Record-high capture of volatile benzene and toluene enabled by activator implant-optimized banana peel-derived engineering carbonaceous adsorbents.

This work developed a super-high performance of engineering carbonaceous adsorbents from waste banana-peel via an optimized KOH-impregnated approach, which affords outstanding structural property (SBET = 3746.5 m2 g-1, Vtotal = 2.50 cm3 g-1), far outperforming KOH-grinding method-induced counterpart and other known banana peel-derived those. Thereby, this triggers a record-high capture value of volatile organic compounds (VOCs) specific to benzene (27.55 mmol g-1) and toluene (23.82 mmol g-1) in the all known results. The structural expression characters were accurately correlated with excellent adsorption efficiency of VOCs by investigating the synthetic factor-controlling comparative samples. Ulteriorly, the adsorption selectivity prediction at different relative humidity was demonstrated through the DIH (difference of the isosteric heats), highlighting the good superiority in selective adsorption of toluene compared to benzene even under humid atmosphere. Our findings provide the possibility for the practical application and fabrication of waste biomass (banana peel)-derived functional biochar adsorbent in the environmental treatment of threatening VOCs pollutants.

Increased serum adiponectin predicts improved coronary flow and clinical outcomes in patients with ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention.

BACKGROUND: Previous studies suggested that adiponectin (APN) could ameliorate ischemia/reperfusion injury and endothelial dysfunction in patients with acute myocardial infarction. However, the relationship between serum APN level and coronary flow after primary percutaneous coronary intervention (PPCI) in patients with ST-segment elevation myocardial infarction (STEMI) is unclear. METHODS: A total of 144 patients with STEMI treated by PPCI were enrolled and divided into two groups based on the mean serum APN level on admission. The data on coronary angiograms and laboratory examinations were collected and compared between groups. The incidence of major adverse cardiac events (MACE) was evaluated in all enrolled patients. RESULTS: The prevalence of Thrombolysis In Myocardial Infarction (TIMI) flow grade <3 after PPCI and corrected TIMI frame count were lower in the high-APN group (P = 0.032 and P = 0.029, respectively). Logistic regression analysis demonstrated that APN was an independent negative predictor of poor coronary flow after PPCI (odds ratio = 0.72, 95% CI: 0.56-0.93, P = 0.011). Kaplan-Meier curves showed that a higher APN level correlated with a better MACE-free survival rate, and multivariate Cox hazard regression analysis indicated that high APN was a significant negative predictor of MACE (hazard ratio = 0.54, 95% CI: 0.29-1.00, P = 0.048). CONCLUSION: Elevated serum levels of APN on admission are associated with improved myocardial blood flow and clinical outcomes in STEMI patients treated with PPCI.

Dynamic fluctuations of advanced glycation end products and its C-terminal truncated receptor level in patients with acute ST-segment elevation myocardial infarction and undergoing diabetes or not: A retrospective study.

The role of advanced glycation end products (AGEs) and its C-terminal truncated receptor (soluble receptor for advanced glycation end products, sRAGE) in ST-segment elevation myocardial infarction (STEMI) patients with or without diabetes is unknown. We compared their levels in patients with and without STEMI, as well as with and without diabetes. A prospective observational study was performed between December 2014 and December 2015. Study group included STEMI patients with coronary artery disease; control group included patients without coronary artery disease. Levels of AGEs and sRAGE were tested on Days 0, 2, and 5 after STEMI. Levels of creatine kinase-MB (CK-MB), cardiac troponin I, and N-terminal pro-brain natriuretic peptide (NT-proBNP) were tested on Days 0, 1, 2, and 3. Patient's diabetic status was determined by medical history or oral glucose tolerance test. Compared to patients in the control group, STEMI patients showed elevated levels of AGEs and sRAGE. In the STEMI group, diabetic patients had higher levels of AGEs and sRAGE compared to nondiabetic patients. The level of AGEs correlated with peak level of CK-MB in the overall population of patients with STEMI and with peak level of NT-proBNP in diabetic patients with STEMI. Levels of AGEs and sRAGE were elevated after STEMI, especially among patients with diabetes. These markers could serve to indicate the severity of myocardial injury and cardiac insufficiency, and play a potential role in predicting the prognosis of patients with STEMI.

