Local vibration therapy increases oxygen re-saturation rate and maintains muscle strength following exercise-induced muscle damage.

Context: Exercise induced muscle damage (EIMD) is associated with transient reductions in strength and athletic performance. Studies conclude aetiology is due in part to muscle micro vascular damage and disruption of blood flow. Previous research on vibration therapy reports modulation in muscle blood flow, oxygenation and strength. Objective: The aim of this study was to observe if local vibration therapy (VT) alleviates the impairments and haemodynamic changes associated with EIMD. Design: Controlled laboratory study. Setting: Laboratory and public gymnasium. Patients or other participants: Ten healthy participants (6 males: 4 females; age: 38±15 yrs; height: 1.72±0.48 m; mass 72.0±10.4 kg) were randomized into experimental (VT) and control (CON) groups. Interventions: Both groups performed 10 sets of 10 eccentric wrist flexions at 70% of 1-repetition maximum to induce muscle damage. Subsequent assessment of wrist flexor strength and flexor carpus ulnaris (FCU) muscle oxygen saturation (SmO2) occurred at 1-, 24- and 48 hr-post exercise. VT group underwent 10 min of local VT (45 Hz) starting 1 hr-post exercise and applied twice daily (separated by 8 hrs) for 48 hrs during habitual waking hours. CON group received no local VT. Main outcome measure(s): Grip strength, resting muscle oxygen (SmO2), muscle oxygen de-saturation and re-saturation rate. Results: No difference in grip strength observed pre EIMD, but the VT group demonstrated greater strength at 1 hr (P=0.004), 24 hr (P=0.031) and 48 hr (P=0.021) post EIMD compared to controls. No difference in SmO2 re-saturation over time (P>0.05), but the VT group had a greater re-saturation rate compared to controls at 1 hr (P=0.007, d = 2.6), 24 hr (P=0.001 d = 3.1) and 48 hr (P=0.035, d = 1.7) post EIMD. Conclusions: Local VT successfully attenuated the effects of EIMD and increased SmO2 re-saturation in FCU muscles. Including local VT as part of a recovery protocol post-EIMD could be beneficial for rehabilitation and athletic training purposes

Seasonal variations in vitamin D do not change the musculoskeletal health of physically active ambulatory men with cerebral palsy: a longitudinal cross-sectional comparison study

Increased levels of vitamin D in the summer months from natural seasonal variations in sun exposure have been linked to improvements in musculoskeletal health and function in UK populations; however, studies have shown that differences in lifestyles because of disability can inhibit the natural vitamin D increase in these populations. We hypothesized that men with cerebral palsy (CP) will experience smaller increases in 25-hydroxyvitamin D (25(OH)D) from winter to summer and men with CP will not experience any improvements in musculoskeletal health and function during the summer. A longitudinal observational study in 16 ambulant men with CP aged 21.0 ± 1.3 years and 16 healthy, physical activity matched, typically developed controls aged 25.4 ± 2.6 years, completed assessments of serum 25(OH)D and parathyroid hormone during winter and summer. Neuromuscular outcomes included vastus lateralis size, knee extensor strength, 10-m sprint, vertical jumps, and grip strength. Bone ultrasounds were performed to obtain radius and tibia T and Z scores. Men with CP and typically developed controls showed a 70.5% and 85.7% increase in serum 25(OH)D from winter to summer months, respectively. Neither group showed seasonal effect on neuromuscular outcomes muscle strength, size, vertical jump, or tibia and radius T and Z scores. A seasonal interaction effect was seen in the tibia T and Z scores (P < .05). In conclusion, there were similar seasonal increases in 25(OH)D observed in men with CP and typically developed controls, but serum 25(OH)D levels were still considered insufficient to improve bone or neuromuscular outcomes

Physical Activity and the Menstrual Cycle: A Mixed-Methods Study of Women’s Experiences

The menstrual cycle is an important biological process in women that is associated with a range of physical symptoms, which can shape how women think, feel, and participate in activities of daily life. This study employed a mixed-methods design to investigate adult women’s physical activity throughout the menstrual cycle. One hundred and twenty-eight participants completed an online questionnaire that explored events of the menstrual cycle (e.g., bleeding, pain, fatigue) and physical activity. Semistructured interviews with 21 questionnaire respondents unpacked individual experiences of physical activity throughout the menstrual cycle. From the questionnaire data, 44 participants were categorized as avoiders and 84 as nonavoiders of physical activity due to menstrual events. Avoiders of physical activity reported longer periods, heavier menstrual flow, and higher levels of fatigue and pain compared with nonavoiders. Interviews revealed that avoidance of physical activity ranged from complete avoidance to adaptation (e.g., types of exercise). Reasons for avoidance and adaptation of physical activity included menstrual symptoms, personal thoughts, and concerns about other people’s views of the period. The present study findings emphasize the importance of not only evaluating prevalent physical symptoms, but also unpacking women’s individual perspectives and established societal norms to better understand and normalize physical activity throughout the menstrual cycle

A quantitative description of self-selected walking in adults with Achondroplasia using the gait profile score.

