INTRODUCTION:Acute kidney injury (AKI) is a significant postoperative complication, particularly following abdominal surgery. Although acetaminophen is widely used for postoperative pain management, its impact on AKI risk in this context remains underexplored. This study investigates the association between postoperative acetaminophen use and AKI incidence in abdominal surgery patients. METHODS:A retrospective cohort study was conducted using the MIMIC-IV database, including 8696 abdominal surgery patients. Multivariable logistic regression and Cox proportional hazards models were used to assess the relationship between acetaminophen administration within 48 h postsurgery and AKI occurrence within 7 days. Subgroup analyses were performed to evaluate effects based on anemia severity, sodium levels, surgery type, and gender. RESULTS:Acetaminophen use within 48 h postsurgery was associated with a 40% reduction in AKI risk (odds ratio = 0.60, 95% confidence interval: 0.54-0.67; hazard ratio [HR] = 0.57, 95% confidence interval: 0.53-0.62). Greater protective effects were observed in females (HR = 0.51 versus males = 0.62), patients with severe anemia (HR = 0.44), hyponatremia (HR = 0.47), and those undergoing open surgery (HR = 0.50). Time-dependent analysis revealed that delayed acetaminophen administration (18-48 h postsurgery) provided stronger protection, with odds ratio values declining from 0.8 to 0.4. CONCLUSIONS:Postoperative acetaminophen use is associated with a reduced risk of AKI in abdominal surgery patients, particularly in high-risk subgroups such as females, anemic patients, and those with hyponatremia or undergoing open surgery. These findings suggest that acetaminophen may serve as a safer alternative to nonsteroidal anti-inflammatory drugs for postoperative pain management. Further prospective studies are needed to optimize dosing and timing strategies.

Dentin hypersensitivity (DH) is a common clinical oral disease. Nano-hydroxyapatite (n-HAP) toothpaste and fluoride toothpaste are widely used treatment options; however, their comparative efficacy is still unclear. This study aimed to systematically evaluate the clinical efficacy of n-HAP toothpaste and fluoride toothpaste in the treatment of DH. This systematic review was prospectively registered on PROSPERO (CRD420251272119) and conducted following the PRISMA 2020 guidelines. Seven databases (PubMed, Embase, Web of Science, Cochrane Library, CNKI, Wanfang Data and SinoMed) were comprehensively retrieved from the establishment of the library to December 2025.Two independent reviewers performed study selection, data extraction, and quality assessment. Risk of bias was evaluated using the Cochrane Risk of Bias (RoB 1) tool. The certainty of evidence for each major outcome was evaluated using the GRADE approach. Statistical analyses were conducted using RevMan 5.4, Stata 17.0, and R 4.2.1 software, with the standardized mean difference (SMD) employed as the effect size measure. This systematic review included a total of 13 randomized controlled trials involving 609 patients (n-HAP group: 296; fluoride group: 313). The majority of included studies raised some concerns regarding risk of bias, primarily related to blinding of participants and outcome assessors .The meta-analysis revealed that at short-term follow-up (2 weeks), compared with fluoride toothpaste, n-HAP toothpaste demonstrated greater reductions in visual analog scale (VAS) scores (standardized mean difference SMD = 8.81, 95

INTRODUCTION:Propofol and midazolam are commonly used sedatives in patients with sepsis-associated acute kidney injury (S-AKI), yet the association of their combined use on patient prognosis remains unclear. This study aimed to compare the associations of propofol monotherapy, midazolam monotherapy, and their combination with 30-day mortality in S-AKI patients. METHODS:This study analyzed 3335 S-AKI patients from the Medical Information Mart for Intensive Care IV database, categorized by sedation strategy: no sedation, propofol alone, midazolam alone, or combination therapy. The primary outcome was 30-day all-cause mortality. Associations were assessed using Kaplan-Meier survival analysis, Cox proportional hazards models, and inverse probability of treatment weighting. Subgroup and mediation analyses were also performed. RESULTS:After multivariable adjustment, both midazolam monotherapy (hazard ratio [HR] = 1.945, 95% confidence interval: 1.519-2.490) and combination therapy (HR = 1.573, 95% confidence interval: 1.275-1.942) were associated with significantly increased 30-day mortality risk compared to propofol monotherapy. This finding was consistent after inverse probability of treatment weighting (HR = 1.742 and 1.328, respectively). Subgroup analyses generally supported this trend across different populations. Mediation analysis indicated that metabolic acidosis significantly mediated part of the increased mortality risk associated with midazolam (alone: 15.84%; combined: 10.21%). CONCLUSIONS:Propofol monotherapy was associated with more significant survival benefits compared to midazolam monotherapy or combination therapy. Metabolic acidosis is a key pathological mechanism mediating this difference, which has important guiding value for improving the prognosis of this high-risk population.

