Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 5 de 5
Filter
1.
Chinese Journal of Preventive Medicine ; (12): 455-458, 2013.
Article in Chinese | WPRIM | ID: wpr-274695

ABSTRACT

<p><b>OBJECTIVE</b>To establish a method for determination of the epichlorohydrin in drinking water by isotope dilution gas chromatography-mass spectrometry (GC-MS).</p><p><b>METHODS</b>The internal standard solution D5-epichlorohydrin was added in drinking water sample. The epichlorohydrin was firstly collected by active carbon, and the adsorbent was then centrifuged at 2739 × g for 10 min to remove water. Finally, the epichlorohydrin was desorbed by dipping the active carbon in 1.0 ml acetone for 1 h. The desorbed solution was tested by GC-MS and quantified with isotopic internal standards. The detection limit, precision and accuracy of the assay were evaluated. This method was adopted to detect the epichlorohydrin in drinking water for 25 batches in a city.</p><p><b>RESULTS</b>The determination method of epichlorohydrin represented a good linear relationship in the range of 0.0645-3.8700 µg/L, the linear regression equation was Y = 2.828X + 4.91 × 10(-2) (r > 0.999). When the epichlorohydrin concentration were 0.0806, 0.3230 and 3.2300 µg/L, the relative standard deviations (RSD) were 7.9%, 4.7% and 3.1%, respectively. The average recoveries were from 95.7% to 98.7%. The limit of detection (LOD) was 0.015 µg/L, limit of quantification (LOQ) was 0.052 µg/L. The content of epichlorohydrin in the 25 cases of drinking water was under the limit of detection.</p><p><b>CONCLUSION</b>The method is more simple than the national standard method, with high sensitivity, accuracy and good reproducibility, which is suitable for detection of the trace amounts of epichlorohydrin in drinking water.</p>


Subject(s)
Drinking Water , Epichlorohydrin , Gas Chromatography-Mass Spectrometry , Methods
2.
Chinese Journal of Applied Physiology ; (6): 510-523, 2012.
Article in English | WPRIM | ID: wpr-358704

ABSTRACT

Hypoxic pulmonary hypertension (HPH) is a syndrome characterized by the increase of pulmonary vascular tone and the structural remodeling of peripheral pulmonary arteries. The aim of specific therapies for hypoxic pulmonary hypertension is to reduce pulmonary vascular resistance, reverse pulmonary vascular remodeling, and thereby improving right ventricular function. Iptakalim, a lipophilic para-amino compound with a low molecular weight, has been demonstrated to be a new selective ATP-sensitive potassium (K(ATP)) channel opener via pharmacological, electrophysiological, biochemical studies, and receptor binding tests. In hypoxia-induced animal models, iptakalim decreases the elevated mean pressure in pulmonary arteries, and attenuates remodeling in the right ventricle, pulmonary arteries and airways. Furthermore, iptakalim has selective antihypertensive effects, selective vasorelaxation effects on smaller arteries, and protective effects on endothelial cells, but no effects on the central nervous, respiratory, digestive or endocrine systems at therapeutic dose. Our previous studies demonstrated that iptakalim inhibited the effects of endothelin-1, reduced the intracellular calcium concentration and inhibited the proliferation of pulmonary artery smooth muscle cells. Since iptakalim has been shown safe and effective in both experimental animal models and phase I clinical trials, it can be a potential candidate of HPH in the future.


Subject(s)
Animals , Antihypertensive Agents , Therapeutic Uses , Calcium , Metabolism , Disease Models, Animal , Endothelin-1 , Metabolism , Hypertension, Pulmonary , Drug Therapy , Hypoxia , Drug Therapy , KATP Channels , Myocytes, Smooth Muscle , Cell Biology , Propylamines , Therapeutic Uses , Pulmonary Artery
3.
Chinese Journal of Endemiology ; (6): 345-347, 2011.
Article in Chinese | WPRIM | ID: wpr-642356

ABSTRACT

Objective Establish a laboratory quality control system to ensure accurate and reliable test data and to contrapose the influence of error factors in current detection methods for urinary iodine measurement. Methods The results of reagent blank absorbance value and uric iodine standard materials were collected, then their relevant technical indexes such as mean, standard deviation, control limit, auxiliary line were worked out. Then the quality control chart of blank test and the relative error control chart were made base on these technical indexes. And different iodine concentrations (high, middle and low concentration) were tested and their mean,relative reduction difference value, weighted mean value and critical limit Rc value were calculated, and then critical limit Rc value precision control chart was made. Results The range of absorbance of blank control test was 1.183 to 1.553. And the limit of the accuracy control Rc value was 0.0883, 0.0572, respectively, when the concentrations of urinary iodine was 0~ < 150 μg/L and 150 ~ 300 μg/L. The control limit of the relative error was 9.3%. Conclusions The method of quality control chart could be satisfactorily applied to identify the quality of the analytical results of urine iodine, and ensure the results of the urine iodine reliable and authentic.

