The purpose of this review was to examine how different relative loads in weight training can improve acceleration over 10 m from a standing or flying start. A systematic review of the literature was undertaken using the following databases: PubMed, MedLine, Google Scholar, and SPORTDiscus. Studies were eligible if they met the following criteria: (1) participants were at least 15 years or older and healthy and injury free, (2) the study included at least one exercise for the lower body with a strength training frequency of at least once a week and included a training period of at least four weeks, and (3) interventions with clear pre- and post-test results on 10 m sprint or 10 m flying start are stated. Non-English-language articles were excluded. Percent change and between-group effect size (ES) were calculated to compare the effects of different training interventions. Forty-nine studies met the inclusion criteria. The results were categorized into four groups: (1) explosive weight training with light loads at 30-60% of 1-RM, (2) explosive weight training with moderate loads at 60-85% of 1-RM, (3) maximal weight training at 85-100% of 1-RM, and (4) hypertrophy training at 60-85% of 1-RM. At 10 m, all methods of weight training demonstrated improvements, and maximal weight training demonstrated the highest results with a large ES, while other approaches varied from very small to moderate ES. Weight training showed little progression with a significantly lower effect on flying start across all training methods, except for one group that trained power cleans (hypertrophy) where progress was large. To improve acceleration over the first 10 m, this review demonstrated maximal weight training as the preferred training method. For athletes with a pre-existing high level of strength, it could be more appropriate to use explosive training with light loads or a combination of the two. To a lesser extent, acceleration from a flying start could be improved using both training methods as well.

Is the use of ART, a proxy for infertility, associated with epigenetic age acceleration?

Parabolic flights provide cost-effective, time-limited access to "weightless" or reduced gravity conditions, facilitating research and validation activities that complement infrequent and costly access to space. Although parabolic flights have been conducted for decades, reference acceleration profiles and processing methods are not widely available. Here we present a solution for collecting, analyzing, and classifying the altered gravity environments experienced during parabolic flights, which we validated during a Boeing 727-200F flight with 20 parabolas. All data and analysis code are freely available. Our solution can be integrated with diverse experimental designs, does not depend upon accelerometer orientation, and allows unsupervised classification of all phases of flight, providing a consistent and open-source approach to quantifying gravito-inertial accelerations (GIA), or g levels. As academic, governmental, and commercial use of space advances, data availability and validated processing methods will enable better planning, execution, and analysis of parabolic flight experiments, and thus facilitate future space activities.

The profusion of high-throughput instruments and the explosion of new results in the scientific literature, particularly in molecular biomedicine, is both a blessing and a curse to the bench researcher. Even knowledgeable and experienced scientists can benefit from computational tools that help navigate this vast and rapidly evolving terrain. In this paper, we describe a novel computational approach to this challenge, a knowledge-based system that combines reading, reasoning, and reporting methods to facilitate analysis of experimental data. Reading methods extract information from external resources, either by parsing structured data or using biomedical language processing to extract information from unstructured data, and track knowledge provenance. Reasoning methods enrich the knowledge that results from reading by, for example, noting two genes that are annotated to the same ontology term or database entry. Reasoning is also used to combine all sources into a knowledge network that represents the integration of all sorts of relationships between a pair of genes, and to calculate a combined reliability score. Reporting methods combine the knowledge network with a congruent network constructed from experimental data and visualize the combined network in a tool that facilitates the knowledge-based analysis of that data. An implementation of this approach, called the Hanalyzer, is demonstrated on a large-scale gene expression array dataset relevant to craniofacial development. The use of the tool was critical in the creation of hypotheses regarding the roles of four genes never previously characterized as involved in craniofacial development; each of these hypotheses was validated by further experimental work.

MRI in presymptomatic autosomal dominant Alzheimer's disease mutation carriers (MC) provides an opportunity to detect changes that pre-date symptoms or clinical diagnosis. We used automated cortical thickness (CTh) measurement to compare the grey matter of such a group with cognitively normal controls.

