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          Clinical implication of crescentic lesions in immunoglobulin A nephropathy

          Lee, Mi Jung,Kim, Seung Jun,Oh, Hyung Jung,Ko, Kwang Il,Koo, Hyang Mo,Kim, Chan Ho,Doh, Fa Mee,Yoo, Tae-Hyun,Kang, Shin-Wook,Choi, Kyu Hun,Lim, Beom Jin,Jeong, Hyeon Joo,Han, Seung Hyeok Oxford University Press 2014 Nephrology, dialysis, transplantation Vol.29 No.2

          <P><B>Background</B></P><P>To date, there has been much controversy about the role of crescentic lesion as a significant prognostic factor in immunoglobulin A nephropathy (IgAN). This study evaluated whether crescentic lesions predict adverse renal outcomes in IgAN patients.</P><P><B>Methods</B></P><P>A total of 430 patients with biopsy-proven IgAN between January 2000 and December 2009 were included. Histological variables of the Oxford classification (Oxford-MEST) and the presence of crescents were assessed. The primary endpoint was a 50% decline in estimated glomerular filtration rate.</P><P><B>Results</B></P><P>Of the 430 patients, 81 (18.8%) had a crescentic lesion. During a mean follow-up of 61 months, the primary outcome occurred in 19 (23.5%) patients with crescents compared with 40 (11.5%) patients without crescents (P = 0.01). A Kaplan–Meier plot showed that the 10-year renal survival rate was significantly lower in patients with crescents than patients without crescents (P = 0.01). However, in a multivariable Cox analysis which included clinical factors and the Oxford-MEST, crescents were not significantly associated with an increased risk of developing the primary outcome [hazard ratio: 0.71, 95% confidence interval (CI) 0.36–1.41, P = 0.33]. Furthermore, adding crescents to the Oxford-MEST did not improve the discriminative ability for the prediction of renal outcomes [<I>c</I>-statistic: 0.86 (0.81–0.91) vs. 0.86 (0.80–0.91), P = 0.21].</P><P><B>Conclusion</B></P><P>Crescentic lesion was not an independent prognostic factor, suggesting that crescents have limited value in predicting renal outcomes of IgAN.</P>

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          First cosmological results using Type Ia supernovae from the Dark Energy Survey: measurement of the Hubble constant

          Macaulay, E,Nichol, R C,Bacon, D,Brout, D,Davis, T M,Zhang, B,Bassett, B A,Scolnic, D,,ller, A,D’Andrea, C B,Hinton, S R,Kessler, R,Kim, A G,Lasker, J,Lidman, C,Sako, M,Smith, M,Sullivan, M,Abbo Oxford University Press 2019 MONTHLY NOTICES- ROYAL ASTRONOMICAL SOCIETY Vol.486 No.2

          <B>ABSTRACT</B><P>We present an improved measurement of the Hubble constant (H0) using the ‘inverse distance ladder’ method, which adds the information from 207 Type Ia supernovae (SNe Ia) from the Dark Energy Survey (DES) at redshift 0.018 &lt; z &lt; 0.85 to existing distance measurements of 122 low-redshift (z &lt; 0.07) SNe Ia (Low-z) and measurements of Baryon Acoustic Oscillations (BAOs). Whereas traditional measurements of H0 with SNe Ia use a distance ladder of parallax and Cepheid variable stars, the inverse distance ladder relies on absolute distance measurements from the BAOs to calibrate the intrinsic magnitude of the SNe Ia. We find H0 = 67.8 ± 1.3 km s−1 Mpc−1 (statistical and systematic uncertainties, 68 per cent confidence). Our measurement makes minimal assumptions about the underlying cosmological model, and our analysis was blinded to reduce confirmation bias. We examine possible systematic uncertainties and all are below the statistical uncertainties. Our H0 value is consistent with estimates derived from the Cosmic Microwave Background assuming a ΛCDM universe.</P>

        • The Oxford classification as a predictor of prognosis in patients with IgA nephropathy.

