Search

Abstract The kink structure in band dispersion usually refers to a certain electron-boson interaction, which is crucial in understanding the pairing in unconventional superconductors. Here we report the evidence of the observation of a kink structure in Fe-based superconductor CsCa2Fe4As4F2 using angle-resolved photoemission spectroscopy. The kink shows an orbital selective and momentum dependent behavior, which is located at 15 meV below Fermi level along the $$\Gamma -{{\rm{{M}}}}$$ Γ − M direction at the band with d xz orbital character and vanishes when approaching the $$\Gamma -{{\rm{{X}}}}$$ Γ − X direction, correlated with a slight decrease of the superconducting gap. Most importantly, this kink structure disappears when the superconducting gap closes, indicating that the corresponding bosonic mode (~ $$9\pm 1$$ 9 ± 1 meV) is closely related to superconductivity. However, the origin of this mode remains unidentified, since it cannot be related to phonons or the spin resonance mode (~15 meV) observed by inelastic neutron scattering. The behavior of this mode is rather unique and challenges our present understanding of the superconducting paring mechanism of the bilayer FeAs-based superconductors.

Abstract Exotic quantum states arise from the interplay of various degrees of freedom such as charge, spin, orbital, and lattice. Recently, a short-ranged charge order (CO) was discovered deep inside the antiferromagnetic phase of Kagome magnet FeGe, exhibiting close relationships with magnetism. Despite extensive investigations, the CO mechanism remains controversial, mainly because the short-ranged behavior hinders precise identification of CO superstructure. Here, combining multiple experimental techniques, we report the observation of a long-ranged CO in high-quality FeGe samples, which is accompanied with a first-order structural transition. With these high-quality samples, the distorted 2 × 2 × 2 CO superstructure is characterized by a strong dimerization along the c-axis of 1/4 of Ge1-sites in Fe3Ge layers, and in response to that, the 2 × 2 in-plane charge modulations are induced. Moreover, we show that the previously reported short-ranged CO might be related to large occupational disorders at Ge1-site, which upsets the equilibrium of the CO state and the ideal 1 × 1 × 1 structure with very close energies, inducing nanoscale coexistence of these two phases. Our study provides important clues for further understanding the CO properties in FeGe and helps to identify the CO mechanism.

Abstract HP1 proteins are essential for establishing and maintaining transcriptionally silent heterochromatin. They dimerize, forming a binding interface to recruit diverse chromatin-associated factors. Although HP1 proteins are known to rapidly evolve, the extent of variation required to achieve functional specialization is unknown. To investigate how changes in amino acid sequence impacts heterochromatin formation, we performed a targeted mutagenesis screen of the S. pombe HP1 homolog, Swi6. Substitutions within an auxiliary surface adjacent to the HP1 dimerization interface produce Swi6 variants with divergent maintenance properties. Remarkably, substitutions at a single amino acid position lead to the persistent gain or loss of epigenetic inheritance. These substitutions increase Swi6 chromatin occupancy in vivo and altered Swi6-protein interactions that reprogram H3K9me maintenance. We show how relatively minor changes in Swi6 amino acid composition in an auxiliary surface can lead to profound changes in epigenetic inheritance providing a redundant mechanism to evolve HP1-effector specificity.

Abstract Background Circular RNAs (circRNAs), one of the major contents of exosomes, have been shown to participate in the occurrence and progression of cancers. The role and the diagnostic potential of exosome-transported circRNAs in non-small-cell lung cancer (NSCLC) remain largely unknown. Methods The NSCLC-associated exosomal circ_0061407 and circ_0008103 were screened by circRNA microarray. The role of circ_0061407 and circ_0008103 in NSCLC was examined in vitro and in vivo. The encapsulation of the two circRNAs into exosomes and the transport to recipient cells were observed by confocal microscopy. The effects of exosome-transported circ_0061407 and circ_0008103 on recipient cells were investigated using a co-culture device. Bioinformatics analyses were performed to predict the mechanisms by which circ_0061407 and circ_0008103 affected NSCLC. The quantitative polymerase chain reaction was used to quantify the exosome-containing circ_0061407 and circ_0008103 in the serum samples of healthy, pneumonia, benign lung tumours, and NSCLC. The diagnostic efficacy was evaluated using receiver operating characteristic curves. Results The levels of circ_0061407 and circ_0008103 within exosomes were down-regulated in the serum of patients with NSCLC. The up-regulation of circ_0061407 and circ_0008103 inhibited the proliferation, migration/invasion, cloning formation of NSCLC cells in vitro and inhibited lung tumour growth in vivo. Circ_0061407 and circ_0008103 were observed to be packaged in exosomes and transported to recipient cells, where they inhibited the proliferation, migration/invasion, and cloning formation abilities of the recipient cells. Moreover, circ_0061407 and circ_0008103 might be involved in the progression of NSCLC by interacting with microRNAs and proteins. Additionally, lower serum exosomal circ_0061407 and circ_0008103 levels were associated with advanced pathological staging and distant metastasis. Conclusions This study identified two novel exosome-transported circRNAs (circ_0061407 and circ_0008103) associated with NSCLC. These findings may provide additional insights into the development of NSCLC and potential diagnostic biomarkers for NSCLC.

