Cartilage regeneration using transforming growth factor-beta 3-loaded injectable crosslinked hyaluronic acid hydrogel.

Cartilage defects can be difficult to heal, potentially leading to complications such as osteoarthritis. Recently, a tissue engineering approach that uses scaffolds and growth factors has been proposed to regenerate new cartilage tissues. Herein, we investigated the application of hyaluronic acid (HA) gel loaded with transforming growth factor-beta 3 (TGF-ß3) for enhanced cartilage regeneration. We assessed the clinical conditions required to efficiently enhance the ability of the modified HA gel to repair defective cartilage. Based on our findings, the prepared HA gel exhibited good physicochemical and mechanical properties and was non-toxic and non-inflammatory. Moreover, HA gel-loaded TGF-ß3 (HAT) had improved biocompatibility and promoted the synthesis of cartilage-specific matrix and collagen, further improving its ability to repair defects. The application of HAT resulted in an initial burst release of HA, which degraded slowly in vivo. Finally, HAT combined with microfracture-inducing bone marrow stem cells could significantly improve the cartilage microenvironment and regeneration of cartilage defects. Our results indicate that HA is a suitable material for developing growth factor carriers, whereas HAT is a promising candidate for cartilage regeneration. Furthermore, this differentiated strategy provides a rapid and effective clinical approach for next-generation cartilage regeneration.

The Taxonomy and Diversity of Proschkinia (Bacillariophyta), A Common But Enigmatic Genus from Marine Coasts.

Detailed morphological documentation is provided for established Proschkinia taxa, including the generitype, P. bulnheimii, and P. complanata, P. complanatula, P. complanatoides and P. hyalosirella, and six new species. All established taxa are characterized from original material from historical collections. The new species described in this paper (P. luticola, P. staurospeciosa, P. impar, P. modesta, P. fistulispectabilis, and P. rosowskii) were isolated from the Western Pacific (Yellow Sea coast of Korea) and the Atlantic (Scottish and Texas coasts). Thorough documentation of the frustule, valve and protoplast architecture revealed the combination of characters diagnostic of the genus Proschkinia: a single-lobed chloroplast; a broad girdle composed of U-shaped, perforated bands; the position of the conopeate raphe-sternum relative to the external and internal valve surface; and the presence of an occluded process through the valve, termed the "fistula". Seven strains of Proschkinia were grown in culture and five of these were sequenced for nuclear ribosomal SSU and plastid-encoded rbcL. Phylogenetic analysis recovered a clade of Proschkinia with Fistulifera, another fistula-bearing diatom genus, and together these were sister to a clade formed of the Stauroneidaceae; in turn, all of these were sister to a clade composed of Parlibellus and two monoraphid genera Astartiella and Schizostauron. Despite morphological similarities between Proschkinia and the Naviculaceae, these two taxa are distant in our analysis. We document the variation in the morphology of Proschkinia, including significant variability in the fistula, suggesting that fistula ultrastructure might be one of the key features for species identification within the genus.

Complete mitochondrial genome of a rare diatom (Bacillariophyta) Proschkinia and its phylogenetic and taxonomic implications.

We obtained the complete mitogenome of Proschkinia sp. strain SZCZR1824, a strain belonging to a poorly known diatom genus with no previous molecular data. This genome is 48,863 bp long, with two group I introns in rnl and three group II introns in cox1. Using mitogenomic data, Proschkinia sp. was recovered with Fistulifera solaris, far distant from Navicula and Nitzschia, two genera with which Proschkinia has sometimes been associated based on morphology.

Influence of the tidal front on the three-dimensional distribution of spring phytoplankton community in the eastern Yellow Sea.

Hydrographic observation and biological samplings were conducted to assess the distribution of phytoplankton community over the sloping shelf of the eastern Yellow Sea in May 2012. The concentration of chlorophyll a was determined and phytoplankton was microscopically examined to conduct quantitative and cluster analyses. A cluster analysis of the phytoplankton species and abundance along four observation lines revealed the three-dimensional structure of the phytoplankton community distribution: the coastal group in the mixed region, the offshore upper layer group preferring stable water column, and the offshore lower layer group. The subsurface maximum of phytoplankton abundance and chlorophyll a concentration appeared as far as 64 km away from the tidal front through the middle layer intrusion. The phytoplankton abundance was high in the shore side of tidal front during the spring tide. The phytoplankton abundance was relatively high at 10-m depth in the mixed region while the concentration of chlorophyll a was high below the depth. The disparity between the profiles of the phytoplankton abundance and the chlorophyll a concentration in the mixed region was related to the depth-dependent species change accompanied by size-fraction of the phytoplankton community.

ARD1 binding to RIP1 mediates doxorubicin-induced NF-κB activation.

NF-κB is activated by several cellular stresses. Of these, the TNFα-induced activation pathway has been examined in detail. It was recently reported that receptor-interacting protein 1 (RIP1) is involved in DNA damage-induced NF-κB activation by forming a complex with the p53 interacting death domain protein (PIDD) and NF-κB essential modulator (NEMO) in the nucleus, although the underlying mechanism of this interaction has yet to be clarified. This study shows that siRNA knock-down of arrest-defective 1 protein (ARD1) abrogated doxorubicin- but not TNFα-induced activation. Conversely, the over-expression of ARD1 greatly enhanced NF-κB activation induced by doxorubicin. Immunoprecipitation experiments revealed that ARD1 interacted with RIP1 via the acetyltransferase domain. Furthermore, the over-expression of several domain-deleted ARD1 constructs demonstrated that the N-terminal and acetyltransferase domains of ARD1 were required for doxorubicin-induced NF-κB activation. Treatment of deacetylase inhibitor, trichostatin A, significantly increased doxorubicin-induced NF-κB activation in the presence of ARD1 but not acetyltransferase-defective ARD1 mutant. Moreover, N-terminal domain-deleted ARD1 could not be localized in the nucleus in response to doxorubicin treatment. These data indicate that the interaction between ARD1 and RIP1 plays an important role in the DNA damage-induced NF-κB activation, and that the acetyltransferase activity of ARD1 and its localization in to the nucleus are involved in such stress response.