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The recently discovered pure-quartic solitons, arising from the interaction of quartic dispersion and Kerr nonlinearity, open the door to unexplored soliton regimes and ultrafast laser science. Here, we report a general analysis of the dispersion and nonlinear properties necessary to observe pure-quartic solitons in optical platforms. We apply this analysis, in combination with numerical calculations, to the design of pure-quartic soliton supporting microstructured optical fibers. The designs presented here, which have realistic fabrication tolerances, support unperturbed pure-quartic soliton propagation providing access to an unmatched platform to study novel soliton physics. (C) 2018 Optical Society of America under the terms of the OSA Open Access Publishing Agreement

We design a photonic crystal fiber suitable for generating the intriguing pure-quartic solitons, so far only demonstrated in silicon photonic crystal waveguides. This platform will enable deeper understanding and applications of this class of solitons.

Through numerical simulations and analytical developments we show the propagation behaviour, stability, and energy scaling of the recently discovered pure quartic solitons, indicating excellent potential for pure-quartic solitons in ultrafast lasers.

We demonstrate, by experiments and analytical developments, that the recently discovered pure-quartic solitons significantly outperform conventional solitons for high-energy ultrafast pulses. This is due to the favorable scaling of their energy and their Kelly sidebands.

A novel strain of influenza A H1N1 emerged in the spring of 2009 and has spread rapidly throughout the world. Although vaccines have recently been developed that are expected to be protective, their availability was delayed until well into the influenza season. While anti-influenza drugs such as neuraminidase inhibitors can be effective, resistance to these drugs has already been reported. Although human saliva was known to inhibit viral infection and may thus prevent viral transmission, the components responsible for this activity on influenza virus, in particular, influenza A swine origin influenza A virus (S-OIV), have not yet been defined. By using a proteomics approach in conjunction with beads that bind alpha 2,6-sialylated glycoprotein, we determined that an alpha-2-macroglobulin (A2M) and a A2M-like protein are essential components in salivary innate immunity against hemagglutination mediated by a clinical isolate of S-OIV [San Diego/01/09 (SD/H1N1-S-OIV)]. A model of an A2M-based “double-edged sword” on competition of alpha 2,6-sialylated glycoprotein receptors and inactivation of host proteases is proposed. We emphasize that endogenous A2M in human innate immunity functions as a natural inhibitor against S-OIV.

Teaching Practice is an essential process for the student teachers before they become formal teachers. The student teachers are placed at different area, so the mentors can not meet the requirement of real-time interaction and guidance. In addition to the demand of professional development, the student teachers encounter many pressures such as the certificate examination. The idea of web 2.0 is widespread, and its advantages include information sharing and collaborative knowledge construction. Appling web 2.0 technologies on overcoming the teaching practice dilemma of student teachers is a feasible approach. The major purpose of this study is to develop a web-based guidance system for the student teachers and mentors. The student teachers can discuss with their peers and mentor, submit and share their homework and information, express their emotion, ask questions and provide solutions or comments for their peers. In addition, the system offers on-line test modular for them to diagnose their concepts of educational subjects which are cornel of certificate examination. In order to survey the suitability of this system, this study conducts a system usage test and evaluation, and the participants are three mentors and 26 student teachers. Through 4-month test, the participants show great appraisal toward this system.

Staphylococcal infection can cause a wide range of diseases resulting either from staphylococcal bacteria invasion or through toxin production. The majority of infections caused by staphylococci are due to Staphylococcus aureus. Moreover, methicillin-resistant Staphylococcus aureus has recently been considered to be one of the major causes of hospital-acquired infections. The treatment of staphylococci infections is difficult because increased antibiotic resistant strains have become more common, increasing the risk of serious health penalty. Delivery of antibiotics via nanoparticles is a promising therapy, as a drug delivery mechanism, particularly for controlled release or depot delivery of drugs to decrease the number of doses required to achieve a clinical effect. This review emphasized the potential of nanoparticles in the targeted antibiotics for therapy of staphylococcal infections.

