Absence of allergenic residues in experimental and commercial wines fined with caseinates

The possible presence of allergenic residues in wines treated with one of the potassium caseinates used as fining agents has been investigated.     

Heaven on Earth

‘By 2050 we will have probed the universe even further, peeling back time as we strive for some sense of creation and meaning.’ The world's first neurologist in space, Roberta L Bondar , who conducted international experiments on space mission STS 42 and has subsequently undertaken neurological research with NASA, urges us to look up and into space, which is set to remain a rich area of exploration, scientific investigation and wonder, with the discovery of new planets, light, patterns and materials on the not-so-distant horizon.     

The Industrial Heritage and the New Architecture： Teaching, Researching, Designing the Place Identity

The new architecture may provide unusual opportunities for the abandoned areas involved by former industrial processes, both in the city centers and in the landscape. In fact, it may create new centralities and give new collective function for deprived areas. The case study of the architectural and educational project for a new museum park devoted to the technique and the science in the Apennine＇ s landscape near Parma （Italy） may give an interesting point of view about the role of the teaching and the research of the architecture in the former industrial heritage, and to avoid the abandonment and the pauperization of the territory around.     

One or infinite optimal city sizes? In search of an equilibrium size for cities

In this paper, the stylized assumption that one single “optimal” city size exists for all cities—achieved when marginal location costs equal marginal location benefits—is abandoned, as well as the opposite view that each city operates on its own cost and production curves, defining a specific optimal size. Instead, this work maintains the comparability among cities and demonstrates that urban specificities in functions performed, quality of life, industrial diversity and social conflicts shift up and down the benefits and costs linked to pure physical size, leading to different “equilibrium” sizes for cities. In order to achieve this result, a model of equilibrium urban size is set up, based on urban costs and urban benefits, merging elements suggested both by the traditional urban economics literature as well as by updated approaches considering also environmental quality, urban form and inter-urban cooperation networks. The model is then estimated on a sample of 59 European cities with data at FUA level. Empirical results allow the identification of city-specific “equilibrium” sizes. The error term, that is, the difference between actual urban population and the “equilibrium” one predicted by the model can be explained, beyond a measure of our ignorance, by good or bad governance, thereby suggesting future strategies for more efficient urban planning.     

Convergence in Diversity: New York City School Food and the Future of the Food Movement

In the context of a global food system that has given rise to widespread concerns for food security and sustainability, reformative efforts have emerged, expanded and multiplied worldwide. To enhance understanding of the multi-faceted nature of this food movement and its scope for convergence and consolidation, in this article we propose frame alignment and alliance-building as a theoretical and analytical framework. Using New York City as a case study, we explore how school food reform may act as a particularly powerful platform for coalescing the interests and goals of diverse food system actors. We conclude with a call to interrogate school food and other reform activities with specific attention to the opportunities they pose for finding ‘convergence in diversity’ — in other words, for aligning the diverse and often fragmented efforts of the ‘food movement’ around an integrated and shared agenda with heightened potential for impact.     

Pectins from Aloe Vera: Extraction and production of gels for regenerative medicine

Extraction, purification, and gel preparation of Aloe Vera pectin and the evaluation of the biocompatibility of the pectin gels were studied, considering as end use as implantable materials for regenerative medicine. A. Vera was chosen as source of pectin, as this pectin was described to possess high molecular weight and a low degree of esterification. As the properties of pectins are strictly dependent upon the extraction methods in combination with the natural source, the extraction method was modified in order to optimize the yield of the final product, its purity, the duration of the process and the selection of non‐toxic chemical reagents. Changing the experimental conditions resulted in four different extraction processes and products with different physical and chemical characteristics. The optimal extraction resulted to be the process: with enzimatic deactivation by microwave and the use of sodium citrate as chelating agent the molecular weight of the pectin extracted was estimated to be 118 kDa and the 2.93% esterification degree. Cytocompatibility of pectin gels, prepared by ionotropic gelation, showing an improved cell adhesion if compared to commercial pectin. The results suggest that the extracted A. Vera pectins possess interesting properties to be exploited for the production of mechanically stable gels by ionotropic gelation and high rhamnose content matrices for application in regenerative medicine. © 2013 Wiley Periodicals, Inc. J. Appl. Polym. Sci. 2014 , 131, 39760.     

Reduced Levels of ABCA1 Transporter Are Responsible for the Cholesterol Efflux Impairment in β-Amyloid-Induced Reactive Astrocytes: Potential Rescue from Biomimetic HDLs

The cerebral synthesis of cholesterol is mainly handled by astrocytes, which are also responsible for apoproteins’ synthesis and lipoproteins’ assembly required for the cholesterol transport in the brain parenchyma. In Alzheimer disease (AD), these processes are impaired, likely because of the astrogliosis, a process characterized by morphological and functional changes in astrocytes. Several ATP-binding cassette transporters expressed by brain cells are involved in the formation of nascent discoidal lipoproteins, but the effect of beta-amyloid (Aβ) assemblies on this process is not fully understood. In this study, we investigated how of Aβ_1-42-induced astrogliosis affects the metabolism of cholesterol in vitro. We detected an impairment in the cholesterol efflux of reactive astrocytes attributable to reduced levels of ABCA1 transporters that could explain the decreased lipoproteins’ levels detected in AD patients. To approach this issue, we designed biomimetic HDLs and evaluated their performance as cholesterol acceptors. The results demonstrated the ability of apoA-I nanodiscs to cross the blood–brain barrier in vitro and to promote the cholesterol efflux from astrocytes, making them suitable as a potential supportive treatment for AD to compensate the depletion of cerebral HDLs.     