          Kang, Seok Hui,Choi, Sun Ryoung,Park, Hoon Suk,Lee, Ja Young,Sun, In O,Hwang, Hyeon Seok,Chung, Byung Ha,Park, Cheol Whee,Yang, Chul Woo,Kim, Yong Soo,Choi, Yeong Jin,Choi, Bum Soon Springer International ; Oxford University Press 2012 Nephrology, dialysis, transplantation Vol.27 No.1

          <P>In 2009, the Oxford classification was developed as a pathological classification system for immunoglobulin A nephropathy (IgAN) to predict the risk of disease progression. The aim of this retrospective study was to evaluate the clinical and pathologic relevance of the Oxford classification in Korean patients with a pathologic diagnosis of IgAN.</P>

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          The prolyl isomerase Pin1 interacts with a ribosomal protein S6 kinase to enhance insulin-induced AP-1 activity and cellular transformation

          Lee, N. Y.,Choi, H.-K.,Shim, J.-H.,Kang, K.-W.,Dong, Z.,Choi, H. S. Oxford University Press 2009 Carcinogenesis Vol.30 No.4

          <P>Phosphorylation of proteins on serine or threonine residues that immediately precede proline (pSer/Thr-Pro) is specifically catalyzed by the peptidyl-prolyl cis-trans isomerase Pin1 and is a central signaling mechanism in cell proliferation and transformation. Although Pin1 is frequently overexpressed in hepatocellular carcinoma (HCC), the molecular mechanism of Pin1 in HCC has not been completely elucidated. Here, we show that Pin1 interacts with p70S6K in vitro and ex vivo. Overexpression of Pin1 resulted in enhanced p70S6K phosphorylation induced by insulin in SK-HEP-1 cells. In contrast, Pin1(-/-) mouse embryonic fibroblasts (MEFs) exhibited significantly decreased insulin-induced p70S6K phosphorylation compared with Pin1(+/+) MEFs. Furthermore, Pin1 enhanced the insulin-induced extracellular signal-regulated protein kinase (ERK)1/2 phosphorylation through its interaction with p70S6K, whereas the inhibition of p70S6K activity by rapamycin suppressed insulin-induced ERK1/2 phosphorylation in SK-HEP-1 cells. Hence, Pin1 affected activator protein-1 activity through p70S6K-ERK1/2 signaling in SK-HEP-1 cells. Most importantly, Pin1-overexpressing JB6 Cl41 cells enhanced neoplastic cell transformation promoted by insulin much more than green fluorescent protein-overexpressing JB6 Cl41 control cells. These results imply that Pin1 amplifies insulin signaling in hepatocarcinoma cells through its interaction with p70S6K, suggesting that Pin1 plays an important role in insulin-induced tumorigenesis and is a potential therapeutic target in hepatocarcinoma.</P>

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          Penta-<i>O</i>-galloyl-beta-<em t='"s"'>d-glucose suppresses tumor growth via inhibition of angiogenesis and stimulation of apoptosis: roles of cyclooxygenase-2 and mitogen-activated protein kinase pathways

          Huh, Jeong-Eun,Lee, Eun-Ok,Kim, Min-Seok,Kang, Kyung-Sun,Kim, Cheol-Ho,Cha, Bae-Cheon,Surh, Young-Joon,Kim, Sung-Hoon Oxford University Press 2005 Carcinogenesis Vol.26 No.8

          <P>Recent studies have revealed that 1,2,3,4,6-penta-<I>O</I>-galloyl-beta-<SMALL>D</SMALL>-glucose (PGG) has anti-tumorigenic activity <I>in vitro</I>. In the present work, we evaluated the <I>in vitro</I> and <I>in vivo</I> antiangiogenic and antitumor activities of PGG and examined its molecular mechanisms. PGG significantly inhibited the proliferation and tube formation in basic fibroblast growth factor (bFGF)-treated human umbilical vein endothelial cells (HUVECs) at non-cytotoxic concentrations. PGG effectively disrupted the bFGF-induced neo-vascularization in chick chorioallantoic membrane (CAM) and in Matrigel plugs in the mice. When mice were intraperitoneally injected, PGG also significantly inhibited tumor angiogenesis induced by Lewis lung carcinoma (LLC) and the growth of LLC by 57 and 91% of control tumor weight at 4 and 20 mg/kg, respectively. Immunohistochemical analysis revealed decreased microvessel density, decreased expression of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF), reduced tumor cell proliferation and increased tumor cell apoptosis. Similarly, PGG significantly attenuated the expression of COX-2 and VEGF and reduced the secretion of VEGF and prostaglandin E<SUB>2</SUB> in bFGF-treated HUVECs. Furthermore, the COX-2 inhibitor NS398 significantly inhibited tube formation and neo-vascularization in CAM, supporting the role of COX-2 in PGG inhibition of angiogenesis. PGG diminished the phosphorylation of extracellular signal regulated kinase 1/2, Jun NH<SUB>2</SUB>-terminal kinase and activated phospho-p38 mitogen-activated protein kinase (MAPK) in a dose-dependent manner in bFGF-treated HUVECs. In addition, p38 inhibitor SB203580 abolished the downregulation of COX-2, VEGF and the antiproliferative activity by PGG. Taken together, our data demonstrate that PGG exerts antitumor activity primarily via inhibition of angiogenesis through COX-2 and MAPK- dependent pathways.</P>

