This investigation was designed to study coach and self-appraised groupings of intercollegiate tennis players who yield to stress and withstand stress and to determine if personality differences existed between groups. Subjects were 75 intercollegiate tennis players from Texas. A stress inventory and the Cattell Sixteen Personality Factor Questionnaire were instruments utilized in the study. Data were subjected to hierarchical profile-groupings, three-way analyses of variance, and a correlational analysis. Conclusions of the study were that intercollegiate tennis players and male and female players respond to stress differently; intercollegiate tennis players and male and female players who experience different levels of stress have different personalities; and players and coaches do not evaluate the ability to cope with stress similarly.

An oft overlooked population in research, firefighters of volunteer and paid-on-call fire departments respond to nighttime calls as a supplement to their normal working hours, making the duties taxing on the autonomic system leading to cardiovascular and endocrine disruptions. These duties also come with a tax burden on the volume and distribution of sleep. The current study was executed in order to gain valuable insight into the impact of nighttime call response in this population and the magnitude and duration of any perturbations. Eight firefighters from Greater Victoria Volunteer and Paid-on-call departments were recruited to wear Equivital EQ02 heart monitors and FitBit Charge 2 devices to record autonomic cardiovascular responses and track sleep between 1900 and 0700. HR MAX was found to significantly increase with a large effect size (p<0.0005) from 97 +/- 20 to 157 +/- 18 beats per minute in the 15 minutes preceding versus following a call within the time period. LF/HF ratios increased during the first 15-minutes following a call to 4.055 +/- 1.316 from 1.911 +/- 0.599 pre-call. HF power, RMSSD, and pNN50 all decreased significantly compared to pre-call values (796.176 +/- 414.296 ms2 vs 244.119 +/- 153.880 ms2, 51.940 +/- 7.119 ms vs 35.072 +/- 2.624 ms, 25.017 +/- 7.034% vs 7.403 +/- 2.411%). Further, all HRV measures with the exception of normalized LF and HF were found to be significantly different when waking for and attending a call versus waking on a normal day despite there being no significant differences among any variables when going to bed on nights with and without a call. Total and REM sleep were the most significantly impacted measurables of sleep. Total sleep fell to 261.11 +/- 61.11 minutes from 417.13 +/- 52.04 minutes while REM absolute and percentage of total sleep dropped from 109.88 +/- 28.47 minutes to 51.44 +/- 17.92 minutes, and 22.25 +/- 3.73% to 16.33 +/- 3.17% respectively. In response to a call, mean salivary cortisol levels increased from pre-call values by 0.426 +/- 0.202 ug/dL (p<.001). Salivary c-reactive protein levels also showed significant increases with a small effect size, though due to secretion kinetics, call response is not the likely cause. The results of this study demonstrate the presence of a significant shift in autonomic control from parasympathetic (PSNS) dominance to sympathetic control and PSNS withdrawal which evokes a cortisol-mediated stress response of comparable magnitude to literature standards for normal waking fluxes. Sleep volume, and arguably the most critical stage of sleep, rapid eye movement, are significantly impacted and the links between cognitive performance and both total and overall REM sleep indicate that call response does not just impact the cardiovascular system but may in fact be reducing mental acuity of firefighters. This is important as it has the potential to impact both self and team health and safety, not only during night time call response, but at the firefighters’ day jobs which they regularly proceed to the very same morning following a call, evidently with significant deprivation in sleep. / Graduate

The purpose of this study was to examine whether physical activity status of healthy adult males (N = 59) while in a coping strategy condition (association, disassociation, or control) influences psychophysiological responses to an acute painful stimulus. Measures of pain tolerance, state anxiety, body awareness, and salivary cortisol were investigated. Results indicated no significant differences between physical activity groups for pain tolerance, stress responses (i.e., self-reported state anxiety and cortisol levels), or body awareness. Though, those who indicated using a disassociation coping technique during the exit interview tolerated the acute, surface pain longer. More research is required to further understand the effects of physical activity and coping strategies on pain perception and psychophysiological responses.

