Background: Predisposition to ACL rupture is multifactorial, resulting from a complex interplay of intrinsic and extrinsic risk factors. Variation in the genome is now considered a key intrinsic risk factor, but the majority of currently implicated loci have been identified through case-control genetic association studies, which are limited by a candidate gene approach and insufficient statistical power. The primary aim of this thesis was to use a whole genome sequencing (WGS) approach within the context of a twin family study to identify novel or previously implicated genetic loci contributing to ACL rupture predisposition (Chapter 2). Additionally, this research aimed to explore prioritised genetic polymorphisms previously associated with ACL rupture and functioning in key biological pathways implicated through the WGS analyses, independently and as a collective, with ACL rupture predisposition in a large combined ACL rupture dataset (Chapter 3 and 4). Methods: The complete genomes of all family members in two unrelated families, each with affected twins were sequenced. Variants with potential loss of function effect were prioritised, and explored for probable biological function in the ACL rupture risk pathway. Furthermore, identity by descent analysis (IBD) was performed to identify potential disease causing mutations, on chromosomal regions shared between family members, and across families. Enriched biological pathway analyses were further explored to prioritise potential candidate genes. Two biological networks were prioritised which highlighted the angiogenesis and proteoglycan family of proteins. Specific polymorphisms within previously investigated candidate genes were further explored in case-control genetic association studies conducted in a large collective data set, including participants from three independent (Sweden, Poland and Australia) cohorts, combined with previously published South African and Polish data. The anterior cruciate ligament (ACL) rupture group included individuals diagnosed with a clinical diagnosis of an ACL rupture based on physical examination, and confirmed by either magnetic resonance imaging or arthroscopy. Only ACL ruptures resulting from a non-contact mechanism of injury were included. The control group comprised individuals of similar age to cases with no prior history of ACL injury or other ligament and tendon injuries, and participating in regular sporting activity, which was similar to cases. Participant samples were genotyped for single nucleotide polymorphisms in the VEGFA (rs699947 C/A rs1570360 G/A, rs2010963 G/C) and KDR (rs2071559 A/G, rs1870377 T/A) genes (Sweden CON: 116 ACL: 95; Poland CON: 149 ACL: 127 and Australia CON: 83 ACL: 342). Additionally, in the ACAN (rs2351491 C/T, rs1042631 T/C, rs1516797 T/G), DCN (rs516115 T/C) and BGN (rs1126499 C/T, rs1042103 G/A) genes (Sweden and Poland). Haplotype analyses were explored (VEGFA, KDR, ACAN and BGN) using the individual genotype data. In addition, inferred allele interactions were presented for VEGFA-KDR, ACAN-BGN ACAN-DCN, BGN-DCN, and VEGFA-DCN as a proxy for gene-gene interactions within the discrete angiogenesis and proteoglycan gene families, and between genes as a proxy for pathway interactions. For association studies, frequencies were calculated for the genotype, allele, inferred haplotypes and allele interactions, and the distributions compared between the control and ACL rupture participants. The statistical programs in R were used for all the analyses, and a p value < 0.05 was accepted to be significant. Results: The WGS analyses highlighted six candidate genetic loci in three genes (COL12A1, CATSPER2, and KCNJ12) with predicted loss of function effects in all affected and unaffected family members within the two studied families. Of the three genes, polymorphisms within COL12A1 were previously associated with ACL rupture predisposition, while CATSPER2 and KCNJ12 are two novel genetic loci with no