Bibliometric analysis of emerging trends and research foci in brainstem tumor field over 30 years (1992-2023).

PURPOSE: Over the past several decades, numerous articles have been published on brainstem tumors. However, there has been limited bibliometric analysis in this field. Therefore, we conducted a bibliometric analysis to elucidate the evolution and current status of brainstem tumor research. METHODS: We retrieved 5525 studies published in English between 1992 and 2023 from the Web of Science Core Collection database. We employed bibliometric tools and VOSviewer to conduct the analysis. RESULTS: We included a total of 5525 publications for further analysis. The annual publications have exhibited steady growth over time. The United States accounted for the highest number of publications and total citations. Among individual researchers, Liwei Zhang had the highest number of publications, while Cynthia Hawkins and Chris Jones shared the most citations, closely followed by Eric Bouffet in this field. The study titled "Diffuse brainstem glioma in children: critical review of clinical trials" stood out as the most cited work in this field. Keyword analysis revealed that immune therapy and epigenetic research are the focal points of this field. CONCLUSIONS: Our bibliometric analysis underscores the enduring significance of brainstem tumors in the realm of neuro-oncology research. The field's hotspots have transitioned from surgery and radiochemotherapy to investigating epigenetic mechanisms and immune therapy.

The clinical significance and oncogenic function of LRRFIP1 in pancreatic cancer.

PURPOSE: Pancreatic cancer is a lethal malignancy with a grim prognosis. Previous studies have proven that Leucine Rich Repeat of Flightless-1 Interacting Protein 1 (LRRFIP1) plays a pivotal role in cell biological processes, while its clinical significance and function in pancreatic cancer remain to be elucidated. Hence, we aimed to explore the roles and mechanisms of LRRFIP1 in pancreatic cancer. METHODS: The expression of LRRFIP1 in pancreatic cancer tissues and its clinical significance for pancreatic cancer were analyzed by immunohistochemistry assay and bioinformatic analysis. The influences of LRRFIP1 on the proliferation and migration of pancreatic cancer cells were assessed in vitro. The underlying mechanisms of LRRFIP1 in pancreatic cancer progression were explored using gene set enrichment analysis (GSEA) and molecular experiments. RESULTS: The results showed that LRRFIP1 expression was significantly upregulated in pancreatic cancer tissues compared to the normal tissues, and such upregulation was associated with poor prognosis of patients with pancreatic cancer. GSEA revealed that LRRFIP1 upregulation was significantly associated with various cancer-associated signaling pathways, including PI3K/AKT signaling pathway and Wnt pathway. Furthermore, LRRFIP1 was found to be associated with the infiltration of various immune cells. Functionally, LRRFIP1 silencing suppressed cell proliferation somewhat and inhibited migration substantially. Further molecular experiments indicated that LRRFIP1 silencing inactivated the AKT/GSK-3ß/ß-catenin signaling axis. CONCLUSION: Taken together, LRRFIP1 is associated with tumorigenesis, immune cell infiltration, and prognosis in pancreatic cancer, which suggests that LRRFIP1 may be a potential biomarker and therapeutic target for pancreatic cancer.

A subset of megakaryocytes regulates development of hematopoietic stem cell precursors.

Understanding the regulatory mechanisms facilitating hematopoietic stem cell (HSC) specification during embryogenesis is important for the generation of HSCs in vitro. Megakaryocyte emerged from the yolk sac and produce platelets, which are involved in multiple biological processes, such as preventing hemorrhage. However, whether megakaryocytes regulate HSC development in the embryonic aorta-gonad-mesonephros (AGM) region is unclear. Here, we use platelet factor 4 (PF4)-Cre;Rosa-tdTomato+ cells to report presence of megakaryocytes in the HSC developmental niche. Further, we use the PF4-Cre;Rosa-DTA (DTA) depletion model to reveal that megakaryocytes control HSC specification in the mouse embryos. Megakaryocyte deficiency blocks the generation and maturation of pre-HSCs and alters HSC activity at the AGM. Furthermore, megakaryocytes promote endothelial-to-hematopoietic transition in a OP9-DL1 coculture system. Single-cell RNA-sequencing identifies megakaryocytes positive for the cell surface marker CD226 as the subpopulation with highest potential in promoting the hemogenic fate of endothelial cells by secreting TNFSF14. In line, TNFSF14 treatment rescues hematopoietic cell function in megakaryocyte-depleted cocultures. Taken together, megakaryocytes promote production and maturation of pre-HSCs, acting as a critical microenvironmental control factor during embryonic hematopoiesis.

