Morphological Reconstruction for Variable Wing Leading Edge Based on the Node Curvature Vectors.

Precise morphology acquisition for the variable wing leading edge is essential for its bio-inspired adaptive control. Therefore, this study proposes a morphological reconstruction method for the variable wing leading edge, utilizing the node curvature vectors-based curvature propagation method (NCV-CPM). By establishing a strain-arc curvature function, the method fundamentally mitigates the impact of surface curvature angle on curvature computation accuracy at sensing points. We introduce a technique that uses high-order curvature fitting functions to determine the curvature vectors of arc segment nodes. This method reduces cumulative errors in curvature computation linked to the linear interpolation-based curvature propagation method (LI-CPM) at unattached sensor positions. Integrating curvature-strain functions aids in wing leading-edge strain field reconstruction, supporting structural health monitoring. Additionally, a particle swarm algorithm optimizes the sensing point distribution, reducing network complexity. This study demonstrates significantly enhanced morphological reconstruction accuracy compared to those obtained with conventional LI-CPM.

Effect of 580 °C (20 h) Heat Treatment on Mechanical Properties of 25Cr2NiMo1V Rotor-Welded Joints of Oscillating Arc (MAG) Narrow Gap Thick Steel.

The thick plate narrow gap welding of 25Cr2NiMo1V rotor steel is achieved by metal active gas arc welding, in which the weld gap was 18.04-19.9 mm. After welding, the weldment was heat treated at 580 °C (20 h). The impact and tensile properties in the as-welded and heat-treated were studied. The results show that after heat treatment, the coarse carbides in the center of the weld were transformed into fine granular carbides distributed along the grain boundaries, and the quantity of carbide precipitates in the weld near the fusion line was reduced. The tensile fracture mode changed from a ductile fracture to a combination of brittle and ductile fractures, and the tensile strength of the weld metal changed from 605 MPa to 543 MPa. After heat-treated, the radiation zone of the weld center changed from a brittle fracture to a combination of brittle and ductile fractures, and the impact energy changed from 141 J to 183 J; the characteristics of the brittle fracture in the radial zone of the fusion line were more obvious, and the impact energy changed from 113 J to 95 J. Therefore, after heat treatment, the toughness of the welded metal was improved, without reducing the strength and hardness of the welded metal to a large extent.

Relationship between Scheuermann disease and symptomatic thoracic spinal stenosis: A retrospective study.

OBJECTIVE: This study aimed to investigate the possible relationship between Scheuermann disease (SD) and the pathophysiological factors of thoracic spinal stenosis (TSS), including ossification of the ligamentum flavum (OLF), ossification of the posterior longitudinal ligament (OPLL), and thoracic disc herniation (TDH) in patients with symptomatic TSS. METHODS: Demographic and radiological data from 66 consecutive patients diagnosed with symptomatic TSS from 2013 to 2018 were retrospectively collected and divided into 3 groups depending on the underlying pathomechanism of TSS: TDH group (18 patients; 6 women; mean age ± standard deviation [Sd] = 59.89 ± 11.34), OPLL group (12 patients; 8 women; mean age ± Sd = 56.08 ± 14.74), and OLF group (36 patients; 20 women; mean age ± Sd = 58.69 ± 9.77). A total of 41 age-matched healthy individuals (19 women; mean age ± Sd = 54.88 ± 13.63) were designated as the control group. In each group, both typical and atypical SD criteria were radiologically examined. The demographic data and presence of SD between the control group and 3 subgroups of TSS pathomechanisms were evaluated. RESULTS: SD characteristics were identified in 83.33% (15/18) of patients in the TDH group, 44.44% (16/36) in the OLF group, 25% (3/12) in the OPLL group, and 17.07% (7/41) of the control individuals. When analyzed by the chi-squared test and logistic regression analysis, the presence of SD was significantly associated with TDH (P < 0.01) and OLF (P < 0.05) but not OPLL (P > 0.05). Patients with TDH and OLF showed peak involvement of T10/11, and patients with OPLL did not. Furthermore, we determined that age, sex, body-mass index, and smoking status were not the risk factors for TDH, OPLL, and OLF (P > 0.05). SD was found to be a risk factor for TDH (P < 0.01) and OLF (P < 0.05) but not for OPLL (P > 0.05). CONCLUSION: Evidence from this study indicated that SD might be a risk factor for OLF and TDH but not for OPLL.

