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We aimed to compare the clinical outcomes of pre-emptive angioplasty versus post-thrombotic percutaneous endovascular restoration of dysfunctional arteriovenous fistula (AVF).This retrospective study reviewed the data from 80 patients who underwent 114 endovascular interventions for a malfunctioning AVF from July 2016 to August 2019. Stenotic AVFs were treated with pre-emptive angioplasty. Thrombosed AVFs were treated with percutaneous pharmacomechanical fibrinolysis with urokinase used only during the operation or continuously infused. The differences in patency rates were evaluated using the Kaplan-Meier method. In addition, univariate and multivariate regression Cox models were used to determine influential factors on the postintervention primary patency.Post-thrombotic interventions and pre-emptive angioplasty yielded statistically similar rates in clinical success (100 vs. 100%), anatomic success (94 vs. 89%; P = 0.52), complication (4 vs. 11%; P = 0.29), as well as postintervention primary, assisted primary and secondary patency (P = 0.80; 0.57; 0.57). The use of pre-emptive angioplasty was associated with reduced total cost (¥25,108 vs. ¥30,833, P 0.001). The patients who used urokinase only during the operation prolonged both the primary and assisted primary patency (P = 0.02; 0.002), while those with continuous infusion of urokinase had worst patency rates and high costs (¥39,275 vs. ¥25,108 vs. ¥27,140, P 0.001). Compared with the other locations, dysfunction in the anastomotic or juxta-anastomotic segment (HR = 0.41, P = 0.001) was associated with prolonged postintervention primary patency.No clinical outcome differences were found between the post-thrombotic percutaneous endovascular interventions and pre-emptive angioplasty. However, pre-emptive angioplasty decreased access expenditure.

The study was aimed at exploring the diagnostic value of artificial intelligence reconstruction algorithm combined with CT image parameters on hepatic ascites, expected to provide a reference for the etiological evaluation of clinical abdominal effusion. Specifically, the adaptive iterative hard threshold (AIHT) algorithm for CT image reconstruction was proposed. Then, 100 patients with peritoneal effusion were selected as the research subjects. After 8 cases were excluded, the remaining was divided into 50 cases of the S1 group (hepatic ascites) and 42 cases of the D0 group (cancerous peritoneal effusion). Gemstone energy spectrum CT scanning was performed on all patients, and CT image parameters of the two groups were compared. It was found that CT value of mixed energy, CT value of 60-100 KeV single energy, concentration value of water (calcium), concentration value of water (iodine), and slope of energy spectrum curve in the S1 group were significantly lower than those in the D0 group ( P < 0.05 ). The effective atomic number in the S1 group was significantly higher than that in the D0 group ( P < 0.05 ). Of the 50 patients in the S1 group, 3 (6%) had an ascending and 47 (94%) had a descending spectral curve. Of the 42 patients in the D0 group, 37 (88.1%) had an ascending and 5 (11.9%) had a descending spectral curve. The sensitivity and specificity of water (iodine) were 0.927 and 0.836, respectively. The sensitivity and specificity of water (calcium) were 0.863 and 0.887, respectively. For different scan ranges ([0,90]; [0,120]), root mean square error (RMSE) of AIHT reconstructed image was significantly smaller than that of traditional algorithm, while peak signal-to-noise ratio (PSNR) was opposite. The differences were statistically significant ( P < 0.05 ). In conclusion, AIHT-based CT images can better display the distribution of hepatic ascites, and the parameters of CT value, effective atomic number, water (iodine), water (calcium), and spectral curve can all provide help for the identification of hepatic ascites. Especially, water (iodine) and water (calcium) demonstrated high diagnostic performance of hepatic ascites.

Multiorgan venous and lymphatic defect (MOVLD) syndrome is a unique visceral vascular malformations with complex etiologies. In this study, primary skin fibroblasts were obtained from three MOVLD patients and reprogrammed into iPSCs by Yamanaka’s classical strategy. The MOVLD- iPSCs carrying the DDX24 p.Glu271Lys mutation were confirmed by Sanger sequencing. The pluripotency of MOVLD-iPSCs was verified by the specific molecular markers and gene expression, trilineage differentiation potential. The establishment of the MOVLD-iPSCs will provide a useful model for understanding the mechanisms involved the MOVLD and promoting the development of medical treatment.

