MicroRNA-30a-5p Promotes Chronic Heart Failure in Rats by Targeting Sirtuin-1 to Activate the Nuclear Factor-κB/NOD-Like Receptor 3 Signaling Pathway.

OBJECTIVE: MicroRNA-30a-5p (miR-30a-5p) has been identified as a marker of heart failure; however, its functional mechanisms in chronic heart failure (CHF) remain unknown. We aim to investigate the role of miR-30a-5p targeting sirtuin-1 (SIRT1) in myocardial remodeling in CHF via the nuclear factor-κB/NOD-like receptor 3 (NF-κB/NLRP3) signaling pathway. METHODS: CHF rat models were established using aortic coarctation. The expression of miR-30a-5p, SIRT1, and the NF-κB/NLRP3 signaling pathway-related factors in CHF rats was determined. The CHF rats were then respectively treated with altered miR-30a-5p or SIRT1 to explore their roles in cardiac function, myocardial function, inflammatory response, pathological changes, and cardiomyocyte apoptosis. The binding relation between miR-30a-5p and SIRT1 was confirmed. RESULTS: MiR-30a-5p was upregulated whereas SIRT1 was downregulated in myocardial tissues of CHF rats. MiR-30a-5p inhibition or SIRT1 overexpression improved cardiac and myocardial function, and suppressed the inflammatory response, alleviated pathological changes and inhibited cardiomyocyte apoptosis in CHF rats. MiR-30a-5p targeted SIRT1 to regulate the NF-κB/NLRP3 signaling pathway. In CHF rats, downregulated miR-30a-5p and silenced SIRT1 could reverse the beneficial effects of downregulated miR-30a-5p. CONCLUSION: Inhibited miR-30a-5p inhibits CHF progression via the SIRT1-mediated NF-κB/NLRP3 signaling pathway.

The value of CT findings combined with inflammatory indicators for preoperative differentiation of benign and malignant gallbladder polypoid lesions.

BACKGROUND: The study aimed to explore the value of CT findings and inflammatory indicators in differentiating benign and malignant gallbladder polypoid lesions before surgery. METHODS: The study comprised a total of 113 pathologically confirmed gallbladder polypoid lesions with a maximum diameter ≥ 1 cm (68 benign and 45 malignant), all of which were enhanced CT-scanned within 1 month before surgery. The CT findings and inflammatory indicators of the patients were analyzed by univariate and multivariate logistic regression analysis to identify independent predictors of gallbladder polypoid lesions, and then a nomogram distinguishing benign and malignant gallbladder polypoid lesions was developed by combining these characteristics. The receiver operating characteristic (ROC) curve and decision curve were plotted to assess the performance of the nomogram. RESULTS: Base status of the lesion (p < 0.001), plain CT value (p < 0.001), neutrophil-lymphocyte ratio (NLR) (p = 0.041), and monocyte-lymphocyte ratio (MLR) (p = 0.022) were independent predictors of malignant polypoid lesions of the gallbladder. The nomogram model established by incorporating the above factors had good performance in differentiating and predicting benign and malignant gallbladder polypoid lesions (AUC = 0.964), with sensitivity and specificity of 82.4% and 97.8%, respectively. The DCA demonstrated the important clinical utility of our nomogram. CONCLUSION: CT findings combined with inflammatory indicators can effectively differentiate benign and malignant gallbladder polypoid lesions before surgery, which is valuable for clinical decision-making.

Quasiparticle dynamics and phonon softening in FeSe0.9S0.1 superconductors.

The quasiparticle and longitudinal acoustic (LA) coherent phonon dynamics of the FeSe0.9S0.1 single crystal were investigated by femtosecond transient optical spectroscopy. The FeSe0.9S0.1 single crystal undergoes metal-superconductor transition at Tc = 9.5 K and structural phase transition at Ts = 72 K. To investigate the correlation between the quasiparticle/LA coherent phonon dynamics and the antiferromagnetic spin/nematic fluctuation, we measured the transient differential reflectivity ΔR(t)/R0 in time series (R is the reflectivity) between 4-130 K. The ΔR(t)/R0 time series showed a negative sign below Ts = 72 K, while its sign reversed from negative to positive above Ts. The ΔR(t)/R0 time series was contributed by a combination of two exponential decays and an oscillation term. The slow decay attributed to electron-phonon and phonon-phonon coupling showed a negative amplitude below Ts and a positive amplitude above Ts. A fast decay with positive amplitude appeared at T ≥ 55 K was induced by the electron-phonon coupling of the high-temperature orthorhombic phase FeSe0.9S0.1. The oscillation contributed by the LA coherent phonon emerged below Ts but was not observed above Ts, indicating that it was impacted by the nematic fluctuation of FeSe0.9S0.1.

