A ratiometric fluorescence sensor based on gold silver nanoclusters and tungsten disulfide quantum dots with simple fabrication for the detection of copper ions in river water.

Copper plays a key role in the human body; meanwhile, excess Cu2+ ions can result in various diseases. Nanoclusters (NCs) are often used to measure Cu2+ ions, but there are two difficulties. On the one hand, a single probe of NCs is easily affected by environmental factors. On the other hand, it is difficult to mask the interference of Pb2+ ions and Cd2+ ions in the process of detecting Cu2+ ions. As a new type of quantum dots (QDs), tungsten disulfide quantum dots (WS2-QDs) have some advantages of simple synthesis and stable luminescence properties. Stable WS2-QDs with blue fluorescence are used as a reference probe, while gold silver nanoclusters (AuAgNCs) with red fluorescence are used as a response probe. A ratiometric fluorescent sensor was constructed by mixing the two styles of fluorescent probes, which is abbreviated as NCs/QDs. This nano-sensor can be used to detect the concentration of Cu2+ ions, in which the fluorescence of QDs does not change significantly, while the fluorescence of NCs can be quenched by Cu2+ ions. The concentration of Cu2+ ions can be determined as low as 0.12 µM with a linear range from 0.3 to 3 µM. The common interference caused by Pb2+ and Cd2+ ions can be eliminated by the phosphate buffer solution (PBS). This sensor was used to detect the concentration of Cu2+ in river water with satisfactory results.

Activin a inhibits foam cell formation and up-regulates ABCA1 and ABCG1 expression through Alk4-Smad signaling pathway in RAW 264.7 macrophages.

BACKGROUND: Activin A has been reported to play important roles in the pathogenesis of atherosclerosis. The purpose of this study is to investigate the effects of activin A on oxidized low-density lipoprotein (ox-LDL)-induced foam cell formation and explore the underlying molecular mechanisms in murine macrophage-like cell line RAW 264.7. METHODS: The effects of activin A on Dil-labeled ox-LDL uptake were examined by confocal microscopy and flow cytometry analysis. The mRNA and protein levels of cholesterol receptors were analyzed by RT-qPCR and western blot analysis, respectively. To investigate whether activin receptor-like kinase 4 (Alk4) is required for activin A-mediated cellular effects, cells were pre-treated with SB-431542. The involvement of Smad2, Smad3 and Smad4 was confirmed by transfection with specific small interfering RNAs (siRNAs). RESULTS: Activin A inhibits ox-ldl-induced foam cell formation and class A scavenger receptors (SR-A) expression, while up-regulates ATP-binding cassette transporter A1 (ABCA1) and ABCG1 expression in RAW 264.7 macrophages. Pre-treatment with SB-431542 abolished activin A-mediated anti-atherogenic effect. Knockdown of Smad2 reversed activin A-induced inhibition of ox-LDL uptake and SR-A expression. However, knockdown of Smad3 or Smad4 did not have such effect. Meanwhile, knockdown of either Smad2, Smad3 or Smad4 reversed the activin A-induced up-regulation of ABCA1 and ABCG1. CONCLUSIONS: Our study provides novel evidence that activin A may exert anti-atherogenic effects through Alk4-Smad signaling pathway in RAW 264.7 macrophages.

Evaluation of Extended-Interval Dabigatran Dosing in Older Patients With Non-Valvular Atrial Fibrillation.

OBJECTIVE: To evaluate the safety and efficacy of extended-interval dabigatran dosing in older Chinese patients with non-valvular atrial fibrillation. METHODS: We conducted an observational study on non-valvular atrial fibrillation patients administered dabigatran at different dosing intervals at the Department of Geriatrics, Peking University First Hospital, China. We enrolled 121 consecutive non-valvular atrial fibrillation patients aged ≥60 years on dabigatran therapy (mean age, 79.6 ± 7.4 years); they were administered conventional low-dose dabigatran (110 mg twice daily) or extended-interval dosing with dabigatran (110 mg every 16 h or every 24 h). All patients received follow-up care, and we evaluated the presence of bleeding and thromboembolic events. RESULTS: All patients exhibited creatinine clearance greater than 30 mL/min with an average of 56.6 ± 17.3 mL/min. Sixty-two patients received extended-interval dosing with dabigatran at a mean dose of 117.1 ± 18.6 mg daily. Patients on extended-interval dosing were older; they exhibited lower creatinine clearance and bodyweight and higher CHA2DS2-VASc and HAS-BLED scores. The mean follow-up time was 25.8 ± 15.6 months. No significant differences were observed in the trough and peak values of the activated partial thromboplastin time and in thromboembolic or bleeding events between the 2 groups. CONCLUSION: Extended-interval dabigatran dosing in older patients with non-valvular atrial fibrillation and lower creatinine clearance can maintain activated partial thromboplastin time trough and peak values comparable to the conventional low dose. Physician-prescribed practices regarding dabigatran dosing intervals do not lead to worse outcomes in the above-mentioned population.

