A novel role of metal response element binding transcription factor 2 at the Hox gene cluster in the regulation of H3K27me3 by polycomb repressive complex 2.

Polycomb repressive complex 2 (PRC2) is known to play an important role in the regulation of early embryonic development, differentiation, and cellular proliferation by introducing methyl groups onto lysine 27 of histone H3 (H3K27me3). PRC2 is tightly associated with silencing of Hox gene clusters and their sequential activation, leading to normal development and differentiation. To investigate epigenetic changes induced by PRC2 during differentiation, deposition of PRC2 components and levels of H3K27me3 were extensively examined using mouse F9 cells as a model system. Contrary to positive correlation between PRC2 deposition and H3K27me3 level, down-regulation of PRC2 components by shRNA and inhibition of EZH1/2 resulted in unexpected elevation of H3K27me3 level at the Hox gene cluster despite its global decrease. We found that metal response element binding transcriptional factor 2 (MTF2), one of sub-stoichiometric components of PRC2, was stably bound to Hox genes. Its binding capability was dependent on other core PRC2 components. A high level of H3K27me3 at Hox genes in Suz12-knock out cells was reversed by knockdown of Mtf2.This shows that MTF2 is necessary to consolidate PRC2-mediated histone methylation. Taken together, our results indicate that expression of Hox gene clusters during differentiation is strictly modulated by the activity of PRC2 secured by MTF2.

A Case of Symptomatic Tracheal Diverticulum and Surgical Resection as a Treatment Modality.

Tracheal diverticulum is often diagnosed incidentally and, due to its rarity, there is no standard treatment. It is a benign entity, but has the potential to cause specific symptoms, such as chronic upper respiratory infection and chronic cough. Symptomatic tracheal diverticulum can be medically treated, but likelihood of recurrence is high. We report a case of surgical resection of symptomatic tracheal diverticulum to prevent recurrence.

ZNF224, Krüppel like zinc finger protein, induces cell growth and apoptosis-resistance by down-regulation of p21 and p53 via miR-663a.

ZNF224 is a Krüppel-associated box-containing zinc-finger protein which represses gene transcription by interacting with various co-repressors. However, its consensus DNA sequences and target genes are not fully identified. In this study, we identified and characterized consensus DNA sequences containing 5'-CAGC-3' recognized by ZNF224 through ChIP-sequencing, which further confirmed by ELISA, SPR, qPCR, and luciferase activity assay. ZNF224 increased miR-663a transcription by binding to miR-663a promoter, which in turn binds to 3' UTR of p53 and p21 to decrease their expression. miR-663a antagonist abolished ZNF224-mediated suppression of p21 and p53, resulting in the enhanced apoptosis by CPT. The analyses using human breast ductal carcinoma tissues exhibited that the expression of ZNF224 and miR-663a was increased in cancer compared to non-cancer region. Consequently, ZNF224 increases cell survival and decreases apoptosis by decreasing the expression of p53 and p21 via miR-663a as a transcriptional activator. Taken together, we identified and characterized DNA binding element of ZNF224, and its target genes, miR-663a, which provides a novel insight in the down-regulation of p21 and p53 via miR-663a by ZNF224 in breast cancer.

A successfully treated case of gorham-stout syndrome with sternal involvement.

Gorham-Stout Syndrome (GSS) is a rare disease characterized by localized bone resorption. Any part of the skeleton may be affected; therefore, symptoms can vary depending on the site involved. Pathological analysis reveals lymphovascular proliferation and osteolysis in the affected lesion, but the etiology of the disease is poorly understood. When GSS occurs in the chest, chylothorax or respiratory failure may occur. Thus far, a standard treatment for GSS has not been established, and the prognosis remains unknown. The following case report describes a successfully treated case of GSS in a 16-year-old boy with an affected sternum and ribs.

Neuromorphic crossbar circuit with nanoscale filamentary-switching binary memristors for speech recognition.

In this paper, a neuromorphic crossbar circuit with binary memristors is proposed for speech recognition. The binary memristors which are based on filamentary-switching mechanism can be found more popularly and are easy to be fabricated than analog memristors that are rare in materials and need a more complicated fabrication process. Thus, we develop a neuromorphic crossbar circuit using filamentary-switching binary memristors not using interface-switching analog memristors. The proposed binary memristor crossbar can recognize five vowels with 4-bit 64 input channels. The proposed crossbar is tested by 2,500 speech samples and verified to be able to recognize 89.2% of the tested samples. From the statistical simulation, the recognition rate of the binary memristor crossbar is estimated to be degraded very little from 89.2% to 80%, though the percentage variation in memristance is increased very much from 0% to 15%. In contrast, the analog memristor crossbar loses its recognition rate significantly from 96% to 9% for the same percentage variation in memristance.

Device/Circuit co-design guide for passive memristor array with non-linear current-voltage behavior.

In this paper, the non-linearity in memristor's current-voltage relationship that can affect half-selected cells is analyzed. From the simulation, for the V(DD)/2 scheme, if the non-linear coefficient is larger than 8, unwanted resistance loss during the write time can be suppressed less than 10%. Comparing the V(DD)/2 and V(DD)/3 scheme, the V(DD)/2 scheme can reduce the current consumption by 2 orders of magnitude with little larger resistance change in half-selected cells than the V(DD)/3.