Predicted 10-year Cardiovascular Disease Risk and Its Association with Sleep Duration among Adults in Beijing-Tianjin-Hebei Region, China / 生物医学与环境科学（英文）

Objective@#The study aims to predict 10-year cardiovascular disease (CVD) risk and explore its association with sleep duration among Chinese urban adults.@*Methods@#We analyzed part of the baseline data of a cohort that recruited adults for health screening by cluster sampling. The simplified Pittsburgh Sleep Quality Index (PSQI) and Framingham 10-year risk score (FRS) were used to measure sleep duration and CVD risk. Demographic characteristics, personal history of chronic diseases, lifestyle factors were collected using a questionnaire. Height, weight, total cholesterol (TC), and high-density lipoprotein cholesterol (HDL-C) were also measured. Multiple logistic regression models were performed to explore the association of sleep duration with the predicted CVD risk.@*Results@#We included 31, 135 participants (median age 44 years, 53.02% males) free of CVD, cerebral stroke, and not taking lipid-lowering agents. Overall, 14.05%, and 25.55% of participants were at medium and high predicted CVD risk, respectively. Short sleep was independently associated with increased odds of medium to high risk of predicted 10-year CVD among males ( @*Conclusion@#A substantial number of adults free of CVD were at high 10-year CVD risk. Short sleep was associated with increased odds of predicted CVD risk.

The effects of low pre-pregnant lead exposure level on maternal bone turnover during gestation and lactation in mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effects of low pre-pregnant lead exposure level on the mobilization of lead and calcium in maternal skeleton during gestation and lactation in mice.</p><p><b>METHODS</b>Seventy Kunming female mice were randomly divided into the lead exposure or control groups, 36 mice were exposed to lead by drinking water (50 mg/L) and 36 mice were exposed to deionized water for 4 weeks. The levels of calcium and lead in blood and femurs were measured on the 1st, 7th and 14th days during gestation and on the 1st,10th and 21st days during lactation with atomic absorption spectrophotometry using a heated graphite atomizer or flame atomic absorption spectrophotometry.</p><p><b>RESULTS</b>As compared with the pre-pregnant, at the end of lactation in exposure group the levels of calcium in blood and bones significantly decreased 18.5% and 17.75%, respectively, the levels of lead in blood significantly increased 65.22% and the levels of lead in bones significantly decreased 28.45% (P < 0.05). There was a significant negative correlation between the blood lead level and the bone lead level during gestation and lactation in exposure group (r = -0.904, P < 0.01). There were significant differences of lead and calcium levels during the gestation and lactation between exposure group and control group (P < 0.05).</p><p><b>CONCLUSION</b>The lead mobilization in maternal bone occurred during gestation and lactation in mice, which could be accelerated by the low pre-pregnant lead exposure.</p>

The effects of the cadmium chloride on the DNA damage and the expression level of gadd gene in HepG2 cell line / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of the cadmium chloride on the DNA damage and the expression of the gadd153 and gadd45beta promoter and mRNA in HepG2 cells.</p><p><b>METHODS</b>DNA damage induced by cadmium chloride was detected by comet assay. The plasmids (pGADD153-Luc and pG45-Luc) containing DNA damage and repair inducible gene 153 and 45 (gadd153 and gadd45beta) promoter and luciferase and gadd45beta reporter gene were constructed. The activity of gadd153 and gadd45beta promoter were represented by the luciferase activity, the inducible luciferase activities was detected by bioluminescence. The expression of gadd153 and gadd45beta mRNA was detected by RT-PCR.</p><p><b>RESULTS</b>The results of comet assay indicated that Olive Tail Moment induced by the cadmium chloride increased significantly at the dose of 100, 300 micromol/L, compared with the control (P < 0.05). The luciferase activity analysis showed that the expression levels of gadd153 promoter increased significantly in 1, 5, 10 micromol/L treatment group, compared with the control (P < 0.05). The expression levels of gadd45beta promoter in 5, 10 micromol/L treatment group were significantly higher than that in control group (P < 0.05). The expression levels of gadd153 mRNA induced by cadmium chloride at the doses of 1, 5, 10 micromol/L and the expression levels of gadd45beta mRNA induced at the doses of 5, 10 micromol/L were significantly higher than thoae in control group (P < 0.05).</p><p><b>CONCLUSION</b>The cadmium chloride can induce the DNA damage and increase the expression levels of the gadd153 and gadd45beta promoters in HepG2 cells.</p>

