Search

This research applied two suppression technologies of atomizing dust suppression (ADS) and spraying dust suppression (SDS) to eliminate fugitive dust emitted from coal stockpiles and further investigated their optimal operating parameters. In field tests, the mass concentrations of TSP, PM10, and PM2.5 were simultaneously measured at both upwind and downwind sites of a simulated coal stockpile to determine the suppression efficiency of fugitive dust. High concentrations of fugitive dust were observed under a strong wind speed of 10 m/s, particularly for particle sizes larger than 7 μm. Overall, the suppression efficiencies of fugitive dust by ADS (75.50–88.17 %) were always higher than those by SDS (70.70–84.50 %). Fine mist atomized by ADS covered a wider surface area of the coal stockpiles and captured more dust in the air than SDS. The suppression efficiencies of fugitive dust for intermittent watering (82.81 %) were higher than those for continuous watering (77.75 %). Intermittent watering could maintain a protective moisture layer over the entire surface of coal stockpiles, thus extending the drying time of moisture from the coal stockpiles. The optimal operating parameter for ADS was intermittent atomizing at an angle of 30°, while that for SDS was intermittent spraying at an angle of 45°.

Background Diabetes has a pronounced effect on the peripheral vasculature. The accumulation of advanced glycation end products (AGEs) is regarded as the crucial mechanism responsible for vascular damage in diabetes, but it is not easy to be avoided from food. In this study, we aimed to investigate the effects of an oral absorbent, AST-120, on the accumulation of AGEs and changes in blood flow recovery in diabetic mice. Methods The mice were divided into four groups, wild-type (WT) mice without treatment, WT mice treated with 5% AST-120 mixed into pulverized chow, streptozotocin-induced diabetes mellitus (DM) mice, and DM mice treated with 5% AST-120. Six weeks after hind-limb ischemia surgery, blood flow reperfusion, histology, plasma AGE, and cytokine were examined. Bone marrow cells were cultured and derived into macrophages to evaluate the effects of AGEs on macrophage polarization. Results Plasma AGEs were significantly increased in diabetic mice. AST-120 could bind to AGEs and reduced their plasma concentrations. Histological analysis revealed fewer collateral vessels with corresponding impairment of blood flow recovery in diabetic mice. In these mice, AGE-positive and AGE receptor-positive macrophages were numerous in ischemic limbs compared with non- diabetic mice. In diabetic mice, macrophages in ischemic tissues demonstrated greater M1 polarization than M2 polarization; this pattern was reversed in the AST-120 treatment group. The change in macrophage polarization was associated with the corresponding expression of pro-inflammatory cytokines in the ischemic tissues. In cell cultures, AGEs triggered the transformation of bone marrow-derived macrophages into the M1 phenotype. The alterations in the polarization of macrophages were reversed after treatment with AST-120. Conclusions Oral administration of AST-120 decreased the serum levels of AGEs in diabetic mice and improved neovascularization of ischemic limbs. This benefit may be due to, at least partially, the alterations in macrophage polarization and the associated changes in inflammatory cytokines.

Recent works on the machine learnings designed for cuffless blood pressure (BP) estimation based on measured photoplethysmogram (PPG) waveforms are reviewed by this study, with future trends of the related technology developments distilled. This review starts with those based on the conventional pulse wave velocity (PWV) theory, by which few equations are derived to calculate BPs based on measured pulse arrival times (PATs) and/or pulse transit time (PTT). Due to the inadequacy of PATs and PPTs to characterize BP, some works were reported to employ more features in PPG waveforms to achieve better accuracy. In these works, varied machine learnings were adopted, such as support vector machine (SVM), regression tree (RT), adaptive boosting (AdaBoost), and artificial neural network (ANN), etc., resulting in satisfactory accuracies based on a large number of data in the databases of Queensland and/or MIMIC II. Most recently, a few studies reported to utilize the deep learning machines like convolution neural network (CNN), recursive neural network (RNN), and long short-term memory (LSTM), etc., to handle feature extraction and establish models integrally, with the aim to cope with the inadequacy of pre-determined (hand-crafted) features to characterize BP and the difficulty of extracting pre-determined features by a designed algorithm. Therefore, the deep learning opens an opportunity of achieving much better BP accuracy by using a single PPG sensor. Favorable accuracies have been resulted by these few studies in comparison with prior works. Finally, future research efforts needed towards successful commercialization of the cuffless BP sensor are distilled.

Inflammation of the vascular microenvironment modulates distinct types of vascular cells, and plays important roles in promoting atherosclerosis, stenosis/restenosis, and vascular-related diseases. Nik-related kinase (Nrk), a member of the Ste20-type kinase family, has been reported to be selectively expressed in embryonic skeletal muscle. However, whether Nrk is expressed in adult vascular smooth muscle, and if it influences intimal hyperplasia is unclear. Here, we found that Nrk is abundantly expressed in cultured vascular smooth muscle cells (VSMC) and mouse arterial intima. Treatment of mouse VSMCs with lipopolysaccharide (LPS) or platelet-derived growth factor significantly reduced Nrk expression. In addition, expression of Nrk was significantly reduced in regions of neointimal formation caused by guide-wire carotid artery injuries in mice, as well as in human atherosclerotic tissues, when compared to normal vessels. We identified that expression of matrix metalloproteinases (MMP3, MMP8 and MMP12) and inflammatory cytokines/chemokines (CCL6, CCL8, CCL11, CXCL1, CXCL3, CXCL5 and CXCL9) are synergistically induced by Nrk siRNA in LPS-treated mouse VSMCs. Moreover, we found that resveratrol significantly impaired LPS- and Nrk siRNA-induced expression of MMP3, CCL8, CCL11, CXCL3 and CXCL5. These results suggested that Nrk may play important roles in regulating pathological progression of atherosclerosis or neointimal- hyperplasia-related vascular diseases.

Objective: Most patients with spinal cerebrospinal fluid (CSF) leakage require an epidural blood patch (EBP); however, the response to treatment is varied. This study aimed to compare the MRI findings at follow-up between EBP effective and non-effective groups and to identify imaging findings that predict EBP treatment failure. Methods: We retrospectively reviewed 48 patients who received EBP treatment for spinal CSF leakage. These patients were stratified into two groups: EBP effective (n = 27) and EBP non-effective (n = 21) using the results of the 3 month MRI as the end point. Results: Compared to the EBP non-effective group, the patients in the EBP effective group had a lower spinal CSF leakage number (2.67 vs 12.48; p = 0.001), lower spinal epidural fluid accumulation levels (3.00 vs 7.48; p = 0.004), brain descend (11.11% vs 38.10%; p = 0.027), pituitary hyperemia (18.52% vs 57.14%; p = 0.007), and decreased likelihood of ≥three numbers of spinal CSF leakage (25.93% vs 90.48%; p = 0.001) in the post-EBP MRI. Clinical non-responsiveness (OR: 57.84; 95% CI: 3.47–972.54; p = 0.005) and ≥three numbers of spinal CSF leakage (OR: 15.13; 95% CI: 1.45–159.06; p = 0.023) were associated with EBP failure. Between these variables, ≥three numbers of spinal CSF leakage identified using the post-EBP MRI demonstrated greater sensitivity in predicting EBP failure compared to clinical non-responsiveness (90.48% vs 61.9%). Conclusion: The number of spinal CSF leakage identified using the post-EBP MRI with a cut-off value of three is an effective predictor of EBP failure. Advances in knowledge: Compared to clinical responsiveness, the post-EBP MRI provided a more objective approach to predict the effectiveness of EBP treatment in patients with spinal CSF leakage.

