Clinicopathological characteristics of endometrial carcinoma with different molecular subtypes and their correlation with lymph node metastasis.

Endometrial carcinoma (EC) is one of the three major malignancies of the female reproductive organs. With intense research of tumor molecular mechanisms and development of precision medicine in recent years, the traditional pathomorphological classification fails to meet the needs of clinical diagnosis and treatment for EC. This study aims to analyze the correlation of different Proactive Molecular Risk Classifier for Endometrial Cancer molecular subtypes with lymph node metastasis (LNM) and other clinical features in EC. 120 treatment-naive EC patients with surgery were enrolled in this study. The molecular subtypes of these patients were classified as follows by Proactive Molecular Risk Classifier for Endometrial Cancer (ProMisE) molecular subtyping: mismatch repair deficiency (MMRd) in 22 cases (18.33%), polymerase epsilon exonuclease domain mutation (POLE EDM) in 2 cases (1.67%), p53 wild-type (p53-wt) in 64 cases (53.33%), and p53 abnormal (p53-abn) in 32 cases (26.67%). The clinicopathological features of 120 patients were retrospectively analyzed. Statistical significance was identified among the four molecular subtypes in terms of histological classification, International Federation of Gynecology and Obstetrics (FIGO) staging, pathological grading, and LNM. Among the enrolled cases, 26 had LNM and 94 had no lymph node involvement. According to the multivariate Logistic regression analysis, p53 wt (P=0.008, OR=0.078, 95% CI: 0.012-0.510) was a protective factor for LNM in EC patients, while poorly differentiated histology (P=0.001, OR=15.137, 95% CI: 3.013-76.044) was a risk factor. ProMisE classification system, being more objective and reproducible, can provide an important reference for preoperative decision-making. The patients with p53 wt by ProMisE had a low risk of LNM in preoperative diagnostic curettage specimens, while there was a higher risk of LNM among the patients with poorly differentiated EC.

Nucleotide polymorphism-based study utilizes human plasma liposomes to discover potential therapeutic targets for intervertebral disc disease.

Background: While intervertebral disc degeneration (IVDD) is crucial in numerous spinally related illnesses and is common among the elderly, the complete understanding of its pathogenic mechanisms is still an area of ongoing study. In recent years, it has revealed that liposomes are crucial in the initiation and progression of IVDD. However, their intrinsic mediators and related mechanisms remain unclear. With the development of genomics, an increasing amount of data points to the contribution of genetics in the etiology of disease. Accordingly, this study explored the causality between liposomes and IVDD by Mendelian randomization (MR) analysis and deeply investigated the intermediary roles of undetected metabolites. Methods: According to MR analysis, 179 liposomes and 1400 metabolites were evaluated for their causal association with IVDD. Single nucleotide polymorphisms (SNPs) are strongly associated with the concentrations of liposomes and metabolites. Consequently, they were employed as instrumental variables (IVs) to deduce if they constituted risk elements or protective elements for IVDD. Furthermore, mediation analysis was conducted to pinpoint possible metabolic mediators that link liposomes to IVDD. The inverse variance weighting (IVW) was the main analytical technique. Various confidence tests in the causality estimates were performed, including consistency, heterogeneity, pleiotropy, and sensitivity analyses. Inverse MR analysis was also utilized to estimate potential reverse causality. Results: MR analysis identified 13 liposomes and 79 metabolites markedly relevant to IVDD. Moreover, the mediation analysis was carried out by choosing the liposome, specifically the triacylglycerol (48:2) levels, which were found to be most notably associated with an increased risk of IVDD. In all, three metabolite-associated mediators were identified (3-methylcytidine levels, inosine 5'-monophosphate (IMP) to phosphate ratio, and adenosine 5'-diphosphate (ADP) to glycine ratio). Conclusion: The analysis's findings suggested possible causal connections between liposomes, metabolites, and IVDD, which could act as both forecast and prognosis clinical indicators, thereby aiding in the exploration of the pathogenesis behind IVDD.

Structural characterization, physicochemical properties and hypoglycemic activity of soluble dietary fibers from salt stressed mung bean sprouts.

