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This paper presents an overview for the Special Issue of Clean Technology and Environmental Policy journal (CTEP), and it includes accepted papers from: 5th South East European Conferences on Sustainable Development of Energy, Water and Environment Systems (SDEWES) held from May 22–26, 2022, in Vlore, Albania. 3rd Latin American Conferences on Sustainable Development of Energy, Water and Environment Systems (SDEWES) held from July 24–28, 2022, in Sao Paulo, Brazil. 17th Conferences on Sustainable Development of Energy, Water and Environment Systems (SDEWES) held from November 6–10, 2022, in Paphos, Cyprus. Considering CTEP's policy of high-quality research papers, guest editors have invited 35 research articles, presented at the SDEWES 2022 conference. After a vigorous review process, 13 papers have been accepted for publication in this special issue. All 13 accepted papers are briefly presented in this overview together with a wider view that presents research efforts within the SDEWES community published through previous SDEWES special issues. [ABSTRACT FROM AUTHOR]

Tuberculosis is a widespread disease all over the world. Early diagnosis plays a crucial role in the treatment of patients and can reduce the mortality rate. A new biosensor based on a binary photonic crystal is designed for the detection of mycobacterium tuberculosis bacteria in the blood. The structure air/(A/B)N/(Defect)/(A/B)N/air is employed, where A, B and N are the first and second layers and the number of periods, respectively. Layers A and B are chosen as GaAs and BaF2, respectively. The defect layer is the blood sample. The transfer matrix method (TMM) is utilized to simulate the structure. Some parameters, such as central wavelength, defect layer thickness and incident angle are optimized to maximize the sensitivity. The optimum sensitivity is found 3197.18 nm/RIU, which is extremely high when compared to the most recent papers published in this field. In addition, our sensor has a simple design, tunable fabrication and low cost and can be useful for the detection of many organisms that can exist in the blood. [ABSTRACT FROM AUTHOR]

Brazil's Atlantic Forest (BAF) is a highly fragmented, strategic environmental and socio-economic region that represents the fourth biodiversity hotspot while also producing many commodities that are exported globally. Human disturbance plays a pivotal role as a driver of BAF's soil dynamics and behaviors. The soils under Late Primary and Secondary Semideciduous Seasonal Forests (LPSF and LSSF) were characterized by high to moderate resilience, with improved chemical properties as human disturbance decreased. The Transitional Forest to Cerrado (TFC) had the worst soil conditions. Disturbed Primary and Secondary Semideciduous Seasonal Forests (DPSF and DSSF) represent a transitional stage between LPSF/LSSF and TFC. Accordingly, SOCs stocks increased from TFC << DPSF, DSSF < LPSF, LSSF. In BAF soils, to avoid unreliable data, SOCs measurements should be (i) conducted to at least 1 m soil depth and (ii) quantified with a CHN analyzer. Human disturbance strongly affected the positive feedback between vegetation succession, SOCs, and soil nutrition. Soil development decreased as human disturbance increased, thus negatively affecting SOCs. Soils in the BAF require a long time to recover after the end of human disturbance, thus suggesting that preservation strategies should be prioritized in remnant BAF fragments. [ABSTRACT FROM AUTHOR]

ATP-dependent chromatin remodeling SWI/SNF complexes exist in three subcomplexes: canonical BAF (cBAF), polybromo BAF (PBAF), and a newly described non-canonical BAF (ncBAF). While cBAF and PBAF regulate fates of multiple cell types, roles for ncBAF in hematopoietic stem cells (HSCs) have not been investigated. Motivated by recent discovery of disrupted expression of BRD9, an essential component of ncBAF, in multiple cancers, including clonal hematopoietic disorders, we evaluate here the role of BRD9 in normal and malignant HSCs. BRD9 loss enhances chromatin accessibility, promoting myeloid lineage skewing while impairing B cell development. BRD9 significantly colocalizes with CTCF, whose chromatin recruitment is augmented by BRD9 loss, leading to altered chromatin state and expression of myeloid-related genes within intact topologically associating domains. These data uncover ncBAF as critical for cell fate specification in HSCs via three-dimensional regulation of gene expression and illuminate roles for ncBAF in normal and malignant hematopoiesis. BRD9 is a core non-canonical BAF component. Here the authors show that BRD9 plays a pivotal role in regulating the disease-related cell fate of hematopoietic stem cells. Its loss promotes myeloid skewing while impairing B cell development by altering CTCF-mediated chromatin states. [ABSTRACT FROM AUTHOR]