LncRNA PVT1 promotes the progression of ovarian cancer by activating TGF-ß pathway via miR-148a-3p/AGO1 axis.

Ovarian cancer is a lethal gynaecologic malignancy with poor diagnosis and prognosis. The long non-coding RNA plasmacytoma variant translocation1 (PVT1) and argonaute 1 (AGO1) are associated with carcinogenesis and chemoresistance; however, the relationship between PVT1 and AGO1 and the downstream mechanisms in ovarian cancer remains poorly known. PVT1 and AGO1 expression was assessed through RT-qPCR and Western blotting in both human tissues and cell lines. The viability and proliferation of ovarian cancer cells were determined by CCK-8 assay and TUNEL assay in vitro and immunohistochemistry in vivo. Cell invasion and migration were investigated through transwell and wound-healing assays. The roles and mechanisms of AGO1 on cell functions were further probed via gain- and loss-of-function analysis. We reveal that PVT1 expression was significantly increased in ovarian cancer tissues which is associated with advanced FIGO stage, lymph-node metastasis, poor survival rate, and high expression of AGO1. PVT1 or AGO1 knockdown significantly reduced the cell viability and increased the cell apoptosis and inhibited ovarian tumour growth and proliferation. Furthermore, we discovered that PVT1 up-regulated the expression of AGO1 and thus regulated the transforming growth factor-ß (TGF-ß) pathway to promote ovarian cancer progression through sponging miR-148a-3p. Additionally, the activation of ERK1/2, smad2 and smad4 is observed to be related to the PVT1/miR-148a-3p/AGO1/TGF-ß pathway-induced cascades. Taken together, the present study reveals that PVT1/miR-148a/AGO1 axis plays an important role in the progression of ovarian cancer and emphasize the potential as a target of value for ovarian cancer therapy.

Deregulation of angiopoietin-like 4 slows ovarian cancer progression through vascular endothelial growth factor receptor 2 phosphorylation.

BACKGROUND: As a tissue-specific proangiogenic or antiangiogenic agent, angiopoietin-like 4 (ANGPTL4) has recently gained attention in many diseases, such as metabolic syndrome, cardiovascular disease and cancer. However, the roles of ANGPTL4 in angiogenesis and tumor growth in epithelial ovarian cancer, the most lethal gynecologic malignancy, remain unclear. OBJECTIVE: To identify a novel mechanism of ANGPTL4 inhibition in epithelial ovarian cancer. METHODS: Western blot, quantitative reverse transcription PCR, and immunofluorescence analyses were applied to evaluate ANGPTL4 expression in ovarian cancer cell lines. Cell proliferation, migration, and invasion were investigated through 5-ethynyl-2'-deoxyuridine (EdU) incorporation, CCK-8 and Transwell assays. The expression of epithelial-mesenchymal transition (EMT)-related proteins in ovarian cancer cells and tumor-bearing mice was evaluated. CD31 staining was used to identify tumor angiogenesis. Immunoprecipitation was performed to examine the regulatory relationship between ANGPTL4 and the vascular endothelial growth factor receptor 2 (VEGFR2)/vascular endothelial (VE)-cadherin/Src complex. VEGFR2 phosphorylation at Y949 and VE-cadherin expression were assessed by western blotting. Inactivation of VEGFR2 Y949 phosphorylation was achieved in a MISIIR-TAg VEGFR2Y949F/Y949F mouse model. RESULTS: Here, we demonstrated that ANGPTL4 was overexpressed in A2780 and CAOV3 ovarian cancer cells. In vitro assays indicated that inhibition of ANGPTL4 by lentiviral small interfering RNA does not alter ovarian cancer cell proliferation, migration, invasion, and EMT, while ANGPTL4 silencing exhibited significant inhibitory effects on tumor angiogenesis, growth, and metastasis in vivo. Immunoprecipitation analysis showed that suppression of ANGPTL4 was accompanied by dissociation of the VEGFR2/VE-cadherin/Src complex and phosphorylation of VEGFR2 Y949 in A2780 and CAOV3 ovarian tumors. Inactivation of VEGFR2 Y949 phosphorylation in MISIIR-TAg VEGFR2Y949F/Y949F mice abolished all tumor-suppressive effects of ANGPTL4 inhibition in spontaneous ovarian carcinoma. CONCLUSIONS: Overall, our results indicate that ANGPLT4 silencing delays tumor progression in specific types of ovarian cancer and may be a potential target for individualized treatment of ovarian cancer.

