Ultrasonographic and pathological features of primary adrenal lymphoma.

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Magnetostriction, piezomagnetism and domain nucleation in a Kagome antiferromagnet.

Whenever the elastic energy of a solid depends on magnetic field, there is a magnetostrictive response. Field-linear magnetostriction implies piezomagnetism and vice versa. Here, we show that Mn3Sn, a non-collinear antiferromanget with Weyl nodes, hosts a large and almost perfectly linear magnetostriction even at room temperature. The longitudinal and transverse magnetostriction, with opposite signs and similar amplitude are restricted to the kagome planes and the out-of-plane response is negligibly small. By studying four different samples with different Mn:Sn ratios, we find a clear correlation between the linear magnetostriction, the spontaneous magnetization and the concentration of Sn vacancies. The recently reported piezomagnetic data fits in our picture. We show that linear magnetostriction and piezomagnetism are both driven by the field-induced in-plane twist of spins. A quantitative account of the experimental data requires the distortion of the spin texture by Sn vacancies. We find that the field-induced domain nucleation within the hysteresis loop corresponds to a phase transition. Within the hysteresis loop, a concomitant mesoscopic modulation of local strain and spin twist angles, leading to twisto-magnetic stripes, arises as a result of the competition between elastic and magnetic energies.

Ultrasound-guided thrombin injection combined with micro-coils embolization for treatment of thoracoacromial artery pseudoaneurysm.

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The ultrasonography and pathological features of primary hepatic pleomorphic undifferentiated sarcoma.

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A recurrence-predictive model based on eight genes and tumor mutational burden/microsatellite instability status in Stage II/III colorectal cancer.

BACKGROUND: Although adjuvant chemotherapy (ACT) is widely used to treat patients with Stage II/III colorectal cancer (CRC), administering ACT to specific patients remains a challenge. The decision to ACT requires an accurate assessment of recurrence risk and absolute treatment benefit. However, the traditional TNM staging system does not accurately assess a patient's individual risk of recurrence. METHODS: To identify recurrence risk-related genetic factors for Stage II/III CRC patients after radical surgery, we conducted an analysis of whole-exome sequencing of 47 patients with Stage II/III CRC who underwent radical surgery at five institutions. Patients were grouped into non-recurrence group (NR, n = 24, recurrence-free survival [RFS] > 5 years) and recurrence group (R, n = 23, RFS <2 years). The TCGA-COAD/READ cohort was employed as the validation dataset. RESULTS: A recurrence-predictive model (G8plus score) based on eight gene (CUL9, PCDHA12, HECTD3, DCX, SMARCA2, FAM193A, AATK, and SORCS2) mutations and tumor mutation burden/microsatellite instability (TMB/MSI) status was constructed, with 97.87% accuracy in our data and 100% negative predictive value in the TCGA-COAD/READ cohort. For the TCGA-COAD/READ cohort, the G8plus-high group had better RFS (HR = 0.22, p = 0.024); the G8plus-high tumors had significantly more infiltrated immune cell types, higher tertiary lymphoid structure signature scores, and higher immunological signature scores. The G8plus score was also a predict biomarker for immunotherapeutic in advanced CRC in the PUCH cohort. CONCLUSIONS: In conclusion, the G8plus score is a powerful biomarker for predicting the risk of recurrence in patients with stage II/III CRC. It can be used to stratify patients who benefit from ACT and immunotherapy.

A Meta-Analysis on the Impact of Prenatal and Early Childhood Antimicrobial Use on Autism Spectrum Disorders.

OBJECTIVE: To investigate the impact of prenatal and early childhood antimicrobial use on autism spectrum disorders (ASD). DATA SOURCES: We searched PubMed and Embase databases for relevant studies from inception to August 2022. STUDY SELECTION AND DATA EXTRACTION: Peer-reviewed, observational studies were all acceptable. Raw data were extracted into a predefined worksheet and quality analysis was performed using the Newcastle-Ottawa Scale. DATA SYNTHESIS: Nineteen studies were identified in the meta-analysis. Prenatal antimicrobial exposure was not associated with ASD (P = 0.06 > 0.05), whereas early childhood antimicrobial exposure was associated with an increased odds ratio of ASD (OR = 1.17, 95% CI = [1.08-1.27], P value < 0.001). The sibling-matched analysis, with a very limited sample size, suggested that neither prenatal (P = 0.47 > 0.05) nor early childhood (P = 0.13 > 0.05) antimicrobial exposure was associated with ASD. Medical professionals may need to take the possible association into consideration when prescribing an antimicrobial in children. CONCLUSIONS: Early childhood antimicrobial exposure could increase the incidence of ASD. In future studies, it would be necessary to control for confounding factors, such as genetic factors, parenteral age at birth, or low birthweight, to further validate the association.

