Home About us Contact
|
Home About us Contact | ||
|
|
||
Stressful Stimuli (stressful + stimulus)
Selected AbstractsThe relationship of some negative events and psychological factors to periodontal disease in an adult Swedish population 50 to 80 years of ageJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 3 2002A. Hugoson Abstract Background: Clinical observations and epidemiological studies suggest that experiences of negative life events, especially those manifested as depression, may contribute to an increased susceptibility to periodontal disease. Objective: In the present study, the prevalence of some negative life events and psychological factors and their relation to periodontal disease were investigated. The sample consisted of individuals 50,80 years of age from an extensive cross-sectional epidemiological study performed in 1993 in the city of Jönköping, Sweden. Method: 298 dentate individuals from the Jönköping study were randomly selected. Clinical and radiographic examinations included registration of the number of existing teeth, plaque index, gingival index, pocket depth, and alveolar bone loss. In addition, a questionnaire about socioeconomic status, life events, and psychological and stress-related factors was used. Results: The results revealed that, in addition to the well-documented periodontal disease risk factors such as increased age, oral hygiene status, and smoking, the loss of a spouse (being a widow or widower) and the personality trait of exercising extreme external control were also associated with severe periodontal disease. Conclusion: The findings support recent studies suggesting that traumatic life events such as the loss of a spouse may increase the risk for periodontal disease. Above all, the present results indicate that an individual's ability to cope with stressful stimuli (coping behavior), as measured by the beliefs of locus of control of reinforcements may play a role in the progression of periodontal disease. Zusammenfassung Hintergrund: Klinische Beobachtungen und epidemiologische Studien legen den Schluss nahe, dass negative Ereignisse im Laufe des Lebens, insbesondere solche, die sich in Depression manifestieren, zu einer erhöhten Empfänglichkeit für Parodontitis beitragen. Zielsetzung: Untersuchung der Prävalenz von negativen Ereignissen im Lebenslauf sowie psychologischen Faktoren und deren Beziehung zu Parodontalerkrankungen in einer Population im Alter zwischen 50 und 80 Jahren, die im Rahmen einer extensiven epidemiologischen Querschnittsstudie im Jahre 1993 in der Stadt Jönköping in Schweden untersucht worden war. Material und Methoden: 298 bezahnte Personen wurden randomisiert aus der Jönköping-Studie ausgewählt. Die klinischen und röntgenologischen Untersuchungen umfassten die Erhebung der vorhandenen Zähne, der Plaque Index, Gingival Index, Sondierungstiefen und alveolärem Knochenabbau. Zusätzlich wurden durch Befragung sozioökonomischer Status, Lebensereignisse sowie psychologische und stressbezogene Faktoren erfasst. Ergebnisse: Die Resultate ergaben, dass zusätzlich zu den bekannten Parodontitisrisikofaktoren wit Alter, Mundhygienestatus und Rauchen der Verlust des Ehepartners, also eine Witwe oder ein Witwer zu sein, und das Persönlichkeitsmuster extreme externe Kontrolle auszuüben, mit schwerer Parodontitis assoziiert waren. Schlussfolgerungn: Diese Ergebnisse unterstützen neuere Studien, die Hinweise dafür gegeben haben, dass traumatische Lebensereignisse wie der Verlust eines Ehenpartners das Risiko an Parodontitis zu erkranken erhöhen. Darüber hinaus legen die Ergebnisse den Schluss nahe, dass die individuelle Fähigkeit mit Stress umzugehen (Coping), die in dieser Studie durch die Erfragung der Überzeugung über die Lokalisation der Kontrolle von Verstärkungen erfasst wurde, eine Rolle in der Progression der Parodontitis spielen. Résumé Origine: Des observations cliniques et des études épidémiologiques suggèrent que des évènements négatifs, particulièrement ceux manifestés par une dépression, puisse contribuer à une susceptibilité augmentée à la maladie parodontale. But: Dans cette étude, la prévalence de ces évènements négatifs et les facteurs psychologiques et leurs relations avec la maladie parodontale ont été recherchés. L'échantillon était composé de personnes âgées de 50 à 80 ans issues d'une étude épidémiologique extensive croisée réalisé en 1993 dans la ville de Jonkoping en Suède. Méthode: 298 individus dentés de cette étude furent sélectionnés au hasard. Les examens cliniques et radiographiques comprenaient l'enregistrement du nombre de dents présentes, l'indice de plaque, l'indice gingival, la profondeur de poche et la perte osseuse alvéolaire. De plus, un questionnaire sur le statut socio économique, les évènements de la vie et les facteurs psychologiques en relation avec le stress, fut utilisé. Résultats: Les résultats montrèrent qu'en plus des facteurs de risque bien documentés de maladie parodontale comme l'âge, l'hygiène orale et le tabagisme, la perte d'un époux (que l'on soit veuf ou veuve) et le trait de personnalité de pouvoir exercer un contrôle externe extrême étaient aussi associés avec une maladie parodontale sévère. Conclusion: Ces résultats soutiennent de récentes études qui suggèrent que des évènements traumatisant de la vie quotidienne comme la perte d'un époux puisse augmenter le risque pour la maladie parodontale. Par-dessus tout, ces résultats indiquent que la capacité d'un individu à gérer des stimuli stressants, (comportement gestionnel), mesurés