Search

Polymorphic microcrystals and their multi-modal/directional optical waveguides (1D, 2D, isotropic and anisotropic) from the first D–A type 5,6,12,13-tetraazaperopyrene are reported.

Micro-nano-level photonic waveguide regulation is essential for future on-chip photonic integrated systems and is still of great challenges. We report a molecular design strategy, changing the position of the methyl substituent makes the arrangement of the three isomer molecules different in their respective crystals. Based on this strategy, three sheet-like crystals with different polygonal morphologies were prepared via solution self-assembly approach. The in-depth optical measurements demonstrated that these three microsheet crystals have different 2D optical waveguide performances related to the shapes. Our work provides a feasible design strategy and material preparation method for realizing precise 2D optical waveguide modulation, which lays the foundation for complex photonic integrated systems in the future.

BackgroundObesity is a complex condition that influences several organ systems and physiologic systems. Obesity (OB) is closely linked to Alzheimer’s disease (AD). However, the interrelationship between them remains unclear. The purpose of this study is to explore the key genes and potential molecular mechanisms in obesity and AD.MethodsThe microarray data for OB and AD were downloaded from the Gene Expression Omnibus (GEO) database. Weighted gene correlation network analysis (WGCNA) was used to delineate the co-expression modules related to OB and AD. The shared genes existing in obesity and AD were identified through biological process analyses using the DAVID website, which then constructed the Protein–Protein Interaction (PPI) Network and selected the hub genes by Cytoscape. The results were validated in other microarray data by differential gene analysis. Moreover, the hub gene expressions were further determined in mice by qPCR.ResultsThe WGCNA identifies five modules and four modules as significant modules with OB and AD, respectively. Functional analysis of shared genes emphasized that inflammation response and mitochondrial functionality were common features in the pathophysiology of OB and AD. The results of differential gene analysis in other microarray data were extremely similar to them. Then six important hub genes were selected and identified using cytoHubba, including MMP9, PECAM1, C3AR1, IL1R1, PPARGC1α, and COQ3. Finally, we validated the hub gene expressions via qPCR.ConclusionsOur work revealed the high inflammation/immune response and mitochondrial impairment in OB patients, which might be a crucial susceptibility factor for AD. Meanwhile, we identified novel gene candidates such as MMP9, PECAM1, C3AR1, IL1R1, PPARGC1α, and COQ3 that could be used as biomarkers or potential therapeutic targets for OB with AD.

Obesity is a complex condition that influences several organ systems and physiologic systems. Obesity (OB) is closely linked to Alzheimer's disease (AD). However, the interrelationship between them remains unclear. The purpose of this study is to explore the key genes and potential molecular mechanisms in obesity and AD.The microarray data for OB and AD were downloaded from the Gene Expression Omnibus (GEO) database. Weighted gene correlation network analysis (WGCNA) was used to delineate the co-expression modules related to OB and AD. The shared genes existing in obesity and AD were identified through biological process analyses using the DAVID website, which then constructed the Protein-Protein Interaction (PPI) Network and selected the hub genes by Cytoscape. The results were validated in other microarray data by differential gene analysis. Moreover, the hub gene expressions were further determined in mice by qPCR.The WGCNA identifies five modules and four modules as significant modules with OB and AD, respectively. Functional analysis of shared genes emphasized that inflammation response and mitochondrial functionality were common features in the pathophysiology of OB and AD. The results of differential gene analysis in other microarray data were extremely similar to them. Then six important hub genes were selected and identified using cytoHubba, including MMP9, PECAM1, C3AR1, IL1R1, PPARGC1α, and COQ3. Finally, we validated the hub gene expressionsOur work revealed the high inflammation/immune response and mitochondrial impairment in OB patients, which might be a crucial susceptibility factor for AD. Meanwhile, we identified novel gene candidates such as MMP9, PECAM1, C3AR1, IL1R1, PPARGC1α, and COQ3 that could be used as biomarkers or potential therapeutic targets for OB with AD.

