Paediatric elbow fractures and public play spaces: adherence to standards for children's playground equipment and surfacing.

Background: Supracondylar humerus fractures (SCHF) are the most common fractures sustained following a fall onto an outstretched hand among healthy children, and one of the leading causes of hospital admission and surgical intervention. The aim of this study was to examine SCHF occurring at public play spaces-particularly to determine whether or not the playground equipment implicated in injurious falls aligned with Canadian playground safety standards. Methods: Cases of children who attended the provincial paediatric orthopaedic clinic following SCHF at a public playground between April 2017 and October 2019 were included in the study. A research assistant visited each playground to measure the play structure type and dimensions, height of the equipment at the point from which the child fell and the type and depth of the surface material, and compare measurements to the 2016 safety standards. Child demographics and injury classification were also noted. Descriptive statistics were calculated and a scatterplot of fall height and surface depth was generated. Results: Forty-three sites, representing 47 SCHF cases (18 female, 29 male), were included in the final analysis. Fourteen children sustained type 1 fracture, 23 had type 2 fracture and the remaining 10 had type 3 fracture. Five children with type 2 fracture and all 10 children with type 3 fracture required surgery. The majority of sites had engineered wood fibre surfacing, with surfacing at 35 sites being less than 300 mm deep. Twenty-six play structures were upper body equipment (ie, monkey bars or similar), seven were track rides, five were rotating structures and the rest comprised a variety of classified and unclassified structures. Twenty-seven children fell from a height exceeding 2 m. Conclusions: The majority of SCHF cases occurred at playgrounds with insufficient surface depth and/or non-compliant equipment. Upper body equipment, track rides and rotating play structures were of particular concern, as the children fell from heights exceeding the recommended standard, likely reflecting the degradation and compaction of the surfacing material over time.

Zinc protects rat liver histo-architecture from detrimental effects of nickel.

This study was designed to examine the protective potential of zinc on the histoarchitecture distortion induced by nickel in rats. Male Sprauge Dawley (S.D) rats received either nickel alone in the form NiSO(4) x 6H(2)O at a dose of 800 mg/l in drinking water, zinc alone in the form of ZnSO(4) x 7H(2)O at a dose of 227 mg/l in drinking water, or nickel plus zinc or drinking water alone for a total duration of eight weeks. The effects of different treatments were studied on rat liver histoarchitecture by using both light and transmission electron microscopes. Normal control and zinc treated animals revealed normal histology of liver, however, nickel treated animals resulted in drastic alterations of normal hepatic histoarchitecture, after 8 weeks of treatment. Administration of zinc to nickel treated rats resulted in marked improvement in the structure of hepatocytes, thus emphasizing the protective potential of zinc in restoring the altered hepatic histoarchitecture close to the histoarchitecture of normal animals.

Oxidative stress due to nickel toxicity in the liver of protein-deficient rats.

This study was designed to determine the oxidative stress induced by nickel sulfate in the liver in the protein-deficient rats. Nickel sulfate in the dose of 800 mg/L in drinking water was administrated to Sprauge Dawley (SD) rats as well as protein-deficient rats for a total duration of 8 weeks. The effects of nickel treatment and protein deficiency separately and in combination were studied on rat liver antioxidant defense system enzymes like catalase, glutathione peroxidase (GPX), glutathione reductase (GR), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione-S-transferase (GST), as well as on lipid peroxidation (LPO). The investigations revealed a significant increase in the activity of enzymes, which include catalase, Gpx, GR and GST, and in the levels with LPO following nickel treatment in combination with protein deficiency. On the contrary, feeding to control rats resulted in a significant depression in the levels of SOD and GSH. However, nickel treatment to normal rats caused a significant increase in the activity of enzymes catalase and GST and in the levels of LPO, whereas the levels of GSH get significantly depressed. Further, nickel treatment to protein-deficient rats did not cause any additional alteration in the status of liver antioxidants as were observed in conditions of protein deficiency.

Role of zinc in regulating the levels of hepatic elements following nickel toxicity in rats.

This study was designed to determine the protective effects of zinc on the hepatotoxicity induced by nickel in rats. Female Sprague-Dawley (SD) rats received either nickel sulfate alone in the dose of 800 mg/L nickel in drinking water, zinc sulfate alone in the dose of 227 mg/L zinc in drinking water, and nickel plus zinc or drinking water alone for a total duration of 8 wk. The effects of different treatments were studied on activities of rat liver marker enzymes like alkaline phosphatase (ALP), alanine aminotransferase (ALT), and aspartate aminotransferases (AST) and on the status of essential elements in rat liver. The study revealed a significant increase in the activities of enzymes ALP and ALT in rats subjected to nickel treatment. Interestingly, zinc supplementation to rats treated with nickel brought back the raised activities of these enzymes to within normal limits. Further, the levels of elements in liver that include zinc, copper, selenium, and potassium were found to be significantly suppressed following nickel treatment, whereas the levels of iron and sulfur were elevated. However, zinc treatment alone did not cause any appreciable change in the concentration of these elements. To the contrary, when zinc was given to nickel-treated rats, the concentrations of zinc, copper, potassium, and phosphorus were not significantly different from that of normal controls, whereas the levels of iron, selenium, and sulfur were improved in comparison to nickel-treated rats but were not within the normal limits. The present study concludes that zinc has the ability to maintain the levels of hepatic elements and has bearing in regulating the liver functions by maintaining the activities of marker enzymes in conditions of nickel toxicity.

