Surface-mediated fluorescent sensor array for identification of gut microbiota and monitoring of colorectal cancer.

The development of efficient, accurate, and high-throughput technology for gut microbiota sensing holds great promise in the maintenance of health and the treatment of diseases. Herein, we developed a rapid fluorescent sensor array based on surface-engineered silver nanoparticles (AgNPs) and vancomycin-modified gold nanoclusters (AuNCs@Van) for gut microbiota sensing. By controlling the surface of AgNPs, the recognition ability of the sensor can be effectively improved. The sensor array was used to successfully discriminate six gut-derived bacteria, including probiotics, neutral, and pathogenic bacteria and even their mixtures. Significantly, the sensing system has also been successfully applied to classify healthy individuals and colorectal cancer (CRC) patients rapidly and accurately within 30 min, demonstrating its clinically relevant specificity.

Tetramethylpyrazine Nitrone Promotes the Clearance of Alpha-Synuclein via Nrf2-Mediated Ubiquitin-Proteasome System Activation.

Aggregation of α-synuclein (α-syn) and α-syn cytotoxicity are hallmarks of sporadic and familial Parkinson's disease (PD). Nuclear factor (erythroid-derived 2)-like 2 (Nrf2)-dependent enhancement of the expression of the 20S proteasome core particles (20S CPs) and regulatory particles (RPs) increases proteasome activity, which can promote α-syn clearance in PD. Activation of peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) may reduce oxidative stress by strongly inducing Nrf2 gene expression. In the present study, tetramethylpyrazine nitrone (TBN), a potent-free radical scavenger, promoted α-syn clearance by the ubiquitin-proteasome system (UPS) in cell models overexpressing the human A53T mutant α-syn. In the α-syn transgenic mice model, TBN improved motor impairment, decreased the products of oxidative damage, and down-regulated the α-syn level in the serum. TBN consistently up-regulated PGC-1α and Nrf2 expression in tested models of PD. Additionally, TBN similarly enhanced the proteasome 20S subunit beta 8 (Psmb8) expression, which is linked to chymotrypsin-like proteasome activity. Furthermore, TBN increased the mRNA levels of both the 11S RPs subunits Pa28αß and a proteasome chaperone, known as the proteasome maturation protein (Pomp). Interestingly, specific siRNA targeting of Nrf2 blocked TBN's effects on Psmb8, Pa28αß, Pomp expression, and α-syn clearance. In conclusion, TBN promotes the clearance of α-syn via Nrf2-mediated UPS activation, and it may serve as a potentially disease-modifying therapeutic agent for PD.

Long-term exposure to ambient ozone and adult-onset asthma: A prospective cohort study.

BACKGROUND: The association between long-term exposure to ozone (O3) and adult-onset asthma (AOA) remains inconclusive, and analysis of causality is lacking. OBJECTIVES: To examine the causal association between long-term O3 exposure and AOA. METHODS: A prospective cohort study of 362,098 participants was conducted using the UK Biobank study. Incident cases of AOA were identified using health administrative data of the National Health Services. O3 exposure at participants' residential addresses was estimated by a spatio-temporal model. Instrumental variable (IV) modelling was used to analyze the causal association between O3 exposure and AOA, by incorporating wind speed and planetary boundary layer height as IVs into time-dependent Cox model. Negative control outcome (accidental injury) was also used to additionally evaluate unmeasured confounding. RESULTS: During a mean follow-up of 11.38 years, a total of 10,973 incident AOA cases were identified. A U-shaped concentration-response relationship was observed between O3 exposure and AOA in the traditional Cox models with HR of 0.917 (95% CI: 0.889, 0.946) for O3 at low levels (<38.17 ppb), and 1.198 (95% CI: 1.162, 1.236) for O3 at high levels (≥38.17 ppb). However, in the IV analysis we only found a statistically significant association between high-level O3 exposure and AOA risk, but not for low-level O3 exposure. No significant associations between O3 exposure and accidental injury were observed. CONCLUSION: Our findings suggest a potential causal relationship between long-term exposure to high-level ambient O3 and increased risks of AOA.

The development of a novel navigation system for reverse shoulder arthroplasty and its accuracy: a phantom and cadaveric study.