Acceleration methods in fMRI aim to reconstruct high fidelity images from under-sampled k-space, allowing fMRI datasets to achieve higher temporal resolution, reduced physiological noise aliasing, and increased statistical degrees of freedom. While low levels of acceleration are typically part of standard fMRI protocols through parallel imaging, there exists the potential for approaches that allow much greater acceleration. One such existing approach is k-t FASTER, which exploits the inherent low-rank nature of fMRI. In this paper, we present a reformulated version of k-t FASTER which includes additional L2 constraints within a low-rank framework. We evaluated the effect of three different constraints against existing low-rank approaches to fMRI reconstruction: Tikhonov constraints, low-resolution priors, and temporal subspace smoothness. The different approaches are separately tested for robustness to under-sampling and thermal noise levels, in both retrospectively and prospectively-undersampled finger-tapping task fMRI data. Reconstruction quality is evaluated by accurate reconstruction of low-rank subspaces and activation maps. The use of L2 constraints was found to achieve consistently improved results, producing high fidelity reconstructions of statistical parameter maps at higher acceleration factors and lower SNR values than existing methods, but at a cost of longer computation time. In particular, the Tikhonov constraint proved very robust across all tested datasets, and the temporal subspace smoothness constraint provided the best reconstruction scores in the prospectively-undersampled dataset. These results demonstrate that regularized low-rank reconstruction of fMRI data can recover functional information at high acceleration factors without the use of any model-based spatial constraints.

Increased rates of brain atrophy measured from serial magnetic resonance imaging precede symptom onset in Alzheimer's disease and may be useful outcome measures for prodromal clinical trials. Appropriate trial design requires a detailed understanding of the relationships between β-amyloid load and accumulation, and rate of brain change at this stage of the disease. Fifty-two healthy individuals (72.3 ± 6.9 years) from Australian Imaging, Biomarkers and Lifestyle Study of Aging had serial (0, 18 m, 36 m) magnetic resonance imaging, (0, 18 m) Pittsburgh compound B positron emission tomography, and clinical assessments. We calculated rates of whole brain and hippocampal atrophy, ventricular enlargement, amyloid accumulation, and cognitive decline. Over 3 years, rates of whole brain atrophy (p < 0.001), left and right hippocampal atrophy (p = 0.001, p = 0.023), and ventricular expansion (p < 0.001) were associated with baseline β-amyloid load. Whole brain atrophy rates were also independently associated with β-amyloid accumulation over the first 18 months (p = 0.003). Acceleration of left hippocampal atrophy rate was associated with baseline β-amyloid load across the cohort (p < 0.02). We provide evidence that rates of atrophy are associated with both baseline β-amyloid load and accumulation, and that there is presymptomatic, amyloid-mediated acceleration of hippocampal atrophy. Clinical trials using rate of hippocampal atrophy as an outcome measure should not assume linear decline in the presymptomatic phase.

Epigenetic age acceleration-the difference between an individual's DNA methylation age and chronological age-is associated with many diseases including cancer. This study aims to evaluate epigenetic age acceleration as a prognostic biomarker for gliomas. DNA methylation data of gliomas patients (516 low-grade and intermediate-grade gliomas and 140 glioblastoma) were obtained from The Cancer Genome Atlas (TCGA) and patient epigenetic ages were computed using Horvath's age prediction model. We used multivariate linear regression to assess the association of epigenetic age acceleration with tumor molecular subtypes, including Codel, Classic-like, G-CIMP-high, G-CIMP-low, Mesenchymal-like and PA-like. Compared with Codel subtype, epigenetic ages in other molecular subtypes show deceleration after controlling age and race. Age deceleration for Classic-like, G-CIMP-high, G-CIMP-low, Mesenchymal-like and PA-like were 15.42 years (CI: 7.98-22.86, p = 5.38E-05), 25.00 years (CI: 20.79-29.22, p = 4.06E-28), 28.56 years (CI: 14.37-42.74, p = 8.75E-05), 45.34 years (CI: 38.80-51.88, p = 2.15E-36), and 53.58 years (CI: 44.90-62.26, p = 4.81E-30), respectively. Then, Cox proportional hazards regression was used to assess the association of epigenetic age acceleration with patient overall survival. Our results show epigenetic age acceleration is positively associated with patient overall survival (per 10-year age acceleration, HR = 0.89; 95%CI: 0.82-0.97; p = 9.04E-03) in multivariate analysis. When stratified by molecular subtypes, epigenetic age acceleration remains positively associated with patient survival after adjusting age and tumor grade. In conclusion, epigenetic age acceleration is significantly associated with molecular subtypes and patient overall survival in gliomas, indication that epigenetic age acceleration has potential as a quantitative prognostic biomarker for gliomas.

