Spatial Transform Decoupling for Oriented Object Detection

Vision Transformers (ViTs) have achieved remarkable success in computer vision tasks. However, their potential in rotation-sensitive scenarios has not been fully explored, and this limitation may be inherently attributed to the lack of spatial invariance in the data-forwarding process. In this study, we present a novel approach, termed Spatial Transform Decoupling (STD), providing a simple-yet-effective solution for oriented object detection with ViTs. Built upon stacked ViT blocks, STD utilizes separate network branches to predict the position, size, and angle of bounding boxes, effectively harnessing the spatial transform potential of ViTs in a divide-and-conquer fashion. Moreover, by aggregating cascaded activation masks (CAMs) computed upon the regressed parameters, STD gradually enhances features within regions of interest (RoIs), which complements the self-attention mechanism. Without bells and whistles, STD achieves state-of-the-art performance on the benchmark datasets including DOTA-v1.0 (82.24% mAP) and HRSC2016 (98.55% mAP), which demonstrates the effectiveness of the proposed method. Source code is available at https://github.com/yuhongtian17/Spatial-Transform-Decoupling

Autophagy regulates the maturation of hematopoietic precursors in the embryo

An understanding of the mechanisms regulating embryonic hematopoietic stem cell (HSC) development would facilitate their regeneration. The aorta-gonad-mesonephros region is the site for HSC production from hemogenic endothelial cells (HEC). While several distinct regulators are involved in this process, it is not yet known whether macroautophagy (autophagy) plays a role in hematopoiesis in the pre-liver stage. Here, we show that different states of autophagy exist in hematopoietic precursors and correlate with hematopoietic potential based on the LC3-RFP-EGFP mouse model. Deficiency of autophagy-related gene 5 (Atg5) specifically in endothelial cells disrupts endothelial to hematopoietic transition (EHT), by blocking the autophagic process. Using combined approaches, including single-cell RNA-sequencing (scRNA-seq), we have confirmed that Atg5 deletion interrupts developmental temporal order of EHT to further affect the pre-HSC I maturation, and that autophagy influences hemogenic potential of HEC and the formation of pre-HSC I likely via the nucleolin pathway. These findings demonstrate a role for autophagy in the formation/maturation of hematopoietic precursors.</p

Transforming Growth Factor beta 1 Gene Play a Novel Role in Innate Immune Response in Pelteobagrus fulvidraco

Transforming growth factor-beta 1 (TGF-beta 1) as a member of TGF-beta superfamily plays crucial roles in regulation of immune responses. Yellow catfish, Pelteobagrus fulvidraco, is one of the most important freshwater aquaculture species in China, but little is known about its genes related to immune response. The present study cloned cDNA encoding TGF-beta 1 from P. fulvidraco. The results showed the full-length cDNA of TGF-beta 1 is 2,816 bp and encodes 461 amino acids. The homology of P. fulvidraco TGF-beta 1 depicted 83% and 81% similarity to the TGF-beta 1 in Stegastes partitus and Pundamilia nyererei respectively. The phylogenetic tree construction revealed that P. fulvidraco is closely related to Astyanax mexicanus. Analysis of mRNA expression of TGF-beta 1 in different tissues (gonads, brain, liver, kidney, spleen, intestine, blood, gills, muscle and heart) revealed that TGF-beta 1 is predominantly expressed in liver and brain, followed by gill and spleen. TGF-beta 1 gene in gill and spleen up-regulated for 48h after Edwardsiella ictaluri and Flavobacterium columnare injection, then the expression showed a significant decrease (p&lt;0.05). These results indicated that TGF-beta 1 contributes to the inherent immune reaction of P. fulvidraco

Selenium-Containing Polysaccharide-Protein Complex in Se-Enriched Ulva fasciata Induces Mitochondria-Mediated Apoptosis in A549 Human Lung Cancer Cells