Development of a computerized tool for the chinese version of the montreal cognitive assessment for screening mild cognitive impairment.

ABSTRACT Background: The Montreal Cognitive Assessment (MoCA) is used for screening mild cognitive impairment (MCI), and the Beijing version (MoCA-BJ) is widely used in China. We aimed to develop a computerized tool for MoCA-BJ (MoCA-CC). Methods: MoCA-CC used person-machine interaction instead of patient-to-physician interaction; other aspects such as the scoring system did not differ from the original test. MoCA-CC, MoCA-BJ and routine neuropsychological tests were administered to 181 elderly participants (MCI = 96, normal controls [NC] = 85). Results: A total of 176 (97.24%) participants were evaluated successfully by MoCA-CC. Cronbach's α for MoCA-CC was 0.72. The test-retest reliability (retesting after six weeks) was good (intraclass correlation coefficient = 0.82; P < 0.001). Significant differences were observed in total scores (t = 9.38, P < 0.001) and individual item scores (t = 2.18-8.62, P < 0.05) between the NC and MCI groups, except for the score for "Naming" (t = 0.24, P = 0.81). The MoCA-CC total scores were highly correlated with the MoCA-BJ total scores (r = 0.93, P < 0.001) in the MCI participants. The area under receiver-operator curve for the prediction of MCI was 0.97 (95% confidence interval = 0.95-1.00). At the optimal cut-off score of 25/26, MoCA-CC demonstrated 95.8% sensitivity and 87.1% specificity. Conclusion: The MoCA-CC tool developed here has several advantages over the paper-pencil method and is reliable for screening MCI in elderly Chinese individuals, especially in the primary clinical setting. It needs to be validated in other diverse and larger populations.

Different risk factors between intracranial and extracranial atherosclerotic stenosis in Asian population: a systematic review and meta-analysis.

Sex, hypertension, diabetes, dyslipidemia, smoking, age and metabolic syndrome (MetS) are major vascular risk factors for intracranial or extracranial atherosclerotic stenosis (ICAS or ECAS) in Asian population. Here, we performed a meta-analysis to evaluate the different influence of these factors on ICAS compared to ECAS in Asian population, by searching PUBMED, EMBASE and Web of Science databases. Sensitivity analysis was performed by repeating the fixed or random effects model meta-analysis with removing each study individually. All statistical analysis was conducted with Stata 11.0. Finally, 15 studies including 3787 patients were identified, 2661 patients in ICAS group and 1126 patients in ECAS group, respectively. Our results showed that female or the patients with MetS were more likely to suffer from ICAS than ECAS, which pooled ORs of ICAS versus ECAS were 2.16 (95% CI: 1.65-2.83, p < 0.0001) and 1.68 (95% CI: 1.32-2.12, p < 0.0001), respectively. Meanwhile, the smoker or the patients with dyslipidemia were more likely to suffer from ECAS than ICAS, which pooled ORs of ICAS versus ECAS were 0.71 (95% CI: 0.61-0.84, p < 0.0001) and 0.75 (95% CI: 0.63-0.90, p = 0.002), respectively. However, age, hypertension and diabetes had not different influence on the location of atherosclerotic stenosis, and the pooled MD and ORs were -0.69 (95% CI: -1.52-0.15, p = 0.11), 1.08 (95% CI: 0.92-1.27, p = 0.34) and 1.02 (95% CI: 0.88-1.19, p = 0.76), respectively. Our results suggested that female sex and MetS were more associated with ICAS, while smoking and dyslipidemia were more associated with ECAS. There was no significant difference between ICAS and ECAS in terms of age, hypertension and diabetes.

[Research on expression and function of phosphorylated DARPP-32 on pentylenetetrazol-induced epilepsy model of rat].

