Deletion of Talin1 in Myeloid Cells Facilitates Atherosclerosis in Mice.

BACKGROUND: Integrin-regulated monocyte recruitment and cellular responses of monocyte-derived macrophages are critical for the pathogenesis of atherosclerosis. In the canonical model, talin1 controls ligand binding to integrins, a prerequisite for integrins to mediate leukocyte recruitment and induce immune responses. However, the role of talin1 in the development of atherosclerosis has not been studied. Our study investigated how talin1 in myeloid cells regulates the progression of atherosclerosis. METHODS: On an Apoe-/- background, myeloid talin1-deficient mice and the control mice were fed with a high-fat diet for 8 or 12 weeks to induce atherosclerosis. The atherosclerosis development in the aorta and monocyte recruitment into atherosclerotic lesions were analyzed. RESULTS: Myeloid talin1 deletion facilitated the formation of atherosclerotic lesions and macrophage deposition in lesions. Talin1 deletion abolished integrin ß2-mediated adhesion of monocytes but did not impair integrin α4ß1-dependent cell adhesion in a flow adhesion assay. Strikingly, talin1 deletion did not prevent Mn2+- or chemokine-induced activation of integrin α4ß1 to the high-affinity state for ligands. In an in vivo competitive homing assay, monocyte infiltration into inflamed tissues was prohibited by antibodies to integrin α4ß1 but was not affected by talin1 deletion or antibodies to integrin ß2. Furthermore, quantitative polymerase chain reaction and ELISA (enzyme-linked immunosorbent assay) analysis showed that macrophages produced cytokines to promote inflammation and the proliferation of smooth muscle cells. Ligand binding to integrin ß3 inhibited cytokine generation in macrophages, although talin1 deletion abolished the negative effects of integrin ß3. CONCLUSIONS: Integrin α4ß1 controls monocyte recruitment during atherosclerosis. Talin1 is dispensable for integrin α4ß1 activation to the high-affinity state and integrin α4ß1-mediated monocyte recruitment. Yet, talin1 is required for integrin ß3 to inhibit the production of inflammatory cytokines in macrophages. Thus, intact monocyte recruitment and elevated inflammatory responses cause enhanced atherosclerosis in talin1-deficient mice. Our study provides novel insights into the roles of myeloid talin1 and integrins in the progression of atherosclerosis.

Deletion of platelet CLEC-2 decreases GPIbα-mediated integrin αIIbß3 activation and decreases thrombosis in TTP.

Microvascular thrombosis in patients with thrombotic thrombocytopenic purpura (TTP) is initiated by GPIbα-mediated platelet binding to von Willebrand factor (VWF). Binding of VWF to GPIbα causes activation of the platelet surface integrin αIIbß3. However, the mechanism of GPIbα-initiated activation of αIIbß3 and its clinical importance for microvascular thrombosis remain elusive. Deletion of platelet C-type lectin-like receptor 2 (CLEC-2) did not prevent VWF binding to platelets but specifically inhibited platelet aggregation induced by VWF binding in mice. Deletion of platelet CLEC-2 also inhibited αIIbß3 activation induced by the binding of VWF to GPIbα. Using a mouse model of TTP, which was created by infusion of anti-mouse ADAMTS13 monoclonal antibodies followed by infusion of VWF, we found that deletion of platelet CLEC-2 decreased pulmonary arterial thrombosis and the severity of thrombocytopenia. Importantly, prophylactic oral administration of aspirin, an inhibitor of platelet activation, and therapeutic treatment of the TTP mice with eptifibatide, an integrin αIIbß3 antagonist, reduced pulmonary arterial thrombosis in the TTP mouse model. Our observations demonstrate that GPIbα-mediated activation of integrin αIIbß3 plays an important role in the formation of thrombosis in TTP. These observations suggest that prevention of platelet activation with aspirin may reduce the risk for thrombosis in patients with TTP.

The rumen microbiota contributed to the development of mastitis induced by subclinical ketosis.

