Metal-Free C60-Doped Mesoporous Carbon Nitride Drives Red-Light Photocatalysis.

The pursuit of novel strategies for synthesizing high-performance nanostructures of graphitic carbon nitride (g-C3N4) has garnered increasing scholarly attention in the field of photocatalysis. Herein, we have successfully designed a metal-free photocatalyst by integrating mesoporous carbon nitride (mpg-C3N4) and C60 through a straightforward and innovative method, marking the first instance of such an achievement. Under red light, the C60/mpg-C3N4 composite exhibited a significantly accelerated rhodamine B (RhB) photodecomposition rate, surpassing bulk g-C3N4 by more than 25.8 times and outperforming pure mpg-C3N4 by 7.8 times. The synergistic effect of C60 and the mesoporous structure significantly enhanced the photocatalytic performance of g-C3N4 by adjusting its electronic structure, broadening the light absorption range, increasing the active sites, and reducing the recombination of photogenerated carriers. This work presents a promising avenue for harnessing a metal-free, stable, efficient photocatalyst driven by red light, with potential for enhancing solar energy utilization in environmental remediation.

GBDT Method Integrating Feature-Enhancement and Active-Learning Strategies-Sea Ice Thickness Inversion in Beaufort Sea.

Sea ice, as an important component of the Earth's ecosystem, has a profound impact on global climate and human activities due to its thickness. Therefore, the inversion of sea ice thickness has important research significance. Due to environmental and equipment-related limitations, the number of samples available for remote sensing inversion is currently insufficient. At high spatial resolutions, remote sensing data contain limited information and noise interference, which seriously affect the accuracy of sea ice thickness inversion. In response to the above issues, we conducted experiments using ice draft data from the Beaufort Sea and designed an improved GBDT method that integrates feature-enhancement and active-learning strategies (IFEAL-GBDT). In this method, the incident angle and time series are used to perform spatiotemporal correction of the data, reducing both temporal and spatial impacts. Meanwhile, based on the original polarization information, effective multi-attribute features are generated to expand the information content and improve the separability of sea ice with different thicknesses. Taking into account the growth cycle and age of sea ice, attributes were added for month and seawater temperature. In addition, we studied an active learning strategy based on the maximum standard deviation to select more informative and representative samples and improve the model's generalization ability. The improved GBDT model was used for training and prediction, offering advantages in dealing with nonlinear, high-dimensional data, and data noise problems, further expanding the effectiveness of feature-enhancement and active-learning strategies. Compared with other methods, the method proposed in this paper achieves the best inversion accuracy, with an average absolute error of 8 cm and a root mean square error of 13.7 cm for IFEAL-GBDT and a correlation coefficient of 0.912. This research proves the effectiveness of our method, which is suitable for the high-precision inversion of sea ice thickness determined using Sentinel-1 data.

SR9009 attenuates inflammation-related NPMSC pyroptosis and IVDD through NR1D1/NLRP3/IL-1ß pathway.

Intervertebral disc is a highly rhythmical tissue. As a key factor linking biorhythm and inflammatory response, the shielding effect of NR1D1 in the process of intervertebral disc degeneration remains unclear. Here, we first confirmed that NR1D1 in the nucleus pulposus tissue presents periodic rhythmic changes and decreases in expression with intervertebral disc degeneration. Second, when NR1D1 was activated by SR9009 in vitro, NLRP3 inflammasome assembly and IL-1ß production were inhibited, while ECM synthesis was increased. Finally, the vivo experiments further confirmed that the activation of NR1D1 can delay the process of disc degeneration to a certain extent. Mechanistically, we demonstrate that NR1D1 can bind to IL-1ß and NLRP3 promoters, and that the NR1D1/NLRP3/IL-1ß pathway is involved in this process. Our results demonstrate that the activation of NR1D1 can effectively reduce IL-1ß secretion, alleviate LPS-induced NPMSC pyroptosis, and protect ECM degeneration.