Identification of a Genomic Instability-Related Long Noncoding RNA Prognostic Model in Colorectal Cancer Based on Bioinformatic Analysis.

Background: In recent years, a growing body of research has revealed that long noncoding RNAs (lncRNAs) participate in regulating genomic instability. Materials and Methods: We obtained RNA expression profiles, somatic mutation profiles, clinical information, and pathological features of colorectal cancer (CRC) from The Cancer Genome Atlas project. We divided the cohort into two groups based on mutation frequency and identified genomic instability-related lncRNAs (GI-lncRNAs) using R software. We further analyzed the function of identified GI-lncRNAs and established a prognostic model through Cox regression. Using the established prognostic model, we divided the cohort into the high- and low-risk groups and further verified the prognostic differences between the two groups as well as the predictive power of prognosis-related lncRNAs in the genomic instability of CRC. Results: We identified a total of 143 GI-lncRNAs that were differentially expressed between the higher mutation frequency group and the lower mutation frequency group. According to Kyoto Encyclopedia of Genes and Genomes pathway and Gene Ontology analyses, a series of cancer-associated terms were enriched. We further constructed a prognostic model that included five GI-lncRNAs (lncRNA PTPRD-AS1, lncRNA AC009237.14, lncRNA LINC00543, lncRNA AP003555.1, and lncRNA AL109615.3). We confirmed that the expression of the five GI-lncRNAs was associated with prognosis and the mutation of critical genes in the CRC patient cohort. Conclusions: The present research further confirmed the vital function of GI-lncRNAs in the genomic instability of CRC. The five GI-lncRNAs identified in our study are potential biomarkers and need to be studied in more depth.

Molecular Characteristics, Oncogenic Roles, and Relevant Immune and Pharmacogenomic Features of EVA1B in Colorectal Cancer.

OBJECTIVE: EVA1B, a protein coding gene, is a critical paralog of EVA1A gene. Herein, our study was conducted to investigate the role of EVA1B in colorectal cancer (CRC) progression and prognosis. METHODS: Pan-cancer analysis was conducted to analyze expression, genetic and epigenetic alterations, and immunological characteristics of EVA1B. Especially, immunological characteristics and mutational landscape were compared between high and low EVA1B expression groups in the combined TCGA-COAD and TCGA-READ datasets. Through random survival forest analysis, an EVA1B-derived genomic model was developed, and its prognostic value was verified in the external datasets (GSE14333, GSE39582, and GSE87211). Drug sensitivity was compared between high- and low-risk subpopulations. A nomogram was conducted through integrating independent factors. RESULTS: EVA1B expression presented a remarkable upregulation in most cancer types, especially CRC. EVA1B expression was significantly correlated to DNA methyltransferases, DNA mismatch repair genes, m6A regulators, TMB, and MSI across pan-cancer. High EVA1B expression indicated an undesirable CRC patients' prognosis. Additionally, its upregulation was correlated to enhanced immune cell infiltration, increased stromal and immune activation, and elevated activities of cancer immunity cycle. Higher frequencies of amplification and deletion were investigated in high EVA1B expression subpopulation. Following verification, the EVA1B-derived genomic model reliably predicted patients' prognosis and drug responses. The nomogram (age, stage, EVA1B-derived risk score) was conducted to quantify an individual's survival probability. Furthermore, our experimental validation based on immunohistochemistry indicated that EVA1B overexpression is correlated with CRC tumorigenesis and poor outcomes in our CRC patients' cohort. CONCLUSION: Collectively, our findings provided valuable resource for guiding the mechanisms and therapeutic analysis of EVA1B in CRC.

Fecal Bacteria as Non-Invasive Biomarkers for Colorectal Adenocarcinoma.