BACKGROUND: Mastitis is a serious disease which affects animal husbandry, particularly in cow breeding. The etiology of mastitis is complex and its pathological mechanism is not yet fully understood. Our previous research in clinical investigation has revealed that subclinical ketosis can increase the number of somatic cell counts (SCC) in milk, although the underlying mechanism remains unclear. Recent studies have further confirmed the significant role of mastitis. RESULTS: In this study, we aimed to examine the SCC, rumen microbiota, and metabolites in the milkmen of cows with subclinical ketosis. Additionally, we conducted a rumen microbiota transplant into mice to investigate the potential association between rumen microbiota disturbance and mastitis induced by subclinical ketosis in dairy cows. The study has found that cows with subclinical ketosis have a higher SCC in their milk compared to healthy cows. Additionally, there were significant differences in the rumen microbiota and the level of volatile fatty acid (VFA) between cows with subclinical ketosis and healthy cows. Moreover, transplanting the rumen microbiota from subclinical ketosis and mastitis cows into mice can induce mammary inflammation and liver function damage than transplanting the rumen flora from healthy dairy cows. CONCLUSIONS: In addition to the infection of mammary gland by pathogenic microorganisms, there is also an endogenous therapeutic pathway mediated by rumen microbiota. Targeted rumen microbiota modulation may be an effective way to prevent and control mastitis in dairy cows.

[Ce3+-OV-Ce4+] Located Surface-Distributed Sheet Cu-Zn-Ce Catalysts for Methanol Production by CO2 Hydrogenation.

The metal-support interaction is crucial for the performance of Cu-based catalysts. However, the distinctive properties of the support metal element itself are often overlooked in catalyst design. In this paper, a sheet Cu-Zn-Ce with [Ce3+-OV-Ce4+] located on the surface was designed by the sol-gel method. Through EPR and X-ray photoelectron spectroscopy (XPS), the relationship between the content of oxygen vacancies and Ce was revealed. Ce itself induces the generation of [Ce3+-OV-Ce4+]. Through ICP-MS, XPS, and SEM-mapping, the Ce-induced formation of [Ce3+-OV-Ce4+] located on the catalyst surface was demonstrated. CO2-TPD and DFT calculations further revealed that [Ce3+-OV-Ce4+] enhanced CO2 adsorption, leading to a 10% increase in methanol selectivity compared to Cu-Zn-Ce synthesized via the coprecipitation method.

In†Silico Analysis Identifies the Anti-Liver Injury Targets of Diammonium Glycyrrhizinate: Validated in Perfluorooctanoic Acid-Lesioned Mouse Model.

Liver injury refers to a pathological condition that causes dysfunction to hepatic parenchymal cells. And diammonium glycyrrhizinate (DG) is clinically prescribed for hepatoprotection. To date, detailed information regarding DG against liver injury in molecular mechanisms remains unrevealed totally. In the present study, we applied network pharmacology and molecular docking to decipher substantial genes, biological functions of DG for treating liver injury. Furthermore, preclinical experiments using perfluorooctanoic acid (PFOA)-induced liver injury in mice were used to validate the bioinformatic findings. Our results showed that the target network of DG and liver injury predominantly shared 90 genes. Eleven core genes of DG treating liver injury including ALB, TP53, TNF, CASP3, PTGS2, JUN, TLR4, IL10, STAT3, NOS3, FOS. The gene ontology and KEGG enrichment further highlighted their importance in regulation of cell proliferation, regulation of transcription, inflammatory response, regulation of NF-kappaB import into nucleus, regulation of apoptotic process, T cell receptor signaling pathway, and Toll-like receptor signaling pathway. Moreover, DG treatment was found to rescue the PFOA-induced liver injury through the modulation of identified genes including TNF, CASP3, PTGS2, and ALB. Current integrated data from bioinformatics method and experimental validation uncovered that DG exerts potent actions to treat liver injury through regulating core targets associated with inflammation and immunomodulation.

Visualizing and Isolating Iron-Reducing Microorganisms at the Single-Cell Level.

Iron-reducing microorganisms (FeRM) play key roles in many natural and engineering processes. Visualizing and isolating FeRM from multispecies samples are essential to understand the in situ location and geochemical role of FeRM. Here, we visualized FeRM by a "turn-on" Fe2+-specific fluorescent chemodosimeter (FSFC) with high sensitivity, selectivity, and stability. This FSFC could selectively identify and locate active FeRM from either pure culture, coculture of different bacteria, or sediment-containing samples. Fluorescent intensity of the FSFC could be used as an indicator of Fe2+ concentration in bacterial cultures. By combining the use of the FSFC with that of a single-cell sorter, we obtained three FSFC-labeled cells from an enriched consortium, and all of them were subsequently shown to be capable of iron reduction; two unlabeled cells were shown to have no iron-reducing capability, further confirming the feasibility of the FSFC.IMPORTANCE Visualization and isolation of FeRM from samples containing multiple species are commonly needed by researchers from different disciplines, such as environmental microbiology, environmental sciences, and geochemistry. However, no available method has been reported. In this study, we provide a method to visualize FeRM and evaluate their activity even at the single-cell level. When this approach is combined with use of a single-cell sorter, FeRM can also be isolated from samples containing multiple species. This method can be used as a powerful tool to uncover the in situ or ex situ role of FeRM and their interactions with ambient microbes or chemicals.

