Fluoxetine and escitalopram are the only antidepressants approved by the Food and Drug Administration of the United States of America (FDA) for treatment of major depression in children and adolescents. Both drugs are selective serotonin reuptake inhibitors (SSRIs). In recent years there has been a growing concern over the long-term developmental effects of early-life exposure to SSRIs. The current study employed male Flinders Sensitive Line (FSL) rats, a well described and validated translational model of depression, to investigate the long term effects of pre-pubertal fluoxetine exposure. First we examined the effect of such early-life exposure on the development of depressive-like behaviour, locomotor activity and anxiety-like behaviour as manifested in early adulthood. Next, the current study investigated the effect of pre-pubertal fluoxetine exposure on the acute monoaminergic stress response, as displayed later in life. Animals received either saline (vehicle control), or 10 mg/kg/day fluoxetine from postnatal day (ND+) 21 to ND+34 (pre-puberty). The treatment period was chosen to coincide with a developmental phase where the serotonergic system’s neurodevelopment had been completed, yet the noradrenergic and dopaminergic systems had not, a scenario comparable to neurodevelopment in human adolescents. Both behavioural and in vivo intra-cerebral microdialysis experiments were conducted after ND+60 (early adulthood). On ND+60 rats allocated to behavioural experiments were evaluated for depressive-like behaviour in the forced swim test (FST), locomotor activity in the open field test (OFT), and anxiety-like behaviour in the OFT. Corticosterone concentrations were shown to be significantly higher in male FSL rats exposed to a 10 minute forced swim stress when compared to male FSL rats not exposed to a forced swim stress on ND+60. In the microdialysis experiments the rats were exposed to an acute 10 minute forced swim stress and the concentrations of the monoamines and their metabolites were measured before, during, and after the acute stressor. Relative to saline-treated (control) rats, fluoxetine-treated FSL rats did not show long-term changes in immobility in the FST (i.e. no anti-depressant-like activity) on ND+60. Like-wise anxiety-like behaviour in the OFT did not change. However, a significant decrease in locomotor activity was observed in fluoxetine-treated FSL rats compared to saline-treated (control) rats. These data suggest that a long-lasting anti-depressant-like effect of fluoxetine may be masked by the effect on locomotor activity. With measurements from the microdialysis experiments a significant attenuation of the noradrenergic stress response was observed in fluoxetine-treated rats compared to saline controls. A similar picture was observed for 5-hydroxyindole-3-acetic acid (5-HIAA), a metabolite of serotonin (5-HT), although the latter was not statistically significant. At baseline, before the stressor, significant increase in dopamine (DA) levels were observed in fluoxetine treated rats when compared to saline controls, suggesting that enhanced dopamine neurotransmission may comprise a long-term effect of pre-pubertal fluoxetine treatment. There were no discernible differences in homovanilllic acid (HVA) concentrations between fluoxetine-treated rats and saline controls. In conclusion significant developmental effects of pre-pubertal fluoxetine exposure were observed later in life and these findings warrant further investigation. / MPharm (Pharmacology), North-West University, Potchefstroom Campus, 2015

Methamphetamine (METH) abuse has become a fast growing drug problem that has developed into a global epidemic. In fact, METH is one of the most commonly abused substances with an estimated 35 million abusers worldwide and is said to be the second most popular illicit drug. The Western Province of South Africa has seen a dramatic increase in drug abuse in recent years where METH is the primary or secondary drug of abuse. Interestingly, more than 50% of these individuals are under the age of 20 years. The longer duration of euphoric effects of METH has attracted many users away from cocaine in favour of METH. In addition to the rapid euphoric effect of METH, the direct short-term effects include arousal, reduced fatigue, an increase in blood pressure, reduced appetite as well as sustained attention. Chronic METH abuse may result in debilitating and long-lasting effects that includes mood disorders such as depression. Studies suggest a strong relationship between exposure to adverse environmental factors early in life and the later development of a neuropsychiatric disorder, such as depression. However, these severe consequences do not seem to invoke cessation of the drug. The euphoric and addictive properties of METH causes users to abuse the drug with an increase in frequency and dose, even though it might not have been their original intention. The primary objective of this study was to investigate the effect of early-life administration of METH to stress-sensitive (Flinders Sensitive Line - FSL) and control (Flinders Resistant Line - FRL) rats on depressive-like behaviour and regional brain monoamine levels later in life. The study implemented a sixteen-day period for administration of METH or a vehicle control from postnatal day 19 (PnD19) to postnatal day 34 (PnD34). The latter developmental stage corresponds to pre-adolescence in the rat when neurological development are similar to that seen in human adolescents, and represents the stage when drug abuse is most common in humans. Chronic dosing of METH and saline was performed twice daily at 09:00 and at 15:00. The animals received a sub-cutaneous (SC) escalating dose regimen of METH during the 16 day period (mimicking binging behaviour in humans), with every dose