The health and fitness profiles of sport studies students at a tertiary institution in South Africa.

Master of Sport Science. University of KwaZulu-Natal, Westville 2014.Introduction The first time most adolescents start to take care of themselves with limited parental support is when they attend university. The watchful guidance of parental support typically wanes and students start to change their habits to suit their lifestyle. This study therefore presents data and related analysis of health and fitness profiles of a selected cohort of students. Aim of the Study: The aim of this study was to determine the health and fitness profiles of Sports Studies students at a tertiary institution in KwaZulu-Natal, South Africa. Methodology: The study was a cross-sectional design of undergraduate students. Three separate year groups (first year, second year and third year) were recruited. A purposive sample of first, (n=70) second (n=90) and third (n=90) year Sport Studies students completed a health questionnaire and a range of physical fitness tests. Descriptive and inferential techniques including the use of correlations and chi square test values were used to analyse data. Results: The sample consisted of 165 students with a mean age of 21.48 years (SD±2.48). First year’s (n = 41) comprised 24.85% of the sample, while second year’s (n = 62) 37.58% and third year’s (n = 62) 37.58%. The sample comprised of 116 males (70.3%) and 49 females (29.7%). According to South African racial classifications the sample consisted of 86.1% of the students who self-identified as Black African, 7.9% Indian, 3.6% Coloured and 2.4% White. The cohort’s mean BMI was 24.09 kg/m², with a general increase from first year (22.65 kg/m²) to second year (24.24 kg/m²) and to third year (24.87 kg/m²). Similarly, there was a mean increase in body weight of 4.09kgs between first and second year, and a mean increase of 3.81kgs from second to third year. In total, there was a mean body weight increase of 7.9kgs from first to third year. The mean body fat was 13.32% for the cohort with first year females at 23.87% and first year males 6.44%. In total, 31.5% males and 4.8% females were overweight or obese. Only 1.8% of the total sample was underweight. There was a mean increase in relative VO₂max in the study cohort (1st years 31.86 ml.kgˉ¹.minˉ¹, 2nd years 33.47 ml.kgˉ¹.minˉ¹ and 3rd years 34.42 ml.kgˉ¹.minˉ¹). The mean VO₂max for the entire sample was 33.43 ml.kgˉ¹.minˉ¹ with male students averaging 36.48 ml.kgˉ¹.minˉ¹ and female students 26.1 ml.kgˉ¹.minˉ¹.. It was reported 78.2% of the sample exercised on a regular basis, with 72.9% being male. Conclusions: Overall results showed that throughout the three years of study, weight and body fat percentage of students increased progressively along with body mass index, waist circumference and waist-to-hip ratios. Such increases are of utmost concern and may be directly associated with low physical activity levels and poor dietary habits. A decrease in physical activity, frequency and participation may be the cause of the reported decrease in physical fitness levels. This area of concern may be a major factor related to the general increase in selected anthropometric measurements. Also prevalent was the variance in results between males and females, with males accounting for 72.9% of regular exercisers. The discrepancy in gender and physical activity and fitness levels is of concern

Polymorphism in the tumour necrosis factor receptor II gene is associated with circulating levels of soluble tumour necrosis factor receptors in rheumatoid arthritis

Levels of soluble tumour necrosis factor receptors (sTNFRs) are elevated in the circulation of patients with rheumatoid arthritis (RA). Although these receptors can act as natural inhibitors of tumour necrosis factor-α, levels of sTNFRs in RA appear to be insufficient to prevent tumour necrosis factor-α induced inflammation. The factors that regulate circulating levels of sTNFRs are unclear, but polymorphisms in the tumour necrosis factor receptor genes may play a role. We investigated the relationship between polymorphisms in the tumour necrosis factor receptor I (TNF-RI) and II (TNF-RII) genes and levels of sTNFRs in two groups of Caucasian RA patients: one with early (disease duration ≤2 years; n = 103) and one with established disease (disease duration ≥5 years; n = 151). PCR restriction fragment length polymorphism analysis was used to genotype patients for the A36G polymorphism in the TNF-RI gene and the T676G polymorphism in TNF-RII. Levels of sTNFRs were measured using ELISA. We also isolated T cells from peripheral blood of 58 patients with established RA with known TNF-R genotypes, and release of sTNFRs into the culture medium was measured in cells incubated with or without phytohaemagglutinin. Serum levels of the two sTNFRs (sTNF-RI and sTNF-RII) were positively correlated in both populations, and the level of each sTNFR was significantly higher in the patients with established disease (P < 0.0001). Multiple regression analyses corrected for age, sex and disease duration revealed a significant trend toward decreasing sTNF-RI and sTNF-RII levels across the TNF-RII genotypes (TT > TG > GG) of patients with established disease (P for trend = 0.01 and P for trend = 0.03, respectively). A similar nonsignificant trend was seen for early disease. No relationship with the TNF-RI A36G polymorphism was observed. sTNFRs released by isolated T cells exhibited a similar trend toward decreasing levels according to TNF-RII genotype, although only the association with levels of sTNF-RII was significant. Strong correlations were found between levels of circulating sTNFRs and levels released by T cells in vitro. Our data indicate that the T676G polymorphism in TNF-RII is associated with levels of sTNFRs released from peripheral blood T cells, and with circulating levels of sTNFR in patients with RA