Malignant rhabdoid tumor (MRT) is a highly malignant and often lethal childhood cancer. MRTs are genetically defined by bi-allelic inactivating mutations in SMARCB1, a member of the BRG1/BRM-associated factors (BAF) chromatin remodeling complex. Mutations in BAF complex members are common in human cancer, yet their contribution to tumorigenesis remains in many cases poorly understood. Here, we study derailed regulatory landscapes as a consequence of SMARCB1 loss in the context of MRT. Our multi-omics approach on patient-derived MRT organoids reveals a dramatic reshaping of the regulatory landscape upon SMARCB1 reconstitution. Chromosome conformation capture experiments subsequently reveal patient-specific looping of distal enhancer regions with the promoter of the MYC oncogene. This intertumoral heterogeneity in MYC enhancer utilization is also present in patient MRT tissues as shown by combined single-cell RNA-seq and ATAC-seq. We show that loss of SMARCB1 activates patient-specific epigenetic reprogramming underlying MRT tumorigenesis. The regulatory landscape of malignant rhabdoid tumor (MRT) due to SMARCB1 loss remains to be explored. Here, the authors perform multi-omics analysis using patient-derived MRT organoids and characterise the epigenetic reprogramming events underlying SMARCB1 loss. [ABSTRACT FROM AUTHOR]

We are living in the 'plasticene' era. Marine plastic pollution is a global problem, and increasing effort and funds are being invested towards identifying and implementing solutions. It is well accepted that the implemented solutions should take into account local specificities and culture, which requires the involvement and engagement of local decision-makers and key actors. This paper presents how the DeCyDe-4 method, which is based on a participatory decision-support concept, was implemented to develop community-based policy tools and action plans to combat marine litter. Through a presentation of the step-by-step implementation of the method at a 3-day workshop in the Paphos District of Cyprus, the DeCyDe-4 method is unfolded so as to showcase how a multi-disciplinary group of local stakeholders can co-create a Policy Tool, and identify and prioritize measures and solutions to marine litter. The case study shows that DeCyDe-4 can support a varied group of stakeholders to negotiate a complex environmental problem such as marine litter, and to make informed, unbiased decisions, through a process that encourages active participation and dialogue, so that opposite opinions are heard, consensus is reached and ownership of the solutions is achieved. [ABSTRACT FROM AUTHOR]

Gammaherpesviruses, including Kaposi sarcoma-associated herpesvirus (KSHV) and Epstein-Barr virus (EBV), are DNA viruses that are globally associated with human cancers and establish lifelong latency in the human population. Detection of gammaherpesviral infection by the cGAS-STING innate immune DNA-sensing pathway is critical for suppressing viral reactivation from latency, a process that promotes viral pathogenesis and transmission. We report that barrier-to-autointegration factor 1 (BAF)-mediated suppression of the cGAS-STING signaling pathway is necessary for reactivation of KSHV and EBV. We demonstrate a role for BAF in destabilizing cGAS expression and show that inhibiting BAF expression in latently infected, reactivating, or uninfected cells leads to increased type I interferon-mediated antiviral responses and decreased viral replication. Furthermore, BAF overexpression resulted in decreased cGAS expression at the protein level. These results establish BAF as a key regulator of the lifecycle of gammaherpesviruses and a potential target for treating viral infections and malignancies. Barrier-to-autointegration factor 1 (BAF) is a DNA binding protein involved in numerous pathways including transcriptional regulation, DNA damage response and nuclear assembly. Here, Broussard and colleagues characterise its role in gammaherpesvirus reactivation. [ABSTRACT FROM AUTHOR]

