Browsing by Author "Marais, E."
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- ItemEiendomsverlies deur verkrygende verjaring : onteiening sonder vergoeding - of nie(LitNet Academic, 2012-12) Van der Walt, A. J.; Marais, E.OPSOMMING: Verkrygende verjaring word meestal beskou as ’n gedeelte van die Suid-Afrikaanse reg wat redelik regseker en onproblematies is. Die klaarblyklik onkontroversiële aard van hierdie regsreël is egter onlangs in twyfel getrek deur die vierde kamer van die Europese hof vir menseregte in die Pye-saak, waar bevind is dat adverse possession – die common law-eweknie van verjaring – ’n onteiening sonder vergoeding behels, welke gevolg strydig met artikel 1 van die eerste protokol tot die Europese Verdrag vir Menseregte, 1950 is. Alhoewel hierdie bevinding op appèl omvergewerp is, beklemtoon dit die belangrikheid van die vraag of verjaring (wat ook eiendomsverlies sonder vergoeding tot gevolg het) op een lyn met artikel 25 van die Suid-Afrikaanse Grondwet is. Om dit te beantwoord, ontleed ons die prosesse oor verjaring met verwysing na die FNB-metodologie. Hierdie artikel fokus spesifiek op die onteieningsvraagstuk, naamlik of verjaring ’n onteiening van regte ingevolge artikel 25(2) meebring. Ten einde dié kwessie aan te spreek ontleed ons hierdie regsreël teen die agtergrond van sekere kernaspekte van die Suid-Afrikaanse onteieningsreg, naamlik die aard van die onteieningsbegrip, die relevansie van staatsverkryging, welke regsbronne onteiening magtig, asook die metodes waarvolgens onteiening kan geskied. Laastens ondersoek ons die vraag of verjaring moontlik konstruktiewe onteiening behels. Deur hierdie ondersoek word getoon dat dit hoogs onwaarskynlik is dat verjaring onteiening meebring. Verjaring vind bykans altyd tussen private individue plaas en dus kan daar geen sprake van staatsverkryging van onteiende regte wees nie. Verder verleen die verjaringswette geensins onteieningsbevoegdheid aan die staat nie en maak hulle ook nie voorsiening vir vergoeding nie. Daarby kan verjaring ook nie maklik onder enige van die bestaande onteieningsmetodes tuisgebring word nie. Laastens redeneer ons dat konstruktiewe onteiening waarskynlik nie in die Suid-Afrikaanse reg bestaan nie. Gevolglik is dit dogmaties beter om verjaring te beskou as ’n nie-arbitrêre ontneming van eiendomsreg, welke ontneming nie ’n onteiening van regte tot gevolg het nie.
- ItemHoarding symptoms in patients on a geriatric psychiatry inpatient unit(Health & Medical Publishing Group, 1997) Stein, D. J.; Laszlo, B.; Marais, E.; Seedat, S.; Potocnik, F.Background. While collecting may be a normal behaviour, hoarding is a symptom of various psychiatric disorders, including obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder (OCPD). Although anecdotal reports suggest that hoarding is not uncommon in geriatric psychiatry populations, its psychopathological correlates in such samples have not been well characterised. Methods. The presence of clinically significant hoarding symptoms was screened for in 100 consecutive patients in a geriatric psychiatry inpatient unit. Both patient and collateral histories were obtained. When hoarding symptoms were present, a detailed history of their phenomenology was obtained by means of a structured questionnaire and the response of hoarding symptoms to treatment during hospitalisation was monitored. Results. Clinically significant hoarding was found in 5/100 subjects. Four of these 5 patients met DSM-IV criteria for schizophrenia (paranoid subtype), with onset of symptoms coinciding with increased symptoms of dementia. The fifth patient met criteria for bipolar disorder (manic episode), also had symptoms of dementia, and had a lifelong history of hoarding. Hoarding behaviours responded to antipsychotic treatment in 3 of the 5 patients. Conclusions. A history of hoarding may be useful in many psychiatric patients, but psychopathological correlates of this symptom are likely to vary with age. In a geriatric psychiatry inpatient population hoarding was associated not with OCD or OCPD, but rather with paranoid schizophrenia and increasing symptoms of dementia. Dopamine blockers appeared useful in decreasing hoarding in some patients, raising interesting questions about the neurobiology of this symptom.
