Bates K.T.,Institute of Aging and Chronic Disease |
Savage R.,Institute of Aging and Chronic Disease |
Pataky T.C.,Shinshu University |
Morse S.A.,Institute of Aging and Chronic Disease |
And 9 more authors.
Journal of the Royal Society Interface | Year: 2013
Footprints are the most direct source of evidence about locomotor biomechanics in extinct vertebrates. One of the principal suppositions underpinning biomechanical inferences is that footprint geometry correlates with dynamic foot pressure, which, in turn, is linked with overall limb motion of the trackmaker. In this study, we perform the first quantitative test of this longstanding assumption, using topological statistical analysis of plantar pressures and experimental and computer-simulated footprints. In computer-simulated footprints, the relative distribution of depth differed from the distribution of both peak and pressure impulse in all simulations. Analysis of footprint samples with common loading inputs and similar depths reveals that only shallow footprints lack significant topological differences between depth and pressure distributions. Topological comparison of plantar pressures and experimental beach footprints demonstrates that geometry is highly dependent on overall print depth; deeper footprints are characterized by greater relative forefoot, and particularly toe, depth than shallowfootprints. The highlighteddifference between 'shallow' and 'deep' footprints clearly emphasizes the need to understand variation in foot mechanics across different degrees of substrate compliance. Overall, our results indicate that extreme caution is required when applying the 'depth equals pressure' paradigm to hominin footprints, and by extension, those of other extant and extinct tetrapods. © 2013 The Author(s) Published by the Royal Society. All rights reserved.
PubMed | University College Dublin, Monaghan Mushrooms Ireland and Institute of Aging and Chronic Disease
Type: | Journal: Journal of nutritional science | Year: 2014
Vitamin D deficiency is emerging worldwide and many studies now suggest its role in the development of several chronic diseases. Due to the low level of vitamin D naturally occurring in food there is a need for supplementation and use of vitamin D-enhanced products. The aim of the present study was to determine if daily consumption of vitamin D2-enhanced mushrooms increased vitamin D status in free-living healthy adults or affected markers of the metabolic syndrome. A total of ninety volunteers (aged 40-65 years) were randomly assigned to one of two 4-week studies: mushroom study (15 g vitamin D2 or placebo mushroom powder) and capsule study (15 g vitamin D3 or placebo capsules). Consumption of vitamin D2-enhanced mushrooms increased serum 25-hydroxyvitamin D2 (25(OH)D2) by 128 % from baseline (39 (sd 19) nmol/l; P<005). Serum 25(OH)D3 increased significantly in the vitamin D3 capsule group (a 55 % increase from a baseline of 44.0 (sd 171) nmol/l; P<005). Vitamin D status (25(OH)D) was affected only in the vitamin D3 group. Plasminogen activator inhibitor-1 was lowered by vitamin D2 intake. Vitamin D2 from enhanced mushrooms was bioavailable and increased serum 25(OH)D2 concentration with no significant effect on 25(OH)D3 or total 25(OH)D.
News Article | December 8, 2016
Metastatic uveal melanoma (UM) is a cancer of the eye that currently has no effective treatment. However researchers from the University of Liverpool have discovered that the gene for the protein p63 can help initiate cancer “cell suicide”, potentially killing the cancer cells and preventing metastasis of the cancer. UM, while still rare, is the leading primary eye cancer in adults and about half of patients develop metastases. Although most cancers have the ability to elude apoptosis, or programmed cell death, a process which is meant to destroy dysfunctional cells, researchers lead by Dr. Luminita Paraoan, found they could initiate apoptosis in cancerous cells if the p63 gene was used in combination with a tumor suppressor gene p53. In patients with cancer, the tumor suppressor gene is typically mutated and can no longer control cell growth, sometimes leading to the growth of tumors. The researchers said that because of this p53 can’t begin the process of apoptosis in UM cancer cells alone. “The study highlights for the first time the requirement of p63 in the initiation of apoptosis in UM,” said Luminita, of the University’s Department of Eye and Vision Science in the Institute of Aging and Chronic Disease, in a statement. “Our findings have broad-ranging implications for other cancers in which apoptosis is evaded or problematic,” Luminita said. “They will hopefully prove advantageous in designing therapeutic approaches to cancerous tumors that are currently resistant to chemotherapy and radiotherapy.” The findings were published in the British Journal of Cancer.