The present study is to explore the change process and distribution of phosphorylated DARPP-32 (p-DARPP-32) in rat brain including cortex, hippocampus and striatum and to further deduce whether p-DARPP-32 was possibly involved in epilepsy induced by repetitive low doses of pentylenetetrazol (PTZ). PTZ-induced epilepsy model in rat was established with 30 male SD rats randomly divided into 6 groups, control group and five trial groups [PTZ 1 h, PTZ 6 h, PTZ 24 h, PTZ 48 h and PTZ 72 h respectively, after onset of status epilepticus (SE)]. Immunohistochemistry and immunofluorescence double-labeling were used to detect the temporal time change and distribution of p-DARPP-32 expression and to analyze the coexpression of DARPP-32 and p-DARPP-32 in rat brain after the onset of PTZ-induced generalized SE. The results showed that there was a temporal time change of p-DARPP-32 expression in rat brain after the onset of SE. The number of p-DARPP-32-positive cells increased significantly and reached the peaks at the ends of 1 hour and 6 hours after the onset of SE, but decreased at the end of 24 hours. The moderate to strong p-DARPP-32-immunopositive neurons were observed in cortex, hippocampus and striatum, and located in cell cytoplasm and cell nucleus. Further immunofluorescence double-labeling revealed that denser colocalization of p-DARPP-32 and DARPP-32 in the neurons existed in the area mentioned above. Therefore, PTZ-induced SE may cause phosphorylation of DARPP-32 in rat brain. The temporal time change and distribution of p-DARPP-32 suggest that phosphorylation of DARPP-32 may be involved in PTZ-induced epilepsy in rat brain including cortex, hippocampus and striatum, and p-DARPP-32 may play a central role in the onset of SE.

ANGPTL3 affects the metastatic potential and the susceptibility of ovarian cancer cells to natural killer cell-mediated cytotoxicity.

High metastatic potential and resistance to immunotherapy lead to poor survival in patients with ovarian cancer. Angiopoietin-like protein 3 is aberrantly expressed and exerts diverse roles in the progression of several cancers. However, its function in ovarian cancer is unknown. Here, decreased expression of angiopoietin-like protein 3 was observed in ovarian cancer tissues and cells. Moreover, patients with high expression of angiopoietin-like protein 3 had longer overall survival and progression-free survival, indicating a good prognosis for patients. Furthermore, angiopoietin-like protein 3 overexpression inhibited ovarian cancer cell proliferation. Concomitantly, high invasion and the occurrence of epithelial-to-mesenchymal transition of cancer cells were restrained after angiopoietin-like protein 3 elevation. Up-regulation of angiopoietin-like protein 3 expression further increased interleukin 2-treated natural killer cell activation by increasing CD69 expression and production of interferon gamma and tumor necrosis factor-alpha when natural killer cells were co-cultured with ovarian cancer cells. Importantly, angiopoietin-like protein 3 overexpression enhanced natural killer cell-evoked cytotoxicity and apoptosis of cancer cells, indicating the pro-tumor killing ability of angiopoietin-like protein 3 for natural killer cells. Mechanistically, angiopoietin-like protein 3 elevation inhibited activation of the Janus Kinase/Signal transducer and activator of transcription 3 signaling in ovarian cancer cells by inhibiting protein expression of phospho-Janus Kinase 2, phospho-Signal transducer and activator of transcription 3, downstream matrix metallopeptidase 2 and programmed cell death 1. Moreover, blocking the Janus Kinase/Signal transducer and activator of transcription 3 pathway via their inhibitor Stattic restrained ovarian cancer cell proliferation, invasion, epithelial-to-mesenchymal transition, and promoted natural killer cell killing to ovarian cancer cells. Thus, these findings reveal that angiopoietin-like protein 3 may act as an anti-oncogenic regulator to inhibit the metastatic potential and enhance the susceptibility of ovarian cancer cells to natural killer cell-mediated killing. Consequently, angiopoietin-like protein 3 may regulate metastatic potential and immune escape from natural killer cells, indicating a promising therapeutic strategy for ovarian cancer.

