The primary aim of this dissertation is to address an important issue of individual susceptibility to false memories. Specifically, what is the role inhibitory control (IC) in children’s and adult’s propensity to producing false memories? Inhibitory control within the context of the current study is defined on the basis of performance on selective attention tasks. Inhibitory control is discussed within this dissertation as it is reflected in two selective attention tasks, Stroop and Negative Priming. While the false memory effect, as reflected in the Deese/Roediger and McDermott paradigm (Roediger & McDermott, 1995), is one of the most widely studied memory phenomenon, the current study is important as it provides some insights into the relation between attention and memory. An interesting finding in the DRM false memory effect is that participants often report having a clear false memory of having seen or heard the non-presented critical lure item (CL item). Such memory illusions have been informative on how memory works. The current study adds to this body of research by providing converging evidence of how individual differences in the sensitivity to the false memory effect may occur, and how this sensitivity may reflect the same IC mechanisms involved in selective attention tasks. The basic notion examined within this dissertation is that when recognition memory is tested in the DRM paradigm, individuals have to select information that was studied and simultaneously inhibit highly activated yet non-presented information in memory, in order to correctly reject the CL item. If the notion that individual differences in sensitivity to the false memory effect is indeed related to a basic IC mechanism, then a relationship should be found between measures of IC in selective attention tasks and rates of false memories in the DRM test. The current study incorporates three experiments. Experiments 1 and 2 are broken down into parts ‘a’ and ‘b’, with each part varying in respect to the IC measure. In part a, participants were assigned to an inhibitory control group (IC group) on the basis of Stroop interference. In part b, participants are assigned to IC groups on the basis of a combined measure of inhibitory control that is, Stroop and Negative Priming. The third experiment assigned participants on the basis of a combined measure of IC, and then considered the relation between the duration of IC over a number of DRM word-lists presented simultaneously prior to the recognition test. Experiment 3 also compared the robust effect of IC on the propensity to produce false memories across all three experiments. The results of this study can be summarized as follows. In each experiment there was clear evidence of a relation between IC estimates and proportion of false memories. As predicted, individuals assigned to a Less IC group produced a higher proportion of false memories than those assigned to the More IC group. Inhibitory control differences did not modulate differences in correct or incorrect recognition in general (hits and false alarms to unrelated distractors). This second finding is important because it suggests a specific effect of IC in false memories, rather than a general breakdown in memory processes. The IC effect in false memories occurred in children (8-year olds and 10-year olds) as well as adults. Furthermore, the IC effect appeared to be additive with age; i.e., all groups produced a similar pattern across all three experiments. Last, the combined estimate of IC was found to be a more sensitive measure of false memories than a single index of IC; however, this was found in relation to adults but not for children. A number of additional manipulations and measures of interest were also included. Experiment 2 found clear evidence of an effect of IC on remember responses, not only were Less IC individuals more likely to produce false alarms to critical lure items, they were also more likely to distinctly respond they “remembered” the CL item as opposed to only “knowing” the CL had been presented. Examination of reaction times (RTs) to false alarms as a function of IC group found the Less IC group were faster to make false alarm responses to CL items, whereas the More IC group were slower to make false responses CL items. As predicted the relation between IC and the false memory effect was modulated by the random versus blocked presentation manipulation in Experiment 3. Specifically, decreased rates of false memories were found in the random presentation format compared to the blocked format. Interestingly however, a small effect of IC group in false memories was found even in the random condition. From this study it can be concluded that individual susceptibility to the false memory effect is in part modulated by inhibitory control. Individuals who demonstrate less effective IC show a greater propensity to false memories than those who demonstrate more effective IC. The IC effect of false memories was found to be robust, with converging evidence found across all three experiments. In relation to the development of inhibitory control, consistent with the research of Pritchard and Neumann (2004, 2009), and Lechuga and colleagues (2006), the results of this study suggest IC is fully developed in young children. However, their ability to accurately encode, retain and retrieve information would appear to develop at a different rate than IC. Specifically, it may be that while younger children are able to utilize IC in memory processes, they have yet to fully develop a richly interconnected semantic network. On the other hand, older children and adults would appear to have a more fully developed semantic network. This series of experiments presents a novel demonstration of the relation between inhibitory control and false memories. As such, this study has the potential to provide new insight into a cognitive mechanism that may be responsible for both developmental trends and for individual differences in the regulation of false memories. Moreover, if the mechanism responsible for mediating false memories is causally linked to performance on selective attention tasks in the systematic way that is proposed, it may be possible in the future to utilize IC measures to assist in identifying individuals who have an exaggerated propensity to form false memories, as well as those more prone to resist them.

