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Kim, Hyemin,Kim, Yejin,Bae, Seyeon,Lim, Seung Hyeon,Jang, Mirim,Choi, Jiyea,Jeon, Jane,Hwang, Young-il,Kang, Jae Seung,Lee, Wang Jae Mary Ann Liebert 2015 ANTIOXIDANTS AND REDOX SIGNALING Vol.23 No.16
<P>Aims: The developing brain of a neonate is particularly susceptible to damage by vitamin C deficiency because of its rapid growth and immature antioxidant system. Cognitive impairment and sensory motor deficits are found in the adult brain upon vitamin C deficiency. Therefore, the aim of this study was to clarify the role of vitamin C in its own right and its related mechanisms in Gulo(-/-) mice incapable of synthesizing vitamin C. Results: When vitamin C supplementation was ceased for 2 weeks until delivery, stillbirths and a significant reduction in neonatal mice were observed and the growth of neonates was remarkably decreased. In addition, intraparenchymal hemorrhages were found in most of the brains, especially in the stillborn neonates. In addition, the levels of malondialdehyde (MDA) and 8-isoprostanes were increased and structural abnormalities were found in the cortex, hippocampus, and cerebellum. Especially, vitamin C deficiency caused the failure of or a delay in the formation of cerebellar fissures accompanied by abnormal foliation and altered Purkinje cell alignment. In the developed adult brains from vitamin C-deficient Gulo(-/-) mice, the levels of glutathione, MDA, nitrate, IL-6, TNF-, and Bax were increased and the expression of the GABRA6 and calbindin-28k was decreased. Due to atrophy of the granule and Purkinje cells, the motor behavior of vitamin C-deficient Gulo(-/-) mice declined. Innovation and Conclusion: Vitamin C deficiency during gestation induces intraparenchymal hemorrhages and severe defects in the development of the cerebellum. In fully developed brains, it induces the functional impairment by altering the cellular composition in the cerebellum. Antioxid. Redox Signal. 23, 1270-1283.</P>
Han, Sangil,Shin, Youngmi,Sharma, Satyasheel,Mishra, Neeraj Kumar,Park, Jihye,Kim, Mirim,Kim, Minyoung,Jang, Jinbong,Kim, In Su American Chemical Society 2014 Organic letters Vol.16 No.9
<P>A rhodium(III)-catalyzed oxidative olefination of 1,2-disubstituted arylhydrazines with alkenes via sp<SUP>2</SUP> C–H bond activation followed by an intramolecular aza-Michael reaction is described. This strategy allows the direct and efficient construction of highly substituted 2,3-dihydro-1<I>H</I>-indazole scaffolds.</P><P><B>Graphic Abstract</B> <IMG SRC='http://pubs.acs.org/appl/literatum/publisher/achs/journals/content/orlef7/2014/orlef7.2014.16.issue-9/ol500865j/production/images/medium/ol-2014-00865j_0003.gif'></P><P><A href='http://pubs.acs.org/doi/suppl/10.1021/ol500865j'>ACS Electronic Supporting Info</A></P>
Mishra, Neeraj Kumar,Park, Jihye,Sharma, Satyasheel,Han, Sangil,Kim, Mirim,Shin, Youngmi,Jang, Jinbong,Kwak, Jong Hwan,Jung, Young Hoon,Kim, In Su The Royal Society of Chemistry 2014 Chemical communications Vol.50 No.18
<P>The rhodium-catalyzed oxidative alkenylation of <I>N</I>-benzyltriflamides with olefins followed by an intramolecular cyclization <I>via</I> C–H bond activation is described. This method results in the direct and efficient synthesis of highly substituted isoindoline frameworks.</P> <P>Graphic Abstract</P><P>The rhodium-catalyzed oxidative alkenylation of <I>N</I>-benzyltriflamides with olefins followed by an intramolecular cyclization <I>via</I> C–H bond activation is described. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c3cc49486a'> </P>
