Relationships of Lead, Mercury and Cadmium Levels with the Timing of Menarche among Korean Girls

Purpose@#This study utilized data from the Korean National Health and Nutrition Examination Survey (KNHANES) to explore differences in the timing of menarche in Korean girls according to blood heavy metal concentrations. @*Methods@#This study performed a secondary analysis of cross-sectional data from the sixth KNHANES. Data from 179 female children and adolescents aged 10~18 were included in this study. The relationships of blood heavy metal concentrations (lead, mercury, and cadmium) with age of menarche were analyzed using complex sample multiple logistic regression. @*Results@#In the participants of this study, the geometric mean values of blood lead, mercury, and cadmium concentrations were 1.15±0.04 μg/dL, 1.80±0.08 μg/L, and 0.30±0.03 μg/L, respectively. Mercury poisoning (>5 μg/L) was found in 1.5% of participants. Furthermore, significant relationships were found between blood lead and mercury concentrations and age at menarche (p for trend: p<.001 and p=.015, respectively). @*Conclusion@#Through an analysis of national big data, this study found evidence that Korean girls showed a younger age at menarche in response to higher blood lead and mercury concentrations. To prevent and manage precocious puberty in Korean children and adolescents, a systematic policy that monitors both exposure to environmental hazards and blood heavy metal concentrations is needed.

Induction of heme oxygenase-1 with dietary quercetin reduces obesity-induced hepatic inflammation through macrophage phenotype switching

BACKGROUND/OBJECTIVES: Obesity-induced steatohepatitis accompanied by activated hepatic macrophages/Kupffer cells facilitates the progression of hepatic fibrinogenesis and exacerbates metabolic derangements such as insulin resistance. Heme oxyganase-1 (HO-1) modulates tissue macrophage phenotypes and thus is implicated in protection against inflammatory diseases. Here, we show that the flavonoid quercetin reduces obesity-induced hepatic inflammation by inducing HO-1, which promotes hepatic macrophage polarization in favor of the M2 phenotype. MATERIALS/METHODS: Male C57BL/6 mice were fed a regular diet (RD), high-fat diet (HFD), or HFD supplemented with quercetin (HF+Que, 0.5g/kg diet) for nine weeks. Inflammatory cytokines and macrophage markers were measured by ELISA and RT-PCR, respectively. HO-1 protein was measured by Western blotting. RESULTS: Quercetin supplementation decreased levels of inflammatory cytokines (TNFα, IL-6) and increased that of the anti-inflammatory cytokine (IL-10) in the livers of HFD-fed mice. This was accompanied by upregulation of M2 macrophage marker genes (Arg-1, Mrc1) and downregulation of M1 macrophage marker genes (TNFα, NOS2). In co-cultures of lipid-laden hepatocytes and macrophages, treatment with quercetin induced HO-1 in the macrophages, markedly suppressed expression of M1 macrophage marker genes, and reduced release of MCP-1. Moreover, these effects of quercetin were blunted by an HO-1 inhibitor and deficiency of nuclear factor E2-related factor 2 (Nrf2) in macrophages. CONCLUSIONS: Quercetin reduces obesity-induced hepatic inflammation by promoting macrophage phenotype switching. The beneficial effect of quercetin is associated with Nrf2-mediated HO-1 induction. Quercetin may be a useful dietary factor for protecting against obesity-induced steatohepatitis.

Relationships among Premenstrual Syndrome, Perfection and Anxiety among the College Student

PURPOSE: The purpose of this study was to compare the premenstrual syndrome (PMS) and the relationships among PMS, perfection, and anxiety in nursing college students and general college students. METHODS: The questionnaire survey was carried out with a convenience sample of 215 college students. The MDQ (Menstrual Distress Questionnaire), APS-R (Almost Perfect Scale-Revised), STAI (State and Trait Anxiety Inventory) were used. The data were collected from June to October, 2011. Data analysis included frequency, chi2-test, t-test, and Pearson correlation. RESULTS: There were significant differences in PMS and perfection but there not in anxiety between nursing college students and general college students. There were significant correlations among PMS, perfection and anxiety in nursing college students, and there were significant correlations among PMS and anxiety in general college students but not significant correlations among PMS and perfection. CONCLUSION: The findings suggest that to provide effective interventions for PMS in college students, it is necessary to design nursing interventions that consider perfection and anxiety.

Effects of Mothers Involved in Dental Health Program for Their Children

PURPOSE: The purpose of this study was to identify the effects of mothers' involvement in a dental health program for their elementary school children. METHODS: This study was a non-equivalent control group pre-post test design in which knowledge and behaviors related to dental health, perceived benefits and barriers, self-efficacy and plaque control scores were compared between the experimental group (n=26) for whom the dental health program included the direct involvement of the mothers, and the control group (n=24) for whom knowledge related to dental health was provided through brochures. RESULTS: Scores for the experimental group in which the mothers were involved in the dental health program were significantly higher for knowledge, behaviors in dental health, self-efficacy and plaque control compared to the control group. CONCLUSION: Results of this study suggest that mothers involvement in the dental health program is effective in reinforcing dental health enhancing behavior in elementary school children.