La réponse au choc thermique est un mécanisme de défense largement décrit au cours duquel l’expression préférentielle des protéines de choc thermique Hsp aide la cellule à récupérer des dommages causés par l’hyperthermie, comme la dénaturation/agrégation des protéines. Une des conséquences du choc thermique mise en évidence au laboratoire, est l’activation du facteur de transcription NFκB. Cette activation a lieu pendant la période de récupération suivant ce stress. Par comparaison de la réponse au choc thermique de cellules témoins ou déficientes en NFκB, nous avons cherché à étudier les conséquences de l’activation de NFκB par le choc thermique. Nous avons montré que NFκB active un mécanisme augmentant la survie des cellules soumises à une hyperthermie : l’autophagie. L’absence d’induction de ce mécanisme conduit à la mort par nécrose des cellules déplétées en NFκB. Dans ces cellules, l’induction artificielle de l’autophagie restaure une survie normale au stress thermique. Nous avons montré que les principaux régulateurs de l’autophagie (complexes mTOR et PI3Kinase de Classe III) ne sont pas des cibles modulées par NFκB, en réponse à une hyperthermie. En revanche, l’accumulation de protéines dénaturées voire agrégées est un élément primordial pour l’activation de l’autophagie-dépendante de NFκB. En effet dans les cellules déficientes pour NFκB, contrairement aux cellules témoins, l’accumulation de protéines agrégées induite par le traitement hyperthermique, mais aussi par l’expression de formes mutées d’HspB5, n’est pas résorbée ; ceci indique que le contrôle qualité des protéines est altéré dans ces cellules. Cette altération pourrait provenir d’un défaut de formation du complexe BAG3-HspB8 en absence de NFκB. En effet, nous avons montré que la forte expression des gènes bag3 et hspb8, induite suite au stress thermique, est dépendante de NFκB et que l’accumulation du complexe BAG3-HspB8, observé dans les cellules témoins soumises au choc thermique, est inhibée dans les cellules déficientes pour NFκB. Nos résultats démontrent que NFκB induit un processus autophagique en réponse à l’agrégation protéique induite par l’hyperthermie. Ce mécanisme, nécessitant la formation du complexe BAG3-HspB8, augmente la survie des cellules probablement par l’élimination des protéines agrégées générées au cours du stress thermique / The heat shock response is a widely described defense mechanism during which the preferential expression of heat shock proteins (Hsps) helps the cell to recover from thermal damages such as protein denaturation/aggregation. We have previously reported that NFκB transcription factor is activated during the recovery period after heat shock. Thus, we aimed to analyze the consequences of NFκB activation during heat shock recovery, by comparing the heat shock response of NFκB competent and incompetent cells. We demonstrated that NFκB plays a major and crucial role during the heat shock response by activating autophagy, which increases the survival of heat-treated cells. Indeed, we observed that autophagy is not activated during heat shock recovery leading to an increased level of necrotic cell death in NFκB incompetent cells. Moreover, when autophagy is artificially induced in these cells, the heat shock cytotoxicity is turned back to normal. We showed that the key regulators of autophagy (mTOR complex, and class III PI3Kinase complex) are not regulated by NFκB after heat shock. In contrast, we observed that aberrantly folded/aggregated proteins accumulation is a prime event in the activation of NFκB -mediated autophagy. Moreover, NFκB -depleted cells accumulate higher levels of protein aggregates induced by either heat shock treatment or mutated form of HspB5, indicating that the protein quality control process seem to be altered in these cells. This alteration could be caused by a defect in BAG3-HspB8 complex formation in NFκB -depleted cells. We demonstrated that heat shock treatment induces a NFB-dependent overexpression of the bag3 and hspb8 genes. Moreover, the accumulation of BAG3-HspB8 complex in heat shocked NFκB -competent cells is inhibited by NFκB depletion. Our findings how / prove / highlight revealed that NFκB -induced autophagy during heat shock recovery is an additional response to protein denaturation/aggregation induced by heat shock. This process depends on the BAG3-HspB8 complex formation and increases cell survival, probably through clearance of aggregated proteins