BACKGROUND: Achondroplasia is characterised by a shorter appendicular limb-to-torso ratio, compared to age matched individuals of average stature (controls). Previous work shows gait kinematics of individuals with Achondroplasia differing to controls, but no global quantification of gait has been made in adults with Achondroplasia. AIM: The aim of this study was to quantify gait differences between a group of adult males with Achondroplasia and controls during self-selected walking (SSW) using the Gait Profile Score (GPS). DESIGN: Whole body motion analysis of 10 adults with Achondroplasia (22 ± 3 yrs) who had not undergone leg lengthening and 17 adult controls (22 ± 2 yrs) was undertaken using a 14 camera VICON system (100 Hz). For each group, fifteen root mean squared Gait Variable Scores (GVS, units °) were computed from lower limb kinematic data and then summed to calculate GPS (°). RESULTS: The group with Achondroplasia had higher GVSs than controls in 10 of the 15 measures (P < 0.05) with the largest differences found in ankle plantar/dorsiflexion (P < 0.001), knee flexion/extension (P < 0.001), and hip internal/external rotation (P < 0.001). The GPS value of the group with Achondroplasia was 64% higher than controls (11.4° (2.0) v 4.1° (1.8), P < 0.001). CONCLUSION: Gait is quantitatively different in adults with Achondroplasia compared to controls. The differences in GPS between groups are due to differences in joint kinematics, which are possibly manifested by maintaining toe-clearance during swing. Gait models derived from the anatomy of individuals with Achondroplasia may improve these data

The Oxygen Consumption and Metabolic Cost of Walking and Running in Adults With Achondroplasia

© 2018 Sims, Onambélé-Pearson, Burden, Payton and Morse. The disproportionate body mass and leg length of Achondroplasic individuals may affect their net oxygen consumption (VO 2 ) and metabolic cost (C) when walking at running compared to those of average stature (controls). The aim of this study was to measure submaximal VO 2 and C during a range of set walking speeds (SWS; 0.56-1.94 m·s-1, increment 0.28 m·s -1 ), set running speeds (SRS; 1.67-3.33 m·s -1 , increment 0.28 m·s -1 ) and a self-selected walking speed (SSW). VO 2 and C was scaled to total body mass (TBM) and fat free mass (FFM) while gait speed was scaled to leg length using Froude's number (Fr). Achondroplasic VO 2FFM x and VO 2FFM were on average 29 and 35% greater during SWS (P 0.05), but CTBM and CFFM at SSW were 23 and 29% higher (P < 0.05) in the Achondroplasic group compared to controls, respectively. VO 2TBM and VO 2FFM correlated with Fr for both groups (r = 0.984-0.999, P < 0.05). Leg length accounted for the majority of the higher VO 2TBM and VO 2FFM in the Achondroplasic group, but further work is required to explain the higher Achondroplasic CTBM and CFFM at all speeds compared to controls. New and Noteworthy: There is a leftward shift of oxygen consumption scaled to total body mass and fat free mass in Achondroplasic adults when walking and running. This is nullified when talking into account leg length. However, despite these scalars, Achondroplasic individuals have a higher walking and metabolic cost compared to age matched non-Achondroplasic individuals, suggesting biomechanical differences between the groups

Effects of nutrient addition and soil drainage on germination of N-fixing and non-N-fixing tropical dry forest tree species

To develop generalised predictions regarding the effects of atmospheric nitrogen (N) and phosphorus (P) deposition on vegetation communities, it is necessary to account for the impacts of increased nutrient availability on the early life history stages of plants. Additionally, it is important to determine if these responses (a) differ between plant functional groups and (b) are modulated by soil drainage, which may affect the persistence of added nutrients. We experimentally assessed seed germination responses (germination proportion and germination energy, i.e. time to germination) of commonly occurring N-fixing and non-N-fixing tropical dry forest tree species found in India to simulated N and P deposition in well-drained soils, as well as soils with impeded drainage. When soils were not allowed to drain, germination proportion declined with nutrient addition, while germination energy remained unchanged. Stronger declines in germination proportion were observed for N-fixing species. In free-draining soils, nutrient addition did not affect germination proportion in either functional group. However, we detected a trend of delayed germination with nutrient addition, especially in N-fixers. Our results suggest that nutrient deposition can lead to potential shifts in functional dominance and tree community composition of tropical dry forests in the long term through its effects on early life stages of trees, although the mechanisms underlying the observed germination responses remain unclear. Further, such effects are likely to be spatially variable across the geographic range in which tropical dry forests occur depending on soil drainage properties

