Background: FAM64A is highly expressed in various cancers (e.g., breast cancer, ovarian cancer), indicating that it promotes tumorigenesis and progression by facilitating epithelial-mesenchymal transition. In the genitourinary system, dihydrotestosterone promotes the expression of FAM64A by binding of the androgen receptor to the FAM64A promoter, thereby enhancing the proliferation, migration, and cell cycle progression of androgen-dependent prostate cancer cell lines. However, its specific role in the initiation and progression of bladder cancer remains unclear. FAM64A overexpression has been observed in cancers such as breast and prostate; however, its role in bladder cancer (BLCA) is less understood. Muscle-invasive BLCA (MIBC) has a poor prognosis, with five-year survival rates below 50%. This study explores FAM64A's molecular mechanisms and therapeutic potential in BLCA. Methods: FAM64A expression was analyzed using TCGA data and clinical BLCA tissues. Functional assays (CCK-8, wound-healing, Transwell) assessed proliferation, migration, and invasion following FAM64A modulation. Western blotting was used to evaluate EMT markers (Vimentin, Slug) and proteins involved in the PI3K/AKT pathway. Bioinformatics (TCGA/GTEx) identified FAM64A-correlated genes, followed by KEGG pathway analysis. Taselisib (PI3K/AKT inhibitor) validated pathway involvement. Results: FAM64A was upregulated in BLCA and correlated with advanced tumor stage, T-stage, and grade. Knockdown suppressed proliferation, migration, and invasion, while overexpression exacerbated these effects. FAM64A promoted G2/M progression (via Cyclin B1/Ki67) and EMT (via Vimentin/Slug). KEGG analysis linked FAM64A to the PI3K/mTORC2/AKT signaling pathway. Taselisib reversed FAM64A-induced EMT and malignant phenotypes. Conclusions: FAM64A drives BLCA progression via PI3K/mTORC2/AKT-mediated EMT, serving as a potential prognostic biomarker and therapeutic target for metastatic BLCA.

Current treatments for chronic neuropathic pain are limited in efficacy, partly due to the complicated etiology of neuropathic pain chronicity. Ongoing nociceptive inputs from peripheral injuries lead to maladaptive alterations in the central nervous system during the transition from acute to chronic pain, which in turn contribute to the maintenance of chronic pain and reduce the effectiveness of peripheral analgesics. Reactive astrocytes are known to contribute to chronic neuropathic pain in the spinal cord, while how astrocytes contribute to chronic pain in supraspinal nuclei remains unclear. This study reveals that continuous painful stimulation from peripheral injury induces astrocyte reactivity and downregulation of astrocytic Kir4.1 (inward rectifying potassium channel protein 4.1) in the paraventricular thalamus (PVT). In turn, these reactive astrocytes help to maintain neuronal hyperactivity in the PVT and enhance neural projections from PVT to the medial prefrontal cortex (mPFC), which contribute to hyperalgesia in chronic neuropathic pain. Therefore, this study identifies a neuro-glial interaction that mediates chronic pain in supraspinal brain.

Pyroptosis is a form of programmed cell death (PCD) that triggers inflammation. Pyroptosis is activated by specific inflammasomes and caspases, leading to the cleavage of gasdermin protein families, especially gasdermin D (GSDMD) and gasdermin E (GSDME). While pyroptosis has been extensively linked to innate immunity and diseases, such as atherosclerosis, the role in cancer remains an area of active investigation. Studies have suggested that pyroptosis influences tumor behavior, including proliferation and invasion, across different tissue types and genetic backgrounds. This process occurs through both canonical and non-canonical pathways involving GSDMD and GSDME. Tumors tend to thrive in the chronic inflammatory environment created by pyroptosis but tumors are more likely to be eradicated if pyroptosis occurs suddenly and extensively. Indeed, targeting pyroptosis pathways holds promise as an anticancer strategy. To date, several drugs are found to have the ability of inducing pyroptosis to enhance tumor clearance. Moreover, pyroptosis-related genes (PRGs) have emerged as valuable biomarkers for prognosis and monitoring the tumor microenvironment (TME). This review explores the mechanisms underlying endogenous and exogenous pyroptosis in cancer, examines the dual role within tumors, discusses the potential for targeting pyroptosis in cancer treatment and prognosis, and highlights the interactions between pyroptosis and other forms of PCD in cancer.