Ligation of cervical lymphatic vessels decelerates blood clearance and worsens outcomes after experimental subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is characterized by the extravasation of blood into the subarachnoid space, in which erythrocyte lysis is the primary contributor to cell death and brain injuries. New evidence has indicated that meningeal lymphatic vessels (mLVs) are essential in guiding fluid and macromolecular waste from cerebrospinal fluid (CSF) into deep cervical lymph nodes (dCLNs). However, the role of mLVs in clearing erythrocytes after SAH has not been completely elucidated. Hence, we conducted a cross-species study. Autologous blood was injected into the subarachnoid space of rabbits and rats to induce SAH. Erythrocytes in the CSF were measured with/without deep cervical lymph vessels (dCLVs) ligation. Additionally, prior to inducing SAH, we administered rats with vascular endothelial growth factor C (VEGF-C), which is essential for meningeal lymphangiogenesis and maintaining integrity and survival of lymphatic vessels. The results showed that the blood clearance rate was significantly lower after dCLVs ligation in both the rat and rabbit models. DCLVs ligation aggravated neuroinflammation, neuronal damage, brain edema, and behavioral impairment after SAH. Conversely, the treatment of VEGF-C enhanced meningeal lymphatic drainage of erythrocytes and improved outcomes in SAH. In summary, our research highlights the indispensable role of the meningeal lymphatic pathway in the clearance of blood and mediating consequences after SAH.

TREM2 Alleviates Subarachnoid Hemorrhage-Induced Brain Injury through Attenuating Neuroinflammation and Programmed Cell Death in Vivo and in Vitro.

BACKGROUND: Apoptosis and pyroptosis are two types of programmed cell death related to the neuroinflammatory reaction after subarachnoid hemorrhage (SAH). Research indicates that triggering receptor expressed on myeloid cells 2 (TREM2) can regulate the SAH-induced inflammatory response. However, whether TREM2 regulates programmed cell death (apoptosis and pyroptosis) remains to be clarified. The purpose of the present study was to investigate the effects of TREM2 on cell death in SAH. METHODS: SAH was induced in adult male C57BL/6J mice by endovascular perforation. An in-vitro cellular model of SAH was established by treating cocultured BV2 microglia and HT22 neuronal cells with oxyhemoglobin. TREM2 overexpression or knockdown was carried out by intraventricular lentivirus injection at 7 d before SAH induction in mice or lentiviral transfection, respectively. Neurobehavioral tests as well as western blot, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), immunofluorescence, Evans blue (EB) staining, Nissl staining, and flow cytometry assays were performed to investigate the neuroprotective role of TREM2 after SAH. RESULTS: After SAH, the TREM2 mRNA and protein levels were elevated in SAH mice, exhibiting a peak at 72 h. TREM2 overexpression improved the SAH-induced neurological deficits in mice, while TREM2 knockdown worsened them. In the brains of mice with TREM2 overexpression, less neuronal death and more neuronal survival were detected at 72 h post SAH. Meanwhile, TREM2 overexpression showed an inhibitory effect on microglial activation, neutrophil infiltration, and the expression of cell death marker proteins. Consistent results were obtained in vitro. CONCLUSIONS: Our research indicates the important role of TREM2 on cell death after SAH, suggesting that targeting TREM2 might be an effective approach for treating SAH.

Revelation of the discrepancy of volatile compounds in fig (Ficus carica) via gas chromatography ion-mobility spectrometry.

The volatile compounds of fig (Ficus carica) are influenced by various factors. To explore the composition and difference of volatile compounds among figs, gas chromatography ion mobility spectrometry (GC-IMS) was used to study the volatiles of figs from various regions, diverse cultivars, and after treatment with different drying methods. Aldehydes were the main volatile compounds in Bojihong from Shandong, while esters, ketones, and alcohols were the main volatile compounds in Bojihong from Sichuan and Guangdong. The volatiles of Branswick and Banane were similar, but differed significantly from those of Bojihong. Drying had the most significant effect on fig volatiles, which greatly reduced the content of benzaldehyde, (E)-2-hexenal, 2-methylbutanal aldehydes, lost the content of esters such as isoamyl acetate, butyl acetate, ethyl butyrate, and generated some ketones and ethers. The results showed that Bojihong from Shandong was more suitable for the processing of subsequent fig drying products.

