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Background: Acellular nerve allografts (ANAs) have been confirmed to improve the repair and reconstruction of long peripheral nerve defects. However, its efficacy is not comparable to that of autologous nerve grafts, which are used as the gold standard for treating peripheral nerve defects. Our study investigated whether fenugreek seed extract (FSE) exhibits neuroprotective potential and enhances the therapeutic outcomes of ANA repair in peripheral nerve defects. Methods: Rat Schwann cells were treated with FSE to assess the effects of FSE on cell proliferation and their secretion function of neurotrophic factors in vitro. Sprague-Dawley rats with a unilateral 15-mm sciatic nerve defect were randomized into the ANA group (the 15-mm defect was replaced by an 18-mm ANA), the ANA + FSE group (the 15-mm defect was repaired with an 18-mm ANA with FSE administration for four weeks), and the Auto group (the 15-mm defect was repaired with an autologous graft). After four weeks post-surgery, various behavioral tests and electrophysiological assays were performed to evaluate the motor and sensory behavior as well as nerve conduction of rats. Then, rats were sacrificed, and the nerve grafts were collected for toluidine blue staining, RT-qPCR, immunofluorescence staining, immunohistochemical staining to evaluate nerve regeneration, neovascularization, and neuroinflammation. Their gastrocnemius was harvested for Masson's trichrome staining to examine gastrocnemius muscle recovery. Results: FSE treatment promoted Schwann cell proliferation and its secretion of neurotrophic factors in vitro. Compared with ANAs alone, FSE treatment combined with ANAs enhanced axonal regeneration, upregulated S100, NF200, P0, MBP, and GAP43 expression, facilitated angiogenesis, and elevated neurotrophic factor expression in regenerating nerves of rats with sciatic nerve defects. In addition, FSE treatment promoted gastrocnemius muscle recovery, stimulated motor and sensory functional recovery and nerve conduction, and mitigated neuroinflammation in rats with sciatic nerve defects after repair with ANAs. Conclusion: FSE treatment improves the beneficial effects of ANA repair on sciatic nerve defects.

Abstract Bone morphogenetic proteins are essential for bone regeneration/fracture healing but can also induce heterotopic ossification (HO). Understanding accessory factors modulating BMP signaling would provide both a means of enhancing BMP-dependent regeneration while preventing HO. This study focuses on the ability of the collagen receptor, discoidin domain receptor 2 (DDR2), to regulate BMP activity. As will be shown, induction of bone formation by subcutaneous BMP2 implants is severely compromised in Ddr2-deficient mice. In addition, Ddr2 deficiency attenuates HO in mice expressing the ACVR1 mutation associated with human fibrodysplasia ossificans progressiva. In cells migrating into BMP2 implants, DDR2 is co-expressed with GLI1, a skeletal stem cell marker, and DDR2/GLI1-positive cells participate in BMP2-induced bone formation where they contribute to chondrogenic and osteogenic lineages. Consistent with this distribution, conditional knockout of Ddr2 in Gli1-expressing cells inhibited bone formation to the same extent seen in globally Ddr2-deficient animals. This response was explained by selective inhibition of Gli1 + cell proliferation without changes in apoptosis. The basis for this DDR2 requirement was explored further using bone marrow stromal cells. Although Ddr2 deficiency inhibited BMP2-dependent chondrocyte and osteoblast differentiation and in vivo, bone formation, early BMP responses including SMAD phosphorylation remained largely intact. Instead, Ddr2 deficiency reduced the nuclear/cytoplasmic ratio of the Hippo pathway intermediates, YAP and TAZ. This suggests that DDR2 regulates Hippo pathway-mediated responses to the collagen matrix, which subsequently affect BMP responsiveness. In summary, DDR2 is an important modulator of BMP signaling and a potential therapeutic target both for enhancing regeneration and treating HO.

Abstract Background The correlation between the triglyceride-glucose (TyG) index and mortality in the general population remains controversial, with inconsistent conclusions emerging from different studies. Objective This study aims to investigate whether there is an association between the TyG index and mortality in the general population in the United States, and to explore whether a new index combining the TyG index with systemic inflammation indicators can better predict all-cause and cardiovascular mortality risks in the general population than using the TyG index alone. Methods Calculate the systemic inflammation indicators and TyG index for each participant based on their complete blood count, as well as their triglyceride and glucose levels in a fasting state. TyG-inflammation indices were obtained by multiplying the TyG index with systemic inflammation indicators (TyG-NLR, TyG-MLR, TyG-lgPLR, TyG-lgSII, and TyG-SIRI). Based on the weighted Cox proportional hazards model, assess whether the TyG and TyG-Inflammation indices are associated with mortality risk in the general population. Restricted cubic splines (RCS) are used to clarify the dose-response relationship between the TyG and TyG-Inflammation indices and mortality, and to visualize the results. Time-dependent receiver operating characteristic (ROC) curves are used to evaluate the accuracy of the TyG and TyG-Inflammation indices in predicting adverse outcomes. Results This study included 17,118 participants. Over a median follow-up period of 125 months, 2595 patients died. The TyG index was not found to be related to mortality after adjusting for potentially confounding factors. However, the TyG-inflammation indices in the highest quartile (Q4), except for TyG-lgPLR, were significantly associated with both all-cause and cardiovascular mortality, compared to those in the lowest quartile (Q1). Among them, TyG-MLR and TyG-lgSII showed the strongest correlations with all-cause mortality and cardiovascular mortality. Specifically, compared to their respective lowest quartiles (Q1), participants in the highest quartile (Q4) of TyG-MLR had a 48% increased risk of all-cause mortality (95% CI: 1.23–1.77, P for trend

Abstract In this paper, a radiation hardened by design StrongARM comparator is proposed to mitigate the radiation effects. With 12 additional transistors compared to the conventional one, the proposed structure shows much higher immunity to single‐event transients. During the amplification phase, when the input differential voltage is 10 mV, the proposed structure can withstand up to 18fC free charge, 45x far surpassing the conventional structure. During the regeneration phase, every sensitive node in the proposed structure can withstand a 200 fC‐injected charge. Compared to other redundant structures with performance deterioration, the proposed architecture exhibits high‐speed characteristics. When the differential voltage between two inputs is 1 mV, the delay of the new structure is 168.26 ps and the speed improvement is 118.02% over the conventional structure.