There is growing evidence that acute changes in fundamental mechanisms of impulse control contribute to the transition from social drinking to abusive drinking. One component of impulsivity concerns the ability to inhibit maladaptive behaviors (i.e., inhibitory control). Inhibitory mechanisms are reliably shown to be sensitive to the impairing effects of alcohol, and studies have begun to show that this impairment fails to recover at the same speed as other aspects of behavior. However, the degree to which inhibitory control develops tolerance to alcohol has only been examined under limited conditions. This dissertation consists of three studies examining contexts in which tolerance has been observed for a host of prototypic behaviors, and will compare the degree to which it fails to develop for inhibitory control. Study 1 examined the rate of recovery for inhibitory control compared with other behaviors as blood alcohol concentrations (BACs) declined to zero following a dose of alcohol in 24 social drinkers. Results revealed prolonged alcohol impairment of inhibitory control along the BAC curve, even as BACs approached zero. By contrast, behaviors including reaction time and motor coordination began to show recovery markedly faster, as BACs were still significantly elevated. Study 2 examined the degree to which recent drinking patterns predict acute alcohol impairment from alcohol in a group of 52 drinkers. Recent, heavy consumption predicted less impairment of motor coordination, but bore no relationship to the magnitude of impairment of inhibitory control. Study 3 examined whether increasing the stimulus strength of environmental cues signaling the need to inhibit behavior could reduce alcohol impairment of inhibitory control in 56 participants. Results showed that increasing stimuli strength reduced alcohol impairment of behavioral activation, but actually increased inhibitory failures. Taken together, the findings contribute to the growing body of evidence suggesting that inhibitory control is especially vulnerable to the impairing effects of alcohol compared with other behaviors. Indeed, these studies systematically assessed the pharmacokinetic and environmental factors that contribute to tolerance, indicating that inhibition is disrupted in circumstances under which response activation is unimpaired. The findings have important implications for understanding the behaviorally-disruptive effects of alcohol.

Impaired inhibition is a deficit of several psychopathological disorders, particularly attention-deficit hyperactivity disorder (ADHD). In the first study, a meta-analysis was conducted to determine whether impaired inhibition as measured by the Stop Signal Task is specific to ADHD, or whether it could be found in other psychopathological disorders. The meta-analysis found an inhibitory deficit in ADHD, but also in obsessive compulsive disorder (OCD) and schizophrenia (SCZ), suggesting that deficient inhibition is not specific to ADHD. A common neural mechanism may underlie deficient inhibition in ADHD, OCD, and SCZ. Study 2 aimed to determine the neural basis of inhibition using a lesion-deficit approach in children with traumatic brain injury (TBI). Only TBI children with white matter lesions in the superior frontal gyrus (SFG) region showed impaired inhibition compared with orthopedic injury controls. This suggests that deficient inhibition may stem from frontal lobe white matter damage, particularly in the SFG.

Impaired inhibition is a deficit of several psychopathological disorders, particularly attention-deficit hyperactivity disorder (ADHD). In the first study, a meta-analysis was conducted to determine whether impaired inhibition as measured by the Stop Signal Task is specific to ADHD, or whether it could be found in other psychopathological disorders. The meta-analysis found an inhibitory deficit in ADHD, but also in obsessive compulsive disorder (OCD) and schizophrenia (SCZ), suggesting that deficient inhibition is not specific to ADHD. A common neural mechanism may underlie deficient inhibition in ADHD, OCD, and SCZ. Study 2 aimed to determine the neural basis of inhibition using a lesion-deficit approach in children with traumatic brain injury (TBI). Only TBI children with white matter lesions in the superior frontal gyrus (SFG) region showed impaired inhibition compared with orthopedic injury controls. This suggests that deficient inhibition may stem from frontal lobe white matter damage, particularly in the SFG.

