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Thanks to its structural characteristics and signal patterns similar to those of human brain synapses, memristors are widely believed to be applicable for neuromorphic computing. However, to our knowledge, memristors have not been effectively applied in the biomedical field, especially in disease diagnosis and health monitoring. In this work, a blood-based biomemristor was prepared for in vitro detection of hyperglycemia and hyperlipidemia. It was found that the device exhibits excellent resistance switching (RS) behavior at lower voltage biases. Through mechanism analysis, it has been confirmed that the RS behavior is driven by Ohmic conduction and ion rearrangement. Furthermore, the hyperglycemia and hyperlipidemia detection devices were constructed for the first time based on memristor logic circuits, and circuit simulations were conducted. These results confirm the feasibility of blood-based biomemristors in detecting hyperglycemia and hyperlipidemia, providing new prospects for the important application of memristors in the biomedical field.

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We experimentally investigate the coherently controllable generation and annihilation of a pseudospin-induced optical vortex in an optically induced honeycomb photonic lattice in a Λ-type 85Rb atomic vapor cell. Three Gaussian coupling beams are coupled into the atomic gases to form a hexagonal interference pattern, which can induce a honeycomb photonic lattice under electromagnetically induced transparency. Then, two probe beams interfere with each other to form periodical fringes and cover one set of sublattice in the honeycomb lattice, corresponding to excite the K or K' valleys in momentum space. By properly adjusting the experimental parameters, the generation and annihilation of the induced optical vortex can be effectively controlled. The theoretical simulations based on the Dirac and Schrödinger equations are performed to explore the underlying mechanisms, which will support the observations. The demonstrated properties of such controllable optical vortex may lay the foundation for the design of vortex-based optical devices with multidimensional tunability.

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Background: The gut microbiota plays a pivotal role in the development of diabetes and kidney disease. However, it is not clear how the intestinal microecological imbalance is involved in the context of diabetic kidney disease (DKD), the leading cause of renal failure. Objectives: To elucidate the gut microbial signatures associated with DKD progression towards end-stage renal disease (ESRD) and explore whether they could reflect renal dysfunction and psychological distress. Methods: A cross-sectional study was conducted to explore the gut microbial signatures of 29 DKD non-ESRD patients and 19 DKD ESRD patients compared to 20 healthy controls. Differential analysis was performed to detect distinct gut microbial alterations in diversities and taxon abundance of DKD with and without ESRD. Renal dysfunction was estimated by urea, creatinine, and estimated glomerular filtration rate. Psychological distress was assessed using the Self-Rating Anxiety Scale, Self-Rating Depression Scale, Hamilton Anxiety Rating Scale, and Hamilton Depression Rating Scale. Results: Alpha diversity indexes were reduced in DKD patients, particularly those with ESRD. Beta diversity analysis revealed that the gut microbial compositions of DKD patients were different with healthy individuals whereas similar compositions were observed in DKD patients. Taxon differential analysis showed that when compared with the controls, DKD patients exhibit distinct microbial profiles including reduced abundances of butyrate-produced, anti-inflammatory bacteria Faecalibacterium, Lachnospira, Roseburia Lachnoclostridium, and increased abundances of pro-inflammatory bacteria Collinsella, Streptococcus etc. These distinctive genera presented consistent associations with renal dysfunction, as well as psychological distress, especially in DKD patients. Conclusions: DKD patients, especially those who have progressed to ESRD, exhibit unique characteristics in their gut microbiota that are associated with both renal dysfunction and psychological distress. The gut microbiota may be a significant factor in the deterioration of DKD and its eventual progression to ESRD.

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Theoretical and experimental studies suggest that both Hermitian and non-Hermitian quasicrystals show localization due to the fractal spectrum and to the transition to diffusive bands via exceptional points, respectively. Here, we present an experimental study of a dodecagonal photonic quasicrystal based on electromagnetically induced transparency in a Rb vapor cell. First, we observe the suppression of the wave packet expansion in the Hermitian case. We then discover a new regime, where increasing the non-Hermiticity leads to delocalization, demonstrating that the behavior in non-Hermitian quasicrystals is richer than previously thought.

