Study on the Strength Performance of Recycled Aggregate Concrete with Different Ages under Direct Shearing.

In order to study the mechanical properties of recycled aggregate concrete (RAC) at different ages, 264 standard cubes were designed to test its direct shear strength and cube compressive strength while considering the parameters of age and recycled aggregate replacement ratio. The failure pattern and load-displacement curve of specimens at direct shearing were obtained; the direct shear strength and residual shear strength were extracted from the load-displacement curves. Experimental results indicate that the influence of the replacement ratio for the front and side cracks of RAC is insignificant, with the former being straight and the latter relatively convoluted. At the age of three days, the damaged interface between aggregate and mortar is almost completely responsible for concrete failure; in addition to the damage of coarse aggregates, aggregate failure is also an important factor in concrete failure at other ages. The load-displacement curve of RAC at direct shearing can be divided into elasticity, elastoplasticity, plasticity, and stabilization stages. The brittleness of concrete decreases with its age, which is reflected in the gradual shortening of the elastoplastic stage. At 28 days of age, the peak direct shear force increases with the replacement ratio, while the trend is opposite at ages of 3 days, 7 days, and 14 days, respectively. The residual strength of RAC decreases inversely to the replacement ratio, with the rate of decline growing over time. A two-parameter RAC direct shear strength calculation formula was established based on the analysis of age and replacement rate to peak shear force of RAC. The relationship between cube compressive strength and direct shear strength of recycled concrete at various ages was investigated.

Sodium P-Aminosalicylic Acid Improved Manganese-Induced Learning and Memory Dysfunction via Restoring the Ultrastructural Alterations and γ-Aminobutyric Acid Metabolism Imbalance in the Basal Ganglia.

Excessive intake of manganese (Mn) may cause neurotoxicity. Sodium para-aminosalicylic acid (PAS-Na) has been used successfully in the treatment of Mn-induced neurotoxicity. The γ-aminobutyric acid (GABA) is related with learning and memory abilities. However, the mechanism of PAS-Na on improving Mn-induced behavioral deficits is unclear. The current study was aimed to investigate the effects of PAS-Na on Mn-induced behavioral deficits and the involvement of ultrastructural alterations and γ-aminobutyric acid (GABA) metabolism in the basal ganglia of rats. Sprague-Dawley rats received daily intraperitoneally injections of 15 mg/kg MnCl2.4H2O, 5d/week for 4 weeks, followed by a daily back subcutaneously (sc.) dose of PAS-Na (100 and 200 mg/kg), 5 days/week for another 3 or 6 weeks. Mn exposure for 4 weeks and then ceased Mn exposure for 3 or 6 weeks impaired spatial learning and memory abilities, and these effects were long-lasting. Moreover, Mn exposure caused ultrastructural alterations in the basal ganglia expressed as swollen neuronal with increasing the electron density in the protrusions structure and fuzzed the interval of neuropil, together with swollen, focal hyperplasia, and hypertrophy of astrocytes. Additionally, the results also indicated that Mn exposure increased Glu/GABA values as by feedback loops controlling GAT-1, GABAA mRNA and GABAA protein expression through decreasing GABA transporter 1(GAT-1) and GABA A receptor (GABAA) mRNA expression, and increasing GABAA protein expression in the basal ganglia. But Mn exposure had no effects on GAT-1 protein expression. PAS-Na treatment for 3 or 6 weeks effectively restored the above-mentioned adverse effects induced by Mn. In conclusion, these findings suggest the involvement of GABA metabolism and ultrastructural alterations of basal ganglia in PAS-Na's protective effects on the spatial learning and memory abilities.

Sodium para-aminosalicylate protected cultured basal ganglia astrocytes from manganese-induced DNA damages and alteration of amino acid neurotransmitter levels.

Sodium para-aminosalicylate (PAS-Na) was first applied successfully in clinical treatment of two manganism patients with good prognosis. However, the mechanism of how PAS-Na protects against Mn-induced neurotoxicity is still elusive. The current study was conducted to explore the effects of PAS-Na on Mn-induced basal ganglia astrocyte injury, and the involvement of amino acid neurotransmitter in vitro. Basal ganglia astrocytes were exposed to 500 µM manganese chloride (MnCl2) for 24 hr, following by 50, 150, or 450 µM PAS-Na treatment for another 24 hr. MnCl2 significantly decreased viability of astrocytes and induced DNA damages via increasing the percentage of tail DNA and Olive tail moment of DNA. Moreover, Mn interrupted amino acid neurotransmitters by decreasing Gln levels and increasing Glu, Gly levels. In contrast, PAS-Na treatment reversed the aforementioned Mn-induced toxic effects on basal ganglia astrocytes. Taken together, our results demonstrated that excessive Mn exposure may induce toxic effects on basal ganglia astrocytes, while PAS-Na could protect basal ganglia astrocytes from Mn-induced neurotoxicity.

The influence of manganese treatment on the distribution of metal elements in rats and the protection by sodium para-amino salicylic acid.