Background Multiple factors, including co-exposure between lifestyle and environmental risks, are important in susceptibility to oxidative DNA damage. However, the underlying mechanism is not fully understood. This study was undertaken to evaluate whether Cytochrome P4501A1 (CYP1A1) methylation can mediate the co-exposure effect between smoking and occupational polycyclic aromatic hydrocarbons (PAH) in development of oxidative DNA damage. Methods We explored the associations between smoking and occupational PAH co-exposure effect, CYP1A1 methylation and oxidative DNA damage among 500 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (1-hydroxypyrene, 1-OHP; 2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; and 9-hydroxyphenanthren, 9-PHE) and a marker of oxidative DNA damage (8-hydroxy- 2′- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. CYP1A1 methylation was measured by pyrosequencing. Finally, mediation analysis was performed to investigate whether CYP1A1 methylation mediated smoking and occupational PAH co-exposure effect on oxidative DNA damage. Results We observed significant associations of smoking and 1-OHP co-exposure with CYP1A1 hypomethylation (OR: 1.87, 95% CI: 1.01–3.47) and high 8-OHdG (OR: 2.13, 95% CI: 1.14–3.97). There was a significant relationship between CYP1A1 hypomethylation and high 8-OHdG (1st vs. 3rd tertile = 1.58, 95% CI: 1.01–2.47, P for trend = 0.046). In addition, mediation analysis suggested CYP1A1 hypomethylation could explain 13.6% of effect of high 8-OHdG related to smoking and 1-OHP co-exposure. Conclusions Our findings suggested that the co-exposure effect of smoking and occupational PAH could increase the risk of oxidative DNA damage by a mechanism partly involving CYP1A1 hypomethylation. Electronic supplementary material The online version of this article (10.1186/s12940-019-0508-0) contains supplementary material, which is available to authorized users.

Polycyclic aromatic hydrocarbons (PAH) are well-known to be carcinogenic and the mechanisms that it contributes to oxidative DNA damage and aryl hydrocarbon receptor (AhR)-dependent induction are also well understood. However, little is known about the associations between PAH exposure, AhR expression, and oxidative DNA damage. We investigated their associations of AhR expression and oxidative DNA damage related to PAH exposure among 310 workers from a coke-oven plant in China. Urine biomarkers of PAH exposure (2-hydroxynaphthalene, 2-NAP; 2-hydroxyfluorene, 2-FLU; 9-hydroxyphenanthren, 9-PHE; and 1-hydroxypyrene, 1-OHP) and a marker of oxidative damage (8-hydroxy- 2′- deoxyguanosine, 8-OHdG) were measured by high performance liquid chromatography. AhR expression in venous blood was measured by reverse transcription -polymerase chain reaction. The results showed that increasing levels of urinary 1-OHP was positively associated with high 8-OHdG (OR (95% CI) was 4.01 (1.41–11.45) for 4th quartile, compared with 1st quartile, P for trend = 0.013). The similar associations were also found between urinary 1-OHP and high-AhR expressions (4th vs. 1st quartile = 3.50, 95% CI: 1.24–9.87, P for trend = 0.029). A significant association between AhR expression and high 8-OHdG was also found (4th vs. 1st quartile = 2.44, 95% CI: 1.05–5.70, P for trend = 0.027). In addition, mediation analysis showed the AhR expression could explain 35.9% of the association of oxidative DNA damage related to PAH exposure. Our findings implicated that the association between PAH exposure and oxidative DNA damage may be mediated by AhR expression among Chinese occupational workers.

Background We calculated the population pharmacokinetics of mizoribine in adult Chinese patients and compared the parameters with those of Japanese patients to determine whether there are any ethnic differences in blood concentration transition between these 2 populations. Methods The blood concentrations of mizoribine in 21 Chinese patients who were administered mizoribine after renal transplantation were measured at 304 time points. The absorption lag time, absorption rate constant, apparent distribution volume, and oral clearance were thereafter calculated and compared with the respective Japanese references. Results The absorption lag time, absorption rate constant, and apparent distribution volume calculated in this study were, respectively, 0.353 hour, 0.856 hour−1, and 0.776 L/kg. The oral clearance was calculated as 2.18 times the creatinine clearance using creatinine clearance as a function. The absorption rate constant, apparent distribution volume, and oral clearance are determinants of the maximum blood concentration, trough, and area under the blood concentration time curve. The relative absorption rate constant, apparent distribution volume, and oral clearance were 0.9-, 0.9-, and 1.2-fold, respectively, in Chinese patients compared with those in Japanese patients. These values are within the confidence limit, suggesting that there is no significant PK difference between the 2 ethnic groups. Conclusions Results of this study showed no ethnic difference in blood mizoribine concentration transition between Chinese and Japanese patients. In addition, the population pharmacokinetic parameters obtained in this study are useful in determining the initial dosage or in the Bayesian analysis of mizoribine concentrations using scarce time points.