Summary: Biomolecular condensates have emerged as major drivers of cellular organization. It remains largely unexplored, however, whether these condensates can impart mechanical function(s) to the cell. The heterochromatin protein HP1α (Swi6 in Schizosaccharomyces pombe) crosslinks histone H3K9 methylated nucleosomes and has been proposed to undergo condensation to drive the liquid-like clustering of heterochromatin domains. Here, we leverage the genetically tractable S. pombe model and a separation-of-function allele to elucidate a mechanical function imparted by Swi6 condensation. Using single-molecule imaging, force spectroscopy, and high-resolution live-cell imaging, we show that Swi6 is critical for nuclear resistance to external force. Strikingly, it is the condensed yet dynamic pool of Swi6, rather than the chromatin-bound molecules, that is essential to imparting mechanical stiffness. Our findings suggest that Swi6 condensates embedded in the chromatin meshwork establish the emergent mechanical behavior of the nucleus as a whole, revealing that biomolecular condensation can influence organelle and cell mechanics.

Abstract Background Extracellular vesicles (EVs) participate in cancer development via cell-to-cell communication. Long non-coding RNAs (lncRNAs), one component of EVs, can play an essential role in non-small-cell lung cancer (NSCLC) through EV-mediated delivery. Methods The NSCLC-associated lncRNA AL139294.1 in EVs was identified via lncRNA microarray analysis. The role of AL139294.1 in NSCLC was examined in vitro and in vivo. Confocal microscopy was used to observe the encapsulation of AL139294.1 into EVs and its transport to recipient cells. A co-culture device was used to examine the effects of transported AL139294.1 on the oncogenic behaviour of recipient cells. Dual-luciferase reporter assay was performed to verify the direct interaction of miR-204-5p with AL139294.1 and bromodomain-containing protein 4 (BRD4). AL139294.1 and miR-204-5p in EVs were quantified using quantitative polymerase chain reaction. Receiver operating characteristic analyses were conducted to evaluate the diagnostic efficiency. Results The lncRNA AL139294.1 in EVs promoted NSCLC progression in vitro and in vivo. After AL139294.1 was encapsulated into EVs and transported to recipient cells, it promoted the cells’ proliferation, migration, and invasion abilities by competitively binding with miR-204-5p to regulate BRD4, leading to the activation of the Wnt and NF-κB2 pathways. Additionally, the expression of serum lncRNA AL139294.1 in EVs was increased, whereas miR-204-5p in EVs was decreased in NSCLC. High levels of lncRNA AL139294.1 and low levels of miR-204-5p in EVs were associated with advanced pathological staging, lymph node metastasis, and distant metastasis, underscoring their promising utility for distinguishing between more and less severe manifestations of the disease. Conclusions This study reveals a novel lncRNA in EVs associated with NSCLC, namely, AL139294.1, providing valuable insights into the development of NSCLC and introducing potential diagnostic biomarkers for NSCLC.

