ZnO nanoparticles coated and stearic acid modified superhydrophobic chitosan film for self-cleaning and oil-water separation.

The aim of this study was to prepare superhydrophobic chitosan films using a ZnO nanoparticle coating and stearic acid hydrophobic modification. A 1 % concentration of ZnO nanoparticles and a 1 % concentration of stearic acid generated a superhydrophobic film with the largest contact angle (WCA) of 156°, which was attributed to the synergy of micro/nano-level hierarchical structure and low surface energy modification. The superhydrophobic film showed better stability to acid, alkali, heat, and UV irradiation than a neat chitosan film and a reduction in light transmittance of 14.4 % at 354 nm. The superhydrophobic chitosan film also showed excellent self-cleaning and oil-water separation performance. Our findings will expand the application of chitosan films in food packaging, outdoor self-cleaning materials and oil-water separations.

Jintiange combined with alfacalcidol improves muscle strength and balance in primary osteoporosis: A randomized, double-blind, double-dummy, positive-controlled, multicenter clinical trial.

Objective: To investigate the effectiveness of a Chinese patent medicine, Jintiange capsules with the main component of artificial tiger bone powder, combined with alfacalcidol on muscle strength and balance of the lower extremities in patients with primary osteoporosis. Design: A randomized, double-blind, double-dummy, positive-controlled, multicenter clinical trial. Subjects and methods: A total of 400 patients diagnosed with primary osteoporosis or osteopenia were recruited and randomized into the Jintiange or control groups. During the 52-week treatment, the participants in the Jintiange group were treated with Jintiange capsules (1.2 â€‹g each time, 3 times per day) and calcium carbonate simulant, while those in the control group were treated with calcium carbonate (element calcium 0.3 â€‹g, twice a day) and a Jintiange capsule simulant. Alfacalcidol (0.25 â€‹µg/d) was applied in both groups. The timed up and go test (TUG), chair rising test (CRT), and tandem gait test (TGT) were performed to evaluate balance, muscle strength and fall risk of the participants. Results: There were 154 participants in the Jintiange group, and 157 participants in the control group were included in the per-protocol set. Comparing the data at week 52 from those at baseline, the TUG time decreased from 9.60 â€‹± â€‹2.25 â€‹s to 8.53 â€‹± â€‹2.06 â€‹s (p â€‹< â€‹0.001) in the Jintiange group and decreased from 9.50 â€‹± â€‹1.91 â€‹s to 9.11 â€‹± â€‹1.95 â€‹s (p â€‹< â€‹0.001) in the control group; the CRT time decreased from 11.49 â€‹± â€‹4.05 â€‹s to 8.57 â€‹± â€‹2.13 â€‹s (p â€‹< â€‹0.001) and 11.17 â€‹± â€‹3.21 â€‹s to 9.74 â€‹± â€‹1.98 â€‹s (p â€‹< â€‹0.001) in the Jintiange and control groups, respectively; the number of correct steps in the TGT increased significantly in both the control (7.40 â€‹± â€‹1.27 vs. 7.69 â€‹± â€‹0.87, p â€‹< â€‹0.01) and Jintiange groups (7.21 â€‹± â€‹1.58 vs. 7.60 â€‹± â€‹1.12, p â€‹< â€‹0.001). At the end of the study, the TUG and CRT results in the Jintiange group were superior to those in the control group (all p value â€‹< â€‹0.05), while no obvious difference was found in the TGT between the two groups. At week 52, the high fall risk proportions in the Jintiange group were significantly lower than those in the control group according to TUG (3.25% vs. 9.55%, p â€‹= â€‹0.023) and CRT (20.78% vs. 33.76%, p â€‹= â€‹0.01). Conclusion: Jintiange capsules combined with alfacalcidol can effectively improve muscle strength and the balance of the lower extremities and reduce fall risk in patients with primary osteoporosis/osteopenia. The translational potential of this article: Artificial tiger bone powder, a traditional Chinese patent medicine, can improve muscle strength and balance and reduce fall risks effectively among patients with primary osteoporosis. It might be a therapeutic option for osteoporosis individuals combined with sarcopenia to improve their muscle function.