Low-salt stress germination is an effective way to improve the nutritional composition of food crops. A novel soluble dietary fiber (MS-SDF) was isolated from low-salt stress mung bean sprouts that were exposed to low-salt stress using anion exchange and gel permeation techniques. Structural analysis revealed that MS-SDF was a homogeneous heteropolysaccharide with an average molecular weight of 164.997 KDa. It featured a loose structure and contained the characteristic functional groups typical of polysaccharides. MS-SDF was composed of arabinose, galactose, glucose, and mannose with a molar ratio of 3.95:3.86:82.69:9.02. The structure was mainly composed of →6)-α-D-Glcp-(1→, →5)-α-L-Araf-(1→, and →3,6)-α-D-Glcp-(1→ as the main chain. Branched at O-3 position with single ß-D-Manp-(1→ as major the side chain. Furthermore, in vitro hypoglycemic assays indicate that MS-SDF exhibits α-glucosidase inhibitory activity, significantly enhancing glucose uptake, glycogen synthesis, and pyruvate kinase activity in insulin-resistant HepG2 cells. Overall, MS-SDF could be used as a promising source of functional hypoglycemic foods.

MGMT promoter methylation is a strong prognostic factor for survival after progression in high-grade gliomas.

BACKGROUND: High-grade gliomas (HGGs) have a rapid relapse and short survival. Studies have identified many clinical characteristics and biomarkers associated with progression-free survival (PFS) and over-survival (OS). However, there has not yet a comprehensive study on survival after the first progression (SAP). METHODS: From CGGA and TCGA, 319 and 308 HGGs were confirmed as the first progression. The data on clinical characteristics and biomarkers were analyzed in accordance with OS, PFS, and SAP. RESULTS: Analysis of 319 patients from CGGA, significant predictors of improved OS/PFS/SAP were WHO grade, MGMT promoter methylation, and Ki-67 expression in univariate analysis. Further multivariate analysis showed MGMT promoter methylation and Ki-67 expression were independent predictors. However, an analysis of 308 patients from TCGA found MGMT promoter methylation is the only prognostic marker. A longer SAP was observed in patients with methylated MGMT promoter after standard chemoradiotherapy. In our data, HGGs could be divided into low, intermediate, and high-risk groups for SAP by MGMT methylation and Ki-67 expression. CONCLUSIONS: Patients with MGMT promoter methylation have a prolonger SAP after standard chemoradiotherapy. HGGs could be divided into low, intermediate, and high-risk groups for SAP according to MGMT status and Ki-67 expression.

Generation and transcriptomic characterization of MIR137 knockout miniature pig model for neurodevelopmental disorders.

BACKGROUND: Neurodevelopmental disorders (NDD), such as autism spectrum disorders (ASD) and intellectual disorders (ID), are highly debilitating childhood psychiatric conditions. Genetic factors are recognized as playing a major role in NDD, with a multitude of genes and genomic regions implicated. While the functional validation of NDD-associated genes has predominantly been carried out using mouse models, the significant differences in brain structure and gene function between mice and humans have limited the effectiveness of mouse models in exploring the underlying mechanisms of NDD. Therefore, it is important to establish alternative animal models that are more evolutionarily aligned with humans. RESULTS: In this study, we employed CRISPR/Cas9 and somatic cell nuclear transplantation technologies to successfully generate a knockout miniature pig model of the MIR137 gene, which encodes the neuropsychiatric disorder-associated microRNA miR-137. The homozygous knockout of MIR137 (MIR137-/-) effectively suppressed the expression of mature miR-137 and led to the birth of stillborn or short-lived piglets. Transcriptomic analysis revealed significant changes in genes associated with neurodevelopment and synaptic signaling in the brains of MIR137-/- miniature pig, mirroring findings from human ASD transcriptomic data. In comparison to miR-137-deficient mouse and human induced pluripotent stem cell (hiPSC)-derived neuron models, the miniature pig model exhibited more consistent changes in critical neuronal genes relevant to humans following the loss of miR-137. Furthermore, a comparative analysis identified differentially expressed genes associated with ASD and ID risk genes in both miniature pig and hiPSC-derived neurons. Notably, human-specific miR-137 targets, such as CAMK2A, known to be linked to cognitive impairments and NDD, exhibited dysregulation in MIR137-/- miniature pigs. These findings suggest that the loss of miR-137 in miniature pigs affects genes crucial for neurodevelopment, potentially contributing to the development of NDD. CONCLUSIONS: Our study highlights the impact of miR-137 loss on critical genes involved in neurodevelopment and related disorders in MIR137-/- miniature pigs. It establishes the miniature pig model as a valuable tool for investigating neurodevelopmental disorders, providing valuable insights for potential applications in human research.

