Faith Leaders\u27 Experiences on Health Counseling Provided to Their Congregation

Numerous faith-based organizations (FBOs), denominations, and religious groups are represented in the United States. Faith leaders have the responsibility of addressing the spiritual needs of the congregation; however, the health needs of parishioners may be a point of discussion faith leaders should address. Communities surrounding FBOs may have limited health care services, lack transportation, and have serious health issues. The purpose of this phenomenological qualitative study was to explore the experiences of faith leaders on giving health counseling to their congregation. Faith leaders play an essential role in providing health counseling on various health topics to their congregation and community. A total of 15 faith leaders were recruited from 6 counties in North Carolina by convenience sampling. Face-to-face face semi-structured interviews was the data collection method. The transformational leadership theory was used to examine how faith leaders motivate parishioners through constructs of the framework. Using NVivo, a qualitative data analysis software tool, the coded results indicated that faith leaders need specialized training to provide health counseling to parishioners about health issues shared beyond their field of expertise. The insight gained from faith leaders was important to understand the health-related resources needed to improve the health of parishioners. This study may be useful for faith leaders, public health educators, health policy makers, and researchers seeking to understand faith leaders\u27 experiences; it could impact positive social change by providing resources and training needed to combat health-related issues within congregations

When do bubbles cause a floating body to sink?

A presentation at NorCal/Nev Meeting of AAPT Lawrence-Berkeley Laboratory, 30-31 March 2001 (Manuscript submitted to American Journal of Physics, 9 March 2001.

Impact de l'obésité sur la détection oro-sensorielle des lipides alimentaires chez la souris et chez l'Homme

La gustation est une composante essentielle de la détection oro-sensorielle des lipides alimentaires. La liaison des AGLC sur le récepteur CD36 joue un rôle prépondérant dans cette lipido-détection orale chez la souris et très probablement chez l Homme. En effet, elle intervient dans le choix alimentaire (sensibilité aux lipides) ainsi que dans la préparation de l organisme à l arrivée de lipides. Ce sensing oral des lipides est fortement régulé. Comme l obésité semble être responsable d une altération de la détection des saveurs primaires, l objectif de cette thèse a été d explorer si l obésité peut également être à l origine de perturbations de la détection orale des lipides à la fois chez l Homme et chez la souris. Nos résultats chez l Homme indiquent qu il existe une altération de la lipido-détection orale chez certains sujets obèses. Nous avons montré que ces derniers présentaient une consommation accrue en lipides. De plus, la sécrétion précoce de triglycérides plasmatiques induite par une stimulation orale observée chez les sujets minces n est plus reproduite chez les sujets obèses. Chez la souris, il a été montré que l obésité provoque une diminution de la sensibilité gustative aux lipides alimentaires. Ce phénomène est la conséquence d une dérégulation de la signalisation calcique CD36-dépendante au niveau des cellules gustatives. Chez ces animaux, la stimulation orale lipidique entraîne, comme chez l Homme, une augmentation transitoire de la triglycéridémie qui pourrait être responsable d une réduction de la taille du repas (rassasiement). En conclusion, l obésité affecte la lipido-détection orale chez l Homme et la souris. Le défaut de détection des lipides alimentaires associé à l abolition de la sécrétion précoce de triglycérides plasmatiques chez les sujets obèses pourrait être à l origine d une perturbation de la régulation de la prise alimentaire, entraînant une surconsommation d aliments riches en lipides et renforçant ainsi l obésitéGustation is an essential parameter in the oro-sensory detection of dietary lipids. In mice and most likely in humans, the binding of long-chain fatty acids to the CD36 receptor plays a major role in this oral fat detection. Gustation is involved in the food choice (fat sensitivity) as well as in the preparation of the body to the fat inflow. This oral lipid sensing is highly regulated. As obesity seems to be responsible for an alteration of the basic tastes detection, the aim of this thesis was to investigate whether obesity can impair the oral lipid detection in both mice and humans. In humans, our data show that there is an alteration of the oral fat detection in some obese subjects who have a higher lipid consumption than the other subjects. Besides, an early secretion of plasma triglycerides induced by an oral fat stimulation was observed in lean subjects but not in obese ones. In mice, a decrease in the dietary lipids taste sensitivity was shown to be caused by obesity. This is the consequence of a deregulation of the CD36-dependent calcium signalling in taste cells. In these mice, as in humans, the oral fat stimulation leads to a temporary increase in the blood triglyceride level which might be responsible for a reduced meal size (satiety). To conclude, obesity impairs oral lipid detection in both mice and humans. An altered dietary fat detection associated with an abolition of the early secretion of plasma triglycerides in obese people might induce an impaired regulation of the food intake, leading to an overconsumption of lipid-rich foods, and so a reinforcement of obesityDIJON-BU Doc.électronique (212319901) / SudocSudocFranceF

The oral lipid sensor GPR120 is not indispensable for the orosensory detectionof dietary lipids in the mouse

