The Effect of Public Education on the Long-Run Income Distribution

We consider public education provided obligatorily and equally for all individuals. It is usually said that compulsory public education ensures an equal opportunity of education for all individuals and contributes to human capital formation. We will discuss how the introduction of public education affects human capital accumulation and income distribution among heterogeneous individuals in an overlapping generation model. Particularly, we discuss those effects on the long-run equilibrium of individual human capital, considering the threshold effects of human capital stock

Popularization in the Higher Education and Optimal Educational Policies

In this paper, we construct a model which explains a change in demand for education, considering an individual preference for the higher education (university). We suppose that the individual preference for education depends on the average level of education in a society and changes drastically at some level. We consider a possibility that diffusion of education brings about discontinuous increase in demand for education, and examine the optimal educational policies in dynamic setting

Combined use of bFGF and GDF-5 enhances the healing of medial collateral ligament injury

Basic fibroblast growth factor (bFGF) and growth and differentiation factor (GDF)-5 stimulate the healing of medial collateral ligament (MCL) injury. However, the effect of isolated and combined use of bFGF/GDF-5 remains still unclear. We investigated cellular proliferation and migration responding to bFGF/GDF-5 using rabbit MCL fibroblasts. Rabbit MCL injury was treated by bFGF and/or GDF-5 with peptide hydrogels. Gene expression and deposition of collagens in healing tissues were evaluated. bFGF/GDF-5 treatment additively enhanced cell proliferation and migration. bFGF/GDF-5 hydrogels stimulated Col1a1 expression without increasing Col3a1 expression. Combined use of bFGF/GDF-5 stimulated type I collagen deposition and the reorganization of fiber alignment, and induced better morphology of fibroblasts in healing MCLs. Our study indicates that combined use of bFGF/GDF-5 might enhance MCL healing by increasing proliferation and migration of MCL fibroblasts, and by regulating collagen synthesis and connective fiber alignment

The Optimal Subsidies to Higher Education, with Reference to Education and Research

We consider a society which consists of two sectors, the educational sector and the production sector. We define the educational sector as one that produces two outputs jointly, higher education forming human capital and research increasing the stock of social knowledge. Social knowledge determines the level of technology in the production of consumption goods. Our purposes are to clarify the nature of higher education and to analyze efficient resource allocation in a two−sector economy, considering the external effects of education and research activities in the context of an endogenous growth model

Anterior cruciate ligament-derived cells have high chondrogenic potential

Anterior cruciate ligament (ACL)-derived cells have a character different from medial collateral ligament (MCL)-derived cells. However, the critical difference between ACL and MCL is still unclear in their healing potential and cellular response. The objective of this study was to investigate the mesenchymal differentiation property of each ligament-derived cell. Both ligament-derived cells differentiated into adipogenic, osteogenic, and chondrogenic lineages. In chondrogenesis, ACL-derived cells had the higher chondrogenic property than MCL-derived cells. The chondrogenic marker genes, Sox9 and α1(II) collagen (Col2a1), were induced faster in ACL-derived pellets than in MCL-derived pellets. Sox9 expression preceded the increase of Col2a1 in both pellet-cultured cells. However, the expression level of Sox9 and a ligament/tendon transcription factor Scleraxis did not parallel the increase of Col2a1 expression along with chondrogenic induction. The present study demonstrates that the balance between Sox9 and Scleraxis have an important role in the chondrogenic differentiation of ligament-derived cells

Histone Acetylation Influences the Activity of Sox9-related Transcriptional Complex

Chondrocyte differentiation is the fundamental process in skeletal development. From the mesenchymal condensation of chondroprogenitors to the hypertrophic maturation of chondrocytes, chondrogenesis is sequentially regulated by cross-talk among transcription factors, growth factors, and chromatin structure. The master transcription factor Sry-type HMG box (Sox) 9 has an essential role in the expression of chondrogenic genes through the association with Sox9-binding sites on its target genes. Several transcription factors and coactivators, such as Scleraxis/E47 and p300, cooperatively modulate the Sox9-dependent transcription by interacting with Sox9. The Sox9-related transcriptional apparatus activates its target gene expression through p300-mediated histone acetylation on chromatin. The transforming growth factor (TGF)-β superfamily also plays a key role in chondrocyte differentiation. The TGF-β-regulated Smad3/4 complex activates Sox9-dependent transcription on chromatin by associating with Sox9 itself, and by recruiting p300 onto Sox9. These findings suggest that the epigenetic status including histone modification and chromatin structure, directly influences Sox9-regulated chondrocyte differentiation. In this article, we review the regulators of Sox9 expression itself, modulators of posttranslational Sox9 function, and Sox9-associating factors in the Sox9-dependent epigenetic regulation during chondrogenesis