The aim of the study was to investigate the effect of immunosuppression therapy early after kidney transplantation, particularly exposure of mycophenolic acid (MPA) and calcineurin inhibitor (CNI), on posttransplantation de novo HLA antibody production. Methods A single-center retrospective cohort study was performed at the First Affiliated Hospital of Sun Yat-sen University, enrolling the kidney transplant or pancreas-kidney transplant recipients who had surgery between January 2010 and February 2016. Results A total of 214 recipients were included in the study with a median follow-up period of 1.06 years. A total of 30 recipients (14.0%) were positive in HLA antibody detection posttransplant with a median follow-up period of 1.46 years. Ten recipients (4.7%) lost their allograft function during follow-up, and 6 of them (60%) developed de novo HLA antibody after graft failure. Multivariate analysis showed that acute rejection significantly increased the risk of de novo HLA antibody (hazard ratio [HR], 2.732). Intensified MPA dosing therapy reduced the risk by 59.8% (HR, 0.402); low-dose CNI therapy increased the risk by 33.3% (HR, 1.333), and the effect of extremely low-dose CNI therapy was even larger (HR, 2.242). Conclusion The risk of de novo HLA antibody can be decreased by reducing the risk of acute rejection. A tendency was seen in low-dose CNI therapy to increase the risk of de novo HLA antibody, but intensified MPA dosing therapy may provide an umbrella protection effect by reducing the risk. Prospective study was required to confirm the effects.

Material decomposition (MD) is an important application of computer tomography (CT). For phase contrast imaging, conventional MD methods are categorized into two types with respect to different operation sequences, i.e., “before” or “after” image reconstruction. Both categories come down to two-step methods, which have the problem of noise amplification. In this study, we incorporate both phase and absorption (PA) information into MD process, and correspondingly develop a simultaneous algebraic reconstruction technique (SART). The proposed method is referred to as phase & absorption material decomposition-SART (PAMD-SART). By iteratively solving an optimization problem, material composition and substance quantification are reconstructed directly from absorption and differential phase projections. Comparing with two-step MD, the proposed one-step method is superior in noise suppression and accurate decomposition. Numerical simulations and synchrotron radiation based experiments show that PAMD-SART outperforms the classical MD method (image-based and dual-energy CT iterative method), especially for the quantitative accuracy of material equivalent atomic number.

Myocardial infarction (MI) is considered as one of the major life-threatening health issues worldwide. Growing number of cases every year is demanding rapid, portable, and early detection by the sensing devices for the identification of MI. This research work introduces a modified interdigitated electrode (IDE) sensing surface constructed with single-walled carbon nanotube (SWCN) to detect the cardiac biomarker, C-reactive protein (CRP). CRP-specific aptamer was conjugated with gold nanoparticle and attached on SWCN-constructed IDE surface. This probe-modified sensing surface has reached the limit of CRP detection to 10 pM on a linear regression curve with the regression coefficient of R² = 0.9223 [y = 0.9198x - 0.4326]. Further, control molecules, such as random aptamer sequence and nontarget cardiac biomarker (Troponin I), did not show the current response, indicating the specific CRP detection. This sensing strategy helps to detect the lower level of CRP and diagnose the MI at its earlier stages.

