A Mendelian randomization study between metabolic syndrome and its components with prostate cancer.

Previous research has produced inconsistent findings concerning the connection between metabolic syndrome and prostate cancer. It is challenging for observational studies to establish a conclusive causal relationship between the two. However, Mendelian randomization can provide stronger evidence of causality in this context. To examine the causal link between a metabolic composite and its components with prostate cancer, we performed a two-sample Mendelian randomization (MR) study utilizing aggregated data from genome-wide association studies, followed by meta-analyses. In our study, we employed inverse variance weighting as the primary method for MR analysis. Additionally, we assessed potential sources of heterogeneity and horizontal pleiotropy through the Cochran's Q test and MR-Egger regression. Moreover, we used multivariate MR to determine whether smoking versus alcohol consumption had an effect on the outcomes. We found no causal relationship between metabolic syndrome and its components and prostate cancer(MetS, odds ratio [OR] = 0.95, 95% confidence interval [CI] = 0.738-1.223, p = 0.691; TG, [OR] = 1.02, 95%[CI] = 0.96-1.08, p = 0.59); HDL, [OR] = 1.02, 95% [CI] = 0.97-1.07, p = 0.47; DBP, [OR] = 1.00, 95%[CI] = 0.99-1.01, p = 0.87; SBP, [OR] = 1.00, 95%[CI] = 0.99-1.00, p = 0.26; FBG [OR] = 0.92, 95%[CI] = 0.81-1.05, p = 0.23; WC, [OR] = 0.93, 95%[CI] = 0.84-1.03, p = 0.16). Finally, the MVMR confirms that the metabolic syndrome and its components are independent of smoking and alcohol consumption in prostate cancer. We didn't find significant evidence to determine a causal relationship between the metabolic syndrome and its components and prostate cancer through MR analysis. Further research is necessary to explore the potential pathogenesis between the two diseases.

SIVA-1 enhances acquired chemotherapeutic drug resistance of gastric cancer in vivo by regulating the ARF/MDM2/p53 pathway.

SIVA-1 has been shown to affect apoptotic processes in various different cell lines, and SIVA-1 significantly contributes to the decreased responsiveness of cancer cells to some chemotherapy agents. However, whether SIVA-1 has potential application in gastric cancer remains unknown. Therefore, the objective of this investigation was to clarify the distinct function of SIVA-1 in chemotherapeutic drug resistance within a living murine model with gastric malignancy, and initially elucidate the underlying mechanisms. In an established multidrug-resistant gastric cancer xenograft mouse model, lentivirus, named Lv-SIVA-1, was injected into xenograft tumors, and increased the mRNA and protein expression of endogenous SIVA-1 in tumors. Immunohistochemical assays of xenograft tumor showed that SIVA-1 was significantly upregulated, and the protein expression levels of SIVA-1 were highly increased, as detected by Western blotting. In addition, we detected the role of SIVA-1 in cell proliferation and cell apoptosis in gastric cancer cells by TUNEL and found that SIVA-1 decreased tumor cell apoptosis and promoted tumor growth in vivo. Using a TMT assay between tumor tissues of experimental and control groups, differentially expressed proteins were examined and three potential biomarkers of multidrug resistance (ARF, MDM2, and p53) were screened. We further investigated the molecular mechanism by which SIVA-1 played an efficient role against chemotherapies and found that overexpressed SIVA-1 leads to increased ARF and MDM2 expression and suppressed expression of p53 in tumor tissue. In conclusion, SIVA-1 plays a significant role in the multidrug resistance of gastric tumors. In addition, overexpressed SIVA-1 positively regulates cell proliferation, adjusts cycle progression, and reduces the response to drug treatment for gastric cancer in an ARF/MDM2/p53-dependent manner. This novel research provides a basis for chemical management of gastric cancer through regulation of SIVA-1 expression.

The Use of Eye-Tracking Technology in Dento-Maxillofacial Esthetics: A Systematic Review.

