Proceedings of the 29th EG-ICE International Workshop on Intelligent Computing in Engineering

This publication is the Proceedings of the 29th EG-ICE International Workshop on Intelligent Computing in Engineering from July 6-8, 2022. The EG-ICE International Workshop on Intelligent Computing in Engineering brings together international experts working on the interface between advanced computing and modern engineering challenges. Many engineering tasks require open-world resolution of challenges such as supporting multi-actor collaboration, coping with approximate models, providing effective engineer-computer interaction, search in multi-dimensional solution spaces, accommodating uncertainty, including specialist domain knowledge, performing sensor-data interpretation and dealing with incomplete knowledge. While results from computer science provide much initial support for resolution, adaptation is unavoidable and most importantly, feedback from addressing engineering challenges drives fundamental computer-science research. Competence and knowledge transfer goes both ways. &nbsp

Proceedings of the 29th EG-ICE International Workshop on Intelligent Computing in Engineering

This publication is the Proceedings of the 29th EG-ICE International Workshop on Intelligent Computing in Engineering from July 6-8, 2022. The EG-ICE International Workshop on Intelligent Computing in Engineering brings together international experts working on the interface between advanced computing and modern engineering challenges. Many engineering tasks require open-world resolution of challenges such as supporting multi-actor collaboration, coping with approximate models, providing effective engineer-computer interaction, search in multi-dimensional solution spaces, accommodating uncertainty, including specialist domain knowledge, performing sensor-data interpretation and dealing with incomplete knowledge. While results from computer science provide much initial support for resolution, adaptation is unavoidable and most importantly, feedback from addressing engineering challenges drives fundamental computer-science research. Competence and knowledge transfer goes both ways. &nbsp

The Effects of Estrogen Receptors' Antagonist on Brain Edema, Intracranial Pressure and Neurological Outcomes after Traumatic Brain Injury in Rat

BACKGROUND: In previous studies, the neuroprotective effect of 17β-estradiol in diffuse traumatic brain injury has been shown. This study used ICI 182,780, a non-selective estrogen receptor antagonist, to test the hypothesis that the neuroprotective effect of 17β-estradiol in traumatic brain injury is mediated by the estrogen receptors. METHODS: The ovariectomized rats were divided into eight groups. Brain injury was induced by Marmarou's method. Estrogen was injected 30 minutes after traumatic brain injury, and ICI 182,780 was injected before traumatic brain injury and also before estrogen treatment. In one group only ICI 182,780 was injected. The brain water content and Evans blue dye content were measured 24 and 5 hours after traumatic brain injury, respectively. The neurologic outcomes and intracranial pressure were assessed before, 4, and 24 hours after traumatic brain injury. RESULTS: Brain water content and Evans blue content were less in estrogen-treated group comparison to vehicle group. ICI 182,780 eliminated the effects of estrogen on brain edema and brain blood barrier permeability. Intracranial pressure was increased significantly after trauma, and estrogen decreased intracranial pressure at 4 and 24 hours after traumatic brain injury in comparison to vehicle. This inhibitory effect was also eliminated by treatment with ICI182,780. ICI 182,780 also inhibited the estrogen induced increase in neurologic outcomes following traumatic brain injury. However, the use of ICI 182,780 alone had no neuroprotective effect after traumatic brain injury. CONCLUSION: The results suggest that classical estrogen receptors have probably a role in the neuroprotective function of estrogen following traumatic brain injury

The brain cytokine levels are modulated by estrogen following traumatic brain injury: Which estrogen receptor serves as modulator?

The present study was designed to explore whether administration of estrogen affects brain cytokine levels in TBI. We also sought determine which one of type of classical estrogen receptors (ERs) is involved. Ovariectomized female rats were divided in to eight groups. Estrogen or vehicle was administered following TBI (E2 and oil groups). Antagonist of ER(ICI 182, 780) or vehicle was also administered following TBI (ICI and DMSO groups). The ICI or vehicle was administered either before induction of TBI and administration of estrogen (ICI+E2 and DMSO+E2 groups). TBI was induced by Marmarou's method. In addition to brain water content, the levels of brain proinflammatory and anti-inflammatory cytokines were measured 24 hours post- TBI. Present results demonstrated that, estrogen reduced TBI- induced brain edema. The antiedema effect of estrogen was attenuated by ICI. The brain measures of IL-1β, IL-6 and TNF-α in TBI were also reduced by estrogen. The anti-inflammatory effect of estrogen was attenuated by ICI. The inhibition level of estrogen by ICI was 53.2%, 12.09% and 48.45% for IL-1β, IL-6 and TNF-α, respectively. Estrogen also elevated IL-10 in TBI. ICI inversely controlled the effect of estrogen on IL-10, by 33.84%. This effect was not observed once ICI was used alone. The estrogen administration following TBI probably results in proinflammatory cytokines reduction, and inversely enhancement of anti-inflammatory cytokines. In our study, the neuroprotective effect of estrogen is proposed to be mediated by both ERα and ERα, and accordingly the inhibition of neuroprotective effect of estrogen by ICI

Functionally distinct POMC-expressing neuron subpopulations in hypothalamus revealed by intersectional targeting

Pro-opiomelanocortin (POMC)-expressing neurons in the arcuate nucleus of the hypothalamus represent key regulators of metabolic homeostasis. Electrophysiological and single-cell sequencing experiments have revealed a remarkable degree of heterogeneity of these neurons. However, the exact molecular basis and functional consequences of this heterogeneity have not yet been addressed. Here, we have developed new mouse models in which intersectional Cre/Dre-dependent recombination allowed for successful labeling, translational profiling and functional characterization of distinct POMC neurons expressing the leptin receptor (Lepr) and glucagon like peptide 1 receptor (Glp1r). Our experiments reveal that POMCLepr+ and POMCGlp1r+ neurons represent largely nonoverlapping subpopulations with distinct basic electrophysiological properties. They exhibit a specific anatomical distribution within the arcuate nucleus and differentially express receptors for energy-state communicating hormones and neurotransmitters. Finally, we identify a differential ability of these subpopulations to suppress feeding. Collectively, we reveal a notably distinct functional microarchitecture of critical metabolism-regulatory neurons. Biglari et al. reveal subgroups of arcuate nucleus hypothalamic neurons that exhibit distinct molecular signatures and feeding-regulatory functions, thus uncovering new regulatory principles in body weight control