Prognostic value of Holliday junction-recognizing protein and its correlation with immune infiltrates in lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is a disease with high morbidity and mortality rates globally. Holliday junction-recognizing protein (HJURP) has recently been shown to be a potentially useful biomarker for diagnosing and determining the progression and prognosis of different cancer types. The present study assessed the prognostic value of HJURP expression in LUAD and investigated the biological pathways related to HJURP that are involved in LUAD pathogenesis. It was found that high HJURP expression was significantly associated with stage (P=0.001), T grade (P=0.012) and N grade (P=0.012). Overall survival analysis demonstrated that patients with LUAD and high HJURP expression had a worse prognosis compared with those patients with low HJURP expression (P<0.001). Multivariate analysis using the Cox proportional hazards model indicated that the expression of HJURP [hazard ratio (HR), 1.32; 95% confidence interval (CI), 1.09-1.60; P=0.004] and stage (HR, 1.90; 95% CI, 1.19-3.03; P=0.007) were independent prognostic factors for patients with LUAD. Gene set enrichment analysis results showed that genes involved with 'basal transcription factors', the 'cell cycle', 'homologous recombination', 'non-small cell lung cancer' (NSCLC), 'oocyte meiosis', 'p53 signaling pathway', 'pathways in cancer', 'RNA degradation' and 'spliceosome' were differentially enriched in the high HJURP expression phenotype. Significant correlations were also found between HJURP and several tumor-infiltrating immune cells, immunomodulators and immune subtypes. Furthermore, western blotting and qPCR analyses confirmed that HJURP was significantly increased in cell lines of NSCLC. In summary, HJURP may be a potentially useful prognostic molecular biomarker of a poor prognosis in LUAD cases. Further experiments are needed to demonstrate the biological effects of HJURP.

Nomograms for Predicting Overall Survival and Cancer-Specific Survival of Young Patients with Epithelial Ovarian Cancer: Analysis Based on SEER Program.

INTRODUCTION: Currently, there is no clinical prediction model for young patients (≤ 45 years old) with epithelial ovarian cancer (EOC) based on large samples of clinical data. The purpose of this study was to construct nomograms using data extracted from the Surveillance, Epidemiology, and End Results (SEER) Program to predict the overall survival (OS) and cancer-specific survival (CSS) of patients and to further guide the choice of clinical treatment options. METHODS: Data from a total of 6376 young patients with EOC collected from 1998 to 2016 were selected from the SEER database. These patients were randomly divided (7:3) into a training cohort (n = 4465) and a validation cohort (n = 1911). Cox and least absolute shrinkage and selection operator (LASSO) analyses were used to select the prognostic factors affecting OS and CSS, and the nomograms of OS and CSS were established. The performance of the nomogram models was assessed by C-index, area under the curve (AUC), calibration curves, and decision curve analysis (DCA). Sample were chosen from patients who underwent surgery in Shengjing Hospital to set external validation. Kaplan-Meier curves were plotted to compare survival outcomes between subgroups. RESULTS: Nomograms showed good predictive power and clinical practicality. The internal and external validation indicated better performance of the nomograms than the American Joint Committee on Cancer (AJCC) staging system and tumor grade system. Significant differences were observed in the survival curves of different risk subgroups. CONCLUSIONS: We constructed predictive nomograms to evaluate the OS and CSS of young patients with EOC. The nomograms will provide an individualized evaluation of OS and CSS for suitable treatment of young patients with EOC.

Multiomics analysis identifies key genes and pathways related to N6-methyladenosine RNA modification in ovarian cancer.