Global surgical volumes continue to rise, yet postoperative morbidity and mortality remain substantial, particularly among geriatric patients. The scarcity of multi-center prospective perioperative cohorts with active follow-up and large-scale, high-quality data limits the understanding of risk profiles and hinders individualized perioperative management in this population. To address this gap, the PeRiOperative sTress risk assEssment and Clinical decision cohorT (PROTECT) was established by creating a dedicated perioperative data platform for geriatric patients. This cohort profile specifically describes the study design, recruitment strategy, data structure, and current status of PROTECT. PROTECT is an ongoing, ambispective, real-world observational cohort across three tertiary medical centers. The study continuously enrolls inpatients aged ≥ 65 years undergoing surgery under anesthesia. Preoperatively, standardized pre-anesthesia assessments are conducted to collect comprehensive medical information. Intraoperatively, anesthetic and surgical data, along with high-frequency biosignals are recorded. Postoperative outcomes are evaluated at 48 hours, 7 days, and 30 days. Descriptive analyses were performed to summarize baseline characteristics and postoperative outcomes. The first participant was enrolled in August 2019. As of May 2025, 61,289 participants aged 65—100 years have been included. The median age is 71 years, and 44.4

BackgroundTriple negative breast cancer (TNBC) is the most malignant type of breast cancer, and its treatment usually uses paclitaxel for chemotherapy. However, TNBC cells are increasingly resistant to paclitaxel. In the context of paclitaxel resistance, we investigated the role of DNA methylation and the DNA methyltransferase DNMT3B methylation regulatory proteins, as well as their interaction with ferroptosis regulator SLC25A6, in regulating paclitaxel resistance and ferroptosis in TNBC.MethodsWe used database integration analysis methods, combined with bioinformatics screening, in vitro and in vivo cell and animal experimental models to analyze DNA methylation and the effect of DNMT3B on SLC25A6 DNA methylation. We explored the effects of the DNMT3B-SLC25A6 regulatory axis on ferroptosis and paclitaxel resistance using electron microscopy, fluorescent probes, and detection of key biomarkers. Statistical significance was evaluated using Student’s t-test and analysis of variance (ANOVA).ResultsDNMT3B was significantly overexpressed in paclitaxel-resistant TNBC tissues and cell lines, correlating with enhanced proliferation, migration, and ferroptosis. Mechanistically, DNMT3B induced DNA methylation of SLC25A6 through its 252-bp CpG island, inhibited its protein expression, and triggered ferroptosis by disrupting mitochondrial function and redox balance, leading to paclitaxel resistance in TNBC.ConclusionIn paclitaxel-resistant TNBC, DNMT3B regulates SLC25A6 expression via DNA methylation, and the DNMT3B-SLC25A6 regulatory axis acts as a central regulator of ferroptosis, promoting paclitaxel resistance in TNBC by suppressing ferroptosis via oxidative stress imbalance. These findings provide promising therapeutic targets for the intervention of TNBC paclitaxel resistance.

Chronic pain is characterized by persistent neural sensitization, yet the cellular processes underlying its maintenance remain incompletely understood. Cell senescence, has recently emerged as a potential contributor to chronic pain. In this review, we summarize evidence of senescence across multiple cell types involved in pain processing and discuss how senescent cells influence neural function through mechanisms including the senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and epigenetic alterations. We further propose that cell senescence acts as a key link between cellular dysfunction and neural sensitization, forming a self-reinforcing network that sustains chronic pain. Importantly, targeting senescence-related pathways, including senolytics and modulators of SASP, may represent promising strategies for chronic pain therapies. This integrative perspective provides a framework for understanding chronic pain and highlights new directions for therapeutic intervention.

