Study on Calculation Method of Bending Performance of Concrete Sandwich Composite Slab.

In order to explore the flexural behavior of a concrete sandwich panel under concentrated boundary conditions, based on Kirachhoff's elastic thin plate theory in this paper, the geometric deformation, physical conditions, and equilibrium relationship of a sandwich panel are deduced by constructing the layered analysis model of the sandwich panel, the basic differential equation of the flexural deformation of the concrete sandwich thin plate is obtained, and the mathematical expression of the internal force and displacement under the boundary condition of concentrated support is given. Combined with an engineering example, the proposed calculation method is verified. The results show that, in the arrangement of reliable connectors for concrete sandwich panels, the concrete wythes bear the load while the contribution of the core layer to the bending capacity of the structure can be ignored. When subjected to a laterally distributed load, the sandwich panel mainly experiences out-of-plane bending deformation, and the bending normal stress in the concrete panel layer shows a linear non-uniform distribution along the thickness direction of the panel. The bending deformation performance and bearing efficiency of a concrete sandwich slab with the change in concentrated support position have significant effects, and the load transfer efficiency can be improved by optimizing the arrangement of supports. Except for small local areas near the supports, the bending stress distribution and deformation behavior of the concrete sandwich panel can be accurately analyzed by the calculation method established in this paper.

Corrigendum: Ribosomal protein L23 drives the metastasis of hepatocellular carcinoma via upregulating MMP9.

[This corrects the article DOI: 10.3389/fonc.2021.779748.].

Circulating sNinj1 as a novel predictor of prognosis and severity in hepatocellular carcinoma.

BACKGROUND: The occurrence and development of HCC are closely associated with cell death. Recently, researchers found that Ninj1 plays a pivotal role in PMR during different types of cell death. However, the importance of Ninj1 in HCC has not been extensively investigated. METHODS: This study included 102 newly diagnosed HCC patients and 102 sex and age-matched NCs. Circulating sNinj1 was assessed by ELISA. Serum LDH and IL-1ß were detected through a chemiluminescence assay. The correlations of these biomarkers with disease severity and their potential as prognostic predictors for HCC were evaluated. The dynamic changes of sNinj1, LDH, and IL-1ß levels before and after treatment were recorded. RESULTS: Serum levels of sNinj1, IL-1ß, and LDH were significantly higher in HCC patients. Our study found that the sNinj1 level was positively correlated with tumor size, metastasis, and staging. ROC analysis indicated that the AUC of sNinj1 in differentiating HCC from NCs was 0.85. As a result of tumor thrombosis and invasion of the hepatic vein, sNinj1's AUCs were 0.71 and 0.73, respectively. After partial resection and TACE treatment, serum sNinj1 and LDH exhibited similar change trends. A one-year follow-up analysis also demonstrated that HCC patients with high sNinj1 had significantly poorer survival than those with low sNinj1. CONCLUSIONS: The serum sNinj1 is another diagnostic biomarker supporting the HCC diagnosis. More importantly, it has been shown that circulating sNinj1 reveals potential as a novel predictor of HCC severity and prognosis.

Comparison of area measurement methods in the routine assessment of diabetic foot ulcers-A consistency analysis method.

BACKGROUND: Ulcer area is a critical parameter in diabetic foot ulcer assessment but existing methods have deficiencies for routine measurement. AIM: We hypothesized that the Image J-based Computer Analysis method has a high level of agreement with the commonly used Maximum Length and Width and the Transparent Dressing-based Square Grid methods and aimed to test the consistency and verify the feasibility of the Image J-based Computer Analysis method in the routine assessment of ulcers. METHODS: Outpatient attendees with diabetic foot ulcers at the Department of Endocrinology of Sun Yat-sen Memorial Hospital were enrolled between October 2020 and October 2021. The three methods sequentially assessed the area of 65 included ulcers. Results were analysed using one-way analysis of variance and Bland-Altman plots to perform consistency analysis. RESULTS: The mean ± standard deviation ulcer area measured using the three methods were 14.79 ± 5.39, 14.35 ± 5.26, and 14.30 ± 5.26 cm2 , respectively. The measurement differences among the three groups or between any two were not statistically significant. Bland-Altman plots showed good consistency between the Image J-based Computer Analysis and the other two methods. CONCLUSION: The Image J-based Computer Analysis method can be interchanged with the other methods to assess ulcer areas. It is freely accessible, accurate and home-operable, thus worth consideration by nurses for routine ulcer area assessment.

