Metal Ruthenium Complexes Treat Spinal Cord Injury By Alleviating Oxidative Stress Through Interaction With Antioxidant 1 Copper Chaperone Protein.

Oxidative stress is a major factor affecting spinal cord injury (SCI) prognosis. A ruthenium metal complex can aid in treating SCI by scavenging reactive oxygen species via a protein-regulated mechanism to alleviate oxidative stress. This study aimed to introduce a pioneering strategy for SCI treatment by designing two novel half-sandwich ruthenium (II) complexes containing diverse N^N-chelating ligands. The general formula is [(η6-Arene)Ru(N^N)Cl]PF6, where arene is either 2-phenylethanol-1-ol (bz-EA) or 3-phenylpropanol-1-ol (bz-PA), and the N^N-chelating ligands are fluorine-based imino-pyridyl ligands. This study shows that these ruthenium metal complexes protect neurons by scavenging reactive oxygen species. Notably, η6-Arene substitution from bz-PA to bz-EA significantly enhances reactive oxygen species scavenging ability and neuroprotective effect. Additionally, molecular dynamics simulations indicate that the ruthenium metal complex increases Antioxidant 1 Copper Chaperone protein expression, reduces oxidative stress, and protects neurons during SCI treatment. Furthermore, ruthenium metal complex protected spinal cord neurons and stimulated their regeneration, which improves electrical signals and motor functions in mice with SCI. Thus, this treatment strategy using ruthenium metal complexes can be a new therapeutic approach for the efficient treatment of SCI.

Curcumin/pEGCG-encapsulated nanoparticles enhance spinal cord injury recovery by regulating CD74 to alleviate oxidative stress and inflammation.

Spinal cord injury (SCI) often accompanies impairment of motor function, yet there is currently no highly effective treatment method specifically for this condition. Oxidative stress and inflammation are pivotal factors contributing to severe neurological deficits after SCI. In this study, a type of curcumin (Cur) nanoparticle (HA-CurNPs) was developed to address this challenge by alleviating oxidative stress and inflammation. Through non-covalent interactions, curcumin (Cur) and poly (-)-epigallocatechin-3-gallate (pEGCG) are co-encapsulated within hyaluronic acid (HA), resulting in nanoparticles termed HA-CurNPs. These nanoparticles gradually release curcumin and pEGCG at the SCI site. The released pEGCG and curcumin not only scavenge reactive oxygen species (ROS) and prevents apoptosis, thereby improving the neuronal microenvironment, but also regulate CD74 to promote microglial polarization toward an M2 phenotype, and inhibits M1 polarization, thereby suppressing the inflammatory response and fostering neuronal regeneration. Moreover, in vivo experiments on SCI mice demonstrate that HA-CurNPs effectively protect neuronal cells and myelin, reduce glial scar formation, thereby facilitating the repair of damaged spinal cord tissues, restoring electrical signaling at the injury site, and improving motor functions. Overall, this study demonstrates that HA-CurNPs significantly reduce oxidative stress and inflammation following SCI, markedly improving motor function in SCI mice. This provides a promising therapeutic approach for the treatment of SCI.

Association of hemoglobin-to-red blood cell distribution width ratio and bone mineral density in older adults.

BACKGROUND: Hemoglobin-to-Red Cell Distribution Width Ratio (HRR) represents novel prognostic markers for diseases. However, there remains a lack of systematic research into the relationship between HRR and Bone Mineral Density (BMD) or osteoporosis in older adults. METHODS: This study utilized information from the NHANES database, selecting individuals over 50 years of age with complete femoral DXA scans and full blood counts. The relationship between HRR and femoral BMD was investigated using weighted linear models and restricted cubic spline (RCS) models. Moreover, the association between HRR and osteoporosis was further explored using logistic regression models and RCS models, with subgroup analysis conducted to test the robustness of the results. RESULTS: This study included a total of 7,149 participants, and the BMD of the group with higher HRR was significantly greater than that of the group with lower HRR. Weighted linear regression analysis found a linear positive correlation between HRR and femoral BMD. When HRR was converted from a continuous variable to a categorical variable, this relationship remained stable. In addition, multivariate logistic regression analysis showed that for each 1-unit increase in HRR, the prevalence of osteoporosis significantly decreased (OR = 0.25, 95% CI: 0.12-0.51), further confirming the findings of this study. Subgroup analysis showed that this association was not significantly affected by confounding factors across different populations. CONCLUSION: HRR may serve as one of the potential indicators for evaluating BMD and assessing the prevalence of osteoporosis in the elderly. Elevating HRR levels may play a crucial role in the prevention and slowing of osteoporosis progression.