Immunometabolomics provides a new perspective for studying systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic multi-organ autoimmune disease characterized by clinical heterogeneity, unpredictable progression, and flare ups. Due to the heterogeneous nature of lupus, it has been challenging to identify sensitive and specific biomarkers for its diagnosis and monitoring. Despite the fact that the mechanism of SLE remains unknown, impressive progress has been made over the last decade towards understanding how different immune cells contribute to its pathogenesis. Research suggests that cellular metabolic programs could affect the immune response by regulating the activation, proliferation, and differentiation of innate and adaptive immune cells. Many studies have shown that the dysregulation of the immune system is associated with changes to metabolite profiles. The study of metabolite profiling may provide a means for mechanism exploration and novel biomarker discovery for disease diagnostic, classification, and monitoring. Here we review the latest advancements in understanding the role of immunometabolism in SLE, as well as the systemic metabolite profiling of this disease along with possible clinical application.

A preoperative model based on gadobenate-enhanced MRI for predicting microvascular invasion in hepatocellular carcinomas (≤ 5 cm).

Purpose: The present study aimed to develop and validate a preoperative model based on gadobenate-enhanced magnetic resonance imaging (MRI) for predicting microvascular invasion (MVI) in patients with hepatocellular carcinoma (HCC) size of ≤5 cm. In order to provide preoperative guidance for clinicians to optimize treatment options. Methods: 164 patients with pathologically confirmed HCC and preoperative gadobenate-enhanced MRI from July 2016 to December 2020 were retrospectively included. Univariate and multivariate logistic regression (forward LR) analyses were used to determine the predictors of MVI and the model was established. Four-fold cross validation was used to verify the model, which was visualized by nomograms. The predictive performance of the model was evaluated based on discrimination, calibration, and clinical utility. Results: Elevated alpha-fetoprotein (HR 1.849, 95% CI: 1.193, 2.867, P=0.006), atypical enhancement pattern (HR 3.441, 95% CI: 1.523, 7.772, P=0.003), peritumoral hypointensity on HBP (HR 7.822, 95% CI: 3.317, 18.445, P<0.001), and HBP hypointensity (HR 3.258, 95% CI: 1.381, 7.687, P=0.007) were independent risk factors to MVI and constituted the HBP model. The mean area under the curve (AUC), sensitivity, specificity, and accuracy values for the HBP model were as follows: 0.830 (95% CI: 0.784, 0.876), 0.71, 0.78, 0.81 in training set; 0.826 (95% CI:0.765, 0.887), 0.8, 0.7, 0.79 in test set. The decision curve analysis (DCA) curve showed that the HBP model achieved great clinical benefits. Conclusion: In conclusion, the HBP imaging features of Gd-BOPTA-enhanced MRI play an important role in predicting MVI for HCC. A preoperative model, mainly based on HBP imaging features of gadobenate-enhanced MRI, was able to excellently predict the MVI for HCC size of ≤5cm. The model may help clinicians preoperatively assess the risk of MVI in HCC patients so as to guide clinicians to optimize treatment options.

Preoperative differentiation of hepatocellular carcinoma with peripheral rim-like enhancement from intrahepatic mass-forming cholangiocarcinoma on contrast-enhanced MRI.

Purpose: The present study aimed to determine the reliable imaging features to distinguish atypical hepatocellular carcinoma (HCC) with peripheral rim-like enhancement from intrahepatic mass-forming cholangiocarcinoma (IMCC) on contrast-enhanced magnetic resonance imaging (MRI). Methods: A total of 168 patients (130 male, 57.10 ± 10.53 years) pathological confirmed HCC or IMCC who underwent contrast-enhanced MRI between July 2019 and February 2022 were retrospectively included. Univariate and multivariate logistic regression analyses were used to determine independent differential factors for distinguishing HCC from IMCC, and the model was established. Bootstrap resampling 1000 times was used to verify the model, which was visualized by nomograms. The predictive performance of the model was evaluated based on discrimination, calibration, and clinical utility. Results: Radiological capsule (OR 0.024, 95% CI: 0.006, 0.095, P<0.001), heterogeneous signal intensity (SI) on T1WI (OR 0.009, 95%CI: 0.001,0.056, P<0.001) were independent differential factors for predicting HCC over IMCC. A lobulated contour (OR 11.732, 95%CI: 2.928,47.007, P = 0.001), target sign on DP (OR 14.269, 95%CI: 2.849,82.106, P = 0.007), bile duct dilatation (OR 12.856, 95%CI: 2.013, P = 0.001) were independent differential factors for predicting IMCCs over HCCs. The independent differential factors constituted a model to distinguish atypical HCCs and IMCCs. The area under receiver operating characteristic (ROC) curve, sensitivity, and specificity values of the model were 0.964(0.940,0.987), 0.88, and 0.906, indicating that the model had an excellent differential diagnostic performance. The decision curve analysis (DCA) curve showed that the model obtained a better net clinical benefit. Conclusion: The present study identified reliable imaging features for distinguishing atypical HCCs with peripheral rim-like enhancement from IMCCs on contrast-enhanced MRI. Our findings may help radiologists provide clinicians with more accurate preoperative imaging diagnoses to select appropriate treatment options.

