In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".

Ex Input:
Abstract: We performed a functional genomic analysis to study the effect of epicatechin and polyphenolic cocoa extract in the human colon adenocarcinoma cell line Caco-2. The specific Human Hematology/Immunology cDNA arrays by Clontech, containing 406 genes in duplicate, were used. The differentially expressed genes were classified according to their level of expression, calculated as the ratio of the value obtained after each treatment relative to control cells, with a statistical significance of P < 0.05 (upregulated: ratio > 1.5; downregulated: ratio < 0.6). Treatment with epicatechin decreased the expression of 21 genes and upregulated 24 genes. Upon incubation with the cocoa polyphenolic extract, 24 genes were underexpressed and 28 were overexpressed. The changes in expression for ferritin heavy polypeptide 1 (FTH1), mitogen-activated protein kinase kinase 1 (MAPKK1), signal transducer and activator of transcription 1 (STAT1), and topoisomerase 1 upon incubation with epicatechin, and for myeloid leukemia factor 2 (MLF2), CCAAT/enhancer binding protein gamma (C/EBPG), MAPKK1, ATP-binding cassette, subfamily c member 1 (MRP1), STAT1, topoisomerase 1, and x-ray repair complementing defective repair 1 (XRCC1) upon incubation with the cocoa polyphenolic extract were validated by RT-PCR. Changes in the messenger RNA levels for MAPKK1, STAT1, MRP1, and topoisomerase 1 upon incubation with either epicatechin or cocoa extract were further confirmed at the protein level by Western blotting. The changes in the expression of STAT1, MAPKK1, MRP1, and FTH1 genes, which are involved in the cellular response to oxidative stress, are in agreement with the antioxidant properties of cocoa flavonoids. In addition, the changes in the expression of C/EBPG, topoisomerase 1, MLF2, and XRCC1 suggest novel mechanisms of action of flavonoids at the molecular level.. Title: Epicatechin and a cocoa polyphenolic extract modulate gene expression in human Caco-2 cells.

Ex Output:
yes

Ex Input:
Abstract: It was recently demonstrated that interleukin (IL)-23driven IL-17producing (ThIL-17) T cells mediate inflammatory pathology in certain autoimmune diseases. We show that the induction of antigen-specific ThIL-17 cells, but not T helper (Th)1 or Th2 cells, by immunization with antigens and adjuvants is abrogated in IL-1 receptor type Ideficient (IL-1RI/) mice. Furthermore, the incidence of experimental autoimmune encephalomyelitis (EAE) was significantly lower in IL-1RI/ compared with wild-type mice, and this correlated with a failure to induce autoantigen-specific ThIL-17 cells, whereas induction of Th1 and Th2 responses was not substantially different. However, EAE was induced in IL-1RI/ mice by adoptive transfer of autoantigen-specific cells from wild-type mice with EAE. IL-23 alone did not induce IL-17 production by T cells from IL-1RI/ mice, and IL-23induced IL-17 production was substantially enhanced by IL-1 or IL-1, even in the absence of T cell receptor stimulation. We demonstrate essential roles for phosphatidylinositol 3-kinase, nuclear factor B, and novel protein kinase C isoforms in IL-1 and IL-23mediated IL-17 production. Tumor necrosis factor also synergized with IL-23 to enhance IL-17 production, and this was IL-1 dependent. Our findings demonstrate that IL-1 functions upstream of IL-17 to promote pathogenic ThIL-17 cells in EAE.. Title: Specificity of sensorymotor connections encoded by Sema3ePlxnd1 recognition

Ex Output:
no

Ex Input:
Abstract: INTRODUCTION The overexpression of human epidermal growth factor receptor (HER)-2 in 20% of human breast cancers and its association with aggressive growth has led to widespread use of HER2-targeted therapies, such as trastuzumab (T) and lapatinib (L). Despite the success of these drugs, their efficacy is limited in patients whose tumors demonstrate de novo or acquired resistance to treatment. The 1 integrin resides on the membrane of the breast cancer cell, activating several elements of breast tumor progression including proliferation and survival.
METHODS We developed a panel of HER2-overexpressing cell lines resistant to L, T, and the potent LT combination through long-term exposure and validated these models in 3D culture. Parental and L/T/LT-resistant cells were subject to HER2 and 1 integrin inhibitors in 3D and monitored for 12 days, followed by quantification of colony number. Parallel experiments were conducted where cells were either stained for Ki-67 and Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) or harvested for protein and analyzed by immunoblot. Results were subjected to statistical testing using analysis of variance and linear contrasts, followed by adjustment with the Sidak method.
RESULTS Using multiple cell lines including BT474 and HCC1954, we reveal that in L and LT resistance, where phosphorylation of EGFR/HER1, HER2, and HER3 are strongly inhibited, kinases downstream of 1 integrin--including focal adhesion kinase (FAK) and Src--are up-regulated. Blockade of 1 by the antibody AIIB2 abrogates this up-regulation and functionally achieves significant growth inhibition of L and LT resistant cells in 3D, without dramatically affecting the parental cells. SiRNA against 1 as well as pharmacologic inhibition of FAK achieve the same growth inhibitory effect. In contrast, trastuzumab-resistant cells, which retain high levels of phosphorylated EGFR/HER1, HER2, and HER3, are only modestly growth-inhibited by AIIB2.
CONCLUSIONS Our data suggest that HER2 activity, which is suppressed in resistance involving L but not T alone, dictates whether 1 mediates an alternative pathway driving resistance. Our findings justify clinical studies investigating the inhibition of 1 or its downstream signaling moieties as strategies to overcome acquired L and LT resistance.. Title: Husbands' involvement in delivery care utilization in rural Bangladesh: A qualitative study

Ex Output:
no