scholarly journals Is Acquired Disgust More Difficult to Extinguish Than Acquired Fear? an Event-Related Potential Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Zeng ◽  
Lishan Lv ◽  
Xifu Zheng

This study used the classical conditioned acquisition and extinction paradigm to compare which of the two emotions, acquired disgust and acquired fear, was more difficult to extinguish, based on behavioral assessments and the event-related potential (ERP) technique. Behavioral assessments revealed that, following successful conditioned extinction, acquired disgust was more difficult to extinguish. The ERP results showed that, at the early stage of P1, the amplitude of conditioned fear was significantly smaller than that of conditioned disgust, and both were significantly different from the amplitude under neutral conditions; at the middle stage of N2, the difference between the amplitudes of conditioned disgust and conditioned fear disappeared, but they were still significantly different from the amplitudes of conditioned neutral stimuli; at the late stage of P3, the difference between conditioned disgust and conditioned neutral stimuli disappeared, but the difference between conditioned fear and neutral stimuli remained, suggesting that acquired fear was more difficult to extinguish than acquired disgust in terms of how the brain works.

2018 ◽  
Author(s):  
Linpei Zhang ◽  
Yuqiu Li ◽  
Wenshu Meng ◽  
Yanying Ni ◽  
Youhe Gao

AbstractPatients with primary and metastatic brain cancer have an extremely poor prognosis, mostly due to the late diagnosis of disease. Urine, which lacks homeostatic mechanisms, is an ideal biomarker source that accumulates early and highly sensitive changes to provides information about the early stage of disease. A rat model mimicking the local tumor growth process in the brain was established with intracerebral Walker 256 (W256) cell injection. Urine samples were collected on days 3, 5 and 8 after injection and then analyzed by LC-MS/MS. In the intracerebral W256 model, no obvious clinical manifestations changes or abnormal MRI signals were found on days 3 and 5; at these time points, nine proteins were changed significantly in the urine of all 8 tumor rats. On day 8, when tumors were detected by MRI, twenty-five differential proteins were identified, including 10 proteins that have been reported to be closely related to tumor metastasis or brain tumors. The differential urinary proteomes were compared with those from the subcutaneous W256 model and the intracerebral C6 model. Few differential proteins overlapped. Specific differential protein patterns were observed among the three models, indicating that the urinary proteome can reflect the difference when tumor cells with different growth characteristics are inoculated into the brain and when identical tumor cells are inoculated into different areas, specifically, the subcutis and the brain.


2021 ◽  
Vol 8 (4) ◽  
pp. 73-76
Author(s):  
Katherine Figarella

Trypanosoma brucei is one of the protozoa parasites that can enter the brain and cause injury associated with toxic effects of parasite-derived molecules or with immune responses against infection. Other protozoa parasites with brain tropism include Toxoplasma, Plasmodium, Amoeba, and, eventually, other Trypano-somatids such as T. cruzi and Leishmania. Together, these parasites affect billions of people worldwide and are responsible for more than 500.000 deaths annually. Factors determining brain tropism, mechanisms of in-vasion as well as processes ongoing inside the brain are not well understood. But, they depend on the par-asite involved. The pathogenesis caused by T. brucei initiates locally in the area of parasite inoculation, soon trypanosomes rich the blood, and the disease enters in the so-called early stage. The pathomecha-nisms in this phase have been described, even mole-cules used to combat the disease are effective during this period. Later, the disease evolves towards a late-stage, characterized by the presence of parasites in the central nervous system (CNS), the so-called meningo-encephalitic stage. This phase of the disease has not been sufficiently examined and remains a matter of investigation. Here, I stress the importance of delve into the study of the neuropathogenesis caused by T. brucei, which will enable the identification of path-ways that may be targeted to overcome parasites that reached the CNS. Finally, I highlight the impact that the application of tools developed in the last years in the field of neuroscience will have on the study of neglect-ed tropical diseases.


2008 ◽  
Vol 600-603 ◽  
pp. 631-634
Author(s):  
Kenichiro Terui ◽  
Atsuko Sekiguchi ◽  
Hiroshi Yoshizaki ◽  
Junichi Koike

The reaction behavior and growth kinetic of reaction layer were investigated in the Ni contact to n-type 6H-SiC. Annealing was performed at temperature in the range between 800 and 1000 °C for 1 to 240 minutes in Ar atmosphere. The interface reaction of Ni/SiC starts with Ni diffusion into SiC. Ni3Si is initially precipitated and subsequently forms the continuous layer of d-Ni2Si. Kirkendall voids are formed at the reaction front. Carbon is segregated in the interface layer of nickel silicide. The growth rate of the interface layer follows a parabolic law, meaning that the growth rate is controlled by diffusion. The growth occurs in two steps at all examined temperatures: a fast growth is followed by a slow growth. In addition, in the late stage, the growth rate changes dramatically below and above 850°C. The observed growth kinetic can be explained by the difference of Ni diffusivity and the required concentration change for phase transition depending on the phase composition and structure. The d-Ni2Si is formed in the early stage, while the e-Ni3Si2 and q-Ni2Si are formed in the late stage below and above 850°C, respectively.