known previous association with predisposition to ACL rupture. The IBD analyses identified several regions shared in each independent family, of which a segment including a long intergenic non-protein coding RNA (lincRNA) LINC01250 gene in the telomeric region of chromosome 2p25.3 was shared between affected twins in both families, and an affected brother. Furthermore, several functional partners were highlighted. Genetic association analyses of the prioritised polymorphisms in a combined cohort identified an independent association of the VEGFA rs2010963 CC genotype and C allele with increased risk (genotype p = 0.0001, FDR p = 0.001, OR 2.16, 95% CI: 1.47-3.19; allele p = 0.0006, FDR p = 0.003, OR 1.29, 95% CI: 1.11-1.49). Furthermore, the association of the VEGFA A-A-G and A-G-G inferred haplotypes (rs699947 A/C-rs1570360 G/Ars2010963 G/C) with reduced risk (p = 0.010, haplo.score: -2.58, OR: 0.85, 95% CI: 0.69-1.05; A-G-G: p = 0.036, haplo.score: -2.09, OR: 0.81, 95% CI: 0.64-1.02) of ACL rupture. Moreover, a reduced interval (rs1570360 G/A-rs2010963 G/C) revealed an association of the VEGFA -GG and -A-G inferred haplotypes with reduced risk (-G-G: p = 0.031, haplo.score: -2.15, OR: 1.00 and -A-G: p = 0.024, haplo.score: -2.25, OR: 0.98, 95% CI: 0.82-1.18) and the -G-C inferred haplotype with increased risk p = 0.012, haplo.score: 2.50, OR: 1.18, 95% CI: 0.99- 1.40). The KDR genotype and haplotype analyses illustrated that it is highly unlikely that the investigated KDR polymorphisms are associated with modulating ACL rupture risk. Inferred allele interactions noted a significant association of the VEGFA (rs699947 A/C, rs2010963 G/C) - KDR (rs2071559 A/G, rs1870377 T/A) A-G-A-A (p = 0.005, OR: 0.51, 95% CI: 0.30- 0.87) and A-G-G-A (p = 0.018, OR: 0.93, 95% CI: 0.54-1.60) combinations with reduced ACL rupture risk. Further, a significant association of the VEGFA (rs699947 C/A, rs1570360 G/A, rs20109630 G/C) - DCN (rs516115 T/C) A-G-G-T (p = 0.010, OR: 0.53, 95% CI: 0.30-0.91), A-A-G-C (p = 0.010, OR: 0.42, 95% CI: 0.21-0.81) and A-A-G-T (p = 0.046, OR: 0.77, CI: 0.49-1.2) allele combinations with reduced risk was noted for male participants in the collective cohort. No independent or haplotype associations with ACL rupture risk were noted for any of the investigated proteoglycan polymorphisms, in the collective cohort. Conclusion: Collectively, this work has expanded current knowledge on the genetic regions contributing to ACL rupture predisposition, and further highlights the polygenic nature of multifactorial phenotypes. Employing whole genome sequencing in a twin family context, together with a pathway based approach, novel and previously implicated genetic loci were identified towards the aims of the thesis. The catalogue of candidate in silico mutations and modifier genes that clustered in pathophysiological pathways important in ACL rupture, and with implications for therapeutic intervention were identified, and need to be interrogated. Of particular interest are the novel CATSPER2, KCNJ12 and LINC01250 genetic loci. Furthermore, additional evidence to support the implication of the VEGFA gene in modulating ACL rupture risk is provided, and highlighted is the potential collaboration of members within the angiogenesis and proteoglycan gene family in modulating risk. The studies in Chapter 3 and 4 suggest genetic association studies in single populations are less informative, and instead larger collective cohorts with increased statistical power should be employed. Further to that, rather than investigating single polymorphisms, larger regions of the genome should be explored to determine the potential interacting components contributing to musculoskeletal injury risk. Going forward, characterisation of the functional biological effect of implicated loci may assist in unravelling the underlying mechanisms altering tissue homeostasis, and subsequently an individual's capacity for healing and adaptive response.