Identification of potential biomarkers for lung adenocarcinoma: a study based on bioinformatics analysis combined with validation experiments.

Background: The prognosis for lung adenocarcinoma (LUAD) remains dismal, with a 5-year survival rate of <20%. Therefore, the purpose of this study was to identify potentially reliable biomarkers in LUAD by machine learning combination with Mendelian randomization (MR). Methods: TCGA-LUAD, GSE40791, and GSE31210 were employed this study. Key module differential genes were identified through differentially expressed analysis and weighted gene co-expression network analysis (WGCNA). Furthermore, candidate biomarkers were derived from protein-protein interaction network (PPI) and machine learning. Ultimately, biomarkers were confirmed using MR analysis. In addition, immunohistochemistry was used to detect the expression levels of genes that have a causal relationship to LUAD in the LUAD group and the control group. Cell experiments were conducted to validate the effect of screening genes on proliferation, migration, and apoptosis of LUAD cells. The correlation between the screened genes and immune infiltration was determined by CIBERSORT algorithm. In the end, the gene-related drugs were predicted through the Drug-Gene Interaction database. Results: In total, 401 key module differential genes were obtained by intersecting of 5,702 differentially expressed genes (DEGs) and 406 key module genes. Thereafter, GIMAP6, CAV1, PECAM1, and TGFBR2 were identified. Among them, only TGFBR2 had a significant causal relationship with LUAD (p=0.04, b=-0.06), and it is a protective factor for LUAD. Subsequently, sensitivity analyses showed that there were no heterogeneity and horizontal pleiotropy in the univariate MR results, and the results were not overly sensitive to individual SNP loci, further validating the reliability of univariate Mendelian randomization (UVMR) results. However, no causal relationship was found between them by reverse MR analysis. Meanwhile, TGFBR2 expression was decreased in LUAD group through immunohistochemistry. TGFBR2 can inhibit proliferation and migration of lung adenocarcinoma cell line A549 and promote apoptosis of A549 cells. Immune infiltration analysis suggested a potential link between TGFBR2 expression and immune infiltration. Finally, Irinotecan and Hesperetin were predicted through DGIDB database. Conclusion: In this study, TGFBR2 was identified as a biomarker of LUAD, which provided a new idea for the treatment strategy of LUAD and may aid in the development of personalized immunotherapy strategies.

Scorpiones, Scolopendra and Gekko Inhibit Lung Cancer Growth and Metastasis by Ameliorating Hypoxic Tumor Microenvironment via PI3K/AKT/mTOR/HIF-1α Signaling Pathway.

OBJECTIVE: To investigate whether Buthus martensii karsch (Scorpiones), Scolopendra subspinipes mutilans L. Koch (Scolopendra) and Gekko gecko Linnaeus (Gekko) could ameliorate the hypoxic tumor microenvironment and inhibit lung cancer growth and metastasis by regulating phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin/hypoxia-inducible factor-1α (PI3K/AKT/mTOR/HIF-1α) signaling pathway. METHODS: Male C57BL/6J mice were inoculated with luciferase labeled LL/2-luc-M38 cell suspension to develop lung cancer models, with rapamycin and cyclophosphamide as positive controls. Carboxy methyl cellulose solutions of Scorpiones, Scolopendra and Gekko were administered intragastrically as 0.33, 0.33, and 0.83 g/kg, respectively once daily for 21 days. Fluorescent expression were detected every 7 days after inoculation, and tumor growth curves were plotted. Immunohistochemistry was performed to determine CD31 and HIF-1α expressions in tumor tissue and microvessel density (MVD) was analyzed. Western blot was performed to detect the expression of PI3K/AKT/mTOR/HIF-1α signaling pathway-related proteins. Enzyme-linked immunosorbent assay was performed to detect serum basic fibroblast growth factor (bFGF), transforming growth factor-ß1 (TGF-ß1) and vascular endothelial growth factor (VEGF) in mice. RESULTS: Scorpiones, Scolopendra and Gekko prolonged the survival time and inhibited lung cancer metastasis and expression of HIF-1α (all P<0.01). Moreover, Scorpiones, Scolopendra and Gekko inhibited the phosphorylation of AKT and ribosomal protein S6 kinase (p70S6K) (P<0.05 or P<0.01). In addition, they also decreased the expression of CD31, MVD, bFGF, TGF-ß1 and VEGF compared with the model group (P<0.05 or P<0.01). CONCLUSION: Scorpiones, Scolopendra and Gekko all showed beneficial effects on lung cancer by ameliorating the hypoxic tumor microenvironment via PI3K/AKT/mTOR/HIF-1α signaling pathway.

