RER-YOLO: improved method for surface defect detection of aluminum ingot alloy based on YOLOv5.

Aluminum ingot alloy is one of the commonly used materials in industrial production and intelligent manufacturing, whose quality directly affects the performance of aluminum processed products. Therefore, the inspection of surface defects of aluminum ingot alloy is extremely valuable for actual industrial engineering. Aiming at the issues of low detecting precision and the slowly processing rate thatexisted in the traditional target detection methods for aluminum ingot alloy dataset, the YOLOv5-based improvement model RER-YOLO is proposed. Firstly, the aluminum ingot alloy dataset is coped with the image pretreatment methods of rotation, translation, contrast and brightness transformations in a random combination so as to boost the capacity of generalization for model training. Secondly, a multi-scale characteristic extraction network block (Res2Net) is utilized to take the place of the C3 block in the previous YOLOv5 to augment the model's ability that can accurately extract rich features. Finally, an over-parameterization-based re-parameterized convolutional block is utilized in place of the 3×3 convolutional blocks in the Res2Net residual block and baseline model, enlarging the search space of the network and boosting the model's fitting ability while maintaining inference rate. The comparison experimental results demonstrate that the RER-YOLO reaches a mean average precision of 75.1% on the aluminum ingot alloy dataset, which is higher 4.9% than the conventional YOLOv5 and does not increase the inference delay. It also improves the detection accuracy by 12.7% for burr defects, which are fewer in number in the dataset and the defect features are difficult to extract. It can be seen that the presented model in this study has an important reference value towards detecting surface defects in aluminum ingot alloy.

Three-dimensional printing technique aids screw insertion into the sustentaculum tali of the internal fixation of intra-articular calcaneal fractures.

INTRODUCTION: Treating complex calcaneus fractures remains challenging. This study evaluated the influence of 3D printing and simulation on precision screw insertion into the calcaneus sustentaculum tali (ST). HYPOTHESIS: 3D printing and simulation improve the treatment for calcaneal fracture. PATIENTS AND METHODS: This retrospective cohort study included 85 patients admitted with 93 Sanders type II-IV intra-articular fractures from January 2015 to June 2020. Multi-slice computed tomography (MSCT) images were used in the conventional group, and MSCT data were used to construct a 3D model of the calcaneus to simulate screw insertion and verify parameter accuracy in the 3D group. RESULTS: The designed parameters (upward and backward oblique angles and screw-path length) were similar to the actual values in the 3D group (p=0.428,0.287,0.585) but not in the conventional group (p=0.01,0.002,0.023). The Maryland foot functional score, accuracy rate, and average screw number were higher and operative time was shorter in the 3D group (p=0.005,0.007,0.000,0.000). DISCUSSION: Preoperative simulation using the 3D printing model helped guide the screws into the ST more accurately, lending better-quality treatment for Sanders type II-IV calcaneal fractures. LEVEL OF PROOF: III; Retrospective case-control study.

Diosmin ameliorates renal fibrosis through inhibition of inflammation by regulating SIRT3-mediated NF-κB p65 nuclear translocation.

