A comparison of floor surfaces for injury prevention in care settings: impact forces and horizontal pulling force required to move wheeled equipment.

Shock-absorbing flooring is one potential solution to prevent fall-related injuries. No standards exist to characterize shock-absorbing healthcare flooring. This study explores two mechanical tests for impact force reduction and horizontal force required to move wheeled objects. An appropriately designed rubber underlay can reduce peak impact by 25% compared with 1% with standard vinyl. INTRODUCTION: Severe falls often occur in hospitals and care homes. Shock-absorbing flooring is one potential solution to prevent fall-related injuries; however, no standards exist for characterizing flooring as an injury prevention measure. Shock-absorbing flooring use in high-risk settings may influence both patients (injury-saving potential) and staff (manoeuvring equipment). We aimed to explore two tests to characterize floors, to determine shock absorbency and horizontal pulling force required to move wheeled objects. METHODS: Mechanical testing was performed according to the Canadian Standards Association Z325 Hip Protectors document. This test was developed for hip protectors but is applicable to compliant surfaces that form part of the floor. Tests were performed on commercially available floor materials (suitable for care settings) to assess the force required to initiate movement of a wheeled object across the floor. We explored the relationships between horizontal force required to pull wheeled objects, impact force, floor thickness, and core material. RESULTS: Considerable differences were identified between floor samples in their ability to reduce the peak impact force (range 0.7-25%). A peak force reduction of up to 25% can be achieved with a specially designed rubber underlay. Horizontal pulling force increased with floor thickness but was lower for rubber floors. There was no direct relationship between impact attenuation and horizontal pulling force. Whilst thickness and core material explain some variations (66.5% for wheel movement; 82.3% for impact), other unmeasured factors clearly influence floor performance. CONCLUSIONS: These results can inform the development of flooring and the establishment of standards needed to underpin practice, research, and development in this field.

Increased spontaneous apoptosis of CD4+CD25+ T cells in patients with active rheumatoid arthritis is reduced by infliximab.

Increased secretion of tumor necrosis factor-alpha (TNF-alpha), along with interleukin-1 (IL-1) and interleukin-6 (IL-6), is important in the pathogenesis of rheumatoid arthritis (RA). T regulatory CD4(+)CD25(+) cells play a role in maintaining self-tolerance by downregulating Th1-induced proinflammation. This function has been found to be altered in active RA, whereas anti-TNF-alpha therapy has been found to improve the suppressive abilities of these cells. Our objectives were to investigate whether T regulatory cells in patients with active RA display a higher sensitivity to spontaneous apoptosis than in normals, and to look into the potential of infliximab (anti-TNF-alpha therapy) to reduce the sensitivity of these cells to spontaneous apoptosis. Seventeen patients suffering from active RA, having failed multiple disease-modifying antirheumatic drug (DMARD) therapies, were treated with infliximab. Spontaneous apoptosis (as detected by annexin V binding) was determined in all patients and compared with a group of normal individuals at baseline and after three months on infliximab treatment. Peripheral blood mononuclear cells were incubated in 24-well plates at 1 x 10(6) cells/mL for 48 hours. Annexin V binding on CD4(+)CD25(+) was assessed using three-color assay by flow cytometry. Prior to infliximab initiation, spontaneous apoptosis of T regulatory cells from active RA patients was found to be increased in comparison with controls (26 +/- 4.2% vs. 19.8 +/- 4.8%, respectively; P = 0.01). Three months later (while still on infliximab) spontaneous apoptosis was comparable in the two groups (20.7 +/- 5.2% vs. 20.9 +/- 3.4%; P 5 0.8). The absolute number of CD4(+)CD25(+) cells/mL in the peripheral blood at baseline was reduced in 11 out of 17 active RA patients when compared with that of the control group (24 +/- 7 vs. 32 +/- 11, respectively; P = 0.02). Following anti-TNF-alpha therapy, CD4(+)CD25(+) cell counts of patients were equivalent to those of normals. The alteration and reversal in both spontaneous apoptosis and cell count of T regulatory cells was found to correlate with RA disease activity. CD4(+)CD25(+) T regulatory cells display increased proclivity to undergo spontaneous apoptosis in active RA. Alterations in CD4(+)CD25(+) cell apoptosis and cell count were found to correlate with RA disease activity. Reversal of these deviations from normal was documented in association with the beneficial outcome of infliximab therapy.