Sleeping more than 8 h: a silent factor contributing to decreased muscle mass in Chinese community-dwelling older adults.

BACKGROUND: Muscle mass loss is an age-related process that can be exacerbated by lifestyle, environmental and other factors, but can be mitigated by good sleep. The objective of this study was to investigate the correlation between varying time lags of sleep duration and the decline in muscle mass among individuals aged 60 years or older by using real-world health monitoring data obtained from wearable devices and smart home health monitoring devices. METHODS: This study included 86,037 observations from 2,869 participants in the Mobile Support System database. Missing data were supplemented by multiple imputation. The investigation utilized generalized estimating equations and restricted cubic spline curve to examine the relationship between sleep duration and low muscle mass. Various lag structures, including 0, 1, 2, 0-1, 0-2, and 1-2 months, were fitted, and the interaction effect of observation time with sleep duration was estimated for each lag structure. Additionally, subgroup analyses were conducted. The models were adjusted for various covariates, including gender, age, body mass index, footsteps, smoking status, drinking status, marital status, number of chronic diseases, number of medications, diabetes mellitus, hyperlipidemia, coronary artery disease, respiratory disease, and musculoskeletal disease and an interaction term between time and sleep duration. RESULTS: The results of the generalized estimating equation showed a significant correlation (p < 0.001) between sleep duration of 8 h or more and low muscle mass in older adults, using 6-7 h of sleep as a reference. This effect was seen over time and prolonged sleep accumulated over multiple months had a greater effect on muscle mass loss than a single month. The effect of long sleep duration on muscle mass loss was significantly greater in females than in males and greater in the over-75 than in the under-75 age group. Restricted cubic spline plots showed a non-linear relationship between sleep duration and low muscle mass (p < 0.001). CONCLUSIONS: This study found an association between sustained nighttime sleep of more than eight hours and decreased muscle mass in older adults, especially older women.

Neoadjuvant chemo-immunotherapy with camrelizumab plus nab-paclitaxel and cisplatin in resectable locally advanced squamous cell carcinoma of the head and neck: a pilot phase II trial.

Neoadjuvant chemoimmunotherapy has emerged as a potential treatment option for resectable head and neck squamous cell carcinoma (HNSCC). In this single-arm phase II trial (NCT04826679), patients with resectable locally advanced HNSCC (T2‒T4, N0‒N3b, M0) received neoadjuvant chemoimmunotherapy with camrelizumab (200 mg), nab-paclitaxel (260 mg/m2), and cisplatin (60 mg/m2) intravenously on day one of each three-week cycle for three cycles. The primary endpoint was the objective response rate (ORR). Secondary endpoints included pathologic complete response (pCR), major pathologic response (MPR), two-year progression-free survival rate, two-year overall survival rate, and toxicities. Here, we report the perioperative outcomes; survival outcomes were not mature at the time of data analysis. Between April 19, 2021 and March 17, 2022, 48 patients were enrolled and received neoadjuvant therapy, 27 of whom proceeded to surgical resection and remaining 21 received non-surgical therapy. The ORR was 89.6% (95% CI: 80.9, 98.2) among 48 patients who completed neoadjuvant therapy. Of the 27 patients who underwent surgery, 17 (63.0%, 95% CI: 44.7, 81.2) achieved a MPR or pCR, with a pCR rate of 55.6% (95% CI: 36.8, 74.3). Treatment-related adverse events of grade 3 or 4 occurred in two patients. This study meets the primary endpoint showing potential efficacy of neoadjuvant camrelizumab plus nab-paclitaxel and cisplatin, with an acceptable safety profile, in patients with resectable locally advanced HNSCC.