Aims: To explore the pathways and target genes related to N6-methyladenosine (m6A) methylation in ovarian cancer and their effect on patient prognosis. Methods & materials: The Cancer Genome Atlas was used to screen genes related to m6A regulators in terms of gene expression, mutation and copy number variation. These genes were subjected to pathway enrichment analysis. Prognosis-related genes were screened and involved in risk signature construction. Immunohistochemistry was used for verification. Results: We obtained 1408 genes dysregulated in parallel to m6A regulators, which were mainly involved in the platelet activation pathway. The m6A-related signature was constructed based on the expression of four prognosis-related genes (RPS6KA2, JUNB, HNF4A and P2RX1). Conclusion: This work provides new insights into the mechanism of m6A methylation in ovarian cancer.

Lay abstract N6-methyladenosine (m⁶A) methylation is the most common type of modification on mRNA. m⁶A methylation can affect the biological function of cells by affecting the protein expression level of mRNA. The process of m⁶A modification is controlled by many m⁶A regulators, which are dysregulated in ovarian cancer. Our research aims to screen the genes that are related to m⁶A regulation to analyze targets and mechanisms in ovarian cancer. We screened 1408 m⁶A-related genes, which are mainly involved in the platelet activation pathway. Among them, RPS6KA2 and JUNB were significantly related to poor prognosis of patients with ovarian cancer. RPS6KA2 was positively correlated with the m⁶A regulator METTL3 in ovarian cancer. Our study provides a basis for future mechanism studies.

Exponentially fitted multisymplectic scheme for conservative Maxwell equations with oscillary solutions.

Aiming at conservative Maxwell equations with periodic oscillatory solutions, we adopt exponentially fitted trapezoidal scheme to approximate the temporal and spatial derivatives. The scheme is a multisymplectic scheme. Under periodic boundary condition, the scheme satisfies two discrete energy conservation laws. The scheme also preserves two discrete divergences. To reduce computation cost, we split the original Maxwell equations into three local one-dimension (LOD) Maxwell equations. Then exponentially fitted trapezoidal scheme, applied to the resulted LOD equations, generates LOD multisymplectic scheme. We prove the unconditional stability and convergence of the LOD multisymplectic scheme. Convergence of numerical dispersion relation is also analyzed. At last, we present two numerical examples with periodic oscillatory solutions to confirm the theoretical analysis. Numerical results indicate that the LOD multisymplectic scheme is efficient, stable and conservative in solving conservative Maxwell equations with oscillatory solutions. In addition, to one-dimension Maxwell equations, we apply least square method and LOD multisymplectic scheme to fit the electric permittivity by using exact solution disturbed with small random errors as measured data. Numerical results of parameter inversion fit well with measured data, which shows that least square method combined with LOD multisymplectic scheme is efficient to estimate the model parameter under small random disturbance.

P76RBE silencing inhibits ovarian cancer cell proliferation, migration, and invasion via suppressing the integrin ß1/NF-κB pathway.

Rhophilin Rho GTPase binding protein 2 (P76RBE) belongs to rhophilin family of Rho-GTPase-binding proteins and is found to contribute to the development of diverse cancers. Data in Oncomine and Kaplan-Meier Plotter databases showed that P76RBE was upregulated in ovarian cancer tissues compared with normal tissues, and patients with high P76RBE expression had worse overall survival, which indicated P76RBE may be associated with the pathogenesis of ovarian cancer. This study aimed to investigate the role of P76RBE in ovarian cancer and to reveal the possible underlying mechanisms. The results demonstrated that P76RBE was highly expressed in ovarian cancer tissues and ovarian cancer cell lines. Functionally, silencing of P76RBE suppressed the proliferation, induced cell cycle arrest, and inhibited migration and invasion in OVCAR-3 and OV-90 cells, while overexpression of P76RBE showed opposite effects on A2780 cells. Mechanically, P76RBE silencing resulted in downregulation of integrin ß1, accompanying the reduced NF-κB p65 phosphorylation and nuclear translocation. Importantly, integrin ß1 knockdown effectively rescued the effects of P76RBE overexpression on ovarian cancer cells with suppressed proliferation, migration, and invasion. Additionally, in the xenograft tumors derived from OVCAR-3 and OV-90 cell lines, P76RBE knockdown inhibited tumor growth. Meanwhile, the expression of integrin ß1 and NF-κB p65 phosphorylation was decreased. In summary, our findings indicate that P76RBE contributes to the progression of ovarian cancer through regulating the integrin ß1/NF-κB signaling, and it may be a promising target for ovarian cancer therapy.

