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ABSTRACT Tracheal obstruction can arise from multiple conditions, including chronic obstructive pulmonary disease, asthma, foreign bodies, tumors, and acute heart failure. We report a case of a 43‐year‐old man with cervical liposarcoma who, following surgical excision, chemotherapy, and radiation, presented with severe dyspnea and was admitted to our hospital. A CT scan detected an endotracheal mass causing significant obstruction, suspected to be malignant. The patient required intensive care due to respiratory distress. Bronchoscopy revealed a red polypoid lesion causing nearly 90% tracheal narrowing, which was successfully resected using high‐frequency electrotrap and argon coagulation, confirming it as a metastasis from the previously treated liposarcoma. Remarkably, there were no significant recurrences after 6 months. While lung metastases are frequent, intratracheal metastasis is rare; this case is the first documenting bronchial and tracheal metastasis of liposarcoma. It highlights the dangers of airway obstruction and the need for timely intervention. Although CT scans are helpful in identifying intrabronchial tumors, bronchoscopy remains the gold standard for diagnosis and treatment, with several options available for urgent cases.

Abstract Background Cervical lymph node metastasis (LNM) is an important prognostic factor for patients with non-small cell lung cancer (NSCLC). We aimed to develop and validate machine learning models that use ultrasound radiomic and descriptive semantic features to diagnose cervical LNM in patients with NSCLC. Methods This study included NSCLC patients who underwent neck ultrasound examination followed by cervical lymph node (LN) biopsy between January 2019 and January 2022 from three institutes. Radiomic features were extracted from the ultrasound images at the maximum cross-sectional areas of cervical LNs. Logistic regression (LR) and random forest (RF) models were developed. Model performance was assessed by the area under the curve (AUC) and accuracy, validated internally and externally by fivefold cross-validation and hold-out method, respectively. Results In total, 313 patients with a median age of 64 years were included, and 276 (88.18%) had cervical LNM. Three descriptive semantic features, including long diameter, shape, and corticomedullary boundary, were selected by multivariate analysis. Out of the 474 identified radiomic features, 9 were determined to fit the LR model, while 15 fit the RF model. The average AUCs of the semantic and radiomics models were 0.876 (range: 0.781–0.961) and 0.883 (range: 0.798–0.966), respectively. However, the average AUC was higher for the semantic-radiomics combined LR model (0.901; range: 0.862–0.927). When the RF algorithm was applied, the average AUCs of the radiomics and semantic-radiomics combined models were improved to 0.908 (range: 0.837–0.966) and 0.922 (range: 0.872–0.982), respectively. The models tested by the hold-out method had similar results, with the semantic-radiomics combined RF model achieving the highest AUC value of 0.901 (95% CI, 0.886–0.968). Conclusions The ultrasound radiomic models showed potential for accurately diagnosing cervical LNM in patients with NSCLC when integrated with descriptive semantic features. The RF model outperformed the conventional LR model in diagnosing cervical LNM in NSCLC patients.

Abstract The spindle assembly checkpoint (SAC) ensures chromosome segregation fidelity by manipulating unattached kinetochore‐dependent assembly of the mitotic checkpoint complex (MCC). The MCC binds to and inhibits the anaphase promoting complex/cyclosome (APC/C) to postpone mitotic exit. However, the mechanism by which unattached kinetochores mediate MCC formation is not yet fully understood. Here, it is shown that CCDC68 is an outer kinetochore protein that preferentially localizes to unattached kinetochores. Furthermore, CCDC68 interacts with the SAC factor CDC20 to inhibit its autoubiquitination and MCC disassembly. Therefore, CCDC68 restrains APC/C activation to ensure a robust SAC and allow sufficient time for chromosome alignment, thus ensuring chromosomal stability. Hence, the study reveals that CCDC68 is required for CDC20‐dependent MCC stabilization to maintain mitotic checkpoint activation.