escalating in increments of 0.2 mg/kg from 0.2 mg/kg to 6.0 mg/kg. The study then investigated whether early-life administration of METH would cause depressive-like behaviours directly after the injection period (immediate drug effects before withdrawal on PnD35) or later in life (after the withdrawal period in early adulthood on PnD60). The behavioural effects were assessed in a battery of tests and thereafter the rats were sacrificed and the frontal cortex removed and snap frozen for later analyses of altered neurochemistry. The study demonstrated that chronic METH treatment during pre-adolescence induces significant behavioural changes related to depression in humans directly after the injection period (PnD35) and later in life (PnD60). The animals displayed antidepressant-like behaviour in the forced swim test (FST) before withdrawal, yet a depressogenic effect was observed 25 days post-withdrawal. This effect also seems to be additive to the congenital depressive-like phenotype of FSL rats, suggesting a role for genetic susceptibility. This observation would be in line with the two-hit hypothesis of depression, suggesting that the manifestation of depression will result when a genetic predisposition is followed by an environmental stressor (i.e. METH) later in life. The data suggests a working hypothesis that individuals that already have a predisposition to depression may be more susceptible to developing depression when abusing METH. The fact that the FSL control rats were more immobile than FRL control rats also confirmed the face validity of the FSL genetic rat model of depression. Locomotor activity assessment indicated that METH treatment decreased locomotor activity in FSL and FRL rats compared to their vehicle controls on PnD35 but not on PnD60. It is important to note that the effects observed in locomotor activity could not have contributed to the immobility observed in the FST, confirming that the immobility in the FST indeed reflects psychomotor and not locomotor effects. The study also demonstrated that METH significantly lowers social interaction behaviour in both FRL and FSL rats, both immediately following drug treatment (PnD35) and after withdrawal (PnD60). It is therefore clear that this effect of METH is long-lasting, putatively related to neurodevelopmental effects. In addition, the rats investigated the familiar object for a greater amount of time in the novel object recognition test (nORT) on PnD35 and PnD60 and may be the result of loss of recognition memory for the familiar object. This data confirms that METH results in cognitive memory deficits probably due to sustained adverse neurodevelopmental effects. Neurochemical analyses of the frontal cortex indicated decreased serotonin (5-HT) and norepinephrine (NE) levels on PnD35. METH is widely recognised for its pro-inflammatory effects, while the reduced 5-HT levels observed may have been the result of an increase in circulating pro-inflammatory cytokines. Neurochemical analyses provided thought-provoking data concerning the role of the permissive hypotheses of depression, indicating that dopamine (DA) is most likely not responsible for the behavioural effects observed, at least under the current study conditions, whereas 5-HT is decidedly more involved than expected. The data also suggest that depletion in NE plays a role in the development of depressive-like behaviours following METH exposure. Based on these findings, we propose that disturbances in 5-HT and NE are a crucial mechanism in how METH abuse may precipitate or worsen depressive-like symptoms in individuals who abuse METH. It should be noted that this study does not discard the role of DA in the development of depression after METH exposure, although under the current study conditions it appears that DA does not play a central role. The current study demonstrated that pre-adolescent exposure to METH can reproduce most of the behavioural changes seen in depressed individuals, and that these behavioural data can be used to identify causal neurochemical factors. Environmental stressors such as METH abuse should be regarded as an additional diagnostic criterion and is relevant to an accumulative risk factor hypothesis. Furthermore, although further study is required, the data suggests that early-life exposure to METH may predispose an individual to mood disorders and behavioural abnormalities later in life. / MSc (Pharmacology), North-West University, Potchefstroom Campus, 2015

Depression is one of the most debilitating, widespread and costly health problems worldwide and has a high prevalence in almost every society. Research suggests that depression affects an individual‟s work engagement levels, burnout levels and the occurrence of stress-related ill health symptoms. However, it is unclear whether these findings would differ among individuals who reported that they suffer from depression and receive medical treatment for it, individuals who reported that they are unsure whether they suffer from depression, and individuals who reported that they do not suffer from depression. This study is quantitative in nature and a cross-sectional design was used. The study population consisted of 15 664 participants from several sectors in South Africa. The participants also differed in terms of gender, age, race, marital status, educational level, language and the province where they reside. The sample population was thus representative of the diverse population of South Africa. The SAEHWS, a self-report instrument based on the dual-process model of work-related well-being, was used to measure all constructs. The participants were divided into three groups, i.e. individuals who reported that they suffer from depression and are currently receiving medical treatment for depression, individuals who reported