• Journal of Environmental Science International
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• v.1 no.2
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• pp.69-80
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• 1992

Effects of light on leaf senescence of Phseolus vulgaris were investigated by measuring the disassembly of chlorophyll-protein complexes in detached leaves which had been kept in the dark or under light. The loss of chlorophyll accompanied by degradation of chlorophyll- protein complexes. PSI (photosystem I) complex containing LHCI (light harvesting complex of PSI) apoproteins was rapidly decreased after the early stage of dark-induced senescence. RC(reaction center)-Cores was slightly increased until 4 d and slowly decreased thereafter. As disassembly of LHCII trimer progressed after the late stage of senescence, there was a steady increase in the relative amount of SC(small complex)-2 containing LHCII monomer. On the other hand, white and red light adaptation caused the structural stability of chlorophyll-protein complexes during dark-induced senescence. Particularly, red light was more effective in the retardation of LHCII breakdown than white light, whereas white light was slightly effect in protecting the disassembly of PSI complex compared to red light. These results suggest, therefore, that light may be a regulatory factor for stability of chlorophyll-protein complexes in the senescent leaves.

• The Journal of Korean Medicine
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• v.26 no.4
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• pp.1-11
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• 2005

This study was to investigate the effect of Danchunwhangagam(DCWGG) extract on the production of proinflammatory cytokines in peripheral blood mononuclear cells (PBMCs) from Cerebral infarction(CI) patients. Methods: We examined how the inhibition rate of tumor necrosis factor (TNF)-$\alpha$, interleukin(IL)-1$\alpha$, IL-1$\beta$, IL-6, and IL-8 productions in DCWGG pretreatment PBMCs culture supernatant in the lipopolysaccaride(LPS)- or desferrioxamine(DFX)treated cells compared to unstimulated cells. Results: DCWGG inhibited the productions of TNF-$\alpha$, IL-1$\alpha$, IL-1$\beta$, IL-6, and IL-8 induced by LPS in a dose-dependent manner. Conclusions: DCWGG might have regulatory effects on LPS or DFX-induced cytokine production, which might explain its beneficial effect in the treatment of CI.

• Applied Microscopy
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• v.23 no.1
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• pp.25-34
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• 1993

Prolactin has been reported to be present in the tear film of humans and prolactin-like immunoreactivity has been detected by immunofluorescence in acinar cells of the lacrimal glands of humans and rats. The present study was aimed at clarifying the intracellular distribution of the prolactin-like immunoreactivity, using the electron microscope immunogold technique. The lacrimal gland acinar cells have two types of secretory granules: 1) Secretory granules containing flocculent materials irregularly shaped and are often coalesced. 2) Secretory granules are fairly round and contain homogenous materials of a moderate electron density. The density of the granular content varies even within a single cell. We found prolactin-like reactivity in secretory granules, some smaller cytosolic vesicles, Golgi cisternae and nuclei in acinar cells from intact glands of rat. Our present results are consistent with the conclusion that prolactin is present in lacrimal cells. The presence of prolactin reactivity in the nucleus suggests that prolactin may be a regulatory factor modulating gene expression.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.323.3-324
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• 2002

Histone deacetylases (HDAC) activity is associated generally with transcriptional repression. We have reported previously that apicidin. a histione deacetylase inhibitor. inhibited the proliferation of tumor cells via induction of p21 WAF/C1P1. We extended our study to identify the effect of apicidin on the expression of other cell cycle regulatory protein. such as cyclin E. a critical regulator of the transition from G1 into S phase. (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.142.2-143
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• 2003

We studied the effect of methanol extract of Carpopeltis affinis (CA) on atopic allergic reaction. CA dose-dependently inhibited interleukin (IL)-8 and tumor necrosis factor (TNF)-$\alpha$ secretion from the PMA- plus A23187- stimulated HMC-1. CA also dose-dependently inhibited the histamine and $\beta$-hexosaminidase release from mast cells. CA had no cytotoxic effect. (omitted)

• BMB Reports
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• v.35 no.1
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• pp.106-115
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• 2002

The serine/threonine kinase Akt has been intensely studied for its role in growth factor-mediated cell survival for the past 5 years. On the other hand, the ongoing research effort has recently uncovered novel regulatory mechanisms and downstream effectors of Akt that demonstrate the involvement of Akt in other cellular functions such as cell cycle progression, angiogenesis, and cancer cell invasion/metastasis. Furthermore, recent studies using whole model organisms suggest additional roles for Akt in important diseases such as aging and diabetes. The following review addresses these recent advances in the understanding of Akt function.

