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Wenhong Zhang,Donghan Wang,Yapu Zhao 기술경영경제학회 2015 ASIAN JOURNAL OF TECHNOLOGY INNOVATION Vol.23 No.3
Drawn on the resource-based view, this study examines the relationships of ties with serviceintermediaries to service innovation and product innovation and the mediations ofinnovation search on these relationships among Chinese manufacturing firms. It finds thatties with service intermediaries have positive relationships with both service innovation andproduct innovation, and technology search and market search mediate these relationships. Moreover, technology search has a stronger impact on product innovation than on serviceinnovation, but the effects of ties with service intermediaries and market search on serviceinnovation are not different from those on product innovation. The findings enrich ourknowledge on the antecedents of service innovation and provide some insight into thedebate on whether the antecedents of product innovation can be generalised to serviceinnovation. Moreover, they draw a more comprehensive picture on how a firm’s externalties affect innovations.
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Zhang, Xinyi Cindy,Xu, Chang,Mitchell, Ryan M,Zhang, Bo,Zhao, Derek,Li, Yao,Huang, Xin,Fan, Wenhong,Wang, Hongwei,Lerma, Luisa Angelica,Upton, Melissa P,Hay, Ashley,M?ndez, Eduardo,Zhao, Lue Ping Stockton Press 2013 Neoplasia Vol.15 No.12
<P>Head and neck squamous cell carcinoma (HNSCC) is characterized by significant genomic instability that could lead to clonal diversity. Intratumor clonal heterogeneity has been proposed as a major attribute underlying tumor evolution, progression, and resistance to chemotherapy and radiation. Understanding genetic heterogeneity could lead to treatments specific to resistant and metastatic tumor cells. To characterize the degree of intratumor genetic heterogeneity within a single tumor, we performed whole-genome sequencing on three separate regions of an human papillomavirus (HPV)-positive oropharyngeal squamous cell carcinoma and two separate regions from one corresponding cervical lymph node metastasis. This approach achieved coverage of approximately 97.9% of the genome across all samples. In total, 5701 somatic point mutations (SPMs) and 4347 small somatic insertions and deletions (indels)were detected in at least one sample. Ninety-two percent of SPMs and 77% of indels were validated in a second set of samples adjacent to the discovery set. All five tumor samples shared 41% of SPMs, 57% of the 1805 genes with SPMs, and 34 of 55 cancer genes. The distribution of SPMs allowed phylogenetic reconstruction of this tumor's evolutionary pathway and showed that the metastatic samples arose as a late event. The degree of intratumor heterogeneity showed that a single biopsy may not represent the entire mutational landscape of HNSCC tumors. This approach may be used to further characterize intratumor heterogeneity in more patients, and their sample-to-sample variations could reveal the evolutionary process of cancer cells, facilitate our understanding of tumorigenesis, and enable the development of novel targeted therapies.</P>
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Jinlin Hou,Edward Gane,Rozalina Balabanska,Wenhong Zhang,Jiming Zhang,Tien Huey Lim,Qing Xie,Chau-Ting Yeh,Sheng-Shun Yang,Xieer Liang,Piyawat Komolmit,Apinya Leerapun,Zenghui Xue,Ethan Chen,Yuchen Zh 대한간학회 2024 Clinical and Molecular Hepatology(대한간학회지) Vol.30 No.2
Background/Aims: Four-week treatment of linvencorvir (RO7049389) was generally safe and well tolerated, and showed anti-viral activity in chronic hepatitis B (CHB) patients. This study evaluated the efficacy, safety, and pharmacokinetics of 48-week treatment with linvencorvir plus standard of care (SoC) in CHB patients. Methods: This was a multicentre, non-randomized, non-controlled, open-label phase 2 study enrolling three cohorts: nucleos(t)ide analogue (NUC)-suppressed patients received linvencorvir plus NUC (Cohort A, n=32); treatment-naïve patients received linvencorvir plus NUC without (Cohort B, n=10) or with (Cohort C, n=30) pegylated interferon-α (Peg-IFN-α). Treatment duration was 48 weeks, followed by NUC alone for 24 weeks. Results: 68 patients completed the study. No patient achieved functional cure (sustained HBsAg loss and unquantifiable HBV DNA). By Week 48, 89% of treatment-naïve patients (10/10 Cohort B; 24/28 Cohort C) reached unquantifiable HBV DNA. Unquantifiable HBV RNA was achieved in 92% of patients with quantifiable baseline HBV RNA (14/15 Cohort A, 8/8 Cohort B, 22/25 Cohort C) at Week 48 along with partially sustained HBV RNA responses in treatment-naïve patients during follow-up period. Pronounced reductions in HBeAg and HBcrAg were observed in treatment-naïve patients, while HBsAg decline was only observed in Cohort C. Most adverse events were grade 1–2, and no linvencorvir-related serious adverse events were reported. Conclusions: 48-week linvencorvir plus SoC was generally safe and well tolerated, and resulted in potent HBV DNA and RNA suppression. However, 48-week linvencorvir plus NUC with or without Peg-IFN did not result in the achievement of functional cure in any patient.
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EVI1 acts as an inducible negative-feedback regulator of NF-κB by inhibiting p65 acetylation.
Xu, Xiangbin,Woo, Chang-Hoon,Steere, Rachel R,Lee, Byung Cheol,Huang, Yuxian,Wu, Jing,Pang, Jinjiang,Lim, Jae Hyang,Xu, Haidong,Zhang, Wenhong,Konduru, Anuhya S,Yan, Chen,Cheeseman, Michael T,Brown, S Williams Wilkins 2012 JOURNAL OF IMMUNOLOGY Vol.188 No.12
<P>Inflammation is a hallmark of many important human diseases. Appropriate inflammation is critical for host defense; however, an overactive response is detrimental to the host. Thus, inflammation must be tightly regulated. The molecular mechanisms underlying the tight regulation of inflammation remain largely unknown. Ecotropic viral integration site 1 (EVI1), a proto-oncogene and zinc finger transcription factor, plays important roles in normal development and leukemogenesis. However, its role in regulating NF-κB-dependent inflammation remains unknown. In this article, we show that EVI1 negatively regulates nontypeable Haemophilus influenzae- and TNF-α-induced NF-κB-dependent inflammation in vitro and in vivo. EVI1 directly binds to the NF-κB p65 subunit and inhibits its acetylation at lysine 310, thereby inhibiting its DNA-binding activity. Moreover, expression of EVI1 itself is induced by nontypeable Haemophilus influenzae and TNF-α in an NF-κB-dependent manner, thereby unveiling a novel inducible negative feedback loop to tightly control NF-κB-dependent inflammation. Thus, our study provides important insights into the novel role for EVI1 in negatively regulating NF-κB-dependent inflammation, and it may also shed light on the future development of novel anti-inflammatory strategies.</P>
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