that they are uncertain whether they suffer from depression, and individuals who reported that they do not suffer from depression. Frequencies were used to determine the prevalence of depression in the three different groups and MANOVA (multivariate analysis of variance) was used to determine the significance of differences between the levels of work engagement, burnout and stress-related ill health symptoms of the three different groups (individuals who reported that they suffer from depression, individuals who reported that they are uncertain whether they suffer from depression, and those who reported that they do not suffer from depression). The results showed that 18,3% of the population reported that they suffer from depression and receive medical treatment for depression, 16,7% of the population reported that they are unsure whether they suffer from depression and 65% reported that they do not suffer from depression. Furthermore, it was found that depression significantly influences work engagement levels negatively and that it significantly influences burnout levels and the occurrence of stress-related ill health symptoms positively. This study will make organisations aware of the effect of depression on an individual‟s well-being and of the fact that depression is a factor to be reckoned with. Employers should consider ways to assist employees who suffer from depression and should learn how to act preventatively to decrease any further occurrence. / Thesis (M.Com. (Industrial Psychology))--North-West University, Potchefstroom Campus, 2011

Depression is one of the most debilitating, widespread and costly health problems worldwide and has a high prevalence in almost every society. Research suggests that depression affects an individual‟s work engagement levels, burnout levels and the occurrence of stress-related ill health symptoms. However, it is unclear whether these findings would differ among individuals who reported that they suffer from depression and receive medical treatment for it, individuals who reported that they are unsure whether they suffer from depression, and individuals who reported that they do not suffer from depression. This study is quantitative in nature and a cross-sectional design was used. The study population consisted of 15 664 participants from several sectors in South Africa. The participants also differed in terms of gender, age, race, marital status, educational level, language and the province where they reside. The sample population was thus representative of the diverse population of South Africa. The SAEHWS, a self-report instrument based on the dual-process model of work-related well-being, was used to measure all constructs. The participants were divided into three groups, i.e. individuals who reported that they suffer from depression and are currently receiving medical treatment for depression, individuals who reported that they are uncertain whether they suffer from depression, and individuals who reported that they do not suffer from depression. Frequencies were used to determine the prevalence of depression in the three different groups and MANOVA (multivariate analysis of variance) was used to determine the significance of differences between the levels of work engagement, burnout and stress-related ill health symptoms of the three different groups (individuals who reported that they suffer from depression, individuals who reported that they are uncertain whether they suffer from depression, and those who reported that they do not suffer from depression). The results showed that 18,3% of the population reported that they suffer from depression and receive medical treatment for depression, 16,7% of the population reported that they are unsure whether they suffer from depression and 65% reported that they do not suffer from depression. Furthermore, it was found that depression significantly influences work engagement levels negatively and that it significantly influences burnout levels and the occurrence of stress-related ill health symptoms positively. This study will make organisations aware of the effect of depression on an individual‟s well-being and of the fact that depression is a factor to be reckoned with. Employers should consider ways to assist employees who suffer from depression and should learn how to act preventatively to decrease any further occurrence. / Thesis (M.Com. (Industrial Psychology))--North-West University, Potchefstroom Campus, 2011

The rising number of the population that present with major depressive disorder has intensified the need to identify and elucidate new biological markers for the diagnosis and treatment of depression. Depression presents with evidence of changes in the nitric oxide (NO) pathway. In this study, levels of various endogenous markers of the NO cascade, viz. nitrite (NO2–), asymmetrical dimethylarginine (ADMA) and arginase II activity, were investigated in the Flinders Sensitive Line (FSL) rat, a genetic animal model of depression. The aim of the current study was to determine if there are differences between these markers in the plasma of the FSL rat compared to its healthy control, the (Flinders Resistant Line) FRL rat, with the possibility of considering their use as biomarkers of depression. Nitrite was chosen as metabolite over nitrate (NO3–) because the dietary intake of nitrite and/or nitrate does not significantly affect nitrite (NO2–) levels in plasma. Although this is of no significance if applied to rats, it is an important factor to be considered when doing clinical studies. For neurochemical determination of nitrite a sensitive fluorometric reversed phase high–performance liquid chromatographic (HPLC) assay was developed to analyze nitrite in human and rat plasma. Derivatization of sample nitrite was performed with 