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Background: Forest musk deer (FMD, Moschus Berezovskii) is a critically endangered species world-widely, the death of which can be caused by pulmonary disease in the farm. Pulmonary fibrosis (PF) was a huge threat to the health and survival of captive FMD. MicroRNAs (miRNAs) and messenger RNAs (mRNAs) have been involved in the regulation of immune genes and disease development. However, the regulatory profiles of mRNAs and miRNAs involved in immune regulation of FMD are unclear. Methods: In this study, mRNA-seq and miRNA-seq in blood were performed to constructed coexpression regulatory networks between PF and healthy groups of FMD. The hub immune- and apoptosis-related genes in the PF blood of FMD were explored through Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. Further, protein-protein interaction (PPI) network of immune-associated and apoptosis-associated key signaling pathways were constructed based on mRNA-miRNA in the PF blood of the FMD. Immune hub DEGs and immune hub DEmiRNAs were selected for experimental verification using RT-qPCR. Results: A total of 2744 differentially expressed genes (DEGs) and 356 differentially expressed miRNAs (DEmiRNAs) were identified in the PF blood group compared to the healthy blood group. Among them, 42 DEmiRNAs were negatively correlated with 20 immune DEGs from a total of 57 correlations. The DEGs were significantly associated with pathways related to CD molecules, immune disease, immune system, cytokine receptors, T cell receptor signaling pathway, Th1 and Th2 cell differentiation, cytokine-cytokine receptor interaction, intestinal immune network for IgA production, and NOD-like receptor signaling pathway. There were 240 immune-related DEGs, in which 186 immune-related DEGs were up-regulated and 54 immune-related DEGs were down-regulated. In the protein-protein interaction (PPI) analysis of immune-related signaling pathway, TYK2, TLR2, TLR4, IL18, CSF1, CXCL13, LCK, ITGB2, PIK3CB, HCK, CD40, CD86, CCL3, CCR7, IL2RA, TLR3, and IL4R were identified as the hub immune genes. The mRNA-miRNA coregulation analysis showed that let-7d, miR-324-3p, miR-760, miR-185, miR-149, miR-149-5p, and miR-1842-5p are key miRNAs that target DEGs involved in immune disease, immune system and immunoregulation. Conclusion: The development and occurrence of PF were significantly influenced by the immune-related and apoptosis-related genes present in PF blood. mRNAs and miRNAs associated with the development and occurrence of PF in the FMD.

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Deep convolutional neural networks approaches often assume that the feature response has a Gaussian distribution with target-centered peak response, which can be used to guide the target location and classification. Nevertheless, such an assumption is implausible when there is progressive interference from other targets and/or background noise, which produces sub-peaks on the tracking response map and causes model drift. In this paper, we propose a feature response regularization approach for sub-peak response suppression and peak response enforcement and aim to handle progressive interference systematically. Our approach, referred to as Peak Response Regularization (PRR), applies simple-yet-efficient method to aggregate and align discriminative features, which convert local extremal response in discrete feature space to extremal response in continuous space, which enforces the localization and representation capability of convolutional features. Experiments on human pose detection, object detection, object tracking, and image classification demonstrate that PRR improves the performance of image tasks with a negligible computational cost.

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The rare-earth telluride compound EuTe4 exhibits a charge density wave (CDW) and an unconventional thermal hysteresis transition. Herein, we report a comprehensive study of the CDW states in EuTe4 by using low-temperature scanning tunneling microscopy. Two types of charge orders are observed at 4 K, including a newly discovered spindle-shaped pattern and a typical stripe-like pattern. As an exotic charge order, the spindle-shaped CDW is off-axis and barely visible at 77 K, indicating that it is a hidden order developed at low temperature. Based on our first-principles calculations, we reveal the origins of the observed electronic instabilities. The spindle-shaped charge order stems from a subsequent transition based on the stripe-like CDW phase. Our work demonstrates that the competition and cooperation between multiple charge orders can generate exotic quantum phases.