Genetic mutation and immune infiltration in embryonal tumor with multilayered rosettes.

PURPOSE: Genetic mutations stand as pivotal factors leading to the occurrence of embryonal tumor with multilayered rosettes (ETMR). This study aims to identify improved treatment approaches by unraveling the genetic drivers and immune infiltration in ETMR. METHODS: Two siblings with ETMR, treated at the General Hospital of Ningxia Medical University, were enrolled. Diagnosis involved MRI, Hematoxylin and Eosin (HE), and immunohistochemical (IHC) staining. Differentially expressed genes (DEGs) in ETMR were identified using GSE122077 and GSE14296 datasets. GO and KEGG analyses were used to determine ETMR-related pathways. Whole exome sequencing (WES) was utilized to annotate genetic variations in ETMR. Core genes, identified by protein-protein interaction (PPI), formed a diagnostic model evaluated by Logistic Regression. Single-sample Gene Set Enrichment Analysis (ssGSEA) assessed immune infiltration in ETMR, examining correlations between immune cells and core genes. RESULTS: Two siblings were diagnosed with ETMR. In ETMR, 135 DEGs were identified, of which 25 genes were annotated with 28 mutation sites. Moreover, ETMR-related pathways included cell cycle, synaptic functions, and neurodegeneration. Three ETMR-related core genes (ALB, PSMD1, and PAK2) were screened by protein-protein interaction (PPI). The diagnostic model constructed using these genes demonstrated an AUC value of 0.901 (95% CI: 0.811-0.991) in the training set, indicating accurate predictions in ETMR. Enhanced ssGSEA scores for 16 immune cells in ETMR tissues suggested a strong immune response. CONCLUSION: This study identifies diagnostic models associated with three core variant genes (ALB, PSMD1, PAK2) and enhanced immune cell activity in ETMR. It reveals crucial genetic features and significant immune responses in ETMR.

Unraveling the immunogenic cell death pathways in gastric adenocarcinoma: A multi-omics study.

BACKGROUND: Gastric cancer (GC) is a prevalent malignant tumor of the gastrointestinal (GI) system. However, the lack of reliable biomarkers has made its diagnosis, prognosis, and treatment challenging. Immunogenic cell death (ICD) is a type of programmed cell death that is strongly related to the immune system. However, its function in GC requires further investigation. METHOD: We used multi-omics and multi-angle approaches to comprehensively explore the prognostic features of ICD in patients with stomach adenocarcinoma (STAD). At the single-cell level, we screened genes associated with ICD at the transcriptome level, selected prognostic genes related to ICD using weighted gene co-expression network analysis (WGCNA) and machine learning, and constructed a prognostic model. In addition, we constructed nomograms that incorporated pertinent clinical features and provided effective tools for prognostic prediction in clinical settings. We also investigated the sensitivity of the risk subgroups to both immunotherapy and drugs. Finally, in addition to quantitative real-time polymerase chain reaction, immunofluorescence was used to validate the expression of ICD-linked genes. RESULTS: Based on single-cell and transcriptome WGCNA analyses, we identified 34 ICD-related genes, of which 11 were related to prognosis. We established a prognostic model using the least absolute shrinkage and selection operator (LASSO) algorithm and identified dissimilarities in overall survival (OS) and progression-free survival (PFS) in risk subgroups. The nomograms associated with the ICD-related signature (ICDRS) demonstrated a good predictive value for clinical applications. Moreover, we detected changes in the tumor microenvironment (TME), including biological functions, mutation landscapes, and immune cell infiltration, between the high- and low-risk groups. CONCLUSION: We constructed an ICD-related prognostic model that incorporated features related to cell death. This model can serve as a useful tool for predicting the prognosis of GC, targeted prevention, and personalized medicine.

AURKB promotes colorectal cancer progression by triggering the phosphorylation of histone H3 at serine 10 to activate CCNE1 expression.