BACKGROUND: Renal fibrosis is considered an irreversible pathological process and the ultimate common pathway for the development of all types of chronic kidney diseases and renal failure. Diosmin is a natural flavonoid glycoside that has antioxidant, anti-inflammatory, and antifibrotic activities. However, whether Diosmin protects kidneys by inhibiting renal fibrosis is unknown. We aimed to investigate the role of Diosmin in renal interstitial fibrosis and to explore the underlying mechanisms. METHODS: The UUO mouse model was established and gavaged with Diosmin (50 mg/kg·d and 100 mg/kg·d) for 14 days. HE staining, Masson staining, immunohistochemistry, western blotting and PCR were used to assess renal tissue injury and fibrosis. Elisa kits were used to detect the expression levels of IL-1ß, IL-6, and TNF-α and the activity of SIRT3 in renal tissues. In addition, enrichment maps of RNA sequencing analyzed changes in signaling pathways. In vitro, human renal tubular epithelial cells (HK-2) were stimulated with TGF-ß1 and then treated with diosmin (75 µM). The protein and mRNA expression levels of SIRT3 were detected in the cells. In addition, 3-TYP (selective inhibitor of SIRT3) and SIRT3 small interfering RNA (siRNA) were used to reduce SIRT3 levels in HK-2. RESULTS: Diosmin attenuated UUO-induced renal fibrosis and TGF-ß1-induced HK-2 fibrosis. In addition, Diosmin reduced IL-1ß, IL-6, and TNF-α levels in kidney tissues and supernatants of HK-2 medium. Interestingly, Diosmin administration increased the enzymatic activity of SIRT3 in UUO kidneys. In addition, Diosmin significantly increased mRNA and protein expression of SIRT3 in vitro and in vivo. Inhibition of SIRT3 expression using 3-TYP or SIRT3 siRNA abolished the anti-inflammatory effects of diosmin in HK-2 cells. Enrichment map analysis by RNA sequencing indicates that the nuclear factor-kappa B (NF-κB) signaling pathway was inhibited in the Diosmin intervention group. Furthermore, we found that TGF-ß1 increased the nuclear expression of nuclear NF-κB p65 but had little significant effect on the total intracellular expression of NF-κB p65. Additionally, Diosmin reduced TGF-ß1-caused NF-κB p65 nuclear translocation. Knockdown of SIRT3 expression by SIRT3 siRNA increased the nuclear expression of NF-κB p65 and abolished the inhibition effect of Diosmin in NF-κB p65 expression. CONCLUSIONS: Diosmin reduces renal inflammation and fibrosis, which is contributed by inhibiting nuclear translocation of NF-κB P65 through activating SIRT3.

The Causal Effect of Obesity on the Risk of 15 Autoimmune Diseases: A Mendelian Randomization Study.

INTRODUCTION: Observational studies have shown that obesity is a risk factor for various autoimmune diseases. However, the causal relationship between obesity and autoimmune diseases is unclear. Mendelian randomization (MR) was used to investigate the causal effects of obesity on 15 autoimmune diseases. METHODS: MR analysis employed instrumental variables, specifically single-nucleotide polymorphisms associated with obesity measures such as body mass index (BMI), waist circumference, hip circumference, and waist-to-hip ratio. The study utilized UK Biobank and FinnGen data to estimate the causal relationship between obesity and autoimmune diseases. RESULTS: Genetically predicted BMI was associated with risk for five autoimmune diseases. The odds ratio per 1-SD increase in genetically predicted BMI, the OR was 1.28 (95% CI, 1.18-1.09; p < 0.001) for asthma, 1.37 (95% CI, 1.24-1.51; p < 0.001) for hypothyroidism, 1.52 (95% CI, 1.27-1.83; p < 0.001) for psoriasis, 1.22 (95% CI, 1.06-1.40; p = 0.005) for rheumatoid arthritis, and 1.55 (95% CI, 1.32-1.83; p < 0.001) for type 1 diabetes. However, after adjusting for genetic susceptibility to drinking and smoking, the correlation between BMI and rheumatoid arthritis was not statistically significant. Genetically predicted waist circumference, hip circumference, and waist and hip circumference were associated with 6, 6, and 1 autoimmune disease, respectively. CONCLUSION: This study suggests that obesity may be associated with an increased risk of several autoimmune diseases, such as asthma, hypothyroidism, psoriasis, rheumatoid arthritis, and type 1 diabetes.

Influencing factors of cardiac valve calcification (CVC) in patients with chronic kidney disease and the impact of CVC on long-term prognosis: a single-center retrospective study.