Astrocyte-derived hepcidin aggravates neuronal iron accumulation after subarachnoid hemorrhage by decreasing neuronal ferroportin1.

Iron accumulation is one of the most essential pathological events after subarachnoid hemorrhage (SAH). Ferroportin1 (FPN1) is the only transmembrane protein responsible for exporting iron. Hepcidin, as the major regulator of FPN1, is responsible for its degradation. Our study investigated how the interaction between FPN1 and hepcidin contributes to iron accumulation after SAH. We found that iron accumulation aggravated after SAH, along with decreased FPN1 in neurons and increased hepcidin in astrocytes. After knocking down hepcidin in astrocytes, the neuronal FPN1 significantly elevated, thus attenuating iron accumulation. After SAH, p-Smad1/5 and Smad4 tended to translocate into the nucleus. Moreover, Smad4 combined more fragments of the promoter region of Hamp after OxyHb stimulation. By knocking down Smad1/5 or Smad4 in astrocytes, FPN1 level restored and iron overload attenuated, leading to alleviated neuronal cell death and improved neurological function. However, the protective role disappeared after recombinant hepcidin administration. Therefore, our study suggests that owing to the nuclear translocation of transcription factors p-Smad1/5 and Smad4, astrocyte-derived hepcidin increased significantly after SAH, leading to a decreased level of neuronal FPN1, aggravation of iron accumulation, and worse neurological outcome.

Melatonin alleviates oxidative stress-induced injury to nucleus pulposus-derived mesenchymal stem cells through activating PI3K/Akt pathway.

Background: The changes in the microenvironment of degenerative intervertebral discs cause oxidative stress injury and excessive apoptosis of intervertebral disc endogenous stem cells. The purpose of this study was to explore the possible mechanism of the protective effect of melatonin on oxidative stress injury in NPMSCs induced by H2O2. Methods: The Cell Counting Kit-8 assay was used to evaluate the cytotoxicity of hydrogen peroxide and the protective effects of melatonin. ROS content was detected by 2'7'-dichlorofluorescin diacetate (DCFH-DA). Mitochondrial membrane potential (MMP) was detected by the JC-1assay. Transferase mediated d-UTP Nick end labeling (TUNEL) and Annexin V/PI double staining were used to determine the apoptosis rate. Additionally, apoptosis-associated proteins and PI3K/Akt signaling pathway-related proteins were evaluated by immunofluorescence, immunoblotting and PCR. ECMs were evaluated by RT‒PCR and immunofluorescence. In vivo, X-ray, Magnetic resonance imaging (MRI) and Histological analyses were used to evaluate the protective effect of melatonin. Results: Melatonin had an obvious protective effect on NPMSCs treated with 0-10 µM melatonin for 24 h. In addition, melatonin also had obvious protective effects on mitochondrial dysfunction, decreased membrane potential and cell senescence induced by H2O2. More importantly, melatonin could significantly reduce the apoptosis of nucleus pulposus mesenchymal stem cells induced by H2O2 by regulating the expression of apoptosis-related proteins and decreasing the rate of apoptosis. After treatment with melatonin, the PI3K/Akt pathway was significantly activated in nucleus pulposus mesenchymal stem cells, while the protective effect was significantly weakened after PI3K-IN-1 treatment. In vivo, the results of X-ray, MRI and histological analyses showed that therapy with melatonin could partially reduce the degree of intervertebral disc degeneration. Conclusion: Our research demonstrated that melatonin can effectively alleviate the excessive apoptosis and mitochondrial dysfunction of nucleus pulposus mesenchymal stem cells induced by oxidative stress via the PI3K/Akt pathway, which provides a novel idea for the therapy of intervertebral disc degeneration. The translational potential of this article: This study indicates that melatonin can effectively alleviate the excessive apoptosis and mitochondrial dysfunction of NPMSCs through activating the PI3K/Akt pathway. Melatonin might serve as a promising candidate for the prevention and treatment of Intervertebral disc degeneration disease (IVDD) in the future.