Abstract Idiopathic pulmonary fibrosis (IPF) is believed to be associated with a notable disruption of cellular energy metabolism. By detecting the changes of energy metabolites in the serum of patients with pulmonary fibrosis, we aimed to investigate the diagnostic and prognostic value of energy metabolites in IPF, and further elucidated the mechanism of their involvement in pulmonary fibrosis. Through metabolomics research, it was discovered that the TCA cycle intermediates changed dramatically in IPF patients. In another validation cohort of 55 patients with IPF compared to 19 healthy controls, it was found that succinate, an intermediate product of TCA cycle, has diagnostic and prognostic value in IPF. The cut-off levels of serum succinate were 98.36 μM for distinguishing IPF from healthy controls (sensitivity, 83.64%; specificity, 63.16%; likelihood ratio, 2.27, respectively). Moreover, a high serum succinate level was independently associated with higher rates of disease progression (OR 13.087, 95%CI (2.819–60.761)) and mortality (HR 3.418, 95% CI (1.308–8.927)). In addition, accumulation of succinate and increased expression of the succinate receptor GPR91 were found in both IPF patients and BLM mouse models of pulmonary fibrosis. Reducing succinate accumulation in BLM mice alleviated pulmonary fibrosis and 21d mortality, while exogenous administration of succinate can aggravate pulmonary fibrosis in BLM mice. Furthermore, GPR91 deficiency protected against lung fibrosis caused by BLM. In vitro, succinate promoted the activation of lung fibroblasts by activating ERK pathway through GPR91. In summary, succinate is a promising biomarker for diagnosis and prognosis of IPF. The accumulation of succinate may promote fibroblast activation through GPR91 and pulmonary fibrosis.

Abstract The spatial organization of molecules in a cell is essential for their functions. While current methods focus on discerning tissue architecture, cell–cell interactions, and spatial expression patterns, they are limited to the multicellular scale. We present Bento, a Python toolkit that takes advantage of single-molecule information to enable spatial analysis at the subcellular scale. Bento ingests molecular coordinates and segmentation boundaries to perform three analyses: defining subcellular domains, annotating localization patterns, and quantifying gene–gene colocalization. We demonstrate MERFISH, seqFISH + , Molecular Cartography, and Xenium datasets. Bento is part of the open-source Scverse ecosystem, enabling integration with other single-cell analysis tools.

The transmembrane protein(TMEM) family exhibits widespread distribution across both the plasma membrane and organelle membranes, actively participating in the intricate regulation of diverse pathophysiological processes. Contemporary investigations have uncovered the pivotal involvement of the TMEM family in the human reproductive system. This family is found to play a crucial role in regulating spermatogenesis, sperm-egg fusion, endometrial receptivity, as well as tumor invasion and migration. These findings highlight its intricate association with the onset and progression of various diseases. A comprehensive identification of the function of TMEM family in human reproductive system holds significant importance, offering profound insights into the nuanced biological functions of this protein family. This in-depth examination not only supports our understanding about the complex mechanisms controlling reproductive processes but also lay a foundation for potential advancements in medical research.

DNA barcoding is an effective modern tool in taxonomy, evolutionary biology, and biodiversity research. Many new species have been discovered and described with DNA barcodes as part of their diagnostic features. We combined morphological examination and molecular species delimitation of the mitochondrial cytochrome c oxidase 1 (COI) gene using the automatic barcode gap discovery (ABGD) to investigate species boundaries. The genus Prochas Walkley (Hymenoptera, Ichneumonidae, Campopleginae) was first reported from China and is new for the Oriental and Eastern Palearctic regions. Using an integrative taxonomy method, two new species P. rugipunctata sp. nov. and P. striata sp. nov. are hereby described and illustrated. A key to the world species and a distribution map are provided.

Campopleginae, the third largest subfamily of Ichneumonidae, has been one of the most investigated ichneumonids from the perspective of biological control. Despite their importance as potential biological control agents, species of campoplegine are among the most poorly studied insect groups. In this study, one new species of the genus Lemophagus Townes, 1965, Lemophagus nanus sp. nov., is described and illustrated. In addition, L. curtus and L. pulcher are recorded from China for the first time.

Abstract Background Patients with Alzheimer’s disease (AD) often exhibit neuropsychiatric symptoms (NPS), particularly delusions. Previous studies have shown an association between white matter hyperintensities (WMH) and specific NPS. This study aims to explore the relationship between WMH volume and delusions in AD patients by comparing the WMH volumes of delusional and non-delusional subgroups. Methods 80 AD patients were divided into a delusion group (n = 36) and a non-delusion group (n = 44) based on the Neuropsychiatric Inventory (NPI). The brain cortical volume and WMH volume were quantitatively calculated for all 80 patients, including total WMH volume, periventricular WMH (PVWMH) volume, deep WMH volume, as well as bilateral frontal lobe, temporal lobe, parietal lobe, and occipital lobe WMH volumes. Firstly, we compared the differences in WMH volumes between the delusion group and non-delusion group. Then, within the delusion group, we further categorized patients based on severity scores of their delusional symptoms into mild (1 point), moderate (2 points), or severe groups (3 points). We compared the WMH volumes among these three groups to investigate the role of WMH volume in delusional symptoms. Results There was a significant difference in left occipital lobe WMH volume between the delusion group and non-delusion group(P

Abstract Background Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial lung disease. Clinical models to accurately evaluate the prognosis of IPF are currently lacking. This study aimed to construct an easy-to-use and robust prediction model for transplant-free survival (TFS) of IPF based on clinical and radiological information. Methods A multicenter prognostic study was conducted involving 166 IPF patients who were followed up for 3 years. The end point of follow-up was death or lung transplantation. Clinical information, lung function tests, and chest computed tomography (CT) scans were collected. Body composition quantification on CT was performed using 3D Slicer software. Risk factors in blood routine examination-radiology-pulmonary function (BRP) were identified by Cox regression and utilized to construct the “BRP Prognosis Model”. The performance of the BRP model and the gender-age-physiology variables (GAP) model was compared using time-ROC curves, calibration curves, and decision curve analysis (DCA). Furthermore, histopathology fibrosis scores in clinical specimens were compared between the different risk stratifications identified by the BRP model. The correlations among body composition, lung function, serum inflammatory factors, and profibrotic factors were analyzed. Results Neutrophil percentage > 68.3%, pericardial adipose tissue (PAT) > 94.91 cm3, pectoralis muscle radiodensity (PMD) ≤ 36.24 HU, diffusing capacity of the lung for carbon monoxide/alveolar ventilation (DLCO/VA) ≤ 56.03%, and maximum vital capacity (VCmax) 3 years; intermediate risk: TFS = 2–3 years; high risk: TFS ≈ 1 year). Patients with a high-risk stratification according to the BRP model had a higher fibrosis score on histopathology. Additionally, serum proinflammatory markers were positively correlated with visceral fat volume and infiltration. Conclusions In this study, the BRP prognostic model of IPF was successfully constructed and validated. Compared with the commonly used GAP model, the BRP model had better performance and generalization with easily obtainable indicators. The BRP model is suitable for clinical promotion.