Background No randomized controlled trials evaluating metformin therapy efficacy in patients with type 2 diabetes mellitus (DM) and acute coronary syndrome (ACS) have been reported. We aimed to examine the mortality benefit of metformin therapy in patients with type 2 DM and ACS, compared with non-metformin anti-diabetes agents users. Methods Data were extracted from the prospective nationwide ACS-DM Taiwan Society of Cardiology registry. Propensity score (PS) matching on baseline characteristics and treatment measures was performed for metformin versus non-metformin users. The Cox proportional hazards model was used to compare mortality outcomes among the PS-matched cohort as the primary analysis. The Cox proportional hazards models adjusting for all pre-determined covariates and quintiles of the PS among the overall population were performed as the secondary analyses. Results Of 1157 patients with type 2 DM and ACS receiving anti-diabetes agents, 78 patients (6.7%) died over the 2-year follow-up period. After PS matching, 318 metformin users were matched with 318 non-metformin users. Metformin users had a lower all-cause mortality rate (adjusted hazard ratio [aHR] 0.50, 95% confidence interval [CI] 0.26–0.95) in the primary analysis. The survival benefit of metformin therapy was consistent in the secondary analyses (aHR 0.30, 95% CI 0.17–0.54 while adjusting for all pre-determined covariates, and aHR 0.34, 95% CI 0.19–0.59 while adjusting for quintiles of the PS). Conclusions Among patients with type 2 DM and ACS, metformin was associated with lower all-cause mortality. However, a detrimental effect of any of the comparators could not be excluded.

Restenosis remains a significant problem after angioplasty of hemodialysis vascular access. Both experimental and clinical studies have shown a protective effect of antioxidants against post-angioplasty restenosis. A prospective, randomized, feasibility study was conducted to investigate the effect of ascorbic acid to prevent restenosis. Ninety-three hemodialysis patients were randomized into three groups after angioplasty: placebo (n = 31), 300 mg ascorbic acid (n = 31), and 600 mg ascorbic acid (n = 31), treated intravenously 3 times per week for 3 months. Eighty-nine completed the clinical follow-up, and 81 had angiographic follow-up. In the angiographic follow-up, the mean (stand deviation) late loss of luminal diameter for the placebo, 300 mg, and 600 mg groups were 3.15 (1.68) mm, 2.52 (1.70) mm (P = 0.39 vs. placebo group), and 1.59 (1.67) mm (P = 0.006, vs. placebo group), with corresponding angiographic binary restenosis of 79%, 67% (P = 0.38 vs. placebo group), and 54% (P = 0.08 vs. placebo group). The post-interventional primary patency rates at 3 months were 47%, 55% (P = 0.59 vs. placebo group), and 70% (P = 0.18 vs. placebo group) for placebo, 300 mg, and 600 mg groups. Our results demonstrated that intravenous 600 mg ascorbic acid was a feasible therapy and might attenuate restenosis after angioplasty; however, its effect on post-interventional primary patency was modest.

Hyperglycemia and inflammation, with their augmented interplay, are involved in cases of stroke with poor outcomes. Interrupting this vicious cycle thus has the potential to prevent stroke disease progression. Tumor necrosis factor-α (TNF-α) is an emerging molecule, which has inflammatory and metabolic roles. Studies have shown that TNF-α receptor inhibitor R-7050 possesses neuroprotective, antihyperglycemic, and anti-inflammatory effects. Using a rat model of permanent cerebral ischemia, pretreatment with R-7050 offered protection against poststroke neurological deficits, brain infarction, edema, oxidative stress, and caspase 3 activation. In the injured cortical tissues, R-7050 reversed the activation of TNF receptor-I (TNFRI), NF-κB, and interleukin-6 (IL-6), as well as the reduction of zonula occludens-1 (ZO-1). In the in vitro study on bEnd.3 endothelial cells, R-7050 reduced the decline of ZO-1 levels after TNF-α-exposure. R-7050 also reduced the metabolic alterations occurring after ischemic stroke, such as hyperglycemia and increased plasma corticosterone, free fatty acids, C reactive protein, and fibroblast growth factor-15 concentrations. In the gastrocnemius muscles of rats with stroke, R-7050 improved activated TNFRI/NF-κB, oxidative stress, and IL-6 pathways, as well as impaired insulin signaling. Overall, our findings highlight a feasible way to combat stroke disease based on an anti-TNF therapy that involves anti-inflammatory and metabolic mechanisms.

Background Hypertrophic cardiomyopathy (HCM), affecting 0.2% of the population, is the leading cause of sudden cardiac arrest (SCA). Incident atrial fibrillation (AF) is associated with an increased risk of SCA in general population. To determine whether AF is associated with an increased risk of SCA in patients with HCM. Methods This nationwide cohort study analyzed data from Registry for Catastrophic Illness, which encompassed almost 100% of the patients with HCM in Taiwan from 1996 to 2013. Follow-up and data analysis ended December 31, 2013. The main outcome was physician-adjudicated SCA, defined as death from a sudden, pulseless condition presumed due to a ventricular tachyarrhythmia. The secondary outcome was non-sudden cardiac death (NSCD), which was heart failure death, stroke death and non-HCM related death. We used Cox proportional hazards models to assess the association between AF and SCA/NSCD, adjusting for baseline demographic and cardiovascular risk factors. Findings A total 10,910 subjects participated in this study with mean age of 62 years. Among enrolled subjects, 1,169 (10.7%) developed AF, which was independently associated with elder age, female sex, and history of heart failure (HF) hospitalization. During follow-up (median, 8.5 years and 2th to 7th interquartile range, 3.6 to 16.5 years), 371 SCA (166 in AF and 205 in non-AF group) and 797 NSCD (417 in AF and 380 in non-AF group) events occurred. The crude incidence rates of SCA were 12.45/1000 person-years (with AF) and 3.57/1000 person-years (without AF). The crude incidence rates for NSCD were 31.29/1000 person-years (with AF) and 6.63/1000 person-years (without AF). The multivariable hazard ratios (HRs) (95% CI) of AF for SCA and NSCD were 3.633 (2.756–4.791) and 2.086 (1.799–2.418), respectively. Furthermore, among the etiologies of NSCD, subjects with AF was at most risk of stroke-related death (HR, 6.609; 95% CI, 3.794–9.725). Interpretation Incident AF is associated with an increased risk of SCA and NSCD in the HCM population. Early detection of AF may provide more comprehensive risk stratification of SCD in HCM population. Because of underuse of oral anticoagulants and the absence of primary prevention ICD therapy in our cohort, the application of our findings was limited for the general HCM population in the current clinical practice. Funding None

Background: Angioplasty-related vessel rupture is a common complication of interventions. The effect of covered stents to treat venous rupture has been evaluated in smaller series, but should be further evaluated. Objective: To report the immediate outcomes and patency rates of a covered stent to rescue angioplasty-related venous rupture of hemodialysis vascular access. Methods: From January 2013 to December 2018, 113 procedures complicated with vessel ruptures were retrospectively analyzed from a prospectively collected database of 8146 hemodialysis access interventions. The strategies to salvage vessel ruptures were based on the discretion of the treating physicians. Follow-up outcomes were obtained via review of the angiographic images, procedural notes, and medical and dialysis records within 12 months after the index procedures. Results: A total of 52 vessel ruptures (21 fistulas, 31 grafts) salvaged by using Viabahn covered stents were enrolled. Vessel ruptures developed in 28 (53.8%) thrombectomy procedures. Device success was achieved in all procedures (100%) and clinical success was achieved in 50 (96.2%). The primary patency of the stent area was 66.0% at 6 months and 50.0% at 12 months. The primary patency of the entire access circuit was 27.4% at 6 months and 16.0% at 12 months. The most common cause of access circuit primary patency loss was thrombotic occlusion for graft accesses and restenosis at stent area for native accesses. Eleven vascular accesses were abandoned within 12 months after vessel ruptures, and the secondary patency rate of the entire access circuit was 78.0% at 12 months. Conclusions: Treatment of angioplasty-induced vessel rupture of hemodialysis vascular accesses by using Viabahn covered stents has good immediate outcomes and patency results at the stent area. Nonetheless, the patency rate of entire access circuit was still below the threshold recommended by guidelines.

Anesthetics, particularly volatile anesthetics, have been shown to impair glucose metabolism and cause hyperglycemia, closely linking them with mortality and morbidity as related to surgery. Beyond being an anesthetic used for general anesthesia and sedation, intravenous hypnotic propofol displays an effect on glucose metabolism. To extend the scope of propofol studies, its effects on glucose metabolism were evaluated in male Sprague-Dawley rats of various ages. Unlike chloral hydrate and isoflurane, propofol had little effect on basal glucose levels in rats at 2 months of age, although it did reduce chloral hydrate- and isoflurane-induced hyperglycemia. Propofol reduced postload glucose levels after either intraperitoneal or oral administration of glucose in both 7- and 12-month-old rats, but not those at 2 months of age. These improved effects regarding propofol on glucose metabolism were accompanied by an increase in insulin, fibroblast growth factor-21 (FGF-21), and glucagon-like peptide-1 (GLP-1) secretion. Additionally, an increase in hepatic FGF-21 expression, GLP-1 signaling, and FGF-21 signaling, along with a decrease in endoplasmic reticulum (ER) stress, were noted in propofol-treated rats at 7 months of age. Current findings imply that propofol may turn into insulin-sensitizing molecules during situations of existing insulin resistance, which involve FGF-21, GLP-1, and ER stress.

