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Ultrasound (US) imaging is a widely used diagnostic method in clinics. Real-time-generated US images are used for rapid diagnosis without harm to patients. The quality of US imaging highly depends on the skill of the physician due to the differences among physicians. Techniques for autonomous robotic ultrasound (AU-RUS) acquisitions are expected to become an effective means to improve the level of US diagnosis, reduce the workload of physicians, and improve the standardization of US imaging quality. This paper aims to summarize the current research status of techniques for AU-RUS acquisitions, and to discuss the research trends and challenges regarding related technologies. Firstly, the techniques for AU-RUS acquisitions and systems are outlined. The techniques for teleoperated or autonomous US acquisitions are briefly discussed. Representative RUS acquisition systems are introduced. Then, the current research status of AU-RUS acquisitions is reviewed from four research directions: force sensitivity and control, scanning path-planning and positioning, US treatment guidance, and US image processing technology and quality assessment optimization. This review provides a decision-oriented autonomy perspective by mapping typical methods to workflow components across the stages of perception, decision-making, and execution. We identify major deployment bottlenecks, including safety-verifiable autonomy and failure recovery, motion compensation under deformation, and the lack of standardized, clinically meaningful US image quality metrics. Finally, the shortcomings of current research are summarized and analyzed, and the research trends and challenges for AU-RUS acquisitions are prospected.

Background Liver carcinoma generally presents as an immunosuppressive microenvironment that promotes tumor evasion. The intercellular crosstalk of immune cells significantly influences the construction of an immunosuppressive microenvironment. This study aimed to investigate the important interactions between immune cells and their targeting drugs in liver carcinoma, by using single-cell and bulk transcriptomic data. Methods Single-cell and bulk transcriptomic data were retrieved from Gene Expression Omnibus (GSE159977, GSE136103, and GSE125449) and The Cancer Genome Atlas (TGCA-LIHC), respectively. Quality control, dimension reduction, clustering, and annotation were performed according to the Scanpy workflow based on Python. Cell–cell interactions were explored using the CellPhone database and CellChat. Trajectory analysis was executed using a partition-based graph abstraction method. The transcriptomic factors (TFs) were predicted using single-cell regulatory network inference and clustering (SCENIC). The target genes from TFs were used to establish a related score based on the TCGA cohort; this score was subsequently validated by survival, gene set enrichment, and immune cell infiltration analyses. Drug prediction was performed based on the Cancer Therapeutics Response Portal and PRISM Repurposing datasets. Results Thirty-one patients at four different states, including health, hepatitis, cirrhosis, and cancer, were enrolled in this study. After dimension reduction and clustering, twenty-two clusters were identified. Cell–cell interaction analyses indicated that macrophage-naive CD4 + T cell interaction significantly affect cancerous state. In brief, macrophages interact with naive CD4 + T cells via different pathways in different states. The results of SCENIC indicated that macrophages present in cancer cells were similar to those present during cirrhosis. A macrophage-naive CD4 + T cell (MNT) score was generated by the SCENIC-derived target genes. Based on the MNT score, five relevant drugs (inhibitor of polo-like kinase 1, inhibitor of kinesin family member 11, dabrafenib, ispinesib, and epothilone-b) were predicted. Conclusions This study reveals the crucial role of macrophage-naive CD4 + T cell interaction in the immunosuppressive microenvironment of liver carcinoma. Tumor-associated macrophages may be derived from cirrhosis and can initiate liver carcinoma. Predictive drugs that target the macrophage-naive CD4 + T cell interaction may help to improve the immunosuppressive microenvironment and prevent immune evasion. The relevant mechanisms need to be further validated in experiments and cohort studies. Graphical Abstract

