Journey of Mesenchymal Stem Cells for Homing: Strategies to Enhance Efficacy and Safety of Stem Cell Therapy

Human mesenchymal stem cells (MSCs) communicate with other cells in the human body and appear to “home” to areas of injury in response to signals of cellular damage, known as homing signals. This review of the state of current research on homing of MSCs suggests that favorable cellular conditions and the in vivo environment facilitate and are required for the migration of MSCs to the site of insult or injury in vivo. We review the current understanding of MSC migration and discuss strategies for enhancing both the environmental and cellular conditions that give rise to effective homing of MSCs. This may allow MSCs to quickly find and migrate to injured tissues, where they may best exert clinical benefits resulting from improved homing and the presence of increased numbers of MSCs

Physical characterization of amorphous In-Ga-Zn-O thin-film transistors with direct-contact asymmetric graphene electrode

High performance a-IGZO thin-film transistors (TFTs) are fabricated using an asymmetric graphene drain electrode structure. A-IGZO TFTs (channel length = 3 μm) were successfully demonstrated with a saturation field-effect mobility of 6.6 cm2/Vs without additional processes between the graphene and a-IGZO layer. The graphene/a-IGZO junction exhibits Schottky characteristics and the contact property is affected not only by the Schottky barrier but also by the parasitic resistance from the depletion region under the graphene electrode. Therefore, to utilize the graphene layer as S/D electrodes for a-IGZO TFTs, an asymmetric electrode is essential, which can be easily applied to the conventional pixel electrode structure. © 2014 Author(s).1

In-situ fabrication of cobalt-doped SrFe2As2 thin films by using pulsed laser deposition with excimer laser

The remarkably high superconducting transition temperature and upper critical field of iron(Fe)-based layered superconductors, despite ferromagnetic material base, open the prospect for superconducting electronics. However, success in superconducting electronics has been limited because of difficulties in fabricating high-quality thin films. We report the growth of high-quality c-axis-oriented cobalt(Co)-doped SrFe2As2 thin films with bulk superconductivity by using an in-situ pulsed laser deposition technique with a 248-nm-wavelength KrF excimer laser and an arsenic(As)-rich phase target. The temperature and field dependences of the magnetization showing strong diamagnetism and transport critical current density with superior Jc-H performance are reported. These results provide necessary information for practical applications of Fe-based superconductors.Comment: 8 pages, 3figures. to be published at Appl. Phys. Let

Antiretroviral Genotypic Resistance Mutations in HIV-1 Infected Korean Patients with Virologic Failure

Resistance assays are useful in guiding decisions for patients experiencing virologic failure (VF) during highly-active antiretroviral therapy (HAART). We investigated antiretroviral resistance mutations in 41 Korean human immunodeficiency virus type 1 (HIV-1) infected patients with VF and observed immunologic/virologic response 6 months after HAART regimen change. Mean HAART duration prior to resistance assay was 45.3±27.5 months and commonly prescribed HAART regimens were zidovudine/lamivudine/nelfinavir (22.0%) and zidovudine/lamivudine/efavirenz (19.5%). Forty patients (97.6%) revealed intermediate to high-level resistance to equal or more than 2 antiretroviral drugs among prescribed HAART regimen. M184V/I mutation was observed in 36 patients (87.7%) followed by T215Y/F (41.5%) and M46I/L (34%). Six months after resistance assay and HAART regimen change, median CD4+ T cell count increased from 168 cells/µL (interquartile range [IQR], 62-253) to 276 cells/µL (IQR, 153-381) and log viral load decreased from 4.65 copies/mL (IQR, 4.18-5.00) to 1.91 copies/mL (IQR, 1.10-3.60) (P<0.001 for both values). The number of patients who accomplished viral load <400 copies/mL was 26 (63.4%) at 6 months follow-up. In conclusion, many Korean HIV-1 infected patients with VF are harboring strains with multiple resistance mutations and immunologic/virologic parameters are improved significantly after genotypic resistance assay and HAART regimen change

Kaempferol inhibits IL‑1β‑induced proliferation of rheumatoid arthritis synovial fibroblasts and the production of COX‑2, PGE2 and MMPs