Abstract Classic heatstroke (CHS) is a life-threatening illness characterized by extreme hyperthermia, dysfunction of the central nervous system and multiorgan failure. Accurate predictive models are useful in the treatment decision-making process and risk stratification. This study was to develop and externally validate a prediction model of survival for hospitalized patients with CHS. In this retrospective study, we enrolled patients with CHS who were hospitalized from June 2022 to September 2022 at 3 hospitals in Southwest Sichuan (training cohort) and 1 hospital in Central Sichuan (external validation cohort). Prognostic factors were identified utilizing least absolute shrinkage and selection operator (LASSO) regression analysis and multivariate Cox regression analysis in the training cohort. A predictive model was developed based on identified prognostic factors, and a nomogram was built for visualization. The areas under the receiver operator characteristic (ROC) curves (AUCs) and the calibration curve were utilized to assess the prognostic performance of the model in both the training and external validation cohorts. The Kaplan‒Meier method was used to calculate survival rates. A total of 225 patients (median age, 74 [68–80] years) were included. Social isolation, self-care ability, comorbidities, body temperature, heart rate, Glasgow Coma Scale (GCS), procalcitonin (PCT), aspartate aminotransferase (AST) and diarrhea were found to have a significant or near-significant association with worse prognosis among hospitalized CHS patients. The AUCs of the model in the training and validation cohorts were 0.994 (95% [CI], 0.975–0.999) and 0.901 (95% [CI], 0.769–0.968), respectively. The model's prediction and actual observation demonstrated strong concordance on the calibration curve regarding 7-day survival probability. According to K‒M survival plots, there were significant differences in survival between the low-risk and high-risk groups in the training and external validation cohorts. We designed and externally validated a prognostic prediction model for CHS. This model has promising predictive performance and could be applied in clinical practice for managing patients with CHS.

Through an empirical analysis of paired sample data from 308 employees in China, this study examines the chain-mediated effects of trust in leaders and defensive silence on the relationship between differentiated empowering leadership and interpersonal counterproductive work behaviors. The study finds that differentiated empowering leadership does not directly influence employees’ interpersonal counterproductive work behaviors. Additionally, it finds that trust in leaders and defensive silence each serve as mediators in the relationship between differentiated empowering leadership and interpersonal counterproductive work behaviors, forming a chained mediation effect. This study is the first empirical research to explore the impact mechanism of differentiated empowering leadership using a chained mediation model. The findings contribute to a deeper understanding of how and why differentiated empowering leadership affects employees’ attitudes, such as trust in leaders, and behaviors, such as interpersonal counterproductive work behaviors.

Non-small cell lung cancer (NSCLC) is one of the main causes of cancer-related death worldwide, with a serious impact on human health and life. The identification of NSCLC at an early stage is a formidable task that frequently culminates in a belated diagnosis. LncRNA is a kind of noncoding RNA with limited protein-coding capacity, and its expression is out of balance in many cancers, especially NSCLC. A large number of studies have reported that lncRNA acts a vital role in regulating angiogenesis, invasion, metastasis, and the proliferation and apoptosis of tumor cells, affecting the occurrence and development of NSCLC. Abundant evidence demonstrates that lncRNAs may serve as potential biomarkers for NSCLC diagnosis and prognosis. In this review, we summarize the latest progress in characterizing the functional mechanism of lncRNAs involved in the development of NSCLC and further discuss the role of lncRNAs in NSCLC therapy and chemotherapy resistance. We also discuss the advantages, limitations, and challenges of using lncRNAs as diagnostic or prognostic biomarkers in the management of NSCLC.

Diffuse large B-cell lymphoma is the most common subtype of lymphoma, representing ∼25 % of non-Hodgkin lymphoid malignancies. EZH2 is highly expressed in Diffuse large B-cell lymphoma and ∼22 % of patients contain EZH2 mutations. EZH2 have been studied as a potential therapeutic target for a decade, but efficient inhibition of EZH2 did not robustly kill lymphoma cells. Here, we found that EZH2 mediates repression of oncogenic genes STAT3 and USP7 in Diffuse large B-cell lymphoma cells. Inhibition of EZH2 leads to upregulation of STAT3 and USP7 at both RNA and protein levels. Along with USP7 upregulation, MDM2 is upregulated and its ubiquitylation substrate, Tumor suppressor P53, is downregulated. Upregulation of STAT3 and downregulation of p53 can strength cell proliferation and prevent cells from apoptosis, which suggests resistance mechanisms by which cells survive EZH2 inhibition-induced cell death. Short-course co-inhibition of USP7 and EZH2 showed increased apoptosis and cell proliferation prevention with the concentration as low as 0.08 μM. In STAT3 and USP7 depleted cells, EZH2 inhibition shows superior efficacy of apoptosis, and in EZH2 depleted cells, USP7 inhibition also shows superior efficacy of apoptosis. Thus, our findings suggest a new precision therapy by combinational inhibition of EZH2 with STAT3 or USP7 for Diffuse large B-cell lymphoma.