Pioglitazone Attenuates Atherosclerosis in Diabetic Mice by Inhibition of Receptor for Advanced Glycation End-Product (RAGE) Signaling.

BACKGROUND Peroxisome proliferator-activated receptor-g (PPAR-g) exhibits anti-inflammatory and anti-diabetic properties, and is protective against cardiovascular diseases. This study aimed to determine the effects of a PPAR-g agonist pioglitazone on atherogenesis in an ApoE knockout mouse (ApoE-/-) diabetic mouse model and in a cultured vascular smooth muscle cells (VSMCs) model. MATERIAL AND METHODS Male ApoE-/- mice were rendered diabetic by 5 daily intraperitoneal injections of streptozotocin. Pioglitazone (20 mg/kg/d) or PPAR-γ inhibitor GW9662 (1 mg/kg/d) were administered for 12 weeks. At the end of treatment, mice were killed and the aortae were isolated. Oil Red O staining was used to evaluate atherosclerotic plaque area. H&E staining was used to evaluate the number of complicated plaques. Western blotting and immunohistochemistry were used to determine the expression of advanced glycation end-products (RAGE) and PPAR-γ. The effects of pioglitazone and GW9662 on RAGE and PPAR-g expression were examined in cultured primary mouse VSMCs in hyperglycemic conditions. RESULTS Administration of pioglitazone in diabetic ApoE-/- mice successfully reduced atherosclerotic plaque area and the number of complicated plaques. Moreover, pioglitazone inhibited RAGE and stimulated PPAR-γ protein expression in atherosclerotic plaques of diabetic ApoE-/- mice. In cultured VSMCs upon high-glucose challenge, pioglitazone downregulated RAGE mRNA and protein expression. Blockade of PPAR-γ activity by GW9662 remarkably attenuated the inhibitory actions of pioglitazone on atherogenesis, both in diabetic ApoE-/- mice and in cultured VSMCs, upon high-glucose challenge. CONCLUSIONS Pioglitazone has a therapeutic effect on atherosclerosis in diabetes, and inhibition of RAGE signaling plays a critical role in mediating the beneficial effects of pioglitazone.

Telmisartan ameliorates adipoR1 and adipoR2 expression via PPAR-γ activation in the coronary artery and VSMCs.

The effects of telmisartan on insulin-resistant properties and expression of adiponectin receptors (AdipoRs) were investigated. A diabetic rat model was established using a high-fat diet and streptozotocin (25mg/kg) and primary rat coronary vascular smooth muscle cells (VSMCs) were used to elucidate the underlying mechanisms. The diabetic rats were insulin-resistant and exhibited weight gain, elevated blood pressures, and increased plasma triglyceride levels. These manifestations were ameliorated by elmisartan treatment. Four-week telmisartan therapy increased plasma adiponectin and decreased TNF-α expression in the coronary artery. Moreover, telmisartan significantly decreased AdipoR1 and AdipoR2 expression. Using high glucose-treated rat coronary VSMCs, telmisartan and PPAR-γ agonist GW1929 prominently stimulated PPAR-γ and decreased TNF-α expression. Interestingly, telmisartan or GW1929 also prevented hyperglycemia-induced downregulation of AdipoR1 and AdipoR2 expression. Additionally, GW9662 (PPAR-γ antagonist) significantly decreased the effects of telmisartan on AdipoR1 and AdipoR2 expression. These results demonstrated that telmisartan effectively ameliorated coronary insulin resistance and inflammation in diabetic rats and upregulated AdipoR1/R2 expression via activation of PPAR-γ in the coronary artery and VSMCs.

