Experiment on Sediment Ammonia Nitrogen Release of Chaohu Lake in Varying Hydrodynamic Disturbance

Shallow water has low depth, and hydrodynamic conditions may change with the effect of wind and waves, resulting in sediment suspension and pollutant release. To investigate the influence of sediment incipient motion on ammonia nitrogen (NH3-N) release in shallow lakes under hydrodynamic disturbance, we monitored ammonia nitrogen concentration in the overlying water of sediments in Chaohu Lake under static, weak, and strong disturbance conditions and analyzed the ammonia nitrogen release rate based on the these concentrations. In static condition, the sediment particles on the surface moved individually (individual movement), and the ammonia nitrogen release rate was 9.59 mg/m2/day. When the disturbance was weak and a small proportion of sediment particles started to move (small movement), the ammonia nitrogen release rate increased to 34.21 mg/m2/day. When the disturbance was further strengthened, and most of the sediment particles moved (general movement), the ammonia nitrogen release rate was 77.04 mg/m2/day. Distribution showed that the release rate varied the most in the western area followed by the eastern area, and the central area had the lowest release rate. The daily release of ammonia nitrogen in Chaohu Lake ranged from 8742.3 kg to 61,008.59 kg. In this experiment, we combined sediment movement and pollutant release, which provides a new reference for the study of pollutant release in shallow lakes and for ammonia nitrogen management in other shallow lakes

Simultaneous identifying the infarct core, collaterals, and penumbra after acute ischemic stroke with a low-immunogenic MRI nanoprobe

Ischemic stroke is one of the leading causes of disability and mortality. The collaterals provide an alternative pathway to preserve the ischemic brain tissue, and determine the penumbra range, where the neurons are salvageable. Therefore, accurately monitoring the collaterals and identifying the penumbra are crucial. Herein, a low-immunogenic nanoprobe-based MRI strategy is developed to simultaneously identify the infarct core, collaterals distribution, and ischemic penumbra distributions. The low-immunogenic nanoprobe was constructed by covalently attaching self-peptide on the surface of biocompatible Fe3O4 nanoparticles as a stealth coating. Both in vitro and in vivo experiments clearly revealed that the nanoprobes can effectively avoid capture by macrophages, and exhibited prolonged blood half-life to continuously enhance the contrast of blood vessels in a longer time window in susceptibility-weighted imaging (SWI), which enabled the delineation of the collaterals and ischemic penumbra. More importantly, combined with the diffusion-weighted imaging (DWI), the infarct core, collateral vessels, and the ischemic penumbra range can be identified simultaneously. In this context, the stroke progress including infarct core growth, collateral vessel formation, and penumbra distribution, can be better understood. This nanoprobe-based strategy thus offers a practical route for precise diagnosis of ischemic stroke, which remains a challenge for conventional MRI strategies

Visualizing the spatial distribution of inflammation in the depressed brain with a targeted MRI nanoprobe in vivo

Abstract Depression is a prevalent mental illness that imposes a substantial public health burden. However, the diverse clinical phenotypes observed in patients make it difficult to realize precise diagnosis. Recently, accumulating preclinical and clinical evidence has suggested that inflammation is involved in the pathophysiology of depression. Herein, a molecular imaging–based strategy was proposed as a means to diagnose depression precisely by specifically visualizing the inflammation status associated with depression. Inflammation-targeting MRI nanoprobes were constructed by attaching an intercellular cell adhesion molecule-1 (ICAM-1)-targeting peptide to biocompatible Fe3O4 nanoparticles. Systematic studies demonstrated that the nanoprobes could specifically target inflamed vascular endothelial cells and visualize the spatial distribution of inflammation in the depressed brain in vivo through susceptibility-weighted imaging (SWI), which was further confirmed by histological analysis. Additionally, these inflammatory brain regions identified by nanoprobe-based imaging are consistent with the focal regions closely associated with the symptoms of depression as reported in previous behavioral studies. Overall, this is the first study to directly visualize the distribution of inflammation in the depressed brain in vivo through a molecular imaging strategy, which may not only facilitate insight into the biological mechanism underlying depression but also provide a potential target within the depressed brain for the further development of anti-inflammatory therapies

DataSheet_1_Comparative cytological and transcriptome analyses of ny2 mutant delayed degeneration of tapetal cells and promotes abnormal microspore development in neo-tetraploid rice.pdf

We aimed to investigate the genetic defects related to pollen development and infertility in NY2, a novel tetraploid rice germplasm known as Neo-tetraploid rice. This rice variety was created through the crossbreeding and selective breeding of various autotetraploid rice lines and has previously shown high fertility. Our previous research has revealed that the NY2 gene, encoding a eukaryotic translation initiation factor 3 subunit E, regulates pollen fertility. However, the underlying mechanism behind this fertility is yet to be understood. To shed light on this matter, we performed a combined cytological and transcriptome analysis of the NY2 gene. Cytological analysis indicated that ny2 underwent abnormal tapetal cells, microspore, and middle layer development, which led to pollen abortion and ultimately to male sterility. Genetic analysis revealed that the F1 plants showed normal fertility and an obvious advantage for seed setting compared to ny2. Global gene expression analysis in ny2 revealed a total of 7545 genes were detected at the meiosis stage, and 3925 and 3620 displayed upregulation and downregulation, respectively. The genes were significantly enriched for the gene ontology (GO) term “carbohydrate metabolic process. Moreover, 9 genes related to tapetum or pollen fertility showed down-regulation, such as OsABCG26 (ATP Binding Cassette G26), TMS9-1 (Thermosensitive Male Sterility), EAT1 (Programmed cell death regulatory), KIN14M (Kinesin Motor), OsMT1a (Metallothionein), and OsSTRL2 (Atypical strictosidine synthase), which were validated by qRT-PCR. Further analyses of DEGs identified nine down-regulated transcription factor genes related to pollen development. NY2 is an important regulator of the development of tapetum and microspore. The regulatory gene network described in this study may offer important understandings into the molecular processes that underlie fertility control in tetraploid rice.</p