In the architecture, engineering, and construction (AEC) industry, the positioning technology for a mobile construction platform (MCP) is critical to achieve on-site, continuous, large-scale construction. During construction, MCP movement and construction actions seldom occur simultaneously. Therefore, this paper categorizes the MCP into stationary and moving states for positioning studies, respectively. When the platform is stationary, it is positioned using an improved ultra-wideband (UWB) sensor. When the platform is in motion, a single UWB positioning technique cannot meet the required accuracy for positioning, and fusion positioning using both UWB and an inertial measurement unit (IMU) is considered. The experimental results show that compared with only UWB positioning, the improved UWB positioning algorithm improves the positioning accuracy by 53% in the stationary state, and the fused UWB/IMU positioning improves the positioning accuracy by 46% in the moving state. As a result, the positioning accuracy of the MCP is significantly improved regardless of whether it is in a stationary or moving state. Furthermore, this paper integrates the positioning technique with the robotic arm construction technique to successfully simulate an on-site continuous construction of a wooden cabin, which provides the potential for large-scale continuous construction in real-world scenarios in the future.

Summary: The rixosome and PRC1 silencing complexes are associated with deSUMOylating and deubiquitinating enzymes, SENP3 and USP7, respectively. How deSUMOylation and deubiquitylation contribute to rixosome- and Polycomb-mediated silencing is not fully understood. Here, we show that the enzymatic activities of SENP3 and USP7 are required for silencing of Polycomb target genes. SENP3 deSUMOylates several rixosome subunits, and this activity is required for association of the rixosome with PRC1. USP7 associates with canonical PRC1 (cPRC1) and deubiquitinates the chromodomain subunits CBX2 and CBX4, and inhibition of USP activity results in disassembly of cPRC1. Finally, both SENP3 and USP7 are required for Polycomb- and rixosome-dependent silencing at an ectopic reporter locus. These findings demonstrate that SUMOylation and ubiquitination regulate the assembly and activities of the rixosome and Polycomb complexes and raise the possibility that these modifications provide regulatory mechanisms that may be utilized during development or in response to environmental challenges.

Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors worldwide. Clinical success is suboptimal owing to late diagnosis, limited treatment options, high recurrence rates, and the development of drug resistance. MicroRNAs (miRNAs), a range of small endogenous non-coding RNAs that are 22 nucleotides in length, have emerged as one of the most important players in cancer initiation and progression in recent decades. Current evidence has revealed the pivotal roles of miRNAs in regulating cell proliferation, migration, invasion, and metastasis in NSCLC. Recently, several studies have demonstrated that miRNAs are strongly associated with resistance to anti-cancer drugs, ranging from traditional chemotherapeutic and immunotherapy drugs to anti-vascular drugs, and even during radiotherapy. In this review, we briefly introduce the mechanism of miRNA dysregulation and resistance to anti-tumor therapy in NSCLC, and summarize the role of miRNAs in the malignant process of NSCLC. We then discuss studies of resistance-related miRNAs in chemotherapy, radiotherapy, targeted therapy, immunotherapy, and anti-vascular therapy in NSCLC. Finally, we will explore the application prospects of miRNA, an emerging small molecule, for future anti-tumor therapy. This review is the first to summarize the latest research progress on miRNAs in anti-cancer drug resistance based on drug classification, and to discuss their potential clinical applications.