Finding Colon Cancer- and Colorectal Cancer-Related Microbes Based on Microbe-Disease Association Prediction.

Microbes are closely associated with the formation and development of diseases. The identification of the potential associations between microbes and diseases can boost the understanding of various complex diseases. Wet experiments applied to microbe-disease association (MDA) identification are costly and time-consuming. In this manuscript, we developed a novel computational model, NLLMDA, to find unobserved MDAs, especially for colon cancer and colorectal carcinoma. NLLMDA integrated negative MDA selection, linear neighborhood similarity, label propagation, information integration, and known biological data. The Gaussian association profile (GAP) similarity of microbes and GAPs similarity and symptom similarity of diseases were firstly computed. Secondly, linear neighborhood method was then applied to the above computed similarity matrices to obtain more stable performance. Thirdly, negative MDA samples were selected, and the label propagation algorithm was used to score for microbe-disease pairs. The final association probabilities can be computed based on the information integration method. NLLMDA was compared with the other five classical MDA methods and obtained the highest area under the curve (AUC) value of 0.9031 and 0.9335 on cross-validations of diseases and microbe-disease pairs. The results suggest that NLLMDA was an effective prediction method. More importantly, we found that Acidobacteriaceae may have a close link with colon cancer and Tannerella may densely associate with colorectal carcinoma.

LncRNA MALAT1 mediates doxorubicin resistance of hepatocellular carcinoma by regulating miR-3129-5p/Nova1 axis.

Drug resistance is one of the major challenges for cancer therapies. In recent years, research on disease-related molecular signaling pathways has become the key ways to understand and overcome obstacles. Dysregulation of MALAT1 could regulate doxorubicin resistance of hepatocellular carcinoma (HCC), but how MALAT1 involving in managing doxorubicin resistance remains unclear yet. We aimed to elucidate the specific molecular mechanism of MALAT1 with doxorubicin resistance in HCC cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was engaged to detect the expression levels of MALAT1, miR-3129-5p and Nova1 mRNA; MTT, western blot, flow cytometry and luciferase reporter assays were executed to identify the influence of MALAT1 on doxorubicin resistance of HCC cells. Xenograft tumor model was created to confirm the biological function of MALAT1 in doxorubicin resistance of HCC cells in vivo. MALAT1 and Nova1 were upregulated, while miR-3129-5p expression was decreased in doxorubicin-resistant HCC tissues and cells. Knockdown of MALAT1 regulated doxorubicin resistance of HCC cells through inhibiting cell proliferation, migration, invasion and promoting apoptosis, but antisense miR-3129-5p released the functional effect of MALAT1 knockdown. Nova1, as a target gene of miR-3129-5p, reversed the results of miR-3129-5p expression and enhanced doxorubicin resistance of HCC cells. Xenograft tumor model suggested that dysregulation of MALAT1 regulated tumor growth and Nova1 to mediate doxorubicin resistance of HCC cells by as a sponge for miR-3129-5p in vivo. Elevation of LncRNA MALAT1 mediated doxorubicin resistance and the progression of HCC via a MALAT1/miR-3129-5p/Nova1 axis. This study would be expected to enrich the understanding of doxorubicin resistance of HCC and provide new ideas for HCC treatment strategies.

A Comparison of Hyperextension versus Neutral Positions for Vertebroplasty to Treat Neurologically Intact Kümmell Disease.

OBJECTIVE: To compare the efficacy between hyperextension position (HPVP) and neutral position for vertebroplasty (NPVP) in treating Kümmell disease. STUDY DESIGN: A Comparative descriptive study. PLACE AND DURATION OF STUDY: Department of Orthopaedics, Yantaishan Hospital, China, from December 2017 to July 2018. METHODOLOGY: This study retrospectively analysed demographic features, operative information, radiologic data, and complications of 58 consecutive patients with single-level Kummel disease (KD) who underwent NPVP (n=27) or HPVP (n=31). All patients were observed preoperatively and at 2 days (POD 2) and one year postoperatively for cement leakage, Cobb's angle, antenior body height ratio, pain and disability. RESULTS: The cement leakage rate was significantly lower in the HPVP group (p<0.01). The visual analogue scale (VAS) scores for pain, and Oswestry disability indices (ODIs) were lower in the HPVP group at one year postoperatively (both p<0.05). For the HPVP group, Cobb's angle was significantly smaller, and the anterior body height ratio (AR) was larger at POD 2 (p<0.05) and one year (p<0.05), postoperatively. CONCLUSION: This study demonstrated that HPVP could achieve a lower cement leakage rate with similar operative time, lower VAS and ODI scores, as well as better kyphosis restoration and AR recovery at the 1-year follow-up than NPVP. HPVP is thus superior to NPVP in treating KD. Key Words: Kyphosis, Cobb's angle, Cement leakage, Intervertebral stability, Surgical outcome, Kümmell disease, Vertebroplasty, Hyperextension position.