The Adult Human Brain Harbors Multipotent Perivascular Mesenchymal Stem Cells

Blood vessels and adjacent cells form perivascular stem cell niches in adult tissues. In this perivascular niche, a stem cell with mesenchymal characteristics was recently identified in some adult somatic tissues. These cells are pericytes that line the microvasculature, express mesenchymal markers and differentiate into mesodermal lineages but might even have the capacity to generate tissue-specific cell types. Here, we isolated, purified and characterized a previously unrecognized progenitor population from two different regions in the adult human brain, the ventricular wall and the neocortex. We show that these cells co-express markers for mesenchymal stem cells and pericytes in vivo and in vitro, but do not express glial, neuronal progenitor, hematopoietic, endothelial or microglial markers in their native state. Furthermore, we demonstrate at a clonal level that these progenitors have true multilineage potential towards both, the mesodermal and neuroectodermal phenotype. They can be epigenetically induced in vitro into adipocytes, chondroblasts and osteoblasts but also into glial cells and immature neurons. This progenitor population exhibits long-term proliferation, karyotype stability and retention of phenotype and multipotency following extensive propagation. Thus, we provide evidence that the vascular niche in the adult human brain harbors a novel progenitor with multilineage capacity that appears to represent mesenchymal stem cells and is different from any previously described human neural stem cell. Future studies will elucidate whether these cells may play a role for disease or may represent a reservoir that can be exploited in efforts to repair the diseased human brain

Do Two Machine-Learning Based Prognostic Signatures for Breast Cancer Capture the Same Biological Processes?

The fact that there is very little if any overlap between the genes of different prognostic signatures for early-discovery breast cancer is well documented. The reasons for this apparent discrepancy have been explained by the limits of simple machine-learning identification and ranking techniques, and the biological relevance and meaning of the prognostic gene lists was questioned. Subsequently, proponents of the prognostic gene lists claimed that different lists do capture similar underlying biological processes and pathways. The present study places under scrutiny the validity of this claim, for two important gene lists that are at the focus of current large-scale validation efforts. We performed careful enrichment analysis, controlling the effects of multiple testing in a manner which takes into account the nested dependent structure of gene ontologies. In contradiction to several previous publications, we find that the only biological process or pathway for which statistically significant concordance can be claimed is cell proliferation, a process whose relevance and prognostic value was well known long before gene expression profiling. We found that the claims reported by others, of wider concordance between the biological processes captured by the two prognostic signatures studied, were found either to be lacking statistical rigor or were in fact based on addressing some other question

Paracrine IL-33 Stimulation Enhances Lipopolysaccharide-Mediated Macrophage Activation

BACKGROUND: IL-33, a member of the IL-1 family of cytokines, provokes Th2-type inflammation accompanied by accumulation of eosinophils through IL-33R, which consists of ST2 and IL-1RAcP. We previously demonstrated that macrophages produce IL-33 in response to LPS. Some immune responses were shown to differ between ST2-deficient mice and soluble ST2-Fc fusion protein-treated mice. Even in anti-ST2 antibody (Ab)-treated mice, the phenotypes differed between distinct Ab clones, because the characterization of such Abs (i.e., depletion, agonistic or blocking Abs) was unclear in some cases. METHODOLOGY/PRINCIPAL FINDINGS: To elucidate the precise role of IL-33, we newly generated neutralizing monoclonal Abs for IL-33. Exogenous IL-33 potentiated LPS-mediated cytokine production by macrophages. That LPS-mediated cytokine production by macrophages was suppressed by inhibition of endogenous IL-33 by the anti-IL-33 neutralizing mAbs. CONCLUSIONS/SIGNIFICANCE: Our findings suggest that LPS-mediated macrophage activation is accelerated by macrophage-derived paracrine IL-33 stimulation

Conscious uncoupling between FANCI and FANCD2 in DNA repair

The Fanconi anemia (FA)-BRCA pathway mediates repair of DNA interstrand crosslinks. The FA core complex, a multi-subunit ubiquitin ligase, participates in the detection of DNA lesions and monoubiquitinates two downstream FA proteins, FANCD2 and FANCI (or the ID complex). However, the regulation of the FA core complex itself is poorly understood. Here we show that the FA core complex proteins are recruited to sites of DNA damage and form nuclear foci in S and G2 phases of the cell cycle. ATR kinase activity, an intact FA core complex and FANCM-FAAP24 were crucial for this recruitment. Surprisingly, FANCI, but not its partner FANCD2, was needed for efficient FA core complex foci formation. Monoubiquitination or ATR-dependent phosphorylation of FANCI were not required for the FA core complex recruitment, but FANCI deubiquitination by USP1 was. Additionally, BRCA1 was required for efficient FA core complex foci formation. These findings indicate that FANCI functions upstream of FA core complex recruitment independently of FANCD2, and alter the current view of the FA-BRCA pathway