908 research outputs found
Graduate Recital: Xingchen Liu, Piano; April 18, 2021
No full textKemp Recital HallApril 18, 2021Sunday Evening6:00 p.m
Chiu et al (2024) -- What To Do (and Not to Do) with Causal Panel Analysis under Parallel Trends
No full textManuscript by Albert Chiu, Xingchen Lan, Ziyi Liu, and Yiqing Xu. Reviews by Andrew Baker and Anton Strezhnev
Altering tensile and crack initiation behavior in a metastable β titanium alloy via designing grain size and precipitates
No full textConvocation Recital: Elliot Godinez, Marimba; Guangxao Xia, Trumpet; Klara Farren, Horn; AJ Nemsick, Trombone; Xingchen Liu, Piano; December 3, 2019
No full textKemp Recital HallDecember 3, 2019Tuesday Morning11:00 a.m
Convocation Recital: Jenn Carver, Timpani and Electronics; Erica Gallermo, Piano; Ya Chun Lee, Piano; Xingchen Liu, Piano; February 23, 2021
No full textCenter for the Performing ArtsFebruary 23, 2021Tuesday Morning11:00 a.m
sj-docx-1-onc-10.1177_11795549231203150 – Supplemental material for The RNA m6A-Binding Protein YTHDC1 Is Downregulated and Associated With M2 Macrophage Infiltration in Muscle-Invasive Bladder Cancer
No full textSupplemental material, sj-docx-1-onc-10.1177_11795549231203150 for The RNA m6A-Binding Protein YTHDC1 Is Downregulated and Associated With M2 Macrophage Infiltration in Muscle-Invasive Bladder Cancer by Lamei Zhao, Dongyan Han, Jianghua Zhu, Dexi Bi, Tingting Ding, Xingchen Zhu, Dengfeng Huang, Youhua Zhang, Ling Lu, Weijun Wu, Yaohui Gao, Hu Liu, Qiongyi Huang, Qing Wei and Xudong Yao in Clinical Medicine Insights: Oncology</p
Point Spread Function Estimation with Blind Deconvolution in Structured Illumination Microscopy
No full textStructured illumination microscopy (SIM) is a kind of wide-field super resolution imaging technique which achieves the resolution improvement by exploiting the interference patterns to obtain the information out of the observable region in Fourier space. The resolution improvement in SIM is done by analyzing the obtained image and restored the observed sample with software. This process is sensitive to the measured PSF, as the PSF is the main factor to do the image deblurring and parameters estimation. Frequently, the PSF of a SIM system is obtained by fitting the recorded beads image with the Gaussian function. However, the Gaussian fitting cannot retrieve the aberration and noise in the PSF. The blind image deconvolution method is a family of algorithms which can be used to restore the object and corresponding PSF from the degraded images. The novel Tangential Iterative Projections (TIP) algorithm is a kind of blind image deconvolution algorithm proposed by Wilding et al.. This algorithm is simple, fast and robust to the noise condition. It is proved that TIP can be implemented on both the multi-frame deconvolution scenario and single-frame scenario. The aim of this thesis is to verify whether TIP algorithm can retrieve a PSF, which can be used to do the SIM image reconstruction, from the SIM data. For this purpose, a simulated SIM optical system is built in Matlab to generate the SIM images, and both the single-frame TIP and multi-frame TIP frameworks are used to do the PSF retrieval. In addition, a new constraint for the PSF which is generated based on the diffraction limit of the optical system is implemented. In order to reduce the execution time and avoid the overfitting of the algorithm, a stop criterion is introduced. The result shows both the multi-frame TIP and single-frame TIP can be used to retrieve an effective PSF from the SIM data, and the single-frame TIP is more applicable and more accuracy compared with the multi-frame TIP.Electrical Engineering | Embedded System
A combined computational and experimental study of the adsorption of sulfur containing molecules on molybdenum disulfide nanoparticles