Comparison Between Hyperextension and Neutral Positions for Vertebroplasty and Kyphoplasty: Which is Best for Osteoporotic Vertebral Compression Fractures?

PURPOSE: This study aimed to compare the demographic features (including total cost), surgical effects, radiographic parameters, and complications of kyphoplasty (KP) and vertebroplasty (VP) in the hyperextension (HP) and neutral positions (NP) and to assess their efficacy and cost-effectiveness for treating single-level osteoporotic vertebral compression fractures (OVCF). PATIENTS AND METHODS: This was a retrospective analysis of 245 consecutive patients who underwent KP or VP from February 2018 to February 2019 with observation on postoperative day 2 and at the one-year follow-up. The first 122 patients (86 KP and 36 VP cases) were treated in the neutral position, and the remaining 123 in the hyperextension position (90 VP and 33 KP cases). Back pain and impact on daily life were evaluated. Cobb's angle and the ratio of the anterior (AR) and middle vertebral (MR) bodies were the main radiographic parameters. The chi-square test, one-way analysis of variance (ANOVA), repeated measurement ANOVA, and post hoc tests (Bonferroni adjustments) were used for statistical analysis. RESULTS: There were no significant differences in the demographic features, operation time, or rate of re-fracture at the one-year follow-up among the groups. The rate of cement leakage was significantly lower in the HPVP group than in the NPKP group. The total cost was significantly lower in the VP groups than in the KP groups. At the one-year follow-up, back pain was significantly lower in the HPVP group than in the NPKP group. The Oswestry Disability Index, Cobb's angle, AR, and MR in the HPVP group were similar to those in the NPKP and HPKP groups, but better than those in the NPVP group. CONCLUSION: HPVP can achieve better pain relief, and similar disability scores, Cobb's angle, AR and MR recovery, with a lower total cost, compared with NPKP. HPVP is the most economically efficacious treatment for OVCF.

Buformin suppresses osteosarcoma via targeting AMPK signaling pathway.

BACKGROUND: Buformin has been reported to be a powerful anticancer drug by activating the AMPK signal. Herein, we aimed to investigate the effects of buformin on osteosarcoma. MATERIAL AND METHODS: Cellular proliferative abilities were determined by cell counting kit-8 and colony formation assays. Cellular invasion was investigated using a transwell system. Cell cycle was examined by flow cytometry. Western blot was performed to measure the expression of key proteins. Synergistic effects of buformin and cisplatin were validated in seven fresh osteosarcoma tissues. RESULTS: Buformin suppressed the growth of U-2 OS cells in a dose-dependent manner (IC50 = 69.1 µM). Moreover, buformin induced cell cycle arrest (P < 0.001) and impaired cellular invasion (P = 0.038). Phosphorylation of AMPK was upregulated by buformin, while phosphorylation of S6, cyclin D1, and MMP9 were significantly downregulated. In addition, buformin notably induced accumulation of reactive oxygen species and lactate and eventually decreased ATP production. In both U-2 OS cells and the primary cultured osteosarcoma tissues, buformin increased tumor sensitivity to cisplatin. CONCLUSIONS: Buformin could suppress tumor growth and invasion of osteosarcoma through directly targeting the AMPK signaling pathway. Moreover, buformin inhibited the abnormal metabolism and notably increased the cytotoxicity of cisplatin, and therefore represents a new potential treatment option for osteosarcoma.

FAM83H-AS1 is upregulated and predicts poor prognosis in colon cancer.