Table_1_Comparative cytological and transcriptome analyses of ny2 mutant delayed degeneration of tapetal cells and promotes abnormal microspore development in neo-tetraploid rice.xlsx

We aimed to investigate the genetic defects related to pollen development and infertility in NY2, a novel tetraploid rice germplasm known as Neo-tetraploid rice. This rice variety was created through the crossbreeding and selective breeding of various autotetraploid rice lines and has previously shown high fertility. Our previous research has revealed that the NY2 gene, encoding a eukaryotic translation initiation factor 3 subunit E, regulates pollen fertility. However, the underlying mechanism behind this fertility is yet to be understood. To shed light on this matter, we performed a combined cytological and transcriptome analysis of the NY2 gene. Cytological analysis indicated that ny2 underwent abnormal tapetal cells, microspore, and middle layer development, which led to pollen abortion and ultimately to male sterility. Genetic analysis revealed that the F1 plants showed normal fertility and an obvious advantage for seed setting compared to ny2. Global gene expression analysis in ny2 revealed a total of 7545 genes were detected at the meiosis stage, and 3925 and 3620 displayed upregulation and downregulation, respectively. The genes were significantly enriched for the gene ontology (GO) term “carbohydrate metabolic process. Moreover, 9 genes related to tapetum or pollen fertility showed down-regulation, such as OsABCG26 (ATP Binding Cassette G26), TMS9-1 (Thermosensitive Male Sterility), EAT1 (Programmed cell death regulatory), KIN14M (Kinesin Motor), OsMT1a (Metallothionein), and OsSTRL2 (Atypical strictosidine synthase), which were validated by qRT-PCR. Further analyses of DEGs identified nine down-regulated transcription factor genes related to pollen development. NY2 is an important regulator of the development of tapetum and microspore. The regulatory gene network described in this study may offer important understandings into the molecular processes that underlie fertility control in tetraploid rice.</p

TGF beta promotes fibrosis by MYST1-dependent epigenetic regulation of autophagy

Activation of fibroblasts is essential for physiological tissue repair. Uncontrolled activation of fibroblasts, however, may lead to tissue fibrosis with organ dysfunction. Although several pathways capable of promoting fibroblast activation and tissue repair have been identified, their interplay in the context of chronic fibrotic diseases remains incompletely understood. Here, we provide evidence that transforming growth factor-beta (TGF beta) activates autophagy by an epigenetic mechanism to amplify its profibrotic effects. TGF beta induces autophagy in fibrotic diseases by SMAD3-dependent downregulation of the H4K16 histone acetyltransferase MYST1, which regulates the expression of core components of the autophagy machinery such as ATG7 and BECLIN1. Activation of autophagy in fibroblasts promotes collagen release and is both, sufficient and required, to induce tissue fibrosis. Forced expression of MYST1 abrogates the stimulatory effects of TGF beta on autophagy and re-establishes the epigenetic control of autophagy in fibrotic conditions. Interference with the aberrant activation of autophagy inhibits TGF beta -induced fibroblast activation and ameliorates experimental dermal and pulmonary fibrosis. These findings link uncontrolled TGF beta signaling to aberrant autophagy and deregulated epigenetics in fibrotic diseases and may contribute to the development of therapeutic interventions in fibrotic diseases. Uncontrolled activation of fibroblasts contributes to tissue fibrosis and organ dysfunction. Here the authors demonstrate that the epigenetic control of autophagy is disturbed by a TGF beta -dependent downregulation of MYST1 in systemic sclerosis patients. Restoration of the epigenetic control of autophagy reduces fibroblast activation and ameliorates fibrotic tissue remodeling

Targeting of canonical WNT signaling ameliorates experimental sclerodermatous chronic graft-versus-host disease

Chronic graft-versus-host disease (cGVHD) is a major life-threatening complication of allogeneic hematopoietic stem cell transplantation. The molecular mechanisms underlying cGVHD remain poorly understood, and targeted therapies for clinical use are not well established. Here, we examined the role of the canonical WNT pathway in sclerodermatous cGVHD (sclGVHD). WNT signaling was activated in human sclGVHD with increased nuclear accumulation of the transcription factor beta-catenin and a WNT-biased gene expression signature in lesional skin. Treatment with the highly selective tankryase inhibitor G007-LK, the CK1 alpha agonist pyrvinium, or the LRP6 inhibitor salinomycin abrogated the activation of WNT signaling and protected against experimental cGVHD, without a significant impact on graft-versus-leukemia effect (GVL). Treatment with G007-LK, pyrvinium, or salinomycin almost completely prevented the development of clinical and histological features in the B10.D2 (H-2(d)) -> BALB/c (H-2(d)) and LP/J (H-2(b)) -> C57BL/6 (H-2(b)) models of sclGVHD. Inhibition of canonical WNT signaling reduced the release of extracellular matrix from fibroblasts and reduced leukocyte influx, suggesting that WNT signaling stimulates fibrotic tissue remodeling by direct effects on fibroblasts and by indirect inflammation-dependent effects in sclGVHD. Our findings may have direct translational potential, because pyrvinium is in clinical use, and tankyrase inhibitors are in clinical trials for other indications