2,3–diaminonaphthalene (DAN) followed by the quantification of the stable and highly fluorescent product, 2,3–naphthotriazole (NAT). Determination of arginase II activity was performed by measuring L–arginine and L–ornithine concentrations in the plasma, while ADMA was measured simultaneously with L–arginine and L–ornithine using liquid chromatography/tandem mass spectrometry, or LC/MS/MS. Plasma nitrite levels of FSL rats were significantly decreased compared to plasma nitrite levels in the FRL rat, but neither the levels of ADMA nor arginase II activity showed a significant difference between the FSL and FRL rat groups. From these results it is concluded that in accordance with previous studies, the NO pathway plays an important role in the pathophysiology of depression, as depicted in the differences found between plasma nitrite levels in the FSL rat compared to its healthy control. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2011.

Major depression is a highly prevalent mood disorder with chronic debilitating effects. Additional to a rising rate in incidence, depression is highly co–morbid with other psychiatric disorders, but also chronic cardiometabolic illnesses that present with an inflammatory component. The exact aetiology of depression is still unknown, being multifactorial in its possible aetiology. Various hypotheses have attempted to shed light on both endogenous and exogenous risk factors as well as the underlying pathology that may lead to the development of the disease. This has led to a wide range of mediators being implicated, including biogenic amines, the HPA–axis, neurotrophic factors, inflammatory agents, the cholinergic system and circadian rhythm, to name a few. The mechanisms of action of current treatment strategies, except for a few atypical and novel treatment approaches, are limited to interactions with monoamines and are at best only 65% effective. Many of these are also plagued by troubling side–effects, relapse and recurrence. It has therefore become imperative to explore novel targets for the treatment of depression that may produce more rapid, robust and lasting antidepressant effects with a less daunting side–effect profile. The strong co–morbidity between depression and various cardiometabolic disorders, including cardiovascular disease, atherosclerosis, type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS) has led to the proposal that a metabolic disturbance may be a vital component that drives inflammatory and immunological dysfunction in depression. Supporting of this is evidence for a role of inflammatory cytokines and neurotrophic factors in the pathogenesis of depression. It has also been demonstrated that a link exists between insulin– and nitric oxide (NO)– mediated pathways in the brain, which further highlights the role of oxidative stress and cell damage. Furthermore, evidence supports a role for oxidative stress and NO in T2DM and/or insulin resistance. Insulin has also been implicated in various physiological processes in the central nervous system (CNS) and may also influence the release and reuptake of neurotransmitters. Preclinical and clinical evidence has provided support for the antidepressant–like effects of insulin–sensitizing peroxisome proliferator activated receptor (PPAR)– agonists, such as rosiglitazone and pioglitazone. In preclinical studies, however, these effects are limited to acute treatment with pioglitazone or sub–chronic (5 days) treatment with rosiglitazone. It is well–recognized that such findings need to be confirmed by chronic treatment paradigms. The aim of the current study was therefore to further investigate the proposed antidepressant–like effects of pioglitazone in a genetic animal model of depression, the Flinders sensitive line (FSL) rat, using a chronic treatment protocol. The FSL rat model was reaffirmed as presenting with inherent depressive–like behaviour compared to its more resilient counterpart, the Flinders resistant line (FRL) rat. Moreover, imipramine demonstrated a robust and reliable antidepressant–like effect in these animals using the forced swim test (FST), thus confirming the face and predictive validity of the FSL rat model for depression. In contrast to previous preclinical studies, acute dose–ranging studies with pioglitazone in Sprague Dawley rats delivered no significant anti–immobility effects in the FST, whereas results similar to that seen in the dose–ranging studies were observed following chronic treatment using FSL rats. Since altered pharmacokinetics could possibly influence the drug’s performance, another route of administration, viz. the subcutaneous route, was utilized as an additional measure to exclude this possibility. The results of the subcutaneous study, however, were congruent with that observed after oral treatment. In order to confirm an association between altered insulin sensitivity and antidepressant action and demonstration by recent studies that thiazolidinediones may augment the efficacy of existing antidepressants, we therefore investigated whether concomitant treatment with gliclazide (an insulin releaser and insulin desensitizer) or pioglitazone (an insulin sensitizer) may alter the antidepressant–like effects evoked by chronic treatment with imipramine. Pioglitazone did not positively or negatively affect the antidepressant effect of imipramine, although gliclazide tended to decrease the anti–immobility effects induced by this antidepressant. Taken together and considering the current available literature, this finding supports evidence linking the insulin–PPAR pathway to depression. However, further explorative studies are required to delineate the role of insulin sensitivity and glucose homeostasis in depression and antidepressant response. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2012.

