Proses Produksi Dan Pengemasan Yoghurtdicv. Cita Nasional Salatiga

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Dynamic Disorder and Potential Fluctuation in Two-Dimensional Perovskite

The structural and electronic properties of 2D perovskite (C₄H₉NH₃)₂PbBr₄ are investigated from first-principles calculations. It is found that despite the existence of carbon chain, the organic molecule C₄H₉NH₃ in 2D perovskite is able to rotate at room temperature, showing a highly dynamic behavior. The dynamic disorder of C₄H₉NH₃ introduces dynamic potential fluctuation, which is sufficient to localize the wave function and to separate the valence band maximum and conduction band minimum states. We further showed that, rather than a pure dipole rotation model, the disorder effect of the molecules can be better described by the motion of the net charge centers of the molecules, which contributes to the potential fluctuation. Hence, polar molecule is not the necessary condition to create potential fluctuation in perovskite, which is further demonstrated by the calculations of 2D inorganic perovskite Cs₂PbBr₄

sj-pdf-3-imr-10.1177_03000605221133655 - Supplemental material for Prediction of homologous recombination deficiency from cancer gene expression data

Supplemental material, sj-pdf-3-imr-10.1177_03000605221133655 for Prediction of homologous recombination deficiency from cancer gene expression data by Jun Kang, Jieun Lee, Ahwon Lee and Youn Soo Lee in Journal of International Medical Research</p

sj-pdf-1-imr-10.1177_03000605221133655 - Supplemental material for Prediction of homologous recombination deficiency from cancer gene expression data

Supplemental material, sj-pdf-1-imr-10.1177_03000605221133655 for Prediction of homologous recombination deficiency from cancer gene expression data by Jun Kang, Jieun Lee, Ahwon Lee and Youn Soo Lee in Journal of International Medical Research</p

sj-pdf-2-imr-10.1177_03000605221133655 - Supplemental material for Prediction of homologous recombination deficiency from cancer gene expression data

Supplemental material, sj-pdf-2-imr-10.1177_03000605221133655 for Prediction of homologous recombination deficiency from cancer gene expression data by Jun Kang, Jieun Lee, Ahwon Lee and Youn Soo Lee in Journal of International Medical Research</p

sj-pdf-4-imr-10.1177_03000605221133655 - Supplemental material for Prediction of homologous recombination deficiency from cancer gene expression data

Supplemental material, sj-pdf-4-imr-10.1177_03000605221133655 for Prediction of homologous recombination deficiency from cancer gene expression data by Jun Kang, Jieun Lee, Ahwon Lee and Youn Soo Lee in Journal of International Medical Research</p

Vapor Phase Growth and Imaging Stacking Order of Bilayer Molybdenum Disulfide

Various stacking patterns have been predicted in few-layer MoS₂, strongly influencing its electronic properties. Bilayer MoS₂ nanosheets have been synthesized by vapor phase growth. It is found that both A-B and A-A′ stacking configurations are present in bilayer MoS₂ nanosheets through optical images, and the different stacking patterns exhibit distinctive line shapes in the Raman spectra. By theory calculation, it is also concluded that the A-B and A-A′ stacking are the most stable and lowest-energy stacking in the five predicted stacking patterns of bilayer MoS₂ nanosheets, which proves the experimental observations

Dysregulation of X Chromosome Inactivation in High Grade Ovarian Serous Adenocarcinoma

<div><p>Background</p><p>One of the two copies of the X chromosome is randomly inactivated in females as a means of dosage compensation. Loss of X chromosome inactivation (XCI) is observed in breast and ovarian cancers, and is frequent in basal-like subtype and <i>BRCA1</i> mutation-associated breast cancers. We investigated the clinical implications of the loss of XCI in ovarian cancer and the association between the loss of XCI and <i>BRCA1</i> dysfunction.</p><p>Materials and Methods</p><p>We used open source data generated by The Cancer Genome Atlas (TCGA) Genome Data Analysis Centers. Ward’s hierarchical clustering method was used to classify the methylation status of the X chromosome.</p><p>Results</p><p>We grouped 584 high grade serous ovarian adenocarcinomas (HG-SOA) according to methylation status, loss of heterozygosity and deletion or gain of X chromosome into the following five groups: preserved inactivated X chromosome (Xi) group (n = 175), partial reactivation of Xi group (n = 100), p arm deletion of Xi group (n = 35), q arm deletion of Xi group (n = 44), and two copies of active X group (n = 230). We found four genes (<i>XAGE3</i>, <i>ZNF711</i>, <i>MAGEA4</i>, and <i>ZDHHC15</i>) that were up-regulated by loss of XCI. HG-SOA with loss of XCI showed aggressive behavior (overall survival of partial reactivation of Xi group: HR 1.7, 95% CI 1.1–2.5, two copies of active X group: HR 1.4, 95% CI 1.0–1.9). Mutation and hypermethylation of <i>BRCA1</i> were not frequent in HG-SOA with loss of XCI.</p><p>Conclusions</p><p>Loss of XCI is common in HG-SOA and is associated with poor clinical outcome. The role of <i>BRCA1</i> in loss of XCI might be limited. XCI induced aberrant expression of cancer-testis antigens, which may have a role in tumor aggressiveness.</p></div

Cancer-Testis Antigen Expression in Serous Endometrial Cancer with Loss of X Chromosome Inactivation

<div><p>Background</p><p>Cancer-testis antigens (CTAs) are potential targets for cancer immunotherapy. Many CTAs are located on the X chromosome and are epigenetically regulated. Loss of X chromosome inactivation (XCI) is observed in breast and ovarian cancers and is thought to be related to the overexpression of CTAs. We investigated the relation between expression of CTAs and loss of XCI in endometrial cancer.</p><p>Materials and Methods</p><p>We used data generated by The Cancer Genome Atlas Genome Data Analysis Centers and data for <i>Xist</i> knockout mice available at the Gene Expression Omnibus.</p><p>Results</p><p>The status of XCI was estimated by methylation status, and deletion or gain of the X chromosome. The endometrial cancers were classified into the following three groups: preserved inactivated X chromosome (Xi) (n = 281), partial reactivation of Xi (n = 52), and two copies of active X group (n = 38). Loss of XCI was more common in serous adenocarcinoma. Expression of CTAs increased in endometrial cancer with loss of XCI, which was accompanied by global hypomethylation. Expression of CTAs did not increase in <i>Xist</i> knockout mice.</p><p>Conclusions</p><p>Loss of XCI is common in serous adenocarcinoma. Global hypomethylation, and not loss of XCI, is the main mechanism of overexpression of CTAs.</p></div

<i>XIST</i> expression and <i>BRCA1</i> mutations and methylation.

<p>*, sample size is different in each analysis</p><p>†, statistically significant</p><p>‡, <i>P</i>-value of fisher’s exact test to compare frequency of <i>BRCA1</i> germline mutations in cluster 4 (33.3%) with other clusters (5.9%)</p><p><i>XIST</i> expression and <i>BRCA1</i> mutations and methylation.</p