4.
Chinese Medical Journal ; (24): 1422-1428, 2005.
Article in English | WPRIM | ID: wpr-320755

ABSTRACT

<p><b>BACKGROUND</b>Nuclear factor kappaB (NF-kappaB) overactivation, requiring phosphorylation and degradation of its inhibitor IkappaBalpha, is the basis for chronicity of airway inflammation in asthma. Based on our previous plasmid pShuttle-IkappaBalpha, carrying an IkappaBalpha gene from human placenta, we optimized a novel IkappaBalpha mutant (IkappaBalphaM) gene, constructed and characterized its replication-deficient recombinant adenovirus (AdIkappaBalphaM), and tested whether AdIkappaBalphaM-mediated overexpression of IkappaBalphaM could inhibit the NF-kappaB activation in endothelial cells.</p><p><b>METHODS</b>IkappaBalphaM gene (203 - 1003 bp) encoding 267 amino acids, acquired by site-directed deleting N-terminal phosphorylation sites of serine 32/36, was subcloned into the pShuttle and pGEM-T vectors for further polymerase chain reaction (PCR), restriction digestion, deoxyribonucleic acid (DNA) sequencing and homology analyses. Subsequent to inserting the expression unit of pShuttle-IkappaBalphaM, containing cytomegalovirus (CMV) promoter, IkappaBalphaM complementary DNA (cDNA) and polyadenylic acid (PolyA) signals, into the type 5 adenovirus (Ad5) vector, the resultant AdIkappaBalphaM was packaged in human embryonic kidney (HEK) 293 cells by cotransfection with lipofectamine. Western blot analysis and electrophoretic mobility shift assay were utilized to detect the AdIkappaBalphaM-mediated overexpression of IkappaBalphaM in HEK293 cells and its suppressive effect on phorbol 12-myristate 13-acetate (PMA)-induced NF-kappaB activation in human umbilical vein endothelial (ECV304) cells, respectively.</p><p><b>RESULTS</b>The relevant nucleotides and deduced amino acids of 801 bp IkappaBalphaM gene were consistent with those of IkappaBalpha gene (GenBank accession number: M69043). The titer of the prepared AdIkappaBalphaM was 4.0 x 10 (12) plaque-forming units (pfu)/L. Moreover, the IkappaBalphaM gene was overexpressed in HEK293 cells, and potently inhibited the PMA-induced NF-kappaB activation in ECV304 cells dose-dependently.</p><p><b>CONCLUSIONS</b>AdIkappaBalphaM is a novel vector for both efficient transfer and specific overexpression of IkappaBalphaM gene, as well as potent inhibition of NF-kappaB activity, providing a promising strategy for gene therapy of asthma.</p>


Subject(s)
Humans , Adenoviridae , Genetics , Cell Line , Endothelial Cells , Metabolism , Genetic Therapy , I-kappa B Proteins , Genetics , Mutation , NF-KappaB Inhibitor alpha , NF-kappa B , Tetradecanoylphorbol Acetate , Pharmacology
5.
Chinese Journal of Applied Physiology ; (6): 4-7, 2003.
Article in Chinese | WPRIM | ID: wpr-339695

ABSTRACT

<p><b>AIM</b>To investigate whether pulmonary vascular remodeling in hypoxic pulmonary hypertensive rats could be prevented by treatment with a selective K(ATP)CO, iptkalim (Ipt).</p><p><b>METHODS</b>Rats were fed in hypoxic and normobaric environment (10% +/- 0.5% O2, 8 h/day and 6 day/week) and divided into control group, hypoxia group (hypoxic rat treated with ig NS 5.0 ml x kg(-1) x d(-1)), treated group I (hypoxic rat treated with ig Ipt 0.75 mg x kg(-1) x d(-1)), treated group II (hypoxic rat treated with ig Ipt 1.5 mg x kg(-1) x d(-1)). After 4 wk, the mean pulmonary arterial pressure (mPAP), right ventricle/left ventricle and septum [RV/(LV + S)] were measured, and the small pulmonary arterial morphologic changes were observed with morphometric analysis under microscopes in four groups.</p><p><b>RESULTS</b>The level of mPAP and RV/(LV+ S) was significantly higher in the hypoxic group than those in control group (P < 0.01). Morphometric analysis revealed that the ratio of vascular medial wall thickness to external diameter (MT%) and the ratio of vascular medial cross-sectional area to total arterial cross-sectional area (MA%) were also significantly increased in the hypoxic group than those in control group (P < 0.01) and the ratio of vessel lumen cross-sectional area to total arterial cross-sectional area (VA%) was significantly lower in the hypoxic group than those in control group (P < 0.01). Ipt 0.75 mg x kg(-1) x d(-1) or 1.5 mg x kg(-1) x d(-1) decreased the level of mPAP(mmHg), RV/(LV+ S), and inhibited the small pulmonary arterial remodeling significantly. Ipt 1.5 mg x kg(-1) x d(-1) reversed all pathological indices.</p><p><b>CONCLUSION</b>K(ATP)CO iptkalim can be a very promising candidate for the treatment of hypoxic pulmonary hypertension.</p>


Subject(s)
Animals , Male , Rats , Hypertension, Pulmonary , Drug Therapy , Hypoxia , KATP Channels , Propylamines , Pharmacology , Rats, Sprague-Dawley
SELECTION OF CITATIONS
SEARCH DETAIL