Validation of a Unique Boxing Monitoring System.

Much development work and scientific research has been conducted in recent years in the field of detecting human activity and the measurement of biomechanical performance parameters using portable sensor technologies, so-called wearable systems. Despite the fact that boxers participating in one of the most vigorous and complex disciplines of all sports, it is one of the disciplines where no noteworthy, advanced performance analytic tools are used for training or for competition purposes worldwide. This research aimed to develop and validate a comprehensive punch performance sensor system for the measurement and analysis of biomechanical parameters in the sport of boxing. A comprehensive validation study on linear regression was conducted following the development of the sensor system, between the gold standard of a Kistler force plate and Vicon motion capture system, to compare sensor-derived measurements with the gold standard-derived measurements. The developed sensor system demonstrated high accuracies ranging from R2 = 0.97 to R2 = 0.99 for punch force, acceleration, velocity and punch-time data. The validation experiments conducted demonstrated the significant accuracy of the sensor-derived measurements for predicting boxing-specific biomechanical movement parameters while punching in field use. Thus, this paper presents a unique sensor system for comprehensive measurements of biomechanical parameters using the developed mobile measurement system in the field of combat sports.

Application of a Validated Innovative Smart Wearable for Performance Analysis by Experienced and Non-Experienced Athletes in Boxing.

An athlete's sporting performance depends to a large extent on the technical execution of the athletic motion in order to achieve maximum effectiveness in physical performance. Performance analysis provides an important means of classifying and quantifying athletic prowess in terms of the significant performance aspects of the sport to provide objective feedback. This study aimed to analyze technical execution in terms of punch trajectory, force, velocity and time, considering the expert-novice paradigm by investigating the technical execution of 31 experienced and non-experienced athletes for the four main punching techniques of the cross, jab, uppercut and hook strike. The kinetic and kinematic data were collected by means of a boxing monitoring system developed and validated for in-field use. The research revealed significant correlation for executed punching trajectory and punch force in intragroup comparison and significant differences in intergroup comparison. No significant differences were detected for punch velocity in either inter- or intra-group paradigms. This study, through use of the sensor system, aligns with the results of existing publications conducted in laboratory conditions, in the assessment of punch force, punch speed and punch time and thus extends the state of research by use of a smart wearable in field method.

Validation of a Novel Boxing Monitoring System to Detect and Analyse the Centre of Pressure Movement on the Boxer's Fist.

The examination of force distribution and centre of pressure (CoP) displacement is a common method to analyse motion, load, and load distribution in biomechanical research. In contrast to gait analysis, the force progression in boxing punches is a new field of investigation. The centre of pressure displacement and distribution of forces on the surface of the fist during a boxing punch is of great interest and crucial to understanding the effect of the punch on the biological structures of the hand as well as the technical biomechanical aspects of the punching action. This paper presents a new method to display the CoP progression on the boxer's fist Therefore, this study presents the validation of the developed novel boxing monitoring system in terms of CoP displacement. In addition, the CoP progression of different punching techniques in boxing is analysed on the athlete's fist. The accuracy of the examination method of the CoP course was validated against the gold standard of a Kistler force plate. High correlations were detected between the developed sensor system and the force plate CoP with a Pearson correlation coefficient ranging from 0.93 to 0.97. The information obtained throughout the experimental study is of great importance in order to gain further knowledge into the technical execution of boxing punches as well as to provide a novel measuring method for determining CoP on the surface of the fist, to improve the understanding of the etiology of boxing-related hand injuries.

A genetic screen identifies BRCA2 and PALB2 as key regulators of G2 checkpoint maintenance.

To identify key connections between DNA-damage repair and checkpoint pathways, we performed RNA interference screens for regulators of the ionizing radiation-induced G2 checkpoint, and we identified the breast cancer gene BRCA2. The checkpoint was also abrogated following depletion of PALB2, an interaction partner of BRCA2. BRCA2 and PALB2 depletion led to premature checkpoint abrogation and earlier activation of the AURORA A-PLK1 checkpoint-recovery pathway. These results indicate that the breast cancer tumour suppressors and homologous recombination repair proteins BRCA2 and PALB2 are main regulators of G2 checkpoint maintenance following DNA-damage.

Gender Identities in Organized Sports-Athletes' Experiences and Organizational Strategies of Inclusion.

In relation to conceptualizing sports, beliefs about sex binary and male hegemony are dominant. To match these assumptions and provide level playing fields, sport systems are based on sex-segregation. Thus, people who do not fit into or reject fitting into sex categories are hindered from participating in sports, particularly organized sports. Studies on social exclusion of gender-identity minorities in sports mainly adopt a qualitative approach and focus on Anglophone countries. This research is the first to provide a comprehensive picture of the experiences of LGBT+ athletes in organized sports settings in Europe and is based on a quantitative online survey (n = 2,282). The current paper draws special attention to differences between cisgender and non-cisgender athletes (including transgender men, transgender women, non-binary, and non-identifying individuals). Besides athletes' experiences, organizational strategies of inclusion, derived from qualitative interviews with stakeholders from sport systems in five European countries (Germany, Scotland, Austria, Italy, and Hungary) are examined. Theoretically anchored in Cunningham's (2012) multilevel model for understanding the experiences of LGBT+ individuals and Meyer's (2003) minority stress model, the paper aims to (1) analyze the assessment of transnegativity and (2) examine negative experiences (prevalence, forms, perpetrators) of LGBT+ athletes from organized sport contexts in Europe; and (3) discuss inclusive strategies in sports organizations in Europe. Data reveal that transnegativity is perceived as a major problem in European sports, and non-cisgender athletes are the most vulnerable group, suffering particularly from structural discrimination. The implementation of inclusive strategies for non-cisgender athletes is perceived as a complex and essential task, but the sports organizations in the five countries differ substantially in terms of the status of implementation.