Schizophrenia (SCZ) is associated with high mortality. DNA methylation levels vary over the life course, and pre-selected combinations of methylation array probes can be used to estimate "methylation age" (mAge). mAge correlates highly with chronological age but when it differs, termed mAge acceleration, it has been previously associated with all-cause mortality. We tested the association between mAge acceleration and mortality in SCZ and controls. We selected 190 SCZ cases and 190 controls from the Sweden Schizophrenia Study. Cases were identified from the Swedish Hospital Discharge Register with ≥5 specialist treatment contacts and ≥5 antipsychotic prescriptions. Controls had no psychotic disorder or antipsychotics. Subjects were selected if they had died or survived during follow-up (2:1 oversampling). Extracted DNA was assayed on the Illumina MethylationEPIC array. mAge was regressed on age at sampling to obtain mAge acceleration. Using Cox proportional hazards regression, the association between mAge acceleration and mortality was tested. After quality control, the following were available: n = 126 SCZ died, 63 SCZ alive, 127 controls died, 62 controls alive. In the primary analyses, we did not find a significant association between mAge acceleration and SCZ mortality (adjusted p > 0.005). Sensitivity analyses excluding SCZ cases with pre-existing cancer demonstrated a significant association between the Hannum mAge acceleration and mortality (hazard ratio = 1.13, 95% confidence interval = 1.04-1.22, p = 0.005). Per our pre-specified criteria, we did not confirm our primary hypothesis that mAge acceleration would predict subsequent mortality in people with SCZ, but we cannot rule out smaller effects or effects in patient subsets.

The recognition that oxidative stress is a major component of several chronic diseases has engendered numerous trials of antioxidant therapies with minimal or no direct benefits. Nanomolar quantities of nitric oxide released into the circulation by pharmacologic stimulation of eNOS have antioxidant properties but physiologic stimulation as through increased pulsatile shear stress of the endothelium has not been assessed. The present study utilized a non-invasive technology, periodic acceleration (pGz) that increases pulsatile shear stress such that upregulation of cardiac eNOS occurs, We assessed its efficacy in normal mice and mouse models with high levels of oxidative stress, e.g. Diabetes type 1 and mdx (Duchene Muscular Dystrophy). pGz increased protein expression and upregulated eNOS in hearts. Application of pGz was associated with significantly increased expression of endogenous antioxidants (Glutathioneperoxidase-1(GPX-1), Catalase (CAT), Superoxide, Superoxide Dismutase 1(SOD1). This led to an increase of total cardiac antioxidant capacity along with an increase in the antioxidant response element transcription factor Nrf2 translocation to the nucleus. pGz decreased reactive oxygen species in both mice models of oxidative stress. Thus, pGz is a novel non-pharmacologic method to harness endogenous antioxidant capacity.

Cardiovascular health (CVH) has been defined by the American Heart Association (AHA) as the presence of the "Life's Simple 7" ideal lifestyle and clinical factors. CVH is known to predict longevity and freedom from cardiovascular disease, the leading cause of death for women in the United States. DNA methylation markers of aging have been aggregated into a composite epigenetic age score, which is associated with cardiovascular morbidity and mortality. However, it is unknown whether poor CVH is associated with acceleration of aging as measured by DNA methylation markers in epigenetic age.

