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Chancellors Distinguished Chair in Biomedical Sciences and Endowed Professor
Professor and Director of Molecular Oncology, Pathology and Laboratory Medicine
Deputy Director, The University of Kansas Cancer Center
Director, Biospecimen Shared Resource
Kansas Bioscience Authority Eminent Scholar
Lab Phone: 913-945-6373
Email: email@example.com
Godwin and members of his group have been involved in both basic and translational research for many years, filling several important niches within the translational research community as a whole (e.g., early detection, predictive biomarkers and clinical trials, molecular pathology, biosample ascertainment). The central theme of his work centers on the idea of obtaining a molecular definition of a tumor to define its treatment-sensitive elements. As such, he has a long-standing interest in the field of cancer genetics and molecular targeted therapies. His studies primarily involve three different types of cancer: breast, ovarian, and gastrointestinal stromal tumor (GIST). His group uses these models to investigate how to improve patient care.
The incidence of epithelial ovarian cancer has remained stable over the last 20 years, with approximately 20,200 cases estimated to occur annually, and a lifetime risk in the general population of 1.4%. Aggressive debulking surgery to remove the primary tumor and its metastatic implants has long been the accepted initial step in the management of ovarian cancer. The achievement of optimum cytoreduction at the end of the initial surgery has been shown as a favorable prognostic factor for the disease course. It has been recently demonstrated that clinical response may not correlate with survival due to the preferential survival of chemotherapy resistant tumor-initiating cells (also referred to as cancer stem cells, cancer progenitor cells, and cancer initiating cells) that eventually grow and repopulate the tumor. Our group studies the origins of ovarian cancer, the role of the extracellular environment (stromal/epithelial/ECM interactions) in regulating tumor cell growth and the use of molecular targeted therapies for the treatment of this disease. Below are examples of ongoing studies in these areas.
The majority of advanced epithelial ovarian, primary peritoneal and fallopian tube cancers are invasive serous adenocarcinomas; recently classified as Type II epithelial ovarian cancers. Identification of morphologic or molecular precursors for Type II ovarian cancer would be paramount to the development of effective prevention strategies. Preliminary studies in hereditary breast-ovarian cancer (HBOC) kindred suggest that Type II ovarian cancer may arise from dysplastic tubal epithelium (tubal intraepithelial carcinoma, TIC) and are related to early mutational loss of TP53. Our preliminary data show strongly stained p53 in both areas of TIC and the concurrent ovarian carcinoma. We hypothesize that TIC represents a precursor of invasive disease for Type II tumors in HBOC (and perhaps sporadic cases). In order to test this hypothesis, we are using molecular genetic approaches to evaluate concurrent TIC and ovarian adenocarcinoma to determine additional molecular alterations that lead to disease development and to determine whether sporadic cases of ovarian cancer share these molecular features. If our data support the model of TIC as an origin of Type II serous tumors, this would justify development of in situ imaging technologies specific to morphologic or molecular changes associated with TIC in the prevention of Type II serous adenocarcinomas.
The tumor microenvironment is complex and contains non-cancerous stromal cells, such as fibroblasts, immune cells, and endothelial cells and products secreted from these cells that intermingle with the tumor cells. Since the trigger for tumor growth and spread may actually come from the stroma, these studies explore how to best use therapies that target the stromal components. We are utilizing 3 dimensional (3D) models to study how the tumor microenvironment supports ovarian tumor cell growth. We have reported that the basement membrane (a thin layer of extracellular proteins that anchors epithelial tissue to underlying connective tissue and provides mechanical structure, separates different cell types, and signals for cell differentiation, migration, and survival) is disturbed very early in the initiation of ovarian cancer. Using this 3D model we have shown that different ovarian cancer cell lines migrate and invade in different ways and these cancer cells change their phenotype by acquiring tumor stem cell characteristics depending on signals provided by their immediate surroundings. Although it is believed that a normal microenvironment has a negative effect on tumor growth, the tumor-associated microenvironment actively contributes to tumor development and progression. Our research is focusing on ways to alter how ovarian tumor cells interact with their microenvironment as a means to interfere with tumor development.
We have utilized recent technological advancements in the field of RNAi and high-throughput screening to perform several types of RNAi screens to identify genes essential for ovarian tumor growth and to identify genes that help sensitize tumor cells to molecular targeted therapies. As a first step we employed a druggable library of 24,088 siRNAs targeting ~6,022 genes (pool of 4 siRNAs/gene) and screened across A1847 cells. From this screen we identified 300 unique human genes that were considered potential targets for drug development and represent essential genes for tumor growth and survival. A custom siRNA library was derived and this library has been screened across a panel of ovarian cancer and non-tumorigenic human ovarian surface epithelium cell lines. For each tumor and non-tumor cell line a gene signature was established. A total of 50 common genes across the 7 ovarian cancer cell lines were discovered and found to induce varying degrees of cytotoxic effects as assessed by a cell viability assay. Of these 50, seven genes were found to have increased cytotoxicity for the tumorigenic cell lines but not for the non-tumorigenic cell lines. These genes were validated by deconvolution of the initial pool of 4 siRNAs targeting each gene and evaluating the effectiveness of individual siRNAs in all of the cell lines. Quantitative RT-PCR was performed to further assess the specificity of the individual siRNAs in all of the cell lines. We will also evaluate the functional significance of these genes in primary cultures obtained by processing ascites from ovarian cancer patients as a basic step towards establishing personalized medicine. As siRNA therapy holds a promising future, we believe that these studies lay the foundation to develop novel molecular approaches and targets that may ultimately improve the treatment of patients with ovarian cancer.
At the time of presentation most epithelial ovarian cancers are no longer dependent on single genetic determinants for growth and/or survival. The overall response to oncogene-targeted therapies used as single agents is not highly significant in the general population, and therefore, treatment of ovarian cancer poses particularly formidable challenges. We hypothesize that targeted agents will become potent when used in combinations that simultaneously block multiple oncogenic pathways, where such simultaneous blockade will reduce the ability of cancer cells to select resistance mutations. Therefore, we have used second-site siRNA lethality screens to help identify critical pathways to target in combination with novel biologics. Our studies have used bioinformatics to devise a tryrosine kinase-centered network, and probed a corresponding siRNA library targeting 638 genes in synthetic lethality screens. Using this library, we have identified a number of genes that synergize with a multi-kinase inhibitor targeting the SRC-family of kinases among other kinases, all of which are implicated in the formation and maintenance of cancer. Our goal is to identify critical pathways which sensitize ovarian cancer cells to this novel biologic that was recently evaluated in a Phase II clinical trial (GOG-0170M) to treat patients with recurrent ovarian cancer. We have completed the siRNA screening and its subsequent validation and are now refining this list of sensitizing genes by performing additional screens using alternate biologics and other tumor cell types to identify drug-specific and ovarian-specific sensitizers. We have analyzed DNA microarray data sets to explore the expression patterns of transcripts for genes identified through our screens in patient samples to assess their clinical relevance. Furthermore, we have access to clinical samples from GOG-0170M (pre- and post-treatment serum samples and tumor tissue) for evaluation of the prognostic value of these dasatinib-sensitizing genes. We have correlated the sensitivity of each cell line to dasatinib with the expression of each of the dasatinib-sensitizing genes using quantitative RT-PCR. We have performed in vitro drug-drug combination experiments using the Chou-Talalay combination index method to evaluate drug combinations and have found strong synergy in several two-drug combinations at various molar ratios of the two drugs across a panel of ovarian cancer cell lines. For highly promising drug combinations, we have initiated in vivo orthotopic xenograft studies to evaluate the efficacy of combination therapy in preventing ovarian tumor growth (see section on "Evaluation of therapeutic agents in treating human ovarian cancer"). The sensitizing genes identified from these studies represent potential targets for combination therapies with biologics in clinical trials. We view this work as ultimately enabling the next-generation approach for cancer therapies: combining targeted drugs in coherently designed multi-agent combinations for use in the clinic.
Our group uses various in vitro and in vivo models to assess the activity of novel anti-tumor drugs alone or in combination for the treatment of ovarian cancer, including 2D- and 3D-cell culture models, subcutaneous/intraperitoneal/intrabursal tumor xenograft models, and bioluminescence-based animal imaging. We are examining many biologics including cetuximab, panitubimab, gefitinib (EGFR inhibitors), dasatinib (SRC family kinases inhibitor), and AMG706 (VEGFR inhibitor) in vitro and in vivo. In addition to drug evaluations, our studies are also focused on understanding the mechanisms of action at the cellular level. The goals of these therapeutic studies are to identify important drug targets, promising agents, and treatment combinations that can ultimately help improve the clinical outcome of human ovarian cancer treatment.
Women who carry mutations in the BRCA1 and BRCA2 (BRCA1/2) genes have a substantially increased risk of developing breast and/or ovarian cancer as compared to the general population. However, risk estimates for breast cancer range from 20-80% suggesting the presence of genetic and/or environmental effect modifiers. We have recently reported that loss of allele specific expression (also referred to as allelic imbalance or AI) of BRCA1 is associated with increased breast cancer risk and demonstrated that these expression patterns can be transmitted by Mendelian inheritance, suggesting that alternate mechanisms, other than deleterious coding mutations, may contribute to breast cancer. We are also participating in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA), an international consortium that is evaluating large cohorts (>20,000) of BRCA1 and BRCA2 mutation carriers for genetic modifiers of breast cancer risk. Our group continues to explore additional high-penetrant breast cancer susceptibility genes. We have shown that BRCC36 is aberrantly expressed in breast cancer, is mutated in cancer prone kindreds, and plays an important role in the regulation of the ubiquitin E3 ligase activities of the BRCA1 containing complex (BRCC). We have also recently initiated studies to identify proteomic markers of benign breast disease (BBD) that can be used to better predict a woman's risk of developing invasive breast cancer. Below are examples of ongoing studies in these areas.
We have previously reported a novel multiprotein complex, termed BRCC, containing seven polypeptides including BRCA1, BRCA2, BARD1, and RAD51 (Dong et al., Mol. Cell 12:1087, 2003). BRCC is an ubiquitin E3 ligase complex exhibiting an E2-dependent ubiquitination of the tumor suppressor p53. In this multiprotein complex, one of these proteins, referred to as BRCC36, was found to be associated with BRCA1 and BRCA2 and was shown to play an important role in the regulation the ubiquitin E3 ligase activity of BRCC. We have shown that cancer-associated mutations in BRCA1 abrogated the association of BRCC36 with BRCC and BRCA1. Furthermore, reconstitution of a recombinant four-subunit BRCC complex containing BRCA1/BARD1/BRCC45/BRCC36 revealed an enhanced E3 ligase activity compared to that of BRCA1/BARD1 heterodimer. In addition, we have reported over-expression of BRCC36 in the majority of breast cancer cell lines and invasive ductal carcinomas. The mechanism and consequences of abnormal BRCC36 expression in breast cancer are presently unknown. To further elucidate the functional consequence of abnormal BRCC36 expression in breast cancer, we performed in vivo silencing studies using small interfering RNAs (siRNA) targeting BRCC36 in the MCF-7 breast cancer cell line. Knock-down of BRCC36 alone did not affect cell growth, but when combined with ionizing radiation (IR) exposure, led to an increase in apoptotic cells when compared to the siRNA control group. Immunoblot analysis showed that inhibition of BRCC36 had no effect on activation of ATM, expression of p21 and p53, or BRCA1- BARD1 interaction following IR exposure (Figure, left panel). Importantly, BRCC36 depletion disrupted IR-induced phosphorylation of BRCA1. Immunofluorescent staining of BRCA1 and g-H2AX indicated that BRCC36 depletion prevented the formation of BRCA1 nuclear foci in response to DNA damage (Figure, right panel). These results imply that down-regulation of BRCC36 expression impairs the DNA repair pathway activated in response to IR via abolishing BRCA1 activation and thereby to sensitizes breast cancer cells to IR-induced apoptosis.
Although breast cancer rates have been declining in recent years, the number of women receiving benign breast diagnoses is increasing. Some benign lesions have a higher relative risk of subsequent breast cancer development than others; however, it is unknown which lesions are most likely to progress to invasive breast cancer. As a proof of principle study, laser capture microdissection was employed to isolate histologically identified regions of BBD (i.e, ductal hyperplasia; DH) and normal breast epithelium from mastectomy specimens. Using 2D gel electrophoresis and mass spectrometry, we identified differentially expressed proteins and demonstrated that a set of these proteins could identify a subpopulation of DH cells exhibiting columnar cell changes (CCC). This is clinically relevant given that cells with atypical CCC have characteristics similar to those observed in atypical DH (ADH) and well-differentiated in situ and invasive carcinomas; thus atypical CCC may represent nonobligate precursors to neoplasia. We have since expanded our studies using more sensitive proteomic technologies to compare ADH from women who remain disease free or subsequently develop invasive disease to those proteins from normal tissue specimens. We compared the proteins and generated a heat map to illustrate proteins that are upregulated in ADH tissues associated with cancer compared to those proteins in normal or ADH tissues not associated with cancer. Together, these markers may prove to be clinically relevant in identifying regions of BBD and in assigning prognostic significance in biopsy samples. We are collaborating with members of the Early Detection Research Network (EDRN) to access clinical specimens to test the value of our markers in predicting women diagnosed with ADH who are at increased risk of developing invasive breast cancer and who might benefit from risk reduction with the use of chemoprevention agents such as Tamoxifen.