The Value of Contrast-Enhanced Magnetic Resonance Imaging Enhancement in the Differential Diagnosis of Hepatocellular Carcinoma and Combined Hepatocellular Cholangiocarinoma.

Background: The distinction between combined hepatocellular-cholangiocarcinoma (cHCC-CC) and hepatocellular carcinoma (HCC) before the operation has an important clinical significance for optimizing the treatment plan and predicting the prognosis of patients. Magnetic resonance imaging (MRI) has been widely used in the preoperative diagnosis and evaluation of primary liver malignant tumors. Purpose: The aim is to study the value of preoperative clinical data and enhanced MRI in the differential diagnosis of HCC and cHCC-CC and obtain independent risk factors for predicting cHCC-CC. Study type. Retrospective. Population. The clinical and imaging data of 157 HCC and 59 cHCC-CC patients confirmed by pathology were collected. Field Strength/Sequence. 1.5T; cross-sectional T1WI (gradient double echo sequence); cross-sectional T2WI (fast spin echo sequence, fat suppression); enhancement (3D LAVA technology). Assessment. The differences between the HCC and cHCC-CC patients were compared. Statistic Tests. Using the t-test, chi-square test, and logistic regression analysis, P < 0.05 was considered statistically significant. Result: 1. CHCC-CC was more likely to show multiple lesions than HCC (28.81% vs. 10.83%, P = 0.001) and more prone to microvascular invasion (MVI) (36.31% vs. 61.02%, P < 0.001). However, HCC had a higher incidence of liver cirrhosis than cHCC-CC (50.85% vs. 72.61%, P = 0.003). 2. The incidence of nonsmooth margin was higher in the cHCC-CC group (84.75% vs. 52.23%, P < 0.001). The incidence of peritumor enhancement in the arterial phase was higher in the cHCC-CC group (11.46% vs. 62.71%, P < 0.001) 3. According to the multivariate analysis, arterial peritumor enhancement (OR = 8.833,95%CI:4.033,19.346, P < 0.001) was an independent risk factor for cHCC-CC (P < 0.001)). It had high sensitivity (62.71%) and specificity (88.54%) in the diagnosis of cHCC-CC. Date Conclusions. Liver cirrhosis and the imaging findings of GD-DTPA-enhanced MRI are helpful for the differential diagnosis of HCC and cHCC-CC. In addition, the imaging sign of peritumoral enhancement in the arterial phase has high sensitivity and specificity for the diagnosis of cHCC-CC.

Use of three-dimensional-printed custom-made prosthesis to treat unicondylar femoral defect secondary to pathological fracture caused by giant cell tumor.

OBJECTIVE: To evaluate the short-term effectiveness of using a three-dimensional (3D)-printed custom-made prosthesis to repair unicondylar femoral defects. METHODS: We retrospectively reviewed 26 patients with a primary pathological fracture of the distal femur caused by a giant cell tumor. All patients had unicondylar defects involving the articular surface. Twelve patients were treated with a 3D-printed custom-made prosthesis to repair the unicondylar defect (3D-printed group). The other 14 patients were treated with total knee replacement (TKR group). The operation time, blood loss, Musculoskeletal Tumor Society score, range of motion, local recurrence, and complications were statistically compared. RESULTS: The operation time was significantly shorter and the blood loss was significantly less in the 3D-printed group than in the TKR group. The Musculoskeletal Tumor Society scores were significantly higher in the 3D-printed group than in the TKR group from 3 to 24 months postoperatively. The range of motion was significantly better in the 3D-printed group than in the TKR group at 6 and 9 months postoperatively. CONCLUSIONS: 3D-printed custom-made prostheses provide better short-term functional results than does TKR.

Robotic single-site surgery versus laparoendoscopic single-site surgery in early-stage endometrial cancer: a case-control study.

