Biochar promotes compost humification by regulating bacterial and fungal communities.

Introduction: Humus can be formed during composting through biological pathways, nonetheless, the mechanisms through which bacterial and fungal communities govern the development of humus in compost with the addition of biochar remain uncertain. Methods: In this study, compost with cow dung and maize stover as feedstock was employed as a control group, and compost with 10% biochar added on top of the feedstock was adopted as a treatment group to investigate the effect of bacterial and fungal communities on humus formation during biochar composting. Results and Discussion: The results demonstrated that the humic acid content increased by 24.82 and 25.10% at the cooling and maturation stages, respectively, after adding biochar. Besides, the degree of polymerization content in the maturation stage was elevated by 90.98%, which accelerated the humification process of the compost. During the thermophilic and maturity stages, there was a respective increase of 51.34 and 31.40% in reducing sugar content, suggesting that the inclusion of biochar could furnish ample reducing sugar substrate for the Maillard reaction. The addition of biochar reduced the number of humus precursor-associated genera by 35, increased the number of genera involved in humus synthesis by two, and enhanced the stability of the cross-domain network between bacteria and fungi, which confirms that microorganisms contribute to the humification process by decreasing humus precursor consumption as well as increasing humus synthesis with the addition of biochar. Additionally, adding biochar could enhance the humification capacity of the compost pile by dominating the Maillard reaction with reducing sugars as the substrate and strengthening the function of humus synthesis-associated genera. This study enhances our comprehension of the regulatory pathways of biochar in the humification process during composting.

Magnetic resonance imaging and clinicopathological findings of primary hepatic angiosarcoma.

PURPOSE: To investigate the magnetic resonance imaging (MRI) and clinicopathological features of primary hepatic angiosarcoma (PHA) and enhance preoperative diagnosis. METHODS: MRI and clinicopathological information of 12 cases proved PHA were reviewed. Summarize the MRI characteristics of PHA combined with literature reviews. RESULTS: Among 12 cases (6 males and 6 females; age range, 23-70 years; mean, 53.3 years), one presented as a large mass, two as a diffuse infiltrating tumor, and nine as a mixed pattern of large masses with multiple nodules, all involving both lobes of the liver and ranging from 0.1 cm to 11 cm in diameter. A total of 63 lesions were analyzed, including 21 masses and 42 nodules. 13 masses (61.9%) demonstrated intratumoral hemorrhage. 18 masses (85.7%) demonstrated heterogeneous patchy, ring-shaped, septate, or irregular shaped enhancing foci on late arterial phase (LAP). On dynamic contrast-enhanced MRI (DCE-MRI), 14 masses (66.7%) showed a centripetal or centrifugal pattern of incomplete progressive enhancement. 6 nodules (14.3%) appeared intratumoral hemorrhage. 31 nodules (73.8%) showed no enhancing foci on LAP images and 27 nodules (64.3%) showed enhancement pattern of complete filling, either centripetal or centrifugal pattern. Moreover, 12 cases (100%) exhibited prominent vessels within or adjacent to at least one lesion. CONCLUSION: PHA exhibits diverse appearances on MRI. Typical MRI signs include multifoci with intratumoral hemorrhage, prominent vessels within or adjacent to the foci, as well as varied degrees of progressive enhancement with incomplete filling in dominant masses of PHA.

CD8+ tissue-resident memory T cells are essential in bleomycin-induced pulmonary fibrosis.

Human tissue-resident memory T (TRM) cells play a crucial role in protecting the body from infections and cancers. Recent research observed increased numbers of TRM cells in the lung tissues of idiopathic pulmonary fibrosis patient. However, the functional consequences of TRM cells in pulmonary fibrosis remain unclear. Here, we found that the numbers of TRM cells, especially the CD8+ subset, were increased in the mouse lung with bleomycin-induced pulmonary fibrosis. Increasing or decreasing CD8+ TRM cells in mouse lungs accordingly altered the severity of fibrosis. In addition, adoptive transfer of CD8+ T cells containing a large number of CD8+ TRM cells from fibrotic lungs was sufficient to induce pulmonary fibrosis in control mice. Treatment with CCL18 to induced CD8+ TRM cell expansion and exacerbated fibrosis, while blocking CCR8 prevented CD8+ TRM recruitment and inhibited pulmonary fibrosis. In conclusion, CD8+ TRM cells are essential for bleomycin-induced pulmonary fibrosis, and targeting CCL18/CCR8/CD8+ TRM cells may be a potential therapeutic approach.

