• Nutrition Research and Practice
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• v.15 no.6
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• pp.673-685
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• 2021

BACKGROUND/OBJECTIVES: Obesity is associated with the impaired regulation of T cells characterized by increased numbers of Th1 and Th17 cells and the dysregulation of vitamin D metabolism. Both obesity and vitamin D have been reported to affect autophagy; however, a limited number of studies have investigated the effects of vitamin D on T cell autophagy in obese mice. Therefore, we aimed to determine whether in vitro treatment with vitamin D affects the proliferation, function, and autophagy of T cells from obese and control mice. MATERIALS/METHODS: Five-week-old male C57BL/6 mice were fed control or high-fat diets (10% or 45% kcal fat: CON or HFDs, respectively) for 12 weeks. Purified T cells were stimulated with anti-CD3 and anti-CD28 monoclonal antibodies and cultured with either 10 nM 1,25(OH)₂D₃ or 0.1% ethanol (vehicle control). The proliferative response; expression of CD25, Foxp3, RORγt, and autophagy-related proteins (LC3A/B, SQSTM1/P62, BECLIN-1, ATG12); and the production of interferon (IFN)-γ, interleukin (IL)-4, IL-17A, and IL-10 by T cells were measured. RESULTS: Compared with the CON group, T cell proliferation tended to be lower, and the production of IFN-γ was higher in the HFD group. IL-17A production was reduced by 1,25(OH)2D₃ treatment in both groups. The LC3 II/I ratio was higher in the HFD group than the CON group, but P62 did not differ. We observed no effect of vitamin D treatment on T cell autophagy. CONCLUSIONS: Our findings suggest that diet-induced obesity may impair the function and inhibit autophagy of T cells, possibly leading to the dysregulation of T cell homeostasis, which may be behind the aggravation of inflammation commonly observed in obesity.

• IMMUNE NETWORK
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• v.21 no.3
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• pp.18.1-18.13
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• 2021

TLR signaling is critical for broad scale immune recognition of pathogens and/or danger molecules. TLRs are particularly important for the activation and the maturation of cells comprising the innate immune response. In recent years it has become apparent that several different TLRs regulate the function of lymphocytes as well, albeit to a lesser degree compared to innate immunity. TLR2 heterodimerizes with either TLR1 or TLR6 to broadly recognize bacterial lipopeptides as well as several danger-associated molecular patterns. In general, TLR2 signaling promotes immune cell activation leading to tissue inflammation, which is advantageous for combating an infection. Conversely, inappropriate or dysfunctional TLR2 signaling leading to an overactive inflammatory response could be detrimental during sterile inflammation and autoimmune disease. This review will highlight and discuss recent research advances linking TLR2 engagement to autoimmune inflammation.

• The Korean Journal of Physiology and Pharmacology
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• v.16 no.1
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• pp.17-24
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• 2012

The hypothalamus-pituitary-adrenocortex (HPA) axis is the central mediator of the stress response. The supramammillary (SuM) region is relatively unique among the hypothalamic structures in that it sends a large, direct projection to the hippocampal formation. It has been shown that mild stress could activate the SuM cells that project to the hippocampus. However, the role of these cell populations in modulating the stress response is not known. The present study examined the effect of stress on different populations of SuM cells that project to the hippocampus by injecting the fluorescent retrograde tracer, fluorogold (FG), into the hippocampus and utilizing the immunohistochemistry of choline acetyltransferase (ChAT), corticotrophin releasing factor (CRF), serotonin (5-HT), glutamate decarboxylase (GAD), tyrosine hydroxylase (TH) and NADPH-d reactivity. Immobilization (IMO) stress (2 hr) produced an increase in the expression of ChAT- immunoreactivity, and tended to increase in CRF, 5-HT, GAD, TH-immunoreactivity and nitric oxide (NO)-reactivity in the SuM cells. Fifty-three percent of 5-HT, 31% of ChAT and 56% of CRF cells were double stained with retrograde cells from the hippocampus. By contrast, a few retrogradely labeled cells projecting to the hippocampus were immunoreactive for dopamine, ${\gamma}$-aminobutyric acid (GABA) and NO. These results suggest that the SuM region contains distinct cell populations that differentially respond to stress. In addition, the findings suggest that serotonergic, cholinergic and corticotropin releasing cells projecting to the hippocampus within the SuM nucleus may play an important role in modulating stress-related behaviors.

