scholarly journals The influence of environmental and core temperature on cyclooxygenase and PGE2 in healthy humans

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Christopher J. Esh ◽  
Bryna C. R. Chrismas ◽  
Alexis R. Mauger ◽  
Anissa Cherif ◽  
John Molphy ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Skin Temperature ◽  
Effect Size ◽  
Mixed Models ◽  
Thermal Perception ◽  
Random Coefficient Models ◽  
Healthy Humans ◽  
Within Subjects ◽  
Thermogenic Response

AbstractWhether cyclooxygenase (COX)/prostaglandin E2 (PGE2) thermoregulatory pathways, observed in rodents, present in humans? Participants (n = 9) were exposed to three environments; cold (20 °C), thermoneutral (30 °C) and hot (40 °C) for 120 min. Core (Tc)/skin temperature and thermal perception were recorded every 15 min, with COX/PGE2 concentrations determined at baseline, 60 and 120 min. Linear mixed models identified differences between and within subjects/conditions. Random coefficient models determined relationships between Tc and COX/PGE2. Tc [mean (range)] increased in hot [+ 0.8 (0.4–1.2) °C; p < 0.0001; effect size (ES): 2.9], decreased in cold [− 0.5 (− 0.8 to − 0.2) °C; p < 0.0001; ES 2.6] and was unchanged in thermoneutral [+ 0.1 (− 0.2 to 0.4) °C; p = 0.3502]. A relationship between COX2/PGE2 in cold (p = 0.0012) and cold/thermoneutral [collapsed, condition and time (p = 0.0243)] was seen, with higher PGE2 associated with higher Tc. A within condition relationship between Tc/PGE2 was observed in thermoneutral (p = 0.0202) and cold/thermoneutral [collapsed, condition and time (p = 0.0079)] but not cold (p = 0.0631). The data suggests a thermogenic response of the COX/PGE2 pathway insufficient to defend Tc in cold. Further human in vivo research which manipulates COX/PGE2 bioavailability and participant acclimation/acclimatization are warranted to elucidate the influence of COX/PGE2 on Tc.

Is prostaglandin E2 (PGE2) involved in the thermogenic response to environmental cooling in healthy humans?

2015 ◽  
Vol 85 (5) ◽  
pp. 607-611 ◽  
Author(s):  
Josh Foster ◽  
Alexis R. Mauger ◽  
Bryna C.R. Chrismas ◽  
Katie Thomasson ◽  
Lee Taylor
Keyword(s):  
Prostaglandin E2 ◽  
Healthy Humans ◽  
Thermogenic Response

scholarly journals Within-Subject Comparison of [11C]-( + )-PHNO and [11C]raclopride Sensitivity to Acute Amphetamine Challenge in Healthy Humans

2011 ◽  
Vol 32 (1) ◽  
pp. 127-136 ◽  
Author(s):  
Paul Shotbolt ◽  
Andri C Tziortzi ◽  
Graham E Searle ◽  
Alessandro Colasanti ◽  
Jasper van der Aart ◽  
...  
Keyword(s):  
Dorsal Striatum ◽  
Binding Potential ◽  
Open Label ◽  
In Vivo Binding ◽  
Healthy Humans ◽  
Positron Emission ◽  
Within Subjects ◽  
Positron Emission Tomography Radiotracer ◽  
Subject Comparison

[11C]PHNO is a D2/D3 agonist positron emission tomography radiotracer, with higher in vivo affinity for D3 than for D2 receptors. As [11C]-( + )-PHNO is an agonist, its in vivo binding is expected to be more affected by acute fluctuations in synaptic dopamine than that of antagonist radiotracers such as [11C]raclopride. In this study, the authors compared the effects of an oral dose of the dopamine releaser amphetamine (0.3 mg/kg) on in vivo binding of [11C]-( + )-PHNO and [11C]raclopride in healthy subjects, using a within-subjects, counterbalanced, open-label design. In the dorsal striatum, where the density of D3 receptors is negligible and both tracers predominantly bind to D2 receptors, the reduction of [11C]-( + )-PHNO binding potential ( BPND) was 1.5 times larger than that of [11C]raclopride. The gain in sensitivity associated with the agonist [11C]-( + )-PHNO implies that ~65% of D2 receptors are in the high-affinity state in vivo. In extrastriatal regions, where [11C]-( + )-PHNO predominantly binds to D3 receptors, the amphetamine effect on [11C]-( + )-PHNO BPND was even larger, consistent with the higher affinity of dopamine for D3. This study indicates that [11C]- ( + )-PHNO is superior to [11C]raclopride for studying acute fluctuations in synaptic dopamine in the human striatum. [11C]-( + )-PHNO also enables measurement of synaptic dopamine in D3 regions.

scholarly journals Evidence that the E2-isoprostane, 15-E2t-isoprostane (8-iso-prostaglandin E2) is formed in vivo

1998 ◽  
Vol 39 (8) ◽  
pp. 1589-1593 ◽  
Author(s):  
Jason D. Morrow ◽  
Jennifer Scruggs ◽  
Yan Chen ◽  
William E. Zackert ◽  
L. Jackson Roberts
Keyword(s):  
Prostaglandin E2

Somatostatin modulates cholinergic neurotransmission in canine antral muscle

1988 ◽  
Vol 254 (2) ◽  
pp. G201-G209 ◽  
Author(s):  
C. B. Koelbel ◽  
G. van Deventer ◽  
S. Khawaja ◽  
M. Mogard ◽  
J. H. Walsh ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Substance P ◽  
Prostaglandin E2 ◽  
Positive Inotropic Effect ◽  
Mechanical Response ◽  
Inhibitory Effect ◽  
Inotropic Effect ◽  
Inotropic Response ◽  
Cholinergic Neurotransmission