PURPOSE: Reverse shoulder arthroplasty has demonstrated excellent clinical efficacy for patients with shoulder joint diseases and is increasingly in demand. Traditional surgery faces challenges such as limited exposed surfaces and a narrow field of vision, leading to a shorter prosthesis lifespan and a higher risk of complications. In this study, an optical navigation system was proposed to assist surgeons in real-time tracking of the surgical scene. METHODS: Our optical navigation system was developed using the NDI Polaris Spectra device and several open-source platforms. The first step involved using the preoperative medical image to plan screw implantation paths. Real-time tracking of the patient phantom or cadaver and the surgical instrument was achieved through registration and calibration algorithms. Surgeons were guided on drilling through visualization methods. Postoperative results were compared with the planned implantation paths, and an algorithm was introduced to correct errors caused by the incorrect beginning points. RESULTS: Experiments involved three scapula cadavers and their corresponding phantoms with identical anatomy. For each experiment, three holes were completed with drills with diameters of 3.2 mm and 8.0 mm, respectively. Comparisons between the postoperative actual screw implantation paths and the preoperative planned implantation paths revealed an entry error of 1.05 ± 0.15 mm and an angle error of 2.47 ± 0.55° for phantom experiments. For cadaver experiments, the entry error was 1.53 ± 0.22 mm, and the angle error was 4.91 ± 0.78°. CONCLUSION: Our proposed optical navigation system successfully achieved real-time tracking of the surgical site, encompassing the patient phantom or cadaver and surgical instrument, thereby aiding surgeons in achieving precise surgical outcomes. Future study will explore the integration of robots to further enhance surgical efficiency and effectiveness.

AMPFLDAP: Adaptive Message Passing and Feature Fusion on Heterogeneous Network for LncRNA-Disease Associations Prediction.

Exploration of the intricate connections between long noncoding RNA (lncRNA) and diseases, referred to as lncRNA-disease associations (LDAs), plays a pivotal and indispensable role in unraveling the underlying molecular mechanisms of diseases and devising practical treatment approaches. It is imperative to employ computational methods for predicting lncRNA-disease associations to circumvent the need for superfluous experimental endeavors. Graph-based learning models have gained substantial popularity in predicting these associations, primarily because of their capacity to leverage node attributes and relationships within the network. Nevertheless, there remains much room for enhancing the performance of these techniques by incorporating and harmonizing the node attributes more effectively. In this context, we introduce a novel model, i.e., Adaptive Message Passing and Feature Fusion (AMPFLDAP), for forecasting lncRNA-disease associations within a heterogeneous network. Firstly, we constructed a heterogeneous network involving lncRNA, microRNA (miRNA), and diseases based on established associations and employing Gaussian interaction profile kernel similarity as a measure. Then, an adaptive topological message passing mechanism is suggested to address the information aggregation for heterogeneous networks. The topological features of nodes in the heterogeneous network were extracted based on the adaptive topological message passing mechanism. Moreover, an attention mechanism is applied to integrate both topological and semantic information to achieve the multimodal features of biomolecules, which are further used to predict potential LDAs. The experimental results demonstrated that the performance of the proposed AMPFLDAP is superior to seven state-of-the-art methods. Furthermore, to validate its efficacy in practical scenarios, we conducted detailed case studies involving three distinct diseases, which conclusively demonstrated AMPFLDAP's effectiveness in the prediction of LDAs.

Tumor burden score and carcinoembryonic antigen predict outcomes in patients with intrahepatic cholangiocarcinoma following liver resection: a multi­institutional analysis.

BACKGROUND: The prognostic significance of tumor burden score (TBS) in relation to carcinoembryonic antigen (CEA) has not been investigated among patients undergoing hepatectomy for intrahepatic cholangiocarcinoma (ICC). This study aimed to develop and validate a simplified model, a combination of TBS and CEA (CTC grade), for predicting the long-term outcomes of postoperative ICC patients. METHODS: Patients who underwent curative - intent resection of ICC between 2011 and 2019 were identified from a large multi - institutional database. The impact of TBS, CEA, and the CTC grade on overall survival (OS) and recurrence - free survival (RFS) was evaluated in both the derivation and validation cohorts. The receiver operating characteristic curve was utilized for assessing the predictive accuracy of the model. Subgroup analyses were performed across 8th TNM stage system stratified by CTC grade to assess the discriminatory capacity within the same TNM stage. RESULTS: A total of 812 patients were included in the derivation cohort and 266 patients in the validation cohort. Survival varied based on CEA (low: 36.7% vs. high: 9.0%) and TBS (low: 40.3% vs. high: 17.6%) in relation to 5 - year survival (both p < 0.001). As expected, patients with low CTC grade (i.e., low TBS/low CEA) were associated with the best OS as well as RFS, while high CTC grade (i.e., high TBS/high CEA) correlated to the worst outcomes. The model exhibited well performance in both the derivation cohort (area under the curve of 0.694) and the validation cohort (0.664). The predictive efficacy of the CTC grade system remains consistently stable across TNM stages I and III/IV. CONCLUSION: The CTC grade, a composite parameter derived from the combination of TBS and CEA levels, served as an easy - to - use tool and performed well in stratifying patients with ICC relative to OS and RFS.

