Hot-iron disbudding: stress responses and behavior of 1- and 4-week-old calves receiving anti-inflammatory analgesia without or with sedation using xylazine

2015 ◽  
Vol 179 ◽  
pp. 22-28 ◽  
Author(s):  
D. Caray ◽  
A. de Boyer des Roches ◽  
S. Frouja ◽  
S. Andanson ◽  
I. Veissier
Keyword(s):  
Stress Responses ◽  
Anti Inflammatory ◽  
And Behavior

scholarly journals Can neuroscience help to understand narcissism? A systematic review of an emerging field

2021 ◽  
Vol 4 ◽  
Author(s):  
Emanuel Jauk ◽  
Philipp Kanske
Keyword(s):  
Systematic Review ◽  
Stress Responses ◽  
Interpersonal Functioning ◽  
Integrative Model ◽  
Experimental Investigations ◽  
Future Research ◽  
Pathological Narcissism ◽  
Ego Threat ◽  
Self Reports ◽  
And Behavior

Abstract Narcissism is a Janusian personality construct, associated with both grandiose self-assuredness and dominance, as well as vulnerable insecurity and reactivity. Central questions of intra- and interpersonal functioning in narcissism are still a matter of debate. Neuroscience could help to understand the paradoxical patterns of experience and behavior beyond the limitations of self-reports. We provide a systematic review of 34 neuroscience studies on grandiose, vulnerable, pathological narcissism, and Narcissistic Personality Disorder (NPD), spanning experimental investigations of intra- and interpersonal mechanisms, research on neurophysiological and neuroendocrine aspects of baseline function, and brain structural correlates. While neuroscience has scarcely directly studied vulnerable narcissism, grandiose narcissism is associated with heightened vigilance to ego threat and stress responses following ego threat, as well as heightened stress indicators in baseline measures. Such responses are not commonly observed in self-reports, highlighting the potential of neuroscience to augment our understanding of self-regulatory dynamics in narcissism. Interpersonal functioning is characterized by deficits in social–affective processes. Both involve altered activity within the salience network, pointing to a double dissociation regarding the expression of narcissism and self/other oriented situational focus. Findings are summarized in an integrative model providing testable hypotheses for future research along with methodological recommendations.

scholarly journals Potential Impact of Statins on Neuronal Stress Responses in Patients at Risk for Cardiovascular Disease

2021 ◽  
Vol 11 (4) ◽  
pp. 261
Author(s):  
Flavia Diggelmann ◽  
Susan Bengs ◽  
Ahmed Haider ◽  
Gioia Epprecht ◽  
Anna Luisa Beeler ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
At Risk ◽  
Bone Marrow ◽  
Metabolic Activity ◽  
Stress Responses ◽  
Cardiovascular Outcomes ◽  
Inflammatory Activity ◽  
18F Fdg ◽  
Anti Inflammatory ◽  
Neuronal Stress

Background: Recent studies indicate that enhanced neuronal stress responses are associated with adverse cardiovascular outcomes. A chronic inflammatory state seems to mediate this detrimental neuro-cardiac communication. Statins are among the most widely prescribed medications in primary and secondary cardiovascular disease (CVD) prevention and not only lower lipid levels but also exhibit strong anti-inflammatory and neuroprotective effects. We therefore sought to investigate the influence of statins on neuronal stress responses in a patient cohort at risk for CVD. Methods: 563 patients (61.5 ± 14.0 years) who underwent echocardiography and 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET) were retrospectively identified. Metabolic activity of the amygdala, a part of the brain’s salience network, was quantified by 18F-FDG uptake, while normal cardiac morphology and function were assured by echocardiography. Vertebral bone marrow metabolism, a marker of inflammatory activity, was measured by 18F-FDG PET. Results: Increased neuronal stress responses were associated with an increased inflammatory activity in the bone marrow (r = 0.152, p = 0.015) as well as with a subclinical reduction in left ventricular ejection fraction (LVEF, r = −0.138, p = 0.025). In a fully-adjusted linear regression model, statin treatment was identified as an independent, negative predictor of amygdalar metabolic activity (B-coefficient −0.171, p = 0.043). Conclusions: Our hypothesis-generating investigation suggests a potential link between the anti-inflammatory actions of statins and reduced neuronal stress responses which could lead to improved cardiovascular outcomes. The latter warrants further studies in a larger and prospective population.