Although China has been the main manufacturer and consumer of phthalate esters (PAEs), human health ambient water quality criteria (AWQCs) have not been proposed for these chemicals. In this study, the distribution and bioaccumulation of six PAEs (dimethyl phthalate (DMP), diethyl phthalate (DEP), di-n-butyl phthalate (DBP), butyl benzyl phthalate (BBP), bis (2-ethylhexyl) phthalate (DEHP), and di-n-octyl phthalate (DnOP)) were investigated in 11 edible fish species collected from Poyang Lake, China. The results showed that the total concentrations of the six PAEs in the fish ranged between 118.63 and 819.84 μg/kg wet weight (mean of 327.50 ± 190.44 μg/kg). DMP, DEP, DBP, and DEHP were detected in all samples, of which DEHP and DBP were two of the most predominant phthalates, accounting for more than 90% of the total PAEs. The DEHP concentrations in fish with different habitat preferences were different, demersal species were significantly higher than pelagic species (p < 0.05). The mean natural logarithmic bioaccumulation factors (log BAFs) of PAEs increased with increasing lipophilicity of the substances, which yielded the following regression equation: log BAF (L/kg) = 0.103 log Kow + 2.158 (r2 = 0.940, p < 0.05, n = 4). Using this quantitative structure–activity relationship to calculate BAFs for the remaining undetected substances (BBP and DnOP) to derive AWQCs. According to the natural parameters, the human health AWQCs relating to PAE concentrations for water and fish consumption were derived as 9.4 × 103 (DMP), 5.0 × 102 (DEP), 4.2 × 101 (DBP), 1.1 (BBP), 8.6 × 10− 2 (DEHP), and 2.0 (DnOP) μg/L. Human health risk assessment indicated that the dietary intake of DEHP may exert a carcinogenic effect on residents of the Poyang Lake region. The results provide important input to assess the health risk posed by PAEs contaminated surface water. [ABSTRACT FROM AUTHOR]

BAF and PBAF are mammalian SWI/SNF family chromatin remodeling complexes that possess multiple histone/DNA-binding subunits and create nucleosome-depleted/free regions for transcription activation. Despite previous structural studies and recent advance of SWI/SNF family complexes, it remains incompletely understood how PBAF-nucleosome complex is organized. Here we determined structure of 13-subunit human PBAF in complex with acetylated nucleosome in ADP-BeF3-bound state. Four PBAF-specific subunits work together with nine BAF/PBAF-shared subunits to generate PBAF-specific modular organization, distinct from that of BAF at various regions. PBAF-nucleosome structure reveals six histone-binding domains and four DNA-binding domains/modules, the majority of which directly bind histone/DNA. This multivalent nucleosome-binding pattern, not observed in previous studies, suggests that PBAF may integrate comprehensive chromatin information to target genomic loci for function. Our study reveals molecular organization of subunits and histone/DNA-binding domains/modules in PBAF-nucleosome complex and provides structural insights into PBAF-mediated nucleosome association complimentary to the recently reported PBAF-nucleosome structure. BAF and PBAF are SWI/SNF family chromatin remodeling complexes that create nucleosome-depleted regions for transcription activation. Here the authors report the structure of a 13-subunit human PBAF in complex with acetylated nucleosome in ADP-BeF3-bound state that provides structural insights into PBAF-mediated nucleosome association. [ABSTRACT FROM AUTHOR]

With an incidence of ~1 in 800 births, Down syndrome (DS) is the most common chromosomal condition linked to intellectual disability worldwide. While the genetic basis of DS has been identified as a triplication of chromosome 21 (HSA21), the genes encoded from HSA21 that directly contribute to cognitive deficits remain incompletely understood. Here, we found that the HSA21-encoded chromatin effector, BRWD1, was upregulated in neurons derived from iPS cells from an individual with Down syndrome and brain of trisomic mice. We showed that selective copy number restoration of Brwd1 in trisomic animals rescued deficits in hippocampal LTP, cognition and gene expression. We demonstrated that Brwd1 tightly binds the BAF chromatin remodeling complex, and that increased Brwd1 expression promotes BAF genomic mistargeting. Importantly, Brwd1 renormalization rescued aberrant BAF localization, along with associated changes in chromatin accessibility and gene expression. These findings establish BRWD1 as a key epigenomic mediator of normal neurodevelopment and an important contributor to DS-related phenotypes. The molecular mechanisms underlying deficits in Down syndrome remain unclear. Here, the authors show that copy number restoration of a chromatin remodeler in trisomic mice is sufficient to rescue epigenomic, physiological and cognitive deficits. [ABSTRACT FROM AUTHOR]