The Interaction between ADK and SCG10 Regulate the Repair of Nerve Damage.

The cytoskeleton must be remodeled during neurite outgrowth, and Superior Cervical Ganglion 10 (SCG10) plays a critical role in this process by depolymerizing Microtubules (MTs), conferring highly dynamic properties to the MTs. However, the precise mechanism of action of SCG10 in the repair of injured neurons remains largely uncertain. Using transcriptomic identification, we discovered that SCG10 expression was downregulated in neurons after Spinal Cord Injury (SCI). Additionally, through mass spectrometry identification, immunoprecipitation, and pull-down assays, we established that SCG10 could interact with Adenosine Kinase (ADK). Furthermore, we developed an excitotoxicity-induced neural injury model and discovered that ADK suppressed injured neurite re-growth, whereas, through overexpression and small molecule interference experiments, SCG10 enhanced it. Moreover, we discovered ADK to be the upstream of SCG10. More importantly, the application of the ADK inhibitor called 5-Iodotubercidin (5-ITu) was found to significantly enhance the recovery of motor function in mice with SCI. Consequently, our findings suggest that ADK plays a negative regulatory role in the repair of injured neurons. Herein, we propose a molecular interaction model of the SCG10-ADK axis to regulate neuronal recovery.

Automated Impactor for Contusive Spinal Cord Injury Model in Mice.

Spinal cord injury (SCI) due to traumatic injuries such as car accidents and falls is associated with permanent spinal cord dysfunction. Creation of contusion models of spinal cord injury by impacting the spinal cord results in similar pathologies to most spinal cord injuries in clinical practice. Accurate, reproducible, and convenient animal models of spinal cord injury are essential for studying spinal cord injury. We present a novel automated spinal cord injury contusion device for mice, the Guangzhou Jinan University smart spinal cord injury system, that can produce spinal cord injury contusion models with accuracy, reproducibility, and convenience. The system accurately produces models of varying degrees of spinal cord injury via laser distance sensors combined with an automated mobile platform and advanced software. We used this system to create three levels of spinal cord injury mice models, determined their Basso mouse scale (BMS) scores, and performed behavioral as well as staining assays to demonstrate its accuracy and reproducibility. We show each step of the development of the injury models using this device, forming a standardized procedure. This method produces reproducible spinal cord injury contusion mice models and reduces human manipulation factors via convenient handling procedures. The developed animal model is reliable for studying spinal cord injury mechanisms and associated treatment approaches.

14-3-3 protein augments the protein stability of phosphorylated spastin and promotes the recovery of spinal cord injury through its agonist intervention.

Axon regeneration is abortive in the central nervous system following injury. Orchestrating microtubule dynamics has emerged as a promising approach to improve axonal regeneration. The microtubule severing enzyme spastin is essential for axonal development and regeneration through remodeling of microtubule arrangement. To date, however, little is known regarding the mechanisms underlying spastin action in neural regeneration after spinal cord injury. Here, we use glutathione transferase pulldown and immunoprecipitation assays to demonstrate that 14-3-3 interacts with spastin, both in vivo and in vitro, via spastin Ser233 phosphorylation. Moreover, we show that 14-3-3 protects spastin from degradation by inhibiting the ubiquitination pathway and upregulates the spastin-dependent severing ability. Furthermore, the 14-3-3 agonist Fusicoccin (FC-A) promotes neurite outgrowth and regeneration in vitro which needs spastin activation. Western blot and immunofluorescence results revealed that 14-3-3 protein is upregulated in the neuronal compartment after spinal cord injury in vivo. In addition, administration of FC-A not only promotes locomotor recovery, but also nerve regeneration following spinal cord injury in both contusion and lateral hemisection models; however, the application of spastin inhibitor spastazoline successfully reverses these phenomena. Taken together, these results indicate that 14-3-3 is a molecular switch that regulates spastin protein levels, and the small molecule 14-3-3 agonist FC-A effectively mediates the recovery of spinal cord injury in mice which requires spastin participation.

