Protective role of ErbB3 signaling in myeloid cells during adaptation to cardiac pressure overload.

BACKGROUND: Myeloid cells play an important role in a wide variety of cardiovascular disorders, including both ischemic and non-ischemic cardiomyopathies. Neuregulin-1 (NRG-1)/ErbB signaling has recently emerged as an important factor contributing to the control of inflammatory activation of myeloid cells after an ischemic injury. However, the role of ErbB signaling in myeloid cells in non-ischemic cardiomyopathy is not fully understood. This study investigated the role of ErbB3 receptors in the regulation of early adaptive response using a mouse model of transverse aortic constriction (TAC) for non-ischemic cardiomyopathy. METHODS AND RESULTS: TAC surgery was performed in groups of age- and sex-matched myeloid cell-specific ErbB3-deficient mice (ErbB3MyeKO) and control animals (ErbB3MyeWT). The number of cardiac CD45 immune cells, CD11b myeloid cells, Ly6G neutrophils, and Ly6C monocytes was determined using flow cytometric analysis. Five days after TAC, survival was dramatically reduced in male but not female ErbB3MyeKO mice or control animals. The examination of lung weight to body weight ratio suggested that acute pulmonary edema was present in ErbB3MyeKO male mice after TAC. To determine the cellular and molecular mechanisms involved in the increased mortality in ErbB3MyeKO male mice, cardiac cell populations were examined at day 3 post-TAC using flow cytometry. Myeloid cells accumulated in control but not in ErbB3MyeKO male mouse hearts. This was accompanied by increased proliferation of Sca-1 positive non-immune cells (endothelial cells and fibroblasts) in control but not ErbB3MyeKO male mice. No significant differences in intramyocardial accumulation of myeloid cells or proliferation of Sca-1 cells were found between the groups of ErbB3MyeKO and ErbB3MyeWT female mice. An antibody-based protein array analysis revealed that IGF-1 expression was significantly downregulated only in ErbB3MyeKO mice hearts compared to control animals after TAC. CONCLUSION: Our data demonstrate the crucial role of myeloid cell-specific ErbB3 signaling in the cardiac accumulation of myeloid cells, which contributes to the activation of cardiac endothelial cells and fibroblasts and development of an early adaptive response to cardiac pressure overload in male mice.

Single-Cell RNA Sequencing Analysis Reveals a Crucial Role for CTHRC1 (Collagen Triple Helix Repeat Containing 1) Cardiac Fibroblasts After Myocardial Infarction.

BACKGROUND: Cardiac fibroblasts (CFs) have a central role in the ventricular remodeling process associated with different types of fibrosis. Recent studies have shown that fibroblasts do not respond homogeneously to heart injury. Because of the limited set of bona fide fibroblast markers, a proper characterization of fibroblast population heterogeneity in response to cardiac damage is lacking. The purpose of this study was to define CF heterogeneity during ventricular remodeling and the underlying mechanisms that regulate CF function. METHODS: Collagen1α1-GFP (green fluorescent protein)-positive CFs were characterized after myocardial infarction (MI) by single-cell and bulk RNA sequencing, assay for transposase-accessible chromatin sequencing, and functional assays. Swine and patient samples were studied using bulk RNA sequencing. RESULTS: We identified and characterized a unique CF subpopulation that emerges after MI in mice. These activated fibroblasts exhibit a clear profibrotic signature, express high levels of Cthrc1 (collagen triple helix repeat containing 1), and localize into the scar. Noncanonical transforming growth factor-ß signaling and different transcription factors including SOX9 are important regulators mediating their response to cardiac injury. Absence of CTHRC1 results in pronounced lethality attributable to ventricular rupture. A population of CFs with a similar transcriptome was identified in a swine model of MI and in heart tissue from patients with MI and dilated cardiomyopathy. CONCLUSIONS: We report CF heterogeneity and their dynamics during the course of MI and redefine the CFs that respond to cardiac injury and participate in myocardial remodeling. Our study identifies CTHRC1 as a novel regulator of the healing scar process and a target for future translational studies.

Forest gaps influence fungal community assembly in a weeping cypress forest.

