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As a biological sound source widely distributed in temperate and tropical coastal waters, snapping shrimp produce strong pulses which can serve as honest signals to indicate habitat-specific soundscape. The past decade has witnessed the growing interest in investigating the acoustical activity of snapping shrimp across many shallow waters including the coastal line of the west Pacific Ocean. It was extended to the Southeast China coastal area where snapping sounds and the associated soundscape were recorded at four sites. Customized codes incorporating bandwidth and amplitude threshold operations were developed to detect snaps from the ambient noise to estimate snap rate and extract snaps individually. The subsequent analysis suggested that snaps recorded at different sites were unanimously stronger than background noise. Sound pressure level of the snaps ranged from 150 dB to 190 dB (re 1 μPa). The characteristics of snaps, including sound pressure level, duration, peak frequency, -3dB bandwidth from different sites are examined to evaluate the variability across the sites. Though snapping pulses had peak frequencies and the -3 dB bandwidth consistently below 10 kHz, snaps had considerable energy extending to the high frequency range over 200 kHz. The analysis of the acoustic data received for 7 consecutive days at one site indicated that the snap rate corresponded to tidal level periodicity. A high tide was accompanied with a local high snap rate regardless of light but this local snap rate peak was much higher at night. The mean rate fluctuated between 2000 and 4000 snaps per minute and more snaps were recorded after sunset suggesting that snapping shrimp living in the area snapped in response to light. These data may indicate that snaps are important communication means in light-limited condition and deepen our understanding on the correlation of snapping behavior and ecological environments.

Chinese bahaba (Bahaba taipingensis) is a critically endangered fish species, which can produce sounds like other Sciaenidae species. In this study, sounds produced by sexually mature Chinese bahaba were recorded during the reproduction season for the first time. Two distinct types of sounds were observed during the reproduction season, termed as single drum and fast drum trains calls. Single drum callings occurred as a series of trains with rapid pulses, while fast drum trains callings were mainly made of a single signal. The single drum and fast drum trains had a peak frequency of 77.8 ± 16.2 Hz and 79.1 ± 8.7 Hz, respectively. Statistical analysis suggested significant differences in −3 dB bandwidth, signal duration, and root-mean-square sound pressure levels, except for peak frequency (p < 0.05) between single drum and fast drum trains sounds. Single drum occurred mainly before dawn (period range from 0:00 to 6:00 am) and less frequently after dusk (18:00–24:00 pm), and the fast drum trains occurred after dawn (6:00 am to 12:00 pm) and dusk (18:00 pm to 24:00 pm). Considering the abundance of Chinese bahaba has significantly declined, passive acoustic monitoring provides a non-invasive and low-cost effective tool to monitor sound production during reproduction season, which may help to facilitate aquaculture management and fishery population conservation in the future.

Abstract We have developed a population-level method for dietary assessment using low-cost wearable cameras. Our approach, EgoDiet, employs an egocentric vision-based pipeline to learn portion sizes, addressing the shortcomings of traditional self-reported dietary methods. To evaluate the functionality of this method, field studies were conducted in London (Study A) and Ghana (Study B) among populations of Ghanaian and Kenyan origin. In Study A, EgoDiet’s estimations were contrasted with dietitians’ assessments, revealing a performance with a Mean Absolute Percentage Error (MAPE) of 31.9% for portion size estimation, compared to 40.1% for estimates made by dietitians. We further evaluated our approach in Study B, comparing its performance to the traditional 24-Hour Dietary Recall (24HR). Our approach demonstrated a MAPE of 28.0%, showing a reduction in error when contrasted with the 24HR, which exhibited a MAPE of 32.5%. This improvement highlights the potential of using passive camera technology to serve as an alternative to the traditional dietary assessment methods.