Platinum nanoparticles reduce ovariectomy-induced bone loss by decreasing osteoclastogenesis

Platinum nanoparticles (PtNP) exhibit remarkable antioxidant activity. There is growing evidence concerning a positive relationship between oxidative stress and bone loss, suggesting that PtNP could protect against bone loss by modulating oxidative stress. Intragastric administration of PtNP reduced ovariectomy (OVX)-induced bone loss with a decreased level of activity and number of osteoclast (OC) in vivo. PtNP inhibited OC formation by impairing the receptor activator of nuclear factor-kappaB ligand (RANKL) signaling. This impairment was due to a decreased activation of nuclear factor-kappaB and a reduced level of nuclear factor in activated T-cells, cytoplasmic 1 (NFAT2). PtNP lowered RANKL-induced long lasting reactive oxygen species as well as intracellular concentrations of Ca2+ oscillation. Our data clearly highlight the potential of PtNP for the amelioration of bone loss after estrogen deficiency by attenuated OC formation.

Rutin inhibits osteoclast formation by decreasing reactive oxygen species and TNF-alpha by inhibiting activation of NF-kappaB

Rutin, a glycoside of flavonol, inhibits osteoclast formation induced by receptor activator of NF-kappaB ligand (RANKL) in bone marrow-derived macrophages. It reduces reactive oxygen species produced by RANKL and its inhibitory effect results from reduced levels of TNF-alpha Rutin also lowers NF-kappaB activation in response to RANKL.

Corn silk induces nitric oxide synthase in murine macrophages

Corn silk has been purified as an anticoagulant previously and the active component is a polysaccharide with a molecular mass of 135 kDa. It activates murine macrophages to induce nitric oxide synthase (NOS) and generate substantial amounts of NO in time and dose-dependent manners. It was detectable first at 15 h after stimulation by corn silk, peaked at 24 h, and undetectable by 48 h. Induction of NOS is inhibited by pyrolidine dithiocarbamate (PDTC) and genistein, an inhibitor of nuclear factor kappa B (NF-kappaB) and tyrosine kinase, respectively, indicating that iNOS stimulated by corn silk is associated with tyrosine kinase and NF-kappaB signaling pathways. IkappaB-alpha degradation was detectible at 10 min, and the level was restored at 120 min after treatment of corn silk. Corn silk induced nuclear translocation of NF-kappaB by phosphorylation and degradation of IkappaB-alpha.

Soluble glucocorticoid-induced TNF receptor (sGITR) induces inflammation in mice

Glucocorticoid-induced TNF receptor (GITR) was a new member of the TNF/nerve growth factor receptor (TNFR/ NGFR) family and induced in murine T cells by dexamathasone. Recombinant soluble GITR (sGITR) induced an inflammation in peritoneal membrane and changes in spleen after i.p. injection of 3 mg/kg in C57BL/6 mice. Spleen was enlarged and percentage of neutrophils and monocytes were increased. The area of red pulp in spleen was increased, while that of white pulp was decreased after GITR injection. The thickening of membrane and neutrophil infiltration was observed in peritoneal membrane with increased myeloperoxidase activity. At later time, neutrophil infiltration moved to inside the tissue with tissue damage. GITR ligand and GITR were expressed constitutively on the surface of spleen cells and cells from peritoneal fluid. In contrast, no significant change in the spleen and in peritoneal membrane was observed in mice treated with LPS. GITR may play a role in body's inflammatory processes.

Induction of nitric oxid esynthase(NOS) by soluble glucocorticoid induced tumor necrosis factor receptor(sGITR) is modulated by IFN-g in murine macrophage

Earlier study showed that glucocorticoid induced tumor necrosis factor receptor (GITR), a new TNFR family, activated murine macrophages to express inducible nitric oxide synthase (iNOS) and to generate nitric oxide (NO). A possible involvement of pro-inflammatory cytokines on NO production by GITR was investigated in vitro systems and signaling molecules contributing to sGITR-induced iNOS production are determined in Raw 264.7 cells, a murine macrophage cell line. The result showed that the synergy was afforded by the combination of GITR with IFN-gamma in a dose-dependent manner but IFN-gamma alone was not able to induce NOS. No effects were observed with TNF-alpha, IL-1beta, or IL-6 co-treated with GITR. To determine signaling molecules contributing to sGITR-induced iNOS production, a specific inhibitor for signal pathway proteins tested showed that PDTC (NF- kB) and genistein (tyrosine kinase) inhibited NOS induction significantly, while sodium orthovanadate (tyrosine phosphatase) potentiated NOS expression. These results suggest that activations of NF-kB were involved in induction of iNOS by GITR and IFN-gamma priming caused earlier and stronger NF-kB activation.