IntroductionDensity management is a key silvicultural tool in management programs that enhances compositional and structural diversity and hence forest growth during the conversion of even-aged pure stands into mixed forests.MethodsTo determine the optimum stand density, a model of maximum size–density relationships was employed to explore the relationship of the self-thinning trajectory with growth, species mixing, latitude, and site conditions during the transition of even-aged pure Chinese fir stands to Chinese fir-dominated mixed forests using stochastic frontier analysis. Data were obtained from a total of 591 permanent plots located in Fujian, Jiangxi, Zhejiang, and Anhui provinces in southern China.ResultsThe results showed that (1) the slope of the maximum size–density relationship of Chinese fir-dominated mixed forests increased and plateaued over time; (2) the slope of the maximum size–density relationship of Chinese fir-dominated mixed forests did not deviate from Reineke’s assumed universal slope of -1.605; and (3) mixing proportion had a positive effect on maximum size–density relationships, and latitude and site conditions had the opposite effect on maximum size–density relationships.ConclusionsOur findings will provide valuable guidance for the forest management of areas in which even-aged pure stands are being converted to mixed forests (i.e., when broadleaved tree species are planted after thinning to improve overall stand density and promote stand growth).

Recent studies suggested that cancer was a risk factor for coronavirus disease 2019 (COVID-19). Toll-like receptor 7 (TLR7), a severe acute respiratory syndrome 2 (SARS-CoV-2) virus's nucleic acid sensor, was discovered to be aberrantly expressed in many types of cancers. However, its expression pattern across cancers and association with COVID-19 has not been systematically studied. In this study, we proposed a computational framework to comprehensively study the roles of TLR7 in COVID-19 and pan-cancers at genetic, gene expression, protein, epigenetic, and single-cell levels. We found TLR7 mRNA expression was significantly up-regulated in 6 cancer types and down-regulated in 6 cancer types, further validated in the HPA database at the protein level. The genes significantly co-expressed with TLR7 were mainly enriched in the toll-like receptor signaling pathway, endolysosome, and signaling pattern recognition receptor activity. In addition, the abnormal TLR7 expression was associated with Mismatch repair (MMR), microsatellite instability (MSI), tumor mutational burden (TMB) in various cancers. Mined by the ESTIMATE algorithm, the expression of TLR7 was also closely linked to various immune infiltration patterns in pan-cancer, and TLR7 was mainly enriched in macrophages, as revealed by single-cell RNA sequencing. Finally, TLR7 expressions were very sensitive to a few targeted drugs, such as Alectinib and Imiquimod. In conclusion, TLR7 might be essential in the pathogenesis of COVID-19 and cancers.

Cobalt sulfides are considered as promising candidates for lithium-ion battery (LIB) anode materials with high energy densities. Their energy storage mechanism is widely understood to involve the traditional intercalation and conversion reaction. However, these conventional mechanisms are unable to explain the storage capacities of certain materials which exceed the theoretical limit. Here, utilizing advanced in situ magnetometry to detect the magnetization evolution of Co1-xS LIBs in real time, it is demonstrated that the Co-catalytic lithium storage process and interfacial space charge storage mechanism are strongly related to the additional capacity of cobalt sulfides. During discharge, a Co/Li2S interface is formed, wherein the Co nanoparticles and Li2S could store a large amount of polarized electrons Li+, respectively. Subsequently, the electrons stored in Co are transferred to the polymeric film, forming radical anions and contributing extra capacity. These findings reveal the charge storage mechanisms of transition metal sulfides and highlight the critical role of magnetic testing in the investigation of energy storage mechanisms.

In recent years, a wide variety of high-performance and versatile nanofiber membranes have been successfully created using different electrospinning methods. As vehicles for medication, they have been receiving more attention because of their exceptional antibacterial characteristics and ability to heal wounds, resulting in improved drug delivery and release. This quality makes them an appealing choice for treating various skin conditions like wounds, fungal infections, skin discoloration disorders, dermatitis, and skin cancer. This article offers comprehensive information on the electrospinning procedure, the categorization of nanofiber membranes, and their use in dermatology. Additionally, it delves into successful case studies, showcasing the utilization of nanofiber membranes in the field of skin diseases to promote their substantial advancement.

The purpose of this work was to use integrated bioinformatics analysis to screen for pyroptosis-related genes (PRGs) and possible immunological phenotypes linked to the development and course of IPF. Transcriptome sequencing datasets GSE70866, GSE47460 and GSE150910 were obtained from GEO database. From the GSE70866 database, 34 PRGs with differential expression were found in IPF as compared to healthy controls. In addition, a diagnostic model containing 4 genes PRGs (CAMP, MKI67, TCEA3 and USP24) was constructed based on LASSO logistic regression. The diagnostic model showed good predictive ability to differentiate between IPF and healthy, with ROC-AUC ranging from 0.910 to 0.997 in GSE70866 and GSE150910 datasets. Moreover, based on a combined cohort of the Freiburg and the Siena cohorts from GSE70866 dataset, we identified ten PRGs that might predict prognosis for IPF. We constructed a prognostic model that included eight PRGs (CLEC5A, TREM2, MMP1, IRF2, SEZ6L2, ADORA3, NOS2, USP24) by LASSO Cox regression and validated it in the Leuven cohort. The risk model divided IPF patients from the combined cohort into high-risk and low-risk subgroups. There were significant differences between the two subgroups in terms of IPF survival and GAP stage. There is a close correlation between leukocyte migration, plasma membrane junction, and poor prognosis in a high-risk subgroup. Furthermore, a high-risk score was associated with more plasma cells, activated NK cells, monocytes, and activated mast cells. Additionally, we identified HDAC inhibitors in the cMAP database that might be therapeutic for IPF. To summarize, pyroptosis and its underlying immunological features are to blame for the onset and progression of IPF. PRG-based predictive models and drugs may offer new treatment options for IPF.

Medical image segmentation of the liver is an important prerequisite for clinical diagnosis and evaluation of liver cancer. For automatic liver segmentation from Computed Tomography (CT) images, we proposed a Multi-scale Feature Extraction and Enhancement U-Net (mfeeU-Net), incorporating Res2Net blocks, Squeeze-and-Excitation (SE) blocks, and Edge Attention (EA) blocks. The Res2Net blocks which are conducive to extracting multi-scale features of the liver were used as the backbone of the encoder, while the SE blocks were also added to the encoder to enhance channel information. The EA blocks were introduced to skip connections between the encoder and the decoder, to facilitate the detection of blurred liver edges where the intensities of nearby organs are close to the liver. The proposed mfeeU-Net was trained and evaluated using a publicly available CT dataset of LiTS2017. The average dice similarity coefficient, intersection-over-union ratio, and sensitivity of the mfeeU-Net for liver segmentation were 95.32%, 91.67%, and 95.53%, respectively, and all these metrics were better than those of U-Net, Res-U-Net, and Attention U-Net. The experimental results demonstrate that the mfeeU-Net can compete with and even outperform recently proposed convolutional neural networks and effectively overcome challenges, such as discontinuous liver regions and fuzzy liver boundaries.