Abstract Circular RNAs (circRNAs) have been reported to play crucial roles in the progression of various cancers, including colorectal cancer (CRC). SP1 (Sp1 transcription factor) is a well-recognized oncogene in CRC and is deemed to trigger the Wnt/β-catenin pathway. The present study was designed to investigate the role of circRNAs which shared the same pre-mRNA with SP1 in CRC cells. We identified that hsa_circ_0026628 (circ_0026628), a circular RNA that originated from SP1 pre-mRNA, was upregulated in CRC cells. Sanger sequencing and agarose gel electrophoresis verified the circular characteristic of circ_0026628. Functional assays including CCK-8, colony formation, transwell, immunofluorescence staining, and sphere formation assay revealed the function of circ_0026628. RNA pull-down and mass spectrometry disclosed the proteins interacting with circ_0026628. Mechanistic assays including RIP, RNA pull-down, CoIP, ChIP, and luciferase reporter assays demonstrated the interplays between molecules. The results depicted that circ_0026628 functioned as a contributor to CRC cell proliferation, migration, EMT, and stemness. Mechanistically, circ_0026628 served as the endogenous sponge of miR-346 and FUS to elevate SP1 expression at the post-transcriptional level, thus strengthening the interaction between SP1 and β-catenin to activate the Wnt/β-catenin pathway. In turn, the downstream gene of Wnt/β-catenin signaling, SOX2 (SRY-box transcription factor 2), transcriptionally activated SP1 and therefore boosted circ_0026628 level. On the whole, SOX2-induced circ_0026628 sponged miR-346 and recruited FUS protein to augment SP1, triggering the downstream Wnt/β-catenin pathway to facilitate CRC progression.

IntroductionPrimary pleural squamous cell carcinoma (PPSCC) is a sporadic disease that is rarely reported in the literature. Due to its low incidence, the pathogenesis of PPSCC is unknown.Case summaryWe report a case of a 68-year-old male with PPSCC and sizable pulmonary bullae. Two months after complete resection of both lesions, a total dose of 50 Gy radiotherapy was administered over the operative field. After more than a year of follow-up, the patient is in steady condition without any sign of recurrence.ConclusionSince PPSCC is rarely reported, our case proposed that complete surgical resection combined with radiotherapy may be a promising therapeutic approach.

Background and objectivesEsophageal squamous cell carcinoma (ESCC) is the most common pathological type of esophageal malignancy in most regions of the world. The study aimed to identify risk factors and develop a predictive model for ESCC following surgical resection.Patients and methodsA total of 533 ESCC patients who underwent surgical resection from Suining Central Hospital were enrolled in the study. Cox proportional hazards regression and Least Absolute Shrinkage and Selection Operator (LASSO) regression were performed to identify significant prognostic factors. A prognostic model was constructed, and the receiver operating characteristic (ROC) curve, concordance index (C-index), and decision cure analysis (DCA) were used to evaluate the discrimination and calibration of the prognostic model. Subsequently, we built a nomogram for overall survival (OS) incorporating the prognostic factors, and a calibration plot was employed to assess the consistency between the predicted survival and the observed survival. Based on the model risk score, we split the patients into two subgroups, low-risk and high-risk, and we analyzed the survival time of these two groups using Kaplan–Meier (K-M) survival plots.ResultsFive independent prognosis factors were identified as independent risk factors for OS in ESCC patients who underwent surgical resection. The C-index, ROC curve, and DCA showed that the prognostic model had good predictive accuracy and discriminatory power in the training cohort and validation cohort than other clinical features. A nomogram consisting of prognosis factors showed some superior net benefit. K-M survival plots showed significant differences in OS between the low-risk and high-risk groups. Similar results were observed in the subgroup analysis based on age, grade, and stage. Univariate and multivariate Cox regression analyses revealed that both risk score and risk group are independent prognostic factors in the patient cohort.ConclusionsThis study put forward a novel prognostic model based on clinical features; biopsy data and blood biomarkers may represent a promising tool for estimating OS in ESCC patients.