The goals of these studies are to evaluate the utility of protein biomarkers in blood at identifying women at increased risk of developing breast or ovarian cancer and to develop a panel of biomarkers to be used to detect these cancers early in their clinical course. To date, we have developed approximately 10 custom bead-based suspension immunoassays (luminex assays) in which fluorescent polystyrene microspheres are coated with antibodies towards the diagnostic biomarkers identified through previous gene microarray studies. We also have in hand approximately 100 commercially available bead-based assays. In many instances, these assays can be multiplexed and provide a fast and effective means to analyze hundreds of biomarkers in precious patient serum or plasma samples. We are currently evaluating our panel of >100 biomarkers by screening blood serum and plasma samples from disease-free women who have a normal level of risk of developing breast and/or ovarian cancer and from women who have an elevated level of risk of developing these cancers due to either being carriers of BRCA1 and/or BRCA2 mutations or by having a family history of these diseases. These tests are being performed to ascertain if single or multiple markers can be used to detect elevated risk in an individual. We have also included blood samples from women who have sporadic breast and/or ovarian tumors to determine the capacity of our marker panel for disease diagnosis in addition to risk diagnosis. Preliminary data show some promising markers for disease diagnosis in ovarian cancer patients as observed by the statistically significant elevation of these markers in women with ovarian cancer relative to healthy women and in women with benign cases. Additional improvements in disease diagnosis were also found when our markers were combined with CA125, a traditional diagnostic marker. Our studies are likely to result in the identification of several single or multi-marker blood-based protein biomarkers which provide the means to assess breast and/or ovarian cancer risk and early detection in women.
Tumor-derived microvesicles or exosomes (TDE) are abundantly found in the plasma and malignant effusions derived from cancer patients. Growing evidence supports the view that tumors constitutively shed exosomes with pleiotropic immunosuppressive effects that are protective and supportive of the tumor to facilitate escape from lymphocyte immunosurveillance. These effects range from regulation of tumor growth, to invasion, angiogenesis and metastasis. Several tudies support a role for exosomes in adapting the host microenvironment to allow escape from immune surveillance via stimulation of angiogenesis and metastasis which suggests that tumors may use exosomes to keep the host immune system under control without a direct interaction with host immune cells. Moreover, TDE are used by tumor cells to remodel the tumor microenvironment into a tumor supportive milieu. The constitutive release and enrichment of certain proteins into TDE prompts consideration of the use of TDE as diagnostic tools in cancer. The use of proteomic analysis on malignant effusion-derived exosomes from various sources has increased our knowledge on exosome protein composition and likewise, our understanding of the role of exosomes in vivo. Exosome-derived proteome studies have been conducted in a number of cancer-derived exosomes including: mesothelioma, melanoma, gastric carcinoma, breast carcinoma, ovarian, prostate, malignant pleural effusions, brain, and colorectal. Since exosomes are known to represent an important mechanism of intercellular communication, numerous studies have been performed which reveal the presence of common subsets of proteins in exosome preparations from different biological fluids, some being unique to the tissue from which they are derived. All of these isolated exosomal proteins constitute a "cancer signature" which may help in improving the diagnosis and follow-up of cancers. We are isolating and characterizing exosomes from blood or ascites fluids as a potentially effective alternative for diagnosis, prognosis, and treatment of cancer.
PATHOGENESIS AND MOLECULARLY TARGETED THERAPY OF GASTROINTESTINAL STROMAL TUMORS (GISTs):
Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal tumors of the digestive tract, with an estimated annual occurrence of 3,300-6,000 in the United States. GISTs are believed to arise from the Interstitial Cells of Cajal (ICCs), the pacemaker cells of the gut, or from interstitial mesenchymal precursor stem cells. GISTs express and are clinically diagnosed by immunohistochemical staining of CD117, the 145 kDa transmembrane glycoprotein KIT. The most common primary sites for these neoplasms are the stomach (60-70%), followed by the small intestine (25-35%). The majority (~80%) of GISTs possess gain-of-function mutations in KIT in either exons 9, 11, 13 or 17, causing constitutive activation of the kinase receptor, whereas smaller subsets of GISTs possess either gain-of-function mutations in PDGFRA (exons 12, 14, or 18) (~5-8%) or no mutations in either KIT or PDGFRA (~12-15%). Imatinib mesylate (IM), an oral drug that inhibits the KIT/PDGFRA is very effective at controlling metastatic disease and preventing recurrence after initial surgery. Unfortunately, in patients with advanced disease, IM stops controlling disease after approximately two years. Our group is studying what happens to GIST cells when they are treated with imatinib and what leads to clinical resistance. Our initial studies identified genetic markers that could predict the response of patients with metastatic/recurrent GIST to imatinib and current studies are focusing on genomic and proteomic changes associated with the pathogenesis of GIST and response to molecular targeted therapies. We have also shown an important role for IGF signaling in adult and pediatric GISTs that lack activating kinase mutations. Based on these studies clinical trials are being developed with the goal of ultimately eradicating this disease. Below are examples of ongoing studies in these areas.
A subset of GISTs lack gain-of-function mutations in the KIT and PDGFRA genes. These GISTs tend to be less responsive to imatinib-based therapies and have a worse prognosis than mutation positive GISTs. We have shown that the aberrant expression of IGF-1R, as opposed to oncogenic RTK-mutations, may be the driving event in these GISTs. This observation suggests an alternative and/or complementary therapeutic regimen in the clinical management of all GISTs, especially in the subset of tumors that respond less favorably to imatinib. Immunoblotting of GIST specimens demonstrated that IGF-1R was present in all tumors but was markedly overexpressed (10- to 30- fold) in GISTs lacking RTK-mutations as compared to mutant GISTs. IGF-1R overexpression in these tumors was confirmed by IHC analysis using an extended set of GIST specimens. In addition, qPCR analysis demonstrated that IGF-1R mRNA is overexpressed ~17- to 19-fold in GISTs lacking RTK-mutations versus mutant GISTs (P = 0.0013). Interestingly, IGF-1R is constitutively activated in all GISTs irrespective of KIT/PDGFRA mutational status. Using a genomic-based qPCR assay, we found that the IGF-1R gene copy number was increased in 70% of GISTs lacking mutation in KIT and PDGFRA (copy number range, 2.5 to 4 copies/tumor cell), as compared with 28% of mutant GISTs (P = 0.04). Fluorescent in situ hybridization analysis confirmed the IGF-1R amplification (3 to 10 copies/tumor cell). Inhibition of IGF-1R signaling with NVP-AEW541 (Novartis, Basel, Switzerland), a specific inhibitor of IGF-1R or down-regulation of expression of IGF-1R with siRNA led to cytotoxicity and induced apoptosis in GIST cells. Combination of NVP-AEW541 and imatinib in GIST cells induced a strong cytotoxicity response. These findings are particularly exciting given the number of agents targeting IGF-1R that are currently being tested in clinical trials. We are currently testing neutralizing monoclonal antibodies and small molecule inhibitors specific for IGF-1R alone and in combination with imatinib, with the hope of improving current therapeutic modalities in GIST patients. Clinical trials using IGF-1R-targeted therapies for imatinib-refractory GIST patients, initially focusing on adult and pediatric GIST patients lacking KIT or PDGFRA mutations are in development within our sarcoma program.
In these studies we have shown that not all GIST that lack mutations in KIT or PDGFRA, the so-called "wild-type" tumors, are alike. Using whole-genome SNP-arrays we have been able to obtain high-resolution maps of the GIST's genome. We used high-density SNP arrays containing ~1.8 million markers genome-wide to analyze GISTs lacking KIT/PDGFRA mutations as well as mutant GISTs. As expected, the mutant GISTs exhibited multiple regions of chromosomal copy number (CN) loss (mean ~ 6.2 per sample) as well as CN gains (mean ~ 2.4 per sample). Importantly, our studies found that the majority of KIT/PDGRFA mutation-negative, both pediatric and adult GISTs which are clinically more resistant to imatinib-based therapies, had either no broad-based CN changes, or CN change across a single chromosome arm. We refer to these tumors as KIT/PDGFRA mutation negative/genome stable GISTs, while the remaining tumors (including both KIT/PDGFRA mutation positive and some mutation negative GISTs) are genome unstable. We also identified smaller (0.2-6 Mb) or focal regions of CN aberration. We have compiled a list of ~80 of these focal CN-variant regions, including 4 regions identified within the mutation-negative, genome stable GISTs. These specific focal changes may be important in the oncogenesis of genome-stable GISTs. Furthermore, as discussed above we have shown that these KIT/PDGFRA mutation negative/genome stable GISTs greatly overexpress IGF1R relative to other GISTs. Importantly, in these studies we have shown the connection between the mutation negative GISTs that have a stable genome and overexpressing of IGF1R. Clinical trials are being developed to explore IGF1R as a target based on these and other molecular studies. Finally, we have shown that a portion of previous classified "wild-type" GISTs that demonstrate genome instability have mutations in the BRAF gene. However, the genetic changes in GISTs without KIT/PDGFRA/BRAF mutations is not known, so we are currently using second-generation sequencing approaches to further explore the GIST genome in these patients to uncover additional clues to help define the origins of these tumors (see Figure "Not all GISTs are created equal").
Despite initial efficacy of imatinib in most GIST patients, many experience primary and secondary drug resistance. Therefore, clinical management of GIST may benefit from further molecular characterization of tumors before and after IM treatment. As part of a recent Phase II Trial of neoadjuvant/adjuvant IM treatment for advanced primary and recurrent operable GISTs (RTOG-S0132), gene expression profiling using oligonucleotide microarrays was performed on tumor samples obtained before and after IM therapy. Patients were classified according to changes in tumor size after treatment based on CT scan measurements. Gene profiling data were evaluated with SAM analysis to identify differentially expressed genes (in pre-treatment GIST samples). Based on SAM analysis, thirty-eight genes were expressed at significantly lower levels in the pre-treatment samples of those tumors that significantly responded to 8 to 12 weeks of IM, i.e., >25% tumor reduction. Eighteen of these genes encoded KRAB domain containing zinc finger (KRAB-ZNF) transcriptional repressors. Interestingly, ten KRAB-ZNF genes mapped to a single chromosomal locus, and a subset of these predicted likely response to IM-based therapy in a naïve panel of GISTs. We designed a custom siRNA library targeting these genes and used a mid-throughput siRNA synthetic lethal screening approach to evaluate the ability of each to sensitize GIST cells to IM. We found that modifying expression of genes within this predictive signature can enhance the sensitivity of GIST cells to IM. These studies are very exciting given that a very high percentage of the siRNAs can sensitize GIST cells to IM, suggesting that many members of the gene signature may not only have predictive value but functional relevance to IM's activity in vivo.
Our group is actively involved in evaluating clinical trial samples for predictive markers of drug response. As such, Dr. Godwin is the Translational Science Co-chair or the lead translational researcher for several Gynecologic Oncology Group (GOG), Eastern Cooperative Oncology Group (ECOG), and Southwestern Oncology Group (SWOG) clinical trials evaluating molecularly targeted agents, such as AMG 102, AMG 386, AMG 479, AMG 706, cetuximab, dasatinib, everolimus, enzastaurin, gefitinib, lapatinib, RAD001, sorafenib, temsirolimus, and VEGF-TRAP. Through the Clinical Molecular Oncology Laboratory (Director, Godwin) at KUMC we are evaluating clinical trial samples for predictive markers of response to therapy. For example, our group demonstrated in a phase II clinical trial that certain serologic markers were predictive of disease control when women with recurrent epithelial ovarian carcinoma were treated with cetuximab alone. We have also recently evaluated a series of tumor vascular proteins identified through gene profiling studies as serum prognostic and diagnostic markers and are assessing the predictive value in large cohorts of patient samples. In a collaborative phase II clinical trial of patients with colorectal cancer we demonstrated that tumors with high gene expression levels of epiregulin, amphiregulin, and/or wild-type K-RAS were more likely to have disease control with cetuximab treatment. This study led to numerous other confirmatory studies and a recent Provisional Clinical Opinion statement by the American Society of Clinical Oncology that all patients with metastatic colorectal cancer who are candidates for anti-EGFR therapy (i.e., cetuximab and panitumumab) have their tumors tested for K-RAS mutations. In general, our translational correlatives are aimed at extracting proteomic and genomic information from patients' blood and/or tumor tissue samples prior to and during the course of treatment to identify potential biomarkers associated with clinical activity and/or predictive of outcome. The ultimate goal of these efforts is to better identify patients more likely to benefit from a particular therapy. A targeted approach to patient selection could potentially improve survival, spare needless toxicity, and reduce expenses associated with futile therapy. Our clinical research efforts will continue to explore and expand the use of molecular pathology in personalizing patient care.


