This thesis deals with the production and characterization of cheese analogues, ie products in which some of the dairy components are mutually or completely replaced by a non-dairy component. Model samples of fresh cheese and analogues of fresh cheese (standard) with the addition of linseed and rapeseed oil were produced by a standard technological procedure in MENDELU Brno. The content of bound and free fatty acids, volatile (aroma) substances and sensory quality was monitored in the samples. The main focus was to evaluate the effect of added vegetable oil on the monitored parameters. The fats from the sample were extracted with a mixture of diethyl ether and petroleum ether. Fatty acids were converted to methyl esters by boron trifluoride-catalyzed acid esterification and subsequently identified by GC-FID. The analysis found a higher content of fatty acids in cheese analogues in comparison with the control sample, also the content of unsaturated fatty acids increased. The HS-SPME-GC-MS method was used for the identification and semi-quantification of volatile substances (aromatic substances). 56 volatile compounds were identified in the samples; The percentage of individual chemical groups differed significantly, the highest content was found in the control sample. Sensory evaluation was performed using a scale and a serial test. In all of monitored indicators (apparence, color, consistency, smell and taste) the control sample was evaluated as best. As for the analogues the taste and smell of used oils were detected, which was unpleasant for the evaluators. The obtained results show that the addition of vegetable oils increases the nutritional value of cheeses (higher content of unsaturated fatty acids), but reduces their sensory quality and overall consumer acceptability.

This paper deals with the manufacture and characterisation of cheese analogues, which are products, where the milk components are totally or partially replaced by non-milk components. Model samples, edam type cheese and the analogue containing hazelnut oil, were manufactured using the standard way at Brno Mendelu. The main parameters chosen to describe the quality of samples were free and bound fatty acids, volatile compounds and sensory quality. The main aim was to judge the influence of added hazelnut oil on mentioned parameters. For the identification and semiquantification of volatile compounds HS-SPME-GC-MS method was used. Fat extraction from sample was made with a mixture of two solvents (diethylether, petrolether), fatty acids were identified and quantified by GC-FID, with their former acid transesterification using methanolic solution of BF3 as a catalyst. For sensory analysis of the appearance, colour, texture, aroma, taste and overall acceptance of the sample descriptive scales and comparison with standard were used, the structure was observed by electron microscopy. The results show that addition of hazelnut oil affects the sensory properties, ripening process (higher amount of volatile compounds, faster lipolysis), nutrition value (higher amount of unsaturated fatty acids), and the stability of the product.

Introduction: Schizophrenia is a neuropsychiatric illness characterized by impairments in cognition and positive and negative symptoms. As currently used antipsychotics do not treat all symptoms of the disease, further research of the therapeutic potential of various drugs in the treatment of this disease is crucial. Psychosis is a condition or a mental state that usually accompany schizophrenia, as well as other disorders. We used MK-801, a non-competitive antagonist of NMDA receptors to induce an experimental model of psychosis in rats. By binding to the NMDA subtype of glutamate receptors located on inhibitory interneurons, MK-801 has been shown to elicit an overactivation of cortical and hippocampal pyramidal neurons, leading to behaviors such as hyperlocomotion, stereotypy or cognitive impairments. LY 379268, an agonist of group II metabotropic glutamate receptors, binds to both presynaptic and postsynaptic receptors on pyramidal neurons. It has been suggested that it could alleviate the MK-801-induced hyperactivity of the principal neurons. In this study, we sought to demonstrate the effects of LY 379268 in the MK-801 animal model of psychosis and hypothesized that LY 379268 will ameliorate deficits in the reversal learning induced by MK-801. Materials and methods: Long Evans rats received...

Magister Artium - MA / In 1987 Ntombikayise Priscilla Kubheka was abducted, tortured, killed and her body dumped by apartheid security police. She was an uMkhonto WeSizwe (MK), the armed wing of the African National Congress (ANC), commander based in Durban and was in charge of weaponry storage and organised safe houses for those returning from exile. Amnesty applications and perpetrator testimony given at the Truth and Reconciliation Commission’s (TRC) amnesty hearings alleged that Kubheka had died, while being interrogated, from a heart attack. The perpetrators claimed the heart attack was possibly as a result of Kubheka being overweight. In 1997 the Truth and Reconciliation Commission (TRC) exhumed skeletal remains and items of clothing, including a floral dress, from a pauper grave in Charlottedale cemetery, Groutville. The exhumed skull indicated a bullet wound. The post-mortem and numerous forensic examinations confirmed the identification of the skeletal remains to be those of Kubheka. The forensic examinations of the items of clothing confirmed the findings of the skeletal examinations in establishing identification. These forensic examinations and its findings contested testimony given by the perpetrators. Through the TRC investigations and its findings, a question of what it may mean to re-humanise the once missing emerges. This mini-thesis underscores a notion of re-humanisation through the work of the TRC in its investigation into the enforced disappearance of Kubheka. It suggests that figuring Kubheka through a notion of re-humanisation in the context of the TRC requires one to understand both de-humanisation and re-humanisation and the ways in which gender complicates these understandings. It does so by examining testimonies, t he exhumation, the forensic examinations, the emergence of a forensic aesthetic and the productions of biographies and forensic memory to understand how these might be processes and strategies of re-humanisation. This mini-thesis then is a forensic history that navigates a politics of the dead by examining the figuring of Kubheka through various fields and in various forums. In so doing, the argument presented in what follows is that the notion of re-humanisation is an inherently unstable one but at its core is a politics of the dead that misses gender it its figuring of the human. / 2023-12-01

No description available.