Recently, few-shot object detection based on fine-tuning has attracted much attention in the field of computer vision. However, due to the scarcity of samples in novel categories, obtaining positive anchors for novel categories is difficult, which implicitly introduces the foreground–background imbalance problem. It is difficult to identify foreground objects from complex backgrounds due to various object sizes and cluttered backgrounds. In this article, we propose a novel context information refinement few-shot detector (CIR-FSD) for remote sensing images. In particular, we design a context information refinement (CIR) module to extract discriminant context features. This module uses dilated convolutions and dense connections to capture rich context information from different receptive fields and then uses a binary map as the supervision label to refine the context information. In addition, we improve the region proposal network (RPN). Concretely, the RPN is fine-tuned on novel categories, and the constraint of non-maximum suppression (NMS) is relaxed, which can obtain more positive anchors for novel categories. Experiments on two remote sensing public datasets show the effectiveness of our detector.

Growth arrest and DNA damage-inducible beta (GADD45B) is closely linked with cell cycle arrest, DNA repair, cell survival, or apoptosis in response to stress and is known to regulate the mitogen-activated protein kinase (MAPK) pathway. Here, using an RNA sequencing approach, we determined that GADD45B was significantly upregulated in diabetic kidneys, which was accompanied by renal tubular epithelial-mesenchymal transition (EMT) and apoptosis, as well as elevated MAPK pathway activation. In vitro, GADD45B expression in cultured human kidney proximal tubular epithelial cells (HK-2 cells) was also stimulated by high glucose (HG). In addition, overexpression of GADD45B in HK-2 cells exacerbated renal tubular EMT and apoptosis and increased p38 MAPK and c-Jun N-terminal kinases (JNK) activation, whereas knockdown of GADD45B reversed these changes. Notably, the activity of extracellular regulated kinase (ERK) was not affected by GADD45B expression. Furthermore, inhibitors of p38 MAPK (SB203580) and JNK (SP600125) alleviated HG‐ and GADD45B overexpression-induced renal tubular epithelial-mesenchymal transition and apoptosis. These findings indicate a role of GADD45B in diabetes-induced renal tubular EMT and apoptosis via the p38 MAPK and JNK pathways, which may be an important mechanism of diabetic kidney injury.

Growth arrest and DNA damage-inducible beta (GADD45B) is closely linked with cell cycle arrest, DNA repair, cell survival, or apoptosis in response to stress and is known to regulate the mitogen-activated protein kinase (MAPK) pathway. Here, using an RNA sequencing approach, we determined that GADD45B was significantly upregulated in diabetic kidneys, which was accompanied by renal tubular epithelial-mesenchymal transition (EMT) and apoptosis, as well as elevated MAPK pathway activation.

Background and purpose Excessive mitochondrial fission was observed in diabetic kidney disease (DKD). Phosphoglycerate mutase family member 5 (PGAM5) plays an important role in mitochondrial fission by dephosphorylating the dynamin-related protein 1 at Ser637 (DRP1S637). Whether PGAM5 participates in the mitochondrial fission in diabetic renal tubular injury is unknown. Clinical trials have observed encouraging effect of Sodium-glucose cotransporter 2 (SGLT2) inhibitors on DKD though the underling mechanisms remain unclear. Experimental approach We used KK-Ay mice as diabetic model and Empagliflozin (Empa) were administrated by oral gavage. The mitochondrial fission and the expressions of phosphorylated AMP-activated protein kinase (p-AMPK), specificityprotein1 (SP1), PGAM5 and DRP1S637 were tested. We also examined these changes in HK2 cells that cultured in normal glucose (NG), high glucose (HG) and high glucose+Empa (HG + Empa) environment. Then we verified our deduction using AMPK activator (5-aminoimidazole-4-carboximide Riboside, AICAR), inhibitor (Compound C), si-SP1 and si-PGAM5. Lastly, we testified the interaction between SP1 and the PGAM5promotor by CHIP assay. Key results The mitochondrial fission and the expression of SP1, PGAM5 increased and the expression of p-AMPK, DRP1S637 decreased in diabetic or HG environment. These changes were all reversed in Empa or AICAR treated groups. These reversal effects of Empa could be diminished by Compound C. Either si-SP1 or si-PGAM5 could alleviate the mitochondrial fission without affection on AMPK phosphorylation. Finally, the CHIP assay confirmed the interaction between SP1 and the PGAM5 promotor. Conclusions and implications The PGAM5 aggravated the development of diabetic renal tubular injury and the Empa could improve the DKD by alleviating mitochondrial fission via AMPK/SP1/PGAM5 pathway.

