Micropatterned biofunctional lubricant-infused surfaces promote selective localized cell adhesion and patterning.

Micropatterned biofunctional surfaces provide a wide range of applications in bioengineering. A key characteristic which is sought in these types of bio-interfaces is prevention of non-specific adhesion for enhanced biofunctionality and targeted binding. Lubricant-infused omniphobic coatings have exhibited superior performance in attenuating non-specific adhesion; however, these coatings completely block the surfaces and do not support targeted adhesion or patterning. In this work, we introduce a novel lubricant-infused surface with biofunctional micropatterned domains integrated within an omniphobic layer. This new class of micropatterned lubricant-infused surfaces simultaneously promotes localized and directed binding of desired targets, as well as repellency of undesired species, especially in human whole blood. Furthermore, this modification method is easily translatable to microfluidic devices offering a wider range of applications and improved performance for immunoassays in whole blood and inhibition of clot formation in microfluidic channels. The biofunctional micropatterned lubricant-infused surfaces were created through a bench-top straight forward process by integrating microcontact printing, chemical vapor deposition (CVD) of self-assembled monolayers (SAMs) of fluorosilanes, and further infusion of the SAMs with a bio-compatible fluorocarbon-based lubricant layer. The developed surfaces, patterned with anti-CD34 antibodies, yield enhanced adhesion and controlled localized binding of target biomolecules (e.g. antibodies) and CD34 positive cells (e.g. HUVECs) inside microfluidic devices, outperforming conventional blocking methods (e.g. bovine serum albumin (BSA) or poly(ethylene glycol) (PEG)) in buffer and human whole blood. These surfaces offer a straightforward and effective way to enhance blocking capabilities while preserving the biofunctionality of a micropatterned system in complex biological environments such as whole blood. We anticipate that these micropatterned biofunctional interfaces will find a wide range of applications in microfluidic devices and biosensors for enhanced and localized targeted binding while preventing non-specific adhesion.

Self-Cleaning Ceramic Tiles Produced via Stable Coating of TiO2 Nanoparticles.

The high photocatalytic power of TiO2 nanoparticles has drawn great attention in environmental and medical applications. Coating surfaces with these particles enables us to benefit from self-cleaning properties and decomposition of pollutants. In this paper, two strategies have been introduced to coat ceramic tiles with TiO2 nanoparticles, and the self-cleaning effect of the surfaces on degradation of an organic dye under ultraviolent (UV) exposure is investigated. In the first approach, a simple one-step heat treatment method is introduced for coating, and different parameters of the heat treatment process are examined. In the second method, TiO2 nanoparticles are first aminosilanized using (3-Aminopropyl)triethoxysilane (APTES) treatment followed by their covalently attachment onto CO2 plasma treated ceramic tiles via N-(3-Dimethylaminopropyl)-N′-ethylcarbodiimide hydrochloride (EDC) and N-Hydroxysuccinimide (NHS) chemistry. We monitor TiO2 nanoparticle sizes throughout the coating process using dynamic light scattering (DLS) and characterize developed surfaces using X-ray photoelectron spectroscopy (XPS). Moreover, hydrophilicity of the coated surfaces is quantified using a contact angle measurement. It is shown that applying a one-step heat treatment process with the optimum temperature of 200 °C for 5 h results in successful coating of nanoparticles and rapid degradation of dye in a short time. In the second strategy, the APTES treatment creates a stable covalent coating, while the photocatalytic capability of the particles is preserved. The results show that coated ceramic tiles are capable of fully degrading the added dyes under UV exposure in less than 24 h.

Snf2l regulates Foxg1-dependent progenitor cell expansion in the developing brain.

Balancing progenitor cell self-renewal and differentiation is essential for brain development and is regulated by the activity of chromatin remodeling complexes. Nevertheless, linking chromatin changes to specific pathways that control cortical histogenesis remains a challenge. Here we identify a genetic interaction between the chromatin remodeler Snf2l and Foxg1, a key regulator of neurogenesis. Snf2l mutant mice exhibit forebrain hypercellularity arising from increased Foxg1 expression, increased progenitor cell expansion, and delayed differentiation. We demonstrate that Snf2l binds to the Foxg1 locus at midneurogenesis and that the phenotype is rescued by reducing Foxg1 dosage, thus revealing that Snf2l and Foxg1 function antagonistically to regulate brain size.

Increasing D4Z4 repeat copy number compromises C2C12 myoblast differentiation.

Facioscapulohumeral muscular dystrophy (FSHD) is an autosomal dominant myopathy associated with deletions of a subtelomeric repeat (D4Z4). A reduction in D4Z4 copy number coincides with increased expression of neighboring 4q35 genes, implying a normal repressive role for the repeats. Here we examine the effect of increasing D4Z4 repeat number on reporter gene activity in C2C12 cells. Repeat size had only a minor cis-effect on reporter gene activity but greatly compromised myotube formation. This latter trans-effect did not result from expression of a gene within the repeat (DUX4) but likely results from squelching of the D4Z4 recognition complex.