scholarly journals Endoplasmic reticulum stress response in the roadway for the effects of non-steroidal anti-inflammatory drugs

2015 ◽  
Vol 2 (1) ◽  
Author(s):  
Fernanda L.B. Mügge ◽  
Aristóbolo M. Silva
Keyword(s):  
Endoplasmic Reticulum ◽  
Stress Response ◽  
Er Stress ◽  
Stress Responses ◽  
Endoplasmic Reticulum Stress Response ◽  
The Road ◽  
Er Stress Response ◽  
Mediated Effects ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

AbstractOver the past decade, a handful of evidence has been provided that nonsteroidal anti-inflammatory drugs (NSAIDs) display effects on the homeostasis of the endoplasmic reticulum (ER). Their uptake into cells will eventually lead to activation or inhibition of key molecules that mediate ER stress responses, raising not only a growing interest for a pharmacological target in ER stress responses but also important questions how the ER-stress mediated effects induced by NSAIDs could be therapeutically advantageous or not. We review here the toxicity effects and therapeutic applications of NSAIDs involving the three majors ER stress arms namely PERK, IRE1, and ATF6. First, we provide brief introduction on the well-established and characterized downstream events mediated by these ER stress players, followed by presentation of the NSAIDs compounds and mode of action, and finally their effects on ER stress response. NSAIDs present promising drug agents targeting the components of ER stress in different aspects of cancer and other diseases, but a better comprehension of the mechanisms underlying their benefits and harms will certainly pave the road for several diseases’ therapy.

scholarly journals The interplay between stress, circadian clocks, and energy metabolism

2020 ◽  
Vol 247 (1) ◽  
pp. R13-R25 ◽  
Author(s):  
Henrik Oster
Keyword(s):  
Circadian Clock ◽  
Stress Responses ◽  
Modern Society ◽  
Well Being ◽  
Circadian Clocks ◽  
Acute And Chronic Stress ◽  
Therapeutic Measures ◽  
Stress Response System ◽  
And Behavior

Endogenous circadian clocks adapt an organism’s physiology and behavior to predictable changes in the environment as a consequence of the Earth’s rotation around its axis. In mammals, circadian rhythms are the output of a ubiquitous network of cellular timers coordinated by a hypothalamic master pacemaker. Circadian clock function is closely connected to the stress response system which has evolved to ensure survival under less predictable situations of danger. Disruptions in both of these functions are highly prevalent in modern society and have been linked to pathologic alterations in metabolic setpoints, promoting overeating, obesity, and type-2 diabetes. This paper describes the different levels of interaction between the circadian clock and acute and chronic stress responses. It summarizes studies assessing clock-stress crosstalk in the context of metabolic homeostasis and outlines options to use this interaction for diagnostic and therapeutic measures targeting metabolic health and well-being in the highly chronodisruptive environment of modern 24-h globalized societies.

scholarly journals IPSE, a urogenital parasite-derived immunomodulatory protein, ameliorates ifosfamide-induced hemorrhagic cystitis through downregulation of pro-inflammatory pathways

2018 ◽  
Author(s):  
Evaristus C. Mbanefo ◽  
Loc Le ◽  
Rebecca Zee ◽  
Nirad Banskota ◽  
Kenji Ishida ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Responses ◽  
Cellular Proliferation ◽  
Transcriptional Profiling ◽  
Hemorrhagic Cystitis ◽  
Underlying Mechanism ◽  
Protective Mechanism ◽  
Therapeutic Effects ◽  
Anti Inflammatory ◽  
Oxidative Stress Responses

AbstractIfosfamide and other oxazaphosphorines can result in hemorrhagic cystitis, a constellation of complications caused by acrolein metabolites. We previously showed that a single dose of IPSE, a schistosome-derived host modulatory protein, can ameliorate ifosfamide-related cystitis; however, the exact mechanisms underlying this urotoxic effect and its prevention are not fully understood. To provide insights into IPSE’s protective mechanism, we undertook transcriptional profiling of bladders from ifosfamide-treated mice, with or without IPSE pretreatment. Following ifosfamide challenge, there was upregulation of a range of pro-inflammatory genes. The pro-inflammatory pathway involving the IL-1β, TNFαand IL-6 triad via NFκB and STAT3 signaling pathways was identified as the key driver of inflammation. The NRF2-mediated oxidative stress response pathway, which regulates bothHmox1-mediated heme homoeostasis and expression of antioxidant enzymes, was highly activated. Anti-inflammatory and cellular proliferation cascades implicated in tissue repair, namely Wnt, Hedgehog and PPAR pathways, were downregulated. IPSE administration before ifosfamide injection resulted in significant downregulation of major proinflammatory pathways including the triad of IL-1β, TNFαand IL-6 pathways, the interferon signaling pathway, and less apparent reduction in oxidative stress responses. Taken together, we have identified signatures of acute phase inflammation and oxidative stress responses in the ifosfamide-injured bladder, which are reversed by pretreatment with IPSE, a parasite derived anti-inflammatory molecule. In addition to providing new insights into the underlying mechanism of IPSE’s therapeutic effects, this work has revealed several pathways that could be therapeutically targeted to prevent and treat ifosfamide-induced hemorrhagic cystitis.

