El objetivo general era estudiar el patrón de relaciones de la psicopatía, entendida como un constructo jerárquico subdividido en dos factores y cuatro facetas (interpersonal, afectiva, estilo impulsivo/irresponsable y antisocial), con variables sociodemográficas, psicológicas, criminológicas y diversos indicadores de la experiencia emocional, utilizando el paradigma de la visión de imágenes. El estudio se realizó en un centro penitenciario con 75 internos penados, evaluados mediante el Psychopathy Checklist-Revised (PCL-R) de R. D. Hare (2003). Las medidas registradas en un contexto de laboratorio incluían indicadores de: a) la experiencia emocional ante distintos estímulos afectivos, evaluada directa (estimaciones en valencia afectiva, arousal y dominancia) e indirectamente (tiempo de reacción de discriminación afectiva); b) la reactividad fisiológica ante esos estímulos, a nivel autonómico (conductancia de la piel y tasa cardíaca) y somático (actividad electromiográfica de los músculos faciales corrugador, cigomático y orbicular del ojo); y c) la reactividad defensiva, mediante la modulación del reflejo de sobresalto. En conjunto, los resultados obtenidos respaldan empíricamente la utilidad del modelo de las cuatro facetas de la psicopatía de Hare en población penitenciaria y, en particular, la asociación exclusiva de las características afectivas del síndrome (crueldad, ausencia de empatía.) con una anomalía emocional de carácter básico y, quizá derivado de lo anterior, con un patrón de comportamiento antisocial y violento.

Macrophages represent long lived immune cells that are remarkably resistant to apoptosis, which allows them to perform in highly stressful environments. Apoptosis resistance is a characteristic that develops during the differentiation process from monocytes to macrophages. However, the signaling pathways that mediate the development of macrophage antiapoptotic phenotype during differentiation remain mostly unknown. Because of their decreased susceptibility to cell death, macrophages are also key viral reservoirs during HIV infection. My research aims to understand the molecular mechanisms and signaling pathways that mediate cell survival during and after monocyte to macrophage differentiation and the involvement of the main families of antiapoptotic proteins, IAPs (inhibitors of apoptosis) and Bcl2 in this process. HIV accessory protein Vpr was used as an apoptotic stimulus, due to its death inducing abilities in other cell types. My results show that survival of macrophages is distinctively regulated during and after differentiation. I have identified a signaling pathway consisting of PI3K/Akt activation of NFκB that is important in survival of differentiating macrophages by specifically sustaining antiapoptotic Bcl-xL expression. However, once differentiated, Mcl-1, but not Bcl-xL is dependent on PI3K/Akt activation. Moreover, differentiated macrophages are resistant to the effect of HIV-Vpr, which is highly apoptotic for monocytes. In contrast, resistance to HIV-Vpr induced apoptosis of human macrophages is specifically mediated by antiapoptotic IAP proteins, with no involvement of the Bcl2 family, which maintains macrophage viability in the absence of any apoptotic stimuli. In addition to their antiapoptotic properties, IAPs are also important regulators of macrophage function. By using chemical compounds (SMAC mimetics) that target IAPs for degradation, I have shown that IAPs positively modulate LPS-induced IL10, IL-27 and MIG (monokine induced by IFNγ) production in human macrophages, by promoting TRAF2, JNK and p38 signaling and NFκB activation. In addition, IAPs also contribute to LPS-induction of CD80/CD86 costimulatory molecules. Overall, my results suggest that both IAPs and Bcl2 families contribute to survival of human macrophages and that IAPs are also involved in innate immune responses. Unraveling the mechanisms that control macrophage survival and function in various settings would provide therapeutic strategies aimed at eliminating cells when their survival is no longer beneficial for the host, as in the case of HIV infection or autoimmune diseases.

Macrophages represent long lived immune cells that are remarkably resistant to apoptosis, which allows them to perform in highly stressful environments. Apoptosis resistance is a characteristic that develops during the differentiation process from monocytes to macrophages. However, the signaling pathways that mediate the development of macrophage antiapoptotic phenotype during differentiation remain mostly unknown. Because of their decreased susceptibility to cell death, macrophages are also key viral reservoirs during HIV infection. My research aims to understand the molecular mechanisms and signaling pathways that mediate cell survival during and after monocyte to macrophage differentiation and the involvement of the main families of antiapoptotic proteins, IAPs (inhibitors of apoptosis) and Bcl2 in this process. HIV accessory protein Vpr was used as an apoptotic stimulus, due to its death inducing abilities in other cell types. My results show that survival of macrophages is distinctively regulated during and after differentiation. I have identified a signaling pathway consisting of PI3K/Akt activation of NFκB that is important in survival of differentiating macrophages by specifically sustaining antiapoptotic Bcl-xL expression. However, once differentiated, Mcl-1, but not Bcl-xL is dependent on PI3K/Akt activation. Moreover, differentiated macrophages are resistant to the effect of HIV-Vpr, which is highly apoptotic for monocytes. In contrast, resistance to HIV-Vpr induced apoptosis of human macrophages is specifically mediated by antiapoptotic IAP proteins, with no involvement of the Bcl2 family, which maintains macrophage viability in the absence of any apoptotic stimuli. In addition to their antiapoptotic properties, IAPs are also important regulators of macrophage function. By using chemical compounds (SMAC mimetics) that target IAPs for degradation, I have shown that IAPs positively modulate LPS-induced IL10, IL-27 and MIG (monokine induced by IFNγ) production in human macrophages, by promoting TRAF2, JNK and p38 signaling and NFκB activation. In addition, IAPs also contribute to LPS-induction of CD80/CD86 costimulatory molecules. Overall, my results suggest that both IAPs and Bcl2 families contribute to survival of human macrophages and that IAPs are also involved in innate immune responses. Unraveling the mechanisms that control macrophage survival and function in various settings would provide therapeutic strategies aimed at eliminating cells when their survival is no longer beneficial for the host, as in the case of HIV infection or autoimmune diseases.

