Sources of Growth in the Turkish Economy: A Non-parametric Approach

Bir ekonomide büyümenin kaynaklarının geleneksel büyüme muhasebesi çerçevesinde tahmini faktör piyasalarının rekabetçi oldukları ve üretim fonksiyonunun belirli bir kalıba uyduğu şeklindeki varsayımların sağlanmasını gerektirmektedir. Bu çalışmada Iwata vd. (2003) çalışmasından hareketle Türkiye ekonomisinde büyümenin kaynakları ve toplam faktör verimliliği (TFV) 1968-2006 dönemi için söz konusu varsayımların sağlanmasını gerektirmeyen parametrik olmayan regresyon analizi ile tahmin edilmiştir. Çıktının sermaye ve işgücü girdisine göre esneklik katsayılarının parametrik olmayan regresyon tahminleri Türkiye ekonomisinde ölçeğe göre azalan getiri olduğunu göstermektedir. Tahmin sonuçlarına göre 1980 öncesi dönemde büyümenin kaynağı sermaye birikimi iken, 1980 sonrası dönemde 1991-95 yılları dışında TFV büyümesidir. İşgücünün büyümeye en önemli katkısını 1991-95 döneminde yaptığı gözlenmiştir.Estimating the sources of economic growth within the framework of the conventional growth accounting approach is based on two assumptions namely the factor markets are competitive and the underlying aggregate production function has a specific form. In this study, following Iwata et al (2003), sources of economic growth and total factor productivity (TFP) growth in the Turkish economy for the period 1968-2006 were estimated with nonparametric regression approach which does not require imposing these restrictive assumptions. Nonparametric estimates of income share of capital and labor indicated there are diminishing returns to scale in the Turkish economy. According to results, capital formation is the main sources of growth before in the pre-1980 period, TFP is the sources of growth with the exception of 1991-95 period and post-1980 period seems to be the sources of growth. It is observed that labor's contribution to economic growth reached the highest level in the 1991-95

ITIH5 mediates epigenetic reprogramming of breast cancer cells

Extracellular matrix (ECM) is known to maintain epithelial integrity. In carcinogenesis ECM degradation triggers metastasis by controlling migration and differentiation including cancer stem cell (CSC) characteristics. The ECM-modulator inter- α-trypsin inhibitor heavy chain family member five (ITIH5) was recently identified as tumor suppressor potentially involved in impairing breast cancer progression but molecular mechanisms underlying its function are still elusive

CCL2 chemokine inhibition primes the tumor vasculature for improved nanomedicine delivery and efficacy

Blood vessel functionality is crucial for efficient tumor-targeted drug delivery. Heterogeneous distribution and perfusion of angiogenic blood vessels contribute to suboptimal accumulation of (nano-) therapeutics in tumors and metastases. To attenuate pathological angiogenesis, an L-RNA aptamer inhibiting the C–C motif chemokine ligand 2 (CCL2) was administered to mice bearing orthotopic 4T1 triple-negative breast cancer tumors. The effect of CCL2 inhibition on tumor blood vessel functionality and tumor-targeted drug delivery was evaluated via multimodal and multiscale optical imaging, employing fluorophore-labeled polymeric (10 nm) and liposomal (100 nm) nanocarriers. Anti-CCL2 treatment induced a dose-dependent anti-angiogenic effect, reflected by a decreased relative blood volume, increased blood vessel maturity and functionality, and reduced macrophage infiltration, accompanied by a shift in the polarization of tumor-associated macrophages (TAM) towards a less M2-like and more M1-like phenotype. In line with this, CCL2 inhibitor treatment improved the delivery of polymers and liposomes to tumors, and enhanced the antitumor efficacy of free and liposomal doxorubicin. Together, these findings demonstrate that blocking the CCL2-CCR2 axis modulates TAM infiltration and polarization, resulting in vascular normalization and improved tumor-targeted drug delivery

Small intestinal mucosa expression of putative chaperone fls485

<p>Abstract</p> <p>Background</p> <p>Maturation of enterocytes along the small intestinal crypt-villus axis is associated with significant changes in gene expression profiles. <it>fls485 </it>coding a putative chaperone protein has been recently suggested as a gene involved in this process. The aim of the present study was to analyze <it>fls48</it>5 expression in human small intestinal mucosa.</p> <p>Methods</p> <p><it>fls485 </it>expression in purified normal or intestinal mucosa affected with celiac disease was investigated with a molecular approach including qRT-PCR, Western blotting, and expression strategies. Molecular data were corroborated with several <it>in situ </it>techniques and usage of newly synthesized mouse monoclonal antibodies.</p> <p>Results</p> <p>fls485 mRNA expression was preferentially found in enterocytes and chromaffine cells of human intestinal mucosa as well as in several cell lines including Rko, Lovo, and CaCo2 cells. Western blot analysis with our new anti-fls485 antibodies revealed at least two fls485 proteins. In a functional CaCo2 model, an increase in fls485 expression was paralleled by cellular maturation stage. Immunohistochemistry demonstrated fls485 as a cytosolic protein with a slightly increasing expression gradient along the crypt-villus axis which was impaired in celiac disease Marsh IIIa-c.</p> <p>Conclusions</p> <p>Expression and synthesis of fls485 are found in surface lining epithelia of normal human intestinal mucosa and deriving epithelial cell lines. An interdependence of enterocyte differentiation along the crypt-villus axis and fls485 chaperone activity might be possible.</p