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713-942-3461 firstname.lastname@example.com
This fall, the University of St. Thomas hosted a public photography contest open to amateur and professional photographers. One of the goals of the contest was to attract people from the Greater Houston area to visit the campus to experience what the University has to offer. UST educates leaders of faith and character who excel not only on campus, but also in the larger Houston community and beyond.
More than 80 photographers entered the contest and shared their points of view through more than 250 photographs submitted on the contest's website. Of the nine photographers selected as winners, two are recent UST graduates and one is currently a student.
People's Choice Award Winner Nicole Christians '12 a chemistry alumna, has great memories of her time at UST and was excited to convey these feelings through her winning photograph, "Chapel of St. Basil." Christians' photo was selected as fan favorite in a public vote held on the University's Facebook page. Her image received 675 votes.
"I wanted to highlight how our campus is nestled right in the heart of the City of Houston," Christians said. "Through teaching by example, UST has made a positive impact on the student body, which in turn, benefits the larger community."
Professional photographer Claudia Arguelles '12 is thankful for UST and the opportunity to spotlight campus architecture through photography. Her photo titled "Home of the Brave," winner in the Campus Life category, captures the sense of community found on campus on the anniversary of 9/11.
Arguelles, an international development alumna, is actively involved in the larger community through UST's Social Entrepreneurship Program, which raises funds for women involved in entrepreneurial ventures such as food and cloth production in locations all over the world. Through the Pennies for Poverty campaign, Arguelles, along with other volunteers, visits local schools to educate students about the effects of poverty around the world.
Rida Qadri, a current UST business student, has an interest in photography and heard about the contest on Facebook. Her photo, "Golden Faith," spotlights a favorite building on campus – the Chapel of St. Basil – and won the amateur Architecture category.
"I took many photos with my camera," Qadri said. "'Golden Faith' captures the emotional, spiritual and mental light of faith."
Qadri credits UST for helping her discover an interest in management information systems and a desire to work in the oil and gas industry upon graduation.
For more information about the photography contest, visit ShineAtUST.com.
Educating Leaders of Faith and Character
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text: Equipment Reviews Heads Warrior Gear Review: Warrior Blade Pro Lacrosse Head Lacrosse Playground / August 28, 2012 The Warrior Blade Pro isn't just for face-off men. It's built for the multi-tasking midfielder and more. The pro-player designed head is built with the new Pro Scoop for easy ground ball pickups for middies and Continue Reading Share