Genome-wide profiling in treatment-naive early rheumatoid arthritis reveals DNA methylome changes in T and B lymphocytes

AIM: Although aberrant DNA methylation has been described in rheumatoid arthritis (RA), no studies have interrogated this epigenetic modification in early disease. Following recent investigations of T- and B-lymphocytes in established disease, we now characterize in these cell populations genome-wide DNA methylation in treatment-naive patients with early RA. PATIENTS & METHODS: HumanMethylation450 BeadChips were used to examine genome-wide DNA methylation in lymphocyte populations from 23 early RA patients and 11 healthy individuals. RESULTS: Approximately 2000 CpGs in each cell type were differentially methylated in early RA. Clustering analysis identified a novel methylation signature in each cell type (150 sites in T-lymphocytes, 113 sites in B-lymphocytes) that clustered all patients separately from controls. A subset of sites differentially methylated in early RA displayed similar changes in established disease. CONCLUSION: Treatment-naive early RA patients display novel disease-specific DNA methylation aberrations, supporting a potential role for these changes in the development of RA

Epigenome-wide profiling identifies significant differences in DNA methylation between matched-pairs of T- and B-lymphocytes from healthy individuals

Multiple reports now describe changes to the DNA methylome in rheumatoid arthritis and in many cases have analyzed methylation in mixed cell populations from whole blood. However, these approaches may preclude the identification of cell type-specific methylation, which may subsequently bias identification of disease-specific changes. To address this possibility, we conducted genome-wide DNA methylation profiling using HumanMethylation450 BeadChips to identify differences within matched pairs of T-lymphocytes and B-lymphocytes isolated from the peripheral blood of 10 healthy females. Array data were processed and differential methylation identified using NIMBL software. Validation of array data was performed by bisulfite Pyrosequencing. Genome-wide DNA methylation was initially determined by analysis of LINE-1 sequences and was higher in B-lymphocytes than matched T-lymphocytes (69.8 vs. 65.2%, p ≤ 0.01). Pairwise analysis identified 679 CpGs, representing 250 genes, which were differentially methylated between T-lymphocytes and B-lymphocytes. The majority of sites (76.6%) were hypermethylated in B-lymphocytes. Pyrosequencing of selected candidates confirmed the array data in all cases. Hierarchical clustering revealed perfect segregation of samples into two distinct clusters based on cell type. Differentially methylated genes showed enrichment for biological functions/pathways associated with leukocytes and T-lymphocytes. Our work for the first time shows that T-lymphocytes and B-lymphocytes possess intrinsic differences in DNA methylation within a restricted set of functionally-related genes. These data provide a foundation for investigating DNA methylation in diseases in which these cell types play important and distinct roles

Quantitative genome-wide methylation analysis of high-grade non-muscle invasive bladder cancer

High-grade non-muscle invasive bladder cancer (HG-NMIBC) is a clinically unpredictable disease with greater risks of recurrence and progression relative to their low-intermediate-grade counterparts. The molecular events, including those affecting the epigenome, that characterise this disease entity in the context of tumour development, recurrence and progression, are incompletely understood. We therefore interrogated genome-wide DNA methylation using HumanMethylation450 BeadChip-arrays in 21 primary HG-NMIBC tumours relative to normal bladder controls. Using strict inclusion-exclusion criteria we identified 1,057 hypermethylated CpGs within gene promoter-associated CpG islands, representing 256 genes. Bisulphite Pyrosequencing validated the array data and examined 25 array-identified candidate genes in an independent cohort of 30 HG-NMIBC and 18 low-intermediate-grade NMIBC. These analyses revealed significantly higher methylation frequencies in high-grade tumours relative to low-intermediate-grade tumours for the ATP5G2, IRX1 and VAX2 genes (p<0.05), and similarly significant increases in mean levels of methylation in high-grade tumours for the ATP5G2, VAX2, INSRR, PRDM14, VSX1, TFAP2b, PRRX1, and HIST1H4F genes (p<0.05). Although inappropriate promoter methylation was not invariantly associated with reduced transcript expression, a significant association was apparent for the ARHGEF4, PON3, STAT5a, and VAX2 gene transcripts (p<0.05). Herein, we present the first genome-wide DNA methylation analysis in a unique HG-NMIBC cohort, showing extensive and discrete methylation changes relative to normal bladder and low-intermediate-grade tumours. The genes we identified hold significant potential as targets for novel therapeutic intervention either alone, or in combination, with more conventional therapeutic options in the treatment of this clinically unpredictable disease

