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The rapid growth of IoT driven by recent advancements in consumer electronics, 5G communication technologies, and cloud-computing-enabled big data analytics, has recently attracted tremendous attention from both the industry and academia. One of the major open challenges for IoT is the limited network lifetime due to massive IoT devices being powered by batteries with finite capacities. The low-power and low-complexity backscatter communications (BackCom), which simply relies on passive reflection and modulation of an incident radio-frequency (RF) wave, has emerged to be a promising technology for tackling this challenge. However, the contemporary BackCom has several major limitations, such as short transmission range, low data rate, and uni-directional information transmission. The article aims at introducing the recent advances in the active area of BackCom. Specifically, we provide a systematic introduction of the next generation BackCom covering basic principles, systems, techniques besides IoT applications. Lastly, we describe the IoT application scenarios with the next generation BackCom.

Gastric cancer (GC) is a leading cause of cancer-related mortality, with a high rate of postoperative recurrence and poor long-term survival. The Eyes Absent (EYA) protein family plays a significant role in cancer progression, with EYA3 being implicated in promoting GC cell proliferation and tumor growth. Utilizing the DepMap database, we identified EYA3 as a gene of interest in GC. We analyzed EYA3 expression in GC tissues and cell lines, performed in vitro assays to assess its role in cell proliferation, and conducted gene set enrichment analysis to explore its relationship with autophagy and the mTORC1 signaling pathway. In vivo, we used a xenograft tumor model to examine the effects of EYA3 expression on tumor progression. EYA3 was consistently upregulated in GC tissues, and its high expression correlated with a decrease in patient survival rates. Silencing EYA3 in GC cell lines resulted in reduced cell proliferation. Inhibition of autophagy and activation of the mTORC1 signaling pathway were observed as mechanisms by which EYA3 may promote GC cell growth. In vivo experiments supported the in vitro findings, showing slower tumor growth with reduced EYA3 expression. Our study confirms the upregulation of EYA3 in GC and its association with poor prognosis. EYA3 promotes GC cell proliferation and tumor growth by activating the mTORC1 signaling pathway and inhibiting autophagy. These findings highlight the potential of EYA3 as a therapeutic target for GC, providing a foundation for future research and treatment strategies. Despite the promising data, the limitations of sample size and the need for further mechanistic studies are acknowledged.

Background Brain injury is the leading cause of death and disability in survivors of cardiac arrest, where neuroinflammation is believed to play a pivotal role, but the underlying mechanism remains unclear. Pyroptosis is a pro-inflammatory form of programmed cell death that triggers inflammatory response upon infection or other stimuli. This study aims to understand the role of microglial pyroptosis in post-cardiac arrest brain injury. Methods Sprague-Dawley male rats underwent 10-min asphyxial cardiac arrest and cardiopulmonary resuscitation or sham-operation. Flow cytometry analysis, Western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), co-immunoprecipitation, and immunofluorescence were used to evaluate activated microglia and CD11b-positive leukocytes after cardiac arrest and assess inflammasome activation and pyroptosis of specific cellular populations. To further explore the underlying mechanism, MCC950 or Ac-YVAD-cmk was administered to block nod-like receptor family protein 3 (NLRP3) or caspase-1, respectively. Results Our results showed that, in a rat model, successful resuscitation from cardiac arrest resulted in microglial pyroptosis and consequential inflammatory infiltration which was mediated by the activation of NLRP3 inflammasome. Targeting NLRP3 and caspase-1, the executor of pyroptosis, with selective inhibitors MCC950 and Ac-YVAD-cmk treatment significantly prevented microglial pyroptosis, reduced infiltration of leukocytes, improved neurologic outcome, and alleviated neuro-pathological damages after cardiac arrest in modeling rats. Conclusions This study demonstrates that microglial pyroptosis mediated by NLRP3 inflammasome is critically involved in the pathogenesis of post-cardiac arrest brain injury and provides a new therapeutic strategy.

As a foundation of large language models, fine-tuning drives rapid progress, broad applicability, and profound impacts on human–AI collaboration, surpassing earlier technological advancements. This paper provides a comprehensive overview of large language model (LLM) fine-tuning by integrating hermeneutic theories of human comprehension, with a focus on the essential cognitive conditions that underpin this process. Drawing on Gadamer’s concepts of Vorverständnis, Distanciation, and the Hermeneutic Circle, the paper explores how LLM fine-tuning evolves from initial learning to deeper comprehension, ultimately advancing toward self-awareness. It examines the core principles, development, and applications of fine-tuning techniques, emphasizing its growing significance across diverse field and industries. The paper introduces a new term, “Tutorial Fine-Tuning (TFT)”, which annotates a process of intensive tuition given by a “tutor” to a small number of “students”, to define the latest round of LLM fine-tuning advancements. By addressing key challenges associated with fine-tuning, including ensuring adaptability, precision, credibility and reliability, this paper explores potential future directions for the co-evolution of humans and AI. By bridging theoretical perspectives with practical implications, this work provides valuable insights into the ongoing development of LLMs, emphasizing their potential to achieve higher levels of cognitive and operational intelligence.

