EMC2A-Net: An Efficient Multibranch Cross-channel Attention Network for SAR Target Classification

In recent years, convolutional neural networks (CNNs) have shown great potential in synthetic aperture radar (SAR) target recognition. SAR images have a strong sense of granularity and have different scales of texture features, such as speckle noise, target dominant scatterers and target contours, which are rarely considered in the traditional CNN model. This paper proposed two residual blocks, namely EMC2A blocks with multiscale receptive fields(RFs), based on a multibranch structure and then designed an efficient isotopic architecture deep CNN (DCNN), EMC2A-Net. EMC2A blocks utilize parallel dilated convolution with different dilation rates, which can effectively capture multiscale context features without significantly increasing the computational burden. To further improve the efficiency of multiscale feature fusion, this paper proposed a multiscale feature cross-channel attention module, namely the EMC2A module, adopting a local multiscale feature interaction strategy without dimensionality reduction. This strategy adaptively adjusts the weights of each channel through efficient one-dimensional (1D)-circular convolution and sigmoid function to guide attention at the global channel wise level. The comparative results on the MSTAR dataset show that EMC2A-Net outperforms the existing available models of the same type and has relatively lightweight network structure. The ablation experiment results show that the EMC2A module significantly improves the performance of the model by using only a few parameters and appropriate cross-channel interactions.Comment: 15 pages, 9 figures, Submitted to IEEE Transactions on Geoscience and Remote Sensing, 202

HMGA1 variant IVS5-13insC is associated with insulin resistance and type 2 diabetes: an updated meta-analysis

Background: High-mobility group A1 (HMGA1) polymorphism has been suspected as a gene variant associated with type 2 diabetes (T2D). However, conflicting outcomes have been reported. Objective: This meta-analysis aimed to predict the association between the HMGA1 variant IVS5-13insC and T2D. Methods: Statistical analyses were performed using Stata/SE 12.0 software. Results: A total of 11 case-control studies in 6 articles were included. Results suggested that the HMGA1 variant IVS5-13insC was associated with an increased risk of insulin resistance (OR = 0.61, 95% CI 0.56 to 0.66, P < 0.0001), T2D (OR = 0.67, 95% CI 0.61 to 0.73, P < 0.0001), particularly for Caucasians with increased risks of T2D (OR = 0.56, 95% CI 0.49 to 0.65, P < 0.0001) compared with wild-type subjects. Conclusion: This meta-analysis indicated that the HMGA1 variant IVS5-13insC can be a risk factor of T2D development, particularly among Caucasians. Significant risks were also found (Asian: OR = 0.74, 95% CI: 0.63 to 0.86, P < 0.0001, Hispanic-American: OR = 0.81, 95% CI: 0.65 to 1.01, P < 0.0001) in non-Caucasian population. However, ethnical studies should be conducted to reveal whether the HMGA1 variant IVS5-13insC is associated with an increased risk of T2D.Keywords: HMGA1, type 2 diabetes, insulin resistance, variant, meta-analysis

Crosstalk between the CBM complex/NF-κB and MAPK/P27 signaling pathways of regulatory T cells contributes to the tumor microenvironment

Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1–BCL10–MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors

HMGA1 variant IVS5-13insC is associated with insulin resistance and type 2 diabetes: an updated meta-analysis

Background: High-mobility group A1 (HMGA1) polymorphism has been suspected as a gene variant associated with type 2 diabetes (T2D). However, conflicting outcomes have been reported. Objective: This meta-analysis aimed to predict the association between the HMGA1 variant IVS5-13insC and T2D. Methods: Statistical analyses were performed using Stata/SE 12.0 software. Results: A total of 11 case-control studies in 6 articles were included. Results suggested that the HMGA1 variant IVS5-13insC was associated with an increased risk of insulin resistance (OR = 0.61, 95% CI 0.56 to 0.66, P < 0.0001), T2D (OR = 0.67, 95% CI 0.61 to 0.73, P < 0.0001), particularly for Caucasians with increased risks of T2D (OR = 0.56, 95% CI 0.49 to 0.65, P < 0.0001) compared with wild-type subjects. Conclusion: This meta-analysis indicated that the HMGA1 variant IVS5-13insC can be a risk factor of T2D development, particularly among Caucasians. Significant risks were also found (Asian: OR = 0.74, 95% CI: 0.63 to 0.86, P < 0.0001, Hispanic-American: OR = 0.81, 95% CI: 0.65 to 1.01, P < 0.0001) in non-Caucasian population. However, ethnical studies should be conducted to reveal whether the HMGA1 variant IVS5-13insC is associated with an increased risk of T2D

The mechanisms of white matter injury and immune system crosstalk in promoting the progression of Parkinson’s disease: a narrative review