Ischemic stroke provokes an inflammatory response concurrent with both sympathetic nervous system activation and hyperglycemia. Currently, their crosstalk and consequences in stroke outcomes are of clinical attraction. We have provided experimental evidence showing the suppressive effects of the nonselective &beta, adrenoreceptor antagonist propranolol on hyperglycemia, inflammation, and brain injury in a rat model experiencing cerebral ischemia. Pretreatment with propranolol protected against postischemic brain infarction, edema, and apoptosis. The neuroprotection caused by propranolol was accompanied by a reduction in fasting glucose, fasting insulin, glucose tolerance impairment, plasma C-reactive protein, plasma free fatty acids, plasma corticosterone, brain oxidative stress, and brain inflammation. Pretreatment with insulin alleviated&mdash, while glucose augmented&mdash, postischemic brain injury and inflammation. Additionally, the impairment of insulin signaling in the gastrocnemius muscles was noted in rats with cerebral ischemia, with propranolol improving the impairment by reducing oxidative stress and tumor necrosis factor-&alpha, signaling. The anti-inflammatory effects of propranolol were further demonstrated in isoproterenol-stimulated BV2 and RAW264.7 cells through its ability to decrease cytokine production. Despite their potential benefits, stroke-associated hyperglycemia and inflammation are commonly linked with harmful consequences. Our findings provide new insight into the anti-inflammatory, neuroprotective, and hypoglycemic mechanisms of propranolol in combating neurodegenerative diseases, such as stroke.

Background: After angioplasty, veins are more prone to intimal hyperplasia than arteries. Veins tend to produce less nitric oxide (NO), which could lead to endothelial dysfunction. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthase and contributes to cardiovascular disease. In humans, dimethylarginine dimethylaminohydrolase 1 (DDAH1) is the major enzyme for ADMA degradation. In this study, we aim to determine whether venous intimal hyperplasia in hemodialysis (HD) vascular access is influenced by common polymorphisms in the DDAH1 genes. Methods: This is a prospective observational cohort study. A total of 473 HD patients referred for the angioplasty of vascular access were enrolled. There were 190 arteriovenous grafts (AVG) and 283 arteriovenous fistulas (AVF). The follow-up lasted for 2 years after the interventions. Seven single nucleotide polymorphisms (SNPs) in DDAH1 were genotyped and ADMA were measured at baseline. The primary outcome was restenosis after angioplasty. Results: Among the 7 SNPs, plasma ADMA levels were significantly different in DDAH1 rs233112 (GA + GG vs. AA, 0.86 ± 0.23 vs. 0.82 ± 0.19 μM, p = 0.03) and rs1498373 (CT + TT vs. CC, 0.87 ± 0.23 vs. 0.82 ± 0.20 μM, p = 0.02) genotypes. The AVF group with GG + GA genotype of rs233112 and CT + TT genotype of rs1498373 had higher risks of early restenosis at 3 months. In the AVG group, only GG + GA genotype of rs233112 was associated with early restenosis. A combined analysis of AVG and AVF groups showed that patients with rs233112 GA + GG genotype and rs1498373 CT + TT genotype had higher risks of early restenosis (both p < 0.001). The multivariate analysis results showed that the association of these genotypes with early restenosis is independent of clinical, access, or biochemical factors. Conclusions: Our findings suggest that certain DDAH1 polymorphisms modulate circulating ADMA levels and are associated with venous intimal hyperplasia.

Recently, multiple ( $k, n$ ) region-incrementing VCSs (RIVCSs) have been proposed that can gradually reconstruct secrets in a single image. In ( $k, n$ )-RIVCS, the secret image is subdivided into multiple regions in such a way that any $t$ shadow images, where $k \le t \le n$ , can be used to reveal the secret in the ( $t-k+1$ )th region. This region-incrementing property provides progressive decoding. However, the regions in previous RIVCSs are disjointed: no two regions have overlapping areas. In this paper, we discuss a ( $k, n$ ) region-in-region progressive VCS (RPVCS). Our ( $k, n$ )-RPVCS has ( $n-k+1$ ) secrecy-level regions, and each region can be located within any previous region. This new type of region allocation not only provides more areas in which to hide the secret compared with the non-overlapping regions in RIVCS but also provides different presentation methods in progressive decoding.

Renal ischemia/reperfusion (I/R) is an alternation of renal hemodynamics, which results in diverse postischemic responses and eventually acute kidney injury. Although renal ischemic preconditioning (IPC) is known to protect the kidney from I/R injury, the precise renoprotective mechanisms are not completely understood. The multiple renoprotective effects of IPC underscore the importance in understanding molecular mechanisms and the targets of action involved. This study aimed to identify the biochemical changes in renal I/R injury and investigate the renoprotective mechanisms of IPC. Herein, renal I/R was produced in adult male Sprague-Dawley rats through the bilateral ligation of renal pedicles for 45 min, followed by reperfusion for 24 h. For the IPC group, rats were subjected to three cycles of 2-min ischemia, followed by a 5-min reperfusion, 15 min prior to renal I/R. Our data confirmed the beneficial effects that IPC has on renal I/R injury. IPC-mediated renoprotection was associated with the resolution of oxidative stress, inflammation, apoptosis, and hyperglycemia. Among the numerous signaling molecules involved in the renoprotective mechanisms of IPC, an elevated protein expression of Nrf2, HO-1, LC3 II conversion, along with Atg12 and protein phosphorylation of AMPK, as well as a decreased protein phosphorylation of ERK, p38 MAPK, and Akt and NF-κB DNA binding activity were identified. Importantly, the post renal I/R overproduction of counter-regulatory hormones, impaired hepatic insulin action, and augmented hepatic gluconeogenesis were improved through IPC. As counter-regulatory hormones have been implicated in the induction of oxidative stress, inflammation, apoptosis, impaired insulin action, hyperglycemia, and tissue destruction, our findings suggest that counter-regulatory hormones may well be valuable targets of IPC for combatting renal I/R injury. © 2018 IUBMB Life, 71(3):321-329, 2019.

Percutaneous transluminal angioplasty (PTA) is widely used as the primary treatment for dialysis vascular access dysfunction. Nonetheless, many patients develop early occlusion after angioplasty. Thus, we investigated the role of thrombophilia in access occlusion within 30 days of angioplasty. This case–control study included patients who underwent PTA for dialysis vascular access dysfunction. Patients who experienced occlusion within 30 days of angioplasty were included in the case group and those without occlusion for at least 30 days after angioplasty were included in the control group. All patients were tested for protein C, protein S, antithrombin III, lupus anticoagulant, and anticardiolipin antibodies. From February to October 2015, 462 patients underwent PTA for dialysis vascular access dysfunction. Forty-one patients (8.9%) had early occlusion within 30 days of angioplasty. The case group had more graft accesses (73 vs. 31%, P

Background: Stent graft is effective for management of balloon-angioplasty-related complications in hemodialysis access. These complications include post-angioplasty venous rupture, dissection/recoil, and acute formation of pseudoaneurysm. Case report: We report a stent-graft complication that caused immediate acute arterial insufficiency by external compression. An 84-year-old woman presented with acute arteriovenous graft thrombosis. During percutaneous balloon thrombectomy, a stent graft was placed because of persistent recoil and mural thrombus, but the flow into the arteriovenous graft immediately ceased. External compression of the brachial artery was observed. A nitinol self-expandable stent was deployed in the brachial artery to oppose the external compression. The flow in the arteriovenous graft was recovered. Conclusion: This case demonstrates the possibility of arterial compression by an adjacent venous stent graft, especially in a patient with a thin habitus and a brachial–brachial arteriovenous graft. Detailed identification of the outflow vein anatomy before stent implantation is mandatory to avoid such a complication.