Long noncoding RNAs (LncRNAs) have been proven to participate in many principal pathways during colonic mucosa tumourigenesis. FAM83H-AS1 has been identified as one of the LncRNAs that is dysregulated in multi-type cancers. Here, our purpose was to determine the expression pattern and clinical significance of FAM83H-AS1 and further analyse its prognostic value in colon cancer. FAM83H-AS1 expression was examined in 90 patients with colon cancer by RNAscope in situhybridization, and the expression levels were analysed with the overall survival (OS) rates for patients with colon cancer. TCGA datasets derived from colon cancer (COAD) were used to further validate the main findings. We demonstrated that the expression of FAM83H-AS1 was significantly higher in cancer tissues than in paired normal mucosa from colon cancer patients (P < 0.001). The prognostic analysis indicated that the OS rates for colon cancer patients with high levels of FAM83H-AS1 were significantly lower than those for patients with low levels of FAM83H-AS1 (P = 0.013). The higher levels of FAM83H-AS1 were found to be associated with a lower expression of SMAD1/5/9, which is involved in TGF-ß signalling in colon cancer tissues (P = 0.0174). In HCT116 and SW480 cell lines, the down regulation of FAM83H-AS1 promoted the expression of SMAD1. Our investigations suggest that the upregulation of FAM83H-AS1 serves as a promising predictor and might be conducive for clinicians to estimate OS time. FAM83H-AS1 might serve as an inhibitor of TGF-ß signalling.

MicroRNA-206 suppresses proliferation and predicts poor prognosis of HR-HPV-positive cervical cancer cells by targeting G6PD.

Cervical cancer (CC) is one of the most frequent gynecological malignancies in females worldwide. Aberrant expression of microRNA (miR)-206 was reported to play an important role in tumor progression. The aim of the present study was to evaluate the potential role of miR-206 and verify its influence on the function of glucose-6-phosphate dehydrogenase (G6PD) in CC. Western blot analysis and RT-PCR were employed to measure miR-206 and G6PD expression. Luciferase assays were performed to validate G6PD as miR-206 targets. CCK-8 assay was performed to examine the regulation of miR-206 and G6PD on CC proliferation. The result showed that miR-206 was downregulated, while G6PD was upregulated in high risk human papillomavirus (HR-HPV)(+) CC. miR-206 directly targeted the 3'-UTR of G6PD. miR-206 overexpressed or G6PD low-expressed suppressed cell proliferation. miR-206 low expressed or G6PD overexpressed predicted poor prognosis. In conclusion, miR-206 reduced cancer growth and suppresses the G6PD expression in CC. This newly identified miR-206 may provide further insight into tumor progression and offers a promising target for the CC therapy.

High Mobility Group Box Protein 1 Serves as a Potential Prognostic Marker of Lung Cancer and Promotes Its Invasion and Metastasis by Matrix Metalloproteinase-2 in a Nuclear Factor-κB-Dependent Manner.

Several studies have reported a significant role of high mobility group box protein 1 (HMGB1) in lung cancer. Nevertheless, there is a lack of knowledge regarding the expression of HMGB1 and its correlation with the clinicopathological features of lung cancer. In addition, the potential molecular mechanisms underlying the role of HMGB1 in lung cancer are still unknown. We therefore investigated the clinicopathological and prognostic significance as well as the potential role of HMGB1 in the development and progression of lung cancer. HMGB1 expression in the tumor tissues of the cohort correlated with clinicopathological features. Moreover, lung cell migration and invasion were significantly increased after treatment with HMGB1. The matrix metalloproteinase-2 (MMP-2) expression and activity were upregulated after treatment with HMGB1, while the upregulated expression of MMP-2 stimulated by HMGB1 in lung cancer cells was significantly reduced with the blockage of si-p65. These results indicated that HMGB1 expression was significantly associated with lung cancer progression. We also showed that HMGB1 promoted lung cancer invasion and metastasis by upregulating the expression and activity of MMP-2 in an NF-κB-dependent manner. Taken together, these data suggested that HMGB1 may be a potential prognosis and therapeutic marker for lung cancer.

Glycyrrhizin Suppresses the Growth of Human NSCLC Cell Line HCC827 by Downregulating HMGB1 Level.

Lung cancer has very high mortality and glycyrrhizin was found to significantly inhibit the growth of lung cancer cells in vitro and tissues in mice. However, the detailed inhibitory role of glycyrrhizin in the growth of lung cancer is still unclear. In this study, we first found that glycyrrhizin inhibited the growth of lung tumor in PDX mice. And high level of HMGB1 promoted the migration and invasion of lung cancer cells, which was suppressed by glycyrrhizin. Moreover, glycyrrhizin reduced the activity of JAK/STAT signaling pathway, which is the upstream regulator of HMGB1. Therefore, this study revealed a potential mechanism by which glycyrrhizin can inhibit the progression of lung cancer.