Abstract Background Few studies have evaluated the effects of the crown-to-implant (C/I) ratio on the marginal bone level (MBL) and bone density in non-splinted single implants. The aim of this study was to assess the effect of C/I ratio on MBL and density of peri-implant bone in non-splinted posterior implants. Methods The C/I ratio, MBL, and grayscale values (GSVs) for bone density were measured from X-rays. Four areas of interest (two at the apical area and two at the middle of the peri-implant area) and two control areas were selected for evaluation. Follow-up radiographs were calibrated according to the control areas. Results In all, 117 non-splinted posterior implants in 73 patients followed up for a mean duration of 36.23 ± 10.40 (range 24–72) months were considered. The mean anatomical C/I ratio was 1.78 ± 0.43 (range 0.93 to 3.06). The mean change in MBL was 0.28 ± 0.97 mm. There were no significant associations between the C/I ratio and MBL changes (r = -0.028, p = 0.766). Pearson correlation showed a significant correlation between changes in GSV and the C/I ratio in the middle peri-implant area (r = 0.301, p = 0.001) and apical area (r = 0.247, p = 0.009). Conclusions A higher C/I ratio of single non-splinted posterior implants is associated with increased peri-implant bone density, but not correlated with changes in MBL.

Abstract Intertwined spin and charge orders have been widely studied in high-temperature superconductors, since their fluctuations may facilitate electron pairing; however, they are rarely identified in heavily electron-doped iron selenides. Here, using scanning tunneling microscopy, we show that when the superconductivity of (Li0.84Fe0.16OH)Fe1-x Se is suppressed by introducing Fe-site defects, a short-ranged checkerboard charge order emerges, propagating along the Fe-Fe directions with an approximately 2aFe period. It persists throughout the whole phase space tuned by Fe-site defect density, from a defect-pinned local pattern in optimally doped samples to an extended order in samples with lower T c or non-superconducting. Intriguingly, our simulations indicate that the charge order is likely driven by multiple-Q spin density waves originating from the spin fluctuations observed by inelastic neutron scattering. Our study proves the presence of a competing order in heavily electron-doped iron selenides, and demonstrates the potential of charge order as a tool to detect spin fluctuations.

Radiation–induced enteritis is an unavoidable complication associated with pelvic tumor radiotherapy, significantly influencing the prognosis of cancer patients. The limited availability of commercial gastrointestinal radioprotectors in clinical settings poses a substantial challenge in preventing radiation enteritis. Despite the inherent radioprotective characteristics of Cur in vitro, its poor solubility in water, instability, and low bioavailability lead to inferior therapeutic effects in vivo. Herein, we developed novel ROS-responsive micelles (CTI) from inulin and curcumin, aimed at mitigating radiation enteritis. CTI micelles had excellent solubility and stability. Importantly, CTI improved the cytotoxicity and bioavailability of curcumin, thereby showing enhanced effectiveness in neutralizing ROS induced by radiation, safeguarding against DNA damage, and reducing radiation-induced cellular mortality. Moreover, in a radiation enteritis mice model, CTI not only alleviated severe radiation-induced intestinal injury but also improved redox-related indicators and reduced inflammatory cytokine expression. Furthermore, CTI effectively increased gut microbiota abundance and maintained gut homeostasis. In conclusion, CTI could be a promising candidate for the clinical management of radiation enteritis. Our study provides a new perspective for radioprotection using natural antioxidants.

BackgroundTraumatic brain injury (TBI) increases the risk of mental disorders and neurodegenerative diseases in the chronic phase. However, there is limited neuropathological or molecular data on the long-term neural dysfunction and its potential mechanism following adolescent TBI.MethodsA total of 160 male mice aged 8 weeks were used to mimic moderate TBI by controlled cortical impact. At 1, 3, 6 and 12 months post-injury (mpi), different neurological functions were evaluated by elevated plus maze, forced swimming test, sucrose preference test and Morris water maze. The levels of oxidative stress, antioxidant response, reactive astrocytes and microglia, and expression of inflammatory cytokines were subsequently assessed in the ipsilateral hippocampus, followed by neuronal apoptosis detection. Additionally, the morphological complexity of hippocampal astrocytes was evaluated by Sholl analysis.ResultsThe adolescent mice exhibited persistent and incremental deficits in memory and anxiety-like behavior after TBI, which were sharply exacerbated at 12 mpi. Depression-like behaviors were observed in TBI mice at 6 mpi and 12 mpi. Compared with the age-matched control mice, apoptotic neurons were observed in the ipsilateral hippocampus during the chronic phase of TBI, which were accompanied by enhanced oxidative stress, and expression of inflammatory cytokines (IL-1β and TNF-α). Moreover, the reactive astrogliosis and microgliosis in the ipsilateral hippocampus were observed in the late phase of TBI, especially at 12 mpi.ConclusionAdolescent TBI leads to incremental cognitive dysfunction, and depression- and anxiety-like behaviors in middle-aged mice. The chronic persistent neuroinflammation and oxidative stress account for the neuronal loss and neural dysfunction in the ipsilateral hippocampus. Our results provide evidence for the pathogenesis of chronic neural damage following TBI and shed new light on the treatment of TBI-induced late-phase neurological dysfunction.