The rising number of the population that present with major depressive disorder has intensified the need to identify and elucidate new biological markers for the diagnosis and treatment of depression. Depression presents with evidence of changes in the nitric oxide (NO) pathway. In this study, levels of various endogenous markers of the NO cascade, viz. nitrite (NO2–), asymmetrical dimethylarginine (ADMA) and arginase II activity, were investigated in the Flinders Sensitive Line (FSL) rat, a genetic animal model of depression. The aim of the current study was to determine if there are differences between these markers in the plasma of the FSL rat compared to its healthy control, the (Flinders Resistant Line) FRL rat, with the possibility of considering their use as biomarkers of depression. Nitrite was chosen as metabolite over nitrate (NO3–) because the dietary intake of nitrite and/or nitrate does not significantly affect nitrite (NO2–) levels in plasma. Although this is of no significance if applied to rats, it is an important factor to be considered when doing clinical studies. For neurochemical determination of nitrite a sensitive fluorometric reversed phase high–performance liquid chromatographic (HPLC) assay was developed to analyze nitrite in human and rat plasma. Derivatization of sample nitrite was performed with 2,3–diaminonaphthalene (DAN) followed by the quantification of the stable and highly fluorescent product, 2,3–naphthotriazole (NAT). Determination of arginase II activity was performed by measuring L–arginine and L–ornithine concentrations in the plasma, while ADMA was measured simultaneously with L–arginine and L–ornithine using liquid chromatography/tandem mass spectrometry, or LC/MS/MS. Plasma nitrite levels of FSL rats were significantly decreased compared to plasma nitrite levels in the FRL rat, but neither the levels of ADMA nor arginase II activity showed a significant difference between the FSL and FRL rat groups. From these results it is concluded that in accordance with previous studies, the NO pathway plays an important role in the pathophysiology of depression, as depicted in the differences found between plasma nitrite levels in the FSL rat compared to its healthy control. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2011.