Colorectal adenocarcinoma (CRC) ranks one of the five most lethal malignant tumors both in China and worldwide. Early diagnosis and treatment of CRC could substantially increase the survival rate. Emerging evidence has revealed the importance of gut microbiome on CRC, thus fecal microbial community could be termed as a potential screen for non-invasive diagnosis. Importantly, few numbers of bacteria genus as non-invasive biomarkers with high sensitivity and specificity causing less cost would be benefitted more in clinical compared with the whole microbial community analysis. Here we analyzed the gut microbiome between CRC patients and healthy people using 16s rRNA sequencing showing the divergence of microbial composition between case and control. Furthermore, ExtraTrees classifier was performed for the classification of CRC gut microbiome and heathy control, and 13 bacteria were screened as biomarkers for CRC. In addition, 13 biomarkers including 12 bacteria genera and FOBT showed an outstanding sensitivity and specificity for discrimination of CRC patients from healthy controls. This method could be used as a non-invasive method for CRC early diagnosis.

Characterization of the Prognostic m6A-Related lncRNA Signature in Gastric Cancer.

N6-methyladenosine (m6A) is a common form of mRNA modification regulated by m6A RNA methylation regulators and play an important role in the progression of gastric cancer (GC). However, the prognostic role of m6A-related lncRNA in gastric cancer has not been fully explored. This study aims at exploring the biological function and prognostic roles of the m6A-related lncRNA signature in gastric cancer. A total of 800 m6A-related lncRNAs were identified through Pearson correlation analysis between m6A regulators and all lncRNAs. Eleven m6A-related lncRNA signatures were identified through a survival analysis and the Kaplan-Meier (KM) curve analysis results suggest that patients in the low-risk group have a better overall survival (OS) and disease-free survival (DFS) outcome than the high-risk group. Also, the lncRNA signature can serve as an independent prognostic factor for OS and DFS. The gene set enrichment analysis (GSEA) result suggests that patients in the high-risk group were mainly enriched in the ECM receptor interaction, focal adhesion, and cytokine-cytokine receptor interaction pathway, while the low-risk group was characterized by the base excision repair pathway. We further constructed an individualized prognostic prediction model via the nomogram based on the independent prognostic factor for the OS and DFS, respectively. In addition, some candidate drugs aimed at GC risk group differentiation were identified using the Connective Map (CMAP) database. Lastly, four subgroups (C1, C2, C3, and C4) were identified based on the m6A-related lncRNA expression, through a consensus clustering algorithm. Among them, C1 and C2 have a greater likelihood to respond to immune checkpoint inhibitor immunotherapy, suggesting that the C1 and C2 subgroup might benefit from immunotherapy. In conclusion, the m6A-related lncRNA signature can independently predict the OS and DFS of GC and may aid in development of personalized immunotherapy strategies.

The predictive and prognostic value of sex in localized colorectal cancer: a SEER-based analysis.

BACKGROUND: Although the influence of sex on different cancer survival has been investigated, the predictive and prognostic value of sex in localized colorectal cancer (CRC) still remain controversial. METHODS: Survival was evaluated in patients who diagnosed with localized CRC in the Surveillance, Epidemiology, and End Results (SEER) database between 2004 and 2016. Overall survival (OS) outcomes were estimated with the Kaplan-Meier method, and multivariable Cox regression was used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: We obtained a dataset that included 70,836 males and 69,705 females of localized CRC patients. Compared with males, females more often had age ≥75 years (55.1% vs. 44%), right-sided colon cancer (56.8% vs. 45.4%), and more advanced pT stage cancer (75.5% vs. 72%). In addition, we found that females had better OS than males and that sex could be an independent factor of OS in T1-3N0M0 (Stage I-II) colon cancer (regardless of right/left-sided tumour) and T1-2N0M0 (Stage I) rectal cancer (each HR <1, each P<0.05). Although a significant OS benefit was not observed in T3N0M0 rectal cancer in the overall analysis (P=0.183), females who underwent postoperative chemotherapy had better OS than males among T3N0M0 (Stage II) rectal cancer patients significantly (P<0.001). CONCLUSIONS: In our study, sex was shown to be a prognostic factor in localized-CRC. In particular, females may benefit more from postoperative chemotherapy than males with T3N0M0 (Stage II) rectal cancer.

Characterization of KH-560-Modified Jute Fabric/Epoxy Laminated Composites: Surface Structure, and Thermal and Mechanical Properties.

