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Li, Fulu,Wu, Kui,Lippman, Andrew The Korea Institute of Information and Commucation 2008 Journal of communications and networks Vol.10 No.2
We study the routing problem in all-wireless networks based on cooperative transmissions. We model the minimum-energy cooperative path (MECP) problem and prove that this problem is NP-complete. We hence design an approximation algorithm called cooperative shortest path (CSP) algorithm that uses Dijkstra's algorithm as the basic building block and utilizes cooperative transmissions in the relaxation procedure. Compared with traditional non-cooperative shortest path algorithms, the CSP algorithm can achieve a higher energy saving and better balanced energy consumption among network nodes, especially when the network is in large scale. The nice features lead to a unique, scalable routing scheme that changes the high network density from the curse of congestion to the blessing of cooperative transmissions.
F. Li,K. Wu,A. Lippman 한국통신학회 2008 Journal of communications and networks Vol.10 No.2
We study the routing problem in all-wireless networks based on cooperative transmissions. We model the minimumenergy cooperative path (MECP) problem and prove that this problem is NP-complete. We hence design an approximation algorithm called cooperative shortest path (CSP) algorithm that uses Dijkstra’s algorithm as the basic building block and utilizes cooperative transmissions in the relaxation procedure. Compared with traditional non-cooperative shortest path algorithms, the CSP algorithm can achieve a higher energy saving and better balanced energy consumption among network nodes, especially when the network is in large scale. The nice features lead to a unique, scalable routing scheme that changes the high network density from the curse of congestion to the blessing of cooperative transmissions.
Kim, Jai-Hyun,Choi, Dong Soon,Lee, Ok-Hee,Oh, Seung-Hyun,Lippman, Scott M.,Lee, Ho-Young American Society of Hematology 2011 Blood Vol.118 No.9
<B>Abstract</B><P>Most antiangiogenic therapies currently being evaluated in clinical trials target the vascular endothelial growth factor pathway; however, the tumor vasculature can acquire resistance to vascular endothelial growth factor-targeted therapy by shifting to other angiogenesis mechanisms. Insulin-like growth factor binding protein-3 (IGFBP-3) has been reported to suppress tumor growth and angiogenesis by both IGF-dependent and IGF-independent mechanisms; however, understanding of its IGF-independent mechanisms is limited. We observed that IGFBP-3 blocked tumor angiogenesis and growth in non-small cell lung cancer and head and neck squamous cell carcinoma. Conditioned media from an IGFBP-3-treated non-small cell lung cancer cell line displayed a significantly decreased capacity to induce HUVEC proliferation and aortic sprouting. In cancer cells, IGFBP-3 directly interacted with Erk1/2, leading to inactivation of Erk1/2 and Elk-1, and suppressed transcription of early growth response protein 1 and its target genes, basic fibroblast growth factor and platelet-derived growth factor. These data suggest that IGF-independent Erk1/2 inactivation and decreased IGFBP-3-induced Egr-1 expression block the autocrine and paracrine loops of angiogenic factors in vascular endothelial and cancer cells. Together, these findings provide a molecular framework of IGFBP-3's IGF-independent antiangiogenic antitumor activities. Future studies are needed for development of IGFBP-3 as a new line of antiangiogengic cancer drug.</P>
Control of inflorescence architecture in tomato by BTB/POZ transcriptional regulators
Xu, Cao,Park, Soon Ju,Van Eck, Joyce,Lippman, Zachary B. Cold Spring Harbor Laboratory 2016 Genes & development Vol.30 No.18
<P>Plant productivity depends on inflorescences, flower-bearing shoots that originate from the stem cell populations of shoot meristems. Inflorescence architecture determines flower production, which can vary dramatically both between and within species. In tomato plants, formation of multiflowered inflorescences depends on a precisely timed process of meristem maturation mediated by the transcription factor gene TERMINATING FLOWER (TMF), but the underlying mechanism is unknown. We show that TMF protein acts together with homologs of the Arabidopsis BLADE-ON-PETIOLE (BOP) transcriptional cofactors, defined by the conserved BTB (Broad complex, Tramtrack, and Bric-a-brac)/POZ (POX virus and zinc finger) domain. TMF and three tomato BOPs (S1BOPs) interact with themselves and each other, and TMF recruits S1BOPs to the nucleus, suggesting formation of a transcriptional complex. Like TMF, S1BOP gene expression is highest during vegetative and transitional stages of meristem maturation, and CRISPR/Cas9 elimination of S1BOP function causes pleiotropic defects, most notably simplification of inflorescences into single flowers, resembling tmf mutants. Flowering defects are enhanced in higher-order s1bop tmf mutants, suggesting that S1BOPs function with additional factors. In support of this, S1BOPs interact with TMF homologs, mutations in which cause phenotypes like sibop mutants. Our findings reveal a new flowering module defined by S1BOP TMF family interactions that ensures a progressive meristem maturation to promote inflorescence complexity.</P>