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          Suppression of NF- B activity by NDRG2 expression attenuates the invasive potential of highly malignant tumor cells

          Kim, A.,Kim, M.-J.,Yang, Y.,Kim, J. W.,Yeom, Y. I.,Lim, J.-S. Oxford University Press 2009 Carcinogenesis Vol.30 No.6

          <P>Downregulation of the N-myc downstream-regulated gene 2 (NDRG2) gene is involved in the progression of aggressive forms of cancer, along with the poor prognosis of cancer patients. In the current study, we examined the effect of NDRG2 expression on the metastatic potential of HT1080 human fibrosarcoma and B16F10 murine melanoma cells in both in vitro and in vivo systems. In gelatin zymography, NDRG2 expression remarkably suppressed the matrix metalloproteinase (MMP)-9 activity and slightly inhibited MMP-2 activity of both cell lines. Tumor migration and invasion in vitro were significantly reduced by NDRG2 expression, and NDRG2 inhibited tumor cell proliferation in an anchorage-independent semisolid agar assay. Specifically, we found that NDRG2 affects invasion through suppression of nuclear factor kappa B (NF-kappa B) activity. In animal experiments, subcutaneously injected B16F10-NDRG2 cells showed delayed tumor growth compared with B16F10-mock cells. Furthermore, severe metastasis from primary tumor mass into the draining lymph nodes was observed after injection of B16F10-mock cells, but not with B16F10-NDRG2 cells. Pulmonary metastasis after intravenous injection of B16F10 cells was also reduced by NDRG2 expression. Intra- and peritumoral angiogenesis that is critical for the tumor growth and metastasis was clearly found in tumors after injection with B16F10-mock cells, whereas it was impaired in tumors after injection with B16F10-NDRG2 cells. Collectively, our data show that NDRG2 expression significantly suppresses tumor invasion by inhibiting MMP activities, which are regulated through the NF-kappa B signaling. Moreover, results from animal experiments provide evidence for the regulatory role of the NDRG2 gene in metastatic tumors.</P>

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          NDRG2 expression decreases with tumor stages and regulates TCF/β-catenin signaling in human colon carcinoma

          Kim, Young-Jun,Yoon, Sun Y.,Kim, Jong-Tae,Song, Eun Y.,Lee, Hee G.,Son, Hyun J.,Kim, Soo Y.,Cho, Daeho,Choi, Inpyo,Kim, Joo H.,Kim, Jae W. Oxford University Press 2009 Carcinogenesis Vol.30 No.4

          <P>NDRG (N-Myc downstream-regulated gene)-2 is a member of the NDRG family. Although it has been suggested that NDRG2 is involved in cellular differentiation and tumor suppression, its intracellular signal and regulatory mechanism are not well known. Here, we show the differential expression of NDRG2 in human colon carcinoma cell lines and tissues by reverse transcription–polymerase chain reaction and immunohistochemical analyses with monoclonal antibody against NDRG2. NDRG2 was strongly expressed in normal colonic mucosa and colonic adenomatous tissues (25 of 25) but not in all invasive cancer tissues [44 of 99 (44%)]. Most distinctive results indicated that the high expression level of NDRG2 has a positive correlation with tumor differentiation and inverse correlation with tumor invasion depth and Dukes’ stage of colon adenocarcinoma. To investigate the roles of NDRG2 in tumorigenesis, we used <I>in vitro</I> cell culture system. SW620 colon cancer cell line with a low level of intrinsic NDRG2 protein was transfected with <I>NDRG2</I>-expressing plasmid. TOPflash luciferase reporter assay showed that the transcriptional activity of T-cell factor (TCF)/lymphoid enhancer factor (LEF) was reduced by NDRG2 introduction, but not by the introduction of mutant NDRG2 generated by deletion or site-directed mutagenesis. Intracellular β-catenin levels were slightly reduced in the NDRG2-transfected SW620 cells and this regulation of β-catenin stability and TCF/LEF activity were mediated through the modulation of glycogen synthase kinase-3beta activity by NDRG2 function. Our results suggest that NDRG2 might play a pivotal role as a potent tumor suppressor by the attenuation of TCF/β-catenin signaling for the maintenance of healthy colon tissues.</P>