Although the differential expression of heat shcok proteins, Hsp90alpha and Hsp90beta was extensively studied in many kinds of cells, the post-transcriptional regulation of Hsp90 isoforms remains unclear. In control and GA-treated rat gliosarcoma cells, it has been reported that the translational efficiency of hsp90alpha is higher than hsp90beta. In this study, we present evidences identifying the roles for leaky scanning and 5'-UTR sequence in translational regulation of Hsp90beta. The result of in vitro transcription and translation (IVTT) experiment showed that hsp90alpha exhibited higher translation efficiency than hsp90beta. Sequence analysis revealed that there is an out-of-frame downstream AUG codon in hsp90beta gene. However, elimination of the downstream AUG by site-directly mutagenesis or introducing Kozak context sequence around the initiator AUG of hsp90beta open reading frame increased its translational efficiency, which indicated that leaky scanning might be a possible mechanism regulating hsp90beta. Furthermore, we also constructed a firefly luciferase reporter system to verify the effect of subsequent translation at the downstream out-of-frame AUG codon in 9L and A549 cells. Furthermore, it is believed that 5'-untranslated region (5'-UTR) also plays a significant role in translational control. We showed hsp90beta 5'-UTR gives rise to the reduction of the translation efficiency in IVTT experiment. Additionally, the reductive effect of hsp90beta 5'-UTR was further confirmed by luciferase reporter assay using truncated deletion analyses of 5'-UTR of hsp90beta. Our results support the hypothesis that ribosome leaky scanning mechanism and 5'-UTR sequence acts as negative regulators in hsp90beta mRNA.

This thesis started by using geldanamycin (GA) to treat rat brain tumor (RBT) 9L cells. By observing cell stress response, we initiated the study of the differentially inductive mechanisms on heat shock protein 90 isoforms. Geldanamycin (GA) is an ansamycin-derivative benzoquinone compound, which was originally isolated as a natural product with anti-fungal activity. GA could inhibit the essential ATPase activity of HSP90 and results in inactivation, destabilization, and degradation of HSP90 client proteins, including a wide variety of signal-transducing proteins that regulate cell growth and differentiation, such as protein kinases and steroid hormone receptors. But reports had shown that GA treatment could also induce heat-shock response; especially including HSP70, GRP78 and GRP94 in RBT 9L cells. In this study, we found only a 1/10 dose of GA (i.e., 0.5 贡M) could induce HSP90, compared to 5 贡M GA to induce those heat shock proteins like HSP70, GRP78 and GRP94. Furthermore, HSP90 exists two highly consistent isoforms, HSP90α and HSP90β, in mammalian cells. We further separated HSP90 isoforms by decrease pH (to 8.0) and percentage (9%) of PAGE gel; the results showed apparently differential induction of HSP90 isoforms through GA treatment (HSP90α > HSP90β). On the other hand, the consistencies were confirmed from RNA to protein level by real time qPCR analysis, Western Blotting and de novo synthetic analysis. Our results demonstrated that gene level regulation controlled the differential induction of HSP90 isoforms. According to the promoter sequences of hsp90α and hsp90β, we evaluated the different importance of some transcriptional elements by Electrophoresis Mobility Shift Assay (EMSA). Interestingly, differential induction of HSP90α and β is related to the differential binding activities to HSEs in hsp90α and hsp90β promoters. In addition, we also observed the binding strengths on HSEs might imply how HSP90α is more inducible isoforms than HSP90β. On the other hand, the results of binding activities on basic transcription elements showed that GC-box (sp-1 site) involved in inductive level of HSP90α汹and HSP90β the binding on TATA-box and CRE were respectively related to the induction of HSP90α and HSP90β. In conclusion, treatment with GA facilitate HSF1 binding to the distinct HSE sites on the promoters of hsp90α and hsp90β and further induce HSP90s. It agreed with the observations of differential induction on mRNA and protein level in 9L cells under treatment with GA.

BackgroundEosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis.ResultsTo address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-α). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-α antibody.ConclusionIn conclusion, our results have demonstrated that ECP increased TNF-α production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.