Diffraction problems for quasilinear parabolic systems with boundary intersecting interfaces

Stability of Unilateral Posterior Crossbite Correction in the Mixed Dentition - an RCT-study with 3-year Follow-Up. Aim: To compare and evaluate long-term stability of crossbite correction with Quad Helix or expansion plate in the mixed dentition. Methods: In this RCT-study 35 patients with unilateral posterior crossbite were randomized to be treated with either Quad Helix or expansion plate. The inclusion criteria were: mixed dentition, unilateral posterior crossbite, no sucking habits or previous orthodontic treatment. Stability was evaluated after 3 years by study cast measurements. Twenty subjects with normal occlusion were included as controls. Success rate, maxillary and mandibular transverse dimensions, overjet, overbite and arch length were registered. Results: Stability was equal for the two treatment methods. Small, albeit significant, differences between the groups were assessed with reference to transverse dimensions. No significant difference was seen for overjet and overbite. The treated patients never reached the same transversal width as the normal control group. Conclusions: The long-term stability of posterior crossbite correction with Quad helix and expansion plate was equal. The maxillary width was greater in the control group than the treated groups

Three-dimensional strain state and spacer thickness-dependent properties of epitaxial Pr0.7Sr0.3MnO3/La0.5Ca0.5MnO3/Pr0.7Sr0.3MnO3 trilayer structure

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Microstructures and resistivity of cuprate/manganite bilayer deposited on SrTiO3 substrate

Thin Yba[SUB2]Cu[SUB3]O[SUB7-δ/La[SUB0.67]Ca[SUB0.33]MnO[SUB3] (YBCO/LCMO) films were grown on SrTiO[SUB3](STO)substrates by magnetron sputtering technique. The microstructures of the bilayers were characterized and a standard four-probe technique was applied to measure the resistivity of the samples. The interdiffusions at the YBCO/LCMO and LCMO/STO interfaces formed two transient layers with the thickness of about 3 and 2 nm, respectively. All the bilayers were well textured along the c axis. At low temperature, the superconductivity can only be observed when the thickness of YBCO is more than 25 nm. When the thickness of YBCO is less than 8 nm, the bilayers show only ferromagnetism. The superconductivity and ferromagnetism perhaps coexist in the bilayer with the YBCO thickness of 12.5 nm. These interesting properties are related to the interaction between spin polarized electrons in the manganites and the cooper pairs in the cuprates. © 2003 American Institute of Physics.published_or_final_versio

Anti-HIV-1 activity of cellulose acetate phthalate: Synergy with soluble CD4 and induction of "dead-end" gp41 six-helix bundles

BACKGROUND: Cellulose acetate phthalate (CAP), a promising candidate microbicide for prevention of sexual transmission of the human immunodeficiency virus type 1 (HIV-1) and other sexually transmitted disease (STD) pathogens, was shown to inactivate HIV-1 and to block the coreceptor binding site on the virus envelope glycoprotein gp120. It did not interfere with virus binding to CD4. Since CD4 is the primary cellular receptor for HIV-1, it was of interest to study CAP binding to HIV-1 complexes with soluble CD4 (sCD4) and its consequences, including changes in the conformation of the envelope glycoprotein gp41 within virus particles. METHODS: Enzyme-linked immunosorbent assays (ELISA) were used to study CAP binding to HIV-1-sCD4 complexes and to detect gp41 six-helix bundles accessible on virus particles using antibodies specific for the α-helical core domain of gp41. RESULTS: 1) Pretreatment of HIV-1 with sCD4 augments subsequent binding of CAP; 2) there is synergism between CAP and sCD4 for inhibition of HIV-1 infection; 3) treatment of HIV-1 with CAP induced the formation of gp41 six-helix bundles. CONCLUSIONS: CAP and sCD4 bind to distinct sites on HIV-1 IIIB and BaL virions and their simultaneous binding has profound effects on virus structure and infectivity. The formation of gp41 six-helical bundles, induced by CAP, is known to render the virus incompetent for fusion with target cells thus preventing infection

Electrically-pumped compact topological bulk lasers driven by band-inverted bound states in the continuum

One of the most exciting breakthroughs in physics is the concept of topology that was recently introduced to photonics, achieving robust functionalities, as manifested in the recently demonstrated topological lasers. However, so far almost all attention was focused on lasing from topological edge states. Bulk bands that reflect the topological bulk-edge correspondence have been largely missed. Here, we demonstrate an electrically pumped topological bulk quantum cascade laser (QCL) operating in the terahertz (THz) frequency range. In addition to the band-inversion induced in-plane reflection due to topological nontrivial cavity surrounded by a trivial domain, we further illustrate the band edges of such topological bulk lasers are recognized as the bound states in the continuum (BICs) due to their nonradiative characteristics and robust topological polarization charges in the momentum space. Therefore, the lasing modes show both in-plane and out-of-plane tight confinements in a compact laser cavity (lateral size ~3λlaser). Experimentally, we realize a miniaturized THz QCL that shows single-mode lasing with a side-mode suppression ratio (SMSR) around 20 dB. We also observe a cylindrical vector beam for the far-field emission, which is evidence for topological bulk BIC lasers. Our demonstration on miniaturization of single-mode beam-engineered THz lasers is promising for many applications including imaging, sensing, and communications