In this study, we present a facile method for preparing oxidation-resistant Cu nanoparticles through a liquid-phase reduction with imidazole compounds (imidazole, 2-methylimidazole, 2-phenylimidazole, and benzimidazole) that serve as protective and dispersing agents. Through a complexation reaction between Cu atoms, the imidazole compounds can form a protective film on the Cu nanoparticles to prevent the particles from rapidly oxidizing. We compared the effects of the four kinds of imidazole compounds on the oxidation resistance and sintering properties of Cu particles. The Cu particles prepared with benzimidazole could be stored in the air for 30 days without being oxidized. After sintering at 300 °C and 2 MPa, the joint of the particles could reach a shear strength of 32 MPa, which meets the requirements for microelectronic packaging.

Abstract Background To observe the clinicopathological and prognostic value of long non-coding RNA five prime to X inactive specific transcript (lncFTX) in multiple tumors. Methods Eligible studies for lncFTX were identified by searching PubMed, Embase, Web of Science and Cochrane Library databases from inception to December 01, 2020. Stata 12.0 software was used to calculate the odds ratio (OR)/hazard ratio (HR) and 95% confidence interval (95% CI). We used The Cancer Genome Atlas (TCGA) dataset to further investigate the differential expression and prognostic value of lncFTX. Results We included 11 studies involving a total of 1633 patients. The results showed that the expression of lncFTX was positively associated with advanced TNM stage (III-IV versus I-II) (OR = 2.30, 95% CI: 1.74–3.03, P

ABSTRACT Bacterial DNA methyltransferases (MTases) function in restriction modification systems, cell cycle control, and the regulation of gene expression. DnmA is a recently described DNA MTase that forms N6-methyladenosine at nonpalindromic 5′-GACGAG-3′ sites in Bacillus subtilis, yet how DnmA activity is regulated is unknown. To address DnmA regulation, we tested substrate binding in vitro and found that DnmA binds poorly to methylated DNA and to an RNA-DNA hybrid with the DNA recognition sequence. Further, DnmA variants with amino acid substitutions that disrupt cognate sequence recognition or catalysis also bind poorly to DNA. Using superresolution fluorescence microscopy and single-molecule tracking of DnmA-PAmCherry, we characterized the subcellular DnmA diffusion and detected its preferential localization to the replisome region and the nucleoid. Under conditions where the chromosome is highly methylated, upon RNA-DNA hybrid accumulation, or with a DnmA variant with severely limited DNA binding activity, DnmA is excluded from the nucleoid, demonstrating that prior methylation or accumulation of RNA-DNA hybrids regulates the association of DnmA with the chromosome in vivo. Furthermore, despite the high percentage of methylated recognition sites and the proximity to putative endonuclease genes conserved across bacterial species, we find that DnmA fails to protect B. subtilis against phage predation, suggesting that DnmA is functionally an orphan MTase involved in regulating gene expression. Our work explores the regulation of a bacterial DNA MTase and identifies prior methylation and RNA-DNA hybrids as regulators of MTase localization. These MTase regulatory features could be common across biology. IMPORTANCE DNA methyltransferases (MTases) influence gene expression, cell cycle control, and host defense through DNA modification. Predicted MTases are pervasive across bacterial genomes, but the vast majority remain uncharacterized. Here, we show that in the soil microorganism Bacillus subtilis, the DNA MTase dnmA and neighboring genes are remnants of a phage defense system that no longer protects against phage predation. This result suggests that portions of the bacterial methylome may originate from inactive restriction modification systems that have maintained methylation activity. Analysis of DnmA movement in vivo shows that active DnmA localizes in the nucleoid, suggesting that DnmA can search for recognition sequences throughout the nucleoid region with some preference for the replisome. Our results further show that prior DNA methylation and RNA-DNA hybrids regulate DnmA dynamics and nucleoid localization, providing new insight into how DNA methylation is coordinated within the cellular environment.