Engineered Multifunctional Zinc-Organic Framework-Based Aggregation-Induced Emission Nanozyme for Accelerating Spinal Cord Injury Recovery.

Functional recovery following a spinal cord injury (SCI) is challenging. Traditional drug therapies focus on the suppression of immune responses; however, strategies for alleviating oxidative stress are lacking. Herein, we developed the zinc-organic framework (Zn@MOF)-based aggregation-induced emission-active nanozymes for accelerating recovery following SCI. A multifunctional Zn@MOF was modified with the aggregation-induced emission-active molecule 2-(4-azidobutyl)-6-(phenyl(4-(1,2,2-triphenylvinyl)phenyl)amino)-1H-phenalene-1,3-dione via a bioorthogonal reaction, and the resulting nanozymes were denoted as Zn@MOF-TPD. These nanozymes gradually released gallic acid and zinc ions (Zn2+) at the SCI site. The released gallic acid, a scavenger of reactive oxygen species (ROS), promoted antioxidation and alleviated inflammation, re-establishing the balance between ROS production and the antioxidant defense system. The released Zn2+ ions inhibited the activity of matrix metalloproteinase 9 (MMP-9) to facilitate the regeneration of neurons via the ROS-mediated NF-κB pathway following secondary SCI. In addition, Zn@MOF-TPD protected neurons and myelin sheaths against trauma, inhibited glial scar formation, and promoted the proliferation and differentiation of neural stem cells, thereby facilitating the repair of neurons and injured spinal cord tissue and promoting functional recovery in rats with contusive SCI. Altogether, this study suggests that Zn@MOF-TPD nanozymes possess a potential for alleviating oxidative stress-mediated pathophysiological damage and promoting motor recovery following SCI.

Inhibition of spastin impairs motor function recovery after spinal cord injury.

Promoting axonal regeneration is an effective strategy for recovery from traumatic spinal cord injury (SCI). Spastin, a microtubule-severing protein, modulates axonal outgrowth and branch formation by regulating microtubule dynamics. However, the exact role of spastin during recovery from SCI remains unknown. Therefore, we utilized a hemisection injury model of the mouse spinal cord and explored the effect of spastin using a spastin inhibitor, spastazoline. Results showed that spastazoline significantly suppressed the microtubule-severing activity of spastin in COS-7 cells and inhibited the promoting effect of spastin on neurite outgrowth in primarily cultured hippocampal neurons. The protein expression level of spastin was significantly upregulated in the injured spinal cord. Injured mice showed impaired motor functions, which included increased toe-off angle and foot fault steps and decreased stride length and Basso mouse scale score. Notably, these motor function impairments were aggravated by the application of spastazoline. Inhibition of spastin exacerbated neurogenesis impairment, as demonstrated by neuronal nuclei antigen staining, the inflammatory response, as shown by Iba-1 and GFAP staining, and axonal regeneration impairment, as shown by 5-hydroxytryptamine staining. Furthermore, mass spectrometry analysis revealed that the inhibition of spastin resulted in numerous dysregulated differentially expressed proteins that were closely associated with vesicle organization and transport. Taken together, our data suggest that spastin is critical for recovery from SCI and may be a potential target for the treatment of SCI.

Iridium metal complex targeting oxidation resistance 1 protein attenuates spinal cord injury by inhibiting oxidative stress-associated reactive oxygen species.