Lactate Protects Intestinal Epithelial Barrier Function from Dextran Sulfate Sodium-Induced Damage by GPR81 Signaling.

The dysregulation of the intestinal epithelial barrier significantly contributes to the inflammatory progression of ulcerative colitis. Recent studies have indicated that lactate, produced by gut bacteria or derived from fermented foods, plays a key role in modulating inflammation via G-protein-coupled receptor 81 (GPR81). In this study, we aimed to investigate the potential role of GPR81 in the progression of colitis and to assess the impact of lactate/GPR81 signaling on intestinal epithelial barrier function. Our findings demonstrated a downregulation of GPR81 protein expression in patients with colitis. Functional verification experiments showed that Gpr81-deficient mice exhibited more severe damage to the intestinal epithelial barrier and increased susceptibility to DSS-induced colitis, characterized by exacerbated oxidative stress, elevated inflammatory cytokine secretion, and impaired expression of tight-junction proteins. Mechanistically, we found that lactate could suppress TNF-α-induced MMP-9 expression and prevent the disruption of tight-junction proteins by inhibiting NF-κB activation through GPR81 in vitro. Furthermore, our study showed that dietary lactate could preserve intestinal epithelial barrier function against DSS-induced damage in a GPR81-dependent manner in vivo. Collectively, these results underscore the crucial involvement of the lactate/GPR81 signaling pathway in maintaining intestinal epithelial barrier function, providing a potential therapeutic strategy for ulcerative colitis.

Effective Interfacing of Surface Homojunctions on Chemically Identical g-C3N4 for Efficient Visible-Light Photocatalysis without Sacrificial Agents.

Developing efficient homojunctions on g-C3N4 promises metal-free photocatalysis to realize truly sustainable artificial photosynthesis. However, current designs are limited by hindered charge separation due to inevitable grain boundaries and random formation of ineffective homojunctions embedded within the photocatalyst. Here, efficient photocatalysis is driven by introducing effective surface homojunctions on chemically and structurally identical g-C3N4 through leveraging its size-dependent electronic properties. Using a top-down approach, the surface layer of bulk g-C3N4 is partially exfoliated to create sheet-like g-C3N4 nanostructures on the bulk material. This hierarchical design establishes a subtle band energy offset between the macroscopic and nanoscopic g-C3N4, generating homojunctions while maintaining the chemical and structural integrities of the original g-C3N4. The optimized g-C3N4 homojunction demonstrates superior photocatalytic degradation of antibiotic pollutants at >96% efficiency in 2 h, even in different real water samples. It achieves reaction kinetics (≈0.041 min-1) up to fourfold better than standalone materials and their physical mixture. Mechanistic studies highlight the importance of the unique design in boosting photocatalysis by effectively promoting interfacial photocarrier manipulation and utilization directly at the point-of-catalysis, without needing co-catalysts or sacrificial agents. This work presents enormous opportunities for developing advanced and green photocatalytic platforms for sustainable light-driven environmental, energy, and chemical applications.

Unlocking the potential of T-cell metabolism reprogramming: Advancing single-cell approaches for precision immunotherapy in tumour immunity.