Kim, Jin‐,Soo,Kim, Edward S.,Liu, Diane,Lee, J. Jack,Solis, Luisa,Behrens, Carmen,Lippman, Scott M.,Hong, Waun Ki,Wistuba, Ignacio I.,Lee, Ho‐,Young Wiley Subscription Services, Inc., A Wiley Company 2012 Cancer Vol.118 No.9
<P><B>Abstract</B></P><P><B>BACKGROUND:</B></P><P>The purpose of this study was to characterize insulin receptor (IR) and insulin‐like growth factor‐1 receptor (IGF‐1R) expression in patients with nonsmall cell lung cancer (NSCLC).</P><P><B>METHODS:</B></P><P>A total of 459 patients who underwent curative resection of NSCLC were studied (median follow‐up duration, 4.01 years). Expression of the IR and IGF‐1R protein in tumor specimens was assessed immunohistochemically using tissue microarrays.</P><P><B>RESULTS:</B></P><P>The cytoplasmic IR score was higher in patients with adenocarcinoma (ADC) than in those with squamous cell carcinoma (SCC), whereas cytoplasmic IGF‐1R score was higher in patients with SCC than those with ADC. Neither IR nor IGF‐1R expression was associated with sex, smoking history, or clinical stage. Patients with positive IR or IGF‐1R expression levels had poor recurrence‐free (RFS) (3.8 vs 3.3 years; 3.8 vs 2.0 years, respectively), but similar overall survival (OS). Patients with high expression levels of IR and IGF‐1R had shorter RFS and OS compared with those with low levels of IR and/or IGF‐1R expression. Finally, a multivariate analysis revealed the impact of IR, but not of IGF‐1R, as an independent predictive marker of NSCLC survival: hazard ratio (HR) for OS, 1.005 (95% confidence interval [CI], 1.001‐1.010], HR for RFS, 1.005 (95% CI, 1.001‐1.009), when IR score was tested as a continuous variable.</P><P><B>CONCLUSIONS:</B></P><P>Overexpression of IR predicts a poor survival among patients with NSCLC, especially those with SCC. These results might serve as future guidance to the clinical trials involving IR or IGR‐1R targeting agents. Cancer 2012;. © 2011 American Cancer Society.</P>
Variation in the flowering gene SELF PRUNING 5G promotes day-neutrality and early yield in tomato
Soyk, Sebastian,Mü,ller, Niels A,Park, Soon Ju,Schmalenbach, Inga,Jiang, Ke,Hayama, Ryosuke,Zhang, Lei,Van Eck, Joyce,Jimé,nez-Gó,mez, José,M,Lippman, Zachary B Nature Publishing Group, a division of Macmillan P 2017 Nature genetics Vol.49 No.1
<P>Plants evolved so that their flowering is triggered by seasonal changes in day lengths. However, day-length sensitivity in crops limits their geographical range of cultivation, and thus modification of the photoperiod response was critical for their domestication(2-11). Here we show that loss of day-length-sensitive flowering in tomato was driven by the florigen paralog and flowering repressor SELF-PRUNING 5G (SP5G). SP5G expression is induced to high levels during long days in wild species, but not in cultivated tomato because of cis-regulatory variation. CRISPR/Cas9-engineered mutations in SP5G cause rapid flowering and enhance the compact determinate growth habit of field tomatoes, resulting in a quick burst of flower production that translates to an early yield. Our findings suggest that pre-existing variation in SP5G facilitated the expansion of cultivated tomato beyond its origin near the equator in South America, and they provide a compelling demonstration of the power of gene editing to rapidly improve yield traits in crop breeding.</P>
Kim, Woo‐,Young,Prudkin, Ludmila,Feng, Lei,Kim, Edward S.,Hennessy, Bryan,Lee, Ju‐,Seog,Lee, J. Jack,Glisson, Bonnie,Lippman, Scott M.,Wistuba, Ignacio I.,Hong, Waun Ki,Lee, Ho‐,Youn Wiley Subscription Services, Inc., A Wiley Company 2012 Cancer Vol.118 No.16
<P><B>Abstract</B></P><P><B>BACKGROUND:</B></P><P>Most patients with nonsmall cell lung cancer (NSCLC) have responded poorly to epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs). The authors investigated the involvement of insulinlike growth factor 1 receptor (IGF‐1R) signaling in primary resistance to EGFR TKIs and the molecular determinants of resistance to IGF‐1R TKIs.</P><P><B>METHODS:</B></P><P>Phosphorylated IGF‐1R/insulin receptor (pIGF‐1R/IR) was immunohistochemically evaluated in an NSCLC tissue microarray. The authors analyzed the antitumor effects of an IGF‐1R TKI (PQIP or OSI‐906), either alone or in combination with a small‐molecular inhibitor (PD98059 or U0126) or with siRNA targeting <I>K‐Ras</I> or mitogen‐activated protein kinase/extracellular signal‐regulated kinase kinase (MEK), in vitro and in vivo in NSCLC cells with variable histologic features and <I>EGFR</I> or <I>K‐Ras</I> mutations.</P><P><B>RESULTS:</B></P><P>pIGF‐1R/IR expression in NSCLC specimens was associated with a history of tobacco smoking, squamous cell carcinoma histology, mutant <I>K‐Ras</I>, and wild‐type (WT) <I>EGFR</I>, all of which have been strongly associated with poor response to EGFR TKIs. IGF‐1R TKIs exhibited significant antitumor activity in NSCLC cells with WT EGFR and WT <I>K‐Ras</I> but not in those with mutations in these genes. Introduction of mutant <I>K‐Ras</I> attenuated the effects of IGF‐1R TKIs on NSCLC cells expressing WT <I>K‐Ras</I>. Conversely, inactivation of MEK restored sensitivity to IGF‐TKIs in cells carrying mutant <I>K‐Ras</I>.</P><P><B>CONCLUSIONS:</B></P><P>The mutation status of both <I>EGFR</I> and <I>K‐Ras</I> could be a predictive marker of response to IGF‐1R TKIs. Also, MEK antagonism can abrogate primary resistance of NSCLC cells to IGF‐1R TKIs. Cancer 2012. © 2012 American Cancer Society.</P>