Channel detection on two-dimensional magnetic recording

Two-dimensional magnetic recording (TDMR) coupled with shingled-magnetic recording (SMR) is one of next generation techniques for increasing the hard disk drive (HDD) capacity up to 10 Tbit/in2 in order to meet the growing demand of mass storage.We focus on solving the tough problems and challenges on the detection end of TDMR. Since the reader works on the overlapped tracks, which are even narrower than the read head, the channel detector works in an environment of low signal-to-noise ratio (SNR), two-dimensional (2-D) inter-symbol interference (ISI) and colored noise, therefore it requires sophisticated detection techniques to provide reliable data recovery. Given that the complexity of optimal 2-D symbol detection is exponential on the data width, we had to choose suboptimal solutions.To build our research environment, we use an innovative Voronoi grain based channel model which captures the important features of SMR, such as squeezed tracks, tilted bit cells, 2-D ISI, electronic and media noise, etc. Then we take an in-depth exploration of channel detection techniques on the TDMR channel model. Our approaches extend the conventional 1-D detection techniques, by using a joint-track equalizer to optimize the 2-D partial-response (PR) target followed by the multi-track detector (MTD) for joint detection, or using the inter-track interference (ITI) canceller to estimate and cancel the ITI from side tracks, followed by a standard BCJR detector. We used the single-track detector (STD) for pre-detecting the side tracks to lower the overall complexity. Then we use pattern-dependent noise prediction (PDNP) techniques to linearly predict the noise sample, so as to improve the detection performance under colored media noise, and especially the data dependent jitter noise. The results show that our 2-D detectors provide significant performance gains against the conventional detectors with manageable complexity

Climate change dominates recent sedimentation and organic carbon burial in Lake Chenghai, southwest China

Lacustrine ecosystems are directly influenced by terrestrial soil erosion, and excessive sediment loading constitutes a significant and widespread environmental issue. In order to investigate the response of catchment soil erosion and organic carbon burial to climate change and human activity, a sediment core spanning the last 160 years was retrieved from Lake Chenghai in southwest China. Multi-proxy analysis including grain-size composition and geochemical indicators were undertaken in this study. The result of grain-size vs. standard deviation method shows that the sensitive component with a modal size of 13.2 μm is related to fluvial processes and sensitive to the catchment soil erosion. The increasing intensity of soil erosion was mainly determined by the weakening of Indian summer monsoon and global warming, as well as intensive human activities during the middle of 20 th century, which resulted in decreasing vegetation cover in Lake Chenghai catchment. The organic carbon burial rate was also attributed to the catchment disturbance, indicating that increased catchment soil erosion may impact the terrestrial carbon recycling

The Role of Factor Inhibiting HIF (FIH-1) in Inhibiting HIF-1 Transcriptional Activity in Glioblastoma Multiforme

<div><p>Glioblastoma multiforme (GBM) accounts for about 38% of primary brain tumors in the United States. GBM is characterized by extensive angiogenesis induced by vascular growth factors and cytokines. The transcription of these growth factors and cytokines is regulated by the <u>H</u>ypoxia-<u>I</u>nducible-<u>F</u>actor-1(HIF-1), which is a key regulator mediating the cellular response to hypoxia. It is known that <u>F</u>actor <u>I</u>nhibiting <u>H</u>IF-1, or FIH-1, is also involved in the cellular response to hypoxia and has the capability to physically interact with HIF-1 and block its transcriptional activity under normoxic conditions. Delineation of the regulatory role of FIH-1 will help us to better understand the molecular mechanism responsible for tumor growth and progression and may lead to the design of new therapies targeting cellular pathways in response to hypoxia. Previous studies have shown that the chromosomal region of 10q24 containing the FIH-1 gene is often deleted in GBM, suggesting a role for the FIH-1 in GBM tumorigenesis and progression. In the current study, we found that FIH-1 is able to inhibit HIF-mediated transcription of GLUT1 and VEGF-A, even under hypoxic conditions in human glioblastoma cells. FIH-1 has been found to be more potent in inhibiting HIF function than PTEN. This observation points to the possibility that deletion of 10q23-24 and loss or decreased expression of FIH-1 gene may lead to a constitutive activation of HIF-1 activity, an alteration of HIF-1 targets such as GLUT-1 and VEGF-A, and may contribute to the survival of cancer cells in hypoxia and the development of hypervascularization observed in GBM. Therefore FIH-1 can be potential therapeutic target for the treatment of GBM patients with poor prognosis.</p></div

Association of HIF-1α with p300 in the presence of FIH-1, PTEN in U87 cells.