Background: Endometrial cancer is highly treatable with timely hysterectomy, yet global survival disparities persist. Whether these differences reflect disease biology or health system capacity remains unclear. We aimed to quantify global inequities and provide policy-relevant projections. Methods: Using GLOBOCAN 2022 data across 185 countries, we extracted incidence and mortality estimates for corpus uteri cancer (ICD-10 C54). Key metrics included age-standardized incidence and mortality rates (ASIR, ASMR), mortality-to-incidence (M:I) ratios, 10-year trends (2008–2017) using estimated annual percentage changes (EAPC), and 2050 projections assuming constant age-specific rates. Stratification was by Human Development Index (HDI) and age (<60 vs ≥60 years). Findings: In 2022, there were 420,173 new cases and 97,670 deaths globally. The M:I ratio—a survival proxy—was 22·0% in very high-HDI versus 33·3% in low-HDI countries, representing a 2·4-fold survival gap. Among women aged ≥60 years in low-HDI settings, the M:I ratio reached 44·1%, exceeding that of pancreatic cancer in high-income countries. Notably, 51·1% of cases in low-HDI countries occurred in women younger than 60 years—opposite to obesity-driven patterns in high-income nations. By 2050, annual deaths are projected to rise 81·6% to 177,331, with the steepest relative increases (338%) in medium-HDI countries. Interpretation: Endometrial cancer outcomes are not biologically predetermined but shaped by structural healthcare inequities. The widening survival gap, projected to exacerbate by 2050, underscores urgent need for targeted investments in diagnostic infrastructure, surgical capacity, and essential cancer medicines in under-resourced settings. Closing this gap would require approximately $0·50–0·80 per capita annually in low-income countries—a fraction of the cost of treating advanced disease. These findings provide quantitative targets for global health policy and cancer control planning.

BACKGROUND:Traumatic brain injury (TBI) results in the release of microparticles from injured brain cells into circulation. These microparticles induce a systemic hypercoagulable state that rapidly transitions into secondary coagulopathy and endotheliopathy. We hypothesize that removing these microparticles from circulation could mitigate the TBI-induced secondary pathologies and improve outcomes. In this study, we investigated the role of Gas-6 (growth arrest-specific 6) as a scavenging factor for microparticles. METHODS:We quantified plasma Gas-6 levels in a mouse model of TBI and administered exogenous Gas-6 either before or after TBI to evaluate its effects on endotheliopathy, coagulopathy, and outcomes. Mechanistic studies assessed Gas-6-mediated clearance of circulating microparticles in TBI mice and investigated the molecular interactions by which Gas-6 binds microparticles and macrophages to facilitate microparticle scavenging. RESULTS:We found that plasma levels of Gas-6 were significantly reduced in mice subjected to severe TBI. Exogenous Gas-6 given either preinjury or postinjury attenuated coagulopathy, protected the integrity of the cerebral and pulmonary endothelium, improved neurological recovery, and increased overall survival of TBI mice. Gas-6 increased the clearance of anionic phospholipid-expressing microparticles from circulation by coupling microparticles with macrophages and monocytes through the γ-carboxyglutamate and the LG1 (laminin G-like domain 1), respectively, to facilitate phagocytosis of microparticles in the liver. CONCLUSIONS:These findings demonstrate the therapeutic potential of Gas-6 for TBI and potentially for other acute pathologies, in which microparticles initiate and propagate coagulation dysfunction and endothelial injuries.

