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Recovery from traumatic muscle injuries is typically prolonged and incomplete, leading to impaired muscle and joint function. We sought to determine whether mechanical stimulation via whole-body low-intensity vibration (LIV) could (1) improve muscle regeneration and (2) reduce muscle fibrosis following traumatic injury. C57BL/6J mice were subjected to a laceration of the gastrocnemius muscle and were treated with LIV (0.2 g at 90 Hz or 0.4 g at 45 Hz for 30 min/day) or non-LIV sham treatment (controls) for seven or 14 days. Muscle regeneration and fibrosis were assessed in hematoxylin and eosin or Masson’s trichrome stained muscle cryosections, respectively. Compared to non-LIV control mice, the myofiber cross-sectional area was larger in mice treated with each LIV protocol after 14 days of treatment. Minimum fiber diameter was also larger in mice treated with LIV of 90 Hz/0.2 g after 14 days of treatment. There was also a trend toward a reduction in collagen deposition after 14 days of treatment with 45 Hz/0.4 g (p = 0.059). These findings suggest that LIV may improve muscle healing by enhancing myofiber growth and reducing fibrosis. The LIV-induced improvements in muscle healing suggest that LIV may represent a novel therapeutic approach for improving the healing of traumatic muscle injuries.

Aim Investigate the immediate effect of low intensity vibration on skin blood flow and its underlying control mechanisms in healthy human participants. Materials and methods One-group pre-post design in a university laboratory setting. Nine adults underwent two bouts of 10-minute vibration (30Hz, peak acceleration 0.4g). Outcome measures include skin blood flow, and skin temperature on the right foot. To examine the control mechanisms underlying the vibration-induced blood flow response, SHORT-TIME Fourier analyses were computed to obtain the spectral densities for three frequency bands: metabolic (0.0095–0.02Hz), neurogenic (0.02–0.06Hz), and myogenic (0.06–0.15Hz). Non-parametric Friedman’s tests were computed to compare changes of the outcome measures and control mechanisms over the course of vibration. Results Vibration increased skin blood flow during both bouts of vibration, however the effect did not last after vibration was terminated. Myogenic spectral density increased during both bouts of vibration, whereas the metabolic and neurogenic spectral densities increased only during the 2nd bout of vibration. Interestingly, only the metabolic spectral density remained elevated after vibration ended. Conclusion Low intensity vibration produced acute increases in skin blood flow mediated in part by vascular control mechanisms of myogenic origin. Further investigation is warranted to determine whether low intensity vibration induces similar increases in skin blood flow in populations prone to developing chronic non-healing wounds, such as spinal cord injury and diabetes.

Recovery from traumatic muscle injuries is typically prolonged and incomplete. Our previous study demonstrated that whole‐body low‐intensity vibration (LIV) enhances healing in a mouse laceration model. We sought to determine whether locally applied LIV (a) improves muscle repair following injury in mice and (b) is directly transduced by cultured muscle cells, via increased IGF‐1 activity. C57BL/6J mice were subjected to laceration of the gastrocnemius muscle and were treated with LIV applied directly to the lower leg for 30 min/day or non‐LIV sham treatment (controls) for 7 or 14 days. LIV was also applied to differentiating myotubes in culture for 30 min/day for 3 or 6 days. Compared with control mice, LIV increased myofiber cross‐sectional area, diameter, and percent area of peripherally nucleated fibers, and decreased percent damaged area after 14 days of treatment. In cultured myotubes, LIV increased fusion and diameter compared with controls after 6 days of treatment. These LIV‐induced effects were associated with increased total Akt on day 7 in injured muscle and on day 3 in myotubes, whereas phosphorylated‐to‐total Akt ratio increased on day 14 in injured muscle and on day 6 in myotubes but were not associated with increased IGF‐1 levels at any time point. These changes were also associated with LIV‐induced suppression of FOXO1 and Atrogin‐1 gene expression at day 7 in injured muscle. These findings demonstrate that muscle cells can directly transduce LIV signals into increased growth and differentiation, and this effect is associated with increased Akt signaling., Our findings demonstrate that muscle cells can directly transduce LIV signals into increased growth and differentiation, and this effect is associated with increased Akt signaling.