Voltage combined with pace mapping is simple and effective for ablation of noninducible premature ventricular contractions originating from the right ventricular outflow tract.

BACKGROUND: Premature ventricular contractions (PVCs) from the right ventricular outflow tract (RVOT) can resist conventional mapping strategies. Studies regarding optimal mapping and ablation methods for patients with noninducible RVOT-PVCs are limited. We retrospectively evaluated the efficacy and safety of a novel mapping strategy for these cases: voltage mapping combined with pace mapping. HYPOTHESIS: METHODS: We retrospectively included symptomatic patients (n = 148; 76 males; age, 44.5 ± 1.4 years) with drug-refractory PVCs originating from the RVOT, who underwent radiofrequency catheter ablation (RFCA), and stratified them as Group 1 and Group 2. Group 1 patients had noninducible RVOT-PVCs, determined after programmed stimulation, burst pacing, and isoproterenol infusion (n = 21; 12 males; age, 39.5 ± 10.8 years). Group 2 patients had inducible PVCs. Group 1 patients were subjected to voltage mapping combined with pace mapping; Group 2 underwent conventional mapping. In all patients prior to RFCA, detailed 3-dimensional electroanatomic voltage maps of the RVOT were obtained during sinus rhythm using the CARTO system. RESULTS: Patients from both groups had similar success and complication rates associated with the RFCA. In Group 2, 89% (113/127) experienced the earliest and the successful ablation points in the voltage transitional zone. During the follow-up (36 ± 8 months), patients from both groups suffered similar rates of PVC relapse (2/21 and 7/127, respectively; P = 0.826). CONCLUSIONS: Voltage mapping combined with pace mapping is effective and safe for patients with noninducible RVOT-PVCs determined by conventional methods.

RhoA/rock signaling mediates peroxynitrite-induced functional impairment of Rat coronary vessels.

BACKGROUND: Diabetes-induced vascular dysfunction may arise from reduced nitric oxide (NO) availability, following interaction with superoxide to form peroxynitrite. Peroxynitrite can induce formation of 3-nitrotyrosine-modified proteins. RhoA/ROCK signaling is also involved in diabetes-induced vascular dysfunction. The study aimed to investigate possible links between Rho/ROCK signaling, hyperglycemia, and peroxynitrite in small coronary arteries. METHODS: Rat small coronary arteries were exposed to normal (NG; 5.5 mM) or high (HG; 23 mM) D-glucose. Vascular ring constriction to 3 mM 4-aminopyridine and dilation to 1 µM forskolin were measured. Protein expression (immunohistochemistry and western blot), mRNA expression (real-time PCR), and protein activity (luminescence-based G-LISA and kinase activity spectroscopy assays) of RhoA, ROCK1, and ROCK2 were determined. RESULTS: Vascular ring constriction and dilation were smaller in the HG group than in the NG group (P < 0.05); inhibition of RhoA or ROCK partially reversed the effects of HG. Peroxynitrite impaired vascular ring constriction/dilation; this was partially reversed by inhibition of RhoA or ROCK. Protein and mRNA expressions of RhoA, ROCK1, and ROCK2 were higher under HG than NG (P < 0.05). This HG-induced upregulation was attenuated by inhibition of RhoA or ROCK (P < 0.05). HG increased RhoA, ROCK1, and ROCK2 activity (P < 0.05). Peroxynitrite also enhanced RhoA, ROCK1, and ROCK2 activity; these actions were partially inhibited by 100 µM urate (peroxynitrite scavenger). Exogenous peroxynitrite had no effect on the expression of the voltage-dependent K+ channels 1.2 and 1.5. CONCLUSIONS: Peroxynitrite-induced coronary vascular dysfunction may be mediated, at least in part, through increased expressions and activities of RhoA, ROCK1, and ROCK2.