Background The reactivation of fetal γ-globin expression is an effective strategy for ameliorating the clinical symptoms of β-hemoglobinopathies. However, the mechanism of globin switching, especially the roles of long non-coding RNAs (lncRNAs) in this process, remains elusive. Methods We compared the in vivo transcriptome profiles of nucleated red blood cells (NRBCs) isolated from the umbilical cord blood of preterm and full-term newborns. We collected 75 umbilical cord blood samples and performed qPCR of the candidate genes. Results In this study, we identified 7,166 differentially expressed protein-coding genes, 3,243 differentially expressed lncRNAs, and 79 differentially expressed microRNAs. Our data show that the Fanconi anemia pathway and the H19/let-7/LIN28B axis may be involved in γ- to β-globin gene switching. Moreover, we constructed the hub gene network of the differentially expressed transcription factors. Based on qPCR, we found that BCL11A was differentially expressed based on biological sex. We also confirmed that H19 is differentially expressed and established the H19-related network to reveal the potential regulatory mechanisms. Conclusion We present the profiles of the in vivo transcriptome differences of NRBCs between preterm and full-term neonates for the first time, and provide novel research targets for β-hemoglobinopathies.

Abstract Background To investigate the correlation between the clinical and pathological characteristics and outcomes in patients with eyelid malignant tumors underwent wide local excision. Methods This retrospective study included 141 cases of eyelid malignant neoplasms from January 2010 to December 2015 in Shanxi eye hospital. Demographic and clinical information were collected. The Kaplan–Meier method was used to calculate survival curves, and the log-rank test method was used to compare survival between groups. Cox proportional regression models were used to calculate the hazard ratios (HR) of total recurrence rate and metastasis rate. Results Overall, there were 141 eyelid malignant neoplasms cases aged 65.34 ± 9.69 (range, 41—88) years old. The duration time range was from 1 to 828 (61.09 ± 122.21) months. Basal cell carcinoma (BCC) is the most common of all eyelid malignancies, accounting for 84 (59.5%), followed by Sebaceous gland carcinoma (SGC, 41, 29%), Squamous Cell Carcinoma (SCC, 11, 7.8%), Malignant Melanoma (MM, 3, 2.1%)。On cox-regression analysis, pathological classification (HR 1.959; 95% CI 1.012–3.790; p = 0.046) and eyelid tumor surgery history (HR 17.168; 95% CI 1.889–156.011; p = 0.012) were independently associated with recurrence in patients with eyelid malignant neoplasm. Pathological classification (HR 2.177; 95% CI 1.423 -3.331; p

Osteoarthritis (OA) is a prevalent musculoskeletal disease that affects approximately 500 million people worldwide. Unfortunately, there is currently no effective treatment available to stop or delay the degenerative progression of joint disease. Wnt signaling pathways play fundamental roles in the regulation of growth, development, and homeostasis of articular cartilage. This review aims to summarize the role of Wnt pathways in joint development during embryonic stages and in cartilage maintenance throughout adult life. Specifically, we focus on aberrant mechanical loading and inflammation as major players in OA progression. Excessive mechanical load activates Wnt pathway in chondrocytes, resulting in chondrocyte apoptosis, matrix destruction and other osteoarthritis-related changes. Additionally, we discuss emerging Wnt-related modulators and present an overview of emerging treatments of OA targeting Wnt signaling. Ultimately, this review provides valuable insights towards discovering new drugs or gene therapies targeting Wnt signaling pathway for diagnosing and treating osteoarthritis and other degenerative joint diseases.

Renal fibrosis is a common pathological outcome of various chronic kidney diseases, and as yet, there is no specific treatment. Dapagliflozin has shown renal protection in some clinical trials as a glucose-lowering drug, but its role and mechanism on renal fibrosis remain unclear. In this study, we used a 0.2% adenine diet-induced renal fibrosis mouse model to investigate whether dapagliflozin could protect renal function and alleviate renal fibrosis in this animal model. In vivo, we found that dapagliflozin’s protective effect on renal fibrosis was associated with 1) sustaining mitochondrial integrity and respiratory chain complex expression, maintained the amount of mitochondria; 2) improving fatty acid oxidation level with increased expression of CPT1-α, PPAR-α, ACOX1, and ACOX2; 3) reducing inflammation and oxidative stress, likely via regulation of IL-1β, IL-6, TNF-α, MCP-1, cxcl-1 expression, and glutathione (GSH) activity, superoxide dismutase (SOD) and malondialdehyde (MDA) levels; and 4) inhibiting the activation of the TGF-β1/MAPK pathway. In HK2 cells treated with TGF-β1, dapagliflozin reduced the expression of FN and α-SMA, improved mitochondrial respiratory chain complex expression, and inhibited activation of the TGF-β1/MAPK pathway.

IntroductionIn December 2019, a novel epidemic of coronavirus pneumonia (COVID-19) was reported，and population-based studies had shown that cancer was a risk factor for death from COVID-19 infection. However, the molecular mechanism between COVID-19 and cancer remains indistinct. In this paper, we analyzed the nucleic acid sensor (DDX58) of SARS-CoV-2 virus, which is a significant gene related to virus infection. For purpose of clarifying the characteristics of DDX58 expression in malignant tumors, this study began to systematically analyze the DDX58 expression profile in the entire cancer type spectrum.MethodsUsing TCGA pan-cancer database and related data resources, we analyzed the expression, survival analysis, methylation expression, mutation status, microsatellite instability (MSI), immune related microenvironment, gene related network, function and drug sensitivity of DDX58.ResultsThe expression level of DDX58 mRNA in most cancers was higher than the expression level in normal tissues. Through TIMER algorithm mining, we found that DDX58 expression was closely related to various levels of immune infiltration in pan-cancer. The promoter methylation level of DDX58 was significantly increased in multiple cancers. In addition, abnormal expression of DDX58 was related to MSI and TMB in multiple cancers, and the most common type of genomic mutation was “mutation.” In the protein–protein interaction (PPI) network, we found that type I interferon, phagocytosis, ubiquitinase, and tumor pathways were significantly enriched. Finally, according to the expression of DDX58 indicated potential sensitive drugs such as Cediranib, VE−821, Itraconazole, JNJ−42756493, IWR−1, and Linsitinib.DiscussionIn conclusion, we had gained new insights into how DDX58 might contribute to tumor development, and DDX58 could be used as an immune-related biomarker and as a potential immunotherapeutic target for COVID-19 infected cancer patients.