Major depression is a highly prevalent mood disorder with chronic debilitating effects. Additional to a rising rate in incidence, depression is highly co–morbid with other psychiatric disorders, but also chronic cardiometabolic illnesses that present with an inflammatory component. The exact aetiology of depression is still unknown, being multifactorial in its possible aetiology. Various hypotheses have attempted to shed light on both endogenous and exogenous risk factors as well as the underlying pathology that may lead to the development of the disease. This has led to a wide range of mediators being implicated, including biogenic amines, the HPA–axis, neurotrophic factors, inflammatory agents, the cholinergic system and circadian rhythm, to name a few. The mechanisms of action of current treatment strategies, except for a few atypical and novel treatment approaches, are limited to interactions with monoamines and are at best only 65% effective. Many of these are also plagued by troubling side–effects, relapse and recurrence. It has therefore become imperative to explore novel targets for the treatment of depression that may produce more rapid, robust and lasting antidepressant effects with a less daunting side–effect profile. The strong co–morbidity between depression and various cardiometabolic disorders, including cardiovascular disease, atherosclerosis, type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS) has led to the proposal that a metabolic disturbance may be a vital component that drives inflammatory and immunological dysfunction in depression. Supporting of this is evidence for a role of inflammatory cytokines and neurotrophic factors in the pathogenesis of depression. It has also been demonstrated that a link exists between insulin– and nitric oxide (NO)– mediated pathways in the brain, which further highlights the role of oxidative stress and cell damage. Furthermore, evidence supports a role for oxidative stress and NO in T2DM and/or insulin resistance. Insulin has also been implicated in various physiological processes in the central nervous system (CNS) and may also influence the release and reuptake of neurotransmitters. Preclinical and clinical evidence has provided support for the antidepressant–like effects of insulin–sensitizing peroxisome proliferator activated receptor (PPAR)– agonists, such as rosiglitazone and pioglitazone. In preclinical studies, however, these effects are limited to acute treatment with pioglitazone or sub–chronic (5 days) treatment with rosiglitazone. It is well–recognized that such findings need to be confirmed by chronic treatment paradigms. The aim of the current study was therefore to further investigate the proposed antidepressant–like effects of pioglitazone in a genetic animal model of depression, the Flinders sensitive line (FSL) rat, using a chronic treatment protocol. The FSL rat model was reaffirmed as presenting with inherent depressive–like behaviour compared to its more resilient counterpart, the Flinders resistant line (FRL) rat. Moreover, imipramine demonstrated a robust and reliable antidepressant–like effect in these animals using the forced swim test (FST), thus confirming the face and predictive validity of the FSL rat model for depression. In contrast to previous preclinical studies, acute dose–ranging studies with pioglitazone in Sprague Dawley rats delivered no significant anti–immobility effects in the FST, whereas results similar to that seen in the dose–ranging studies were observed following chronic treatment using FSL rats. Since altered pharmacokinetics could possibly influence the drug’s performance, another route of administration, viz. the subcutaneous route, was utilized as an additional measure to exclude this possibility. The results of the subcutaneous study, however, were congruent with that observed after oral treatment. In order to confirm an association between altered insulin sensitivity and antidepressant action and demonstration by recent studies that thiazolidinediones may augment the efficacy of existing antidepressants, we therefore investigated whether concomitant treatment with gliclazide (an insulin releaser and insulin desensitizer) or pioglitazone (an insulin sensitizer) may alter the antidepressant–like effects evoked by chronic treatment with imipramine. Pioglitazone did not positively or negatively affect the antidepressant effect of imipramine, although gliclazide tended to decrease the anti–immobility effects induced by this antidepressant. Taken together and considering the current available literature, this finding supports evidence linking the insulin–PPAR pathway to depression. However, further explorative studies are required to delineate the role of insulin sensitivity and glucose homeostasis in depression and antidepressant response. / Thesis (M.Sc. (Pharmacology))--North-West University, Potchefstroom Campus, 2012.