PSMC2/CCND1 axis promotes development of ovarian cancer through regulating cell growth, apoptosis and migration.

Ovarian cancer is known as one of the most common malignancies of the gynecological system, whose treatment is still not satisfactory because of the unclear understanding of molecular mechanism. PSMC2 is an essential component of 19 S regulatory granules in 26 S proteasome and its relationship with ovarian cancer is still not clear. In this study, we found that PSMC2 was upregulated in ovarian cancer tissues, associated with tumor grade and could probably predict poor prognosis. Knocking down the endogenous PSMC2 expression in ovarian cancer cells could decrease colony formation ability, cell motility and cell proliferation rate, along with increasing cell apoptosis rate. Cells models or xenografts formed by cells with relatively lower expression of PSMC2 exhibited weaker oncogenicity and slower growth rate in vivo. Moreover, gene microarray was used to analyze the alteration of gene expression profiling of ovarian cancer induced by PSMC2 knockdown and identify CCND1 as a potential downstream of PSMC2. Further study revealed the mutual regulation between PSMC2 and CCND1, and demonstrated that knockdown of CCND1 could enhance the regulatory effects induced by PSMC2 knockdown and overexpression of CCND1 reverses it. In summary, PSMC2 may promote the development of ovarian cancer through CCND1, which may predict poor prognosis of ovarian cancer patients.

A Novel Clinical Nomogram for Predicting Cancer-Specific Survival in Adult Patients After Primary Surgery for Epithelial Ovarian Cancer: A Real-World Analysis Based on the Surveillance, Epidemiology, and End Results Database and External Validation in a Tertiary Center.

BACKGROUND: The present study aimed to construct and validate a nomogram that can be used to predict cancer-specific survival (CSS) in patients with epithelial ovarian cancer (EOC). METHODS: A total of 7,129 adult patients with EOC were extracted from the Surveillance, Epidemiology, and End Results database between 2010 and 2015. Patients were randomly divided into the training and validation cohorts (7:3). Cox regression was conducted to evaluate prognostic factors of CSS. The internal validation of the nomogram was performed using concordance index (C-index), AUC, calibration curves, and decision curve analyses (DCAs). Data from 53 adult EOC patients at Shengjing Hospital of China Medical University from 2008 to 2012 were collected for external verification. Kaplan-Meier curves were plotted to compare survival outcomes among risk subgroups. RESULTS: Age, grade, histological types, stage, residual lesion size, number of regional lymph nodes resected, number of positive lymph nodes, and chemotherapy were independent risk factors for CSS. Based on the above factors, we constructed a nomogram. The C-indices of the training cohort, internal validation cohort, and external verification group were 0.763, 0.750, and 0.920, respectively. The calibration curve indicated good agreement between the nomogram prediction and actual survival. AUC and DCA results indicated great clinical usefulness of the nomogram. The differences in the Kaplan-Meier curves among different risk subgroups were statistically significant. CONCLUSIONS: We constructed a nomogram to predict CSS in adult patients with EOC after primary surgery, which can assist in counseling and guiding treatment decision making.

The Overexpression of Acyl-CoA Medium-Chain Synthetase-3 (ACSM3) Suppresses the Ovarian Cancer Progression via the Inhibition of Integrin ß1/AKT Signaling Pathway.

