IL-10 is an immunosuppressive cytokine in the immune system. It was in clinical trail as an anti-inflammatory therapy for inflammatory bowel disease and various autoimmune diseases such as psoriasis, rheumatoid arthritis, and multiple sclerosis. IL-19 belongs to the IL-10 family, which includes IL-10, IL-19, IL-20, IL-22, melanoma differentiation-associated gene (MDA-7, IL-24), and AK155 (IL-26). Despite a partial homology in their amino acid sequences, they are dissimilar in their biologic functions. Little is known about the biologic function and gene regulation of IL-19. To understand the gene regulation of human IL-19, we identified a human IL-19 genomic clone and analyzed its promoter region. Five fusion genes containing different regions upstream of exon 1 linked to a luciferase reporter gene were expressed in the canine kidney epithelial-like Madin-Darby canine kidney cells. A fusion gene containing 394 bp showed luciferase activity 7- to 8-fold higher than the negative control of the promoterless fusion gene. We also isolated a full-length mouse cDNA clone. Mouse IL-19 shared 71% amino acid identity with human IL-19. Treatment of monocytes with mouse IL-19 induced the production of IL-6 and TNF-α. It also induced mouse monocyte apoptosis and the production of reactive oxygen species. Taken together, our results indicate that mouse IL-19 may play some important roles in inflammatory responses because it up-regulates IL-6 and TNF-α and induces apoptosis.
In this study, we developed a simple and powerful method to fabricate flexible and lightweight graphene-based composites that provide high electromagnetic interference (EMI) shielding performance. Electrospun waterborne polyurethane (WPU) that featured sulfonate functional groups was used as the polymer matrix, which was light and flexible. First, graphene oxide (GO)/WPU composites were prepared through layer-by-layer (L-b-L) assembly of two oppositely charged suspensions of GO, the cationic surfactant (didodecyldimethylammonium bromide, DDAB)-adsorbed GO and intrinsic negatively charged GO, depositing on the negatively charged WPU fibers. After the L-b-L assembly cycles, the GO bilayers wrapped the WPU fiber matrix completely and revealed fine connections guided by the electrospun WPU fibers. Then, we used hydroiodic acid (HI) to obtain highly reduced GO (r-GO)/WPU composites, which exhibited substantially enhanced electrical conductivity (approximately 16.8 S/m) and, moreover, showed a high EMI-shielding effectiveness (approximately 34 dB) over the frequency range from 8.2 to 12.4 GHz.
Abstract.Apart from SERPINB2 and SERPINB5, the roles of the remaining 13 members of the human SERPINB family in cancer metastasis are still unknown. In the present study, we demonstrated that most of these genes are differentially expressed in tumor tissues compared to matched normal tissues from lung or breast cancer patients. Overexpression of each SERPINB gene effectively suppressed the invasiveness and motility of malignant cancer cells. Among all of the genes, the SERPINB1, SERPINB5 and SERPINB7 genes were more potent, and the inhibitory effect was further enhanced by co-expression of any two of them. In addition, single treatment of the synthetic peptides corresponding to the P5-P5' sequences of the reactive center loop (RCL) of SERPINB1, SERPINB5 or SERPINB7 markedly suppressed the invasive and migratory properties of the cancer cells in a dose-dependent manner. More significantly, combination treatment of these peptides in cancer cells further improved the suppressive effect by 20-40%. Here, we determined the expression of all SERPINB family members in lung and breast cancer patients, and identified those members with potent inhibitory ability toward invasion and migration, and designed RCL-derived peptides to suppress the malignancy of cancer cells. Forced re-expression of these anti-invasive SERPINB genes or application of the SERPINB RCL-peptides may provide a reasonable strategy against lethal cancer metastasis. IntroductionCancer metastasis is the leading cause of morbidity and mortality in cancer patients. It is a highly complex process, including cell detachment, migration, invasion, circulation in blood