Ethanol extract of Cyathulae Radix inhibits osteoclast differentiation and bone loss.

Cyathulae Radix, a traditional Chinese medicine and a common vegetable, boasts a history spanning millennia. It enhances bone density, boosts metabolism, and effectively alleviates osteoporosis-induced pain. Despite its historical use, the molecular mechanisms behind Cyathulae Radix's impact on osteoporosis remain unexplored. In this study, we investigated the effects and mechanisms of Cyathulae Radix ethanol extract (CEE) in inhibiting osteoporosis and osteoclastogenesis. Eight-week-old female mice underwent ovariectomy and were treated with CEE for eight weeks. Micro-computed tomography (micro-CT) assessed histomorphometric parameters, bone tissue staining observed distal femur histomorphology, and three-point bending tests evaluated tibia mechanical properties. Enzyme-linked immunosorbent assay (ELISA) measured serum estradiol (E2), receptor activator for nuclear factor B ligand (RANKL), and osteoprotegerin (OPG) levels. Osteoclastogenesis-related markers were analyzed via Western blotting (WB) and quantitative real-time polymerase chain reaction (qRT-PCR). Additionally, CEE effects on RANKL-induced osteoclast formation and bone resorption were investigated in vitro using tartrate-resistant acid phosphatase (TRAP) staining, qRT-PCR, and WB assay. Compared with the ovariectomy (OVX) group, CEE treatment enhanced trabecular bone density, maximal load-bearing capacity, and various histomorphometric parameters. Serum E2 and OPG levels significantly increased, while Receptor activator of nuclear factor-κB (RANK) decreased in the CEE group. CEE downregulated matrix metallopeptidase 9 (MMP-9), Cathepsin K (CTSK), and TRAP gene and protein expression. In bone marrow macrophages (BMMs), CEE reduced mature osteoclasts, bone resorption pit areas, and MMP-9, CTSK, and TRAP expression during osteoclast differentiation. Compared with DMSO treatment, CEE markedly inhibited RANK, TNF receptor associated factor 6 (TRAF6), Proto-oncogene c-Fos (c-Fos), Nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) expressions, and Extracellular regulated protein kinases (ERK), c-Jun N-terminal kinase (JNK), NF-kappa B-p65 (p65) phosphorylation in osteoclasts. In conclusion, CEE significantly inhibits OVX-induced osteoporosis and RANKL-induced osteoclastogenesis, potentially through modulating the Estrogen Receptor (ER)/RANK/NFATc1 signaling pathway.

Easy conversion perovskite fluorides KCo1-xFexF3 for efficient oxygen evolution reaction.

Herein, we report an easily oxidized Co-Fe perovskite fluoride as an efficient catalyst for the oxygen evolution reaction (OER). In situ Raman spectroscopy showed that the presence of F promotes reconstruction to form highly active (Co3+Fe3+)OOH, and the current density of 10 mA cm-2 can be achieved at the overpotential of only 118 mV in 1 M KOH aqueous solution. This work helps to understand the role of fluoride during the OER.

H5N1 high pathogenicity avian influenza virus in migratory birds exhibiting low pathogenicity in mallards increases its risk of transmission and spread in poultry.