All living tissues and cells on Earth are subject to gravitational acceleration, but no reports have verified whether acceleration mode influences bone formation and healing. Therefore, this study was to compare the effects of two acceleration modes, vibration and constant (centrifugal) accelerations, on bone formation and healing in the trunk using BMP 2-induced ectopic bone formation (EBF) mouse model and a rib fracture healing (RFH) rat model. Additionally, we tried to verify the difference in mechanism of effect on bone formation by accelerations between these two models. Three groups (low- and high-magnitude vibration and control-VA groups) were evaluated in the vibration acceleration study, and two groups (centrifuge acceleration and control-CA groups) were used in the constant acceleration study. In each model, the intervention was applied for ten minutes per day from three days after surgery for eleven days (EBF model) or nine days (RFH model). All animals were sacrificed the day after the intervention ended. In the EBF model, ectopic bone was evaluated by macroscopic and histological observations, wet weight, radiography and microfocus computed tomography (micro-CT). In the RFH model, whole fracture-repaired ribs were excised with removal of soft tissue, and evaluated radiologically and histologically. Ectopic bones in the low-magnitude group (EBF model) had significantly greater wet weight and were significantly larger (macroscopically and radiographically) than those in the other two groups, whereas the size and wet weight of ectopic bones in the centrifuge acceleration group showed no significant difference compared those in control-CA group. All ectopic bones showed calcified trabeculae and maturated bone marrow. Micro-CT showed that bone volume (BV) in the low-magnitude group of EBF model was significantly higher than those in the other two groups (3.1±1.2mm3 v.s. 1.8±1.2mm3 in high-magnitude group and 1.3±0.9mm3 in control-VA group), but BV in the centrifuge acceleration group had no significant difference compared those in control-CA group. Union rate and BV in the low-magnitude group of RFH model were also significantly higher than those in the other groups (Union rate: 60% v.s. 0% in the high-magnitude group and 10% in the control-VA group, BV: 0.69±0.30mm3 v.s. 0.15±0.09mm3 in high-magnitude group and 0.22±0.17mm3 in control-VA group). BV/TV in the low-magnitude group of RFH model was significantly higher than that in control-VA group (59.4±14.9% v.s. 35.8±13.5%). On the other hand, radiographic union rate (10% in centrifuge acceleration group v.s. 20% in control-CA group) and micro-CT parameters in RFH model were not significantly different between two groups in the constant acceleration studies. Radiographic images of non-union rib fractures showed cartilage at the fracture site and poor new bone formation, whereas union samples showed only new bone. In conclusion, low-magnitude vibration acceleration promoted bone formation at the trunk in both BMP-induced ectopic bone formation and rib fracture healing models. However, the micro-CT parameters were not similar between two models, which suggested that there might be difference in the mechanism of effect by vibration between two models.

This study investigated relationships between 10 m sprint acceleration, step kinematics (step length and frequency, contact and flight time), and leg muscle performance (power, stiffness, strength). Twenty-eight field sport athletes completed 10 m sprints that were timed and filmed. Velocity and step kinematics were measured for the 0-5, 5-10, and 0-10 m intervals to assess acceleration. Leg power was measured via countermovement jumps (CMJ), a five-bound test (5BT), and the reactive strength index (RSI) defined by 40 cm drop jumps. Leg stiffness was measured by bilateral and unilateral hopping. A three-repetition maximum squat determined strength. Pearson's correlations and stepwise regression (p ≤ 0.05) determined velocity, step kinematics, and leg muscle performance relationships. CMJ height correlated with and predicted velocity in all intervals (r = 0.40-0.54). The 5BT (5-10 and 0-10 m intervals) and RSI (5-10 m interval) also related to velocity (r = 0.37-0.47). Leg stiffness did not correlate with acceleration kinematics. Greater leg strength related to and predicted lower 0-5 m flight times (r = -0.46 to -0.51), and a longer 0-10 m step length (r = 0.38). Although results supported research emphasizing the value of leg power and strength for acceleration, the correlations and predictive relationships (r(2) = 0.14-0.29) tended to be low, which highlights the complex interaction between sprint technique and leg muscle performance. Nonetheless, given the established relationships between speed, leg power and strength, strength and conditioning coaches should ensure these qualities are expressed during acceleration in field sport athletes.

The emergence and spread of antibiotic resistance in bacteria is becoming a global public health problem. Combination therapy, i.e., the simultaneous use of multiple antibiotics, is used for long-term treatment to suppress the emergence of resistant strains. However, the effect of the combinatorial use of multiple drugs on the development of resistance remains elusive, especially in a quantitative assessment.

The rate of molecular evolution varies widely between proteins, both within and among lineages. To what extent is this variation influenced by genome-wide, lineage-specific effects? To answer this question, we assess the rate variation between insect lineages for a large number of orthologous genes.

Dolomite (CaMg(CO3)2) plays a key role in the global carbon cycle. Yet, the chemical mechanisms that catalyze its formation remain an enigma. Here, using batch reactor experiments, we demonstrate an unexpected acceleration of dolomite formation by zinc in saline fluids, reflecting a not uncommon spatial association of dolomite with Mississippi Valley-type ores. The acceleration correlates with dissolved zinc concentration, irrespective of the zinc source tested (ZnCl2 and ZnO). Moreover, the addition of dissolved zinc counteracts the inhibiting effect of dissolved sulfate on dolomite formation. Integration with previous studies enables us to develop an understanding of the dolomitization pathway. Our findings suggest that the fluids' high ionic strength and zinc complexation facilitate magnesium ion dehydration, resulting in a dramatic decrease in induction time. This study establishes a previously unrecognized role of zinc in dolomite formation, and may help explain the changes in dolomite abundance through geological time.

