Si(100)-SiO2 interface properties following rapid thermal processing

An experimental examination of the properties of the Si(100)-SiO2 interface measured following rapid thermal processing (RTP) is presented. The interface properties have been examined using high frequency and quasi-static capacitance-voltage (CV) analysis of metal-oxide-silicon (MOS) capacitor structures immediately following either rapid thermal oxidation (RTO) or rapid thermal annealing (RTA). The experimental results reveal a characteristic peak in the CV response measured following dry RTO and RTA (T > 800 degreesC), as the Fermi level at the Si(100)-SiO2 interface approaches the conduction band edge. Analysis of the QSCV responses reveals a high interface state density across the energy gap following dry RTO and RTA processing, with a characteristic peak density in the range 5.5x10(12) to 1.7x10(13) cm(-2) eV(-1) located at approximately 0.85-0.88 eV above the valence band edge. When the background density of states for a hydrogen-passivated interface is subtracted, another peak of lower density (3x10(12) to 7x10(12) cm(-2) eV(-1)) is observed at approximately 0.25-0.33 eV above the valence band edge. The experimental results point to a common interface state defect present after processes involving rapid cooling (10(1)-10(2) degreesC/s) from a temperature of 800 degreesC or above, in a hydrogen free ambient. This work demonstrates that the interface states measured following RTP (T > 800 degreesC) are the net contribution of the P-b0/P-b1 silicon dangling bond defects for the oxidized Si(100) orientation. An important conclusion arising from this work is that the primary effect of an RTA in nitrogen (600-1050 degreesC) is to cause hydrogen desorption from pre-existing P-b0/P-b1 silicon dangling bond defects. The implications of this work to the study of the Si-SiO2 interface, and the technological implications for silicon based MOS processes, are briefly discussed. The significance of these new results to thin oxide growth and optimization by RTO are also considered

Suppression of ablation in femtosecond double pulse experiments

We report the physical reasons of a curious decrease in the crater depth observed for long delays in experiments with femtosecond double pulses. Detailed hydrodynamic modeling demonstrates that the ablation mechanism is dumped when the delay between the pulses exceeds the electron-ion relaxation time. In this case, the interaction of the second laser pulse with the expanding target material leads to the formation of the second shock wave suppressing the rarefaction wave created by the first pulse. The evidence of this effect follows from the pressure and density profiles obtained at different delays after the first laser pulse.Comment: Submitted to one of the APS Journal

In vitro culture with gemcitabine augments death receptor and NKG2D ligand expression on tumour cells

Much effort has been made to try to understand the relationship between chemotherapeutic treatment of cancer and the immune system. Whereas much of that focus has been on the direct effect of chemotherapy drugs on immune cells and the release of antigens and danger signals by malignant cells killed by chemotherapy, the effect of chemotherapy on cells surviving treatment has often been overlooked. In the present study, tumour cell lines: A549 (lung), HCT116 (colon) and MCF-7 (breast), were treated with various concentrations of the chemotherapeutic drugs cyclophosphamide, gemcitabine (GEM) and oxaliplatin (OXP) for 24 hours in vitro. In line with other reports, GEM and OXP upregulated expression of the death receptor CD95 (fas) on live cells even at sub-cytotoxic concentrations. Further investigation revealed that the increase in CD95 in response to GEM sensitised the cells to fas ligand treatment, was associated with increased phosphorylation of stress activated protein kinase/c-Jun N-terminal kinase and that other death receptors and activatory immune receptors were co-ordinately upregulated with CD95 in certain cell lines. The upregulation of death receptors and NKG2D ligands together on cells after chemotherapy suggest that although the cells have survived preliminary treatment with chemotherapy they may now be more susceptible to immune cell-mediated challenge. This re-enforces the idea that chemotherapy-immunotherapy combinations may be useful clinically and has implications for the make-up and scheduling of such treatments

Transcription profiling reveals potential mechanisms of dysbiosis in the oral microbiome of rhesus macaques with chronic untreated SIV infection.

A majority of individuals infected with human immunodeficiency virus (HIV) have inadequate access to antiretroviral therapy and ultimately develop debilitating oral infections that often correlate with disease progression. Due to the impracticalities of conducting host-microbe systems-based studies in HIV infected patients, we have evaluated the potential of simian immunodeficiency virus (SIV) infected rhesus macaques to serve as a non-human primate model for oral manifestations of HIV disease. We present the first description of the rhesus macaque oral microbiota and show that a mixture of human commensal bacteria and "macaque versions" of human commensals colonize the tongue dorsum and dental plaque. Our findings indicate that SIV infection results in chronic activation of antiviral and inflammatory responses in the tongue mucosa that may collectively lead to repression of epithelial development and impact the microbiome. In addition, we show that dysbiosis of the lingual microbiome in SIV infection is characterized by outgrowth of Gemella morbillorum that may result from impaired macrophage function. Finally, we provide evidence that the increased capacity of opportunistic pathogens (e.g. E. coli) to colonize the microbiome is associated with reduced production of antimicrobial peptides

EPGD: a comprehensive web resource for integrating and displaying eukaryotic paralog/paralogon information