Parkinson’s disease (PD) is neurodegenerative disease in middle-aged and elderly people with some pathological mechanisms including immune disorder, neuroinflammation, white matter injury and abnormal aggregation of alpha-synuclein, etc. New research suggests that white matter injury may be important in the development of PD, but how inflammation, the immune system, and white matter damage interact to harm dopamine neurons is not yet understood. Therefore, it is particularly important to delve into the crosstalk between immune cells in the central and peripheral nervous system based on the study of white matter damage in PD. This crosstalk could not only exacerbate the pathological process of PD but may also reveal new therapeutic targets. By understanding how immune cells penetrate through the blood–brain barrier and activate inflammatory responses within the central nervous system, we can better grasp the impact of structural destruction of white matter in PD and explore how this process can be modulated to mitigate or combat disease progression. Microglia, astrocytes, oligodendrocytes and peripheral immune cells (especially T cells) play a central role in its pathological process where these immune cells produce and respond to pro-inflammatory cytokines such as tumor necrosis factor (TNF-α), interleukin-1β(IL-1β) and interleukin-6(IL-6), and white matter injury causes microglia to become pro-inflammatory and release inflammatory mediators, which attract more immune cells to the damaged area, increasing the inflammatory response. Moreover, white matter damage also causes dysfunction of blood–brain barrier, allows peripheral immune cells and inflammatory factors to invade the brain further, and enhances microglia activation forming a vicious circle that intensifies neuroinflammation. And these factors collectively promote the neuroinflammatory environment and neurodegeneration changes of PD. Overall, these findings not only deepen our understanding of the complexity of PD, but also provide new targets for the development of therapeutic strategies focused on inflammation and immune regulation mechanisms. In summary, this review provided the theoretical basis for clarifying the pathogenesis of PD, summarized the association between white matter damage and the immune cells in the central and peripheral nervous systems, and then emphasized their potential specific mechanisms of achieving crosstalk with further aggravating the pathological process of PD

Metabolic reprogramming in the tumor microenvironment: unleashing T cell stemness for enhanced cancer immunotherapy

T cells play a pivotal role in the immune system by distinguishing between various harmful pathogens and cancerous cells within the human body and initiating an immune response. Within the tumor microenvironment (TME), immune effector T cells encounter both immunosuppressive cells and factors that hinder their functionality. Additionally, they endure robust and persistent antigenic stimulation, often leading to exhaustion and apoptosis. However, the stemness of T cells, characterized by their ability to survive and self-renew over extended periods, represents a primary target in immune checkpoint therapies such as anti-PD-1 therapy. T cell stemness encompasses specific memory T cell subsets and progenitor-exhausted T cells with stem cell-like properties. Therefore, understanding the impact of the TME on T cell stemness, including factors like K+, lactate, and H+, holds significant importance and can facilitate the mitigation of terminal T-cell depletion, the identification of potential resilient biomarkers or therapeutic targets resistant to immune checkpoint therapies, and ultimately lead to sustained anti-tumor effects. Thus, it offers a novel perspective for advancing tumor immunotherapy

Aging Kit Mutant Mice Develop Cardiomyopathy

Both bone marrow (BM) and myocardium contain progenitor cells expressing the c-Kit tyrosine kinase. The aims of this study were to determine the effects of c-Kit mutations on: i. myocardial c-Kit+ cells counts and ii. the stability of left ventricular (LV) contractile function and structure during aging. LV structure and contractile function were evaluated (echocardiography) in two groups of Kit mutant (W/Wv and W41/W42) and in wild type (WT) mice at 4 and 12 months of age and the effects of the mutations on LV mass, vascular density and the numbers of proliferating cells were also determined. In 4 month old Kit mutant and WT mice, LV ejection fractions (EF) and LV fractional shortening rates (FS) were comparable. At 12 months of age EF and FS were significantly decreased and LV mass was significantly increased only in W41/W42 mice. Myocardial vascular densities and c-Kit+ cell numbers were significantly reduced in both mutant groups when compared to WT hearts. Replacement of mutant BM with WT BM at 4 months of age did not prevent these abnormalities in either mutant group although they were somewhat attenuated in the W/Wv group. Notably BM transplantation did not prevent the development of cardiomyopathy in 12 month W41/W42 mice. The data suggest that decreased numbers and functional capacities of c-Kit+ cardiac resident progenitor cells may be the basis of the cardiomyopathy in W41/W42 mice and although defects in mutant BM progenitor cells may prove to be contributory, they are not causal

Mandatory IFRS adoption and executive compensation: Evidence from China

This study investigates how the mandatory adoption of International Financial Reporting Standards (IFRS) affects the contractual benefits of using accounting information to determine executive compensation in China. After controlling for firm and corporate governance characteristics, we find strong evidence supporting the positive role of mandatory IFRS adoption on the accounting-based performance sensitivity of executive compensation. Subsample analysis suggests that improvements in accounting-based performance sensitivity after IFRS adoption differ across regions with various levels of institutional quality and across firms that are affected to a different extent by the adoption. Additional analysis supports the argument that the positive effects of IFRS adoption on the use of accounting performance in executive compensation are driven by the reduction in accounting conservatism associated with IFRS adoption