The use of eye-tracking technology in dental esthetics has gained popularity over the past decade because of its ability to assess observers' visual preferences in an objective manner. The goal of this study was to provide a comprehensive review of eye-tracking studies in dentistry, which could provide a reference for the rational and effective application of eye-tracking technology by dentists in the future. A comprehensive search of articles on eye tracking, published from January 1946 to June 2023, was conducted across several databases using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. The major criterion for inclusion was that the study evaluated the use of eye-tracking technology in the field of dentistry. Two independent reviewers screened the eligible studies. A total of 67 articles were identified, 41 of which met our inclusion criteria. The most common application of eye tracking was the assessment of perceptions of changes in specific dental conditions among different classes of observers. Overall differences between groups (different classes of observers, different types of conditions) among different areas or regions of interest were analyzed. This systematic review demonstrated the utility of eye-tracking technology as a quantifiable objective assessment and emerging research tool for evaluating outcomes in several domains of dentistry.

Didymin alleviates metabolic dysfunction-associated fatty liver disease (MAFLD) via the stimulation of Sirt1-mediated lipophagy and mitochondrial biogenesis.

BACKGROUND: Metabolic dysfunction-associated fatty liver disease (MAFLD) is one of the most prevalent metabolic syndromes worldwide. However, no approved pharmacological treatments are available for MAFLD. Chenpi, one kind of dried peel of citrus fruits, has traditionally been utilized as a medicinal herb for liver diseases. Didymin is a newly identified oral bioactive dietary flavonoid glycoside derived from Chenpi. In this study, we investigated the therapeutic potential of Didymin as an anti-MAFLD drug and elucidated its underlying mechanisms. METHODS: High-fat diet (HFD)-induced MAFLD mice and alpha mouse liver 12 (AML12) cells were utilized to evaluate the effects and mechanisms of Didymin in the treatment of MAFLD. Liver weight, serum biochemical parameters, and liver morphology were examined to demonstrate the therapeutic efficacy of Didymin in MAFLD treatment. RNA-seq analysis was performed to identify potential pathways that could be affected by Didymin. The impact of Didymin on Sirt1 was corroborated through western blot, molecular docking analysis, microscale thermophoresis (MST), and deacetylase activity assay. Then, a Sirt1 inhibitor (EX-527) was utilized to confirm that Didymin alleviates MAFLD via Sirt1. Western blot and additional assays were used to investigate the underlying mechanisms. RESULTS: Our results suggested that Didymin may possess therapeutic potential against MAFLD in vitro and in vivo. By promoting Sirt1 expression as well as directly binding to and activating Sirt1, Didymin triggers downstream pathways that enhance mitochondrial biogenesis and function while reducing apoptosis and enhancing lipophagy. CONCLUSIONS: These suggest that Didymin could be a promising medication for MAFLD treatment. Furthermore, its therapeutic effects are mediated by Sirt1.

Reconstruction of the temporomandibular joint using a vascularized medial femoral condyle osteocartilaginous flap: an experimental investigation in miniature pigs.

BACKGROUND: Reconstruction of the temporomandibular joint (TMJ) is a significant challenge in maxillofacial surgery. A vascularized medial femoral condyle (MFC) osteocartilaginous flap is a good choice for TMJ reconstruction. In this study, we evaluated the radiographic and histological changes of MFC after TMJ reconstruction. METHODS: A ramus-condyle unit (RCU) defect was created unilaterally in five adult male Bama miniature pigs. The ipsilateral vascularized MFC osteocartilaginous flap was used to reconstruct the TMJ, and the non-operative sides served as controls. Multislice spiral computed tomography (CT) was performed preoperatively, immediately postoperatively, and at two weeks, three months, and six months postoperatively. Three animals were euthanized at 6 months postoperatively. Their reconstructed condyles, natural condyles and the MFCs on the opposite side were collected and subjected to µCT and histological evaluation. RESULTS: In the miniature pigs, the vascularized MFC osteocartilaginous flap was fused to the mandible, thus restoring the structure and function of the RCU. The postoperative radiographic changes and histological results showed that the reconstructed condyle was remodeled toward the natural condyle, forming a similar structure, which was significantly different from the MFC. CONCLUSIONS: In miniature pigs, the RCU can be successfully reconstructed by vascularized osteocartilaginous MFC flap. The reconstructed condyle had almost the same appearance and histological characteristics as the natural condyle.

Immunogenic cell death-associated biomarkers classification predicts prognosis and immunotherapy efficacy in pancreatic ductal adenocarcinoma.

