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01 - Yoksulluğa Son

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Yoksulluğun her biçiminin ortadan kaldırılması günümüzde insanlığın karşı karşıya olduğu en büyük sorun olmaya devam ediyor. Aşırı yoksulluk içinde yaşayan insanların sayısı 1990 ile 2015 arasında 1,9 milyardan 836 milyona düşmek suretiyle, yarıdan fazla azalmış olsa da, hala çok sayıda insan en temel insani gereksinimlerini karşılama savaşı vermektedir. Sürdürülebilir Kalkınma Amaçları, başlamış olduğumuz şeyi bitirme ve yoksulluğun her biçimi ve boyutunu ortadan kaldırma yönünde oldukça cesur bir taahhüttür. En korunmasız durumda olanların hedeflenmesi, temel kaynaklar ve hizmetlere erişimin artırılması ve çatışmalar ile iklim temelli afetlerden etkilenen toplumların desteklenmesini içerir.

Publication Search Results

Now showing 1 - 3 of 3
  • PublicationMetadata only
    SIRT1 gene variants are related to risk of childhood obesity
    (2015-04-01) Kilic, Ulkan; GOK, Ozlem; ELIBOL-CAN, BİRSEN; Ozgen, Ilker Tolga; Erenberk, UFUK; Uysal, Omer; DUNDAROZ, Mehmet Rusen; ELİBOL, BİRSEN; ÖZGEN, İLKER TOLGA; ERENBERK, UFUK; UYSAL, ÖMER
    Obesity is a multifactorial disorder resulting from the interaction between genetic, psychological, physical, environmental, and socioeconomic factors. SIRT1 gene has important effects on the regulation of adiponectin, caloric restriction, insulin sensitivity, coronary atherosclerosis, and cardiovascular diseases. The aim of this study was to investigate the association between childhood obesity and SIRT1 gene polymorphisms regarding rs7895833 A > G in the promoter region, rs7069102 C > G in intron 4, and rs2273773 C > T in exon 5 using PCR-CTPP method in 120 obese and 120 normal weight children. In this study, BMI, systolic and diastolic blood pressure, LDL cholesterol, triglyceride, and insulin levels were significantly higher and HDL-cholesterol levels were significantly lower in obese children compared to normal weight children. For rs7895833 A > G, the rate of having AG genotype and G allele was significantly higher in obese children compared to non-obese group (p T. There was no significant difference for rs7069102 C > G gene polymorphism between groups.
  • PublicationMetadata only
    SOCIO-ECONOMIC FACTORS THAT AFFECT PERCEIVED HEALTH STATUS OF TURKISH ADOLESCENTS
    (2011-02-01T00:00:00Z) Erginoz, Ethem; Alikasifoglu, Mujgan; Ercan, Oya; Albayearak-Kaymak, Deniz; Uysal, Omer; UYSAL, ÖMER
  • PublicationOpen Access
    Vitamin D Receptor Gene Haplotype Is Associated with Late-Onset Alzheimer-s Disease
    (2012-11-01T00:00:00Z) Gezen-Ak, Duygu; Dursun, Erdinc; Bilgic, Basar; Hanagasi, Hasmet; Ertan, Turan; Gurvit, Hakan; Emre, Murat; Eker, Engin; Ulutin, Turgut; Uysal, Omer; Yilmazer, Selma; UYSAL, ÖMER
    Vitamin D-3 is a neurosteroid that mediates its effects via the vitamin D receptor (VDR). The VDR gene is located on chromosome 12q13 and consists of 9 exons. VDR contains the DNA-binding site encoded by exons 2 and 3 and the ligand-binding site encoded by exons 4 - 9. Our earlier study showed that the ApaI polymorphic site of the VDR gene is associated with late-onset Alzheimer-s disease (AD). Here, we investigated the association between additional polymorphisms of the VDR gene and AD using the same samples. Two single nucleotide polymorphisms (SNPs) in intron 8 (BsmI and Tru9I polymorphisms) and one in exon 2 (FokI polymorphism) of the VDR gene were examined in up to 108 AD patients and 115 age-matched controls. Genotypes were determined with polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. Haplotype analysis also included the previously studied polymorphic sites that were recognized by TaqI (in exon 9) and ApaI (in intron 8) restriction enzymes. There was no significant difference between AD patients and controls when their genotypes for BsmI, Tru9I and FokI polymorphic sites were compared. However, the frequency of -TaubF- haplotype (alleles of TaqI, ApaI, Tru9I, BsmI and FokI, respectively), which was determined by analyzing 5 polymorphisms together, was significantly higher in the AD patient group, suggesting that this haplotype is a risk factor in AD. Our results point out a possible link between AD and certain VDR polymorphisms and indicate that individuals with these polymorphisms might be vulnerable to AD.