In 2020, an H5N1 avian influenza virus of clade 2.3.4.4b was detected in Europe for the first time and was spread throughout the world by wild migratory birds, resulting in the culling of an unprecedented number of wild birds and poultry due to the epidemic. In February 2023, we isolated and identified a strain of H5N1 high pathogenicity avian influenza virus from a swab sample from a grey crane in Ningxia, China. Phylogenetic analysis of the Hemagglutinin (HA) gene showed that the virus belonged to clade 2.3.4.4b, and several gene segments were closely related to H5N1 viruses infecting humans in China. Analysis of key amino acid sites revealed that the virus contained multiple amino acid substitutions that facilitate enhanced viral replication and mammalian pathogenicity. The results of animal challenge experiments showed that the virus is highly pathogenic to chickens, moderately pathogenic to BALB/c mice, and highly infectious but not lethal to mallards. Moreover, the virus exhibited minor antigenic drift compared with the H5-Re14 vaccine strain. To this end, we need to pay more attention to the monitoring of wild birds to prevent further spread of viruses to poultry and mammals, including humans.

Autophagy regulates the maturation of hematopoietic precursors in the embryo.

An understanding of the mechanisms regulating embryonic hematopoietic stem cell (HSC) development would facilitate their regeneration. The aorta-gonad-mesonephros region is the site for HSC production from hemogenic endothelial cells (HEC). While several distinct regulators are involved in this process, it is not yet known whether macroautophagy (autophagy) plays a role in hematopoiesis in the pre-liver stage. Here, we show that different states of autophagy exist in hematopoietic precursors and correlate with hematopoietic potential based on the LC3-RFP-EGFP mouse model. Deficiency of autophagy-related gene 5 (Atg5) specifically in endothelial cells disrupts endothelial to hematopoietic transition (EHT), by blocking the autophagic process. Using combined approaches, including single-cell RNA-sequencing (scRNA-seq), we have confirmed that Atg5 deletion interrupts developmental temporal order of EHT to further affect the pre-HSC I maturation, and that autophagy influences hemogenic potential of HEC and the formation of pre-HSC I likely via the nucleolin pathway. These findings demonstrate a role for autophagy in the formation/maturation of hematopoietic precursors.

Peritoneal Phosphate Clearance: Determinants and Association With Mortality.

BACKGROUND: Dialytic phosphate removal is a cornerstone of the management of hyperphosphatemia in peritoneal dialysis (PD) patients, but the influencing factors on peritoneal phosphate clearance (PPC) are incompletely understood. Our objective was to explore clinically relevant factors associated with PPC in patients with different PD modality and peritoneal transport status and the association of PPC with mortality. METHODS: This is a cross-sectional and prospective observational study. Four hundred eighty-five PD patients were enrolled and divided into 2 groups according to PPC. All-cause mortality was evaluated after followed-up for at least 3 months. RESULTS: High PPC group showed lower mortality compared with Low PPC group by Kaplan-Meier analysis and log-rank test. Both multivariate linear regression and multivariate logistic regression revealed that high transport status, total effluent dialysate volume per day, continuous ambulatory PD (CAPD), and protein in total effluent dialysate volume appeared to be positively correlated with PPC; body mass index (BMI) and the normalized protein equivalent of total nitrogen appearance (nPNA) were negatively correlated with PPC. Besides PD modality and membrane transport status, total effluent dialysate volume showed a strong relationship with PPC, but the correlation differed among PD modalities. CONCLUSIONS: Higher PPC was associated with lower all-cause mortality risk in PD patients. Higher PPC correlated with CAPD modality, fast transport status, higher effluent dialysate volume and protein content, and with lower BMI and nPNA.

Risk factors and a nomogram for predicting cognitive frailty in Chinese patients with lung cancer receiving drug therapy: A single-center cross-sectional study.

BACKGROUND: To identify independent factors of cognitive frailty (CF) and construct a nomogram to predict cognitive frailty risk in patients with lung cancer receiving drug therapy. METHODS: In this cross-sectional study, patients with lung cancer undergoing drug therapy from October 2022 to July 2023 were enrolled. The data collected includes general demographic characteristics, clinical data characteristics and assessment of tools for cognitive frailty and other factors. Logistic regression was harnessed to determine the influencing factors, R software was used to establish a nomogram model to predict the risk of cognitive frailty. The enhanced bootstrap method was employed for internal verification of the model. The performance of the nomogram was evaluated by using calibration curves, the area under the receiver operating characteristic curve, and decision curve analysis. RESULTS: A total of 372 patients were recruited, with a cognitive frailty prevalence of 56.2%. Age, education background, diabetes mellitus, insomnia, sarcopenia, and nutrition status were identified as independent factors. Then, a nomogram model was constructed and patients were classified into high- and low-risk groups with a cutoff value of 0.552. The internal validation results revealed good concordance, calibration and discrimination. The decision curve analysis presented prominent clinical utility. CONCLUSIONS: The prevalence of cognitive frailty was higher in lung cancer patients receiving drug therapy. The nomogram could identify the risk of cognitive frailty intuitively and simply in patients with lung cancer, so as to provide references for early screening and intervention for cognitive frailty at the early phases of drug treatment.