Introduction: Immunogenic cell death (ICD) is a sort of regulated cell death (RCD) sufficient to trigger an adaptive immunological response. According to the current findings, ICD has the capacity to alter the tumor immune microenvironment by generating danger signals or damage-associated molecular patterns (DAMPs), which may contribute in immunotherapy. It would be beneficial to develop ICD-related biomarkers that classify individuals depending on how well they respond to ICD immunotherapy. Methods and results: We used consensus clustering to identify two ICD-related groupings. The ICD-high subtype was associated with favorable clinical outcomes, significant immune cell infiltration, and powerful immune response signaling activity. In addition, we developed and validated an ICD-related prognostic model for PDAC survival based on the tumor immune microenvironment. We also collected clinical and pathological data from 48 patients with PDAC, and patients with high EIF2A expression had a poor prognosis. Finally, based on ICD signatures, we developed a novel PDAC categorization method. This categorization had significant clinical implications for determining prognosis and immunotherapy. Conclusion: Our work emphasizes the connections between ICD subtype variations and alterations in the immune tumor microenvironment in PDAC. These findings may help the immune therapy-based therapies for patients with PDAC. We also created and validated an ICD-related prognostic signature, which had a substantial impact on estimating patients' overall survival times (OS).

Da-Yuan-Yin decoction polyphenol fraction attenuates acute lung injury induced by lipopolysaccharide.

CONTEXT: Da-Yuan-Yin is a Chinese traditional prescription. OBJECTIVE: This study explores the therapeutic effects of the Da-Yuan-Yin decoction polyphenol fraction (DYY-4) on acute lung injury (ALI) in mice induced by lipopolysaccharide (LPS). MATERIALS AND METHODS: The mice (n = 10) were orally administrated with DYY-4 (15, 30, and 60 mg/kg) or DXM (5 mg/kg), half an hour after LPS (2 mg/kg) instilled intratracheally. The protein content and the levels of inflammatory factors, the levels of complements, the mRNA expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the level of myeloperoxidase (MPO) and superoxide dismutase (SOD), the expression of the IkB kinase (IKK) and nuclear factor-kappa B (NF-κB), the lung wet-to-dry weight (W/D) ratio and lung tissue were evaluated, 24 h after LPS challenge. Network pharmacology predicted potential targets. RESULTS: DYY-4 (30, 60 mg/kg, p < 0.01, p < 0.01) decreased the lung W/D ratio, total protein concentration, the levels of C3, C3c and C5a, the levels of TNF-α, IL-6, and IL-1ß, while increased the levels of IL-4 and IL-10. DYY-4 (60 mg/kg) decreased the levels of C5aR1, C5b-9 and COX-2 mRNA (p < 0.05), the levels of MPO and iNOS mRNA, the activation of the IKK/NF-κB pathway (p < 0.01), and increased the levels of IL-13 and SOD (p < 0.01). DYY-4 (60 mg/kg) relieved the lung tissue pathological changes and reduced the C3c deposition. DISCUSSION AND CONCLUSIONS: Network pharmacology combined with animal experiments revealed the targets of DYY-4 alleviating ALI.

Comparison of Postoperative Enophthalmos Between Fresh and Delayed Unilateral Orbital Fractures After Orbital Reconstruction With Titanium Mesh Using Computer-Assisted Navigation.

This study compares postoperative enophthalmos between fresh and delayed unilateral orbital fractures after orbital reconstruction with titanium mesh using computer-assisted navigation. The sample was composed of 45 patients with post-traumatic unilateral enophthalmos who were divided into the fresh fracture group and the delayed fracture group. They underwent orbital reconstruction with standard preformed orbital implants and computer-assisted navigation system. The following parameters were measured with computed tomography images: the degree of enophthalmos, orbital volume, and fracture defect area. Patients were reviewed preoperatively (T0), 1 week postoperatively (T1), and 6 months postoperatively (T2). Computed tomography measurements showed that in both groups, the degree of enophthalmos decreased after surgery but increased significantly from T1 to T2 ( P <0.05). ΔE (difference in the degree of enophthalmos between T1 and T2) was similar in patients with fresh and delayed fractures. There was a significant difference in the degree of ΔE between patients with single-wall orbital fractures and those with two-wall orbital fractures. The findings indicate that postoperative enophthalmos is common in both the groups and is closely related to the degree of preoperative enophthalmos. Furthermore, the recurrence of enophthalmos is similar between the 2 groups, but it is higher in patients with orbital fractures involving 2 walls.

Case Report: A rare case of primary paraganglioma of the gallbladder with a literature review.