Effect of zinc on biological half-lives of 65Zn in whole body and liver and on distribution of 65Zn in different organs of rats following nickel toxicity.

This study was designed to determine the effect of zinc on the biological half-lives of 65Zn in whole body and liver and on distribution of 65Zn in different organs of rats following nickel toxicity. Sprague-Dawley (SD) rats received either nickel in the form NiSO4.6H2O at a dose of 800 mg/L in drinking water, zinc in the form of ZnSO4.7H2O at a dose of 227 mg/L in drinking water, and nickel plus zinc or drinking water alone for a total duration of 8 wk. All of the rats were injected with a tracer dose of 0.37 MBq 65Zn at the end of the treatment period. The effects of different treatments were studied on biological half-lives of 65Zn in whole body and liver and on the distribution of 65Zn in different organs of rats. In the present study, we have noted that nickel treatment to normal rats caused a significant decrease in the slow component (Tb2) in liver, which improved following zinc supplementation. Nickel administration to normal-diet-fed animals caused significant lowering in the percentage uptake of 65Zn values in the brain, liver, and intestine. However, the administration of zinc to nickel-treated rats improved the status of 65Zn in different organs. The Tb2 in the liver and the percentage uptake of 65Zn values elevated following zinc supplementation to nickel-treated rats.

Protective role of zinc in nickel induced hepatotoxicity in rats.

This study was planned to determine the protective role of zinc, if any, in attenuating the toxicity induced by nickel sulfate in rat liver. Female Sprague Dawley (SD) rats received either nickel alone in the dose of 800 mg/l in drinking water, zinc alone in the dose of 227 mg/l in drinking water, and nickel plus zinc or drinking water alone for a total duration of eight weeks. The effects of different treatments were studied on various parameters in rat liver which include antioxidant enzymes, levels of nickel and zinc and histoarchitecture at the light microscopic level. Further, the activities of hepatic marker enzymes AST and ALT were also studied in rat serum. Nickel treatment to the normal control animals, resulted in a significant increase in lipid peroxidation and enzyme activities of catalase and glutathione-S-transferase. On the contrary, nickel treatment to normal rats caused a significant inhibition in the levels of reduced glutathione. Superoxide dismutase activity was found to be decreased which however was not significant. Interestingly, when Zn was supplemented to nickel treated rats, the activities of catalase, and glutathione-S-transferase and the levels of GSH and lipid peroxidation came back to within normal limits. Activities of serum AST and ALT were increased significantly following nickel treatment to normal rats. Simultaneous zinc administration to nickel treated rats tended to restore the altered levels of AST and ALT. Normal control and zinc treated animals revealed normal histology of liver. On the other hand, nickel treated animals showed alterations in normal hepatic histoarchitecture which comprise of vacuolization of the hepatocytes and dilatation of sinusoids as well as increase in the number of bi-nucleated cells. Administration of zinc to nickel treated rats resulted in marked improvement in the structure of hepatocytes, thus emphasizing the protective potential of zinc in restoring the altered hepatic histoarchitecture. The nickel administration to normal rats indicated increased concentrations of nickel and decreased concentrations of zinc. However, zinc effectively brought the altered levels of nickel and zinc to within normal range. The study concludes that zinc has the potential in alleviating the toxic effects of nickel in rat liver because of its property to induce metallothionein (S-rich protein) as a free radical scavenger, or its indirect action in reducing the levels of oxygen reactive species.

Biokinetics of 65Zn in liver and whole body and its bio-distribution in nickel treated protein deficient rats.

This study was designed to determine the effect of nickel treatment on biological half-lives of 65Zn in whole body and liver as well as on distribution of 65Zn in different organs of protein deficient rats. Nickel sulfate at a dose level of 800mg/l in drinking water was administrated to normal control as well as to protein deficient rats for 8 weeks. A significant increase was found in fast and slow components of biological half lives of 65Zn in whole body and only fast component in liver of protein deficient rats. Interestingly, slow component in whole body and fast component in liver of nickel treated protein deficient rats were not different from normal controls though they were significantly elevated in protein deficient rats. On the other hand, slow component of 65Zn was also not altered in nickel treated protein deficient rats, which however, was significantly decreased in nickel treated rats. Protein deficiency led to a marked elevation in per cent uptake of 65Zn in brain and caused significant depression in liver, kidney and intestine. However, uptake of 65Zn in brain showed a significant depression in nickel treated rats, whereas the uptake was elevated in brain in nickel treated protein deficient rats. In conclusion, protein deficient conditions seem to be playing a dominant role in context with the distribution of 65Zn in different organs when nickel is administered to protein deficient rats. However nickel alone is seen to cause adverse effect on the distribution of 65Zn.