Rheumatoid arthritis (RA), a chronic inflammatory disease, deprives patients' walking ability and reduces their life quality worldwide. Though recent studies have indicated the role of long noncoding RNA (lncRNA) ZFAS1 in several diseases, however, its role in RA remains uncharacterized. The present study aimed to unravel the the effect of ZFAS1 on RA. Herein, the RA mouse model and the human RA synoviocyte MH7A cell lines stimulated with TNF-α were established. ZFAS1 was next determined to be highly expressed in the mice with RA-like symptoms and TNF-α-stimulated MH7A cells while inhibiting ZFAS1 was demonstrated to promote proliferation and suppress apoptosis of MH7A cells. Furthermore, ZFAS1 knockdown exerted anti-inflammation effect in vitro and in vivo and reduced the arthritis index value. Moreover, RNA immunoprecipitation and dual-luciferase reporter assays identified the binding of ZFAS1 to microRNA (miR)-296-5p as well as the binding of miR-296-5p to matrix metalloproteinase-15 (MMP-15). Of note, ZFAS1 could bind miR-296-5p to up-regulate the expression of MMP-15. Our results from in vitro and in vivo experiments demonstrated silencing ZFAS1 mitigated RA-like symptoms such as inflammation and hyperplasia via miR-296-5p-dependent inhibition of MMP-15. Taken altogether, our study confirmed that ZFAS1 involved in RA progression by competitively binding to miR-296-5p and regulating MMP-15 expression.

Coke oven emissions (COE) containing polycyclic aromatic hydrocarbons (PAHs) are predominant toxic constituents of particulate air pollution that have been linked to increased risk of lung cancer. Aberrant DNA methylation is one of the best known epigenetic changes in human cancers and healthy subjects exposed to carcinogens. The purpose of this study is to explore the factors influencing the methylation of long interspersed nuclear element-1 (LINE-1) and aryl-hydrocarbon receptor repressor (AhRR) in coke oven workers. The study population is composed by coke oven workers (348) and water treatment workers (131). And their urinary PAH metabolites were analyzed by high performance liquid chromatography; DNA methylation were measured by pyrosequencing. The urinary PAHs metabolites were significantly elevated in coke oven workers (P 0.01). The results from multivariate logistic regression analysis showed that a high level of urinary 1-hydroxypyrene was associated with a significantly increased risk of hypomethylation of LINE-1 (OR: 1.80; 95% CI: 1.25, 2.60), and heavy smoking was associated with a significantly increased risk of hypomethylation of AhRR (OR: 1.44; 95% CI: 1.04, 2.00). Our findings demonstrate that urinary 1-hydroxypyrene may be a useful biomarker for evaluating the role of PAHs exposure on hypomethylation of LINE-1 among coke oven workers and that smoking may be an important factor affecting hypomethylation of AhRR.

Coke oven emissions containing polycyclic aromatic hydrocarbons (PAHs) are predominant toxic constituents of particulate air pollution that have been linked to increased risk of lung cancer. Numerous epidemiological studies have suggested that oxidative DNA damage may play a pivotal role in the carcinogenic mechanism of lung cancer. Little is known about the effect of interaction between PAHs exposure and lifestyle on DNA oxidative damage. The study population is composed by coke oven workers (365) and water treatment workers (144), and their urinary levels of four PAH metabolites and 8-hydroxydeoxyguanosine (8-OHdG) were determined. Airborne samples of exposed sites (4) and control sites (3) were collected, and eight carcinogenic PAHs were detected by high-performance liquid chromatography. The median values of the sum of eight carcinogenic PAHs and BaP in exposed sites were significantly higher than control sites (P

Glomerulonephritis recurrence has emerged as one of the leading causes of allograft loss. We aimed to investigate the effect of living-related and deceased donation on the incidence of renal allograft glomerulonephritis and its effect on renal allograft survival.Adult renal allograft recipients with primary glomerulonephritis were enrolled. Transplantation date was from Feb 2004 to Dec 2015. Exclusion criteria included combined organ transplantation, structural abnormality, diabetic nephropathy, hypertension nephropathy, obstructive nephropathy, and primary uric acid nephropathy. The incidence of biopsy-proven allograft glomerulonephritis was compared between the living-related donor group and the deceased donor group. Graft survival was assessed with Kaplan-Meier method, and Cox proportional hazard model was used to evaluate the effect of posttransplant glomerulonephritis on graft outcome.There were 525 living-related donor kidney transplant recipients (LRKTx) and 456 deceased donor kidney transplant recipients (DDKTx) enrolled. The incidence of IgA nephropathy was 8.8% in the LRKTx group and 1.3% in the DDKTx group (P .001); the incidence of focal segmental glomerulosclerosis (FSGS) was 3.8% in the LRKTx group and 1.5% in the DDKTx group (P = .03). FSGS increased the risk of graft failure compared with non-FSGS (hazard ratio [HR], 3.703 [1.459-9.397]; P = .006). IgA nephropathy increased the risk of graft failure by over 5 times 5 years after kidney transplantation compared with non-IgA nephropathy, but it did not affect early allograft survival (HR for ≥5 years, 6.139; 95% CI, 1.766-21.345; P = .004; HR for 5 years, 0.385 [0.053-2.814]; P = .35).Higher incidence of IgA nephropathy and FSGS in renal allograft was observed in living-related donor kidney transplantation compared with deceased donor kidney transplantation. De novo or recurrent IgA nephropathy and FSGS impaired long-term renal allograft survival.

