Improvement of the Abrasion and Corrosion Resistance of a Waterborne Epoxy Coating by α-ZrP@PTA-Ce(III) with Dual Corrosion Inhibition Effects.

The introduction of poly(tannic acid) (PTA) and cerium ion [Ce(III)] on the surface of α-zirconium phosphate (α-ZrP) endowed the α-ZrP@PTA-Ce(III)/waterborne epoxy composite coating with enhanced corrosion protection and wear resistance performances. The successful preparation of α-ZrP@PTA-Ce(III) was confirmed through X-ray diffraction, X-ray photoelectron spectroscopy, and Fourier transform infrared spectra. PTA improved the compatibility between α-ZrP@PTA-Ce(III) and the waterborne epoxy resin due to the presence of organic groups from tannic acid. The wear resistance test indicated that the incorporation of α-ZrP@PTA-Ce(III) effectively reduced the coefficient of friction and the wear rate. Electrochemical impedance spectroscopy was used to analyze the corrosion protection performance of unbroken coatings and the self-healing ability of scratched coatings. The incorporation of α-ZrP@PTA-Ce(III) improved the protection performace distinctly. In addition, α-ZrP@PTA-Ce(III) endowed the composite coating with dual corrosion inhibition effects, originating from the PTA film, to prevent the penetration of corrosive media and a dense film that came from the Ce(III) cation. The waterborne epoxy system with enhanced corrosion and wear resistance in this paper broadens the application of α-ZrP.

[Efficacy of Decitabine Combined with Preexcitation Regimen in Treatment of Newly Diagnosed AML Patients Who Did not Respond to Initial Standard Induction Chemotherapy].

OBJECTIVE: To investigate the efficacy of decitabine combined with preexcitation regimen in the treatment of newly diagnosed acute myeloid leukemia (AML) patients who have not been relieved by the first standard induction chemotherapy and its influence on the relative content of regulatory T lymphocytes (Tregs). METHODS: The clinical data of 102 newly diagnosed AML patients (except acute promyelocytic leukemia) who did not relieve after initial standard induction chemotherapy in Shaanxi Provincial People's Hospital from March 2013 to March 2019 were retrospectively analyzed. Fifty-one patients who accepted pre-excitation regimen were divided into regular group, while another 51 patients treated with decitabine combined with pre-excitation regimen were divided into combination group. The efficacy, incidence of toxic and side effects, Core Scale of Quality of Life (QLQ-C30) score before and after treatment, T lymphocyte subsets (CD3+, CD4+, CD4+/CD8+, Tregs) and 3-year overall survival (OS) rate were compared between the two groups. RESULTS: The total effective rate of combination group was 80.39%, which was significantly higher than 62.75% of regular group (P < 0.05). After treatment, the QLQ-C30 score of combination group was 60.27±6.96, which was significantly lower than 65.73±7.96 of regular group (P < 0.001). There was no statistical difference in the incidence of toxic and side effects between the two groups (P >0.05). After treatment, the levels of CD3+, CD4+, CD4+/CD8+ in the combination group were higher than those in the regular group (all P < 0.001), while Treg was lower (P < 0.001). The 3-year OS rate in the combination group was 72.55%, which was significantly higher than 52.94% in the regular group (P < 0.001). CONCLUSION: Decitabine combined with preexcitation regimen has a significant effect on AML patients who have not been alleviated by standard induction chemotherapy in the first course of treatment. It can reduce anti-tumor immune suppression and improve immune function by regulating the relative content of Tregs, thus prolongs survival time and improves life quality of patients without increasing adverse reactions.

Association between serum albumin levels and survival in elderly patients with diffuse large B-cell lymphoma: a single-center retrospective study.

Background: In clinical hematology, diffuse large B-cell lymphoma (DLBCL) is notably heterogeneous and varies in prognosis. Serum albumin (SA) is considered a biomarker of prognostic value in a number of hematologic malignancies. However, current knowledge of the association between SA levels and survival is limited, especially in DLBCL patients aged ≥70 years. Thus, this study sought to assess the prognostic value of SA levels among this age group of patients. Methods: The data of DLBCL patients aged ≥70 years at the Shaanxi Provincial People's Hospital in China from 2010 to 2021 were retrospectively reviewed. The SA levels were measured using standard procedures. The Kaplan-Meier method was used to estimate survival time, and the Cox proportional hazards model for time-to-event data was used to identify potential risk factors. Results: The data of 96 participants were included in the study. The univariate analysis showed that B symptoms, Ann Arbor stage III or IV of the disease, high International Prognostic Index (IPI) scores, high NCCN-IPI scores, and low SA levels were prognostic factors for an undesirable overall survival (OS) rate. The multivariate analysis showed that a high SA level (hazard ratio: 0.43; 95% confidence interval: 0.2-0.88; P=0.022) was an independent prognostic factor of superior outcomes. Conclusions: An SA level ≥4.0 g/dL was identified as an independent biomarker of prognostic value for DLBCL patients aged ≥70 years.