Background Acute myocardial ischemia/reper fusion (MI/R) increases risk for cognitive decline, yet the underlying mechanisms mediating heart-brain communication remain poorly understood. Small extracellular vesicles (sEVs) have emerged as novel long-range signaling mediators and may play a critical role. MethodsMI/R was induced by transient ligation of the left anterior descending artery. Cognitive performance was assessed using multiple behavioral tests. sEVs derived from cardiomyocytes were labeled to track their distribution and cellular uptake in the brain. Heart and brain tissues were analyzed for microRNAs (miRNAs) expression using bioinformatics, qPCR, and RNAScope. The role of specific miRNAs was investigated through genetic inhibition of cardiomyocyte-derived sEVs release using Rab27a(f/f)Myh6-Cre(+) mice, pharmacological blockade of exosome, and AAV-mediated overexpression or knockdown. Results MI/R mice exhibited significant cognition deficits along with hypothalamic paraventricular nucleus (PVN) synaptic ultrastructural injury and dysfunction. sEVs released from injured cardiomyocytes were significantly elevated and preferentially accumulated in oxytocin neurons from the PVN. Inhibiting cardiomyocyte-derived sEVs ameliorated cognitive impairments and synaptic pathology. Conversely, injection of cardiomyocyte-derived sEVs into the PVN recapitulated MI/R-induced cognitive deficits. Among candidate miRNAs, miR-574-5p was identified as a key mediator. Its inhibition via miRNA sponge restored cognitive function. Bioinformatic analyses revealed that miR-574-5p targets genes involved in synaptic structure and GABA(B) receptor signaling. Conclusions Cardiomyocyte-derived sEVs contribute to MI/R-induced cognitive impairment through miR-574-5p. Upon delivery to the PVN and uptake by oxytocin neurons, miR-574-5p suppresses synaptic and GABA(B) receptor-related proteins, leading to synaptic disruption and cognitive decline. Targeting this pathway may represent a promising therapeutic approach for cognitive dysfunction associated with heart disease.

Background: Coughing and hemodynamic fluctuations during emergence from anesthesia after a craniotomy can result in serious complications. This study evaluated whether the ultrasound-guided superior laryngeal nerve block (SLNB) attenuates these tracheal tube-related responses. Methods: Eighty patients scheduled for elective craniotomy were randomized into the control (Group C, 2 ml 0.9% saline per side) and SLNB (Group S, 2 ml 1% lidocaine per side) group. The primary outcome was the incidence of coughing during the recovery period. Secondary outcomes included the severity of coughing, hemodynamic fluctuations, need for rescue interventions, anesthesia-related parameters, and complications.Results: Compared to controls, the patients in Group S experienced a significantly reduced incidence (78.9% vs. 48.6%; P = 0.006) and severity (P < 0.001) of coughing during emergence. The mean arterial pressure and heart rate were also more stable during and after extubation in Group S than in Group C. Furthermore, Group S required a significantly lower dose of nicardipine during the emergence period (P = 0.032), and both the incidence of and visual analog scale scores for postoperative sore throat at 6 h after extubation were markedly reduced (P = 0.035). No significant differences were noted between the groups in terms of propofol consumption, emergence agitation, extubation time, post-anesthesia care unit stay duration, or complications.Conclusions: The SLNB significantly suppressed extubation-related responses during anesthetic emergence after craniotomy by reducing coughing and attenuating hemodynamic fluctuations, thereby contributing to a smoother emergence profile.

BackgroundPlasmodium infection has been proven to activate antitumor immune responses. This study comprehensively analyzes the immune cell populations in peripheral blood and tumor microenvironment to elucidate the potential immunological mechanisms by which Plasmodium infection inhibits tumor growth.MethodsWe established a subcutaneous Lewis lung cancer model in C57BL/6J mice and treated them with intraperitoneal injection of Plasmodium yoelii. The long and short diameters of tumors were measured. Then, high-dimensional flow cytometry was used to analyze the T cell subsets, macrophages and myeloid-derived suppressor cells (MDSCs) in peripheral blood and tumor tissues. Immunosuppression-related phosphorylated signal transducer and activator of transcription 3 (pSTAT3) and TGFβ in tumor tissues were also measured through Western blotting assay.ResultsPlasmodium infection inhibited the growth of Lewis lung cancer in mice. The infection increased in the numbers of CD3+ T cells, including CD4+ and CD8+ T, CD4+ central memory T (Tcm), CD4+ effector memory T (Tem), CD8+ Tcm, CD8+ Tem, CD8+ virtual memory T (Tvm), CD8+ short-lived effector cells (SLEC), and CD8+ memory precursor effector cells (CD8+ MPEC) in peripheral blood. Concurrently, the infection also increased the numbers of CD3+ T cells, including CD4+ and CD8+ T, CD4+ Tcm, CD4+ Tem, CD4+ tissue resident memory T (Trm), CD8+ Tcm, CD8+ Tem, CD8+ Trm and CD8+ SLEC in tumor tissues. In addition, Plasmodium infection reduced the expression levels of PD-1 on CD4+ and CD8+ T, the number of polymorphonuclear MDSCs, and increased the ratio of M1/M2 macrophages in the tumor tissues. The initial mechanism study revealed that Plasmodium infection significantly reduced the expression levels of pSTAT3 and TGFβ in tumor tissues, providing direct evidence that Plasmodium infection activated the antitumor immune responses.ConclusionBased on our past and current studies, we can draw the following conclusion: Plasmodium infection fully remodels and activates the immune system, targets and inhibits the entire tumor ecosystem through the key signals of pSTAT3 and TGFβ. This is completely different from the mechanisms of action of the current immune checkpoint blockade therapies, representing a new form of cancer immunotherapy, namely, the immune ecotherapy.