Objective: To investigate the effect of cardiac valve calcification (CVC) on the prognosis of patients with chronic kidney disease (CKD). Methods: A total of 343 CKD patients were retrospectively analyzed, and divided into two groups according to the presence or absence of cardiac valve calcification. All patients were followed until death, loss to follow-up, or the end point of the study (December 2021). Results: The incidence of CVC among the 343 CKD patients was 29.7%, including 21 cases of mitral valve calcification, 63 cases of aortic valve calcification, and 18 cases of mitral valve combined with aortic valve calcification. The incidence of CVC in CKD stages 1-2 was 0.3%, 5.2% in CKD stages 3-4, and 24.2% in CKD stage 5 (P < 0.05). Advanced age, higher serum albumin, higher cystatin C and lower uric acid levels were all associated with a higher risk of CVC. After six years of follow-up, 77 patients (22.4%) died. The causes of death were cardiovascular and cerebrovascular diseases in 36 cases (46.7%), infection in 29 cases (37.7%), gastrointestinal bleeding in nine cases (11.7%), and "other" in the remaining three cases (3.9%). A Kaplan Meier survival analysis showed that the overall survival rate of patients with CVC was lower than that of patients without CVC. Conclusion: The incidence of CVC, mainly aortic calcification, is high in patients with CKD. Advanced age, higher serum albumin and higher cystatin C levels were associated with a higher risk of CVC. Hyperuricemia was associated with a lower risk of CVC. The overall survival rate of patients with CVC was lower than that of patients without CVC.

LncRNA GAS5 as an Inflammatory Regulator Acting through Pathway in Human Lupus.

AIM: To investigate the contribution of GAS5 in the pathogenesis of SLE. BACKGROUND: Systemic Lupus Erythematosus (SLE) is characterized by aberrant activity of the immune system, leading to variable clinical symptoms. The etiology of SLE is multifactor, and growing evidence has shown that long noncoding RNAs (lncRNAs) are related to human SLE. Recently, lncRNA growth arrest-specific transcript 5 (GAS5) has been reported to be associated with SLE. However, the mechanism between GAS5 and SLE is still unknown. OBJECTIVE: Find the specific mechanism of action of lncRNA GAS5 in SLE. METHODS: Collecting samples of the SLE patients, Cell culture and treatment, Plasmid construction, and transfection, Quantitative real-time PCR analysis, Enzyme-linked immunosorbent assay (ELISA), Cell viability analysis, Cell apoptosis analysis, Western blot. RESULTS: In this research, we investigated the contribution of GAS5 in the pathogenesis of SLE. We confirmed that, compared to healthy people, the expression of GAS5 was significantly decreased in peripheral monocytes of SLE patients. Subsequently, we found that GAS5 can inhibit the proliferation and promote the apoptosis of monocytes by over-expressing or knocking down the expression of GAS5. Additionally, the expression of GAS5 was suppressed by LPS. Silencing GAS5 significantly increased the expression of a group of chemokines and cytokines, including IL-1ß, IL-6, and THFα, which were induced by LPS. Furthermore, it was identified the involvement of GAS5 in the TLR4-mediated inflammatory process was through affecting the activation of the MAPK signaling pathway. CONCLUSION: In general, the decreased GAS5 expression may be a potential contributor to the elevated production of a great number of cytokines and chemokines in SLE patients. And our research suggests that GAS5 contributes a regulatory role in the pathogenesis of SLE, and may provide a potential target for therapeutic intervention.

Analysis of the potential biological mechanisms of diosmin against renal fibrosis based on network pharmacology and molecular docking approach.