Atorvastatin prevents advanced glycation end products (AGEs)-induced cardiac fibrosis via activating peroxisome proliferator-activated receptor gamma (PPAR-γ).

BACKGROUND: Previous studies have shown that the activation of advanced glycation end products (AGEs) contributed to the cardiac fibrosis in diabetic patients. Although it had been reported that statins have beneficial effects on cardiac fibrosis in hypertension and myocardial ischemia models, their effects on AGEs models have not been studied. We aimed to investigate the effects of atorvastatin (Ator) on the AGEs-induced cardiac fibrosis both in vitro and vivo. METHODS: Male Sprague-Dawley rats were randomly divided into four groups: Control, AGEs, Ator or AGEs+Ator. The cardiac function was evaluated with the echocardiography at the second and the third month. Fibrosis area, α-SMA and RAGE expression in cardiac tissue were measured. For in vitro study, rat cardiac fibroblasts were treated with PD98059 (ERK inhibitor), Ator or Ator+GW9662 (PPAR-γ antagonist), and then were stimulated with AGEs. Fibroblasts proliferation, ERK1/2, phosphorylated ERK1/2, α-SMA, and RAGE expression were studied. RESULTS: Compared with the control group, in vivo treatment with Ator significantly retarded the AGEs-induced diastolic function and attenuated cardiac fibrosis, α-SMA, and RAGE over expression induced by AGEs. Consistently, Ator prominently downregulated RAGE and α-SMA, while inhibited phosphorylation of ERK1/2 and fibroblast proliferation induced by AGEs in vitro. The GW9662 neutralized these effects of Ator on cardiac fibroblasts stimulated by AGEs. CONCLUSION: In this study, we demonstrated that AGEs-induced fibroblast proliferation and differentiation were dependent on AGEs-RAGE-ERK1/2 pathway and that atorvastatin could block this pathway via activating PPAR-γ.

Pioglitazone inhibits high glucose-induced expression of receptor for advanced glycation end products in coronary artery smooth muscle cells.

Receptor for advanced glycation end products (RAGE) is critical in inflammatory diseases, including diabetes and atherosclerosis. The mechanism underlying the effect of peroxisome proliferator­activated receptor γ (PPARγ) agonist pioglitazone (PIO) on RAGE expression in coronary artery smooth muscle cells (SMCs) stimulated by high glucose concentrations remains to be elucidated. In the present study, the effect and mechanism of action of PIO on RAGE expression in SMCs was investigated following treatment with high glucose concentrations. Rat coronary artery SMCs were pretreated with PIO alone, PIO and GW9662 (a PPARγ antagonist), diphenyleneiodonium (DPI; a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor) or the antioxidant pyrrolidine dithiocarbamate (PDTC; a nuclear factor­κB (NF­κB) inhibitor), followed by treatment with high glucose. RAGE mRNA and protein expression, reactive oxygen species (ROS) production and NF­κB nuclear translocation were investigated. Glucose induced RAGE expression in a dose­dependent manner, with maximal effect at a concentration of 25 mmol/l following treatment for 48 h. PIO, DPI and PDTC reduced high glucose­induced increases in RAGE protein and mRNA expression. PIO prominently downregulated RAGE expression and inhibited high glucose­induced increases in ROS production and NF­κB activation (P<0.05). Pretreatment with PIO and GW9662 did not exhibit this inhibitory effect. High glucose may stimulate RAGE expression in coronary artery SMCs through NADPH oxidase­mediated ROS generation and NF­κB activation. PIO downregulated RAGE expression and inhibited ROS production and NF­κB activation via PPARγ activation, which may prevent the inflammatory effect of AGE/RAGE system in diabetes.

Pioglitazone prevents hyperglycemia induced decrease of AdipoR1 and AdipoR2 in coronary arteries and coronary VSMCs.