In this study, jute fabrics were used to reinforce epoxy resin to prepare laminated composites. KH-560 silane coupling agent modification was used to improve the interfacial compatibility between fibers and epoxy. The effects of different immersion times (0 min, 10 min, 30 min, 60 min, 90 min, and 120 min) on the jute fiber's element content, crystal structure, and thermal stability, and the mechanical properties of laminated composites were studied. X-ray diffractometry (XRD) analysis showed that the KH-560 modification improved the crystallinity index (CI) and crystallite sizes (CS) of jute fibers. Scanning electron microscopy (SEM) analysis of the tensile fracture surfaces revealed a thick epoxy on the modified pulled fiber surfaces. Fourier transform infrared spectroscopy (FTIR) and energy dispersive spectrometer (EDS) analysis identified the presence of silicon and C-O-Si/Si-O-Si cross-linked structures on the surface of modified jute fibers. These cross-linked structures improved the thermal stability and mechanical properties of the laminated composites. When the immersion time was 60 min, the CI, CS, tensile strength, tensile modulus, flexural strength, and flexural modulus of the modified samples were 42.39%, 3.62 nm, 34.6 ± 1.1 MPa, 2.11 ± 0.12 GPa, 83.7 ± 1.8 MPa, and 4.08 ± 0.12 GPa, respectively, which were better than that of unmodified and other modified composites.

An anti-windup INDI fault-tolerant control scheme for flying wing aircraft with actuator faults.

In this paper, an anti-windup incremental nonlinear dynamic inversion (INDI) fault-tolerant scheme is proposed for flying wing aircraft with actuator faults, actuator saturation and uncertainties of aerodynamic parameters. An optimal anti-windup compensator based on nonlinear partial differential inequalities is used to compensate the actuator saturation. INDI is used to control the fault system and compensate the uncertainties of the flight dynamics. Control allocation strategy is designed in consideration of the control scheme and configuration of the control surfaces. The proposed control method can guarantee the bounded tracking of the reference signals. Simulation results are given to show the effectiveness of the proposed method.

MicroRNA-761 is downregulated in colorectal cancer and regulates tumor progression by targeting Rab3D.

The purpose of the present study was to investigate the biological role of microRNA-761 (miR-761) in colorectal cancer (CRC) and the underlying mechanisms by which miR-761 regulates CRC cell proliferation and migration. Quantitative polymerase chain reaction was performed to measure miR-761 expression in CRC tumor tissues and cell lines. It was demonstrated that miR-761 expression was dramatically reduced in CRC tumor tissues and cell lines compared with in normal tissues and cell lines. Overexpression of miR-761 significantly decreased CRC cell growth and migration. Using bioinformatics analysis and luciferase reporter assays, Rab3D was identified as a novel target of miR-761. In addition, it was demonstrated that Rab3D expression was negatively correlated with miR-761. Furthermore, overexpression of Rab3D could reverse the inhibitory effects of miR-761 on cell proliferation and migration. Collectively, the present study demonstrated that miR-761 overexpression could inhibit the proliferation and migration of CRC cell lines, partly at least, via directly targeting Rab3D.

Is adjuvant chemotherapy necessary for locally advanced rectal cancer patients with pathological complete response after neoadjuvant chemoradiotherapy and radical surgery? A systematic review and meta-analysis.

PURPOSE: Current clinical guidelines recommended the routine use of adjuvant chemotherapy for locally advanced rectal cancer (LARC) patients. However, the effects of adjuvant chemotherapy in patients with pathological complete response (pCR) after neoadjuvant chemoradiotherapy and radical surgery showed discrepancies in different investigations. METHODS: A systematic review and meta-analysis were conducted using PubMed, Embase and Web of Science databases. All original comparative studies published in English that were related to adjuvant versus non-adjuvant chemotherapy for LARC patients with pCR were included. RESULTS: A total of 6 studies based on 18 centres or databases involving 2948 rectal cancer patients with pCR (adjuvant group = 1324, non-adjuvant group = 1624) were included in our overall analysis. Based on our meta-analysis, LARC patients with pCR who received adjuvant chemotherapy showed a significantly improved overall survival (OS) when compared to patients with observation (HR = 0.65, 95% CI = 0.46-0.90, P = 0.01). In addition, investigations focused on this issue based on the National Cancer Database (NCDB) were systematically reviewed in our current study. Evidence from all three analyses demonstrated that LARC patients with clinical nodal positive disease that achieved pCR might benefit the most from additional adjuvant chemotherapy. CONCLUSION: Our meta-analysis indicated that adjuvant chemotherapy is associated with improved OS in LARC patients with pCR after neoadjuvant chemoradiotherapy and radical surgery.

miR-135a Protects Dextran Sodium Sulfate-Induced Inflammation in Human Colorectal Cell Lines by Activating STAT3 Signal.