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The 5th generation M5 has the V8 S63 TU engine with twin turbos under the hood producing 550hp. The engine and DCT gear box pusses the M5 0-60 in just 4.2 seconds.
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My 2013 M5, Singapore Gray on Sakhir/Black, Loaded (Now available to public.)
Hey y'all!
Here's the scoop, I've been 1st on the list @ my local dealer for 1 year 6 months ( 02/12/2011 : 7 months before the car was even revealed at the '11 Frankfurt show!
It finally got to the dealership and I changed my mind and placed an order for a slightly different configuration + ED + PCD. Also, depending on how far down the line I'm placed (11th I think) and how long it'll take. I just might hold out for a CC brake car. I'll see as the information becomes available to me.
The car is now available to go to a new home and my SA went out of his way to accommodate my desires so I'm trying to recoop some CARma by trying to speed the process of finding this M5 a warm home.
I hope you all will see this not as spam, but as a heads up to those who don't want to wait in line for one OR a lucky break for someone who shares my taste in F10 M5 configuration.
Brand New, 0 owner, 11 delivery miles.
Here is the Vehicle Inquiry Report.
Model Code 135G M5 Sedan USD 89,900.00
Color B41 Singapore Grey Metallic
Upholstery LKDA Sakhir Orange / Black Merino Leather
Options ZDA Driver Assistance Package 1,900.00
5AD Lane Departure Warning N/C
5AG Active Blind Spot Detection N/C
5DL Side and Top View Cameras N/C
8TH Speed Limit Info N/C
ZEC Executive Package 5,500.00
248 Heated Steering Wheel N/C
316 Power tailgate N/C
322 Comfort Access keyless entry N/C
323 Soft-close automatic doors N/C
415 Power rear sunshade N/C
416 Power rear sunshade with rear manual side window shades N/C
453 Front ventilated seats N/C
455 Active front seats N/C
496 Heated rear seats N/C
4NB 4-zone automatic climate control N/C
610 Head-up Display N/C
655 Satellite radio with 1 year subscription N/C
6NF Smartphone Integration N/C
6NR BMW Apps N/C
2NK M Carbon Ceramic Brakes 8,700.00 (ORDERED BUT NOT DELIVERED AS YOU WELL KNOW )
2NZ 20" M light alloy wheels Style 343M 1,300.00
320 Delete badge N/C
4CE Anthracite Wood Trim N/C
6F2 Bang & Olufsen Sound System 3,700.00
6FH Rear-seat entertainment Professional 2,200.00
6UK Night Vision with Pedestrian Detection 2,600.00
776 Anthracite Alcantara Headliner N/C
8S4 Variable Light Decoding N/C
As you can see the car is loaded. The Sakhir 'Orange' in real life is much like Coral/Fox, I adore it and I feel it's still pretty red-ish instead of orange.
Here are a few pictures:
Feel free to ask any questions via this thread or PM.
Or if you've seen/heard enough you should directly contact my SA @ BMW of Sterling.
Felix B. Bighem
Senior Sales & Leasing Client Advisor
Regional Sales Council / Honors
Phone: 571 434-1944 ex 1105
Fax: 571.434.9690
Thanks for looking, have a great life. :thumbsup:
Stg V N/A
Last edited by Turbo Squid; 09-06-2012 at 10:00 PM.
Why delete the badge? Isn't that for guys who want a real M car, but don't quite have the means?
I'm pretty sure you meant to say: "Isn't that for people who make put the M-look on their regular 5'er but debadge the 5XX badge so people think it's an M5."
Either way, No. It's for guys who don't need people to know it's an M5 and just want the car for the car and not for the flash factor. (As if it had any flash...)
Badge delete because I don't care much for labels, people who know enough about cars will recognize that it is an M5. I don't feel the need to show off. Plus I think it cleans up the rear of the car, less features that break up the end of it, giving it a somewhat wider-ish look.
Added benefit is that when I take this car to Paris haters will just think it is a taxi rather than scold it for being a gas guzzler. (Not really an issue for USA.)
It is for discretion.
You can always just buy the emblem and slap it on there later on though...
Stg V N/A
Last edited by Turbo Squid; 09-08-2012 at 02:06 PM.
Yes, of course I meant guys who debadge a 5 series or 3 in hopes of passing it off as an M. But, as you say, the M5 is already the most discrete super sedan available and it looks so classy in stock form. Dfferent strokes, but just an observation on your choice.
Saw one in this same color combo earlier this week and then a black on black today. I don't know what color o would choose of I went that route, but the lines and proportions of the car are just perfect IMO. I just love the subtle muscular look of it.
I wish I didn't need AWD more than a few days each year. Maybe an X5M will be the compromise, of sorts.
Hope you love yours when it arrives.
Although I must say that these days even high powered sedans perform admirably in the snow. The trick is to just have a dedicated set of winter tires/wheels. As long as you know how to drive on the snow you'll be fine. My C-AMG's were driven daily when there'd be snow on the ground. Plus, look at everyone in Europe, when I'm in the Alps I see tons of RWD cars driving on snow (literally on snow and not cleared roads.) It's just a matter of experience I guess. (Note: Maybe if you live in BumF$*K, Alaska snow tires aren't enough to cut it.)
Stg V N/A
M5 is all about the badge which of course comes performance.
It's like buying a 1st class ticket but sitting in couch...I bet you could. But if u but a coach ticket and want to sit in 1st class ... You have no chance in hell.
Doesn't make sense to remove the badging!!!!
The M5 is not all about the badge. Only materialistic people think that way.
Your analogy on plane tickets makes no sense... What you're saying corresponds to buying an M5 and trying to pass it off as a 520d -or- buying a 520d and trying to pass it off as an M5. Neither is the case here.
If I had to analogize this M5 debadging scenario I would put it like this: I'm the kind of person who would buy a ~$27k White Gold Rolex Daytona even though by the naked eye it looks pretty much identical to the ~$8k Stainless Steel Rolex Daytona. I don't need everyone to know its a big shot piece, I know, and that is what matters most. (Needless to say that most people worth their salt can instantly recognize that this is an M5 and not a subordinate trim 5'er.)
If you need a badge to feel better about yourself then you are missing the point of the M5 entirely. It is meant to be visually understated, and professional.
If you wanna be flashy go buy something that you think doesn't need a badge to be recognized as what it is.
Side note, ANYONE can slap an M5 badge back on there. (Preferably done by a legit dealer or bodyshop so the spacing is correct and doesn't look off.)
Just sayin'.
Stg V N/A
Personally, I like the look of debadged cars, but I eventually went with rebadging on my xDrive and yes I have dedicated snow tires for the winter too.
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The Golden Griffins extend their winning streak to 12 games, which is the longest winning streak in program history and is the second-longest active winning streak in the country.
The combination of the Canisius win along with a victory by Quinnipiac has locked up a first-round bye for the Golden Griffins in the six-team 2014 MAAC Championship (May 21-25 at Lakewood, N.J.). The Griffs now need a combination of two Canisius wins and Siena losses to lock up the No. 1 seed and outright regular-season title.
Canisius collected 18 hits in the game, with freshman Christ Conley recording a career-high four hits to go along with two runs scored and three RBI. Senior Jose Torralba and junior Jesse Puscheck each went 3-for-4 with three RBI as Torralba also scored three runs.
After the Griffs scored a run in the top of the first, Niagara (16-30, 8-14 MAAC) took its only lead of the day by scoring two runs in the bottom of the first. Canisius then scored 14 consecutive runs, starting with three unearned runs in the second. Senior Shane Zimmer scored on a wild pitch in the third, which included an RBI groundout from Torralba and RBI single from Puscheck.
Canisius broke the game open in the fourth with an RBI single from Conley, two-RBI single from Torralba and another RBI single from Puscheck to make it 11-2. The Griffs added four runs in the sixth on an RBI double from Puscheck, sacrifice fly from junior Connor Panas and two-RBI double from Conley to put the Griffs up by 13 runs.
Junior Devon Stewart (5-5) went six innings, and allowed two runs on four hits. Of the 18 outs recorded by Stewart, 13 were of the ground-ball variety. Freshmen Zachary Trumpler and Zachary Sloan along with junior Tyler Vavra each threw an inning of relief.
Canisius has four home games remaining on its schedule, starting with a non-conference game on Tuesday against Niagara at the Demske Sports Complex with first pitch set for 2 p.m. The Griffs will wrap up the MAAC schedule against red-hot Monmouth, who has won 10-consecutive games. That series starts on Thursday, with first pitch for the doubleheader set for noon.
Notes: Canisius finishes the regular season with 22 road wins… The Griffs have now won 11 consecutive games over the Purple Eagles… Canisius scored double-digit runs for the 13th time this season… Junior Sean Ritter, sophomore Auston Ingram and freshman Kyle Collins each made pinch-hit appearances for the Griffs in the ninth inning… Stewart went six or more innings for the eighth time in the last nine starts… The 17 MAAC wins are the third-most in program history, trailing the 2008 and 2010 teams that each won 19 conference games. Both of those teams won the MAAC regular-season title.