Compulsive eating behavior is a transdiagnostic construct observed in certain forms of obesity and eating disorders, as well as in the recently proposed ‘food addiction.’ Compulsive eating has been conceptualized as being comprised of three elements: i) habitual overeating, ii) overeating to relieve a negative emotional state, and iii) overeating despite adverse consequences. Neurobiological processes that include maladaptive habit formation, the emergence of a negative affect, and dysfunctions in inhibitory control are thought to drive the development and persistence of compulsive eating behavior. These complex psychobehavioral processes are under the control of various neuropharmacological systems. Here, we describe the current evidence implicating these systems in compulsive eating behavior, and contextualize them within the three elements. A better understanding of the neuropharmacological substrates of compulsive eating behavior has the potential to significantly advance the pharmacotherapy for feeding-related pathologies. / 2018-10-31T00:00:00Z

abstract: A model of the effects of early adolescents' temperament (negative emotionality and inhibitory control) and threat appraisals on resulting status in the bullying dynamic was examined. Specifically, I examined the hypothesis that negative emotionality and passive victim versus bully-victim status would be mediated by threat appraisals, and that mediated effect would be moderated by levels of inhibitory control. The study used a sample of 56 early adolescents ages 7–16. Temperament characteristics were measured using the EATQ–R (Capaldi & Rothbart, 1992). Threat appraisals were assessed using items from Hunter, Boyle, and Warden (2004). Bullying and victimization were measured using items created for this study and additional cyber bullying items (Smith, Mahdavi, Carvalho, & Tippett, 2006). A multinomial logistic regression and test of moderated mediation were analyzed to examine the model (Hayes, 2012). Higher levels of negative emotionality were correlated with being a victim of bullying. The moderated mediation model was not statistically significant, however the direction of the patterns fit the hypotheses. Future directions and limitations are discussed. / Dissertation/Thesis / M.S. Psychology 2012

Prospective memory (PM) is the ability to remember to carry out one's intentions. This is a critical ability for children to develop in order to function independently in their daily activities. This dissertation examines the role of executive functioning in preschoolers' PM in two studies that vary the executive demand at different stages of the PM task. Study 1 investigated the role of task difficulty during the retention interval prior to the PM task. A difficult working memory task during the delay period resulted in worse PM performance in 4- and 5-year-olds compared to an easy working memory task. In addition, children's working memory, planning ability, and theory of mind correlated with PM but only in the difficult filler task condition. Study 2 examined age differences between 4- and 5-year-olds in PM task performance when the task: (1) was embedded in an easy or difficult ongoing task, (2) had an instruction to focus on the intention versus an instruction to focus on the distractor activity during the retention interval, and (3) varied in the salience of prospective targets. Overall, 5-year-olds performed better on the PM task than 4-year-olds. Children also had superior PM when targets were salient compared to non-salient and marginally superior PM when they received an instruction to monitor their intention compared to when they received an instruction to focus on the distractor activity. In addition, positive relations between executive functioning and PM were documented. Taken together, these studies suggest that disrupting or encouraging monitoring has a direct impact on PM performance in certain conditions. The implications of these results for theories that suggest differing roles for controlled processes in PM are discussed.

This diploma thesis deals with acidic proteins contained in the potato (Solanum tuberosum) tubers, or rather about their separation with chromatography techniques. For the analysis were chosen tubers of two czech potato varieties, Adéla and Westamyl. From the concentrated potato juice were eliminated basic and most of the patatin proteins with the gravity column chromatography. In the next step were applied the chromatography techniques on the anion and hydroxyapatite columns by the fast protein liquid chromatography (FPLC) system. On the anion column were separated protein fractions which contained proteins of molecular weight in the range of 15 kDa to 60 kDa (Adéla) and 15 kDa to 100 kDa (Westamyl). The most abundant were the proteins with molecular weight 15 kDa a 20 kDa. In the last step was used the mass spectrometry for the identification of chosen protein fractions.