scholarly journals IL-37 expression reduces acute and chronic neuroinflammation and rescues cognitive impairment in an Alzheimer s disease mouse model

2021 ◽  
Author(s):  
Niklas Lonnemann ◽  
Shirin Hosseini ◽  
Melanie Ohm ◽  
Karsten Hiller ◽  
Charles A. Dinarello ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cognitive Abilities ◽  
Long Term Potentiation ◽  
Spine Density ◽  
Chronic Neuroinflammation ◽  
Model Of Alzheimer’S Disease ◽  
Term Potentiation ◽  
Anti Inflammatory ◽  
And Function ◽  
And Behavior

The anti-inflammatory cytokine interleukin-37 (IL-37) is a member of the IL-1 family but not expressed in mice. We used a human IL 37 (hIL-37tg) expressing mouse, which has been subjected to various models of local and systemic inflammation as well as immunological challenges. Those studies demonstrate an immune-modulatory role of IL-37 which can be characterized as an important suppressor of innate immunity. We investigated the functions of IL-37 in the CNS and explored the effects of IL-37 on neuronal architecture and function, microglia phenotype, cytokine production and behavior after inflammatory challenge by intraperitoneal LPS-injection. Reduced spine density, activated microglia phenotype and impaired long-term potentiation (LTP) were observed in wild-type mice after LPS injection, whereas hIL-37tg mice showed no impairment. In addition, we crossed the hIL-37tg mouse with an animal model of Alzheimer's disease (APP/PS1) to investigate the anti-inflammatory properties of IL-37 under chronic neuroinflammatory conditions. Our results show that IL-37 is able to limit inflammation in the brain after acute inflammatory events and prevent the loss of cognitive abilities in a mouse model of AD.

scholarly journals Differential behavioral, stress, and sleep responses in mice with different delays of fear extinction

SLEEP ◽  
2019 ◽  
Vol 42 (10) ◽  
Author(s):  
Mayumi Machida ◽  
Amy M Sutton ◽  
Brook L Williams ◽  
Laurie L Wellman ◽  
Larry D Sanford
Keyword(s):  
Body Temperature ◽  
Stress Responses ◽  
Dark Period ◽  
Contextual Fear Conditioning ◽  
Fear Learning ◽  
Contextual Fear ◽  
Behavioral Stress ◽  
And Behavior ◽  
Sleep Amount ◽  
Shock Training

Abstract Study Objectives Sleep, in particular rapid eye movement (REM), has been linked to fear learning and extinction; however, their relationship is poorly understood. We determined how different delays of extinction training (ET) impact fear-conditioned behaviors, changes in sleep, and stress responses. Methods EEG activity, movement, and body temperature in mice were monitored via telemetry. Following contextual fear conditioning (shock training [ST]), separate groups of mice were reexposed to the context at 24-hour post-ST (24h ET-1) and at 48-hour post-ST (48h ET-1). Post-ET sleep amount and sleep-associated EEG (delta and theta) activity were compared to baseline and to post-ST sleep. Freezing, locomotion, grooming, and rearing were monitored to determine effects of ET on fear behaviors. Body temperature immediately after ET was monitored to assess stress-induced hyperthermia (SIH). Results 24h ET-1 and 48h ET-1 produced similar freezing and REM reductions, but dissimilar rearing activity and SIH. 24h ET-1 was followed by periods of suppressed REM-associated theta (REM-θ) activity, immediately after ET and during the subsequent dark period. Suppressed REM-θ was specific to sleep after 24h ET-1, and did not occur after ST, nor after 48h ET-1. Conclusions ET-1 at 24 and 48 hours after ST was associated with similar freezing and REM amounts, but with differences in other overt behaviors, in REM-θ, and in SIH. Freezing was not predictive of changes in other fear-associated responses. This study demonstrated that consideration of time delay from fear acquisition to extinction is important when assessing the relationships between extinction and behavior, sleep, and stress responses.

