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( Jihyun Yang ),( Geun Eog Ji ),( Myeong Soo Park ),( Yeong-je Seong ),( Yoon Sook Go ),( Hee Young Lee ),( Yina Fang ),( Myung-gyu Kim ),( Se Won Oh ),( Won Yong Cho ),( Sang-kyung Jo ) 대한신장학회 2021 Kidney Research and Clinical Practice Vol.40 No.4
Background: A healthy microbiome helps maintain the gut barrier and mucosal immune tolerance. Previously, we demonstrated that acute kidney injury (AKI) provoked dysbiosis, gut inflammation, and increased permeability. Here, we investigated the renoprotective effects of the probiotic Bifidobacterium bifidum BGN4 and the underlying mechanisms thereof. Methods: C57BL/6 mice were subjected to bilateral renal ischemia-reperfusion injury (IRI) or sham operation. In the probiotic-treated group, BGN4 was administered by gavage once daily, starting 2 weeks before injury. Results: Administration of BGN4 significantly increased gut microbiome diversity and prevented expansion of the Enterobacteriaceae and Bacteroidetes that were the hallmarks of AKI-induced dysbiosis. Further, BGN4 administration also significantly reduced other IRI-induced changes in the colon microenvironment, including effects on permeability, apoptosis of colon epithelial cells, and neutrophil and proinflammatory macrophage infiltration. Mononuclear cells co-cultured with BGN4 expressed significantly increased proportions of CD103<sup>+</sup>/ CD11c<sup>+</sup> and CD4<sup>+</sup> CD25<sup>+</sup> Treg cells, suggesting a direct immunomodulatory effect. BGN4 induced Treg expansion in colon, mesenteric lymph nodes (MNL), and kidney. BGN4 also reduced CX<sub>3</sub>CR<sub>1</sub><sup>intermediate</sup>Ly6C<sup>high</sup> monocyte infiltration and interleukin (IL)-17A suppression in the small intestine, which may have attenuated AKI severity, kidney IL-6 messenger RNA expression, and AKI-induced liver injury. Conclusion: Prior supplementation with BGN4 significantly attenuated the severity of IRI and secondary liver injury. This renoprotective effect was associated with increased Foxp3 and reduced IL-17A expression in the colon, MNL, and kidney, suggesting that BGN4-induced immunomodulation might contribute to its renoprotective effects. Probiotics may therefore be a promising strategy to reduce AKI severity and/or remote organ injury.
Risk factors and outcomes of acute renal infarction
( Jihyun Yang ),( Jun Yong Lee ),( Young Ju Na ),( Sung Yoon Lim ),( Myung Gyu Kim ),( Sang Kyung Jo ),( Wonyong Cho ) 대한신장학회 2016 Kidney Research and Clinical Practice Vol.35 No.2
Background: Renal infarction (RI) is an uncommon disease that is difficult to diagnose. As little is known about clinical characteristics of this disease, we investigated its underlying risk factors and outcomes. Methods: We performed a retrospective single-center study of 89 patients newly diagnosed with acute RI between January 2002 and March 2015 using imaging modalities. Clinical features, possible etiologies, and long-term renal outcome data were reviewed. Results: The patients`` mean age was 63.5 ± 15.42 years; 23.6% had diabetes and 56.2% had hypertension. Unilateral and bilateral involvements were shown in 80.9% and 19.1% of patients, respectively; proteinuria and hematuria were reported in 40.4% and 41.6%, respectively. Cardiovascular disease was the most common underlying disease, followed by renal vascular injury and hypercoagulability disorder. Fourteen patients had no specific underlying disease. At the time of diagnosis, acute kidney injury (AKI) was found in 34.8% of patients. Univariate analysis revealed diabetes mellitus (DM), leukocytosis, and high C-reactive protein (CRP) as significant risk factors for the development of AKI. On multivariate analysis, DM and high CRP levels were independent predictors for AKI. During follow-up, chronic kidney disease developed in 27.4% of patients. Univariate and multivariate Cox regression analyses showed old age to be an independent risk factor for this disease, whereas AKI history was a negative risk factor. Conclusion: DM patients or those with high CRP levels should be observed for renal function deterioration. Clinicians should also monitor for RI in elderly patients.