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          Phosphatidylinositol 3-kinase p85 regulatory subunit gene Met326Ile polymorphism in women with polycystic ovary syndrome

          Kim, J. J.,Choi, Y. M.,Hong, M. A.,Hwang, S. S.,Yoon, S. H.,Chae, S. J.,Jee, B. C.,Ku, S. Y.,Kim, J. G.,Moon, S. Y. Oxford University Press 2009 Human reproduction Vol.24 No.5

          <P>BACKGROUND: Insulin resistance is a core feature of polycystic ovary syndrome (PCOS). Phosphatidylinositol (PI) 3-kinase is an important enzyme in the early insulin signaling cascade and plays a key role in insulin-mediated glucose transport. In its regulatory subunit, p85alpha, there is a common amino acid substitution (the Met326Ile polymorphism), and this amino acid may be crucial for the function of the p85alpha regulatory subunit and PI3-kinase. METHODS: Analysis of the Met326Ile polymorphism was carried out on DNA samples from 256 PCOS patients and 283 controls. Clinical and biochemical profiles of participants were also compared. RESULTS: The genotype distribution of the Met326Ile polymorphism in the PCOS group was not different from that of the controls (Met326Met/Met326Ile/Ile326Ile rates were 73.4%/23.4%/3.2% and 70.3%/26.1%/3.6% for the PCOS and control groups, respectively, P = 0.72). The PCOS group was divided into two subgroups according to the presence of the variant 326Ile allele. Compared with those carrying at least one variant 326Ile allele, carriers with the Met326Met genotype had higher serum 17-hydroxyprogesterone (17-OHP) {1.1 [95% confidence interval (CI) 1.1-1.3] ng/ml in those with the Met326Met genotype versus 0.8 (95% CI 0.7-1.0) ng/ml in those with Ile326Ile and Met326Ile genotypes, P = 0.0073} and free testosterone levels [1.2 (95% CI 1.1-1.4) pg/ml for Met326Met genotype versus 0.9 (95% CI 0.6-1.3) pg/ml for Ile326Ile and Met326Ile genotypes, P = 0.038]. CONCLUSIONS: Our results suggest that the PI3-kinase gene Met326Ile polymorphism may not be a major determinant for the development of PCOS, but it may modulate the concentrations of serum 17-OHP or free testosterone in PCOS patients.</P>

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          Polymorphic expression of DAZ proteins in the human testis

          Kim, Byunghyuk,Lee, Youngbin,Kim, Yeonwha,Lee, Kyung Ho,Chun, Sunhye,Rhee, Kunsoo,Seo, Ju Tae,Kim, Soo Woong,Paick, Jae-Seung Oxford University Press 2009 Human reproduction Vol.24 No.6

          <P>BACKGROUND:DAZ is a male infertility gene located at the AZFc region of the Y chromosome. There are four copies of the DAZ gene that share a strong homology but are not identical to one another. In the present study, we carried out cDNA cloning and immunoblot analyses to determine whether all of the DAZ genes are actively expressed in the human testis. METHODS:AZFc deletion was detected by sequence-tagged site polymerase chain reaction (PCR) of genomic DNA isolated from blood samples. DAZ cDNAs were cloned with RT-PCR followed by sequence analysis. The expression of DAZ proteins in human testis was determined by immunoblot and compared with DAZ cDNA expression. RESULTS:Immunoblot analysis revealed four DAZ protein bands in testis samples that showed no deletions in the AZFc region. No specific bands were observed in samples from AZFc deletion patients. Testis samples from individuals with the partial AZFc deletion, gr/gr, showed two DAZ-specific bands. Interestingly, the sizes of DAZ-specific bands varied among individuals. Analysis of DAZ transcripts in testis samples revealed that the DAZ proteins were translated from the largest of the multiple transcripts originating from each single DAZ gene. CONCLUSIONS:All four DAZ genes are expressed in the human testis, and their products are highly polymorphic among men.</P>

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