Introduction: Paragangliomas of the gallbladder are exceptionally rare. To date, only a few cases of this disease have been reported globally, and the majority were found incidentally during surgery. Although complete resection can achieve a curative effect, specific targeted drugs may have survival benefits for patients with potential recurrence and metastasis risks. Case presentation: A 48-year-old woman was scheduled for anatomical central hepatectomy due to the discovery of a liver mass. Surprisingly, a gallbladder tumor accompanied by intrahepatic invasion was found rather than primary liver lesions during the operation. Postoperatively, the lesion was confirmed to be a paraganglioma originating from the gallbladder with intrahepatic invasion detectable on histopathology. After surgery, the patient was treated with a new targeted drug, surufatinib {200 mg, q.d. [quaque die (every day)]}, and no recurrence was observed during the regular follow-up. Discussion: Gallbladder paraganglioma is rare and occult, and surgeons do not know it well, so it is easily misdiagnosed before surgery. Postoperative pathological examination is the gold standard for diagnosis. Conclusion: Given that the tumor contained abundant blood sinuses, the early and continuous enhancement of dynamic enhanced CT scanning was its characteristic manifestation. We presented a case in which a primary gallbladder paraganglioma was identified accidentally in a patient who was misdiagnosed with a liver lesion before surgery. Based on our experience in this work, the en bloc resection technique in combination with surufatinib might have a survival benefit to patients at risk of potential recurrence or metastasis; however, further follow-up observations are needed.

Value of glycogen synthase 2 in intrahepatic cholangiocarcinoma prognosis assessment and its influence on the activity of cancer cells.

Intrahepatic cholangiocarcinoma (ICC) is the second most common primary liver tumor with increasing incidence worldwide. Metabolic reprogramming caused by metabolic related gene disorders is a prominent hallmark of tumors, among which Glycogen Synthase 2 (GYS2) is the key gene responsible for regulating cellular energy metabolism, and its expression disorders are closely related to various tumors and glycometabolic diseases. However, we still know nothing about its role in ICC. This study is intended to reveal the functional role of GYS2 in the ICC progress and explore the underlying mechanism. Based on the integrated pan-cancer analysis of GYS2 in the GEPIA database, the expression of GYS2 in paired ICC and adjacent non tumor tissues was detected by qPCR. It was found that the expression of GYS2 was significantly down-regulated in ICC. Further analysis showed that its low expression was not only associated with the degree of pathological differentiation, tumor size, microvascular invasion and lymph node metastasis, but also an independent risk factor for unfavorable prognosis. Functional studies have shown that GYS2 overexpression can significantly impair the proliferation, replication, cloning, migration and invasion of cholangiocarcinoma cells, while the silencing GYS2 dramatically promotes the development of the aforementioned phenotypes, the underlying mechanism may be that GYS2 activates the P53 pathway. In conclusions,low GYS2 expression in ICC predicted unfavorable patient outcomes; GYS2 overexpression could significantly impair the proliferation, migration and invasion of cholangiocarcinoma cells via activating the P53 pathway and GYS2 was expected to become a potential therapeutic target for such patients.

An Adaptive Transfer-Learning-Based Deep Cox Neural Network for Hepatocellular Carcinoma Prognosis Prediction.

BACKGROUND: Predicting hepatocellular carcinoma (HCC) prognosis is important for treatment selection, and it is increasingly interesting to predict prognosis through gene expression data. Currently, the prognosis remains of low accuracy due to the high dimension but small sample size of liver cancer omics data. In previous studies, a transfer learning strategy has been developed by pre-training models on similar cancer types and then fine-tuning the pre-trained models on the target dataset. However, transfer learning has limited performance since other cancer types are similar at different levels, and it is not trivial to balance the relations with different cancer types. METHODS: Here, we propose an adaptive transfer-learning-based deep Cox neural network (ATRCN), where cancers are represented by 12 phenotype and 10 genotype features, and suitable cancers were adaptively selected for model pre-training. In this way, the pre-trained model can learn valuable prior knowledge from other cancer types while reducing the biases. RESULTS: ATRCN chose pancreatic and stomach adenocarcinomas as the pre-training cancers, and the experiments indicated that our method improved the C-index of 3.8% by comparing with traditional transfer learning methods. The independent tests on three additional HCC datasets proved the robustness of our model. Based on the divided risk subgroups, we identified 10 HCC prognostic markers, including one new prognostic marker, TTC36. Further wet experiments indicated that TTC36 is associated with the progression of liver cancer cells. CONCLUSION: These results proved that our proposed deep-learning-based method for HCC prognosis prediction is robust, accurate, and biologically meaningful.

