Comparative analysis of growth rate reductions on shadow masked substrates

The growth on shadow masked substrates by atmospheric pressure metalorganic vapor phase epitaxy is investigated. An analytical description based on simple concepts for a complex geometry shows good agreement with the experimental results and enables the determination of quantum well thickness variations in optical waveguide structures. The growth rate reduction (or: ratio of growth rates) r(u) in the middle of the channel increases as the width-to-height ratio of the mask opening is increased

Selective MOVPE growth of GaAs on Si and its applications to LEDs

The two main problems still encountered during the growth of GaAs on Si are the lattice mismatch and the difference in thermal expansion coefficient. In this paper we will concentrate on the use of selective MOVPE growth of GaAs on Si and its applications to LED fabrication. The two reported techniques - small area selective growth and spatial control of microcrack formation through selective growth - resulted in higher yield and higher output power of IR-DH LEDs. By the implementation of thermal cycling procedures and the growth of an InGaAs/GaAs strained layer superlattice in the LED buffer layer we succeeded in increasing the output power over a factor of 5. For 3-mu-m GaAs on Si layers, we obtained X-ray FWHM values of 125 arc sec and etch pit density values of (1.0 +/- 0.5) x 10(6) cm-2

Monolithic integration of a spot size transformer with a planar buried heterostructure InGaAsP/InP-laser using the shadow masked growth technique

We present a vertically tapered InGaAsP/InP planar buried heterostructure (PBB) laser for low loss coupling to single-mode fibers. To achieve the vertical tapering we make use of the shadow masked growth technique. Tapered lasers with beam divergences of 15° in both lateral and transverse directions were realized. In comparison with untapered lasers, the coupling losses to cleaved single-mode fibers could be reduced by 4.8 dB down to 5.8 dB

Activated epithelial cells lead to reduction in both volume of saliva produced and Mucin 10 present in saliva.

<p>A) Whole stimulated saliva produced by A20^-/- mice and WT littermate controls. <i>n</i> = 6 mice per group per time point Two Way ANOVA testing showed significant difference at the 30 week time point. ** p < 0.01 B) Area under curve analysis of saliva production in A. Student’s <i>t</i>-test was performed for statistical analysis, ** <i>p</i> < 0.01. C) Coomassie and Periodic Acid Shift stained gel of whole stimulated saliva from WT and A20^-/- mice. Position of bands representing Mucins 10 is shown. Each lane represents saliva from a separate biological replicate. D) Quantification amount of Mucin 10 in saliva, relative to total protein. Each data point represents a separate biological replicate. *** <i>p</i> < 0.001, student’s <i>t</i>-test.</p

A20 inhibition of STAT1 expression in myeloid cells: a novel endogenous regulatory mechanism preventing development of enthesitis

Objectives: A20 is an important endogenous regulator of inflammation. Single nucleotide polymorphisms in A20 have been associated with various immune-mediated inflammatory diseases, and cell-specific deletion of A20 results in diverse inflammatory phenotypes. Our goal was to delineate the underlying mechanisms of joint inflammation in myeloid-specific A20-deficient mice (A20myelKO mice). Methods: Inflammation in A20myelKO mice was assessed in a time-dependent manner. Western blot analysis and quantitative PCR analysis were performed on bone marrow-derived macrophages from A20myelKO and littermate control mice to study the effect of A20 on STAT1/STAT3 expression and STAT1/STAT3-dependent gene transcription in myeloid cells. The in vivo role of Janus kinase-Signal Transducer and Activator of Transcription (JAK-STAT) signalling in the development of enthesitis in A20myelKO mice was assessed following administration of a JAK inhibitor versus placebo control. Results: Enthesitis was found to be an early inflammatory lesion in A20myelKO mice. A20 negatively modulated STAT1-dependent, but generally not STAT3-dependent gene transcription in myeloid cells by suppressing STAT1 but not STAT3 expression, both in unstimulated conditions and after interferon-γ or interleukin-6 stimulation. The increase in STAT1 gene transcription in the absence of A20 was shown to be JAK-STAT-dependent. Moreover, JAK inhibition in vivo resulted in significant reduction of enthesitis, both clinically and histopathologically. Conclusions: Our data reveal an important and novel interplay between myeloid cells and tissue resident cells at entheseal sites that is regulated by A20. In the absence of A20, STAT1 but not STAT3 expression is enhanced leading to STAT1-dependent inflammation. Therefore, A20 acts as a novel endogenous regulator of STAT1 that prevents onset of enthesitis

Activated epithelial cells cause leukocyte striated duct invasion and local increased cytokine production.

<p>A) Leukocytic (CD45⁺) invasion of a striated duct in A20^-/- mice at 30 weeks of age. B) CD3⁺ T cell invasion of a striated duct in serial section to A. C) B220⁺ B cell invasion of a striated duct in serial section to A. Second panels in A-C are high resolution images of inset boxes. D) Quantification of invaded striated ducts frequency per 4 mm² of glandular tissue. *** = p< 0.001, Two Way ANOVA. E) Relative expression of the pro-inflammatory cytokines (IFNα, IFNɣ, TNFα and IL-6) and pSS-associated chemokines (CXCL10, CXCL13) in A20^-/- mice at 20 and 30 weeks of age. <i>n</i> ≥ 5 per group. * p < 0.05, ** p < 0.01, *** p < 0.001, student’s <i>t</i>-test.</p

Dysregulation of NF-kB in glandular epithelial cells results in Sjögren’s-like features

<div><p>The autoimmune disease primary Sjögren’s syndrome (pSS) is characterized by hypofunction of the salivary glands (SGs), the cause of which is not correlated to lymphocytic SG infiltration, as prevailing dogma often states. We knocked out the NF-κB proinflammatory pathway inhibitor A20 in keratin14⁺ epithelial cells, to investigate if immune activated epithelial cells are capable of initiating pSS SG hallmarks. We show that immune activated epithelial cells can cause T cell dominated leukocytic infiltration and immune foci development of the SGs, reflecting the early clinical picture. Infiltrating leukocytes invaded striated ducts, similar to early stage lymphoepithelial lesions observed clinically. Expression of proinflammatory cyto-/chemokines IFNɣ, TNFα, IL-6, CXCL10 and CXCL13 increased in A20^-/- SGs, and functionally both volume and mucin 10 content of whole stimulated saliva from A20^-/- mice was significantly reduced. Epithelial cells may therefore represent the initial trigger for pSS SG pathologies, as opposed to simple reactionaries to pre-existing stimuli.</p></div