Fitness and body composition profiling of elite junior South African rugby players

Objective. The aim of this study was to describe the body composition, strength and speed characteristics of elite junior South African rugby players. Design. Cross-sectional. Setting. Field study. Subjects. Rugby players (16 and 18 years old, N = 174) selected for the South African Rugby Union National Green Squad. Outcome measures. Body composition, 10 m and 40 m speed, agility, 1RM bench press, underhand pull-ups, push-ups, multistage shuttle run. Results. The under-16 players were on average shorter (175.6 ± 5.7 v. 179.2 ± 6.7 cm), weighed less (76.5 ± 8.2 v. 84.8 ± 8.3 kg) had less upper body absolute strength (77.1 ± 11.8 kg v. 95.3 ± 16.7 kg) and muscular endurance (41 ± 12 v. 52 ± 15 push-ups) and aerobic fitness (87.1 ± 19.4 v. 93.5 ± 15.3 shuttles) than the under-18 players. There were no differences in body fat, sprinting speed (10 m and 40 m) or agility between the two age groups. There were differences between playing positions, with the props having the most body fat, strongest upper bodies, slowest sprinting speed, least agility and lowest aerobic capacity compared with players in the other positions. Conclusion. This study provides data for elite junior rugby players and can be used to monitor the progression of players after intervention while also assisting with talent identification for the different playing positions

Fitness and body composition profiling of elite junior South African rugby players

Objective. The aim of this study was to describe the body composition, strength and speed characteristics of elite junior South African rugby players. Design. Cross-sectional. Setting. Field study. Subjects. Rugby players (16 and 18 years old, N = 174) selected for the South African Rugby Union National Green Squad. Outcome measures. Body composition, 10 m and 40 m speed, agility, 1RM bench press, underhand pull-ups, push-ups, multistage shuttle run. Results. The under-16 players were on average shorter (175.6 ± 5.7 v. 179.2 ± 6.7 cm), weighed less (76.5 ± 8.2 v. 84.8 ± 8.3 kg) had less upper body absolute strength (77.1 ± 11.8 kg v. 95.3 ± 16.7 kg) and muscular endurance (41 ± 12 v. 52 ± 15 push-ups) and aerobic fitness (87.1 ± 19.4 v. 93.5 ± 15.3 shuttles) than the under-18 players. There were no differences in body fat, sprinting speed (10 m and 40 m) or agility between the two age groups. There were differences between playing positions, with the props having the most body fat, strongest upper bodies, slowest sprinting speed, least agility and lowest aerobic capacity compared with players in the other positions. Conclusion. This study provides data for elite junior rugby players and can be used to monitor the progression of players after intervention while also assisting with talent identification for the different playing positions. South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 38-4

Fitness and body composition profiling of elite junior South African rugby players

Objective. The aim of this study was to describe the body composition, strength and speed characteristics of elite junior South African rugby players. Design. Cross-sectional. Setting. Field study. Subjects. Rugby players (16 and 18 years old, N = 174) selected for the South African Rugby Union National Green Squad. Outcome measures. Body composition, 10 m and 40 m speed, agility, 1RM bench press, underhand pull-ups, push-ups, multistage shuttle run. Results. The under-16 players were on average shorter (175.6 ± 5.7 v. 179.2 ± 6.7 cm), weighed less (76.5 ± 8.2 v. 84.8 ± 8.3 kg) had less upper body absolute strength (77.1 ± 11.8 kg v. 95.3 ± 16.7 kg) and muscular endurance (41 ± 12 v. 52 ± 15 push-ups) and aerobic fitness (87.1 ± 19.4 v. 93.5 ± 15.3 shuttles) than the under-18 players. There were no differences in body fat, sprinting speed (10 m and 40 m) or agility between the two age groups. There were differences between playing positions, with the props having the most body fat, strongest upper bodies, slowest sprinting speed, least agility and lowest aerobic capacity compared with players in the other positions. Conclusion. This study provides data for elite junior rugby players and can be used to monitor the progression of players after intervention while also assisting with talent identification for the different playing positions. South African Journal of Sports Medicine Vol. 18 (2) 2006: pp. 38-4

TP53 mutations in ovarian carcinomas from sporadic cases and carriers of two distinct BRCA1 founder mutations; relation to age at diagnosis and survival

BACKGROUND: Ovarian carcinomas from 30 BRCA1 germ-line carriers of two distinct high penetrant founder mutations, 20 carrying the 1675delA and 10 the 1135insA, and 100 sporadic cases were characterized for somatic mutations in the TP53 gene. We analyzed differences in relation to BRCA1 germline status, TP53 status, survival and age at diagnosis, as previous studies have not been conclusive. METHODS: DNA was extracted from paraffin embedded formalin fixed tissues for the familial cases, and from fresh frozen specimen from the sporadic cases. All cases were treated at our hospital according to protocol. Mutation analyses of exon 2 – 11 were performed using TTGE, followed by sequencing. RESULTS: Survival rates for BRCA1-familial cases with TP53 mutations were not significantly lower than for familial cases without TP53 mutations (p = 0.25, RR = 1.64, 95% CI [0.71–3.78]). Median age at diagnosis for sporadic (59 years) and familial (49 years) cases differed significantly (p < 0.001) with or without TP53 mutations. Age at diagnosis between the two types of familial carriers were not significantly different, with median age of 47 for 1675delA and 52.5 for 1135insA carriers (p = 0.245). For cases ≥50 years at diagnosis, a trend toward longer survival for sporadic over familial cases was observed (p = 0.08). The opposite trend was observed for cases <50 years at diagnosis. CONCLUSION: There do not seem to be a protective advantage for familial BRCA1 carriers without TP53 mutations over familial cases with TP53 mutations. However, there seem to be a trend towards initial advantage in survival for familial cases compared to sporadic cases diagnosed before the age of 50 both with and without TP53 mutations. However, this trend diminishes over time and for cases diagnosed ≥50 years the sporadic cases show a trend towards an advantage in survival over familial cases. Although this data set is small, if confirmed, this may be a link in the evidence that the differences in ovarian cancer survival reported, are not due to the type of BRCA1 mutation, but may be secondary to genetic factors shared. This may have clinical implications for follow-up such as prophylactic surgery within carriers of the two most frequent Norwegian BRCA1 founder mutations