Transposable elements (TEs) through evolutionary exaptation have become an integral part of the human genome, offering ample regulatory sequences and shaping chromatin 3D architecture. While the functional impacts of TE-derived sequences on early embryogenesis have been recognized, their roles in malignancy are only starting to emerge. Here we show that many TEs, especially the pluripotency-related human endogenous retrovirus H (HERVH), are abnormally activated in colorectal cancer (CRC) samples. Transcriptional upregulation of HERVH is associated with mutations of several tumor suppressors, particularly ARID1A. Knockout of ARID1A in CRC cells leads to increased transcription at several HERVH loci, which involves compensatory contribution by ARID1B. Suppression of HERVH in CRC cells and patient-derived organoids impairs tumor growth. Mechanistically, HERVH transcripts colocalize with nuclear BRD4 foci, modulating their dynamics and co-regulating many target genes. Altogether, we uncover a critical role for ARID1A in restraining HERVH, whose abnormal activation can promote tumorigenesis by stimulating BRD4-dependent transcription. Here the authors show mutation of the BAF chromatin remodeler subunit ARID1A results in an ARID1B-dependent upregulation of HERVH, an ERV required for the pluripotency regulatory network. These HERVH RNAs can partition into BRD4 foci, affecting BRD4-dependent transcription. Suppression of HERVH in colorectal cancer cells and patient-derived organoids impairs tumor growth. [ABSTRACT FROM AUTHOR]

Over millions of years, eukaryotes evolved from unicellular to multicellular organisms with increasingly complex genomes and sophisticated gene expression networks. Consequently, chromatin regulators evolved to support this increased complexity. The ATP-dependent chromatin remodelers of the SWI/SNF family are multiprotein complexes that modulate nucleosome positioning and appear under different configurations, which perform distinct functions. While the composition, architecture, and activity of these subclasses are well understood in a limited number of fungal and animal model organisms, the lack of comprehensive information in other eukaryotic organisms precludes the identification of a reliable evolutionary model of SWI/SNF complexes. Here, we performed a systematic analysis using 36 species from animal, fungal, and plant lineages to assess the conservation of known SWI/SNF subunits across eukaryotes. We identified evolutionary relationships that allowed us to propose the composition of a hypothetical ancestral SWI/SNF complex in the last eukaryotic common ancestor. This last common ancestor appears to have undergone several rounds of lineage-specific subunit gains and losses, shaping the current conformation of the known subclasses in animals and fungi. In addition, our results unravel a plant SWI/SNF complex, reminiscent of the animal BAF subclass, which incorporates a set of plant-specific subunits of still unknown function. The ancestral history of SWI/SNF subunits, responsible for nucleosome positioning, are explored in this work, revealing a plant SWI/SNF complex similar to the animal BAF subclass. [ABSTRACT FROM AUTHOR]

Single crystals of Ca1– хBaхF2 (x = 0.001–0.05 and 0.85–0.99) solid solutions have been grown by the Bridgman method, and their thermal conductivity has been measured in the range 50–300 K by an absolute steady-state axial heat flow technique. The thermal conductivity of all samples has been shown to decrease with increasing temperature. At 300 K, the lowest thermal conductivity of the samples with x ≤ 0.05 exceeds 6 W/(m K), and that of the samples with x ≥ 0.85 is a factor of 2 lower. [ABSTRACT FROM AUTHOR]

The process of epigenetic silencing, while fundamentally important, is not yet completely understood. Here we report a replenishable female mouse embryonic stem cell (mESC) system, Xmas, that allows rapid assessment of X chromosome inactivation (XCI), the epigenetic silencing mechanism of one of the two X chromosomes that enables dosage compensation in female mammals. Through a targeted genetic screen in differentiating Xmas mESCs, we reveal that the BAF complex is required to create nucleosome-depleted regions at promoters on the inactive X chromosome during the earliest stages of establishment of XCI. Without this action gene silencing fails. Xmas mESCs provide a tractable model for screen-based approaches that enable the discovery of unknown facets of the female-specific process of XCI and epigenetic silencing more broadly. Female embryonic stem cells (ESCs) are the ideal model to study X chromosome inactivation (XCI) establishment; however, these cells are challenging to keep in culture. Here the authors create fluorescent 'Xmas' reporter mice as a renewable source of ESCs and show nucleosome remodelers Smarcc1 and Smarca4 create a nucleosome-free promoter region prior to the establishment of silencing. [ABSTRACT FROM AUTHOR]

Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state while blocking terminal differentiation. Here, we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define the mSWI/SNF functional repertoire in FP-RMS. We find that SMARCA4 (encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes localize to sites of de novo histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes, which is recapitulated by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor. Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage with an aggressive subtype caused by translocations involving PAX3- /PAX7-FOXO1 chimeric transcription factors. Here the authors show that the BRG1-containing BAF complex is overexpressed and acts largely independently of the PAX3-FOXO1 chimera on chromatin to result in a myogenic differentiation blockade in this malignancy. [ABSTRACT FROM AUTHOR]

Subunit switches in the BAF chromatin remodeler are essential during development. ARID1B and its paralog ARID1A encode for mutually exclusive BAF subunits. De novo ARID1B haploinsufficient mutations cause neurodevelopmental disorders, including Coffin-Siris syndrome, which is characterized by neurological and craniofacial features. Here, we leveraged ARID1B+/− Coffin-Siris patient-derived iPSCs and modeled cranial neural crest cell (CNCC) formation. We discovered that ARID1B is active only during the first stage of this process, coinciding with neuroectoderm specification, where it is part of a lineage-specific BAF configuration (ARID1B-BAF). ARID1B-BAF regulates exit from pluripotency and lineage commitment by attenuating thousands of enhancers and genes of the NANOG and SOX2 networks. In iPSCs, these enhancers are maintained active by ARID1A-containing BAF. At the onset of differentiation, cells transition from ARID1A- to ARID1B-BAF, eliciting attenuation of the NANOG/SOX2 networks and triggering pluripotency exit. Coffin-Siris patient cells fail to perform the ARID1A/ARID1B switch, and maintain ARID1A-BAF at the pluripotency enhancers throughout all stages of CNCC formation. This leads to persistent NANOG/SOX2 activity which impairs CNCC formation. Despite showing the typical neural crest signature (TFAP2A/SOX9-positive), ARID1B-haploinsufficient CNCCs are also aberrantly NANOG-positive. These findings suggest a connection between ARID1B mutations, neuroectoderm specification and a pathogenic mechanism for Coffin-Siris syndrome. Mutations in the ARID1B subunit of the BAF chromatin remodeling complex are associated with the neurodevelopmental Coffin-Siris syndrome. Here the authors reveal that there is a transition from ARID1A-containing complexes to ARID1B during cranial neural crest cell differentiation that is impaired in Coffin-Siris patient-derived cells, which is important for exit from pluripotency. [ABSTRACT FROM AUTHOR]

We present far ultraviolet (FUV) observations of globular cluster NGC 4147 using three FUV filters, BaF 2 (F154W), sapphire (F169M), and silica (F172M) of Ultra-Violet Imaging Telescope (UVIT) on-board the AstroSat satellite. We confirmed the cluster membership of the UVIT observed sources using proper motions from Gaia data release 2 (GAIA DR2). We identified 37 blue horizontal branch stars (BHBs), one blue straggler star (BSS) and 15 variable stars using UV-optical color magnitude diagrams (CMDs). We find that all the FUV bright BHBs are second generation population stars. Using UV-optical CMDs, we identify two sub-populations, BHB1 and BHB2, among the UV-bright BHBs in the cluster with stars count ratio of 24:13 for BHB1 and BHB2. The effective temperatures ( T eff ) of BHB1 and BHB2 were derived using color-temperature relation of BaSTI-IAC zero-age horizontal branch (ZAHB). We found that BHB1 stars are more centrally concentrated than BHB2 stars. We also derive physical parameters of the detected FUV bright BSS by fitting younger age BaSTI-IAC isochrones on optical and UV-optical CMDs. [ABSTRACT FROM AUTHOR]

The structure of our Galaxy has been studied from ultraviolet (UV) star counts obtained with the Ultra-Violet Imaging Telescope (UVIT) on board the AstroSat satellite, in Far-UV (FUV) and Near-UV (NUV) bands. The F154W (BaF2) and N263M (NUVB4) filters were used in the FUV and NUV bands, respectively. The point sources are separated from the extra-galactic sources of UVIT observations using infrared (IR) color cut method. The observed UVIT star counts match well with the simulations obtained from the Besançon model of stellar population synthesis towards several Galactic directions. We also estimated the scale length and scale height of the thick disc and the scale height of the thin disc using the space density function and the exponential density law for the stars of intermediate galactic latitudes. The scale length of the thick disc ranges from 3.11 to 5.40 kpc whereas the scale height ranges from 530 ± 32 pc to 630 ± 29 pc. The scale height of the thin disc comes out to be in the range of 230 ± 20 pc to 330 ± 11 pc. [ABSTRACT FROM AUTHOR]