Association of Sleep Duration with Weight Gain and General and Central Obesity Risk in Chinese Adults: A Prospective Study.

OBJECTIVE: Evidence on the association between sleep duration and obesity among adults is inconsistent. Prospective studies investigating the association in Chinese adults have been limited. This study aims to prospectively evaluate sleep duration in relation to subsequent weight gain and general and central obesity risk among Chinese adults. METHODS: A total of 21,958 participants aged 30 to 79 years reported their daily sleep duration. Obesity indicators were objectively measured; then significant weight gain (≥ 5 kg) and general and central obesity were modeled as the outcome. Logistic regression models were used to estimate odds ratios and 95% CIs. RESULTS: Average sleep duration was 7.5 hours at baseline. During 8.0 ± 0.8 years of follow-up, participants who reported sleeping ≤ 6 hours had higher risk for significant weight gain than those who slept 7 hours (multivariable-adjusted odds ratio: 1.13; 95% CI: 1.02-1.29). The association was stronger among those who were physically inactive at baseline (P = 0.04 for interaction). Short sleep duration was also associated with subsequent incident central obesity, with odds ratio of 1.13 (95% CI: 1.00-1.28), but not with incident general obesity (P = 0.31). CONCLUSIONS: Compared with those who slept 7 hours per day, short sleepers had an increased risk of significant weight gain and central obesity.

Upper esophageal sphincter augmentation reduces pharyngeal reflux in nasogastric tube-fed patients.

OBJECTIVES/HYPOTHESIS: Aspiration of gastric refluxate is one of the most commonly observed complications among long-term nasogastric tube (NGT) fed patients. The upper esophageal sphincter (UES) pressure barrier is the main defense mechanism against pharyngeal reflux of gastric contents. Our objective was to investigate the efficacy and safety of the UES assist device (UES-AD) in preventing gastric reflux through the UES in long-term NGT-fed patients. STUDY DESIGN: Self-Controlled Case series. METHODS: We studied 10 patients (mean age = 90.6 ± 3.4 years, four females) with dysphagia caused by stroke or dementia who were fed for 0.5 to 5 years (median = 3 years) by NGT. External pressures of 20 to 30 mm Hg were applied by using a handmade UES-AD, which was started 2 hours after the beginning of NGT infusion and was alternated between periods of 2 hours on and 2 hours off, for a total of 12 hours. Placement of the impedance sensors within the UES was guided by high-resolution manometry. Trans-UES and intraesophageal reflux events were recorded by using 24-hour combined pH-impedance measurements. RESULTS: No aspiration pneumonia events were noted in the period 1 month before or during the study in any of the cohort. Baseline UES pressure averaged 17.5 ± 9.4 mm Hg and was increased to 38.9 ± 11.9mm Hg after application of the UES-AD. Overall frequency of trans-UES reflux decreased significantly with the UES-AD compared to without (0.8 ± 0.9 vs. 3.3 ± 2.8, P < .05 for the 12-hour study period). There was no effect of the UES-AD on esophageal reflux events (7.4 ± 4.4 vs. 6.4 ± 3.0, P > .05). CONCLUSIONS: UES-AD significantly decreases the number of trans-UES reflux events and can potentially reduce the aspiration risk associated with NGT feeding. LEVEL OF EVIDENCE: 4. Laryngoscope, 128:1310-1315, 2018.

Synthesis, characterization and luminescence of europium perchlorate with MABA-Si complex and coating structure SiO2 @Eu(MABA-Si) luminescence nanoparticles.

This article reports a novel category of coating structure SiO2 @Eu(MABA-Si) luminescence nanoparticles (NPs) consisting of a unique organic shell, composed of perchlorate europium(III) complex, and an inorganic core, composed of silica. The binary complex Eu(MABA-Si)3 ·(ClO4 )3 ·5H2 O was synthesized using HOOCC6 H4 N(CONH(CH2 )3 Si(OCH2 CH3 )3 )2 (MABA-Si) and was used as a ligand. Furthermore, the as-prepared silica NPs were successfully coated with the -Si(OCH2 CH3 )3 group of MABA-Si to form Si-O-Si chemical bonds by means of the hydrolyzation of MABA-Si. The binary complexes were characterized by elemental analysis, molar conductivity and coordination titration analysis. The results indicated that the composition of the binary complex was Eu(MABA-Si)3 ·(ClO4 )3 ·5H2 O. Coating structure SiO2 @Eu(MABA-Si) NPs were characterized using transmission electron microscopy (TEM), scanning electron microscopy (SEM) and infrared (IR) spectra. Based on the SEM and TEM measurements, the diameter of core-SiO2 particles was ~400 and 600 nm, and the thickness of the cladding layer Eu(MABA-Si) was ~20 nm. In the binary complex Eu(MABA-Si)3 ·(ClO4 )3 ·5H2 O, the fluorescence spectra illustrated that the energy of the ligand MABA-Si transferred to the energy level for the excitation state of europium(III) ion. Coating structure SiO2 @Eu(MABA-Si) NPs exhibited intense red luminescence compared with the binary complex. The fluorescence lifetime and fluorescence quantum efficiency of the binary complex and of the coating structure NPs were also calculated. The way in which the size of core-SiO2 spheres influences the luminescence was also studied. Moreover, the luminescent mechanisms of the complex were studied and explained.