"We are still doing some magic": Exploring the effectiveness of online therapeutic clowning.

BACKGROUND: Therapeutic clowns use embodied practices to engage with clients, their families and healthcare staff to empower patients and create therapeutic relationships. This study explored the effectiveness of a virtual therapeutic clown initiative. METHODS: Thirteen therapeutic clowns participated in a semi-structured interview to discuss their experiences with online clowning; additionally, four dyads consisting of a clown duo and a client explored multiple perspectives of a shared online clowning experience. Data were analyzed according to the six core competencies of therapeutic clowning. RESULTS: Although all therapeutic clowns and caregivers reported challenges and limitations with the medium, virtual therapeutic clowning was effective for empowering clients and forming therapeutic relationships. Clowns successfully used many strategies to maintain their core clowning competencies in the virtual environment. CONCLUSIONS: Virtual clowning may be more beneficial for some clients than in-person clowning and has the potential to extend therapeutic clowning beyond its traditional domains of practice.

An integrated microfluidics platform with high-throughput single-cell cloning array and concentration gradient generator for efficient cancer drug effect screening.

BACKGROUND: Tumor cell heterogeneity mediated drug resistance has been recognized as the stumbling block of cancer treatment. Elucidating the cytotoxicity of anticancer drugs at single-cell level in a high-throughput way is thus of great value for developing precision therapy. However, current techniques suffer from limitations in dynamically characterizing the responses of thousands of single cells or cell clones presented to multiple drug conditions. METHODS: We developed a new microfluidics-based "SMART" platform that is Simple to operate, able to generate a Massive single-cell array and Multiplex drug concentrations, capable of keeping cells Alive, Retainable and Trackable in the microchambers. These features are achieved by integrating a Microfluidic chamber Array (4320 units) and a six-Concentration gradient generator (MAC), which enables highly efficient analysis of leukemia drug effects on single cells and cell clones in a high-throughput way. RESULTS: A simple procedure produces 6 on-chip drug gradients to treat more than 3000 single cells or single-cell derived clones and thus allows an efficient and precise analysis of cell heterogeneity. The statistic results reveal that Imatinib (Ima) and Resveratrol (Res) combination treatment on single cells or clones is much more efficient than Ima or Res single drug treatment, indicated by the markedly reduced half maximal inhibitory concentration (IC50). Additionally, single-cell derived clones demonstrate a higher IC50 in each drug treatment compared to single cells. Moreover, primary cells isolated from two leukemia patients are also found with apparent heterogeneity upon drug treatment on MAC. CONCLUSION: This microfluidics-based "SMART" platform allows high-throughput single-cell capture and culture, dynamic drug-gradient treatment and cell response monitoring, which represents a new approach to efficiently investigate anticancer drug effects and should benefit drug discovery for leukemia and other cancers.

Differential expression of MSTN, IGF2BP1, and FABP2 across different embryonic ages and sexes in white Muscovy ducks.