The role of selenium (Se) and Ulva fasciata as potent cancer chemopreventive and chemotherapeutic agents has been supported by epidemiological, preclinical, and clinical studies. In this study, Se-containing polysaccharide-protein complex (Se-PPC), a novel organoselenium compound, a Se-containing polysaccharide-protein complex in Se-enriched Ulva fasciata, is a potent anti-proliferative agent against human lung cancer A549 cells. Se-PPC markedly inhibited the growth of cancer cells via induction of apoptosis which was accompanied by the formation of apoptotic bodies, an increase in the population of apoptotic sub-G1 phase cells, upregulation of p53, and activation of caspase-3 in A549 cells. Further investigation on intracellular mechanisms indicated that cytochrome C was released from mitochondria into cytosol in A549 cells after Se-PPC treatment. Se-PPC induced depletion of mitochondrial membrane potential (ΔΨm) in A549 cells through regulating the expression of anti-apoptotic (Bcl-2, Bcl-XL) and pro-apoptotic (Bax, Bid) proteins, resulting in disruption of the activation of caspase-9. This is the first report to demonstrate the cytotoxic effect of Se-PPC on human cancer cells and to provide a possible mechanism for this activity. Thus, Se-PPC is a promising novel organoselenium compound with potential to treat human cancers

Protection of Siganus oramin, rabbitfish, from heavy metal toxicity by the selenium-enriched seaweed Gracilaria lemaneiformis

Seaweed is an inherently important entity in marine ecosystems. It is not only consumed by aquatic animals but also improves environmental quality in the mariculture. Seaweed is also part of the diet of human beings. The purpose of the present study was to evaluate the antagonism of selenium (Se)-enriched Gracilaria lemaneiformis against heavy metals, specifically, the potential of dietary Se-enriched Gracilaria to protect against heavy metal toxicity in rabbitfish (Siganus oramin). Growth rate, heavy metal (Se, Cd, Pb, Cu, Zn and Cr) concentrations, malondialdehyde (MDA), metallothionein (MT), and the activity of the antioxidants, glutathione peroxidase (GPX), catalase (CAT) and superoxide dismutase (SOD) were all assessed. The results showed that the total organic and inorganic Se concentration for the 250 mg L-1 Se-enriched Gracilaria was significantly higher than those of the 50 and 10 mg L-1 treatments after 3 days of enrichment. The mean total Se concentrations in Gracilaria were 42.5 mu g g(-1)- in the 250 mg L-1 treatment, 13.5 mu g g(-1)- in the 50 mg L-1 treatment and 2.5 mu g g(-1) in the 10 mg L-1 treatment, respectively. Organic Se accounts for 80-82% of total Se in Se-enriched Gracilaria. The Se concentration of rabbitfish fed Se-enriched Gracilaria was significantly higher than control. Furthermore, Se increased Cu and Zn absorption, and enhanced MT generation, and improved GPX, CAT, and SOD antioxidant activity, and decreased MDA concentrations and lipid pemxidation levels, all antagonistic to Cd, Pb and Cr. The effects of Se-enriched Gracilaria on waterborne Cd, Pb and Cr-induced toxicity occurred via both enzymatic and non-enzymatic antioxidative mechanisms in rabbitfish. Selenium had synergistic effects on Zn and Cu in rabbitfish. For the 50 mg L-1 Se-enriched Gracilaria treatment, the Se, Cu, Zn, and antagonistic Cd, Pb, Cr, and the antioxidant enzymes CAT, SOD, GPX activities, and MT concentrations in rabbitfish were higher than that with the 250 mg L-1 and 10 mg L-1 Se-enriched Gracilaria treatments. The 50 mg L-1 Se treatment of Gracilaria was deemed to be the optimum concentration to promote growth of rabbitfish. Therefore, the obtained results suggest Se-enriched Gracilaria can antagonize heavy metal toxicity, and is an advisable Se supplement to improve the edible safety of cultured animals

HDAC6 Deficiency Has Moderate Effects on Behaviors and Parkinson’s Disease Pathology in Mice

Histone deacetylase 6 (HDAC6) is involved in the regulation of protein aggregation and neuroinflammation, but its role in Parkinson’s disease (PD) remains controversial. In this study, Hdac6−/− mice were generated by CRISPR-Cas9 technology for exploring the effect of HDAC6 on the pathological progression of PD. We found that male Hdac6−/− mice exhibit hyperactivity and certain anxiety. In the acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mice, though motor injury was slightly alleviated by HDAC6 deficiency, dopamine (DA) depletion in the striatum, the decrease in the number of DA neurons in the substantia nigra (SN) and the reduction in DA neuronal terminals were not affected. In addition, activation of glial cells and the expression of α-synuclein, as well as the levels of apoptosis-related proteins in the nigrostriatal pathway, were not changed in MPTP-injected wild-type and Hdac6−/− mice. Therefore, HDAC6 deficiency leads to moderate alterations of behaviors and Parkinson’s disease pathology in mice

