17 research outputs found
Eating attitudes, body image satisfaction and self-esteem in Turkish adolescents.
No full textBatı ülkelerinde bozulmuş yeme davranışları ve zayıflık arzusunun ergenler arasında yaygın olduğu bilinmesine rağmen, gelişmekte olan ülkelerde bu konuyla ilgili veriler kısıtlıdır. Türkiye hızla gelişen bir ülkedir ve Türk ergenler Avrupa ve Asya değerlerinden etkilenmektedir. Özellikle genç Türk popülasyonunda yeme davranışlarındaki değişimi takip edebilmek için klinik dışı örneklemlerde gerçekleştirilecek çalışmalar ihtiyaç vardır.
Bu çalışmanın temel amacı Türk ergen grupta bozulmuş yeme tutum ve davranışlarını değerlendirmektir. 38 soruluk bir sosyo-demografik değerlendirme formu, Yeme Bozuklukları Değerlendirme Ölçeği (EDE-Q), Yeme Tutumu Testi (EAT-40), Beden İmgesi Memnuniyeti Anketi (BISQ) ve Rosenberg Benlik Değeri Skalası kullanılmıştır. Farklı sosyo-ekonomik düzeylerden, İstanbul'u temsil eden bir kaç orta okul ve liseden ortalama yaşları 15.52 (min-max=12-18, SD=1.88) olan 626 kız ve 299 erkek çalışmaya dahil edildi. Ergenlerin çoğu (%90) anne ve babalarıyla yaşıyordu. Annelerin çoğu (%47.4) ilkokul mezunuyken, babaların çoğu (%37.8)lise mezunuydu.
Ortalama BKİ 20.90 (SD=3.38)'dı. Sadece 11 kız (%1.8) ve 4 erkek (%1.3) için BKİ>30 iken, 84 kız (%14) ve 29 erkek (%10) için BKİ<17.5 (p<0.05) idi. BKİ kategorilerinin, beden imgesi memnuniyetsizliği, zayıflık arzusu, bozulmuş yeme tutumunun bir fonksiyonu olarak kız ve erkeklerin sıklık dağılımları farklılaşmakta idi. Karşılaştırmalı sonuçlar kız ve erkekler arasında SES açısından anlamlı bir fark göstermezken, BKİ, EDE-Q toplam ve alt-ölçekler, EAT-40 ve BISQ skorlarının cinsiyetin bir fonksiyonu olarak farklılaştığını göstermektedir. SES'e göre düşük benlik saygısı skorları olan kişiler, tüm alt ölçeklerde ve toplam EDE-Q da yüksek skorlar almışlardı.
Bu çalışma bozulmuş yeme tutumu ve davranışlarının özellikle pek çok Türk kız lise öğrencisi arasında bulunduğuna işaret etmektedir. Bu veriler, ergen kızların yeme bozuklukları açısından taranması ve bu grup için birincil ve ikincil müdahalelerin hedeflenmesi gerektiğini düşündürmektedir
Visualisation, VISC and scientific insight
No full textFirst paragraph:The report by McCormick et al (1987) on Visualisation in Scientific Computing (ViSC) played a major role in drawing attention to the increasing need and scope for visual computing. There is no doubt that developments in computer-based technology will greatly extend human capacity for visualisation. The invention of the microscope and telescope led to breakthroughs in many scientific disciplines. These tools not only enabled Man to see the otherwise unseeable but they also enabled empirical evaluation of pre-existing theory. Similarly, imaging systems and computer graphics are further enabling Man to see the unseeabl~ and are becoming vital tools of research in some disciplines . A wide range of phenomena , which exist either outside our sensory limits or which exist only in our imagination, may berendered visual. The technology for this is already well developed and the euphoria over ViSC is justifiable
Visualisation, VISC and scientific insight
No full textFirst paragraph:The report by McCormick et al (1987) on Visualisation in Scientific Computing (ViSC) played a major role in drawing attention to the increasing need and scope for visual computing. There is no doubt that developments in computer-based technology will greatly extend human capacity for visualisation. The invention of the microscope and telescope led to breakthroughs in many scientific disciplines. These tools not only enabled Man to see the otherwise unseeable but they also enabled empirical evaluation of pre-existing theory. Similarly, imaging systems and computer graphics are further enabling Man to see the unseeabl~ and are becoming vital tools of research in some disciplines . A wide range of phenomena , which exist either outside our sensory limits or which exist only in our imagination, may berendered visual. The technology for this is already well developed and the euphoria over ViSC is justifiable
NDRG1 expression in trophoblast cell lines in response to hypoxia or CoCl<sub>2</sub>.
No full text<p>NDRG1 (upper panels) and tubulin (loading control, lower panels) were detected using Western immunoblot. (A) NDRG1 expression in trophoblasts and trophoblast-derived choriocarcinoma cell lines, as well as in other cell types under standard conditions. (B) NDRG1 expression in JEG-3 cells cultured in standard conditions, 24 h of hypoxia (<1% O<sub>2</sub>) or the hypoxia mimetic CoCl<sub>2</sub> (200 µM). The expression of HIF-1α (middle panel) confirmed the effect of CoCl<sub>2</sub> or hypoxia. (C) A time course and concentration-dependent stimulation of NDRG1 expression in JEG-3 cells exposed to the hypoxia mimetic agent CoCl<sub>2</sub>. Data are representative of at least three independent experiments.</p
The impact of non-hypoxic cell injury on NDRG1 expression in trophoblast lines.
