Prospective randomized controlled pilot study on the effects of almond consumption on skin lipids and wrinkles.

ObjectiveAlmonds are a rich source of fatty acids and antioxidants, and their supplementation is known to significantly modulate serum lipids. The effects of almond on the skin's lipid barrier and the appearance of wrinkles have not yet been elucidated. The aim of this study was to investigate the effects of almond consumption on facial sebum production and wrinkles.MethodsThis was a prospective, investigator-blinded, randomized controlled trial in which subjects consumed 20% of their daily energy consumption in either almonds or a calorie-matched snack for 16 weeks. This study was completed at the UC Davis Dermatology clinic. Participants were a volunteer sample of generally healthy postmenopausal females with Fitzpatrick skin types 1 and 2. A facial photograph and image analysis system was used to obtain standardized photographs and information on wrinkle width and severity at 0, 8, and 16 weeks. Measurements of transepidermal water loss and sebum production were also completed at 0, 8, and 16 weeks.ResultsFifty healthy postmenopausal females were recruited, 31 participants were enrolled, and 28 completed the study. Under photographic analysis, the almond group had significantly decreased wrinkle severity and width compared with the control group at 16 weeks (p < .02). Changes in skin barrier function were nonsignificant, measured by the transepidermal water loss (p = .65) between the almond and control groups relative to baseline after 16 weeks. No adverse effects were reported.ConclusionOur study demonstrates that daily almond consumption may reduce wrinkle severity in postmenopausal females to potentially have natural antiaging benefits

Quantitative assessment of disease resistance by real-time PCR

Dissertação de Mestrado Integrado em Arquitectura, apresentada ao Departamento de Arquitectura da Faculdade de Ciências e Tecnologia da Universidade de Coimbra, sob a orientação do Prof. Doutor Rui Lobo.O centro histórico de Coimbra, como muitos outros, sofre as consequências do grave problema da desocupação. A gravidade deste problema nota-se ao olhar para o estado de degradação e ruína dos edifícios, mas também, e principalmente, ao percorrer o espaço no período noturno, altura em que o comércio fecha deixando a área totalmente sem vida e consequentemente pouco convidativa e perigosa. A quem cabe a função de animar este espaço? Ao comércio? O prolongar o seu horário de funcionamento ou o manter as luzes das montras acesas durante a noite acarretam custos e alteração de dinâmicas que são dificilmente compensados. Aos turistas? Estes têm um caráter transitório. Então cabe a quem? Tem de caber á população residente na área. Mas, se o espaço está desabitado, quem o vai dinamizar? A reabilitação tem de passar pela criação de condições para que se recupere e desenvolva a função habitacional. Como proliferar a função habitacional em edifícios que não respondem às exigências mínimas de habitabilidade dos dias de hoje? Já lá vai o tempo em que se demolia para construir de novo. Hoje, mais do que nunca, o valor patrimonial do legado arquitetónico é valorizado (e bem!) pois é parte essencial da identidade da cidade e da nossa identidade. Num espaço como o centro histórico a reabilitação da casa corrente deve promover as melhorias das condições de habitabilidade e ao mesmo tempo o seu valor enquanto parte constituinte de um conjunto com identidade própria. A questão fundamental a que esta tese se propõe tentar responder é: ‘Como reabilitar?’The historical center of Coimbra, like many others, suffers from serious problems of emptiness. The severity of this problem is noticed when looking at the state of degradation and ruin of buildings, but also, and especially, at night, when the shops close leaving the area lifeless and consequently uninviting and dangerous. Who has the function of animating this space? The shops? To extend their opening hours or to keep the shop lights lit at night entail costs and changing dynamics that are rarely compensated. The tourists? These have a temporary character. So it’s up to who? It must fit to the resident population in the area. However, if space is uninhabited, who will animate it? Rehabilitation has to go through the creation of conditions to recover and develop the housing function. How can we proliferate housing function in buildings that do not have the minimum habitability requirements of today? Gone are the days of demolishion to build again. Today, more than ever, the asset value of the architectural heritage is considered (and well!) because it is an essential part of the city’s identity. In an area as the historical center the rehabilitation of the ‘current house’ must promote improvements on living conditions and at the same time its value as a constituent part of a set with its own identity. The key question this thesis will try to answer is: ‘How to rehabilitate?