The use of photomedicine in ancient civilizations dates back 4000 years ago but it wasn't until the beginning of the 20th century that photodynamic therapy was discovered by man. The “trinity” of photodynamic therapy (PDT) comprises a photosensitizer, light and molecular oxygen. Following cellular uptake of the photosensitizer, its activation by light produces reactive oxygen species in the presence of oxygen. The resulting cytotoxic oxidative stress elicits cancer cell death by various mechanisms including apoptosis, necrosis and autophagy. Hypericin, an extract from St John's Wort, is a promising photosensitizer in the context of clinical photodynamic therapy due to its excellent photosensitizing properties and tumoritropic characteristics. However, limited reports on the efficacy of this photomedicine for the treatment of melanoma have been published. South Africa has the second highest incidence of malignant melanoma skin cancer in the world; a highly aggressive tumor due to its metastasizing potential and resistance to conventional cancer therapies. The aim of this study was to investigate the response mechanisms of melanoma cells to hypericinPDT in an in vitro tissue culture model. This investigation was three-fold. Firstly, the susceptibility of melanoma cells to the treatment was determined using cell viability assays. We found a dose of 3 µM light-activated hypericin was effective in reducing cell viability to 50 % or less than the control, for all melanoma cells employed in this study. We therefore used this killing-dose for further experiments. Next, hypericin uptake and its specific association with intracellular organelles was characterized using organelle-specific fluorescent-fusion proteins and dyes, in conjunction with the red fluorescent nature of hypericin and visualization by live confocal fluorescent microscopy. The intracellular localization of a photosensitizer directly influences its cytotoxic action and is thus crucial for effective cell death induction. Hypericin was taken up by all melanoma cells and co-localized with lysosomes and variably with melanosomes, the pigment producing organelles. No co-localization with the cell membrane, mitochondria, endoplasmic reticulum or nucleus was found. Investigating intracellular hypericin after treatment revealed a time-dependent decrease in all melanoma cells. Finally, melanoma cell death mechanisms were elucidated in response to the killing-dose of lightactivated hypericin. Ultrastructural examination of the cells with transmission electron microscopy 2 revealed extensive cytoplasmic vacuolisation, at 4 hours after treatment. In pigmented melanoma cells, the treatment furthermore induced the formation of glycogen aggregations. Fluorescent activated cell sorting analyses revealed a time-dependent increase in phosphatidylserine exposure, indicating apoptosis, in conjunction with a loss of cell membrane integrity, indicating necrosis, in all melanoma cells. An initial early necrotic population was found which decreased with time after treatment, whereas the late apoptotic/necrotic population increased. Minimal early apoptotic populations were found in all cell lines. In addition, melanoma cells showed a decrease in cellular size accompanied by an increase in granularity/pigmentation after treatment. Western blot analyses of proteins involved in specific cell death cascades furthermore verified the induction of apoptosis in melanoma cells by hypericin-PDT. The extrinsic apoptotic cascade was initiated in unpigmented A375 melanoma cells at 24 hours after treatment, mediated by activation of the suicidal proteases caspase 8 and caspase 3. Intrinsic apoptosis was found in pigmented UCT Mel-1 cells at 4 and 7 hours, mediated by activation of caspase 3 and cleavage of poly(ADP-ribose)polymerase 1 (PARP1). Induction of apoptosis by cleavage of PARP1 was furthermore evident in 501mel cells at 7 hours after treatment; however this cleavage was not mediated by caspase 3. Apoptosis inducing factor was found in its vital form in all melanoma cells, indicating that caspase-independent apoptosis or regulated necrosis by parthanatos were not induced by hypericin-PDT. In summary, this study demonstrated the effectiveness of hypericin-PDT in killing both unpigmented and pigmented melanoma cells by the induction of apoptosis. Further investigations into the exact mechanisms of the cell death response, including the observed loss of cell membrane integrity and the involvement of lysosomes and melanosomes are interesting avenues to explore in future studies. Translation of hypericin-PDT into a three-dimensional skin model with melanoma invasion is of particular interest, to further simulate the natural environment of this aggressive cancer and thereby enable the identification of enhanced treatment options.