ObjectiveThe psychological problems of frontline nurses in COVID-19 prevention and control are very prominent, and targeted intervention is needed to alleviate them. This study was to assess the impact of online intervention programs on psychological crisis of anxiety, depression levels and physical symptoms among frontline nurses fighting the COVID-19 pandemic.MethodsA three-stage online psychological crisis intervention program was established. The General Anxiety 7 (GAD-7) assessment, Patient Health Questionnaire-9 (PHQ-9), and the Self-rating Somatic Symptom Scale (SSS) were used to evaluate the effect of intervention on the day before entering isolation wards (Time 1), the first day after leaving the isolation ward (Time 2), and at the end of the intervention (Time 3).ResultsSixty-two nurses completed the study, including 59 female (95.2%) and three male nurses (4.8%) with an age range of 23–49 (mean 33.37 ± 6.01). A significant (P < 0.01) difference existed in the scores of GAD-7, PHQ-9, and SSS at different intervention periods. The GAD-7 score was significantly (P < 0.001) lower at the end of quarantine period (time 3) than that before entering the isolation wards (time 1) or after leaving the isolation wards (time 2), the PHQ-9 score was significantly (P = 0.016) lower at the end of quarantine period (time 3) than that after leaving the isolation wards (time 2), and the SSS score was significantly (P < 0.001) lower at the end of quarantine period (time 3) than that before entering the isolation wards (time 1) or after leaving the isolation wards (time 2).ConclusionThe three-stage online intervention program based on the psychological crisis can be effective in reducing negative emotions and somatic symptoms and improving the mental health of frontline nurses in prevention and control of the COVID-19 epidemic. It may provide an empirical basis for psychological crisis intervention of frontline medical staff when facing public health emergencies.

Abstract Colorectal cancer (CRC) is a fatal disease ranking the third among the commonplace cancer types around the world. It is extremely significant to exploit effective treatments against CRC. FAM225A was proved to influence cell progression and forecast unfavorable prognosis in nasopharyngeal carcinoma. The role and function mechanism of FAM225A are still unclear in CRC. In this research, FAM225A was discovered presenting much higher expression in CRC tissues and cell lines. In addition, depleting FAM225A was capable of inhibiting cell proliferation, migration, and epithelial‐to‐mesenchymal transition (EMT) progress, and enhancing cell apoptosis ability. Furthermore, miR‐613 exerted important effects as a mediator between FAM225A and NOTCH3. NOTCH3 was negatively correlated with miR‐613, whereas was positively associated with FAM225A. Via competitively binding with miR‐613, FAM225A positively regulated NOTCH3 expression. FAM225A facilitated CRC occurrence and development through positively regulating NOTCH3 expression by binding with miR‐613. In a word, FAM225A/miR‐613/NOTCH3 axis may play a tumor‐facilitator in CRC cell progression. These data manifested the pivotal effect of FAM225A/miR‐613/NOTCH3 pathway in CRC cell proliferation, apoptosis, and migration process. The findings may provide some theoretical basis and different perspective for CRC treatment.

Lung cancer is the leading cause of cancer-related deaths worldwide and in China. Screening for lung cancer by low dose computed tomography (LDCT) can reduce mortality but has resulted in a dramatic rise in the incidence of indeterminate pulmonary nodules, which presents a major diagnostic challenge for clinicians regarding their underlying pathology and can lead to overdiagnosis. To address the significant gap in evaluating pulmonary nodules, we conducted a prospective study to develop a prediction model for individuals at intermediate to high risk of developing lung cancer. Univariate and multivariate logistic analyses were applied to the training cohort (n = 560) to develop an early lung cancer prediction model. The results indicated that a model integrating clinical characteristics (age and smoking history), radiological characteristics of pulmonary nodules (nodule diameter, nodule count, upper lobe location, malignant sign at the nodule edge, subsolid status), artificial intelligence analysis of LDCT data, and liquid biopsy achieved the best diagnostic performance in the training cohort (sensitivity 89.53%, specificity 81.31%, area under the curve [AUC] = 0.880). In the independent validation cohort (n = 168), this model had an AUC of 0.895, which was greater than that of the Mayo Clinic Model (AUC = 0.772) and Veterans’ Affairs Model (AUC = 0.740). These results were significantly better for predicting the presence of cancer than radiological features and artificial intelligence risk scores alone. Applying this classifier prospectively may lead to improved early lung cancer diagnosis and early treatment for patients with malignant nodules while sparing patients with benign entities from unnecessary and potentially harmful surgery.Clinical Trial Registration NumberChiCTR1900026233, URL: http://www.chictr.org.cn/showproj.aspx?proj=43370.

