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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>
Macaulay, E,Nichol, R C,Bacon, D,Brout, D,Davis, T M,Zhang, B,Bassett, B A,Scolnic, D,Mö,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 < z < 0.85 to existing distance measurements of 122 low-redshift (z < 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>
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>
<P>AtCYP19-4 (also known as CYP5) was previously identified as interacting <I>in vitro</I> with GNOM, a member of a large family of ARF guanine nucleotide exchange factors that is required for proper polar localization of the auxin efflux carrier PIN1. The present study demonstrated that <I>OsCYP19-4,</I> a gene encoding a putative homologue of AtCYP19-4, was up-regulated by several stresses and showed over 10-fold up-regulation in response to cold. The study further demonstrated that the promoter of <I>OsCYP19-4</I> was activated in response to cold stress. An OsCYP19-4-GFP fusion protein was targeted to the outside of the plasma membrane via the endoplasmic reticulum as determined using brefeldin A, a vesicle trafficking inhibitor. An <I>in vitro</I> assay with a synthetic substrate oligomer confirmed that OsCYP19-4 had peptidyl-prolyl <I>cis-trans</I> isomerase activity, as was previously reported for AtCYP19-4. Rice plants overexpressing <I>OsCYP19-4</I> showed cold-resistance phenotypes with significantly increased tiller and spike numbers, and consequently enhanced grain weight, compared with wild-type plants. Based on these results, the authors suggest that OsCYP19-4 is required for developmental acclimation to environmental stresses, especially cold. Furthermore, the results point to the potential of manipulating <I>OsCYP19-4</I> expression to enhance cold tolerance or to increase biomass.</P>
Brassinosteroid-Induced Transcriptional Repression and Dephosphorylation-Dependent Protein Degradation Negatively Regulate BIN2-Interacting AIF2 (a BR Signaling-Negative Regulator) bHLH Transcription Factor
<P>Rec8 is a prominent component of the meiotic prophase chromosome axis that mediates sister chromatid cohesion, homologous recombination and chromosome synapsis. Here, we explore the prophase roles of Rec8. (i) During the meiotic divisions, Rec8 phosphorylation mediates its separase-mediated cleavage. We show here that such cleavage plays no detectable role for chromosomal events of prophase. (ii) We have analyzed in detail three <I>rec8</I> phospho-mutants, with 6, 24 or 29 alanine substitutions. A distinct ‘separation of function’ phenotype is revealed. In the mutants, axis formation and recombination initiation are normal, as is non-crossover recombination; in contrast, crossover (CO)-related events are defective. Moreover, the severities of these defects increase coordinately with the number of substitution mutations, consistent with the possibility that global phosphorylation of Rec8 is important for these effects. (iii) We have analyzed the roles of three kinases that phosphorylate Rec8 during prophase. Timed inhibition of Dbf4-dependent Cdc7 kinase confers defects concordant with <I>rec8</I> phospho-mutant phenotypes. Inhibition of Hrr25 or Cdc5/polo-like kinase does not. Our results suggest that Rec8's prophase function, independently of cohesin cleavage, contributes to CO-specific events in conjunction with the maintenance of homolog bias at the leptotene/zygotene transition of meiotic prophase.</P>
<P>Motivation: Gene-gene interaction (GGI) is one of the most popular approaches for finding and explaining the missing heritability of common complex traits in genome-wide association studies. The multifactor dimensionality reduction (MDR) method has been widely studied for detecting GGI effects. However, there are several disadvantages of the existing MDR-based approaches, such as the lack of an efficient way of evaluating the significance of multi-locus models and the high computational burden due to intensive permutation. Furthermore, the MDR method does not distinguish marginal effects from pure interaction effects. Methods: We propose a two-step unified model based MDR approach (UM-MDR), in which, the significance of a multi-locus model, even a high-order model, can be easily obtained through a regression framework with a semi-parametric correction procedure for controlling Type I error rates. In comparison to the conventional permutation approach, the proposed semi-parametric correction procedure avoids heavy computation in order to achieve the significance of a multi-locus model. The proposed UM-MDR approach is flexible in the sense that it is able to incorporate different types of traits and evaluate significances of the existing MDR extensions. Results: The simulation studies and the analysis of a real example are provided to demonstrate the utility of the proposed method. UM-MDR can achieve at least the same power as MDR for most scenarios, and it outperforms MDR especially when there are some single nucleotide polymorphisms that only have marginal effects, which masks the detection of causal epistasis for the existing MDR approaches. Conclusions: UM-MDR provides a very good supplement of existing MDR method due to its efficiency in achieving significance for every multi-locus model, its power and its flexibility of handling different types of traits.</P>
<P>Hepatocellular carcinoma (HCC) has a high mortality rate and early detection of HCC is crucial for the application of effective treatment strategies. HCC is typically caused by either viral hepatitis infection or by fatty liver disease. To diagnose and treat HCC it is necessary to elucidate the underlying molecular mechanisms. As a major cause for development of HCC is fatty liver disease, we here investigated anomalies in regulation of lipid metabolism in the liver. We applied a tailored network-based approach to identify signaling hubs associated with regulation of this part of metabolism. Using transcriptomics data of HCC patients, we identified significant dysregulated expressions of lipid-regulated genes, across many different lipid metabolic pathways. Our findings, however, show that viral hepatitis causes HCC by a distinct mechanism, less likely involving lipid anomalies. Based on our analysis we suggest signaling hub genes governing overall catabolic or anabolic pathways, as novel drug targets for treatment of HCC that involves lipid anomalies.</P>
Ding, Xuheng,Treu, Tommaso,Suyu, Sherry H.,Wong, Kenneth C.,Morishita, Takahiro,Park, Daeseong,Sluse, Dominique,Auger, Matthew W.,Agnello, Adriano,Bennert, Vardha N.,Collett, Thomas E. Oxford University Press 2017 MONTHLY NOTICES- ROYAL ASTRONOMICAL SOCIETY Vol.472 No.1