Excessive iron released by hemoglobin and necrotic tissues is the predominant factor that aggravates the outcome of traumatic brain injury (TBI). Regulating the levels of iron and its metabolism is a feasible way to alleviate damage due to TBI. However, the spatial-temporal iron metabolism and iron deposition in neurons and glial cells after TBI remains unclear. In our study, male C57BL/6 mice (8–12 weeks old, weighing 20–26 g) were conducted using controlled cortical impact (CCI) models, combined with treatment of iron chelator deferoxamine (DFO), followed by systematical evaluation on iron deposition, cell-specific expression of iron metabolic proteins and ferroptosis in ipsilateral cortex. Herein, ferroptosis manifest by iron overload and lipid peroxidation was noticed in ipsilateral cortex. Furthermore, iron deposition and cell-specific expression of iron metabolic proteins were observed in the ipsilateral cortical neurons at 1–3 days post-injury. However, iron overload was absent in astrocytes, even though they had intense TBI-induced oxidative stress. In addition, iron accumulation in oligodendrocytes was only observed at 7–14 days post-injury, which was in accordance with the corresponding interval of cellular repair. Microglia play significant roles in iron engulfment and metabolism after TBI, and excessive affects the transformation of M1 and M2 subtypes and activation of microglial cells. Our study revealed that TBI led to ferroptosis in ipsilateral cortex, iron deposition and metabolism exhibited cell-type-specific spatial-temporal changes in neurons and glial cells after TBI. The different effects and dynamic changes in iron deposition and iron metabolism in neurons and glial cells are conducive to providing new insights into the iron-metabolic mechanism and strategies for improving the treatment of TBI.

Ferroptosis and iron-related redox imbalance aggravate traumatic brain injury (TBI) outcomes. NRF2 is the predominant transcription factor regulating oxidative stress and neuroinflammation in TBI, but its role in iron-induced post-TBI damage is unclear. We investigated ferroptotic neuronal damage in the injured cortex and observed neurological deficits post-TBI. These were ameliorated by the iron chelator deferoxamine (DFO) in wild-type mice. In Nrf2-knockout (Nrf2−/−) mice, more sever ferroptosis and neurological deficits were detected. Dimethyl fumarate (DMF)-mediated NRF2 activation alleviated neural dysfunction in TBI mice, partly due to TBI-induced ferroptosis mitigation. Additionally, FTH-FTL and FSP1 protein levels, associated with iron metabolism and the ferroptotic redox balance, were highly NRF2-dependent post-TBI. Thus, NRF2 is neuroprotective against TBI-induced ferroptosis through both the xCT-GPX4- and FTH-FTL-determined free iron level and the FSP1-regulated redox status. This yields insights into the neuroprotective role of NRF2 in TBI-induced neuronal damage and its potential use in TBI treatment.

Identifying crop disease fast, intelligently and accurately, plays a vital role in agricultural informatization development, while existing methods are almost performed manually, which depends on expert experience, and thus the identifying result is inevitably influenced by personal preferences. To address these issues, an improved crop disease identification method based on convolutional neural network is proposed to process images of crops for identifying diseases. Firstly, the original crop images were cut and normalized, and the irrelevant noises were removed by image data enhancement to improve the generalization ability and recognition accuracy of the training network. Then a neural network with nine convolutional layers is built to work on crop images, the first stage of training loads data samples, and divide the training set and verification set, and then set the learning rate, image intensifier, and optimizer and compile the training convolution model. Finally, it saves the loss and accuracy data during the training process and evaluates the accuracy of the model. In order to improve the training learning rate, Adam optimizer combining momentum algorithm and RMSprop algorithm is used to dynamically adjust the learning rate; the combination of the two algorithms makes the loss function converge to the lowest point faster. Then the feature map after each convolution is obtained by using transferred revolution, and the model is adjusted according to the feature map to further improve the effect of model recognition. Finally, validations were carried out by PlantVillage dataset, which consists of images of about 38 kinds of crops. The experiment result shows that the validation accuracy and the test accuracy are 95.7% and 94.3%, respectively; in addition, the recognition accuracy of apple, corn, grape, and other single classes is about 97%, which proves that the convolutional neural network in this paper has faster training speed and higher accuracy. In addition, the proposed method is less time consuming, which is of great significance to promote the development of smart agriculture and precision agriculture.