As single-cell RNA sequencing enables the detailed clustering of T-cell subpopulations and facilitates the analysis of T-cell metabolic states and metabolite dynamics, it has gained prominence as the preferred tool for understanding heterogeneous cellular metabolism. Furthermore, the synergistic or inhibitory effects of various metabolic pathways within T cells in the tumour microenvironment are coordinated, and increased activity of specific metabolic pathways generally corresponds to increased functional activity, leading to diverse T-cell behaviours related to the effects of tumour immune cells, which shows the potential of tumour-specific T cells to induce persistent immune responses. A holistic understanding of how metabolic heterogeneity governs the immune function of specific T-cell subsets is key to obtaining field-level insights into immunometabolism. Therefore, exploring the mechanisms underlying the interplay between T-cell metabolism and immune functions will pave the way for precise immunotherapy approaches in the future, which will empower us to explore new methods for combating tumours with enhanced efficacy.

Evaluation of the ecological status of shallow-water coral reefs in China using a novel method and identification of environmental factors for coral decline.

Coral reefs worldwide have faced extensive damage due to natural catastrophes and anthropogenic disturbances.The decline can cause their widespread collapse and an inability to recover from natural disturbances, highlighting the urgent need for their protection. This study conducted an extensive ecological condition assessment of seven coral reef regions in China's offshore. Our findings revealed the presence of 204 species of scleractinian corals belonging to 16 families. Massive corals were the predominant reef-building corals in all regions. The degradation of coral reef ecosystems was apparent in the present compared to historical reef conditions. The ecosystem suffered varying degrees of damage in surveyed regions according to a novel assessment approach, impling more effective measures should be taken to mitigate the local pressures. Our research establishes a baseline for understanding the status of coral reefs that can be used in future and provides a crucial foundation to designate protective zones for their conservation.

Mechanochemical evolution of coal microscopic groups: A new pathway for mechanical forces acting on coal spontaneous combustion.

Coal spontaneous combustion (CSC) remains a significant threat to regional ecological environments. As coal mining operations extend deeper into the earth, the increasingly complex mechanical force conditions in deep-seated mines escalate the potential risk of CSC. Mechanical forces such as ground stress and mechanical cutting are traditionally believed to be linked to CSC through the following pathway: mechanical forces act → mechanical energy is input → mechanical crushing and pulverization occur → coal-oxygen contact area increases → CSC accelerates. Noteworthily, these forces do more than just physically break coal; they also trigger a mechanochemical effect (MCE) that alters coal's microscopic chemistry. However, an independent evaluation of its influence on CSC was lacking. This study characterized coal's microscopic chemical group responses to the MCE. It was found that the MCE led to the degradation of aliphatic side chains while enhancing the polycondensation of aromatic ring structures, indicating a synergistic effect. Additionally, an increase in oxygen-containing functional groups, such as alkyl/aryl ethers, suggested enhanced interactions of the coal microscopic groups with oxygen due to mechanical forces. Based on these findings, an MCE-modified coal macromolecular model was developed and molecular quantum mechanical calculations were conducted. The results indicated that the MCE boosted coal macromolecule reactivity, thus facilitating easier activation. These conclusions were validated through modern thermal analysis tests. Finally, this study proposed a new pathway of mechanical forces acting on CSC: mechanical forces act → mechanical energy is input → the MCE occurs → evolutions of the microscopic groups within coal are induced → Activity of coal molecules is enhanced → CSC accelerates.

Exopolysaccharides Produced by Bifidobacterium longum subsp. longum YS108R Ameliorates DSS-Induced Ulcerative Colitis in Mice by Improving the Gut Barrier and Regulating the Gut Microbiota.

Ulcerative colitis (UC) is a major disease that has endangered human health. Our previous study demonstrated that Bifidobacterium longum subsp. longum YS108R, a ropy exopolysaccharide (EPS)-producing bacterium, could alleviate UC in mice, but it is unclear whether EPS is the key substance responsible for its action. In this study, we proposed to investigate the remitting effect of EPS from B. longum subsp. longum YS108R on UC in a DSS-induced UC mouse model. Water extraction and alcohol precipitation were applied to extract EPS from the supernatant of B. longum subsp. longum YS108R culture. Then the animal trial was performed, and the results indicated that YS108R EPS ameliorated colonic pathological damage and the intestinal barrier. YS108R EPS suppressed inflammation via NF-κB signaling pathway inhibition and attenuated oxidative stress via the Nrf2 signaling pathway activation. Remarkably, YS108R EPS regulated gut microbiota, as evidenced by an increase in short-chain fatty acid (SCFA)-producing bacteria and a decline in Gram-negative bacteria, resulting in an increase of propionate and butyrate and a reduction of lipopolysaccharide (LPS). Collectively, YS108R EPS manipulated the intestinal microbiota and its metabolites, which further improved the intestinal barrier and inhibited inflammation and oxidative stress, thereby alleviating UC.