Human apolipoprotein E glycosylation and sialylation: from structure to function.

Human apolipoprotein E (ApoE) was first identified as a polymorphic gene in the 1970s; however, the genetic association of ApoE genotypes with late-onset sporadic Alzheimer's disease (sAD) was only discovered 20 years later. Since then, intensive research has been undertaken to understand the molecular effects of ApoE in the development of sAD. Despite three decades' worth of effort and over 10,000 papers published, the greatest mystery in the ApoE field remains: human ApoE isoforms differ by only one or two amino acid residues; what is responsible for their significantly distinct roles in the etiology of sAD, with ApoE4 conferring the greatest genetic risk for sAD whereas ApoE2 providing exceptional neuroprotection against sAD. Emerging research starts to point to a novel and compelling hypothesis that the sialoglycans posttranslationally appended to human ApoE may serve as a critical structural modifier that alters the biology of ApoE, leading to the opposing impacts of ApoE isoforms on sAD and likely in the peripheral systems as well. ApoE has been shown to be posttranslationally glycosylated in a species-, tissue-, and cell-specific manner. Human ApoE, particularly in brain tissue and cerebrospinal fluid (CSF), is highly glycosylated, and the glycan chains are exclusively attached via an O-linkage to serine or threonine residues. Moreover, studies have indicated that human ApoE glycans undergo sialic acid modification or sialylation, a structural alteration found to be more prominent in ApoE derived from the brain and CSF than plasma. However, whether the sialylation modification of human ApoE has a biological role is largely unexplored. Our group recently first reported that the three major isoforms of human ApoE in the brain undergo varying degrees of sialylation, with ApoE2 exhibiting the most abundant sialic acid modification, whereas ApoE4 is the least sialylated. Our findings further indicate that the sialic acid moiety on human ApoE glycans may serve as a critical modulator of the interaction of ApoE with amyloid ß (Aß) and downstream Aß pathogenesis, a prominent pathologic feature in AD. In this review, we seek to provide a comprehensive summary of this exciting and rapidly evolving area of ApoE research, including the current state of knowledge and opportunities for future exploration.

EDAC-modified chitosan/imidazolium-polysulfone composite beads for removal of Cr(VI) from aqueous solution.

To enhance the stability and adsorption performance of chitosan in Cr(VI)-contaminated acidic wastewater, a novel EDAC-modified-EDTA-crosslinked chitosan derivative (CSEC) was synthesized via a one-pot method with chitosan, 1-Ethyl-3-(3-dimethylaminopropyl) carbodiimide hydrochloride (EDAC), and Na2EDTA as raw materials. To further improve the mechanical strength and separation performance of CSEC, a novel composite bead (CSEP) of CSEC and imidazolium-functionalized polysulfone (IMPSF) was prepared through a phase inversion method. The chemical composition and microstructure of CSEC and CSEP were characterized by FESEM, FTIR, NMR and XPS techniques. The maximum adsorption capacities of CSEC and CSEP for Cr(VI) were 145.96 and 135.82 mg g-1 at pH 3, respectively, and the equilibrium time for Cr(VI) adsorption by CSEC and CSEP was 5 min and 8 h, respectively. The adsorption process of Cr(VI) by both CSEC and CSEP was exothermic and spontaneous. Compared to CSEC, CSEP has significantly enhanced resistance to interference from coexisting anions. The removal mechanism of Cr(VI) by CSEP might involve redox reaction as well as electrostatic attraction between Cr(VI) oxyanions and various nitrogen cations, including protonated amino groups, guanidinium groups, protonated tertiary amine groups, and imidazolium cations. The CSEP beads have potential application value in the treatment of acidic wastewater containing Cr(VI).

The role of cattle manure-driven polysaccharide precursors in humus formation during composting of spent mushroom substrate.