Melicope pteleifolia commonly known as thin evodia, is an herb used to therapy eczema, dermatitis, and other ailments in traditional Chinese medicine. Here, we reported the third complete chloroplast genome of M. pteleifolia based on next-generation sequencing. The third chloroplast genome of M. pteleifolia is 158,933 bp in length consisting of large and small single-copy regions of length 85,020 and 18,607 bp, separated by two IR regions of 27,683 bp. The overall GC content was 38.30%. De novo assembly and annotation showed the chloroplast genome of M. pteleifolia encodes 134 genes, including 89 protein-coding genes, 37 tRNA genes, and eight rRNA genes. A huge intraspecies variation was found with 248 SNPs and 97 INDELs among three assemblies of M. pteleifolia. Phylogenetic tree indicated that three assemblies of M. pteleifolia form a clade, sister to the genus Phellodendron and Casimiroa.

Single particle tracking (SPT) enables the investigation of biomolecular dynamics at a high temporal and spatial resolution in living cells, and the analysis of these SPT datasets can reveal biochemical interactions and mechanisms. Still, how to make the best use of these tracking data for a broad set of experimental conditions remains an analysis challenge in the field. Here, we develop a new SPT analysis framework: NOBIAS (NOnparametric Bayesian Inference for Anomalous Diffusion in Single-Molecule Tracking), which applies nonparametric Bayesian statistics and deep learning approaches to thoroughly analyze SPT datasets. In particular, NOBIAS handles complicated live-cell SPT data for which: the number of diffusive states is unknown, mixtures of different diffusive populations may exist within single trajectories, symmetry cannot be assumed between the x and y directions, and anomalous diffusion is possible. NOBIAS provides the number of diffusive states without manual supervision, it quantifies the dynamics and relative populations of each diffusive state, it provides the transition probabilities between states, and it assesses the anomalous diffusion behavior for each state. We validate the performance of NOBIAS with simulated datasets and apply it to the diffusion of single outer-membrane proteins in Bacteroides thetaiotaomicron. Furthermore, we compare NOBIAS with other SPT analysis methods and find that, in addition to these advantages, NOBIAS is robust and has high computational efficiency and is particularly advantageous due to its ability to treat experimental trajectories with asymmetry and anomalous diffusion.

The electroencephalogram (EEG) can objectively reflect the emotional state of human beings, and has attracted much attention in the academic circles in recent years. However, due to its weak, non-stationary, and low signal-to-noise properties, it is inclined to cause noise in the collected EEG data. In addition, EEG features extracted from different frequency bands and channels usually exhibit different levels of emotional expression abilities in emotion recognition tasks. In this paper, we fully consider the characteristics of EEG and propose a new model RSRRW (retargeted semi-supervised regression with robust weights). The advantages of the new model can be listed as follows. (1) The probability weight is added to each sample so that it could help effectively search noisy samples in the dataset, and lower the effect of them at the same time. (2) The distance between samples from different categories is much wider than before by extending the ϵ-dragging method to a semi-supervised paradigm. (3) Automatically discover the EEG emotional activation mode by adaptively measuring the contribution of sample features through feature weights. In the three cross-session emotion recognition tasks, the average accuracy of the RSRRW model is 81.51%, which can be seen in the experimental results on the SEED-IV dataset. In addition, with the support of the Friedman test and Nemenyi test, the classification of RSRRW model is much more accurate than that of other models.