BACKGROUND: Interstitial fibrosis is involved in the progression of various chronic kidney diseases and renal failure. Diosmin is a naturally occurring flavonoid glycoside that has antioxidant, anti-inflammatory, and antifibrotic activities. However, whether diosmin protects kidneys by inhibiting renal fibrosis is unknown. METHODS: The molecular formula of diosmin was obtained, targets related to diosmin and renal fibrosis were screened, and interactions among overlapping genes were analyzed. Overlapping genes were used for gene function and KEGG pathway enrichment analysis. TGF-ß1 was used to induce fibrosis in HK-2 cells, and diosmin treatment was administered. The expression levels of relevant mRNA were then detected. RESULTS: Network analysis identified 295 potential target genes for diosmin, 6828 for renal fibrosis, and 150 hub genes. Protein-protein interaction network results showed that CASP3, SRC, ANXA5, MMP9, HSP90AA1, IGF1, RHOA, ESR1, EGFR, and CDC42 were identified as key therapeutic targets. GO analysis revealed that these key targets may be involved in the negative regulation of apoptosis and protein phosphorylation. KEGG indicated that pathways in cancer, MAPK signaling pathway, Ras signaling pathway, PI3K-Akt signaling pathway, and HIF-1 signaling pathway were key pathways for renal fibrosis treatment. Molecular docking results showed that CASP3, ANXA5, MMP9, and HSP90AA1 stably bind to diosmin. Diosmin treatment inhibited the protein and mRNA levels of CASP3, MMP9, ANXA5, and HSP90AA1. Network pharmacology analysis and experimental results suggest that diosmin ameliorates renal fibrosis by decreasing the expression of CASP3, ANXA5, MMP9, and HSP90AA1. CONCLUSIONS: Diosmin has a potential multi-component, multi-target, and multi-pathway molecular mechanism of action in the treatment of renal fibrosis. CASP3, MMP9, ANXA5, and HSP90AA1 might be the most important direct targets of diosmin.

Causal effect of polyunsaturated fatty acids on bone mineral density and fracture.

Background: Polyunsaturated fatty acids (PUFAs) are closely related to osteoporosis. To test their causal relationship, we conducted a Mendelian randomization (MR) analysis. Methods: We analyzed the causal relationship between four PUFAs measures, n-3 PUFAs (n-3), n-6 PUFAs (n-6), the ratio of n-3 PUFAs to total fatty acids (n-3 pct), and the ratio of n-6 PUFAs to n-3 PUFAs (n-6 to n-3), and five measures of osteoporosis, including estimated bone mineral density (eBMD), forearm (FA) BMD, femoral neck (FN) BMD, lumbar spine (LS) BMD, and fracture, using two-sample MR analysis. In order to verify the direct effect between PUFAs and BMD, we chose interleukin-6 (IL-6), tumor necrosis factor-ß (TNF-ß), and bone morphogenetic proteins 7 (BMP-7), three markers or cytokines strongly related to BMD, as possible confounding factors, and analyzed the possible causal relationships between them and PUFAs or BMD by MR. Inverse variance weighting (IVW), MR-Egger, weighted and weighted median were conducted. MR Pleiotropy RESidual Sum and Outlier (MR-PRESSO) and MR-Egger regression methods were used to evaluate the potential pleiotropy of instrumental variables (IVs) and outliers were identified by MR-PRESSO. Cochran's Q statistic was used to detect the heterogeneity among IVs. Leave-one-out sensitivity analysis was used to find SNPs that have a significant impact on the results. All results were corrected by the Bonferroni correction. Results: The IVW results showed that n-3 PUFAs (OR = 1.030, 95% CI: 1.013, 1.047, P = 0.001) and n-6 PUFAs (OR = 1.053, 95% CI: 1.034, 1.072, P < 0.001) were positively correlated with eBMD, while n-6 to n-3 (OR = 0.947, 95% CI: 0.924, 0.970, P < 0.001) were negatively correlated with eBMD. These casual relationships still existed after Bonferroni correction. There were positive effects of n-3 PUFAs on FA BMD (OR = 1.090, 95% CI: 1.011, 1.176, P = 0.025) and LS BMD (OR = 1.056, 95% CI: 1.011, 1.104, P = 0.014), n-3 pct on eBMD (OR = 1.028, 95% CI: 1.002, 1.055, P = 0.035) and FA BMD (OR = 1.090, 95% CI: 1.011, 1.174, P = 0.025), n-6 to n-3 on LS BMD (OR = 1.071, 95% CI: 1.021, 1.124, P = 0.005); negative effects of n-3 pct on fracture (OR = 0.953, 95% CI: 0.918, 0.988, P = 0.009) and n-6 to n-3 on FA BMD (OR = 0.910, 95% CI: 0.837, 0.988, P = 0.025). However, these causal effects all disappeared after Bonferroni correction (all P > 0.0025). None of IL-6, TNF-ß, and BMP-7 had a causal effect on PUFA and BMD simultaneously (all P > 0.05). Conclusion: Evidence from this MR study supports the genetically predicted causal effects of n-3, n-6, n-3 pct, and n-6 to n-3 on eBMD. In addition, n-3 not only associate with FA BMD and LS BMD through its own level and n-6 to n-3, but also link to fracture through n-3 pct.

