Effects of a multi-component exercise program and calcium–vitamin-D3-fortified milk on bone mineral density in older men : a randomised controlled trial

Summary We examined the independent and combined effects of a multi-component exercise program and calcium&ndash;vitamin-D3-fortified milk on bone mineral density (BMD) in older men. Exercise resulted in a 1.8% net gain in femoral neck BMD, but additional calcium&ndash;vitamin D3 did not enhance the response in this group of older well-nourished men.Introduction This 12-month randomised controlled trial assessed whether calcium&ndash;vitamin-D3-fortified milk could enhance the effects of a multi-component exercise program on BMD in older men.Methods Men (n&thinsp; =&thinsp;180) aged 50&ndash;79 years were randomised into: (1) exercise + fortified milk; (2) exercise; (3) fortified milk; or (4) controls. Exercise consisted of high intensity progressive resistance training with weight-bearing impact exercise. Men assigned to fortified milk consumed 400 mL/day of low fat milk providing an additional 1,000 mg/day calcium and 800 IU/day vitamin D3. Femoral neck (FN), total hip, lumbar spine and trochanter BMD and body composition (DXA), muscle strength 25-hydroxyvitamin D and parathyroid hormone (PTH) were assessed.Results There were no exercise-by-fortified milk interactions at any skeletal site. Exercise resulted in a 1.8% net gain in FN BMD relative to no-exercise (p&thinsp;&lt;&thinsp;0.001); lean mass (0.6 kg, p&thinsp;&lt;&thinsp;0.05) and muscle strength (20&ndash;52%, p&thinsp;&lt;&thinsp;0.001) also increased in response to exercise. For lumbar spine BMD, there was a net 1.4&ndash;1.5% increase in all treatment groups relative to controls (all p&thinsp;&lt;&thinsp;0.01). There were no main effects of fortified milk at any skeletal site.Conclusion A multi-component community-based exercise program was effective for increasing FN BMD in older men, but additional calcium&ndash;vitamin D3 did not enhance the osteogenic response.<br /

Temperature compensation of aerobic capacity and performance in the Antarctic pteropod, \u3cem\u3eClione antarctica\u3c/em\u3e, compared with its northern congener, \u3cem\u3eC. limacina\u3c/em\u3e

In ectotherms living in cold waters, locomotory performance is constrained by a slower generation of the ATP that is needed to fuel muscle contraction. Both polar and temperate pteropods of the genus Clione, however, are able to swim continuously by flapping their parapodia (wings) at comparable frequencies at their respective habitat temperatures. Therefore, we expected polar species to have increased aerobic capacities in their wing muscles when measured at common temperatures. We investigated muscle and mitochondrial ultrastructure of Clione antarctica from the Southern Ocean (−1.8°C) and populations of a sister species, Clione limacina, from the Arctic (−0.5 to 3°C) and from the North Atlantic (10°C). We also measured oxygen consumption and the activity of the mitochondrial enzyme citrate synthase (CS) in isolated wings of the two species. The Antarctic species showed a substantial up-regulation of the density of oxidative muscle fibers, but at the expense of fast-twitch muscle fibers. Mitochondrial capacity was also substantially increased in the Antarctic species, with the cristae surface density (58.2±1.3μm2μm−3) more than twice that found in temperate species (34.3±0.8μm2μm−3). Arctic C. limacina was intermediate between these two populations (43.7±0.5μm2μm−3). The values for cold-adapted populations are on par with those found in high-performance vertebrates. As a result of oxidative muscle proliferation, CS activity was 4-fold greater in C. antarctica wings than in temperate C. limacina when measured at a common temperature (20°C). Oxygen consumption of isolated wing preparations was comparable in the two species when measured at their respective habitat temperatures. These findings indicate complete compensation of ATP generation in wing muscles across a 10°C temperature range, which supports similar wing-beat frequencies during locomotion at each species\u27 respective temperature. The elevated capacity in the wing muscles is reflected in the partial compensation of whole-animal oxygen consumption and feeding rates

Axonopathy in the central nervous system is the hallmark of mice with a novel intragenic null mutation of dystonin.

Dystonia musculorum is a neurodegenerative disorder caused by a mutation in the dystonin gene. It has been described in mice and humans where it is called hereditary sensory autonomic neuropathy. Mutated mice show severe movement disorders and die at the age of 3-4 weeks. This study describes the discovery and molecular, clinical, as well as pathological characterization of a new spontaneously occurring mutation in the dystonin gene in C57BL/6N mice. The mutation represents a 40-kb intragenic deletion allele of the dystonin gene on chromosome 1 with exactly defined deletion borders. It was demonstrated by Western blot, mass spectrometry, and immunohistology that mice with a homozygous mutation were entirely devoid of the dystonin protein. Pathomorphological lesions were restricted to the brain stem and spinal cord and consisted of swollen, argyrophilic axons and dilated myelin sheaths in the white matter and, less frequently, total chromatolysis of neurons in the gray matter. Axonal damage was detected by amyloid precursor protein and nonphosphorylated neurofilament immunohistology. Axonopathy in the central nervous system (CNS) represents the hallmark of this disease. Mice with the dystonin mutation also showed suppurative inflammation in the respiratory tract, presumably due to brain stem lesion-associated food aspiration, whereas skeletal muscles showed no pathomorphological changes. This study describes a novel mutation in the dystonin gene in mice leading to axonopathy in the CNS. In further studies, this model may provide new insights into the pathogenesis of neurodegenerative diseases and may elucidate the complex interactions of dystonin with various other cellular proteins especially in the CNS

Community-dwelling men with dementia are at high risk of hip but not any other fracture: The Concord Health and Ageing in Men Project