A Nomogram for Preoperative Estimation of Microvascular Invasion Risk in Hepatocellular Carcinoma: Single-Center Analyses With Internal Validation.

BACKGROUND: Microvascular invasion (MVI) is highly associated with poor prognosis in patients with liver cancer. Predicting MVI before surgery is helpful for surgeons to better make surgical plan. In this study, we aim at establishing a nomogram to preoperatively predict the occurrence of microvascular invasion in liver cancer. METHOD: A total of 405 patients with postoperative pathological reports who underwent curative hepatocellular carcinoma resection in the Third Affiliated Hospital of Sun Yat-sen University from 2013 to 2015 were collected in this study. Among these patients, 290 were randomly assigned to the development group while others were assigned to the validation group. The MVI predictive factors were selected by Lasso regression analysis. Nomogram was established to preoperatively predict the MVI risk in HCC based on these predictive factors. The discrimination, calibration, and effectiveness of nomogram were evaluated by internal validation. RESULTS: Lasso regression analysis revealed that discomfort of right upper abdomen, vascular invasion, lymph node metastases, unclear tumor boundary, tumor necrosis, tumor size, higher alkaline phosphatase were predictive MVI factors in HCC. The nomogram was established with the value of AUROC 0.757 (0.716-0.809) and 0.768 (0.703-0.814) in the development and the validation groups. Well-fitted calibration was in both development and validation groups. Decision curve analysis confirmed that the predictive model provided more benefit than treat all or none patients. The predictive model demonstrated sensitivity of 58.7%, specificity of 80.7% at the cut-off value of 0.312. CONCLUSION: Nomogram was established for predicting preoperative risk of MVI in HCC. Better treatment plans can be formulated according to the predicted results.

Three-dimensional network-like structure formed by silicon coated carbon nanotubes for enhanced microwave absorption.

The rapid development of electronic technology generates a great deal of electromagnetic wave (EMW) that is tremendously hazardous to environment and human health. Correspondingly, the high efficient EMW absorption materials with lightweight, high capacity and broad bandwidth are highly required. Herein, a series of three-dimensional (3D) network-like structure formed by silicon coated carbon nanotubes (NW-CNT@SiO2) are massively prepared through an improved sol-gel process. The as-obtained 3D NW-CNT@SiO2 exhibit low densities of about 1.6 ± 0.2 g/cm3. The formation of this special 3D structure can provide high dielectric loss and good impedance matching for EMW absorption. As expected, a minimum reflection loss (RL) of -54.076 dB is obtained when uses the sample prepared by 0.1 g of CNTs and 0.2 mL of tetraethoxysilane as absorbent with a low loading rate of 10 wt% and thin absorber thickness of 1.08 mm. This specific minimum RL value exceeds many other CNT based EMW absorbers reported in previous literature. These findings featured with a green and scalable preparation process provides a facile strategy to design and fabricate high-performance EMW absorption materials, which can be applied to other materials such as carbon fibers and graphene.

ß-Arrestin-2 attenuates hepatic ischemia-reperfusion injury by activating PI3K/Akt signaling.

Hepatic ischemia-reperfusion injury (IRI) remains a common complication during liver transplantation (LT), partial hepatectomy and hemorrhagic shock in patients. As a member of the G protein-coupled receptors adaptors, ARRB2 has been reported to be involved in a variety of physiological and pathological processes. However, whether ß-arrestin-2 affects the pathogenesis of hepatic IRI remains unknown. The goal of the present study was to determine whether ARRB2 protects against hepatic IR injury and elucidate the underlying mechanisms. To this end, 70% hepatic IR models were established in ARRB2 knockdown mice and wild-type littermates, with blood and liver samples collected at 1, 6 and 12 h after reperfusion to evaluate liver injury. The effect of ARBB2 on PI3K/Akt signaling during IR injury was evaluated in vivo, and PI3K/Akt pathway regulation by ARRB2 was further assessed in vitro. Our results showed that ARRB2 knockdown aggravates hepatic IR injury by promoting the apoptosis of hepatocytes and inhibiting their proliferation. In addition, ARRB2 deficiency inhibited PI3K/Akt pathway activation, while the administration of the PI3K/Akt inhibitor PX866 resulted in severe IR injury in mice. Furthermore, the liver-protecting effect of ARRB2 was shown to depend on PI3K/Akt pathway activation. In summary, our results suggest that ß-Arrestin-2 protects against hepatic IRI by activating PI3K/Akt signaling, which may provide a novel therapeutic strategy for treating liver ischemia-reperfusion injury.

