Solar Furnace: Heliostat and Concentrator Design

In recent decades, solar energy has been shown as a viable, clean, and abundant alternative to fossil fuels. Many methods of solar energy collection are being researched, with solar thermal electrochemistry being one of the most promising. Solar thermal electrochemistry uses sunlight to heat a furnace to temperatures nearing 2000 K. At these temperatures, metallic oxides can be decomposed to metals and oxygen with minimal electrical work. Achieving these high temperatures requires a solar furnace that consists of a heliostat to track and reflect the sun’s rays into a concentrator, which then focuses the sunlight to a single point in a solar thermal chemical reactor. A system of louvers regulates the amount of sunlight entering the system. Our research focuses on the design and development of the solar furnace components; specifically, the design and construction of the heliostat structure, the heliostat control system, and the concentrator

TRAIL promotes membrane blebbing, detachment and migration of cells displaying a dysfunctional intrinsic pathway of apoptosis

Recently, tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL/Apo2L) has been shown to be a potential candidate for cancer therapy. TRAIL induces apoptosis in various cancer cells but not in normal tissues. Here we show that HCT116 and SW480 cells with a deficient mitochondrial apoptotic pathway were resistant to TRAIL-induced apoptosis, whereas HCT116 and SW480 cells with a functional mitochondrial apoptotic pathway underwent apoptosis upon exposure to TRAIL. Surprisingly, TRAIL induced phenotypic changes in cells with a dysfunctional mitochondrial apoptotic pathway, including membrane blebbing and a transient loss of adhesion properties to the substratum. Accordingly, TRAIL stimulated the ability of these cells to migrate. This behavior was the consequence of a transient TRAIL-induced ROCK1 cleavage. In addition, we report that Bax-deficient HCT116 cells exposed to TRAIL for a prolonged period lost their sensitivity to TRAIL as a result of downregulation of TRAIL receptor expression, and became resistant to combination of TRAIL and other drugs such as MG-132 and bortezomib. These findings may have important consequences for TRAIL anti-cancer therap

Thousands of cold-water coral mounds along the Moroccan Atlantic continental margin : distribution and morphometry

Coral mounds formed by framework-forming cold-water corals pierce the seabed along most continental margins of the Atlantic Ocean and new sites are continuously being discovered. Here, we describe an extremely high accumulation of coral mounds at the NW Moroccan Atlantic margin between 35 degrees N and 35.5 degrees N. Within an area of only 1440 km(2), > 3400 mounds were found exposed at the seabed. The coral mounds are nowadays characterized by an almost complete lack of living cold-water corals. In addition, numerous buried mounds were identified in hydroacoustic sub-bottom profiles, and are estimated to be similar to 3.7 times more frequent than the exposed mounds. Consequently, a total of similar to 16,000 buried and exposed mounds is estimated for the entire study area. The exposed mounds are rather small with a mean height of 18 m and show a conspicuous arrangement in two slope-parallel belts that centre in water depths between 720 and 870 m and 890-980 m, respectively, putting them among the deepest mound occurrences discovered so far in the Atlantic. The mostly elongated mounds largely stretch downslope pointing to a significant influence of internal waves in the mound formation process. Moreover, based on their average dimensions, the entire coral mound volume can be estimated as 1.3 km(3), which means the mounds store a considerable amount of coral carbonate highlighting their potentially important role as regional carbonate factories. In combination with further occurrences of coral mounds along the Moroccan margin, both in the Mediterranean and in the Atlantic Ocean, these new findings underline Morocco's role as a hotspot for the occurrence of cold-water coral mounds

Biological activity of ectodysplasin A is conditioned by its collagen and heparan sulfate proteoglycan-binding domains.

Mutations in the TNF family ligand EDA1 cause X-linked hypohidrotic ectodermal dysplasia (XLHED), a condition characterized by defective development of skin appendages. The EDA1 protein displays a proteolytic processing site responsible for its conversion to a soluble form, a collagen domain, and a trimeric TNF homology domain (THD) that binds the receptor EDAR. In-frame deletions in the collagen domain reduced the thermal stability of EDA1. Removal of the collagen domain decreased its activity about 100-fold, as measured with natural and engineered EDA1-responsive cell lines. The collagen domain could be functionally replaced by multimerization domains or by cross-linking antibodies, suggesting that it functions as an oligomerization unit. Surprisingly, mature soluble EDA1 containing the collagen domain was poorly active when administered in newborn, EDA-deficient (Tabby) mice. This was due to a short stretch of basic amino acids located at the N terminus of the collagen domain that confers EDA1 with proteoglycan binding ability. In contrast to wild-type EDA1, EDA1 with mutations in this basic sequence was a potent inducer of tail hair development in vivo. Thus, the collagen domain activates EDA1 by multimerization, whereas the proteoglycan-binding domain may restrict the distribution of endogeneous EDA1 in vivo

Malt1 protease inactivation efficiently dampens immune responses but causes spontaneous autoimmunity.