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Tell me where it says a word about ADD.
As always, I say fix the system rather than trash the whole thing.
Maybe I'm reading the site wrong, but it appears to be aimed at adults who can't function well enough to work. I'm not finding anything about children and SSI. I cannot fathom a reason they would qualify for SSI for a learning issue. And I've never, ever heard of that.
Hard to imagine why a family would need SSI if the school is dealing with it, though


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Come join the FotoFreaks on their scenic journey of Newfoundland and Labrador in Canada. You will be glad you did.
Comments welcome on the site and photography.
New Scenic Web Site
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Hi everybody!
I just wanted to drop in and say hi! I am currently in Kuwait and I will be heading up to Baghdad in the next couple of days. Right now, everything is going smoothly. The internet connection out here is slow as heck, so I can't upload any pics right now. But I'll definately upload some when I get to Iraq.


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By Rob Kelly
Santi Cazorla says the key to victory at Old Trafford on Saturday will rest in Arsenal's ability to control possession.
The Spain international has made a superb start to life in the Premier League and is looking forward to the challenge of facing Manchester United.
While the 27-year-old says a win would be a huge boost to the team's self-belief, he accepts they will have to work extremely hard to achieve it.
"I think the key to modern football is having possession, the more you have the more you control the game," Cazorla told Arsenal Player. "At Old Trafford we need to control the game and keep hold of the ball.
"[A win] would be great for the team's confidence. To beat such a strong side at their own ground makes you stronger in all aspects.
"Let's take the example of our match against Manchester City, which was a difficult game against a tough side. The team showed incredible quality and could even have won the game, so we came out of that match much stronger than before.
"Therefore, as well as the three points you can hopefully take from those games, you can come out stronger and take away more confidence too."
Cazorla admits Saturday's game is one he has been looking forward to ever since he arrived in England this summer.
"It's a great fixture," he said. "It's a great stadium, they're a good side and it's a big game. It will be a brilliant experience. They've got brilliant players like Robin [Van Persie], Rooney and many more who are first class, so it will be very difficult to beat them.
"But all the players in our squad have played against some of the biggest teams in the world so it's nothing new for us."
Watch the full interview with Santi on Arsenal Player now.
Join the conversation on Twitter: #MUFCvAFCCopyright 2017 The Arsenal Football Club plc. Permission to use quotations from this article is granted subject to appropriate credit being given to www.arsenal.com as the source


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On Saturday(10/04/2010) we climbed Devil's Advocate. Between the 2nd and 3rd bolts you get this undercling type hold to reach up from, well you don't get it no more as it broke off. In my opinion the route grade should stay the same as you can still get to the side pull/pinch underneath the roof without too much drama as there are still sufficiant holds where the undercling used to be. Might be a little harder...
Devil's Advocate-Bronkies
Swop tips on moves, route conditions, etc.
4 posts • Page 1 of 1
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- Location: Johannesburg
Re: Devil's Advocate-Bronkies
I dunno. I needed that undercling to do it. So for me it's gonna be a lot harder now!
- Posts: 84
- Joined: Tue Feb 26, 2008 9:33 am
- Location: Johannesburg
Re: Devil's Advocate-Bronkies
Daniel found a heel hook out right which helped him, I could'nt get a size 9 in there though.
- Posts: 61
- Joined: Sat Jan 26, 2008 9:49 pm
Re: Devil's Advocate-Bronkies
with a name like that, I am not surprised. the rock is probably playing 'devil's advocate'...
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The online programme is available as a downloadable PDF file.
This allows the online version to accurately mirror the award-winning design of our official matchday programme.
Simply click on the button below to download.
Total file size: 16.44 MB
In today's programme...
- Arsène Wenger - On Sparta Prague, the Champions League draw and recent tragic events
- William Gallas - Looking to the challenges ahead
- Voice of Arsenal - Including the Group Stage draw in full
- Theo Walcott - Waiting to be unleashed on his old rivals
- Young Gun - Jay Emmanuel-Thomas - fresh from scoring a Beckham-style goal
- Reserves and Youth - Reviewing the Under-18s' draw with Charlton
- Photographic Memory - A new picture - and a new chance to win
- Arsenal Ladies - World Cup build-up, and Vic's views
- Creating Chances - A look at this new Premier League initiative
- Emirates Examination - More fiendish half-time teasers
- Junior Gunners - The latest news for our young fans
- Scene Around Europe - What's happening on the Continent
- Mariner Memories - Paul Mariner is a familiar face to both sets of fans today
- Country File - Gunners called up for their national squads
- Portsmouth - Welcoming some old faces - and some new ones too
- Arsenal A-Z - Did you know legendary cricketer Brian Close was once a Gunner?
- Sparta Prague Action - Eduardo off the mark
- The Interview - Club Physio Gary Lewin
- Arsenal Opus - Another extract from this remarkable production
- Gael Clichy - Summing up the start of the season
Copyright 2017 The Arsenal Football Club plc. Permission to use quotations from this article is granted subject to appropriate credit being given to www.arsenal.com as the source


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Arsenal supporter Paul Smith is set to finish yet another remarkable challenge, as he continues his now long-standing tradition of supporting Arsenal Football Club's charity partners.
After successfully completing an arduous three-day journey in his wheelchair from Fratton Park in Portsmouth to Emirates Stadium last season, raising £25,000 in the process, Paul set himself an even tougher challenge this season as he looks to raise double that amount for Save the Children.
On April 16 2012, Paul set off on his fourth and most ambitious challenge to date, as he travels from Portland in Dorset to Emirates Stadium on a five-day journey. The entire trip has seen him self-propel himself in his wheelchair towards London, in an epic journey of approximately 200 miles.
Portsmouth resident Paul, 52, suffers with brain injury, crush injuries to his hips and chest, as well as long-term damage to his neck and shoulder following a road traffic accident back in 1991. The Arsenal supporter is determined to complete this challenge with a dedicated crew who will help him through this latest gruelling test.
To support Paul's challenge, visit www.justgiving.com/challenge200. You can also follow his progress on Twitter at www.twitter.com/challenge200.
Alternatively, supporters can cheer on Paul as he crosses the finish line at the Queensland Road slope outside Emirates Stadium on Friday at approximately 3pm.Copyright 2017 The Arsenal Football Club plc. Permission to use quotations from this article is granted subject to appropriate credit being given to www.arsenal.com as the source


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Rolex daytona STAINLESS STEEL white or black dial best
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After 5 days have passed all sales will be considered FINAL and no claims whatsoever shall be entertained.
The item must not be altered and must not have any wear & tear marks.
We accept Checks, Money Orders, Bidpay, Bank to bank wire Transfer or Paypal.
We also accept Amex, Visa or MC only via paypal. Shipping & Handling for US Customers is $19.50 & for Customers outside USA its $29.50 per package.
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Insurance cost is $25.00 for shipments equal to or less than $2000 in value. Insurance cost is $50.00 for shipments over $2000 in value.
Although we do our best to accurately describe our items we do not guarantee accuracy of the information, we obtain information from other sources such as suppliers , third parties, etc. In case of diamond grading, being basically subjective in nature,the grades of diamonds' depend upon the personal opinion of the person grading the stones.Any difference in opinion is beyond our control. Grading, appraisals etc. from jewelers, appraisers, etc. are/is not binding on this sale.


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Orlando Florida Chrysler, Jeep, Dodge and RAM in Clermont, FL does so much more than just sell you a car. We provide customers with guaranteed auto financing, up to $10,000 minimum for your trade on select vehicles, as well as plenty more benefits. We are located at 15859 State Road 50, Clermont, FL 34711 . We service customers in cities such as Ocoee, The Villages, Winter Haven and throughout Central Florida. We always have more than 500 new Chrysler, Jeep, Dodge and RAM vehicles in stock to ensure that you find the right new car for you. In addition to our new car stock, we carry an extensive array of pre-owned luxury and domestic cars as well as many Chrysler, Jeep, Dodge and RAM cars. Beyond the sales department, we continue to care for your car with a state-of-the-art service and parts department that are open seven days a week to service your car at your convenience. Please, feel free to call us at (877) 356-6859 or stop by any day of the week. Your Orlando New Chrysler Jeep Dodge RAM Dealerships
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Injury Updates
Pirates Notebook: Tabata Returns, Will Burnett Pitch a Rehab Start?
Injury Updates
This content is for Pirates Prospects subscribers only. Subscribers get access to all of our daily articles on the Pirates and their minor league system, with live coverage throughout the system on a daily basis. Our lowest rates are $2.22 per month under our Top Prospect Plan, which also gets you a 40% discount on the 2017 Prospect Guide. Subscribe today to access all of our daily coverage of the Pirates' system.
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James dabbles in the baseballey-writey world. He won the SABR Analytics Conference Research Award for contemporary baseball analysis. It was for that defensive shifts piece, you remember that? Not a huge deal, he also lost a bunch of other awards. He has also written for NBCOlympics.com, Pittsburgh Magazine, Pittsburgh Sports Report and the official websites of the Los Angeles Clippers and Pittsburgh Penguins. By night, James is a television news reporter and weekend anchor for WKBN and WYTV in Youngstown, Ohio. Makes sense, seeing as how his degree from the University of Southern California is in Broadcast Journalism. James dispenses more bad jokes at his Twitter account, @JamesSantelli. It's there that he promises to write in the first-person.
Agreed, getting all three would obviously be perfect, but they're…
Do they still have enough money under their allotted amount…


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Hello folks,
A few things, I've been wondering about:
1. What colour are your eyes vs. what is the colour of your eyes?
Which is correct? Why?
2. What tense is used in the following sentences?
I am tempted to give an examination.
I am scared to do the test.
She is disgusted with his attitude.
I am finished
I finished.
In your answer, please focus on the verb to be + words which end with ed.
3. What's the rule about punctuating interrogative sentences which express exclamation?
For example: excitedly greeting a friend you´ve not seen a long time -
How are you? (!)