BackgroundRecently, cancer neuroscience has become the focus for scientists. Interactions between the nervous system and cancer (both systemic and local) can regulate tumorigenesis, progression, treatment resistance, compromise of anti-cancer immunity, and provocation of tumor-promoting inflammation. We assessed the related research on cancer neuroscience through bibliometric analysis and explored the research status and hotspots from 2020 to 2024.MethodsPublications on cancer neuroscience retrieved from the Web of Science Core Collection. CiteSpace, VOSviewer, and Scimago Graphica were used to analyze and visualize the result.ResultsA total of 744 publications were retrieved, with an upward trend in the overall number of articles published over the last 5 years. As it has the highest number of publications (n = 242) and citations (average 13.63 citations per article), the United States holds an absolute voice in the field of cancer neuroscience. The most productive organizations and journals were Shanghai Jiaotong University (n = 24) and Cancers (n = 45), respectively. Monje M (H-index = 53), Hondermarck H (H-index = 42), and Amit M (H-index = 39) were the three researchers who have contributed most to the field. From a global perspective, research hotspots in cancer neuroscience comprise nerve/neuron-tumor cell interactions, crosstalk between the nervous system and other components of the tumor microenvironment (such as immune cells), as well as the impact of tumors and tumor therapies on nervous system function.ConclusionThe United States and European countries are dominating the field of cancer neuroscience, while developing countries such as China are growing rapidly but with limited impact. The next focal point in this field is likely to be neurotrophic factors. Cancer neuroscience is still in its infancy, which means that many of the interactions and mechanisms between the nervous system and cancer are not yet fully understood. Further investigation is necessary to probe the interactions of the nervous system with cancer cell subpopulations and other components of the tumor microenvironment.

Abstract In the process of photocatalytic synthesis of ammonia, the kinetics of carrier separation and transport, adsorption of nitrogen, and activation of the NN triple bond are key factors that directly affect the efficiency of converting nitrogen to ammonia. Here, we report a new strategy for anchoring MXene quantum dots (MXene QDs) onto the surface of ZnIn2S4 by forming TiS bonds, which provide a channel for the rapid separation and transport of charge carriers and effectively extend the lifespan of photogenerated carriers. The unique charge distribution caused by the sulfurization of the MXene QDs further enhances the performance of the photocatalysts for the adsorption and activation of nitrogen. The photocatalytic ammonia synthesis efficiency of MXene QDs–ZnIn2S4 can reach up to 360.5 μmol g−1 h−1. Density functional theory calculations, various in situ techniques, and ultrafast spectroscopy are used to characterize the successful construction of TiS bonds and the dynamic nature of excited state charge carriers in MXene QDs–ZnIn2S4, as well as their impact on nitrogen adsorption activation and photocatalytic ammonia synthesis efficiency. This study provides a new example of how to improve nitrogen adsorption and activation in photocatalytic material systems and enhance charge carrier dynamics to achieve efficient photocatalytic nitrogen conversion.

The RNA modification 5-methylcytosine (m5C) is widespread across various RNA types, significantly impacting RNA stability and translational efficiency. Accumulating evidence highlights its significant role within the tumorigenesis and progression of multiple malignancies. Nevertheless, the specific process through m5C is implicated in Glioblastoma (GBM) remains unclear. We conducted acomprehensive analysis of m5C expression distribution in single-cell GBM data. Our findings revealed elevated m5C scores in GBM single-cell data compared to the normal group. Additionally, multiple tumors exhibited significantly higher m5C scores than the normal group. Moreover, there was a positive correlation observed between the m5C score and inflammation score. m5C regulatory factor YBX1 exhibited a heightened expression in GBM, correlating closely with metastatic tendencies and an unfavorable prognosis across various cancer types. YBX1 has different biological functions in myeloid cells 1 and myeloid cells 2. YBX1 may act as immunosuppressive regulator by inhibiting the NF-κB pathway and inflammatory response in myeloid cells 1. YBX1 is essential for immune infiltrates, which creates a highly immunosuppressive tumor microenvironment by TNF signaling pathway in myeloid cells 2. YBX1+ neoplastic cells promote cell proliferation by NF-κB pathway. APOE mediates the interaction of YBX1+ myeloid cells and neoplastic cells by NF-κB.