Yang, Jihyun,Ryu, Young Hee,Yun, Cheol-Heui,Han, Seung Hyun Wiley (John WileySons) 2009 Journal of leukocyte biology Vol.86 No.4
<P>Degenerative bone disease, marked by excessive loss of calcified matrix, is often associated with bacterial infections. Osteoclasts, which mediate the bone-resorptive process, are derived mainly from myeloid precursor cells of the monocyte/macrophage lineage, from which cells with phagocytic and inflammatory capacities may alternatively arise. Here, we investigated the effect of LTA, a major cell-wall virulence factor of Gram-positive bacteria, on osteoclast differentiation. Osteoclast precursors were prepared from C57BL/6 mouse BM using M-CSF and RANKL. When osteoclastogenesis was induced in the presence of staphylococcal LTA, LTA dose-dependently inhibited the differentiation of osteoclast precursors to mature osteoclasts. A corresponding inhibition of bone-resorptive function was observed in the reduced resorption area on calcium phosphate-coated culture plates. In contrast, the phagocytic and inflammatory potential of the osteoclast precursors increased in the presence of LTA. TLR2, known to recognize LTA, might be essential for the LTA inhibition of osteoclastogenesis, as the inhibition did not occur in the precursors from TLR2-deficient mice. Importantly, MyD88-dependent and MyD88-independent pathways would participate in the inhibition, as determined using MyD88-deficient cells. Moreover, LTA inhibited phosphorylation of ERK and JNK in osteoclast precursors stimulated with M-CSF and RANKL, concomitantly with a decreased DNA-binding activity of AP-1. These results suggest that staphylococcal LTA inhibits osteoclast differentiation primarily through TLR2 but also in part through MyD88 signaling, which in turn, inhibits activation of ERK, JNK, and AP-1.</P>
Yang, Jihyun,Park, Ok Jin,Lee, Yeon Ju,Jung, Hong-Moon,Woo, Kyung Mi,Choi, Youngnim WILEY-VCH Verlag 2008 European journal of immunology Vol.38 No.6
<P>The 4–1BB is a costimulatory molecule similar to the receptor activator of NF-&kgr;B ligand (RANKL), both of which are key factors for the differentiation of osteoclasts and are expressed mainly by activated T cells. The 4–1BB shares common signaling pathways with RANK, suggesting a potential role in osteoclastogenesis. In this study, the role of 4–1BB and 4–1BB ligand (4–1BBL) in osteoclastogenesis was investigated using 4–1BB<SUP>–/–</SUP> and 4–1BB<SUP>+/+</SUP> mice. Osteoclast precursors normally express 4–1BB and 4–1BBL after exposure to RANKL, which was confirmed by semi-quantitative RT-PCR and flow cytometry. The 4–1BB<SUP>–/– </SUP>mice had a slightly increased bone mass accompanied by a reduced osteoclastogenic ability of 4–1BB<SUP>–/–</SUP> bone marrow-derived macrophages (BMM) ex vivo. In addition, 4–1BB<SUP>–/–</SUP> BMM demonstrated hypophosphorylation of JNK and p38 and decreased induction of c-Fos in response to RANKL stimulation. Retroviral transduction of wild-type as well as partial-length 4–1BB, which lacks TNF receptor-associated factor 2-binding sites for signaling, restored the osteoclastogenic ability of 4–1BB<SUP>–/–</SUP> BMM. Furthermore, both recombinant 4–1BB and 4–1BBL enhanced RANKL-induced osteoclastogenesis by 4–1BB<SUP>+/+</SUP> BMM and the induction of c-Fos and NFATc1.Together, these results indicate that 4–1BBL and 4–1BB expressed on osteoclast precursors enhance RANKL-induced osteoclastogenesis via bi–directional signaling, findings that may delineate the complex nature of the 4–1BBL and 4–1BB interaction.</P><P>Supporting Information for this article is available at www.wiley-vch.de/contents/jc_2040/2008/37650_s.pdf</P>
Flexible graphene-based chemical sensors on paper substrates
Yang, Gwangseok,Lee, Chongmin,Kim, Jihyun,Ren, Fan,Pearton, Stephen J. The Royal Society of Chemistry 2013 Physical chemistry chemical physics Vol.15 No.6
<P>Graphene-based, flexible NO<SUB>2</SUB> sensors on paper substrates exhibited an immediate response (32–39%) once exposed to 200 ppm NO<SUB>2</SUB> gas under a strain of 0.5%. Chemical vapor deposition-grown graphene with a supporting poly(methyl methacrylate) layer was transferred onto paper substrates, followed by formation of two electrodes using silver paste. Current–voltage characteristics and dynamic sensing response were obtained under both relaxed and strained conditions. We demonstrate a facile method without complex photo-lithography and high vacuum processes for fabricating graphene-based flexible NO<SUB>2</SUB> sensors on paper substrates with high sensing response.</P> <P>Graphic Abstract</P><P>We demonstrate a simple method for fabricating graphene-based flexible chemical sensors on paper substrates with high sensing response. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c2cp43717a'> </P>