The study examined the impact of adding cattle manure to the composting process of Agaricus bisporus mushroom substrate on compost humification. A control group CK comprised entirely of Agaricus bisporus mushroom substrate, while the experimental group CD (70 percent Agaricus bisporus mushroom substrate and 30 percent cattle manure) comprised the two composting treatments that were established. The study determined that the addition of cow dung has promoted the formation of humus components. Particularly, humic substance (HS-C) and humic acid (HA) increased by 41.3 and 74.7%, respectively, and the ratio of humic acid to fulvic acid (HA/FA) also increased by 2.78. It showed that the addition of cow dung accelerated the synthesis and decomposition of precursors, such as polysaccharides, polyphenols, and reducing sugars. Thereby promoting the formation of humic acid. Network analysis revealed that adding cow dung promoted microbial interactions increased the complexity and stability of the bacterial and fungal symbiotic network, enhanced cooperation and reciprocity among microbes, and assisted in transforming fulvic acid (FA) components. Structural equation modeling (SEM) is a multivariate data analysis method for analyzing complex relationships among constructs and core indicators. SEM illustrated that introducing cattle manure into the composting process resulted in alterations to the correlation between physicochemical parameters and the microbial community, in addition to humus formation. Polysaccharides are the primary precursors for polymerization to form HA, which is an essential prerequisite for the conversion of fulvic acid to humic acid. Additionally, microbes affected the formation of humus, with bacteria substantially more influential than fungi. These findings provide new ideas for regulating the degree of humification in the composting process and have important practical implications for optimizing mushroom cultivation and composting techniques today.

Development of a non-invasive diagnostic model for high-risk esophageal varices based on radiomics of spleen CT.

PURPOSE: To evaluate the diagnostic performance of radiomics models derived from multi-phase spleen CT for high-risk esophageal varices (HREV) in cirrhotic patients. METHODS: We retrospectively selected cirrhotic patients with esophageal varices from two hospitals from September 2019 to September 2023. Patients underwent non-contrast and contrast-enhanced CT scans and were categorized into HREV and non-HREV groups based on endoscopic evaluations. Radiomics features were extracted from spleen CT images in non-contrast, arterial, and portal venous phases, with feature selection via lasso regression and Pearson's correlation. Ten machine learning models were developed to diagnose HREV, evaluated by area under the curve (AUC). The AUC values of the three groups of models were statistically compared by the Kruskal-Wallis H test and Bonferroni-corrected Mann-Whitney U test. A p-value less than 0.05 was considered statistically significant. RESULTS: Among 233 patients, 11, 6, and 11 features were selected from non-contrast, arterial, and portal venous phases, respectively. Significant differences in AUC values were observed across phases (p < 0.05), and the arterial phase models showed the highest AUC values. The best model in arterial phase was the logical regression model, whose AUC value was 0.85, sensitivity was 83.3%, specificity was 80% and F1 score was 0.81. CONCLUSION: Radiomics models based on spleen CT, especially the arterial phase models, demonstrate high diagnostic accuracy for HREV, offering the potential for early detection and intervention.

Predicting High-Risk Esophageal Varices in Cirrhosis: A Multi-Parameter Splenic CT Study.

RATIONALE AND OBJECTIVES: To explore the value of splenic hemodynamic parameters from low-dose one-stop dual-energy and perfusion CT (LD-DE&PCT) in non-invasively predicting high-risk esophageal varices (HREV) in cirrhotic patients. METHODS: We retrospectively analyzed cirrhotic patients diagnosed with esophageal varices (EV) through clinical, laboratory, imaging, and endoscopic examinations from September 2021 to December 2023 in our hospital. All patients underwent LD-DE&PCT to acquire splenic iodine concentration and perfusion parameters. Radiation dose was recorded. Patients were classified into non-HREV and HREV groups based on endoscopy. Univariate and multivariate logistic regression analysis were performed, and the prediction model for HREV was constructed. P < 0.05 was considered statistically significant. RESULTS: Univariate analysis revealed that significant differences were found in portal iodine concentration (PIC), blood flow (BF), permeability surface (PS), spleen volume (V-S), total iodine concentration (TIC), and total blood volume of the spleen (BV-S) between groups. TIC demonstrated the highest predictive value with an area under the curve (AUC) value of 0.87. Multivariate analysis showed that PIC, PS, and BV-S were independent risk factors for HREV. The logistic regression model for predicting HREV had an AUC of 0.93. The total radiation dose was 20.66 ± 4.07 mSv. CONCLUSION: Splenic hemodynamic parameters obtained from LD-DE&PCT can non-invasively and accurately assess the hemodynamic status of the spleen in cirrhotic patients with EV and predict the occurrence of HREV. Despite the retrospective study design and limited sample size of this study, these findings deserve further validation through prospective studies with larger cohorts.