Aloperine targets lysosomes to inhibit late autophagy and induces cell death through apoptosis and paraptosis in glioblastoma.

Glioblastoma (GBM) is an aggressive intracranial tumour, and current chemotherapy regimens have limited efficacy. Aloperine (ALO), a natural alkaline compound, has shown potential as an antitumor agent. However, the effect of ALO against GBM remains unclear. This study aimed to investigate the function of ALO in treating GBM. U87, A172, and GL261 cell lines were used for in vitro experiments, and GL261 was also used to establish in vivo models. The results showed that ALO inhibited the proliferation of GBM cells by cell cycle arrest and apoptosis. Furthermore, autophagy was found to play a critical role, suggested by observation of autophagosomes under the transmission electron microscopy. It was discovered for the first time that ALO targeted lysosomes directly in glioma cells, tested by fluo-rescence-labelled ALO and organelle-localizing probes. In addition, ALO inhibited late autophagy and induced paraptosis in GBM, verified by classical gene expression changes in qPCR and western blotting. Also, ALO inhibited tumour growth and acted synergistically with temozolomide in intracranial glioma mice models in vivo. Our findings suggest that ALO targets lysosomes to inhibit late autophagy in GBM, inducing cell cycle arrest, paraptosis, and apoptosis. ALO may therefore be a promising therapeutic agent for the treatment of GBM.

Red Tide Detection Method Based on Improved U-Net Model-Taking GOCI Data in East China Sea as an Example.

In the coastal areas of China, the eutrophication of seawater leads to the continuous occurrence of red tide, which has caused great damage to Marine fisheries and aquatic resources. Therefore, the detection and prediction of red tide have important research significance. The rapid development of optical remote sensing technology and deep-learning technology provides technical means for realizing large-scale and high-precision red tide detection. However, the difficulty of the accurate detection of red tide edges with complex boundaries limits the further improvement of red tide detection accuracy. In view of the above problems, this paper takes GOCI data in the East China Sea as an example and proposes an improved U-Net red tide detection method. In the improved U-Net method, NDVI was introduced to enhance the characteristic information of the red tide to improve the separability between the red tide and seawater. At the same time, the ECA channel attention mechanism was introduced to give different weights according to the influence of different bands on red tide detection, and the spectral characteristics of different channels were fully mined to further extract red tide characteristics. A shallow feature extraction module based on Atrous Spatial Pyramid Convolution (ASPC) was designed to improve the U-Net model. The red tide feature information in a multi-scale context was fused under multiple sampling rates to enhance the model's ability to extract features at different scales. The problem of limited accuracy improvement in red tide edge detection with complex boundaries is solved via the fusion of deep and shallow features and multi-scale spatial features. Compared with other methods, the method proposed in this paper achieves better results and can detect red tide edges with complex boundaries, and the accuracy, precision, recall, and F1-score are 95.90%, 97.15%, 91.53%, and 0.94, respectively. In addition, the red tide detection experiments in other regions with relatively concentrated distribution also prove that the method has good applicability.

Underwater Fish Segmentation Algorithm Based on Improved PSPNet Network.

With the sustainable development of intelligent fisheries, accurate underwater fish segmentation is a key step toward intelligently obtaining fish morphology data. However, the blurred, distorted and low-contrast features of fish images in underwater scenes affect the improvement in fish segmentation accuracy. To solve these problems, this paper proposes a method of underwater fish segmentation based on an improved PSPNet network (IST-PSPNet). First, in the feature extraction stage, to fully perceive features and context information of different scales, we propose an iterative attention feature fusion mechanism, which realizes the depth mining of fish features of different scales and the full perception of context information. Then, a SoftPool pooling method based on fast index weighted activation is used to reduce the numbers of parameters and computations while retaining more feature information, which improves segmentation accuracy and efficiency. Finally, a triad attention mechanism module, triplet attention (TA), is added to the different scale features in the golden tower pool module so that the space attention can focus more on the specific position of the fish body features in the channel through cross-dimensional interaction to suppress the fuzzy distortion caused by background interference in underwater scenes. Additionally, the parameter-sharing strategy is used in this process to make different scale features share the same learning weight parameters and further reduce the numbers of parameters and calculations. The experimental results show that the method presented in this paper yielded better results for the DeepFish underwater fish image dataset than other methods, with 91.56% for the Miou, 46.68 M for Params and 40.27 G for GFLOPS. In the underwater fish segmentation task, the method improved the segmentation accuracy of fish with similar colors and water quality backgrounds, improved fuzziness and small size and made the edge location of fish clearer.

