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202. Thou Shalt Not Reject the P-value

Author

Chén, Oliver Y., Saraiva, Raúl G., Nagels, Guy, Phan, Huy, Schwantje, Tom, Cao, Hengyi, Gou, Jiangtao, Reinen, Jenna M., Xiong, Bin, Zhi, Bangdong, Wang, Xiaojun, and de Vos, Maarten

Subjects
Statistics - Methodology
Abstract

Since its debut in the 18th century, the P-value has been an important part of hypothesis testing-based scientific discoveries. As the statistical engine accelerates, questions are beginning to be raised, asking to what extent scientific discoveries based on P-values are reliable and reproducible, and the voice calling for adjusting the significance level or banning the P-value has been increasingly heard. Inspired by these questions and discussions, here we enquire into the useful roles and misuses of the P-value in scientific studies. For common misuses and misinterpretations, we provide modest recommendations for practitioners. Additionally, we compare statistical significance with clinical relevance. In parallel, we review the Bayesian alternatives for seeking evidence. Finally, we discuss the promises and risks of using meta-analysis to pool P-values from multiple studies to aggregate evidence. Taken together, the P-value underpins a useful probabilistic decision-making system and provides evidence at a continuous scale. But its interpretation must be contextual, considering the scientific question, experimental design (including the model specification, sample size, and significance level), statistical power, effect size, and reproducibility.

Published
2020

204. On the Radiality Constraints for Distribution System Restoration and Reconfiguration Problems

Author

Wang, Ying, Xu, Yin, Li, Jiaxu, He, Jinghan, and Wang, Xiaojun

Subjects
Electrical Engineering and Systems Science - Systems and Control
Abstract

Radiality constraints are involved in both distribution system restoration and reconfiguration problems. However, a set of widely used radiality constraints, i.e., the spanning tree (ST) constraints, has its limitations which have not been well recognized. In this letter, the limitation of the ST constraints is analyzed and an effective set of constraints, referred to as the single-commodity flow constraints, is presented. Furthermore, a combined set of constraints is proposed and case studies indicate that the combined constraints can gain computational efficiency in the reconfiguration problem. Recommendations on the use of radiality constraints are also provided., Comment: 4 pages, 3 figures, IEEE PES letters

Published
2019

226. A novel HIV-1 restriction factor that is biologically distinct from APOBEC3 cytidine deaminases in a human T cell line CEM.NKR

Author

Zhou Tao, Han Yanxing, Dang Ying, Wang Xiaojun, and Zheng Yong-Hui

Subjects
Immunologic diseases. Allergy, RC581-607
Abstract

Abstract Background Isolation of novel retroviral restriction factors will open new avenues for anti-HIV/AIDS treatment. Although HIV-1 replication is restricted by APOBEC3G/APOBEC3F, TRIM5α, and CD317, none defend HIV-1 infection under natural conditions. Previously, we demonstrated a host factor from the human T cell line CEM.NKR that potently restricted wild-type HIV-1 replication. Interestingly, this restriction resembled the APOBEC3G/APOBEC3F pattern in that viral replication was inhibited from the second round of replication cycle at a post-entry step. Results Here, we further characterized this factor and found it distinguishable from the known anti-HIV APOBEC3 proteins. Although CEM.NKR cells expressed both APOBEC3G and APOBEC3F, their levels were at least 10 or 4-fold lower than those in H9 cells, and importantly, Vif effectively neutralized their activity. Among eight subclones isolated from CEM.NKR cells, one was relatively permissive, four were semi-permissive, and three were completely non-permissive for HIV-1 replication. When the levels of APOBEC3 expression were determined, all these clones retained similar low levels of APOBEC3DE, APOBEC3F, APOBEC3G and APOBEC3H expression, and no APOBEC3B expression was detected. Since the vif from SIVmac can effectively neutralize APOBEC3B and APOBEC3H, recombinant HIV-1 expressing this SIV gene were created. However, these viruses still failed to replicate in CEM.NKR cells. We also confirmed that HIV-1 restriction in CEM.NKR was not due to a loss of calnexin expression. Conclusion Taken together, these results not only demonstrate that all these aforementioned anti-HIV APOBEC3 proteins do not contribute to this HIV-1 restriction, but also shed light on a novel and potent HIV-1 inhibitor in CEM.NKR cells.

Published
2009
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227. Hepatitis B virus infection disrupts homologous recombination in hepatocellular carcinoma by stabilizing resection inhibitor ADRM1

Author

Zeng, Ming, Tang, Zizhi, Ren, Laifeng, Wang, Haibin, Wang, Xiaojun, Zhu, Wenyuan, Mao, Xiaobing, Li, Zeyang, Mo, Xianming, Chen, Jun, Han, Junhong, Kong, Daochun, Ji, Jianguo, Carr, Antony M., and Liu, Cong

Subjects
R and D Systems -- International economic relations, Computer software industry -- International economic relations, Chromatin -- Health aspects -- Genetic aspects, Biotechnology -- Genetic aspects -- Health aspects, Ubiquitin -- Genetic aspects -- Health aspects, Ligases -- Health aspects -- Genetic aspects, Hepatitis B -- Development and progression -- Genetic aspects, Hepatitis B virus -- Genetic aspects -- Development and progression, Hepatoma -- Development and progression -- Genetic aspects, Surgery -- Health aspects, Health care industry
Abstract

Many cancers harbor homologous recombination defects (HRDs). A HRD is a therapeutic target that is being successfully utilized in treatment of breast/ovarian cancer via synthetic lethality. However, canonical HRD caused by BRCAness mutations do not prevail in liver cancer. Here we report a subtype of HRD caused by the perturbation of a proteasome variant (CDW19S) in hepatitis B virus-bearing (HBV-bearing) cells. This amalgamate protein complex contained the 19S proteasome decorated with [CRL4.sup.WDR70] ubiquitin ligase, and assembled at broken chromatin in a [PSMD4.sup.Rpn10]-and ATM-MDC1-RNF8-dependent manner. CDW19S promoted DNA end processing via segregated modules that promote nuclease activities of MRE11 and EXO1. Contrarily, a proteasomal component, [ADRM1.sup.Rpn13], inhibited resection and was removed by [CRL4WDR.sup.70]-catalyzed ubiquitination upon commitment of extensive resection. HBx interfered with [ADRM1.sup.Rpn13] degradation, leading to the imposition of [ADRM1.sup.Rpn13]- dependent resection barrier and consequent viral HRD subtype distinguishable from that caused by BRCA1 defect. Finally, we demonstrated that viral HRD in HBV-associated hepatocellular carcinoma can be exploited to restrict tumor progression. Our work clarifies the underlying mechanism of a virus-induced HRD subtype., Introduction Long-term liver infection with hepatitis B virus (HBV) predisposes carriers to hepatocellular carcinoma (1). Therapy for late-stage HBV-associated hepatocellular carcinoma remains a major challenge, with poor therapy responses and [...]

Published
2023
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