Abstract Background Progress of the aortic disease after the stent graft treatment of aortic dissection implicates the potential risks of stent graft-induced new entry (SINE). Although rarely reported, it should be vigilant in patients who might incur serious complication in early period after the thoracic endovascular aortic repair (TEVAR). Thus, the development of aortic disease-specific stent grafts would assist in achieving positive patient outcomes when suffering SINE. However, it is an extremely rare for SINE between two non-overlapping stent-grafts. Case presentation We here reported a 59-year-old male patient with sudden onset of chest pain for 4 h. Multi-detector computed tomography (MDCT) revealed a huge SINE formed between two non-overlapping stent-grafts. The re-TEVAR surgery was performed and the patient experienced a good recovery. Conclusion The SINE between two non-overlapping stent-grafts treated by re-TEVAR operation was alternative and feasible. The short-term and medium-term follow-up results were satisfactory.

Abstract Background Spindle microtubule organization, regulated by microtubule-associated proteins, is critical for cell division. Proper organization of kinetochore fiber (K-fiber), connecting spindle poles and kinetochores, is a prerequisite for precise chromosomal alignment and faithful genetic material transmission. However, the mechanisms of K-fiber organization and dynamic maintenance are still not fully understood. Results We reveal that two previously uncharacterized coiled-coil domain proteins CCDC74A and CCDC74B (CCDC74A/B) are spindle-localized proteins in mammalian cells. They bind directly to microtubules through two separate domains and bundle microtubules both in vivo and in vitro. These functions are required for K-fiber organization, bipolar spindle formation, and chromosomal alignment. Moreover, CCDC74A/B form homodimers in vivo, and their self-association activity is necessary for microtubule bundling and K-fiber formation. Conclusions We characterize CCDC74A and CCDC74B as microtubule-associated proteins that localize to spindles and are important K-fiber crosslinkers required for bipolar spindle formation and chromosome alignment.

Ciliated muconodular papillary tumor (CMPT) is a rare type of pulmonary tumor with mucoid features. Only a few cases confirmed by surgery have been reported worldwide. We report a case of CMPT following sublobectomy, with no recurrence detected in 10 months of follow‐up. The accumulation of similar cases is essential for pathologists and surgeons to improve their understanding of such tumors.

Although robotic spatial printing (RSP) has demonstrated a new way of fabricating building components with a good stiffness-to-weight ratio, the complexity of the applied geometries is still limited. Among them are branching geometries, which refer to the bio-inspired branching structures (BIBSs) in the building industry. This paper presents a cutting-edge approach to tackle this bottleneck problem, in which we propose an automated printing path generation (APPG) approach for the RSP of branching geometries, including an original hierarchical framework of printing node permutations and a linear workflow that incorporates five core algorithms: the heat method, graph generation, graph traversal, curve adjustment, and lattice generation. Through the execution of this workflow, a lattice structure and its corresponding printing path can be generated. This work is validated by the simulation of three prototypes: two-branch geometry, multi-branch geometry, and multi-level-branch geometry. Printing expenses are compared with each of the related algorithms to validate the efficiency of this proposed approach. Along with the appropriate APPG solutions, an analytical tool for topological type is also presented in this paper.

Non-small-cell lung cancer (NSCLC) is one of the most common malignancies and the leading causes of cancer-related death worldwide. Despite many therapeutic advances in the past decade, NSCLC remains an incurable disease for the majority of patients. Molecular targeted therapies and immunotherapies have significantly improved the prognosis of NSCLC. However, the vast majority of advanced NSCLC develop resistance to current therapies and eventually progress. In this review, we discuss current and potential therapies for NSCLC, focusing on targeted therapies and immunotherapies. We highlight the future role of metabolic therapies and combination therapies in NSCLC.

Abstract Background TRIP13 is highly expressed in several cancers and is closely connected with cancer progression. However, its roles on the growth and metastasis of hepatocellular carcinoma (HCC), and the underlying mechanism are still unclear. Methods Combining bioinformatics with previous studies, the correlation between TRIP13 and HCC was predicted. TRIP13 expressions from 52 HCC patients and several cell lines were determined. The effects of silencing TRIP13 on cell viability, apoptosis, migration and invasion were respectively detected using CCK-8, flow cytometry and Transwell. qRT-PCR and western blot were performed to reveal associated mechanism. A HCC model was established in BALB/c-nu mice by transplanting HepG2 cells. TRIP13 protein expression and apoptosis in mice tissues were accordingly detected by Immunohistochemistry and TUNEL. Results High expression of TRIP13 in HCC affected the survival rate and it was enriched in RNA degradation and fatty acid metabolism according to bioinformatics and prediction from previous literature. Increased expression of TRIP13 in HCC patient tissues was associated with the progression of HCC. Silencing TRIP13 inhibited cell viability, migration and invasion, and induced cell apoptosis. TRIP13 knockdown also suppressed the formation of tumor in vivo. Meanwhile, silencing TRIP13 decreased the expressions of Ki67 and MMP-2 and increased the expressions of TIMP-2, active-caspase-3 and TGF-β1/smad3 signaling- related genes. Conclusions Silencing TRIP13 acts as a tumor suppresser of HCC to repress cell growth and metastasis in vitro and in vivo, and such a phenomenon possibly involved activation of TGF-β1/smad3 signaling.