Increased NOX2 expression in astrocytes leads to eNOS uncoupling through dihydrofolate reductase in endothelial cells after subarachnoid hemorrhage.

Introduction: Endothelial nitric oxide synthase (eNOS) uncoupling plays a significant role in acute vasoconstriction during early brain injury (EBI) after subarachnoid hemorrhage (SAH). Astrocytes in the neurovascular unit extend their foot processes around endothelia. In our study, we tested the hypothesis that increased nicotinamide adenine dinucleotide phosphate oxidase 2 (NOX2) expression in astrocytes after SAH leads to eNOS uncoupling. Methods: We utilized laser speckle contrast imaging for monitoring cortical blood flow changes in mice, nitric oxide (NO) kits to measure the level of NO, and a co-culture system to study the effect of astrocytes on endothelial cells. Moreover, the protein levels were assessed by Western blot and immunofluorescence staining. We used CCK-8 to measure the viability of astrocytes and endothelial cells, and we used the H2O2 kit to measure the H2O2 released from astrocytes. We used GSK2795039 as an inhibitor of NOX2, whereas lentivirus and adeno-associated virus were used for dihydrofolate reductase (DHFR) knockdown in vivo and in vitro. Results: The expression of NOX2 and the release of H2O2 in astrocytes are increased, which was accompanied by a decrease in endothelial DHFR 12 h after SAH. Moreover, the eNOS monomer/dimer ratio increased, leading to a decrease in NO and acute cerebral ischemia. All of the above were significantly alleviated after the administration of GSK2795039. However, after knocking down DHFR both in vivo and in vitro, the protective effect of GSK2795039 was greatly reversed. Discussion: The increased level of NOX2 in astrocytes contributes to decreased DHFR in endothelial cells, thus aggravating eNOS uncoupling, which is an essential mechanism underlying acute vasoconstriction after SAH.

Neuroprotective mechanisms of OXCT1 via the SIRT3-SOD2 pathway after traumatic brain injury.

BACKGROUND: Ketones are not only utilized to produce energy but also play a neuroprotective role in many neurodegenerative diseases. However, whether this process has an impact on secondary brain damage after traumatic brain injury (TBI) remains unknown. OXCT1 (3-Oxoacid CoA-Transferase 1) is the rate-limiting enzyme in the intra-neuronal utilization of ketones. In this study, we investigated whether reduced expression of OXCT1 after TBI could impact neuroprotective mechanisms and exacerbate neurological dysfunction. MATERIALS AND METHODS: Experimental TBI was induced by a modified version of the weight drop model, it is a model of severe head trauma. Expression of OXCT1 in the injured hippocampus of mice was measured at different time points using immunoblotting assays. The release of abnormal mitochondrial cytochrome c from neurons of the mouse injured lateral hippocampus was measured 1 week after TBI using immunoblotting assays. Neuronal death was assessed by Nissl staining and the level of reactive oxygen species (ROS) within the neurons of the injured lateral hippocampus was assessed by Dihydroethidium staining. RESULTS: OXCT1 was overexpressed in hippocampal neurons by injection of adeno-associated virus into the lateral ventricle. OXCT1 expression levels decreased significantly 1 week post-TBI. After comparing the data obtained from different groups of mice, OXCT1 was found to significantly increase the expression of SIRT3 and reduce the proportion of acetylated SOD2, thus decreasing the production of ROS in the injured hippocampal neurons, reducing neuronal death, and improving cognitive function. CONCLUSIONS: OXCT1 has a critical previously unappreciated protective role in neurological impairment following TBI via the SIR3-SOD2 pathway. These findings highlight the potential of OXCT1 as a simple treatment for patients with TBI.