Effects of paraquat on the learning and memory ability in developing mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the damages of paraquat to the learning and memory ability of developing mice and explore the possible mechanism involving oxidative stress.</p><p><b>METHODS</b>Eighty healthy Kunming mice in aged 21 days were divided into 4 groups randomly: a control group (distilled water) and three paraquat treatment groups. The doses of paraquat were 0.89, 2.67 and 8mg/kg body weight, respectively. Paraquat was administered orally in doses of 0.1 ml/10 g body weight, respectively, once a day and for 28 consecutive days. The Morris water maze test and the shuttling and avoid dark box test were used to detect the learning and memory abilities of mice. The levels of MDA and the activities of SOD and GSH-PX were detected according to the commercial kits manual using a microplate reader.</p><p><b>RESULTS</b>Morris water maze test showed that the escape latency of mice after paraquat treatment (57.98 +/- 2.78, 62.35 +/- 3.18, 85.57 +/- 5.10) were significantly increase compared with the control (21.74 +/- 1.36), respectively (P < 0.05). There were good dose-response relationship (R = 0.8629, P < 0.05). The shuttling and avoid dark box test showed that initiative avoidance latency of mice after paraquat treatment (5.56 +/- 0.29, 6.08 +/- 0.22, 8.32 +/- 0.38) were significantly increase compared with the control (3.50 +/- 0.13), respectively (P < 0.05). There were good dose-response relationship (R = 0.9579, P < 0.05). The levels of MDA in serum of mice in paraquat treatment groups (2.67 and 8 mg/kg) (24.76 +/- 1.76, 31.10 +/- 4.57) and in hippocampus of mice in each paraquat treatment groups were significantly increase compared with the control (serum: 16.38 +/- 6.26, hippocampus: 1.93 +/- 0.39) (P < 0.05, respectively). The activities of SOD in serum and hippocampus of mice in each paraquat treatment groups were significantly decrease compared with the control (serum: 213.25 +/- 6.78, hippocampus: 197.36 +/- 6.37) (P < 0.05, respectively). The activities of GSH-PX in serum and hippocampus of mice in each paraquat treatment groups were significantly decrease compared with the control (serum: 583.47 +/- 11.23, hippocampus: 412.38 +/- 13.16) (P < 0.05, respectively).</p><p><b>CONCLUSION</b>Paraquat can induce the oxidative damage in hippocampus, and then influence the learning and memory abilities of developing mice.</p>

Effects of different sized titanium dioxide particles on reactive oxygen species in mice / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effects of different sized titanium dioxide on reactive oxygen species (ROS) levels.</p><p><b>METHODS</b>Forty-eight healthy mice were divided into 3 groups randomly: control group (distilled water), 50 nm TiO₂ (5 g/kg) group and 120 nm TiO₂ (5 g/kg) group. The mice were exposed to distilled water or TiO₂ by a syringe via gastrointestinal tract in a minute. One week later, the mice were sacrificed and the liver, kidney and brain (cortex, hippocampus) were collected. The contents of Ti in the above tissues of mice were measured by ICP-MS. The ROS levels in the tissues were measured by flow cytometry.</p><p><b>RESULTS</b>There was no significant difference in organ coefficient between two exposure groups and control group (P > 0.05). The Ti contents in liver, kidney, cortex and hippocampus of two exposure groups were higher than those of control group (P < 0.05); The Ti contents of above four tissues in 50 nm TiO₂ group were higher than those in 120 nm group (P < 0.05). The ROS levels in liver, kidney and cortex cells of two exposure groups (273.2 ± 32.5, 160.2 ± 28.5, 74.9 ± 8.9; 159.4 ± 15.9, 64.4 ± 7.5, 41.2 ± 5.6) significantly increased, as compared with control group (74.9 ± 6.4, 24.9 ± 2.8, 32.8 ± 3.1) (P < 0.05). The ROS levels in hippocampus cells in 50 nm TiO₂ group were significantly higher than those in control group (P < 0.05). The ROS levels of above four tissues in 50 nm group were significantly higher than those in 120 nm TiO₂ group (P < 0.05).</p><p><b>CONCLUSION</b>After mice were exposed to 50 nm and 120 nm TiO₂ particles via gastrointestinal tract, Ti could be distributed into the liver, kidney and the brain tissues in mice, resulting in the enhanced ROS levels in liver, kidney, cortex and hippocampus cells. Moreover, the ROS levels induced by 50 nm TiO₂ particles are significantly higher than those induced by 120 nm TiO₂ particles.</p>