Simulation of Drosophila Circadian Oscillations, Mutations, and Light Responses by a Model with VRI, PDP-1, and CLK

A model of Drosophila circadian rhythm generation was developed to represent feedback loops based on transcriptional regulation of per, Clk (dclock), Pdp-1, and vri (vrille). The model postulates that histone acetylation kinetics make transcriptional activation a nonlinear function of [CLK]. Such a nonlinearity is essential to simulate robust circadian oscillations of transcription in our model and in previous models. Simulations suggest two positive feedback loops involving Clk are not essential for oscillations, because oscillations of [PER] were preserved when Clk, vri, or Pdp-1 expression was fixed. Eliminating the negative feedback loop in which PER represses per expression abolished oscillations. Simulations of per or Clk null mutations and of vri, Clk, or Pdp-1 heterozygous null mutations altered model behavior in ways similar to experimental data. The model simulated a photic phase-response curve resembling experimental curves, and oscillations entrained to simulated light-dark cycles. The model makes experimental predictions, some of which could be tested in transgenic Drosophila.Comment: Accepted to Biophysical Journal, 1/16/04. Single PDF file, 7 figures at en

Undergraduate teaching of surgical skills in the UK: systematic review

Background: Students must be proficient in surgical skills according to General Medical Council and Royal College of Surgeons of England guidelines. If these skills are not appropriately taught, there is a risk of an incoming junior workforce with inadequate surgical skills. This paper aimed to review the literature relating to undergraduate teaching of surgical skills in the UK and summarize future suggested training methods. Methods: The databases MEDLINE, Embase and SCOPUS were searched, and the existing literature relating to methodology of undergraduate teaching of surgical skills in the UK over the past 10 years was summarized. The Medical Education Research Quality Instrument was used to assess research quality. Results: A total of 19 papers were included. Cross-sectional evaluations and survey-based studies highlight a clear deficit in surgical skills teaching in the UK. Medical students are currently unable to fulfil their own learning needs and meet requirements set out by the General Medical Council. This lack of surgical teaching appears to negatively affect student desire to pursue a surgical career. The three main themes for improvement are extracurricular surgical skills days, near-peer teaching and simulation. Each method appeared to improve learning, although no studies utilized medium- to long-term follow-up to demonstrate efficacy and there lacks a clear consensus as to the ‘standard’ of undergraduate surgical skill education. There was also potential for selection bias and response shift bias in many of the studies assessing pre- and postintervention confidence and opinions. Conclusion: There is a concerning lack of surgical skills teaching that has resulted in medical students and junior doctors not having the necessary surgical skills as per General Medical Council guidance and students feel that their own learning needs are not met. This failure to address the learning deficit may be responsible for the fall in surgical competition ratios. While surgical skills teaching must be improved urgently, more robust evidence is required to evaluate the optimal ways of approaching this issue

DNA methylation at diagnosis is associated with response to disease-modifying drugs in early rheumatoid arthritis

Aim: A proof-of-concept study to explore whether DNA methylation at first diagnosis is associated with response to disease-modifying antirheumatic drugs (DMARDs) in patients with early rheumatoid arthritis (RA). Patients & methods: DNA methylation was quantified in T-lymphocytes from 46 treatment-naive patients using HumanMethylation450 BeadChips. Treatment response was determined in 6 months using the European League Against Rheumatism (EULAR) response criteria. Results: Initial filtering identified 21 cytosine-phosphate-guanines (CpGs) that were differentially methylated between responders and nonresponders. After conservative adjustment for multiple testing, six sites remained statistically significant, of which four showed high sensitivity and/or specificity (?75%) for response to treatment. Moreover, methylation at two sites in combination was the strongest factor associated with response (80.0% sensitivity, 90.9% specificity, AUC 0.85). Conclusion: DNA methylation at diagnosis is associated with disease-modifying antirheumatic drug treatment response in early RA

Maternal genome-wide DNA methylation profiling in gestational diabetes shows distinctive disease-associated changes relative to matched healthy pregnancies

Several recent reports have described associations between gestational diabetes (GDM) and changes to the epigenomic landscape where the DNA samples were derived from either cord or placental sources. We employed genome-wide 450Karray analysis to determine changes to the epigenome in a unique cohort of maternal blood DNA from 11 pregnant women prior to GDM development relative to matched controls. Hierarchical clustering segregated the samples into two distinct clusters comprising GDM and healthy pregnancies. Screening identified 100 CpGs with a mean β-value difference of ≥0.2 between cases and controls. Using stringent criteria, 5 CpGs (within COPS8, PIK3R5, HAAO, CCDC124, and C5orf34 genes) demonstrated potentials to be clinical biomarkers as revealed by differential methylation in 8 of 11 women who developed GDM relative to matched controls. We identified, for the first time, maternal methylation changes prior to the onset of GDM that may prove useful as biomarkers for early therapeutic intervention