COMP promotes pancreatic fibrosis by activating pancreatic stellate cells through CD36-ERK/AKT signaling pathways.

BACKGROUND: Pancreatic fibrosis is one of the most important pathological features of chronic pancreatitis (CP) and pancreatic stellate cells (PSCs) are the key cells of fibrosis. As an extracellular matrix (ECM) glycoprotein, cartilage oligomeric matrix protein (COMP) is critical for collagen assembly and ECM stability and recent studies showed that COMP exert promoting fibrosis effect in the skin, lungs and liver. However, the role of COMP in activation of PSCs and pancreatic fibrosis remain unclear. We aimed to investigate the role and specific mechanisms of COMP in regulating the profibrotic phenotype of PSCs and pancreatic fibrosis. METHODS: ELISA method was used to determine serum COMP in patients with CP. Mice model of CP was established by repeated intraperitoneal injection of cerulein and pancreatic fibrosis was evaluated by Hematoxylin-Eosin staining (H&E) and Sirius red staining. Immunohistochemical staining was used to detect the expression changes of COMP and fibrosis marker such as α-SMA and Fibronectin in pancreatic tissue of mice. Cell Counting Kit-8, Wound Healing and Transwell assessed the proliferation and migration of human pancreatic stellate cells (HPSCs). Western blotting, qRT-PCR and immunofluorescence staining were performed to detect the expression of fibrosis marker, AKT and MAPK family proteins in HPSCs. RNA-seq omics analysis as well as small interfering RNA of COMP, recombinant human COMP (rCOMP), MEK inhibitors and PI3K inhibitors were used to study the effect and mechanism of COMP on activation of HPSCs. RESULTS: ELISA showed that the expression of COMP significantly increased in the serum of CP patients. H&E and Sirius red staining analysis showed that there was a large amount of collagen deposition in the mice in the CP model group and high expression of COMP, α-SMA, Fibronectin and Vimentin were observed in fibrotic tissues. TGF-ß1 stimulates the activation of HPSCs and increases the expression of COMP. Knockdown of COMP inhibited proliferation and migration of HPSCs. Further, RNA-seq omics analysis and validation experiments in vitro showed that rCOMP could significantly promote the proliferation and activation of HPSCs, which may be due to promoting the phosphorylation of ERK and AKT through membrane protein receptor CD36. rCOMP simultaneously increased the expression of α-SMA, Fibronectin and Collagen I in HPSCs. CONCLUSION: In conclusion, this study showed that COMP was up-regulated in CP fibrotic tissues and COMP induced the activation, proliferation and migration of PSCs through the CD36-ERK/AKT signaling pathway. COMP may be a potential therapeutic candidate for the treatment of CP. Interfering with the expression of COMP or the communication between COMP and CD36 on PSCs may be the next direction for therapeutic research.

Comprehensive analysis based on the disulfidptosis-related genes identifies hub genes and immune infiltration for pancreatic adenocarcinoma.

Pancreatic adenocarcinoma (PAAD) is a prevalent and aggressive malignancy in the digestive tract, requiring accurate prediction and effective treatment strategies. Recently, the discovery of disulfidptosis, a novel form of programmed cell death characterized by abnormal disulfide accumulation, has sparked interest in its role in PAAD. In this study, we aimed to investigate the involvement of disulfidptosis-related genes (DRGs) in PAAD. Using publicly available databases, we conducted a comprehensive analysis exploring the complex relationships between DRGs and important aspects of PAAD, including gene expression, immune response, mutation, drug sensitivity, and functional enrichment. Notably, we observed significant heterogeneity among different disulfidptosis subclusters and identified specific differentially expressed genes in PAAD. Through machine learning techniques, we identified SLC7A11, S100A4, DIAPH3, PRDX1, and SLC7A7 as the most relevant hub genes. We further validated their significance in PAAD by considering their expression patterns, prognostic value, diagnostic potential, diagnostic model, and immune infiltration. This study presents exciting opportunities and challenges in unraveling the underlying mechanisms of PAAD prognosis. It also establishes a foundation for personalized cancer care and the development of innovative immunotherapeutic strategies. By shedding light on the role of DRGs, particularly hub genes, we enhance our understanding and management of PAAD.

