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Search Results: 1 - 10 of 269954 matches for " Alice L. Yu "
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Monoclonal antibodies targeting the synthetic peptide corresponding to the polybasic cleavage site on H5N1 influenza hemagglutinin
Henry J Tsai, Li-Ann Chi, Alice L Yu
Journal of Biomedical Science , 2012, DOI: 10.1186/1423-0127-19-37
Abstract: Monoclonal antibodies (mAb) specific to the synthetic peptide of hemagglutinin polybasic cleavage site of H5N1 virus were raised and tested for their neutralizing potential.Purified mAb showed suppression of H5N1 pseudovirus infection on Madin-Darby Canine Kidney (MDCK) cells but the efficacy was less than 50%. Since those mAb are specific to the intact uncut polybasic cleavage site of hemagglutinin, their efficacy depends on the extent of hemagglutinin cleavage on the viral surface.Proteolytic analysis suggests the low efficacy associated with those mAb may be due to proteolytic cleavage already present on the majority of hemagglutinin prior to the infection of virus.Avian H5N1 highly pathogenic influenza virus was first isolated from sick geese in China during 1996 and later transmitted to human in Hon Kong during 1997 [1]. This H5N1 virus was spread throughout Asia and over as far as Europe or Africa by migratory birds in 2005 [1], which prompted a fear of global pandemic. Avian H5N1 Influenza virus has two major antigenic surface proteins, hemagglutinin (HA) and neuraminidase (NA), and a RNA genome which accumulates mutations rapidly over its life cycles [2]. The rapid accumulation of genomic mutations results in frequent alterations on the surface epitopes that is known as antigenic drift [3]. The function of HA is to recognize host sialic acid residue as an entry receptor [4,5], and to fuse viral envelope with vesicle's membrane [5,6] after the linker peptide between subdomain HA1 and HA2 of HA is cleaved by host trypsin-like proteases. Virulent H5 and H7 hemagglutinins [7] have a polybasic cleavage site that is exposed and cleavable by furin or other proprotein convertases [8,9] which enables the virus to infect multiple organs and leads to multisystem failure [7]. A second factor correlating to the high pathogenicity of H5N1 influenza virus is the PB2 subunit in polymerase complex [10,11]. The adaptation of viral polymerase complex to replicate in mammalian
Biological Effects of Cigarette Smoke in Cultured Human Retinal Pigment Epithelial Cells
Alice L. Yu, Kerstin Birke, Johannes Burger, Ulrich Welge-Lussen
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0048501
Abstract: The goal of the present study was to determine whether treatment with cigarette smoke extract (CSE) induces cell loss, cellular senescence, and extracellular matrix (ECM) synthesis in primary human retinal pigment epithelial (RPE) cells. Primary cultured human RPE cells were exposed to 2, 4, 8, and 12% of CSE concentration for 24 hours. Cell loss was detected by cell viability assay. Lipid peroxidation was assessed by loss of cis-parinaric acid (PNA) fluorescence. Senescence-associated ?-galactosidase (SA-?-Gal) activity was detected by histochemical staining. Expression of apolipoprotein J (Apo J), connective tissue growth factor (CTGF), fibronectin, and laminin were examined by real-time PCR, western blot, or ELISA experiments. The results showed that exposure of cells to 12% of CSE concentration induced cell death, while treatment of cells with 2, 4, and 8% CSE increased lipid peroxidation. Exposure to 8% of CSE markedly increased the number of SA-?-Gal positive cells to up to 82%, and the mRNA expression of Apo J, CTGF, and fibronectin by approximately 3–4 fold. Treatment with 8% of CSE also increased the protein expression of Apo J and CTGF and the secretion of fibronectin and laminin. Thus, treatment with CSE can induce cell loss, senescent changes, and ECM synthesis in primary human RPE cells. It may be speculated that cigarette smoke could be involved in cellular events in RPE cells as seen in age-related macular degeneration.
On the matrix equation $XA+AX^T =0$, II: Type 0-I interactions
Alice Zhuo-Yu Chan,Luis Alberto Garcia German,Stephan Ramon Garcia,Amy L. Shoemaker
Mathematics , 2013,
Abstract: The matrix equation $XA + AX^T = 0$ was recently introduced by De Ter\'an and Dopico to study the dimension of congruence orbits. They reduced the study of this equation to a number of special cases, several of which have not been explicitly solved. In this note we obtain an explicit, closed-form solution in the difficult Type 0-I interaction case.