The search for highly sensitive and specific tumor biomarkers is essential for the evaluation of prognosis and new therapeutic targets. Immune cells in the tumor microenvironment (TME) have dual roles in promoting and suppressing tumor growth, which is crucial for the development and treatment of cancer. According to previous studies, syndecan binding protein (SDCBP) participated in biological processes like epithelial-mesenchymal transformation, angiogenesis, and exosome formation and secretion during cancer metastasis, but whether SDCBP affects immune cells infiltration in the TME remains unclear. Here, we conducted a comprehensive analysis of multiple databases to explore the expression and prognosis of SDCBP in pan-cancer and focused on the effect of SDCBP on the immune cells, particularly on macrophages. The study found that SDCBP was expressed at different levels in most tumor tissues and cells. Upregulation of SDCBP was associated with malignant progression, poor patient prognosis and treatment non-response in certain tumors. Gene set enrichment analysis suggested that SDCBP was mainly involved in regulating immunity and inflammation-related pathways, which may be closely associated with the high levels of immune cells infiltration. Further experiments confirmed that SDCBP is highly expressed in macrophages, and knockdown of SDCBP in THP-1-derived macrophages reduces their chemotaxis but does not affect their polarization and phagocytic function. Our study indicated that SDCBP involves in tumor progression and macrophages infiltration, providing novel perspectives for cancer, particularly in combination with immunotherapy.

BACKGROUND:Gastric cancer invades local tissue extensively and metastasizes through the circulation to remote organs. Patients with metastasized gastric cancer have poor clinical outcomes. The vasculature in the cancer niche is developed poorly, thus allowing cancer cells to be released into the circulation. However, it is poorly understood how cancer cells adhere to and transmigrate through the fully developed endothelium in remote organs and what key adhesive ligands are involved in the process. Here, we report results from a study designed to investigate the role of hyperadhesive VWF (von Willebrand factor) in promoting the pulmonary metastasis of gastric cancer. METHODS:We used mouse models to investigate the roles of hyperadhesive VWF in the pulmonary metastasis of gastric cancer. The findings from these mouse models were validated through in vitro experiments that specifically examined how VWF promoted gastric cancer-derived extracellular vesicles to activate endothelial cells and analyzed established databases of patients with gastric cancer. RESULTS:VWF in cancer-bearing mice became hyperadhesive and mediated the adhesion of gastric cancer-derived extracellular vesicles to the endothelium, where gastric cancer-derived extracellular vesicles caused endothelial permeability and promoted the transmigration of cancer cells to the interstitial tissue of the lungs. Reducing VWF adhesive activity by the metalloprotease ADAMTS-13 (A disintegrin and metalloprotease with thrombospondin type motifs, type 13) prevented the pulmonary metastasis of gastric cancer cells in mice. We further validated the findings in mice through targeted in vitro experiments and by associating VWF with the outcomes of patients with gastric cancer through established databases of patients with gastric cancer using bioinformatics tools. CONCLUSIONS:We show how VWF becomes hyperadhesive to promote the pulmonary metastasis of gastric cancer through its interaction with gastric cancer-derived extracellular vesicles and that the hyperadhesive activity of VWF is reduced by ADAMTS-13 to prevent the metastasis.

To study the changes in the vertical and sagittal craniomaxillofacial morphology in Chinese adult patients with bilateral anterior temporomandibular joint(TMJ)disc displacement and to explore their correlation. This may provide valuable insights for clinical diagnosis and treatment planning. Ninety-eight Chinese adult patients were divided into 3 groups: 29 patients in bilateral disc Normal Position group (BN), 33 patients in bilateral Anterior Disc Displacement With Reduction group (ADDWR) and 36 patients in bilateral Anterior Disc Displacement Without Reduction group (ADDWoR). Uceph software was used to measure 6 items of occlusal plane and 13 items of craniomaxillofacial morphology for comparison and correlation analysis between groups. Compared to the BN group, subjects with anterior TMJ disc displacement (ADD) were more likely to exhibit a steeper posterior occlusal plane and an extended craniofacial posture with a Class II hyperdivergent pattern characteristics. Nevertheless, there were no statistically significant differences between the ADDWR and ADDWoR groups. The results of Pearson correlation analysis revealed a significant association between a steep occlusal plane in ADD patients and both skeletal mandibular retraction and vertical overgrowth. Chinese patients with anterior disc displacement of the TMJ have a steeper posterior occlusal plane and hyperdivergent skeletal Class II malocclusions tendency, which may be associated with occlusal function or condylar remodeling.