No full textCombining density functional theory calculations and temperature programmed desorption (TPD)
experiments, the adsorption behavior of various sulfur containing compounds, including C2H5SH,
CH3SCH3, tetrahydrothiophene, thiophene, benzothiophene, dibenzothiophene, and their
derivatives on the coordinately unsaturated sites of Mo27Sx model nanoparticles, are studied
systematically. Sulfur molecules with aromaticity prefer flat adsorption than perpendicular
adsorption. The adsorption of nonaromatic molecules is stronger than the perpendicular
adsorption of aromatic molecules, but weaker than the flat adsorption of them. With gradual
hydrogenation (HYD), the binding affinity in the perpendicular adsorption modes increases, while
in flat adsorption modes it increases first, then decreases. Significant steric effects on the
adsorption of dimethyldibenzothiophene were revealed in perpendicular adsorption modes. The
steric effect, besides weakening adsorption, could also activate the S–C bonds through
a compensation effect. Finally, by comparing the theoretical adsorption energies with the TPD
results, we suggest that HYD and direct-desulfurization path may happen simultaneously, but on
different active sites
Epigenetic regulation of gene expression by BRD4 in cancer and innate immune response
No full textEpigenetic regulation of gene expression plays essential roles in controlling normal cellular functions as well as abnormal cellular activities in human diseases like inflammatory diseases and cancers. The bromodomain-containing protein 4 (BRD4), one of the BET (bromodomain and extra terminal) family proteins, represents a class of epigenetic readers that regulate gene transcription by binding to acetylated lysine of histone and non-histone proteins via their bromodomains (BDs). This interaction either changes the availabilities of cis-regulatory elements by altering chromatin compacity or activates specific transcription factors, both of which contribute to transcriptional activation of BRD4’s target genes. BRD4 has been implicated in the dysregulated transcription of oncogenes and inflammatory genes during disease progression; thus, the small molecule inhibitors that target the bromodomains of BRD4, as well as other BET family proteins, are under clinical investigations.
Gastric cancer has become one of the leading malignancies that cause death with a 5-year survival rate of 10%. Although BET inhibitors (BETis) have shown potential therapeutic effects against gastric cancer, the detailed mechanism by which BRD4 facilities gastric cancer cell proliferation remains elusive. In an effort to understand the contribution of BET to gastric cancer development, we confirmed that BRD4 was overexpressed in gastric cancer patient tissues compared to normal tissue. Meanwhile, BET inhibitor JQ1 inhibited multiple gastric cancer cell proliferation by inducing BRD4-dependent cellular senescence. Depletion of BRD4, but not other BET proteins, recapitulated JQ1-induced cellular senescence with increased cellular SA--Galactose activity and elevated p21 levels. BRD4 inhibited p21 expression at the post-transcriptional level through activating the transcription of miR-106b-5p, which targets the 3’-UTR of p21 mRNA. Overexpression of miR-106b-5p prevented JQ1-induced p21 expression and BRD4 inhibition-associated cellular senescence, whereas miR-106b-5p inhibitor upregulated p21 and induced cellular senescence. Finally, we demonstrated that inhibition of E2F suppressed the binding of BRD4 to the promoter of miR-106b-5p and inhibited its transcription, leading to the increased p21 levels and cellular senescence in gastric cancer cells. Our results reveal a novel mechanism by which BRD4 regulates cancer cell proliferation by modulating the cellular senescence through the E2F/miR-106b-5p/p21 axis and provide new insights into using BET inhibitors as potential anti-cancer drugs.