Mounting evidence suggests that physical exercise shows health benefits in a range of diseases, including psychiatric disorders. Perinatal opioid exposure produces neurobehavioral abnormality, which includes depression symptoms, in patients and their offspring following chronic use of buprenorphine, a mixed agonist/antagonist with a high affinity to opioid receptors, for pain control. Previously, we demonstrated that prenatal buprenorphine exposure in pregnant Sprague-Dawley rats starting from gestation day 7 and lasting for 14 days caused the development of depression-like phenotypes in pups at postnatal day 21. Using the same prenatal buprenorphine exposure model, we further demonstrated that a 4-week course of moderate treadmill exercise conducted on pups starting from postnatal day 22 improved depression-like neurobehaviors. Prenatal buprenorphine exposure-induced neurobehavioral changes were accompanied by reductions of neuronal survival, neural stem cell-associated genes, plasma level of brain-derived neurotrophic factor (BDNF) and serotonin, phosphorylated tropomyosin-related kinase receptor type B (TrkB), phosphorylated extracellular signal-regulated kinase (ERK), PKA activity, phosphorylated cAMP response element-binding protein (CREB), and CREB DNA binding activity, as well as elevation of repressor element-1 silencing transcription factor (REST), oxidative stress, and inflammatory responses. Those changes in parameters of plasma and brain were improved by treadmill exercise. In conclusion, the findings of the current study suggest that a non-pharmacological option, i.e., moderate treadmill exercise, alleviated the development of depression-like neurobehaviors by resolving the oxidative and inflammatory burden as well as by enhancing neurochemical and neuroendocrine signaling.

CKD is an independent risk factor for cardiovascular disease (CVD). The accumulation of uremic toxins in CKD induces oxidative stress and endothelial dysfunction. MicroRNA-92a (miR-92a) is induced by oxidative stress in endothelial cells (ECs) and involved in angiogenesis and atherosclerosis. We investigated a role for oxidative stress–responsive miR-92a in CKD. Our study of patients at three clinical sites showed increased serum miR-92a level with decreased kidney function. In cultured ECs, human CKD serum or uremic toxins (such as indoxyl sulfate), compared with non-CKD serum, induced the levels of miR-92a and suppressed the expression of miR-92a targets, including key endothelial-protective molecules. The antioxidant N-acetylcysteine inhibited these vasculopathic properties. In rats, adenine-induced CKD associated with increased levels of miR-92a in aortas, serum, and CD144+ endothelial microparticles. Furthermore, CD144+ microparticles from human uremic serum contained more miR-92a than those from control serum. Additional analysis showed a positive correlation between serum levels of miR-92a and indoxyl sulfate in a cohort of patients with ESRD undergoing hemodialysis. Collectively, our findings suggest that the uremic toxins accumulated in CKD can upregulate miR-92a in ECs, which impairs EC function and predisposes patients to CVD.

Obesity is associated with a wide range of chronic diseases, including cancer. It has been noted that the integration of metabolic mechanisms in obese patients may predispose them to suffer from cancer incidence and its progression. Thus, a better understanding of metabolic alterations in obesity, along with the development of feasible therapeutic approaches for intervention, are theoretically relevant to the prevention and treatment of cancer malignancy. Using a syngeneic tumor model involving Lewis Lung Carcinoma (LLC) cells and C57BL/6 mice fed with a high fat diet, obesity was found to be associated with dysregulated glucose and glutamine metabolism, inflammation, along with platelet activation and the promotion of tumor growth. Tumor-bearing lowered glucose levels while moderately increasing inflammation, platelet activation, and glutamine levels. The antiplatelet drug aspirin, mitigated tumor growth in obese mice, paralleled by a decrease in systemic glucose, insulin, inflammation, platelet activation, glutamine and tumor expression of cell proliferation, aerobic glycolysis, glutaminolysis, platelets, and leukocyte molecules. The anti- and pro-cell proliferation, aerobic glycolysis, and glutaminolysis effects of aspirin and glutamine were further demonstrated in a LLC cell study. Although there remains limitations to our experiments, glucose and glutamine metabolism are proposed targets for the anticancer effects of aspirin.

BACKGROUND Restenosis remains a significant problem in endovascular therapy for hemodialysis vascular access. Drug-coated balloon (DCB) angioplasty decreases restenosis in peripheral and coronary artery diseases. The aim of this systematic review and meta-analysis is to assess the patency outcomes following DCB angioplasty, as compared to conventional balloon (CB) angioplasty for the stenosis of hemodialysis vascular access. METHODS A comprehensive search in the MEDLINE, EMBASE, and CENTRAL databases was conducted in order to identify eligible randomized controlled trials evaluating DCB angioplasty for hemodialysis vascular access dysfunction. The primary endpoint was the 6-month target lesion primary patency and the secondary endpoints were 12-month target lesion primary patency and procedure-related complications. Risk ratios (RR) were pooled and relevant subgroups were analyzed separately. RESULTS Eleven randomized controlled trials comprised of 487 patients treated with DCB angioplasty and 489 patients treated with CB angioplasty were included. There were no significant differences in the target lesion primary patency at 6 months [RR, 0.75; 95% confidence interval (CI), 0.56, 1.01; p = 0.06] and at 12 months (RR 0.89; 95% CI, 0.79, 1.00; p = 0.06). The absence of benefit for the DCB group remained, even in the arteriovenous fistula subgroup or the subgroup of studies excluding central vein stenosis. The risk of procedure-related complication did not differ between the two groups (RR 1.00; 95% CI 0.98, 1.02; p = 0.95). CONCLUSION DCB angioplasty did not demonstrate significant patency benefit for the treatment of hemodialysis vascular access dysfunction. Wide variations in patency outcomes across studies were noted. Further studies focusing on specific types of access or lesions are warranted to clarify the value of DCB for hemodialysis vascular access. (PROSPERO Number CRD42019119938).

The article is motivated by a nephrology study in Taiwan, which enrolled hemodialysis patients who suffered from vascular access thrombosis. After treatment, some patients were cured of thrombosis, while some may experience recurrence of either type (acute or nonacute) of vascular access thrombosis. Our major interest is to estimate the cumulative incidence probability of time to the first recurrence of acute thrombosis after therapy. Since the occurrence of one type of vascular access thrombosis precludes occurrence of the other type, patients are subject to competing risks. To account for the presence of competing risks and cured patients, we develop a mixture model approach to the regression analysis of competing-risks data with a cure fraction. We make inference about the effects of factors on both the cure rate and cumulative incidence function (CIF) for a failure of interest, which are separately specified in the logistic regression model and semiparametric regression model with time-varying and time-invariant effects. Based on two-stage method, we develop novel estimation equations using the inverse probability censoring weight techniques. The asymptotic properties of the estimators are rigorously studied and the plug-in variance estimators can be obtained for constructing interval estimators. We also propose a lack-of-fit test for assessing the adequacy of the proposed model and several tests for time-varying effects. The simulation studies and vascular access thrombosis data analysis are conducted to illustrate the proposed method.

Endovascular therapy is the principal therapy for haemodialysis vascular access dysfunction. Nonetheless, the incidence and determinants of post-intervention thrombotic events are unclear. This prospective cohort study evaluated the incidence and timing of thrombotic events after endovascular therapy and analysed the clinical, angiographic, and biological determinants of thrombosis. Of the 236 patients enrolled, 91 experienced post-intervention thrombotic events within 1 year. The 1-year thrombosis-free patency was 28% for thrombosed accesses, 53% for non-thrombosed grafts, and 78% for non-thrombosed fistulas. Forty-one of the 91 thrombotic events (45%) occurred within 3 months post-intervention. In the univariate analysis, early thrombosis was associated with longer haemodialysis duration (hazard ratio [HR], 1.01; 95% confidence interval [CI], 1.01–1.02), graft access (HR, 7.69; 95% CI, 3.33–20.0), multiple stenoses (HR, 2.69; 95% CI, 1.36–5.37), and high indoxyl sulphate (IS) levels (HR, 1.55; 95% CI, 1.32–1.82). Late thrombosis was associated with diabetes (HR, 1.89; 95% CI, 1.01–3.57), cardiovascular disease (HR, 2.38; 95% CI, 1.27–4.54), and endothelial progenitor cell counts (HR, 0.97; 95% CI, 0.93–0.99). After multivariate adjustment, high IS was the major predisposing factor for early post-intervention thrombosis (HR, 1.41; 95% CI, 1.18–1.69). Our findings suggest that measures to decrease IS could target the most critical period of thrombosis.

