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( Darlene Mae D. Ortiz ),( Mikyung Kim ),( Hyun Jun Lee ),( Chrislean Jun Botanas ),( Raly James Perez Custodio ),( Leandro Val Sayson ),( Nicole Bon Campomayor ),( Chaeyeon Lee ),( Yong Sup Lee ),( J 한국응용약물학회 2023 Biomolecules & Therapeutics(구 응용약물학회지) Vol.31 No.2
Major depressive disorder is a leading cause of disability in more than 280 million people worldwide. Monoamine-based antidepressants are currently used to treat depression, but delays in treatment effects and lack of responses are major reasons for the need to develop faster and more efficient antidepressants. Studies show that ketamine (KET), a PCP analog, produces antidepressant effects within a few hours of administration that lasts up to a week. However, the use of KET has raised concerns about side effects, as well as the risk of abuse. 4 -F-PCP analog is a novel PCP analog that is also an NMDA receptor antagonist, structurally similar to KET, and might potentially elicit similar antidepressant effects, however, there has been no study on this subject yet. Herein, we investigate whether 4-F-PCP displays antidepressant effects and explored their potential therapeutic mechanisms. 4-F-PCP at 3 and 10 mg/kg doses showed antidepressant-like effects and repeated treatments maintained its effects. Furthermore, treatment with 4-F-PCP rescued the decreased expression of proteins most likely involved in depression and synaptic plasticity. Changes in the excitatory amino acid transporters (EAAT2, EAAT3, EAAT4) were also seen following drug treatment. Lastly, we assessed the possible side effects of 4-F-PCP after long-term treatment (up to 21 days). Results show that 4-F-PCP at 3 mg/kg dose did not alter the cognitive function of mice. Overall, current findings provide significant implications for future research not only with PCP analogs but also on the next generation of different types of antidepressants.
김학균,Walsh, Darlene 한국상품학회 2012 商品學硏究 Vol.30 No.6
How does mood affect our predictions about the preferences of other people? This paper proposes a psychological mechanism by which positive affect influences people’s perceptions of the similarity between their own preferences and those of other people by decreasing the psychological distance between them. In two experiments, this research shows that people in a positive mood tend to assume that their own preferences are similar to others’more often than those in a negative mood do. These findings add to the growing evidence that affect influences how people process information and demonstrate that mood affects people’s predictions about others.
Kim,Hakkyun.Walsh,Darlene 한국상품학회 2012 商品學硏究 Vol.30 No.6
How does mood affect our predictions about the preferences of other people? This paper proposes a psychological mechanism bywhich positive affect influences people’s perceptions of the similarity between their own preferences and those of other people by decreasing the psychological distance between them. In two experiments, this research shows that people in a positive mood tend to assume that their own preferences are similar to others’more often than those in a negative mood do. These findings add to the growing evidence that affect influences how people process information and demonstrate that mood affects people’s predictions about others.
Models of multiple system atrophy
이혜진,Diadem Ricarte,Darlene Ortiz,이승재 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Multiple system atrophy (MSA) is a neurodegenerative disease with diverse clinical manifestations, including parkinsonism, cerebellar syndrome, and autonomic failure. Pathologically, MSA is characterized by glial cytoplasmic inclusions in oligodendrocytes, which contain fibrillary forms of α-synuclein. MSA is categorized as one of the αsynucleinopathy, and α-synuclein aggregation is thought to be the culprit of the disease pathogenesis. Studies on MSA pathogenesis are scarce relative to studies on the pathogenesis of other synucleinopathies, such as Parkinson’s disease and dementia with Lewy bodies. However, recent developments in cellular and animal models of MSA, especially α-synuclein transgenic models, have driven advancements in research on this disease. Here, we review the currently available models of MSA, which include toxicant-induced animal models, α-synuclein-overexpressing cellular models, and mouse models that express α-synuclein specifically in oligodendrocytes through cell type-specific promoters. We will also discuss the results of studies in recently developed transmission mouse models, into which MSA brain extracts were intracerebrally injected. By reviewing the findings obtained from these model systems, we will discuss what we have learned about the disease and describe the strengths and limitations of the models, thereby ultimately providing direction for the design of better models and future research.