Inflammatory cytokines, matrix metalloproteinases (MMPs) and cyclooxygenase (COX)‑2 released from rheumatoid arthritis synovial fibroblasts (RASFs) are involved in the destruction of both articular bone and cartilage. Kaempferol has been reported to act as an antioxidant and anti‑inflammatory agent by inhibiting nitric oxide synthase and COX enzymes. The aim of the present study was to determine the effects of kaempferol on the interleukin‑1β (IL‑1β)‑induced proliferation of RASFs and the production of MMPs, COX and prostaglandin E2 (PGE2) by RASFs. The proliferation of the RASFs stimulated with IL‑1β and treated with/without kaempferol was evaluated by CCK‑8 assay. The expression of MMPs, TIMP metallopeptidase inhibitor‑1 (TIMP‑1), COXs, PGE2 and that of intracellular MAPK signaling molecules, including p‑ERK, p‑p38, p‑JNK and nuclear factor‑κB (NF‑κB) was examined by immunoblotting or semi‑quantitative reverse transcription‑polymerase chain reaction (RT‑PCR) and ELISA under the conditions described above. Kaempferol inhibited the proliferation of both unstimulated and IL‑1β‑stimulated RASFs, as well as the mRNA and protein expression of MMP‑1, MMP-3, COX‑2 and PGE2 induced by IL‑1β. Kaempferol also inhibited the phosphorylation of ERK‑1/2, p38 and JNK, as well as the activation of NF‑κB induced by IL‑1β. These results indicate that kaempferol inhibits synovial fibroblast proliferation, as well as the production of and MMPs, COX‑2 and PGE2, which is involved in articular inflammation and destruction in rheumatoid arthritis (RA). Our data suggest that kaempferol may be a novel therapeutic agent for the treatment of RA

Ethyl acetate fraction from Angelica sinensis inhibits IL-1β-induced rheumatoid synovial fibroblast proliferation and COX-2, PGE2, and MMPs production

BACKGROUND: The root of Angelica sinensis (AS), also known as "Dang-gui," was a popular herbal medicine widely used in the treatment of gynecological diseases in China, Korea, and Japan for a long time. This study aimed to determine the effects of ethyl acetate fraction from Angelica sinensis (EAAS) on the interleukin-1β (IL-1β)-induced proliferation of rheumatoid arthritis synovial fibroblasts (RASFs), and production of matrix metalloproteinases (MMPs), cyclooxygenase (COX) 2, and prostaglandin E2 (PGE2), involved in articular bone and cartilage destruction, by RASFs. RESULTS: RASF proliferation was evaluated with cholecystokinin octapeptide (CCK-8) reagent in the presence of IL-1β with/without EAAS. Expression of MMPs, tissue inhibitor of metalloproteinases-1 (TIMP-1), COXs, PGE2, and intracellular mitogen-activated protein kinase (MAPK) signaling molecules, including p-ERK, p-p38, p-JNK, and NF-κB, were examined using immunoblotting or semi-quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. EAAS inhibited IL-1β-induced RASF proliferation; MMP-1, MMP-3, and COX-2 mRNA and protein expressions; and PGE2 production. EAAS also inhibits the phosphorylation of ERK-1/2, p38, and JNK, and activation of NF-κB by IL-1β. CONCLUSION: EAAS might be a new therapeutic modality for rheumatoid arthritis management

Peritonsillar Abscess in a 40-Day-Old Infant

A peritonsillar abscess is one of the most commonly occurring deep space infections of the head and neck in adults and children. A peritonsillar abscess that appears in newborns, however, is extremely rare. The treatment of a peritonsillar abscess requires both the selection of appropriate antibiotics and the best procedure to remove the abscessed material. We report a case of a peritonsillar abscess in a 40-day-old infant who was treated with antibiotic therapy alone

Serum immunoglobulin fused interferon-α inhibited tumor growth in athymic mice bearing colon 26 adenocarcinoma cells

Interferon (IFN) has therapeutic potential for a wide range of infectious and proliferative disorders. However, the half-life of IFN is too short to have a stable therapeutic effect. To overcome this problem, serum immunoglobulin has been fused to IFN. In this study, the efficacy of serum immunoglobulin fused INFs (si-IFN1 and si-IFN2) was evaluated on athymic mice bearing colon 26 adenocarcinoma cells. Seven days after the implantation of tumor cells, each group of mice was injected once a week with si-IFN1 and si-IFN2 at two different concentrations (10 × : 30 µg/kg and 50 × : 150 µg/kg). A slight anti-tumoral effect was observed in all 10 × groups compared to the control. In the 50 × groups, however, si-IFN1 and si-IFN2 showed significant anti- tumoral effects compared to the control. To gain more information on the mechanisms associated with the decrease of tumor size, a Western blot assay of apoptosis-related molecules was performed. The protein expression of cytochrome c, caspase 9, 6, and 3 were increased by si-IFN1 and si-IFN2. These 2 IFNs also increased the expressions of p53, p21, Bax and Bad. Interestingly, si-IFN1 and si-IFN2 decreased the expression of VEGF-β. Taken together, serum immunoglobulin fused IFNs increased therapeutic efficacy under current experimental condition