The protease activity of the paracaspase Malt1 has recently gained interest as a drug target for immunomodulation and the treatment of diffuse large B-cell lymphomas. To address the consequences of Malt1 protease inactivation on the immune response in vivo, we generated knock-in mice expressing a catalytically inactive C472A mutant of Malt1 that conserves its scaffold function. Like Malt1-deficient mice, knock-in mice had strong defects in the activation of lymphocytes, NK and dendritic cells, and the development of B1 and marginal zone B cells and were completely protected against the induction of autoimmune encephalomyelitis. Malt1 inactivation also protected the mice from experimental induction of colitis. However, Malt1 knock-in mice but not Malt1-deficient mice spontaneously developed signs of autoimmune gastritis that correlated with an absence of Treg cells, an accumulation of T cells with an activated phenotype and high serum levels of IgE and IgG1. Thus, removal of the enzymatic activity of Malt1 efficiently dampens the immune response, but favors autoimmunity through impaired Treg development, which could be relevant for therapeutic Malt1-targeting strategies

Generation and characterization of function-blocking anti-ectodysplasin A (EDA) monoclonal antibodies that induce ectodermal dysplasia.

Development of ectodermal appendages, such as hair, teeth, sweat glands, sebaceous glands, and mammary glands, requires the action of the TNF family ligand ectodysplasin A (EDA). Mutations of the X-linked EDA gene cause reduction or absence of many ectodermal appendages and have been identified as a cause of ectodermal dysplasia in humans, mice, dogs, and cattle. We have generated blocking antibodies, raised in Eda-deficient mice, against the conserved, receptor-binding domain of EDA. These antibodies recognize epitopes overlapping the receptor-binding site and prevent EDA from binding and activating EDAR at close to stoichiometric ratios in in vitro binding and activity assays. The antibodies block EDA1 and EDA2 of both mammalian and avian origin and, in vivo, suppress the ability of recombinant Fc-EDA1 to rescue ectodermal dysplasia in Eda-deficient Tabby mice. Moreover, administration of EDA blocking antibodies to pregnant wild type mice induced in developing wild type fetuses a marked and permanent ectodermal dysplasia. These function-blocking anti-EDA antibodies with wide cross-species reactivity will enable study of the developmental and postdevelopmental roles of EDA in a variety of organisms and open the route to therapeutic intervention in conditions in which EDA may be implicated

FRAUD ONLINE

E-fraud involves fraudulent online payments and e-commerce sites, soliciting personal data or cheating on virtual currency. In recent years, a new type of criminal e-transaction has been identified in Latvia - illegal access to bank accounts and fraud, which tends to Smart-ID users. Criminals are coming up with new ways to obtain money illegally. Often these crimes are transnational in nature, making it difficult for victims to return the money lost. Funds are transferred to payment systems such as cryptocurrencies, which makes it very difficult to track their progress. Police statistics show that hundreds of Latvians suffer from various forms of Internet fraud every year. However, it must be acknowledged that this is largely due to people's credulity and the lack of cyber hygiene in society

STING activation of tumor endothelial cells initiates spontaneous and therapeutic antitumor immunity.

Spontaneous CD8 T-cell responses occur in growing tumors but are usually poorly effective. Understanding the molecular and cellular mechanisms that drive these responses is of major interest as they could be exploited to generate a more efficacious antitumor immunity. As such, stimulator of IFN genes (STING), an adaptor molecule involved in cytosolic DNA sensing, is required for the induction of antitumor CD8 T responses in mouse models of cancer. Here, we find that enforced activation of STING by intratumoral injection of cyclic dinucleotide GMP-AMP (cGAMP), potently enhanced antitumor CD8 T responses leading to growth control of injected and contralateral tumors in mouse models of melanoma and colon cancer. The ability of cGAMP to trigger antitumor immunity was further enhanced by the blockade of both PD1 and CTLA4. The STING-dependent antitumor immunity, either induced spontaneously in growing tumors or induced by intratumoral cGAMP injection was dependent on type I IFNs produced in the tumor microenvironment. In response to cGAMP injection, both in the mouse melanoma model and an ex vivo model of cultured human melanoma explants, the principal source of type I IFN was not dendritic cells, but instead endothelial cells. Similarly, endothelial cells but not dendritic cells were found to be the principal source of spontaneously induced type I IFNs in growing tumors. These data identify an unexpected role of the tumor vasculature in the initiation of CD8 T-cell antitumor immunity and demonstrate that tumor endothelial cells can be targeted for immunotherapy of melanoma