• The Korean journal of internal medicine
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• v.33 no.6
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• pp.1210-1223
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• 2018

Background/Aims: The co-occurrence of obesity aggravates asthma symptoms. Diet-induced obesity increases helper T cell (TH) 17 cell differentiation in adipose tissue and the spleen. The 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor pravastatin can potentially be used to treat asthma in obese patients by inhibiting interleukin 17 (IL-17) expression. This study investigated the combined effects of pravastatin and anti-IL-17 antibody treatment on allergic inflammation in a mouse model of obesity-related asthma. Methods: High-fat diet (HFD)-induced obesity was induced in C57BL/6 mice with or without ovalbumin (OVA) sensitization and challenge. Mice were administered the anti-IL-17 antibody, pravastatin, or both, and pathophysiological and immunological responses were analyzed. Results: HFD exacerbated allergic airway inflammation in the bronchoalveolar lavage fluid of HFD-OVA mice as compared to OVA mice. Blockading of the IL-17 in the HFD-OVA mice decreased airway hyper-responsiveness (AHR) and airway inflammation compared to the HFD-OVA mice. Moreover, the administration of the anti-IL-17 antibody decreased the leptin/adiponectin ratio in the HFD-OVA but not the OVA mice. Co-administration of pravastatin and anti-IL-17 inhibited airway inflammation and AHR, decreased goblet cell numbers, and increased adipokine levels in obese asthmatic mice. Conclusions: These results suggest that the IL-17-leptin/adiponectin axis plays a key role in airway inflammation in obesity-related asthma. Our findings suggest a potential new treatment for IL-17 as a target that may benefit obesity-related asthma patients who respond poorly to typical asthma medications.

• Korean Journal of Environmental Biology
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• v.17 no.3
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• pp.331-335
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• 1999

The present study was carried out to investigate the combined effect of radiation and photoperiod (PP) regimes on Tradescantia 4430 somatic cell mutations. Potted plants were irradiated with 0.3, 0.5 and 1.0 Gy of gamma radiation from 60Co source. The plants irradiated only with gamma radiation were used as control group (CT). The somatic cell mutation rate in 0.5 Gy irradiated CT and PP20 group started to increase on the 6th day and reached a maximum value on the l0th day and 9th day after irradiation while the rate in the experimental group under 4 hours of photoperiod a day (PP4) started to increase on the l0th day and reached a maximal value on the 16th day post-irradiation. The slope of dose-response curve in CT was 5.99 ($r^2$=0.99), while it was 6.93 ($r^2$=0.98) in PP20 and 11.74 ($r^2$=0.99) in PP4, respectively. The biological efficacy of radiation in the induction of pink mutation increased by 15.7% in PP20 and 95.9 % in PP4, respectively. It is suggested that photoperiod regimes unfavorable to the plant have an additive effect on radiation-induced mutations and a delaying or inhibiting effect on cell damage repair, as well.

• Applied Chemistry for Engineering
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• v.29 no.6
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• pp.696-702
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• 2018

Recently, the current thermal battery technology needs new materials for electrodes in the power and energy density to meet various space and defense requirements. In this paper, to replace the pellet type Li(Si) anode having limitations of the formability and capacity, electrochemical properties of the lithium anode with high density for thermal batteries were investigated. The lithium anode (Li 17, 15, 13 wt%) was fabricated by mixing the molten lithium and iron powder used as a binder to hold the molten lithium at $500^{\circ}C$. The single cell with 13 wt% lithium showed a stable performance. The 2.06 V (OCV) of the lithium anode was significantly improved compared to 1.93 V (OCV) of the Li(Si) anode. Specific capacities during the first phase of the lithium anode and Li(Si) were 1,632 and $1,181As{\cdot}g^{-1}$, respectively. As a result of the thermal battery performance test at both room and high temperatures, the voltage and operating time of lithium anode thermal batteries were superior to those of using Li(Si) anode thermal batteries. The power and energy densities of Li anode thermal batteries were also remarkably improved.

• Biomedical Science Letters
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• v.19 no.2
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• pp.142-146
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• 2013

Enterotoxigenic Bacteroides fragilis (ETBF) causes inflammatory diarrhea in humans and animals and is also implicated in colorectal cancer. ETBF-infected mice exhibit a prominent large intestinal inflammation characterized by neutrophil infiltration and induction of the Th17 response. In this study, we examined differences in the secreted cytokine profile of the cecum and proximal colon of ETBF-infected mice using an antibody array. Of the cytokines examined, we found that the cecal tissues from ETBF-infected mice secreted elevated levels of G-CSF, IL-6, IL-17 and LIX compared to non-toxigenic Bacteroides fragilis (NTBF) and Mock infected mice. The proximal colon tissues from ETBF-infected mice secreted higher levels of G-CSF, IL-6, KC, LIX, MIP-1g and MCP-1. This study demonstrates that the cecum and colon should be considered separately when assays are used to determine immune responsiveness to enteric infections.