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Conventional implantable electronics based on von Neumann architectures encounter significant limitations in computing and processing vast biological information due to computational bottlenecks. The memristor with integrated memory-computing and low power consumption offer a promising solution to overcome the computational bottleneck and Moore's law limitations of traditional silicon-based implantable devices, making them the most promising candidates for next-generation implantable devices. In this work, a highly stable memristor with an Ag/BaTiO3/MnO2/FTO structure was fabricated, demonstrating retention characteristics exceeding 1200 cycles and endurance above 1000 s. The device successfully exhibited three-stage responses to biological signals after implantation in SD (Sprague-Dawley) rats. Importantly, the memristor perform remarkable reversibility, maintaining over 100 cycles of stable repetition even after extraction from the rat. This study provides a new perspective on the biomedical application of memristors, expanding the potential of implantable memristive devices in intelligent medical fields such as health monitoring and auxiliary diagnostics.

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Precise control of gene expression levels is essential for normal cell functions, yet how they are defined and tightly maintained, particularly at intermediate levels, remains elusive. Here, using a series of newly developed sequencing, imaging, and functional assays, we uncover a class of transcription factors with dual roles as activators and repressors, referred to as condensate-forming level-regulating dual-action transcription factors (TFs). They reduce high expression but increase low expression to achieve stable intermediate levels. Dual-action TFs directly exert activating and repressing functions via condensate-forming domains that compartmentalize core transcriptional unit selectively. Clinically relevant mutations in these domains, which are linked to a range of developmental disorders, impair condensate selectivity and dual-action TF activity. These results collectively address a fundamental question in expression regulation and demonstrate the potential of level-regulating dual-action TFs as powerful effectors for engineering controlled expression levels.

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Objective: This study aimed to assess the value of PLK4 as a biomarker in papillary thyroid carcinoma (PTC). Methods: This study reviewed 230 PTC patients receiving surgical resections. PLK4 was detected in tumor tissues and samples of normal thyroid gland tissues by immunohistochemistry. Results: PLK4 was elevated in tumor tissues versus normal thyroid gland tissues (p < 0.001). Tumor PLK4 was linked with extrathyroidal invasion (p = 0.036), higher pathological tumor stage (p = 0.030), node stage (p = 0.045) and tumor/node/metastasis stage (p = 0.022) in PTC patients. Tumor PLK4 immunohistochemistry score >3 was linked with shortened disease-free survival (p = 0.026) and overall survival (p = 0.028) and independently predicted poorer disease-free survival (hazard ratio: 2.797; p = 0.040). Conclusion: Tumor PLK4 reflects extrathyroidal invasion, higher tumor stage and shortened survival in PTC.

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Different aspects of cognitive functions are affected in patients with Alzheimer's disease. To date, little is known about the associations between features from brain-imaging and individual Alzheimer's disease (AD)-related cognitive functional changes. In addition, how these associations differ among different imaging modalities is unclear. Here, we trained and investigated 3D convolutional neural network (CNN) models that predicted sub-scores of the 13-item Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog13) based on MRI and FDG-PET brain-imaging data. Analysis of the trained network showed that each key ADAS-Cog13 sub-score was associated with a specific set of brain features within an imaging modality. Furthermore, different association patterns were observed in MRI and FDG-PET modalities. According to MRI, cognitive sub-scores were typically associated with structural changes of subcortical regions, including amygdala, hippocampus, and putamen. Comparatively, according to FDG-PET, cognitive functions were typically associated with metabolic changes of cortical regions, including the cingulated gyrus, occipital cortex, middle front gyrus, precuneus cortex, and the cerebellum. These findings brought insights into complex AD etiology and emphasized the importance of investigating different brain-imaging modalities.