Primary ciliary dyskinesia (PCD) is a rare autosomal recessive disorder that affects the structure and function of motile cilia, leading to classic clinical phenotypes, such as situs inversus, chronic sinusitis, bronchiectasis, repeated pneumonia and infertility. In this study, we diagnosed a female patient with PCD who was born in a consanguineous family through classic clinical manifestations, transmission electron microscopy and immunofluorescence staining. A novel DNAAF4 variant NM_130810: c.1118G>A (p. G373E) was filtered through Whole-exome sequencing. Subsequently, we explored the effect of the mutation on DNAAF4 protein from three aspects: protein expression, stability and interaction with downstream DNAAF2 protein through a series of experiments, such as transfection of plasmids and Co-immunoprecipitation. Finally, we confirmed that the mutation of DNAAF4 lead to PCD by reducing the stability of DNAAF4 protein, but the expression and function of DNAAF4 protein were not affected.

Chronic kidney disease (CKD) is a serious disease that endangers human health. It is reported that inhibiting renal cell apoptosis can delay the progress of CKD. Our previous study found that the mice with protein phosphatase Mg2+/Mn2+ dependent 1K (PPM1K) gene deletion had obvious symptoms of glomerular vascular and interstitial vascular dilatation, congestion and hemorrhage, glomerular hemorrhage and necrosis, interstitial fibrous tissue proliferation, decreased urinary creatinine clearance, and increased urinary protein level. In addition, studies have found that PPM1K is essential for cell survival, apoptosis and metabolism. However, no study has confirmed that PPM1K can inhibit renal cell apoptosis. In this study, PPM1K was overexpressed in human kidney-2 cells (HK-2), and the biological process of differentially expressed genes and its effect on apoptosis were comprehensively screened by RNA sequencing (RNA-seq). Through sequencing analysis, we found that there were 796 differentially expressed genes in human renal tubular epithelial cells transfected with PPM1K gene, of which 553 were down-regulated and 243 were up-regulated. Enrichment analysis found that differentially expressed genes may play an important role in amino acid metabolism and biosynthesis. In the GO analysis functional pathway list, we also found that multiple genes can be enriched in apoptosis related pathways, such as G0S2, GADD45A, TRIB3, VEGFA, NUPR1 and other up-regulated genes, and IL-6, MAGED1, CCL2, TP53INP1 and other down-regulated genes. Then we verified these differentially expressed genes by RT-PCR, and found that only the RT-PCR results of G0S2, VEGFA and NUPR1 were consistent with the transcriptome sequencing results. We believe that G0S2, VEGFA, NUPR1 and other genes may participate in the apoptosis process of HK-2 cells induced by PPM1K.In conclusion, these findings provide some data support for the study of HK-2 cell apoptosis mechanism, and also provide a scientific theoretical basis for further study of the effect of PPM1K on kidney disease.

Schistosoma sinensium belongs to the Asian Schistosoma and is transmitted by freshwater snails of the genus Tricula. Rodents are known definitive hosts of S. sinensium. In 2016, suspected schistosome eggs were found in the feces of the northern tree shrew (Tupaia belangeri) in a field in Lufeng County (latitude, 25°04′50″ N; longitude, 102°19′30″ E; altitude 1820 m), Yunnan Province, China. Morphological analysis suggested that the schistosome was S. sinensium. 18S, 12S and CO1 genes sequencing and phylogenetic analysis showed that this species had the highest similarity to and occupied the same evolutionary branch as S. sinensium from Mianzhu, Sichuan, China. Meanwhile, based on 16S and 28S rDNA sequencing and morphological identification, the snail intermediate host was identified as a species of Tricula, and was found in irrigation channels. Phylogeny indicated that Tricula sp. LF was a sister taxon to T. bambooensis, T. ludongbini. The S. sinensium was able to experimentally infect the captive-bred Tupaia belangeri, and Schistosoma eggs were recovered from all Tupaia belangeri exposed. In this study, we report the infection of Tupaia belangeri and Tricula sp. LF with S. sinensium in Lufeng, Yunnan, southwest China. These findings may improve our understanding of the host range, evolution, distribution, and phylogenetic position of S. sinensium.

ObjectiveProviding protection against aggregation and guiding hydrophobic precursors through the mitochondria’s intermembrane space, this protein functions as a chaperone-like protein. SLC25A12 is imported by TIMM8 as a result of its interaction with TIMM13. In spite of this, it is still unknown how TIMM13 interacts with skin cutaneous melanoma (SKCM) and tumor-infiltrating lymphocytes (TILs).MethodsAberrant expression of TIMM13 in SKCM and its clinical outcome was evaluated with the help of multiple databases, including the Xiantao tool (https://www.xiantao.love/), HPA, and UALCAN. TISIDB and Tumor Immune Estimation Resources (TIMER) databases were applied to explore the association between TIMM13 and tumor infiltration immune cells. OS nomogram was constructed, and model performance was examined. Finally, TIMM13 protein expression was validated by immunohistochemistry (IHC).ResultsTIMM13 expression was higher in SKCM samples than in peritumor samples. TIMM13 was strongly associated with sample type, subgroup, cancer stage, lymph node stage, and worse survival. Further, upregulation of TIMM13 was significantly associated with immunoregulators, and chemokines, as well as T cells, B cells, monocytes, neutrophils, macrophages, and T-cell regulators. An analysis of bioinformatic data uncovered that TIMM13 expression was strongly associated with PD1 (T-cell exhaustion marker). The nomogram showed good predictive performance based on calibration plot. TIMM13 was highly expressed in melanoma tissue samples than in normal samples.ConclusionIn brief, TIMM13 may be a prognostic biomarker for SKCM. It might modulate the tumor immune microenvironment and lead to a poorer prognosis. In addition, it is necessary to study the targeted therapy of TIMM13.

Clostridioides difficile is the predominant antibiotic-associated enteropathogen associated with diarrhoea or pseudomembranous colitis in patients worldwide. Previously, we identified C. difficile RT078 isolates (CD21062) from elderly patients in China, including two new ribotype strains (CD10010 and CD12038) belonging to the ST11 group, and their genomic features were also investigated. This study compared sporulation, spore germination, toxin expression, flagellar characteristics, and adhesion among these strains in vitro and analysed their pathogenic ability in vivo using animal models. The results showed sporulation and spore germination did not significantly differ among the three C. difficile strains. CD10010 and CD12038 showed higher transcriptional levels of toxins until 48 h; thereafter, the transcriptional levels of toxins remained constant among RT078, CD10010, and CD12038. RT078 showed a loss of flagellum and its related genes, whereas CD12038 showed the highest motility in vitro. Both CD10010 and CD12038 initially showed flg phase OFF, and the flagellar switch reversed to phase ON after 48 h in swim agar. Flagellar proteins and toxins were both upregulated when flg phase OFF changed to flg phase ON status, enhancing their pathogenic ability. CD12038 showed the highest adhesion to Hep-2 cells. Histopathology and inflammation scores demonstrated that CD12038 caused the most severe tissue damage and infection in vivo. The new ribotype strains, particularly CD12038, exhibit higher pathogenic ability than the typical RT078 strain, both in vitro and in vivo. Therefore, more attention should be paid to this new C. difficile strain in epidemiological research; further studies are warranted.