Axial and frontal X-ray fluoroscopy technique of the sustentaculum tali can improve the accuracy of sustentacular screw placement.

INTRODUCTION: Calcaneal fractures, especially those involving the articular surface, should be anatomically reduced as much as possible. Fixing the fracture by placing a screw into the sustentaculum tali from the lateral side of the calcaneus is generally considered to be the key to successful surgery. However, due to the limited visibility during surgery, it is not easy to place screws into the sustentaculum tali accurately. The purpose of this study was to explore a new fluoroscopy method for the sustentaculum tali and verify the value of this method in improving screw placement accuracy. METHODS: In this study, a total of 42 human foot and ankle specimens were dissected and measured. The shape and position of the sustentaculum tali were observed, and the influence of adjacent bones on imaging findings was analysed. The axial and frontal X-ray fluoroscopy method to view the sustentaculum tali was formulated, and the appropriate projection angle through anatomical and image measurements was explored. Thirty specimens were randomly selected for screw placement, and the direction of the screw was dynamically adjusted under the new imaging method. The success rate of sustentacular screw placement was evaluated. RESULTS: The anteversion angles of the sustentaculum tali were 30.81 ± 2.21° and 30.68 ± 2.86° by anatomical and imaging measurements, respectively. There was no statistically significant difference in the anteversion angle between the two measurement methods. Harris heel views should be obtained at 30° to identify the sustentaculum tali on axial X-ray images. Frontal X-ray imaging was performed perpendicular to this projection angle. Through frontal and axial X-ray imaging, the position and shape of the sustentaculum tali can be clearly observed, and these factors are seldom affected by adjacent bones. Under the new fluoroscopy method, the screws were placed from the anterior region of the lateral wall of the calcaneus to the sustentaculum tali. A total of 60 screws were placed in the 30 specimens; of these, 54 screws were in good position, 2 screws penetrated the cortical bone, and 4 screws did not enter the sustentaculum tali. The success rate of sustentacular screw placement was 90% (54/60). CONCLUSIONS: Axial and frontal X-ray images of the sustentaculum tali can clearly show the shape of the structure, which improves sustentacular screw placement accuracy.

Environmental factors influencing the risk of ANCA-associated vasculitis.

Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a group of diseases characterized by inflammation and destruction of small and medium-sized blood vessels. Clinical disease phenotypes include microscopic polyangiitis (MPA), granulomatosis with polyangiitis (GPA), and eosinophilic granulomatosis with polyangiitis (EGPA). The incidence of AAV has been on the rise in recent years with advances in ANCA testing. The etiology and pathogenesis of AAV are multifactorial and influenced by both genetic and environmental factors, as well as innate and adaptive immune system responses. Multiple case reports have shown that sustained exposure to silica in an occupational environment resulted in a significantly increased risk of ANCA positivity. A meta-analysis involving six case-control studies showed that silica exposure was positively associated with AAV incidence. Additionally, exposure to air pollutants, such as carbon monoxide (CO), is a risk factor for AAV. AAV has seasonal trends. Studies have shown that various environmental factors stimulate the body to activate neutrophils and expose their own antigens, resulting in the release of proteases and neutrophil extracellular traps, which damage vascular endothelial cells. Additionally, the activation of complement replacement pathways may exacerbate vascular inflammation. However, the role of environmental factors in the etiology of AAV remains unclear and has received little attention. In this review, we summarized the recent literature on the study of environmental factors, such as seasons, air pollution, latitude, silica, and microbial infection, in AAV with the aim of exploring the relationship between environmental factors and AAV and possible mechanisms of action to provide a scientific basis for the prevention and treatment of AAV.

U-Net combined with multi-scale attention mechanism for liver segmentation in CT images.

