Improved GaN-based HEMT performance by nanocrystalline diamond capping

As a wide-bandgap semiconductor, gallium nitride (GaN) is an attractive material for next-generation power devices. To date, the capabilities of GaN-based high electron mobility transistors (HEMTs) have been limited by self-heating effects (drain current decreases due to phonon scattering-induced carrier velocity reductions at high drain fields). Despite awareness of this, attempts to mitigate thermal impairment have been limited due to the difficulties involved with placing high thermal conductivity materials close to heat sources in the device. Heat spreading schemes have involved growth of AIGaN/GaN on single crystal or CVD diamond, or capping of fullyprocessed HEMTs using nanocrystalline diamond (NCD). All approaches have suffered from reduced HEMT performance or limited substrate size. Recently, a "gate after diamond" approach has been successfully demonstrated to improve the thermal budget of the process by depositing NCD before the thermally sensitive Schottky gate and also to enable large-area diamond implementation.

Profiling the temperature distribution in AlGaN/GaN HEMTs with nanocrystalline diamond heat spreading layers

Reduced performance in Gallium Nitride (GaN) based high electron mobility transistors (HEMTs) as a result of self-heating has been well-documented. A new approach, termed “diamond-before-gate" is shown to improve the thermal budget of the deposition process and enables large area diamond without degrading the gate metal NCD capped devices had a 20% lower channel temperature at equivalent power dissipation.

PADRÕES DE PRODUTIVIDADE EM PESQUISA NA LITERATURA DE FINANÇAS: UM ESTUDO BIBLIOMÉTRICO NOS PRINCIPAIS PERIÓDICOS CIENTÍFICOS NACIONAIS NO PERÍODO DE 2005 A 2014

A Administração Financeira surge no início do século XIX juntamente com o movimento de consolidação das grandes empresas e a formação dos mercados nacionais americano enquanto que no Brasil os primeiros estudos ocorrem a partir da segunda metade do século XX. Desde entãoo país conseguiu consolidar alguns centros de excelência em pesquisa, formar grupo significativo de pesquisadores seniores e expandir as áreas de pesquisa no campo, contudo, ainda são poucos os trabalhos que buscam retratar as características da produtividade científica em Finanças. Buscando contribuir para a melhor compreensão do comportamento produtivo dessa área a presente pesquisa estuda sua produção científica, materializada na forma de artigos digitais, publicados em 24 conceituados periódicos nacionais classificados nos estratos Qualis/CAPES A2, B1 e B2 da Área de Administração, Ciências Contábeis e Turismo. Para tanto são aplicadas a Lei de Bradford, Lei do Elitismo de Price e Lei de Lotka. Pela Lei de Bradford são identificadas três zonas de produtividade sendo o núcleo formado por três revistas, estando uma delas classificada no estrato Qualis/CAPES B2, o que evidencia a limitação de um recorte tendo como único critério a classificação Qualis/CAPES. Para a Lei do Elitismo de Price, seja pela contagem direta ou completa, não identificamos comportamento de uma elite semelhante ao apontado pela teoria e que conta com grande número de autores com apenas uma publicação.Aplicando-se o modelo do Poder Inverso Generalizado, calculado por Mínimos Quadrados Ordinários (MQO), verificamos que produtividade dos pesquisadores, quando feita pela contagem direta, se adequa àquela definida pela Lei de Lotka ao nível de α = 0,01 de significância, contudo, pela contagem completa não podemos confirmar a hipótese de homogeneidade das distribuições, além do fato de que nas duas contagens a produtividade analisada pelo parâmetro n é maior que 2 e, portanto, a produtividade do pesquisadores de finanças é menor que a defendida pela teoria.