Abstract Background Clostridioides difficile is a major cause of antibiotic associated diarrhea. Several animal models are used to study C. difficile infection (CDI). The tree shrew has recently been developed as a model of primate processes. C. difficile infection has not been examined in tree shrews. We infected tree shrews with hyper-virulent C. difficile strains and examined the alterations in gut microbiota using 16S rRNA gene sequencing. Results C. difficile colonized the gastrointestinal tract of tree shrew and caused diarrhea and weight loss. Histopathologic examination indicated structures and mucosal cell destruction in ileal and colonic tissues. The gut microbial community was highly diversity before infection and was dominated by Firmicutes, Fusobacteria, Bacteroidetes, and Proteobacteria. Antibiotic administration decreased the diversity of the gut microbiota and led to an outgrowth of Lactobacillus. The relative abundance of Proteobacteria, Gammaproteobacteria, Enterobacteriales, Lachnospiraceae, Enterobacteriaceae, Escherichia, Blautia, and Tyzzerella increased following C. difficile infection. These taxa could be biomarkers for C. difficile colonization. Conclusions In general, the disease symptoms, histopathology, and gut microbiota changes following C. difficile infection in tree shrews were similar to those observed in humans.

Abstract Diffuse intrinsic pontine glioma (DIPG) is most commonly diagnosed based on imaging criteria, with biopsy often reserved for pontine tumors with imaging features not typical for DIPG (atypical DIPG, ‘aDIPG’). The histopathologic and molecular spectra of the clinical entity aDIPG remain to be studied systematically. In this study, thirty-three patients with newly diagnosed pontine-centered tumors with imaging inconsistent with DIPG for whom a pathologic diagnosis was subsequently obtained were included. Neoplasms were characterized by routine histology, immunohistochemistry, interphase fluorescence in situ hybridization, Sanger and next-generation DNA/RNA sequencing, and genome-wide DNA methylome profiling. Clinicopathologic features and survival outcomes were analyzed and compared to those of a contemporary cohort with imaging features consistent with DIPG (typical DIPG, ‘tDIPG’). Blinded retrospective neuroimaging review assessed the consistency of the initial imaging-based diagnosis and correlation with histopathology. WHO grade II-IV infiltrating gliomas were observed in 54.6% of the cases; the remaining were low-grade gliomas/glioneuronal tumors or CNS embryonal tumors. Histone H3 K27M mutation, identified in 36% of the cases, was the major prognostic determinant. H3 K27M–mutant aDIPG and H3 K27M–mutant tDIPG had similar methylome profiles but clustered separately from diffuse midline gliomas of the diencephalon and spinal cord. In the aDIPG cohort, clinicoradiographic features did not differ by H3 status, yet significant differences in clinical and imaging features were observed between aDIPG without H3 K27M mutation and tDIPG. Neuroimaging review revealed discordance between the classification of aDIPG and tDIPG and did not correlate with the histology of glial/glioneuronal tumors or tumor grade. One patient (3.1%) developed persistent neurologic deficits after surgery; there were no surgery-related deaths. Our study demonstrates that surgical sampling of aDIPG is well-tolerated and provides significant diagnostic, therapeutic, and prognostic implications, and that neuroimaging alone is insufficient to distinguish aDIPG from tDIPG. H3 K27M-mutant aDIPG is epigenetically and clinically similar to H3 K27M-mutant tDIPG.

BackgroundGastric cancer (GC) is the fifth commonest cancer and the third commonest reason of death causing by cancer worldwide. Currently, tumor immunology and ferropotosis develop rapidly that has made gastric cancer be treated in new directions. So, finding the potential targets and prognostic biomarkers for immunotherapy combined with ferropotosis is urgent.MethodsBy mining TCGA, immune-related genes, ferropotosis-related genes and immune-ferropotosis-related differentially expressed genes (IFR-DEGs) were identified. The independent prognostic value of IFR-DEGs was determined by differential expression analysis, prognostic analysis, and univariate and lasso regression analysis. Then, based on the prognostic risk model, the correlation between IFR-DEGs and immune scores, immune checkpoints were evaluated. Besides, we predicted the response of high and low risk groups to drugs.ResultsA 15-gene prognostic feature was constructed. The high-risk group had a poorer prognosis than the low-risk group. High-risk group had higher level of Treg immune cell infiltration compared with that in the low-risk group, and the tumor purity, immune checkpoint PD-1 and CTLA4, and immunity in the high-risk group were higher than those in the low-risk group. These results indicate that immune ferropotosis-related genes migh be potential predictors of STAD’s response to ICI immunotherapy biomarkers. In addition, the response of small molecule drugs such as Nilotini, Sunitinib, Imatinib, etc. for high and low risk groups was predicted.ConclusionIFRSig can be regarded as an independent prognostic feature and may estimate OS and clinical treatment response in patients with STAD. IFRSig also has important correlation with immune microenvironment. A new understanding of the immune-ferropotosis-related genes during the occurrence and development of STAD is provided in this study.

Introduction: Diabetic nephropathy (DN) is related to type 1 and type 2 diabetes. They are the leading cause of end-stage renal disease, but the underling specific pathogenesis of DN is not yet clear. Our study was conducted to explore how DN changed the transcriptome profiles in the kidney. Methods: The gene expression profile of microdissected glomeruli of 41 type 2 DN patients and 20 healthy controls were included. The sample dataset GSE96804 was obtained from the GEO database. Differentially expressed genes (DEGs) were analyzed in R with the limma package and the important modules were found by weighted gene co-expression network analysis (WGCNA) clustering. The modules were then analyzed based on Gene Ontology (GO) gene set enrichment analysis, and the hub genes were found out. We next validated the hub gene, PDK4, in a cell model of DN. We also constructed the PDK4-related PPI network to investigate the correlation between PDK4 expression and other genes. Results: Heatmap and volcano map were drawn to illustrate the mRNA expression profile of 1,204 DEGs in both samples of DN patients and the control group. Using WGCNA, we selected the blue module in which genes showed the strongest correlation with the phenotype and the smallest p value. We also identified PDK4 as a hub gene. PDK4 expression was upregulated in human diabetic kidney tissue. Moreover, PDK4 was speculated to play a role in glomerular basement membrane development and kidney development according to the enrichment of functions and signaling pathways. Furthermore, PDK4 and two key genes GSTA2 and G6PC protein expression were verified highly expressed in the cell model of DN. Conclusion: During the pathogenesis of DN, many genes may change expression in a coordinated manner. The discovery of PDK4 as key gene using WGCNA is of great significance for the development of new treatment strategies to block the development of DN.