Microglia are immune cells within the central nervous system (CNS) closely linked to brain health and neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In response to changes in the surrounding environment, microglia activate and change their state and function. Several factors, example for circadian rhythm disruption and the development of neurodegenerative diseases, influence microglia activation. In this review, we explore microglia’s function and the associated neural mechanisms. We elucidate that circadian rhythms are essential factors influencing microglia activation and function. Circadian rhythm disruption affects microglia activation and, consequently, neurodegenerative diseases. In addition, we found that abnormal microglia activation is a common feature of neurodegenerative diseases and an essential factor of disease development. Here we highlight the importance of microglia activation in neurodegenerative diseases. Targeting microglia for neurodegenerative disease treatment is a promising direction. We introduce the progress of methods targeting microglia for the treatment of neurodegenerative diseases and summarize the progress of drugs developed with microglia as targets, hoping to provide new ideas for treating neurodegenerative diseases.

Abstract Background Plants are continuously challenged with biotic stress from environmental pathogens, and precise regulation of defense responses is critical for plant survival. Defense systems require considerable amounts of energy and resources, impairing plant growth, and plant hormones controlling transcriptional regulation play essential roles in establishing the appropriate balance between defense response to pathogens and growth. Chromatin regulators modulating gene transcription are broadly involved in regulating stress-responsive genes. However, which chromatin factors are involved in coordinating hormone signaling and immune responses in plants, and their functional mechanisms, remains unclear. Here, we identified a role of bromodomain-containing protein GTE4 in negatively regulating defense responses in Arabidopsis thaliana. Results GTE4 mainly functions as activator of gene expression upon infection with Pseudomonas syringe. Genome-wide profiling of GTE4 occupancy shows that GTE4 tends to bind to active genes, including ribosome biogenesis related genes and maintains their high expression levels during pathogen infection. However, GTE4 is also able to repress gene expression. GTE4 binds to and represses jasmonate biosynthesis gene OPR3. Disruption of GTE4 results in overaccumulation of jasmonic acid (JA) and enhanced JA-responsive gene expression. Unexpectedly, over-accumulated JA content in gte4 mutant is coupled with downregulation of JA-mediated immune defense genes and upregulation of salicylic acid (SA)-mediated immune defense genes, and enhanced resistance to Pseudomonas, likely through a noncanonical pathway. Conclusions Overall, we identified a new role of the chromatin factor GTE4 as negative regulator of plant immune response through inhibition of JA biosynthesis, which in turn noncanonically activates the defense system against Pseudomonas. These findings provide new knowledge of chromatic regulation of plant hormone signaling during defense responses.

A small indentation embedded in a microchannel creates a surface energy well (SEW) for a confined droplet due to surface energy release. Inspired by this, we developed a SEW-based microfluidic platform to realize high spatiotemporal-resolved signal profiling at the single-cell level applying droplet stimulus on a single chip. The method allows for controlled droplet replacement within only 3 s with almost 100% exchange efficiency, reliable single-cell patterning of adherent cells and successive treatment of adherent cells with reagent droplets. Furthermore, the PDGFR/Akt pathway served as a model system for evaluating the performance of the SEW-based method in determining the effects of ligand stimulation duration (3 s to 3 min) on receptor phosphorylation. The novel strategy offers a general platform for probing the temporal dynamics of single cells, as well for monitoring rapid chemical reactions in various applications.

With the increasing demands on quality healthcare and the raising cost of care, pervasive healthcare is considered as a technological solutions to address the global health issues. In particular, the recent advances in Internet of Things have led to the development of Internet of Medical Things (IoMT). Although such low cost and pervasive sensing devices could potentially transform the current reactive care to preventative care, the security and privacy issues of such sensing system are often overlooked. As the medical devices capture and process very sensitive personal health data, the devices and their associated communications have to be very secured to protect the user's privacy. However, the miniaturized IoMT devices have very limited computation power and fairly limited security schemes can be implemented in such devices. In addition, with the widespread use of IoMT devices, managing and ensuring the security of IoMT systems are very challenging and which are the major issues hindering the adoption of IoMT for clinical applications. In this paper, the security and privacy challenges, requirements, threats, and future research directions in the domain of IoMT are reviewed providing a general overview of the state-of-the-art approaches.