Gene duplication is common in all three domains of life, especially in eukaryotic genomes. The duplicates provide new material for the action of evolutionary forces such as selection or genetic drift. Here we describe a sophisticated procedure to extract duplicated genes (paralogs) from 26 available eukaryotic genomes, to pre-calculate several evolutionary indexes (evolutionary rate, synonymous distance/clock, transition redundant exchange clock, etc.) based on the paralog family, and to identify block or segmental duplications (paralogons). We also constructed an internet-accessible Eukaryotic Paralog Group Database (EPGD; http://epgd.biosino.org/EPGD/). The database is gene-centered and organized by paralog family. It focuses on paralogs and evolutionary duplication events. The paralog families and paralogons can be searched by text or sequence, and are downloadable from the website as plain text files. The database will be very useful for both experimentalists and bioinformaticians interested in the study of duplication events or paralog families

Effects of Heparin and Enoxaparin on APP Processing and Aβ Production in Primary Cortical Neurons from Tg2576 Mice

Alzheimer's disease (AD) is caused by accumulation of Aβ, which is produced through sequential cleavage of β-amyloid precursor protein (APP) by the β-site APP cleaving enzyme (BACE1) and γ-secretase. Enoxaparin, a low molecular weight form of the glycosaminoglycan (GAG) heparin, has been reported to lower Aβ plaque deposition and improve cognitive function in AD transgenic mice

Cereal Domestication and Evolution of Branching: Evidence for Soft Selection in the Tb1 Orthologue of Pearl Millet (Pennisetum glaucum [L.] R. Br.)

BACKGROUND: During the Neolithic revolution, early farmers altered plant development to domesticate crops. Similar traits were often selected independently in different wild species; yet the genetic basis of this parallel phenotypic evolution remains elusive. Plant architecture ranks among these target traits composing the domestication syndrome. We focused on the reduction of branching which occurred in several cereals, an adaptation known to rely on the major gene Teosinte-branched1 (Tb1) in maize. We investigate the role of the Tb1 orthologue (Pgtb1) in the domestication of pearl millet (Pennisetum glaucum), an African outcrossing cereal. METHODOLOGY/PRINCIPAL FINDINGS: Gene cloning, expression profiling, QTL mapping and molecular evolution analysis were combined in a comparative approach between pearl millet and maize. Our results in pearl millet support a role for PgTb1 in domestication despite important differences in the genetic basis of branching adaptation in that species compared to maize (e.g. weaker effects of PgTb1). Genetic maps suggest this pattern to be consistent in other cereals with reduced branching (e.g. sorghum, foxtail millet). Moreover, although the adaptive sites underlying domestication were not formerly identified, signatures of selection pointed to putative regulatory regions upstream of both Tb1 orthologues in maize and pearl millet. However, the signature of human selection in the pearl millet Tb1 is much weaker in pearl millet than in maize. CONCLUSIONS/SIGNIFICANCE: Our results suggest that some level of parallel evolution involved at least regions directly upstream of Tb1 for the domestication of pearl millet and maize. This was unanticipated given the multigenic basis of domestication traits and the divergence of wild progenitor species for over 30 million years prior to human selection. We also hypothesized that regular introgression of domestic pearl millet phenotypes by genes from the wild gene pool could explain why the selective sweep in pearl millet is softer than in maize

Parallel Expansions of Sox Transcription Factor Group B Predating the Diversifications of the Arthropods and Jawed Vertebrates

Group B of the Sox transcription factor family is crucial in embryo development in the insects and vertebrates. Sox group B, unlike the other Sox groups, has an unusually enlarged functional repertoire in insects, but the timing and mechanism of the expansion of this group were unclear. We collected and analyzed data for Sox group B from 36 species of 12 phyla representing the major metazoan clades, with an emphasis on arthropods, to reconstruct the evolutionary history of SoxB in bilaterians and to date the expansion of Sox group B in insects. We found that the genome of the bilaterian last common ancestor probably contained one SoxB1 and one SoxB2 gene only and that tandem duplications of SoxB2 occurred before the arthropod diversification but after the arthropod-nematode divergence, resulting in the basal repertoire of Sox group B in diverse arthropod lineages. The arthropod Sox group B repertoire expanded differently from the vertebrate repertoire, which resulted from genome duplications. The parallel increases in the Sox group B repertoires of the arthropods and vertebrates are consistent with the parallel increases in the complexity and diversification of these two important organismal groups

Role of Fas/FasL in regulation of inflammation in vaginal tissue during HSV-2 infection

To assess the role of Fas in lesion development during genital HSV-2 infection, we used a well-established HSV-2 murine model applied to MRL-Faslpr/J (Fas−/−) and C3-Faslgld/J (FasL−/−) C57BL6 mice. In vitro infection of murine keratinocytes and epithelial cells was used to clarify molecular details of HSV-2 infection. Despite upregulation of Fas and FasL, HSV-2-infected keratinocytes and epithelial cells showed a moderate level of apoptosis due to upregulated expression of the anti-apoptotic factors Bcl-2, Akt kinase and NF-κB. Inflammatory lesions within the HSV-2-infected epithelium of C57BL6 mice consisted of infected cells upregulating Fas, FasL and Bcl-2, uninfected cells upregulating Fas and neutrophils expressing both Fas and FasL. Apoptosis was detected in HSV-2-infected cells and to even higher extent in non-infected cells surrounding HSV-2 infection sites. HSV-2 infection of Fas- and FasL-deficient mice led to increased apoptosis and stronger recruitment of neutrophils within the infection sites. We conclude that the Fas pathway participates in regulation of inflammatory response in the vaginal epithelium at the initial stage of HSV-2 infection