The ubiquitin-like protein UBTD1 promotes colorectal cancer progression by stabilizing c-Myc to upregulate glycolysis.

Dysfunction of the ubiquitin-proteasome system (UPS) is involved in the pathogenesis of various malignancies including colorectal cancer (CRC). Ubiquitin domain containing 1 (UBTD1), a ubiquitin-like protein, regulates UPS-mediated protein degradation and tumor progression in some cancer types. However, the biological function and mechanism of UBTD1 are far from being well elucidated, and its role in CRC has not been explored yet. In our study, we analyzed CRC patients' clinical information and UBTD1 expression data, and found that the expression of UBTD1 in cancer tissue was significantly higher than that in adjacent normal tissue. Higher UBTD1 expression was significantly associated with poorer survival and more lymph node metastasis. Overexpression of UBTD1 could facilitate, while knockdown could inhibit CRC cell proliferation and migration, respectively. RNA-seq and proteomics indicated that c-Myc is an important downstream target of UBTD1. Metabolomics showed the products of the glycolysis pathway were significantly increased in UBTD1 overexpression cells. In vitro, we verified UBTD1 upregulating c-Myc protein and promoting CRC cell proliferation and migration via regulating c-Myc. UBTD1 promoted CRC cells' glycolysis, evidenced by the increased lactate production and glucose uptake following UBTD1 overexpression. Mechanistically, UBTD1 prolonged the half-life of the c-Myc protein by binding to E3 ligase ß-transducin repeat-containing protein (ß-TrCP), thereby upregulated the expression of glycolysis rate-limiting enzyme hexokinase II (HK2), and enhanced glycolysis and promoted CRC progression. In conclusion, our study revealed that UBTD1 promotes CRC progression by upregulating glycolysis via the ß-TrCP/c-Myc/HK2 pathway, suggesting its potential as a prognostic biomarker and therapeutic target in CRC.

Efficacy and safety of intranasal insulin on postoperative cognitive dysfunction in elderly patients after laparoscopic radical resection of colorectal cancer: a double-blind pilot study.

Objective: To evaluate the efficacy and safety of intranasal insulin on postoperative cognitive dysfunction (POCD) in elderly patients after laparoscopic radical resection of colorectal cancer. Methods: Older patients scheduled for laparoscopic radical resection of colorectal cancer at Beijing Luhe Hospital, Capital Medical University, between August 2023 and November 2023, were enrolled in this double-blind pilot study. Patients were randomized to the control and insulin groups at a 1:1 ratio. The primary outcome was the rate of POCD at postoperative 7 days. Results: A total of 61 patients (30 in the insulin group) were analyzed. The insulin group had a significantly lower POCD rate compared with the control group at postoperative day 7 [4(13.3%) vs. 12 (38.7%), p = 0.024]. The serum levels of IL-6, TNF-α and S100ß at T2-5 in the insulin group were significantly lower than those of the control group (IL-6: mean difference at T2, -4.14, p = 0.036; T3, -3.84, p = 0.039; T4, -3.37, p = 0.013; T5, -2.57, p = 0.042; TNF-α: mean difference at T2, -3.19, p = 0.002; T3, -2.35, p = 0.028; T4, -2.30, p = 0.019; T5, -1.96, p = 0.0181; S100ß: mean difference at T2, -8.30, p = 0.019; T3, -23.95, p = 0.020; T4, -20.01, p = 0.023; T5, -17.67, p = 0.010). No insulin allergic reactions, nasal irritation, or hypoglycemic reactions were observed in either of the groups. Conclusion: Intranasal insulin may decrease the risk of POCD and inhibit the elevated serum IL-6, TNF-α, and S100ß levels in elderly patients after laparoscopic radical resection of colorectal cancer, which proves that intranasal insulin may be a promising therapeutic option for POCD. Clinical trial registration: Identifier, ChiCTR2300074423.

Electrohydrodynamic Direct-Writing Micro/Nanofibrous Architectures: Principle, Materials, and Biomedical Applications.