BACKGROUND: The liver is an important organ that undertakes the metabolic function of the human body. Liver cancer has become one of the cancers with the highest mortality. In clinic, it is an important work to extract the liver region accurately before the diagnosis and treatment of liver lesions. However, manual liver segmentation is a time-consuming and boring process. Not only that, but the segmentation results usually varies from person to person due to different work experience. In order to assist in clinical automatic liver segmentation, this paper proposes a U-shaped network with multi-scale attention mechanism for liver organ segmentation in CT images, which is called MSA-UNet. Our method makes a new design of U-Net encoder, decoder, skip connection, and context transition structure. These structures greatly enhance the feature extraction ability of encoder and the efficiency of decoder to recover spatial location information. We have designed many experiments on publicly available datasets to show the effectiveness of MSA-UNet. Compared with some other advanced segmentation methods, MSA-UNet finally achieved the best segmentation effect, reaching 98.00% dice similarity coefficient (DSC) and 96.08% intersection over union (IOU).

Emerging role of air pollution in chronic kidney disease.

Chronic kidney disease (CKD), a global disease burden related to high rates of incidence and mortality, manifests as progressive and irretrievable nephron loss and decreased kidney regeneration capacity. Emerging studies have suggested that exposure to air pollution is closely relevant to increased risk of CKD, CKD progression and end-stage kidney disease (ESKD). Inhaled airborne particles may cause vascular injury, intraglomerular hypertension, or glomerulosclerosis through non-hemodynamic and hemodynamic factors with multiple complex interactions. The mechanisms linking air pollutants exposure to CKD include elevated blood pressure, worsening oxidative stress and inflammatory response, DNA damage and abnormal metabolic changes to aggravate kidney damage. In the present review, we will discuss the epidemiologic observations linking air pollutants exposure to the incidence and progression of CKD. Then, we elaborate the potential roles of several air pollutants including particulate matter and gaseous co-pollutants, environmental tobacco smoke, and gaseous heavy metals in its pathogenesis. Finally, this review outlines the latent effect of air pollution in ESKD patients undergoing dialysis or renal transplant, kidney cancer and other kidney diseases. The information obtained may be beneficial for further elucidating the pathogenesis of CKD and making proper preventive strategies for this disease.

Predictors of coronary artery calcification and its association with cardiovascular events in patients with chronic kidney disease.

OBJECTIVE: To investigate the predictors of coronary artery calcification (CAC) and its association with cardiovascular events (CVE) in patients with stage 3-5 chronic kidney disease (CKD). METHOD: Two hundred ninety CKD patients in our nephrology department were enrolled from 2018 to May 2019. The levels of matrix Gla protein (MGP) and interleukin 6 (IL-6) were measured via enzyme-linked immunosorbent assay (ELISA) method in 131 CKD patients of all. CAC was evaluated via computed tomography (CT). The covariate factors were analyzed by binary logistic regression analysis. We conducted the visits to explore the prevalence of CVE in 276 CKD patients, and covariate factors were analyzed by Cox proportional hazard model. RESULTS: The prevalence of CAC was up to 57.93%. We found that age, diabetes mellitus, hyperphosphatemia, dialysis duration, and the neutrophil-lymphocyte ratio (NLR) were positively associated with CAC in all patients. In 131 patients, we demonstrated that higher IL-6 and lower MGP levels were associated with CAC. A Cox proportional hazard model demonstrated that moderate to severe CAC was correlated with an increased risk for CVE [Hazard Ratio (HR): 7.250; 95% confidence interval (CI): 3.192-16.470], and a higher MGP level was associated with a reduced risk for CVE (HR: 0.340; 95% CI: 0.124-0.933). CONCLUSIONS: The prevalence of CAC in patients with CKD is a significant issue. Older age, hyperphosphatemia, dialysis duration, diabetes mellitus, IL-6, and the NLR are associated with CAC. In addition, higher MGP levels represent protective factor for CAC. Moderate to severe CAC, and lower MGP levels are associated with an increased risk for CVE. Abbreviations: AGEs: Advanced glycosylation end products; CAC: Coronary artery calcification; CACS: Coronary artery calcification score; Ca: Calcium; CI: confidence interval; CKD: Chronic kidney disease; CVE: Cardiovascular events; CT: Computed tomography; ELISA: Enzyme-linked immunosorbent assay; Hb: hemoglobin; HR: Hazard ratio; hs-CRP: high-sensitivity C-reactive protein; IL-6: Interleukin 6; iPTH: Intact parathyroid hormone; Mg: Magnesium; MGP: Matrix Gla protein; NF-κB: nuclear factor-kappa gene binding; NRL: Neutrophil-lymphocyte ratio; Runx2: Runt-related transcription factor 2; RRT: Renal replacement therapy; P: Phosphorus; Scr: Serum creatinine; TNF--alpha: Tumor necrosis factor--alpha; TC: Total cholesterol; TG: Triglyceride; VSMC: vascular smooth muscle cel.