A YakA é uma proteína quinase necessária para a regulação da resposta a diversos estresses em Dictyostelium e é uma efetora chave da transição do crescimento para desenvolvimento nesse organismo. O gene keaA foi isolado como um supressor do mutante yakA- em uma busca para revelar genes envolvidos na sobrevivência a estresse nitrosoativo. O gene keaA codifica uma proteína com seis repetições kelch na porção C-terminal, um domínio zf-C3HC4 na porção N-terminal, também chamado RING-finger, e uma sequência rica em cisteínas localizada na porção mediana da proteína. Mutantes deficientes em keaA foram avaliados revelando-se um papel para esse gene também no processo de desenvolvimento. A expressão de mRNA de keaA é induzida quando células selvagens crescem e a fonte de alimento começa a esgotar. A indução do mRNA de keaA também ocorre durante o desenvolvimento. Essa indução não é observada em células yakA- indicando que YakA regula KeaA. Células deficientes em keaA expressam baixos níveis de mRNA de pkaC, acaA e carA durante a agregação em baixa densidade celular, o que pode explicar porque as células deficientes em keaA apresentam o processo de desenvolvimento mais lento em baixa densidade celular. Células deficientes em keaA são mais resistentes a estresses nitrosoativo e oxidativo e keaA é necessário para a produção e detecção de AMPc. A análise da agregação de células deficientes em keaA durante o desenvolvimento multicelular indica que KeaA é necessário para que as células participem eficientemente desse processo. Células que super-expressam o domínio rico em cisteínas levam o mesmo tempo que as células selvagens para atingir o estágio de agregação. No entanto, essas células apresentam agregados, culminantes e corpos de frutificação menores. Células que super-expressam o domínio Kelch expressam altos níveis de acaA e carA depois de 8 horas de desenvolvimento, mas os níveis de pkaC são similares aos observados em células selvagens. Isso poderia indicar que o domínio Kelch induz a ativação da PKA. No entanto, essa interação não foi observada em experimentos de duplo híbrido. Adicionalmente, a expressão gênica em resposta a compostos que geram estresse oxidativo e nitrosoativo foi estudada utilizando-se microarranjos de cDNA. Os resultados revelaram um papel de keaA na resposta à pré-carência e no controle do ciclo celular / The YakA is a protein kinase required for the regulation of several stress responses in Dictyostelium and is a key effector of the transition from growth to development in this microorganism. The gene keaA was isolated as suppressor of the yakA- mutant in a screen targeted to reveal genes involved in the survival to nitrosoative stress. The keaA gene codes a protein with six kelch domain repeats at the C-terminus, a zf-C3HC4 domain at the N-terminus, also called RING-finger, and a cysteine-rich sequence located in the mid-portion of the protein. The analysis of mutants deficient in keaA revealed a role for this gene also in the development process. keaA mRNA expression is induced when wild type cells grow and the food source becomes scarce. An induction of keaA mRNA expression also occurs during development. This induction is not observed in yakA- cells, indicating that YakA regulates KeaA. keaA deficient cells express low levels of pkaC, acaA and carA mRNA during aggregation in low cell densities, which may explain why the keaA deficient cells present a delay in development in low cell densities. keaA deficient cells are more resistant to nitrosoative and oxidative stress and keaA is necessary for the production and detection of cAMP. The analysis of agreggation of keaA deficient cells during multicellular development indicated that KeaA is required for the cells to efficiently participate in the process. Cells over-expressing the cisteine-rich domain took the same time as the wild-type cells to reach the aggregation stage. However, these cells present smaller aggregates, culminants and fruiting bodies. Cells over-expressing the Kelch domain express high levels of acaA and carA after 8 hours of development, but the levels of pkaC are kept similar to those in wild-type cells. This could indicate that the Kelch domain induces the activation of PKA. However, this interaction was not observed when we conducted tests in a two-hybrid system. Additionally, gene expression in response to compounds that generate redox stresses was studied using cDNA microarrays. The results revealed a role of keaA in response to pre-starvation and control of cell cycle