International audienceImplication of the long-chain fatty acid (LCFA) receptor GPR120, also termed free fatty acid receptor 4 (FFAR4), in the taste-guided preference for lipids is a matter of debate. To further unravel the role of GPR120 in the "taste of fat", the present study was conducted on GPR120-null mice and their wild-type littermates. Using a combination of morphological (i.e. immunohistochemical staining of circumvallate papillae - CVP), behavioral (i.e. two-bottle preference tests, licking tests and conditioned taste aversion) and functional studies (i.e. calcium imaging in freshly isolated taste bud cells - TBC), we show that absence of GPR120 in oral cavity was not associated with changes in i) the gross anatomy of CVP, ii) the LCFA-mediated increases in [Ca2+]i, iii) the preference for oily and LCFA solutions and iv) the conditioned avoidance of LCFA solutions. In contrast, the rise in [Ca2+]i triggered by grifolic acid (GA), a specific GPR120 agonist, was dramatically curtailed when GPR120 gene was lacking. Taken together these data demonstrate that activation of lingual GPR120 and preference for fat are disconnected, suggesting that GPR120 expressed in TBC is not absolutely required for the oral fat detection in the mouse

A Scoping Review of the Literature on Trauma Cue-Induced Drug Craving in Substance Users with Trauma Histories or PTSD

Among trauma-exposed individuals, substances may be used as a means of obtaining symptom relief following exposure to trauma reminders. Repeated pairing of trauma cues with substance use may lead to the development of classically conditioned craving to trauma cues. Conditioned craving following cue exposure can be studied in-lab using the cue-reactivity paradigm. To map cue-reactivity research conducted with trauma-exposed substance users, we aimed to synthesize research which studied our population of interest, used a cue-reactivity paradigm, and measured craving as an outcome. Three databases were searched using relevant keywords. Twenty-eight studies met our criteria. Four key 19 themes are discussed in our review of these scoped studies—(1) craving as an outcome; (2) methodological subtypes across paradigms; (3) affect as an additional outcome or as a mediator of cue-induced craving; and (4) cue-reactivity paradigms as an intervention outcome assessment tool. Overall, there is strong evidence for cue-reactivity paradigms as a useful means of eliciting craving in response to trauma cues. Our scoping review suggests the need for a meta-analysis to determine the magnitude of the trauma cue-induced craving effect in substance users with trauma histories, and to determine significant moderators (e.g., PTSD symptom severity) and mediators of this effect (e.g., negative affect)

CB1 Antagonism Exerts Specific Molecular Effects on Visceral and Subcutaneous Fat and Reverses Liver Steatosis in Diet-Induced Obese Mice

International audienceThe beneficial effects of the inactivation of endocannabinoid system (ECS) by administration of antagonists of the cannabinoid receptor (CB) 1 on several pathological features associated with obesity is well demonstrated, but the relative contribution of central versus peripheral mechanisms is unclear. We examined the impact of CB1 antagonism on liver and adipose tissue lipid metabolism in a mouse model of diet-induced obesity. Mice were fed either with a standard diet or a high-sucrose high-fat (HSHF) diet for 19 weeks and then treated with the CB1-specific antagonist SR141716 (10 mg x kg(-1) x day(-1)) for 6 weeks. Treatment with SR141716 reduced fat mass, insulin levels, and liver triglycerides primarily increased by HSHF feeding. Serum adiponectin levels were restored after being reduced in HSHF mice. Gene expression of scavenger receptor class B type I and hepatic lipase was induced by CB1 blockade and associated with an increase in HDL-cholesteryl ether uptake. Concomitantly, the expression of CB1, which was strongly increased in the liver and adipose tissue of HSHF mice, was totally normalized by the treatment. Interestingly, in visceral but not subcutaneous fat, genes involved in transport, synthesis, oxidation, and release of fatty acids were upregulated by HSHF feeding, while this effect was counteracted by CB1 antagonism. A reduction in the CB1-mediated ECS activity in visceral fat is associated with a normalization of adipocyte metabolism, which may be a determining factor in the reversion of liver steatosis induced by treatment with SR141716

Do trauma cue exposure and/or PTSD symptom severity intensify selective approach bias toward cannabis cues in regular cannabis users with trauma histories?

Trauma cue-elicited activation of automatic cannabis-related cognitive biases are theorized to contribute to comorbid posttraumatic stress disorder and cannabis use disorder. This phenomenon can be studied experimentally by combining the trauma cue reactivity paradigm (CRP) with cannabis-related cognitive processing tasks. In this study, we used a computerized cannabis approach-avoidance task (AAT) to assess automatic cannabis (vs. neutral) approach bias following personalized trauma (vs. neutral) CRP exposure. We hypothesized that selective cannabis (vs. neutral) approach biases on the AAT would be larger among participants with higher PTSD symptom severity, particularly following trauma (vs. neutral) cue exposure. We used a within-subjects experimental design with a continuous between-subjects moderator (PTSD symptom severity). Participants were exposed to both a trauma and neutral CRP in random order, completing a cannabis AAT (cannabis vs. neutral stimuli) following each cue exposure. Current cannabis users with histories of psychological trauma (n = 50; 34% male; mean age = 37.8 years) described their most traumatic lifetime event, and a similarly-detailed neutral event, according to an established interview protocol that served as the CRP. As hypothesized, an AAT stimulus type x PTSD symptom severity interaction emerged (p = .042) with approach bias greater to cannabis than neutral stimuli for participants with higher (p = .006), but not lower (p = .36), PTSD symptom severity. Contrasting expectations, the stimulus type x PTSD symptoms effect was not intensified by trauma cue exposure (p = .19). Selective cannabis approach bias may be chronically activated in cannabis users with higher PTSD symptom severity and may serve as an automatic cognitive mechanism to help explain PTSD-CUD co-morbidity.</p