Abstract Background Traumatic aortic arch rupture with pseudoaneurysm is a rare high fatal injury. Thoracic endovascular aortic repair(TEVAR) is widely used in the treatment of aortic diseases. However a unified traumatic aortic injury risk stratification tool still lacks. The patients’ disease assessment and operation method still rely on the doctors’ subjective anticipation of disease and surgical results. Case presentation A 31-year-old male presented with chest pain and hoarseness of recent onset. Imageological examination showed aortic rupture with mediastinal pseudoaneurysm in Zone 1. Debranching + TEVAR hybrid operation was considered: Using artificial blood vessels rebuild the arch branches, the covered stent was placed in aortic arch for endovascular repair via femoral artery. The follow-up was good in postoperative 7d, 1 year and > 2 years. Conclusion The traumatic aortic arch rupture with pseudoaneurysm treated by Debranching+TEVAR hybrid operation is feasible. The short-term and medium-term follow-up results are satisfactory. For traumatic aortic arch injury, hybrid operation is recommended to reduce the risk of cardiopulmonary bypass and deep hypothermia circulatory arrest under no open operation conditions or emergency situation.

Non-small cell lung cancer is one of the most common types of malignances worldwide and the main cause of cancer-related deaths. Current treatment for NSCLC is based on surgical resection, chemotherapy, radiotherapy, and targeted therapy, with poor therapeutic effectiveness. In recent years, immune checkpoint inhibitors have applied in NSCLC treatment. A large number of experimental studies have shown that immune checkpoint inhibitors are safer and more effective than traditional therapeutic modalities and have allowed for the development of better guidance in the clinical treatment of advanced NSCLC patients. In this review, we describe clinical trials using ICI immunotherapies for NSCLC treatment, the available data on clinical efficacy, and the emerging evidence regarding biomarkers.

Abstract Background Pulmonary sequestration is a rare congenital pulmonary dysplasia, which requires surgical resection (either via open thoracotomy or video-assisted thoracoscopic surgery [VATS] or via endoluminal occlusion of the abnormal feeding vessel). Case presentation We described a 51-year-old female patient with a history of recurrent cough and repeated pneumonia. She was referred to our hospital for further work-up of pulmonary sequestration. We performed a hybrid surgery (i.e., embolization of the aberrant feeding vessel of the sequestration combined with wedge resection of the left lower lobe lesion through VATS). The patient was discharged on the sixth postoperative day in good condition and without complications. Conclusions We believe that a hybrid operation is safer, more feasible, and more comprehensive than other treatments.

The spindle assembly checkpoint relies on the accumulation of Mad1-Mad2 at kinetochores, but the mechanism of regulation is not known. Here Zhou et al. show that the centrosomal protein Cep57 interacts with the kinetochore proteins Mis12 and Mad1, and regulates the recruitment of Mad1/Mad2 to kinetochores.

During interphase, centrosomes are connected by a proteinaceous linker between the proximal ends of the centrioles, which is important for the centrosomes to function as a single microtubule-organizing center. However, the composition and regulation of centrosomal linker remain largely unknown. Here, we show that LRRC45 is a centrosome linker that localizes at the proximal ends of the centrioles and forms fiber-like structures between them. Depletion of LRRC45 results in centrosome splitting during interphase. Moreover, LRRC45 interacts with both C-Nap1 and rootletin and is phosphorylated by Nek2A at S661 during mitosis. After phosphorylation, both LRRC45 centrosomal localization and fiber-like structures are significantly reduced, which subsequently leads to centrosome separation. Thus, LRRC45 is a critical component of the proteinaceous linker between two centrioles and is required for centrosome cohesion.