The purpose of this study was to determine whether thrombospondin (TSP)-1 promotes macrophage activity and disease progression in dysferlinopathy. First, we found that levels of TSP-1 are elevated in blood of non-ambulant dysferlinopathy patients compared with ambulant patients and healthy controls, supporting the idea that TSP-1 levels are correlated with disease progression. We then crossed dysferlinopathic BlaJ mice with TSP-1 knockout mice and assessed disease progression longitudinally with magnetic resonance imaging (MRI). In these mice, deletion of TSP-1 ameliorated loss in volume and mass of the moderately affected gluteal muscle but not of the severely affected psoas muscle. T2 MRI parameters revealed that loss of TSP-1 modestly inhibited inflammation only in gluteal muscle of male mice. Histological assessment indicated that deletion of TSP-1 reduced inflammatory cell infiltration of muscle fibers, but only early in disease progression. In addition, flow cytometry analysis revealed that, in males, TSP-1 knockout reduced macrophage infiltration and phagocytic activity, which is consistent with TSP-1-enhanced phagocytosis and pro-inflammatory cytokine induction in cultured macrophages. In summary, TSP-1 appears to play an accessory role in modulating Mp activity in BlaJ mice in a gender, age and muscle-dependent manner, but is unlikely a primary driver of disease progression of dysferlinopathy.

The aim of this study was to evaluate the diagnostic accuracy of 5 indirect methods that may be used in veterinary practices to assess the success of maternal immunoglobulins transfer in neonatal calves. Blood samples (n = 245) were collected from 2- to 6-d-old calves. Serum immunoglobulin concentrations were determined by radial immunodiffusion. Serum total protein and albumin concentrations and γ-glutamyl transferase activity were determined by veterinary practitioners using their own biochemistry analyzer. Globulin concentration was calculated. Veterinary practitioners were also asked to assess serum total protein using a digital Brix refractometer (%Brix) and an optical refractometer (g/L). Test sensitivity (Se) and specificity (Sp) were calculated using radial immunodiffusion as the reference standard, with failure of transfer of passive immunity defined as IgG10.0 g/L. Receiver operating characteristics curves were created and optimal cutoff values for each of the 5 indirect measurement methods were selected based on the maximization of the Youden's

This review is based on an invited presentation at the 65th Annual Meeting of the European Association for Animal Production held in Copenhagen, Denmark, August 2014; Neonatal mortality in small ruminant livestock has remained stubbornly unchanging over the past 40 years, and represents a significant loss of farm income, contributes to wastage and affects animal welfare. Scientific knowledge about the biology of neonatal adaptation after birth has been accumulating but does not appear to have had an impact in improving survival. In this paper, we ask what might be the reasons for the lack of impact of the scientific studies of lamb and kid mortality, and suggest strategies to move forward. Biologically, it is clear that achieving a good intake of colostrum, as soon as possible after birth, is crucial for neonatal survival. This provides fuel for thermoregulation, passive immunological protection and is involved in the development of attachment between the ewe and lamb. The behaviour of the lamb in finding the udder and sucking rapidly after birth is a key component in ensuring sufficient colostrum is ingested. In experimental studies, the main risk factors for lamb mortality are low birthweight, particularly owing to poor maternal nutrition during gestation, birth difficulty, litter size and genetics, which can all be partly attributed to their effect on the speed with which the lamb reaches the udder and sucks. Similarly, on commercial farms, low birthweight and issues with sucking were identified as important contributors to mortality. In epidemiological studies, management factors such as providing assistance with difficult births, were found to be more important than risk factors associated with housing. Social science studies suggest that farmers generally have a positive attitude to improving neonatal mortality but may differ in beliefs about how this can be achieved, with some farmers believing they had no control over early lamb mortality. Facilitative approaches, where farmers and advisors work together to develop neonatal survival strategies, have been shown to be effective in achieving management goals, such as optimising ewe nutrition, that lead to reductions in lamb mortality. We conclude that scientific research is providing useful information on the biology underpinning neonatal survival, such as optimal birthweights, lamb vigour and understanding the importance of sufficient colostrum intake, but the transfer of that knowledge would benefit from an improved understanding of the psychology of management change on farm. Developing tailored solutions, on the basis of adequate farm records, that make use of the now substantial body of scientific literature on neonatal mortality will help to achieve lower neonatal mortality.

The purpose of this work is to present how structural changes in the conventional Flash Analog to Digital Converter can secure it for a harsh radiation environment. The method consists in a coupling of two complementary techniques: a robust reconfiguration of the logical structure joined to a design hardening of the individual blocks. This approach preserves the ADC performances.