To explore the effects of growth-related genes in both sexes and at different growth and development stages, male and female white Muscovy ducks at embryonic day E13, E17, E21, E25 and E29 were assessed in this study. RT-qPCR was used to determine the mRNA transcription levels of selected growth-related genes in the leg muscles of Muscovy ducks of both sexes and at different growth and developmental stages. MSTN, IGF2BP1 and FABP2 mRNAs were expressed in the leg muscles of male and female Muscovy ducks, but with different expression patterns. The MSTN and IGF2BP1 mRNA expression patterns were wavelike. MSTN mRNA expression was elevated at E13, increased at E17, decreased rapidly to the lowest level at E21, increased again at E25, and then decreased. IGF2BP1 mRNA expression was elevated at E13, increased at E17, decreased rapidly at E21, decreased rapidly to the lowest level at E25, and increased at E29. The expression trend of FABP2 mRNA was approximately "⊥" shape; the expression was the lowest at E13, increased slowly from E17 to E25, and increased extremely significantly at E29. In addition, the expression of MSTN in male Muscovy ducks was significantly higher than that in female ducks at E25 (P < 0.05). The expression of IGF2BP1 in male Muscovy ducks was extremely significantly higher than that in female ducks at E17 (P < 0.01). However, the expression of FABP2 in female Muscovy ducks was extremely significantly higher than that in male Muscovy ducks at E21 and E29 (P < 0.01). In conclusion, the mRNA expression of MSTN, IGF2BP1 and FABP2 in white Muscovy ducks is gestational age specific and sex specific. The differential gene expression patterns observed in this study provide a basis for understanding the physiological changes in white Muscovy ducks at different embryonic ages and in both sexes, supplementing the existing research on duck embryo muscle development. In addition, the findings provide a new framework for further discussion of poultry breeding.

LncRNA SNHG3 promotes gastric cancer cell proliferation and metastasis by regulating the miR-139-5p/MYB axis.

The long non-coding RNA (lncRNA) SNHG3 has been shown to play oncogenic roles in several cancer types, but the mechanisms underlying its activity are poorly understood. In this study, we aimed to explore the clinical relevance and mechanistic role of SNHG3 in gastric cancer (GC). We found that SNHG3 expression in GC cell lines and tissues was significantly increased, and the upregulation of this lncRNA was correlated with tumor clinical stage and decreased patient survival. Knocking down SNHG3 in GC cells impaired the proliferative, migratory, and invasive activity in vitro and constrained in vivo GC xenograft tumor growth. Mechanistically, SNHG3 was found to bind and sequester miR-139-5p, thereby indirectly promoting the upregulation of the miR-139-5p target gene MYB. These data demonstrated that SNHG3 functions in an oncogenic manner to drive GC proliferation, migration, and invasion by regulating the miR-139-5p/MYB axis.

Ribosomal Protein L23 Drives the Metastasis of Hepatocellular Carcinoma via Upregulating MMP9.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths globally. Tumor metastasis is one of the major causes of high mortality of HCC. Identifying underlying key factors contributing to invasion and metastasis is critical to understand the molecular mechanisms of HCC metastasis. Here, we identified RNA binding protein L23 (RPL23) as a tumor metastasis driver in HCC. RPL23 was significantly upregulated in HCC tissues compared to adjacent normal tissues, and closely related to poor clinical outcomes in HCC patients. RPL23 depletion inhibited HCC cell proliferation, migration and invasion, and distant metastasis. Mechanistically, RPL23 directly associated with 3'UTR of MMP9, therefore positively regulated MMP9 expression. In conclusion, we identified that RPL23 might play an important role in HCC metastasis in an MMP9-dependent manner and be a potential therapeutic target for HCC tumorigenesis and metastasis.

[Simulation analysis of the radial growth characteristics of Pinus sylvestris var. mongolica in Hulunbuir Sandy Land by Vaganov-Shashkin Model]. / 呼伦贝尔沙地樟子松径向生长特征的VS模型模拟分析.