The Multifaceted Effects of Polysaccharides Isolated from Dendrobium huoshanense on Immune Functions with the Induction of Interleukin-1 Receptor Antagonist (IL-1ra) in Monocytes
Juway Lin, Ya-Jen Chang, Wen-Bin Yang, Alice L. Yu, Chi-Huey Wong
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0094040
Abstract: Dendrobium huoshanense is a valuable and versatile Chinese herbal medicine with the anecdotal claims of cancer prevention and anti-inflammation. However, its immunological activities are limited to in vitro studies on a few cytokines and immune cell functions. First, we investigated the effects of polysaccharides isolated from DH (DH-PS) on inducing a panel of cytokines/chemokines in mice in vivo and human in vitro. We found that DH polysaccharides (DH-PS) induced TH1, TH2, inflammatory cytokines and chemokines in mouse in vivo and human cells in vitro. Secondly, we demonstrated that DH-PS expanded mouse splenocytes in vivo including CD4+ T cells, CD8+ T cells, B cells, NK cells, NKT cells, monocytes/macrophages, granulocytes and regulatory T cells. Notably, DH-PS induced an anti-inflammatory molecule, IL-1ra, in mouse and human immune cells, especially monocytes. The serum level of IL-1ra elicited by the injection of DH-PS was over 10 folds of IL-1β, suggesting that DH-PS-induced anti-inflammatory activities might over-ride the inflammatory ones mediated by IL-1β. The signaling pathways of DH-PS-induced IL-1ra production was shown to involve ERK/ELK, p38 MAPK, PI3K and NFκB. Finally, we observed that IL-1ra level induced by DH-PS was significantly higher than that by F3, a polysaccharide extract isolated from another popular Chinese herbal medicine, Ganoderma lucidum. These results indicated that DH-PS might have potential applications for ameliorating IL-1-induced pathogenic conditions.
Possibilities of Differentiated Approach Implementation into Disadvantaged Children’s Legal Instruction
Alice Yu. Kolomiets
European Researcher , 2012,
Abstract: The article is focused on differentiated approach to disadvantaged children’s legal culture development. Special attention is attached to disadvantaged families and different approaches to schoolchildren’s legal culture development and differentiated approach.
Concordant and Discordant Regulation of Target Genes by miR-31 and Its Isoforms
Yu-Tzu Chan, You-Chin Lin, Ruey-Jen Lin, Huan-Hsien Kuo, Wai-Cheng Thang, Kuo-Ping Chiu, Alice L. Yu
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0058169
Abstract: It has been shown that imprecise cleavage of a primary or precursor RNA by Drosha or Dicer, respectively, may yield a group of microRNA (miRNA) variants designated as “isomiR”. Variations in the relative abundance of isoforms for a given miRNA among different species and different cell types beg the question whether these isomiRs might regulate target genes differentially. We compared the capacity of three miR-31 isoforms (miR-31-H, miR-31-P, and miR-31-M), which differ only slightly in their 5′- and/or 3′-end sequences, to regulate several known targets and a predicted target, Dicer. Notably, we found isomiR-31s displayed concordant and discordant regulation of 6 known target genes. Furthermore, we validated a predicted target gene, Dicer, to be a novel target of miR-31 but only miR-31-P could directly repress Dicer expression in both MCF-7 breast cancer cells and A549 lung cancer cells, resulting in their enhanced sensitivity to cisplatin, a known attribute of Dicer knockdown. This was further supported by reporter assay using full length 3′-untranslated region (UTR) of Dicer. Our findings not only revealed Dicer to be a direct target of miR-31, but also demonstrated that isomiRs displayed similar and disparate regulation of target genes in cell-based systems. Coupled with the variations in the distribution of isomiRs among different cells or conditions, our findings support the possibility of fine-tuning gene expression by miRNAs.