Aurora kinase B (AURKB) initiates the phosphorylation of serine 10 on histone H3 (pH3S10), a crucial process for chromosome condensation and cytokinesis in mammalian mitosis. Nonetheless, the precise mechanisms through which AURKB regulates the cell cycle and contributes to tumorigenesis as an oncogenic factor in colorectal cancer (CRC) remain unclear. Here, we report that AURKB was highly expressed and positively correlated with Ki-67 expression in CRC. The abundant expression of AURKB promotes the growth of CRC cells and xenograft tumors in animal model. AURKB knockdown substantially suppressed CRC proliferation and triggered cell cycle arrest in G2/M phase. Interestingly, cyclin E1 (CCNE1) was discovered as a direct downstream target of AURKB and functioned synergistically with AURKB to promote CRC cell proliferation. Mechanically, AURKB activated CCNE1 expression by triggering pH3S10 in the promoter region of CCNE1. Furthermore, it was showed that the inhibitor specific for AURKB (AZD1152) can suppress CCNE1 expression in CRC cells and inhibit tumor cell growth. To conclude, this research demonstrates that AURKB accelerated the tumorigenesis of CRC through its potential to epigenetically activate CCNE1 expression, suggesting AURKB as a promising therapeutic target in CRC.

Prognostic and Immunotherapeutic Predictive Value of CAD Gene in Hepatocellular Carcinoma: Integrated Bioinformatics and Experimental Analysis.

Hepatocellular carcinoma (HCC) is a common type of cancer that ranks first in cancer-associated death worldwide. Carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase (CAD) are the key components of the pyrimidine pathway, which promotes cancer development. However, the function of CAD in HCC needs to be clarified. In this study, the clinical and transcriptome data of 424 TCGA-derived HCC cases were analyzed. The results demonstrated that high CAD expression was associated with poor prognosis in HCC patients. The effect of CAD on HCC was then investigated comprehensively using GO annotation analysis, KEGG enrichment analysis, Gene Set Enrichment Analysis (GSEA), and CIBERSORT algorithm. The results showed that CAD expression was correlated with immune checkpoint inhibitors and immune cell infiltration. In addition, low CAD levels in HCC patients predicted increased sensitivity to anti-CTLA4 and PD1, while HCC patients with high CAD expression exhibited high sensitivity to chemotherapeutic and molecular-targeted agents, including gemcitabine, paclitaxel, and sorafenib. Finally, the results from clinical sample suggested that CAD expression increased remarkably in HCC compared with non-cancerous tissues. Loss of function experiments demonstrated that CAD knockdown could significantly inhibit HCC cell growth and migration both in vitro and in vivo. Collectively, the results indicated that CAD is a potential oncogene during HCC metastasis and progression. Therefore, CAD is recommended as a candidate marker and target for HCC prediction and treatment.

Salvage Surgery for Initially Unresectable HCC With PVTT Converted by Locoregional Treatment Plus Tyrosine Kinase Inhibitor and Anti-PD-1 Antibody.

BACKGROUND: This study aimed to compare the survival outcomes of patients with initially unresectable hepatocellular carcinoma (HCC) and portal vein tumor thrombus (PVTT) who underwent or did not undergo salvage surgery followed by a triple combination conversion treatment consisted of locoregional treatment (LRT), tyrosine kinase inhibitors (TKIs), and anti-PD-1 antibodies. METHODS: The data from 93 consecutive patients with initially unresectable HCC and PVTT across 4 medical centers were retrospectively reviewed. They were converted successfully by the triple combination treatment and underwent or did not undergo salvage resection. The baseline characteristics, conversion schemes, conversion treatment-related adverse events (CTRAEs), overall survival (OS), and progression-free survival (PFS) of the salvage surgery and non-surgery groups were compared. Multivariate Cox regression analysis was performed to identify independent risk factors for OS and PFS. Additionally, subgroup survival analysis was conducted by stratification of degree of tumor response and type of PVTT. RESULTS: Of the 93 patients, 44 underwent salvage surgery, and 49 did not undergo salvage surgery. The OS and PFS of the salvage surgery and non-surgery groups were not significantly different (P = .370 and .334, respectively). The incidence and severity of CTRAEs of the 2 groups were also comparable. Subgroup analyses revealed that for patients with complete response (CR) or types III-IV PVTT, there was a trend toward better survival in patients who did not undergo salvage surgery. Multivariate analysis showed that baseline α-fetoprotein and best tumor response per mRECIST criteria were independent prognostic factors for OS and PFS. CONCLUSIONS: For patients with initially unresectable HCC and PVTT who were successfully converted by the triple combination therapy, salvage liver resection may not be necessary, especially for the patients with CR or types III-IV PVTT.