Objective Paclitaxel-coated balloons are used to reduce neointimal hyperplasia in native arteriovenous (AV) fistulas. However, no study specifically evaluated their effect on venous anastomotic stenosis of dialysis grafts. We aimed to compare the efficacy of angioplasty with drug-coated balloons (DCBs) and angioplasty with conventional balloons (CBs) for venous anastomotic stenosis in dysfunctional AV grafts. Methods In this investigator-initiated, single-center, single-blinded, prospective randomized controlled trial, we randomly assigned 44 patients who had venous anastomotic stenosis to undergo angioplasty with DCBs (n = 22) or CBs (n = 22) from July 2015 to August 2018. Access function was observed per the hemodialysis center's protocols; ancillary angiographic follow-up was performed every 2 months for 1 year after the interventions. The primary end point was target lesion primary patency at 6 months. Secondary outcomes included anatomic and clinical success after angioplasty, circuit primary patency at 6 months and 1 year, and target lesion primary patency at 1 year. Results At 6 months, target lesion primary patency in the DCB group was significantly greater than that in the CB group (41% vs 9%; hazard ratio [HR], 0.393; 95% confidence interval [CI], 0.194-0.795; P = .006), as was the primary patency of the entire access circuit (36% vs 9%; HR, 0.436; 95% CI, 0.218-0.870; P = .013). At 1 year, the target lesion primary patency in the DCB group remained greater than that in the CB group (23% vs 9%; HR, 0.477; 95% CI, 0.243-0.933; P = .019) but not the primary patency of the access circuit (14% vs 9%; HR, 0.552; 95% CI, 0.288-1.059; P = .056). No difference in anatomic or clinical success was observed; no major complications were noted. Conclusions Angioplasty with DCBs showed a modest improvement in primary patency of venous anastomotic stenosis and all dialysis AV grafts at 6 months. The short-term benefit was not durable to 1 year, and reinterventions were eventually needed.

Background The aim of this study was to determine the influence of various antidiabetic therapies on the relationship between body mass index and all‐cause mortality in patients with diabetes mellitus and acute coronary syndrome. Methods and Results This was a prospective, observational study comprising 1193 patients diagnosed with type 2 diabetes mellitus and acute coronary syndrome. The patients were stratified into 4 body mass index categories, and their mortality rates were compared using time‐dependent Cox regression analysis using normal weight (body mass index, 18.5–23.9) as the reference. Subsequently, the influence of antidiabetic therapies on the association between BMI and mortality were analyzed. Seventy‐four patients (6.2%) died over 2 years of follow‐up. The mortality rate was lowest in the class I obese group (3.35%) and highest in the normal‐weight group (9.67%). After adjusting for covariates, class I obesity paradoxically remained significantly protective against mortality compared with normal weight (hazard ratio, 0.141; P =0.049); interaction term analysis showed that insulin therapy influenced this “obesity paradox” ( P =0.045). When the patients were stratified by insulin use, the protective effect of obesity disappeared in the insulin‐treated patients but persisted in the non–insulin‐treated patients. Conclusions In patients with type 2 diabetes mellitus and acute coronary syndrome, the relationship between body mass index and mortality rate is U‐shaped, with class I obesity representing the nadir and normal weight the peak. The protective effect of obesity disappeared in patients treated with insulin.

Background Hemodialysis (HD) patients have an increased risk of thrombosis. Endothelial progenitor cells (EPCs), which function in vascular repair, are deficient in HD patients. Nonetheless, the relationship between EPC deficiency and thrombosis in HD patients is unknown. Methods From January 2010 to December 2012, circulating levels of EPCs that were positive for CD34 and kinase insert domain receptor (KDR) were measured in 269 HD patients. Patients received prospective follow-ups at 6-month intervals until May 2015. The primary outcome was the composite of HD access thrombosis and systemic vascular thrombosis. Results There were 141 thrombotic events, 50 systemic vascular thrombotic events and 116 HD access thrombotic events. We found significantly negative associations between CD34 + KDR + tertile and overall thrombotic events (low: 61%; middle: 56%; high: 40%; P = 0.02), systemic vascular thrombotic events (low: 27%; middle: 18%; high: 10%; P = 0.03) and HD access thrombotic events (low: 52%; middle: 46%; high: 36%; P = 0.02). Univariate analysis indicated that systemic vascular thrombotic events were positively associated with age, diabetes, dyslipidemia, vascular disease history, urea clearance, albumin and C-reactive protein (CRP), and negatively associated with CD34 + KDR + cell count. HD access thrombosis was positively associated with vascular disease history and CRP, and negatively associated with CD34 + KDR + cell count. Multivariate analysis indicated that a low CD34 + KDR + cell count was an independent risk factor for both types of thrombosis. Conclusions Our study of a population of HD patients showed that a low level of circulating EPCs is associated with thrombosis.

ObjectiveThe pain prevalence of inpatients is not a well-studied medical issue in Asia. We have aimed to evaluate pain prevalence and characterize those patients who have suffered from severe, persistent pain.MethodsWe investigated pain prevalence using a quota sampling from 19 general wards during the year 2018. Using a structured questionnaire, eight interviewers visited patients at an age ≥ 20 years, and who had been staying in general wards for ≥ 3 days. Those patients were excluded if they were unable to respond to the interview questions. If they reported pain during hospitalization, the maximum pain level and the duration of pain suffered in the past 24 hours were assessed. Care-related pain was also surveyed.ResultsA total of 1,034 patients (M/F, 537/497) completed the survey. Amongst them, 719 patients (69.5%) experienced pain, with moderate and severe pain levels being 27.3% and 43%, respectively. Surgery was considered as it related to pain, including significantly severe pain. The top 3 care-related pain causes were needle pain, wound dressing, and change in position/chest percussion. Change in position/chest percussion and rehabilitation were associated with severe, persistent pain.ConclusionsPain is common in approximately 70% of inpatients, with surgery being associated with severe pain. Mobilization and rehabilitation may lead to severe, persistent pain. The periodic study of pain prevalence is essential in order to provide precise pain management.

Contains fulltext : 215333.pdf (Publisher’s version ) (Closed access) BACKGROUND: Patients with stable coronary artery disease and diabetes with previous percutaneous coronary intervention (PCI), particularly those with previous stenting, are at high risk of ischaemic events. These patients are generally treated with aspirin. In this trial, we aimed to investigate if these patients would benefit from treatment with aspirin plus ticagrelor. METHODS: The Effect of Ticagrelor on Health Outcomes in diabEtes Mellitus patients Intervention Study (THEMIS) was a phase 3 randomised, double-blinded, placebo-controlled trial, done in 1315 sites in 42 countries. Patients were eligible if 50 years or older, with type 2 diabetes, receiving anti-hyperglycaemic drugs for at least 6 months, with stable coronary artery disease, and one of three other mutually non-exclusive criteria: a history of previous PCI or of coronary artery bypass grafting, or documentation of angiographic stenosis of 50% or more in at least one coronary artery. Eligible patients were randomly assigned (1:1) to either ticagrelor or placebo, by use of an interactive voice-response or web-response system. The THEMIS-PCI trial comprised a prespecified subgroup of patients with previous PCI. The primary efficacy outcome was a composite of cardiovascular death, myocardial infarction, or stroke (measured in the intention-to-treat population). FINDINGS: Between Feb 17, 2014, and May 24, 2016, 11 154 patients (58% of the overall THEMIS trial) with a history of previous PCI were enrolled in the THEMIS-PCI trial. Median follow-up was 3.3 years (IQR 2.8-3.8). In the previous PCI group, fewer patients receiving ticagrelor had a primary efficacy outcome event than in the placebo group (404 [7.3%] of 5558 vs 480 [8.6%] of 5596; HR 0.85 [95% CI 0.74-0.97], p=0.013). The same effect was not observed in patients without PCI (p=0.76, pinteraction=0.16). The proportion of patients with cardiovascular death was similar in both treatment groups (174 [3.1%] with ticagrelor vs 183 (3.3%) with placebo; HR 0.96 [95% CI 0.78-1.18], p=0.68), as well as all-cause death (282 [5.1%] vs 323 [5.8%]; 0.88 [0.75-1.03], p=0.11). TIMI major bleeding occurred in 111 (2.0%) of 5536 patients receiving ticagrelor and 62 (1.1%) of 5564 patients receiving placebo (HR 2.03 [95% CI 1.48-2.76], p