The forest gap crucially influences forest environments, but its effects on local fungal community assembly are not fully understood. In this study, the fungal community in a weeping cypress forest was investigated as a function of forest gap locations based on forest clearing, using amplicon sequencing of the ITS2 region. The results showed that the fungal community significantly varied with the variations in soil properties related to gap location. Deterministic processes played pivotal roles in fungal community assembly, which was mainly driven by the temperature, moisture, available nitrogen, and microbial carbon in soil. Beta diversity of the fungal community increased from the gap center to the closed canopy. The relative abundances of dominant orders such as Microascales, Sordariales, and Chaetothyriales regularly varied as a function of gap location, and they were potential indicators for different gap locations. Based on network analysis, gap locations caused distinct co-occurrence patterns of fungal communities. This study shed light on the roles of forest gaps in the assembly of local fungal communities and provided additional strategies to manage forest ecosystems.

Cardioprotective Role of Tumor Necrosis Factor Receptor-Associated Factor 2 by Suppressing Apoptosis and Necroptosis.

BACKGROUND: Programmed cell death, including apoptosis, mitochondria-mediated necrosis, and necroptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and heart failure progression. Whereas apoptosis and mitochondria-mediated necrosis signaling is well established, the regulatory mechanisms of necroptosis and its significance in the pathogenesis of heart failure remain elusive. METHODS: We examined the role of tumor necrosis factor receptor-associated factor 2 (Traf2) in regulating myocardial necroptosis and remodeling using genetic mouse models. We also performed molecular and cellular biology studies to elucidate the mechanisms by which Traf2 regulates necroptosis signaling. RESULTS: We identified a critical role for Traf2 in myocardial survival and homeostasis by suppressing necroptosis. Cardiac-specific deletion of Traf2 in mice triggered necroptotic cardiac cell death, pathological remodeling, and heart failure. Plasma tumor necrosis factor α level was significantly elevated in Traf2-deficient mice, and genetic ablation of TNFR1 largely abrogated pathological cardiac remodeling and dysfunction associated with Traf2 deletion. Mechanistically, Traf2 critically regulates receptor-interacting proteins 1 and 3 and mixed lineage kinase domain-like protein necroptotic signaling with the adaptor protein tumor necrosis factor receptor-associated protein with death domain as an upstream regulator and transforming growth factor ß-activated kinase 1 as a downstream effector. It is important to note that genetic deletion of RIP3 largely rescued the cardiac phenotype triggered by Traf2 deletion, validating a critical role of necroptosis in regulating pathological remodeling and heart failure propensity. CONCLUSIONS: These results identify an important Traf2-mediated, NFκB-independent, prosurvival pathway in the heart by suppressing necroptotic signaling, which may serve as a new therapeutic target for pathological remodeling and heart failure.

Neural development is dependent on the function of specificity protein 2 in cell cycle progression.

Faithful progression through the cell cycle is crucial to the maintenance and developmental potential of stem cells. Here, we demonstrate that neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in two temporally and spatially distinct progenitor domains. Differential conditional deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal olfactory bulb progenitors disrupted transitions through G1, G2 and M phases, whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified by deletion of Sp2 using mosaic analysis with double markers, which clearly established that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly, conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis in the embryonic and postnatal brain.

Interindividual differences of dietary fat-inducible Mest in white adipose tissue of C57BL/6J mice are not heritable.

OBJECTIVE: Differences in white adipose tissue (WAT) expression of mesoderm-specific transcript (Mest) in C57BL6/J mice fed a high-fat diet (HFD) are concomitant with and predictive for the development of obesity. However, the basis for differences in WAT Mest among mice is unknown. This study investigated whether HFD-inducible WAT Mest, as well as susceptibility to obesity, is transmissible from parents to offspring. METHODS: WAT biopsies of mice fed an HFD for 2 weeks identified parents with low and high WAT Mest for breeding. Obesity phenotypes, WAT Mest, hepatic gene expression, and serum metabolites were determined in offspring fed an HFD for 2 weeks. RESULTS: Offspring showed no heritability of obesity or WAT Mest phenotypes from parents but did show hepatic and serum metabolite changes consistent with their WAT Mest. Importantly, retired male breeders showed WAT Mest expression congruent with initial WAT biopsies even though HFD exposure occurred early in life. CONCLUSIONS: Disparity of HFD-induced Mest in mice is not heritable but, rather, is reestablished during each generation and remains fixed from an early age to adulthood. Short-term HFD feeding reveals variation of WAT Mest expression within isogenic mice that is positively associated with the development of obesity.

Skin-inspired, sensory robots for electronic implants.