The breakdown of the blood‐brain barrier (BBB) is related to the occurrence and deterioration of neurological dysfunction in ischemic stroke, which leads to the extravasation of blood‐borne substances, resulting in vasogenic edema and increased mortality. However, a limited understanding of the molecular mechanisms that control the restrictive properties of the BBB hinders the manipulation of the BBB in disease and treatment. Here, we found that the glycocalyx (GCX) is a critical factor in the regulation of brain endothelial barrier integrity. First, endothelial GCX displayed a biphasic change pattern, of which the timescale matched well with the biphasic evolution of BBB permeability to tracers within the first week after t‐MCAO. Moreover, GCX destruction with hyaluronidase increased BBB permeability in healthy mice and aggravated BBB leakage in transient middle cerebral artery occlusion (t‐MCAO) mice. Surprisingly, ultrastructural observation showed that GCX destruction was accompanied by increased endothelial transcytosis at the ischemic BBB, while the tight junctions remained morphologically and functionally intact. Knockdown of caveolin1 (Cav1) suppressed endothelial transcytosis, leading to reduced BBB permeability, and brain edema. Lastly, a coimmunoprecipitation assay showed that GCX degradation enhanced the interaction between syndecan1 and Src by promoting the binding of phosphorylated syndecan1 to the Src SH2 domain, which led to rapid modulation of cytoskeletal proteins to promote caveolae‐mediated endocytosis. Overall, these findings demonstrate that the dynamic degradation and reconstruction of GCX may account for the biphasic changes in BBB permeability in ischemic stroke, and reveal an essential role of GCX in suppressing transcellular transport in brain endothelial cells to maintain BBB integrity. Targeting GCX may provide a novel strategy for managing BBB dysfunction and central nervous system drug delivery. Glycocalyx‐regulated transcellular transport across the BBB contributes significantly to the barrier function of the BBB in both normal and diseased conditions. GCX may be an essential target for manipulating BBB permeability to help with drug delivery to the brain or to protect against BBB injury under diseased conditions.

Colorectal cancer (CRC) remains a major cause of cancer-related morbidity and mortality, with high recurrence rates and limited treatment options for metastatic disease. The tumor microenvironment (TME) and metabolic reprogramming are critical drivers of CRC progression, influencing immune responses, therapeutic resistance, and patient outcomes. This study explores the interplay between metabolic reprogramming and the TME in CRC using transcriptomic data and bioinformatics approaches to identify metabolically and microenvironmentally defined CRC subtypes and candidate biomarkers. Gene expression and clinical data were obtained from TCGA colorectal adenocarcinoma (COAD), rectal adenocarcinoma (READ), and six GEO CRC datasets. Immunohistochemistry (IHC) was performed to validate PDE2A and CKMT2 expression in CRC tissues. Bioinformatic analyses were conducted using R software v4.0.3. We identified 220 TME- and 40 metabolism-related differentially expressed genes (DEGs) in CRC. Consensus clustering of these TMET genes revealed two distinct subtypes: Cluster 1 (C1), associated with poorer survival, an immune-mesenchymal phenotype, and frequent mutations in TTN and BRAF, and Cluster 2 (C2), characterized by enriched TP53 and APC mutations, classic tumor suppressor pathway activation, and higher genomic instability. Metabolically, C1 was characterized by lipid metabolism and extracellular matrix remodeling, whereas C2 showed enrichment of nucleotide and amino acid metabolism linked to cell cycle progression and DNA repair. Single-cell RNA sequencing confirmed these distinctions, revealing that C1-upregulated genes were predominantly expressed in immune and stromal compartments, whereas C2-upregulated genes were enriched in epithelial and malignant cells. PDE2A, primarily expressed by endothelial cells, was identified as a metabolic biomarker of C1, while CKMT2, expressed in malignant cells, defined C2. These genes serve as key metabolic markers distinguishing CRC subtypes based on molecular heterogeneity and prognosis. PDE2A and CKMT2 were identified as critical metabolic biomarkers associated with distinct CRC subtypes and TME compositions. These findings highlight the intricate relationship between metabolic reprogramming, the tumor microenvironment, and tumor heterogeneity, providing insights into CRC molecular subtypes and their prognostic significance.