The mammalian testis is divided into two distinct compartments which carry out its principal functions. Spermatogenesis occurs within the seminiferous tubules and androgen biosynthesis primarily occurs in the interstitial space. Both these processes are entirely dependent upon the two major testicular somatic cell populations - the Sertoli and Leydig cells respectively. In human males, testicular spermatogenic and endocrine function declines during the ageing process. Of particular significance is the reported age-related decrease in Leydig cell androgen production as androgens have been suggested to play a crucial role in supporting lifelong general health in men, with low circulating testosterone linked to an increased risk of developing chronic age-related cardiometabolic diseases. However, the relationship between ageing, testicular function and disease is not fully understood, impeding the development of novel therapeutic strategies to treat age-related testicular dysfunction. In one set of studies undertaken herein, a series of novel mouse models of premature ageing were utilised to begin to dissect the process of age-related testicular degeneration. Firstly, a novel knockout-first conditional allele of a previously reported premature-ageing model driven by Cisd2 (CDGSH Iron Sulphur Domain 2) deficiency was validated and the testicular phenotype characterised and compared to that of naturally aged mice at 18-months of age. Histological analyses revealed premature testicular atrophy at 6-months of age in CISD2 deficient mice, consistent with observations of the naturally aged testis. Circulating testosterone was significantly lower in CISD2-deficient mice compared to wild-type controls at 6-months of age and the luteinising hormone/testosterone ratio was significantly elevated, indicative of compensated Leydig cell failure. mRNA expression of key genes involved in androgen production were also significantly reduced in the CISD2-deficient testis, pointing to Leydig cell dysfunction in this model of premature aging. Next, Cre/LoxP technology was used to delete Cisd2 from specific testicular cell populations to determine which cell types control/support Leydig cell function during the ageing process. Testosterone production was unaffected when Cisd2 was disrupted in either the Leydig cell population or Sertoli cell population. These observations suggest that disruption to the testicular microenvironment in which Leydig cells reside, rather than intrinsic Leydig cell ageing, may play a significant role in age-associated Leydig cell dysfunction. A second set of studies were carried out to investigate the role of leukemia inhibitory factor (LIF) signalling in the maintenance of testicular function. LIF is a pleiotropic cytokine belonging to the interleukin-6 family. In the rodent testis, LIF is expressed in fetal life and adulthood; the peritubular myoid cells thought to be the main site of production. Given their anatomical location within the testis, LIF produced by peritubular myoid cells may act on both intratubular and interstitial cells to influence spermatogenesis and steroidogenesis respectively. Indeed, LIFR is expressed in germ cells, Sertoli cells, Leydig cells as well as testicular macrophages suggesting that LIF may be a key paracrine regulator of testicular function. However, the precise role of LIF/LIFR signalling in the testis is largely unknown. As such, models of testicular cell-specific Lifr deletion were generated using Cre/LoxP technology. Analysis of these novel models of conditional LIFR ablation revealed that LIFR is dispensable in germ cells for normal spermatogenesis. However, LIFR ablation from Sertoli cells resulted in a progressive degenerative phenotype, characterised by abnormal germ cell loss, sperm stasis, seminiferous tubule distention and subsequent atrophy of the seminiferous tubules. In a final set of studies, a rat model of Leydig cell ablation-regeneration was used to determine the regenerative capacity of human adipose-derived perivascular stem cells (hAd-PSC) as a potential therapy for testicular dysfunction. Following ethane dimethanesulphonate (EDS) mediated Leydig cell ablation, primary hAd-PSCs, cultured with or without LH, IGF-1, PDGFBB, T3 and ITS supplement, were transplanted into the rat testis and Leydig cell regeneration was monitored via serial measurements of circulating luteinising hormone (LH) and testosterone. Overall, hAd- PSCs had no impact on the recovery of circulating testosterone levels. However, when pre-cultured with the cocktail of hormone/growth factor supplements, the LH spike induced by the removal of testosterone negative feedback was dampened, suggesting the transplanted cells may promote Leydig cell regeneration. Whether these cells differentiate into Leydig cells, or simply provide paracrine support to the regenerating Leydig cells remains to be determined. Although Ad-PSCs may enhance regeneration kinetics, the transplanted cells were undetectable in the testis 5 weeks post transplantation suggesting they may not survive in the context of long term xenogeneic transplantation.

