Planetary period magnetic field oscillations in Saturn's magnetosphere: Postequinox abrupt nonmonotonic transitions to northern system dominance

[1] We examine the “planetary period” magnetic field oscillations observed in the “core” region of Saturn's magnetosphere (dipole L ≤ 12), on 56 near‐equatorial Cassini periapsis passes that took place between vernal equinox in August 2009 and November 2012. Previous studies have shown that these consist of the sum of two oscillations related to the northern and southern polar regions having differing amplitudes and periods that had reached near‐equal amplitudes and near‐converged periods ~10.68 h in the interval to ~1 year after equinox. The present analysis shows that an interval of strongly differing behavior then began ~1.5 years after equinox, in which abrupt changes in properties took place at ~6‐ to 8‐month intervals, with three clear transitions occurring in February 2011, August 2011, and April 2012, respectively. These are characterized by large simultaneous changes in the amplitudes of the two systems, together with small changes in period about otherwise near‐constant values of ~10.63 h for the northern system and ~10.69 h for the southern (thus, not reversed postequinox) and on occasion jumps in phase. The first transition produced a resumption of strong southern system dominance unexpected under northern spring conditions, while the second introduced comparably strong northern system dominance for the first time in these data. The third resulted in suppression of all core oscillations followed by re‐emergence of both systems on a time scale of ~85 days, with the northern system remaining dominant but not as strongly as before. This behavior poses interesting questions for presently proposed theoretical scenarios

DNA Methylation Profile Distinguishes Clear Cell Sarcoma of the Kidney from Other Pediatric Renal Tumors

<div><p></p><p>A number of specific, distinct neoplastic entities occur in the pediatric kidney, including Wilms’ tumor, clear cell sarcoma of the kidney (CCSK), congenital mesoblastic nephroma (CMN), rhabdoid tumor of the kidney (RTK), and the Ewing’s sarcoma family of tumors (ESFT). By employing DNA methylation profiling using Illumina Infinium HumanMethylation27, we analyzed the epigenetic characteristics of the sarcomas including CCSK, RTK, and ESFT in comparison with those of the non-neoplastic kidney (NK), and these tumors exhibited distinct DNA methylation profiles in a tumor-type-specific manner. CCSK is the most frequently hypermethylated, but least frequently hypomethylated, at CpG sites among these sarcomas, and exhibited 490 hypermethylated and 46 hypomethylated CpG sites in compared with NK. We further validated the results by MassARRAY, and revealed that a combination of four genes was sufficient for the DNA methylation profile-based differentiation of these tumors by clustering analysis. Furthermore, <i>THBS1</i> CpG sites were found to be specifically hypermethylated in CCSK and, thus, the DNA methylation status of these <i>THBS1</i> sites alone was sufficient for the distinction of CCSK from other pediatric renal tumors, including Wilms’ tumor and CMN. Moreover, combined bisulfite restriction analysis could be applied for the detection of hypermethylation of a <i>THBS1</i> CpG site. Besides the biological significance in the pathogenesis, the DNA methylation profile should be useful for the differential diagnosis of pediatric renal tumors.</p></div

Development of a Method To Measure DNA Methylation Levels by Using Methyl CpG-Binding Protein and Luciferase-Fused Zinc Finger Protein

DNA methylation, which is an important epigenetic event for transcriptional regulation, is regarded as a biomarker for cancer. A rapid and sensitive method for measuring DNA methylation levels in target genomic regions may enable early diagnosis of cancer. To detect DNA methylation levels conveniently, we developed a detection system for DNA methylation, designated as methylated DNA precipitation combined luciferase-fused zinc finger assay (MELZA), which uses methyl CpG-binding domain (MBD) and luciferase-fused zinc finger protein. This system comprises the following 3 steps: (1) MBD-based methylated DNA precipitation, (2) PCR amplification of the target genomic region, and (3) detection of the PCR product quantity by using luciferase-fused zinc finger protein. Using this system, we have accurately measured methylation levels of the androgen receptor gene promoter region in LNCaP, PC3, Du145, and whole blood cells. This system does not require bisulfite treatment, and all the steps can be automated. Therefore, it might be useful for measuring DNA methylation levels in clinical cancer diagnoses

Primers used for MassARRAY.

<p>F, forward; R, reverse. Lower case letters indicate tag sequences.</p

Hierarchical cluster analysis of methylation value (β) in Infinium assay on pediatric tumors.

<p>Two-way hierarchical cluster analysis of the methylation level of 1,494 probes (rows, equivalent to hyper- and hypomethylated genes shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062233#pone-0062233-t002" target="_blank">Table 2</a>) and three cases for each of clear cell sarcoma of the kidney (CCSK), rhabdoid tumor of the kidney (RTK), the Ewing’s sarcoma family of tumors (ESFT), and non-neoplastic kidney (NK) (columns) were performed using hclust in the R clustering package. The β-values ranged from 0 (unmethylated) to 1 (fully methylated) on a continuous scale.</p

Combined bisulfite restriction analysis (COBRA) of <i>THBS1</i> in pediatric renal tumors.

<p>Using the same PCR products as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062233#pone-0062233-g003" target="_blank">Figure 3</a>, COBRA analysis was performed by digesting with the HpyCH4IV enzyme. The HpyCH4IV site is equivalent to CpG18 (chr15:37,660,642-37,660,645/hg18) in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062233#pone-0062233-g003" target="_blank">Figure 3</a>. The positions of bands representing methylated and unmethylated DNA are indicated by arrows. As the control of HpyCH4IV digestion, 0, 50, and 100% methylated DNA were loaded on the same gel. WT: Wilms’ tumor.</p

The number of specifically methylated genes compared with other each of tumors and non-neoplastic kidney.

<p>Hypermethylation: difference of average β-value >0.3. Hypomethylation: difference of average β-value<−0.3.</p

The number of hyper- and hypomethylated genes in comparison with non-neoplastic kidney.

<p>Hypermethylation: difference of average β-value >0.3. Hypomethylation: difference of average β-value<−0.3.</p

Frequency of <i>THBS1</i> methylation by COBRA.

<p>Frequency of <i>THBS1</i> methylation by COBRA.</p

MassARRAY analysis of methylation in <i>THBS1</i>.

<p>In addition to the 6 cases for each tumor group, 9 and 21 cases of CMN and Wilms’ tumor (WT), respectively, were analyzed for DNA methylation of the <i>THBS1</i> CpG site, as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0062233#pone-0062233-g002" target="_blank">Figure 2A</a>. Different colored of circles mark the position of CpG within the sequence (straight line) and the levels of methylation are shown in color (red, low methylation level; yellow, high methylation level). Gray circles represent the unanalyzed CpG sites. WT: Wilms’ tumor.</p