Breast cancer is the second most commonly diagnosed cancer and the leading cause of cancer deaths in women. Several factors, such as the costs of anti-cancer drugs, drug resistance and relapse, make it difficult to treat this disease effectively. In the South African context this is exacerbated by poor socio-economic conditions. Thus, there is a dire need to develop novel anti-breast cancer drugs which are safe, effective and cheap. In this regard, natural products serve as a highly exploitable medicinal resource and indeed, many successful commercially available drugs have been derived from natural products. Plants, especially those used as food or medicine, are a particularly robust source of beneficial phytochemicals. Thus, this study investigated the anti-cancer effects of extracts derived from three varieties of African millets as well as from the indigenous Kraalbos plant, Galenia africana, against the MCF-7 oestrogen receptor positive and the MDA-MB-231 triple negative breast cancer cell lines. The millet extracts tested were derived from Sorghum bicolor (Enforcer), Pennisetum glaucum (Babala) and Eragrostis tef (Tef) using both a reflux-based and a cold extraction procedure. MTT assays reveal that the millet extracts derived from the reflux-based extraction show no short-term cytotoxicity against both breast cancer cell lines tested. Extracts derived from the cold extraction were subjected to fractionation using HPTLC. Results from these extracts show that only the methanol fractions of the Babala and Enforcer millets exhibited short-term cytotoxic activity against the MCF-7 and the MDAMB- 231 breast cancer cell lines. Five Kraalbos extracts (KB1, KB2, KB3, KB4 and KB5) were tested for their short-term cytotoxicity against the MCF-7 and MDA-MB-231 breast cancer cell lines. KB2 was found to display the most potent activity and its anti-cancer activity was characterized further. Clonogenic assays revealed that KB2 also displayed long-term cytotoxicity against breast cancer cells but not normal breast epithelial cells. Scratch motility assays and western blotting with antibodies to epithelial to mesenchymal transition markers showed that KB2 inhibited the migratory ability of breast cancer cells. To understand the mechanism(s) underpinning the anti-cancer activity of KB2, ROS-GloTM H2O2 and GSH-GloTM Glutathione assays were performed and the results revealed that KB2 induced the production of reactive oxygen species. Furthermore, western blotting with antibodies to γH2AX showed that KB2 induced double strand DNA breaks in breast cancer cells. Flow cytometry and western blotting with antibodies to p53, p21, cyclin A and cyclin B1 further revealed that KB2 causes breast cancer cells to arrest in the S and G2/M phases. A sub-G1 peak, indicative of cell death, was also observed in the flow cytometry analyses. Indeed, using western blotting with antibodies to markers of apoptosis (caspases 3, 7, 8, and 9 and PARP) and necroptosis (p-MLKL and p-RIP3) KB2 was found to induce cell death via the intrinsic and extrinsic apoptotic pathways and necroptosis. Western blotting and immunocytochemistry with an antibody to LC-3 also showed that KB2 induces autophagy in the breast cancer cells but whether it functions as a pro-death or pro-survival mechanism remains to be elucidated. Taken together, this study demonstrates that extracts derived from millets and Kraalbos show anti-cancer activity against oestrogen receptor positive and triple negative breast cancer cells and that KB2 is worth progressing to pre-clinical studies.

Background Achilles tendinopathy (AT) is a common injury in athletes and sedentary individuals, which presents as pain and loss of function in the lower limb. Tendon pathology can exist without pain, but the hallmark of the condition is pain, which is classically of insidious onset, related to loading activity and often resistant to treatment. While the biology of pain in general is well described, the mechanisms of pain in AT are not fully understood. Most commonly, the nociceptive driver associated with AT is thought to be a result of the structural changes that occur in the tendon or the inflammatory cascades that occur in the pathological tendon and/or reflective of altered central pain mechanisms. Evidence from other chronic pain conditions also shows that genetic variation explains, at least in part, some of the heterogeneity observed in chronic pain conditions. The