Hsp27 participates in the maintenance of breast cancer stem cells through regulation of epithelial-mesenchymal transition and nuclear factor-κB
Li Wei, Tsung-Ta Liu, Hsiu-Huan Wang, Hui-Mei Hong, Alice L Yu, Hsiang-Pu Feng, Wen-Wei Chang
Breast Cancer Research , 2011, DOI: 10.1186/bcr3042
Abstract: Mitogen-activated protein kinase antibody array and Western blot were used to discover the expression of Hsp27 and its phosphorylation in ALDH + BCSCs. To study the involvement of Hsp27 in BCSC biology, siRNA mediated gene silencing and quercetin treatment were used to inhibit Hsp27 expression and the characters of BCSCs, which include ALDH+ population, mammosphere formation and cell migration, were analyzed simultaneously. The tumorigenicity of breast cancer cells after knockdown of Hsp27 was analyzed by xenograftment assay in NOD/SCID mice. The epithelial-mesenchymal transition (EMT) of breast cancer cells was analyzed by wound-healing assay and Western blot of snail, vimentin and E-cadherin expression. The activation of nuclear factor kappa B (NF-κB) was analyzed by luciferase-based reporter assay and nuclear translocation.Hsp27 and its phosphorylation were increased in ALDH+ BCSCs in comparison with ALDH- non-BCSCs. Knockdown of Hsp27 in breast cancer cells decreased characters of BCSCs, such as ALDH+ population, mammosphere formation and cell migration. In addition, the in vivo CSC frequency could be diminished in Hsp27 knockdown breast cancer cells. The inhibitory effects could also be observed in cells treated with quercetin, a plant flavonoid inhibitor of Hsp27, and it could be reversed by overexpression of Hsp27. Knockdown of Hsp27 also suppressed EMT signatures, such as decreasing the expression of snail and vimentin and increasing the expression of E-cadherin. Furthermore, knockdown of Hsp27 decreased the nuclear translocation as well as the activity of NF-κB in ALDH + BCSCs, which resulted from increasing expression of IκBα. Restored activation of NF-κB by knockdown of IκBα could reverse the inhibitory effect of Hsp27 siRNA in suppression of ALDH+ cells.Our data suggest that Hsp27 regulates the EMT process and NF-κB activity to contribute the maintenance of BCSCs. Targeting Hsp27 may be considered as a novel strategy in breast cancer therapy.Heat shock p
Chimeras of p14ARF and p16: Functional Hybrids with the Ability to Arrest Growth
Richard T. Williams, Lisa M. Barnhill, Huan-Hsien Kuo, Wen-Der Lin, Ayse Batova, Alice L. Yu, Mitchell B. Diccianni
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0088219
Abstract: The INK4A locus codes for two independent tumor suppressors, p14ARF and p16/CDKN2A, and is frequently mutated in many cancers. Here we report a novel deletion/substitution from CC to T in the shared exon 2 of p14ARF/p16 in a melanoma cell line. This mutation aligns the reading frames of p14ARF and p16 mid-transcript, producing one protein which is half p14ARF and half p16, chimera ARF (chARF), and another which is half p16 and half non-p14ARF/non-p16 amino acids, p16-Alternate Carboxyl Terminal (p16-ACT). In an effort to understand the cellular impact of this novel mutation and others like it, we expressed the two protein products in a tumor cell line and analyzed common p14ARF and p16 pathways, including the p53/p21 and CDK4/cyclin D1 pathways, as well as the influence of the two proteins on growth and the cell cycle. We report that chARF mimicked wild-type p14ARF by inducing the p53/p21 pathway, inhibiting cell growth through G2/M arrest and maintaining a certain percentage of cells in G1 during nocodazole-induced G2 arrest. chARF also demonstrated p16 activity by binding CDK4. However, rather than preventing cyclin D1 from binding CDK4, chARF stabilized this interaction through p21 which bound CDK4. p16-ACT had no p16-related function as it was unable to inhibit cyclin D1/CDK4 complex formation and was unable to arrest the cell cycle, though it did inhibit colony formation. We conclude that these novel chimeric proteins, which are very similar to predicted p16/p14ARF chimeric proteins found in other primary cancers, result in maintained p14ARF-p53-p21 signaling while p16-dependent CDK4 inhibition is lost.
Contributions in the First 21st Century Decade to Environmental Health Vector Borne Disease Research
Alice L. Anderson
Infectious Diseases: Research and Treatment , 2012, DOI: 10.4137/IDRT.S2832
Abstract: A selective review of recent concepts, events and major recent research methodologies, and educational approaches in the field of vector-borne disease are drawn together in this article. Since vector borne disease is a major contributor to world disease bur- dens, and also comprises list of neglected diseases, recent research in the field elucidates the uncertain and far-reaching consequences of these diseases to human health and well-being. Some of the specific findings included in this review are the following: Chickungunya virus disease range is changing as a result of global climate change; Tick-borne disease vaccinations are being pursued with the help of PCR techniques; the wide availability of remote sensing and ecology are providing habitat surveillance tools to improve predictability of risk areas; environmental health education approaches are incorporating community and cultural aspects to improve success and reduce risk.
Contributions in the First 21st Century Decade to Environmental Health Vector Borne Disease Research
Alice L. Anderson
Infectious Diseases: Research and Treatment , 2010,
Abstract:
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