Other than its critical role in facilitating tumor cell proliferation, BRD4 has also been investigated in the dysregulated cytokine production at the transcriptional level during inflammatory disease progression. BRD4 has been shown to activate NF-B-dependent inflammatory gene expression by binding to acetylated RelA subunit of NF-B through its bromodomains, highlighting its essential role in transcriptional regulation of cytokine production. Although the production of inflammatory cytokines is heavily regulated at the transcriptional level, a group of functional cytokines, such as interleukin-1 (IL-1) and IL-18, require post-translational maturation mediated by the activation of the inflammasome complex. In order to study the comprehensive role of BRD4 in cytokine production, we seek to investigate if BRD4 plays a role in regulating inflammasome activation and cytokine maturation. Using Salmonella enterica serovar Typhimurium (S. Typhimurium) as a NLRC4 inflammasome activator, we found that Brd4-deficient bone marrow-derived macrophages (BMDMs) displayed blunted NLRC4 inflammasome activation with decreased caspase-1 activation, Asc oligomerization, IL-1 maturation, gasdermin-D (Gsdmd) cleavage, and pyroptosis upon bacterial infection. RNA-seq results unveiled that the ablation of Brd4 in BMDMs suppressed the transcription of Naips and Nlrc4. Mechanistically, ChIP-seq analysis revealed that Brd4 co-localized with Irf8 and Pu.1 at the promoter regions of Naips, activating their transcriptions. Moreover, myeloid lineage-specific Brd4 conditional-knockout (Brd4-CKO) mice were more sensitive to S. Typhimurium infection with the significantly enhanced bacterial burden and tissue damages. Altogether, our findings emphasize the unexpected role of Brd4 in NLRC4 inflammasome activation through modulating the transcription of Naips and Nlrc4. ¬¬
In summary, BRD4, as an epigenetic reader, activates the transcription of diverse sets of genes through engaging distinct transcription factors in the cell context- and disease-dependent manner. In the gastric cancer cells, BRD4 controls cancer cell proliferation by modulating the cellular senescence through the E2F/miR-106b-5p/p21 axis. Meanwhile, in the innate immune response, Brd4 engages Irf8 and Pu.1 in maintaining the transcription of Naips and Nlrc4, which confers a prompt inflammasome activation against invading pathogens. Of note, mechanistically, BRD4’s transcriptional activities highly, but not exclusively, depend on the interaction between its bromodomains and acetylated lysine on histone or transcription factors, which supports the clinical investigations using BETis as anti-cancer and -inflammatory disease drugs.Submission published under a 24 month embargo labeled 'U of I Access', the embargo will last until 2022-08-01The student, Xingchen Dong, accepted the attached license on 2020-07-08 at 14:30.The student, Xingchen Dong, submitted this Dissertation for approval on 2020-07-08 at 14:41.This Dissertation was approved for publication on 2020-07-14 at 06:57.DSpace SAF Submission Ingestion Package generated from Vireo submission #15525 on 2020-10-02 at 15:31:38Made available in DSpace on 2020-10-07T22:44:26Z (GMT). No. of bitstreams: 2
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Previous issue date: 2020-07-14Embargo set by: Seth Robbins for item 116210
Lift date: 2022-10-07T22:44:53Z
Reason: Author requested U of Illinois access only (OA after 2yrs) in Vireo ETD systemAuthor requested U of Illinois access only (OA after 2yrs) in Vireo ETD systemU of I Onl
Mechanism of Sliding Clamp Loading During DNA Replication and Repair in Atomic Detail
No full textDNA replication is a fundamental process that is essential for all forms of life, and it is made efficient by ring-shaped sliding clamp proteins. One such protein is the eukaryotic sliding clamp, Proliferating Cellular Nuclear Antigen (PCNA), which not only facilitates replication but also coordinates multiple cellular pathways, such as DNA repair, cell cycle regulation, and apoptosis. The proper function of PCNA is critical for maintaining genome stability, making it a crucial factor in human health.
The clamp loader complex is the primary regulator of sliding clamp activity. Replication Factor C (RFC), the eukaryotic clamp loader, is responsible for opening the closed PCNA and loading it onto DNA. However, the mechanism by which RFC accomplishes this task has been elusive for years. Our research has contributed to this field by revealing multiple cryo-electron microscopy (cryo-EM) structures of the RFC:PCNA complex that describe the steps involved in the clamp loading reaction. Specifically, we found that RFC opens PCNA with a 'crab-claw' motion, allowing it to preferentially bind to PCNA before DNA. Additionally, during replication, primer-template DNA, which is RFC's primary DNA substrate, directly binds to the central chamber of the complex.
Our study also sheds light on the mechanism by which RFC performs its role in loading PCNA during DNA repair. When RFC binds to gapped or nicked DNA during DNA repair, it uses an additional DNA binding site, and both sites work together to melt the DNA strands with their 'separation pins.' This discovery provides the first structural insight into how RFC accomplishes its crucial functions in DNA replication and repair. Overall, our findings provide detailed atomic-level insights into how RFC efficiently loads PCNA onto different DNA substrates, advancing our understanding of this essential biological process.Biochemistry and Molecular Biotechnolog
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