BACKGROUND: Adiponectin receptors play an important role in inflammatory diseases like diabetes and atherosclerosis. Former studies revealed that the regulation of adiponectin receptors expression differs in the receptor responses to pioglitazone. However, expression of AdipoRs has not been investigated in the coronary arteries or the coronary vascular smooth muscle cells (VSMCs). In the present study we investigated the effect of pioglitazone on the adiponectin receptors both in vitro and in vivo. METHODS: Male Sprague-Dawley rats were randomly divided in three groups. One of them fed with regular chow (the Control group) and two of them fed with high-fat diet and then received low-dose Streptozotocin once by intraperitoneal injection (the DM groups). Rats in one of the DM groups were further treated with pioglitazone (the PIO group). Blood pressure, serum adiponectin, fasting blood glucose, fasting serum insulin, cholesterol, triglyceride, AdipoR1 and AdipoR2 expression, and TNF-α expression in coronary arteries of these groups were investigated. For the in vitro study, the rat coronary VSMCs maintained under defined in vitro conditions were treated with either PIO or the PIO+ GW9662 (PPAR-γ antagonist), and then stimulated with high glucose. AdipoR1 and AdipoR2 expression, TNF-α expression and PPAR-γ expression were investigated. RESULTS: Compared to the DM group, treatment with PIO in vivo significantly attenuated cholesterol level, triglyceride level, fasting serum insulin and TNF-α overexpression (p<0.05). PIO also increased AdipoR1 and AdipoR2 expression in coronary arteries, which were reduced notably in the DM group (p<0.05). Consistently, in the study with rat coronary VSMCs, PIO prominently downregulated TNF-α expression and induced PPAR-γ expression, as well as prevented hyperglycemia induced decrease of AdipoR1 and AdipoR2 expression (p<0.05). And pretreatment of PIO+GW9662 did not manifest the prevention effect. CONCLUSION: In this study, we showed that treatment with PIO could ameliorate coronary insulin resistant and upregulate the expression of AdipoR1/R2. PIO showed an anti-atherogenic property via the activation of PPAR-γ, suppression of TNF-α overexpression in coronary and coronary VSMCs.

[Transurethral resection of bladder neck for female bladder neck sclerosis: a prospective urodynamics study].

OBJECTIVE: To explore the probable unsuccessful reasons for transurethral resection of bladder neck (TUR-BN) of female bladder neck sclerosis. METHODS: Thirty eligible cases received urodynamic inspections at pre-operation, post-operation of months 1, 2, 3 and 6 and year 1. RESULTS: TUR-BN was effective in 27 patients (90%), but ineffective in 3 (10%). Among the effective cases, the urodynamic parameters of Qmax and Qave increased (P < 0.05) while the residual urine volume and maximum pressure of detrusor contraction decreased (P < 0.05). The above four parameters showed no difference in those ineffective cases (P > 0.05). CONCLUSION: TUR-BN is an effective therapy for female bladder neck sclerosis. Those ineffective cases are probably caused by functional obstruction. Further urodynamic imaging studies may help to confirm the causes.

Association of neutrophil/lymphocyte ratio with long-term mortality after ST elevation myocardial infarction treated with primary percutaneous coronary intervention.

BACKGROUND: Primary percutaneous coronary interventions (PCI) have been proposed as a novel superior management strategy in patients with ST elevation myocardial infarction (STEMI). This study tested the hypothesis that in the acute phase of myocardial infarction with ST-segment elevation, the neutrophil/lymphocyte (N/L) ratio is a predictor of long-term prognosis. METHODS: We analyzed 551 consecutive STEMI patients treated with primary PCI at a single university center. Patients were stratified according to quartiles of the mean neutrophil/lymphocyte ratio. RESULTS: Kaplan-Meier survival analysis showed a cumulative eight-year survival of 94.2% in the first quartile, 92.0% in the second quartile, 91.3% in the third quartile, and 75.4% in the fourth quartile (P < 0.001 by log rank). Relative to patients in the other three lower N/L ratio quartiles, patients in the highest quartile were more than four times more likely to die during hospitalization (P < 0.001) and during long-term follow-up (P < 0.001). By multivariate Cox regression analysis including baseline demographic, clinical, and angiographic covariables, the N/L ratio in the highest quartile remained an independent predictor of mortality (hazard ratio 2.38, 95% confidence interval (CI) 1.42 to 3.98; P = 0.001). CONCLUSION: The neutrophil/lymphocyte ratio is a strong independent predictor of long-term mortality after ST elevation myocardial infarction treated with very early revascularization.