BackgroundBreast cancer (BRCA) has become the most frequently appearing, lethal, and aggressive cancer with increasing morbidity and mortality. Previously, it was discovered that the HAUS5 protein is involved in centrosome integrity, spindle assembly, and the completion of the cytoplasmic division process during mitosis. By encouraging chromosome misdivision and aneuploidy, HAUS5 has the potential to cause cancer. The significance of HAUS5 in BRCA and the relationship between its expression and clinical outcomes or immune infiltration remains unclear.MethodsPan-cancer was analyzed by TIMER2 web and the expression differential of HAUS5 was discovered. The prognostic value of HAUS5 for BRCA was evaluated with KM plotter and confirmed with Gene Expression Omnibus (GEO) dataset. Following that, we looked at the relationship between the high and low expression groups of HAUS5 and breast cancer clinical indications. Signaling pathways linked to HAUS5 expression were discovered using Gene Set Enrichment Analysis (GSEA). The relative immune cell infiltrations of each sample were assessed using the CIBERSORT algorithm and ESTIMATE method. We evaluated the Tumor Mutation Burden (TMB) value between the two sets of samples with high and low HAUS5 expression, as well as the differences in gene mutations between the two groups. The proliferation changes of BRCA cells after knockdown of HAUS5 were evaluated by fluorescence cell counting and colony formation assay.ResultHAUS5 is strongly expressed in most malignancies, and distinct associations exist between HAUS5 and prognosis in BRCA patients. Upregulated HAUS5 was associated with poor clinicopathological characteristics such as tumor T stage, ER, PR, and HER2 status. mitotic prometaphase, primary immunodeficiency, DNA replication, cell cycle related signaling pathways were all enriched in the presence of elevated HAUS5 expression, according to GSEA analysis. The BRCA microenvironment’s core gene, HAUS5, was shown to be related with invading immune cell subtypes and tumor cell stemness. TMB in the HAUS5-low expression group was significantly higher than that in the high expression group. The mutation frequency of 15 genes was substantially different in the high expression group compared to the low expression group. BRCA cells’ capacity to proliferate was decreased when HAUS5 was knocked down.ConclusionThese findings show that HAUS5 is a positive regulator of BRCA progression that contributes to BRCA cells proliferation. As a result, HAUS5 might be a novel prognostic indicator and therapeutic target for BRCA patients.

Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is a hereditary cerebral small vascular disease caused by a homozygous mutation in the high-temperature requirement A serine peptidase 1 (HTRA1) gene. Cerebral microbleeds (CMBs) are increasingly being recognized as neuroimaging findings occurring with cerebrovascular disease and have different etiologies. Mild to moderate CMBs are not unusual in CARASIL, and they are observed to affect cortical and subcortical structures; in contrast, diffuse CMBs, especially in the cerebellum, are rare. In this case, we report a novel mutation of HTRA1 in a 43-year-old woman whose imaging indicated multiple CMBs in all lobes, brain stem, and cerebellum. The amount and location of CMBs vary in CARASIL cases, and the potential cause is not fully understood. This study revealed that specific imaging findings of this patient may be related to a new genetic mutation.

Reactivation of fetal hemoglobin (HbF, α2γ2) alleviates clinical symptoms in patients with β-thalassemia and sickle cell disease, although the regulatory mechanisms of γ-globin expression have not yet been fully elucidated. Recent studies found that interfering with the expression of the membrane protein ANTXR1 gene upregulated γ-globin levels. However, the exact mechanism by which ANTXR1 regulates γ-globin levels remains unclear. Our study showed that overexpression and knockdown of ANTXR1 in K562, cord blood CD34+, and HUDEP-2 cells decreased and increased γ-globin expression, respectively. ANTXR1 regulates the reactivation of fetal hemoglobin (HbF, α2γ2) in K562, cord blood CD34+, and adult peripheral blood CD34+ cells through interaction with LRP6 to promote the nuclear entry of β-catenin and activate the Wnt/β-catenin signaling pathway. The overexpression or knockdown of ANTXR1 on γ-globin and Wnt/β-catenin signaling in K562 cells was reversed by the inhibitor XAV939 and the activator LiCl, respectively, where XAV939 inhibits the transcription of β-catenin in the Wnt pathway, but LiCl inhibits GSK3-β. We also showed that the binding ability of the rank4 site in the transcriptional regulatory region of the SOX6 gene to c-Jun was significantly increased after overexpression of ANTXR1 in K562 cells. SOX6 protein expression was increased significantly after overexpression of the c-Jun gene, indicating that the transcription factor c-Jun initiated the transcription of SOX6, thereby silencing γ-globin. Our findings may provide a new intervention target for the treatment of β-hemoglobinopathies.

It is hard to grasp the deformation law of the surrounding rock and the force characteristics of the support structure during the construction of ultra-small clearance tunnels in upper soil and lower rock composite strata. Based on the ultra-small clearance tunnel in Li Shuping, Tongxin Expressway, Guizhou, this paper adopted a combination of numerical simulation and field monitoring to analyze the influence of different burial depths and soil-rock interface positions on the deformation of the surrounding rock and the internal forces of the support structure of the ultra-small clearance tunnel. The conclusions are: (1) the monitoring data show that the stress in the steel frame of the leading tunnel increases first by the influence of proximity construction, and then decreases and reaches a stable value after the secondary lining is applied, and the stress at the arch waist of the soft soil layer furtherest from the side of the middle rock column is greater than that in the rock layer on the side of the middle rock column; (2) the position of the soil-rock interface has a significant influence on the initial support force of the first tunnel, and the bending moment of the structure increases with the downward movement of the soil-rock interface and the increase in the burial depth; (3) the influence of the soil-rock interface position on the initial support moment of the first tunnel is greater than the influence of proximity construction, a point to which attention should be paid during construction; and (4) when the soil-rock interface is located below the foot of the arch, the deformation of the surrounding rock of the following tunnel will be larger than that of the first tunnel. The results can provide a reference for the design and construction of ultra-small clearance tunnels in upper soil and lower rock composite soft strata and soil strata.