Background Diabetic retinopathy (DR) is the most common microvascular complication of diabetes and the main cause of non-traumatic blindness in adults. Pericyte loss is known to be an early pathological change of DR. Our group's previous research indicated that prostaglandin F2α (PGF2α) acts as an eicosanoidal protector against non-proliferative DR that can regulate the mobility of pericytes in a RhoA-mediated manner. However, the effect of PGF2α on pericyte apoptosis has yet to be described. Methods Two animal models were constructed: a high-fat diet (HFD) and streptozotocin (STZ)-induced type 2 diabetes mouse model and a spontaneous type 2 diabetes db/db mouse model. We analyzed pathological changes, and performed TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling) staining and western blot to detect apoptosis in the retinas of diabetic mice. For our in vitro experiments, we selected human retinal pericytes and subjected them to high-glucose (HG), PGF2α, and AL8810 (an antagonist of the PGF2α receptor) treatment. Subsequently, apoptosis and the levels of PI3K/Akt/GSK3β/β-catenin pathway-related proteins were detected by TUNEL staining and western blot, respectively. Results The levels of apoptosis were increased in the retinas of diabetic mice in both T2DM models. In vitro, HG treatment increased apoptosis and inhibited PI3K/Akt/GSK3β/β-catenin signaling in pericytes. In contrast, PGF2α treatment inhibited pericyte apoptosis while increasing the levels of the PI3K, p-Akt/t-Akt, p-GSK3β/t-GSK3β, and β-catenin proteins; however, these PGF2α-induced effects were eliminated by ALL80. Conclusions PGF2α may make a key contribution to reducing pericyte apoptosis and protecting against DR via its inhibition of the PI3K/Akt/GSK3β/β-catenin signaling pathway.

Modern agriculture, based on the improved single-genotype crop varieties and the intensive and monocultural managements, has contributed tremendously to the world’s food supply. However, it is also challenged by stagnant yield growth, increasingly high input, mounting environmental pollution and pressing sustainability of development. In comparison, old agriculture of 100 years ago, based on the traditional multi-genotype landraces and low-input cultivation, prevailed thousands of years and still exists now in subsistence farming in marginal areas in spite of its low productivity. Crop multi-genotype breeding, which combines the advantages of both old and modern agriculture at the high level of productivity, will give us a promising strategy to break the predicament of modern agriculture. The concept, necessity, principle, technical tactics and characteristics of crop multi-genotype breeding are first elucidated in detail here. Two successful cases of application in rice and cotton are presented. Firstly, rice multi-genotype inbred varieties (colony variety) have commercialized using MAGIC lines. In cotton, a multi-genotype hybrid variety Jing-Mi 1 revealed superiority in seeded cotton and lint yields over the check variety in regional trial. Multigenotype variety could be maintained and recover the genetic diversity in production system. In their progenies of the MAGIC lines, most of them could be transmitted to the multi-genotype varieties, implying that the genetic diversity of agro-ecosystem could be effectively restored by crop multi-genotype varieties. We believe crop multi-genotype breeding will make a substantial contribution to restoring genetic diversity of agro-ecosystem, preventing the exacerbation of vulnerable environment and promoting the sustainable development of agriculture. We call for ever-increasing efforts to develop and apply the crop multi-genotype breeding in agriculture.