Epithelial ovarian cancer (EOC) is the most malignant gynecological carcinoma and is of a high incidence of death due to detection at late stages when metastasis already occurs. However, the mechanism underlying metastasis of EOC remains unclear. Analysis of the open database and experiments with immunochemistry showed that LRRC4 is lowly expressed in high-grade serous ovarian cancer (HGSC) cells and during EOC metastasis. The 3D cell culture system and the orthotopic ovarian xenograft model infected with LRRC4-containing adeno-associated virus serotype 9 (AAV9) were used to confirm collective invasion and metastasis of cells in vitro and in vivo. Phos-tag SDS-PAGE was used to detect the phosphorylation of LRRC4 and PIK3R1. A number of experiments with methods such as co-immunoprecipitation and immunoblotting were performed to explore the mechanism for the actions of LRRC4 and PIK3R1 in EOC metastasis. An inverse correlation between LRRC4 and E-cadherin expression was detected in the regions of invasion in primary EOC tissues and metastatic ascites. LRRC4 binds to the cSH2 domain of PIK3R1 and inhibits the activity of PIK3R1, without disrupting the physical interactions between PIK3R1 and PIK3CA. LRRC4 inhibits EOC metastasis by targeting E-cadherin-dependent collective cell invasion and does so by inhibiting the PIK3R1-mediated AKT/GSK3β/β-catenin signaling pathway. LRRC4 functions as a tumor suppressor gene to inhibit EOC collective invasion and metastasis in vitro and in vivo and does so by directly binding to the cSH2 domain of PIK3R1 to exert its regulatory function. Our findings provide a potential novel approach for metastasis prognosis and a new strategy for the treatment of EOC.

Abstract Background Despite the overwhelming number of investigations on AKT, little is known about lncRNA on AKT regulation, especially in GBM cells. Methods RNA-binding protein immunoprecipitation assay (RIP) and RNA pulldown were used to confirm the binding of LINC00470 and fused in sarcoma (FUS). Confocal imaging, co-immunoprecipitation (Co-IP) and GST pulldown assays were used to detect the interaction between FUS and AKT. EdU assay, CCK-8 assay, and intracranial xenograft assays were performed to demonstrate the effect of LINC00470 on the malignant phenotype of GBM cells. RT-qPCR and Western blotting were performed to test the effect of LINC00470 on AKT and pAKT. Results In this study, we demonstrated that LINC00470 was a positive regulator for AKT activation in GBM. LINC00470 bound to FUS and AKT to form a ternary complex, anchoring FUS in the cytoplasm to increase AKT activity. Higher pAKT activated by LINC00470 inhibited ubiquitination of HK1, which affected glycolysis, and inhibited cell autophagy. Furthermore, higher LINC00470 expression was associated with GBM tumorigenesis and poor patient prognosis. Conclusions Our findings revealed a noncanonical AKT activation signaling pathway, i.e., LINC00470 directly interacts with FUS, serving as an AKT activator to promote GBM progression. LINC00470 has an important referential significance to evaluate the prognosis of patients.

Abstract Background SIX homeobox 3 (SIX3) is a member of the sine oculis homeobox transcription factor family. It plays a vital role in the nervous system development. Our previous study showed that the SIX3 gene is hypermethylated, and its expression is decreased in astrocytoma, but the role of SIX3 remains unknown. Methods Chromatin-immunoprecipitation (ChIP) and luciferase reporter assay were used to confirm the binding of SIX3 to the promoter regions of aurora kinase A (AURKA) and aurora kinase B (AURKB). Confocal imaging and co-immunoprecipitation (Co-IP) were used to detect the interaction between AURKA and AURKB. Flow cytometry was performed to assess the effect of SIX3 on cell cycle distribution. Colony formation, EdU incorporation, transwell, and intracranial xenograft assays were performed to demonstrate the effect of SIX3 on the malignant phenotype of astrocytoma cells. Results SIX3 is identified as a novel negative transcriptional regulator of AURKA and AURKB, and it decreases the expression of AURKA and AURKB in a dose-dependent manner in astrocytoma cells. Importantly, interactions between AURKA and AURKB stabilize and protect AURKA/B from degradation, and overexpression of SIX3 does not affect these interactions; SIX3 also acts as a tumor suppressor, and it increases p53 activity and expression at the post-translational level by the negative regulation of AURKA or AURKB, reduces the events of numerical centrosomal aberrations and misaligned chromosomes, and significantly inhibits the proliferation, invasion, and tumorigenesis of astrocytoma in vitro and in vivo. Moreover, experiments using primary cultured astrocytoma cells indicate that astrocytoma patients with a low expression of SIX3 and mutant p53 are more sensitive to treatment with aurora kinase inhibitors. Conclusion SIX3 is a novel negative transcriptional regulator and acts as a tumor suppressor that directly represses the transcription of AURKA and AURKB in astrocytoma. For the first time, the functional interaction of AURKA and AURKB has been found, which aids in the protection of their stability, and partially explains their constant high expression and activity in cancers. SIX3 is a potential biomarker that could be used to predict the response of astrocytoma patients to aurora kinase inhibitors.