Background Parenteral anticoagulants and vitamin K antagonists (VKAs) have constituted the cornerstone of venous thromboembolism (VTE) treatment. Meanwhile, direct oral anticoagulants (DOACs) provide physicians with an alternative. The Global Anticoagulant Registry in the FIELD (GARFIELD)-VTE observes real-world treatment practices. Objectives Describe initial anticoagulation (AC) treatment patterns in VTE patients who received parenteral AC, VKAs, and/or DOACs within ±30 days of diagnosis. Methods VTE patients were categorized into parenteral AC only, parenteral AC with transition to VKA, VKA only, parenteral AC with transition to DOAC, and DOAC only. Results A total of 9647 patients were initiated on AC treatment alone. 4781 (49.6%) patients received DOACs ± parenteral ACs; 3187 (33.0%), VKA ± parenteral ACs; and 1679 (17.4%) parenteral ACs alone. Rivaroxaban was the most frequently used DOAC (79.4%). DOACs were more frequently used in North America/Australia (58.1%), Europe (52.2%), and Asia (47.6%) than in Latin America (29.7%) and the Middle East/South Africa (32.5%). In patients with suspected VTE, most received parenteral AC monotherapy (67.7%). Patients with deep vein thrombosis were more likely to receive DOACs alone than those with pulmonary embolism with or without deep vein thrombosis (36.2% vs 25.9%). Active cancer patients received parenteral AC alone (58.9%), with 25.5% receiving DOAC ± parenteral AC and 12.8% parenteral AC and VKA. A total of 46.5% of pregnant patients received parenteral AC monotherapy, 34.0% were treated with VKA ± parenteral AC, and 19.5% received a DOAC (± parenteral AC). Conclusion AC treatment patterns vary by patient population, geographic region and site of VTE. Guidelines for AC therapy are not always adhered to.

Chronic kidney disease (CKD) accelerates the development of neointima formation at the anastomosis site of arteriovenous (AV) fistulas. Accumulation of certain uremic toxins has a deleterious effect on the cardiovascular system. The oral charcoal adsorbent, AST-120, reduces circulating and tissue uremic toxins, but its effect on neointima formation at an AV fistula is unknown. To understand the effect of CKD and AST-120 on neointima formation, we created AV fistulas (common carotid artery to the external jugular vein in an end-to-side anastomosis) in mice with and without CKD. AST-120 was administered in chow before and after AV fistula creation. Administration of AST-120 significantly decreased serum indoxyl sulfate levels in CKD mice. CKD mice had a larger neointima area than non-CKD mice, and administration of AST-120 in CKD mice attenuated neointima formation. Both smooth muscle cell and fibrin components were increased in CKD mice, and AST-120 decreased both. RNA expression of MMP-2, MMP-9, TNF&alpha, and TGF&beta, was increased in neointima tissue of CKD mice, and AST-120 administration neutralized the expression. Our results provided in vivo evidence to support the role of uremic toxin-binding therapy on the prevention of neointima formation. Peri-operative AST-120 administration deserves further investigation as a potential therapy to improve AV fistula patency.

Background and objectives There is increasing evidence that microRNAs (miRNAs) play crucial roles in the regulation of neointima formation. However, the translational evidence of the role of miRNAs in dialysis vascular access is limited. Design, setting, participants, & measurements miRNA expression in tissues was assessed by using venous tissues harvested from ten patients on dialysis who received revision or removal surgery, and ten patients who were predialysis and received creation surgery of arteriovenous fistulas served as controls. To extend these findings, 60 patients who received angioplasty of dialysis access were enrolled and the levels of circulating miRNAs were determined before and 2 days after angioplasty. Clinical follow-up was continued monthly for 6 months. The primary outcome of angioplasty cohort was target lesion restenosis within 6 months after angioplasty. Results In the surgery cohort, the expressions of miR-21, miR-130a, and miR-221 were upregulated in stenotic tissues, whereas those of miR-133 and miR-145 were downregulated. In situ hybridization revealed similar expression patterns of these miRNAs, localized predominantly in the neointima region. Twenty eight patients in the angioplasty cohort developed restenosis within 6 months. The levels of circulating miR-21, miR-130a, miR-221, miR-133, and miR-145 significantly increased 2 days after angioplasty. Kaplan–Meier plots showed that patients with an increase of miR-21 expression level >0.35 have a higher risk of patency loss (hazard ratio, 4.45; 95% confidence interval, 1.68 to 11.7). In a multivariable analysis, postangioplasty increase of miR-21 expression was independently associated with restenosis (hazard ratio, 1.20; 95% confidence interval, 1.07 to 1.35 per one unit increase of miR-21 expression level; P=0.001). Conclusions Certain miRNAs are differentially expressed in the stenotic venous segments of dialysis accesses. An increase in blood miR-21 level with angioplasty is associated with a higher risk of restenosis.

Recently, Hou and others introduced a (2, n) block-based progressive visual cryptographic scheme (BPVCS) in which image blocks can be gradually recovered step by step. In Hou and others' (2, n)-BPVCS, a secret image is subdivided into n non-overlapping image blocks. When t () participants stack their shadow images, all the image blocks associated with these t participants will be recovered. However, Hou and others' scheme is only a simple 2-out-of-n case. In this paper, we discuss a general (k, n)-BPVCS for any k and n. Our main contribution is to give two constructions (Construction 1 and Construction 2) of this general (k, n)-BPVCS. Also, we theoretically prove that both constructions satisfy a threshold property and progressive recovery of the proposed (k, n)-BPVCS. For k = 2, Construction 1 is reduced to Hou and others' (2, n)-BPVCS.

Objective To explore the point-specific clinical effect of 2 Hz electroacupuncture (EA) in treating postoperative pain in patients undergoing total knee arthroplasty (TKA), Methods In a randomised, partially single-blinded preliminary study, 47patients with TKA were randomly divided into three groups: control group (CG, n=17) using only patient-controlled analgesia (PCA); EA group (EAG, n=16) with 2 Hz EA applied at ST36 ( Zusanli) and GB34 ( Yanglingquan) contralateral to the operated leg for 30 min on the first two postoperative days, also receiving PCA; and non-point group (NPG, n=14), with EA identical to the EAG except given 1 cm lateral to both ST36 and GB34. The Mann–Whitney test was used to show the difference between two groups and the Kruskal–Wallis test to show the difference between the three groups. Results The time until patients first required PCA in the CG was 34.1±22.0 min, which was significantly shorter than the 92.0±82.7 min in the EAG (p0.05). The total dosage of PCA solution given was 4.6±0.9 mL/kg body weight in the CG, 4.2±1.0 mL/kg in the EAG and 4.5±1.0 mL/kg in the NPG; there were no significant differences (p>0.05) among the three groups. Conclusions In this small preliminary study, EA retarded the first demand for PCA in comparison with no EA. No effect was seen on the total dosage of PCA required and no point-specific effect was seen.

Background: No randomized controlled trials evaluating metformin therapy efficacy in patients with type 2 diabetes mellitus (DM) and acute coronary syndrome (ACS) have been reported. Well-designed retrospective studies controlling for imbalance in baseline patient characteristics are scarce. We aimed to examine the mortality benefit of metformin therapy in patients with type 2 DM and ACS, compared with non-metformin anti-diabetes agent users. Method: Data were extracted from the prospective nationwide ACS-DM Taiwan Society of Cardiology registry. Propensity score (PS) matching on baseline characteristics and treatment measures was performed for metformin versus non-metformin users. Cox proportional hazard models were used to compare mortality outcomes among the PS-matched cohort as a primary analysis. Traditional Cox proportional hazard models adjusting for all pre-determined covariates and quintiles of the PS among the overall population were performed as a secondary analysis. Findings: Of 1157 patients with type 2 DM and ACS receiving anti-diabetes agents, 78 patients (6.7%) died over the 2-year follow-up period. After PS matching, 318 metformin users were matched with 318 non-metformin users. Metformin users had a lower all-cause mortality rate (adjusted hazard ratio [aHR] 0·50, 95% confidence interval [CI] 0·26-0·95) in the primary analysis. The survival benefit of metformin therapy was consistent in the secondary analyses (aHR 0·30, 95% CI 0·17-0·54 while adjusting for all pre-determined covariates, and aHR 0·34, 95% CI 0·19-0·59 while adjusting for quintiles of the PS). Interpretation: Among patients with type 2 DM and ACS, metformin was associated with lower all-cause mortality. Funding Statement: This work was supported with grants from the Hsin-Chu branch of the National Taiwan University Hospital (HCH-106036). The funding source also provided technical help (Biotechnology R&D Center) with data analysis and interpretation of the findings. Declaration of Interest: All authors report no relationships that could be construed as a conflict of interest. Ethics Approval Statement: Patients are treated according to international or local guidelines and evidence-based strategies. The protocol and consent forms used in this study were consistent with the Declaration of Helsinki and relevant regulations. The ethics committees of each participating hospital approved the study, and all enrolled patients provided written informed consent.