Drawing inspiration from cohesive integration of skeletal muscles and sensory skins in vertebrate animals, we present a design strategy of soft robots, primarily consisting of an electronic skin (e-skin) and an artificial muscle. These robots integrate multifunctional sensing and on-demand actuation into a biocompatible platform using an in-situ solution-based method. They feature biomimetic designs that enable adaptive motions and stress-free contact with tissues, supported by a battery-free wireless module for untethered operation. Demonstrations range from a robotic cuff for detecting blood pressure, to a robotic gripper for tracking bladder volume, an ingestible robot for pH sensing and on-site drug delivery, and a robotic patch for quantifying cardiac function and delivering electrotherapy, highlighting the application versatilities and potentials of the bio-inspired soft robots. Our designs establish a universal strategy with a broad range of sensing and responsive materials, to form integrated soft robots for medical technology and beyond.

[Effects of target tree management of Pinus massoniana plantation on soil nematode community structure at different soil depths]. / ç›®æ ‡æ ‘ç»è¥å¯¹é©¬å°¾æ¾äººå·¥æž—ä¸åŒåœŸå±‚æ·±åº¦åœŸå£¤çº¿è™«ç¾¤è½ç»“æž„çš„å½±å“.

To understand soil nematode community structure at different soil depths and its responses to target tree management, we collected soil samples (0-10, 10-20, and 20-50 cm) and litter samples from the target tree management plots and control plots of Pinus massoniana plantation and analyzed community structure, soil environmental factors, and their relationship. The results showed that target tree management increased the abundance of soil nematodes, with the most significant effect at a depth of 0-10 cm. The highest abundance of herbivores was found in the target tree management treatment, while that of bacterivores was found in the control. Compared with the control, Shannon diversity index, richness index, maturity index of nematodes at 10-20 cm soil layer and Shannon diversity index at 20-50 cm soil layer of target trees were significantly improved. According to the results of Pearson correlation and redundancy analysis, soil pH, total phosphorus, available phosphorus, total potassium, and available potassium were the main environmental factors affecting community structure and composition of soil nematodes. In general, target tree management was conducive to the survival and development of soil nematodes and promoted the sustainable development of P. massoniana plantations.

ZipperCells Exhibit Enhanced Accumulation and Retention at the Site of Myocardial Infarction.

There has been extensive interest in cellular therapies for the treatment of myocardial infarction, but bottlenecks concerning cellular accumulation and retention remain. Here, a novel system of in situ crosslinking mesenchymal stem cells (MSCs) for the formation of a living depot at the infarct site is reported. Bone marrow-derived mesenchymal stem cells that are surface decorated with heterodimerizing leucine zippers, termed ZipperCells, are engineered. When delivered intravenously in sequential doses, it is demonstrated that ZipperCells can migrate to the infarct site, crosslink, and show ≈500% enhanced accumulation and ≈600% improvement in prolonged retention at 10 days after injection compared to unmodified MSCs. This study introduces an advanced approach to creating noninvasive therapeutics depots using cellular crosslinking and provides the framework for future scaffold-free delivery methods for cardiac repair.

Immunoglobulin G inhibits glucocorticoid-induced osteoporosis through occupation of FcγRI.

Glucocorticoid-induced osteoporosis (GIOP) is a severe and common complication of long-term usage of glucocorticoids (GCs) and lacks of efficient therapy. Here, we investigated the mechanism of anti-inflammation effect and osteoclastogenesis side effect of GCs and immunoglobulin G (IgG) treatment against GIOP. GCs inhibited SLE IgG-induced inflammation, while IgG inhibited GCs-induced osteoclastogenesis. FcγRI and glucocorticoid receptor (GR) were found directly interacted with each other. GCs and IgG could reduce the expression of FcγRI on macrophages. The deficiency of FcγRI affected osteoclastogenesis by GCs and systemic lupus erythematosus (SLE) IgG-induced inflammation. Also, IgG efficiently reduced GIOP in mice. These data showed that GCs could induce osteoporosis and inhibit IgG-induced inflammation through FcγRI while IgG efficiently suppressed osteoporosis induced by GCs through FcγRI. Hence, our findings may help in developing a feasible therapeutic strategy against osteoporosis, such as GIOP.

Skin-inspired, sensory robots for electronic implants.