presentation of chronic Achilles tendon pain is variable and therefore it is reasonable to propose that this variability may be influenced by a genetic component. The absence of a definitive cause or mechanism of pain in AT is reflected in the plethora of treatment strategies available to manage it, most of which are not universally effective. In order to improve the management of pain in chronic AT, it is imperative that its mechanisms be better understood. Aims of the thesis The aims of this thesis were therefore to characterise Achilles tendon pain using other pain questionnaires, to investigate the relationship between structural changes and central pain mechanisms with self-reported tendon pain. Additionally, the thesis sought to evaluate the relationship between selected gene variants and pain in a cohort of recreational athletes with chronic Achilles tendinopathy using a candidate gene approach. Candidate genes: COMT rs4818 (C/G), COMT rs4633 (C/T), TAC1rs2072100 (C/T), TACR1 rs3771829 (C/G) and SCN9A rs6746030 (G/A) were selected based on the biological function of their encoded proteins within the pain pathways. The objectives of the specific chapters which addressed these aims were: • Describe Achilles tendon pain using multidimensional pain scales; the short forms of the McGill pain questionnaire (sf-MPQ) and Brief Pain Inventory (sf-BPI), as well as the Victorian Institute of Sports Assessment – Achilles questionnaire (VISA-A) (Chapter 2). • Evaluate the relationship between self- reported tendon pain, the grey scale ultrasound and colour Doppler characteristics in chronic AT (Chapter 3). • Evaluate the relationship between conditioned pain modulation and chronic AT (Chapter 4). • Explore and evaluate if variants in genes [COMT rs4818 (C/G), COMT rs4633 (C/T), TAC1 rs2072100 (C/T), TACR1 rs3771829 (C/G) and SCN9A rs6746030 (G/A)] involved in the pain pathways are associated with either self-reported tendon pain and/or conditioned pain modulation (Chapter 5). Methods Two hundred and eighty-two (282) recreational athletes with at least one year's experience in their main sport were recruited for the studies in this thesis but fifty-two (52) were excluded for not meeting the inclusion criteria of the studies. Hence, 103 recreational athletes without a history of chronic AT (CON) and 127 participants clinically diagnosed with chronic AT (TEN) were included in the study. All participants completed demographic questionnaires on their medical, sporting, training, and injury history. Participants with AT (TEN) also completed the self-administered eight question VISA-A questionnaire, the sf-MPQ and the sf-BPI. Additionally, all participants had grey scale ultrasound (US) and colour Doppler (CD) assessments of both their tendons performed and had conditioned pain modulation (CPM) assessed using pressure and cold pain. Lastly, participants were genotyped for variants in COMT rs4818 (C/G), COMT rs4633 (C/T), TAC1 rs2072100 (C/T), TACR1 rs3771829 (C/G) and SCN9A rs6746030 (G/A) using standard PCR methods. Data were analysed using Statistica Version 13.2.50. Normality of data was assessed using the Shapiro-Wilks test. Evaluations of differences between normally distributed quantitative data were conducted with the independent students t-test or one-way ANOVA, while Mann-Whitney-U and Kruskall-Wallis tests were used for non-normally distributed data. The Fisher's exact and χ2 tests were used for categorical data. For post-hoc analyses, the Kruskal-Wallis associated multiple comparisons test with Bonferroni adjustment was used for quantitative data. For the genotyping data, Hardy– Weinberg equilibrium (HWE) was calculated using ‘HardyWeinberg' version 1.6.3. package. The overall level of significance was set at p<0.05. Results From the sf-MPQ, the most frequent descriptors in the sensory index were ‘aching' (n=73, 60.3%), ‘tender' (n=64, 52.9%) and ‘throbbing' (n=41, 33.9%). Words from the affective index of the sf-MPQ were seldom used to describe tendon pain. From the sf BPI, in addition to interfering with walking ability, AT pain also interfered with mood (n=61, 50.8%), sleep (n=40, 34.8%) and relationships with others (n=30, 25.0%). Additionally, there were weak to moderate correlations between corresponding indices on the sf-MPQ, VISA-A and sf-BPI (r2>0.3; p<0.05) and the VISA-A scores were lower when participants reported severe tenderness (p=0.005), sharp (p=0.030) and/or stabbing pain (p=0.048) on the sf-MPQ. On US and CD, the TEN participants had thicker tendons [median (IQR)] [TEN 6.3mm (5.4 - 7.9) vs CON 5.5mm (4.8 - 6.0), p<0,001]; relative abnormal ultrasound appearances (TEN 48.7%, n=38 vs CON 22.4%, n=19, p=0.001) and had more neovessels (TEN 20.5%, n=16 vs CON 1.0%, n=1, p=0.001) (p<0.001) than the CON participants. In the TEN group, no significant differences were noted between the self reported total pain scores of the sf-MPQ, sf-BPI and VISA-A scales or their separate indices and tendon diameter, US abnormalities or presence of neovessels (p>0.05). However, the median interference index scores of the VISA-A questionnaire of participants with US abnormalities [median (IQR)] [35.5 (30.0 - 41.0), n=36] was significantly higher than those without US abnormalities [32.5 (26.0 - 37.0), n=39, p=0.046]. Additionally, participants from the TEN group who reported no stabbing pain, those who reported mild, moderate or severe stabbing pain on the sf-MPQ had significantly thicker tendons [median (IQR)] [6.0mm (5.2 - 7.6) vs 7.0mm (5.9 - 8.9), 7.7mm (6.2 - 9.1) and 6.3mm (4.9 - 7.4), p=0.037]. From the CPM analysis, participants with tendinopathy had a lower pressure pain threshold (PPT) before [median (IQR)] [TEN: 417kPa (364 - 516) vs CON 601kPa (459 - 724), p<0.001] and during [TEN: 458kPa (358 - 550) vs CON 633kPa (506 - 753), p<0.001] the cold pressor test. However, there was no difference in the CPM effect between the two groups [median (IQR)] [TEN: 34kPa (-2 - 79) vs CON: 45kPa (4 - 94), p=0.490]. From the sf-BPI, PPT before the cold pressor test were significantly lower in individuals who reported mild to severe interferences in mood (p=0.023), general activity (p=0.038) and walking ability (p=0.004) when compared to those who reported no interferences. Pressure pain thresholds before the cold pressor test were also significantly lower in those participants who reported mild to severe pain at the time of testing (p=0.024) or reported moderate to severe pain on average (p=0.014) on the sf- BPI. Additionally, from the sf-BPI, a low CPM effect was significantly associated with mild to severe interference with sleep (p=0.043). The genotype analysis showed that the median total scores of self-reported tendon pain from the sf-MPQ were significantly different (p=0.019) among the three COMT rs4818 (G/C) genotype groups [median (IQR)] [CC: 9.1 (4.0 - 13.0) n=61; CG: 7.3 (4.0 - 0.0) n=50; GG: 4.0 (1.0 - 5.0) n=7], with the CC genotype having a significantly higher pain score (p=0.018) than the GG genotype. No other associations were observed between genotype distributions of COMT rs4633, TAC1 rs2072100, TACR1 rs3771829, SCN9A rs746030 and the median self-reported total tendon pain scores for the sf-MPQ, sf-BPI, VISA-A, or their subscales. Conclusion The novel findings of this thesis suggest that the language of chronic AT pain ought to be further investigated as it may help extend our knowledge of the underlying mechanisms in chronic AT pain. In addition, that AT pain interferes with more than physical and sporting ability should be considered in the overall management of this condition in athletes. While no associations were observed between imaging findings and tendon pain, the relationship between imaging findings and physical limitations suggests that using pain as a primary outcome measure in rehabilitation may be insufficient and highlights the need to further study the relationship between tendon structure, imaging and pain. Furthermore, impaired CPM was associated with interferences with sleep which suggests that, though not quite clear, some central mechanisms are at play in chronic AT pain. This finding also reaffirms the need to consider factors other than physical function in AT management. Another novel finding of this thesis was the association between COMT rs4818 (C/G) and chronic tendon pain. This finding suggests that the catecholaminergic pathway is involved in the chronic AT pain pathway. COMT variants are associated with maladaptive coping mechanisms which may be important to consider in managing chronic pain conditions such as AT. In future, larger studies are required in order to replicate these findings and large, prospective cohort studies are required to confirm the role of genetic variation in chronic AT pain. Overall, the mechanisms of pain in tendinopathy are complex and not yet well described, emphasising the further need for multi-sectorial research.

