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Time‐dependent diffusion MRI (td‐dMRI) has potential in characterizing microstructural features; however, its value in imaging endometrioid endometrial adenocarcinoma (EEA) remains uncertain. Patients surgically confirmed with EEA were finally enrolled in our study. The td‐dMRI data were acquired using pulsed gradient spin echo sequence and oscillating gradient spin echo sequences. The microstructural markers, including cell diameter, intracellular volume fraction (Vin), cellularity, and extracellular diffusivity (Dex), were fitted with the imaging microstructural parameters using a limited spectrally edited diffusion (IMPULSED) model. The parameters were compared between low‐ and high‐risk groups and between low‐ and high‐proliferation groups. The diagnostic performance was evaluated using receiver‐operating characteristic curve and logistic regression analysis. Diameter, Dex, ADCPGSE, ADCN1, and ADCN2 were significantly low, whereas cellularity, ΔADC1 and ΔADC2 were significantly high in the high‐risk and high‐proliferation groups. Cellularity, ΔADC1, and ΔADC2 demonstrated excellent diagnostic efficacy in predicting both risk stratification and proliferation status. Cellularity was the only independent predictor for risk stratification, which exhibited a satisfactory positive correlation with cell density in histopathologic examination. The diagnostic potential of td‐dMRI‐based microstructural mapping was demonstrated to noninvasively probe the pathologic characteristics of patients with EEA in a clinical setting, which provided a valuable contribution to surgical guidance. This work, demonstrating the diagnostic potential of td‐dMRI‐based microstructural mapping in noninvasively probing the pathologic characteristics of patients with EEA in a clinical setting and providing a valuable contribution to surgical guidance, would be of interest to a broad readership in the fields of oncology, preoperative evaluation, and cancer treatment strategies.

Rheumatoid arthritis (RA) is a chronic inflammatory disease with a serious pre-vascular inflammatory phase, followed by significant increase in vessel growth. Inhibition of angiogenesis is a novel therapeutic strategy against RA. The Chinese herbal remedy Tripterygium wilfordii, Hook. f. (TwHf) has been reported to be therapeutically efficacious in the treatment of RA. Recent studies have revealed that treatment with TwHf extracts inhibit angiogenesis of RA, thereby elaborately attenuation RA symptom. This review mainly addresses the anti-angiogenesis effect of TwHf in treatment of RA.

Introduction: Ablation therapy is a commonly used tool in the management of hepatocellular carcinoma (HCC). After ablation, dying cancer cells release a variety of substances that trigger subsequent immune responses. Immunogenic cell death (ICD) has been a trending topic in recent years and has been discussed many times along with oncologic chemotherapy. However, the subject of ablative therapy and ICDs has been little discussed. The purpose of this study was to investigate whether ablation treatment induces ICD in HCC cells and whether different types of ICDs arise because of different ablation temperatures. Methods: Four different HCC cell lines (H22, Hepa-16, HepG2 and SMMC7221) were cultured and treated under different temperatures (−80°C, −40°C, 0°C, 37°C, and 60°C). Cell Counting Kit-8 assay was performed to analyze the viability of different cell lines. Apoptosis was detected by flow cytometry assay, and a few ICD-related cytokines (calreticulin, ATP, high mobility group box 1, and CXCL10) were detected by immunofluorescence or enzyme-linked immunosorbent assay. Results: The apoptosis rate of all kinds of cells increased significantly in −80°C group ( p < 0.01) and 60°C group ( p < 0.01). The expression levels of ICD-related cytokines were mostly significantly different between the different groups. For calreticulin, Hepa1-6 cells and SMMC7221 cells showed significantly higher protein expression levels in 60°C group ( p < 0.01) and significantly lower protein expression levels −80°C group ( p < 0.01). The ATP, high mobility group box 1 and CXCL10 expression levels were significantly higher in 60°C, −80°C and −40°C group of all four cell lines ( p < 0.01). Conclusion: Different ablative treatments could induce different types of ICDs in HCC cells, providing a promising track for the development of individualized cancer therapies.