Knockdown of Nrf2 radiosensitizes glioma cells by inducing redox stress and apoptosis in hypoxia.

Background: Radiotherapy remains a mainstream treatment for patients with glioma. Yet intrinsic radioresistance has largely compromised the efficacy of the treatment. Increasing concerns have been raised that overexpression of the Nrf2, along with a hypoxic tumor microenvironment, may have contributed to the deterioration of radiotherapy in tumors. So, this study investigated the role of Nrf2 in the radiation therapy of glioma cells in hypoxia. Methods: To determine the expression levels of Nrf2 and HIF-1α, surgical mastectomy specimens from patients with glioma in our institute were analyzed by immunohistochemical staining. Glioblastoma multiforme (GBM) cell lines U251 and U87 with Nrf2 knocked down were produced by transfection with lentiviral particles. Cell lines were treated with ionizing radiation in hypoxia in vitro, with expression and activity of Nrf2 examined by polymerase chain reaction and western blot. Reactive oxygen species (ROS) generation and cell apoptosis analysis were analyzed by flow cytometry. Results: Nrf2 and its downstream pathway were upregulated in surgical specimens after radiotherapy, verified by GBM cell lines treated with in vitro ionizing radiation in hypoxia. Furthermore, knockdown of Nrf2 could induce the ROS generation and cell apoptosis levels after radiation. Conclusions: Downregulation of Nrf2 could sensitize the lethal effect on GBM cells in vitro by enhancing oxidative stress and apoptosis in hypoxia.

A novel nomogram model for clinical outcomes of severe subarachnoid hemorrhage patients.

Background: Systemic responses, especially inflammatory responses, after aneurysmal subarachnoid hemorrhage (SAH) are closely related to clinical outcomes. Our study aimed to explore the correlation between the systemic responses in the acute stage and the mid-term outcomes of severe SAH patients (Hunt-Hess grade III-V). Materials and methods: Severe SAH patients admitted to Jinling Hospital from January 2015 to December 2019 were retrospectively analyzed in the study. The univariate and multivariate logistic regression analyses were used to explore the risk factors of 6-month clinical outcomes in severe SAH patients. A predictive model was established based on those risk factors and was visualized by a nomogram. Then, the predictive nomogram model was validated in another severe SAH patient cohort from January 2020 to January 2022. Results: A total of 194 patients were enrolled in this study. 123 (63.4%, 123 of 194) patients achieved good clinical outcomes at the 6-month follow-up. Univariate and multivariate logistic regression analysis revealed that age, Hunt-Hess grade, neutrophil-to-lymphocyte ratio (NLR), and complications not related to operations were independent risk factors for unfavorable outcomes at 6-month follow-up. The areas under the curve (AUC) analysis showed that the predictive model based on the above four variables was significantly better than the Hunt-Hess grade (0.812 vs. 0.685, P = 0.013). In the validation cohort with 44 severe SAH patients from three different clinical centers, the AUC of the prognostic nomogram model was 0.893. Conclusion: The predictive nomogram model could be a reliable predictive tool for the outcome of severe SAH patients. Systemic inflammatory responses after SAH and complications not related to operations, especially hydrocephalus, delayed cerebral ischemia, and pneumonia, might be the important risk factors that lead to poor outcomes in severe SAH patients.

Endothelial NOX4 aggravates eNOS uncoupling by decreasing dihydrofolate reductase after subarachnoid hemorrhage.