INTRODUCTION: Laparoendoscopic single-site surgery (LESS) can reduce the limited invasiveness of conventional laparoscopy while providing superior cosmetic results. Robotic single-site surgery (RSSS) can overcome this shortcoming to a certain extent. AIM: To evaluate the advantages of RSSS in treating early-stage endometrial cancer by comparing RSSS with LESS. MATERIAL AND METHODS: From January 2018 to August 2018, patients diagnosed with endometrial cancer from endometrial curettage and imaging studies were selected for this prospective cohort study, with 22 undergoing RSSS and 18 undergoing LESS. All surgical procedures were performed using the conventional da Vinci Si surgical system with the Lagiport single port or a conventional laparoendoscopic instrument with the Lagiport single port. Operative time was recorded electronically. Intraoperative parameters and postoperative parameters were recorded and further analyzed. RESULTS: The operation was successfully completed, and a pure single-point approach was adopted. There were no laparotomy or intraoperative complications. Compared with the LESS group, the RSSS group had significantly longer pre-surgical time, significantly lower median operation time, significantly lower median blood loss, and significantly lower vaginal cuff closure time. The median length of hospital stay in the RSSS group was significantly lower than that in the LESS group. There was no significant difference in the incidence of early and late complications between the two groups. No recurrence events were observed in either the RSSS or the LESS group. CONCLUSIONS: RSSS is feasible and safe in patients with early-stage endometrial cancer. RSSS can reduce operating time, blood loss and length of hospital stay compared with LESS.

Clinical Guideline for Microwave Ablation of Bone Tumors in Extremities.

Microwave ablation has been used to treat bone tumors in extremities for more than 30 years. With improved recognition, updated microwave equipment, and expanded clinical application, microwave ablation has recently been widely used to treat bone tumors. To standardize the application of microwave ablation in the clinical treatment of bone tumors in the limbs, research results and clinical experience involving the use of microwave ablation to treat bone tumors in the limbs have been summarized, and a clinical guideline has been designed. This guideline is aimed at providing a reliable clinical basis for indications, preoperative evaluation and decision-making, perioperative treatment, complications, and other issues via evidence-based medicine. Two aspects are considered-percutaneous microwave ablation and intraoperative microwave ablation of bone tumors in extremities. Ultimately, the guideline is intended to standardize treatment and improve the clinical efficacy of microwave ablation of bone tumors in extremities.

Long non-coding RNA H19 mediates ovarian cancer cell cisplatin-resistance and migration during EMT.

OBJECTIVE: (1) to investigate the expression of long non-coding RNA (lncRNA) H19 in OVCAR3 and cisplatin-resistant OVCAR3/DDP cells; (2) to explore the effects of lncRNA H19 on cisplatin-resistance in ovarian cancer (OC) cells; (3) to determine the roles of lncRNA H19 on OC cell migration and epithelial to mesenchymal transition (EMT)-related factors. METHODS: The human ovarian cancer OVCAR3 cell line was obtained from ATCC; the cisplatin-resistant OVCAR3/DDP cell line was induced from OVCAR3 cells through a progressive cisplatin concentration; OVCAR3 cells that overexpress lncRNA H19 and OVCAR3/DDP cells that silence the lncRNA H19 expression were established by the transfection of a recombinant lentivirus. A cell counting kit-8 (CCK-8) assay was used to determine the cell viability of OVCAR3 and OVCAR3/DDP. A reverse transcription-quantitative polymerase chain reaction (RT-qPCR) demonstrated the expressions of lncRNA H19, E-cadherin, twist, slug, and snail mRNA in OVCAR3 and OVCAR3/DDP cells. A Transwell assay was used to investigate the migration of OVCAR3 and OVCAR3/DDP cells. The expressions of E-cadherin, twist, slug, and snail proteins were determined by Western blot. RESULTS: The cisplatin-resistant OVCAR3/DPP cells were successfully established. The level of lncRNA H19 in the OVCAR3/DDP cells was significantly elevated compared with the OVCAR3 cells (P < 0.05). The overexpression of lncRNA in the OVCAR3 cells improved the cisplatin-resistance, and the inhibition of lncRNA H19 expression in OVCAR3/DDP cells eliminated the cisplatin resistance. Furthermore, the migration ability and the expressions of the EMT positive regulator, twist, slug, snail mRNA, and protein in OVCAR3/DDP were dramatically up-regulated compared with the OVCAR3 group, and the expressions of the EMT negative regulator, E-cadherin mRNA, and protein were decreased compared with the OVCAR3 group, suggesting an increase of migration and EMT ability was observed in the OVCAR3/DDP cells. A gain of lncRNA expression in the OVCAR3 cells promoted migration and EMT-related activity; the loss of lncRNA H19 expression eliminated the enhanced ability of migration and EMT in the OVCAR3/DDP cells. CONCLUSIONS: LncRNA H19 is responsible for the cisplatin-resistance, migration, and MET regulation in OVCAR3 cells.