β-actin is a crucial component of several chromatin remodeling complexes that control chromatin structure and accessibility. The mammalian Brahma-associated factor (BAF) is one such complex that plays essential roles in development and differentiation by regulating the chromatin state of critical genes and opposing the repressive activity of polycomb repressive complexes (PRCs). While previous work has shown that β-actin loss can lead to extensive changes in gene expression and heterochromatin organization, it is not known if changes in β-actin levels can directly influence chromatin remodeling activities of BAF and polycomb proteins. Here we conduct a comprehensive genomic analysis of β-actin knockout mouse embryonic fibroblasts (MEFs) using ATAC-Seq, HiC-seq, RNA-Seq and ChIP-Seq of various epigenetic marks. We demonstrate that β-actin levels can induce changes in chromatin structure by affecting the complex interplay between chromatin remodelers such as BAF/BRG1 and EZH2. Our results show that changes in β-actin levels and associated chromatin remodeling activities can not only impact local chromatin accessibility but also induce reversible changes in 3D genome architecture. Our findings reveal that β-actin-dependent chromatin remodeling plays a role in shaping the chromatin landscape and influences the regulation of genes involved in development and differentiation. β-actin loss can affect gene expression and heterochromatin organization. Here the authors conduct a comprehensive genomic analysis of β-actin knockout mouse embryonic fibroblasts (MEFs) to investigate the impact of changes in β-actin levels on 3d genome architecture and chromatin remodeling activities of BAF and polycomb proteins. [ABSTRACT FROM AUTHOR]

The system xBa(PO3)2·(99 – x)(AlF3–BaF2–CaF2–MgF2–SrF2)–1NdF3, where x = 2, 5, 10, 15, 20, 30, and 40 mol %, is considered. The dependences of the thermal coefficient of linear expansion, Tg, Tx. Tx–Tg, HV, and K1C on the concentration of Ba(PO3)2 are determined. It is found that an increase in the concentration of Ba(PO3)2 with the uniform replacement of the fluoride component leads to a decrease in the thermal coefficient of linear expansion, an increase in the glass transition temperature and crystallization, and a broadening of the interval Tx–Tg. It is shown that an increase in Ba(PO3)2 in the glass leads to an increase in microhardness HV and fracture toughness K1C of the glasses. The main thermomechanical characteristics of the studied glasses are compared with those of their commercial analogs. [ABSTRACT FROM AUTHOR]

The transition from pluripotent to somatic states marks a critical event in mammalian development, but remains largely unresolved. Here we report the identification of SS18 as a regulator for pluripotent to somatic transition or PST by CRISPR-based whole genome screens. Mechanistically, SS18 forms microscopic condensates in nuclei through a C-terminal intrinsically disordered region (IDR) rich in tyrosine, which, once mutated, no longer form condensates nor rescue SS18−/− defect in PST. Yet, the IDR alone is not sufficient to rescue the defect even though it can form condensates indistinguishable from the wild type protein. We further show that its N-terminal 70aa is required for PST by interacting with the Brg/Brahma-associated factor (BAF) complex, and remains functional even swapped onto unrelated IDRs or even an artificial 24 tyrosine polypeptide. Finally, we show that SS18 mediates BAF assembly through phase separation to regulate PST. These studies suggest that SS18 plays a role in the pluripotent to somatic interface and undergoes liquid-liquid phase separation through a unique tyrosine-based mechanism. Emerging evidence suggests that exit from pluripotency is a regulated, rather than passive process. Here the authors identify a requirement for SS18-mediated Brg/Brahma-associated factors (BAF) chromatin remodeling complex assembly during exit from pluripotency, and that SS18 promotes BAF assembly through liquidliquid phase separation. [ABSTRACT FROM AUTHOR]

