• BMB Reports
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• 제56권11호
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• pp.575-583
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• 2023

Mitochondria, fundamental cellular organelles that govern energy metabolism, hold a pivotal role in cellular vitality. While consuming dioxygen to produce adenosine triphosphate (ATP), the electron transfer process within mitochondria can engender the formation of reactive oxygen species that exert dual roles in endothelial homeostatic signaling and oxidative stress. In the context of the intricate electron transfer process, several metal ions that include copper, iron, zinc, and manganese serve as crucial cofactors in mitochondrial metalloenzymes to mediate the synthesis of ATP and antioxidant defense. In this mini review, we provide a comprehensive understanding of the coordination chemistry of mitochondrial cuproenzymes. In detail, cytochrome c oxidase (CcO) reduces dioxygen to water coupled with proton pumping to generate an electrochemical gradient, while superoxide dismutase 1 (SOD1) functions in detoxifying superoxide into hydrogen peroxide. With an emphasis on the catalytic reactions of the copper metalloenzymes and insights into their ligand environment, we also outline the metalation process of these enzymes throughout the copper trafficking system. The impairment of copper homeostasis can trigger mitochondrial dysfunction, and potentially lead to the development of copper-related disorders. We describe the current knowledge regarding copper-mediated toxicity mechanisms, thereby shedding light on prospective therapeutic strategies for pathologies intertwined with copper dyshomeostasis.

• Asian Pacific Journal of Cancer Prevention
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• 제14권10호
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• pp.5543-5552
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• 2013

Colorectal cancer (CRC), a complex multi-step process involving progressive disruption of homeostatic mechanisms controlling intestinal epithelial proliferation/inflammation, differentiation, and programmed cell death, is the third most common malignant neoplasm worldwide. A number of promising targets such as inducible nitric acid (iNOS), cyclooxygenase (COX)-2, NF-E2-related factor 2 (Nrf2), $Wnt/{\beta}$-catenin, Notch and apoptotic signaling have been identified by researchers as useful targets to prevent or therapeutically inhibit colon cancer development. In this review article, we aimed to explore the current targets available to eliminate colon cancer with an update of dietary and non-nutritional compounds that could be of potential use for interaction with regulatory molecules to prevent CRC.

• Journal of Electrical Engineering and Technology
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• 제5권1호
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• pp.1-7
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• 2010

Recently, smart grid has been considered a very important new energy delivery technology, and one that can help ensure a cleaner environment by making use of information and communication technology (ICT) in countries around the world. The many technological benefits smart grid offers is expected to bring about a huge change in the electric energy supply chain. In particular, smart grid with advanced ICT is likely to allow market agents to participate in the decision-making process in the restructured electricity industry, easily facilitating Homeostatic Utility Control. In this paper, we examine smart grid as a market externality, and then illustrate issues from the commercial market perspective as it relates to electricity market design. Finally, our paper identifies some of the impacts of smart grid on electricity market design, which may possibly be incorporated into the evolution of the electricity market, thus ensuring market efficiency.

• Journal of Oral Medicine and Pain
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• 제48권2호
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• pp.39-44
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• 2023

Primary Sjögren's syndrome (pSS) is an autoimmune progressive disease characterized by dysfunction and inflammation of the salivary glands. The underlying mechanisms of salivary gland involvement in pSS remain unclear, and researchers have primarily focused on immunological phenomena, making it difficult to distinguish between the cause and effect of the disease. Consequently, our research aims to directly investigate changes in homeostasis occurring in acinar cells, specifically in the context of muscarinic signaling, mucins, aquaporins, and forkhead box protein O1, to elucidate the initial step of pSS. We compare the disease-related phenomena observed in salivary gland acinar cells in pSS with the overall process of salivary secretion.