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Schistosomiasis, the second largest parasitic disease in the world after malaria, poses a significant threat to human health and causes public health issues. The disease primarily affects populations in economically underdeveloped tropical regions, earning it the title of "neglected tropical disease". Schistosomiasis is difficult to eradicate globally if medication alone is used. One of the essential elements of thorough schistosomiasis prevention and control is the management and disruption of the life cycle of intermediate host snails. The key approach to controlling the transmission of schistosomiasis is to control the intermediate hosts of the schistosome to disrupt its life cycle. We believe that approaching it from the perspective of the intermediate host's immunity could be an environmentally friendly and potentially effective method. Currently, globally significant intermediate host snails for schistosomes include Oncomelania hupensis, Biomphalaria glabrata, and Bulinus truncatus. The immune interaction research between B. glabrata and Schistosoma mansoni has a history of several decades, and the complete genome sequencing of both B. glabrata and B. truncatus has been accomplished. We have summarized the immune-related factors and research progress primarily studied in B. glabrata and B. truncatus and compared them with several humoral immune factors that O. hupensis research focuses on: macrophage migration inhibitory factor (MIF), Toll-like receptors (TLRs), and thioredoxin (Trx). We believe that continued exploration of the immune interactions between O. hupensis and Schistosoma japonicum is valuable. This comparative analysis can provide some direction and clues for further in-depth research. Comparative immunological studies between them not only expand our understanding of the immune defense responses of snails that act as intermediaries for schistosomes but also facilitate the development of more comprehensive and integrated strategies for schistosomiasis prevention and control. Furthermore, it offers an excellent opportunity to study the immune system of gastropods and their co-evolution with pathogenic organisms.

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BACKGROUND: The gut microbiota plays a crucial role in regulating host metabolism and producing uremic toxins in patients with end-stage renal disease (ESRD). Our objective is to advance toward a holistic understanding of the gut ecosystem and its functional capacity in such patients, which is still lacking. RESULTS: Herein, we explore the gut microbiome of 378 hemodialytic ESRD patients and 290 healthy volunteers from two independent cohorts via deep metagenomic sequencing and metagenome-assembled-genome-based characterization of their feces. Our findings reveal fundamental alterations in the ESRD microbiome, characterized by a panel of 348 differentially abundant species, including ESRD-elevated representatives of Blautia spp., Dorea spp., and Eggerthellaceae, and ESRD-depleted Prevotella and Roseburia species. Through functional annotation of the ESRD-associated species, we uncover various taxon-specific functions linked to the disease, such as antimicrobial resistance, aromatic compound degradation, and biosynthesis of small bioactive molecules. Additionally, we show that the gut microbial composition can be utilized to predict serum uremic toxin concentrations, and based on this, we identify the key toxin-contributing species. Furthermore, our investigation extended to 47 additional non-dialyzed chronic kidney disease (CKD) patients, revealing a significant correlation between the abundance of ESRD-associated microbial signatures and CKD progression. CONCLUSION: This study delineates the taxonomic and functional landscapes and biomarkers of the ESRD microbiome. Understanding the role of gut microbiota in ESRD could open new avenues for therapeutic interventions and personalized treatment approaches in patients with this condition.

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PURPOSE: To investigate the differences in intracranial culprit plaque characteristics of the middle cerebral artery (MCA), collateral circulation and hypoperfusion in patients with and without recurrent ischemic stroke and to identify the association with the recurrent ischemic cerebrovascular events. METHOD: Eighty-six patients with acute/subacute ischemic stroke caused by atherosclerotic plaques of the MCA were retrospectively enrolled and grouped into patients with recurrence (n = 36) and without recurrence (n = 50). All patients underwent high-resolution vessel wall imaging and dynamic susceptibility contrast-enhanced perfusion weighted imaging. The differences in culprit plaque characteristics, collateral circulation and hypoperfusion in the territory of the stenotic MCA were assessed between the two groups. The relationship between plaque characteristics and hypoperfusion was evaluated. The independent factors of recurrent ischemic stroke were identified by logistic regression analyses. RESULTS: Higher HbA1c, culprit plaque enhancement grade, culprit plaque enhancement ratio, and lower time to peak map based on the Alberta Stroke Program Early CT score (TTP-ASPECTS) were observed in the recurrence group(all p < 0.050). Both plaque enhancement grade and enhancement ratio were significantly associated with TTP-ASPECTS (p = 0.030 and 0.039, respectively). HbA1c, culprit plaque enhancement ratio and TTP-ASPECTS were independent factors of the recurrence of ischemic stroke (all p < 0.050). The area under the curve of the combination including the above factors (AUC = 0.819) was significantly higher than that of any variable alone after adjustment (all p < 0.050). CONCLUSIONS: Culprit plaque enhancement ratio, TTP-ASPECTS and HbA1c were independent factors of recurrent ischemic stroke. Their combination improved the accuracy in identifying the risk of recurrent ischemic stroke.

