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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>
Lee, Jong Seok,Krause, Roland,Schreiber, Jö,rg,Mollenkopf, Hans-Joachim,Kowall, Jane,Stein, Robert,Jeon, Bo-Young,Kwak, Jeong-Yeon,Song, Min-Kyong,Patron, Juan Pablo,Jorg, Sabine,Roh, Kyoungmin,Ch Elsevier 2008 Cell host & microbe Vol.3 No.2
<P><B>Summary</B></P><P>Attenuated strains of mycobacteria can be exploited to determine genes essential for their pathogenesis and persistence. To this goal, we sequenced the genome of H37Ra, an attenuated variant of <I>Mycobacterium tuberculosis</I> H37Rv strain. Comparison with H37Rv revealed three unique coding region polymorphisms. One polymorphism was located in the DNA-binding domain of the transcriptional regulator PhoP, causing the protein's diminished DNA-binding capacity. Temporal gene expression profiles showed that several genes with reduced expression in H37Ra were also repressed in an H37Rv phoP knockout strain. At later time points, genes of the dormancy regulon, typically expressed in a state of nonreplicating persistence, were upregulated in H37Ra. Complementation of H37Ra with H37Rv <I>phoP</I> partially restored its persistence in a murine macrophage infection model. Our approach demonstrates the feasibility of identifying minute but distinct differences between isogenic strains and illustrates the consequences of single point mutations on the survival stratagem of <I>M. tuberculosis.</I></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.