[The vitamin D nutritional status in Chinese urban women of child-bearing age from 2010 to 2012].

Objective: To evaluate the vitamin D nutritional status in Chinese women of child-bearing age by analyzing serum 25-hydroxyvitamin D level in 2010-2012. Methods: Data were obtained from the China Nutrition and Health Survey in 2010-2012. Using cluster sampling and proportional stratified random sampling, 1 514 women of child-bearing age (18-44 years old) from 34 metropolis and 41 small and medium-sized cities were included in this study. Demographic information was collected by questionnaire and serum 25-hydroxyvitamin D concentration was determined by radioimmunoassay, in accordance with the 2010 Institute of Medicine of the National Academies standards. We compared differences in vitamin D levels, specifically serious deficiency, lack of deficiency, insufficiency, and excess. Results: The overall serum 25-hydroxyvitamin D level of Chinese urban women of child-bearing age (P(50) (P(25)-P(75))) was 20.1 (15.1-26.3) ng/ml; minorities had a significantly higher serum 25-hydroxyvitamin D level of 22.0 (15.9-27.5) ng/ml compared with women of Han nationality (19.8 (14.9-26.2) ng/ml) (χ(2)=7.02, P=0.008). The proportions of women with serious deficiency, lack of deficiency, insufficiency, and excess vitamin D were 11.6% (n=175), 37.9% (n=574), 35.1% (n=531), and 0.3% (n=5), respectively. Only 15.1% (n=229) of women of child-bearing age had normal vitamin D nutritional status. No significant differences in vitamin D nutritional status were observed according to age, body mass index, city, nationality, educational level, marital status, or household income per capita (P>0.05). Conclusion: Most Chinese urban women of child-bearing age have poor vitamin D levels and require vitamin D supplementation.

[Study on vitamin A nutritional status of 6- to 17-year-old urban children and adolescents between 2010 and 2012 in China].

Objective: To investigate the vitamin A nutritional status of 6- to 17-year-old urban children and adolescents by analyzing serum retinol level, between 2010 and 2012 in China. Methods: Data were obtained from the China Nutrition and Health Survey in 2010-2012. Using multi-stage stratified sampling and the population proportional stratified random sampling method, 6 617 children aged 6-17 years from 32 metropolis and 41 middle-sized and small cities of China were selected. The questionnaire survey was used to collect demographic information. Blood samples were analyzed using high-performance liquid chromatography to determine serum retinol concentration, and the World Health Organization guidelines were used to evaluate the nutritional status of vitamin A. Vitamin A levels, vitamin A deficiency, and marginal vitamin A deficiency in children with different characteristics were compared. Results: A total of 3 785 cases with valid samples were obtained. The overall mean serum retinol concentration level was (1.49±0.71) µmol/L; the mean serum retinol concentration was (1.55±0.69) µmol/L for metropolis and (1.49±0.75) µmol/L for middle-sized and small cities (P>0.05). The mean serum retinol concentration was (1.52±0.78) µmol/L for boys and (1.47±0.68) µmol/L for girls (P>0.05). The mean serum retinol concentration level was (1.46±0.70) µmol/L for 6- to 11-year-old children and (1.54±0.65) µmol/L for 12- to 17-year-old children (P<0.05). The total vitamin A deficiency rate and marginal vitamin A deficiency rate was 7.69% (291/3 785) and 18.57% (703/3 785), respectively. The vitamin A deficiency rate was 8.00% (36/450) for metropolis and 7.64% (65/3 335) for middle-sized and small cities; 8.12% (155/1 908) for boys and 7.25% (136/1 877) for girls; and 8.04% (171/2 115) for 6- to 11-year-old children and 7.18% (120/1 670) for 12- to 17-year-old children. No significant differences were observed for region, sex, or age (P>0.05). The marginal vitamin A deficiency rate was 19.11% (86/450) for metropolis and 18.50% (617/3 335) for middle-sized and small cities; 18.19% (347/1 908) for boys and 18.97% (356/1 877) for girls, with no significant differences observed (P>0.05). The marginal vitamin A deficiency rate was 16.54% (350/2 115) for 6- to 11-year-old children and 21.13% (353/1 670) for 12- to 17-year-old children (P<0.05). Conclusion: The vitamin A nutritional status of 6- to 17-year-old Chinese urban children and adolescents between 2010 and 2012 has improved, and the gap between cities is narrowing. However, vitamin A deficiency overall remains high, especially in younger children, and requires specific attention.

Reactive oxygen species mediate crosstalk between NF-kappaB and JNK.

The activation of NF-kappaB inhibits apoptosis via a mechanism involving upregulation of various antiapoptotic genes, such as cellular FLICE-inhibitory protein (c-FLIP), Bcl-xL, A1/Bfl-1, and X chromosome-liked inhibitor of apoptosis (XIAP). In contrast, the activation of c-Jun N-terminal kinase (JNK) promotes apoptosis in a manner that is dependent on the cell type and the context of the stimulus. Recent studies have indicated that one of the antiapoptotic functions of NF-kappaB is to downregulate JNK activation. Further studies have also revealed that NF-kappaB inhibits JNK activation by suppressing accumulation of reactive oxygen species (ROS). In this review, we will focus on the signaling crosstalk between the NF-kappaB and JNK cascades via ROS.

Novel SH3 protein encoded by the AF3p21 gene is fused to the mixed lineage leukemia protein in a therapy-related leukemia with t(3;11) (p21;q23).