Recently, Li et al. proposed a ( t , s , k , n ) essential secret image sharing (ESIS) scheme with different importance of shadows, which has s essential shadow images and n − s non-essential shadow images. This ( t , s , k , n )-ESIS scheme can simultaneously provide the conventional threshold property ( k or more shadow images are required in reconstruction) and the essential-threshold property (these involved k shadow images should include at least t essential shadow images). Generally, small shadow images have advantages in storage or transmission, and will be suitable for modern visual communication applications where features such as secure transmission and storage are required. Therefore, the size of shadow image is a critical consideration for designing ESIS-( t , s , k , n ) scheme. In this paper, we propose a ( t , s , k , n )-ESIS scheme to achieve the less size of total shadow images and the less size of required shadow images in reconstruction when compared with Li et al.’s ( t , s , k , n )-ESIS scheme.

// I-Chun Chen 1 , Chin-Sung Kuo 1, 2 , Chih-Cheng Wu 3, 4, 5, 6 , Hsiao-Ya Tsai 1 , Chih-Pei Lin 7, 8 , Szu-Yuan Li 1, 9 , Ruey-Hsing Chou 1, 3, 10 , Po-Hsun Huang 1, 3, 10 , Jaw-Wen Chen 3, 10, 11, 12 and Shing-Jong Lin 1, 3, 10, 11, 13 1 Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan 2 Division of Endocrinology and Metabolism, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan 3 Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan 4 National Tsing-Hua University, Institute of Biomedical Engineering, Hsinchu, Taiwan 5 National Taiwan University Hospital, College of Medicine, Taipei, Taiwan 6 Cardiovascular Center, National Taiwan University Hospital, Hsinchu Branch, Hsinchu, Taiwan 7 Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan 8 Department of Biotechnology and Laboratory Science in Medicine and Institute of Biotechnology in Medicine, National Yang-Ming University, Taipei, Taiwan 9 Division of Nephrology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan 10 Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan 11 Department of Medical Research, Taipei Veterans General Hospital, Taipei, Taiwan 12 Institute and Department of Pharmacology, National Yang-Ming University, Taipei, Taiwan 13 Taipei Medical University, Taipei, Taiwan Correspondence to: Po-Hsun Huang, email: huangbsvgh@gmail.com Chih-Cheng Wu, email: chihchengwumd@gmail.com Chin-Sung Kuo, email: cskuo241@yahoo.com.tw Keywords: hyperuricemia; endothelial progenitor cell; ischemia; neovascularization Received: August 14, 2017 Accepted: January 02, 2018 Published: January 22, 2018 ABSTRACT Objective: Chronic hyperuricemia is associated with cardiovascular disease, but its impact on endothelial progenitor cells (EPC) and ischemia-induced neovascularization remains unclear. Herein we investigated whether chronic hyperuricemia could impede blood flow recovery in response to tissue ischemia by suppression of EPC. Methods: Human EPC were isolated and cultured in a high-level uric acid medium for functional testing. Cell proliferation, nitric oxide (NO) production and apoptosis assay were examined. A chronic hyperuricemia mouse model was established by potassium oxonate treatment and/or a high-level uric acid diet to evaluate the actions of chronic hyperuricemia on ischemia-induced blood flow recovery. After 4 weeks of drug treatment, hindlimb ischemia surgery was performed in the control and hyperuricemia mice. Blood flow recovery was followed up every week before and after ischemic surgery using a laser Doppler Perfusion Imager System. The circulating EPC number in the peripheral blood was determined by flow cytometry (Sca-1 + /Flk-1 + ). Results: Incubation with a high-level uric acid medium (10 mg/dL) significantly suppressed EPC proliferation, reduced NO production, and lessened phosphorylation of Akt and eNOS. Moreover, EPC treated with high-level uric acid increased reactive oxygen species production, promoted cellular apoptosis and senescence, and also inhibited EPC tube formation. Four weeks after hindlimb ischemia surgery, the chronic hyperuricemia mice had significantly reduced tissue reperfusion, EPC mobilization, and impaired neovascularization in the ischemic hindlimbs compared with the control mice. Conclusions: Chronic hyperuricemia impaired blood flow recovery and EPC mobilization in response to tissue ischemia, and these effects could have occurred through suppression of EPC.

The urgency with which salvage of thrombosed vascular accesses for dialysis should be attempted remains unknown. We examined the effect of a timely thrombectomy approach on vascular access outcomes for dialysis.A before-and-after study was conducted with patients on hemodialysis who had undergone endovascular thrombectomy. A timely thrombectomy initiative (ie, salvage within 24 hours of thrombosis diagnosis) was started in July 2015 at our institution. Data about thrombectomy procedures, performed within 1 year before and after the initiative was introduced, were abstracted from an electronic database. Immediate outcomes and patency outcomes were compared between the preinitiative (control) and postinitiative (intervention) groups.During the study period, 329 patients were enrolled, including 165 cases before and 164 cases after the initiative. The intervention group had more thrombectomy procedures performed within 24 hours (93% vs 55%; P .01) and within 48 hours (97% vs 79%; P .01) than the control group. No between-group differences in procedural success or clinical success rates were found. At 3 months, the intervention group had a higher postintervention primary patency rate than the control group, although this did not reach statistical significance (58% vs 48%; P = .06). After stratification into native or graft accesses, the patency benefit was observed in the native access group (68% vs 50%; P = .03) but not in the graft access group (50% vs 46%; P = .65). After adjusting for potential confounders, timely thrombectomy remained an independent predictor of postintervention primary patency (hazard ratio, 0.449; 95% confidence interval, 0.224-0.900; P = .02) for native dialysis accesses.Our results suggest that a timely thrombectomy approach, in which salvage is attempted within 24 hours of thrombosis diagnosis, improves postintervention primary patency of native but not graft accesses for dialysis.

Background and aim Atrial fibrillation (AF) is an important cardiovascular disease in the elderly. The association between hyperuricemia and AF is unclear. Therefore, we aimed to investigate the prospective relationship between uric acid and development of AF in a nationally representative cohort of elderly people. Methods and results A total of 1485 elderly people (age ≥ 65 yrs) from the Elderly Nutrition and Health Survey in Taiwan (1999–2000) were without AF on “electrocardiography” at baseline. Incident AF events (International Classification of Diseases, Ninth Revision, Clinical Modification, ICD-9-CM: 427.31) were identified using data from the National Health Insurance Dataset. Hyperuricemia was defined as levels of uric acid >7.0 mg/dL in men and 6.0 mg/dL in women. A Cox proportional hazards model was used to evaluate the association between hyperuricemia and incident AF. The follow-up period was from 1999 to 2000 to 2008. During the follow-up period (median: 9.16 yrs), 90 AF events occurred (44 in men and 46 in women). Older age, elevated systolic blood pressure, being an ex-smoker, and high uric acid were positively associated with incident AF. Hyperuricemia was positively associated with incident AF in normotensive (age-adjusted hazard ratio (HR): 2.65 and 95% confidence intervals: 1.05–6.69), but not in (1.20:0.74–1.94) hypertensive individuals (systolic blood pressure ≥130 or diastolic blood pressure ≥85 or using hypertensive medicine). A significant association between hyperuricemia and AF (3.78; 1.24–11.59) remained after adjusting for other potential confounders among normotensive older persons. Conclusion Hyperuricemia is associated with the development of AF in elderly people with normal blood pressure.