Living organisms with motor and sensor units integrated seamlessly demonstrate effective adaptation to dynamically changing environments. Drawing inspiration from cohesive integration of skeletal muscles and sensory skins in these organisms, we present a design strategy of soft robots, primarily consisting of an electronic skin (e-skin) and an artificial muscle, that naturally couples multifunctional sensing and on-demand actuation in a biocompatible platform. We introduce an in situ solution-based method to create an e-skin layer with diverse sensing materials (e.g., silver nanowires, reduced graphene oxide, MXene, and conductive polymers) incorporated within a polymer matrix (e.g., polyimide), imitating complex skin receptors to perceive various stimuli. Biomimicry designs (e.g., starfish and chiral seedpods) of the robots enable various motions (e.g., bending, expanding, and twisting) on demand and realize good fixation and stress-free contact with tissues. Furthermore, integration of a battery-free wireless module into these robots enables operation and communication without tethering, thus enhancing the safety and biocompatibility as minimally invasive implants. Demonstrations range from a robotic cuff encircling a blood vessel for detecting blood pressure, to a robotic gripper holding onto a bladder for tracking bladder volume, an ingestible robot residing inside stomach for pH sensing and on-site drug delivery, and a robotic patch wrapping onto a beating heart for quantifying cardiac contractility, temperature and applying cardiac pacing, highlighting the application versatilities and potentials of the nature-inspired soft robots. Our designs establish a universal strategy with a broad range of sensing and responsive materials, to form integrated soft robots for medical technology and beyond.

TAB2 deficiency induces dilated cardiomyopathy by promoting RIPK1-dependent apoptosis and necroptosis.

Mutations in TGF-ß-activated kinase 1 binding protein 2 (TAB2) have been implicated in the pathogenesis of dilated cardiomyopathy and/or congenital heart disease in humans, but the underlying mechanisms are currently unknown. Here, we identified an indispensable role for TAB2 in regulating myocardial homeostasis and remodeling by suppressing receptor-interacting protein kinase 1 (RIPK1) activation and RIPK1-dependent apoptosis and necroptosis. Cardiomyocyte-specific deletion of Tab2 in mice triggered dilated cardiomyopathy with massive apoptotic and necroptotic cell death. Moreover, Tab2-deficient mice were also predisposed to myocardial injury and adverse remodeling after pathological stress. In cardiomyocytes, deletion of TAB2 but not its close homolog TAB3 promoted TNF-α-induced apoptosis and necroptosis, which was rescued by forced activation of TAK1 or inhibition of RIPK1 kinase activity. Mechanistically, TAB2 critically mediates RIPK1 phosphorylation at Ser321 via a TAK1-dependent mechanism, which prevents RIPK1 kinase activation and the formation of RIPK1-FADD-caspase-8 apoptotic complex or RIPK1-RIPK3 necroptotic complex. Strikingly, genetic inactivation of RIPK1 with Ripk1-K45A knockin effectively rescued cardiac remodeling and dysfunction in Tab2-deficient mice. Together, these data demonstrated that TAB2 is a key regulator of myocardial homeostasis and remodeling by suppressing RIPK1-dependent apoptosis and necroptosis. Our results also suggest that targeting RIPK1-mediated cell death signaling may represent a promising therapeutic strategy for TAB2 deficiency-induced dilated cardiomyopathy.

3D morphable systems via deterministic microfolding for vibrational sensing, robotic implants, and reconfigurable telecommunication.

DNA and proteins fold in three dimensions (3D) to enable functions that sustain life. Emulation of such folding schemes for functional materials can unleash enormous potential in advancing a wide range of technologies, especially in robotics, medicine, and telecommunication. Here, we report a microfolding strategy that enables formation of 3D morphable microelectronic systems integrated with various functional materials, including monocrystalline silicon, metallic nanomembranes, and polymers. By predesigning folding hosts and configuring folding pathways, 3D microelectronic systems in freestanding forms can transform across various complex configurations with modulated functionalities. Nearly all transitional states of 3D microelectronic systems achieved via the microfolding assembly can be easily accessed and modulated in situ, offering functional versatility and adaptability. Advanced morphable microelectronic systems including a reconfigurable microantenna for customizable telecommunication, a 3D vibration sensor for hand-tremor monitoring, and a bloomable robot for cardiac mapping demonstrate broad utility of these assembly schemes to realize advanced functionalities.

Sp2 is a maternally inherited transcription factor required for embryonic development.