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Papillary thyroid cancer (PTC) is the most common form of thyroid cancer and is characterized by its tendency for lymphatic metastasis, leading to a poor prognosis. Tetraspanin 1 (TSPAN1) is a member of the tetra-transmembrane protein superfamily and has been implicated in tumorigenesis and cancer metastasis in various studies. However, the role of TSPAN1 in PTC tumor development remains unclear. In this study, we aimed to investigate the impact of TSPAN1 on PTC cell behavior. Our results demonstrate that knockdown of TSPAN1 inhibits PTC cell proliferation, migration, and invasion, while overexpression of TSPAN1 has the opposite effect. These findings suggest that TSPAN1 might play a role in the tumorigenesis and invasiveness of PTC. Mechanistically, we found that TSPAN1 activates the ERK pathway by increasing its phosphorylation, subsequently leading to upregulated expression of c-Myc. Additionally, we observed that TSPAN1-ERK-c-Myc axis activation promotes glycolytic activity in PTC cells, as evidenced by the upregulation of glycolytic genes such as LDHA. Taken together, our findings indicate that TSPAN1 acts as an oncogene in PTC by regulating glycolytic metabolism. This discovery highlights the potential of TSPAN1 as a promising therapeutic target for PTC treatment. Further research in this area could provide valuable insights into the development of targeted therapies for PTC patients.

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Organic pollutants in paddy fields may undergo different processes from those in dryland due to the anaerobic environment. The integrated use of compound-specific stable isotope analysis (CSIA) and enantiomer-specific analysis is a promising technique for understanding the behavior and fate of organic pollutants in soils. In this study, soil samples were collected from paddy fields in three major rice cultivation regions of China, spanning a transect of 4000 km. The mean concentrations of Æ©HCHs in paddy soils from the Taihu Plain were the highest (1.44 ng/g). The ratios of α-HCH/ß-HCH (all below 11.8) and α-HCH/γ-HCH (92% below 4.64), as well as the enantiomeric fractions (EFs) of chiral α-HCH (mean of 0.81), reflected that the distribution of HCHs was affected by the use of both technical HCHs and lindane. The preferential depletion of (-)-α-HCH and pronounced carbon isotope fractionation of α-HCH (δ13C of -28.22 ± 0.92‰ -23.63 ± 1.89‰) demonstrated its effective transformation. Factors such as altitude, soil temperature, soil pH, soil conductivity and soil organic matter significantly influenced the fate and transformation of HCHs. The current study highlights the integrated application of CSIA and enantiomer-specific analysis to provide multiple lines of evidence for the transformation of HCHs in soils.

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Diabetic kidney disease (DKD) is one of the main complications of diabetic microangiopathy. The pathogenesis of DKD is very complex, including autophagy, inflammation, oxidative stress. Although a series of treatment intervention have achieved certain results in the treatment of diabetic nephropathy, still cannot reverse the kidney injury of diabetic nephropathy. The kidney is one of the most important organs of energy metabolism. Renal function is highly dependent on phagocytosis of mitochondria, and aberrant or defective autophagic mechanisms are central to the pathology of many renal diseases. Under high glucose conditions, mitochondrial fragments accumulate in the kidney, suggesting that mitochondrial clearance mechanisms may be attenuated with changes in mitochondrial transformation mechanisms. However, the exact mechanism of mitophagy regulation in DKD has not been elucidated. Recent advances in autophagy have renewed interest in these signaling pathways and molecules in the pathogenesis of DKD. Investigating autophagy and its associated signaling molecules may provide potential unique targets for therapeutic intervention in DKD.