Cyclin F suppresses B-Myb activity to promote cell cycle checkpoint control.

Cells respond to DNA damage by activating cell cycle checkpoints to delay proliferation and facilitate DNA repair. Here, to uncover new checkpoint regulators, we perform RNA interference screening targeting genes involved in ubiquitylation processes. We show that the F-box protein cyclin F plays an important role in checkpoint control following ionizing radiation. Cyclin F-depleted cells initiate checkpoint signalling after ionizing radiation, but fail to maintain G2 phase arrest and progress into mitosis prematurely. Importantly, cyclin F suppresses the B-Myb-driven transcriptional programme that promotes accumulation of crucial mitosis-promoting proteins. Cyclin F interacts with B-Myb via the cyclin box domain. This interaction is important to suppress cyclin A-mediated phosphorylation of B-Myb, a key step in B-Myb activation. In summary, we uncover a regulatory mechanism linking the F-box protein cyclin F with suppression of the B-Myb/cyclin A pathway to ensure a DNA damage-induced checkpoint response in G2.

Correction: Kousholt, A.N. et al. Pathways for Genome Integrity in G2 Phase of the Cell Cycle. Biomolecules 2012, 2, 579-607.

We have discovered an error in our paper published in Biomolecules [1], in Figure 1 on page 589. The protein names ATR and ATRIP have been swapped. A corrected version of the Figure 1 is provided below. [...].

Pathways for genome integrity in G2 phase of the cell cycle.

The maintenance of genome integrity is important for normal cellular functions, organism development and the prevention of diseases, such as cancer. Cellular pathways respond immediately to DNA breaks leading to the initiation of a multi-facetted DNA damage response, which leads to DNA repair and cell cycle arrest. Cell cycle checkpoints provide the cell time to complete replication and repair the DNA damage before it can continue to the next cell cycle phase. The G2/M checkpoint plays an especially important role in ensuring the propagation of error-free copies of the genome to each daughter cell. Here, we review recent progress in our understanding of DNA repair and checkpoint pathways in late S and G2 phases. This review will first describe the current understanding of normal cell cycle progression through G2 phase to mitosis. It will also discuss the DNA damage response including cell cycle checkpoint control and DNA double-strand break repair. Finally, we discuss the emerging concept that DNA repair pathways play a major role in the G2/M checkpoint pathway thereby blocking cell division as long as DNA lesions are present.

CtIP-dependent DNA resection is required for DNA damage checkpoint maintenance but not initiation.

To prevent accumulation of mutations, cells respond to DNA lesions by blocking cell cycle progression and initiating DNA repair. Homology-directed repair of DNA breaks requires CtIP-dependent resection of the DNA ends, which is thought to play a key role in activation of ATR (ataxia telangiectasia mutated and Rad3 related) and CHK1 kinases to induce the cell cycle checkpoint. In this paper, we show that CHK1 was rapidly and robustly activated before detectable end resection. Moreover, we show that the key resection factor CtIP was dispensable for initial ATR-CHK1 activation after DNA damage by camptothecin and ionizing radiation. In contrast, we find that DNA end resection was critically required for sustained ATR-CHK1 checkpoint signaling and for maintaining both the intra-S- and G2-phase checkpoints. Consequently, resection-deficient cells entered mitosis with persistent DNA damage. In conclusion, we have uncovered a temporal program of checkpoint activation, where CtIP-dependent DNA end resection is required for sustained checkpoint signaling.

The histone methyltransferase SET8 is required for S-phase progression.

Chromatin structure and function is influenced by histone posttranslational modifications. SET8 (also known as PR-Set7 and SETD8) is a histone methyltransferase that monomethylates histonfe H4-K20. However, a function for SET8 in mammalian cell proliferation has not been determined. We show that small interfering RNA inhibition of SET8 expression leads to decreased cell proliferation and accumulation of cells in S phase. This is accompanied by DNA double-strand break (DSB) induction and recruitment of the DNA repair proteins replication protein A, Rad51, and 53BP1 to damaged regions. SET8 depletion causes DNA damage specifically during replication, which induces a Chk1-mediated S-phase checkpoint. Furthermore, we find that SET8 interacts with proliferating cell nuclear antigen through a conserved motif, and SET8 is required for DNA replication fork progression. Finally, codepletion of Rad51, an important homologous recombination repair protein, abrogates the DNA damage after SET8 depletion. Overall, we show that SET8 is essential for genomic stability in mammalian cells and that decreased expression of SET8 results in DNA damage and Chk1-dependent S-phase arrest.