Evaluation of Fourier transform infrared (FTIR) spectroscopy with multivariate analysis as a novel diagnostic tool for lymph node metastasis in gastric cancer.

Fourier transform infrared (FTIR) spectroscopy is a vibration spectroscopy that uses infrared radiation to vibrate to absorb the molecular bonds in its absorbed sample. The main purpose of this study was to evaluate FTIR spectroscopy as a novel diagnostic tool for lymph node metastasis (LNM) of gastric cancer. We collected 160 fresh non-metastatic and metastatic lymph nodes (80 each) from 60 patients with gastric cancer for spectral analysis. FTIR spectra of lymph node (LN) samples were obtained in the wavenumber range of 4000 cm-1 to 900 cm-1. We calculated the changes in the ratio of spectral intensity (/ I1460). Principal component analysis (PCA) and Fisher's discriminant analysis (FDA) were used to distinguish malignant from normal LN. Four significant bands at 1080 cm-1, 1640 cm-1, 1740 cm-1 and 3260 cm-1 separated metastatic and non-metastatic LN spectra into two distinct groups by PCA.T-tests showed that, along with the relative intensity ratios (I1080/I1460, I1640/I1460, I3260/I1460, I1740/I1460), these band ratios were also able to differentiate between malignant and benign LN spectra. Six parameters (P1080 cm-1, P1300 cm-1, I1080/I1460, I1640/I1460, I3260/I1460, I1740/I1460) were selected as independent factors to set up discriminant functions. The sensitivity of FTIR spectroscopy in diagnosing LNM was 95 % by discriminant analysis. Our study suggested that FTIR spectroscopy can be a useful tool to examine LNM with high sensitivity and specificity for LNM diagnosis. Therefore it can be used in clinical practice as a non-invasive method.

Marine collagen peptides: A novel biomaterial for the healing of oral mucosal ulcers.

The purpose of this study was to analyze the therapeutic effects of marine collagen peptides (MCPs) from tilapia skin on oral mucosal ulcers in a rat model. CCK-8 and wound healing assays were performed in vitro to evaluate proliferation and migration of L929 cells after treatment with MCPs. The effects of MCPs on the healing of oral mucosal ulcers in a rat model were macroscopically and microscopically analyzed in vivo. Results showed that MCPs promoted proliferation and migration of L929 cells. Moreover, 75%MCPs enhanced the ulcer healing process, suppressed inflammatory response and up-regulated the expression levels of vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF). MCPs are potentially used as a new therapeutic strategy for oral mucosal ulceration.

Postsurgical Pain and Implant Osseointegration Failure: A Case Control Study.

Aim: The relationship between postsurgical pain and osseointegration was evaluated and analyzed in this study. Material and method. 27 patients, ranging in age from 35 to 72 years old, 12 males and 15 females, who received dental implants and failed to achieve osseointegration from Tianjin Medical University Second Hospital, were analyzed and studied in the following aspects: bone density, initial torque, one- or two-stage surgery, postsurgical pain, postsurgical swelling, and radiographic evidence of osseointegration failure. Result: 5 patients were assessed to be D4 bone density and 7 cases were assessed to be D3 bone density, 2 patients were assessed to be D2 bone density and 13 patients were assessed to be D1 bone density. All cases were documented with clinically acceptable initial torque. Among the 27 cases, 2 of them were one-stage nonsubmerged surgery and 25 cases were two-stage submerged surgery. 25 out of 27 patients reported moderate to severe pain lasting for more than 72 hours. Radiologic examinations failed to offer any indication of poor osseointegration in the 7-day postsurgical follow-up. Conclusion: Moderate to severe postsurgical pain lasting more than 72 hours displays high odd ratio of poor osseointegrate. The radiological examinations alone failed to offer any valuable evidence for the early detection of osseointegration failure in this study.

circSTRN3 aggravates sepsis-induced acute kidney injury by regulating miR-578/ toll like receptor 4 axis.