Passively Q-Switched Operation of a Tm,Ho:LuVO4 Laser with a Graphene Saturable Absorber

A passively Q-switched (PQS) operation of Tm,Ho:LuVO4 laser is experimentally demonstrated with a graphene saturable absorber (SA) mirror. An average output power of 1034 mW at 54.5 kHz is acquired with an 8% optical&ndash;optical conversion efficiency. The energy per pulse of 40.4 &mu;J and a peak power of 56.07 W are achieved; the narrowest pulse width of 300 ns is acquired, and the output wavelengths of Tm,Ho:LuVO4 are 2075.02 nm in a continuous wave (CW) regime and 2057.03 nm in a PQS regime

Image_1_Protein phosphatase-1 inhibitor-2 promotes PP1γ positive regulation of synaptic transmission.tiff

Inhibitor-2 (I-2) is a prototypic inhibitor of protein phosphatase-1 (PP1), a major serine-threonine phosphatase that regulates synaptic plasticity and learning and memory. Although I-2 is a potent inhibitor of PP1 in vitro, our previous work has elucidated that, in vivo, I-2 may act as a positive regulator of PP1. Here we show that I-2 and PP1γ, but not PP1α, positively regulate synaptic transmission in hippocampal neurons. Moreover, we demonstrated that I-2 enhanced PP1γ interaction with its major synaptic scaffold, neurabin, by Förster resonance energy transfer (FRET)/Fluorescence lifetime imaging microscopy (FLIM) studies, while having a limited effect on PP1 auto-inhibitory phosphorylation. Furthermore, our study indicates that the effect of I-2 on PP1 activity in vivo is dictated by I-2 threonine-72 phosphorylation. Our work thus demonstrates a molecular mechanism by which I-2 positively regulates PP1 function in synaptic transmission.</p

Additional file 1 of NOD-like receptor NLRC5 promotes neuroinflammation and inhibits neuronal survival in Parkinson’s disease models

Additional file 1. Additional figures and Tables

Data_Sheet_1_Deficiency of miR-29a/b1 leads to premature aging and dopaminergic neuroprotection in mice.pdf

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by progressive degeneration of midbrain dopaminergic neurons. The miR-29s family, including miR-29a and miR-29b1 as well as miR-29b2 and miR-29c, are implicated in aging, metabolism, neuronal survival, and neurological disorders. In this study, the roles of miR-29a/b1 in aging and PD were investigated. miR-29a/b1 knockout mice (named as 29a KO hereafter) and their wild-type (WT) controls were used to analyze aging-related phenotypes. After challenged with the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), dopaminergic injuries, glial activation, and mouse behaviors were evaluated. Primary glial cells were further cultured to explore the underlying mechanisms. Additionally, the levels of miR-29s in the cerebrospinal fluid (CSF) of PD patients (n = 18) and healthy subjects (n = 17) were quantified. 29a KO mice showed dramatic weight loss, kyphosis, and along with increased and deepened wrinkles in skins, when compared with WT mice. Moreover, both abdominal and brown adipose tissues reduced in 29a KO mice, compared to their WT counterpart. However, in MPTP-induced PD mouse model, the deficiency of miR-29a/b1 led to less severe damages of dopaminergic system and mitigated glial activation in the nigrostriatal pathway, and subsequently alleviated the motor impairments in 3-month-old mice. Eight-month-old mutant mice maintained such a resistance to MPTP intoxication. Mechanistically, the deficiency of miR-29a/b-1 promoted the expression of neurotrophic factors in 1-Methyl-4-phenylpyridinium (MPP+)-treated primary mixed glia and primary astrocytes. In lipopolysaccharide (LPS)-treated primary microglia, knockout of miR-29a/b-1 inhibited the expression of inflammatory factors, and promoted the expression of anti-inflammatory factors and neurotrophic factors. Knockout of miR-29a/b1 increased the activity of AMP-activated protein kinase (AMPK) and repressed NF-κB/p65 signaling in glial cells. Moreover, we found miR-29a level was increased in the CSF of patients with PD. Our results suggest that 29a KO mice display the peripheral premature senility. The combined effects of less activated glial cells might contribute to the mitigated inflammatory responses and elicit resistance to MPTP intoxication in miR-29a/b1 KO mice.</p