Characterization of anti-anti-idiotypic antibodies that bind antigen and an anti-idiotype

Two mouse monoclonal anti-anti-idiotopic antibodies (anti-anti-Id, Ab3), AF14 and AF52, were prepared by immunizing BALB/c mice with rabbit polyclonal anti-idiotypic antibodies (anti-Id, Ab2) raised against antibody D1.3 (Ab1) specific for the antigen hen egg lysozyme. AF14 and AF52 react with an “internal image” monoclonal mouse anti-Id antibody E5.2 (Ab2), previously raised against D1.3, with affinity constants (1.0 × 109 M−1 and 2.4 × 107 M−1, respectively) usually observed in secondary responses against protein antigens. They also react with the antigen but with lower affinity (1.8 × 106 M−1 and 3.8 × 106 M−1). This pattern of affinities for the anti-Id and for the antigen also was displayed by the sera of the immunized mice. The amino acid sequences of AF14 and AF52 are very close to that of D1.3. In particular, the amino acid side chains that contribute to contacts with both antigen and anti-Id are largely conserved in AF14 and AF52 compared with D1.3. Therapeutic immunizations against different pathogenic antigens using anti-Id antibodies have been proposed. Our experiments show that a response to an anti-Id immunogen elicits anti-anti-Id antibodies that are optimized for binding the anti-Id antibodies rather than the antigen.

Thrombospondin-1 Induces Tyrosine Phosphorylation of Adherens Junction Proteins and Regulates an Endothelial Paracellular Pathway

Thrombospondin-1 (TSP) induces endothelial cell (EC) actin reorganization and focal adhesion disassembly and influences multiple EC functions. To determine whether TSP might regulate EC–EC interactions, we studied the effect of exogenous TSP on the movement of albumin across postconfluent EC monolayers. TSP increased transendothelial albumin flux in a dose-dependent manner at concentrations ≥1 μg/ml (2.2 nM). Increases in albumin flux were observed as early as 1 h after exposure to 30 μg/ml (71 nM) TSP. Inhibition of tyrosine kinases with herbimycin A or genistein protected against the TSP-induced barrier dysfunction by >80% and >50%, respectively. TSP-exposed monolayers exhibited actin reorganization and intercellular gap formation, whereas pretreatment with herbimycin A protected against this effect. Increased staining of phosphotyrosine-containing proteins was observed in plaque-like structures and at the intercellular boundaries of TSP-treated cells. In the presence of protein tyrosine phosphatase inhibition, TSP induced dose- and time-dependent increments in levels of phosphotyrosine-containing proteins; these TSP dose and time requirements were compatible with those defined for EC barrier dysfunction. Phosphoproteins that were identified include the adherens junction proteins focal adhesion kinase, paxillin, γ-catenin, and p120Cas. These combined data indicate that TSP can modulate endothelial barrier function, in part, through tyrosine phosphorylation of EC proteins.

A Millennial Myosin Census

The past decade has seen a remarkable explosion in our knowledge of the size and diversity of the myosin superfamily. Since these actin-based motors are candidates to provide the molecular basis for many cellular movements, it is essential that motility researchers be aware of the complete set of myosins in a given organism. The availability of cDNA and/or draft genomic sequences from humans, Drosophila melanogaster, Caenorhabditis elegans, Arabidopsis thaliana, Saccharomyces cerevisiae, Schizosaccharomyces pombe, and Dictyostelium discoideum has allowed us to tentatively define and compare the sets of myosin genes in these organisms. This analysis has also led to the identification of several putative myosin genes that may be of general interest. In humans, for example, we find a total of 40 known or predicted myosin genes including two new myosins-I, three new class II (conventional) myosins, a second member of the class III/ninaC myosins, a gene similar to the class XV deafness myosin, and a novel myosin sharing at most 33% identity with other members of the superfamily. These myosins are in addition to the recently discovered class XVI myosin with N-terminal ankyrin repeats and two human genes with similarity to the class XVIII PDZ-myosin from mouse. We briefly describe these newly recognized myosins and extend our previous phylogenetic analysis of the myosin superfamily to include a comparison of the complete or nearly complete inventories of myosin genes from several experimentally important organisms.