[Glucose level on admission and outcome after primary percutaneous coronary intervention in patients with acute myocardial infarction].

OBJECTIVE: To investigate the influence of elevated glucose level on epicardial/microvascular flow and survival in patients with acute ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (PCI). METHODS: A total of 308 patients with STEMI underwent primary PCI were divided into 3 groups according to the glucose level on admission: group 1, < 7.8 mmol/L; group 2, 7.8-11.0 mmol/L, and group 3, > or = 11.0 mmol/L. RESULTS: Compared with group 1, patients in the group 2 and 3 were older, had higher triglycerides levels and more 2-vessel or 3-vessel diseases. Although TIMI flow after PCI were similar among groups (89.7%, 86.0% and 86.3%, P = > 0.05), corrected TIMI frame count (CTFC) in group 2 and group 3 were higher than that in group 1. Moreover, TIMI myocardial perfusion grade (TMPG) 0-1 grade rate post PCI was higher in group 2 and 3 (30.3% and 29.0%) than that of group 1 (17.3%, P < 0.05). There was less frequently complete ST-segment resolution (56.7%) and early T wave inversion (58.3%) in group 3 than that of group 1 after PCI (72.0% and 73.4% respectively, P < 0.05). Mortality rate at 30 days post PCI was significantly higher in the group 3 (10.4%) than that in the group 1 (2.6%, P < 0.05). CONCLUSION: Elevated glucose level on admission in ST-segment elevation myocardial infarction patients treated with primary PCI is associated with reduced myocardial microvascular flow. Abnormal myocardial microvascular flow might contribute to the poor outcomes observed in patients with hyperglycemia on admission.

The influence of admission glucose on epicardial and microvascular flow after primary angioplasty.

BACKGROUND: Patients with elevated admission glucose levels may be at increased risk of death after myocardial infarction, independent of other baseline risk factors and more severe coronary artery disease. However, data regarding admission glucose and epicardial and microvascular flow after primary angioplasty is limited. METHODS: Angioplasty was performed in 308 ST-segment elevated myocardial infarction patients. Patients were divided into 3 groups on the basis of admission glucose level: group 1, < 7.8 mmol/L; group 2, (7.8 - 11.0) mmol/L; and group 3, >or= 11.0 mmol/L. RESULTS: Compared with group 1, patients in group 2 and group 3 were more often female and older. Triglycerides (TG) in group 3 were significantly higher than group 1. At angiography, they more frequently had 2-vessel or 3-vessel disease. In the infarct-related artery, there was no relationship between hyperglycemia and thrombolysis in myocardial infarction (TIMI) 3 flow after percutaneous coronary intervention (PCI) (89.7%, 86.0% and 86.3%, P = NS). However, corrected TIMI frame count (CTFC) in group 2 and group 3 were more than group 1. TIMI myocardial perfusion grade (TMPG) 0 - 1 grade among patients with hyperglycemia after PCI were more frequent (30.9% and 29.0% vs 17.3%, P < 0.05). There was less frequent complete ST - segment resolution (STR) and early T wave inversion among patients with hyperglycemia after PCI. CONCLUSION: Elevated admission glucose levels in ST - segment elevation myocardial infarction patients treated with primary PCI are independently associated with impaired microvascular flow. Abnormal microvascular flow may contribute at least in part to the poor outcomes observed in patients with elevated admission glucose.