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The accumulation of pollutants in water is dangerous for the environment and human lives. Some of them are considered as persistent organic pollutants (POPs) that cannot be eliminated from wastewater effluent. Thus, many researchers have devoted their efforts to improving the existing technology or providing an alternative strategy to solve this environmental problem. One of the attractive materials for this purpose are metal-organic frameworks (MOFs) due to their superior high surface area, high porosity, and the tunable features of their structures and function. This review provides an up-to-date and comprehensive description of MOFs and their crucial role as adsorbent, catalyst, and membrane in wastewater treatment. This study also highlighted several strategies to improve their capability to remove pollutants from water effluent.

The transcription factor NRF2 is the major mediator of oxidative stress responses and is closely connected to therapy resistance in tumors harboring activating mutations in the NRF2 pathway. In melanoma, such mutations are rare, and it is unclear to what extent melanomas rely on NRF2. Here we show that NRF2 suppresses the activity of the melanocyte lineage marker MITF in melanoma, thereby reducing the expression of pigmentation markers. Intriguingly, we furthermore identified NRF2 as key regulator of immune-modulating genes, linking oxidative stress with the induction of cyclooxygenase 2 (COX2) in an ATF4-dependent manner. COX2 is critical for the secretion of prostaglandin E2 and was strongly induced by H2O2 or TNFα only in presence of NRF2. Induction of MITF and depletion of COX2 and PGE2 were also observed in NRF2-deleted melanoma cells in vivo. Furthermore, genes corresponding to the innate immune response such as RSAD2 and IFIH1 were strongly elevated in absence of NRF2 and coincided with immune evasion parameters in human melanoma datasets. Even in vitro, NRF2 activation or prostaglandin E2 supplementation blunted the induction of the innate immune response in melanoma cells. Transcriptome analyses from lung adenocarcinomas indicate that the observed link between NRF2 and the innate immune response is not restricted to melanoma.

The blackbody radiation left over from the Big Bang has been transformed by the expansion of the Universe into the nearly isotropic 2.73 K cosmic microwave background. Tiny inhomogeneities in the early Universe left their imprint on the microwave background in the form of small anisotropies in its temperature. These anisotropies contain information about basic cosmological parameters, particularly the total energy density and curvature of the Universe. Here we report the first images of resolved structure in the microwave background anisotropies over a significant part of the sky. Maps at four frequencies clearly distinguish the microwave background from foreground emission. We compute the angular power spectrum of the microwave background, and find a peak at Legendre multipole l peak = (197 ± 6), with an amplitude Δ T 200 = (69 ± 8) µK. This is consistent with that expected for cold dark matter models in a flat (euclidean) Universe, as favoured by standard inflationary models.

The Hippo signalling pathway and its central effector YAP regulate proliferation of cardiomyocytes and growth of the heart. Using genetic models in mice we show that the increased proliferation of embryonal and postnatal cardiomyocytes due to loss of the Hippo-signaling component SAV1 depends on the Myb-MuvB (MMB) complex. Similarly, proliferation of postnatal cardiomyocytes induced by constitutive active YAP requires MMB. Genome studies revealed that YAP and MMB regulate an overlapping set of cell cycle genes in cardiomyocytes. Protein-protein interaction studies in cell lines and with recombinant proteins showed that YAP binds directly to B-MYB, a subunit of MMB, in a manner dependent on the YAP WW domains and a PPXY motif in B-MYB. Disruption of the interaction by overexpression of the YAP binding domain of B-MYB strongly inhibits the proliferation of cardiomyocytes. Our results point to MMB as a critical downstream effector of YAP in the control of cardiomyocyte proliferation.

The EXperiment for Cryogenic Large-Aperture Intensity Mapping (EXCLAIM) is a cryogenic balloon-borne instrument that will survey galaxy and star formation history over cosmological timescales. Rather than identifying individual objects, EXCLAIM will be a pathfinder to demonstrate an intensity mapping approach, which measures the cumulative redshifted line emission. EXCLAIM will operate at 420–540 GHz with a spectral resolution R = 512 to measure the integrated CO and [CII] in redshift windows spanning 0 < z < 3.5 . CO and [CII] line emissions are key tracers of the gas phases in the interstellar medium involved in star formation processes. EXCLAIM will shed light on questions such as why the star formation rate declines at z < 2 , despite continued clustering of the dark matter. The instrument will employ an array of six superconducting integrated grating-analog spectrometers ( μ -Spec) coupled to microwave kinetic inductance detectors. Here we present an overview of the EXCLAIM instrument design and status.

We report on the status of an ongoing effort to develop arrays of horn-coupled, polarization-sensitive microwave kinetic inductance detectors (MKIDs) that are each sensitive to two spectral bands between 125 and 280 GHz. These multi-chroic MKID arrays are tailored for next-generation, large-detector-count experiments that are being designed to simultaneously characterize the polarization properties of both the cosmic microwave background and Galactic dust emission. We present our device design and describe laboratory-based measurement results from two 23-element prototype arrays. From dark measurements of our first engineering array, we demonstrated a multiplexing factor of 92, showed the resonators respond to bath temperature changes as expected, and found that the fabrication yield was 100%. From our first optically loaded array, we found the MKIDs respond to millimeter-wave pulses; additional optical characterization measurements are ongoing. We end by discussing our plans for scaling up this technology to kilo-pixel arrays over the next 2 years.