Sepsis is a systemic inflammatory response caused by infection, and severe sepsis is commonly associated with the development of acute kidney injury (AKI). Accumulating evidence has revealed the implication of circular RNAs in AKI. In this study, we explored the potential engagement and the underlying mechanism of hsa_circ_010157 (circSTRN3) in sepsis-induced AKI. CircSTRN3 levels in HK2 cells and serum samples of patients were determined by RT-PCR. The protein levels of TLR4 (Toll Like Receptor 4), bax (Bcl-2-associated X protein), cleaved caspase 3 and bcl-2 (B-cell lymphoma-2) were detected by Western blotting (WB), and the levels of proinflammatory cytokines were detected by ELISA. The molecular interactions between mir-578/TLR4 and circSTRN3/miR-578 were analyzed by dual luciferase reporter assay as well as RNA pull-down experiment. Lipopolysaccharide (LPS) treated HK2 cells were used as an in vitro model to investigate the functional interaction of circSTRN3/miR-578/TLR4 axis. We found that the expression level of circSTRN3 in patients with sepsis-induced AKI and LPS-induced HK2 cells was higher. Silencing cicrSTRN3 alleviated LPS-induced cell proliferation, and suppressed the inflammatory response and apoptosis in LPS-treated HK2 cells. In contrast, the overexpression of circSTRN3 aggravated the cellular damages induced by LPS treatment. CircSTRN3 targeted miR-578/TLR4 axis to influence the damage effect induced by LPS. miR-578 inhibitor or TLR4 overexpression impaired the rescue effect of circSTRN3 knockdown. These results indicate that circSTRN3 upregulation in sepsis-induced AKI modulates miR-578/TLR4 axis to promote the pathogenesis of AKI, which could serve as future therapeutic targets for AKI treatment.

DACT3 has a tumor-inhibiting role in acute myeloid leukemia via the suppression of Wnt/ß-catenin signaling by DVL2.

Dapper antagonist of catenin-3 (DACT3) is a new tumor-related protein associated with a diverse set of tumors. However, whether DACT3 plays a role in acute myeloid leukemia (AML) is not fully understood. Our findings showed low DACT3 level in AML tissue, which was corrected with shorter survival rates. Upregulation of DACT3 effectively repressed cellular proliferation, and promoted cell cycle arrest and apoptosis of AML cells. Upregulation of DACT3 decreased levels of Dishevelled2 (DVL2), phospho-glycogen synthase kinase-3ß (GSK-3ß), and active ß-catenin, which collectively suppressed Wnt/ß-catenin-mediated transcriptional activity. Overexpression of DVL2 reversed DACT3-mediated suppression of Wnt/ß-catenin pathway. Reactivation of Wnt/ß-catenin abrogated DACT3-upregulation-evoked tumor-suppression in AML cells. Overexpression of DACT3 impeded the formation and growth of AML-derived xenograft tumor. Collectively, our work reveals a tumor-suppressive role of DACT3, a protein that negatively adjusts Wnt/ß-catenin pathway via downregulation of DVL2 in AML.

TMIGD1 Inhibited Abdominal Adhesion Formation by Alleviating Oxidative Stress in the Mitochondria of Peritoneal Mesothelial Cells.

BACKGROUND: Postoperative abdominal adhesion remains one of the frequent complications after abdominal surgery and lacks effective intervention. Peritoneal mesothelial cell injury and healing play crucial roles in the process of adhesion formation, and identifying this mechanism might provide new insight into possible new therapeutic strategies for this disease. Transmembrane and immunoglobulin domain-containing 1 (TMIGD1) has been proven to protect renal epithelial cells from injury induced by oxidative stress and has also been identified as a novel adhesion molecule. Here, we investigated the role of TMIGD1 and its possible mechanism in adhesion formation. MATERIALS AND METHODS: Immunohistochemistry (IHC), qPCR, and immunofluorescence (IHF) were used to detect the expression of TMIGD1. The grade and tenacity score of adhesion were used to evaluate the adhesion formation conditions. A TMIGD1-overexpressing HMrSV5 cell line was established. MTT assay, Western blotting, Annexin V apoptosis analysis, and CK19 staining were used to measure mesothelial cell viability, apoptosis, and completeness. ROS and MDA detection were used to measure mesothelial cell oxidative stress levels. JC-1 staining, IHF, and transmission electron microscopy were performed to assess mitochondrial function. Scratch-wound and adhesion assays were used to evaluate the adhesion ability of mesothelial cells. RESULTS: First, we showed that TMIGD1 was decreased in mouse abdominal adhesion tissue and peritoneal mesothelial cells. Second, TMIGD1 overexpression inhibited adhesion formation. Third, TMIGD1 overexpression protected mesothelial cells from hydrogen peroxide- (H2O2-) induced oxidative stress injury. Fourth, TMIGD1 overexpression alleviated oxidative stress by protecting the mitochondrial function of mesothelial cells. In addition, TMIGD1 overexpression enhanced mesothelial cell adhesion. CONCLUSION: Our findings suggest that TMIGD1 protects mesothelial cells from oxidative stress injury by protecting their mitochondrial function, which is decreased in regular abdominal adhesion tissue. In addition, TMIGD1 enhances peritoneal mesothelial cell adhesion to promote healing.