Effects of prenatal exposure to lead on hippocampal nephroblastoma over-expressed gene expression of offspring / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effects of prenatal exposure to lead on nephroblastoma over-expressed gene (NOV) protein and mRNA expression in hippocampus of rats' offspring, and to explore the molecular mechanism of lead on learning and memory.</p><p><b>METHODS</b>The pregnant rats were divided into 1 control group and 3 lead expose groups randomly: low( 125 mg/L), middle (250 mg/L) and high (500 mg/L). 8 rats in each group. From pregnancy ld until birth, the rats were given double evaporated water or lead acetate water of different doses according to their groups. The samples of descendants were taken on embryo 18 th day, postnatal 1st day, 21st day, 60th day. The contents of lead in blood and hippocampus were determined by hydride generation atomic absorption spectrometry method. The expression of NOV protein and mRNA in hippocampus were observed by immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>The lead contents of blood [(312.46 +/- 43.55), (419.35 +/- 62.25), (541.45 +/- 47.90) microg/L] and hippocampus[(2.10 +/- 0.18), (2.58 +/- 0.12), (3.41 +/- 0.23) microg/L] were significantly higher in lead exposed groups than that of control [(214.31 +/- 40.77), (0.76 +/- 0.13) microg/L] (P < 0.05) on the embryo 18th, 1st and 21 st day, while there was no significantly difference among them on 60 th day. The expression of NOV protein in all lead exposed groups were significantly decreased compared with control group (P < 0.05) on 1st and 21 st day, while there was no significantly difference among them on 60th day. The expression of NOV mRNA of all the lead exposed groups were significantly decreased compared with control group (P < 0.05) on the embryo 18th, 1st and 21st day, while there was significantly difference only in the high dose group (0.0355 +/- 0.0100) compared with control (0.0900 +/- 0.0200) (P < 0.01) on 60th day.</p><p><b>CONCLUSION</b>Pregnancy low level lead exposure could decrease the NOV protein and mRNA expression in hippocampus of offspring, which might be one of the molecular mechanisms of effect of lead on learning and memory.</p>

Effects of prenatal exposure to low level lead on expression of GAP-43 in hippocampus of rat's offspring / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To observe the effects of prenatal exposure to low level lead on the protein and mRNA expression of growth-associated protein (GAP-43) in hippocampus of rat's offspring, and to explore the molecular mechanisms of lead on learning and memory.</p><p><b>METHODS</b>The pregnant rats were randomizedly divided into 4 groups and provided with doubly evaporated water in control group and 125, 250, 500 mg/L lead acetate solution via drinking water in treatment groups respectively during pregnancy. When the rat's offspring was 1, 21, 60 days old, the lead content in hippocampus was measured by hydride generation atomic absorption spectrometry, and the GFAP protein and mRNA expression at hippocampal CA1 region were observed by immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>The content of lead in the hippocampus was (1.64 +/- 0.32), (2.33 +/- 0.42) and (3.28 +/- 0.58) microg/L, and (0.94 +/- 0.18), (1.27 +/- 0.26) and (1.79 +/- 0.42) microg/L respectively in the low, middle and high lead dosage group when the rat's offspring was one day and 21 day old. When the rat's offspring was 1, 21 days old, the content of lead in hippocampus in treatment groups was significant higher than that of control (P < 0.05), the integral optical density of GAP-43 protein and mRNA expression (except low dosage treatment at 21 d) were significantly decreased compared with the control (P < 0.01, P < 0.05), but there was no significant difference at 60-day old offsprings for the parameters above.</p><p><b>CONCLUSION</b>Exposure to low level lead during pregnancy could inhibit the GAP-43 protein and mRNA expression in hippocampus of rat's offspring, which may be one of the molecular mechanisms of lead on learning and memory.</p>