The Sp family of transcription factors is required for the expression of cell cycle- and developmentally regulated genes, and the deregulated expression of a handful of family members is associated with human tumorigenesis. Sp2 is a relatively poorly characterized member of the Sp family that, although widely expressed, exhibits little or no DNA binding or transcriptional activity in human and mouse cell lines. To begin to address the role(s) played by Sp2 in early metazoan development we have cloned and characterized Sp2 from zebrafish (Danio rerio). We report that 1) the intron/exon organization and amino acid sequence of zebrafish Sp2 is closely conserved with its mammalian orthologues, 2) zebrafish Sp2 weakly stimulates an Sp-dependent promoter in vitro and associates with the nuclear matrix in a DNA-independent fashion, 3) zebrafish Sp2 is inherited as a maternal transcript, is transcribed in zebrafish embryos and adult tissues, and is required for completion of gastrulation, and 4) zebrafish lines carrying transgenes regulated by the Sp2 promoter recapitulate patterns of endogenous Sp2 expression.

Transcription of mouse Sp2 yields alternatively spliced and sub-genomic mRNAs in a tissue- and cell-type-specific fashion.

The Sp-family of transcription factors is comprised by nine members, Sp1-9, that share a highly conserved DNA-binding domain. Sp2 is a poorly characterized member of this transcription factor family that is widely expressed in murine and human cell lines yet exhibits little DNA-binding or trans-activation activity in these settings. As a prelude to the generation of a "knock-out" mouse strain, we isolated a mouse Sp2 cDNA and performed a detailed analysis of Sp2 transcription in embryonic and adult mouse tissues. We report that (1) the 5' untranslated region of Sp2 is subject to alternative splicing, (2) Sp2 transcription is regulated by at least two promoters that differ in their cell-type specificity, (3) one Sp2 promoter is highly active in nine mammalian cell lines and strains and is regulated by at least five discrete stimulatory and inhibitory elements, (4) a variety of sub-genomic messages are synthesized from the Sp2 locus in a tissue- and cell-type-specific fashion and these transcripts have the capacity to encode a novel partial-Sp2 protein, and (5) RNA in situ hybridization assays indicate that Sp2 is widely expressed during mouse embryogenesis, particularly in the embryonic brain, and robust Sp2 expression occurs in neurogenic regions of the post-natal and adult brain.

Short-Term Thinning Influences the Rhizosphere Fungal Community Assembly of Pinus massoniana by Altering the Understory Vegetation Diversity.

Thinning can significantly promote forest productivity and ecological function. Rhizosphere fungi play an indispensable role in regulating nutrient cycling between plants and the environment, and their community composition can positively respond to anthropogenic disturbance. However, the initial effects of thinning on rhizosphere fungal community assembly have seldom been reported. In this research, we studied the alterations in the rhizosphere fungal communities of 29-year-old Pinus massoniana in East Sichuan 2 years after three different thinning intensity treatments. In addition, the responses of fungal community and functional group composition to alterations in understory vegetation and soil physiochemical properties were analyzed. Three thinning intensities were set, which were 0 (CK), 25% (LIT), and 50% (HIT), respectively. The results suggested that the richness index and Shannon index of understory vegetation increased significantly with increasing thinning intensity. The alpha diversity indices of rhizosphere fungal community and soil physiochemical properties did not show significant differences among the three treatments. The relative abundances of 17 fungal indicator species varied regularly with increasing thinning intensity, and most of them belong to Hypocreales and Eurotiales, indicating that these two orders were potential indicators for different thinning treatments. Rhizosphere fungal community assembly was determined by deterministic process, and it was driven by the diversity of understory vegetation in the initial stage of thinning. The Simpson index and Pielou index of herbs were useful measures of the main environmental factors driving the differentiation of fungal functional group composition. Based on network analysis, thinning resulted in distinct co-occurrence patterns of rhizosphere fungal functional groups. This research elucidates the initial role of thinning in rhizosphere fungal community assembly of P. massoniana and has practical significance for the functional restoration and protection of local forest ecosystem.

Impact of Hydroiodic Acid on Resistive Switching Performance of Lead-Free Cs3Cu2I5 Perovskite Memory.

Herein, we employed lead-free Cs3Cu2I5 perovskite films as the functional layers to construct Al/Cs3Cu2I5/ITO memory devices and systematically investigated the impact on the corresponding resistive switching (RS) performance via adding different amounts of hydroiodic acid (HI) in Cs3Cu2I5 precursor solution. The results demonstrated that the crystallinity and morphology of the Cs3Cu2I5 films can be improved and the resistive switching performance can be modulated by adding an appropriate amount of HI. The obtained Cs3Cu2I5 films by adding 5 µL HI exhibit the fewest lattice defects and flattest surface (RMS = 13.3 nm). Besides, the memory device, utilizing the optimized films, has a low electroforming voltage (1.44 V), a large on/off ratio (∼65), and a long retention time (104 s). The RS performance impacted by adding HI, providing a scientific strategy for improving the RS performance of iodine halide perovskite-based memories.