• 수면정신생리
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• 제4권1호
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• pp.57-65
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• 1997

누구나 시차가 큰 여행을 할 때 몇일 간 비행시차증이라고 불리우는 증상을 경험하게 된다. 비행시차증은 수면박탈, 비행요인, 지연요인의 복합적인 원인으로 인해 생기는 하나의 증상군이라고 말할 수 있다. 특히 빠른 시차변화로 인한 생리적 지연효과(Jet lag)는 외적 비동조화, 내적 비동조화, 그리고 수면상실의 결과를 낳는다. 인간의 수면을 조절하는 기전에 있어 일중체계가 중요하다. 즉, 평균적인 수면-각성주기는 중심체온의 주기와 내적 비동조화가 일어나더라도 수면경향, 졸리움, 자발적 수면 기간, 그리고 렘수면 경향은 중심체온의 내인성 일중주기에 따라 통제된다. 수면의 구성요소중에서 서파수면은 중심체온의 주기보다는 수면시작시간에 따라 나타나며 이전에 깨어있었던 기간이 길수록 강력하게 나타난다. 따라서 수면은 일중체계와 항상성 기전의 상호작용으로 조절된다. 비행시차 후에 변화되는 수면양상을 이해하는데 있어 일중 체계 이외에 도항상성 기전을 고려하여야한다. 수면에 대한 일중리듬체계의 영향과 수면의 항상성 과정이 비행시차후 도착지에서의 수면양상을 설 명할 수 있을 것이다. 도착지에서의 적응은 통과한 시간대 수, 여행 방향, 일주기 리듬의 부조화에 적응 할 수 있는 개인별 능력에 따라 다르다. 도착지의 시간적 단서에 빨리 노출되어 일중체계의 위상반응곡선에 의한 재동조화를 촉진시키고 수면의 항상성 과정을 고려하여 도착지의 밤 이전까지 충분히 깨어 있는 것이 Jet Lag를 극복하고 적응하는 지름길일 것이다.

• Molecules and Cells
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• 제40권9호
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• pp.607-612
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• 2017

When mammalian cells and animals face a variety of internal or external stresses, they need to make homeostatic changes so as to cope with various stresses. To this end, mammalian cells are equipped with two critical stress responses, autophagy and cellular senescence. Autophagy and cellular senescence share a number of stimuli including telomere shortening, DNA damage, oncogenic stress and oxidative stress, suggesting their intimate relationship. Autophagy is originally thought to suppress cellular senescence by removing damaged macromolecules or organelles, yet recent studies also indicated that autophagy promotes cellular senescence by facilitating the synthesis of senescence-associated secretory proteins. These seemingly opposite roles of autophagy may reflect a complex picture of autophagic regulation on cellular senescence, including different types of autophagy or a unique spatiotemporal activation of autophagy. Thus, a better understanding of autophagy process will lead us to not only elucidate the conundrum how autophagy plays dual roles in the regulation of cellular senescence but also helps the development of new therapeutic strategies for many human diseases associated with cellular senescence. We address the pro-senescence and anti-senescence roles of autophagy while focusing on the potential mechanistic aspects of this complex relationship between autophagy and cellular senescence.

• 한국발생생물학회지:발생과생식
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• 제18권4호
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• pp.225-231
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• 2014

Autophagy is a homeostatic degradation process that is involved in tumor development and normal development. Autophagy is induced in cancer cells in response to chemotherapeutic agents, and inhibition of autophagy results in enhanced cancer cell death or survival. Chloroquine (CQ), an anti-malarial drug, is a lysosomotropic agent and is currently used as a potential anticancer agent as well as an autophagy inhibitor. Here, we evaluate the characteristics of these dual activities of CQ using human colorectal cancer cell line HCT15. The results show that CQ inhibited cell viability in dose- and time-dependent manner in the range between 20 to 80 uM, while CQ did not show any antiproliferative activity at 5 and 10 uM. Cotreatment of CQ with antitumor agent NVP-BEZ235, a dual inhibitor of PI3K/mTOR, rescued the cell viability at low concentrations meaning that CQ acted as an autophagy inhibitor, but CQ induced the lethal effect at high concentrations. Acridine orange staining revealed that CQ at high doses induced lysosomal membrane permeabilization (LMP). High doses of CQ produced cellular reactive oxygen species (ROS) and cotreatment of antioxidants, such as NAC and trolox, with high doses of CQ rescued the cell viability. These results suggest that CQ may exert its dual activities, as autophagy inhibitor or LMP inducer, in concentration-dependent manner.