Effects of prenatal exposure to low level lead on learning and memory of rats' offspring / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore the effects of prenatal exposure to low level lead on learning and memory of rat's offspring.</p><p><b>METHODS</b>The pregnant rats were randomizedly divided into 4 groups and provided with doubly evaporated water in the control group and 125, 250 and 500 mg/L lead acetate solution via drinking water in three exposed groups respectively during the pregnancy. The learning and memory ability of 21-day old and 60-day old offsprings were tested by the Morris water maze and the shuttling and avoiding dark box respectively.</p><p><b>RESULTS</b>The blood and hippocampus lead concentrations of 1-day old and 21-day old offspring in the 3 lead-exposed groups were significantly increased compared with the control group (P < 0.05), while at the period of 60-day old there was no significant difference between them. The time to find the platform in Morris water maze for 21-day old and 60-day old offsprings of the 3 lead in the exposed groups was significantly increased compared with the control group during the 4 days training (P < 0.05). The times of initiative avoiding in the shuttling and avoiding dark box for 21-day old and 60-day old offsprings in the 3 lead-exposed groups were significantly decreased, while the latency of the initiative avoiding and latency of the passive avoiding were significantly increased compared with the control group (P < 0.05).</p><p><b>CONCLUSION</b>Prenatal exposure to low level lead impaired the space learning and memory ability of offsprings of the rats, and this kind of influence will continue till the offspring's maturity.</p>

Effects of lead acetate on expression of brain-derived neurotropic factor and P75NTR in rat brain / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effects of lead acetate on the expression of brain-derived neurotropic factor (BDNF) and its receptor P75NTR in rat brain.</p><p><b>METHODS</b>Lead acetate was given to SD rats by intraperitoneal injection (ip) for 5 days at the dosage of 25, 50 and 100mg/kg body weight respectively. The contents of lead in serum, cerebral cortex and hippocampus were measured by atomic absorption spectrophotochemistry. The levels of BDNF mRNA and protein expression in cerebral cortex and hippocampus were observed by RT-PCR and immunohistochemistry, respectively. The levels of P75NTR protein expression in rat brain were measured by immunohistochemistry.</p><p><b>RESULTS</b>Compared with the control, the contents of lead were significantly increased in serum, cerebral cortex and hippocampus in the treatment groups respectively (P < 0.01, P < 0.05). The BDNF mRNA expression in the cerebral cortex (0.52 +/- 0.05, 0.33 +/- 0.03) and hippocampus (0.77 +/- 0.10, 0.92 +/- 0.08) of 50, 100 mg/kg treated groups was significantly higher than that of the control group (0.52 +/- 0.05, 0.33 +/- 0.03), respectively (P < 0.05). The results of immunohistochemistry showed that the area density of BDNF protein in cerebral cortex of every treatment group (0.040 +/- 0.027, 0.048 +/- 0.027, 0.086 +/- 0.040) was significantly increased whereas the average gray value (187.11 +/- 11.15, 180.53 +/- 5.82, 180.15 +/- 8.01) was significantly lower than that of the control (0.026 +/- 0.005, 204.98 +/- 3.45) (P < 0.05, P < 0.01). The area density of BDNF protein in hippocampus of every treatment group was 0.040 +/- 0.027, 0.048 +/- 0.027, 0.086 +/- 0.040, respectively, which was significantly increased compared with the control (0.045 +/- 0.019, P < 0.05). The average gray value of BDNF protein in hippocampus (181.03 +/- 5.16, 171.25 +/- 12.65) of 50, 100 mg/kg were significantly lower than that of the control (198.98 +/- 6.40, P < 0.01). There was no positive expression of P75NTR protein in the control and 25 mg/kg body weight groups. The positive expression of P75NTR protein was detected in 50 and 100 mg/kg body weight groups.</p><p><b>CONCLUSION</b>Lead can increase the BDNF and P75NTR expression in rat brain which might play an important role in the neural damage and repair.</p>