Application of near-infrared fluorescent cholangiography using indocyanine green in laparoscopic cholecystectomy.

OBJECTIVE: Near-infrared fluorescence cholangiography (NIRF-C) can help to identify the bile duct during laparoscopic cholecystectomy. This retrospective study was performed to investigate the effect of NIRF-C in laparoscopic cholecystectomy. METHODS: Consecutive patients who underwent NIRF-C-assisted laparoscopic cholecystectomy (n = 34) or conventional laparoscopic cholecystectomy (n = 36) were enrolled in this study. Identification of biliary structures, the operation time, intraoperative blood loss, and postoperative complications were analyzed. RESULTS: Laparoscopic cholecystectomy was completed in all patients without conversion to laparotomy. The median operation time and intraoperative blood loss were not significantly different between the two groups. No intraoperative injuries or postoperative complications occurred in either group. In the NIRF-C group, the visualization rate of the cystic duct, common bile duct, and common hepatic duct prior to dissection was 91%, 79%, and 53%, respectively. The success rate of cholangiography was 100% in the NIRF-C group. NIRF-C was more effective for visualizing biliary structures in patients with a BMI of <25 than >25 kg/m2. CONCLUSIONS: NIRF-C is a safe and effective technique that enables real-time identification of the biliary anatomy during laparoscopic cholecystectomy. NIRF-C helps to improve the efficiency of dissection.

Primary hepatic neuroendocrine tumor with multiple liver metastases: A case report with literature review.

Primary hepatic neuroendocrine tumors (PHNETs) are a group of extremely rare tumors that are difficult to differentiate from common hepatic malignancies on routine imaging studies. By presenting a case of PHNET, we herein introduce our experience with the diagnosis, differential diagnosis, and management of patients with this rare disease. The patient was preoperatively diagnosed with hepatic hydatidosis but postoperatively diagnosed with a PHNET with multiple liver metastases. He was successfully treated with transcatheter arterial chemoembolization. This case indicates that the clinical diagnosis of PHNET is a medical challenge. Although peptide receptor radionuclide therapy has been suggested as the mainstay of treatment for well-differentiated somatostatin receptor-positive PHNETs, patients with a large tumor burden may also benefit from transcatheter arterial chemoembolization.

A novel protein encoded by circFNDC3B inhibits tumor progression and EMT through regulating Snail in colon cancer.

BACKGROUND: Colon cancer (CC) is a common malignant cancer. Recently, circFNDC3B was found to exert biological function in multiple cancers. However, it was unclear whether the potential protein encoded by circFNDC3B is involved in carcinogenesis of CC. METHODS: We used Sanger sequence and RNase R digestion assay to confirm the existence of circFNDC3B, and quantitative real-time PCR was used to evaluate the circRNA's expression. Then fluorescence in situ hybridization (FISH) was performed to study location of circFNDC3B. The identification of protein encoded by circFNDC3B was performed using LC-MS/MS. The function of circFNDC3B-218aa on proliferation, invasion and migration were assessed by CCK8 assays, colony formation assays, transwell assays, wound-healing assays and animal experiments. RNA-sequencing and western blot were used to identify the gene regulated by circFNDC3B-218aa. Finally, glucose metabolism-related assays were performed to further investigate function of circFNDC3B-218aa. RESULTS: CircFNDC3B was localized mostly in the cytoplasm, and was decreased in CC cell lines and tissues. The patients with low circFNDC3B expression had a shorter OS (P = 0.0014) than patients with high expression. Moreover, circFNDC3B inhibited the proliferation, invasion and migration of CC cells. Next, we identified that circFNDC3B could encode a novel protein circFNDC3B-218aa. Furthermore, circFNDC3B-218aa, not circFNDC3B, inhibited the proliferation, invasion and migration of CC. Additionally, the in vivo experiments implied that up-regulated circFNDC3B-218aa exhibited an inhibitory effect on CC progression. By RNA-sequencing, western blot and glucose metabolism-related assays, we found that circFNDC3B-218aa inhibited the expression of Snail, and subsequently promoted the tumor-suppressive effect of FBP1 in CC. CONCLUSIONS: The novel circFNDC3B-218aa may serve as a tumor suppressive factor and potential biomarker which may supply the potential therapeutic target for CC.