>Magister Scientiae - MSc / The occurrence and spread of Invasive Alien Plants (IAPs) is a threat to global water resources and natural ecosystems due to high water use rates. With the current climate change projections and their ability to survive extreme environmental conditions, these species pose a huge threat to grazing resources, water availability and ecosystems in general. Routine monitoring and understanding their distribution and potential vulnerable areas is fundamental as it provides the requisite baseline information to guide clearing efforts and other related management and rehabilitation initiatives.

The inflammatory and anti-inflammatory macrophages have been implicated in many diseases including rheumatoid arthritis, inflammatory bowel disease and chronic rhinosinusitis. Recent studies suggest targeting macrophage function and activation may represent a potential target to treat these diseases. Herein, I investigated the effect of second mitochondria-derived activator of caspases (SMAC) mimetics (SMs), the inhibitors of apoptosis (IAPs) proteins, on the killing of normal human pro- and anti-inflammatory macrophage subsets. It has been shown that human monocytes are highly susceptible to the cytotoxic effects of SMs, however, differentiated macrophages (M0) develop resistance to the cytocidal abilities of SMs. Whether human macrophage subsets are also resistant to the cytotoxic effects of SM remains unknown. My results show that differentiation of M0 macrophages towards M1 state rendered them highly susceptible to SM-induced cell death, whereas M2a, M2b and M2c differentiated subsets were resistant, with M2c being the most resistant. SM-induced cell death in M1 macrophages was mediated by apoptosis as well as necroptosis and activated both extrinsic and intrinsic pathways of apoptosis. The susceptibility of M1 macrophages to SM-induced cell death was attributed to the IFN-𝛾-mediated polarization as JAK inhibitor reversed their susceptibility. In contrast, M2c and M0 macrophages experienced cell death through necroptosis pathway following simultaneous blockage of the IAPs pathways by SM-LCL161 and the caspase pathways by the pan-caspase inhibitors (zVAD.fmk). I investigated the molecular mechanism governing SM-induced cell death in M1 macrophages. My results show that in contrast to the cancer cell lines, SM-induced cell death in M1 macrophages is independent of endogenously produced TNF-⍺, the canonical and non- canonical NF-𝜅B pathways. The susceptibility of M1 macrophages to SM-induced cell death was found to be dependent on IFN-𝛾-mediated differentiation through the JAK-STAT pathway and subsequent activation of IRF-1. In addition, the selective cell death in SM-treated M1 macrophages is mediated by simultaneous degradation of cellular IAP-2 (cIAP-2) and RIPK-1/3 through the activation of mTORC signaling pathway. Overall, the results suggest that survival of human macrophages is critically linked to the activation of the IAPs pathways. Moreover, agents blocking cIAP-1/2, mTORC and IRF-1 can be exploited therapeutically to address inflammation-related diseases. These observations hold a promising therapeutic strategy to limit the activation of proinflammatory M1 macrophages and eventually controlling the M1-associated diseases.

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Both pictures and films are widely used elicitors in experimental approach to emotions. However, there is no consensus regarding their relative impact. I describe conceptual underpinning of these methods, their theoretical comparison, and related methods. In a study of 124 students I assess and compare the impact of pictures and films on experiential, behavioural and physiological reactions. There were stronger reactions in response to positive film than to positive pictures. Negative film and pictures were similar in strength yet different in kind of reactions they yielded. The difference can be explained by different temporal characteristics of both methods. Present study is the second study dealing with this topic, and the only study that engaged multiple reaction levels. Powered by TCPDF (www.tcpdf.org)