Ovarian cancer is considered as one of the most fatal gynecologic malignancies. This work aimed to explore the effects and regulatory mechanism of Acyl-CoA medium-chain synthetase-3 (ACSM3, a subunit of CoA ligases) in ovarian cancer progression. As well as employing CCK-8 assay, clone formation assay, and cell cycle analysis were carried out to investigate cell proliferation ability. Wound healing assay and transwell assay were subsequently used to assess cell migration and invasion. Mice xenografts were then conducted to measure the effects of ACSM3 on tumor development in vivo. Our bioinformatics analysis suggested that the expression of ACSM3 was down-regulated in ovarian cancer tissues, and the low expression level of ACSM3 might related with poorer overall survival than high mRNA expression of ACSM3 in ovarian cancer patients. We artificially regulated the expression of ACSM3 to evaluate its effects on ovarian cancer malignant phenotypes. Our data revealed that the overexpression of ACSM3 inhibited cell proliferation, migration, and invasion of ovarian cancer cells. In contrast, the knock-down of ACSM3 received the opposite results. Our western blot results showed that the Integrin ß1/AKT signaling pathway was negatively regulated by ACSM3 expression. Moreover, ACSM3 overexpression-induced suppression of cell migration and invasion activities were abolished by the overexpression of ITG ß1 (Integrin ß1). Additionally, the growth of ovarian cancer xenograft tumors was also repressed by the overexpression of ACSM3. And ACSM3 interference obtained the contrary effects in vivo. In summary, ACSM3 acts as a tumor suppressor gene and may be a potential therapeutic target of ovarian cancer.

Low-dose naltrexone plays antineoplastic role in cervical cancer progression through suppressing PI3K/AKT/mTOR pathway.

The incidence of cervical cancer is increasing annually worldwide. Low-dose naltrexone (LDN) has been reported to delay tumor progression, but the mechanism remains unclear. Here, we found that low-dose naltrexone could upregulate the expression of OGFr. Additionally, LDN could suppress the abilities of colony formation, migration and invasion in cervical cancer cells. LDN could also inhibit cervical cancer progression in mice model. Moreover, LDN indirectly reduced the expressions of PI3K, pAKT and mTOR in vitro and in vivo. Therefore, LDN may be considered a potential treatment option for cervical cancer.

Identification of PKP 2/3 as potential biomarkers of ovarian cancer based on bioinformatics and experiments.

BACKGROUND: Plakophilins (PKPs) are widely involved in gene transcription, translation, and signal transduction, playing a crucial role in tumorigenesis and progression. However, the function and potential mechanism of PKP1/2/3 in ovarian cancer (OC) remains unclear. It's of great value to explore the expression and prognostic values of PKP1/2/3 and their potential mechanisms, immune infiltration in OC. METHODS: The expression levels, prognostic values and genetic variations of PKP1/2/3 in OC were explored by various bioinformatics tools and databases, and PKP2/3 were selected for further analyzing their regulation network and immune infiltration. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes pathways (KEGG) enrichment were also conducted. Finally, the expression and prognosis of PKP2 were validated by immunohistochemistry. RESULTS: The expression level and prognosis of PKP1 showed little significance in ovarian cancer, and the expression of PKP2/3 mRNA and protein were upregulated in OC, showing significant correlations with poor prognosis of OC. Functional enrichment analysis showed that PKP2/3 and their correlated genes were significantly enriched in adaptive immune response, cytokine receptor activity, organization of cell-cell junction and extracellular matrix; KEGG analysis showed that PKP2/3 and their significantly correlated genes were involved in signaling pathways including cytokine-mediated signaling pathway, receptor signaling pathway and pathways in cancer. Moreover, PKP2/3 were correlated with lymphocytes and immunomodulators. We confirmed that high expression of PKP2 was significantly associated with advanced stage, poor differentiation and poor prognosis of OC patients. CONCLUSION: Members of plakophilins family showed various degrees of abnormal expressions and prognostic values in ovarian cancer. PKP2/3 played crucial roles in tumorigenesis, aggressiveness, malignant biological behavior and immune infiltration of OC, and can be regarded as potential biomarker for early diagnosis and prognosis evaluation in OC.