BackgroundChromobox family genes (CBXs) are known to play roles in numerous modifications of the chromatin in order to inhibit the transcription of target genes. CBXs have been shown to be expressed at high levels in many types of cancer and can also serve as a target gene for therapeutic purposes. However, little is known about the expression and prognostic value of CBXs in human sarcomas.MethodsThe transcription level of CBXs was analyzed using the Oncomine dataset, and the differential expression of CBXs in sarcoma was reported by the Gene Expression Profiling Interactive Analysis (GEPIA) dataset. We also used the CCLE dataset to evaluate the expression of CBXs in a sarcoma cell line. The prognostic value of CBXs was analyzed using GEPIA and Kaplan–Meier analysis. In addition, the corrections between CBXs and their co-expressed genes were reported using Oncomine and GEPIA datasets. DAVID was used to perform GO function enrichment analysis for the CBXs and their co-expression genes. Finally, TIMER was used to analyze the immune cell infiltration of CBXs in patients with sarcoma.ResultsHP1-α/β/γ (CBX1/3/5) and CBX4/6/8 were found to be overexpressed in human sarcoma, and CBXs were upregulated in almost all the sarcoma cell line. The expression levels of HP1-α/β/γ (CBX1/3/5) and CBX7 were associated with overall survival (OS) in patients with sarcoma, while high expression levels of CBX7 were related to disease-free survival (DFS). In addition, the expression levels of CBX2/6/7 were related to recurrence-free survival (RFS). We also found that the CBX family was positively correlated with the infiltration of immune cells, including CD8+ T cells, CD4+ T cells, B cells, macrophages, neutrophils, and dendritic cells, in sarcoma.ConclusionsThe results from the present study indicated that CBXs were significantly associated with prognosis and immunological status in sarcoma. These data suggest that CBXs could serve as potential biomarkers for prognosis and immune infiltration in human sarcoma.

Abstract Background HER2+ and hormone receptor (HoR)‐negative breast cancer usually associated with poor outcome. However, it remained elusive for the prognosis of small (T1a‐T1c) HER2+/HoR‐ breast cancer. The present study retrospectively analyzed the Surveillance, Epidemiology, and End Results (SEER) database to explore the clinicopathological characteristics and prognosis of T1a‐T1c HER2+/HoR‐ breast cancer. Material and Methods Data for patients diagnosed with either HER2‐/HoR+or HER2+/HoR‐ T1a‐T1c breast cancer between 2010 and 2012 were obtained from SEER program. Survival analyses were conducted by Kaplan‐Meier method and Cox proportion hazard regression. Results Totally, 2648 HER2+/HoR‐ and 56387 HER2‐/HoR+T1a‐T1c breast cancer patients were enrolled. There was a clear trend that tumor size had a positive correlation with advanced AJCC stage (P

Abstract Background Epilepsy is a major complication of stroke. We aimed to establish whether there is an association between intravenous thrombolysis, intra-arterial thrombolysis and post stroke seizure (PSS) development. Improved understanding of the relationship between reperfusion therapies and seizure development may improve post-stroke monitoring and follow-up. Methods This was a retrospective, multicentre cohort study conducted at the Royal Melbourne Hospital and Jingling Hospital Nanjing. We included patients with anterior circulation ischemic stroke admitted 2008–2015. Patients were divided into four treatment groups 1. IV-tPA only, 2. Intra-arterial therapies (IAT) only, 3. IAT + IV-tPA and 4. stroke unit care only (i.e. no IV-tPA or IAT). To assess the association between type of reperfusion treatment and seizure incidence we used multivariable logistic regression models adjusted for age, stroke severity, 3-month functional outcome and prognostic factors. Results There were 1375 stroke unit care-only patients, of whom 28 (2%) developed PSS. There were 363 patients who received only IV-tPA, of whom 21 (5.8%) developed PSS. There were 93 patients who received IAT only, of whom 12 (12.9%) developed PSS and 112 that received both IV-tPA + IAT, of which 5 (4.5%) developed PSS. All reperfusion treatments were associated with seizure development compared to stroke unit care-only patients: IV-tPA only adjusted odds ratio (aOR) 3.7, 95%CI 1.8–7.4, p

