Parylene-C, which is traditionally used to coat implantable devices, has emerged as a promising material to generate miniaturized devices due to its unique mechanical properties and inertness. In this paper we compared the surface properties and cell and protein compatibility of parylene-C relative to other commonly used BioMEMS materials. We evaluated the surface hydrophobicity and roughness of parylene-C and compared these results to those of tissue culture-treated polystyrene, poly(dimethylsiloxane) (PDMS), and glass. We also treated parylene-C and PDMS with air plasma, and coated the surfaces with fibronectin to demonstrate that biochemical treatments modify the surface properties of parylene-C. Although plasma treatment caused both parylene-C and PDMS to become hydrophilic, only parylene-C substrates retained their hydrophilic properties over time. Furthermore, parylene-C substrates display a higher degree of nanoscale surface roughness (>20 nm) than the other substrates. We also examined the level of BSA and IgG protein adsorption on various surfaces and found that surface plasma treatment decreased the degree of protein adsorption on both PDMS and parylene-C substrates. After testing the degree of cell adhesion and spreading of two mammalian cell types, NIH-3T3 fibroblasts and AML-12 hepatocytes, we found that the adhesion of both cell types to surface-treated parylene-C variants were comparable to standard tissue culture substrates, such as polystyrene. Overall, these results indicate that parylene-C, along with its surface-treated variants, could potentially be a useful material for fabricating cell-based microdevices.

We report a technique to characterize adhesion of monolayered/multilayered graphene sheets on silicon wafer. Nanoparticles trapped at graphene-silicon interface act as point wedges to support axisymmetric blisters. Local adhesion strength is found by measuring the particle height and blister radius using a scanning electron microscope. Adhesion energy of the typical graphene-silicon interface is measured to be 151Ϯ 28 mJ/ m 2 . The proposed method and our measurements provide insights in fabrication and reliability of microelectromechanical/nanoelectromechanical systems. © 2010 American Institute of Physics. ͓doi:10.1063/1.3294960͔Graphene, the monolayer of carbon atoms packed into a two-dimensional honeycomb lattice, has attracted much attention in the scientific community because of its ultrahigh mechanical strength, conductivity with high electron mobility, and optical transparency. Whether graphene is a promising material for transparent or stretchable electronics 1-4 depends predominantly on the nanostructure's mechanical integrity and ability to integrate or to adhere to electronic substrates. There is, therefore, an urgent need for experimental methods to characterize the mechanical properties and adhesion behavior. However, viable techniques remain scarce despite the voluminous literature on theoretical and molecular dynamics simulations. Recently, direct force measurements using atomic force microscope ͑AFM͒ indentations were performed on graphene beams clamped at opposite ends, 5 and also on freestanding graphene sheets suspended over lithographically etched holes. 6 The measured changes in indenter displacement as a function of the applied load allowed researchers to find the elastic modulus in the range of 0.5-1.0 TPa and an ultimate strength of 130 GPa. 5,6 These results are consistent with theoretical computation. 7 On the other hand, measuring graphene adhesion on dissimilar substrates is difficult since the extremely thin sheet is hard to handle and prone to damage by clamps and fixtures as in the conventional peel test. In this paper, we describe a simple method to quantitatively measure local graphene adhesion on silicon surface, and report the value of adhesion energy of the dissimilar interface.Silicon wafer ͑100͒ with a 280-nm-thick oxide layer was chosen as the substrate. 8,9 The wafer was diced into 1 ϫ 1 cm 2 square pieces, cleaned with alcohol, and dried with nitrogen. Gold nanoparticles ͑from BBInternational Ltd., Cardiff, UK͒ in diameter 2R Ϸ 50 nm in an aqueous colloidal suspension with concentration of 4.5 ϫ 10 10 particles/ ml or silver particles with diameter 2R Ϸ 80 nm and 1.1ϫ 10 9 particles/ ml were used in the experiments. They were spread as randomly and evenly as possible on the silicon substrate and then left to completely dry out under ambient conditions. Clustering of the particles was inevitable among the isolated ones. Graphene sheets were mechanically cleaved from the surface of highly oriented pyrolytic graphite ͑HOPG͒ ͑ZYH grade from NT-MDT Co., Moscow, Russia. Note t...

Background Trichoderma reesei (Ascomycota, Pezizomycotina) QM6a is a model fungus for a broad spectrum of physiological phenomena, including plant cell wall degradation, industrial production of enzymes, light responses, conidiation, sexual development, polyketide biosynthesis, and plant–fungal interactions. The genomes of QM6a and its high enzyme-producing mutants have been sequenced by second-generation-sequencing methods and are publicly available from the Joint Genome Institute. While these genome sequences have offered useful information for genomic and transcriptomic studies, their limitations and especially their short read lengths make them poorly suited for some particular biological problems, including assembly, genome-wide determination of chromosome architecture, and genetic modification or engineering.ResultsWe integrated Pacific Biosciences and Illumina sequencing platforms for the highest-quality genome assembly yet achieved, revealing seven telomere-to-telomere chromosomes (34,922,528 bp; 10877 genes) with 1630 newly predicted genes and >1.5 Mb of new sequences. Most new sequences are located on AT-rich blocks, including 7 centromeres, 14 subtelomeres, and 2329 interspersed AT-rich blocks. The seven QM6a centromeres separately consist of 24 conserved repeats and 37 putative centromere-encoded genes. These findings open up a new perspective for future centromere and chromosome architecture studies. Next, we demonstrate that sexual crossing readily induced cytosine-to-thymine point mutations on both tandem and unlinked duplicated sequences. We also show by bioinformatic analysis that T. reesei has evolved a robust repeat-induced point mutation (RIP) system to accumulate AT-rich sequences, with longer AT-rich blocks having more RIP mutations. The widespread distribution of AT-rich blocks correlates genome-wide partitions with gene clusters, explaining why clustering of genes has been reported to not influence gene expression in T. reesei.ConclusionCompartmentation of ancestral gene clusters by AT-rich blocks might promote flexibilities that are evolutionarily advantageous in this fungus’ soil habitats and other natural environments. Our analyses, together with the complete genome sequence, provide a better blueprint for biotechnological and industrial applications.Electronic supplementary materialThe online version of this article (doi:10.1186/s13068-017-0825-x) contains supplementary material, which is available to authorized users.