Este estudo teve por objetivo avaliar a ação inibitória de duas soluções de quitosana através da determinação da concentração inibitória mínima (CIM) e concentração bactericida mínima (CBM) de duas soluções de quitosana de diferentes procedências. A primeira solução de quitosana derivada de camarão, do tipo comercial Fluka, de PM 600.000 g/mol, G.A. 76% e a segunda solução de quitosana derivada de lula, de PM: '10 POT.7' g/mol e G.A.: 83%. As duas soluções foram ajustadas ao pH 5,0 e na concentração de 0,5% em solução acética a 1%. A melhor atividade antimicrobiana da quitosana ocorre em pH igual ou menor que cinco e ela sofre precipitação em pH superiores a 6,5. Estas duas características foram determinantes na escolha do pH utilizado no teste da CIM. Para confirmar que a inibição do crescimento dos enteropatógenos ocorreu pela ação da quitosana e não pelo pH ácido dos meios, vários testes foram realizados. A avaliação do crescimento dos enteropatógenos em ágar MacConkey, pH 5,0 (ótimo para quitosana) e 7,4(ótimo para o cultivo das bactérias utilizadas), o inóculo de cada bactéria foi preparado segundo o tubo 0,5 de Mc Farland (controle positivo), e a avaliação foi repetida utilizando o inóculo diluído 1:1000 para contagem do número de colônias, e não apresentaram diferenças significativas. Para confirmar estes dados foram realizados os controles negativos das duas soluções de quitosana e do meio de cultura MacConkey em pH 5,0 e 7,4, incubados a 37°C e lidos por 72 horas, sem qualquer alteração. A avaliação da reação de precipitação foi feita em caldo Müeller Hinton em pH 4,0; 5,0; 6,0; 7,0 e 8,0 para as duas soluções de quitosana (v/v), incubados a 37°C e lidos por 72 horas. A avaliação da CIM das duas soluções de quitosana para os enteropatógenos foi realizada por diluição seriada e os inóculos comparados ao tubo 0,5 de Mc Farland, sendo 10 'mü'L da suspensão bacteriana acrescida a cada tubo, incubados a 37°C por 24 horas. A leitura da ausência de turvação visível caracterizou a CIM. Todos os tubos que não apresentaram turvação visível foram plaqueados em ágar MacConkey, em pH 7,4 e incubados a 37°C por 24 horas para determinação da CBM, a qual foi determinada pela menor concentração capaz de causar morte total da população dos enteropatógenos. Todas as técnicas foram realizadas em triplicata para confirmação dos resultados / The aim of this study was to evaluate the inhibitory action of chitosan solutions derived from shrimp (Fluka commercial type, MW 600.000 g/mol, acetylation degree of 76%) and squid (MW '10 POT.7' g/mol, acetylation degree of 83%) through determination of minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) against enteropathogens: Salmonella enterica, Shigella sonnei and Escherichia coli EPEC. Those solutions were set to pH 5,0 and a 0,5% concentration in a 1% acetic acid solution. The best antimicrobial activity of chitosan occurs in pH less than or equal to 5,0 and it shows precipitation in pH greater than 6,5. Those features were decisive to choose the pH used in the MIC test. In order to confirm that the growth inhibition of enteropathogens occurred by the action of chitosan and not for the acid pH of the environments, growth evaluation tests of enteropathogens were accomplished in MacConkey agar, pH 5,0 (excellent for chitosan) and pH 7,4 (excellent for culture of used bacteria). The inoculum of each bacterium was prepared comparing with the 0,5 tube of McFarland (positive control) and the evaluation was repeated using the inoculum diluted in a salt solution 1:1000 to count the number of colonies, which did not show significant differences. The reaction evaluation of precipitation of chitosan was done in Müeller Hinton broth with pH ranging 4,0 - 8,0 for both solutions of chitosan (v/v), which were incubated at 37°C and read for 72 hours. The MIC evaluation for both solutions of chitosan for the enteropathogens was done by serial dilution and the inocula were compared to the 0,5 tube of McFarland, adding 10 'mü'L of bacterial suspension to each tube, which were incubated at 37°C for 24 hours. The MIC was distinguished by the absence of visible turbidity. Each tube that did not show visible turbidity was spread on MacConkey agar plates in pH 7,4, and incubated at 37°C for 24 hours to find the MBC, which was determined by the smallest concentration able to cause total death to the enteropathogen population. In both cases, the solutions of chitosan presented a high antimicrobial activity against the enteropathogens Salmonella enterica and Escherichia coli EPEC. However, the higher antimicrobial activity was observed in the enteropathogen Shigella sonnei