text:
|Topic Review (Newest First)
|Super Streeter
Thats exactly why I have a 1/4" longer rod in my 427,but again it depends on the application.If it meant running a narrow ring package in a street engine instead of a wider more durable package I would say no.If it meant putting the top ring less then .100" from the top of the piston on just about any engine I would say no.If it meant not being able to get an extra half inch of stroke in the engine I would say no.If it meant going over about 1.85:1 on the rod ratio I would say no unless it was some oddball exmaple of some super short stroke engine that would need 1000 gram pistons just to make it go together,and even then I would be skeptical.
As for induction signals,increasing the speed at which the piston moves away from TDC on the intake stroke causes the demand on the intake to be greater at this part of the cycle,while being weaker at the end of the intake cycle.This isnt good since this requires that the valvetrain be timed to get as much lift at the valve as possible at or around the time the piston crosses TDC to take advantage of the high piston speed,and it means that the slow approach to BDC will somewhat deminish to velocity in the port as the piston crosses BDC and will require an earlier intake closing event which limits RPM potential.This problem was a big issue when Comp eliminator drag engines had to run standard deck height blocks.These engines had a surplus of cylinder head and intake flow,but poor velocity because the ports were typically larger then optimum for these super destroked engines,The problem was made worse by the fact that the only was to get a sane piston weight out of a 3" stroke smallblock with a 9.2" deck height was to run 6" rods which created the induction pulse problems I mentioned above.The problem was further aggitaged be the fact that in order to get more signal up to the carb through the already too big indiuction system,builders took plenum volume out of the intakes which helped low speed signal to the carbs but caused reversion at high speeds.
Think of it like this,a 3" stroke or even 2.75" stroke Comp smallblock could easily run a 6.25" rod in a stock height block with no issues,and a 3.650" stroke 500 cube prostocker could easily run 6.800" rods in a stock height block with no compromise to piston design,but for the same reason
both classes use very expensive and very trick "low deck" blocks that let them use much shorter rods with these combinations.
3 hp per cube normally asperated on gas isnt something to scoff at the last time I checked.
Induction signal that's too strong! Never heard that one before.
many of you have said that this debate will never be solved, that there are no true facts. I could go on to quote famous tuners, or something from the 100's of pages of literature I've read on the subject, But the general concensus seems to be that the longer rods make more power. Though small and not worth the effort, in most's opinion's. But more still.
Let's ask this question. If you could get a quarter inch longer rod, at the same price, pistons and all, would you? or not?
sorry if I sounded like a ***** saying it like that.
|Super Streeter
There are some basic ideas about rod length.I never gove it much though as a means of increasing performance,but here is what I think about it anyway.
I would never pass up the chance to gain stroke if I needed it just because it would hurt the rod ratio.Of course there are extremes,but in most well rounded combinations this can be taken as fact.I would also never give up piston strength or resort to using a comprimised ring package just to get more rod into an engine.
Short stroke engines can sometime use longer rods as a means of reducing piston weight and improving ring stability,but too much rod can make an induction signal that is too strong on an engine with a limited induction system,so even on an unlimited induction engine,I wouldnt go over about 1.9:1 on the rod ratio.My preference would be to shorten the deck height of the motor and get the rod ratio back down to 1.7:1.
My last theory is the most noteworthy.When in doubt and room permits,build any 90 degree V8 engine with a rod ratio of 1.7:1.I say this not because this is a magic number,but because it is in the middle of where rod ratios typically fall,so matter what anybody else in your class has or claims to have,they will never have any signifigant amount more or less power then you just because of rod ratio.
As a point of interest,my own personal engine is a bigblock chevy built for class racing at 440 cubes,and I use a 3.76" stroke and 6.385 rods with a standard deck height block,and the combination is about as well rounded as it gets,and guess what the rod ratio is.
|machine shop tom
I agree with k-star and camaroman. For most engine builds short of professional circle track or drag racing, rod length is a small issue in a total engine build. I would look at the whole picture. If an engine combination came with only one choice of rod length, your choice is made. If more than one rod length is available, use the cheaper one and use the left over money for something that will make a tangible difference. If the price is the same, flip a coin.
|A heavier rod will result however, not in direct proportion to the piston weight reduction with longer rods. I agree that with a street engine a long rod doesn't make a lot difference. But it's an additional tuning tool with competition engines.
There was/is an article that was done about this exact subject and the differences are minute. I wish I could find it. Anyway, my "opinion" is that people make much too big of a deal about this subject. The side loading vs. time at TDC, etc.. the difference is so tiny it is really not worth the effort. While I agree in most cases the longer rod will have a lighter piston BUT, you will usually have a heavier rod (since it's longer). Like 99% of hot rodding it is all give and take. Buy what works best for your application and is priced best.
I have built 383's with 5.565" (stock length 400 rods), 5.7" and 6" rods, there really is no difference when it comes to performance.
This is one of those topics that will probably never really be agreed on. Build it either way and it will probably run about the same, so there is no real risk or reward.
Theoretical power differences are offset by the additional frictional losses.
As for Smoky Yunick = That is a correct quote that has a distorted meaning......
What he actually meant was.... longer rods flop back and forth less so there is less force trying to break them.... at least that is what he told us.
So Smoky said put as long a rod as possible into it.
IMO, i think you are going to be very limited with your rod choices with that engine....
At any rate i would be more concerned about getting the bob weight as light as you can. That will get you far more results then any planning of the rod ratio......
There is almost no hard facts on this subject. There are however a ton of opinions on it. Many have been hyjacked from someone elses opinion... Unless you are at the end of your ropes and are looking for that last 1 or 2 hp don't even spend the time on it.......
I assume this is going to be a drag race engine????
Keep in mind that going from 1.55 rod ratio to 1.60 is more dramatic and makes more of a difference then from 1.70 to 1.75. Just like camshaft duration and compression ratio it only helps to a point. Someone mentioned Smokey Yunicks says go for the longest rod. For his type of racing this was probably true. They never saw more then 500miles and probably never saw anything under 5000rpm. For the street this couldnt be more wrong. Johngrass hit it dead on, its not about long or short rods, its about how you match your setup for it. To take advantage of it, you need to match the cam, even more important are the heads. The intake runner size is very important when considering your rod length.
IMO anything above 1.7 is not worth it. The advantages are so small that its not going to make a difference unless your a professional racer limited to a class and every .5hp makes a difference. Your money could be spent somewhere else with probably better gains per dollar.
Wow, awsome resposes guys,many many thanks , looks like i may have opened a can of worms here!
DoubleVision, i did that but couldn't find what i was after, best i look again or perhaps get the wife too as she has a knack of finding things.....lol
Huskinhano,Thanks for the info, very interesting.
johnsongrass1, thanks for the reply, higher rev capability would be a bonus forsure as this engine will see 8-8500rpm.
ap72, thanks for your input
k-star, I'm building a boosted Mazda Fe3 2.0L stroked to 2.3-2.4 Ltrs depending on overbore.Its going in a MX5/Miata.
predator carb guru, That reply deserves a medal and certainly clears a few things up for me, big thanks for taking the time to post it all
Cheers Rob
|predator carb guru
ok, i'm no expert here, but i'll just make a quick couple of quotes:
warren "the professor of pro stock" johnson - a connecting rod is there simply for nothing more than to link the piston to the crankshaft.
reher-morrison - We also wanted to point out some of the common myths and misconceptions about high-performance motors. For example, I've seen dozens of magazine articles on supposedly "magic" connecting rod ratios. If you believe these stories, you would think that the ratio of the connecting rod length to the crankshaft stroke is vitally important to performance. Well, in my view, the most important thing about a connecting rod is whether or not the bolts are torqued! If I had to make a list of the ten most important specifications in a racing engine, connecting rod length would rank about fiftieth. Back in the days when Buddy Morrison and I built dozens of small-block Modified motors, we earnestly believed that an engine needed a 1.9:1 rod/stroke ratio. Today every Pro Stock team uses blocks with super-short deck heights, and we couldn't care less about the rod ratio. A short deck height improves the alignment between the intake manifold runners and the cylinder head intake ports, and helps to stabilize the valvetrain. These are much more important considerations than the rod-to-stroke ratio. There's no magic - a rod's function is to connect the piston to the crankshaft. Period.
ed iskenderian - Rod Lengths/Ratios: Much ado about almost nothing.
Why do people change connecting rod lengths or alter their rod length to stroke ratios? I know why, they think they are changing them. They expect to gain (usually based upon the hype of some magazine article or the sales pitch of someone in the parts business) Torque or Horsepower here or there in rather significant "chunks". Well, they will experience some gains and losses here or there in torque and or H.P., but unfortunately these "chunks" everyone talks about are more like "chips".
To hear the hype about running a longer Rod and making more Torque @ low to mid RPM or mid to high RPM (yes, it is, believe it or not actually pitched both ways) you'd think that there must be a tremendous potential for gain, otherwise, why would anyone even bother? Good question. Let's begin with the basics. The manufacture's (Chevy, Ford, Chrysler etc.) employ automotive engineers and designers to do their best (especially today) in creating engine packages that are both powerful and efficient. They of course, must also consider longevity, for what good would come form designing an engine with say 5% more power at a price of one half the life factor? Obviously none. You usually don't get something for nothing - everything usually has its price. For example: I can design a cam with tremendous high RPM/H.P. potential, but it would be silly of me (not to mention the height of arrogance) to criticize the engineer who designed the stock camshaft. For this engine when I know how poorly this cam would perform at the lower operating RPM range in which this engineer was concerned with as his design objective!
Yet, I read of and hear about people who do this all the time with Rod lengths. They actually speak of the automotive engine designer responsible for running "such a short Rod" as a "stupid SOB." Well, folks I am here to tell you that those who spew such garbage should be ashamed of themselves - and not just because the original designer had different design criteria and objectives. I may shock some of you, but in your wildest dreams you are never going to achieve the level of power increase by changing your connecting rod lengths that you would, say in increasing compression ratio, cam duration or cylinder head flow capacity. To illustrate my point, take a look at the chart below. I have illustrated the crank angles and relative piston positions of today's most popular racing engine, the 3.48" stroke small block 350 V8 Chevy in standard 5.7", 6.00", 6.125" and 6.250" long rod lengths in 5 degree increments. Notice the infinitesimal (look it up in the dictionary) change in piston position for a given crank angle with the 4 different length rods. Not much here folks, but "oh, there must be a big difference in piston velocity, right?" Wrong! Again it's a marginal difference (check the source yourself - its performance calculator).
To hear all this hype about rod lengths I'm sure you were prepared for a nice 30, 40, or 50 HP increase, weren't you? Well its more like a 5-7 HP increase at best, and guess what? It comes at a price. The longer the rod, the closer your wrist pin boss will be to your ring lands. In extreme situations, 6.125" & 6.250" lengths for example, both ring and piston life are affected. The rings get a double whammy affect. First, with the pin boss crowding the rings, the normally designed space between the lands must be reduced to accommodate the higher wrist pin boss. Second, the rings wobble more and lose the seal of their fine edge as the piston rocks. A longer Rod influences the piston to dwell a bit longer at TDC than a shorter rod would and conversely, to dwell somewhat less at BDC. This is another area where people often get the information backwards.
In fact, this may surprise you, but I know of a gentleman who runs a 5.5" Rod in a 350 Small Block Chevy who makes more horsepower (we're talking top end here) than he would with a longer rod. Why? Because with a longer dwell time at BDC the short rod will actually allow you a slightly later intake closing point (about 1 or 2 degrees) in terms of crank angle, with the same piston rise in the cylinder. So in terms of the engines sensitivity to "reversion" with the shorter rod lengths you can run about 2-4 degrees more duration (1-2 degrees on both the opening & closing sides) without suffering this adverse affect! So much for the belief that longer rod's always enhance top end power!
Now to the subject of rod to stroke ratios. People are always looking for the "magic number" here - as if like Pythagoras they could possibly discover a mathematical relationship which would secure them a place in history. Rod to stroke ratios are for the most part the naturally occurring result of other engine design criteria. In other-words, much like with ignition timing (spark advance) they are what they are. In regards to the later, the actual number is not as important as finding the right point for a given engine. Why worry for example that a Chrysler "hemi" needs less spark advance that a Chevrolet "wedge" combustion chamber? The number in and of itself is not important and it is much the same with rod to stroke ratios. Unless you want to completely redesign the engine (including your block deck height etc.) leave your rod lengths alone. Let's not forget after all, most of us are not racing at the Indy 500 but rather are hot rodding stock blocks.
Only professional engine builders who have exhausted every other possible avenue of performance should ever consider a rod length change and even they should exercise care so as not to get caught up in the hype.
sorry for such a long post, but i feel it's worth posting. if you get caught up in all this stuff about rod length in your engine, i honestly believe that you're wasting money and time with something that is pretty much futile. spend your money on high quality parts, and match the parts that count, intake system, camshaft, compression, exhaust, etc...............just my $5.00 (adjusted for inflation, 2 cents just doesn't get what it used to anymore.....)
What typ of engine are you building???
drag race, dirt track???
Pump gas,race gas????
400 hp or 1000 hp????
|less rod fatigue with shorter rods, also as far as I see it they have the advantage at higher rpms too.
Regardless of opinions, a few fact's are: delayed TDC dwell time for restricted head and intakes, less thrust wear on cyl. walls, Higher rpm capability. Cam choice is critical to gain the advantage.
My opinion?
The price is the same, the pistons are lighter, they'er many pro's, and not many cons.
|From my bench racing point of view is this. I'm a long rod fan. Well over 10 years ago I read an article where a sbc was built using 2 sets of rods & pistons, one long rod and the other short. They swapped the two during dyno tests, keeping everything else the same to keep variables to a minimum. The long rod set up made a modest amount more. But as I said, this was over 10 years ago. I've read so many different point of views, I don't know who to believe. With todays heads, cams and intake systems it may not be such a big deal anymore. Most likely you'd be better of spending money on a custom cam, headers or some dyno time IMO. There comes a pratical limit, is the expense having a custom set of rods and pistons in search for the idea rod ratio worth it over readily and cheaper off the shelf parts? Look athe the Ford 428 and Chevy 454. Two well respected engines know for their power and both have so called lousy rod ratios, something like 1.43 or something like that IIRC. It'll be interesting to hear what a profession engine builder has to say.
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As some of you know I'm working on a servo kit. It has been more difficult than I had anticipated, but I think I will eventually figure it out. One issue that may speed that up is the switches. I know the screen used switches were the alco mpe106d which are push on push off SPDT switches. My question to you are is would it be a big deal if the switch were the alco mpe106f? It looks exactly the same as the 106d, it's just a momentary on/off instead of the push on push off 106d.
Post your thoughts below and I will go with whatever the majority of you think is better.


