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Huang, Yisong,Samawi, Hani M.,Vogel, Robert,Yin, Jingjing,Gato, Worlanyo Eric,Linder, Daniel F. The Korean Statistical Society 2016 Communications for statistical applications and me Vol.23 No.6
The validity of statistical inference depends on proper randomization methods. However, even with proper randomization, we can have imbalanced with respect to important characteristics. In this paper, we introduce a method based on ranked auxiliary variables for treatment allocation in crossover designs using Latin squares models. We evaluate the improvement of the efficiency in treatment comparisons using the proposed method. Our simulation study reveals that our proposed method provides a more powerful test compared to simple randomization with the same sample size. The proposed method is illustrated by conducting an experiment to compare two different concentrations of titanium dioxide nanofiber (TDNF) on rats for the purpose of comparing weight gain.
The Wilms Tumor Suppressor WT1 Encodes a Transcriptional Activator of Amphiregulin
Lee, Sean-Bong,Huang, Karen,Palmer, Rachel,Truong, Vivi B,Doris Herzlinger,Kolquist, Kathryn A.,Wong, Jenise,Paulding, Charles,Woon, Seung-Kew,Gerald, William,Oliner, JonathanD.,Haber, Daniel A. 가톨릭대학교 2000 Bulletin of The Catholic Research Institutes of Me Vol.28 No.-
WT1 encodes a zinc finger transcription factor implicated in kidney differentiation and tumorigenesis. In reporter assays, WT1 represses transcription from GC- and TC-rich promoters, but its physiological targets remain uncertain. We used hybridization to high-density oligonucleotide arrays to search for native genes whose expression is altered following inducible expression of WT1. The major target of WT1 was amphiregulin, a member of the epidermal growth factor family. The WT1(-KTS) isoform binds directly to the amphiregulin promoter, resulting in potent transcriptional activation. The in vivo expression profile of amphiregulin during fetal kidney development mirrors the highly specific pattern of WT1 itself, and recombinant Amphiregulin stimulates epithelial branching in organ cultures of embryonic mouse kidney. These observations suggest a model for WT1 as a transcriptional regulator during kidney differentiation. (Cell 98:663-673, 1999)
Cheng Han Ng,Daniel Q. Huang,Mindie H. Nguyen 대한간학회 2022 Clinical and Molecular Hepatology(대한간학회지) Vol.28 No.4
Nonalcoholic fatty liver disease (NAFLD) affects about a third of the world’s adult population and is a major public health concern. NAFLD is defined by the presence of hepatic steatosis and the absence of other causes of liver disease. As NAFLD is closely associated with the presence of the metabolic syndrome, several experts have called for a change in nomenclature from NAFLD to metabolic-associated fatty liver disease (MAFLD) to better reflect the underlying pathophysiology of NAFLD as a metabolically driven disease and shift to a “positive” diagnostic criteria rather than one of exclusion. Recent studies have suggested that the global prevalence of MAFLD is higher than that of NAFLD, and patients with MAFLD have more metabolic comorbidities compared to those with NAFLD. Emerging data also suggest that all-cause and cardiovascular mortality may be higher in MAFLD compared with NAFLD. In this synopsis, we discuss differences in clinical features, prevalence and clinical outcomes between NAFLD and MAFLD. In addition, we highlight the advantages and disadvantages of a name change from NAFLD to MAFLD from the perspective of the scientific community, care providers and patients.