[Effects of thinning intensity on species composition and diversity of undergrowth vegetation community in Pinus massoniana plantation at initial stage of thinning]. / é—´ä¼å¼ºåº¦å¯¹é©¬å°¾æ¾äººå·¥æž—é—´ä¼åˆæœŸæž—ä¸‹æ¤è¢«ç¾¤è½ç‰©ç§ç»„æˆå’Œå¤šæ ·æ€§çš„å½±å“.

Species composition and diversity of undergrowth vegetation community under different thinning intensities (0, 10%, 20%, 30%, 40%, 50%) were examined at the initial stage of thinning in 29-year-old Pinus massoniana plantation in the low mountain region of eastern Sichuan. The results show that all the thinning treatments could reduce the absolute dominance of Miscanthus sinensis and Dicranopteris dichotoma. The dominant species composition of shrubs in each treatment was different. There were more extensive species in the medium thinning intensity (20%, 30% and 40%) treatments than other treatments. The diversity indices increased first and then decreased with increasing thinning intensity. The variation degree of herbs was stronger than shrubs. The diversity indices of herbs were positively correlated with soil water content. The explanation amount of thinning intensity and soil physicochemical properties to community differentiation was 81%. The vegetation communities in the medium thinning intensity forests showed positive correlation with all the factors except total phosphorus. At the initial stage of thinning, herbaceous communities were more sensitive to disturbance than shrub communities. The 40% thinning intensity treatment was more closely related to soil environmental factors, with high stability and the most abundant species, which would be the best thinning measure under the experimental condition.

Sp2 localizes to subnuclear foci associated with the nuclear matrix.

We have reported that extracts prepared from many human and mouse cell lines show little or no Sp2 DNA-binding activity and that Sp2 has little or no capacity to stimulate transcription of promoters that are activated by Sp1, Sp3, and Sp4. Using an array of chimeric Sp1/Sp2 proteins we showed further that Sp2 DNA-binding activity and trans-activation are each negatively regulated in mammalian cells. As part of an ongoing effort to study Sp2 function and regulation we characterized its subcellular localization in comparison with other Sp-family members in fixed and live cells. We report that 1) Sp2 localizes largely within subnuclear foci associated with the nuclear matrix, and 2) these foci are distinct from promyelocytic oncogenic domains and appear to be stable during an 18-h time course of observation. Deletion analyses identified a 37 amino acid sequence spanning the first zinc-"finger" that is sufficient to direct nuclear matrix association, and this region also encodes a bipartite nuclear localization sequence. A second nuclear matrix targeting sequence is encoded within the Sp2 trans-activation domain. We conclude that Sp2 preferentially associates with the nuclear matrix and speculate that this subcellular localization plays an important role in the regulation of Sp2 function.

Intermediate-calcium based cementitious materials prepared by MSWI fly ash and other solid wastes: hydration characteristics and heavy metals solidification behavior.

Municipal solid waste incineration (MSWI) fly ash is a by-product of garbage incineration power generation, and its disposal is currently a world problem because it contains over standard heavy metals. This research aims to solidify the heavy metals in MSWI fly ash and make it to be utilizable construction materials under the guidance of intermediate-calcium cementitious materials (ICCM), and meanwhile figure out the solidification and hydration mechanism. The hydration characteristics of ICCM were characterized by XRD, FTIR, 29Si MAS-NMR and SEM techniques, and the environmental properties are investigated by TCLP and EPMA. The results indicate that the optimal ratio of (CaO + MgO)/(SiO2 + Al2O3) for ICCM is at the range of 0.76-0.88. The compressive strengths of ICCM reach the 42.5R normal Portland cement level, and the leaching concentrations of heavy metals meet the Chinese integrated wastewater discharge standard GB 8978-1996. As predominant hydration products, ettringite, hydrocalumite and amorphous C-S-H gel are principally responsible for the strength development of ICCM, and the (Ca + Mg)/(Si + Al) ratio at 0.88 has the best polymerized structure. The heavy metals are well solidified through combining with the C-S-H gel or absorbed in the hydration pastes. This paper provides an effective solution to use the MSWI fly ash in building material.