Electrohydrodynamic (EHD) direct-writing has recently gained attention as a highly promising additive manufacturing strategy for fabricating intricate micro/nanoscale architectures. This technique is particularly well-suited for mimicking the extracellular matrix (ECM) present in biological tissue, which serves a vital function in facilitating cell colonization, migration, and growth. The integration of EHD direct-writing with other techniques has been employed to enhance the biological performance of scaffolds, and significant advancements have been made in the development of tailored scaffold architectures and constituents to meet the specific requirements of various biomedical applications. Here, a comprehensive overview of EHD direct-writing is provided, including its underlying principles, demonstrated materials systems, and biomedical applications. A brief chronology of EHD direct-writing is provided, along with an examination of the observed phenomena that occur during the printing process. The impact of biomaterial selection and architectural topographic cues on biological performance is also highlighted. Finally, the major limitations associated with EHD direct-writing are discussed.

Potentially functional genetic variants in interferon regulatory factor family genes are associated with colorectal cancer survival.

Interferon regulatory factor (IRF) family genes play a critical role in colorectal cancer (CRC) development and impact patient survival. This study evaluated the influence of functional single nucleotide polymorphisms (SNPs) in IRF genes on CRC survival, including functional predictions and experimental validations. Multivariate Cox regression analysis identified three linked SNPs as significant survival predictors, with the rs141112353 T/T genotype in the 3'UTR region of IRF6 significantly associated with decreased survival (HR = 1.60, P = 6E-04). Expression quantitative trait loci (eQTL) analysis indicated that the rs141112353 TA > T alteration reduced IRF6 expression. Dual luciferase assays showed lower activity for the T allele in the presence of hsa-miR-548ap-3p. Data from The Cancer Genome Atlas (TCGA) and other databases confirmed lower IRF6 levels in CRC tissues, correlating with worse survival and inversely with M2 macrophage infiltration. In vitro, IRF6 overexpression inhibited CRC cell proliferation and M2 macrophage polarization by downregulating MIF expression. These findings suggest that the IRF6 rs141112353 TA > T variant significantly affects CRC survival, potentially by enhancing miR-548-ap-3p binding affinity.

DEC1 is involved in circadian rhythm disruption-exacerbated pulmonary fibrosis.

BACKGROUND: The alveolar epithelial type II cell (AT2) and its senescence play a pivotal role in alveolar damage and pulmonary fibrosis. Cell circadian rhythm is strongly associated with cell senescence. Differentiated embryonic chondrocyte expressed gene 1 (DEC1) is a very important circadian clock gene. However, the role of DEC1 in AT2 senescence and pulmonary fibrosis was still unclear. RESULTS: In this study, a circadian disruption model of light intervention was used. It was found that circadian disruption exacerbated pulmonary fibrosis in mice. To understand the underlying mechanism, DEC1 levels were investigated. Results showed that DEC1 levels increased in lung tissues of IPF patients and in bleomycin-induced mouse fibrotic lungs. In vitro study revealed that bleomycin and TGF-ß1 increased the expressions of DEC1, collagen-I, and fibronectin in AT2 cells. Inhibition of DEC1 mitigated bleomycin-induced fibrotic changes in vitro and in vivo. After that, cell senescence was observed in bleomycin-treated AT2 cells and mouse models, but these were prevented by DEC1 inhibition. At last, p21 was confirmed having circadian rhythm followed DEC1 in normal conditions. But bleomycin disrupted the circadian rhythm and increased DEC1 which promoted p21 expression, increased p21 mediated AT2 senescence and pulmonary fibrosis. CONCLUSIONS: Taken together, circadian clock protein DEC1 mediated pulmonary fibrosis via p21 and cell senescence in alveolar epithelial type II cells.

Improving osseointegration and antimicrobial properties of titanium implants with black phosphorus nanosheets-hydroxyapatite composite coatings for vascularized bone regeneration.

For decades, titanium implants have shown impressive advantages in bone repair. However, the preparation of implants with excellent antimicrobial properties as well as better osseointegration ability remains difficult for clinical application. In this study, black phosphorus nanosheets (BPNSs) were doped into hydroxyapatite (HA) coatings using electrophoretic deposition. The coatings' surface morphology, roughness, water contact angle, photothermal properties, and antibacterial properties were investigated. The BP/HA coating exhibited a surface roughness of 59.1 nm, providing an ideal substrate for cell attachment and growth. The water contact angle on the BP/HA coating was measured to be approximately 8.55°, indicating its hydrophilic nature. The BPNSs demonstrated efficient photothermal conversion, with a temperature increase of 42.2°C under laser irradiation. The BP/HA composite coating exhibited a significant reduction in bacterial growth, with inhibition rates of 95.6% and 96.1% against Staphylococcus aureus and Escherichia coli. In addition, the cytocompatibility of the composite coating was evaluated by cell adhesion, CCK8 and AM/PI staining; the effect of the composite coating in promoting angiogenesis was assessed by scratch assay, transwell assay, and protein blotting; and the osteoinductivity of the composite coating was evaluated by alkaline phosphatase assay, alizarin red staining, and Western blot. The results showed that the BP/HA composite coating exhibited superior performance in promoting biological functions such as cell proliferation and adhesion, antibacterial activity, osteogenic differentiation, and angiogenesis, and had potential applications in vascularized bone regeneration.