The mixed lineage leukemia (MLL) gene located at chromosome band 11q23 is frequently rearranged in patients with therapy-related acute monocytic leukemia who received topoisomerase II inhibitors. We have identified a novel fusion partner of MLL (FAB M5b) in a patient who developed t-AML 9 years after treatment for acute lymphoblastic leukemia (ALL). The leukemic cells had a sole karyotypic abnormality of t(3;11) (p21;q23). Screening of a genomic DNA library, prepared from leukemic cell DNA, identified rearranged clones composed of MLL and a novel gene on chromosome 3p21 (AF3p21). The AF3p21 gene encodes a protein of 722 amino acids, which contains an Src homology 3 (SH3) domain, a proline-rich domain, and a bipartite nuclear localizing signal (NLS). RNA analysis demonstrated that exon 6 of the MLL gene fused to exon 2 of the AF3p21 gene. The resulting chimeric protein consists of AT-hooks, methyltransferase, and transcription repressor domains of MLL in addition to the AF3p21 proline-rich domain and NLS but not the AF3p21 SH3 domain.

Genomic structure and promoter analysis of the ecto-phosphodiesterase I gene (PDNP3) expressed in glial cells.

PDNP (phosphodiesterase I/nucleotide pyrophosphatase) is one of a series of ectoenzymes that are involved in hydrolysis of extracellular nucleotides. PDNP possesses ATPase (EC 3.6.1.3) and ATP pyrophosphatase (EC 3.6.1.8) activities. Mammalian PDNP consists of three closely related family proteins (PDNP1, -2, and -3), and they are expressed in different cell types and at different developmental stages. Rat PDNP3 is expressed in a subset of immature glial cells and in the alimentary tract. Human PDNP3 is expressed in glioma cells, prostate, and uterus, but not in the alimentary tract. We have cloned genomic DNA containing the whole coding region of the human PDNP3 gene and determined its exon-intron structure. The human PDNP3 gene spans over 60 kb and is organized into 25 exons and 24 introns. We determined the nucleotide sequence of the 5'-flanking region of human and rat PDNP3 genes. The upstream region of both species lacks a canonical TATA box and contains a putative binding site for CCAAT enhancer-binding proteins near the transcription start site. Promoter activity analysis of the 5'-flanking region revealed that the sequence around the CCAAT box is required for its transcriptional activity in 9L rat glioma cells. A gel shift assay demonstrated that 9L nuclear extract contains proteins that bind to this region.

Assignment of Pdnp2, the gene encoding phosphodiesterase I/nucleotide pyrophosphatase 2, to mouse chromosome 15D2.

We have isolated cDNA and genomic DNA encoding mouse PDNP2 (PD-Ialpha). The mouse Pdnp2 cDNA contains a 2,589-nucleotide open reading frame encoding a polypeptide of 863 amino acids. The 5' region of the mouse Pdnp2 gene contains Sp1, Max1, HNF-3B, and AP1 putative transcription factor binding sites, without typical TATA or CAAT boxes. Fluorescence in situ hybridization showed that Pdnp2 is located at Chromosome 15D2, as expected based on mouse-human conserved regions.

Biochemical and morphological changes in the lenses of selenium and/or vitamin E deficient rats.

The activities of glutathione peroxidase (GSH-Px), glutathione reductase (GSSG-R), superoxide dismutase (SOD) and the contents of malondialdehyde (MDA) and free radicals were measured, and the morphological changes were observed in the lens of control rats, selenium-deficient (SeD) and/or vitamin E deficient (VED) rats. The activities of GSH-Px in the lens of SeD rats decreased significantly. The GSH-Px activities of lens were positively related to erythrocytes selenium level. There was a free radical at g = 2.0015 in the rat lens of all groups, but the content of free radicals in the lens of SeD group was significantly higher than that of the control group. The free radical content of lens was negatively related to erythrocytes selenium level, as well as the GSH-Px activities in the lens. In vitro, ultraviolet radiation caused the generation of another kind of free radical (g = 2.0097) in the lens of all groups, but the amount of the free radical in the lens of the SeD group was also significantly higher than that of the control group. The activities of SOD and GSSG-R in VED rat lens were significantly decreased. The amount of MDA in the lens of SeD and/or VED rats were significantly increased. The results showed that the decrease of antioxidative capability in the lenses of SeD and/or VED rats accelerated the lipid peroxidation and generation of free radicals. Although only early morphological changes in SeD and/or VED rat lens were observed, it is considered that selenium and vitamin E deficiency may be involved in the occurrence of cataract.

Effect of selenium deficiency on tissue taurine concentration and urinary taurine excretion in the rat.

The purpose of this study was to determine the effect of selenium deficiency on tissue taurine levels and urinary taurine excretion. Weanling male Sprague-Dawley rats were fed selenium-deficient or selenium-adequate diets for 20 weeks. As selenium deficiency developed, urinary taurine excretion increased in selenium-deficient rats compared to controls. At 12 weeks, the selenium-deficient rats excreted 1.7-fold more taurine than control rats. At the same time plasma glutathione peroxidase was 1.2% of control and plasma glutathione was 226% of control. At 20 weeks, renal taurine was decreased but renal glutathione was increased in selenium-deficient rats compared to controls. Feeding the experimental diet for 6 weeks without methionine supplementation caused a fall in urinary taurine excretion. However, there was no difference between selenium-deficient and control rats. These results indicate that selenium deficiency affects renal handling of taurine in the rat when dietary sulfur amino acids are not restricted.