• Journal of Korean Neurosurgical Society
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• v.59 no.1
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• pp.1-5
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• 2016

Chronic subdural hematomas (CSHs) are generally regarded to be a traumatic lesion. It was regarded as a stroke in 17th century, an inflammatory disease in 19th century. From 20th century, it became a traumatic lesion. CSH frequently occur after a trauma, however, it cannot occur when there is no enough subdural space even after a severe head injury. CSH may occur without trauma, when there is sufficient subdural space. The author tried to investigate trends in the causation of CSH. By a review of literature, the author suggested a different view on the causation of CSH. CSH usually originated from either a subdural hygroma or an acute subdural hematoma. Development of CSH starts from the separation of the dural border cell (DBC) layer, which induces proliferation of DBCs with production of neomembrane. Capillaries will follow along the neomembrane. Hemorrhage would occur into the subdural fluid either by tearing of bridge veins or repeated microhemorrhage from the neomembrane. That is the mechanism of hematoma enlargement. Trauma or bleeding tendency may precipitate development of CSH, however, it cannot lead CSH, if there is no sufficient subdural space. The key determinant for development of CSH is a sufficient subdural space, in other words, brain atrophy. The most common and universal cause of brain atrophy is the aging. Modifying Virchow's description, CSH is sometimes traumatic, but most often caused by degeneration of the brain. Now, it is reasonable that degeneration of brain might play pivotal role in development of CSH in the aged persons.

• Biomolecules & Therapeutics
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• v.31 no.6
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• pp.611-618
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• 2023

Rhizome of Alisma orientale has been used as a traditional medicine for treating kidney diseases in East Asian countries. Its inhibitory effects on hypersensitivity responses have been reported for methanol extracts, with alisol B 23-acetate (AB23Ac) being the most active constituent among six terpenes in inhibiting the direct passive Arthus reaction. However, whether AB23Ac has efficacy against allergic asthma has not been tested to date. The in vivo efficacy of AB23Ac in an ovalbumin (OVA)-induced allergic asthma mouse model was evaluated by administrating AB23Ac before OVA sensitization or OVA challenge in BALB/c mice. AB23Ac suppressed antigen-induced degranulation of RBL-2H3 mast cells in a concentration-dependent manner. The administration of AB23Ac both before OVA sensitization and OVA challenge greatly lowered pulmonary resistance and the increase in immune cell counts and inflammatory responses around the peribronchial and perivascular regions. In addition, the inflammatory cytokine levels of Th1/Th2/Th17 cells in the bronchoalveolar lavage fluid decreased in the AB23Ac-treated groups. AB23Ac reduced the number of PAS-stained cells in the lungs. Furthermore, a computer modeling study indicated that AB23Ac can bind tightly to spleen tyrosine kinase (Syk). These results suggest that AB23Ac may ameliorate allergic asthma by suppressing immune responses in dendritic cells during sensitization and in mast cells during challenge periods.

• The Korean Journal of Food And Nutrition
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• v.36 no.6
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• pp.452-461
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• 2023

Hypertension caused by high-fat and high-salt diets is is a well-known significant risk factor for cardiovascular and cerebrovascular diseases. In this study, to confirm the relationship between hypertension and immune cells, angiotensin (Ang) II was administered to Dahl salt-sensitive (SS) rats and Dahl salt-resistant (SR) rats. Then the expression of immune cells and the proinflammatory cytokines were compared between the SS and SR rats. It was observed that after administration of Ang II (50ng/kg/min) for three weeks, blood pressure was increased in the SS rats, but there was no significant change in the SR rats. In addition, the expression of T helper (Th) cells and Th 17 cells in the spleen and the expression of Th cell Rorγt and regulatory T regulatory (Treg) cells in the peripheral blood mononuclear cells did not show a significant difference between the two experimental groups even after the administration of Ang II.IL-1β expression was significantly increased in the kidney tissue of the SS rats, while there was no significant difference in the IL-6 expression in all the experimental groups. The results of this study suggest that Ang II induces hypertension by stimulating IL-1β secretion from renal macrophage in SS rats.