Endothelial malfunction is a major contributor to early or delayed vasospasm after subarachnoid hemorrhage (SAH). As a representative form of endothelial dysfunction, endothelial nitric oxide synthase (eNOS) uncoupling leads to a reduction in nitric oxide (NO) generated by endothelial cells. In this study, we investigated how the interaction between endothelial NOX4 (nicotinamide adenine dinucleotide phosphate oxidase 4) and DHFR (dihydrofolate reductase) contributes to eNOS uncoupling after SAH. Setanaxib and the adeno-associated virus (AAV) targeting brain vascular endothelia were injected through the tail vein and the expression and localization of proteins were examined by western blot and immunofluorescence staining. The NO content was measured using the NO assay kit, and laser speckle contrast imaging was used to assess cortical perfusion. ROS (reactive oxygen species) level was detected by DHE (dihydroethidium) staining, DCFH-DA (2',7'-dichlorofluorescin diacetate) staining and H2O2 (hydrogen peroxide) measurement. The Garcia score was employed to examine neurological function. Setanaxib is widely used for its preferential inhibition for NOX1/4 over other NOX isoforms. After endothelial NOX4 was inhibited by Setanaxib in a mouse model of SAH, the endothelial DHFR level was significantly elevated, which attenuated eNOS uncoupling, increased cortical perfusion, and improved the neurological function. The protective role of inhibiting endothelial NOX4, however, disappeared after knocking down endothelial DHFR. Our results suggest that endothelial DHFR decreased significantly because of the elevated level of endothelial NOX4, which aggravated eNOS uncoupling after SAH, leading to decreased cortical perfusion and worse neurological outcome.

Underwater Holothurian Target-Detection Algorithm Based on Improved CenterNet and Scene Feature Fusion.

Aiming at the common problems, such as noise pollution, low contrast, and color distortion in underwater images, and the characteristics of holothurian recognition, such as morphological ambiguity, high similarity with the background, and coexistence of special ecological scenes, this paper proposes an underwater holothurian target-detection algorithm (FA-CenterNet), based on improved CenterNet and scene feature fusion. First, to reduce the model's occupancy of embedded device resources, we use EfficientNet-B3 as the backbone network to reduce the model's Params and FLOPs. At the same time, EfficientNet-B3 increases the depth and width of the model, which improves the accuracy of the model. Then, we design an effective FPT (feature pyramid transformer) combination module to fully focus and mine the information on holothurian ecological scenarios of different scales and spaces (e.g., holothurian spines, reefs, and waterweeds are often present in the same scenario as holothurians). The co-existing scene information can be used as auxiliary features to detect holothurians, which can improve the detection ability of fuzzy and small-sized holothurians. Finally, we add the AFF module to realize the deep fusion of the shallow-detail and high-level semantic features of holothurians. The results show that the method presented in this paper yields better results on the 2020 CURPC underwater target-detection image dataset with an AP50 of 83.43%, Params of 15.90 M, and FLOPs of 25.12 G compared to other methods. In the underwater holothurian-detection task, this method improves the accuracy of detecting holothurians with fuzzy features, a small size, and dense scene. It also achieves a good balance between detection accuracy, Params, and FLOPs, and is suitable for underwater holothurian detection in most situations.

BTB domain and CNC homolog 1 promotes glioma invasion mainly through regulating extracellular matrix and increases ferroptosis sensitivity.

BTB Domain and CNC Homolog 1 (Bach1) has been implicated in cancer progression, particularly in invasion, but little is unknown about its effect on glioma. Here, we confirmed that highly expressed Bach1 prominently promoted glioma invasion. Similar to the reported mechanisms in other tumors, Bach1 upregulation was also correlated with epithelial mesenchymal transition (EMT) in glioma cells. More importantly, proteomic analysis indicated that the main mechanism of Bach1 promoting invasion in glioma involved extracellular matrix (ECM). We further found thatBach1 upregulation was associated with the multiple mechanisms of ECM remodeling in glioma, including increasing the expression and deposition of ECM components, activating TGFBR2-smad2/3 signaling, promoting invadopodia formation and inducing the expression and secretion of MMP2. Meanwhile, Bach1 overexpression increased ferroptosis sensitivity in glioma cells. The ferroptosis inducer (sulfasalazine) obviously suppressed the gliomas with Bach1 upregulation in vitro and in vivo. Overall, Bach1 has a two-faced role in glioma. Highly expressed Bach1 promotes glioma invasion. Conversely, Bach1 upregulation is also a potential indicator of the sensitivity of ferroptosis inducers.