Introduction: Androgen deprivation therapy (ADT) is considered the basic treatment for advanced prostate cancer, but it is highly associated with detrimental changes in muscle mass and muscle strength. The aim of this meta-analysis was to investigate the effects of supervised physical training on lean mass and muscle strength in prostate cancer patients undergoing ADT.Methods: A systematic literature search was performed using MEDLINE, Embase, and ScienceDirect until October 2018. Only studies that examined both muscle mass and strength in prostate cancer patients undergoing ADT were included. Outcomes of interest were changes in lean body mass (surrogate for muscle mass) as well as upper and lower body muscle strength. The meta-analysis was performed with fixed-effects models to calculate mean differences between intervention and no-training control groups.Results: We identified 8,521 publications through the search of the following key words: prostate cancer, prostate tumor, prostate carcinoma, prostate neoplasm, exercise, and training. Out of these studies, seven randomized controlled trials met the inclusion criteria and where included in the analysis. No significant mean differences for changes in lean mass were observed between the intervention and control groups (0.49 kg, 95% CI: −0.76, 1.74; P = 0.44). In contrast, the mean difference for muscle strength was significant both in chest (3.15 kg, 95% CI: 2.46, 3.83; P < 0.001) and in leg press (27.46 kg, 95% CI: 15.05, 39.87; p < 0.001).Conclusion: This meta-analysis provides evidence that low- to moderate-intensity resistance and aerobic training is effective for increasing muscle strength but may not be sufficient to affect muscle mass in prostate cancer patients undergoing ADT. The underlying mechanisms for this maladaptation may in part be explained by an insufficient stimulus induced by the training regimens as well as a delayed initiation of training in relation to the start of ADT. When interpreting the present findings, one should bear in mind that the overall number of studies included in this review was rather low, emphasizing the need for further studies in this field.

The world produces vast quantities of high-dimensional multi-semantic data. However, extracting valuable information from such a large amount of high-dimensional and multi-label data is undoubtedly arduous and challenging. Feature selection aims to mitigate the adverse impacts of high dimensionality in multi-label data by eliminating redundant and irrelevant features. The ant colony optimization algorithm has demonstrated encouraging outcomes in multi-label feature selection, because of its simplicity, efficiency, and similarity to reinforcement learning. Nevertheless, existing methods do not consider crucial correlation information, such as dynamic redundancy and label correlation. To tackle these concerns, the paper proposes a multi-label feature selection technique based on ant colony optimization algorithm (MFACO), focusing on dynamic redundancy and label correlation. Initially, the dynamic redundancy is assessed between the selected feature subset and potential features. Meanwhile, the ant colony optimization algorithm extracts label correlation from the label set, which is then combined into the heuristic factor as label weights. Experimental results demonstrate that our proposed strategies can effectively enhance the optimal search ability of ant colony, outperforming the other algorithms involved in the paper. [ABSTRACT FROM AUTHOR]

Background: Traumatic brain injury (TBI) increases the risk of mental disorders and neurodegenerative diseases in the chronic phase. However, there is limited neuropathological or molecular data on the long-term neural dysfunction and its potential mechanism following adolescent TBI. Methods: A total of 160 male mice aged 8 weeks were used to mimic moderate TBI by controlled cortical impact. At 1, 3, 6 and 12 months post-injury (mpi), different neurological functions were evaluated by elevated plus maze, forced swimming test, sucrose preference test and Morris water maze. The levels of oxidative stress, antioxidant response, reactive astrocytes and microglia, and expression of inflammatory cytokines were subsequently assessed in the ipsilateral hippocampus, followed by neuronal apoptosis detection. Additionally, the morphological complexity of hippocampal astrocytes was evaluated by Sholl analysis. Results: The adolescent mice exhibited persistent and incremental deficits in memory and anxiety-like behavior after TBI, which were sharply exacerbated at 12 mpi. Depression-like behaviors were observed in TBI mice at 6 mpi and 12 mpi. Compared with the age-matched control mice, apoptotic neurons were observed in the ipsilateral hippocampus during the chronic phase of TBI, which were accompanied by enhanced oxidative stress, and expression of inflammatory cytokines (IL-1ß and TNF-a). Moreover, the reactive astrogliosis and microgliosis in the ipsilateral hippocampus were observed in the late phase of TBI, especially at 12 mpi. Conclusion: Adolescent TBI leads to incremental cognitive dysfunction, and depression- and anxiety-like behaviors in middle-aged mice. The chronic persistent neuroinflammation and oxidative stress account for the neuronal loss and neural dysfunction in the ipsilateral hippocampus. Our results provide evidence for the pathogenesis of chronic neural damage following TBI and shed new light on the treatment of TBI-induced late-phase neurological dysfunction. [ABSTRACT FROM AUTHOR]