Oxidative stress is a key factor leading to profound neurological deficits following spinal cord injury (SCI). In this study, we present the development and potential application of an iridium (iii) complex, (CpxbiPh) Ir (N^N) Cl, where CpxbiPh represents 1-biphenyl-2,3,4,5-tetramethyl cyclopentadienyl, and N^N denotes 2-(3-(4-nitrophenyl)-1H-1,2,4-triazol-5-yl) pyridine chelating agents, to address this challenge through a mechanism governed by the regulation of an antioxidant protein. This iridium complex, IrPHtz, can modulate the Oxidation Resistance 1 (OXR1) protein levels within spinal cord tissues, thus showcasing its antioxidative potential. By eliminating reactive oxygen species (ROS) and preventing apoptosis, the IrPHtz demonstrated neuroprotective and neural healing characteristics on injured neurons. Our molecular docking analysis unveiled the presence of π stacking within the IrPHtz-OXR1 complex, an interaction that enhanced OXR1 expression, subsequently diminishing oxidative stress, thwarting neuroinflammation, and averting neuronal apoptosis. Furthermore, in in vivo experimentation with SCI-afflicted mice, IrPHtz was efficacious in shielding spinal cord neurons, promoting their regrowth, restoring electrical signaling, and improving motor performance. Collectively, these findings underscore the potential of employing the iridium metal complex in a novel, protein-regulated antioxidant strategy, presenting a promising avenue for therapeutic intervention in SCI.

Compound Kushen Injection Reduces Severe Toxicity and Symptom Burden Associated With Curative Radiotherapy in Patients With Lung Cancer.

BACKGROUND: Radiotherapy (RT) causes adverse events for which there are no effective treatments. This study investigated the clinical benefits of compound Kushen injection (CKI) in managing radiation injury in patients with lung cancer. METHODS: A multicenter, open-label, randomized clinical trial randomly assigned patients with lung cancer to receive either CKI (20 mL/d for at least 4 weeks) integrated with curative RT (RT + CKI group; n=130) or RT alone (control group; n=130). The primary outcome was the incidence of grade ≥2 radiation-induced lung injury (RILI) in the lungs, esophagus, or heart. Secondary outcomes included patient-reported symptoms, quality of life, objective response rate (ORR), and toxic effects. RESULTS: During the 16-week trial, the RT + CKI group had a significantly lower incidence of grade ≥2 RT-related injury than the control group (12.3% [n=16] vs 23.1% [n=30]; P=.02). Compared with the control group, the RT + CKI group experienced a significant decrease in moderate-to-severe symptoms of fatigue, cough, and pain (P<.001 for the treatment and time interaction term); significantly less physical symptom interference (P=.01); and significantly better quality of life by the end of the trial (P<.05). No statistically significant difference in ORR was found. Adverse reactions associated with CKI were rare. CONCLUSIONS: This study demonstrated low toxicity of CKI and its effectiveness in patients with lung cancer in reducing the incidence of grade ≥2 RILI and symptom burden, improving patients' quality of life.

Molecular subtypes based on DNA sensors predict prognosis and tumor immunophenotype in hepatocellular carcinoma.

DNA sensors play crucial roles in inflammation and have been indicated to be involved in antitumor or tumorigenesis, while it is still unclear whether DNA sensors have potential roles in the prognosis and immunotherapy of hepatocellular carcinoma (HCC). Herein, The Cancer Genome Atlas and Gene Expression Omnibus databases were used to analyze RNA sequencing data and clinical information. A total of 14 DNA sensors were collected and performed consensus clustering to determine their molecular mechanisms in HCC. Two distinct molecular subtypes (Clusters C1 and C2) were identified and were associated with different overall survival (OS). Immune subtype analysis revealed that C1 was mainly characterized by inflammation, while C2 was characterized by lymphocyte depletion. Immune scoring and immunomodulatory function analysis confirmed the different immune microenvironment of C1 and C2. Notably, significant differences in "Hot Tumor" Immunophenotype were observed between the two subtypes. Moreover, the prognostic model based on DNA sensors is capable of effectively predicting the OS of HCC patients. Besides, the chemotherapeutic drug analysis showed the different sensitivity of two subtypes. Taken together, our study shows that the proposed DNA sensors were a reliable signature to predict the prognosis and immunotherapy response with potential application in the clinical decision and treatment of HCC.

Publication trends and hotspots of colorectal adenoma during 2002-2022: a bibliometric and visualized analysis.