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- Part of our perfect-fitting Platinum Denim collection.
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- 98% cotton, 2% spandex.
- Machine wash. Imported.


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Posted by Julie Ask on September 12, 2012
I listened to the Mark Zuckerberg interview from the TechCrunch Disrupt event in San Francisco this week.
There were a few choice quotes (I'll paraphrase them here - these are not literally a transcription. You can find the video/audio on the TechCrunch site):
"The biggest mistake we made (with our mobile services) was relying too much on HTML5 and for too long."
"We finally realized that a good enough mobile experience would fall short. We needed a great mobile experience. The only path to great is native on iOS and Android."
"Our mobile users are more engaged and use our services more frequently."
"All of our code is for mobile."
"We'll build native code for iOS and Android." (And it is building for iOS first)
"Ads can't be standalone on a sidebar in mobile. They need to be integrated into our product."
"We reorganized. A year ago, 90% of the code check-ins were from the core mobile team. Now 90% comes from other parts of the organization."
"We reorganized. We were in functional silos. We now have product teams (responsible for delivery)."
"A Facebook phone doesn't make any sense."
Some context. Certainly, Facebook is unique with it being a media-centric company and very global. It does need mobile Web to reach much of its audience - now nearing 950M. For many companies, mobile Web will continue to be a relatively low-cost, broad-reach play to get to most of the phones. Mobile Web doesn't go away, but it is not where the differentiation will happen - at least in the near term.


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This weekend see's ACB return for it's sixth installment. With many great amateur fights on the card it is set to be an explosive night of fights.
Some of the many fights on the night see Martin Chester aiming to win his third amateur title as he takes on HAMMA star Callum Gaghan.
Also on the card is Conor Hignett. Who has a 9-2 record at just 17.
Check out the full preview here


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Kathy Griffin gets in shape for her celebrity boxing match with Demi Lovato. See, people would watch that.
Katherine Heigl in NYC, with what looks like a wig.
Kelly Rowland is also in NYC.
Kevin Spacey is in Miami taking in men's tennis.
Ali Landry smiles every day knowing she dumped Mario Lopez.
Anthony Mackie surfs in front of a green screen.
Miranda Kerr looks great here.
Rosario Dawson headed through the airport.


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Winter is here for me, so I usually spend it down in my shop working on armor or at the forge working on a knife. Ever since I finished my 2.0 armor that most people have seen me in over the last few months...the only thing I can think about is the next set and making it better. So, as I do on Mercs I'll be posting a work log here also.
This set of armor is very special to me, because it will encompass every ounce of skill I have in metalwork and electonics. I'm sure I'll be learning some new tricks and techniques as I put it together...as you just can't know it all. For all intents and purposes, this is also my last personal set of armor for hopefully many years as I begin working on sets to sell.
I'm installing quite a few new innovations that I've been working on over the last year. A working RF, compressed jet-firing JP, and modular armor system are the three big projects that go into this set. Many future upgrades are planned, and with the nature of this build there will be no need to replace an entire set, just add on. =)
So, lets start with the Jet Pack. Firstly, I used Skupilkinson's JP patterns for a Jango arena pack. I've always loved the arena pack because of it's more sleek look. Now there will be quite a few customizations to the pack itself before the internals are even installed. Pictures are in sequence of order, with the final picture being acompairison of it next to my modified Boba fiberglass pack. I still have the center strut to add to the ouside of the canister as well as a couple small parts before the fuel canisters can be added.
The metals used are 26gu plate steel for the base, top, bottom and outer fuel canister holders. 25gu aluminum for everything else to keep it light. At this point it weighs about 5oz less than my fiber pack, and I don't expect the weight to be that much more in it's blank state. Once the NOS jets and canister are added, I expect it to put on a few pounds. The goal of this pack is not to *fire* but to blow out 2 jets of N20 gas illuminated by 2 ultra-bright red LED's for a working effect. Anyone worried about N20 shouldn't as it's a stable inert gas. =)