Previous studies in our laboratory demonstrated that Ring2 may affect DNA damage and repair through pathways other than through regulating the expression of the nucleotide excision repair protein. In a series of experiments using wild-type cell (16HBE and WI38) and small interfering RNA (siRNA) Ring2 cells exposed to benzo[a]pyrene (BaP), we evaluated the cell cycle and DNA damage. The benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE-DNA) adduct assay demonstrated that in vitro exposure to BaP increased DNA damage in a time- and dose-dependent manner in wild-type and siRNA Ring2 cells. Analysis of covariance showed that a decrease of Ring2 caused DNA hypersensitivity to BaP. Flow cytometry results and proliferating cell nuclear antigen levels indicated that inhibition of Ring2 attenuated the effect of BaP on S-phase arrest. Taken together, these data implied that the lower proportion of cells in the S phase induced by inhibition of Ring2 may play an important role in DNA hypersensitivity to BaP.

The vacuolar-type H+ adenosine triphosphatase (V-ATPase) plays an important role in cellular acidification and bone resorption by osteoclasts. However, the direct effect of bovine parathyroid hormone (bPTH) on V-ATPase has not yet been elucidated. The aim of the present study was to assess the effects of bPTH on V-ATPase and osteoclasts. Osteoclasts from bone marrow (BM)-derived monocytes of C57BL/6 mice were cultured with or without bPTH. The mRNA and protein expression levels of the V-ATPase a3-subunit and d2-subunit (by RT-qPCR and western blot analysis), V-ATPase activity (using the V type ATPase Activity Assay kit) and the bone resorption function of osteoclasts (by bone resorption assay) were examined following treatment with various concentrations of bPTH (0.1, 1.0, 10 and 100 ng/ml) alone or with bPTH and its inhibitor, bafilomycin A1. Furthermore, the expression of parathyroid hormone (PTH) receptors in osteoclasts was also detected. The results revealed that the mRNA and protein expression levels of V-ATPase a3-subunit and d2-subunit increased in a dose‑dependent manner, paralleling the level of bPTH present. In addition, an increase in the concentration of bPTH was accompanied by the increased resorption capability of osteoclasts, whereas bone resorption was inhibited in the presence of bafilomycin A1. In addition, we confirmed the existence of parathyroid hormone 1 receptor (PTH1R) in osteoclasts using three different methods (RT-qPCR, western blot analysis and immunofluorescence staining). We found that bPTH enhanced the bone resorption capability of osteoclasts by modulating the expression of V-ATPase subunits, intracellular acidification and V-ATPase activity. Thus, we propose that PTH has a direct effect on osteoblasts and osteoclasts, and that this effect is mediated through PTH1R, thus contributing to bone remodeling.

The aim of this study was to explore the expression and clinical significance of miR-494 and PTEN (phosphatase and tensin homologue deleted on chromosome ten) in non-small cell lung cancer (NSCLC). Immunohistochemistry for PTEN and in situ hybridization (ISH) for miR-494 were performed in 92 NSCLC tissues and 10 normal lung tissues to detect their expression, and correlation between their expression with clinical characteristics and prognosis was analyzed. The expression of miR-494 was significantly higher in NSCLC than in normal lung tissues (P = 0.004). The positive expression of PTEN protein in the lung carcinoma tissues was significantly lower than that in the normal lung tissues (P = 0.013), while the level of miR-494 expression was negatively correlated with PTEN expression (r = −0.577, P