Objective To develop a simple, rapid, accurate method to determine selenium in human hair. Methods Digested in the superior grade pure nitric acid, Ni(NO3)2?6H2O was used as the improver and the content of selenium in the hair samples was determined by graphite furnace atomic absorption spectrometer. Results Under the designed standard conditions, the detection limit was 0.004 mg/L, in the range of 0.008-0.04 mg/L, the linearity relevance coefficient of absorbency and concentration was 0.996 9, the RSD was 3.7%. At the level of 0.01 mg/L, the recovery rates were 93.8%-98.8%. Conclusion The method is simple, rapid, accurate and is suitable for the determination of selenium in the hair.

Objective To determine the prognostic significance of non-thyroidal illness syndrome(NTIS) and FT3 on long-term all-cause and cardiovascular mortality in patients with coronary artery disease(CAD).Methods A total of 1 354 patients underwent coronary angiograhy and participated in the study.After screening,984 patients with CAD were enrolled finally and divided into NTIS group and euthyroid group.The admitted patients were also classified into Tertile 1-3 groups based on FT3 value.The relationship of long-term all-cause and cardiovascular mortality with FT3 was investigated by multivariate Cox regression analysis.Results 129 out of 984 patients had NTIS.As FT3 value decreased,both long-term all-cause mortality (Tertile 1 group 9.6％,Tertile 2 group 11.5％,Tertile 3 group 20.9％,P＜0.01) and cardiovascular mortality (Tertile 1 group 4.5 ％,Tertile 2 group 7.2％,Tertile 3 group 11.0％,P＜0.01) gradually increased.After adjusting for all factors,FT3 (HR =0.614,95％ CI 0.439-0.859)was independently associated with long-term all-cause mortality.FT3 (HR =0.605,95％ CI 0.370-0.986)was also a risk factor for cardiovascular mortality.Conclusion NTIS exists in patients with CAD without myocardial infarction.FT3 reduction is an independent risk factor for long-term all-cause and cardiovascular mortality in patients with CAD.

AIM:To study the effect of astragalus polysaccharides(Aps)on cholesterol efflux in THP-1 macrophage-derived foam cells.METHODS:After exposed to Aps at different doses,cholesterol efflux and ABCA1 protein levels in cultured THP-1 macrophage-derived foam cells were determined by a ? counter and flow cytometry,respectively.RESULTS:Aps increased cholesterol efflux in THP-1 macrophage-derived foam cells with dose dependent pattern and resulted in an increase in the expression of ABCA1 protein in THP-1 macrophage-derived foam cells.CONCLUSION:The increase in cholesterol efflux by Aps might be related to the up-regulation of ABCA1.

Objective To is ol ate novel thyroid hormone-response genes, to study the characterizations of the ir expressions and to predict their possible functions in neonatal rats. Methods A neonatal rat model with congenital hypothyr oidism was established and cDNA fragments of novel thyroid hormone-response gen es from cerebral cortex of neonatal rats were obtained by fluorescence-labeled DD-PCR analysis, subcloning and sequencing. Complete cDNAs of novel thyroid hor mone-response genes were cloned by the techniques of electronic clone, RT-PCR and sequencing, their expressions regulated by thyroid hormone were confirmed b y Northern blot analysis, their distributions, transcription levels in different tissues and different brain areas were further observed by semiquantitative RT -PCR analysis, and their possible functions were postulated through bioinformat ic techniques. Results A novel complete cDNA of thyroid hormone-response protein-1 (TRP-1) gene is cloned. It is 973 bp in f ull-length (Gene Bank accession no. AF348365), and its transcription was enhanc ed in cerebral cortex in neonatal hypothyroidism rats. The expression of its mRN A was very extensive, but more abundant in brain. Its transcriptional level in d ifferent brain areas was not uniform, much higher in olfactory bulb. Its encodin g protein had some significant domains and motifs. Conclusion TRP-1 gene is a new thyroid hormone-response gene and may play an important role during normal brain development. Its abnormal expression may b e partially responsible for neurological defects in brain arising from thyroid h ormone deficiency during critical period for perinatal rats.