Leu promotes C2C12 cell differentiation by regulating the GSK3ß/ß-catenin signaling pathway through facilitating the interaction between SESN2 and RPN2.

BACKGROUND: Leucine (Leu) is an essential amino acid that facilitates skeletal muscle satellite cell differentiation, yet its mechanism remains underexplored. Sestrin2 (SESN2) serves as a Leu sensor, binding directly to Leu, while ribophorin II (RPN2) acts as a signaling factor in multiple pathways. This study aimed to elucidate Leu's impact on mouse C2C12 cell differentiation and skeletal muscle injury repair by modulating RPN2 expression through SESN2, offering a theoretical foundation for clinical skeletal muscle injury prevention and treatment. RESULTS: Leu addition promoted C2C12 cell differentiation compared to the control, enhancing early differentiation via myogenic determinant (MYOD) up-regulation. Sequencing revealed SESN2 binding to and interacting with RPN2. RPN2 overexpression up-regulated MYOD, myogenin and myosin heavy chain 2, concurrently decreased p-GSK3ß and increased nuclear ß-catenin. Conversely, RPN2 knockdown yielded opposite results. Combining RPN2 knockdown with Leu rescued increased p-GSK3ß and decreased nuclear ß-catenin compared to Leu absence. Hematoxylin and eosin staining results showed that Leu addition accelerated mouse muscle damage repair, up-regulating Pax7, MYOD and RPN2 in the cytoplasm, and nuclear ß-catenin, confirming that the role of Leu in muscle injury repair was consistent with the results for C2C12 cells. CONCLUSION: Leu, bound with SESN2, up-regulated RPN2 expression, activated the GSK3ß/ß-catenin pathway, enhanced C2C12 differentiation and expedited skeletal muscle damage repair. © 2024 Society of Chemical Industry.

Hydrophobic functionalization of a metal-organic framework as an ammonia visual sensing material under high humidity conditions.

Since exhaled ammonia (NH3) is one of the metabolic markers of liver and kidney diseases, ammonia visual sensing materials in humid environments have received extensive attention and investigation. Herein, through a tailor-made pore environment provided by metal-organic framework (MOF) materials (CH3-Cu(BDC)), we achieved NH3 anti-interference sensing with apparent color changing under humid conditions. With methyl (CH3-) functionalization, CH3-Cu(BDC) demonstrated a strong response for trace ammonia and showed high selectivity under a humid environment. Grand canonical Monte Carlo (GCMC) simulations indicated that CH3-Cu(BDC) showed stronger attraction towards NH3 molecules than H2O. Benefiting from the target changing coordination environment, CH3-Cu(BDC) showed a rapid response and simple analysis properties for patients' exhaled air. The strategy used in this study not only provides a demonstration case for NH3 colorimetric sensing with high humidity and anti-interference but also introduces a new method for painless and quick exhaled breath analysis for diagnosis of patients with kidney and liver diseases.

Stable hydrogen evolution reaction at high current densities via designing the Ni single atoms and Ru nanoparticles linked by carbon bridges.

Continuous and effective hydrogen evolution under high current densities remains a challenge for water electrolysis owing to the rapid performance degradation under continuous large-current operation. In this study, theoretical calculations, operando Raman spectroscopy, and CO stripping experiments confirm that Ru nanocrystals have a high resistance against deactivation because of the synergistic adsorption of OH intermediates (OHad) on the Ru and single atoms. Based on this conceptual model, we design the Ni single atoms modifying ultra-small Ru nanoparticle with defect carbon bridging structure (UP-RuNiSAs/C) via a unique unipolar pulse electrodeposition (UPED) strategy. As a result, the UP-RuNiSAs/C is found capable of running steadily for 100 h at 3 A cm-2, and shows a low overpotential of 9 mV at a current density of 10 mA cm-2 under alkaline conditions. Moreover, the UP-RuNiSAs/C allows an anion exchange membrane (AEM) electrolyzer to operate stably at 1.95 Vcell for 250 h at 1 A cm-2.