Evaluating the remodeling of condyles reconstructed by transport distraction osteogenesis in the treatment of temporomandibular joint ankylosis.

PURPOSE: This study aimed to evaluate the remodeling of condyles reconstructed by transport distraction osteogenesis (DO) in patients with temporomandibular joint (TMJ) ankylosis. PATIENTS AND METHODS: Twenty-one patients with 26 affected joints were followed up for 34.1 ± 13.3 months. Patients who had undergone gap arthroplasty and TMJ reconstruction by DO were included. Maximal mouth opening (MMO) and occlusion were recorded. Computed tomography images were obtained preoperatively (T0), upon completing distraction (T1), upon removal of the distraction device (T2), and >2 years postoperatively (T3). The following were measured: mandibular ramus height, distance between gonion and Frankfurt plane (Go-FN), condylar width, and condyle-ramus angulation. RESULTS: Of the 21 patients, one showed re-ankylosis, while five exhibited anterior open bite. From T1 to T3, the total amount of resorption of ramus height reached up to 8.2 ± 4.6 mm (p < 0.001), in comparison with a total distraction length of 13.8 ± 4.1 mm; the mean resorption rate was 59.4%. Similarly, Go-FN decreased by 6.2 ± 4.0 mm (p < 0.001). CONCLUSION: Our findings indicated that DO combined with gap arthroplasty was an effective method for the treatment of TMJ ankylosis to improve MMO. The reconstructed condyle exhibited a high frequency of resorption in height.

Long Non-Coding RNA-PAICC Promotes the Tumorigenesis of Human Intrahepatic Cholangiocarcinoma by Increasing YAP1 Transcription.

Intrahepatic cholangiocarcinoma (ICC) is a heterogeneous hepatobiliary tumor with poor prognosis, and it lacks reliable prognostic biomarkers and effective therapeutic targets. Long non-coding RNAs (lncRNAs) have been documented to be involved in the progression of various cancers. However, the role of lncRNAs in ICC remains largely unknown. In the present work, we used bioinformatics analysis to identify the differentially expressed lncRNAs in human ICC tissues, among which lncRNA-PAICC was found to be an independent prognostic marker in ICC. Moreover, lncRNA-PAICC promoted the proliferation and invasion of ICC cells. Mechanistically, lncRNA-PAICC acted as a competitive endogenous RNA (ceRNA) that directly sponged the tumor suppressive microRNAs miR-141-3p and miR-27a-3p. The competitive binding property was essential for lncRNA-PAICC to promote tumor growth and metastasis through activating the Hippo pathway. In summary, our results highlighted the important role of the lncRNA-PAICC-miR-141-3p/27a-3p-Yap1 axis in ICC, which offers a novel perspective on the molecular pathogenesis and may serve as a potential target for antimetastatic molecular therapies of ICC.

SOX11 promotes osteoarthritis through induction of TNF-α.

OBJECTIVE: Osteoarthritis (OA) is a degenerative disease and the molecular mechanism of OA remains unclear. Transcription factor SOX11 has been proved to be involved in the development progress of OA. The present study aimed to evaluate the potential function of SOX11 during the development of OA. METHODS: SOX11 expression in patients with OA and health donator was determined with qRT-PCR. Subsequently, in vitro OA model was established by treating the chondrocyte cells CHON-001 with IL-1ß. Next, we validated the function of SOX11 in in vitro OA model by using siRNAs. Finally, the relationship between SOX11 and TNF-α was explored. RESULTS: SOX11 was upregulated in patients with OA and in IL-1ß treated cells. IL-1ß significantly increased both the mRNA and protein levels of MMP13 and cleaved caspase 3, while decreased collagen II and aggrecan in CHON-001 cells. In addition, knockdown of SOX11 could significantly decrease IL-1ß-induced apoptosis in CHON-001 cells. Meanwhile, IL-1ß induced OA like phenomenon was significantly reversed by siRNA interference. Moreover, inhibition of SOX11 decreased the level of TNF-α in patients with OA and in IL-1ß treated cell supernatant. CONCLUSION: Inhibition of SOX11 could improve IL-1ß-induced OA like phenomenon in CHON-001 cells, which suggesting SOX11 played an important role during the pathogenesis of OA. Thus, we hypothesized that SOX11 could be a potential target for the treatment of patients with OA.