Incidence, Risk Factors, and Prognosis of Patients with Hepatocellular Carcinoma and Brain Metastases.

OBJECTIVE: Brain metastases significantly impact the clinical course of patients with hepatocellular carcinoma (HCC). This study aimed to examine the age-related incidence, demographics, and survival of patients with HCC and brain metastases. METHODS: Data of HCC patients from 2010 to 2015 in the Surveillance, Epidemiology, and End Results (SEER) Registry were screened for the presence of brain metastases. They were stratified by age and ethnicity. Multivariable logistic and Cox regression analyses were used to identify factors associated with brain metastases and those with overall survival (OS) and liver cancer-specific survival (CSS), respectively. RESULTS: A total of 141 HCC patients presenting with brain metastases were identified, accounting for 0.35% of all HCC patients and 2.37% of patients with metastatic disease. Among all HCC patients, the incidence rate was the highest among patients aged 30-49 years old (0.47%). Ethnicity was not associated with the presence of brain metastases at the time of HCC diagnosis. However, African-American patients presented with a significantly lower disease-specific survival [median time: 1 month; interquartile range (IQR): 0-3.0 months)]. Initial lung or bone metastasis was independently associated with an increased risk of the presence of brain metastases [odds ratio (OR): 12.62, 95% confidence interval (CI): 8.40-18.97] but was not associated with a worse OS or CSS among those with brain metastases. CONCLUSION: This study identified the age-related incidence and risk factors of brain metastases in HCC patients. These results may contribute to the consideration of brain screening among patients with initial metastatic HCC with lung or bone metastases, and influence the counseling of this patient population regarding their prognosis.

Stent Insertion for Inoperable Hilar Cholangiocarcinoma: Comparison Between Unilateral Radioactive Stent and Bilateral Normal Stent.

OBJECTIVE: To comparatively analyze the clinical efficacy and safety of unilateral radioactive stent (RS) insertion versus bilateral normal stent (NS) insertion in patients with inoperable hilar cholangiocarcinoma (HC). PATIENTS AND METHODS: Patients with inoperable HC were treated in our hospital from January 2016 to December 2020. The treatment approach included the insertion of either unilateral RS or bilateral NS, evaluating the efficacy and safety of therapy in 2 distinct groups. RESULTS: A total of 58 individuals experienced the insertion of a unilateral RS, whereas 57 patients underwent the insertion of bilateral NS. No statistically significant difference between the unilateral RS and bilateral NS groups was seen in the technical success rates (98.3% vs 94.7%, P = 0.598) and clinical success rates (98.2% vs 100%, P = 0.514). While there is no statistically significant difference in the rates of stent restenosis (19.3% vs 9.3%, P = 0.132) between the two groups, the unilateral RS group demonstrated substantially longer stent patency (202 vs 119 d, P = 0.016) and overall survival (229 vs 122 d, P = 0.004) compared with the bilateral NS group. Moreover, 8 patients (14.0%) in the unilateral RS group and 14 patients (25.9%) in the bilateral NS group had postoperative complications with no significant difference ( P = 0.116). CONCLUSION: When inserting stents for inoperable HC, both unilateral RS and bilateral NS insertion procedures have demonstrated favorable therapeutic efficacy. Nevertheless, inserting a unilateral RS provided a longer duration of stent patency and overall survival than implantation of bilateral NS.

Treatment outcomes and risk factors of patients with intracranial germ cell tumour with choriocarcinoma element or ß-HCG level higher than 500 IU/L.

BACKGROUND: In previous studies, patients with intracranial germ cell tumour (iGCT) with pure choriocarcinoma or mixed germ cell tumours with choriocarcinoma element showed similar dismal prognoses, with median overall survival (OS) of 22 months and 1-year survival rate of approximately 60%. However, these conclusions need to be updated because radiotherapy, which is the mainstay for this disease, was not applied in a number of patients. Additionally, prognostic factors need to be explored in this population. METHODS: Clinical data of patients with iGCTs with histologically confirmed choriocarcinoma element or beta-human chorionic gonadotropin (ß-HCG) > 500 IU/L were collected from the archives of our institution and retrospectively studied. RESULTS: A total of 76 patients were eligible for this study. Except for two early deaths, all patients received radiotherapy (craniospinal irradiation [CSI], n = 23; non-CSI, n = 51). The median follow-up duration for the entire series was 63 months (range, 6-188 months). The 5-year event-free survival (EFS) and OS rates were 81.5% and 84.1%, respectively. Among patients who did not have early death or progressive disease after induction chemotherapy, multivariate analysis revealed that chemotherapy cycles (> 4 vs. ≤ 4) (hazard ratio [HR] for EFS 0.144, p = 0.020; HR for OS 0.111, p = 0.028) and ß-HCG levels (> 3000 IU/L vs. ≤ 3000 IU/L) (HR for EFS 4.342, p = 0.059; HR for OS 6.614, p = 0.033) were independent factors for survival. CONCLUSIONS: Patients with iGCTs with choriocarcinoma element or ß-HCG > 500 IU/L showed improved survival with radiotherapy-based treatments. Additional chemotherapy cycles could result in additional survival benefits. Patients with ß-HCG level > 3000 IU/L had poorer prognosis.