Disruption of Neuronal Autophagy by Infected Microglia Results in Neurodegeneration

There is compelling evidence to support the idea that autophagy has a protective function in neurons and its disruption results in neurodegenerative disorders. Neuronal damage is well-documented in the brains of HIV-infected individuals, and evidence of inflammation, oxidative stress, damage to synaptic and dendritic structures, and neuronal loss are present in the brains of those with HIV-associated dementia. We investigated the role of autophagy in microglia-induced neurotoxicity in primary rodent neurons, primate and human models. We demonstrate here that products of simian immunodeficiency virus (SIV)-infected microglia inhibit neuronal autophagy, resulting in decreased neuronal survival. Quantitative analysis of autophagy vacuole numbers in rat primary neurons revealed a striking loss from the processes. Assessment of multiple biochemical markers of autophagic activity confirmed the inhibition of autophagy in neurons. Importantly, autophagy could be induced in neurons through rapamycin treatment, and such treatment conferred significant protection to neurons. Two major mediators of HIV-induced neurotoxicity, tumor necrosis factor-α and glutamate, had similar effects on reducing autophagy in neurons. The mRNA level of p62 was increased in the brain in SIV encephalitis and as well as in brains from individuals with HIV dementia, and abnormal neuronal p62 dot structures immunoreactivity was present and had a similar pattern with abnormal ubiquitinylated proteins. Taken together, these results identify that induction of deficits in autophagy is a significant mechanism for neurodegenerative processes that arise from glial, as opposed to neuronal, sources, and that the maintenance of autophagy may have a pivotal role in neuroprotection in the setting of HIV infection

Complementation of diverse HIV-1 Env defects through cooperative subunit interactions: a general property of the functional trimer

<p>Abstract</p> <p>Background</p> <p>The HIV-1 Env glycoprotein mediates virus entry by catalyzing direct fusion between the virion membrane and the target cell plasma membrane. Env is composed of two subunits: gp120, which binds to CD4 and the coreceptor, and gp41, which is triggered upon coreceptor binding to promote the membrane fusion reaction. Env on the surface of infected cells is a trimer consisting of three gp120/gp41 homo-dimeric protomers. An emerging question concerns cooperative interactions between the protomers in the trimer, and possible implications for Env function.</p> <p>Results</p> <p>We extended studies on cooperative subunit interactions within the HIV-1 Env trimer, using analysis of functional complementation between coexpressed inactive variants harboring different functional deficiencies. In assays of Env-mediated cell fusion, complementation was observed between variants with a wide range of defects in both the gp120 and gp41 subunits. The former included gp120 subunits mutated in the CD4 binding site or incapable of coreceptor interaction due either to mismatched specificity or V3 loop mutation. Defective gp41 variants included point mutations at different residues within the fusion peptide or heptad repeat regions, as well as constructs with modifications or deletions of the membrane proximal tryptophan-rich region or the transmembrane domain. Complementation required the defective variants to be coexpressed in the same cell. The observed complementation activities were highly dependent on the assay system. The most robust activities were obtained with a vaccinia virus-based expression and reporter gene activation assay for cell fusion. In an alternative system involving Env expression from integrated provirus, complementation was detected in cell fusion assays, but not in virus particle entry assays.</p> <p>Conclusion</p> <p>Our results indicate that Env function does not require every subunit in the trimer to be competent for all essential activities. Through cross-talk between subunits, the functional determinants on one defective protomer can cooperatively interact to trigger the functional determinants on an adjacent protomer(s) harboring a different defect, leading to fusion. Cooperative subunit interaction is a general feature of the Env trimer, based on complementation activities observed for a highly diverse range of functional defects.</p

Broadly Neutralizing Human Anti-HIV Antibody 2G12 Is Effective in Protection against Mucosal SHIV Challenge Even at Low Serum Neutralizing Titers

Developing an immunogen that elicits broadly neutralizing antibodies (bNAbs) is an elusive but important goal of HIV vaccine research, especially after the recent failure of the leading T cell based HIV vaccine in human efficacy trials. Even if such an immunogen can be developed, most animal model studies indicate that high serum neutralizing concentrations of bNAbs are required to provide significant benefit in typical protection experiments. One possible exception is provided by the anti-glycan bNAb 2G12, which has been reported to protect macaques against CXCR4-using SHIV challenge at relatively low serum neutralizing titers. Here, we investigated the ability of 2G12 administered intravenously (i.v.) to protect against vaginal challenge of rhesus macaques with the CCR5-using SHIVSF162P3. The results show that, at 2G12 serum neutralizing titers of the order of 1∶1 (IC90), 3/5 antibody-treated animals were protected with sterilizing immunity, i.e. no detectable virus replication following challenge; one animal showed a delayed and lowered primary viremia and the other animal showed a course of infection similar to 4 control animals. This result contrasts strongly with the typically high titers observed for protection by other neutralizing antibodies, including the bNAb b12. We compared b12 and 2G12 for characteristics that might explain the differences in protective ability relative to neutralizing activity. We found no evidence to suggest that 2G12 transudation to the vaginal surface was significantly superior to b12. We also observed that the ability of 2G12 to inhibit virus replication in target cells through antibody-mediated effector cell activity in vitro was equivalent or inferior to b12. The results raise the possibility that some epitopes on HIV may be better vaccine targets than others and support targeting the glycan shield of the envelope