Magnetic Resonance Imaging Segmentation via Weighted Level Set Model Based on Local Kernel Metric and Spatial Constraint.

Magnetic resonance imaging (MRI) segmentation is a fundamental and significant task since it can guide subsequent clinic diagnosis and treatment. However, images are often corrupted by defects such as low-contrast, noise, intensity inhomogeneity, and so on. Therefore, a weighted level set model (WLSM) is proposed in this study to segment inhomogeneous intensity MRI destroyed by noise and weak boundaries. First, in order to segment the intertwined regions of brain tissue accurately, a weighted neighborhood information measure scheme based on local multi information and kernel function is designed. Then, the membership function of fuzzy c-means clustering is used as the spatial constraint of level set model to overcome the sensitivity of level set to initialization, and the evolution of level set function can be adaptively changed according to different tissue information. Finally, the distance regularization term in level set function is replaced by a double potential function to ensure the stability of the energy function in the evolution process. Both real and synthetic MRI images can show the effectiveness and performance of WLSM. In addition, compared with several state-of-the-art models, segmentation accuracy and Jaccard similarity coefficient obtained by WLSM are increased by 0.0586, 0.0362 and 0.1087, 0.0703, respectively.

Sialylation on O-glycans protects platelets from clearance by liver Kupffer cells.

Most platelet membrane proteins are modified by mucin-type core 1-derived glycans (O-glycans). However, the biological importance of O-glycans in platelet clearance is unclear. Here, we generated mice with a hematopoietic cell-specific loss of O-glycans (HC C1galt1-/- ). These mice lack O-glycans on platelets and exhibit reduced peripheral platelet numbers. Platelets from HC C1galt1-/- mice show reduced levels of α-2,3-linked sialic acids and increased accumulation in the liver relative to wild-type platelets. The preferential accumulation of HC C1galt1-/- platelets in the liver was reduced in mice lacking the hepatic asialoglycoprotein receptor [Ashwell-Morell receptor (AMR)]. However, we found that Kupffer cells are the primary cells phagocytosing HC C1galt1-/- platelets in the liver. Our results demonstrate that hepatic AMR promotes preferential adherence to and phagocytosis of desialylated and/or HC C1galt1-/- platelets by the Kupffer cell through its C-type lectin receptor CLEC4F. These findings provide insights into an essential role for core 1 O-glycosylation of platelets in their clearance in the liver.

Loss of mucin-type O-glycans impairs the integrity of the glomerular filtration barrier in the mouse kidney.

The kidney's filtration activity is essential for removing toxins and waste products from the body. The vascular endothelial cells of the glomerulus are fenestrated, flattened, and surrounded by podocytes, specialized cells that support glomerular endothelial cells. Mucin-type core 1-derived O-glycans (O-glycans) are highly expressed on both glomerular capillary endothelial cells and their supporting podocytes, but their biological role is unclear. Biosynthesis of core 1-derived O-glycans is catalyzed by the glycosyltransferase core 1 ß1,3-galactosyltransferase (C1galt1). Here we report that neonatal or adult mice with inducible deletion of C1galt1 (iC1galt1-/-) exhibit spontaneous proteinuria and rapidly progressing glomerulosclerosis. Ultrastructural analysis of the glomerular filtration barrier components revealed that loss of O-glycans results in altered podocyte foot processes. Further analysis indicated that O-glycan is essential for the normal signaling function of podocalyxin, a podocyte foot process-associated glycoprotein. Our results reveal a new function of O-glycosylation in the integrity of the glomerular filtration barrier.

One-pot engineering TiO2/graphene interface for enhanced adsorption and photocatalytic degradation of multiple organics.