Spatial navigation, cognitive coordination and behavioral flexibility belong amongst cognitive functions, which play a role in many neuropsychiatric disorders. Behavioral tasks have proved to be useful paradigms to test these functions in pharmacological or genetic animal models. First aim was to determine a potential interaction between β-adrenergic and α1-adrenergic or D2-dopaminergic systems. Spatial navigation and coordination were impaired in both studies during co-aplication of subthreshold doses of drugs. Used substances belong to group of widely prescribed drugs, thus our results could be implicated in clinical practice. Another study examined an acute effect of MK-801 (animal model of schizophrenia) on behavioral flexibility in Carousel maze and the Morris water maze (MWM). Carousel maze showed higher sensitivity with impairments from 0.08 mg.kg-1 compared to 0.10 mg.kg- 1 in MWM. The final experiment aimed at testing the effect of reduced expression of Nogo-A protein on spatial navigation and behavioral flexibility of rats. A battery of tests in the Carousel maze revealed impairment in cognitive functions, MWM showed unaffected working memory of rats. Our results support the hypothesis linking Nogo-A knock-down rats with neuropsychiatric symptoms and cognitive disorders. Key words:...

Spatial navigation, cognitive coordination and behavioral flexibility belong amongst cognitive functions, which play a role in many neuropsychiatric disorders. Behavioral tasks have proved to be useful paradigms to test these functions in pharmacological or genetic animal models. First aim was to determine a potential interaction between β-adrenergic and α1-adrenergic or D2-dopaminergic systems. Spatial navigation and coordination were impaired in both studies during co-aplication of subthreshold doses of drugs. Used substances belong to group of widely prescribed drugs, thus our results could be implicated in clinical practice. Another study examined an acute effect of MK-801 (animal model of schizophrenia) on behavioral flexibility in Carousel maze and the Morris water maze (MWM). Carousel maze showed higher sensitivity with impairments from 0.08 mg.kg-1 compared to 0.10 mg.kg- 1 in MWM. The final experiment aimed at testing the effect of reduced expression of Nogo-A protein on spatial navigation and behavioral flexibility of rats. A battery of tests in the Carousel maze revealed impairment in cognitive functions, MWM showed unaffected working memory of rats. Our results support the hypothesis linking Nogo-A knock-down rats with neuropsychiatric symptoms and cognitive disorders. Key words:...

Schizophrenia is a troubling and severe mental illness that is only incompletely treated by currently available drugs. New drug development is hindered by a scarcity of functionally relevant pharmacodynamic biomarkers that are translatable across preclinical and human subjects. Although psychosis is a major feature of schizophrenia, cognitive and negative symptoms determine the long-term functional outcomes for patients. Stimulus-evoked neural synchrony at gamma (~ 40 Hz) frequency plays an important role in the processing and integration of sensory information. Not surprisingly, schizophrenia patients show deficits in gamma oscillations. NMDA receptor (NMDAR) activation on fast-spiking parvalbumin-positive interneurons is deemed important for the generation of gamma oscillations. NMDA hypofunction has been proposed as an alternative hypothesis to the well-known dopamine dysregulation to explain the neurochemical abnormalities associated with schizophrenia. For this dissertation, we validated a preclinical model to pharmacologically probe NMDA-mediated gamma oscillations by further characterizing the auditory-steady state response (ASSR) in female Sprague Dawley rats. The ASSR is a measure of cortical neural synchrony evoked in response to periodic auditory stimuli. ASSR at 40 Hz is consistently disrupted in patients. First, we established the reliability of click train-evoked 40 Hz ASSR and tone-evoked gamma oscillations in 6 separate sessions, spread over a 3-week period. Then we established the sensitivity of these neural synchrony measures to acute NMDAR blockade using the high affinity NMDA channel blocker MK-801, using a repeated measures design. Next, we compared the reliability and sensitivity of the 40 Hz ASSR from two distinct recording sites. Results from this study showed that as compared to vertex, temporal recording showed a greater gamma synchrony. However, the temporal recording had poor test-retest reliability and lower sensitivity to MK-801-induced disruption. Lastly, we characterized the dose-response profiles of an NMDA co-agonist D-serine, an atypical (clozapine) and a typical (haloperidol) antipsychotic, on the 40 Hz ASSR. Results from these studies showed that only clozapine was effective in robustly augmenting 40 Hz ASSR. Furthermore, only clozapine pretreatment had partial protective effect against MK-801 induced ASSR disruption. Overall, this work establishes that vertex recorded 40 Hz ASSR is a reliable neural synchrony biomarker in female SD rats that is amenable for bidirectional pharmacodynamic modulation.