Introduction: In 2021, South Africans had a 51.9 percent chance of dying from an NCD. The Western Cape on Wellness (WoW!) program advocates for wellness, through partnership, innovation and policy, including health in communities, worksites and schools. Increasing knowledge and awareness regarding health behaviors and NCD risk factors is an important pathway in preventing and mitigating the problem at hand through a combination of structural and social policy change. Social media provides an unprecedented opportunity and innovative way to provide a solution to the problem. The internet has increasingly become a popular source of health information by connecting individuals with health content, experts, and support. Aim &amp; Objective: To use a social media campaign with expert knowledge to change healthy lifestyle actions and increase health knowledge and engagement in a para-social western cape on wellness social media group. Methods: A mixed methods quantitative and qualitative analysis was undertaken to assess key messages, which were publicly available on the WoW! Facebook group. 60 lifestyle messages were posted on the WoW! Facebook group 5 times a week from Monday through to Friday. Each message was disseminated by a moderator and followed a theme for the day. Three icons were used to measure levels of participant engagement likes, shares, comments. Associated comments were extracted and coded using a codebook based on items from the supportive accountability model and peer social support analysis. The identified search material was reviewed allowing removal of any personally identifying or geographical material in order that that the comments were rendered anonymous. One –way ANOVA was performed to determine whether level of likes, shares and comments differed between posts. One-way ANOVA was performed to determine whether level of engagement differed between post types, with Tukey–Kramer test used to determine post hoc differences. An independent samples t-test was conducted to determine whether total engagement differed between moderator initiated posts and Facebook user-initiated posts. Results: The most common form of engagement was "likes," and engagement was higher for moderator initiated rather than participant-initiated posts. Overall traffic to the page increased over the 3 month period from 1083 WoW! Facebook users to 1300. Likes were the most common and easiest form of engagement (M=7.6, SD 9.8) with comments being the lowest (m=0.81, SD 2.3). The most engaged with and resonative messages were the #transformationthursday posts. Empirically physical activity behaviour and change in eating patterns did increase over time. The 7 main themes that were identified constituted 53.3% (112/210) of all comments in the pre and during campaign analyses. The most prevalent theme was social cohesion and connectedness at 29% (33/112). The least common theme was developing professional communication and organisational support at 4.5% (5/112). Overall, there were more comments before the campaign (n=63), than during (n=49). In terms of Geographical proximity most of the comments and posts came from participants in the Metro (58.3%) and rural districts Paarl (48.3%) and George (40%). A proximal or virtual tie to a place adds connection and thus value to the information. Conclusion: The favourable results of the WoW! Facebook campaign shows promise for future social media-driven health campaigns to educate and prevent lifestyle related chronic conditions. Social media content for knowledge sharing should be created through a well-intentioned process with the support of moderators to facilitate the conversation and drive engagement.

No description available.

The adoption of an agricultural lifestyle had profound implications for nutritional ecology, health and behaviour of human populations. The goal of this project was to generate information about the health status and disease patterns of early farming populations from central and southern Africa. Skeletal material was obtained from various 'Iron Age' sites in South Africa, Ingombe Ilede from Zambia, and Sanga and Katoto from the Democratic Republic of Congo. Palaeopathological analyses was done through the examination of non-specific stress indicators that included cribra orbitalia/porotic hyperostosis, Harris lines, linear enamel hypoplasias, subperiosteal bone lesions and dental diseases. The evidence from palaeopathology indicated that the environments played a major role in causing differences observed at micro-scale level. It is suggested that the health problems of these agricultural peoples are a result of their sedentary lifestyle and aggregation, which promoted maintenance and spread of infectious diseases; as well as high carbohydrate diets and dependence on a few main foodstuffs that affected their iron levels. The individuals from the forest region were less healthy than those in the dry or wet savanna zones. Also, the impact of the stress experienced by these societies was not sufficient to cause stunted growth and thus did not affect their terminal heights. The complex relationship between the environment, socio-cultural factors and biology has shown that subsistence economy only influences a fraction of human behaviour, health and well being. The results of this study argue that generalisations about prehistoric farming peoples cannot be made, until further research work is done.

No description available.

Neurociências / Doctoral Programme in Neurosciences

Neurociências / Doctoral Programme in Neurosciences