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*03/12/08 UPDATE..I will be going through the text and editing some things as well.
*update 5/7/06- On the paint master of the MR I used an all topical method and here's the interesting part I think. I used a complete masking method on the 2nd helmet which should be on display at comic con. Also the color updates below are what I found out while under the gun trying to get it for everyone who may want an MR helmet. One last thing the MR helmet is outrageously accurate for not being a direct casting and unless you have an uber sized head it'll be just fine for all sizes.
Also some of these methods are intermixed between topical and scratch methods so if you see the word "seal" that applies to topical. I highly recommend using all Floquil ENAMELS and do a scratch method laying all of the scratches and peeling off. The original was done this way and enamel paints allow accuracy when peeling. If you seee topical on an original helmet that means it was done as a repait or after the fact.
On the paint master of the MR proto #1 I used an all topical method and here's the interesting part I think. I used a complete masking method on the 2nd helmet. Also the color updates below are what I found out while under the gun trying to get it for everyone who may want an MR helmet. One last thing the MR helmet is outrageously accurate for not being a direct casting and unless you have an uber sized head it'll be just fine for all sizes.
This is where I have it now and unless labeled 'unsure' I'm fairly confident it is the correct color based on input research and opinions of actual obeservations made by people who have seen the helmet and suit. All colors are Floquil or Polly Scale paints it really doesn't matter which you purchase as long as the color is the same they are the same paints for the most part. If you have questions please let me know or post them here and I'll help you out.
I almost forgot. You have to tone down the helmet with an acrylic wash in a few cases depends on how the helmet looks after painting. Basically get some of that blue window wash you use for the car 95 cents a gallon at your local store. put in a cup but keep it away from children it's poisonous believe it or not. Add a few drops of black acylic paint thus making a dirty cloudy water type mixture(not very much paint is used in this). Get a mister bottle and put the blue window cleaner in it so you can mist down dark spots and even out the finish. Don't go too heavy and using your mixture in the cup brush it on and if it's too dark just mist it and dabb with a paper towel. Do a little bit at a time and I would suggest not to do it all in one sitting or it will come out too dark. This blends the helmet and reduces the contrast of some colors I'm fairly confident this was done on the original.
Helmet (Empire version)
* German Field Gray or Panzer Olive Green (Cheeks and dome) court is out on this one but GFG is a very old Floquil and was produced back in the day but not now so you'll have to buy it from Tamiya.
* Caboose (not caboose red) (mandibles) * Reefer Yellow Vertical stripes (update) also the look of this strictly dependent on heavily applied it is and don't apply heavily on frontal stripes
* Reefer Gray update (Gray around scratches)
* Rust (various locations)
* Chrome (scratches) I think this was actually a color called bright silver but this works best.
* Main color back of helmet- RLM73
* Back of helmet scratches- Concrete
* Earth Enamel(Rangefinder ear) I hate this paint.
* POG Green Update!(Left ear)
* PRR Green(I like weathered black better) (Inside cheeks) this is practically black.
* Caboose (Red scratches on left ear).
* Light Gray (on left ear) any light gray will do.
* PRR Maroon for the dark color on mands may need to darken this color with a touch of black. I know the original color but Floquil hasn't made the color for almost 20 years so it's very very hard to find and this will do trust me.
Jet Pack (AOSW version)
* Light Blue
* Chrome
* Grimey black (weathering for exhausts etc.)
* Boxcar Red
* UP armor Yellow
* White
Armor (AOSW version)
* Reefer Yellow (Shoulders and knees put on heavier on knees but not much this color gets darker the more you throw down).
* ATSF Catwhisker Yellow (Shoulders and knees the trim around the scratches).
* UP Armor Yellow (Shoulders and knees to highlight darker spots).
* US Med. Green (Chest, cod, back, buttplate).
* Yellow Zinc Chromate (I could not locate in floquil so I used testors for trim around scratches)
* Black (For speckles and weahtering)
* Chrome
Guants (AOSW)
* Wisconson Central Maroon
* Weathered Black (weathering and highlights creates that purplish look you see)
* Chrome
* Rock Island Maroon (calc buttons)
Ok, Using the dome as an example first and then we'll move onto the mandible.
Primer coat your helmet if you choose. Grab a can of chrome spray paint whatever works best for you but make sure the surface is free of dust and it's not real humid outside this paint can get real tricky. Spray it on if it looks crappy let it dry and put on another coat or sand it down and start over (I hate that part) *NOTE let this dry for a few days. Apply the POG(Panzer olive green). Ok there is a real trick here make sure you get it on good otherwise the chrome shows through and it also lightens up the green a lot.
Mandibles are the toughest. After chrome has dried apply the Caboose and it let dry. Then apply the Gray areas and then the PRR maroon (Dark over the light color thinking) that's it on that as well.
There will be issues with masking off with tape for example the cheek area. This is a toughie for me but use your best judgement but I hand painted the inside cheek so no masking issue there and I airbrushed on the green cheek so basically airbrush the cheek green and then hand paint the inside cheek. If you have to mask with tape seal the paint with a coat dulcoat or semi gloss(yes semi-gloss(Testors) it creates a hardcoat which prevents future scratches and you can dulcoat the helmet later).
When masking for the verticle stripes you can seal the green and then paint the stripes and then scratche helmet it will just take more than a tooth pick but it's not a worry. After all is said and done apply the acylic coat and a little scotchbrite to smooth it out.
*Note also if the Lark gray doesn't look dark enough try Euro Dark gray instead it's a matter of choice but I felt the gray had bluish tones to it so I used the lark. Also your colors are going to look funky until you apply the acrylic coat so don't worry. You see evidence of this on the real stuff.
I hope this helps and I did not hold back this is how I did it.


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Yes, it's a guest post! My friend and all-around wise dude Charlie Gilkey graciously offered me this guest post as a way to rouse Remarkable Communication gently from its slumber.
This is the second part of the How To Blog Like Shakespeare series from Charlie Gilkey. Check out How To Write For New Readers if you missed Part 1.
Regular readers are familiar with you and your content, so they're already keyed into how you write and what you're about. They're also likely to be your friends, fans, champions, and customers.
The fact that they're familiar with what you're up to, though, can also make it more difficult to write for them. They might have already learned some of the stuff you've written for your new readers, so the way you write for your new readers won't provide a lot of value to them. While they may have some favored themes and topics, to keep their attention, you'll have to provide them something new.


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I live in Nodak and my party and I are having a hard time with the early season. Basically we scout hard, find the X, then set up and no birds are coming when there was 350 there the day before. This has happened several times so far and we have been skunked twice. Any advice? We are hunting over 3 doz, and light calling and flagging if we do at all. Geese just dont want to decoy with us when we do have geese. Only twice have we had small flocks of 4 or 5 decoy with us. Any suggestions?
As much as a pain as it has been, it sure feels good to be back in the blind. Cant wait until I can see all the pics from around the country as Early Season opens.


text: I think any singles skater that did not achieve success by the early twenties could be considered a late bloomer. For pairs that age limit has to approach high twenties. I know that's quite arbitrary, so feel free to shift them if you wish. Here is my list of late bloomers: Paul Wylie (27 yrs.- Oly silver; no world medal prior to that) Rudy Galindo (1st US title at age 26; 96 world bronze) I would probably add Petr Barna to the list. Before his bronze at the 92 Olympics, his success was pretty limited Maria Butyrskaya- world champ at 26; not a lot of previous success, other than making the Russian world team Shizuka Arakawa (24 yrs.- OGM)- she is a borderline case, IMO. She won the worlds 2 years before the OGM. She is a late bloomer only when you compare her with the ladies that won the OGM before her (Sarah, Tara, Oksana) The Protopopovs- won their first OGM at ages 32 & 35.


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CHAPEL HILL --- No. 8 North Carolina won a tight doubles point and took four singles matches in straight sets to post a 5-2 win over No. 16 Michigan Sunday afternoon at the Cone-Kenfield Tennis Center. Gina Suarez-Malaguti and Zoe De Brucyker clinched doubles with a 10-8 tiebreak win on court two before the Tar Heels took care of business in singles.
No. 21 Emina Bektas and Brooke Bolender bested No. 8 Ashley Dai and Whitney Kay at No. 1 doubles, 8-2, before Carolina (5-0) rallied on the other two courts. No. 51 Lauren McHale and Tessa Lyons topped Ronit Yurovsky and Kristen Dodge on court three, 8-4, to set up the dramatic finish on court two.
De Bruycker and Suarez-Malaguti trailed 6-3 in the tiebreak before winning three straight points to even the breaker at 6. Michigan (3-1) got a fourth match point at 7-6 but the Tar Heel seniors spoiled that one as well and eventually took the tiebreak, 10-8, and the match, 8-7.
No. 65 Dai got Carolina off to a hot start in singles as the Temple City, Calif., freshman drilled Mimi Nguyen on court five, 6-1, 6-1. No. 11 Suarez-Malaguti then pushed it to 3-0 in the dual with an impressive 6-2, 6-2 win over Bektas on court one.
No. 36 Caroline Price clinched the win on court four after rallying to win a second-set tiebreak. The Duluth, Ga., sophomore was in control early against Michigan's Sarah Lee, winning the opening set, 6-1. Price then outlasted Lee in the breaker to take the match, 6-1, 7-6.
No. 21 Kay gave the Tar Heels their final point of the day on court three, besting Bolender in straight sets, 6-3, 6-4.
Michigan got wins from #61 Yurovsky on court two and #94 Amy Zhu on court six to round out the scoring.
Both teams will now turn their attention to the ITA National Team Indoor Championships next weekend in Charlottesville, Va. With the win Sunday, UNC is expected to receive a seed in Tuesday's draw.
No. 8 North Carolina 5, No. 16 Michigan 2
1. #21 Emina Bektas/Brooke Bolender (MICH) def. #8 Ashley Dai/Whitney Kay (NC), 8-2
2. Zoe De Bruycker/Gina Suarez-Malaguti (NC) def. Sarah Lee/Mimi Nguyen (MICH), 8-7
3. #51 Tessa Lyons/Lauren McHale (NC) def. Ronit Yurovsky/Kristen Dodge (MICH), 8-4
Order of finish: 1, 3, 2
1. #11 Gina Suarez-Malaguti (NC) def. Emina Bektas (MICH), 6-2, 6-2
2. #61 Ronit Yurovsky (MICH) def. #28 Zoe De Bruycker (NC), 6-1, 3-6, 10-6
3. #21 Whitney Kay (NC) def. Brooke Bolender (MICH), 6-3, 6-4
4. #36 Caroline Price (NC) def. Sarah Lee (MICH), 6-1, 7-6
5. #65 Ashley Dai (NC) def. Mimi Nguyen (MICH), 6-1, 6-1
6. #94 Amy Zhu (MICH) def. #101 Tessa Lyons (NC), 7-5, 6-3
Order of finish: 5, 1, 4*, 3, 2, 6


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convivium wrote:Yes, thank you! So it is an attitude with regard to "practice." How far does practice extend into daily life? Do you take it as an additional meditation object/contemplation? Or is it a continuous attitude that you apply while attending to your primary meditation object? Does it help keep the precepts and your daily practice?
convivium wrote:Could you say more about how it works? You seem to be saying that metta either allows you to relax into each experience, or that it is the act of relaxing into each experience. If it is the former, then could you descibe in more detail what it is or what it looks like (the act or perception of metta) that results in relaxing into each experience? Or if it's just relaxing into each experience, then how is it different then, for example, equanimity or patience? Then there's the idea of directing metta towards some recipient as against the experience of metta qua metta. How is this experience of metta qua metta different then, for example, attending to the blissful aspects of breathing?


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