The transient, dynamic response of soft materials to mechanical impact has become increasingly relevant due to the emergence of numerous biomedical applications, e.g., accurate assessment of blunt injuries to the human body. Despite these important implications, acceleration-induced pressure gradients in soft materials during impact and the corresponding material response, from small deformations to sudden bubble bursts, are not fully understood. Both through experiments and theoretical analyses, we empirically show, using collagen and agarose model systems, that the local pressure in a soft sample is proportional to the square of the sample depth in the impact direction. The critical acceleration that corresponds to bubble bursts increases with increasing gel stiffness. Bubble bursts are also highly sensitive to the initial bubble size, e.g., bubble bursts can occur only when the initial bubble diameter is smaller than a critical size (≈10 μm). Our study gives fundamental insight into the physics of injury mechanisms, from blunt trauma to cavitation-induced brain injury.

Lipoproteins and lipid membranes accelerate •NO autoxidation by increasing local concentration of •NO and O2. Although the idea that proteins could also accelerate this reaction was presented some time ago, it was largely criticized and dismissed. Herein the effect of proteins on •NO autoxidation rates was studied following •NO disappearance with a selective electrode. It was found that human serum albumin (HSA) accelerated •NO autoxidation by a factor of 9 per g/mL of protein, much less than previously suggested. The acceleration by HSA was sensitive to pH and significantly decreased at pH lower than 4.5 coincident with the acid structure transition of HSA to a partially unfolded and rigid conformation. Other proteins with different surface hydrophobicity also accelerated •NO autoxidation and it was found to depend mostly on the protein size and dynamics. Mathematical simulations were performed to assess the physiological importance of this acceleration. It was calculated that in plasma the autoxidation of •NO is accelerated 1.38 times by HSA relative to water alone, but this becomes of little relevance when whole blood is simulated because of the rapid rate of •NO consumption by red blood cells.

The gut microbiota (GM) exerts a strong influence over the host immune system and dysbiosis of this microbial community can affect the clinical phenotype in chronic inflammatory conditions. To explore the role of the GM in lupus nephritis, we colonized NZM2410 mice with Segmented Filamentous Bacteria (SFB). Gut colonization with SFB was associated with worsening glomerulonephritis, glomerular and tubular immune complex deposition and interstitial inflammation compared to NZM2410 mice free of SFB. With SFB colonization mice experienced an increase in small intestinal lamina propria Th17 cells and group 3 innate lymphoid cells (ILC3s). However, although serum IL-17A expression was elevated in these mice, Th17 cells and ILC3s were not detected in the inflammatory infiltrate in the kidney. In contrast, serum and kidney tissue expression of the macrophage chemoattractants MCP-1 and CXCL1 were significantly elevated in SFB colonized mice. Furthermore, kidney infiltrating F4/80+CD206+M2-like macrophages were significantly increased in these mice. Evidence of increased gut permeability or "leakiness" was also detected in SFB colonized mice. Finally, the intestinal microbiome of SFB colonized mice at 15 and 30 weeks of age exhibited dysbiosis when compared to uncolonized mice at the same time points. Both microbial relative abundance as well as biodiversity of colonized mice was found to be altered. Collectively, SFB gut colonization in the NZM2410 mouse exacerbates kidney disease, promotes kidney M2-like macrophage infiltration and overall intestinal microbiota dysbiosis.

A superresolution imaging approach that localizes very small targets, such as red blood cells or droplets of injected photoacoustic dye, has significantly improved spatial resolution in various biological and medical imaging modalities. However, this superior spatial resolution is achieved by sacrificing temporal resolution because many raw image frames, each containing the localization target, must be superimposed to form a sufficiently sampled high-density superresolution image. Here, we demonstrate a computational strategy based on deep neural networks (DNNs) to reconstruct high-density superresolution images from far fewer raw image frames. The localization strategy can be applied for both 3D label-free localization optical-resolution photoacoustic microscopy (OR-PAM) and 2D labeled localization photoacoustic computed tomography (PACT). For the former, the required number of raw volumetric frames is reduced from tens to fewer than ten. For the latter, the required number of raw 2D frames is reduced by 12 fold. Therefore, our proposed method has simultaneously improved temporal (via the DNN) and spatial (via the localization method) resolutions in both label-free microscopy and labeled tomography. Deep-learning powered localization PA imaging can potentially provide a practical tool in preclinical and clinical studies requiring fast temporal and fine spatial resolutions.