Gastric cancer is one of the most common malignant tumors in the world. The occurrence of chemotherapy resistance seriously affects the survival and prognosis of middle and advanced patients. Enhancing DNA repair ability is one of the important mechanisms of chemotherapy resistance. ADAM9, a member of the disintegrin and metalloproteinase family, is involved in many biological processes, such as tumor cells proliferation, apoptosis, invasion and migration, vascular invasion, and drug resistance. In this study, we found that the high expression of ADAM9 in gastric cancer tissues was associated with a variety of clinicopathological factors and poor prognosis in patients. Gastric cancer cells with high ADAM9 expression reduced sensitivity to Cisplatin, decreased DNA damage, increased expression of ATM and CHK2, the key proteins in DNA damage repair pathway, and improved cancer cells survival rate. Further studies showed that the expression of ADAM9 was selectively interfered with gastric cancer cells, the expression levels of ATM and CHK2 were decreased, while the expression of damage protein γ-H2AX was significantly increased, the degree of DNA damage was increased, and the sensitivity of gastric cancer cells to Cisplatin was significantly enhanced. It is suggested that ADAM9 is involved in Cisplatin resistance in gastric cancer cells, and its mechanism is related to the activation of ATM-CHK2 pathway in DNA damage repair. These data demonstrate that ADAM9 plays a pro-cancer role and mediates Cisplatin resistance in gastric cancer, which may be a new target to overcome chemotherapy resistance.

Extracellular vesicles (EVs) play a pivotal role in intercellular communication and are closely linked to cancer progression and metastasis. Our previous studies have shown that gastric cancer cell-derived EVs can promote tumor metastasis by increasing the permeability of the endothelial barrier. However, it remains unclear which effector molecule in the EV structure is the key factor of EV-mediated tumor metastasis and the underlying molecular mechanism. In this study, we found that CD147 is a key molecule highly expressed in gastric cancer-derived EVs and confirmed the role of CD147-high EVs from gastric cancer cells in promoting endothelial dysfunction and tumor metastasis. Our results showed that CD147-high EVs activated the VEGF/AKT/eNOS/NO and AKT/mTOR/p70S6K signaling pathways, leading to endothelial cytoskeletal reorganization and internalization of VE-cadherin, which significantly compromised endothelial barrier integrity, increased vascular leakage, enhanced transendothelial migration of tumor cell, and promoted the formation of metastatic tumors. Furthermore, detection of CD147 levels in gastric cancer tissues and plasma EVs indicated that high CD147 expression was associated with advanced tumor stage, poor prognosis, and reduced survival. Our findings suggest that CD147-high EVs are critical mediators of tumor-endothelial interactions and potential diagnostic and prognostic biomarkers for gastric cancer. Their potential as therapeutic targets for gastric cancer is underscored.

Gastric cancer remains a significant global health burden with limited treatment options and high mortality. Syndecan-binding protein (SDCBP), a scaffolding protein involved in tumor differentiation, has attracted attention as a potential therapeutic target in cancers. However, its precise role in gastric cancer progression is not fully understood. In this study, through bioinformatics analysis and gastric cancer samples detection, we discovered that SDCBP was highly expressed in gastric cancer tissues, which was correlated with clinicopathological features such as tumor invasion depth and distant metastasis, and exhibited heterogeneity across histological or molecular subtypes. Elevated SDCBP expression promoted the proliferation, invasion and migration of gastric cancer cells, and modulated epithelial-mesenchymal transition (EMT) via the ERK signaling pathway. Xenograft experiments in mice confirmed that inhibiting SDCBP or ERK signaling could delay cancer progression. We also found that gastric cancer cells with SDCBP knockdown were able to inhibit the M2 polarization of cocultured macrophages, reduce chemotaxis and enhance phagocytosis of macrophages. Therefore, SDCBP plays a crucial role in driving gastric cancer progression. Targeting SDCBP in gastric cancer can partially reverse the malignant phenotype, and SDCBP is expected to be a promising therapeutic target for gastric cancer.