[Effects of predator stress on the expression of cAMP responsive element binding protein in hippocampus: experiment with rats].

OBJECTIVE: To explore the neurobiological basis involved in the pathogenesis of the lasting emotionality and cognitive impairment following severe psychological stress. METHODS: Ninety-six male Wistar rats were divided randomly into 2 equal groups: group of predator stress (Group PS) put into a cage in the experimental box singly to be exposed to a cat in the box but outside the cage for 23-57 min until tremor, polypnea, and nares flaring appeared for 6 min so as to establish predator stress models, and control group, put into the cage without non-injurious exposure of cat. 1, 12, and 24 hours later 8 rats from each group were killed with the hippocampus taken out. Western blotting was used to detect the protein expressions of cAMP response element-binding protein (CREB), phosphorylated CREB (pCREB) and CREB binding protein (CBP). Twelve hours after the experiment 24 rats from each group were killed with their brains taken out to obtain serial coronary sections. Immunohistochemistry was used to detect the positive immunoreactivities of CREB, pCREB, and CBP. RESULTS: Immunohistochemistry revealed that the absorbance (A) value of CREB-in the tissues of hippocampus and frontal cortex 12h after the cat exposure of Group PS were 0.55 +/- 0.13 and 0.88 +/- 0.20 respectively, both significantly lower than those of the control group (1.78 +/- 0.40 and 1.18 +/- 0.26 respectively, both P < 0.01), the A values of. pCREB in the hippocampus and frontal cortex of Group PS were 1.51 +/- 0.34 and 1.07 +/- 0.24 respectively, both significantly higher than those of the control group (0.47 +/- 0.11 and 0.48 +/- 0.11 respectively, both P < 0.01), and the A values of CBP in the hippocampus and frontal cortex of Group PS were 1.01 +/- 0.23 and 0.81 +/- 0.18 respectively, both significantly higher than those of the control group (0.52 +/- 0.12 and 0.29 +/- 0.07 respectively, both P < 0.01). Western blotting showed that the CREB protein expression levels 1 h and 24 h after the cat exposure of Group PS were 2.82 +/- 0.65 and 5.12 +/- 1.13 respectively, both significantly lower than those of the control group (11.86 +/- 2.47 and 10.56 +/- 2.38 respectively, both P < 0.01), the CBP protein expression levels 1 h and 24 h after the cat exposure of Group PS were 1.77 +/- 0.39 and 2.44 +/- 0.55 respectively, both significantly higher than those of the control group (1.06 +/- 0.24 and 0.86 +/- 0.20 respectively, both P < 0.01), and the pCREB protein expression levels 1 h and 12 h after the cat exposure of Group PS were 2.56 +/- 0.59 and 1.93 +/- 0.41 respectively, both significantly higher than those of the control group (1.04 +/- 0.22 and 0.96 +/- 0.21 respectively, both P < 0.01). CONCLUSION: The dysfunction of CREB signaling in the central nervous system, especially in the hippocampal formation after predation stress may play an important role in the long-term neuropsychological sequelae following severe stress.

1,25-dihydroxyvitamin D3 reduces mouse airway inflammation of neutrophilic asthma by transcriptional modulation of interleukin-17A.

Corticosteroid resistance and severe airflow obstruction have been proved to participate in the neutrophilic inflammation of airway in uncontrollable asthmatics. IL-17 is one of the pro-inflammatory cytokines produced by Th17 cells, and it plays an important role in the neutrophilic inflammation of airway in steroid-resistant asthmatics. Recent data have proved that 1,25(OH)2D3 represses IL-17A in inflammation and Th17-mediated autoimmunity through vitamin D receptors(VDR) at the level of transcription. Our study validated that 1,25-(OH)2D3 can modulate IL-17A on the transcriptional level by using Runx1, thus reducing inflammation in the airway of mice with neutrophilic asthma. 1,25(OH)2D3 may be promising for the therapeutic applications of neutrophilic asthma.