Chez les bactéries, la régulation de l’expression génétique est fondamentale pour permettre une adaptation optimale à l’environnement. De nombreux contrôles existent, notamment au niveau post-transcriptionnel par de nombreux ARN régulateurs (sRNA pour « small RNAs »). Ceux-ci ciblent des ARN messager (ARNm), permettant une régulation rapide de la synthèse de protéines. Le plus souvent, ces sRNAs interagissent avec leur(s) cible(s) au niveau du site de fixation du ribosome (RBS pour « ribosome binding site »), entrant dès lors en compétition avec le ribosome pour la fixation à l’ARNm et entraînant une régulation négative de l’expression des gènes cibles. Pour autant, il existe de nombreux mécanismes alternatifs de régulation par les sRNA. Nous avons ainsi pu démontrer que les deux sRNAs OmrA et OmrB, conservés au sein des entérobactéries, répriment la synthèse du récepteur FepA aux complexes fer-entérobactine en ciblant une structure de l’ARNm fepA. Cette structure en tige-boucle est située en aval du RBS de fepA, et de façon surprenante, elle contrôle positivement la synthèse de FepA via une activation de la fixation de la sous-unité 30S du ribosome à l’ARNm. Des structures similaires ont pu être prédites dans d’autres ARNm, à l’image de bamA, codant la sous-unité essentielle du complexe Bam d’adressage des protéines de membrane externe en tonneaux β. Comme pour fepA, la tige-boucle de l'ARNm bamA favorise la fixation du ribosome, suggérant que ce mécanisme de régulation pourrait être bien plus général du fait de la grande conservation de bamA au sein des bactéries à Gram négatif. De surcroît, ces résultats constituent la première illustration que les structures d'ARNm peuvent avoir un effet positif sur la traduction. Par ailleurs, deux autres sRNAs répriment également et indépendamment l’expression de fepA, à savoir SdsR et RseX. A chaque fois, le mécanisme de régulation impliqué est différent. Ainsi, SdsR s’apparie vraisemblablement à deux régions différentes de l’ARNm fepA, impliquant notamment une compétition classique avec la fixation du ribosome. La répression par RseX nécessite quant à elle la présence d’autres séquences du 5’UTR de fepA, à plus d’une centaine de nucléotides (nts) en amont du RBS. Enfin, chacun de ces sRNAs semble répondre à des stimuli différents, ce qui enrichit considérablement notre connaissance des signaux contribuant à la régulation de fepA, dont jusqu’ici seule la carence en fer était connue comme un signal de dérépression par le facteur de transcription Fur. Ce travail est une nouvelle illustration de l’immense diversité des mécanismes de régulation impliquant des ARN, dont la grande flexibilité de structure et de séquence constitue une importante source de diversité à la disposition de l’évolution / In order to perfectly adapt to their environment, bacteria require a tight gene expression regulation. This can occur through post-transcriptional control by numerous regulatory RNAs (or small RNAs, sRNAs). These sRNAs can target mRNAs, leading to a fast regulation of protein synthesis. Most often, sRNAs base-pair with their target mRNAs at the ribosome binding site (RBS), therefore competing with the ribosome for the binding with the mRNA and repressing gene expression. However, many other regulatory mechanisms involve sRNAs. We have demonstrated that the two sRNAs OmrA and OmrB, conserved among enterobacteria, repress the synthesis of the FepA receptor for iron-enterobactin complexes through base-pairing with a secondary structure within fepA mRNA. This stem-loop structure is located downstream of fepA RBS, and most surprisingly, promotes 30S ribosomal subunit binding to fepA mRNA, therefore activating FepA synthesis. Similar stem-loop structures have been predicted in other mRNAs, such as the bamA mRNA encoding the essential subunit of the Bam outer membrane protein assembly complex. As for fepA mRNA, the stem-loop found in bamA mRNA also promotes ribosome binding, showing that this regulatory mechanism could be widespread considering the strong conservation of bamA among Gram negative bacteria. Moreover, these results challenge the commonly admitted view of mRNA secondary structures being repressors of gene expression. Two other sRNAs also repress fepA expression in an OmrA/B-independent fashion, namely SdsR and RseX. For each of these sRNAs, the regulatory mechanism involved is different. Indeed, SdsR most likely acts through two distinct binding sites, one of which leading to a classical competition with the ribosome binding. Meanwhile, RseX repression requires most of fepA 5’UTR, including sequences at about 100nt upstream of the start codon. Finally, each of these sRNAs is expressed upon diverse stimuli, considerably extending our knowledge of the signals leading to fepA regulation, for which only the Fur-dependent derepression upon iron starvation was known. This work highlights the great versatility of regulatory mechanisms involving RNAs. This illustrates how RNAs structural flexibility and sequence diversity is a key source of diversity for evolution