MKP1 may be involved in the occurrence of depression by regulating hippocampal autophagy in rats.

BACKGROUND: Mitogen-activated protein kinase (MAPK) phosphatase-1 (MKP1) is upregulated in the hippocampus of patients with depression, while pharmacological inhibition of hippocampal MKP1 can mitigate depression-like behaviors in rodents. In addition, MAPK signaling regulates autophagy, and antidepressants were recently shown to target autophagic signaling pathways. We speculated that MKP1 contributes to depression by enhancing hippocampal autophagy through dephosphorylation of the MAPK isoform ERK1/2. METHODS: We established a rat depression model by exposure to chronic unpredictable mild stress (CUMS), and then examined depression-like behaviors in the sucrose preference test (SPT) and forced swimming test (FST) as well as expression changes in hippocampal MKP1, ERK1/2, phosphorylated ERK1/2, and autophagy-related proteins LC3II by Western blotting and immunostaining. These same measurements were repeated in rats exposed to CUMS following hippocampal infusion of a MKP1-targeted shRNA. Finally, the effects of MKP1 expression level on autophagy we examined in rat GMI-R1 microglia. RESULTS: CUMS-exposed rats demonstrated anhedonia in the SPT and helplessness in the FST, two core depression-like behaviors. Expression levels of MKP1 and LC3II were upregulated in the hippocampus of CUMS rats, suggesting enhanced autophagy, while pERK/ERK was downregulated. Knockdown of hippocampal MKP1 mitigated depression-like behaviors, downregulated hippocampal LC3II expression, and upregulated hippocampal pERK/ERK. Similarly, MKP1 knockdown in GMI-R1 cells upregulated pERK/ERK and reduced the number of LC3II autophagosomes, while MKP1 overexpression had the opposite effects. CONCLUSION: Enhanced hippocampal autophagy via MKP1-mediated ERK dephosphorylation may contribute to the development of depression.

Preparation of black phosphorus@sodium alginate microspheres with bone matrix vesicle structure via electrospraying for bone regeneration.

Bone matrix vesicles are commonly acknowledged as the primary site of biomineralization in human skeletal tissue. Black phosphorus has exhibited favorable properties across various chemical and physical domains. In this investigation, a novel composite microsphere was synthesized through the amalgamation of sodium alginate (ALG) with black phosphorus nanosheets (BP) utilizing the electrospray (ES) technique. These microspheres were tailored to mimic the regulatory function of matrix vesicles (MV) upon exposure to a biomimetic mineralization fluid (SBF) during the biomineralization process. Results revealed that black phosphorus nanosheets facilitated the generation of hydroxyapatite (HA) on the microsphere surface. Live-dead assays and cell proliferation experiments showcased a cell survival rate exceeding 85 %. Moreover, wound healing assessments unveiled that M-ALG-BP microspheres exhibited superior migration capacity, with a migration rate surpassing 50 %. Furthermore, after 7 days of osteogenic induction, M-ALG-BP microspheres notably stimulated osteoblast differentiation. Particularly noteworthy, M-ALG-BP microspheres significantly enhanced osteogenic differentiation of osteoblasts and induced collagen production in vitro. Additionally, experiments involving microsphere implantation into mouse skeletal muscle demonstrated the potential for ectopic mineralization by ALG-BP microspheres. This investigation underscores the outstanding mineralization properties of ALG-BP microspheres and their promising clinical prospects in bone tissue engineering.

A hybrid prediction model of dissolved oxygen concentration based on secondary decomposition and bidirectional gate recurrent unit.