A Clinical Study on Video Bronchoscopy-guided Coblation for Benign Central Airway Stenosis.

Background: Benign central airway stenosis poses a significant challenge to respiratory and thoracic surgeons due to the high recurrence rate associated with current treatment methods, causing severe breathing difficulties and potentially life-threatening complications. This article aims to investigate the therapeutic efficacy and prospects of using coblation in the management of benign central airway stenosis in adults. Moreover, the pathogenesis of benign central airway stenosis was deeply explored to provide better guidance for future clinical treatments. Materials and Methods: This retrospective study examined patients with benign central airway stenosis who were treated at The Second Hospital of Hebei Medical University from 2017 to 2020. In addition, a comparative analysis of whole-genome sequencing was conducted between the aforementioned patient group and healthy populations to investigate the underlying etiology of this stenotic condition. Results: The present study encompassed 32 patients who underwent 43 treatments in total between 2017 and 2020. All patients exhibited alleviation of airway stenosis and an improvement in clinical symptoms following surgery, without any significant surgical or postoperative complications. Whole-genome analysis revealed significant changes in gene expression in the airway mucosa of patients with benign airway stenosis in comparison to healthy populations. A total of 91 differentially expressed genes were identified, among which 44 upregulated genes displayed characteristics of promoting inflammatory responses. Conclusion: Coblation demonstrates promise as an efficacious treatment modality for adults suffering from benign central airway stenosis, and its widespread application in clinical settings is anticipated. The direct pathogenesis of benign central airway stenosis involves airway lumen narrowing and obstruction resulting from excessive inflammation and proliferative granulation.

Causal association between long-term exposure to air pollution and incident Parkinson's disease.

Epidemiological evidence for long-term air pollution exposure and Parkinson's disease (PD) is controversial, and analysis of causality is limited. We identified 293,888 participants who were free of PD at baseline in the UK Biobank (2006-2010). Time-varying air pollution [fine particulate (PM2.5) and ozone (O3)] exposures were estimated using spatio-temporal models. Incident cases of PD were identified using validated algorithms. Four methods were used to investigate the associations between air pollution and PD, including (1) standard time-varying Cox proportional-hazard model; (2) Cox models weighted by generalized propensity score (GPS) and inverse-probability weights (IPW); (3) instrumental variable (IV) analysis; and (4) negative control outcome analysis. During a median of 11.6 years of follow-up, 1822 incident PD cases were identified. Based on standard Cox regression, the hazard ratios (95% confidence interval) for a 1 µg/m3 or ppb increase in PM2.5 and O3 were 1.23 (1.17, 1.30) and 1.02 (0.98, 1.05), respectively. Consistent results were found in models weighted by GPS and IPW, and in IV analysis. There were no significant associations between air pollution and negative control outcomes. This study provides evidence to support a causal association between PM2.5 exposure and PD. Mitigation of air pollution could be a protective measure against PD.

Fluorescent Probe for Investigating the Mitochondrial Viscosity and Hydrogen Peroxide Changes in Cerebral Ischemia/Reperfusion Injury.

Cerebral ischemia-reperfusion injury (CIRI), a cause of cerebral dysfunction during cerebral infarction treatment, is closely associated with mitochondrial viscosity and hydrogen peroxide (H2O2). However, the accurate measurement of mitochondrial viscosity and H2O2 levels in CIRI is challenging because of the lack of sufficient selectivity and blood-brain barrier (BBB) penetration of existing monitoring tools related to CIRI, hampering the exploration of the role of mitochondrial viscosity and H2O2 in CIRI. To address this issue, we designed an activatable fluorescent probe, mitochondria-targeting styryl-quinolin-ium (Mito-IQS), with excellent properties including high selectivity, mitochondrial targeting, and BBB penetration, for the visualization of mitochondrial viscosity and H2O2 in the brain. Based on the real-time monitoring capabilities of the probe, bursts of mitochondrial viscosity and H2O2 levels were visualized during CIRI. This probe can be used to monitor the therapeutic effects of butylphthalein treatment. More importantly, in vivo experiments further confirmed that CIRI was closely associated with the mitochondrial viscosity and H2O2 levels. This discovery provides new insights and tools for the study of CIRI and is expected to accelerate the process of CIRI diagnosis, treatment, and drug design.