Coronary heart disease is the leading cause of death in American women, accounting for one in six deaths in 2004. One third of women over the age of forty will develop coronary heart disease in their lifetime. The role of chronic and excessive inflammation and risk factors, such as smoking and high cholesterol, are now well-established factors contributing to coronary heart disease pathology. A knowledge gap exists in that little is known about the mechanisms by which psychosocial factors, such as anger, may be associated with pro-inflammatory processes that contribute to cardiovascular morbidity and mortality in women. The purpose of this study was to determine if there were differences in serum levels of the proinflammatory biomarker, C-reactive protein, in post-menopausal women who scored high on anger characteristics compared to those with low anger characteristics. Mean levels of C-reactive protein were not found to be different in a sample of 42 women with high trait anger or high anger expression compared to those with low trait anger or low anger expression. Significant relationships were found in C-reactive protein and some anger control characteristics (anger control-in) and might imply that certain anger expression styles may play a role in pro-inflammatory responses in post-menopausal women.

Hwa-Byung, known as an anger illness, was conceptualized in Korean culture and listed in the glossary under Culture-Bound Syndromes in the Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994). Hwa-Byung develops when the emotions of anger have been suppressed for a long period of time and it becomes difficult to control those feelings. Common complaints of Hwa-Byung have two dimensions, psychological and physical symptoms. The prevalence of Hwa-Byung exhibits gender differences in that the majority of individuals who experience Hwa-Byung are women between the ages of 40 and 60. However, as the number of Korean immigrants in the United States continues to increase and their issues draw attention from researchers, the topic of Hwa-Byung receives little. Because Korean immigrants in the United States share a cultural background with their origin of ethnicity, and at the same time, may also assimilate the American culture during the acculturation process, this study will address the cultural differences in Hwa-Byung between native Koreans who live in South Korea and Korean immigrants in the United States. Accordingly, the purpose of this study was to examine the differences and similarities of Hwa-Byung in native Korean middle-aged women in South Korea and Korean immigrants in the United States, roughly between the age range of late-30's to middle 60's, by investigating the influencing factors of stressful life events, stress response, anger expression, and demographic background. A sample size of at least 200 participants, required for each group, using both paper-pencil and web-based methods, depended on participants' preferences, which were influenced by a gap in ages and the level of familiarity with and/or ability to access Internet. Participants were randomly selected from major cities, both in South Korea (including Seoul, Incheon, Busan, Daejeon, and Gyeonggi Province) and the United States (including Chicago, New York, and Los Angeles), using similar proportions of ages for both groups for the equivalences of participants in cross-cultural research. Survey measures included five instruments: (a) the Hwa-Byung scale (Kwon, Kim, Park, Lee, Min, & Kwon, 2008); (b) Life Stress for Korean women (Chon & Kim, 2003); (c) stress response inventory (SRI) (Koh, Park, & Kim, 2000); (d) anger expression (Hahn, Chon, Lee, & Spielberger, 1997), and (e) demographic background that measured the variables used in this study. To minimize the weakness of language differences used in the different cultural contexts, survey packages for Korean immigrant participants in the United States were formatted in both Korean and English for each item. Thus, a translation process became necessary, especially for the Korean instruments of the Hwa-Byung Scale, Life Stress for Korean women and Stress Response Inventory (SRI), from Korean into Englishtwo of which were (originally developed by Korean researchers) . On the other hand, native Koreans submitted only the Korean version of questionnaires because they fully understood the meaning of questionnaire statements, as well as in order to get rid of possible distractions by the inclusion of English sentences.