BACKGROUND:Traumatic brain injury (TBI) induces endothelial injury (endotheliopathy) that disrupts the vascular barrier to cause cerebral hemorrhage and inflammation and allows the release of extracellular vesicles (EVs) from injured brain cells into the circulation. These EVs are highly procoagulant, causing a systemic hypercoagulable state that rapidly turns into consumptive coagulopathy. Protecting endothelial integrity and removing procoagulant EVs is, therefore, critical to preventing secondary cerebral and extracranial injuries from TBI. METHODS:We measured plasma Del-1 (developmental endothelial locus 1) levels in severe TBI mouse models and administered exogenous Del-1 pre-TBI or post-TBI to assess its effects on endotheliopathy, coagulopathy, and outcomes. Mechanistic studies involved administering exogenous Del-1 to TBI mice, followed by EV-scavenging analysis, and evaluating adhesion and apoptosis in Del-1-treated cultured endothelial cells, with key findings validated in both wild-type and Del-1-deficient mice. RESULTS:Plasma levels of Del-1 were reduced by 69% in mice subjected to severe TBI. Exogenous Del-1, given as either a preconditioning or a therapeutic agent, prevented mice with severe TBI from developing local and systemic endotheliopathy and coagulopathy, improving their outcomes. Del-1 protected TBI mice by scavenging anionic phospholipid-expressing EVs, including extracellular mitochondria from the circulation, by promoting endothelial cell adhesion and survival to protect endothelial integrity in wild-type and Del-1-deficient mice subjected to severe TBI. CONCLUSIONS:This study demonstrates the importance of reducing anionic phospholipid-expressing EVs for TBI resuscitation and identifies Del-1 as a potential therapeutic agent to reduce EV-induced endotheliopathy and coagulopathy.

Neurodegenerative diseases, mostly occurring in the elderly population, are the significant cause of disability and death worldwide. The pathogenesis of neurodegenerative diseases is still largely unknown yet, although they have been continuously explored. Thus, there is still a lack of safe, effective, and low side effect drugs in clinical practice for the treatment of neurodegenerative diseases. Pieces of accumulating evidence have demonstrated that licorice played neuroprotective roles in various neurodegenerative diseases. In the past two decades, increasing studies have indicated that glycyrrhizic acid (GL), the main active ingredient from traditional Chinese medicine licorice (widely used in the food industry) and a triterpenoid saponin with multiple pharmacological effects (such as anti-oxidant, anti-inflammatory, and immune regulation), and its metabolites (glycyrrhetinic acid and carbenoxolone) play a neuroprotective role in a range of neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Huntington's disease and epilepsy. This review will elaborate on the multiple neuroprotective mechanisms of GL and its metabolites in this series of diseases, aiming to provide a basis for further research on these protective drugs for neurodegenerative diseases and their clinical application. In summary, GL may be a promising candidate drug for the therapy of neurodegenerative diseases.

Considering the excellent properties such as deep tissue penetration, high signal-to-noise ratio, and in-situ recharge and reactivation, near-infrared luminescence long afterglow nanoparticles show considerable promise for biological application, especially in multifunctional imaging, targeting, and synergistic therapeutic. In this paper, Zn3Ga4GeO11: 0.1% Cr3+, 1% Yb3+, 0.1% Tm3+@Ag-FA (ZGGO@Ag-FA, ZGA-FA) nanoparticles were synthesized by in-situ growth of Ag nanoparticles on the surface of long afterglow nanoparticles, and further modified with folic acid. Through precise adjustments, the luminescent properties of ZnGa2O4 were enhanced and notably boosted the photothermal effect of Ag by leveraging the upconversion emission of ZGGO, with a photothermal conversion efficiency reaching about 59.9%. The ZGA-FA nanoparticles are ultra-small, measuring less than 50 nm. The modification with folic acid provides the ZGA-FA nanoparticles with excellent tumor-targeting capabilities, demonstrating effective enrichment and retention in tumor tissues, thus enabling long-term imaging and therapy through in vivo re-excitation. Due to its stable photothermal effect, outstanding near-infrared (NIR) afterglow imaging, and red-light charged characteristics, combined with effective tumor-targeting abilities, the therapeutic strategy proposed by this study has significant potential for clinical applications.

In patients with abdominal or pelvic tumors, radiotherapy can result in radiation-induced intestinal injury (RIII), a potentially severe complication for which there are few effective therapeutic options. Sitagliptin (SI) is an oral hypoglycemic drug that exhibits antiapoptotic, antioxidant, and anti-inflammatory activity, but how it influences RIII-associated outcomes has yet to be established. In this study, a pH-responsive metal-organic framework-based nanoparticle platform was developed for the delivery of SI (SI@ZIF-8@MS NP). These NPs incorporated mPEG-b-PLLA (MS) as an agent capable of resisting the effects of gastric acid, and are capable of releasing Zn2+ ions. MS was able to effectively shield these SI@ZIF-8 NPs from rapid degradation when exposed to an acidic environment, enabling the subsequent release of SI and Zn2+ within the intestinal fluid. Notably, SI@ZIF-8@MS treatment was able to mitigate radiation-induced intestinal dysbiosis in these mice. restored radiation-induced changes in bacterial composition. In summary, these data demonstrate the ability of SI@ZIF-8@MS to protect against WAI-induced intestinal damage in mice, suggesting that these NPs represent a multimodal targeted therapy that can effectively be used in the prevention or treatment of RIII.