- ItemMyocardial susceptibility to ischaemia/reperfusion in obesity : a re-evaluation of the effects of age(BioMed Central, 2017-03-17) Webster, I.; Salie, R.; Marais, E.; Fan, W. J.; Maarman, G.; Huisamen, B.; Lochner, A.Background Reports on the effect of age and obesity on myocardial ischaemia/reperfusion (I/R) injury and ischaemic preconditioning are contradictory. The aim of this study was to re-evaluate the effects of age and diet-induced obesity (DIO) on myocardial I/R injury and preconditioning potential. Methods Four groups of Wistar male rats were used: age-matched controls (AMC) receiving standard rat chow for (i) 16 weeks and (ii) 16 months respectively; DIO rats receiving a sucrose-supplemented diet for (iii) 16 weeks and (iv) 16 months respectively. The ages of groups (i) and (iii) were 22 weeks (“young”) and groups (ii) and (iv) 17 months (“middle-aged”) at time of experimentation. Isolated perfused working hearts were subjected to 35 min regional ischaemia/1 h reperfusion. Endpoints were infarct size (tetrazolium staining) and functional recovery. Hearts were preconditioned by 3 × 5 min ischaemia/5 min reperfusion. Results were processed using GraphPad Prism statistical software. Results Age did not affect baseline heart function before induction of ischaemia and I/R damage as indicated by infarct size and similar values were obtained in hearts from both age groups. Age also had no effect on functional recovery of hearts during reperfusion after regional ischaemia in AMC rats, but cardiac output during reperfusion was better in hearts from middle-aged than young DIO rats. The diet reduced infarct size in hearts from young rats (% of area at risk: AMC: 32.4 ± 3.6; DIO: 20.7 ± 2.9, p < 0.05), with no differences in hearts from middle-aged rats (AMC: 24.6 ± 4.6; DIO: 28.3 ± 13.5, p = NS). Compared to their respective AMC, diet-induced obesity had no significant effect on functional recovery of hearts from both age groups after exposure to regional ischaemia. When exposed to the more severe stress of global ischaemia, the functional recovery potential of middle-aged DIO rats appeared to be impeded compared to hearts of young DIO rats, while age had no effect on the functional recovery of AMC hearts. Preconditioning reduced infarct size in hearts from young control rats and both middle-aged groups, but not from young DIO rats. Age had a significant effect on functional recovery in preconditioning: it was improved in hearts from young control and DIO rats, but depressed in both middle-aged groups. Conclusions The data showed that middle-age and obesity had no effect on baseline myocardial function and did not increase susceptibility to I/R damage upon exposure to regional ischaemia. On the contrary, obesity reduced I/R damage in young rats. Preconditioned aging hearts showed a decreased infarct size, but a reduction in functional recovery.
- ItemProtection of the ischaemic heart : investigations into the phenomenon of ischaemic preconditioning(Clinics Cardiv Publishing, 2009-02) Lochner, A.; Marais, E.; Genade, S.; Huisamen, B.; Du Toit, E. F.; Moolman, J. A.Exposure of the heart to one or more short episodes of ischaemia/reperfusion protects the heart against a subsequent prolonged period of ischaemia, as evidenced by a reduction in infarct size and an improvement in functional recovery during reperfusion. Elucidation of the mechanism of this endogenous protection could lead to the development of pharmacological mimetics to be used in the clinical setting. The aim of our studies was therefore to gain more information regarding the mechanism of ischaemic preconditioning, using the isolated perfused working rat heart as model. A preconditioning protocol of 1 × 5 or 3 × 5 min of ischaemia, interspersed with 5 min of reperfusion was found to protect hearts exposed to 25 min of global ischaemia or 35–45 min of regional ischaemia. These models were used throughout our studies. In view of the release of catecholamines by ischaemic tissue, our first aim was to evaluate the role of the alphaadrenergic receptor in ischaemic preconditioning. However, using a multi-cycle ischaemic preconditioning protocol, we could not find any evidence for alpha-1 adrenergic or PKC activation in the mechanism of preconditioning. Cyclic increases in the tissue cyclic nucleotides, cAMP and cGMP were found, however, to occur during a multi-cycle preconditioning protocol, suggesting roles for the beta-adrenergic signalling pathway and nitric oxide (NO) as triggers of cardioprotection. This was substantiated by the findings that (1) administration of the beta-adrenergic agonist, isoproterenol, or the NO donors SNAP or SNP before sustained ischaemia also elicited cardioprotection similar to ischaemic preconditioning; (2) beta-adrenergic blockade or nitric oxide synthase inhibition during an ischaemic preconditioning protocol abolished protection. Effectors downstream of cAMP, such as p38MAPK and CREB, were also demonstrated to be involved in the triggering process. Our next step was to evaluate intracellular signalling during sustained ischaemia and reperfusion. Our results showed that ischaemic preconditioned-induced cardioprotection was associated with a significant reduction in tissue cAMP, attenuation of p38MAPK activation and increased tissue cGMP levels and HSP27 activation, compared to non-preconditioned hearts. The role of the stress kinase p38MAPK was further investigated by using the inhibitor SB203580. Our results suggested that injury by necrosis and apoptosis share activation of p38MAPK as a common signal transduction pathway and that pharmacological targeting of this kinase offers a tenable option to manipulate both these processes during ischaemia/reperfusion injury.