Dissolved oxygen is one of the important comprehensive indicators of river water quality, which reflects the degree of pollution in the water body. Monitoring and predicting dissolved oxygen are an important tool for water quality management, which helps to effectively maintain water ecological balance and prevent environmental problems. A single model cannot describe the dynamic characteristics of dissolved oxygen sequence, which affects the prediction accuracy. In order to obtain more accurate dissolved oxygen prediction results, decomposition techniques are commonly used to extract the main fluctuations and trends of water quality sequences. However, the high-frequency modes obtained from decomposition are still unstable. To solve this problem, this paper proposed a hybrid prediction model of dissolved oxygen concentration based on secondary decomposition and bidirectional gate recurrent unit. Firstly, dissolved oxygen sequence is preliminarily decomposed by complete ensemble empirical mode decomposition with adaptive noise (CEEMDAN) and obtain several intrinsic mode functions (IMF). The fuzzy entropy (FE) is calculated to quantify the complexity of the IMF. Then, variational mode decomposition improved by northern goshawk optimization is used to decompose the IMF with higher entropy. The nonlinearity and instability of the sequence are further weakened. Finally, the bidirectional gate recurrent unit (BiGRU) neural network is used to predict each IMF component, and the final prediction result is obtained by reconstructing the prediction results of each component. In order to verify the effectiveness of the proposed model, this paper selects the dissolved oxygen data of Xin'anjiang Reservoir as the research object. The experimental results show that the RMSE, MAE, MAPE, and R2 of the proposed model are 0.1164, 0.0894, 1.0403%, and 0.9939, respectively, which is best among other comparative prediction models (BP, LSTM, GRU, BiGRU, EMD-BiGRU, CEEMDAN-BiGRU, VMD-BiGRU, and GNO-VMD-BiGRU). Therefore, this model effectively deals with high volatility and nonlinear dissolved oxygen data and provides reference for water environment management and ecological protection.

LncRNA SNHG26 promotes gastric cancer progression and metastasis by inducing c-Myc protein translation and an energy metabolism positive feedback loop.

Metastasis is a bottleneck in cancer treatment. Studies have shown the pivotal roles of long noncoding RNAs (lncRNAs) in regulating cancer metastasis; however, our understanding of lncRNAs in gastric cancer (GC) remains limited. RNA-seq was performed on metastasis-inclined GC tissues to uncover metastasis-associated lncRNAs, revealing upregulated small nucleolar RNA host gene 26 (SNHG26) expression, which predicted poor GC patient prognosis. Functional experiments revealed that SNHG26 promoted cellular epithelial-mesenchymal transition and proliferation in vitro and in vivo. Mechanistically, SNHG26 was found to interact with nucleolin (NCL), thereby modulating c-Myc expression by increasing its translation, and in turn promoting energy metabolism via hexokinase 2 (HK2), which facilitates GC malignancy. The increase in energy metabolism supplies sufficient energy to promote c-Myc translation and expression, forming a positive feedback loop. In addition, metabolic and translation inhibitors can block this loop, thus inhibiting cell proliferation and mobility, indicating potential therapeutic prospects in GC.

Blocking EGR1/TGF-ß1 and CD44s/STAT3 Crosstalk Inhibits Peritoneal Metastasis of Gastric Cancer.

Peritoneal metastasis (PM) continues to limit the clinical efficacy of gastric cancer (GC). Early growth response 1 (EGR1) plays an important role in tumor cell proliferation, angiogenesis and invasion. However, the role of EGR1 derived from the tumor microenvironment in reshaping the phenotypes of GC cells and its specific molecular mechanisms in increasing the potential for PM are still unclear. In this study, we reported that EGR1 was significantly up-regulated in mesothelial cells from GC peritoneal metastases, leading to enhanced epithelial-mesenchymal transformation (EMT) and stemness phenotypes of GC cells under co-culture conditions. These phenotypes were achieved through the transcription and secretion of TGF-ß1 by EGR1 in mesothelial cells, which could regulate the expression and internalization of CD44s. After being internalized into the cytoplasm, CD44s interacted with STAT3 to promote STAT3 phosphorylation and activation, and induced EMT and stemness gene transcription, thus positively regulating the metastasis of GC cells. Moreover, TGF-ß1 secretion in the PM microenvironment was significantly increased compared with the matched primary tumor. The blocking effect of SHR-1701 on TGF-ß1 was verified by inhibiting peritoneal metastases in xenografts. Collectively, the interplay of EGR1/TGF-ß1/CD44s/STAT3 signaling between mesothelial cells and GC cells induces EMT and stemness phenotypes, offering potential as a therapeutic target for PM of GC.