The Vaganov-Shashkin model was used to simulate the standardized ring-width chrono-logy of Pinus sylvestris var. mongolica on the sandy land in Hulunbuir. The results showed that the fitting degree was better in the period before 2000 than that after 2000. Thus, the simulation results before 2000 were selected to analyze the radial growth. The results showed that the main growing season of P. sylvestris var. mongolica in Hulunbuir Sandy Land was from May to September each year. Temperature had a significant impact on the early and late growth of P. sylvestris var. mongo-lica. In the prosperous period of the growing season, insufficient soil moisture was the main factor restricting the radial growth. The radial growth rates of P. sylvestris var. mongolica in extremely narrow years were more limited by soil moisture than that in extremely wide years. The radial growth rates in the middle of the growing season (from July to August) showed a decreasing trend in wide and narrow years, indicating that the growth of P. sylvestris var. mongolica was affected by drought stress. Our results were consistent with the characteristics of tree-ring physiological models in semi-arid areas of China. The model was applicable to the radial growth simulation of P. sylvestris var. mongolica in Hulunbuir Sandy Land.

High expression of citron kinase predicts poor prognosis of prostate cancer.

Citron kinase (CIT) is a Rho-effector protein kinase that is associated with several types of cancer. However, the role of CIT in prostate cancer (PCa) is unclear. The current study utilized microarray data obtained from The Cancer Genome Atlas, which was analyzed via Biometric Research Program array tools. Additionally, reverse transcription-quantitative (RT-q)PCR was performed to compare the mRNA expression of CIT in PCa tissue and in benign prostatic hyperplasia. The protein expression of CIT was detected in a consecutive cohort via immunochemistry and CIT was screened as a potential oncogene in PCa. The results of RT-qPCR demonstrated that the mRNA expression of CIT was increased in PCa tissues. Furthermore, immunochemistry revealed that CIT protein expression was positively associated with age at diagnosis, Gleason grade, serum PSA, clinical T stage, risk group, lymph node invasion and metastasis. When compared with the low expression group, patients with a high CIT expression exhibited shorter survival rates, cancer specific mortalities (CSM) and biochemical recurrence (BCR). In addition, multivariate analysis revealed that CIT was a potential predictor of CSM and BCR. The results revealed that CIT is overexpressed during the malignant progression of PCa and may be a predictor of a poor patient prognosis.

Abnormal Ca2+ handling contributes to the impairment of aortic smooth muscle contractility in Zucker diabetic fatty rats.

Vascular dysfunction is a common pathological basis for complications in individuals affected by diabetes. Previous studies have established that endothelial dysfunction is the primary contributor to vascular complications in type 2 diabetes (T2DM). However, the role of vascular smooth muscle cells (VSMCs) in vascular complications associated with T2DM is still not completely understood. The aim of this study is to explore the potential mechanisms associated with Ca2+ handling dysfunction and how this dysfunction contributes to diabetic vascular smooth muscle impairment. The results indicated that endothelium-dependent vasodilation was impaired in diabetic aortae, but endothelium-independent vasodilation was not altered. Various vasoconstrictors such as phenylephrine, U46619 and 5-HT could induce vasoconstriction in a concentration-dependent manner, such that the dose-response curve was parallel shifted to the right in diabetic aortae, compared to the control. Vasoconstrictions mediated by L-type calcium (Cav1.2) channels were attenuated in diabetic aortae, but effects mediated by store-operated calcium (SOC) channels were enhanced. Intracellular Ca2+ concentration ([Ca2+]i) in VSMCs was detected by Fluo-4 calcium fluorescent probes, and demonstrated that SOC-mediated Ca2+ entry was increased in diabetic VSMCs. VSMC-specific knockout of STIM1 genes decreased SOC-mediated and phenylephrine-induced vasoconstrictive response in mice aortae. Additionally, Orai1 expression was up-regulated, Cav1.2 expression was downregulated, and the phenotypic transformation of diabetic VSMCs was determined in diabetic aortae. The overexpression of Orai1 markedly promoted the OPN expression of VSMCs, whereas SKF96365 (SOC channel blocker) reversed the phenotypic transformation of diabetic VSMCs. Our results demonstrated that the vasoconstriction response of aortic smooth muscle was weakened in type 2 diabetic rats, which was related to the downregulation of the Cav1.2 channel and the up-regulation of the SOC channel signaling pathway.