Epigenetic Regulation in Chondrogenesis

Epigenetics is an essential mechanism to control gene expression and fundamental cellular processes. DNA methylation in CpG-rich promoters correlates with gene silencing. Histone modification including histone acetylation and deacetylation determines the stability of the chromatin structure. Condensed chromatin (heterochromatin), which has a higher-order histone-DNA structure, prevents the access of transcriptional activators to their target genes. The fundamental unit of eukaryotic chromatin consists of 146 bp of DNA wrapped around a histone octamer. Posttranslational modifications of the histone tail and the chromatin remodeling complex disrupt histone-DNA contacts and induce nucleosome mobilization. Histone acetylation of specific lysine residues in the histone tail plays a crucial role in epigenetic regulation. Histone acetylation is a dynamic process regulated by the antagonistic actions of 2 families of enzymes - the histone acetyltransferases (HATs) and the histone deacetylases (HDACs). The balance between histone acetylation and deacetylation serves as a key epigenetic mechanism for transcription factor-dependent gene expression and the developmental process. We review emerging evidence that DNA methylation, histone acetylation modified by HAT and/or HDAC, and transcription factor-associated molecules contribute to a mechanism that can alter chromatin structure, gene expression, and cellular differentiation during chondrogenesis

Histological Analysis of Failed Cartilage Repair after Marrow Stimulation for the Treatment of Large Cartilage Defect in Medial Compartmental Osteoarthritis of the Knee

Bone marrow-stimulating techniques such as microfracture and subchondral drilling are valuable treatments for full-thickness cartilage defects. However, marrow stimulation-derived reparative tissues are not histologically well-documented in human osteoarthritis. We retrospectively investigated cartilage repairs after marrow stimulation for the treatment of large cartilage defects in osteoarthritic knees. Tissues were obtained from patients who underwent total knee arthroplasty (TKA) after arthroscopic marrow stimulation in medial compartmental osteoarthritis. Clinical findings and cartilage repair were assessed. Sections of medial femoral condyles were histologically investigated by safranin O staining and anti-type II collagen antibody. Marrow stimulation decreased the knee pain in the short term. However, varus leg alignment gradually progressed, and TKA conversions were required. The grade of cartilage repair was not improved. Marrow stimulations resulted in insufficient cartilage regeneration on medial femoral condyles. Safranin O-stained proteoglycans and type II collagen were observed in the deep zone of marrow-stimulated holes. This study demonstrated that marrow stimulation resulted in failed cartilage repair for the treatment of large cartilage defects in osteoarthritic knees. Our results suggest that arthroscopic marrow stimulation might not improve clinical symptoms for the long term in patients suffering large osteoarthritic cartilage defects

Pullout Repair Associated With a Bridging Suture Using FiberLink for the Medial Meniscus Posterior Horn/Root Tear

Transtibial pullout repair for the medial meniscus (MM) posterior root tear has become the gold standard. However, an optimal repair technique has not yet been established for MM posterior horn (MMPH) tear with a sufficient root remnant. We describe a pullout repair technique associated with a bridging suture using FiberLink (Arthrex, Naples, FL) for the MMPH tear. In this bridging suture technique, the simple cinch stitch is applied to the root remnant and MMPH. The loop end of the FiberLink is inserted into the MMPH, and its free-end is inserted into the root remnant. Next, the suture is tensioned and tied on the superior surface of the MMPH. The bridging suture and the additional simple stitch applied to the MMPH are pulled out through the tibial tunnel and fixed to the tibia on an expected tension. This technique might lead to better meniscal healing of the tear site, because it involves bridging of the MMPH and root remnant, and lower risk of suture cut-out owing to the biomechanical strength