Field-based, portable motion-capture systems can be used to help identify individuals at greater risk of lower extremity injury. Microsoft Kinect-based markerless motion-capture systems meet these requirements; however, until recently, these systems were generally not automated, required substantial data postprocessing, and were not commercially available.
 
  To validate the kinematic measures of a commercially available markerless motion-capture system.
 
  Descriptive laboratory study.
 
  Laboratory.
 
  A total of 20 healthy, physically active university students (10 males, 10 females; age = 20.50 ± 2.78 years, height = 170.36 ± 9.82 cm, mass = 68.38 ± 10.07 kg, body mass index = 23.50 ± 2.40 kg/m2).
 
  Participants completed 5 jump-landing trials. Kinematic data were simultaneously recorded using Kinect-based markerless and stereophotogrammetric motion-capture systems.
 
  Sagittal- and frontal-plane trunk, hip-joint, and knee-joint angles were identified at initial ground contact of the jump landing (IC), for tIC measures (20.00%; 2/10). The markerless system underestimated sagittal-plane measures (86.67%; 13/15) and overestimated frontal-plane measures (76.47%; 13/17). No trends were observed for overestimating or underestimating IC, MAX, or DSP measures.
 
  Moderate agreement existed between markerless and stereophotogrammetric motion-capture systems. Better agreement existed for larger (eg, sagittal plane, MAX) than for smaller (eg, frontal plane, IC) joint angles. The DSP angles had the worst agreement. Markerless motion-capture systems may help clinicians identify individuals at greater risk of lower extremity injury.
 Moderate agreement existed between markerless and stereophotogrammetric motion-capture systems. Better agreement existed for larger (eg, sagittal plane, MAX) than for smaller (eg, frontal plane, IC) joint angles. The DSP angles had the worst agreement. Markerless motion-capture systems may help clinicians identify individuals at greater risk of lower extremity injury.Nonribosomal peptides (NRP) are crucial molecular mediators in microbial ecology and provide indispensable drugs. Nevertheless, the evolution of the flexible biosynthetic machineries that correlates with the stunning structural diversity of NRPs is poorly understood. Here, we show that recombination is a key driver in the evolution of bacterial NRP synthetase (NRPS) genes across distant bacterial phyla, which has guided structural diversification in a plethora of NRP families by extensive mixing and matching of biosynthesis genes. The systematic dissection of a large number of individual recombination events did not only unveil a striking plurality in the nature and origin of the exchange units but allowed the deduction of overarching principles that enable the efficient exchange of adenylation (A) domain substrates while keeping the functionality of the dynamic multienzyme complexes. In the majority of cases, recombination events have targeted variable portions of the Acore domains, yet domain interfaces and the flexible Asub domain remained untapped. Our results strongly contradict the widespread assumption that adenylation and condensation (C) domains coevolve and significantly challenge the attributed role of C domains as stringent selectivity filter during NRP synthesis. Moreover, they teach valuable lessons on the choice of natural exchange units in the evolution of NRPS diversity, which may guide future engineering approaches.Telomere fusions lead to a state of genomic instability, and are thought to drive clonal evolution and tumorigenesis. Telomere fusions occur via both Classical and Alternative Non-Homologous End Joining repair pathways. AsiDNA is a DNA repair inhibitor that acts by mimicking a DNA double strand break (DSB) and hijacking the recruitment of proteins involved in various DNA repair pathways. In this study, we investigated whether the inhibition of DSB-repair pathways by AsiDNA could prevent telomere fusions during crisis.  https://www.selleckchem.com/products/semaxanib-su5416.html  The present study showed that AsiDNA decreased the frequency of telomere fusions without affecting the rate of telomere erosion. Further, it indicated that AsiDNA does not impact the choice of the repair pathway used for the fusion of short dysfunctional telomeres. AsiDNA is thought to prevent short telomeres from fusing by inhibiting DNA repair. An alternative, non-mutually exclusive possibility is that cells harbouring fusions preferentially die in the presence of AsiDNA, thus resulting in a reduction in fusion frequency. This important work could open the way for investigating the use of AsiDNA in the treatment of tumours that have short dysfunctional telomeres and/or are experiencing genomic instability.
  Prevention of frailty is paramount in older adults. We evaluated the efficacy of a tailored multidomain intervention, monitored with the My Active and Healthy Aging platform, in reducing conversion from a prefrail status to overt frailty and preventing decline in quality of life.
 
  We performed a multicentre, multicultural, randomised control study. The effects of multidomain interventions on frailty parameters, quality of life, physical, cognitive, psychosocial function, nutrition and sleep were evaluated in a group of 101 prefrail older subjects and compared with 100 prefrail controls, receiving general health advice.
 
  At the 12-month assessment, controls showed a decline in quality of life that was absent in the active group. In addition, active participants showed an increase in mood and nutrition function. No effect on remaining parameter was observed.
 
  Our study supports the use of personalised multidomain intervention, monitored with an information and communication technology platform, in preventing quality of life decline in older adults.
 Our study supports the use of personalised multidomain intervention, monitored with an information and communication technology platform, in preventing quality of life decline in older adults.Emerging evidence indicates that microRNAs (miRNAs) play a critical role in breast cancer development. We recently reported that a higher expression of miR-374b in tumor tissues was associated with a better disease-free survival of triple-negative breast cancer (TNBC). However, the functional significance and molecular mechanisms underlying the role of miR-374b in breast cancer are largely unknown. In this current study, we evaluated the biological functions and potential mechanisms of miR-374b in both TNBC and non-TNBC. We found that miR-374b was significantly downregulated in breast cancer tissues, compared to adjacent tissues. MiR-374b levels were also lower in breast cancer cell lines, as compared to breast epithelial cells. In vitro and in vivo studies demonstrated that miR-374b modulates the malignant behavior of breast cancer cells, such as cell proliferation in 2D and 3D, cell invasion ability, colony-forming ability and tumor growth in mice. By using bioinformatics tools, we predicted that miR-374b plays a role in breast cancer cells through negatively regulating cyclin D1 (CCND1) and transforming growth factor alpha (TGFA).