Brain Temporal-Spectral Functional Variability Reveals Neural Improvements of DBS Treatment for Disorders of Consciousness.

Deep brain stimulation (DBS) is establishing itself as a promising treatment for disorders of consciousness (DOC). Measuring consciousness changes is crucial in the optimization of DBS therapy for DOC patients. However, conventional measures use subjective metrics that limit the investigations of treatment-induced neural improvements. The focus of this study is to analyze the regulatory effects of DBS and explain the regulatory mechanism at the brain functional level for DOC patients. Specifically, this paper proposed a dynamic brain temporal-spectral analysis method to quantify DBS-induced brain functional variations in DOC patients. Functional near-infrared spectroscopy (fNIRS) that promised to evaluate consciousness levels was used to monitor brain variations of DOC patients. Specifically, a fNIRS-based experimental procedure with auditory stimuli was developed, and the brain activities during the procedure from thirteen DOC patients before and after the DBS treatment were recorded. Then, dynamic brain functional networks were formulated with a sliding-window correlation analysis of phase lag index. Afterwards, with respect to the temporal variations of global and regional networks, the variability of global efficiency, local efficiency, and clustering coefficient were extracted. Further, dynamic networks were converted into spectral representations by graph Fourier transform, and graph energy and diversity were formulated to assess the spectral global and regional variability. The results showed that DOC patients under DBS treatment exhibited increased global and regional functional variability that was significantly associated with consciousness improvements. Moreover, the functional variability in the right brain regions had a stronger correlation with consciousness enhancements than that in the left brain regions. Therefore, the proposed method well signifies DBS-induced brain functional variations in DOC patients, and the functional variability may serve as promising biomarkers for consciousness evaluations in DOC patients.

Improving Carbon Nanotube-Based Radiofrequency Field-Effect Transistors by the Device Architecture and Doping Process.

The semiconducting carbon nanotube (CNT) has been considered a promising candidate for future radiofrequency (RF) electronics due to its excellent electrical properties of high mobility and small capacitance. After decades of development, great progress has been achieved on CNT-based RF field-effect transistors (FETs). However, almost all elevations are owing to advancement of the CNT materials and fabrication process, while the study of device architecture is seldom considered and reported. In this work, we innovatively combined device architecture and related doping processes to further optimize CNT-based RF FETs by guiding process or materials with collaborative optimization for the first time and explore their effect on device performance carefully and statistically. Based on more mature random-oriented CNT materials, we fabricated CNT-based RF FETs having three different gate positions of device architecture variation accompanied by suitable doping schemes. The optimized FETs obtained 2-3 times of current density (transconductance) and 1.3 times the cutoff frequency and maximum oscillation frequency compared with unoptimized devices at the same channel length. After transistor-level verification of effect, we further built a CNT RF amplifier and demonstrated almost 10 dB of transducer gain improvement operating at 8 GHz for X-band application. The achieved results from this work would help further improve CNT RF performance beyond the materials and process point of view.

Quasi-type-II Cu-In-Zn-S/Ni-MOF heterostructure with prolonged carrier lifetime for photocatalytic hydrogen production.

Visible-driven photocatalytic hydrogen production using narrow-bandgap semiconductors has great potential for clean energy development. However, the widespread use of these semiconductors is limited due to problems such as severe charge recombination and slow surface reactions. Herein, a quasi-type-II heterostructure was constructed by combining bifunctional Ni-based metal-organic framework (Ni-MOF) nanosheets with BDC (1,4-benzenedicarboxylic acid) linker coupled with Cu-In-Zn-S quantum dots (CIZS QDs). This heterostructure exhibited a prolonged charge carrier lifetime and abundant active sites, leading to significantly improved hydrogen production rate. The optimized rate achieved by the CIZS/Ni-MOF heterostructure was 2642 µmol g-1 h-1, which is 5.28 times higher than that of the CIZS QDs. This improved performance can be attributed to the quasi-type-II band alignment between the CIZS QDs and Ni-MOF, which facilitates effective delocalization of the photogenerated electrons within the system. Additional photoelectrochemical tests confirmed the well-maintained photoluminescence and prolonged charge carrier lifetime of the CIZS/Ni-MOF heterostructure. This study provides valuable insights into the use of multifunctional MOFs in the development of highly efficient composite photocatalysts, extending beyond their role in light harvesting and charge separation.