vessels, adhesion, colonization at other sites and formation of secondary tumors (1). Prior to tumor cell detachment from the primary site, which leads to cell migration and invasion in the metastasis process, the extracellular matrix (ECM) microenvironment must be degraded by proteases, such as urokinase plasminogen activator (uPA), uPA receptor (uPAR) and the plasmin network (2,3) and matrix metalloproteinases (MMPs) (4). On the other hand, protease inhibitors negatively regulate the proteolysis process in cancer metastasis, e.g. plasminogen activator inhibitors (PAIs), PAI-1 (SERPINE1) and PAI-2 (SERPINB2) against uPA/uPAR/plasmin network and the tissue inhibitor of matrix metalloproteinases (TIMPs), TIMP-1 to TIMP-4 against MMPs.Serine protease inhibitors (serpins) regulate many physiological processes, such as blood coagulation, fibrinolysis, inflammation, complement activation and cell migration (5). Based on their phylogenic relationships, the superfamily is divided into 16 different clades (A-P), in which human serpins are the first 9 clades (A-I) (6). The clade B serpins (SERPINB family) is the largest one within the human serpin superfamily. It contains 13 genes located on chromosome 6p25 (SERPINB1, SERPINB6 and SERPINB9) and 18q21 (the remaining members of the family). Unlike circulating serpins, the SERPINB family genes lack the N and C terminus extension regions common to other serpin...
Interleukin-22 (IL-22), a member of IL-10 family, plays some important roles in immune response through activation of the STAT 3 signal transduction pathway. Two types of IL-22-binding receptor have been discovered, a membrane-bound receptor and a soluble receptor, both encoded by different genes. IL-22 may be involved in inflammatory processes specifically regulated by soluble receptors. By screening a mouse genomic library for a human IL-22 binding protein homologue, we identified the mouse genomic clone of IL-22 binding protein. Its coding sequence was verified and isolated by RT-PCR. The gene encodes a protein of 230 amino acids that share 67.1% amino-acid sequence identity with human IL-22 binding protein.We designated this receptor 'mouse IL-22 binding protein' (mIL-22BP). mIL-22BP could be upregulated by LPS stimulation in mouse monocytes. mIL-22BP binds to mouse and human IL-22 and neutralizes STAT3 activation induced by both cytokines in human and rat hepatoma cell lines. Treating B cells with mouse IL-22 induces production of reactive oxygen species, which mIL-22BP blocks.
Dielectric and structural properties of aqueous nonpolar solute mixtures J. Chem. Phys. 137, 124501 (2012) The thickness and stretch dependence of the electrical breakdown strength of an acrylic dielectric elastomer Appl. Phys. Lett. 101, 122905 (2012) Surface tension and phase coexistence for fluids of molecules with extended dipoles J. Chem. Phys. 137, 114708 (2012) Structure, magnetic, and dielectric characteristics of Ln2NiMnO6 (Ln=Nd and Sm) ceramics J. Appl. Phys. 112, 064104 (2012) Anisotropy in the dielectric spectrum of hydration water and its relation to water dynamics Flake-shaped carbonyl iron (FCI) powder was prepared by ball milling spherical carbonyl iron (SCI) powder for 20 h. The thicknesses of the FCI particles were $0.1-0.3 lm with a diameter of $5-10 lm. The milling process increased the aspect ratio from $1 for spherical powder to an aspect ratio of $20-100 for flake one. The complex permittivity (e 0 À je 00 ) and permeability (l 0 À jl 00 ) were measured by the transmission/reflection method in the frequency range of 2-18 GHz for composites with various weight ratios of SCI and FCI. The results show that all e 0 , e 00 , l 0 and l 00 substantially increased after the milling treatment. Compared to SCI particles, the FCI particles exhibit higher permeability, higher permittivity, and better absorbing properties within the frequency test range. The magnetic loss tangent of FCI composites shows that FCI, with their large shape anisotropy, may have a higher resonance frequency and exceed the Snoek's limit in the gigahertz frequency range. For the 50 wt. % FCI composite with a thickness of 3 mm, the reflection loss at 5.5 GHz reaches À23.0 dB.
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