Background: Prevention and treatment of colorectal adenoma (CRA) are great significant to reduce morbidity and mortality of colorectal cancer. Although there have been numerous studies on CRA recently, few publications utilized the bibliometrics to evaluate this field. The objective of current study was to provide a comprehensive analysis of the current state and frontier progress of CRA over the past 20 years. Methods: The Web of Science Core Collection was utilized to extracted all studies of CRA during 2002-2022. Bibliometric tools including CiteSpace, VOSviewer, and the Online Analysis Platform of Literature Metrology were used for statistical analysis. CiteSpace and the Online Analysis Platform were used to evaluate the contributions of various countries/regions, institutions, authors, and journals in this field. Research hotspots and trends were identified through keywords and references analysis by VOSviewer and CiteSpace. Results: 2,268 publications from 2002 to 2022 in total were identified. The number of global publications in this field has increased annually. The USA was the most productive country, contributing nearly 30% of global publications. But in recent years, China's publications grew rapidly and had the highest citation strength. The most productive institutions was the National Cancer Institute. Baron JA from the USA was the most productive and the one of most co-cited authors. Cancer Epidemiology Biomarkers & Prevention had the highest number of publications and Gastroenterology was the most co-cited journals. Analysis of keywords clusters showed that "mechanism/pathophysiology", "risk factors and prevention", "colonoscopy screening and treatment", "metabolism", and "microbiota" were the major frontier topics and the main research directions. Conclusions: CRA publications have shown a gradual upward trend in recent years, most of which have been published by developed countries. Developing countries should further focus on CRA research and transnational cooperation with developed countries in the future, in order to better improve the situation of the increasing morbidity and mortality of CRC. Baron JA was the most outstanding researcher in this field. More attention should be devoted to "pathogenesis of CRA", "less invasive diagnostic methods", "chemoprevention", and "screening and risk prediction of CRA including gut microbiome and metabolism", which will be frontiers in the future.

Lifestyles and the risk of an asthma attack in adult asthma patients: a cross-sectional study using NHANES database.

BACKGROUND: The influence of physical activity, diet and sleep on asthma has been well documented by recent studies respectively. However, few studies focus on the relationship between asthma attack and the overall lifestyle, which comprises interrelated lifestyle factors. This study aims to investigate the influence of lifestyles on the ratio of asthma attack. Data were extracted from the NHANES database (2017 to May 2020). METHODS: A total of 834 asthmatic patients were enrolled and divided into non-asthma attack (N.=460) and asthma attack (N.=374) groups. The risk factors for asthma attacks were preliminarily identified by univariate logistic analysis, then multivariate logistic analysis was employed to select independent risk factors other than lifestyles and further determine the association between lifestyles and asthma attacks. RESULTS: After multivariate logistic analysis, engagement of vigorous activity (Model 1 P=0.010, Model 2 P=0.016, Model 3 P=0.012), engagement of moderate activity (Model 1 P=0.006, Model 2 P=0.008, Model 3 P=0.003) and sleep disorder (Model1 P=0.001, Model 2 P<0.001, Model 3 P=0.008) were determined as independent risk factors of lifestyles for an asthma attack in the past year. CONCLUSIONS: This research documented that, for asthmatic patients, engagement of vigorous activity, engagement of moderate activity, and sleep disorder will make an asthma attack more likely to happen.

Emergency Treatment and Photoacoustic Assessment of Spinal Cord Injury Using Reversible Dual-Signal Transform-Based Selenium Antioxidant.

Spinal cord injury (SCI), following explosive oxidative stress, causes an abrupt and irreversible pathological deterioration of the central nervous system. Thus, preventing secondary injuries caused by reactive oxygen species (ROS), as well as monitoring and assessing the recovery from SCI are critical for the emergency treatment of SCI. Herein, an emergency treatment strategy is developed for SCI based on the selenium (Se) matrix antioxidant system to effectively inhibit oxidative stress-induced damage and simultaneously real-time evaluate the severity of SCI using a reversible dual-photoacoustic signal (680 and 750 nm). Within the emergency treatment and photoacoustic severity assessment (ETPSA) strategy, the designed Se loaded boron dipyrromethene dye with a double hydroxyl group (Se@BDP-DOH) is simultaneously used as a sensitive reporter group and an excellent antioxidant for effectively eliminating explosive oxidative stress. Se@BDP-DOH is found to promote the recovery of both spinal cord tissue and locomotor function in mice with SCI. Furthermore, ETPSA strategy synergistically enhanced ROS consumption via the caveolin 1 (Cav 1)-related pathways, as confirmed upon treatment with Cav 1 siRNA. Therefore, the ETPSA strategy is a potential tool for improving emergency treatment and photoacoustic assessment of SCI.