Traditional Chinese opera, such as , requires actors to master sophisticated performance skills and cultural knowledge, potentially influencing brain function. This study aimed to explore the effects of long-term opera training on the dynamic amplitude of low-frequency fluctuation (dALFF) and dynamic functional connectivity (dFC). Twenty professional well-trained actors and twenty demographically matched untrained subjects were recruited. Resting-state functional magnetic resonance imaging (fMRI) data were collected to assess dALFF differences in spontaneous regional brain activity between the actors and untrained participants. Brain regions with altered dALFF were selected as the seeds for the subsequent dFC analysis. Statistical comparisons examined differences between groups, while correlation analyses explored the relationships between dALFF and dFC, as well as the associations between these neural measures and the duration of training. Compared with untrained subjects, professional actors exhibited significantly lower dALFF in the right lingual gyrus. Additionally, actors showed increased dFC between the right lingual gyrus and the bilateral cerebellum, as well as between the right lingual gyrus and the bilateral midbrain/red nucleus/thalamus, compared with untrained subjects. Furthermore, a negative correlation was found between the dALFF in the right lingual gyrus and its dFC, and a significant association was found between dFC in the bilateral midbrain/red nucleus/thalamus and the duration of training. Long-term engagement in training induces neuroplastic changes, reflected in altered dALFF and dFC. These findings provide evidence for the interaction between artistic training and brain function, highlighting the need for further research into the impact of professional training on cognitive functions.

White matter microstructure, essential for neural communication, is genetically influenced and often disrupted in schizophrenia. Large-scale genome-wide association studies have identified over 200 genome-wide significant loci for schizophrenia, yet the extent to which schizophrenia shares genetic architecture with white matter microstructure—particularly across multidimensional diffusion tensor imaging (DTI) metrics and hemispheric distinctions—remains incompletely understood. Here, we employed the conditional/conjunctional false discovery rate (cond/conjFDR) approach to investigate the genetic overlap between schizophrenia and white matter microstructure. These analyses utilized large-scale genome-wide association datasets for schizophrenia ( N case = 53,386, N control = 77,258) and the microstructure of 48 white matter tracts ( N = 33,224), derived from individuals of European ancestry. White matter integrity was assessed using fractional anisotropy (FA), mean diffusivity (MD), and 3 eigenvalues. Additionally, we performed comprehensive functional and validation analyses for the shared loci. We identified 435 shared loci, including 154 loci exclusive to 3 eigenvalues. Hemisphere-specific analysis of white matter tracts revealed lateralized patterns, with 25.5% to 34.4% of loci being left-specific and 23.9% to 33.7% right-specific. Enrichment analysis highlighted the shared loci related to nervous system and central nervous system development, supporting their role in neurodevelopmental mechanisms. Validation analyses across diverse methods and datasets further confirmed the reliability of the shared loci. This study demonstrates a complex, shared genetic architecture between schizophrenia and white matter microstructure, highlighting hemispheric genetic asymmetry and the value of multidimensional DTI metrics in uncovering the genetic basis of structural brain abnormalities.

Because of the high heterogeneity and low incidence of rare mutations in EGFR, it has been difficult to evaluate the efficacy of EGFR‐TKIs in the treatment of NSCLC with rare EGFR mutations. The results indicated that osimertinib had a response rate comparable to other EGFR‐TKIs in patients with Gly719Xaa or Leu861Gln mutations. [...]in patients with Ser768Ile mutations, the response rate of osimertinib was better than the first‐generation EGFR‐TKIs. [...]there were some accompanying limitations of this study that are worth mentioning: (i) Instead of whole‐genome sequencing, the authors used a low sensitivity and small sequencing coverage method (PCR combined with direct sequencing) to detect EGFR mutations. [...]there are certain limitations in detecting EFGR mutations; (ii) in addition to patients receiving first‐line osimertinib therapy, this study also included patients receiving second‐ and third‐line osimertinib therapy.