Tris{2-[(2,6-dimethyl­phen­yl)amino]­eth­yl}amine

The title compound, C30H42N4, is an aryl­ated tris­(amino­eth­yl)amine derivative which was obtained by reducing the corresponding tris-amide with AlH3. The asymmetric unit consists of one third of a C 3v-symmetric mol­ecule with the tertiary N atom lying on a crystallographic threefold axis

Dissecting the role of histidine kinase and Hog1 mitogen-activated protein kinase signalling in stress tolerance and pathogenicity of Parastagonospora nodorum on wheat.

The HOG1 mitogen-activated protein kinase (MAPK) pathway is activated through two-component histidine kinase (HK) signalling. This pathway was first characterized in the budding yeast Saccharomyces cerevisiae as a regulator of osmotolerance. The fungus Parastagonospora nodorum is the causal agent of septoria nodorum blotch of wheat. This pathogen uses host-specific effectors in tandem with general pathogenicity mechanisms to carry out its infection process. Genes showing strong sequence homology to S. cerevisiae HOG1 signalling pathway genes have been identified in the genome of P. nodorum. In this study, we examined the role of the pathway in the virulence of P. nodorum on wheat by disrupting putative pathway component genes: HOG1 (SNOG_13296) MAPK and NIK1 (SNOG_11631) hybrid HK. Mutants deleted in NIK1 and HOG1 were insensitive to dicarboximide and phenylpyrrole fungicides, but not a fungicide that targets ergosterol biosynthesis. Furthermore, both Δnik1 and Δhog1 mutants showed increased sensitivity to hyperosmotic stress. However, HOG1, but not NIK1, is required for tolerance to elevated temperatures. HOG1 deletion conferred increased tolerance to 6-methoxy-2-benzoxazolinone, a cereal phytoalexin. This suggests that the HOG1 signalling pathway is not exclusively associated with NIK1. Both Δnik1 and Δhog1 mutants retained the ability to infect and cause necrotic lesions on wheat. However, we observed that the Δhog1 mutation resulted in reduced production of pycnidia, asexual fruiting bodies that facilitate spore dispersal during late infection. Our study demonstrated the overlapping and distinct roles of a HOG1 MAPK and two-component HK signalling in P. nodorum growth and pathogenicity

The impact of pulsed electric field on the extraction of bioactive compounds from beetroot

Beetroot is a root vegetable rich in different bioactive components, such as vitamins, minerals, phenolics, carotenoids, nitrate, ascorbic acids, and betalains, that can have a positive effect on human health. The aim of this work was to study the influence of the pulsed electric field (PEF) at different electric field strengths (4.38 and 6.25 kV/cm), pulse number 10\u201330, and energy input 0\u201312.5 kJ/kg as a pretreatment method on the extraction of betalains from beetroot. The obtained results showed that the application of PEF pre-treatment significantly (p < 0.05) influenced the efficiency of extraction of bioactive compounds from beetroot. The highest increase in the content of betalain compounds in the red beet\u2019s extract (betanin by 329%, vulgaxanthin by 244%, compared to the control sample), was noted for 20 pulses of electric field at 4.38 kV/cm of strength. Treatment of the plant material with a PEF also resulted in an increase in the electrical conductivity compared to the non-treated sample due to the increase in cell membrane permeability, which was associated with leakage of substances able to conduct electricity, including mineral salts, into the intercellular space

Differential effector gene expression underpins epistasis in a plant fungal disease.