Teng Pai-Chi,Huang Daniel Q.,Lin Ting-Yi,Noureddin Mazen,Yang Ju Dong 거트앤리버 소화기연관학회협의회 2023 Gut and Liver Vol.17 No.1
Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in the world. NAFLD is a hepatic manifestation of insulin resistance, the core pathophysiology of diabetes. Multiple clinical studies show that diabetes increases the risk of liver disease progression and cirrhosis development in patients with NAFLD. Diabetes has causal associations with many different cancers, including hepatocellular carcinoma (HCC). More recent studies demonstrate that diabetes increases the risk of HCC in patients with underlying NAFLD cirrhosis, confirming the direct hepatocarcinogenic effect of diabetes among cirrhosis patients. Diabetes promotes hepatocarcinogenesis via the activation of inflammatory cascades producing reactive oxygen species and proinflammatory cytokines, leading to genomic instability, cellular proliferation, and inhibition of apoptosis. Given the global increase in the burden of NAFLD and HCC, high-risk patients such as older diabetic individuals should be carefully monitored for HCC development. Future larger studies should explore whether the effect of diabetes on HCC risk in NAFLD cirrhosis is modifiable by the type of antidiabetic medication and the effectiveness of diabetes control.
Zhao, Ling,Kwon, Myung-Ja,Huang, Shurong,Lee, Joo Y.,Fukase, Koichi,Inohara, Naohiro,Hwang, Daniel H. American Society for Biochemistry and Molecular Bi 2007 The Journal of biological chemistry Vol.282 No.16
<P>Nucleotide-binding oligomerization domain-containing proteins (Nods) are intracellular pattern recognition receptors recognizing conserved moieties of bacterial peptidoglycan through their leucine-rich repeats domain. The agonists for Nods activate proinflammatory signaling pathways, including NF-kappaB pathways. The results from our previous studies showed that the activation of TLR4 and TLR2, leucine-rich repeat-containing pattern recognition receptors, were differentially modulated by saturated and n-3 polyunsaturated fatty acids in macrophages and dendritic cells. Here, we show the differential modulation of NF-kappaB activation and interleukin-8 (IL-8) expression in colonic epithelial cells HCT116 by saturated and unsaturated fatty acids mediated through Nods proteins. Lauric acid (C12:0) dose dependently activated NF-kappaB and induced IL-8 expression in HCT116 cells, which express both Nod1 and Nod2, but not detectable amounts of TLR2 and TLR4. These effects of lauric acid were inhibited by dominant negative forms of Nod1 or Nod2, but not by dominant negative forms of TLR2, TLR4, and TLR5. The effects of lauric acid were also attenuated by small RNA interference targeting Nod1 or Nod2. In contrast, polyunsaturated fatty acids, especially n-3 polyunsaturated fatty acids, inhibited the activation of NF-kappaB and IL-8 expression induced by lauric acid or known Nods ligands in HCT116. Furthermore, lauric acid induced, but docosahexaenoic acid inhibited lauric acid- or Nod2 ligand MDP-induced, Nod2 oligomerization in HEK293T cells transfected with Nod2. Together, these results provide new insights into the role of dietary fatty acids in modulating inflammation in colon epithelial cells. The results suggest that Nods may be involved in inducing sterile inflammation, one of the key etiological conditions in the development of many chronic inflammatory diseases.</P>
Changing PEO coating formation on Mg alloys by particle additions to the treatment electrolyte
Carsten Blawert,Bala Srinivasan,Jun Liang,Yuanding Huang,Daniel Hoche,Nico Scharnagl,Volker Heitmann,Ulrich Burmester 한국표면공학회 2012 한국표면공학회 학술발표회 초록집 Vol.2012 No.11
Plasma electrolytic oxidation of magnesium alloys is a well known technique to produce corrosion and wear resistant coatings. The addition of particles to the electrolyte provides a possibility to produce coatings with an increasing range of composition by in-situ incorporation of those particles into the coating. An extensive literature review has revealed that the mode of incorporation depends mainly on the melting point of the used particles and the energy provided by the discharges of the PEO process. The spectrum ranges from inert to partly reactive incorporation, but a complete reactive incorporation and a formation of a new single phase coating was not observed so far. Thus a new approach in PEO processing is introduced using specific particles as a kind of sintering additive, changing not only the composition but lowering the melting temperature and increase the liquid phase fraction during the discharges, resulting in a new amorphous coating.