Gastric-type adenocarcinoma of the uterine cervix (GAS) is a rare, aggressive cervical cancer unrelated to HPV infection that is frequently misdiagnosed because it closely resembles both benign cervical glands and HPV-related cervical adenocarcinoma. This diagnostic confusion can lead to inappropriate treatment, highlighting the need for objective molecular markers. Here, we performed the systematic multi-center proteomic analysis of GAS, profiling 407 cervical tissue samples to map its molecular landscape. To overcome limited sample size and biological noise, we developed WEDGE. First, generative AI synthesizes realistic artificial proteomic profiles to augment the training data. Biologically informed network analysis then leverages known biological relationships to surface diagnostically meaningful patterns. WEDGE identified a two-protein signature, Pepsinogen C (PGC) and DNA Methyltransferase 1 (DNMT1), that distinguished GAS from HPV-related cervical cancer with 93% accuracy in the test cohort and 97% accuracy in an external proteomic cohort, outperforming existing biomarker-discovery methods. Tissue staining of an IHC validation cohort confirmed the expression patterns and reached a diagnostic accuracy of 87.9%. Beyond diagnosis, PGC independently predicted patient outcomes, and combining PGC with routine clinical features improved risk prediction (C-index 0.701). Together, these results establish an AI-driven framework for biomarker discovery and provide clinically relevant candidate tools for diagnosing and prognosticating for GAS. ### Competing Interest Statement The authors have declared no competing interest. ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: Ethics committee/IRB of Zhejiang Cancer Hospital gave ethical approval for this work (Approval No. IRB-2025-76 (IIT)). I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes All data and code produced in this work are available online. The mass spectrometry proteomics data are deposited in the ProteomeXchange Consortium via the iProX repository (identifier: PXD074127 / IPX0013995000) and will be released publicly upon manuscript publication at https://www.iprox.cn/page/PSV023.html;?url=1782219624318PdxleQ1V. Source code is openly accessible at https://github.com/HuangHan-LabAccount/WEDGE-for-biomarker-discovery. Zhejiang Provincial Natural Science Foundation, LRG25H310001(Q.W.) Noncommunicable Chronic Diseases–National Science and Technology Major Project, 2025ZD0545600 (T.Z.) Fundamental Research Funds for the Central Universities, 226-2024-00094 (T.Z.) National Natural Science Foundation of China, 82470623 (J.W.) Science and Technology Cooperation Project of Sanmen Collaborative Innovation Center, Taizhou Institute of Zhejiang University, 2025SIC02 (J.W.)

BACKGROUND:Forty Hz light flicker has shown promise in mitigating cognitive impairments, though its mechanisms remain unclear. AIMS:This study aimed to use perioperative neurocognitive dysfunction (PND) as a unique model of neural damage to provide a broader understanding of the neural mechanisms underlying the cognitive improvements associated with 40 Hz visual stimulation and offer new insights into the clinical application of PND treatment. MATERIALS AND METHODS:Postoperative cognitive function was assessed through behavioral tests. Male and female mice received various visual light flicker stimuli, including 40 Hz, random, continuous, or no light. Local field potentials were recorded from the hippocampal dentate gyrus (DG) and primary visual cortex. RESULTS:Our results show that among the stimuli, only the 40 Hz flicker improved cognitive function, impaired by anesthesia or surgery. Intraoperative 40 Hz stimulation activated the primary visual cortex and was correlated with enhanced gamma coherence between this region and the hippocampal DG, a coherence that surgery itself notably reduced. This preserved functional connectivity. Additionally, hippocampal DG activity was enhanced, particularly in the gamma frequency range. CONCLUSION:Our results suggest that 40 Hz flicker mitigates anesthesia/surgery-induced cognitive deficits, potentially through modulating gamma coherence between the visual cortex and hippocampus. These findings provide insights into PND prevention and the neural mechanisms underlying 40 Hz-induced cognitive benefits.