The aim of this study was to examine the effect of a positive emotion-based exercise intervention on quality of life (QOL), fatigue, and mental health status in patients with lung cancer undergoing chemotherapy. A total of 80 patients with lung cancer undergoing chemotherapy were selected and divided into an observation group and a control group, with 40 patients in each group. Patients in the control group received routine care and were educated about the benefits of exercise, while patients in the experimental group received an additional exercise intervention based on positive emotions. We assessed patients' quality of life, fatigue, and mental health at the time of recruitment and 12 weeks after the exercise intervention. After the intervention, patients in the experimental group had a higher overall QOL score than those in the control group, with statistically significant differences in body, role, and emotions (p < .05). After the intervention, patients in the experimental group had less fatigue than those in the control group, with statistical differences between the two groups (p = .047). After the intervention, patients in the experimental group had lower scores in depression (p = .008) and anxiety (p = .245) than those in the control group. We found that patients with lung cancer receiving chemotherapy benefited from an exercise intervention based on positive emotions in terms of improvements in quality of life, fatigue, and mental health status.

ABSTRACT Cells of gastric cancer invade local tissue extensively and also metastasize through the circulation to remote organs. Patients with metastasized gastric cancer have poor outcomes. Cancer cells are known to release extracellular vesicles (EVs) that contribute to cancer progression, but how cancer cell-derived EVs promote cancer growth and metastasis remains poorly understood. We have recently reported that levels of circulating gastric cancer cell-derived EVs (gcEVs) and the adhesive ligand von Willebrand factor (VWF) are associated with cancer metastasis and poor prognosis of patients, but the underlying mechanism of this gcEV-VWF interaction was not known. Here we report results from a study designed to investigate the synergistic action of VWF and gcEVs in vitro and in mouse models. We showed that VWF in cancer-bearing mice was hyperadhesive and became microvesicle-bound. EV-bound VWF mediated the adhesion of gcEVs to the endothelium to disrupt endothelial integrity and facilitate the transendothelial migration of cancer cells and pulmonary metastasis. Reducing VWF adhesive activity by the metalloprotease ADAMTS-13 or promoting gcEV clearance by the scavenging factor lactadherin prevented pulmonary metastasis in mice. These results highlight the synergistic action of gcEVs and VWF in promoting gastric cancer metastasis and identifying new targets for its prevention. Key point: Author contributions Hyperadhesive VWF becomes microvesicle-bound to induce endothelial leakage and promote the pulmonary metastasis of gastric cancer in mice. Reducing VWF activity by ADAMTS-13 and accelerating microvesicle clearance by lactadherin reduces pulmonary metastasis of gastric cancer.

Persistent luminescence nanoparticle scintillators (PLNS) have been attempted for X-ray-induced photodynamic therapy (X-PDT) because persistent luminescence after ceasing radiation can make PLNS use less cumulative irradiation time and dose to generate the same amount of reactive oxygen species (ROS) compared with conventional scintillators to combat cancer cells. However, excessive surface defects in PLNS reduce the luminescence efficiency and quench the persistent luminescence, which is fatal to the efficacy of X-PDT. Herein, the PLNS of SiO2@Zn2SiO4:Mn2+, Yb3+, Li+ was designed by the energy trap engineering and synthesized by a simple template method, which has excellent X-ray and UV-excited persistent luminescence and continuously tunable emission spectra from 520 to 550 nm. Its luminescence intensity and afterglow time are more than 7 times that of the reported Zn2SiO4:Mn2+ used for X-PDT. By loading a Rose Bengal (RB) photosensitizer, an effective persistent energy transfer from the PLNS to photosensitizer is observed even after the removal of X-ray irradiation. The X-ray dose of nanoplatform SiO2@Zn2SiO4:Mn2+, Yb3+, Li+@RB in X-PDT of HeLa cancer cells was reduced to 0.18 Gy compared to the X-ray dose of 1.0 Gy for Zn2SiO4:Mn for X-PDT. This indicates that the Zn2SiO4:Mn2+, Yb3+, Li+ PLNS have great potential for X-PDT applications.