METFORMIN MITIGATES SEPSIS-ASSOCIATED PULMONARY FIBROSIS BY PROMOTING AMPK ACTIVATION AND INHIBITING HIF-1α-INDUCED AEROBIC GLYCOLYSIS.

ABSTRACT: Recent research has revealed that aerobic glycolysis has a strong correlation with sepsis-associated pulmonary fibrosis (PF). However, at present, the mechanism and pathogenesis remain unclear. We aimed to test the hypothesis that the adenosine monophosphate-activated protein kinase (AMPK) activation and suppression of hypoxia-inducible factor 1α (HIF-1α)-induced aerobic glycolysis play a central role in septic pulmonary fibrogenesis. Cellular experiments demonstrated that lipopolysaccharide increased fibroblast activation through AMPK inactivation, HIF-1α induction, alongside an augmentation of aerobic glycolysis. By contrast, the effects were reversed by AMPK activation or HIF-1α inhibition. In addition, pretreatment with metformin, which is an AMPK activator, suppresses HIF-1α expression and alleviates PF associated with sepsis, which is caused by aerobic glycolysis, in mice. Hypoxia-inducible factor 1α knockdown demonstrated similar protective effects in vivo . Our research implies that targeting AMPK activation and HIF-1α-induced aerobic glycolysis with metformin might be a practical and useful therapeutic alternative for sepsis-associated PF.

Computed tomography-guided biopsy for sub-centimetre pulmonary nodules: a meta-analysis.

Introduction: Pulmonary nodules (PNs) with a diameter from 5 to 10 mm exhibit malignancy rates anywhere from 47.5 to 61.5%. Despite the potential danger posed by these lesions, their small size makes the biopsy of these sub-centimetre (≤ 10 mm) PNs under computed tomography (CT) guidance very difficult. Aim: A meta-analysis was performed with the goal of evaluating the safety and diagnostic utility of CT-guided biopsy procedures for sub-centimetre PNs. Material and methods: Relevant studies published through April 2023 were identified in the PubMed, Web of Science, and Wanfang databases and used to conduct pooled analyses of selected endpoints, including technical success, diagnostic yield, diagnostic accuracy, pulmonary haemorrhage, and pneumothorax rates. Results: In total, this meta-analysis incorporated 10 studies in which 1482 patients with sub-centimetre PNs underwent CT-guided biopsy procedures. Among these patients, the respective pooled rates of technical success, diagnostic yield, diagnostic accuracy, pulmonary haemorrhage, and pneumothorax were 90%, 60%, 91%, 11%, and 24%, and significant heterogeneity was detected for all of these endpoints (I2 = 93.6%, 96%, 76.9%, 80.8%, and 93.6%). A substantial difference in diagnostic accuracy was observed when comparing biopsy procedures performed using fine- and core-needle biopsy approaches (85% vs. 95%), whereas the use of the co-axial method or the selected guidance approach (conventional vs. cone-beam CT) had no impact on diagnostic accuracy. Needle type, guidance method, and co-axial method use had no impact on the rates of pulmonary haemorrhage or pneumothorax. Conclusions: CT-guided biopsy represents a safe and effective means of accurately diagnosing sub-centimetre PNs.

Preoperative and Prognostic Prediction of Microvascular Invasion in Hepatocellular Carcinoma: A Review Based on Artificial Intelligence.