Comparison of transradial coronary intervention for left main bifurcation disease using the new Braidin® slender 7 Fr sheath and a standard 6 Fr sheath.

OBJECTIVES: To compare the effectiveness and safety of the Braidin® slender 7 Fr sheath with a standard 6 Fr sheath for treating left main bifurcation disease. METHODS: From January 2017 to March 2019, 277 patients with left main bifurcation disease who underwent the transradial approach for percutaneous coronary intervention were divided into the slender 7 Fr sheath group (Braidin® slender 7 Fr sheath, n = 154) and standard 6 Fr sheath group (n = 123). Pathological features, surgical effect, and complications were evaluated. RESULTS: The rate of using the classic crush technique was significantly higher in the slender 7 Fr sheath group than in the standard 6 Fr sheath group. The slender 7 Fr sheath group had a significantly shorter operation time than the standard 6 Fr sheath group. There were no significant differences in the radial artery occlusion rate after surgery and at 1 month of follow-up between the groups. Multivariate logistic regression analysis showed that 6 Fr and Braidin slender 7 Fr sheaths did not predict radial artery occlusion. CONCLUSION: The Braidin slender 7 Fr sheath has a superior operative process and similar safety for the radial artery as that of the standard 6 Fr sheath for treating left main bifurcation disease.

Study on the mechanism and intervention strategy of sunitinib induced nephrotoxicity.

Sunitinib is an oral small molecular tyrosine kinase inhibitor that exhibits potent antiangiogenic and antitumor activity. Unfortunately, sunitinib kidney toxicity limits its clinical use. Renal injury caused by sunitinib treatment can not only lead to the failure of cancer treatment, but also jeopardizes the health and life of patients. Currently, there is no better intervention measure for renal injury caused by sunitinib therapy except reducing the dosage or stopping the medication. In this study, we learned from clinical case report that sunitinib can cause severe renal injury. Subsequently, we compiled the clinical trials data of sunitinib found that sunitinib can cause general renal damage. Based on this finding, we conducted a study on the mechanism of sunitinib-induced renal injury. The results showed that sunitinib can inhibit the survival of HK-2 cells (human tubule epithelial cells) in a dose- and time-dependent manner. The survival inhibition is mainly due to the activation apoptotic signaling pathway by sunitinib in HK-2 cells and induces apoptosis of HK-2 cells. Subsequently, we found that natural compound oxypeucedanin can significantly alleviate the apoptosis of HK-2 cells induced by sunitinib. Through clinical investigation and experimental study of sunitinib, we found that sunitinib can cause extensive renal damage by inducing apoptosis of renal tubular epithelial cells and natural compound oxypeucedanin is a potentially effective intervention for nephrotoxicity of sunitinib. Thus, our research will provide a theoretical basis for the future rational use of sunitinib and the search for appropriate interventions for sunitinib-induced kidney damage.

The synergistic action of phosphate and interleukin-6 enhances senescence-associated calcification in vascular smooth muscle cells depending on p53.