BackgroundPrevious studies have reported the potential of aryl hydrocarbon receptor (AhR) in cancer immunotherapy. However, the mechanisms underpinning its therapeutic value have yet to be comprehensively investigated. Thus, this research aimed to explore the underlying association between AhR and cancer immunotherapy in 33 human cancers.MethodsThe gene expression data and clinical characteristics of 33 cancers were retrieved from The Cancer Genome Atlas database. The immunotherapeutic cohorts included GSE67501 and GSE78220 as well as IMvigor210, which were obtained from the Gene Expression Omnibus database and included in a previously published study respectively. Clinical parameters, including patient age, gender, survival, and tumor stage were analyzed to assess the prognostic value of AhR. The activity of AhR was generated by single sample gene set enrichment analysis and used to evaluate the difference between the AhR transcriptome and protein expression level. To better understand the role of AhR in cancer immunotherapy, the correlation between AhR and tumor microenvironment, as well as its relation to immune processes/elements, such as immune cell infiltration, immune inhibitors and stimulators, and the major histocompatibility complex were analyzed. The relevant underlying pathways associated with AhR signaling in cancer were also explored. Furthermore, the correlation between AhR and two immunotherapeutic biomarkers (tumor mutational burden and microsatellite instability) was investigated. Finally, the relationship between AhR and immunotherapeutic response was explored using three independent immunotherapeutic cohorts.ResultsAlthough AhR was not closely associated with age (5/33), gender (3/33), or tumor stage (3/21) in any of the studied human cancers, it exhibited potential prognostic value for predicting patient survival. Consistency has been observed between AhR activity and expression in some cancers (7/33). Generally, AhR presented a robust correlation with immune cell infiltration, immune modulators, and immunotherapeutic markers. Moreover, high AhR expression was significantly related to immune-relevant pathways. However, no significant correlation was observed between AhR and the immunotherapeutic response.ConclusionsThis research investigated the immunotherapeutic value of AhR in 33 human cancers, providing evidence regarding the function of AhR and its role in clinical treatment. However, considering that a bioinformatics approach was adopted, the current results are preliminary and require further validation.

Hepatocellular carcinoma (HCC) is one of the most common primary cancers, and its pathogenesis is complicated and difficult to screen. Currently, there is no effective treatment. In traditional Chinese medicine, a large proportion of patients with HCC have been diagnosed with spleen deficiency (SD) syndrome and treated with tonifying traditional Chinese medicine, which has significant clinical efficacy. However, the role and molecular mechanism of SD in HCC remain unclear. In this study, 40 mice were randomly divided into four groups: control, SD, HCC, and SD-HCC groups. The liver cancer model of SD was established by reserpine induction and orthotopic transplantation. The effects of SD on the proliferation, apoptosis, invasion, and metastasis of HCC cells were studied by cell proliferation, cell apoptosis, cell scratch, and transwell assay. We found that compared with the HCC group, the protein expressions of cytotoxic T lymphocyte antigen 4 (CTLA-4), programmed cell death protein 1 (PD-1), phosphatase and tensin homolog (PTEN), and AKT (also known as protein kinase B or PKB) in the exosomes of the SD-HCC group were upregulated. In addition, the metastases and self-renewal of exosomes in the SD-HCC group were more aggressive than those in the HCC group, which could be partially reversed with the addition of CTLA-4 inhibitors. Further studies showed that in the internal environment of SD, CTLA-4 promoted tumor invasion and metastasis by regulating the PTEN/CD44 pathway. In conclusion, our findings suggest that during SD in the internal environment, exosome CTLA-4 regulates the PTEN/CD44 signal pathway to promote the proliferation, self-renewal, and metastasis of liver cancer.

Background. Tuina, acupuncture, traction, and Chinese herbs play an important role in the treatment of lumbar disc herniation. However, the comparative effectiveness and safety of the four commonly utilized treatment modalities are still unclear. Objective. To compare the effectiveness and safety of the four interventions for lumbar disc herniation. Methods. Randomized controlled trials comparing any two of the four interventions in the treatment of lumbar disc herniation were identified using the following databases: PubMed, the Cochrane Library, Embase, Web of Science, the China National Knowledge Infrastructure, Chinese Science and Technology Periodical Database, and Wanfang data, and network meta-analysis was performed using STATA 14.0. Results. One hundred and twenty-one studies involving a total of 13075 patients were included. In all the outcome measurements, traction demonstrated a worst effectiveness, and Tuina and acupuncture demonstrated a best effectiveness, but no significant differences were found between Tuina and acupuncture. Compared with Tuina or acupuncture, Chinese herbs showed a similar effectiveness in Visual Analogue Score and Japanese Orthopedic Association Scores, but an inferior effectiveness in invalid rate and cure rate. Conclusions. In the treatment of lumbar disc herniation, Tuina and acupuncture were superior to traction or Chinese herbs, and the effectiveness of traction was the worst. However, considering the limitations of this review, more high-quality trials, especially those comparing Chinese herbs with the other three interventions, should be carried out in the future to further confirm the current findings.