Fungal effector-host sensitivity gene interactions play a key role in determining the outcome of septoria nodorum blotch disease (SNB) caused by Parastagonospora nodorum on wheat. The pathosystem is complex and mediated by interaction of multiple fungal necrotrophic effector-host sensitivity gene systems. Three effector-sensitivity gene systems are well characterised in this pathosystem; SnToxA-Tsn1, SnTox1-Snn1 and SnTox3-Snn3. We tested a wheat mapping population that segregated for Snn1 and Snn3 with SN15, an aggressive P. nodorum isolate that produces SnToxA, SnTox1 and SnTox3, to study the inheritance of sensitivity to SnTox1 and SnTox3 and disease susceptibility. Interval quantitative trait locus (QTL) mapping showed that the SnTox1-Snn1 interaction was paramount in SNB development on both seedlings and adult plants. No effect of the SnTox3-Snn3 interaction was observed under SN15 infection. The SnTox3-Snn3 interaction was however, detected in a strain of SN15 in which SnTox1 had been deleted (tox1-6). Gene expression analysis indicates increased SnTox3 expression in tox1-6 compared to SN15. This indicates that the failure to detect the SnTox3-Snn3 interaction in SN15 is due - at last in part - to suppressed expression of SnTox3 mediated by SnTox1 Furthermore, infection of the mapping population with a strain deleted in SnToxA, SnTox1 and SnTox3 (toxa13) unmasked a significant SNB QTL on 2DS where the SnTox2 effector sensitivity gene, Snn2, is located.This QTL was not observed in SN15 and tox1–6 infections and thus suggesting that SnToxA and/or SnTox3 were epistatic. Additional QTLs responding to SNB and effectors sensitivity were detected on 2AS1 and 3AL

Controlling magnetic exchange and anisotropy by non-magnetic ligand substitution in layered MPX3 (M = Ni, Mn; X = S, Se)

Recent discoveries in two-dimensional (2D) magnetism have intensified the investigation of van der Waals (vdW) magnetic materials and further improved our ability to tune their magnetic properties. Tunable magnetism has been widely studied in antiferromagnetic metal thiophosphates MPX3. Substitution of metal ions M has been adopted as an important technique to engineer the magnetism in MPX3. In this work, we have studied the previously unexplored chalcogen X substitutions in MPX3 (M = Mn/Ni; X = S/Se). We synthesized the single crystals of MnPS3-xSex (0 < x < 3) and NiPS3-xSex (0 < x < 1.3) and investigated the systematic evolution of the magnetism with varying x. Our study reveals the effective tuning of magnetic interactions and anisotropies in both MnPS3 and NiPS3 upon Se substitution. Such efficient engineering of the magnetism provides a suitable platform to understand the low-dimensional magnetism and develop future magnetic devices

Functional redundancy of necrotrophic effectors – consequences for exploitation for breeding

Necrotrophic diseases of wheat cause major losses in most wheat growing areas of world. Tan spot (caused by Pyrenophora tritici-repentis) and septoria nodorum blotch (SNB; Parastagonospora nodorum) have been shown to reduce yields by 10–20% across entire agri-ecological zones despite the application of fungicides and a heavy focus over the last 30 years on resistance breeding. Efforts by breeders to improve the resistance of cultivars has been compromised by the universal finding that resistance was quantitative and governed by multiple quantitative trait loci (QTL). Most QTL had a limited effect that was hard to measure precisely and varied significantly from site to site and season to season. The discovery of necrotrophic effectors has given breeding for disease resistance new methods and tools. In the case of tan spot in West Australia, a single effector, PtrToxA and its recogniser gene Tsn1, has a dominating impact in disease resistance. The delivery of ToxA to breeders has had a major impact on cultivar choice and breeding strategies. For P. nodorum, three effectors – SnToxA, SnTox1, and SnTox3 – have been well characterized. Unlike tan spot, no one effector has a dominating role. Genetic analysis of various mapping populations and pathogen isolates has shown that different effectors have varying impact and that epistatic interactions also occur. As a result of these factors the deployment of these effectors for SNB resistance breeding is more complex. We have deleted the three effectors in a strain of P. nodorum and measured effector activity and disease potential of the triple knockout mutant. The culture filtrate causes necrosis in several cultivars and the strain causes disease, albeit the overall levels are less than in the wild type. Modeling of the field disease resistance scores of cultivars from their reactions to the microbially expressed effectors SnToxA, SnTox1, and SnTox3 is significantly improved by including the response to the triple knockout mutant culture filtrate. This indicates that one or more further effectors are secreted into the culture filtrate. We conclude that the in vitro-secreted necrotrophic effectors explain a very large part of the disease response of wheat germplasm and that this method of resistance breeding promises to further reduce the impact of these globally significant diseases