Additional file 1: of Epidemiology of burns in pediatric patients of Beijing City

Raw data of epidemiology in pediatric burned patients of Beijing City. (XLSX 64 kb

Role of α‑Dicarbonyl Compounds in the Inhibition Effect of Reducing Sugars on the Formation of 2‑Amino-1-methyl-6-phenylimidazo[4,5‑<i>b</i>]pyridine

The effect of reducing sugars on formation of PhIP in fried pork was investigated, and the underlying mechanisms were revealed by studying the reaction pathways between α-dicarbonyl compounds (α-DCs) and PhIP. The addition of reducing sugars (such as glucose) greatly reduced the amount of PhIP in fried pork from 15.5 ng/g to less than 1.0 ng/g. The amount of PhIP decreased significantly with an increasing level of added α-DCs in model systems. Similarly, the addition of methylglyoxal (MGO) decreased significantly the levels of phenylalanine (Phe) and creatinine (Crn) but increased significantly the level of phenylacetaldehyde (PEA). 2-Amino-1-methyl-5-(2-oxopropylidene)-imidazol-4-one and <i>N</i>-(1-methyl-4-oxoimidazolidin-2-ylidene) amino propionic acids were identified in MGO/Crn and MGO/Crn/Phe model systems and fried pork with glucose. These results revealed that the degradation products of reducing sugarsα-DCsplay an important role in inhibiting formation of PhIP by reacting with key precursors of PhIP and itself

Cardioprotective Effects of a Novel Hydrogen Sulfide Agent–Controlled Release Formulation of S-Propargyl-Cysteine on Heart Failure Rats and Molecular Mechanisms

<div><p>Objective</p><p>Heart failure (HF) is one of the most serious diseases worldwide. S-propargyl-cysteine (SPRC), a novel modulator of endogenous hydrogen sulfide, is proved to be able to protect against acute myocardial ischemia. In order to produce more stable and sustainable hydrogen sulfide, we used controlled release formulation of SPRC (CR-SPRC) to elucidate possible cardioprotective effects on HF rats and investigate involved mechanisms on apoptosis and oxidation.</p><p>Methods</p><p>Left coronary artery was occluded to induce HF model of rat. The survival rats were randomly divided into 7 groups after 24 hours and treated with drugs for 6 weeks. Echocardiographic indexes were recorded to determine cardiac function. TTC staining was performed to determine infarct size. Plasmatic level of hydrogen sulfide was detected by modified sulfide electrode. Activity of enzyme and expression of protein were determined by colorimetry and Western blot, respectively.</p><p>Results</p><p>The cardioprotective effects of CR-SPRC on HF rats were confirmed by significant reduction of infarct size and improvement of cardiac function, with better effects compared to normal SPRC. CR-SPRC modulated antioxidant defenses by preserving levels of GSH, CAT and SOD and reducing CK leakage. In addition, CR-SPRC elevated ratio of Bcl-2/Bax and inhibited activity of caspases to protect against myocardial apoptosis. The cardioprotective effects of CR-SPRC were mediated by hydrogen sulfide.</p><p>Conclusions</p><p>All experiment data indicated cardioprotective effects of CR-SPRC on HF rats. More importantly, CR-SPRC exerted better effects than normal SPRC in all respects, providing a new perspective on hydrogen sulfide-mediated drug therapy.</p></div

CR-SPRC preserved oxidative stress and prevented cell damage.

<p>The levels of CK (A), CAT (B), GSH (C) and SOD (D) in tissue extract of ventricular myocardium were determined by colorimetry, and statistically analyzed. Data were presented as means ± standard deviations (n = 5–6). ^#P<0.01 versus sham, ^*P<0.01 versus HF, ^**P<0.05 versus HF, ^&P<0.01 versus CR-SPRC, ^&&P<0.05 versus CR-SPRC. All experiments repeated at least 3 times.</p

In-Situ Grafting MPEG on the Surface of Cell-Loaded Microcapsules for Protein Repellency

<div><p>The protein repelled alginate-graft-BAT/chitosan/MPEG-norbornene (A_BCP_N) hydrogel microcapsules were achieved by copper-free ‘click’ reaction between azides from BAT and alkylenes from norbornene. The MPEG modified polyelectrolyte microcapsules showed significant resistance to immune protein adsorption and good biocompatibility in vivo. Moreover, the mild reaction condition made it feasible that the microcapsules could be formed and modified <i>in situ</i> even when live cells were encapsulated, and precluded the damage cause by other voilent modifications methods to transplanted cells or tissues.</p></div

CR-SPRC inhibited activity of caspases.

<p>The levels of caspase 3 and caspase 9 in tissue extract of ventricular myocardium were determined by colorimetry, and statistically analyzed. Data were presented as means ± standard deviations (n = 5–6). ^#<i>P</i><0.01 versus sham, ^##<i>P</i><0.05 versus sham, ^*<i>P</i><0.01 versus HF, ^**<i>P</i><0.01 versus HF, ^&<i>P</i><0.01 versus CR-SPRC. All experiments repeated at least 3 times.</p

Effects of CR-SPRC on expression of proteins.

<p>(A) The expression of Bax, Bcl-2 and CSE were detected by Western blot. β-Tubulin was used as a loading control. (B), (C) and (D) were statistical analysis of (A). Data were presented as means ± standard deviations (n = 5–6). ^#<i>P</i><0.01 versus sham, ^*<i>P</i><0.01 versus HF, ^**<i>P</i><0.05 versus HF, ^&<i>P</i><0.01 versus CR-SPRC. All experiments repeated at least 3 times.</p

CR-SPRC improved cardiac function of HF rats.

<p>(A) Representative echocardiographic records obtained from a short-axis mid-ventrical view of hearts of the HF rats. (B), (C), (D) and (E) were statistical analysis of the data obtained or derived from original echocardiographic records. Data were presented as means ± standard deviations (n = 6). ^#<i>P</i><0.01 versus sham, ^*<i>P</i><0.01 versus HF, ^**<i>P</i><0.05 versus HF, ^&<i>P</i><0.01 versus CR-SPRC, ^&&<i>P</i><0.05 versus CR-SPRC.</p

CR-SPRC reduced infarct size of left ventricle.

<p>(A) Representative photograph of infarct size which was determined by 1% triphenyltetrazolium chloride (TTC) staining. (B) Statistical analysis of infarct size. Data were presented as means ± standard deviations (n = 5–8). ^#<i>P</i><0.01 versus sham, ^*<i>P</i><0.01 versus HF, ^&<i>P</i><0.01 versus CR-SPRC.</p

Effects of CR-SPRC on body weight and survival rate of HF rats.

<p>(A) Body weight curve. Data were presented as means ± standard deviations (n = 10–16). ^*<i>P</i><0.01 HF versus sham, CR-SPRC versus HF, CR-SPRC versus SPRC, CR-SPRC+PAG versus CR-SPRC. (B) Kaplan–Meier survival curve. <i>P</i> = 0.041 CR-SPRC versus HF.</p