( Joo Kyung Park ),( Hye Min Kim ),( Ye Jin Kim ),( Mirim Jang ),( Ji Yea Choi ),( Jane Jeon ),( Sang Hyub Lee ),( Ji Kon Ryu ),( Yong Tae Kim ),( Wang Jae Lee ),( Jae Seung Kang ) 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background: The aim of this study was to evaluate the combination benefi t of telomerase peptide vaccination, GV1001 combined with gemcitabine in PDAC.Methods: Human pancreatic cancer cell lines (PANC1 and AsPC1) and pancreatic cancer stem cells (CD133+) were used in vitro experiment and to establish PDAC xenograft mouse model. Treatment groups were divided as follows; control, gemcitabine, GV 1001, gemcitabine+GV 1001. The changes of weight and tumor size were evaluated in regular intervals. The infi ammatory cytokines (IL-1ß, IL-6, TNF-a, INF-γ), leptin and ghrelin were measured from the serum of xenograft tumor model. Results: GV1001 did not have anti-cancer effects on PDAC cells. Gemcitabine and gemcitabine+GV 1001 treatment group had signifi cantly reduced tumor size among the different treatment groups (P < 0.001). Interestingly, study animals of gemcitabine+ GV 1001 treatment group did not have significant weight loss compared to gemcitabine group. Serum level of IL-1ß showed signifi cant decrease in groups with GV1001+gemcitabine and GV1001 alone (p=0.01). On the other hands, serum level of IFN -γ and TNF-a signifi cantly increased in GV1001 including treatment groups (p<0.001). Xenograft tumor tissue in gemcitabine treatment group showed that tumor tissue had been replaced by severe fi brosis whereas fi brosis was scarcely found in thetumor of gemcitabine+GV1001 treatment group. Conclusions: GV1001 showed benefi cial effects combined with gemcitabine in PDAC xenograft mice model preventing from emaciation. Moreover, GV 1001 combined with gemcitabine treatment showed signifi cant loss of fi brosis in tumor tissue as well as tumor cell death. Therefore, further investigation of GV1001 effect may give us useful insights to understand the biology of PDAC progression and the synergistic effects of anti-cancer drug delivery in PDAC treatment.
Won Kim,Seyeon Bae,Hyemin Kim,Yejin Kim,Jiwon Choi,Sun Young Lim,Hei Jin Lee,Jihyuk Lee,Jiyea Choi,Mirim Jang,Kyoung Eun Lee,Sun G,Chung,Young-il Hwang,Jae Seung Kang,Wang Jae Lee 대한해부학회 2013 Anatomy & Cell Biology Vol.46 No.4
The L-gulono-γ-lactone oxidase gene (Gulo) encodes an essential enzyme in the synthesis of ascorbic acid from glucose. On the basis of previous findings of bone abnormalities in Gulo-/- mice under conditions of ascorbic acid insufficiency, we investigated the effect of ascorbic acid insufficiency on factors related to bone metabolism in Gulo-/- mice. Four groups of mice were raised for 4 weeks under differing conditions of ascorbic acid insufficiency, namely, wild type; ascorbic acid-sufficient Gulo-/- mice, 3-week ascorbic acid-insufficient Gulo-/- mice, and 4-week ascorbic acid-insufficient Gulo-/- mice. Four weeks of ascorbic acid insufficiency resulted in significant weight loss in Gulo-/- mice. Interestingly, average plasma osteocalcin levels were significantly decreased in Gulo-/- mice after 3 weeks of ascorbic acid insufficiency. In addition, the tibia weight in ascorbic acid-sufficient Gulo-/- mice was significantly higher than that in the other three groups. Moreover, significant decreases in trabecular bone volume near to the growth plate, as well as in trabecular bone attachment to the growth plate, were evident in 3- or 4-week ascorbic acid-insufficient Gulo-/-. In summary, ascorbic acid insufficiency in Gulo-/- mice results in severe defects in normal bone formation, which are closely related to a decrease in plasma osteocalcin levels.