[Postprandial changes of blood lipid after ordinary Chinese diet and the influencing factors thereof].

OBJECTIVE: To investigate the postprandial changes of blood lipid after ordinary Chinese diet and the influencing factors thereof. METHODS: Peripheral venous blood samples were collected from 88 patients, 72 males and 16 females, aged (65 +/- 12), 53 with hypertension, 35 with coronary heart diseases, and 27 with diabetes, while fasting and 4 h after breakfast and lunch to measure the levels of lipoproteins, including total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), apolipoprotein A (ApoA), ApoB, lipoprotein (Lp) (a), oxidized LDL (ox-LDL). Homeostasis model assessment insulin resistance index (HOMA-IR) was calculated. Weight, height, waist circumference, and hip circumference were examined, and body mass index (BMI) and waist/hip ratio (WHR) were calculated. RESULTS: The TG level after breakfast was (2.79 +/- 0.19) mmol/L, significantly higher than the fasting level by 49.5% [(1.94 +/- 0.13) mmol/L, P < 0.05]. The TG level after lunch was (3.08 +/- 0.26) mmol/L, significantly higher than the fasting level by 58.8% [(1.94 +/- 0.13) mmol/L, P < 0.05]. The ox-LDL after breakfast was (430 +/- 21) microg/L, significantly higher than the fasting level by 32.6% [(324 +/- 14) microg/L, P < 0.05] and the ox-LDL level after lunch was (448 +/- 17) microg/L, significantly higher than the fasting level by 38.1% [(324 +/- 14) microg/L, P < 0.05]. The fasting insulin level was (62 +/- 4) pmol/L, and the HOMA-IR was (15.27 +/- 1.08). The fasting insulin level was positively correlated with the fasting and postprandial TG levels (all P < 0.01). The IR index was positively correlated with the fasting TG and TG after breakfast (both P < 0.05). Fasting insulin and HOMA-IR were negatively correlated with the fasting and postprandial HDL-C levels (all P < 0.05), and positively correlated with the fasting and postprandial TC/HDL-C levels (all P < 0.05). BMI and WHR were negatively correlated with the fasting and postprandial HDL-C (both P < 0.01). BMI was positively correlated with fasting and postprandial TG (both P < 0.05). The insulin level, HOMA-IR, and BMI were negatively correlated with LPL (r = -0.232 - 0.297, P < 0.05). LPL were positively correlated with fasting and postprandial HDL-C levels (r = 0.37, 0.31, 0.35, all P < 0.01). CONCLUSION: The TG and ox-LDL levels significantly increased postprandially. The postprandial blood lipid levels are significantly correlated with the fasting blood lipids.

Hydrogen sulfide protects rat lung from ischemia-reperfusion injury.

Recent studies have indicated that hydrogen sulfide (H(2)S) is capable of modulating many physiological processes, which prompted us to investigate the potential of H(2)S as a lung protective agent. To explore changes in the generation of endogenous H(2)S and the role of H(2)S in the pathogenesis of pulmonary ischemia-reperfusion (I/R) injury in rats, we built an isolated rat lung I/R model. Lungs were subjected to 45 min ischemia followed by reperfusion (45 min) and were pretreated with H(2)S (50 micromol/l or 100 micromol/l) or an irreversible inhibitor of cystathionine-gamma-lyase (CSE), propargylglycine (PPG; 2 mmol/l). We examined indices of lung injury: lung histological change, perfusion flow rate, ratio of lung wet weight to dry weight (w/d), and lung compliance. H(2)S content and CSE protein expression in lung tissues were measured. Malondialdehyde (MDA) content, activities of superoxide dismutase (SOD) and catalase (CAT), and restraint of superoxide anion (O(2)(-)) production in lung tissues were measured to reflect oxidative stress. In the current study, we demonstrated that H(2)S content and CSE activity in lungs after I/R were significantly higher than those in the control group. Preperfusion with H(2)S attenuated the lung I/R injury while preperfusion with PPG aggravated the lung I/R injury. H(2)S preperfusion reduced I/R-induced MDA production and potentiated SOD and CAT activities and the restraint of O(2)(-) production in the lungs under I/R, which attenuated lung oxidative injury. These findings suggest that endogenous CSE/H(2)S pathway might be involved in the pathogenesis of lung I/R injury and that administration of H(2)S might be of clinical benefit in lung I/R injury.