No full text<p>(A) BeWo cells were incubated for either 24 or 48 h in standard, serum-containing medium or in serum-free medium. NDRG1 was detected by Western immunoblot (upper panel), and tubulin (lower panel) used for loading control. (B) JEG-3 cells were exposed to UV irradiation at the energy dosage indicated, and harvested after 6 or 24 h after the brief (1-3 seconds) pulse of UV irradiation. Analysis was performed as described in panel A. (C) Immunofluorescent staining of NDRG1 in JEG-3 cells 24 h after exposure to CoCl<sub>2</sub> (200 µM), serum-free medium, or UV irradiation (6 mJ/cm<sup>2</sup>). Panels are NDRG1 alone, or channel merge of NDRG1 (green) and Hoechst 33342 (blue), used for nuclear staining. Bar = 20 µm(D) The expression of NDRG members in PHT cells 24 h after exposure to ionizing radiation at the energy dose shown. Left panel shows RT-qPCR analysis, performed as described in Materials and Methods. None of the differences were significant. Right panel depicts NDRG1 expression, detected as in panel A, in cells exposed to ionizing radiation at the energy dosage shown. Analysis was performed as described in panel A. Data are representative of at least three independent experiments.</p
The sub-cellular localization of NDRG1 in response to hypoxic injury.
No full text<p> Wild type or myc-tagged NDRG1, as well as cell nuclei, were detected as described in Materials and Methods. (A) The impact of hypoxia on NDRG1 expression level and localization in PHT cells exposed to hypoxia at the time period indicated. NDRG1 (green) is shown in the left panels, and a merged channel of NDRG1 and nuclei (blue) is shown in the right panels. (B) JEG-3 cells were exposed to CoCl<sub>2</sub> (200 µM) for 24 h, and data analyzed as in (A). (C) A Western immunoblot of NDRG1 expression in the cytoplasmic (upper panel) or nuclear (lower panel) fraction of JEG-3 cells cultured in standard or hypoxic conditions for the period of time indicated. Tubulin and lamin A/C were used as markers of the cytoplasm and nucleus, respectively. (D) The impact of CoCl<sub>2</sub> (200 µM for 24 h) on the localization of myc-tagged NDRG1 in JEG-3 cells. Myc-tagged NDRG1 (red), E-cadherin (green), and nuclei (blue) are shown. (E) The impact of hypoxia (24 h, <1% O<sub>2</sub>) on the localization of myc-tagged NDRG1 in BeWo cells. Myc-tagged NDRG1 (red) and nuclei (green) are shown. Data are representative of at least three independent experiments. Bar = 20 µm in all panels.</p
The expression and nuclear localization of NDRG1 deletion mutants.
No full text<p>(A) Schematic representation of human NDRG1 protein structure, depicting protein domains, including those mutated in NDRG1-related human diseases, as well as NDRG1 deletion mutants generated in this study. (B) The subcellular localization of PPAS-deleted NDRG1 mutants in BeWo cells, cultured in hypoxia (24 h, <1% O<sub>2</sub>). Myc-tagged NDRG1 wild type and ΔCAP but not ΔPPAS (red, upper panels) were co-localized with nuclei (SYTOX Green, lower panels). Bar = 20 µm. (C) Upper panel: The expression of myc-tagged NDRG1 wild type or mutants (mRNA, upper gel; protein, lower gel) in BeWo cells. Lower panels: the effect of the proteasome inhibitor MG-132 (5 µM, 16 h) on the expression of myc-tagged NDRG1 mutant in PPAS domain in BeWo cells, detected using Western immunoblot. (D) The effect of the proteasome inhibitor MG-132 (5 µM, 16 h) on the subcellular localization of transfected mutant PPAS domain of NDRG1 (red) in hypoxic BeWo cells. Bar = 10 µm. Data are representative of at least three independent experiments.</p
The expression of NDRG1 in cytoplasmic membranes or membrane-associated structures in hypoxic (24 h) trophoblastic lines.
No full text<p>The nuclei (blue), in all panels, were detected using Hoechst 33342 and each organelle was detected using a specific antibody as described in Materials and Methods. (A-D) NDRG1 (green) co-localizes with desmosomes (red) in JEG-3 cells. (E-H) Myc-tagged NDRG1 (red) co-localizes with E-Cadherin (green) in BeWo cells. (I-L) Myc-tagged NDRG1 (green) co-localizes with calreticulin (red) in BeWo cells. (M-P) Myc-tagged NDRG1 (green) co-localizes with tubulin (red) in BeWo cells. Arrow points to perinuclear NDRG1 and tubulin signals. Arrowheads point to peripheral microtubules. Data are representative of at least three independent experiments. Bar = 20 µm in panels A-H, and Bar = 10 µm in panels I-P.</p
Unadjusted and adjusted odds ratios (OR) and 95% confidence intervals (CI) for prematurity (adjusted for mom’s age, mom’s education, pre-pregnancy weight, gender of infant, prenatal visits, smoking during pregnancy, gestational diabetes, WIC, race, and birth order).
No full text<p>Key: Referent (First quartile), <0.87 wells per mile; Second quartile (2Q), 0.87 to 2.59 wells per mile; Third quartile (3Q), 2.60 to 5.99 wells per mile; Fourth quartile (4Q), ≥6.00 wells per mile.</p
