD +294T/C and APOE genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism technique. The PPARD and APOE genotype distributions were the same between study groups ( p>0.05). In the nondiabetic CHD patients, the PPARD +294 C allele showed higher serum low-density lipoprotein cholesterol (LDL-C) level than the common +294 TT homozygote genotype (3.83±1.01 vs. 3.33±1.14, p=0.015). In addition, a significant association between APOE 4 and PPARD +294 C alleles was detected based on their effects on LDL-C in the nondiabetic CHD patients (+294 C/ APOE4: 4.43±0.88 vs. +294 TT/non APOE 4: 3.48±1.09, p=0.009). This association indicated the interaction of two genes on plasma LDL-C levels ascended in the order +294 T<+294 T- APOE 4<+294 C< APOE 4<+294 C- APOE 4. The PPARD +294 C allele was associated with higher incidence of left ventricular hypertrophy (LVH) in all male patients with body mass index >27. In addition, the CHD patients who were +294 C allele carriers had a 2.48-fold higher risk of LVH than subjects homozygous for the T allele. An increasing effect of the PPARD +294 C allele was shown on serum LDL-C levels in nondiabetic CHD patients. In addition, the results suggested that the +294 C allele might be associated with an increased LVH risk especially in male CHD patients. Furthermore, gene-gene interaction between the PPARD +294T/C and the APOE polymorphisms was observed regarding LDL-C concentrations. [ABSTRACT FROM AUTHOR]

In coronary artery disease (CAD), a potentially reversible factor leading to cardiac death is left ventricular hypertrophy (LVH). The 3'untranslated region (3'UTR) 188CT polymorphism of lectin-like oxidized low-density lipoproteins receptor-1 (LOX-1) gene has been associated with an increased risk for CAD. We aim to investigate, in a Turkish population, whether 3'UTR188CT variation could affect the development of LVH in CAD patients. In a population-based case-control study, we compared 83 cases with CAD and 99 healthy controls for this polymorphism. The LOX-1 3'UTR188CT genotypes were determined by PCR-RFLP technique. LOX-1 3'UTR188 TT genotype was associated with significantly increased systolic blood pressure (P = 0.047) and risk of LVH (P = 0.014, OR: 3.541) when compared with the C allele carriers. In addition, the TT genotype was positively associated with decreased levels of HDL-cholesterol in the control subjects (P = 0.031) and increased levels of VLDL-C in the patient group (P = 0.009). The LOX-1 3'UTR188CT gene polymorphism may predispose to the development of LVH in CAD patients, dependent on blood pressure.

Background: Human lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1, OLR1) has been identified as a cell surface endocytosis receptor for oxidized low-density lipoprotein (oxLDL) on vascular endothelial cells. OxLDLs are avidly ingested by macrophages, resulting in foam cell formation. OxLDLs are also involved in inducing smooth muscle cell migration, proliferation and transformation. A single nucleotide polymorphism K167N (G501C) of the LOX-1 gene results in an amino acid dimorphism (Lys/Asn) at residue 167. Replacement of this Lys residue causes reduced binding and internalization of oxLDL. The purpose of this study was to investigate the effect of the LOX-1 K167N gene polymorphism in Turkish patients with coronary artery disease (CAD)., Materials and Methods: K167N polymorphism were studied in 91 patients with CAD and 72 healthy controls by the PCR-RFLP method., Results: The frequencies of the KK genotype and the K allele were higher in the CAD group than the controls (p<0.05), while the frequency of the NN genotype was higher in the control group than in the CAD group (p<0.05). It was observed that the decreased CAD risk in patients who had the N allele was reversed by male sex (OR: 0.400 -->0.481) and smoking (OR: 0.400 -->0.949). Although male sex and smoking were lower than other cardiovascular risk factors in patients with the N allele they were higher than other cardiovascular risk factors in patients with the K allele., Conclusion: Male sex and smoking decrease the protective effects of the N allele. The adverse effects of the K allele on the CAD risk resulting from the K167N polymorphism appear to be independent of other cardiovascular risk factors.

Background: This study investigated associations of specific lipoprotein lipase (LPL) S447X and apolipoprotein (Apo)E allelic patterns with low-density lipoprotein (LDL) size and subfraction profiles in patients with coronary artery disease (CAD) and healthy individuals., Patients and Methods: Forty-one cases with CAD and 23 controls were compared regarding the occurrence of the Ser-->Stop codon of the LPL and ApoE polymorphism. Polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) techniques were utilized to perform genotyping, and LDL size and subfractions were assessed by a high-resolution, nongradient polyacrylamide gel electrophoresis technique., Results: The lowest small dense (sd) LDL level was observed for the homozygous LPLX447 genotype (6.00 +/- 4.00 mg/dl) while the highest sdLDL level was observed for LPLX447(+)/ApoE4(+) carriers (14.33 +/- 20.55 mg/dl) in the patient group. No protective effect of LPLX447 allele on the atherogenic LDL profile was observed when it was together with the ApoE4 allele. Furthermore, the detrimental effect of LPLS447 on the atherogenic LDL profile increased when it was present together with the ApoE4 allele., Conclusion: The X447 allele of the LPL gene may protect from atherogenic LDL subfraction, although this effect is small. We suggest that the S447X polymorphism of the LPL gene may modify the risk of atherogenic sdLDL fraction in an ApoE-dependent fashion.