Expression and Clinical Significance of miR-26a and Pleomorphic Adenoma Gene 1 (PLAG1) in Invasive Pituitary Adenoma.

BACKGROUND Although pituitary adenoma is a malignant tumor, it can present as invasive growth in some cases. MicroRNA (miR)-26a has been found to be abnormally highly expressed in pituitary adenoma, indicating possible involvement in pathogenesis. As a known target gene of miR-26a, PLAG1 has abnormally low expression in pituitary adenoma. The correlation between miR-26a or PLAG1 expressional abnormality and occurrence of pituitary adenoma is still unknown, as is its association with invasiveness of pituitary adenoma. MATERIAL AND METHODS Pituitary adenoma tissues, including both invasive and non-invasive subtypes, were collected from our Neurosurgery Department, in parallel with normal pituitary tissues from postmortem autopsy. qRT-PCR was used to detect mRNA expression of miR-26a and PLAG1, while Western blotting was used to test PLAG1 protein expression. The correlation between miR-26a and PLAG1, and with pathological features, were analyzed. ROC analysis revealed the utility of miR-26a and PLAG1 in differential diagnosis of invasive/non-invasive pituitary tumors and in analyzing their effects on patient prognosis. RESULTS MiR-26a was remarkably upregulated in pituitary tumors, while PLAG1 was downregulated, especially in invasive pituitary tumors. miR-26a and PLAG1 had higher diagnostic values for differentiating between invasive and non-invasive pituitary tumors (AUC=0.889 and 0.818, respectively). Those patients with miR-26 overexpression and PLAG1 downregulation had unfavorable prognosis. miR-26 and PLAG1 are independent factors affecting patient diagnosis. CONCLUSIONS MiR-26a can facilitate occurrence of pituitary tumor and invasiveness, probably via inhibiting PLAG1 expression.

Characterization of nuclear localization signal in the N terminus of CUL4B and its essential role in cyclin E degradation and cell cycle progression.

CUL4A and CUL4B, which are derived from the same ancestor, CUL4, encode scaffold proteins that organize cullin-RING ubiquitin ligase (E3) complexes. Recent genetic studies have shown that germ line mutation in CUL4B can cause mental retardation, short stature, and other abnormalities in humans. CUL4A was observed to be overexpressed in breast and hepatocellular cancers, although no germ line mutation in human CUL4A has been reported. Although CUL4A has been known to be involved in a number of cellular processes, including DNA repair and cell cycle regulation, little is known about whether CUL4B has similar functions. In this report, we tested the functional importance of CUL4B in cell proliferation and characterized the nuclear localization signal (NLS) that is essential for its function. We found that RNA interference silencing of CUL4B led to an inhibition of cell proliferation and a prolonged S phase, due to the overaccumulation of cyclin E, a substrate targeted by CUL4B for ubiquitination. We showed that, unlike CUL4A and other cullins that carry their NLS in their C termini, NLS in CUL4B is located in its N terminus, between amino acid 37 and 40, KKRK. This NLS could bind to importin alpha1, alpha3, and alpha5. NLS-deleted CUL4B was distributed in cytoplasm and failed to promote cell proliferation. Therefore, the nuclear localization of CUL4B mediated by NLS is critical for its normal function in cell proliferation.

RpoS as an intermediate in RsmA-dependent regulation of secondary antifungal metabolites biosynthesis in Pseudomonas sp. M18.

To investigate the regulatory mechanism governing antifungal metabolite biosynthesis, two kinds of global regulator genes in Pseudomonas sp. M18, an rpoS and an rsmA gene, were cloned and mutated by inserting with an aacC1 cassette, respectively. Two mutants showed the same regulatory mode with repression of phenazine-1-carboxylic acid and remarkable enhancement of pyoluteorin. In the rpoS-mutant, a translational rsmA'-'lacZ fusion was expressed at the same level corresponding to that in the wild-type strain. In the rsmA-mutant, however, expression of the translational rpoS'-'lacZ fusion was only about 30% of that in the wild-type strain. The results indicated that the absence of RsmA leads to repression of the rpoS gene expression, which has further been confirmed with construction of chromosomal rpoS-lacZ fusion in the rsmA-mutant and the wild-type strain, respectively. The findings showed a new regulatory cascade controlling antifungal metabolite production in Pseudomonas sp. M18, suggesting that RpoS may serve as a mediator in RsmA-dependent regulation of secondary metabolite biosynthesis.