Are joint torque models limited by an assumption of monoarticularity?

This study determines whether maximal voluntary ankle plantar flexor torque could be more accurately represented using a torque generator that is a function of both knee and ankle kinematics. Iso velocity and isometric ankle plantar flexor torques were measured on a single participant for knee joint angles of 111° to 169° (approximately full extension) using a Contrex M J dynamometer. Maximal voluntary torque was represented by a 19-parameter two-joint function of ankle and knee joint angles and angular velocities with the parameters determined by minimizing a weighted root mean square difference between measured torques and the two-joint function. The weighted root mean square difference between the two-joint function and the measured torques was 10 N-m or 3% of maximum torque. The two-joint function was a more accurate representation of maximal voluntary ankle plantar flexor torques than an existing single-joint function where differences of 19% of maximum torque were found. It is concluded that when the knee is flexed by more than 40°, a two-joint representation is necessary

An isovelocity dynamometer method to determine monoarticular and biarticular muscle parameters

This study aimed to determine whether subject-specific individual muscle models for the ankle plantar flexors could be obtained from single joint isometric and isovelocity maximum torque measurements in combination with a model of plantar flexion. Maximum plantar flexion torque measurements were taken on one subject at six knee angles spanning full flexion to full extension. A planar three-segment (foot, shank and thigh), two muscle (soleus and gastrocnemius) model of plantar flexion was developed. Seven parameters per muscle were determined by minimizing a weighted root mean square difference (wRMSD) between the model output and the experimental torque data. Valid individual muscle models were obtained using experimental data from only two knee angles giving a wRMSD score of 16 N m, with values ranging from 11 to 17 N m for each of the six knee angles. The robustness of the methodology was confirmed through repeating the optimization with perturbed experimental torques (±20%) and segment lengths (±10%) resulting in wRMSD scores of between 13 and 20 N m. Hence, good representations of maximum torque can be achieved from subject-specific individual muscle models determined from single joint maximum torque measurements. The proposed methodology could be applied to muscle-driven models of human movement with the potential to improve their validity

Optimal initial position and technique for the front foot contact phase of cricket fast bowling: commonalities between individual-specific simulations of elite bowlers

Group-based and individual-based studies in cricket fast bowling have identified common technique characteristics associated with ball release speed. The applicability of these findings to individual bowlers is often questioned, however, due to research approach limitations. This study aims to identify whether the optimal initial body position at front foot contact and subsequent technique to maximise ball release speed exhibit common characteristics for elite male cricket fast bowlers using individual-specific computer optimisations. A planar 16-segment whole-body torque-driven simulation model of the front foot contact phase of fast bowling was customised, evaluated, and the initial body position and subsequent movement pattern optimised, for ten elite male fast bowlers. The optimised techniques significantly increased ball release speed by 4.8 ± 1.3 ms−1 (13.5 ± 4.1%) and ranged between 37.8 and 42.9 ms−1, and in lower peak ground reaction forces and loading rates. Common characteristics were observed within the optimal initial body position with more extended front knees, as well as more flexion of the front and bowling arm shoulders than in current performances. Delays to the onset of trunk flexion, front arm and bowling arm shoulder extension, and wrist flexion were also common in the subsequent movement during the front foot contact phase. Lower front hip extensor and front shoulder flexor torques, as well as greater bowling shoulder extensor torques were also evident. This is useful knowledge for coach development, talent identification, and coaching practice

Jumping without Using Legs: The Jump of the Click-Beetles (Elateridae) Is Morphologically Constrained

To return to their feet, inverted click-beetles (Elateridae) jump without using their legs. When a beetle is resting on its dorsal side, a hinge mechanism is locked to store elastic energy in the body and releases it abruptly to launch the beetle into the air. While the functional morphology of the jumping mechanism is well known, the level of control that the beetle has over this jumping technique and the mechanical constraints governing the jumps are not entirely clear. Here we show that while body rotations in air are highly variable, the jumps are morphologically constrained to a constant “takeoff” angle (79.9°±1.56°, n = 9 beetles) that directs 98% of the jumping force vertically against gravity. A physical-mathematical model of the jumping action, combined with measurements from live beetle, imply that the beetle may control the speed at takeoff but not the jumping angle. In addition, the model shows that very subtle changes in the exact point of contact with the ground can explain the vigorous rotations of the body seen while the beetle is airborne. These findings suggest that the evolution of this unique non-legged jumping mechanism resulted in a jumping technique that is capable of launching the body high into the air but it is too constrained and unstable to allow control of body orientation at landing

Germline variation at 8q24 and prostate cancer risk in men of European ancestry

An Author Correction to this article was published on 17 January 2019.Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10 −15 ), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification. © 2018, The Author(s).Chromosome 8q24 is a susceptibility locus for multiple cancers, including prostate cancer. Here we combine genetic data across the 8q24 susceptibility region from 71,535 prostate cancer cases and 52,935 controls of European ancestry to define the overall contribution of germline variation at 8q24 to prostate cancer risk. We identify 12 independent risk signals for prostate cancer (p < 4.28 × 10 −15 ), including three risk variants that have yet to be reported. From a polygenic risk score (PRS) model, derived to assess the cumulative effect of risk variants at 8q24, men in the top 1% of the PRS have a 4-fold (95%CI = 3.62–4.40) greater risk compared to the population average. These 12 variants account for ~25% of what can be currently explained of the familial risk of prostate cancer by known genetic risk factors. These findings highlight the overwhelming contribution of germline variation at 8q24 on prostate cancer risk which has implications for population risk stratification. © 2018, The Author(s).Peer reviewe

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation

Although genome-wide association studies have identified over 100 risk loci that explain ~33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa

Atlas of prostate cancer heritability in European and African-American men pinpoints tissue-specific regulation

Although genome-wide association studies have identified over 100 risk loci that explain similar to 33% of familial risk for prostate cancer (PrCa), their functional effects on risk remain largely unknown. Here we use genotype data from 59,089 men of European and African American ancestries combined with cell-type-specific epigenetic data to build a genomic atlas of single-nucleotide polymorphism (SNP) heritability in PrCa. We find significant differences in heritability between variants in prostate-relevant epigenetic marks defined in normal versus tumour tissue as well as between tissue and cell lines. The majority of SNP heritability lies in regions marked by H3k27 acetylation in prostate adenoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines. We find a high degree of similarity between European and African American ancestries suggesting a similar genetic architecture from common variation underlying PrCa risk. Our findings showcase the power of integrating functional annotation with genetic data to understand the genetic basis of PrCa