It is challenging to design a multifunctional structure or composite for the simultaneous adsorption and photocatalytic degradation of organic pollutants in water. Towards this goal, in this work we innovatively engineered interfacial sites between TiO2 particles and reduced graphene oxide (RGO) sheets by employing an in situ one-pot one-step solvothermal method. The interface was associated with the content of RGO, solvothermal time and solvent ratio of n-pentanol to n-hexane. It was found that with a moderate amount of RGO (25%), TiO2 nanoparticles were well dispersed on the surface of the RGO or wrapped by the RGO, thus leading to full contact and strong interactions to form a Ti-O-C interfacial structure. But with low content of RGO (6%), TiO2 aggregates were a mixture of nanosheets, nanoparticles and nanorods. 25%RGO/TiO2 also had 175% higher surface area (146 m2 g-1), 95% larger volume (0.339 cm3 g-1) and smaller band gap than 6%RGO/TiO2. More importantly, 25%RGO/TiO2 demonstrated higher adsorption efficiency (25%) and four times faster degradation rate than TiO2 (0%). It also exhibited good capability to eliminate multiple organics and stable long-term cycle performance (up to 93% retention after 30 cycles). Its superiority was attributed to the large surface area and unique interface between the TiO2 and RGO, which not only provided more active sites to capture pollutants, but enhanced charge transfer (3 µA cm-2, five times higher than TiO2). This work offers a promising way to purify water through engineering new material structure and integrating adsorption and photodegradation technologies.

A Fluorescein-Based Colorimetric and Fluorescent Probe for Hydrazine and its Bioimaging in Live Cells.

A turn-on fluorescent probe (FN) for detection of hydrazine has been developed. Probe FN exhibited high selectivity and excellent sensitivity towards hydrazine with a detection limit as low as 4.6 × 10-10 M. Probe FN selectively reacts with hydrazine (N2H4) in a physiological environment, leading to an off-on fluorescence response along with the color change from colorless to yellow, allowing colorimetric detection of hydrazine by the naked eye. Furthermore, probe FN was successfully applied for visualizing hydrazine in living cells.

Structure of the human cohesin inhibitor Wapl.

Cohesin, along with positive regulators, establishes sister-chromatid cohesion by forming a ring to circle chromatin. The wings apart-like protein (Wapl) is a key negative regulator of cohesin and forms a complex with precocious dissociation of sisters protein 5 (Pds5) to promote cohesin release from chromatin. Here we report the crystal structure and functional characterization of human Wapl. Wapl contains a flexible, variable N-terminal region (Wapl-N) and a conserved C-terminal domain (Wapl-C) consisting of eight HEAT (Huntingtin, Elongation factor 3, A subunit, and target of rapamycin) repeats. Wapl-C folds into an elongated structure with two lobes. Structure-based mutagenesis maps the functional surface of Wapl-C to two distinct patches (I and II) on the N lobe and a localized patch (III) on the C lobe. Mutating critical patch I residues weaken Wapl binding to cohesin and diminish sister-chromatid resolution and cohesin release from mitotic chromosomes in human cells and Xenopus egg extracts. Surprisingly, patch III on the C lobe does not contribute to Wapl binding to cohesin or its known regulators. Although patch I mutations reduce Wapl binding to intact cohesin, they do not affect Wapl-Pds5 binding to the cohesin subcomplex of sister chromatid cohesion protein 1 (Scc1) and stromal antigen 2 (SA2) in vitro, which is instead mediated by Wapl-N. Thus, Wapl-N forms extensive interactions with Pds5 and Scc1-SA2. Wapl-C interacts with other cohesin subunits and possibly unknown effectors to trigger cohesin release from chromatin.

Baccalaureate nursing students' perspectives on learning about caring in China: a qualitative descriptive study.

BACKGROUND: The need to provide humanistic care in the contemporary healthcare system is more imperative now and the importance of cultivating caring in nursing education is urgent. Caring as the primary work of nursing has been discussed extensively, such as the meaning of caring, and teaching and learning strategies to improve nursing students' caring ability. Yet attempts to understand students' perspectives on learning about caring and to know their learning needs are seldom presented. The aim of this qualitative descriptive study was to explore the baccalaureate nursing students' perspectives on learning about caring in China. METHODS: A qualitative descriptive study using focus group interviews were undertaken in two colleges in Yunnan Province, China from February 2010 to April 2010. Purposeful sampling of 20 baccalaureate nursing students were recruited. Content analysis of the transcribed data was adopted to identify the themes. RESULTS: Four categories with some sub-categories related to students' perspectives on learning about caring were identified from the data: 1) Learning caring by role model; 2) conducive learning environment as the incentive to the learning about caring; 3) lack of directive substantive way of learning as the hindrance to the learning about caring; 4) lack of cultural competency as the barrier to the learning about caring. CONCLUSIONS: Both caring and uncaring experiences can promote the learning about caring in a way of reflective practice. The formal, informal and hidden curricula play an important role in the learning about caring. Cultural awareness, sensitivity and humility are important in the process of learning to care in a multicultural area.