Objective. To investigate the potential active ingredients and underlying mechanisms of Artemisia annua (AA) on the treatment of hepatocellular carcinoma (HCC) based on network pharmacology. Methods. In the present study, we used a network pharmacological method to predict its underlying complex mechanism of treating HCC. First, we obtained relative compounds of AA based on the traditional Chinese medicine systems pharmacology (TCMSP) database and collected potential targets of these compounds by target fishing. Then, we built HCC-related targets target by the oncogenomic database of hepatocellular carcinoma (OncoDB.HCC) and biopharmacological network (PharmDB-K) database. Based on the matching results between AA potential targets and HCC targets, we built a protein-protein interaction (PPI) network to analyze the interactions among these targets and screen the hub targets by topology. Furthermore, the function annotation and signaling pathways of key targets were performed by Gene Oncology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis using DAVID tools. Finally, the binding capacity between active ingredients and key targets was validated by molecular docking. Results. A total of 19 main active ingredients of AA were screened as target prediction; then, 25 HCC-related common targets were seeked out via multiple HCC databases. The areas of nodes and corresponding degree values of EGFR, ESR1, CCND1, MYC, EGF, and PTGS2 were larger and could be easily found in the PPI network. Furthermore, GO and KEGG enrichment analysis showed that these key targets were significantly involved in multiple biological processes and pathways which participated in tumor cell proliferation, apoptosis, angiogenesis, tumor invasion, and metastasis to accomplish the anti-HCC activity. The molecular docking analysis showed that quercetin could stably bind to the active pocket of EGFR protein 4RJ5 via LibDock. Conclusion. The anticancer effects of AA on HCC were predicted to be associated with regulating tumor cell proliferation, apoptosis, angiogenesis, tumor invasion, and metastasis via various pathways such as the EGFR signaling pathway, ESR1 signaling pathway, and CCND1 signaling pathway. It is suggested that AA might be developed as a broad-spectrum antitumor drug based on its characteristics of multicomponent, multipath, and multitarget.

Hepatocellular carcinoma (HCC) is a major contributor to global cancer-related mortality. Serglycin (SRGN) is involved in the progression of various cancers, and its overexpression is related to poor prognosis in HCC patients. Its biological role in HCC aggressiveness is unknown. This study aims to elucidate the mechanism of SRGN in HCC. Via and vivo experiments, we identified SRGN as a critical regulator of HCC cells migratory capability and metastasis. SRGN significantly correlated with maintaining stemness-like characteristics, emphasizing its central role in HCC progression. Mechanistically, SRGN activated YAP into the tumor cells' nucleus. Moreover, SRGN selectively upregulated CRISPLD2, establishing the SRGN/YAP/CRISPLD2 axis and promoting metastatic behavior in HCC cells. Our results revealed that CRISPLD2 is a direct target of the SRGN-mediated YAP/TEAD1 complex. SRGN orchestrated stemness maintenance, tumorigenesis, and metastasis in an autocrine way by selectively reactivating the novel YAP/CRISPLD2 axis. Besides, sorafenib with verteporfin showed a certain therapeutic effect in SRGN-positive individuals. Our work clarifies the mechanism by which SRGN promotes the invasiveness of HCC. It provides insights into targeting the SRGN-triggered signaling pathway as a potential new direction in treating HCC.