Beneficial and Sexually Dimorphic Response to Combined HDAC Inhibitor Valproate and AMPK/SIRT1 Pathway Activator Resveratrol in the Treatment of ALS Mice

Amyotrophic lateral sclerosis (ALS) is a fatal adult-onset neurodegenerative disorder. There is no cure and current treatments fail to slow the progression of the disease. Epigenetic modulation in the acetylation state of NF-kB RelA and the histone 3 (H3) protein, involved in the development of neurodegeneration, is a drugable target for the class-I histone deacetylases (HDAC) inhibitors, entinostat or valproate, and the AMP-activated kinase (AMPK)-sirtuin 1 pathway activator, resveratrol. In this study, we demonstrated that the combination of valproate and resveratrol can restore the normal acetylation state of RelA in the SOD1(G93A) murine model of ALS, in order to obtain the neuroprotective form of NF-kB. We also investigated the sexually dimorphic development of the disease, as well as the sex-sensibility to the treatment administered. We showed that the combined drugs, which rescued AMPK activation, RelA and the histone 3 acetylation state, reduced the motor deficit and the disease pathology associated with motor neuron loss and microglial reactivity, Brain-Derived Neurotrophic Factor (BDNF) and B-cell lymphoma-extra large (Bcl-xL) level decline. Specifically, vehicle-administered males showed earlier onset and slower progression of the disease when compared to females. The treatment, administered at 50 days of life, postponed the time of onset in the male by 22 days, but not in a significant way in females. Nevertheless, in females, the drugs significantly reduced symptom severity of the later phase of the disease and prolonged the mice’s survival. Only minor beneficial effects were produced in the latter stage in males. Overall, this study shows a beneficial and sexually dimorphic response to valproate and resveratrol treatment in ALS mice.     

CD26 Induces Colorectal Cancer Angiogenesis and Metastasis through CAV1/MMP1 Signaling

CD26 has been reported as a marker for colorectal cancer stem cells endowed with tumor-initiating properties and capable of colorectal cancer (CRC) metastasis. In this study, we investigated the functional effect of CD26 on CRC angiogenesis and metastasis, and the potential underlying mechanism. The functional effects of CD26 overexpression or repression were determined by a wound healing experiment, and cell migration and invasion assays in vitro and in mouse models. Differentially expressed genes regulated by CD26 were identified by genome-wide mRNA expression array and validated by quantitative PCR. CD26 functionally regulated CRC cell migration and invasion in vitro and angiogenesis and metastasis in vivo. Genome-wide mRNA expression array and qPCR showed that MMP1 was up-regulated in CD26+ subpopulation, and a subsequent experiment demonstrated the regulatory effect of CD26 on MMP1 in CRC cell lines with CD26 repression or overexpression. Furthermore, overexpression of CAV1 abrogated the CD26-regulated MMP1 induction in CRC cell lines. This study demonstrated the functional roles of CD26 in inducing CRC migration, invasion, angiogenesis and metastasis and identified the potential involvement of MMP1 and CAV1 in such process. CD26 is an attractive therapeutic target for combating tumor progression to improve the prognosis of CRC patients.     

SEC23B Loss-of-Function Suppresses Hepcidin Expression by Impairing Glycosylation Pathway in Human Hepatic Cells

Biallelic pathogenic variants in the SEC23B gene cause congenital dyserythropoietic anemia type II (CDA II), a rare hereditary disorder hallmarked by ineffective erythropoiesis, hemolysis, erythroblast morphological abnormalities, and hypo-glycosylation of some red blood cell membrane proteins. Abnormalities in SEC23B, which encodes the homonymous cytoplasmic COPII (coat protein complex II) component, disturb the endoplasmic reticulum to Golgi trafficking and affect different glycosylation pathways. The most harmful complication of CDA II is the severe iron overload. Within our case series (28 CDA II patients), approximately 36% of them exhibit severe iron overload despite mild degree of anemia and slightly increased levels of ERFE (the only erythroid regulator of hepcidin suppression). Thus, we hypothesized a direct role of SEC23B loss-of-function in the pathomechanism of hepatic iron overload. We established a hepatic cell line, HuH7, stably silenced for SEC23B. In silenced cells, we observed significant alterations of the iron status, due to both the alteration in BMP/SMADs pathway effectors and a reduced capability to sense BMP6 stimulus. We demonstrated that the loss-of-function of SEC23B is responsible of the impairment in glycosylation of the membrane proteins involved in the activation of the BMP/SMADs pathway with subsequent hepcidin suppression. Most of these data were confirmed in another hepatic cell line, HepG2, stably silenced for SEC23B. Our findings suggested that the pathogenic mechanism of iron overload in CDA II is associated to both ineffective erythropoiesis and to a specific involvement of SEC23B pathogenic variants at hepatic level. Finally, we demonstrated the ability of SEC23B paralog, i.e., SEC23A, to rescue the hepcidin suppression, highlighting the functional overlap between the two SEC23 paralogs in human hepatic cells.