Background Intermittent theta burst stimulation (iTBS) is a form of repetitive transcranial stimulation that has been used to enhance upper limb (UL) motor recovery. However, only limited studies have examined its efficacy in patients with chronic stroke and therefore it remains controversial. Methods This was a randomized controlled trial that enrolled patients from a rehabilitation department. Twenty-two patients with first-ever chronic and unilateral cerebral stroke, aged 30–70 years, were randomly assigned to the iTBS or control group. All patients received 1 session per day for 10 days of either iTBS or sham stimulation over the ipsilesional primary motor cortex in addition to conventional neurorehabilitation. Outcome measures were assessed before and immediately after the intervention period: Modified Ashworth Scale (MAS), Fugl-Meyer Assessment Upper Extremity (FMA-UE), Action Research Arm Test (ARAT), Box and Block test (BBT), and Motor Activity Log (MAL). Analysis of covariance was adopted to compare the treatment effects between groups. Results The iTBS group had greater improvement in the MAS and FMA than the control group ( η 2 = 0.151–0.233; p < 0.05), as well as in the ARAT and BBT ( η 2 = 0.161–0.460; p < 0.05) with large effect size. Both groups showed an improvement in the BBT, and there were no significant between-group differences in MAL changes. Conclusions The iTBS induced greater gains in spasticity decrease and UL function improvement, especially in fine motor function, than sham TBS. This is a promising finding because patients with chronic stroke have a relatively low potential for fine motor function recovery. Overall, iTBS may be a beneficial adjunct therapy to neurorehabilitation for enhancing UL function. Further larger-scale study is warranted to confirm the findings and its long-term effect. Trial registration This trial was registered under ClinicalTrials.gov ID No. NCT01947413 on September 20, 2013.

Background and purpose: Excessive inflammation and apoptosis are pathological features of endotoxaemic acute renal failure. Activation of glycogen synthase kinase-3 (GSK-3) is involved in inflammation and apoptosis. We investigated the effects of inhibiting GSK-3 on lipopolysaccharide (LPS)-induced acute renal failure, nuclear factor-kB (NF-kB), inflammation and apoptosis. Experimental approach: The effects of inhibiting GSK-3 with inhibitors, including lithium chloride (LiCl) and 6-bromoindirubin-3′-oxime (BIO), on LPS-treated (15 mg·kg ) renal epithelial cells (LiCl, 20 mM and BIO, 5 mM) were studied. Mouse survival was monitored and renal function was analysed by histological and serological examination. Cytokine and chemokine production, and cell apoptosis were measured by enzyme-linked immunosorbent assay and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labelling staining, respectively. Activation of NF-kB and GSK-3 was determined by immunostaining and Western blotting, respectively. Key results: Mice treated with GSK-3 inhibitors showed decreased mortality, renal tubular dilatation, vacuolization and sloughing, blood urea nitrogen, creatinine and renal cell apoptosis in response to endotoxaemia. Inhibiting GSK-3 reduced LPS-induced tumour necrosis factor-a (TNF-a) and CCL5/RANTES (released upon activation of normal T-cells) in vivo in mice and in vitro in murine kidney cortical collecting duct epithelial M1 cells. Inhibiting GSK-3 did not block TNF-a-induced cytotoxicity in rat kidney proximal tubular epithelial NRK52E or in M1 cells. Conclusions and implications:These results suggest that GSK-3 inhibition protects against endotoxaemic acute renal failure mainly by down-regulating pro-inflammatory TNF-a and RANTES.

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Immune interferon (IFN), also known as IFN-γ, promotes not only immunomodulation but also antimicrobial and anticancer activity. After IFN-γ binds to the complex of IFN-γ receptor (IFNGR) 1-IFNGR2 and subsequently activates its downstream signaling pathways, IFN-γ immediately causes transcriptional stimulation of a variety of genes that are principally involved in its biological activities. Regarding IFN-γ-dependent immunosurveillance, IFN-γ can directly suppress tumorigenesis and infection and/or can modulate the immunological status in both cancer cells and infected cells. Regarding the anticancer effects of IFN-γ, cancer cells develop strategies to escape from IFN-γ-dependent cancer immunosurveillance. Immune evasion, including the recruitment of immunosuppressive cells, secretion of immunosuppressive factors, and suppression of cytotoxic T lymphocyte responses, is speculated to be elicited by the oncogenic microenvironment. All of these events effectively downregulate IFN-γ-expressing cells and IFN-γ production. In addition to these extrinsic pathways, cancer cells may develop cellular tolerance that manifests as hyporesponsiveness to IFN-γ stimulation. This review discusses the potential escape mechanisms from IFN-γ-dependent immunosurveillance in tumorigenesis.

The preliminary findings indicate that brain adaptation may be modulated by specific rehabilitation practices, although generalization of the functional magnetic resonance imaging findings is limited by sample size. Further research is needed to identify the specific neural correlates of the behavioral gains achieved after rehabilitation therapies.