Inkjet printed TiO2 nanoparticles from aqueous solutions for dye sensitized solar cells (DSSCs)

This is the accepted version of the following article: Cherrington, R., Hughes, D. J., Senthilarasu, S. and Goodship, V. (2015), Inkjet-Printed TiO2 Nanoparticles from Aqueous Solutions for Dye-Sensitized Solar Cells (DSSCs). Energy Technology., which has been published in final form at http://dx.doi.org/10.1002/ente.201500096This work reports on the formulation of suitable ink for inkjet printing of TiO2 by investigating the critical parame- ters of particle size, pH, viscosity, and stability. Aqueous sus- pensions of TiO2 nanoparticles (Degussa, P25) were pre- pared with the addition of 25 wt % polyethylene glycol 400 as a humectant to minimize drying at the printer nozzles and reduce the likelihood of nozzle blockage. The inkjet-printed TiO2 layers were assembled into dye-sensitized solar cells. The current–voltage (I–V) characteristics were measured under one sun (air mass 1.5, 100 mW cm 2) using a source meter (Model 2400, Keithley Instrument, Inc.), and the active area of the cell was 0.25 cm2. The inkjet-printed TiO2 photoanode produced a device with a short-circuit current (Isc) of 9.42 mA cm 2, an open-circuit voltage (Voc) of 0.76 V, and a fill factor (FF) of 0.49, resulting in a power conversion efficiency (PCE) of 3.50 %.Engineering and Physical Sciences Research Council (EPSRC

Clinical features of a novel TIMP-3 mutation causing Sorsby's fundus dystrophy: implications for disease mechanism

AIMS: To describe the phenotype in three family members affected by a novel mutation in the gene coding for the enzyme tissue inhibitor of metalloproteinase-3 (TIMP-3). METHODS: Three members of the same family were seen with a history of nyctalopia and visual loss due to maculopathy. Clinical features were consistent with Sorsby's fundus dystrophy. Exon 5 of the gene coding for TIMP-3 was amplified by the polymerase chain reaction, single strand conformation polymorphism analysis undertaken and exon 5 amplicons were directly sequenced. RESULTS: Onset of symptoms was in the third to fourth decade. Five of six eyes had geographic macular atrophy rather than neovascularisation as a cause for central visual loss. Peripheral retinal pigmentary disturbances were present. Scotopic ERGs were abnormal in all three. Mutation analysis showed a GT transversion in all three resulting in a premature termination codon, E139X, deleting most of the carboxy terminal domain of TIMP-3. CONCLUSIONS: The patients described had a form of Sorsby's fundus dystrophy which fell at the severe end of the spectrum of this disease. Postulated disease mechanisms include deposition of dimerised TIMP-3 protein

Building in multifunctionality in plastic components : complexity, cost and sustainability

Multifunctionality can be embedded into material systems by three distinct design processes. These are: firstly multifunction can be embedded at a material level such as the use of nanomaterials within a polymer. In the second instance, discrete material systems can be added together. Examples are laminate systems in food pouches consisting of thin layers of metal and polymer. In the third process this can be achieved by integrating these materials systems together to form one holistically behaving component with multifunctionality. An example is an embedded antenna in an automotive windscreen.Drivers for multifunctionality include the increased push towards intelligent objects, such as the creation of the internet of things. Here, the embedding of communication and electronic function into daily consumer objects, such as milk cartons and food packaging are demanded. This must be offset by consideration of the related rise of a new wave of short-lifetime waste electronic and electronic equipment, incapable with current plastic recycling infrastructure, for disposal systems to adapt too. Designing integrated and multifunctional plastic components however, is complicated by the sheer number of material choices, multiple processing platforms, cost implications and environmental legislation. Considering just the processes of injection moulding, compression moulding and additive manufacturing, a designer is confronted with considerable complexity and numerous engineering design and stakeholder issues to consider. This paper presents examples of current state of art in multifunctional systems and discusses the barriers and potential solutions to creating fully realized multifunctional systems within a polymeric manufacturing environment. Impacts on material lifecycles and disposal infrastructures must be considered, as is the necessity to retain diversity with new integrated and advanced manufacturing processes suitable for the demands of mass customization, automation and Industry 4.0

Is the collagen primed for mineralization in specific regions of the Turkey tendon?:an investigation of the protein-mineral interface using Raman spectroscopy

The tendons in the turkey leg have specific well-defined areas which become mineralized as the animal ages and they are a thoroughly characterized model system for studying the mineralization process of bone. In this study, nondestructive Raman spectroscopic analysis was used to explore the hypothesis that regions of the turkey tendon that are associated with mineralization exhibit distinct and observable chemical modifications of the collagen prior to the onset of mineralization. The Raman spectroscopy features associated with mineralization were identified by probing (on the micrometer scale) the transition zone between mineralized and nonmineralized regions of turkey leg tendons. These features were then measured in whole tendons and identified in regions of tendon which are destined to become rapidly mineralized around 14 weeks of age. The data show there is a site-specific difference in collagen prior to the deposition of mineral, specifically the amide III band at 1270 cm(-1) increases as the collagen becomes more ordered (increased amide III:amide I ratio) in regions that become mineralized compared to collagen destined to remain nonmineralized. If this mechanism were present in materials of different mineral fraction (and thus material properties), it could provide a target for controlling mineralization in metabolic bone disease

Compressive loading of the murine tibia reveals site-specific micro-scale differences in adaptation and maturation rates of bone