Microvascular invasion of hepatocellular carcinoma is an important factor affecting tumor recurrence after liver resection and liver transplantation. There are many ways to classify microvascular invasion, however, an international consensus is urgently needed. Recently, artificial intelligence has emerged as an important tool for improving the clinical management of hepatocellular carcinoma. Many studies about microvascular invasion currently focus on preoperative and prognosis prediction of microvascular invasion using artificial intelligence. In this paper, we review the definition and staging of microvascular invasion, especially the diagnosis of it by using artificial intelligence. In preoperative prediction, deep learning based on multimodal data modeling of radiomics-screened features, clinical features, and medical images is currently the most effective means. In prognostic prediction, pathology is the gold standard, and the techniques used should more effectively utilize the global features of the pathology images.

Arctium lappa L. roots inhibit the intestinal inflammation of dietary obese rats through TLR4/NF-κB pathway.

Long-term consumption of Arctium lappa L. roots can lead to weight loss. To explore the relationship between anti-obesity and anti-inflammation, the effects and mechanism of A. lappa L. root powder (ARP) on intestinal inflammation in obese rats were investigated. Dietary obese rats were successfully established by feeding a high-fat and high-sugar diet. The control group (n = 6) consumed a normal diet. The intestines were compared among the groups (each n = 6) with and without the administration of ARP (intragastric 7.5 g/kg·bw/d). Real-time quantitative reverse transcription-polymerase chain reaction and western blotting analysis revealed that ARP effectively inhibited the expression of pro-inflammatory and inflammatory cytokines in the colons of obese rats. These cytokines included interleukin (IL)-1ß, IL-8, IL-6, tumor necrosis factor-α (TNF-α), monocyte chemoattractant protein-1, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1. The inhibition rates for all these cytokines exceeded 88 %. Moreover, ARP demonstrated the ability to down-regulate key genes involved in Toll-like receptor 4 (TLR4) complexes, namely Tlr4, myeloid differentiation protein-2 (Md2), and myeloid differentiation factor 88 (Myd88), along with downstream signaling molecules such as tumor necrosis factor receptor associated factor 6 (TRAF6) and nuclear factor-κB (NF-κB), with inhibition rates over 81 %. Additionally, ARP was observed to inhibit protein levels of TLR4, NF-κB, IL-1ß, and TNF-α in the colons of obese rats, with inhibition rates of 65.6 ± 10.9 %, 84.4 ± 19.9 %, 80.8 ± 14.4 %, and 68.4 ± 17.5 %, respectively. This study confirmed the effectiveness of ARP in inhibiting intestinal inflammation through the blockade of the TLR4/NF-κB signaling pathway. It also suggested that ARP holds potential in improving intestinal health in the context of obesity, implying its possible application in the prevention and treatment of obesity and related metabolic diseases.

Primary thyroid smooth muscle tumour.

Not required for Clinical Vignette.

Genome-wide identification and expression analysis of the NRT genes in Ginkgo biloba under nitrate treatment reveal the potential roles during calluses browning.

Nitrate is a primary nitrogen source for plant growth, and previous studies have indicated a correlation between nitrogen and browning. Nitrate transporters (NRTs) are crucial in nitrate allocation. Here, we utilized a genome-wide approach to identify and analyze the expression pattern of 74 potential GbNRTs under nitrate treatments during calluses browning in Ginkgo, including 68 NITRATE TRANSPORTER 1 (NRT1)/PEPTIDE TRANSPORTER (PTR) (NPF), 4 NRT2 and 2 NRT3. Conserved domains, motifs, phylogeny, and cis-acting elements (CREs) were analyzed to demonstrate the evolutionary conservation and functional diversity of GbNRTs. Our analysis showed that the NPF family was divided into eight branches, with the GbNPF2 and GbNPF6 subfamilies split into three groups. Each GbNRT contained 108-214 CREs of 19-36 types, especially with binding sites of auxin and transcription factors v-myb avian myeloblastosis viral oncogene homolog (MYB) and basic helix-loop-helix (bHLH). The E1X1X2E2R motif had significant variations in GbNPFs, indicating changes in the potential dynamic proton transporting ability. The expression profiles of GbNRTs indicated that they may function in regulating nitrate uptake and modulating the signaling of auxin and polyphenols biosynthesis, thereby affecting browning in Ginkgo callus induction. These findings provide a better understanding of the role of NRTs during NO3- uptake and utilization in vitro culture, which is crucial to prevent browning and develop an efficient regeneration and suspension production system in Ginkgo.