Cell type-specific enhancers are activated by coordinated actions of lineage-determining transcription factors (LDTFs) and chromatin regulators. The SWI/SNF chromatin remodeling complex BAF and the histone H3K4 methyltransferase MLL4 (KMT2D) are both implicated in enhancer activation. However, the interplay between BAF and MLL4 in enhancer activation remains unclear. Using adipogenesis as a model system, we identify BAF as the major SWI/SNF complex that colocalizes with MLL4 and LDTFs on active enhancers and is required for cell differentiation. In contrast, the promoter enriched SWI/SNF complex PBAF is dispensable for adipogenesis. By depleting BAF subunits SMARCA4 (BRG1) and SMARCB1 (SNF5) as well as MLL4 in cells, we show that BAF and MLL4 reciprocally regulate each other's binding on active enhancers before and during adipogenesis. By focusing on enhancer activation by the adipogenic pioneer transcription factor C/EBPβ without inducing cell differentiation, we provide direct evidence for an interdependent relationship between BAF and MLL4 in activating cell type-specific enhancers. Together, these findings reveal a positive feedback between BAF and MLL4 in promoting LDTF-dependent activation of cell type-specific enhancers. The SWI/SNF complex BAF and the histone H3K4 methyltransferase MLL4 (KMT2D) play critical roles in enhancer activation, however the interplay between them has remained unclear. Here the authors show that BAF and MLL4 are interdependent in promoting enhancer activation by lineage-determining transcription factors during adipogenesis. [ABSTRACT FROM AUTHOR]

We have prepared ErF3-doped glasses in the ZrF4–BaF2–LaF3–AlF3–NaF system containing chlorine ions substituted for fluorine ions. The crystallization behavior of the chlorine-substituted glasses has been studied at various BaCl2 and ErF3 concentrations. We have identified phases precipitating during heat treatment of the glasses and assessed the effect of chlorine substitution for fluoride on the optical absorption and IR luminescence in the glasses. The results demonstrate that chlorine substitution for fluorine causes the UV absorption edge of the glass to shift to longer wavelengths and produces an additional absorption in the visible spectral region. The formation of crystalline phases during heat treatment of the glasses leads to significant changes in the shape of the Er3+ luminescence bands at 0.98 and 1.55 μm. [ABSTRACT FROM AUTHOR]

Background: The double sampling method known as "big BAF sampling" has been advocated as a way to reduce sampling effort while still maintaining a reasonably precise estimate of volume. A well-known method for variance determination, Bruce's method, is customarily used because the volume estimator takes the form of a product of random variables. However, the genesis of Bruce's method is not known to most foresters who use the method in practice. Methods: We establish that the Taylor series approximation known as the Delta method provides a plausible explanation for the origins of Bruce's method. Simulations were conducted on two different tree populations to ascertain the similarities of the Delta method to the exact variance of a product. Additionally, two alternative estimators for the variance of individual tree volume-basal area ratios, which are part of the estimation process, were compared within the overall variance estimation procedure. Results: The simulation results demonstrate that Bruce's method provides a robust method for estimating the variance of inventories conducted with the big BAF method. The simulations also demonstrate that the variance of the mean volume-basal area ratios can be computed using either the usual sample variance of the mean or the ratio variance estimators with equal accuracy, which had not been shown previously for Big BAF sampling. Conclusions: A plausible explanation for the origins of Bruce's method has been set forth both historically and mathematically in the Delta Method. In most settings, there is evidently no practical difference between applying the exact variance of a product or the Delta method—either can be used. A caution is articulated concerning the aggregation of tree-wise attributes into point-wise summaries in order to test the correlation between the two as a possible indicator of the need for further covariance augmentation. [ABSTRACT FROM AUTHOR]

We report a study of upconversion luminescence in BaF2–HoF3 crystals in the visible spectral region under excitation to the 5I5 level of Ho3+ ions by laser radiation with a wavelength of 890 nm. For these excitation conditions, we propose mechanisms responsible for upconversion luminescence from the 5F3, 5S2(5F4) and 5F5 levels of Ho3+ ions. [ABSTRACT FROM AUTHOR]

We have studied luminescence and electron paramagnetic resonance (EPR) spectra of manganese- and europium-activated fluorozirconate glasses in the ZrF4–BaF2–LaF3–AlF3–NaF (ZBLAN) system and fluorohafnate glasses in the HfF4–BaF2–LaF3–AlF3–NaF (HBLAN) system in order to assess the oxidation state and spatial distribution of the activator ions. The manganese luminescence band has been shown to shift from the green (545 nm) to the red (610 nm) spectral region, and additional lines in the EPR spectrum of manganese have been observed to emerge in the EPR spectrum of manganese as a result of BaCl2 substitution for BaF2 in the ZBLAN glass. The ratio of the concentration of free activator ions to that of clustered ions has been estimated quantitatively. It has been shown that, at high doping levels, the manganese and europium ions in the glasses are predominantly clustered, and only a small part of them are present as isolated ions. [ABSTRACT FROM AUTHOR]