MCNMF-Unet: a mixture Conv-MLP network with multi-scale features fusion Unet for medical image segmentation.

Recently, the medical image segmentation scheme combining Vision Transformer (ViT) and multilayer perceptron (MLP) has been widely used. However, one of its disadvantages is that the feature fusion ability of different levels is weak and lacks flexible localization information. To reduce the semantic gap between the encoding and decoding stages, we propose a mixture conv-MLP network with multi-scale features fusion Unet (MCNMF-Unet) for medical image segmentation. MCNMF-Unet is a U-shaped network based on convolution and MLP, which not only inherits the advantages of convolutional in extracting underlying features and visual structures, but also utilizes MLP to fuse local and global information of each layer of the network. MCNMF-Unet performs multi-layer fusion and multi-scale feature map skip connections in each network stage so that all the feature information can be fully utilized and the gradient disappearance problem can be alleviated. Additionally, MCNMF-Unet incorporates a multi-axis and multi-windows MLP module. This module is fully end-to-end and eliminates the need to consider the negative impact of image cropping. It not only fuses information from multiple dimensions and receptive fields but also reduces the number of parameters and computational complexity. We evaluated the proposed model on BUSI, ISIC2018 and CVC-ClinicDB datasets. The experimental results show that the performance of our proposed model is superior to most existing networks, with an IoU of 84.04% and a F1-score of 91.18%.

The potential crosstalk genes and molecular mechanisms between glioblastoma and periodontitis.

Despite clinical and epidemiological evidence suggestive of a link between glioblastoma (GBM) and periodontitis (PD), the shared mechanisms of gene regulation remain elusive. In this study, we identify differentially expressed genes (DEGs) that overlap between the GEO datasets GSE4290 [GBM] and GSE10334 [PD]. Functional enrichment analysis was conducted, and key modules were identified using protein-protein interaction (PPI) network and weighted gene co-expression network analysis (WGCNA). The expression levels of CXCR4, LY96, and C3 were found to be significantly elevated in both the test dataset and external validation dataset, making them key crosstalk genes. Additionally, immune cell landscape analysis revealed elevated expression levels of multiple immune cells in GBM and PD compared to controls, with the key crosstalk genes negatively associated with Macrophages M2. FLI1 was identified as a potential key transcription factor (TF) regulating the three key crosstalk genes, with increased expression in the full dataset. These findings contribute to our understanding of the immune and inflammatory aspects of the comorbidity mechanism between GBM and PD.

Bioinformatics analysis revealed the potential crosstalk genes and molecular mechanisms between intracranial aneurysms and periodontitis.

OBJECTIVES: The risk of intracranial aneurysms (IAs) development and rupture is significantly higher in patients with periodontitis (PD), suggesting an association between the two. However, the specific mechanisms of association between these two diseases have not been fully investigated. MATERIALS AND METHODS: In this study, we downloaded IAs and PD data from the Gene Expression Omnibus. Differentially expressed genes (DEGs) were identified, and functional enrichment analysis was performed. The protein-protein interaction (PPI) network and weighted gene co-expression network analysis (WGCNA) was performed to identified key modules and key crosstalk genes. In addition, the immune cell landscape was assessed and the correlation of key crosstalk genes with each immune cell was calculated. Finally, transcription factors (TFs) regulating key crosstalk genes were explored. RESULTS: 127 overlapping DEGs were identified and functional enrichment analysis highlighted the important role of immune reflection in the pathogenesis of IAs and PD. We identified ITGAX and COL4A2 as key crosstalk genes. In addition, the expression of multiple immune cells was significantly elevated in PDs and IAs compared to controls, and both key crosstalk genes were significantly negatively associated with Macrophages M2. Finally, GATA2 was identified as a potential key transcription factor (TF), which regulates two key crosstalk gene. CONCLUSIONS: The present study identifies key crosstalk genes and TF in PD and IAs, providing new insights for further study of the co-pathogenesis of PD and IAs from an immune and inflammatory perspective. Also, this is the first study to report the above findings.

Cohesin acetylation promotes sister chromatid cohesion only in association with the replication machinery.