The South Pole Telescope (SPT) is a 10 m diameter, wide-field, offset Gregorian telescope with a 966 pixel, multicolor, millimeter-wave, bolometer camera. It is located at the Amundsen-Scott South Pole station in Antarctica. The design of the SPT emphasizes careful control of spillover and scattering, to minimize noise and false signals due to ground pickup. The key initial project is a large-area survey at wavelengths of 3, 2, and 1.3 mm, to detect clusters of galaxies via the Sunyaev-Zel’dovich effect and to measure the small-scale angular power spectrum of the cosmic microwave background (CMB). The data will be used to characterize the primordial matter power spectrum and to place constraints on the equation of state of dark energy. A second-generation camera will measure the polarization of the CMB, potentially leading to constraints on the neutrino mass and the energy scale of inflation.

The opportunistic human pathogen Staphylococcus aureus causes serious infectious diseases that range from superficial skin and soft tissue infections to necrotizing pneumonia and sepsis. While classically regarded as an extracellular pathogen, S. aureus is able to invade and survive within human cells. Host cell exit is associated with cell death, tissue destruction, and the spread of infection. The exact molecular mechanism employed by S. aureus to escape the host cell is still unclear. In this study, we performed a genome-wide small hairpin RNA (shRNA) screen and identified the calcium signaling pathway as being involved in intracellular infection. S. aureus induced a massive cytosolic Ca2+ increase in epithelial host cells after invasion and intracellular replication of the pathogen. This was paralleled by a decrease in endoplasmic reticulum Ca2+ concentration. Additionally, calcium ions from the extracellular space contributed to the cytosolic Ca2+ increase. As a consequence, we observed that the cytoplasmic Ca2+ rise led to an increase in mitochondrial Ca2+ concentration, the activation of calpains and caspases, and eventually to cell lysis of S. aureus-infected cells. Our study therefore suggests that intracellular S. aureus disturbs the host cell Ca2+ homeostasis and induces cytoplasmic Ca2+ overload, which results in both apoptotic and necrotic cell death in parallel or succession.IMPORTANCE Despite being regarded as an extracellular bacterium, the pathogen Staphylococcus aureus can invade and survive within human cells. The intracellular niche is considered a hideout from the host immune system and antibiotic treatment and allows bacterial proliferation. Subsequently, the intracellular bacterium induces host cell death, which may facilitate the spread of infection and tissue destruction. So far, host cell factors exploited by intracellular S. aureus to promote cell death are only poorly characterized. We performed a genome-wide screen and found the calcium signaling pathway to play a role in S. aureus invasion and cytotoxicity. The intracellular bacterium induces a cytoplasmic and mitochondrial Ca2+ overload, which results in host cell death. Thus, this study first showed how an intracellular bacterium perturbs the host cell Ca2+ homeostasis.

The objective of this study is to measure the effectiveness of GLЀH in enhancing ecological intelligence across eight indicators: environmental awareness, ecological knowledge, environmental concern, eco-friendly behavior, critical thinking about environmental impacts, ecological responsibility, sustainable lifestyle, and collaboration in environmental actions. The research employed an experimental method with a quantitative approach. All data were obtained through testing and analyzed using inferential statistical techniques, specifically R square, to determine the contribution of GLЀH to each individual indicator. Our general findings show a significant improvement in ecological intelligence following the GLЀH intervention. Moreover, we identified the specific contribution of GLЀH to each indicator: environmental awareness (48.3%), ecological knowledge (52.1%), environmental concern (70.5%), eco-friendly behavior (60.6%), critical thinking about environmental impacts (53.2%), ecological responsibility (69.1%), sustainable lifestyle (61%), and collaboration in environmental actions (65.4%). These results indicate that GLЀH contributes substantially to shaping students’ environmental awareness and attitudes in the school context.

In pancreatic ductal adenocarcinoma (PDAC), endogenous MYC is required for S-phase progression and escape from immune surveillance. Here we show that MYC in PDAC cells is needed for the recruitment of the PAF1c transcription elongation complex to RNA polymerase and that depletion of CTR9, a PAF1c subunit, enables long-term survival of PDAC-bearing mice. PAF1c is largely dispensable for normal proliferation and regulation of MYC target genes. Instead, PAF1c limits DNA damage associated with S-phase progression by being essential for the expression of long genes involved in replication and DNA repair. Surprisingly, the survival benefit conferred by CTR9 depletion is not due to DNA damage, but to T-cell activation and restoration of immune surveillance. This is because CTR9 depletion releases RNA polymerase and elongation factors from the body of long genes and promotes the transcription of short genes, including MHC class I genes. The data argue that functionally distinct gene sets compete for elongation factors and directly link MYC-driven S-phase progression to tumor immune evasion. MYC drives S-phase progression and immune invasion in pancreatic ductal adenocarcinoma (PDAC), but the underlying mechanisms are not fully understood. Here, the authors show that the transcription elongation complex PAF1c controls the competition of different gene sets for RNA polymerase and elongation factors to regulate these MYC-associated mechanisms in PDAC.