Unprecedented and highly stable lithium storage capacity of (001) faceted nanosheet-constructed hierarchically porous TiO2/rGO hybrid architecture for high-performance Li-ion batteries.

Active crystal facets can generate special properties for various applications. Herein, we report a (001) faceted nanosheet-constructed hierarchically porous TiO2/rGO hybrid architecture with unprecedented and highly stable lithium storage performance. Density functional theory calculations show that the (001) faceted TiO2 nanosheets enable enhanced reaction kinetics by reinforcing their contact with the electrolyte and shortening the path length of Li+ diffusion and insertion-extraction. The reduced graphene oxide (rGO) nanosheets in this TiO2/rGO hybrid largely improve charge transport, while the porous hierarchy at different length scales favors continuous electrolyte permeation and accommodates volume change. This hierarchically porous TiO2/rGO hybrid anode material demonstrates an excellent reversible capacity of 250 mAh g-1 at 1 C (1 C = 335 mA g-1) at a voltage window of 1.0-3.0 V. Even after 1000 cycles at 5 C and 500 cycles at 10 C, the anode retains exceptional and stable capacities of 176 and 160 mAh g-1, respectively. Moreover, the formed Li2Ti2O4 nanodots facilitate reversed Li+ insertion-extraction during the cycling process. The above results indicate the best performance of TiO2-based materials as anodes for lithium-ion batteries reported in the literature.

Mechanisms of U46619-induced contraction in mouse intrarenal artery.

Thromboxane A2 (TXA2 ) has been implicated in the pathogenesis of vascular complications, but the underlying mechanism remains unclear. The contraction of renal arterial rings in mice was measured by a Multi Myograph System. The intracellular calcium concentration ([Ca2+ ]i ) in vascular smooth muscle cells (VSMCs) was obtained by using a fluo-4/AM dye and a confocal laser scanning microscopy. The results show that the U46619-induced vasoconstriction of renal artery was completely blocked by a TXA2 receptor antagonist GR32191, significantly inhibited by a selective phospholipase C (PI-PLC) inhibitor U73122 at 10 µmol/L and partially inhibited by a Phosphatidylcholine - specific phospholipase C (PC-PLC) inhibitor D609 at 50 µmol/L. Moreover, the U46619-induced vasoconstriction was inhibited by a general protein kinase C (PKC) inhibitor chelerythrine at 10 µmol/L, and a selective PKCδ inhibitor rottlerin at 10 µmol/L. In addition, the PKC-induced vasoconstriction was partially inhibited by a Rho-kinase inhibitor Y-27632 at 10 µmol/L and was further completely inhibited together with a putative IP3 receptor antagonist and store-operated Ca2+ (SOC) entry inhibitor 2-APB at 100 µmol/L. On the other hand, U46619-induced vasoconstriction was partially inhibited by L-type calcium channel (Cav1.2) inhibitor nifedipine at 1 µmol/L and 2-APB at 50 and 100 µmol/L. Last, U46619-induced vasoconstriction was partially inhibited by a cell membrane Ca2+ activated C1- channel blocker 5-Nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) at 50 and 100 µmol/L. Our results suggest that the U46619-induced contraction of mouse intrarenal arteries is mediated by Cav1.2 and SOC channel, through the activation of thromboxane-prostanoid receptors and its downstream signaling pathway.

PRR11 and SKA2 gene pair is overexpressed and regulated by p53 in breast cancer.