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La Vitamine K (VK) est largement reconnue pour son rôle dans la coagulation sanguine toutefois, de plus en plus de travaux indiquent son implication dans la fonction cérébrale. La VK est requise pour l'activation de différentes protéines, par exemple la protéine Gas6, et la ménaquinone-4 (MK-4), le principal vitamère K dans le cerveau, est impliquée dans le métabolisme des sphingolipides. Dans un rapport précédent, nous avons montré qu'un régime alimentaire faible en VK tout au long de la vie était associé à des déficits cognitifs chez des rats âgés. La warfarine sodique est un puissant antagoniste de la VK qui agit en bloquant le cycle de la VK, provoquant un «déficit relatif de VK » au niveau cellulaire. À la lumière du rôle émergent de la VK dans le cerveau, la warfarine pourrait représenter un facteur de risque pour la fonction cérébrale. Ce travail est donc pertinente en raison de la forte proportion d'adultes traîtés à la warfarine sodique. Dans la présente étude, 14 rats mâles Wistar ont été traités avec 14 mg de warfarine/kg /jour (dans l'eau potable) et des injections sous-cutanées de VK (85 mg/kg), 3x/sem, pendant 10 semaines. Quatorze rats témoins ont été traités avec de l'eau normale et injectés avec une solution saline. Les rats ont été soumis à différents tests comportementaux après quoi les niveaux de phylloquinone, MK-4, sphingolipides (cérébroside, sulfatide, sphingomyéline, céramide et gangliosides), et les sous-types de gangliosides (GT1b, GD1a, GM1, GD1b), ont été évalués dans différentes régions du cerveau. Comparativement aux rats du groupe contrôle, les rats traités à la warfarine présentaient des latences plus longues au test de la piscine de Morris (p <0,05) ainsi qu'une hypoactivité et un comportement exploratoire plus faible au test de « l’open field » (p <0,05). Le traitement par warfarine a également entraîné une diminution spectaculaire du niveau de MK-4 dans toutes les régions du cerveau (p <0,001), une altération des concentrations de sphingolipidiques, en particulier dans le cortex frontal et le mésencéphale (p <0,05), et une perte de différences régionales sphingolipidiques, notamment pour les gangliosides. Le traitement par warfarine a été associé à un niveau inférieur de GD1a dans l'hippocampe et un niveau supérieur de GT1b dans le cortex préfrontal et le striatum. En conclusion, la déficience en VK induite par warfarine altère les niveaux de VK et sphingolipides dans le cerveau, avec de potentiels effets néfastes sur les fonctions cérébrales. / Vitamin K (VK) is widely known for its role in blood coagulation, however many studies suggest its involvement in brain function. VK is required for the activation of various cerebral proteins (e.g., Gas6) and menaquinone-4 (MK-4), the main K vitamer in brain, is involved in sphingolipid metabolism. Furthermore, life-long intake of a low VK diet has been associated with cognitive deficits in old rats. Warfarin (W) is a potent VK antagonist that acts by blocking the VK cycle causing a “relative VK deficiency” at the cellular level. In light of this and the emerging role of VK in brain, W could represent a risk factor for cerebral function. The finding of this study is important according to the large proportion of adults with thromboembolic diseases being treated with warfarin drugs. This study was conducted in a rat model where the impact of W was investigated with respect to cognition, behavior, and brain menaquinone-4 (MK-4) and sphingolipid status. Fourteen Wistar male rats were treated with 15 mg W/kg/d (in drinking water) and subcutaneous VK (85 mg/kg), 3X/wk, for 10 wks; 14 control rats were treated with normal water and injected with saline. At the end of the treatment period, rats were subjected to different behavioral tests, afterwhich their brains assessed for VK (phylloquinone and MK-4) and sphingolipids (gangliosides, ceramides, cerebrosides, sphingomyelin and sulfatides) and gangliosides subtypes (GT1b, GD1a, GM1, GD1b). Mean latencies to find the hidden platform were higher in the W compared to the control group (p<0.05) suggesting cognitive deficits as well as hypoactivity and lower exploratory behaviour in the open field test (p<0.05). Warfarin treatment also resulted in a dramatic decrease in MK-4 concentration in all brain regions (p<0.001), altered sphingolipid level, especially in frontal cortex and midbrain (p<0.05), and in a loss of sphingolipid regional differences, notably for gangliosides. W treatment was associated with lower GD1a in the hippocampus and higher GT1b in the striatum and prefrontal cortex. In conclusion, warfarin-induced VK deficiency alters VK and sphingolipid status in brain with potential detrimental effects on brain functions.