Acute lung injury (ALI) is a severe disease that presents serious damage and excessive inflammation in lungs with high mortality without effective pharmacological therapy. Fluorofenidone (AKFPD) is a novel pyridone agent that has anti-fibrosis, anti-inflammation, and other pharmacological activities, while the effect of fluorofenidone on ALI is unclarified. Here, we elucidated the protective effects and underlying mechanism of fluorofenidone on lipopolysaccharide (LPS)-induced ALI. In this study, fluorofenidone alleviated lung tissue structure injury and reduced mortality, decreased the pulmonary inflammatory cell accumulation and level of inflammatory cytokines IL-1β, IL-6, and TNF-α in the bronchoalveolar lavage fluid, and attenuated pulmonary apoptosis in LPS-induced ALI mice. Moreover, fluorofenidone could block LPS-activated phosphorylation of ERK, JNK, and P38 and further inhibited the phosphorylation of IκB and P65. These results suggested that fluorofenidone can significantly contrast LPS-induced ALI through suppressing the activation of the MAPK/NF-κB signaling pathway, which indicates that fluorofenidone could be considered as a novel therapeutic candidate for ALI.

Skin cutaneous melanoma (SKCM) is the most aggressive and fatal type of skin cancer. Its highly heterogeneous features make personalized treatments difficult, so there is an urgent need to identify markers for early diagnosis and therapy. Detailed profiles are useful for assessing malignancy potential and treatment in various cancers. In this study, we constructed a co-expression module using expression data for cutaneous melanoma. A weighted gene co-expression network analysis was used to discover a co-expression gene module for the pathogenesis of this disease, followed by a comprehensive bioinformatics analysis of selected hub genes. A connectivity map (CMap) was used to predict drugs for the treatment of SKCM based on hub genes, and immunohistochemical (IHC) staining was performed to validate the protein levels. After discovering a co-expression gene module for the pathogenesis of this disease, we combined GWAS validation and DEG analysis to identify 10 hub genes in the most relevant module. Survival curves indicated that eight hub genes were significantly and negatively associated with overall survival. A total of eight hub genes were positively correlated with SKCM tumor purity, and 10 hub genes were negatively correlated with the infiltration level of CD4+ T cells and B cells. Methylation levels of seven hub genes in stage 2 SKCM were significantly lower than those in stage 3. We also analyzed the isomer expression levels of 10 hub genes to explore the therapeutic target value of 10 hub genes in terms of alternative splicing (AS). All 10 hub genes had mutations in skin tissue. Furthermore, CMap analysis identified cefamandole, ursolic acid, podophyllotoxin, and Gly-His-Lys as four targeted therapy drugs that may be effective treatments for SKCM. Finally, IHC staining results showed that all 10 molecules were highly expressed in melanoma specimens compared to normal samples. These findings provide new insights into SKCM pathogenesis based on multi-omics profiles of key prognostic biomarkers and drug targets. GPR143 and SLC45A2 may serve as drug targets for immunotherapy and prognostic biomarkers for SKCM. This study identified four drugs with significant potential in treating SKCM patients.

As the foundational element of sports dance, music serves as its quintessential "soul," profoundly influencing the artistic allure and evolutionary trajectory of the discipline. Frequently, it unveils the distinctive charisma of sports dance to global audiences through its intricate rhythmic patterns, melodious compositions, and fervent and uninhibited style. Given the imperative of harmoniously integrating sports dance technique with musical artistry to enhance its expressive capacities, this research endeavours to scrutinize the impact of piano accompaniment music on the psychology and expressive dimensions of sports dancers. Experimental findings substantiate the noteworthy influence of piano accompaniment music training on the expressive prowess exhibited by sports dance athletes. This investigation systematically scrutinized the expressive capacity inherent in sports dance art through the lens of music. By methodically analysing pertinent factors encompassing music training and the expressive capabilities inherent in sports dance art, the pivotal role of music training in augmenting the expressive potency of sports dance art was validated. To corroborate this assertion, a pedagogical experiment employing a single-factor comparative analysis was adopted, elucidating the artistic manifestation within sports dance from an empirical vantage point. Following the experimental intervention, the measurement scores of students within the experimental cohort exhibited a statistically significant elevation in comparison to those of the control group (P < 0.05). These outcomes underscore the pronounced impact of music training on the rhythmic acuity and coordination of sports dancers. Moreover, post-experiment performance in sports skills demonstrated a notable enhancement within the experimental cohort relative to the control group (P < 0.05), further affirming the beneficial effects of music training on sports performance. By honing the rhythmic sensibility instilled through dance music, mastering sequences of movements, grasping the intricacies of dance music, and undergoing collaborative training integrating music with choreographed routines, the artistic expression of dance athletes can be significantly enhanced. Facilitating the fusion of artistry and athleticism, policymakers are encouraged to advocate for the amalgamation of art and sports, thereby fostering an environment conducive to the development of sports dance. This entails provisioning of enhanced artistic resources and training opportunities tailored specifically for sports dance athletes, including guidance and collaboration in musical accompaniment. Provision of professional accompaniment teams is recommended, with policymakers contemplating the establishment of dedicated piano accompaniment teams for sports dance athletes to ensure the calibre and adaptability of musical accompaniment, thereby elevating athletes' performance standards. [ABSTRACT FROM AUTHOR]

Abstract. Erythropoiesis is a complex and sophisticated multi-stage process regulated by a variety of factors, including the transcription factor GATA1 and non-coding RNA. GATA1 is regarded as an essential transcriptional regulator promoting transcription of erythroid-specific genes—such as long non-coding RNAs (lncRNA). Here, we comprehensively screened lncRNAs that were potentially regulated by GATA1 in erythroid cells. We identified a novel lncRNA—PCED1B-AS1—and verified its role in promoting erythroid differentiation of K562 erythroid cells. We also predicted a model in which PCED1B-AS1 participates in erythroid differentiation via dynamic chromatin remodeling involving GATA1. The relationship between lncRNA and chromatin in the process of erythroid differentiation remains to be revealed, and in our study we have carried out preliminary explorations.

Abstract Background Tree shrew is a novel laboratory animal with specific characters for human disease researches in recent years. However, little is known about its characteristics of gut microbial community and intestinal commensal bacteria. In this study, 16S rRNA sequencing method was used to illustrate the gut microbiota structure and commensal Enterobacteriaceae bacteria were isolated to demonstrate their features. Results The results showed Epsilonbacteraeota (30%), Proteobacteria (25%), Firmicutes (19%), Fusobacteria (13%), and Bacteroidetes (8%) were the most abundant phyla in the gut of tree shrew. Campylobacteria, Campylobacterales, Helicobacteraceae and Helicobacter were the predominant abundance for class, order, family and genus levels respectively. The alpha diversity analysis showed statistical significance (P