Our previous study found that two novel cancer-related genes, PRR11 and SKA2, constituted a classic gene pair that was regulated by p53 and NF-Y in lung cancer. However, their role and regulatory mechanism in breast cancer remain elusive. In this study, we found that the expression levels of PRR11 and SKA2 were upregulated and have a negative prognotic value in breast cancer. Loss-of-function experiments showed that RNAi-mediated knockdown of PRR11 and/or SKA2 inhibited proliferation, migration, and invasion of breast cancer cells. Mechanistic experiments revealed that knockdown of PRR11 and/or SKA2 caused dysregulation of several downstream genes, including CDK6, TPM3, and USP12, etc. Luciferase reporter assays demonstrated that wild type p53 significantly repressed the PRR11-SKA2 bidirectional promoter activity, but not NF-Y. Interestingly, NF-Y was only essential for and correlated with the expression of PRR11, but not SKA2. Consistently, adriamycin-induced (ADR) activation of endogenous p53 also caused significant repression of the PRR11 and SKA2 gene pair expression. Notably, breast cancer patients with lower expression levels of either PRR11 or SKA2, along with wild type p53, exhibited better disease-free survival compared to others with p53 mutations and/or higher expression levels of either PRR11 or SKA2. Collectively, our study indicates that the PRR11 and SKA2 transcription unit might be an oncogenic contributor and might serve as a novel diagnostic and therapeutic target in breast cancer. [BMB Reports 2019; 52(2): 157-162].

Study on the Effect Mechanism of Iridoid Glycosides of Scrophularia ningpoensis Inhibiting Cardiomyocytes Apoptosis in Myo- cardial Infarction Model Rats Based on Different Caspase Apoptosis Pathways / 中国药房

OBJECTIVE： To study the effect mechanism of iridoid glycosides extracted from Scrophularia ningpoensis inhibiting cardiomyocytes apoptosis in myocardial infarction model rats. METHODS： The male Wistar rats were randomly divided into sham operation group， model group and S. ningpoensis iridoid glycosides low-dose， medium-dose and high-dose groups， with 10 rats in each group. Myocardial infarction models were established by ligating the left anterior descending coronary artery of the rats， and sham operation group was only threaded without ligation. After the model was established， each administration group was given S. ningpoensis iridoid glycosides suspension intragastrically at three different doses of 50，100，200 mg/kg （by the amount of total glycosides extract） with 10 mL/time， twice a day， for consecutive 7 days. Sham operation group and model group were given constant volume of normal saline intragastrically with same method. The changes of S-T segment of lead ECG Ⅱ were recorded before， after and during 7 days of administration. Cardiac function of rats was examined. The serum levels of LDH， CK-MB， cTnⅠ， NT-pro BNP and TNF-α were determined by colorimetry， immunosuppression or ELISA. The apoptosis of myocardial cells was observed by TUNEL method. SOD activity and MDA content in cardiac myocytes were detected by colorimetry. The expressions of Bcl-2， Bax， Cyt C， Caspase-8， Caspase-9， Caspase-12， Caspase-3 and Calpain in cardiac myocytes were detected by ELISA， enzymolysis colorimetry or enzymatic fluorescence assay. RESULTS： Compared with sham operation， electrocardiogram S-T segment was significantly elevated and the left ventricular end-diastolic diameter and left ventricular end-systolic diameter were significantly increased in the model group； left ventricular ejection fraction and short axis shortening rate decreased significantly； serum levels of LDH， CK-MB， cTnⅠ， NT-pro BNP and TNF-α were increased significantly； there were a large number of yellow-brown apoptotic cells in myocardial tissue； the activity of SOD in myocardial tissue was significantly decreased while the content of MDA was significantly increased； the protein expression level of Bcl-2 and Bcl-2/Bax were significantly decreased， while the levels of Bax， Cyt C， Caspase-3， Caspase-8， Caspase-9， Caspase-12 and Calpain were significantly increased （P＜0.05 or P＜0.01）. Compared with model group， above indexes and pathological changes of myocardial tissue were improved significantly in administration group； the level of Bcl-2 and Bcl-2/Bax in cardiomyocytes increased significantly， while the levels of Bax， Cyt C， Caspase-3， Caspase-8， Caspase-9， Caspase-12 and Calpain decreased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS： S. ningpoensis iridoid glycosides can inhibit the activation of Caspase-3 by inhibiting three apoptotic pathways related to Caspase-8， Caspase-9 and Caspase-12， and then inhibit the apoptosis of cardiomyocytes.