Development of potent nonopioid analgesics (NOAs) has attracted great attentions from both academic and industrial worlds, aiming at replacing current opioid drugs in acute and chronic pain management. Among the diverse proposed pathways toward nonopioid analgesia, voltage-gated sodium channel stood out as one of the most promising targets in developing potent NOA. Diverging from the prevailing focus on highly subtype-selective blockers, we report here the access of potent analgesia via the simultaneous inhibition on multianalgesic-related sodium channel subtypes. Originated from AI-driven drug discovery and computer-aided drug design, the hit and lead compounds exhibited efficient inhibitory effect on analgesic-related sodium channel subtypes, robust analgesic effect in various rat models and no opioid-related adverse reactions. Furthermore, the potential of such a multi-subtype sodium channel blocker for perioperative use was validated through a surgical simulation. These findings represent a meaningful leap toward the goal of replacing opioids in perioperative period and provide fresh insights for future NOA development.

Early detection of hypertension is challenging due to the absence of overt symptoms. To address this, we developed an attention-based deep learning model for predicting hypertension risk, offering detailed interpretability and a comprehensive assessment of an individual's future disease likelihood based on electronic health records (EHRs). Our findings show that incorporating time series data significantly enhances the accuracy of hypertension prediction, achieving an AUC of 0.835 across the entire dataset. The model consistently surpasses traditional machine learning approaches and simple sequential model across various evaluation metrics, underscoring its potential for broad clinical application. The interpretability analysis, grounded in attention scores, effectively identifies decision thresholds for dynamic features and tracks individual risk trajectories. By aligning these risk thresholds with a causal diagram, our model supports clinicians in making informed decisions. This study provides a valuable platform for healthcare providers, aiding in the early identification of high-risk populations and improving long-term management of hypertension, thereby addressing the diverse needs of stakeholders.

ABSTRACT Approximately 10%–30% of elderly patients experience cognitive decline after general anesthesia and surgery. However, how specific brain regions coordinate cellular and molecular networks to mediate cognitive decline remains unknown. Here, we revealed that the hippocampus, but not other cognitive‐related brain regions, exhibits increased blood–brain barrier (BBB) permeability, leading to neuroinflammation activation and cognitive decline after general anesthesia and surgery in aged mice. Mechanistically, anesthesia and surgery induce expression of the mechanosensitive channel Piezo1 in hippocampal endothelial cells (ECs) of aged mice. Inducible EC‐specific deletion of Piezo1 restores hippocampal BBB integrity, inhibits neuroinflammation activation, and improves cognitive decline in aged mice following anesthesia and surgery. Conversely, injection of the Piezo1 agonist Yoda1 promotes hippocampal BBB breakdown. Moreover, activation of Piezo1 induces Nox4, which mediates hippocampal BBB breakdown and neuroinflammation activation after anesthesia and surgery in aged mice. Therapeutically, AAV‐BR1 transduction to brain microvascular ECs for the knockdown of endothelial Nox4 blocks Piezo1‐mediated hippocampal BBB breakdown and neuroinflammation activation. Overall, inhibiting the endothelial Piezo1‐Nox4 axis restores hippocampal BBB integrity to improve anesthesia‐ and surgery‐induced cognitive decline in aged mice, highlighting potential therapeutic strategies.

Intraoperative Neurophysiological Monitoring (IONM) is an indispensable surgical tool that offers invaluable insights into neurological function across a spectrum of anatomical areas. By comprehensively assessing the integrity of the brain, brainstem, spinal cord, cranial nerves, and peripheral nerves, IONM plays a pivotal role in guiding surgical decision-making and optimizing patient outcomes, particularly in the context of high-risk procedures. Intraoperative drugs, especially anesthetics and/or analgesics, differentially modulate neurophysiological monitoring, which remarkably affects the application of neurophysiological monitoring under specific conditions and indicates the neurobiological mechanisms of anesthetics/analgesics. This review will describe various neurophysiological modalities utilized in intraoperative procedures, each employing a wide variety of physiological principles; summarize the modulatory effects of anesthetics/analgesics on these neurophysiological monitoring parameters; and elucidate their underlying mechanisms, with a particular emphasis on evoked potentials. Insights gleaned from this review can inform strategies of anesthesia management for surgeries that require IONM and guide future investigations on the mechanisms of anesthesia/analgesia.

