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Chen, Xuan

Publications and source records attributed to Chen, Xuan.

Expression profile analysis of differentially expressed genes in ruptured intracranial aneurysms: In search of biomarkers

Highlights: • Bioinformatics can identify potential biomarkers of ruptured intracranial aneurysm. • BASP1, CD74, CEBPB, ECHDC2, GZMK, HLA-DRB3, KLHL3, SLC2A3 & SOCS3 affect IA rupture. • DEGs are involved in antigen processing and presentation and immune response. • Vascular brain injury affects gene expression in IA tissue. Intracranial aneurysms (IAs) result from the bulging of arterial walls secondary to several factors such as flow, vessel morphology, and genetics. Subarachnoid hemorrhage occurs when such walls rupture, leading to high disability and mortality. Despite numerous investigations pertaining to the relationship between geometric characteristics and IA rupture, only a few have obtained consistent results. This study aimed to further identify the potential genes associated with the pathogenesis of IAs, which may provide novel molecular biomarkers. We downloaded and reanalyzed six datasets, which were divided into four groups. IA walls and blood samples were screened for differentially expressed genes (DEGs); then, functional and pathway enrichment analyses were conducted. In total, 158 common DEGs were identified from Groups 1–3 and 396 genes (187 upregulated and 209 downregulated genes) were differentially expressed in Group 4. The functional analysis revealed that the DEGs were mainly associated with the major histocompatibility complex class II protein complex and antigen processing and presentation. Finally, we identified nine key genes, both in aneurysm tissue samples and blood samples, of which three were mostly associated with the progression and rupture of IAs. Bioinformatics was used to analyze the datasets of the ruptured IAs and identify potential biomarkers, which may provide information for the early detection and treatment of IAs.

60 APPLIED LIFE SCIENCES↗

FSPA Report [Slides]

Fermilab Student & Postdoc Association: Form deeper connections between early career researchers; Share cultural events and activities from various backgrounds; Provide support to the community of early career researchers at Fermilab; Act as liaison to the Fermilab directorate.

99 GENERAL AND MISCELLANEOUS↗

Q482H mutation of procaspase-8 in acute myeloid leukemia abolishes caspase-8-mediated apoptosis by impairing procaspase-8 dimerization

Highlights: • The Q482H mutation of procaspase-8 was identified from AML patients. • The Q482H mutation was associated with poor chemotherapy response in AML patients. • The Q482H mutation abolished procaspase-8 mediated apoptotic signaling cascade. • The Q482H inhibited TRAIL-induced apoptosis. • The Q482H mutation disrupted the dimeriztion of procaspase-8. Certain procaspase-8 mutations are reported to be associated with the progression and prognosis of multiple tumors. However, it remains unclear whether the poor chemotherapy response and frequent relapse after complete remission of patients with acute myeloid leukemia (AML) is also related to procaspase-8 abnormalities.

60 APPLIED LIFE SCIENCES↗