Variations of training load, monotony, and strain and dose-response relationships with maximal aerobic speed, maximal oxygen uptake, and isokinetic strength in professional soccer players

This study aimed to identify variations in weekly training load, training monotony, and training strain across a 10-week period (during both, pre- and in-season phases); and to analyze the dose-response relationships between training markers and maximal aerobic speed (MAS), maximal oxygen uptake, and isokinetic strength. Twenty-seven professional soccer players (24.9±3.5 years old) were monitored across the 10-week period using global positioning system units. Players were also tested for maximal aerobic speed, maximal oxygen uptake, and isokinetic strength before and after 10 weeks of training. Large positive correlations were found between sum of training load and extension peak torque in the right lower limb (r = 0.57, 90%CI[0.15;0.82]) and the ratio agonist/antagonist in the right lower limb (r = 0.51, [0.06;0.78]). It was observed that loading measures fluctuated across the period of the study and that the load was meaningfully associated with changes in the fitness status of players. However, those magnitudes of correlations were small-to-large, suggesting that variations in fitness level cannot be exclusively explained by the accumulated load and loading profile

Triple-negative breast cancer: Present challenges and new perspectives

Contains fulltext : 83751.pdf (publisher's version ) (Open Access)21 p

Gene expression patterns associated with p53 status in breast cancer

BACKGROUND: Breast cancer subtypes identified in genomic studies have different underlying genetic defects. Mutations in the tumor suppressor p53 occur more frequently in estrogen receptor (ER) negative, basal-like and HER2-amplified tumors than in luminal, ER positive tumors. Thus, because p53 mutation status is tightly linked to other characteristics of prognostic importance, it is difficult to identify p53's independent prognostic effects. The relation between p53 status and subtype can be better studied by combining data from primary tumors with data from isogenic cell line pairs (with and without p53 function). METHODS: The p53-dependent gene expression signatures of four cell lines (MCF-7, ZR-75-1, and two immortalized human mammary epithelial cell lines) were identified by comparing p53-RNAi transduced cell lines to their parent cell lines. Cell lines were treated with vehicle only or doxorubicin to identify p53 responses in both non-induced and induced states. The cell line signatures were compared with p53-mutation associated genes in breast tumors. RESULTS: Each cell line displayed distinct patterns of p53-dependent gene expression, but cell type specific (basal vs. luminal) commonalities were evident. Further, a common gene expression signature associated with p53 loss across all four cell lines was identified. This signature showed overlap with the signature of p53 loss/mutation status in primary breast tumors. Moreover, the common cell-line tumor signature excluded genes that were breast cancer subtype-associated, but not downstream of p53. To validate the biological relevance of the common signature, we demonstrated that this gene set predicted relapse-free, disease-specific, and overall survival in independent test data. CONCLUSION: In the presence of breast cancer heterogeneity, experimental and biologically-based methods for assessing gene expression in relation to p53 status provide prognostic and biologically-relevant gene lists. Our biologically-based refinements excluded genes that were associated with subtype but not downstream of p53 signaling, and identified a signature for p53 loss that is shared across breast cancer subtypes

Microarray analysis reveals a major direct role of DNA copy number alteration in the transcriptional program of human breast tumors

Genomic DNA copy number alterations are key genetic events in the development and progression of human cancers. Here we report a genome-wide microarray comparative genomic hybridization (array CGH) analysis of DNA copy number variation in a series of primary human breast tumors. We have profiled DNA copy number alteration across 6,691 mapped human genes, in 44 predominantly advanced, primary breast tumors and 10 breast cancer cell lines. While the overall patterns of DNA amplification and deletion corroborate previous cytogenetic studies, the high-resolution (gene-by-gene) mapping of amplicon boundaries and the quantitative analysis of amplicon shape provide significant improvement in the localization of candidate oncogenes. Parallel microarray measurements of mRNA levels reveal the remarkable degree to which variation in gene copy number contributes to variation in gene expression in tumor cells. Specifically, we find that 62% of highly amplified genes show moderately or highly elevated expression, that DNA copy number influences gene expression across a wide range of DNA copy number alterations (deletion, low-, mid- and high-level amplification), that on average, a 2-fold change in DNA copy number is associated with a corresponding 1.5-fold change in mRNA levels, and that overall, at least 12% of all the variation in gene expression among the breast tumors is directly attributable to underlying variation in gene copy number. These findings provide evidence that widespread DNA copy number alteration can lead directly to global deregulation of gene expression, which may contribute to the development or progression of cancer