LncRNA SNHG1 contributes to the regulation of acute myeloid leukemia cell growth by modulating miR-489-3p/SOX12/Wnt/ß-catenin signaling.

The long noncoding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) is a critical regulator for the development and progression of multiple tumors. Yet, the role of SNHG1 in acute myeloid leukemia (AML) is unknown. The present study demonstrated that SNHG1 expression was upregulated in AML. SNHG1 silencing markedly repressed AML cell growth, whereas SNHG1 overexpression had the opposite effect. MicroRNA-489-3p (miR-489-3p) was identified as a SNHG1-targeting miRNA. SNHG1 knockdown increased miR-489-3p expression. Low expression of miR-489-3p was correlated with high expression of SNHG1 in AML tissues. miR-489-3p overexpression restricted AML cell growth, and SRY-related high-mobility-group box 12 (SOX12) was identified as a miR-489-3p-targeting gene. SNHG1 inhibition or miR-489-3p overexpression inactivated Wnt/ß-catenin signaling through downregulation of SOX12. SOX12 overexpression partially reversed the SNHG1 knockdown- or miR-489-3p overexpression-mediated effects. Taken together, these data indicate that suppression of SNHG1 downregulates AML cell growth by inactivating SOX12/Wnt/ß-catenin signaling via upregulating miR-489-3p.

Solanine inhibits proliferation and promotes apoptosis of the human leukemia cells by targeting the miR-16/Bcl-2 axis.

PURPOSE: Leukemia causes tremendous human mortality especially in children and young adults. This study was undertaken to investigate the anticancer effects of Solanine against the normal human NCI-H526 and human leukemia AML-193 cell lines. METHODS: Cell proliferation was determined by MTT assay. DAPI and annexin V/propidium iodide (PI) assays were used for the determination of apoptosis. The expression analysis was done by qRT-PCR. Protein concentrations were determined by western blot analysis. RESULTS: DAPI staining showed that Solanine causes nuclear morphological changes. The annexin V/PI staining showed that Solanine increased the leukemia apoptotic cell death dose-dependently. The expression of Bax was increased while of Bcl-2 was decreased. The qRT-PCR analysis showed that microRNA (miR)-16 was significantly (p<0.05) downregulated in leukemia AML-193 cells as compared to normal NCI-H526 cells. CONCLUSION: Taken together, these results showed that Solanine inhibits the proliferation of leukemia cells via induction of apoptosis and modulation of miR-16/Bcl-2 axis.

Identification of a robust subpathway-based signature for acute myeloid leukemia prognosis using an miRNA integrated strategy.

Acute myeloid leukemia (AML) is a heterogeneous disease, and survival signatures are urgently needed to better monitor treatment. MiRNAs displayed vital regulatory roles on target genes, which was necessary involved in the complex disease. We therefore examined the expression levels of miRNAs and genes to identify robust signatures for survival benefit analyses. First, we reconstructed subpathway graphs by embedding miRNA components that were derived from low-throughput miRNA-gene interactions. Then, we randomly divided the data sets from The Cancer Genome Atlas (TCGA) into training and testing sets, and further formed 100 subsets based on the training set. Using each subset, we identified survival-related miRNAs and genes, and identified survival subpathways based on the reconstructed subpathway graphs. After statistical analyses of these survival subpathways, the most robust subpathways with the top three ranks were identified, and risk scores were calculated based on these robust subpathways for AML patient prognoses. Among these robust subpathways, three representative subpathways, path: 05200_10 from Pathways in cancer, path: 04110_20 from Cell cycle, and path: 04510_8 from Focal adhesion, were significantly associated with patient survival in the TCGA training and testing sets based on subpathway risk scores. In conclusion, we performed integrated analyses of miRNAs and genes to identify robust prognostic subpathways, and calculated subpathway risk scores to characterize AML patient survival.