Brain tumors are the second leading cause of cancer deaths in young adults ages 20- 39. (Armstrong et al., 2004) According to the South African Medical Research Council, there was an estimate 801 deaths because of brain cancer in South Africa in 2000. If these statistics are compared to other types of cancers like breast-, lung- and prostate cancers, is the prevalence of the diagnoses of brain tumors, a very small percentage. According to the Mayo clinic in South Africa, the estimate number of brain tumor incidences was 3% in 2007. Despite of these statistics with regards Brain tumors, one in six South African men and one in seven South African women will be diagnosed with cancer during their life times. Despite this small percentage, the diagnoses of brain tumors have escalated the last few years. The reason for these new statistics is still unknown. With exercise that is becoming one of the most important adjuvant therapies for most diseases or illnesses, we may sustain this idea of using exercise intervention as an adjuvant therapy for brain tumor cancers we can prove this through many researches that has been done in the last few years. (Schwartz, 2003) Studies done by different researchers they found that exercise intervention is becoming increasingly recognized as a safe, feasible and beneficial supportive therapy for cancer patients both during and after the cessation of adjuvant therapy. (Jones et al., 2006) Exercise influences a lot of different systems in the body, to the advantage of the cancer patient (Schwartz, 2003) and emerging new research shows that physical exercise may boost brain function, which include improve mood. (Kong, 1999) Exercise, according to Cotman and Berchtold (2002) is commonly believed to be a behavioral strategy to relieve stress, and reduce depression and anxiety in humans. Exercise intervention further influence following aspects of the human body, namely brain deprived neurotrophic factor (BDNF) and 5-HT (Serotonin). Improvement of these could, in fact, lead to a better quality of life (QoL) of a brain tumor patient (Cotman&Berchtold, 2002). Fatigue that sets in, due to the different cancer therapies, is also a factor that has an affect on depression and anxiety of the patient. Keeping still and rest to prevent fatigue were followed in previous regiment when working with cancer patients was followed. This approach, in fact, has a very negative effect on the patient. Being diagnosed with a brain tumor the patient will never be emotionally prepared for this type of information and it usually shatters their sense of well being and their personal security. All of these factors, especially depression, affect the patient’s QoL. (Vaynman et al., 2004) An exercise regiment for brain tumor patients has not yet been developed properly, because exercise intervention for familiar cancers could be problematic and not suitable for brain tumor patients. (Schwartz, 2003) Therefore, the purpose of this study is to further the knowledge and the field of expertise of exercise as an adjuvant therapy in brain tumor patients to better QoL over a larger period of time. AFRIKAANS : Die tweede grootste leier in siektes tussen die ouderdomme van 20-39 jaar wat lewens eis is Brein gewasse (brein kanker). (Armstrong et al., 2004) Volgens die Suid- Afrikaanse Mediese Navorsingraad, is daar tot 801 gevalle van breingewas sterftes in die jaar 2000 aangemeld. As hierdie statistieke vergelyk word met statistieke van kanker wat meer prominent voorkom soos byvoorbeeld bors-, long-, en protaatkanker, lyk die voorkoms van breinkanker diagnosis maar na ‘n baie klein persentasie. Die Mayo Kliniek in Suid-Afrika het in 2007 bevind dat die voorkoms van breinkanker in Suid-Afrika ‘n persentasie van 3% uitgemaak het. Ten spyte van hierdie statistieke betreffende breingewasse, sal een uit elke ses mans en een uit elke sewe vroue, gediagnoseer word met een of ander kanker gedurende hulle leeftyd. Alhoewel die persentasie wat reeds genoem is maar na ‘n klein hoeveelheid lyk, het die voorkoms van breingewasse baie toegeneem in die laaste paar jaar en selfs maande. Die rede vir hierdie aansienlike toename is steeds onbekend. Oefening word al hoe belangriker en word al hoe meer deur verskeie dokters voorgeskryf om te dien as ‘n bykomende behandeling vir verskeie siekte toestande. Dit word veral ook vir kanker pasiënte voorgeskryf. Oefen intervensie kan dus gebruik word vir breinkanker pasiënte, hierdie stelling gestaaf kan word, aangesien daar verskeie navorsings reeds bewys het dat oefening as bykomende terapie gebruik is vir kanker pasiënte. (Schwartz, 2003) Hierdie studies het bevind dat oefening as ‘n veilige, uitvoerbare en voordelige bykomende intervensie vir kanker pasiënte erken word. Hierdie intervensie kan tydens en na hoof kanker behandeling gebruik word (Jones et al., 2006). Oefening beinvloed verskeie sisteme in die liggaam, tot voordeel van die kanker pasiënt. (Schwartz, 2003) Nuwe navorsing het ook aan die lig laat kom dat fisieke aktiwiteit ‘n persoon se breinfunksie bevorder, wat onder andere ‘n baie groot invloed het om die pasiënt