Aim The aim of the present longitudinal study of community‐dwelling older men was to examine the association between cognitive status at baseline, and falls, fractures and bone loss over time. Methods In the Concord Health and Aging in Men Project, 1705 community‐dwelling men aged 70–97 years had detailed baseline clinical assessment of cognitive status (dementia, mild cognitive impairment [MCI] and normal cognition), as well as depression, physical activity, neuromuscular function, health status, sociodemographics, comorbidities, medication use and serum 25 hydroxyvitamin D, 1,25 dihydroxyvitamin D and parathyroid hormone levels. During a mean follow‐up period of 6 years, participants were contacted 4‐monthly to ascertain incident falls and fractures, the latter being confirmed by radiographic reports. Bone mineral density was measured by dual X‐ray absorptiometry at multiple time‐points. Results At baseline, 120 men were assessed to have MCI and 93 men to have dementia. Over time, there were 162 first incident fractures, including 43 hip and 32 vertebral fractures. In univariate models, baseline dementia, but not MCI, predicted an increased incidence of hip fracture (HR 6.95, 95% CI 3.47–13.96), but not vertebral (HR 2.26, 95% CI 0.79–6.46) or non‐hip non‐vertebral fracture (HR 0.73, 95% CI 0.27–1.99). The strong risk of hip fractures associated with dementia remained after accounting for potential confounders (HR 4.44, 95% CI 1.97–9.98). In multivariate analyses, dementia (incidence rate ratio 2.26, 95% CI 1.70–2.99), but not MCI, was associated with an increased risk of falls compared with normal cognition. There was no association between baseline dementia and change in bone mineral density. Conclusions Older men with dementia, but not MCI, have a greater tendency to fall and sustain hip fractures, but not any other types of fractures.NHMRC, Ageing and Alzheimer's Institute, Sydney Medical School Foundatio

Direct Neutron Capture for Magic-Shell Nuclei

In neutron capture for magic--shell nuclei the direct reaction mechanism can be important and may even dominate. As an example we investigated the reaction $^{48}$Ca(n,$\gamma)^{49}$Ca for projectile energies below 250\,keV in a direct capture model using the folding procedure for optical and bound state potentials. The obtained theoretical cross sections are in agreement with the experimental data showing the dominance of the direct reaction mechanism in this case. The above method was also used to calculate the cross section for $^{50}$Ca(n,$\gamma)^{51}$Ca.Comment: REVTeX, 7 pages plus 3 uuencoded figures, the complete uuencoded postscript file is available at ftp://is1.kph.tuwien.ac.at/pub/ohu/calcium.u

Metabolic suppression in thecosomatous pteropods as an effect of low temperature and hypoxia in the eastern tropical North Pacific

Author Posting. © The Author(s), 2011. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Marine Biology 159 (2012): 1955-1967, doi:10.1007/s00227-012-1982-x.Many pteropod species in the eastern tropical north Pacific Ocean migrate vertically each day, transporting organic matter and respiratory carbon below the thermocline. These migrations take species into cold (15-10ºC) hypoxic water (< 20 µmol O2 kg-1) at depth. We measured the vertical distribution, oxygen consumption and ammonia excretion for seven species of pteropod, some of which migrate and some which remain in oxygenated surface waters throughout the day. Within the upper 200 meters of the water column, changes in water temperature result in a ~60-75% reduction in respiration for most species. All three species tested under hypoxic conditions responded to low O2 with an additional ~35-50% reduction in respiratory rate. Combined, low temperature and hypoxia suppress the metabolic rate of pteropods by ~80-90%. These results shed light on the ways in which expanding regions of hypoxia and surface ocean warming may impact pelagic ecology.This work was funded by National Science Foundation grants to K. Wishner and B. Seibel (OCE – 0526502 and OCE – 0851043) and to K. Daly (OCE – 0526545), the University of Rhode Island, and the Rhode Island Experimental Program to Stimulate Competitive Research Fellowship program.2013-06-3

The Fall Armyworm Spodoptera frugiperda Utilizes Specific UDP-Glycosyltransferases to Inactivate Maize Defensive Benzoxazinoids

The relationship between plants and insects is continuously evolving, and many insects rely on biochemical strategies to mitigate the effects of toxic chemicals in their food plants, allowing them to feed on well-defended plants. Spodoptera frugiperda, the fall armyworm (FAW), accepts a number of plants as hosts, and has particular success on plants of the Poaceae family such as maize, despite their benzoxazinoid (BXD) defenses. BXDs stored as inert glucosides are converted into toxic aglucones by plant glucosidases upon herbivory. DIMBOA, the main BXD aglucone released by maize leaves, can be stereoselectively re-glucosylated by UDP-glycosyltransferases (UGTs) in the insect gut, rendering it non-toxic. Here, we identify UGTs involved in BXD detoxification by FAW larvae and examine how RNAi-mediated manipulation of the larval glucosylation capacity toward the major maize BXD, DIMBOA, affects larval growth. Our findings highlight the involvement of members of two major UGT families, UGT33 and UGT40, in the glycosylation of BXDs. Most of the BXD excretion in the frass occurs in the form of glucosylated products. Furthermore, the DIMBOA-associated activity was enriched in the gut tissue, with a single conserved UGT33 enzyme (SfUGT33F28) being dedicated to DIMBOA re-glucosylation in the FAW gut. The knock-down of its encoding gene reduces larval performance in a strain-specific manner. This study thus reveals that a single UGT enzyme is responsible for detoxification of the major maize-defensive BXD in this pest insect. © Copyright © 2020 Israni, Wouters, Luck, Seibel, Ahn, Paetz, Reinert, Vogel, Erb, Heckel, Gershenzon and Vassão