BACKGROUND/AIMS: miR-135a is reduced in several cancers and has been suggested to mediate immune and inflammatory responses. However, the effect of miR-135a on inflammatory bowel diseases was obscure. This study firstly attempted to investigate the hypothesis that miR-135a alleviates dextran sodium sulfate (DSS)-induced inflammation in colonic cells and potential mechanisms are also studied. METHODS: Caco-2 and HT-29 cells in this study were treated with DSS, miR-135a mimic, and S3I-201, and then CKK-8 assay was used to test cell viability. Expressions of miR-135a, cytokines, and signal transducers and activators of transcription factors (STATs) were determined by RT-PCR. Also, cytokine productions were further tested by using ELISA kits. Activation or inactivation of STAT3 signal was validated by western blotting analysis. RESULTS: The results showed that DSS markedly downregulated miR-135a expression (P< 0.05) and induced inflammatory response in Caco-2 and HT-29 cells evidenced by the up regulations and productions of interleukin-1ß (IL-1ß) and tumor necrosis factor-ɑ (TNF-ɑ) (P< 0.05). Transfection with miR-135a mimic significantly alleviated DSS-induced upregulation and productions of IL-1ß and TNF-ɑ in Caco-2 and HT-29 cells (P< 0.05). STATs were analyzed and miR-135a mimic treatment reversed STAT3 downregulation in DSS-challenged Caco-2 and HT-29 cells compared with the mimic control (P< 0.05). Also, STAT3 phosphorylation was inhibited in DSS-challenged Caco-2 cells and miR-135a mimic activated STAT3 signal (P< 0.05). S3I-201, an inhibitor of STAT3 signal, further used to inactivate STAT3 signal and the results showed that S3I-201 blocked the anti-inflammatory effect of miR-135a mimic on Caco-2 and HT-29 cells evidenced by the lowered expressions and productions of proinflammatory cytokines ((IL-1ß and TNF-ɑ) (P< 0.05). CONCLUSION: Our results indicated that miR-135a alleviated DSS-induced inflammation and activated STAT3 signal in colonic cells. Inhibition of STAT3 reversed the anti-inflammatory function of miR-135a by regulating proinflammatory cytokines. Thus, STAT3 signal might serve, at least in part, as the potential mechanism of miR-135a-mediated anti-inflammatory effect in colonic cells.

miR­218 promotes apoptosis of SW1417 human colon cancer cells by targeting c­FLIP.

MicroRNAs (miRNAs) are suggested to act as either tumor oncogenes or tumor suppressors in different types of cancer. miRNA­218 (miR­218) is a type of short, non-coding RNA which is involved in gastric cancer development. In the present study, we evaluated the functions of miR­218 in SW1417 human colon cancer cells and its potential mechanisms. Following overexpression of miR­218 in human colon cancer cells, cell viability was determined by CKK­8 assay, cell apoptosis was observed using a TUNEL Kit, the expression of caspase­8, and its inhibitor cellular Fas­associated death domain­like interleukin­1ß­converting enzyme inhibitory protein (c­FLIP) was assessed by RT­PCR, western blot analysis and immunohistochemistry. The results indicated that miR­218 and caspase­8 expression was decreased while c­FLIP expression was elevated in human colon cancer tissues. In cultured SW1417 human colon cancer cells, miR­218 overexpression potently inhibited cell viability and promoted cell apoptosis. Furthermore, downregulation of c­FLIP expression and upregulation of caspase­8 expression were detected in miR­218­stimulated SW1417 cells. In addition, following the knockdown of c­FLIP using c­FLIP siRNA, the apoptotic effects of miR­218 on SW1417 cells were significantly reduced. Collectively, the present study demonstrated that miR­218 induced the apoptosis of SW1417 cells by targeting c­FLIP. Therefore, miR­218 may represent a potential therapeutic method for screening and treating colon cancer.