Background We investigated the relationship between small cell lung cancer (SCLC) and non‐small cell lung cancer (NSCLC) based on micro ribonucleic acid (miRNA) and messenger (m)RNA expression profiles. Methods Utilizing the differentially expressed mRNAs and the targeting miRNAs, the mRNA‐miRNA network for the two cancers was constructed. By integrating the miRNA expression profile, drug, and drug targets, miRNA‐drug target‐drug networks were established and the mechanisms in drug therapy efficacy were compared between SCLC and NSCLC. Results Drug targets of different expressed miRNAs of SCLC are mainly located in the organelle, act in the electron carrier activity, and consist of the synapse; while drug targets of NSCLC are the membrane‐enclosed lumen, mainly distributed in the extracellular region and synapse, and function in the binding. Drug targets of miRNA expressed commonly in the two cancers are involved in the reproduction multi‐organism process. In SCLC, the miR‐16 in the miRNA‐drug target‐drug network is significant and follows the result of the mRNA‐miRNA network. The pigmentation and rhythmic process of SCLC is different from NSCLC, while the process of cellular component biogenesis and cellular component organization are important for the occurrence of NSCLC. miR‐16 in the miRNA‐mRNA‐drug network of SCLC is significant and we acquired 11 potential drugs, such as dexamethasone and budesonide. The miR‐124 for NSCLC is important in the network and 17 potential drugs were screened, including dexamethasone and budesonide. Conclusions These findings suggest that miR‐16 and miR‐124 might be novel diagnostic and prognostics markers for SCLC and NSCLC, respectively.

4,5 In the 2010s, immunotherapy, especially treatment with pembrolizumab (a monoclonal antibody of programmed cell death protein 1 [PD-1] antibody), altered the treatment landscape for NSCLC patients without driver mutations. 6,7 Previous clinical trials have shown that pembrolizumab monotherapy more effectively improved the OS of advanced NSCLC patients without programmed death-ligand 1 (PD-L1) expression and oncogenic epidermal growth factor receptor (EGFR), or anaplastic lymphoma kinase (ALK) mutations compared with platinum-based chemotherapy. 8,9 Additionally, pembrolizumab in combination with chemotherapy has been shown to improve OS versus chemotherapy alone for advanced NSCLC patients without driver mutations, regardless of PD-L1 expression. 10,11 The first randomized, phase III study comparing the efficacy of pembrolizumab monotherapy and platinum-based chemotherapy is KEYNOTE-024. 12 The subsequent analysis of KEYNOTE-024 demonstrated that OS continued to be improved for pembrolizumab monotherapy versus platinum-based chemotherapy (HR = 0.63, 95% CI: 0.47–0.86). [...]5-year survival is considered to be an important milestone in the treatment of NSCLC. [...]the vast majority of patients who completed 35 cycles of pembrolizumab monotherapy were still alive at data cutoff, and nearly half of them survived without progressive disease or subsequent treatment, indicating that the treatment duration of pembrolizumab continued for at least 2 years. [...]of the 12 patients who received a second course of pembrolizumab due to subsequent progression, eight patients were still alive at data cutoff, and five survived without progressive disease, which indicated that pembrolizumab retreatment upon progressive disease is feasible and effective.

Schizophrenia progresses through high-risk, first-episode, and chronic stages, each associated with altered spontaneous brain activity. Resting state functional MRI studies highlight these changes, but inconsistencies persist, and the genetic basis remains unclear. A neuroimaging meta-analysis was conducted to assess spontaneous brain activity alterations in each schizophrenia stage. The largest available genome-wide association study (GWAS) summary statistics for schizophrenia (  = 53,386 cases, 77,258 controls) were used, followed by Hi-C-coupled multimarker analysis of genomic annotation (H-MAGMA) to identify schizophrenia-associated genes. Transcriptome-neuroimaging association and gene prioritization analyses were performed to identify genes consistently linked to brain activity alterations. Biological relevance was explored by functional enrichment. Fifty-two studies met the inclusion criteria, covering the high-risk (  = 409,  = 475), first-episode (  = 1842,  = 1735), and chronic (  = 1242,  = 1300) stages. High-risk stage showed reduced brain activity in the right median cingulate and paracingulate gyri. First-episode stage revealed increased activity in the right putamen and decreased activity in the left gyrus rectus and right postcentral gyrus. Chronic stage showed heightened activity in the right inferior frontal gyrus and reduced activity in the superior occipital gyrus and right postcentral gyrus. Across all stages, 199 genes were consistently linked to brain activity changes, involved in biological processes such as nervous system development, synaptic transmission, and synaptic plasticity. Brain activity alterations across schizophrenia stages and genes consistently associated with these changes highlight their potential as universal biomarkers and therapeutic targets for schizophrenia.