Acetylation of the Smc3 subunit of cohesin is essential to establish functional cohesion between sister chromatids. Smc3 acetylation is catalyzed by members of the Eco family of acetyltransferases, although the mechanism by which acetylation is regulated and how it promotes cohesion are largely unknown. In vertebrates, the cohesin complex binds to chromatin during mitotic exit and is converted to a functional form during or shortly after DNA replication. The conserved proliferating cell nuclear antigen-interacting protein box motif in yeast Eco1 is required for function, and cohesin is acetylated during the S phase. This has led to the notion that acetylation of cohesin is stimulated by interaction of Eco1 with the replication machinery. Here we show that in vertebrates Smc3 acetylation occurs independently of DNA replication. Smc3 is readily acetylated before replication is initiated and after DNA replication is complete. However, we also show that functional acetylation occurs only in association with the replication machinery: disruption of the interaction between XEco2 and proliferating cell nuclear antigen prevents cohesion establishment while having little impact on the overall levels of Smc3 acetylation. These results demonstrate that Smc3 acetylation can occur throughout interphase but that only acetylation in association with the replication fork promotes sister chromatid cohesion. These data reveal how the generation of cohesion is limited to the appropriate time and place during the cell cycle and provide insight into the mechanism by which acetylation ensures cohesion.

Confronting the caring crisis in clinical practice.

CONTEXT: In light of the call for humanistic caring in the contemporary health care system globally and in China, the issue of improving the caring skills that are essential to student success, high-quality nursing practice and positive patient outcomes is at the forefront of nursing education. OBJECTIVES: The aim of this mixed-methods quantitative and qualitative study was to investigate baccalaureate nursing students' caring ability in the context of China and to explore the role of clinical practice learning in the development of students' caring skills. METHODS: A two-phase, descriptive study utilising a mixed methodology consisting of a caring ability survey and focus group interviews was conducted. In the quantitative phase, 598 baccalaureate nursing students at two colleges in Yunnan Province in southwest China were surveyed using the Caring Ability Inventory (CAI). In the qualitative phase, 16 of the students who had participated in the quantitative phase were interviewed. RESULTS: Students obtained lower scores on the CAI than have been reported elsewhere by other researchers. In addition, students in the clinical stage of training scored lower than students in the pre-clinical stage. Three themes concerning facilitation by and three themes concerning the obstructive effects of clinical practice learning in the development of caring ability were identified. Themes pertaining to facilitation were: (i) promoting a sense of professional responsibility and ethics; (ii) providing an arena in which to practise caring, and (iii) learning from positive role models. Themes pertaining to obstruction were: (i) a critical practice learning environment; (ii) encountering inappropriate clinical teachers, and (iii) experiencing shock at the contrast between an idealised and the real environment. CONCLUSIONS: The key to developing students' ability to care lies in highlighting caring across the entire health care system. By diminishing exposure to negative role models, and adopting appropriate pedagogical ideas about education in caring, such as truth telling and helping students to think in a critical manner, educators can help students to improve their caring ability.

Sororin cooperates with the acetyltransferase Eco2 to ensure DNA replication-dependent sister chromatid cohesion.

Sister chromatids are held together, from the time they are made during S phase until they are pulled apart just before cell division, by a protein complex called cohesin. The mechanistic details by which sister chromatid cohesion is established and maintained have remained elusive, particularly in vertebrate systems. Sororin, a protein that interacts with the cohesin complex, is essential for cohesion in vertebrates, but how it participates in the process is unknown. Here we demonstrate that sororin recruitment depends on active DNA replication and that sororin loading onto chromosomes depends upon another essential cohesion factor, the acetyltransferase Eco2. We find that Eco2, like sororin, is a substrate of the anaphase-promoting complex (APC), which ensures that protein levels remain low before S phase. These findings demonstrate that sororin and Eco2 work together to form a unique regulatory module that limits cohesion to cells with replicated chromatin and support a model in which cohesion in vertebrates is not fully established until the G2 phase of the cell cycle.

FM-Unet: Biomedical image segmentation based on feedback mechanism Unet.

With the development of deep learning, medical image segmentation technology has made significant progress in the field of computer vision. The Unet is a pioneering work, and many researchers have conducted further research based on this architecture. However, we found that most of these architectures are improvements in the backward propagation and integration of the network, and few changes are made to the forward propagation and information integration of the network. Therefore, we propose a feedback mechanism Unet (FM-Unet) model, which adds feedback paths to the encoder and decoder paths of the network, respectively, to help the network fuse the information of the next step in the current encoder and decoder. The problem of encoder information loss and decoder information shortage can be well solved. The proposed model has more moderate network parameters, and the simultaneous multi-node information fusion can alleviate the gradient disappearance. We have conducted experiments on two public datasets, and the results show that FM-Unet achieves satisfactory results.