Loading increases bone mass and strength in a site-specific manner; however, possible effects of loading on bone matrix composition have not been evaluated. Site-specific structural and material properties of mouse bone were analyzed on the macro- and micro/molecular scale in the presence and absence of axial loading. The response of bone to load is heterogeneous, adapting at molecular, micro-, and macro-levels. INTRODUCTION: Osteoporosis is a degenerative disease resulting in reduced bone mineral density, structure, and strength. The overall aim was to explore the hypothesis that changes in loading environment result in site-specific adaptations at molecular/micro- and macro-scale in mouse bone. METHODS: Right tibiae of adult mice were subjected to well-defined cyclic axial loading for 2 weeks; left tibiae were used as physiologically loaded controls. The bones were analyzed with μCT (structure), reference point indentation (material properties), Raman spectroscopy (chemical), and small-angle X-ray scattering (mineral crystallization and structure). RESULTS: The cranial and caudal sites of tibiae are structurally and biochemically different within control bones. In response to loading, cranial and caudal sites increase in cortical thickness with reduced mineralization (-14 and -3%, p < 0.01, respectively) and crystallinity (-1.4 and -0.3%, p < 0.05, respectively). Along the length of the loaded bones, collagen content becomes more heterogeneous on the caudal site and the mineral/collagen increases distally at both sites. CONCLUSION: Bone structure and composition are heterogeneous, finely tuned, adaptive, and site-specifically responsive at the micro-scale to maintain optimal function. Manipulation of this heterogeneity may affect bone strength, relative to specific applied loads

Use of the complement inhibitor Coversin to treat HSCT-associated TMA

Finding an inherited complement abnormality in HSCT-associated TMA provides a rationale for the use of a complement inhibitor.Alternative complement inhibitors such as Coversin should be considered in patients who are resistant to eculizumab

Phenotype-specific effect of chromosome 1q21.1 rearrangements and GJA5 duplications in 2436 congenital heart disease patients and 6760 controls

Recurrent rearrangements of chromosome 1q21.1 that occur via non-allelic homologous recombination have been associated with variable phenotypes exhibiting incomplete penetrance, including congenital heart disease (CHD). However, the gene or genes within the ∼1 Mb critical region responsible for each of the associated phenotypes remains unknown. We examined the 1q21.1 locus in 948 patients with tetralogy of Fallot (TOF), 1488 patients with other forms of CHD and 6760 ethnically matched controls using single nucleotide polymorphism genotyping arrays (Illumina 660W and Affymetrix 6.0) and multiplex ligation-dependent probe amplification. We found that duplication of 1q21.1 was more common in cases of TOF than in controls [odds ratio (OR) 30.9, 95% confidence interval (CI) 8.9-107.6); P = 2.2 × 10−7], but deletion was not. In contrast, deletion of 1q21.1 was more common in cases of non-TOF CHD than in controls [OR 5.5 (95% CI 1.4-22.0); P = 0.04] while duplication was not. We also detected rare (n = 3) 100-200 kb duplications within the critical region of 1q21.1 in cases of TOF. These small duplications encompassed a single gene in common, GJA5, and were enriched in cases of TOF in comparison to controls [OR = 10.7 (95% CI 1.8-64.3), P = 0.01]. These findings show that duplication and deletion at chromosome 1q21.1 exhibit a degree of phenotypic specificity in CHD, and implicate GJA5 as the gene responsible for the CHD phenotypes observed with copy number imbalances at this locu

Identification of the first ATRIP-deficient patient and novel mutations in ATR define a clinical spectrum for ATR-ATRIP Seckel Syndrome

A homozygous mutational change in the Ataxia-Telangiectasia and RAD3 related (ATR) gene was previously reported in two related families displaying Seckel Syndrome (SS). Here, we provide the first identification of a Seckel Syndrome patient with mutations in ATRIP, the gene encoding ATR-Interacting Protein (ATRIP), the partner protein of ATR required for ATR stability and recruitment to the site of DNA damage. The patient has compound heterozygous mutations in ATRIP resulting in reduced ATRIP and ATR expression. A nonsense mutational change in one ATRIP allele results in a C-terminal truncated protein, which impairs ATR-ATRIP interaction; the other allele is abnormally spliced. We additionally describe two further unrelated patients native to the UK with the same novel, heterozygous mutations in ATR, which cause dramatically reduced ATR expression. All patient-derived cells showed defective DNA damage responses that can be attributed to impaired ATR-ATRIP function. Seckel Syndrome is characterised by microcephaly and growth delay, features also displayed by several related disorders including Majewski (microcephalic) osteodysplastic primordial dwarfism (MOPD) type II and Meier-Gorlin Syndrome (MGS). The identification of an ATRIP-deficient patient provides a novel genetic defect for Seckel Syndrome. Coupled with the identification of further ATR-deficient patients, our findings allow a spectrum of clinical features that can be ascribed to the ATR-ATRIP deficient sub-class of Seckel Syndrome. ATR-ATRIP patients are characterised by extremely severe microcephaly and growth delay, microtia (small ears), micrognathia (small and receding chin), and dental crowding. While aberrant bone development was mild in the original ATR-SS patient, some of the patients described here display skeletal abnormalities including, in one patient, small patellae, a feature characteristically observed in Meier-Gorlin Syndrome. Collectively, our analysis exposes an overlapping clinical manifestation between the disorders but allows an expanded spectrum of clinical features for ATR-ATRIP Seckel Syndrome to be define