Background Coughing caused by tracheal extubation is common following general anaesthesia. Heavy aerosol production by coughing during recovery from general anaesthesia in patients with respiratory infections (especially COVID-19) may be one of the highest risk factors for infection in healthcare workers. The application of local anaesthetics to the endotracheal tube is an effective method to reduce coughing. The most commonly used anaesthetics are compound lidocaine/prilocaine cream and tetracaine spray. However, coughing still occurs when the two anaesthetics are used alone. We speculated that the application of compound lidocaine/prilocaine combined with tetracaine spray would better prevent coughing caused by tracheal extubation. Methods Patients scheduled for laparoscopic cholecystectomy or cholecystectomy combined with common bile duct exploration under general anaesthesia were randomly assigned to Group C (saline spray), Group L (2 g compound lidocaine/prilocaine cream contains 5 mg of lidocaine and 5 mg prilocaine)), Group T (tetracaine) and Group F (compound lidocaine/prilocaine cream combined with tetracaine). The incidence of coughing, the endotracheal tube tolerance assessment, the incidence of agitation, the active extubation rate, the incidence of postoperative pharyngeal pain and the incidence of postoperative cough were recorded and analysed. Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), and the plasma concentrations of epinephrine and norepinephrine were measured immediately before extubation and 1 min after extubation. Results A total of 211 patients were randomly assigned to Group C (53 cases), Group L (52 cases), Group T (52 cases) and Group F (54 cases). The primary result is assessment of the incidence of cough. The patients emerged from general anaesthesia, 96% of Group C had cough, which was significantly reduced in Group L (61.5%, P < 0.001), Group T (75%, P < 0.05) and Group F (22.2%, P < 0.001). Group F had a significantly reduced incidence of cough compared to Group L and Group T ( P < 0.05 or P < 0.01, respectively). The secondary results were assessed. The endotracheal tube tolerance score in Group C ((1, 3) 4, P < 0.001) was higher than Group L ((0, 1) 2), Group T ((0, 1.25) 3) and Group F ((0, 0) 1). Group F had a significantly lower score than Group L and Group T ( P < 0.05, P < 0.01, respectively). The incidence of agitation and the active extubation rate were also higher in Group C (96.2% and 71.7%, respectively, P < 0.001) than Group L (48.1% and 15.4%, respectively), Group T (61.5% and 26.9%, respectively) and Group F (17.3% and 7.7%, respectively). Blood pressure, HR and plasma concentrations of epinephrine and norepinephrine were significantly higher in Group C than in all other groups at the time of extubation and 1 min after extubation ( P < 0.001). Group F exhibited significantly reduced blood pressure, heart rate and plasma concentrations of epinephrine and norepinephrine compared to Group L and Group T ( P < 0.05, P < 0.01 or P < 0.001, respectively). The incidence of postoperative pharyngeal pain and the incidence of postoperative cough were not significantly different among the groups. Conclusions Compound lidocaine/prilocaine cream combined with tetracaine may be a more effective approach for preventing coughing and stabilising circulation during extubation following general anaesthesia. This may play an important role in preventing medical staff from contracting respiratory infectious diseases. Trial registration Chinese Clinical Trial Registry: ChiCTR2200058429 (registration date: 09–04-2022) “retrospectively registered”.

铁死亡是一种不同于自噬、凋亡和坏死的新型细胞死亡方式,通过细胞铁过载和脂质过氧化启动.近年来,越来越多的研究探索铁死亡相关机制在卵巢癌中的作用,发现改变卵巢癌细胞内铁和脂质的代谢,以及P53、Yes相关蛋白(Yes-associated protein,YAP)和基于PDZ结合基序的转录共激活因子(transcriptional co-activator with PDZ-binding motif,TAZ)的表达可以调控癌细胞铁死亡,进而影响卵巢癌进展.研究还证实铁死亡不仅可以提高卵巢癌细胞对铂类药物的敏感性,增强化疗效果,而且可以改善卵巢癌细胞对多腺苷二磷酸核糖聚合酶[poly(ADP-ribose)polymerase,PARP]抑制剂的耐药性,提高卵巢癌患者PARP抑制剂治疗的临床获益,而PARP抑制剂与免疫治疗又能促进卵巢癌细胞铁死亡,表明铁死亡与化疗、PARP抑制剂和免疫治疗在抑制卵巢癌细胞生长方面具有协同作用,铁死亡可能成为未来卵巢癌治疗的一个新靶点.