Somatostatin has been shown to inhibit antral motility in vivo. To examine the effect of somatostatin on cholinergic neurotransmission in the canine antrum, we studied the mechanical response of and the release of [3H]acetylcholine from canine longitudinal antral muscle in response to substance P, gastrin 17, and electrical stimulation. In unstimulated tissues, somatostatin had a positive inotropic effect on spontaneous phasic contractions. In tissues stimulated with substance P and gastrin 17, but not with electrical stimulation, somatostatin inhibited the phasic inotropic response dose dependently. This inhibitory effect was abolished by indomethacin. Somatostatin stimulated the release of prostaglandin E2 radioimmunoreactivity, and prostaglandin E2 inhibited the release of [3H]acetylcholine induced by substance P and electrical stimulation. Somatostatin increased the release of [3H]acetylcholine from unstimulated tissues by a tetrodotoxin-sensitive mechanism but inhibited the release induced by substance P and electrical stimulation. These results suggest that somatostatin has a dual modulatory effect on cholinergic neurotransmission in canine longitudinal antral muscle. This effect is excitatory in unstimulated tissues and inhibitory in stimulated tissues. The inhibitory effect is partially mediated by prostaglandins.

Physical exercise increases autophagic signaling through ULK1 in human skeletal muscle

2015 ◽  
Vol 118 (8) ◽  
pp. 971-979 ◽  
Author(s):  
Andreas Buch Møller ◽  
Mikkel Holm Vendelbo ◽  
Britt Christensen ◽  
Berthil Forrest Clasen ◽  
Ann Mosegaard Bak ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Light Chain ◽  
Human Skeletal Muscle ◽  
Transgenic Animal ◽  
Dependent Manner ◽  
Healthy Humans ◽  
Transgenic Animal Models ◽  
Exercise Induced

Data from transgenic animal models suggest that exercise-induced autophagy is critical for adaptation to physical training, and that Unc-51 like kinase-1 (ULK1) serves as an important regulator of autophagy. Phosphorylation of ULK1 at Ser555 stimulates autophagy, whereas phosphorylation at Ser757 is inhibitory. To determine whether exercise regulates ULK1 phosphorylation in humans in vivo in a nutrient-dependent manner, we examined skeletal muscle biopsies from healthy humans after 1-h cycling exercise at 50% maximal O2 uptake on two occasions: 1) during a 36-h fast, and 2) during continuous glucose infusion at 0.2 kg/h. Physical exercise increased ULK1 phosphorylation at Ser555 and decreased lipidation of light chain 3B. ULK1 phosphorylation at Ser555 correlated positively with AMP-activated protein kinase-α Thr172 phosphorylation and negatively with light chain 3B lipidation. ULK1 phosphorylation at Ser757 was not affected by exercise. Fasting increased ULK1 and p62 protein expression, but did not affect exercise-induced ULK1 phosphorylation. These data demonstrate that autophagy signaling is activated in human skeletal muscle after 60 min of exercise, independently of nutritional status, and suggest that initiation of autophagy constitutes an important physiological response to exercise in humans.

scholarly journals Measuring arterial pulsatility with Dynamic Inflow MAgnitude Contrast (DIMAC)

2021 ◽  
Author(s):  
Joseph R Whittaker ◽  
Fabrizio Fasano ◽  
Marcello Venzi ◽  
Patrick Liebig ◽  
Daniel Gallichan ◽  
...  
Keyword(s):  
Flow Velocity ◽  
Pulsatile Flow ◽  
Cerebral Arteries ◽  
Mr Image ◽  
Signal Contrast ◽  
Within Subjects ◽  
Fast Gradient ◽  
Arterial Tone ◽  
Reliable Methods

Poor arterial health is increasingly recognised as an independent risk factor for cerebrovascular disease, however there remain relatively few reliable methods for assessing the function and health of cerebral arteries. In this study, we outline a new MRI approach to measuring pulsatile flow in cerebral arteries that is based on the inflow phenomenon associated with fast gradient-recalled-echo acquisitions. Unlike traditional phase-contrast techniques, this new method, which we dub Dynamic Inflow MAgnitude Contrast (DIMAC), does not require velocity-encoding gradients as sensitivity to flow velocity results purely from the inflow effect. We achieved this desired effect using a highly accelerated single slice EPI acquisition with very short TR (15 ms) and a 90 degree flip angle, thus maximising inflow contrast. Simulating the spoiled GRE signal in the presence of large arteries and perform a sensitivity analysis to demonstrate that in the regime of high inflow contrast it shows much greater sensitivity to flow velocity over blood volume changes. We support this theoretical prediction with in-vivo data collected in two separate experiments designed to demonstrate the utility of the DIMAC signal contrast. We perform a hypercapnia challenge experiment in order to experimentally modulate arterial tone within subjects, and thus modulate the arterial pulsatile flow waveform. We also perform a thigh-cuff release challenge, designed to induce a transient drop in blood pressure, and demonstrate that the continuous DIMAC signal captures the complex transient change in the pulsatile and non-pulsatile components of flow. In summary, this study proposes a new role for a well established source of MR image contrast, and demonstrate its potential for measuring both steady-state and dynamic changes in arterial tone.

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