se gemoedstoestand. (Kong, 1999) Volgens, Cotman and Berchtold (2002), is daarvolgens studies bewys dat oefenterapie ‘n manier is om stres te verlig, sowel as depressie en angstigheid in meeste mense. Oefenterapie beinvloed ook die volgende aspekte positief in die menslike liggaam naamlik, Brein ontnemende neurtrofiese-faktor (BDNF) en 5-HT (Serotonien). Verbetering van hierdie faktore, kan ly tot ‘n beter kwaliteit van lewe van ‘n pasiënt wat met ‘n breingewas gediagnoseer is (Cotman&Berchtold, 2002). Uitputting (moegheid) wat gewoonlik intree as gevolg van kanker terapie, is ook ‘n faktor wat ‘n effek het op die depressie- en angsvlakke van ‘n pasiënt. In vroeë behandelingsprotokol van kankerpasiënte, moes die pasiënt so stil as moontlik verkeer om sodoende uitputting of moegheid te voorkom. Hierdie benadering het in die uiteinde ‘n baie negatiewe effek op die pasiënte tot gevolg gehad. ‘n Persoon wat met ‘n breingewas gediagnoseer word sal nooit emosioneel voorbereid wees op hierdie diagnose nie en sodoende kan dit lei tot ‘n ineenstorting van die persoon se geestestoestand en persoonlike sekuriteit. Hierdie “ineenstorting” kan ‘n groot invloed hê op die kwaliteit van lewe van hierdie pasiënt (Vaynman et al., 2004). ‘n Oefenintervensie protokol vir breinkanker pasiënte is nog nie voldoende vasgestel nie, aangesien oefenterapie intervensies wat vir bekende kankers problematies en selfs gevaarlik kan wees vir breingewas pasiënte nie. (Schwartz, 2003) Daarom is die doel van die studie, om inligting te verkry en kennis in te samel om die veld van deskundiges uit te brei om sodoende ‘n oefenterapie protokol neer te lê vir breinkanker pasiënte. Hierdie protokol sal dus dien as ‘n bevordering van kwaliteit van lewe van hierdie pasiente deur middel van oefen intervensie as bykomende behandeling. Copyright / Dissertation (MA)--University of Pretoria, 2012. / Biokinetics, Sport and Leisure Sciences / unrestricted

Die doel van hierdie navorsingstudie is om riglyne vir 'n groepsterapeutiese program te ontwikkel waarin adolessente in rou (in besonder na die afsterwe van 'n betekenisvolle ander) die geleentheid kry om hul emosies rondom sterwe en rou te verwerk. In 'n omvattende literatuurstudie is bestaande teorieë aangaande die ontwikkelingsfase adolessensie, rou-, verdriet- en verliesreaksies asook terapeutiese groepe en groepsprogramme, bespreek. Die navorsingsprosedures is vervolgens bespreek gedurende die eerste en laaste sessies is vir die doel van evaluering 'n persoonlike vraelys, die Beck Depressie-vraelys en spesifieke T.A.T.-kaarte aan die groeplede voorgelê. Die groepsprosedures is op oudioband opgeneem vir analise en interpretasie van prosesnotas. Die verwerking van die data wat ingesamel is, is kwalitatief ontleed. Elf Afrikaanssprekende adolessente is op 'n hoërskoolkamp genader om vrywillig aan die program deel te neem. Vyf het aan die program deelgeneem. Die studie het die volgende resultate opgelewer: <ul> <li> Groepsterapie en die -programme beinvloed die emosionele verliese van adolessente in rou.</li> <li> Groepsterapie en die -programme dra by tot die konstruktiewe vermindering van gevoelens van rou, verlies en gepaardgaande depressie by adolessente.</li> <li> Groepsterapie dra by tot 'n adolessent se hernude ingesteldheid op hoop en die toekoms.</li></ul> Op grond van hierdie bevindings word riglyne vir 'n groepsterapeutiese program vir adolessente in rou voorgestel. ENGLISH : The purpose of this research study is to develop guidelines for a group therapy programme for adolescents in mourning (especially after the death of a significant other). The programme offers an opportunity to come to terms with emotions relating to death and bereavement. In a comprehensive literature study of existing theories regarding the development phase of adolescence, mourning-, grief- and loss reactions as well as therapeutic groups and group programmes are discussed. The research procedures are subsequently discussed. For evaluations purposes a personal questionnaire, the Beck Depression questionnaire as well as specific T.A.T. cards were submitted to the group members at their first and final sessions. Audio tapes were used during the group procedures. The processing of the collected data was analysed qualitatively. Eleven Afrikaans speaking adolescents were approached at a high school camp to participate in the programme on a voluntary basis. Five of them participated. The following results were obtained from the study: <ul> <li> Group therapy and the -programme influence the emotional losses of adolescents in the process of mourning.</li> <li> Group therapy and the -programme alleviate feelings of grief, loss and depression in adolescents.</li> <li> Group therapy contributes to an adolescents' renewed feelings of hope and the future.</li></ul> On the basis of these findings guidelines for a group therapy programme for adolescents in mourning are suggested. / Dissertation (MA)--University of Pretoria, 1997. / Psychology / unrestricted