Aims. Abundant evidences in traditional Chinese medicine (TCM) supported the therapeutic value of herbal medicine Yinchen in hepatocellular carcinoma (HCC), but the underlying mechanism remains to be investigated. Main Methods. The intersection of immune gene set, module genes, HCC-associated genes, and target genes of Yinchen was employed for further analyses. The module genes were identified by weighted gene coexpression network analysis, and the other three gene sets were obtained from public databases. Subsequently, we further explored the clinical value and immunoregulation of the hub gene of intersection. The relevant pathways related to hub gene expression were investigated by gene set enrichment analysis. Finally, the interaction of active compounds and target genes was validated by molecular docking. Key Findings. Thirteen active compounds and 90 target genes of Yinchen were included. After constructing the network among Yinchen, target genes, and HCC, BIRC5 was identified as the hub gene. Significant difference was found between the high-expressed group and the low-expressed group in survival and stage. Different immune subtypes also presented significant difference in BIRC5 expression. Moreover, NK cell and T cell (CD4+ effector memory and CD4+ memory resting) were negatively correlated with BIRC5 expression, while CTLA4 and LAG3 were positively correlated. The results of molecular docking further validated a good binding activity of quercetin-BIRC5 interaction. Significance. In summary, our research identified for the first time a novel underlying association among herbal medicine Yinchen, BIRC5, immunotherapy, and HCC. We speculated that Yinchen may target the immune checkpoints (CTLA4 and LAG3) and activate the immune cells by suppressing BIRC5.

•PLIF has its limitations in the treatment of lumbar degenerative diseases.•The interspinous process devices have advantages in lowering the incidence of ASD.•PLIF, Coflex, Wallis, and X-stop have the same effects in clinical outcomes. Posterior lumbar interbody fusion and lumbar interspinous non-fusion technique are common surgical procedures for lumbar degenerative diseases, but the effectiveness and safety of these two techniques are still unclear. We performed this network meta-analysis to evaluate the comparative effectiveness and safety of posterior lumbar interbody fusion and the three commonly used interspinous devices including Coflex, Wallis, and X-stop for lumbar degenerative diseases. Randomized controlled trials and cohort studies comparing among posterior lumbar interbody fusion, Coflex, Wallis, and X-stop for lumbar degenerative diseases were identified using the databases including PubMed, the Cochrane Library, Web of Science, the China National Knowledge Infrastructure, Chinese Science and Technology Periodical Database, and Wanfang data. A network meta-analysis was performed using R 3.4.3 software. 27 studies with 2241 patients were included. The results of network meta-analysis revealed that no significant differences in Oswestry Disability Index, Visual Analogue Scale, Japanese Orthopedic Association Scores, and posterior disc height were found among posterior lumbar interbody fusion group, Coflex, Wallis, or X-stop. However, compared with posterior lumbar interbody fusion, the three interspinous process devices presented with significantly more range of motion in surgical segment, but no significant difference was found among these three interspinous process devices. Node-splitting analysis showed no significant inconsistency in our network meta-analysis. We concluded that compared with posterior lumbar interbody fusion, Coflex, Wallis and X-stop had the same effectiveness in relieving pain, improving quality of life, recovering disc space height and lumbar function, but may lower incidence of adjacent segment degeneration.

Retinal dehydrogenase 5 (RDH5) is an important enzyme in the visual cycle. Several studies have reported that the RDH family may play crucial roles in tumor prognosis. However, the role of RDH5 in tumor prognosis is still unclear. We examined the mRNA level of RDH5 by using q-PCR in hepatocellular carcinoma (HCC) and adjacent non-cancerous tissues. The proliferation rate of HCC cells was detected by MTS assay, and the invasive ability was examined by transwell and scratch wound assays. The YAP protein localization and expression were visualized by immunofluorescence in two different cell lines. CpG islands in the promoter region were predicted by using the methprimer database. Clinical characteristics of a patient cohort data came from The Cancer Genome Atlas database. RDH5 was significantly downregulated in hepatocellular carcinoma tissues, and low RDH5 expression was associated with metastasis and poor patient prognosis. Functional assays revealed that the RDH5 promoter is methylated in HCC cell lines. Moreover, overexpressing RDH5 can suppress metastasis by reversing the epithelial-mesenchymal transition (EMT) process, and RDH5 also inhibits cell proliferation in HCC cell lines. Furthermore, suppressing RDH5 can activate the Hippo/YAP signaling pathway and promote the nuclear translocation of YAP. Clinical data demonstrated that RDH5 is an independent prognostic factor in HCC. In our study, we provided the first evidence that RDH5 plays a crucial role in suppressing proliferation and metastasis, and the RDH5 promoter is methylated in hepatocellular carcinoma. And as an important regulator, RDH5 can suppress the Hippo/YAP signaling pathway. Taken together, it revealed that RDH5 might be a potential therapeutic target in HCC patients.