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在心理與認知科學領域中常使用生理訊號來測量受試者的反應，並反映出人們的心理狀態起伏。本研究探討應用生理訊號識別情緒之可能性，以及將生理訊號與其他情緒辨識結果整合之方法。 在過去的研究中，生理與心理的對應關係，並無太多著墨，可稱為一黑盒子(black-box)的方式。並因上述類別式實驗長時間收集的生理訊號，對於誘發特定情緒反應之因果(cause-effect)並未進行深入的討論。本研究由於實驗的設計與選用材料之故，可一探純粹由刺激引發的情緒下情緒在生理與心理之因果關係，在輸入輸出對應間能有較明確的解釋。 本研究中嘗試監測較短時間(<10sec)的生理資訊，期望以一近乎即時的方式判讀並回饋使用者適當的資訊，對於生理訊號與情緒狀態的關聯性研究，將以IAPS(International Affective Picture System) 素材為來源，進行較過去嚴謹的實驗設計與程序，以探究生理訊號特徵如何應用於情緒分類。 雖然本研究以維度式情緒學說為理論基礎，然考慮到實際應用情境，若有其他以類別式的理論為基礎之系統，如何整合維度式與類別式兩類的資訊，提出可行的轉換方式，亦是本研究的主要課題。 / Physiological signals can be used to measure a subject’s response to a particular stimulus, and infer the emotional status accordingly. This research investigates the feasibility of emotion recognition using physiological measurements in a smart living space. It also addresses important issues regarding the integration of classification results from multiple modalities. Most past research regarded the recognition of emotion from physiological data as a mapping mechanism which can be learned from training data. These data were collected over a long period of time, and can not model the immediate cause-effect relationship effectively. Our research employs a more rigorous experiment design to study the relationship between a specific physiological signal and the emotion status. The newly designed procedure will enable us to identify and validate the discriminating power of each type of physiological signal in recognizing emotion. Our research monitors short term (< 10s) physiological signals. We use the IAPS (International Affective Picture System) as our experiment material. Physiological data were collected during the presentation of various genres of pictures. With such controlled experiments, we expect the cause-effect relation to be better explained than previous black-box approaches. Our research employs dimensional approach for emotion modeling. However, emotion recognition based on audio and/or visual clues mostly adopt categorical method (or basic emotion types). It becomes necessary to integrate results from these different modalities. Toward this end, we have also developed a mapping process to convert the result encoded in dimensional format into categorical data.

人們對於錯誤訊息處理經由自我覺察或外在回饋之管道，可藉由事件關聯電位分別測得ERN (error-related negativity) 及FRN (feedback-related negativity)。過去研究曾指出雙側作業(Flanker task)中錯誤所引發的ERN會受到以圖片呈現的短期情緒所調節，然而對於回饋誘發的FRN與個體情緒調節的關係則未曾被探討過。過去FRN的研究認為唯有當受試者所進行的作業為增強學習作業時，受試者對於回饋結果的預期狀態才能反映於FRN的反應強度。本研究利用兩個實驗分別採用非增強學習作業及增強學習作業，其中並以IAPS情緒圖片進行短期情緒的引發，在受試者於實驗中對其反應結果的不同預期狀態，探測受試者FRN受短期情緒調節的效果。 實驗一利用非增強學習作業，結果顯示FRN的強度可以反映受試者對於回饋結果的預期狀態，其中以非預期時FRN的強度為最大，預期時FRN的強度為最小；另外，正向情緒圖片對於FRN具有調節效果，正向情緒下FRN反應強度小於中性以及負向情緒下FRN反應強度。實驗二利用增強學習作業，前述的FRN強度反映受試者對回饋結果的預期效果，只有在實驗前半段的嘗試次中被觀測到，此效果未見於全部嘗試次納入分析；另外，實驗二中沒有觀察到情緒對於FRN的調節效果。 綜合而言，本研究發現受試者唯有持續處於學習的情形下，FRN才能反映受試者對於回饋結果的預期狀態，情緒對FRN的調節效果也僅於此情況下才能被觀測到。 / Error-related information in human can be processed via self-awareness and/or feedback given externally, which are measurable by the use of event-related potential (ERP) and termed error-related negativity (ERN) and feedback-related negativity (FRN) respectively. Previous studies showed that short-term affective stimuli would modulate the magnitude of ERN elicited by Flanker task. However, such modulation effect has not been tested on FRN. Furthermore, the magnitude of FRN is indicated to be related to the expectancy states toward feedback when the subject is undergoing a reinforcement learning task. Present study, thus, was designed to test the affective modulation effect on FRN in two separate tasks. In which, emotional pictures adopted from IAPS were used as the short-term affective stimuli, and different expectancy states in both non-reinforcement learning task (Experiment1) and reinforcement learning task (Experiment 2) were manipulated. In the results of Experiment 1, the magnitude of FRN was larger under the unexpected condition in comparing to the expected one. Modulation effect of short-term affective stimuli on FRN was obtained when positive emotion pictures were presented in non-reinforcement learning task, which FRN amplitude was significantly smaller in comparing to those measured after the presentation of neutral and negative pictures. In the results of Experiment 2, FRN elicited in the unexpected condition was only obtained from analyzing the dada collected in the first half of trails. Such effect was not confirmed when the data from all trials were analyzed. A lack of modulation effect of short-term affective stimuli on FRN appeared in Experiment 2. In conclusion, it is indicated that the expectancy depended FRN is most apparent when the subject is undergoing a continuous learning-demanded process. Meanwhile, short-term affective stimuli can modulate such FRN.