Fluid shear stress inhibits TNF-α activation of JNK but not ERK1/2 or p38 in human umbilical vein endothelial cells: Inhibitory crosstalk among MAPK family members

Atherosclerosis preferentially occurs in areas of turbulent flow and low fluid shear stress, whereas laminar flow and high shear stress are atheroprotective. Inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and IL-1 stimulate expression of endothelial cell (EC) genes that may promote atherosclerosis. TNF-α and IL-1 regulate gene expression in ECs, in part, by stimulating mitogen-activated protein kinases (MAPK), which phosphorylate transcription factors. We hypothesized that steady laminar flow inhibits cytokine-mediated activation of MAPK in EC. To test this hypothesis, we determined the effects of flow (shear stress = 12 dynes/cm2) on TNF-α and IL-1-stimulated activity of three MAPK in human umbilical vein ECs (HUVEC): extracellular signal-regulated kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK). Flow alone stimulated ERK1/2 and p38 activity but decreased JNK activity compared with static controls. TNF-α or IL-1 alone activated ERK1/2, p38, and JNK maximally at 15 min in HUVEC. Preexposing HUVEC for 10 min to flow inhibited TNF-α and IL-1 activation of JNK by 46% and 49%, respectively, but had no significant effect on ERK1/2 or p38 activation. Incubation of HUVEC with PD98059, which inhibits flow-mediated ERK1/2 activation, prevented flow from inhibiting cytokine activation of JNK. Phorbol 12-myristate 13-acetate, which strongly activates ERK1/2, also inhibited TNF-α activation of JNK. These findings indicate that fluid shear stress inhibits TNF-α-mediated signaling events in HUVEC via the activation of the ERK1/2 signaling pathway. Inhibition of TNF-α signal transduction represents a mechanism by which steady laminar flow may exert atheroprotective effects on the endothelium.

Callose Deposition Is Responsible for Apoplastic Semipermeability of the Endosperm Envelope of Muskmelon Seeds1

Semipermeable cell walls or apoplastic “membranes” have been hypothesized to be present in various plant tissues. Although often associated with suberized or lignified walls, the wall component that confers osmotic semipermeability is not known. In muskmelon (Cucumis melo L.) seeds, a thin, membranous endosperm completely encloses the embryo, creating a semipermeable apoplastic envelope. When dead muskmelon seeds are allowed to imbibe, solutes leaking from the embryo are retained within the envelope, resulting in osmotic water uptake and swelling called osmotic distention (OD). The endosperm envelope of muskmelon seeds stained with aniline blue, which is specific for callose (β-1,3-glucan). Outside of the aniline-blue-stained layer was a Sudan III- and IV-staining (lipid-containing) layer. In young developing seeds 25 d after anthesis (DAA) that did not exhibit OD, the lipid layer was already present but callose had not been deposited. At 35 DAA, callose was detected as distinct vesicles or globules in the endosperm envelope. A thick callose layer was evident at 40 DAA, coinciding with development of the capacity for OD. Removal of the outer lipid layer by brief chloroform treatment resulted in more rapid water uptake by both viable and nonviable (boiled) seeds, but did not affect semipermeability of the endosperm envelope. The aniline-blue-staining layer was digested by β-1,3-glucanase, and these envelopes lost OD. Thus, apoplastic semipermeability of the muskmelon endosperm envelope is dependent on the deposition of a thick callose-containing layer outside of the endosperm cell walls.

Mapping the literature of cytotechnology

The major purpose of this study was to identify and assess indexing coverage of core journals in cytotechnology. It was part of a larger project sponsored by the Nursing and Allied Health Resources Section of the Medical Library Association to map the literature of allied health. Three representative journals in cytotechnology were selected and subjected to citation analysis to determine what journals, other publication types, and years were cited and how often. Bradford's Law of Scattering was applied to the resulting list of cited journals to identify core titles in the discipline, and five indexes were searched to assess coverage of these core titles. Results indicated that the cytotechnology journal literature had a small core but wide dispersion: one third of the 21,021 journal citations appeared in only 3 titles; another third appeared in an additional 26 titles; the remaining third were scattered in 1,069 different titles. Science Citation Index Expanded rated highest in indexing coverage of the core titles, followed by MEDLINE, EMBASE/Excerpta Medica, HealthSTAR, and Cumulative Index to Nursing and Allied Health Literature (CINAHL). The study's results also showed that journals were the predominantly cited format and that citing authors relied strongly on more recent literature.