The use of electromagnetic devices such as microwave ovens and mobile phones has certainly brought convenience to our lives. At the same time, the proliferation of said devices has increased public awareness of the potential health hazards. It is generally assumed that there is little or no risk associated with the use of electromagnetic devices, based on the small amount of power associated with those devices. However, case studies on animals indicate that the risk cannot be entirely ruled out. It has long been known that proteins are sensitive to stress, arising from various sources such as temperature, chemical, pressure, and changes in pH condition. In all of these cases, the protein exhibits clear signs of damage and distress, which range from slight unfolding to complete loss of structure. Frequently, the damage to the protein is alleviated by refolding, either by itself or by the aid of molecular chaperones. However, if the damage to the protein is too great, the protein will generally undergo proteolysis. Opinion has been divided over the implication of prolonged use of electromagnetic devices to human health. Studies conducted on animals so far have given conflicting results. The studies on the separate components, electric and magnetic fields, also give inconclusive results. This indicates that our understanding on how electric and magnetic fields interact with biological matter is incomplete. In this project, we use molecular dynamics to explore the behaviour of two forms of insulin chain-B, isolated and monomeric (in the presence of chain-A with all disulfide bonds intact), at ambient conditions and under the influence of various stress. Specifically, we focus our attention to thermal stress and electric field stress. The electric field stress considered in this study takes several forms: static and oscillating with three different frequencies. These fields have strength ranging from 1806 V/m to 109 V/m. By performing molecular dynamics simulations totalling over 500 ns, we have gained valuable insights into the effects of elevated temperature and electric field on insulin chain-B. We observed differences in the damage mechanisms by the application of static electric field and oscillating field. The application of static fields restricts the conformational freedom of a protein, whereas the application of oscillating fields increases the mobility and flexibility of the protein, similar to the effect of thermal stress. Both of these interfere with the normal behaviour of a protein. We have also observed frequency-dependent effects, with low frequency fields having static field-like characteristics in damage mechanism.

Background: Biological systems adapt to changing environments by reorganizing their cellula r and physiological program with metabolites representing one important response level. Different stresses lead to both conserved and specific responses on the metabolite level which should be reflected in the underl ying metabolic network. Methodology/Principal Findings: Starting from experimental data obtained by a GC-MS based high-throughput metabolic profiling technology we here develop an approach that: (1) extracts network representations from metabolic conditiondependent data by using pairwise correlations, (2) determines the sets of stable and condition-dependent correlations based on a combination of statistical significance and homogeneity tests, and (3) can identify metabolites related to the stress response, which goes beyond simple ob servation s about the changes of metabolic concentrations. The approach was tested with Escherichia colias a model organism observed under four different environmental stress conditions (cold stress, heat stress, oxidative stress, lactose diau xie) and control unperturbed conditions. By constructing the stable network component, which displays a scale free topology and small-world characteristics, we demonstrated that: (1) metabolite hubs in this reconstructed correlation networks are significantly enriched for those contained in biochemical networks such as EcoCyc, (2) particular components of the stable network are enriched for functionally related biochemical path ways, and (3) ind ependently of the response scale, based on their importance in the reorganization of the cor relation network a set of metabolites can be identified which represent hypothetical candidates for adjusting to a stress-specific response. Conclusions/Significance: Network-based tools allowed the identification of stress-dependent and general metabolic correlation networks. This correlation-network-ba sed approach does not rely on major changes in concentration to identify metabolites important for st ress adaptation, but rather on the changes in network properties with respect to metabolites. This should represent a useful complementary technique in addition to more classical approaches.