Optimisation of Air Source Heat Pumps in Residential Retrofits

Correctly applied air source heat pumps (ASHPs) are a proven technology that can reliably and effectively replace fossil fuel heating systems and achieve targeted heating-related CO2 reductions. However, poor-quality system design, installation or commissioning can lead to higher than expected running costs and poorly-performing heating systems, thus resulting in lower than expected CO2 savings. The retrofit ASHP systems studied in this research in residential retrofits in Ireland had significant engineering input at design stage, and comprehensive oversight during the installation and commissioning stages by the engineering team. Following analysis, most of the systems performed in line with, or exceeded, predictions but further opportunities for optimisation were identified. The research highlights the need for increased focus and resources to be applied by commissioning engineers to ensure that all ASHP installations are successful, a point that is especially critical in the context of the Irish Climate Action Plan targets of 500,000 retrofitted homes and the installation of 400,000 retrofit heat pumps by 2030 (Government of Ireland, 2019). This paper presents recommendations on how the ASHP installation process can deliver systems that operate to their full potential in terms of energy efficiency and CO2 reductions

Time-Resolved Thickness and Shape-Change Quantification using a Dual-Band Nanoplasmonic Ruler with Sub-Nanometer Resolution

Time-resolved measurements of changes in the size and shape of nanobiological objects and layers are crucial to understand their properties and optimize their performance. Optical sensing is particularly attractive with high throughput and sensitivity, and label-free operation. However, most state-of-the-art solutions require intricate modeling or multiparameter measurements to disentangle conformational or thickness changes of biomolecular layers from complex interfacial refractive index variations. Here, we present a dual-band nanoplasmonic ruler comprising mixed arrays of plasmonic nanoparticles with spectrally separated resonance peaks. As electrodynamic simulations and model experiments show, the ruler enables real-time simultaneous measurements of thickness and refractive index variations in uniform and heterogeneous layers with sub-nanometer resolution. Additionally, nanostructure shape changes can be tracked, as demonstrated by quantifying the degree of lipid vesicle deformation at the critical coverage prior to rupture and supported lipid bilayer formation. In a broader context, the presented nanofabrication approach constitutes a generic route for multimodal nanoplasmonic optical sensing

Activation of human invariant natural killer T cells with a thioglycoside analogue of ?-galactosylceramide

Activation of CD1d-restricted invariant NKT (iNKT) cells with the glycolipid ?-galactosylceramide (?-GalCer) confers protection against disease in murine models, however, clinical trials in humans have had limited impact. We synthesised a novel thioglycoside analogue of ?-GalCer, denoted ?-S-GalCer, and tested its efficacy for stimulating human iNKT cells in vitro. ?-S-GalCer stimulated cytokine release by iNKT cells in a CD1d-dependent manner and primed CD1d+ target cells for lysis. ?-S-GalCer-stimulated iNKT cells induced maturation of monocyte-derived dendritic cells into antigen-presenting cells that released IL-12 and small amounts of IL-10. The nature and potency of ?-S-GalCer and ?-GalCer in human iNKT cell activation were similar. However, in contrast to ?-GalCer, ?-S-GalCer did not activate murine iNKT cells in vivo. Because of its enhanced stability in biological systems, ?-S-GalCer may be superior to ?-GalCer as a parent compound for developing adjuvant therapies for humans. ?We tested if a thioglycoside analogue of ?-galactosylceramide could activate human iNKT cells ??-S-GalCer stimulated CD1d-dependent cytokine release and cytotoxicity by iNKT cells ??-S-GalCer-stimulated iNKT cells induced maturation of dendritic cells ??-S-GalCer did not activate murine iNKT cells in vivo ??-S-GalCer may be superior to ?-GalCer as a parent compound for developing adjuvant therapie

Nanopatterned Monolayers of Bioinspired, Sequence-Defined Polypeptoid Brushes for Semiconductor/Bio Interfaces

The ability to control and manipulate semiconductor/bio interfaces is essential to enable biological nanofabrication pathways and new bioelectronic devices. Traditional surface functionalization methods, like self-assembled monolayers (SAMs), provide limited customization for these interfaces. Polymer brushes offer a wider range of chemistries, but choices that maintain compatibility with both lithographic patterning and biological systems are scarce. Here we developed a class of bioinspired, sequence-defined polymers, i.e., polypeptoids, as tailored polymer brushes for surface modification of semiconductor substrates. Polypeptoids featuring a terminal hydroxyl (–OH) group are designed and synthesized for efficient melt grafting onto the native oxide layer of Si substrates, forming ultrathin (~1 nm) monolayers. By programming monomer chemistry, our polypeptoid brush platform offers versatile surface modification, including adjustments to surface energy, passivation, preferential biomolecule attachment, and specific biomolecule binding. Importantly, the polypeptoid brush monolayers remain compatible with electron-beam lithographic patterning and retain their chemical characteristics even under harsh lithographic conditions. Electron-beam lithography is used over polypeptoid brushes to generate highly precise, binary nanoscale patterns with localized functionality for the selective immobilization (or passivation) of biomacromolecules such as DNA origami or streptavidin onto addressable arrays. This surface modification strategy with bioinspired, sequence-defined polypeptoid brushes enables monomer-level control over surface properties with a large parameter space of monomer chemistry and sequence, and therefore is a highly versatile platform to precisely engineer semiconductor/bio interfaces for bioelectronics applications

Toll-like receptor 3 L412F polymorphism promotes a persistent clinical phenotype in pulmonary sarcoidosis

Background/Introduction: Sarcoidosis is a multi-systemic disorder of unknown etiology, characterized by the presence of non-caseating granulomas in target organs. In 90% of cases, there is thoracic involvement. Fifty to seventy percent of pulmonary sarcoidosis patients will experience acute, self-limiting disease. For the subgroup of patients who develop persistent disease, no targeted therapy is currently available. Aim: To investigate the potential of the single nucleotide polymorphism (SNP), Toll-like receptor 3 Leu412Phe (TLR3 L412F; rs3775291), as a causative factor in the development of and in disease persistence in pulmonary sarcoidosis. To investigate the functionality of TLR3 L412F in vitro in primary human lung fibroblasts from pulmonary sarcoidosis patients. Design: SNP-genotyping and cellular assays, respectively, were used to investigate the role of TLR3 L412F in the development of persistent pulmonary sarcoidosis. Methods: Cohorts of Irish sarcoidosis patients (n=228), healthy Irish controls (n=263) and a secondary cohort of American sarcoidosis patients (n=123) were genotyped for TLR3 L412F. Additionally, the effect of TLR3 L412F in primary lung fibroblasts from pulmonary sarcoidosis patients was quantitated following TLR3 activation in the context of cytokine and type I interferon production, TLR3 expression and apoptotic- and fibroproliferative-responses. Results: We report a significant association between TLR3 L412F and persistent clinical disease in two cohorts of Irish and American Caucasians with pulmonary sarcoidosis. Furthermore, activation of TLR3 in primary lung fibroblasts from 412 Fhomozygous pulmonary sarcoidosis patients resulted in reduced IFN-? and TLR3 expression, reduced apoptosis- and dysregulated fibroproliferative-responses compared with TLR3 wild-type patients. Discussion/Conclusion: This study identifies defective TLR3 function as a previously unidentified factor in persistent clinical disease in pulmonary sarcoidosis and reveals TLR3 L412F as a candidate biomarke