scholarly journals The Effect of Virtual Fencing Stimuli on Stress Responses and Behavior in Sheep

Animals ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 30 ◽  
Author(s):  
Tellisa Kearton ◽  
Danila Marini ◽  
Frances Cowley ◽  
Susan Belson ◽  
Caroline Lee
Keyword(s):  
Animal Welfare ◽  
Stress Responses ◽  
Electrical Stimulus ◽  
The Other ◽  
Cortisol Response ◽  
Treatment Control ◽  
Welfare Impact ◽  
Electrical Stimuli ◽  
And Behavior ◽  
Vaginal Temperature

To understand the animal welfare impact of virtual fencing stimuli (audio cue ‘beep’ and electrical stimulus) on naïve sheep, it is necessary to assess stress responses during the animal’s first encounters with these stimuli. Eighty Merino ewes were exposed to one of the following treatments (n = 16 animals per treatment): Control (no stimuli), beep, dog bark, manual restraint, and electrical stimulus. Collars were used to apply the audio and electrical stimuli. The restraint treatment showed an elevated cortisol response compared with the control (p < 0.05), but there were no differences between the other treatments and the control. There were no differences between treatments in vaginal temperature (p > 0.05). For behaviors, the sheep receiving the bark and beep treatments were more vigilant compared to the control (p < 0.05), there were more aversive responses observed in the electrical stimulus treatment compared to the control. Together, the responses showed that the beep stimuli were largely benign, the bark stimuli was minimally aversive, the electrical stimuli was acutely aversive, and the restraint was moderately aversive. These data suggest that, for sheep, their first exposure to the virtual fencing stimuli should be perceived as less aversive than a commonly used restraint procedure.

scholarly journals Neuroprotective and Anti-Inflammatory Effects of Kuwanon C from Cudrania tricuspidata Are Mediated by Heme Oxygenase-1 in HT22 Hippocampal Cells, RAW264.7 Macrophage, and BV2 Microglia

2020 ◽  
Vol 21 (14) ◽  
pp. 4839 ◽  
Author(s):  
Wonmin Ko ◽  
Chi-Su Yoon ◽  
Kwan-Woo Kim ◽  
Hwan Lee ◽  
Nayeon Kim ◽  
...  
Keyword(s):  
Heme Oxygenase ◽  
Stress Responses ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Neuroprotective Effects ◽  
Bv2 Cells ◽  
Bv2 Microglia ◽  
Anti Inflammatory ◽  
Nrf2 Expression ◽  
Raw264.7 Macrophage

Heme oxygenase (HO)-1 is a detoxifying phase II enzyme that plays a role in both inflammatory and oxidative stress responses. Curdrania tricuspidata is widespread throughout East Asia and is used as a therapeutic agent in traditional medicine. We investigated whether treatment with sixteen flavonoid or xanthone compounds from C. tricuspidata could induce HO-1 expression in HT22 hippocampal cells, RAW264.7 macrophage, and BV2 microglia. In these compounds, kuwanon C showed the most remarkable HO-1 expression effects. In addition, treatment with kuwanon C reduced cytoplasmic nuclear erythroid 2-related factor (Nrf2) expression and increased Nrf2 expression in the nucleus. Significant inhibition of glutamate-induced oxidative injury and induction of reactive oxygen species (ROS) occurred when HT22 hippocampal cells were pretreated with kuwanon C. The levels of inflammatory mediator and cytokine, which increased following lipopolysaccharide (LPS) stimulation, were suppressed in RAW264.7 macrophage and BV2 microglia after kuwanon C pretreatment. Kuwanon C also attenuated p65 DNA binding and translocation into the nucleus in LPS-induced RAW264.7 and BV2 cells. The anti-inflammatory, anti-neuroinflammatory, and neuroprotective effects of kuwanon C were reversed when co-treatment with HO-1 inhibitor of tin protoporphyrin-IX (SnPP). These results suggest that the neuroprotective and anti-inflammatory effects of kuwanon C are regulated by HO-1 expression.

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