Venous thromboembolism prophylaxis and mortality in patients with spinal fractures in ICUs.

BACKGROUND: Spinal fracture is a common traumatic condition in orthopaedics, accounting for 5%-6% of total body fractures, and is a high-risk factor for venous thromboembolism (VTE), which seriously affects patient prognosis. AIM: The aim of this study was to determine the impact of VTE prophylaxis on the prognosis of patients with spinal fractures in intensive care units (ICUs) and to provide a scientific basis for clinical treatment and nursing. DESIGN: A retrospective study of patients with spinal fractures from the multicenter eICU Collaborative Research Database. METHOD: The outcomes of this study were ICU mortality and in-hospital mortality. Patients were divided into the VTE prophylaxis (VP) and no VTE prophylaxis (NVP) groups according to whether they had undergone VTE prophylaxis during their ICU admission. The association between groups and outcomes were analysed using Kaplan-Meier (KM) survival curve, log-rank test and the Cox proportional-hazards regression model. RESULTS: This study included 1146 patients with spinal fractures: 330 in the VP group and 816 in the NVP group. KM survival curves and log-rank tests revealed that both ICU and in-hospital survival probabilities in the VP group were significantly higher than in the NVP group. After the Cox model was adjusted for all covariates, the hazard ratio for ICU mortality in the VP group was 0.38 (0.19-0.75); the corresponding value for in-hospital mortality in the VP group was 0.38 (0.21-0.68). CONCLUSIONS: VTE prophylaxis is associated with reduced ICU and in-hospital mortality in patients with spinal fractures in ICUs. More research is necessary to further define specific strategies and optimal timing for VTE prophylaxis. RELEVANCE TO CLINICAL PRACTICE: This study provides the basis that VTE prophylaxis may be associated with improved prognosis in patients with spinal fractures in ICUs. In clinical practice, an appropriate modality should be selected for VTE prophylaxis in such patients.

The comparison of the Effect of double reverse traction repositor (DRTR) and traction table assisted Anterograde Intramedullary nail in treatment of femoral shaft fractures.

OBJECTIVE: The objective of this study was to compare the clinical efficacy of DRTR (Double Reverse Traction Repositor, DRTR)and traction table in the treatment of femoral shaft fractures with the aid of AN-IMN (Antegrade intramedullary nailing). PATIENTS AND METHODS: In this study, patients with femoral shaft fractures admitted to the Department of Orthopedics at Zhaoqing First People's Hospital from May 2018 to October 2022 were recruited. All patients were treated with anterograde intramedullary nailing, with 23 patients in the DRTR-assisted group and 21 patients in the traction table-assisted group. The demographic characteristics, fracture classification, intraoperative data, postoperative data, and prognostic indicators of the two groups were recorded and analyzed retrospectively. All procedures were performed by the same team of experienced physicians. RESULTS: All the patients in the two groups were followed up for more than 12 months. Both traction methods could provide stable traction for the operator during AN-IMN, and there was no significant difference in demographic characteristics and fracture classification. The intraoperative fluoroscopy times and opening reduction rate of the DRTR group were lower than those of the traction table group (P < 0.05), and the postoperative Harris Hip Score, as well as the Lyshol Lysholm knee function Score of the DRTR group, were significantly higher than the traction table group members (P < 0.05). Postoperative complications such as perineal soft tissue injury and lateral femoral cutaneous nerve injury occurred in the traction table group, but not in the DRTR group. CONCLUSION: DRTR can safely and effectively provide continuous and stable traction in the femoral shaft fractures surgery, and outperforms the traction table in the number of intraoperative fluoroscopy, opening reduction rate, reduction of complications, and postoperative joint function score.