2014 ◽  
Vol 88 ◽  
pp. 83-89 ◽  
Author(s):  
Hannah A.D. Keage ◽  
Scott Coussens ◽  
Mark Kohler ◽  
Myra Thiessen ◽  
Owen F. Churches

Religions ◽  
2020 ◽  
Vol 11 (11) ◽  
pp. 608
Author(s):  
Byeongdae Bae

The purpose of this study was to characterize early Donghak thought as the fusion of two horizons, one Confucian and the other Catholic. In particular, the study divided the Donghak founder Su-un Choe Je-u’s view of divinity into three stages, and showed how the evolution of his thought through these stages can be explained as the product of a dialogue between the Confucian monist tradition based on qi or vital energy and the Catholic dualist tradition based on Thomistic scholasticism. The study adopted a comparative and historical methodology, whereby comparison was limited to similarities and differences between Su-un’s works and sources in the Confucian or Catholic tradition that we can reasonably assume to have been available to Su-un. It was found that Su-un’s thought in the early stage was marked by theistic features similar to the scholastic view of God, and that in the middle stage Su-un sought to accommodate this theism within a pantheistic framework based on the Confucian monist tradition. For convenience’ sake, this theism-within-pantheism can be referred to as Su-un’s “panentheism”. It is suggested that the creative tension within this panentheism motivated Su-un to introduce innovations in his thought. First, in the middle stage, Su-un rejected the monism of li or pattern that was prevalent in the Neo-Confucian orthodoxy of his day, reverting to the older tradition of qi-monism. Second, in the late stage of his thought, he appears to have rehabilitated li as intelligent pattern that is the source of all signs of intelligence in the natural and moral order. As for the value of the approach adopted in this study, it enables us to make better sense of obscure details in Su-un’s works by placing them in their proper historical context, as evinced by the reading of Su-un’s late stage work “Buryeon Giyeon” presented herein. It is hoped that this approach will be applied more rigorously in future studies to deepen our understanding of the intellectual history of Donghak and Cheondogyo, along with various other new religions that emerged in Korea’s modern history.


2019 ◽  
Vol 5 (1) ◽  
pp. 20 ◽  
Author(s):  
Jakub Godlewski ◽  
Jacek Lenart ◽  
Elzbieta Salinska

The mammalian brain is made up of billions of neurons and supporting cells (glial cells), intricately connected. Molecular perturbations often lead to neurodegeneration by progressive loss of structure and malfunction of neurons, including their death. On the other side, a combination of genetic and cellular factors in glial cells, and less frequently in neurons, drive oncogenic transformation. In both situations, microenvironmental niches influence the progression of diseases and therapeutic responses. Dynamic changes that occur in cellular transcriptomes during the progression of developmental lineages and pathogenesis are controlled through a variety of regulatory networks. These include epigenetic modifications, signaling pathways, and transcriptional and post-transcriptional mechanisms. One prominent component of the latter is small non-coding RNAs, including microRNAs, that control the vast majority of these networks including genes regulating neural stemness, differentiation, apoptosis, projection fates, migration and many others. These cellular processes are also profoundly dependent on the microenvironment, stemness niche, hypoxic microenvironment, and interactions with associated cells including endothelial and immune cells. Significantly, the brain of all other mammalian organs expresses the highest number of microRNAs, with an additional gain in expression in the early stage of neurodegeneration and loss in expression in oncogenesis. However, a mechanistic explanation of the concept of an apparent inverse correlation between the odds of cancer and neurodegenerative diseases is only weakly developed. In this review, we thus will discuss widespread de-regulation of microRNAome observed in these two major groups of brain pathologies. The deciphering of these intricacies is of importance, as therapeutic restoration of pre-pathological microRNA landscape in neurodegeneration must not lead to oncogenesis and vice versa. We thus focus on microRNAs engaged in cellular processes that are inversely regulated in these diseases. We also aim to define the difference in microRNA networks between pro-survival and pro-apoptotic signaling in the brain.


1997 ◽  
Vol 6 (1) ◽  
pp. 37-52 ◽  
Author(s):  
Martina Penke ◽  
Helga Weyerts ◽  
Matthias Gross ◽  
Elke Zander ◽  
Thomas F Münte ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document