Effects of microwave radiation on thymocytes in mice at different power densities / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effects of microwave radiation on thymocytes in mice at different power densities.</p><p><b>METHODS</b>The experimental animals were whole-body exposed to microwave radiation with frequency of 2,450 MHz, power density of 1, 5, 15 mW/cm(2) respectively 1 h everyday for 30 days. Then the thymus were taken out after the mice were decapitated. Thymus index, morphological characteristics of thymus were examined. The changes of thymus T-cell subgroups, cell cycle progression in thymocytes and cellular apoptosis were detected with flow cytometry (FCM).</p><p><b>RESULTS</b>The body weights of animals in 5, 15 mW/cm(2) irradiation groups [(28.10 +/- 1.46), (27.50 +/- 2.52) g] were lower than that of the control [(31.95 +/- 2.51) g] (P < 0.05). Pathological observation showed dark red piece of nucleus, some nuclei inclined to one side, slight increase in hassall body. The expressions of CD8 in 5, 15 mW/cm(2) irradiation groups (29.14% +/- 1.68%, 29.18% +/- 0.81%) were higher than that in control group (26.95% +/- 1.27%) (P < 0.05). The percentages of G(2) + M phase thymocytes in both radiation groups (12.24% +/- 1.82%, 11.19% +/- 1.36%) were lower than that in control group (14.58% +/- 0.64%) (P < 0.01). Thymocytic apoptosis rates in the three experimental groups (7.18% +/- 0.99%, 10.06% +/- 1.58%, 9.45% +/- 0.92%) were higher than that in control (4.25% +/- 1.63%) (P < 0.01), but the evident difference between 5 mW/cm(2) and 15 mW/cm(2) was not found (P > 0.05).</p><p><b>CONCLUSION</b>Sub-chronic microwave exposure (2 450 MHz, 5, 15 mW/cm(2)) could induce thymocyte apoptosis, cause pathological changes in thymus, and affect cell cycle progression, thus may inhibit the immune function of the animal.</p>

Effect of lead acetate on the nerve growth factor protein expression and the regulation of thyroid hormone / 中华劳动卫生职业病杂志

<p><b>OBJECTIVES</b>To study the effect of lead acetate on the expression of nerve growth factor (NGF) protein in rat brain and the regulation of thyroid hormone.</p><p><b>METHODS</b>Lead acetate was given to SD rats intraperitoneally ip. at the dosage of 25, 50 and 100 mg/kg respectively. 6-n-propyl-2-thiouracil (PTU) was used to make a hypothyroid model and then lead acetate was given at the dosage of 50 mg/kg body weight through i.p. The NGF protein expression in rat brain was observed by immunohistochemistry Triiodothyronine (T3), thyroxin (T4), TSH in serum and T3, T4 in brain tissue were determined by radio immunoassays (RIAs).</p><p><b>RESULTS</b>The average gray value of NGF protein in cerebral cortex of 50 mg, 100 mg treated groups (180.49 +/- 10.33, 169.72 +/- 19.75, respectively) were lower than the control (200.75 +/- 3.27, P<0.01). The area density of NGF protein in hippocampus of three treated groups (0.08 +/- 0.14, 0.12 +/- 0.02, 0.13 +/- 0.04, respectively) were significantly different from the control (0.025 +/- 0.015, P<0.05). The area density and the average gray value of NGF protein in lead acetate treated hypothyroid rat brain were of no significant changes. The levels of serum T3 in three treated groups [(0.68 +/- 0.02), (0.57 +/- 0.04), (0.54 +/- 0.02) microg/L respectively] and T4 [(28.30 +/- 1.83), (27.35 +/- 2.55), (24.00 +/- 3.01) microg/L] in serum were significantly lower while TSH [(6.34 +/- 1.13), (7.74 +/- 0.79), (9.16 +/- 0.77) IU] higher than those in the control [T3 (0.97 +/- 0.14) microg/L, T4 (54.50 +/- 3.70) microg/L and TSH (4.62 +/- 2.16) IU], and there was a good dose-response relationship. The levels of T3 in cerebral cortex of three treated groups [(13.26 +/- 0.81), (11.49 +/- 0.10), (10.42 +/- 1.19) pg/mg pro respectively] and T4 [(0.50 +/- 0.03), (0.49 +/- 0.13), (0.42 +/- 0.01) ng/mg pro] were significantly lower than those in control [(20.85 +/- 11.01) pg/mg pro, (0.76 +/- 0.14) ng/mg pro, P<0.05, P<0.01].</p><p><b>CONCLUSION</b>Lead could increase the NGF protein expression in rat brain, which may be regulated by thyroid hormone.</p>