par les convictions de contrôle des renforcements pourrait jouer un rôle dans la progression de la maladie parodontale. [source] ,-Endorphin Mediates Behavioral Despair and the Effect of Ethanol on the Tail Suspension Test in MiceALCOHOLISM, Issue 6 2010Elizabeth T. Barfield Background:, The opioid peptide ,-endorphin (,-E) is synthesized and released in response to stressful stimuli as well as acute alcohol administration. The release of ,-E following exposure to an inescapable aversive situation may mediate behaviors that contribute to allostasis of the stress response. The present study examines the effects of ,-E on immobility in assays involving inescapable stress, both under basal conditions and after acute administration of EtOH. Methods:, Female and male transgenic mice with varying capacities to translate ,-E were subjected to either the forced swim (FST, Experiment 1) or the tail suspension test (TST, Experiment 2). In Experiment 3, mice were divided into three groups based on hormonal status (male, female-estrous, and female-nonestrous) and injected with either 1 g/kg EtOH or equivolume saline 14 minutes prior to behavioral assessment on the TST. Results:, Experiments 1 and 2 demonstrated a direct relationship between ,-E levels and immobility. There were also sex differences in behavior in these tests, with males displaying more immobility than females. A main effect of genotype in Experiment 3 replicated findings in Experiments 1 and 2. There was also an effect of EtOH (increasing immobility) and a significant interaction reflecting a particularly robust effect of the drug in mice with low ,-E. In addition, there were interactions between ,-E, EtOH effects, and hormonal status. Conclusions:, These findings support the contention that ,-E moderates behavioral responses to stressful stimuli and suggest a role for this peptide in coping behavior. Furthermore, the effects of EtOH on the response to stress may be mediated by ,-E. Sex differences in this influence may contribute to sex differences in disease susceptibility and expression. [source] Hypothalamic Function in Response to 2-Deoxy- d -Glucose in Long-Term Abstinent AlcoholicsALCOHOLISM, Issue 5 2001John C. Umhau Background: The body adapts to diverse stressful stimuli with a response characterized by activation of the hypothalamic-pituitary-adrenal (HPA) axis. Chronic alcohol consumption can cause changes in the function of this neuroendocrine system. Although many studies have examined this phenomenon in drinking and recently sober alcoholics, few studies have examined HPA axis function in long-term sober alcoholics. Methods: To characterize HPA axis function in long-term sober alcoholics, we used a challenge paradigm with 2-deoxy-d-glucose (2-DG). An infusion of 2-DG (a nonmetabolizable glucose analog) induces a well-characterized stress response. In a previous study, our laboratory found an exaggerated corticotropin and cortisol response in alcoholics abstinent 3 weeks; in this investigation we compared the effects of an infusion of 2-DG on 19 healthy volunteers and 20 community-living alcoholics who had been abstinent more than 6 months. Results: In contrast to the previous study, long-term sober alcoholics did not have an exaggerated corticotropin and cortisol response after 2-DG. Conclusions: Previously observed abnormalities in cortisol regulation in 3-week-sober alcoholics may be related to the acute effects of recent alcohol consumption and withdrawal. Future investigations into the metabolic function of alcoholics, particularly investigations involving the HPA system, should consider the possibility that normalization may not occur until long-term abstinence has been achieved. [source] Apoptosis signal-regulating kinase 1-mediated sustained p38 mitogen-activated protein kinase activation regulates mycoplasmal lipoprotein- and staphylococcal peptidoglycan-triggered Toll-like receptor 2 signalling pathwaysCELLULAR MICROBIOLOGY, Issue 9 2005Takeshi Into Summary Toll-like receptor (TLR) 2 functions as a sensor for detecting various microbial components conserved in bacteria or fungi in innate immunity. TLR2 induces several signalling pathways linking to activation of the transcriptional factors NF-,B and AP-1 as well as induction of cell death. In human embryonic kidney 293 cells expressed human TLR2, mycoplasmal lipoproteins (MLP) or staphylococcal peptidoglycans (PGN) induced sustained phosphorylation of p38 mitogen-activated protein kinase (MAPK), accompanied by generation of reactive oxygen species. This observation encouraged us to examine roles of apoptosis signal-regulating kinase 1 (ASK1) in TLR2 signalling, because ASK1 is an upstream activator of p38 MAPK during exposure to oxidative stress and other stressful stimuli. A kinase-inactive mutant of ASK1 greatly impaired the sustained phosphorylation of p38 MAPK induced by MLP or PGN. This mutant also attenuated MLP- or PGN-induced transcriptional activities of NF-,B and AP-1 via inhibition of p38 MAPK activation. MLP- or PGN-induced cell death reactions, including DNA fragmentation and caspase-3/7 activation, were also downregulated by the ASK1 mutant via p38 MAPK inhibition. Furthermore, TLR2 signalling had a potential to phosphorylate and dephosphorylate ASK1 at Ser83 residue. Thus, MLP and PGN have capabilities to induce ASK1-dependent signalling pathways which regulate p38 MAPK activation through TLR2, leading to activation of NF-,B and AP-1 as well as induction of cell death. [source] | ||||||||||