Effects of PON1 Gene Promoter DNA Methylation and Genetic Variations on the Clinical Outcomes of Dual Antiplatelet Therapy for Patients Undergoing Percutaneous Coronary Intervention.

INTRODUCTION AND OBJECTIVE: The relationship between either paraoxonase 1 (PON1) gene promoter DNA methylation or genetic variations and bleeding or major adverse cardiac events after dual antiplatelet therapy has been incompletely characterized. We aimed to systematically investigate the role of genetic variations and DNA methylation of the PON1 CpG island promoter on the clinical outcomes of dual antiplatelet therapy for patients with coronary artery disease (CAD) who underwent percutaneous coronary intervention (PCI). METHODS: This study included 653 patients with CAD undergoing PCI and receiving dual antiplatelet therapy. Genomic DNAs were isolated from whole blood and were genotyped for the three single nucleotide polymorphisms (SNPs) of the PON1 gene. The DNA methylation levels in the PON1 promoter region were determined by bisulfite sequencing or pyrosequencing at five CpG sites (positions -142, -161, -163, -170, and -184 from the transcription start site). Clopidogrel and its metabolites in plasma were examined using high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), and platelet function analysis was performed using the VerifyNow assay. RESULTS: Statistically significant associations between methylation levels at five PON1 CpG sites and bleeding were observed: -184 [odds ratio (OR) 0.98, 95% confidence interval (CI) 0.96-1.00, p = 0.028]; -170 (OR 0.99, 95% CI 0.97-1.00, p = 0.048); -163 (OR 0.98, 95% CI 0.96-1.00, p = 0.029); -161 (OR 0.98, 95% CI 0.97-1.00, p = 0.026); and -142 (OR 0.98, 95% CI 0.97-1.00, p = 0.042) at a false discovery rate of <5%. Statistical analysis also revealed that aspirin reaction units (ARUs) were significantly associated with PON1 methylation level at CpG site -163 (p = 0.0342). The ARUs of patients with the PON1 126 CC genotype was 527 ± 94, which was higher than the ARUs (473 ± 89) of patients with the 126 CG genotype (p = 0.0163). Multivariate logistic regression analysis indicated that the PON1 methylation level at CpG site -161 (OR 0.95, 95% CI 0.92-0.98, p = 0.002) and the use of angiotensin-converting enzyme inhibitors (OR 0.48, 95% CI 0.26-0.89, p = 0.021) were associated with a decreased risk of bleeding events. CONCLUSIONS: Hypomethylation of CpGs in the PON1 promoter may be a weak, albeit statistically significant, risk factor of bleeding after dual antiplatelet therapy. Further large-scale studies are needed to verify our results.

Synovial fluid­derived synovial fragments represent an improved source of synovial mesenchymal stem cells in the temporomandibular joint.

Surgery-obtained synovium specimens (SSSs) can provide a source of synovial mesenchymal stem cells (SMSCs) for experimental studies. However, these specimens contain diverse tissues, including the intima and subintima; therefore, these SMSCs are not entirely derived from the intima and their cell source is heterogeneous. The present study isolated synovial fragments (SFs) from synovial fluid dilutions extracted from patients with temporomandibular joint (TMJ) osteoarthrosis. Unlike SSSs, SFs, which are membranous and translucent, consist of only several cell layers, indicating the presence of only the intima. In the present study, SF cells (SFCs) and SSS cells (SSSCs) exhibited a homogeneous, fibroblast­like, spindle­shaped morphology after passaging in vitro. Furthermore, both cell types exhibited similar proliferative and differentiation potentials in vitro. However, SFCs exhibited more uniform surface markers compared with SSSCs when analysed by flow cytometry. Taken together, these results indicated that SFs contained a greater amount of unmixed intima than SSSs, and that SFCs exhibited more homogeneous characteristics than SSSCs, thereby offering an improved source of SMSCs in the TMJ.