<p>A: Western blot of HIF-1α from protein lysates of U87 cells incubated overnight either in hypoxic (3% oxygen) or normoxic (21% oxygen) conditions (top panel). No change of p300 protein levels was observed in the same samples (middle panel). β-actin was used as a loading control (lower panel). B: Association of HIF-1α with p300 in U87 cells: cells were transiently transfected with either FIH-1 or a PTEN expression plasmid, or both of them together for 24 hrs, and then incubated overnight under both normoxic and hypoxic conditions. Nuclear extracts were collected and subjected to immunoprecipitation with anti-p300 antibody followed by Western blot analysis with anti-HIF-1α (top panel) and IgG (middle panel). Nuclear extracts were also subjected to western blot analysis with anti- HIF-1α antibody (bottom panel).</p

Inhibition of VEGF-A expression by FIH-1.

<p>VEGF-A expression was controlled by FIH-1 in both normoxia and hypoxia. U87 cells were transfected with the FIH-1 expression plasmid at different doses (e.g. 0.5 µg/ml, 1.5 µg/ml) and cultured under both hypoxic and normoxic conditions. Total RNA was obtained and then RQ-PCR was performed using primers specific for VEGF-A and 36B4 (internal control). VEGF-A mRNA levels were decreased with FIH-1 overexpresssion under both normoxic and hypoxic conditions (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086102#pone-0086102-g004" target="_blank">Figure 4A</a>). FIH-1 mRNA levels were also measured as a control experiment (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0086102#pone-0086102-g004" target="_blank">Figure 4B</a>). The data here represent the mean of three independent experiments, and * represents p<0.05.</p

The mRNA levels of GLUT-1 were reduced with FIH-1 overexpression.

<p>1A and 1B: U87 cells were transfected with FIH-1-expression plasmid and cultured in both hypoxic (1B) and normoxic (1A) conditions. Total RNA was harvested and RQ-PCR was performed using primers specific for GLUT-1 and 36B4 (internal control). A significant decrease of GLUT-1 mRNA levels was observed in cells transfected with FIH-1 expression plasmid in both normoxia and hypoxia. The data here is the mean from three independent results. * Represents p value less than 0.05. 1C and 1D: The expression levels of GLUT-1 were decreased by overexpression of FIH-1 in U87 cells. U87 cells were transfected with constructs either expressing FIH-1 or with vector alone and incubated for 48 hrs under normoxic condition. Cells were collected and subjected to flow cytometry analysis. A reduction in GLUT-1 levels was detected in cells transfected with FIH-1 plasmid (1D) compared with cells transfected with control vector (1C), as shown in the P3 population.</p

Inhibit GLUT-1 transcription by FIH-I in U87 under hypoxia GLUT-1 expression was inhibited by PTEN under normoxic condition.

<p>U87 cells were transfected with FIH-1 and PTEN expression plasmids either alone or in combination and cultured in both hypoxic and normoxic conditions. 2A: Total RNA was obtained and followed with RQ-PCR using primers specific for GLUT-1 and 36B4 (internal control). A significant reduction of GLUT-1 mRNA levels was observed in cells expressing PTEN, FIH-1, or both under normoxic conditions, but interestingly, GLUT-1 mRNA levels were not changed in cells expressing PTEN under hypoxic conditions. Average and standard deviation of three independent experiments were calculated. * Represents p value less than 0.05. 2B: Whole cell lysates from each experimental condition were collected and protein levels of FIH-1 (top panel) and PTEN (middle panel) were examined by Western blot. β-actin was used as a loading control (lower panel).</p

The expression pattern of FIH-1 and VEGF-A in serially transplantable GBM cell lines.

<p>5A: The levels of VEGF-A mRNA were determined in different transplantable GBM xenografts by RQ-PCR. All values were normalized to the housekeeping gene 36B4. 5B: The levels of FIH-1 mRNA were determined in different transplantable GBM xenografts by real-time PCR. Values were normalized to the housekeeping gene 36B4. The levels of VEGF-A mRNA is inversely correlated with the levels of FIH-1 mRNA (correlation coefficient value r = −0.869, p = 0.025 (2-tailed), Pearson regression analysis was performed using SPSS software version 19.0). 5C: The association of p300 and HIF-1α was confirmed in GBM mouse xenograft cell line 6 and 44. The amount of p300 protein immunoprecipitated was same for each line. They also expressed similar levels of HIF-1α (bottom panel). 5D: FIH-1 expression in GBM xenografts by Immunohistostaining. High expression of FIH-1 was detected in GBM-44 line (brown color, marked as arrows), whereas no detectable levels of FIH-1 were found GBM-6, -12AT and -14.</p