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Non-Hermitian systems with complex-valued energy spectra provide an extraordinary platform for manipulating unconventional dynamics of light. Here, we demonstrate the localization of light in an instantaneously reconfigurable non-Hermitian honeycomb photonic lattice that is established in a coherently prepared atomic system. One set of the sublattices is optically modulated to introduce the absorptive difference between neighboring lattice sites, where the Dirac points in reciprocal space are extended into dispersionless local flat bands, with two shared eigenstates: low-loss (high-loss) one with fields confined at sublattice B (A). When these local flat bands are broad enough due to larger loss difference, the incident beam with its tangential wave vector being at the K point in reciprocal space is effectively localized at sublattice B with weaker absorption, namely, the commonly seen power exchange between adjacent channels in photonic lattices is effectively prohibited. The current work unlocks a new capability from non-Hermitian two-dimensional photonic lattices and provides an alternative route for engineering tunable local flat bands in photonic structures.

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Regioselective B-H activation of o-carboranes is an effective way for constructing o-carborane derivatives, which have broad applications in medicine, catalysis and the wider chemical industry. However, the mechanistic basis for the observed selectivities remains unresolved. Herein, a series of density functional theory (DFT) calculations were employed to characterise the palladium N-heterocyclic carbene (Pd-NHC) catalysed regioselective B(3,6)-diarylation of o-carboranes. Computational results at the IDSCRF(ether)-LC-ωPBE/BS1 and IDSCRF(ether)-LC-ωPBE/BS2 levels showed that the reaction undergoes a Pd(0) → Pd(II) → Pd(0) oxidation/reduction cycle, with the regioselective B(3)-H activation being the rate-determining step (RDS) for the full reaction profile. The computed RDS free energy barrier of 24.3 kcal mol-1 agrees well with the 82% yield of B(3,6)-diphenyl-o-carborane in ether solution at 298 K after 24 hours of reaction. The Ag2CO3 additive was shown to play a crucial role in lowering the RDS free energy barrier and facilitating the reaction. Natural charge population (NPA) and molecular surface electrostatic potential (ESP) analyses successfully predicted the experimentally observed regioselectivities, with electronic effects being revealed to be the dominant contributors to product selectivity. Steric hindrance was also shown to impact the reaction rate, as revealed by experimental and computational characterisation studies of substituents and ligand effects. Furthermore, computational predictions aligned with the experimental findings that NHC ligands outperform the phosphine ones for this particular reaction. Overall, the observed trends reported in this work are expected to assist in the rational optimisation of the efficiency and regioselectivity of this and related reactions.

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We assessed interactions between the astrocytic volume-regulated anion channel (VRAC) and aquaporin 4 (AQP4) in the supraoptic nucleus (SON). Acute SON slices and cultures of hypothalamic astrocytes prepared from rats received hyposmotic challenge (HOC) with/without VRAC or AQP4 blockers. In acute slices, HOC caused an early decrease with a late rebound in the neuronal firing rate of vasopressin neurons, which required activity of astrocytic AQP4 and VRAC. HOC also caused a persistent decrease in the excitatory postsynaptic current frequency, supported by VRAC and AQP4 activity in early HOC; late HOC required only VRAC activity. These events were associated with the dynamics of glial fibrillary acidic protein (GFAP) filaments, the late retraction of which was mediated by VRAC activity; this activity also mediated an HOC-evoked early increase in AQP4 expression and late subside in GFAP-AQP4 colocalization. AQP4 activity supported an early HOC-evoked increase in VRAC levels and its colocalization with GFAP. In cultured astrocytes, late HOC augmented VRAC currents, the activation of which depended on AQP4 pre-HOC/HOC activity. HOC caused an early increase in VRAC expression followed by a late rebound, requiring AQP4 and VRAC, or only AQP4 activity, respectively. Astrocytic swelling in early HOC depended on AQP4 activity, and so did the early extension of GFAP filaments. VRAC and AQP4 activity supported late regulatory volume decrease, the retraction of GFAP filaments, and subside in GFAP-VRAC colocalization. Taken together, astrocytic morphological plasticity relies on the coordinated activities of VRAC and AQP4, which are mutually regulated in the astrocytic mediation of HOC-evoked modulation of vasopressin neuronal activity.

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