The mechanisms by which circRNAs regulate estrogen receptor (ER)-positive breast progression and therapeutic resistance remain poorly defined. By screening circRNAs involved in ER signaling, circESR1 was identified as a novel circRNA exhibiting high specificity of expression in ER+ breast cancer. CircESR1 interacted with HNRNPAB, which was transcriptionally activated by ER/SP1 signaling. HNRNPAB promoted the back-splicing and expression of circESR1 by binding to the Alu elements of cognate pre-mRNA; and circESR1 transcripts increased the stability and expression of HNRNPAB, ensuring an efficient positive feedback loop as reflected in antiestrogen-resistant breast cancer cells. Furthermore, HNRNPAB interacted and stabilized CDK1 and CDK6 mRNA, which was facilitated by its asymmetrical binding of circESR1, to promote cell cycle progression. Patients whose cancer exhibited high levels of circESR1 and/or HNRNPAB exhibited advanced prognostic stage and poor survival. Combined use of circESR1 ASO and CDK4/6 inhibitors were shown to be an effective therapeutic approach overcoming antiestrogen resistance in breast cancer xenograft models. Hence, these findings elucidated a novel signaling complex centered around circESR1 and HNRNPAB in ER+ breast cancer, and suggested that circESR1 might represent a potential therapeutic target for this disease.

Immune checkpoint blockade holds promise in hepatocellular carcinoma (HCC) treatment, but its efficacy remains limited. Dysregulated polyamine metabolism and its interaction with oncogenic pathways promote tumor progression. However, the heterogeneity of polyamine metabolism and its effects on the immune microenvironment and response to immunotherapy in HCC remain unclear. Here, we aimed to investigate the prognostic and immunotherapeutic implications of polyamine metabolism in HCC. Based on polyamine-related genes, HCC patients were categorized into two clusters with distinct survival outcomes. We developed a polyamine-related signature, termed PAscore, which was found to be a strong predictor of both poor prognosis and reduced immunocyte infiltration. Notably, a high PAscore was also associated with decreased sensitivity to immunotherapy. Within the HCC microenvironment, malignant cells exhibited polyamine metabolic heterogeneity, those with high polyamine metabolic activity showed altered hallmark pathway signatures and increased communication with myeloid cells. In vitro experiments suggested that FIRRE, the gene with the greatest impact on the PAscore, significantly contributed to HCC proliferation and metastasis. This study underscores the potential of our polyamine-related signature in predicting the prognosis and immunotherapy response in HCC patients, and also reveals the polyamine metabolic heterogeneity among HCC cells that influences their crosstalk with infiltrating myeloid cells.

Purpose Emergence agitation (EA) after (adeno)tonsillectomy (AT) surgery impairs recovery in children. Adequate analgesia plays a crucial role in reducing EA incidence. This study investigated whether hydromorphone infusion (30 mu g/kg) during anesthesia induction could reduce EA following AT surgery for obstructive sleep apnea in children.Patients and methods A total of 186 ASA I-III children aged 3-7 years undergoing AT surgery were enrolled in a blinded randomized trial comparing hydromorphone (30 mu g/kg) to fentanyl (4 mu g/kg). The primary outcome was EA incidence within 30 min post-extubation. Secondary outcomes included pediatric anesthesia emergence delirium (PAED), face, legs, activity, crying, consolability (FLACC), Ramsay sedation scores, extubation time, rescue analgesia incidence, and adverse events.Results The incidence of EA was significantly lower in the hydromorphone group [48.4% (45/93) vs 64.5% (60/93); absolute difference: 16.1%; 95% CI: 18.9-29.5%; P = 0.027]. Hydromorphone improved PAED, FLACC, and Ramsay scores and reduced moderate-to-severe pain and rescue analgesia. No postoperative complications occurred in either group.Conclusion Hydromorphone at 30 mu g/kg effectively reduces the incidence of EA within 30 min post-extubation in children after AT surgery compared to fentanyl. It shows superior analgesia and has a low incidence of adverse effects.

Type 2 diabetes mellitus affects over 500 million people globally, with 10%-20% requiring surgery. Patients with diabetes are at increased risk for perioperative complications, including prolonged hospital stays and higher mortality, primarily due to perioperative hyperglycemia. Managing blood glucose during the perioperative period is challenging, and conventional monitoring is often inadequate to detect rapid fluctuations. Clinical decision support systems (CDSS) are emerging tools to improve perioperative diabetes management by providing real-time glucose data and medication recommendations. This viewpoint examines the role of CDSS in perioperative diabetes care, highlighting their benefits and limitations. CDSS can help manage blood glucose more effectively, preventing both hyperglycemia and hypoglycemia. However, technical and integration challenges, along with clinician acceptance, remain significant barriers.