• The Korean Journal of Physiology and Pharmacology
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• 제14권5호
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• pp.291-297
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• 2010

The sleep homeostatic response significantly affects the state of anesthesia. In addition, sleep recovery may occur during anesthesia, either via a natural sleep-like process to occur or via a direct restorative effect. Little is known about the effects of isoflurane anesthesia on sleep homeostasis. We investigated whether 1) isoflurane anesthesia could provide a sleep-like process, and 2) the depth of anesthesia could differently affect the post-anesthesia sleep response. Nine rats were treated for 2 hours with $ad$ $libitum$ sleep (Control), sleep deprivation (SD), and isoflurane anesthesia with delta-wave- predominant state (ISO-1) or burst suppression pattern-predominant state (ISO-2) with at least a 1-week interval. Electroencephalogram and electromyogram were recorded and sleep-wake architecture was evaluated for 4 hours after each treatment. In the post-treatment period, the duration of transition to slow-wave-sleep decreased but slow wave sleep (SWS) increased in the SD group, but no sleep stages were significantly changed in ISO-1 and ISO-2 groups compared to Control. Different levels of anesthesia did not significantly affect the post-anesthesia sleep responses, but the deep level of anesthesia significantly delayed the latency to sleep compared to Control. The present results indicate that a natural sleep-like process likely occurs during isoflurane anesthesia and that the post-anesthesia sleep response occurs irrespective to the level of anesthesia.

• 수면정신생리
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• 제3권2호
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• pp.18-31
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• 1996

Jet-lag can be defined as the cumulative physiological and psychological effects of rapid air travel across multiple time zones. Many reports have suggested that age-related changes in sleep reflect fundamental changes in the circadian system and in significant declines in slow wave sleep. Jet lag is a dramatic situation in which the changes of the phase of circadian process and homeostatic process of sleep occur. Thus the authors evaluatead the changes of sleep-wake cycle from jet lag by age. Thirty-eight healthy travellers were studied for 3 days before and 7 days after jet-flights across seven to ten time zone. They were aged 19-70, They trareled eastbound, Seoul to North America (USA, Canada). Sleep onset time, wake-up time, sleep latency, awakening frequency on night sleep, awakening duration on night sleep, sleepiness at wake-up and nap length were evaluated. Our results suggest that by the 7 to 10 time zone shift, the old age group was significantly influenced in sleep-wake cycles. The date on which subjective physical condition was recovered was $6.23{\pm}83$ day after arrivals for old age group, while for young and middle age group, $4.46{\pm}1.50$ day and $4.83{\pm}1.52$ day, respectively. In old age group, sleep onset time was later than baselines and could not recover untill 7th day. But in other groups, the recovery was within 5th day. Nap dura fion was longer in old age group through jet lag than younger age group. In other parameters, there was no definite difference among three age groups. Our results suggested that the old age was significantly influenced by the disharmony between internal body clock and sleep-wake cycle needed at the travel site. Thus we proved that recovery ability from jet lag was age-dependent as well as travelling direction-dependent. To demonstrate more definite evidence, EEG monitoring and staging of sleep were funthun encouraged.

• Biomolecules & Therapeutics
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• 제19권1호
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• pp.70-76
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• 2011

Bone remodeling is a dynamic process involving a constant balance between osteoclast-induced bone resorption and osteoblast-induced bone formation. Osteoclasts play a crucial homeostatic role in skeletal modeling and remodeling, and destroy bone in many pathological conditions. Previously, we reported that the hexane soluble fraction of Ficus carica inhibited osteoclast differentiation. Poly unsaturated fatty acids, such as ethyl docosahexaenoate (E-DHA), docosahexaenoic acid (DHA), cis-11,14-eicosadienoic acid (EDA) and eicosapentaenoic acid (EPA), were identified from the hexane soluble fraction of Ficus carica. Among them, E-DHA most potently inhibited osteoclastogenesis in RAW264.7 cells. E-DHA reduced the activities of JNK and NF-$\kappa}B$. E-DHA suppressed the expression of c-Fos and nuclear factor of activated T cells c1 (NFATc1). Interestingly, DHA increased the activity of alkaline phosphatase and expression of bone morphogenetic protein 2 (BMP2) more than E-DHA in MC3T3-E1 cells, suggesting that DHA may induce osteoblast differentiation. The data suggests that a combination of E-DHA and DHA has potential use in the treatment of diseases involving abnormal bone lysis, such as osteoporosis, rheumatoid arthritis and periodontal bone erosion.