We have prepared glasses in the ZrF4–BaF2–LaF3–AlF3–NaF (ZBLAN) and HfF4–BaF2–LaF3–AlF3–NaF (HBLAN) systems in which fluorine anions are partially replaced by chlorine and bromine anions. Structural changes in the chlorine-substituted glasses have been investigated by Raman spectroscopy and their crystallization behavior has been studied by differential thermal analysis and X-ray diffraction. The results demonstrate a characteristic decrease in glass transition temperature (Tg) and the precipitation of fine-particle crystalline chloride and bromide phases in a temperature range well below the crystallization temperature (Tx) of the fluoride analogues. We have identified phases that crystallize during heat treatment of the glasses at various temperatures. [ABSTRACT FROM AUTHOR]

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Background: To explore the effects of topographical modification of titanium substrates at submicron level by oxalic acid treatment on bone quality and quantity around dental implants in rabbit tibiae. Methods: A total of 60 blasted CP-grade IV titanium dental implants were used. Twenty-eight control implant surfaces were treated with a mixture of HCl/H2SO4, whereas 28 other test implant surfaces were treated with oxalic acid following HCl/H2SO4 treatment. Two randomly selected sets of control or test implants were placed in randomly selected proximal tibiae of 14 female Japanese white rabbits. Euthanasia was performed 4 and 8 weeks post-implant placement. Bone to implant contact (BIC), bone area fraction (BAF), ratios of mature and immature bone to total bone, and the amount and types of collagen fibers were evaluated quantitatively. Two control and two test implants were used to analyze surface characteristics. Results: Treatment by oxalic acid significantly decreased Sa and increased Ra of test implant surfaces. BIC in test implants was increased without alteration of BAF and collagen contents at 4 and 8 weeks after implant placement when compared with control implants. The ratios of immature and mature bone to total bone differed significantly between groups at 4 weeks post-implantation. Treatment by oxalic acid increased type I collagen and decreased type III collagen in bone matrices around test implants when compared with control implants at 8 weeks after implant placement. The effects of topographical changes of implant surfaces induced by oxalic acid on BAF, mature bone, collagen contents, and type I collagen were significantly promoted with decreased immature bone formation and type III collagen in the later 4 weeks post-implantation. Conclusions: Treatment of implant surfaces with oxalic acid rapidly increases osseointegration from the early stages after implantation. Moreover, submicron topographical changes of dental implants induced by oxalic acid improve bone quality based on bone maturation and increased production of type I collagen surrounding dental implants in the late stage after implant placement. [ABSTRACT FROM AUTHOR]

Genomic studies performed in cancer patients and tumor-derived cell lines have identified a high frequency of alterations in components of the mammalian switch/sucrose non-fermentable (mSWI/SNF or BAF) chromatin remodeling complex, including its core catalytic subunit, SMARCA4. Cells exhibiting loss of SMARCA4 rely on its paralog, SMARCA2, making SMARCA2 an attractive therapeutic target. Here we report the genomic profiling of solid tumors from 131,668 cancer patients, identifying 9434 patients with one or more SMARCA4 gene alterations. Homozygous SMARCA4 mutations were highly prevalent in certain tumor types, notably non-small cell lung cancer (NSCLC), and associated with reduced survival. The large sample size revealed previously uncharacterized hotspot missense mutations within the SMARCA4 helicase domain. Functional characterization of these mutations demonstrated markedly reduced remodeling activity. Surprisingly, a few SMARCA4 missense variants partially or fully rescued paralog dependency, underscoring that careful selection criteria must be employed to identify patients with inactivating, homozygous SMARCA4 missense mutations who may benefit from SMARCA2-targeted therapy. SMARCA4 is the core catalytic subunit of the mammalian SWI/SNF complex and is known to be mutated in many cancers. Here, the authors detect more than 10,000 SMARCA4 variants across different cancer subtypes and find hotspot mutations throughout the helicase domain, which reduce remodeling activity. [ABSTRACT FROM AUTHOR]