Stroke is a significant health concern impacting society and the health care system. Reperfusion therapy for acute ischemic stroke and standard rehabilitative therapies may not always be effective at improving post-stroke neurological function, and developing alternative strategies is particularly important. Vagus nerve stimulation (VNS) is a treatment option currently approved by the Food and Drug Administration (FDA) for intractable epilepsy, refractory depression, primary headache disorders, obesity, and moderate to severe upper-limb motor dysfunction in chronic ischemic stroke patients. Moreover, VNS has demonstrated potential efficacy in various conditions, including autoimmune diseases, disorders of consciousness, Alzheimer’s disease, Parkinson’s disease, traumatic brain injury, stroke, and other diseases. Although the popularity and application of VNS continue to increase rapidly, the field generally lacks a consensus on the optimal stimulation parameters. The stimulation parameters for VNS are directly related to the clinical outcome, and determining the optimal stimulation conditions for VNS has become an essential concern in its clinical application. This review summarizes the current evidence on VNS for stroke in preclinical models and clinical trials in humans, paying attention to the current types and stimulation parameters of VNS, highlighting the mechanistic pathways involved in the beneficial effects of VNS, critically evaluating clinical implementation challenges and proposing some suggestions for its future research directions. Achieving safe and effective clinical transformation of VNS requires further animal and clinical studies to determine the optimal stimulation parameters and therapeutic mechanisms.

We introduce Password Authenticated Searchable Encryption (PASE), a novel searchable encryption scheme where a single human-memorizable password can be used to outsource (encrypted) data with associated keywords to a group of servers and later retrieve this data through the encrypted keyword search procedure. PASE ensures that only the legitimate user who knows the initially registered password can perform these operations. In particular, PASE guarantees that no single server can mount an offline attack on the user’s password or learn any information about the encrypted keywords. The concept behind PASE protocols extends previous concepts behind searchable encryption by removing the requirement on the client to store high-entropy keys, thus making the protocol device-agnostic on the user side. In this paper, we model the functionality of PASE along with two security requirements (indistinguishability against chosen keyword attacks and authentication) and propose an efficient direct construction in a two-server setting those security we prove in the standard model under the Decisional Diffie–Hellman assumption. Our constructions support outsourcing and retrieval procedures based on multiple keywords and allow users to change their passwords without any need for the re-encryption of the outsourced data. Our theoretical efficiency comparisons and experimental performance and scalability measurements show that the proposed scheme is practical and offers high performance in relation to computations and communications on the user side. The practicality of our PASE scheme is further demonstrated through its implementation within a JavaScript-based web application that can readily be executed on any (mobile) browser and remains practical for commodity user devices such as laptops and smartphones.

Prediction of extubation failure, particularly in neurocritical patients, is unique and controversial. We conducted a systematic review and meta-analysis to identify the risk factors for extubation failure in these patients. A literature search of databases (MEDLINE, EMBASE, the Cochrane Library, and Web of Science) was performed up to August of 2013 to identify trials that evaluated extubation failure predictors. Included trials were either prospective or retrospective cohort studies. Nine studies involving 928 participants were included. The systematic review and meta-analysis revealed that the following were predictive for extubation failure: pneumonia, atelectasis, mechanical ventilation of >24 h, a low Glasgow Coma Scale score (7-9T) (OR = 4.96, 95% CI = 1.61-15.26, P = 0.005), the inability to follow commands (OR = 2.07, 95% CI = 1.15-3.71, P = 0.02), especially the command to close the eyes, thick secretion, and no intact gag reflex. Meanwhile, the following were not predictive for extubation failure: sex, secretion volume, coughing upon suctioning, and the inability to follow one command among showing two fingers, wiggling the toes, or coughing on command. Additionally, some traditional weaning parameters were shown to poorly predict extubation failure in neurocritical patients. Besides pneumonia, atelectasis, and the duration of mechanical ventilation, other factors that should be taken into consideration in the prediction of extubation failure when neurocritical patients are weaned from tracheal intubation include neurologic abilities (Glasgow Coma Scale score and following commands), the secretion texture, and the presence of a gag reflex.

Radiation-induced brain injury (RBI) is a common complication of radiotherapy for head and neck tumors while its mechanism is not fully understood. Animal whole-brain radiation (WBR) models are of key importance in experimental radiation research, and an appropriate radiation source is essential. Previous animal WBR models were administered by clinical linear accelerator to induce the pathophysiological changes of RBI. In the current study, we adopted Faxitron MultiRad 225 X-ray irradiation system to construct a mouse WBR model with a single dose of 30 Gy. In the acute phase of this mouse WBR model, brain edema and blood–brain barrier (BBB) damage were found mild. However, two months later, the results of immunofluorescence showed that astrocytes and microglia were activated continuously, and the number of immature neurons in dentate gyrus (DG) area of hippocampus was significantly reduced, in accordance with the features of chronic pathophysiological changes. Besides, data of MRI scans and behavior tests illustrated the structural changes of brain tissue and cognitive impairment in the chronic phase. To sum up, this mouse WBR model using the Faxitron MultiRad 225 irradiation system with a single dose of 30 Gy is feasible to simulate the RBI-related chronic pathophysiological changes.