• BMB Reports
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• v.49 no.8
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• pp.403-404
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• 2016

The Wnt/β-catenin signaling is an evolutionarily conserved pathway that plays a pivotal role in embryonic development and adult homeostasis. However, we have limited information about the involvement of Wnt/β-catenin signaling in the lymphatic vascular system that regulates fluid homeostasis by absorbing interstitial fluid and returning it to blood circulation. In this recent publication we report that canonical Wnt/β-catenin signaling is highly active and critical for the formation of lymphovenus valves (LVVs) and lymphatic valves (LVs). β-catenin directly associates with the regulatory elements of the lymphedema-associated transcription factor, FOXC2 and activates its expression in an oscillatory shear stress (OSS)-dependent manner. The phenotype of β-catenin null embryos was rescued by FOXC2 overexpression. These results suggest that Wnt/β-catenin signaling is a mechanotransducer that links fluid force with lymphatic vascular development.

• Sleep Medicine and Psychophysiology
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• v.12 no.2
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• pp.87-92
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• 2005

Cytokines are the main regulatory molecules of not only immune system but also sleep system. Research on the role of cytokines on sleep has greatly been expanding since the first report of sleep-promoting effects of interleukin-1, the first cytokine molecule. Interleukin-1 and tumor necrosis factor are most widely studied among various cytokines. Studies over about twenty years demonstrate that most cytokines promote sleep but several cytokines inhibit sleep. Slow wave sleep is the main part that cytokines have effects on. Besides normal sleep physiology, cytokines have more major roles on pathophysiology of various sleep disorders. Obstructive sleep apnea is the representative sleep disorder that shows how deeply cytokines are involved in their pathophysiologic mechanisms of sleep disorders. Though there are many controversial issues on this topic, more mysterious part of normal sleep physiology and sleep disorders will be revealed in near future through thorough studies on sleep and cytokine.

• BMB Reports
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• v.49 no.9
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• pp.459-473
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• 2016

Neurodegenerative diseases (NDs) often involve the formation of abnormal and toxic protein aggregates, which are thought to be the primary factor in ND occurrence and progression. Aged neurons exhibit marked increases in aggregated protein levels, which can lead to increased cell death in specific brain regions. As no specific drugs/therapies for treating the symptoms or/and progression of NDs are available, obtaining a complete understanding of the mechanism underlying the formation of protein aggregates is needed for designing a novel and efficient removal strategy. Intracellular proteolysis generally involves either the lysosomal or ubiquitin-proteasome system. In this review, we focus on the structure and assembly of the proteasome, proteasome-mediated protein degradation, and the multiple dynamic regulatory mechanisms governing proteasome activity. We also discuss the plausibility of the correlation between changes in proteasome activity and the occurrence of NDs.

• Biomolecules & Therapeutics
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• v.22 no.1
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• pp.1-9
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• 2014

Vascular endothelial growth factor (VEGF)-VEGF receptor (VEGFR) system has been shown to play central roles not only in physiological angiogenesis, but also in pathological angiogenesis in diseases such as cancer. Based on these findings, a variety of anti-angiogenic drugs, including anti-VEGF antibodies and VEGFR/multi-receptor kinase inhibitors have been developed and approved for the clinical use. While the clinical efficacy of these drugs has been clearly demonstrated in cancer patients, they have not been shown to be effective in curing cancer, suggesting that further improvement in their design is necessary. Abnormal expression of an endogenous VEGF-inhibitor sFlt-1 has been shown to be involved in a variety of diseases, such as preeclampsia and aged macular degeneration. In addition, various factors modulating angiogenic processes have been recently isolated. Given this complexity then, extensive studies on the interrelationship between VEGF signals and other angiogenesis-regulatory systems will be important for developing future strategies to suppress diseases with an angiogenic component.