Empirical Antibiotic Treatment in Diabetic Foot Infection: A Study Focusing on the Culture and Antibiotic Sensitivity in a Population From Southern China.

Diabetic foot and subsequent diabetic ulcer infections are the most devastating complication of diabetes. This study was conducted to explore the bacterial spectrum, sensitivity of microbials, and analysis of the empirical antibiotic regimens in our health center. The study included patients with diabetic foot ulcer infection (DFI) seen from 2009 to 2014. The patients included had all information covering the physical examination, laboratory tests, and image examinations. We sent appropriately obtained specimens for culture prior to starting empirical antibiotic therapy in all participants. A total of 312 patients were included: 52, 112, 95 and 53 patients within uninfected, mild, moderate, and severe infection groups. The total percentages of Gram-positive cocci (GPCs) and Gram-negative rods (GNRs) were 54% and 48.8% ( P = 0.63). The most common GPC was Staphylococcus aureus (22.4%) and GNR was Pseudomonas aeruginosa (11.9%). Methicillin-resistant Staphylococcus aureus was isolated from 21 patients (6.7%). Even in the mild infection group, there was no significant difference between GPC and GNR infection, irrespective of recent antibiotic use ( P = 0.053). The most frequently used empirical antibiotics in our center were second-/third-generation cephalosporin ± clindamycin, both in the mild and moderate/severe infection groups. In our center, the amoxicillin/clavulanate or ampicillin/sulbactam (ß-L-ase 1) and second-/third-generation cephalosporins were highly resistant to the common GNR (30%-60%). The ticarcillin/clavulanate, piperacillin/tazuobactam (ß-L-ase 2), fluoroquinolone, and group 2 carbapenem had good sensitivity. This study presents a comprehensive microbiological survey of diabetic foot ulcers in inpatients and provides reliable evidence of the local microbial epidemiology and sensitivity of antibiotics, which may help us improve clinical outcomes in DFI patients.

Rce1 expression in renal cell carcinoma and its regulatory effect on 786-O cell apoptosis through endoplasmic reticulum stress.

Ras and a-factor-converting enzyme 1 (Rce1) is located in the endoplasmic reticulum (ER) and is thought to be responsible for endoproteolytic processing of the vast majority of CAAX proteins. Endoplasmic reticulum stress (ERS) plays an important role in renal cell carcinoma (RCC); however, the expression and role of Rce1 in RCC have not been extensively studied. We aimed to investigate the expression of Rce1 in RCC tissues and its molecular mechanism in ERS-induced apoptosis in RCC 786-O cells. We first used western blotting, quantitative reverse transcriptase-polymerase chain reaction, and immunohistochemistry to detect the Rce1 expression in renal carcinoma tissues and paracancerous tissues. It was found that Rce1 expression was upregulated in RCC tissues, and its positive expression level was strongly associated with clinicopathologic features. Next, we detected the expression of Rce1 in human embryonic kidney cell line HEK293 and human renal carcinoma cell lines 786-O, ACHN, and A498. Higher expression of Rce1 was found in human renal carcinoma cell lines, especially in 786-O cells. Knockdown of Rce1 in 786-O cells increased apoptosis and inhibited proliferation (P < 0.05). Moreover, downregulation of Rce1 upregulated the expression of the pro-apoptotic protein Bax, but downregulated the expression of the anti-apoptotic protein Bcl-2. Further studies showed that downregulation of Rce1 also affected the expression of ERS factors. In conclusion, our results indicated that Rce1 plays a key role in RCC. Low expression of Rce1 might indirectly increase apoptosis and inhibit proliferation of renal carcinoma cells through ERS.