Rationale: Stellate Ganglion Block (SGB) provides a blockade of sympathetic signals from the sympathetic chain and appears to be a promising method of controlling refractory ventricular arrhythmias, but there are scanty data in the literature. Patient concerns: Herein, we describe a 59-year-old male patient with a history of non-ischemic cardiomyopathy and suffering from frequent VT episodes, who received ICD implantation and regular amiodarone medication control. Diagnoses: Monomorphic VT refractory to standard medication control and focal extensive catheter ablation. Interventions: Left Stellate Ganglion Block (LSGB) was performed under ultrasound-assisted injection at the C6 level using a 10 ml solution of 0.4% lidocaine and 0.5% bupivacaine. Outcomes: In our case, refractory VT subsided and sinus rhythm was retained immediately after LSGB. There were no VT episodes for at least 3 hours during the inter-hospital transfer, which did not involve any specific complications. Lessons: LSGB may provide effective VT control and play an important role in rescue and bridge therapy before catheter ablation.

BACKGROUND:Little is known about the components and contributing factors of door-to-balloon time after implementation of Door-to-Balloon Alliance quality-improving (QI) strategies, including the impact of door-to-ECG time on door-to-balloon time. OBJECTIVE:We investigated whether modification of emergency department (ED) triage processes could improve door-to-ECG and door-to-balloon times after implementation of QI strategies. METHODS:This was a retrospective before-and-after study of a prospectively collected database. From June 2014 to October 2014, interventions were implemented in our ED, including a protocol-driven ECG initiation and moving an ECG station and technician to the triage area. The primary outcome was the percentage of patients with ST-elevation myocardial infarction (STEMI) who received ECG within 10 min of arrival; the secondary outcome was the percentage of patients with door-to-balloon times of

BackgroundPrescription of guideline-recommended medicines after acute coronary syndrome (ACS) has been suboptimal. Tools for improving the use of medications have been developed, but they mainly targeted physicians.ObjectiveWe evaluated the effects of reinforcement of patient and family education on the usage of guideline-recommended secondary prevention medications.MethodsThis was a retrospective analysis of a prospectively collected registry of patients with ACS who were admitted to a regional teaching hospital in Taiwan between February 2015 and April 2017. The control group included 76 patients discharged before implementing the electronic-based patient and family education (PFE) system. The intervention group included 206 patients discharged after implementation. The primary outcome was the prescription rate of all four guideline-recommended drugs. Predictors of adherence were also evaluated.ResultsThe study cohort included 282 ACS patients (188 men and 94 women) with a mean age of 68.5 years (standard deviation, 14.2). The intervention group patients were younger, had more family history of premature cardiovascular disease, more dyslipidemia, and underwent more reperfusion therapy. The intervention group was prescribed more guideline-recommended drugs than the control group: dual antiplatelet agents, 79.61% vs. 47.37% (pConclusionsReinforcement of patient education was associated with significant improvements in physicians' adherence to guideline-recommended medical therapy after acute coronary syndrome.

Arteriovenous graft (AVG) dysfunction is mainly caused by neointimal hyperplasia. Endovascular intervention can salvage the stenosis. But the long-term patent rate doesn’t improve due to repeated restenosis. Paclitaxel-coated balloon (PCB) is used to reduce neointimal hyperplasia in patients with

Patient initials or identifier number 607300 ### Relevant clinical history and physical exam A 33-year-old man came for a 12-hour history of totally occluded arteriovenous fistula (AVF). Past history: polycystic kidney disease with regular hemodialysis since childhood and active smoker.

Patient initials or identifier number CSC ### Relevant clinical history and physical exam A 52 y/o man with hyperlipidemia presented with exertional chest tightness and dyspnea for 1 year. He had received PCI with a BMS implanted in LAD one year ago in a local hospital; however, his chest

In (k, n) secret image sharing (SIS), a scheme encrypts a secret image into n shadow images. Any k or more shadow images can be collaborated together to reveal the secret image. Most of the previous SIS schemes don't distinguish the importance of shadows. However, in some application environments, some participants are accorded special privileges due to their status or importance. Thus, some shadows may be more important than others. In this paper, we consider the (t, s, k, n) essential SIS (ESIS) scheme. All n shadows are classified into s essential shadows and (n-s) non-essential shadows. When reconstructing the secret image, the (t, s, k, n)-ESIS scheme needs k shadows, which should include at least t essential shadows.

Many micropayment schemes have been proposed in the desire to support the low-value and the high-volume purchases of some e-commerce applications such as mobile commerce services or web-based interactive video services. However it seems that no one studies how to add the ability of returning changes in micropayment schemes. In this paper, we take the lead in studying a micropayment scheme with the ability to return changes (MSRC), which reduces the hash operations in the transaction phase. When compared with previous micropayment schemes, the proposed MSRC has low computation costs and thus is more suitable and practical for mobile commerce environments, which have a limited computation capability and limited bandwidth.

We report the novel use of a Sengstaken-Blakemore tube in an 82-year-old man with severe upper gastrointestinal bleeding and subsequent hypovolemic shock. When exploratory laparotomy failed to locate the source of the bleeding, a Sengstaken-Blakemore tube was placed retrograde to the gastroesophageal junction using a previously inserted nasogastric tube for guidance. The bleeding stopped immediately after mechanical compression by the inflated gastric and esophageal balloons. Hemodynamic stability permitted a thorough evaluation of the surgical field. The balloons were deflated intermittently to allow the surgeon to address the major and other smaller bleeding vessels in a stepwise manner. The intraoperative insertion of a Sengstaken-Blakemore tube can be used to control disastrous upper gastrointestinal bleeding located at or above the gastroesophagealjunction. It helps to achieve hemodynamic stability with less transfusion required and results in fewer complications. However, the lack of experience with the direct placement of a Sengstaken-Blakemore tube and the need for the equipment-dependent confirmation of the SengstakenBlakemore tube position reduces its clinical usage. The retrograde Sengstaken-Blakemore tube insertion strategy does not require assistance by ultrasonography or endoscopy and avoids most procedure-related complications.

Chronic kidney disease (CKD) is now clearly recognized as a public health problem worldwide. Patients with CKD display a substantial increase in end‐stage renal disease (ESRD) and cardiovascular disease (CVD).[1][1] Moreover, the prognosis of CVD in CKD is extremely poor.[2][2] Understanding the

Ethnopharmacological relevance In traditional Chinese medicine, Glechoma hederacea is frequently prescribed to patients with cholelithiasis, dropsy, abscess, diabetes, inflammation, and jaundice. Polyphenolic compounds are main bioactive components of Glechoma hederacea. Aim of the study This study was aimed to investigate the hepatoprotective potential of hot water extract of Glechoma hederacea against cholestatic liver injury in rats. Materials and methods Cholestatic liver injury was produced by ligating common bile ducts in Sprague-Dawley rats. Saline and hot water extract of Glechoma hederacea were orally administrated using gastric gavages. Liver tissues and bloods were collected and subjected to evaluation using histological, molecular, and biochemical approaches. Results Using a rat model of cholestasis caused by bile duct ligation (BDL), daily oral administration of Glechoma hederacea hot water extracts showed protective effects against cholestatic liver injury, as evidenced by the improvement of serum biochemicals, ductular reaction, oxidative stress, inflammation, and fibrosis. Glechoma hederacea extracts alleviated BDL-induced transforming growth factor beta-1 (TGF-β1), connective tissue growth factor, and collagen expression, and the anti-fibrotic effects were accompanied by reductions in α-smooth muscle actin-positive matrix-producing cells and Smad2/3 activity. Glechoma hederacea extracts attenuated BDL-induced inflammatory cell infiltration/accumulation, NF-κB and AP-1 activation, and inflammatory cytokine production. Further studies demonstrated an inhibitory effect of Glechoma hederacea extracts on the axis of high mobility group box-1 (HMGB1)/toll-like receptor-4 (TLR4) intracellular signaling pathways. Conclusions The hepatoprotective, anti-oxidative, anti-inflammatory, and anti-fibrotic effects of Glechoma hederacea extracts seem to be multifactorial. The beneficial effects of daily Glechoma hederacea extracts supplementation were associated with anti-oxidative, anti-inflammatory, and anti-fibrotic potential, as well as down-regulation of NF-κB, AP-1, and TGF-β/Smad signaling, probably via interference with the HMGB1/TLR4 axis.