A New Synthesized Dicarboxylated Oxy-Heparin Efficiently Attenuates Tumor Growth and Metastasis.

Heparanase (Hpa1) is expressed by tumor cells and cells of the tumor microenvironment and functions to remodel the extracellular matrix (ECM) and regulate the bioavailability of ECM-bound factors that support tumor growth. Heparanase expression is upregulated in human carcinomas, sarcomas, and hematological malignancies, correlating with increased tumor metastasis, vascular density, and shorter postoperative survival of cancer patients, and encouraging the development of heparanase inhibitors as anti-cancer drugs. Among these are heparin/HS mimetics, the only heparanase-inhibiting compounds that are being evaluated in clinical trials. We have synthesized dicarboxylated oxy-heparins (DCoxHs) containing three carboxylate groups per split residue (DC-Hep). The resulting lead compound (termed XII) was upscaled, characterized, and examined for its effectiveness in tumor models. Potent anti-tumorigenic effects were obtained in models of pancreatic carcinoma, breast cancer, mesothelioma, and myeloma, yielding tumor growth inhibition (TGI) values ranging from 21 to 70% and extending the survival time of the mice. Of particular significance was the inhibition of spontaneous metastasis in an orthotopic model of breast carcinoma following resection of the primary tumor. It appears that apart from inhibition of heparanase enzymatic activity, compound XII reduces the levels of heparanase protein and inhibits its cellular uptake and activation. Heparanase-dependent and -independent effects of XII are being investigated. Collectively, our pre-clinical studies with compound XII strongly justify its examination in cancer patients.

Bioaugmented ensiling of sweet sorghum with Pichia anomala and cellulase and improved enzymatic hydrolysis of silage via ball milling.

Sweet sorghum, as a seasonal energy crop, is rich in cellulose and hemicellulose that can be converted into biofuels. This work aims at investigating the effects of synergistic regulation of Pichia anomala and cellulase on ensiling quality and microbial community of sweet sorghum silages as a storage and pretreatment method. Furthermore, the combined pretreatment effects of ensiling and ball milling on sweet sorghum were evaluated by microstructure change and enzymatic hydrolysis. Based on membership function analysis, the combination of P. anomala and cellulase (PA + CE) significantly improved the silage quality by preserving organic components and promoting fermentation characteristics. The bioaugmented ensiling with PA + CE restructured the bacterial community by facilitating Lactobacillus and inhibiting undesired microorganisms by killer activity of P. anomala. The combined bioaugmented ensiling pretreatment with ball milling significantly increased the enzymatic hydrolysis efficiency (EHE) to 71%, accompanied by the increased specific surface area and decreased pore size/crystallinity of sweet sorghum. Moreover, the EHE after combined pretreatment was increased by 1.37 times compared with raw material. Hence, the combined pretreatment was demonstrated as a novel strategy to effectively enhance enzymatic hydrolysis of sweet sorghum.

Regulatory T cells use heparanase to access IL-2 bound to extracellular matrix in inflamed tissue.

Although FOXP3+ regulatory T cells (Treg) depend on IL-2 produced by other cells for their survival and function, the levels of IL-2 in inflamed tissue are low, making it unclear how Treg access this critical resource. Here, we show that Treg use heparanase (HPSE) to access IL-2 sequestered by heparan sulfate (HS) within the extracellular matrix (ECM) of inflamed central nervous system tissue. HPSE expression distinguishes human and murine Treg from conventional T cells and is regulated by the availability of IL-2. HPSE-/- Treg have impaired stability and function in vivo, including in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis. Conversely, endowing monoclonal antibody-directed chimeric antigen receptor (mAbCAR) Treg with HPSE enhances their ability to access HS-sequestered IL-2 and their ability to suppress neuroinflammation in vivo. Together, these data identify a role for HPSE and the ECM in immune tolerance, providing new avenues for improving Treg-based therapy of autoimmunity.

