Application of metabolomics in establishing primary nephrotic syndrome diagnosis model / 中华肾脏病杂志

Objective To establish diagnosis model and explore related metabolic pathways by analyzing the serum metabolic profile of patients with primary nephrotic syndrome (PNS) through metabolomics.Methods Thirty PNS patients hospitalized in Huai'an First People's Hospital between December 2010 and April 2012 were enrolled.High performance liquid chromatography-mass spectrometry (LC-MS) was employed to detect metabolites in the serum of 30 PNS patients and 30 healthy controls.Metabolic fingerprint profiling and multivariate pattern recognition analysis were combined to establish disease-specific metabolic diagnosis model,and metabolic pathway analysis was performed.Results PNS group and control group could be well separated by principal component analysis (PCA) model as well as partial least-squares discriminant analysis (PLS-DA) model with Q2 of 0.300.There was well interpretation in PLA-DA model (R2X=0.581,R2Y=0.452).Compared with healthy controls,PNS patients had decreased cholestane 3,7,12,15 alcohol,acyl glycerine,phytosphingosine and tryptophan,and increased sphingomyelin,arginine and glutamic acid (all VIP ＞ 1,P ＜ 0.05).The metabolic disorders pathways of PNS patients included sphingolipid metabolism,arginine and proline metabolism,linoleic acid metabolism and pyrimidine metabolism (all impact ＞0.10 and P ＜ 0.05).Conclusions Metabolomics combined with multivariate pattern recognition analysis may be a new tool for diagnosis and monitoring of PNS.

A investigation of thirdhand smoke pollution in 3 types of places of Nanjing, 2014 / 中华预防医学杂志

<p><b>OBJECTIVE</b>To investigate thirdhand smoke (THS) pollution in certain places of Nanjing, as well as to analyze its distribution characteristics.</p><p><b>METHODS</b>From March to May, 2014, we selected 3 types of places (residencies, public places and transportation vehicles) that were close to people's living in Jianye,Yuhua,Jiangning,Xuanwu,Gulou and Pukou districts of Nanjing city.For each of the above 3 types of places, 2-3 smoking and non-smoking (smoking ban) locations were investigated, totally 51 locations, 9-10 samples were collected each location, totally 477 samples. The surface wipe sampling method in conjunction with liquid chromatography-tandem mass spectrometry (LC-MS/MS) was utilized to quantify the levels of nicotine that served as the tracer of THS pollution.One-way ANOVA and t-tests were employed to compare the levels of nicotine collected at different places and locations.</p><p><b>RESULTS</b>Totally 477 samples were collected in this study, of which 27.0% was from residencies (129/477), 61.0% (291/477) from public places and 11.9% (57/477) from transportations. The levels of indoor surface nicotine in smoking residences, public places and transportations were (214 ± 55),(1 408 ± 177) and (1 511 ± 785) µg/m(2), respectively, which were all higher than those in the corresponding non-smoking places ((23 ± 9),(62 ± 11), and (46 ± 15) µg/m(2); t values were 13.79, 13.15, 3.45, respectively. P values were <0.001, <0.001 and 0.006, respectively).In the smoking places, the levels of surface nicotine on walls, desks, sofas, cabinets, door backsides and air conditioning openings were (171 ± 62),(232 ± 38),(373 ± 151),(903 ± 239), (978 ± 212), (1 721 ± 517) µg/m(2) (F = 7.06, P = 0.009).In the smoking condition, the levels of surface nicotine collected from public places were higher (F = 9.25, P = 0.024), while under non-smoking (smoking ban) conditions, the levels of surface nicotine collected from residences were lower (F = 7.88, P < 0.001).</p><p><b>CONCLUSION</b>THS pollution was widespread in public places, residences and transportations in Nanjing city, which was more serious in the smoking environments than non-smoking (smoking ban) environments; the contamination was less serious in non-smoking (smoking ban) private residences; in the smoking condition, the levels of surface nicotine were relatively high at locations close to air conditioning openings, door backsides and cabinets.</p>

Effect of carbon disulfide exposure on fatty acid metabolism in ApoE knockout and C57BL/6J mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the influences of carbon disulfide (CS2) exposure on fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice.</p><p><b>METHODS</b>Twenty-four male ApoE knockout mice were randomly and equally divided into four groups: a CS2-exposed normal diet group, a CS2-unexposed normal diet group, a CS2-exposed high-fat diet group, and a CS2-unexposed high-fat diet group. Twenty-four C57BL/6J male mice were divided into four groups in the same way. The CS2-exposed groups were exposed to CS2 (1 g/m(3)) by static inhalation for 5 hours a day, 5 days a week. After two weeks, the whole blood of mice was collected. Methyl ester derivatization of fatty acids was performed using an acid-catalyzed method. Fatty acid contents before and after exposure were compared by gas chromatography-mass spectroscopy.</p><p><b>RESULTS</b>There were significant differences in fatty acid contents of mice between the four groups. For the C57BL/6J mice, the arachidic acid contents in the CS2-exposed high-fat diet group were significantly lower than those in the CS2-unexposed high-fat diet group (P = 0.045 0). For the ApoE knockout mice, the arachidonic acid contents in the CS2-exposed normal diet group were significantly lower than those in the CS2-unexposed control diet group (P = 0.045 2). For the ApoE knockout mice, the γ-linolenic acid contents in the CS2-exposed high-fat diet group were significantly higher than those in the unexposed high-fat diet group (P = 0.044 7).</p><p><b>CONCLUSION</b>Exposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.</p>

Effects of carbon disulfide inhalation on lipid levels of ApoE gene knockout mice and C57BL/6J mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of carbon disulfide (CS(2)) inhalation on the lipid levels of ApoE knockout gene mice and C57BL/6J mice.</p><p><b>METHODS</b>Fifty-one male ApoE gene knockout mice were randomly divided into four groups: CS(2)-exposed normal diet group, CS(2)-unexposed normal diet group, CS(2)-exposed high-fat diet group, and CS(2)-unexposed high-fat diet group. Fifty male C57BL/6J mice were divided into four groups in the same way. The exposed groups received 1000 mg/m3 CS(2) by static inhalation (5h/d, 5d/w) for four weeks. The weight of each mouse was determined and recorded once a week. On the 14th day of exposure, six mice in each group were randomly selected to measure serum total cholesterol (TC) levels. On the 28th day of exposure, the serum levels of TC and low-density lipoprotein (LDL) in the remaining mice were measured.</p><p><b>RESULTS</b>The mean weight gain of exposed groups was less than that of the unexposed groups. On the 14th and 28th days of experiment, the TC levels of the CS2-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P < 0.01 for both). On the 14th day of experiment, the TC levels of the CS(2)-unexposed high-fat diet group were significantly higher than those of the CS(2)-unexposed normal-diet group among C57BL/6J mice group (P < 0.05). On the 28th day of experiment, the LDL levels of the CS(2)-exposed high-fat diet group were significantly higher than those of the CS(2)-unexposed high-fat diet group among ApoE knockout gene mice (P = 0.003).</p><p><b>CONCLUSION</b>CS(2) exposure, high-fat diet, and ApoE gene knockout can elevate blood lipids in mice, thus increasing the risk of atherosclerosis.</p>