Abstract Background As a well-characterized key player in various signal transduction networks, extracellular-signal-regulated kinase (ERK1/2) has been widely implicated in the development of many malignancies. We previously found that Leucine-rich repeat containing 4 (LRRC4) was a tumor suppressor and a negative regulator of the ERK/MAPK pathway in glioma tumorigenesis. However, the precise molecular role of LRRC4 in ERK signal transmission is unclear. Methods The interaction between LRRC4 and ERK1/2 was assessed by co-immunoprecipitation and GST pull-down assays in vivo and in vitro. We also investigated the interaction of LRRC4 and ERK1/2 and the role of the D domain in ERK activation in glioma cells. Results Here, we showed that LRRC4 and ERK1/2 interact via the D domain and CD domain, respectively. Following EGF stimuli, the D domain of LRRC4 anchors ERK1/2 in the cytoplasm and abrogates ERK1/2 activation and nuclear translocation. In glioblastoma cells, ectopic LRRC4 expression competitively inhibited the interaction of endogenous mitogen-activated protein kinase (MEK) and ERK1/2. Mutation of the D domain decreased the LRRC4-mediated inhibition of MAPK signaling and its anti-proliferation and anti-invasion roles. Conclusions Our results demonstrated that the D domain of LRRC4 anchors ERK1/2 in the cytoplasm and competitively inhibits MEK/ERK activation in glioma cells. These findings identify a new mechanism underlying glioblastoma progression and suggest a novel therapeutic strategy by restoring the activity of LRRC4 to decrease MAPK cascade activation.

Tumor-associated macrophages (TAMs) constitute a major component of inflammatory cells in the glioblastoma multiforme (GBM) tumor microenvironment. TAMs have been implicated in GBM angiogenesis, invasion, local tumor recurrence, and immunosuppression. Coagulation factor X (FX) is a vitamin K-dependent plasma protein that plays a role in the regulation of blood coagulation. In this study, we first found that FX was highly expressed and positively correlated with TAM density in human GBM. FX exhibited a potent chemotactic capacity to recruit macrophages and promoted macrophages toward M2 subtype polarization, accelerating GBM growth. FX bound to extracellular signal-related kinase (ERK)1/2 and inhibited p-ERK1/2 in GBM cells. FX was secreted in the tumor microenvironment and increased the phosphorylation and activation of ERK1/2 and AKT in macrophages, which may have been responsible for the M2 subtype macrophage polarization. Moreover, although the lncRNA CASC2c has been verified to function as a miR-101 competing endogenous RNA (ceRNA) to promote miR-101 target genes in GBM cells, we first confirmed that CASC2c did not function as a miR-338-3p ceRNA to promote FX expression, and that FX was a target gene of miR-338-3p. CASC2c interacted with and reciprocally repressed miR-338-3p. Both CASC2c and miR-388-3p bound to FX and commonly inhibited its expression and secretion. CASC2c repressed M2 subtype macrophage polarization. Taken together, our findings revealed a novel mechanism highlighting CASC2c and FX as potential therapeutic targets to improve GBM patients by altering the GBM microenvironment.