Manufacturing non-sintered ceramsite from dredged sediment, steel slag, and fly ash for lightweight aggregate: production and characterization.

Green and low-carbon materialization for dredged sediment (DS) is limited due to its low pozzolanic activity. In this study, a novel DS-based non-sintered lightweight aggregate (LWA) is developed by steel slag (SS) and fly ash (FA) activation. Process optimization is performed by the response surfaces, and the basic properties and characterization of the optimal product are investigated. Results indicated that the optimized design ceramic aggregate (ODCA) was prepared as follows: raw pellets comprising of 59.2% DS, 5% SS, 35.8% FA, 5% MK, 5% H2O2, and 2‰ foam stabilizer were activated by alkali activator (1.5 weight ratio of 14 M NaOH to water glass) and then cured at 80 °C and 95% humidity for 24 h. The basic and environmental performances of ODCA were in accordance with standards, whose bulk density was as low as 665.8 kg/m3, the high cylinder compressive strength was 6.143 MPa, and leaching concentrations of heavy metals were controllable. The regulation mechanism of LWA performances could be summarized as follows. SS and FA additives played the role for the mechanical strength enhancement and passivation of heavy metals, which promoted the formation of sillimanite, chabazite, and C-S-H / C-S-A-H gels in ODCA. The bulk density of ODCA was greatly reduced by H2O2 addition, where ODCA had an open-pore structure with a median pore size of 4969.75 nm. Note that C-S-H/C-S-A-H were the key hydration products to give ODCA light density and high mechanical strength, simultaneously.

Pediococcus acidilactici reduces tau pathology and ameliorates behavioral deficits in models of neurodegenerative disorders.

BACKGROUND: Alzheimer's disease (AD), affecting many elders worldwide, is characterized by A-beta and tau-related cognitive decline. Accumulating evidence suggests that brain iron accumulation is an important characteristic of AD. However, the function and mechanism of the iron-mediated gut-brain axis on AD is still unclear. METHODS: A Caenorhabditis elegans model with tau-overexpression and a high-Fe diet mouse model of cognitive impairment was used for probiotic function evaluation. With the use of qPCR, and immunoblotting, the probiotic regulated differential expression of AD markers and iron related transporting genes was determined. Colorimetric kits, IHC staining, and immunofluorescence have been performed to explore the probiotic mechanism on the development of gut-brain links and brain iron accumulation. RESULTS: In the present study, a high-Fe diet mouse model was used for evaluation in which cognitive impairment, higher A-beta, tau and phosphorylated (p)-tau expression, and dysfunctional phosphate distribution were observed. Considering the close crosstalk between intestine and brain, probiotics were then employed to delay the process of cognitive impairment in the HFe mouse model. Pediococcus acidilactici (PA), but not Bacillus subtilis (BN) administration in HFe-fed mice reduced brain iron accumulation, enhanced global alkaline phosphatase (AP) activity, accelerated dephosphorylation, lowered phosphate levels and increased brain urate production. In addition, because PA regulated cognitive behavior in HFe fed mice, we used the transgenic Caenorhabditis elegans with over-expressed human p-tau for model, and then PA fed worms became more active and longer lived than E.coli fed worms, as well as p-tau was down-regulated. These results suggest that brain iron accumulation influences AD risk proteins and various metabolites. Furthermore, PA was shown to reverse tau-induced pathogenesis via iron transporters and AP-urate interaction. CONCLUSIONS: PA administration studies demonstrate that PA is an important mediator of tau protein reduction, p-tau expression and neurodegenerative behavior both in Caenorhabditis elegans and iron-overload mice. Finally, our results provide candidates for AP modulation strategies as preventive tools for promoting brain health. Video Abstract.

GCF2 mediates nicotine-induced cancer stemness and progression in hepatocellular carcinoma.