Cardiovascular calcification is associated with cardiovascular morbidity and mortality of patients with end-stage renal diseases (ESRD). Hyperphosphatemia and many of the inflammatory markers and mediators, including interleukin-6 (IL-6), are considered as the major risk factors of cardiovascular calcification. Although cellular senescence may be involved in cardiovascular calcification caused by phosphate overload and (or) IL-6 in patients with ESRD, less is known about the underlying mechanisms for phosphate- and IL-6-induced senescence-associated calcification of vascular smooth muscle cells (VSMCs). In the present study, we investigated the correlation between cellular senescence and vascular calcification induced by loading phosphate and (or) IL-6 in VSMCs. Our findings show that p53 plays a major role in senescence-associated vascular calcification induced by phosphate overload. IL-6 induces senescence-associated calcification in VSMCs depending upon activation of the IL-6/soluble IL-6 receptor (sIL-6R)/signal transducer and activator of transcription 3 (STAT3)/p53/p21 pathway. We demonstrate that the synergistic action of phosphate overload and IL-6 enhances senescence-associated calcification in a p53-dependent manner and is inhibited by an anti-aging agent (resveratrol) in a dose-dependent manner.

Association study of TRAP1 gene polymorphisms with susceptibility and glucocorticoids efficacy of systemic lupus erythematosus.

New functions of tumor necrosis factor receptor-associated protein 1 (TRAP1) have been investigated recently. This study explored if TRAP1 gene polymorphisms in patients with systemic lupus erythematosus (SLE) are associated with disease susceptibility and the efficacy of glucocorticoids (GCs). A case control study was performed to explore the association between TRAP1 gene polymorphisms and susceptibility to SLE, then the SLE patients included in the case control study were followed to investigate the relationship between TRAP1 gene polymorphisms and efficacy of GCs. We also compared the improvement in health related quality of life (HRQOL) of patients among different genotypes of TRAP1 gene. The Benjamini-Hochberg (BH) method was used to correct for multiple comparison. In case control study, the significant association between rs8055172 and the susceptibility to SLE was discovered in the dominant model (p = 3.54 × 10-7), which is further supported by the different distributions of haplotype TT and TC of rs2072379 and rs8055172 (p = 4.26 × 10-4 and p = 6.93 × 10-9). In the dominant model, rs3751842 and rs1639150 may be associated with fever of SLE patients (p = 0.035 and p = 0.028), while rs2072379 and rs12597773 related to oral ulcers (p = 0.021) and hematologic disorder (p = 0.035) respectively. In the follow-up study, rs6500552 showed a significant relationship with the efficacy of GCs in SLE patients in the dominant model (p = 0.004). Besides, rs3794701 was associated with the improvement in role-emotional (RE) of SLE patients in dominant model (p = 0.029). The results supported that TRAP1 gene polymorphisms may be associated with susceptibility to SLE and efficacy of GCs in SLE patients.

Identification of long non-coding RNAs GAS5, linc0597 and lnc-DC in plasma as novel biomarkers for systemic lupus erythematosus.

Despite increasing evidence that long non-coding RNAs (lncRNAs) widely take part in human diseases, the role of lncRNAs in systemic lupus erythematosus (SLE) is largely unknown. In this study, we performed a two-stage study to explore the plasma levels of five lncRNAs (GAS5, linc0949, linc0597, HOTAIRM1 and lnc-DC) and their potential as SLE biomarkers. Compared with healthy controls, plasma levels of GAS5 and lnc-DC were significantly decreased (P < 0.001 and P = 0.002, respectively) while linc0597 were overexpressed in SLE patients (P < 0.001). When SLE patients were divided into SLE without nephritis and lupus nephritis (LN), the levels of lnc-DC were significantly higher in LN compared with SLE without nephritis (P = 0.018), but no significant difference in levels of GAS5 and linc0597 were found between LN and SLE without nephritis; plasma linc0949 level showed no significant difference in all comparisons. Further evaluation on potential biomarkers showed that GAS5, linc0597 and lnc-DC may specifically identify patients with SLE, the combination of GAS5 and linc0597 provided better diagnostic accuracy; lnc-DC may discriminate LN from SLE without nephritis. In summary, GAS5, linc0597 and lnc-DC in plasma could be potential biomarkers for SLE.