Manganese (Mn) overexposure induced neurological damages, which could be potentially protected by sodium para-aminosalicylic acid (PAS-Na). In this study, we systematically detected the changes of divalent metal elements in most of the organs and analyzed the distribution of the metals in Mn-exposed rats and the protection by PAS-Na. Sprague Dawley (SD) rats received intraperitoneal injections of 15mg/kg MnCl2·4H2O (5d/week for 3 weeks), followed by subcutaneous (back) injections of PAS-Na (100 and 200mg/kg, everyday for 5 weeks). The concentrations of Mn and other metal elements [Iron (Fe), Copper (Cu), Zinc (Zn), Magnesium (Mg), Calcium (Ca)] in major organs (liver, spleen, kidney, thighbone and iliac bone, cerebral cortex, hippocampus and testes) and blood by Inductively Coupled Plasma-Atomic Emission Spectrometry (ICP-AES). The results showed that Mn overexposure significantly increased Mn in most organs, Fe and Zn in liver, Fe and Mg in blood; however decreased Fe, Cu, Zn, Mg and Ca in cortex, Cu and Zn in kidney, Cu and Mg in iliac bone, and Zn in blood. In contrast, PAS-Na treatment restored most changes particularly in cortex. In conclusion, excessive Mn exposure disturbed the balance of other metal elements but PAS-Na post-treatments could restore these alterations.

Sodium Para-aminosalicylic Acid Protected Primary Cultured Basal Ganglia Neurons of Rat from Manganese-Induced Oxidative Impairment and Changes of Amino Acid Neurotransmitters.

Manganese (Mn), an essential trace metal for protein synthesis and particularly neurotransmitter metabolism, preferentially accumulates in basal ganglia. However, excessive Mn accumulation may cause neurotoxicity referred to as manganism. Sodium para-aminosalicylic acid (PAS-Na) has been used to treat manganism with unclear molecular mechanisms. Thus, we aim to explore whether PAS-Na can inhibit Mn-induced neuronal injury in basal ganglia in vitro. We exposed basal ganglia neurons with 50 µM manganese chloride (MnCl2) for 24 h and then replaced with 50, 150, and 450 µM PAS-Na treatment for another 24 h. MnCl2 significantly decreased cell viability but increased leakage rate of lactate dehydrogenase and DNA damage (as shown by increasing percentage of DNA tail and Olive tail moment). Mechanically, Mn reduced glutathione peroxidase and catalase activity and interrupted amino acid neurotransmitter balance. However, PAS-Na treatment reversed the aforementioned Mn-induced toxic effects. Taken together, these results showed that PAS-Na could protect basal ganglia neurons from Mn-induced neurotoxicity.

Relationship of lead and essential elements in whole blood from school-age children in Nanning, China.

OBJECTIVES: The aim of this study was to investigate blood lead level and its relationship to essential elements (zinc, copper, iron, calcium and magnesium) in school-age children from Nanning, China. METHODS: A total of 2457 children aged from 6 to 14 years were enrolled in Nanning, China. The levels of lead (Pb), zinc (Zn), copper (Cu), iron (Fe), calcium (Ca) and magnesium (Mg) were determined by an atomic absorption spectrometer. RESULTS: The mean blood lead level (BLL) was 57.21±35.00µg/L. 188 (7.65%) asymptomatic children had toxic lead level higher than 100µg/L. The school-age boys had similar lead level among different age groups, while the elder girls had less BLL. The blood Zn and Fe were found to be increased in the boys with elevated BLL, but similar trends were not observed in the girls. Positive correlations between Pb and Fe or Mg (r=0.112, 0.062, respectively, p<0.01) and a negative correlation between Pb and Ca (r=-0.047, p<0.05) were further established in the studied children. CONCLUSIONS: Lead exposure in school-age children was still prevalent in Nanning. The boys and girls differed in blood levels of lead and other metallic elements. Lead exposure may induce metabolic disorder of other metallic elements in body.

Blood lead level and its relationship to essential elements in preschool children from Nanning, China.

OBJECTIVE: Our study aimed to assess the distribution of blood lead level and its relationship to essential elements in preschool children in an urban area of China. DESIGN AND METHODS: A total of 6741 children aged 0- to 6-year-old were recruited. Levels of lead, zinc, copper, iron, calcium, and magnesium in whole blood samples were determined using atomic absorption spectrometry. RESULTS: The mean blood lead level (BLL) and the prevalence of BLL≥10µg/dl (5.26±4.08µg/dl and 6.84%, respectively) increased with age gradually, and there was a gender-difference for blood lead, copper, zinc and iron levels. Compared with the group of children who had BLLs<5µg/dl, the groups of 5≤BLLs<10µg/dl and 10≤BLLs<15µg/dl showed higher blood zinc, iron and magnesium levels, and a lower blood calcium level. A positive correlation of lead with zinc, iron and magnesium, and a negative correlation of lead with calcium were found in the group of children with BLL<5µg/dl. CONCLUSION: Age- and gender-differences were found when assessing the BLL and intoxication prevalence in preschool children. Metabolic disorder of essential elements was found even with a low level of lead exposure.