Cigarette smoking is one of the most impactful behavior-related risk factors for multiple cancers including hepatocellular carcinoma (HCC). Nicotine, as the principal component of tobacco, is not only responsible for smoking addiction but also a carcinogen; nevertheless, the underlying mechanisms remain unclear. Here we report that nicotine enhances HCC cancer stemness and malignant progression by upregulating the expression of GC-rich binding factor 2 (GCF2), a gene that was revealed to be upregulated in HCC and whose upregulation predicts poor prognosis, and subsequently activating the Wnt/ꞵ-catenin/SOX2 signaling pathway. We found that nicotine significantly increased GCF2 expression and that silencing of GCF2 reduced nicotine-induced cancer stemness and progression. Mechanistically, nicotine could stabilize the protein level of GCF2, and then GCF2 could robustly activate its downstream Wnt/ß-catenin signaling pathway. Taken together, our results thus suggest that GCF2 is a potential target for a therapeutic strategy against nicotine-promoted HCC.

A systematic review of risk prediction model of venous thromboembolism for patients with lung cancer.

BACKGROUND: Venous thromboembolism (VTE) increases the risk of death or adverse outcomes in patients with lung cancer. Therefore, early identification and treatment of high-risk groups of VTE have been the research focus. In this systematic review, the risk assessment tools of VTE in patients with lung cancer were systematically analyzed and evaluated to provide a reference for VTE management. METHODS: Relevant studies were retrieved from major English databases (The Cochrane Library, Embase, Web of Science, PubMed, Scopus, Medline) and Chinese databases (China National Knowledge Infrastructure [CNKI] and WanFang Data) until July 2023 and extracted by two researchers. This systematic review was registered at PROSPERO (no. CRD42023409748). RESULTS: Finally, two prospective cohort studies and four retrospective cohort studies were included from 2019. There was a high risk of bias in all included studies according to the Prediction Model Risk of Bias Assessment tool (PROBAST). In the included studies, Cox and logistic regression were used to construct models. The area under the receiver operating characteristic curve (AUC) of the model ranged from 0.670 to 0.904, and the number of predictors ranged from 4 to 11. The D-dimer index was included in five studies, but significant differences existed in optimal cutoff values from 0.0005 mg/L to 2.06 mg/L. Then, three studies validated the model externally, two studies only validated the model internally, and only one study validated the model using a combination of internal and external validation. CONCLUSION: VTE risk prediction models for patients with lung cancer have received attention for no more than 5 years. The included model shows a good predictive effect and may help identify the risk population of VTE at an early stage. In the future, it is necessary to improve data modeling and statistical analysis methods, develop predictive models with good performance and low risk of bias, and focus on external validation and recalibration of models.

MRI-based radiomics model for preoperative prediction of extramural venous invasion of rectal adenocarcinoma.

BACKGROUND: Extramural venous invasion (EMVI) is an important prognostic factor of rectal adenocarcinoma. However, accurate preoperative assessment of EMVI remains difficult. PURPOSE: To assess EMVI preoperatively through radiomics technology, and use different algorithms combined with clinical factors to establish a variety of models in order to make the most accurate judgments before surgery. MATERIAL AND METHODS: A total of 212 patients with rectal adenocarcinoma between September 2012 and July 2019 were included and distributed to training and validation datasets. Radiomics features were extracted from pretreatment T2-weighted images. Different prediction models (clinical model, logistic regression [LR], random forest [RF], support vector machine [SVM], clinical-LR model, clinical-RF model, and clinical-SVM model) were constructed on the basis of radiomics features and clinical factors, respectively. The area under the curve (AUC) and accuracy were used to assess the predictive efficacy of different models. Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were also calculated. RESULTS: The clinical-LR model exhibited the best diagnostic efficiency with an AUC of 0.962 (95% confidence interval [CI] = 0.936-0.988) and 0.865 (95% CI = 0.770-0.959), accuracy of 0.899 and 0.828, sensitivity of 0.867 and 0.818, specificity of 0.913 and 0.833, PPV of 0.813 and 0.720, and NPV of 0.940 and 0.897 for the training and validation datasets, respectively. CONCLUSION: The radiomics-based prediction model is a valuable tool in EMVI detection and can assist decision-making in clinical practice.