For Love\u27s Sweet Sake

https://digitalcommons.library.umaine.edu/mmb-vp/1471/thumbnail.jp

Avenge the Good Ship Maine

https://digitalcommons.library.umaine.edu/mmb-me/1320/thumbnail.jp

Again

https://digitalcommons.library.umaine.edu/mmb-vp/1159/thumbnail.jp

Whisper

Text on white backgroundhttps://scholarsjunction.msstate.edu/cht-sheet-music/1232/thumbnail.jp

Picadilly

Title Onlyhttps://scholarsjunction.msstate.edu/cht-sheet-music/7915/thumbnail.jp

The Sweetest Story Ever Told

Man and woman embracing in heart surrounded by roses and ribbonshttps://scholarsjunction.msstate.edu/cht-sheet-music/10524/thumbnail.jp

Mechanical Effects of Rice Hush Ash in Ultra-High Performance Concretes: A Matrix Study,

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/84784/1/stults-RHA-2009.pd

Recombination phenotypes of the NCI-60 collection of human cancer cells

<p>Abstract</p> <p>Background</p> <p>The NCI-60 is a collection of tumor cell lines derived from a variety of human adult cancer tissue types and is commonly used for genetic analysis and screening of potential chemotherapeutic agents. We wanted to understand the contributions of specific mechanisms of genomic instability to the etiology of cancers represented by the NCI-60.</p> <p>Results</p> <p>We screened the NCI-60 for dysregulated homologous recombination by using the gene cluster instability (GCI) assay we pioneered, and for defects in base excision repair by sensitivity to 5-hydroxymethyl-2'-deoxyuridine (hmdUrd). We identified subsets of the NCI-60 lines that either displayed the characteristic molecular signature of GCI or were sensitive to hmdUrd. With the exception of the NCI-H23 lung cancer line, these phenotypes were not found to overlap. None of the lines examined in either subset exhibited significant changes in the frequency of sister chromatid exchanges (SCE), neither did any of the lines in either subset exhibit microsatellite instability (MSI) indicative of defects in DNA mismatch repair.</p> <p>Conclusions</p> <p>Gene cluster instability, sensitivity to hmdUrd and sister chromatid exchange are mechanistically distinct phenomena. Genomic instability in the NCI-60 appears to involve only one mechanism of instability for each individual cell line.</p

The Prevalence and Clinical Correlates of an Auscultatory Gap in Systemic Sclerosis Patients

Introduction. Accurate blood pressure (BP) measurement is essential to the diagnosis and management of hypertension in patients with systemic sclerosis (SSc) to help prevent renal and cardiovascular complications. The presence of an auscultatory gap during manual BP measurement—the temporary disappearance of the Korotkoff sounds during cuff deflation—leads to a potentially important underestimate of systolic BP if undetected. Objectives. Since the presence of an auscultatory gap is frequently associated with increased vascular stiffness, we investigated its presence and correlates in 50 consecutive SSc patients. Methods. For each patient, BP was measured sequentially using three different approaches performed in the same order. Results. Sixteen of 50 patients (32%) had an auscultatory gap which if undetected would have resulted in clinically important underestimates of systolic BP in 4 patients. The presence of an auscultatory gap was statistically associated with the presence of antibodies to RNA polymerase III (P<0.0068) and SSc diagnosis type (P<0.01). Conclusions. Our study demonstrates that auscultatory gaps are relatively common in SSc and correlate with markers for SSc vasculopathy. If undetected auscultatory gaps may result in clinically important underestimation of BP. Thus, electronic oscillometric BP may be preferred in SSc patients

Escherichia Coli RecG Functionally Suppresses Human Bloom Syndrome Phenotypes

Defects in the human BLM gene cause Bloom syndrome, notable for early development of tumors in a broad variety of tissues. On the basis of sequence similarity, BLM has been identified as one of the five human homologs of RecQ from Escherichia coli. Nevertheless, biochemical characterization of the BLM protein indicates far greater functional similarity to the E. coli RecG protein and there is no known RecG homolog in human cells. To explore the possibility that the shared biochemistries of BLM and RecG may represent an example of convergent evolution of cellular function where in humans BLM has evolved to fulfill the genomic stabilization role of RecG, we determined whether expression of RecG in human BLM-deficient cells could suppress established functional cellular Bloom syndrome phenotypes. We found that RecG can indeed largely suppress both the definitive elevated sister chromatid exchange phenotype and the more recently demonstrated gene cluster instability phenotype of BLM-deficient cells. In contrast, expression of RecG has no impact on either of these phenotypes in human cells with functional BLM protein. These results suggest that the combination of biochemical activities shared by RecG and BLM fill the same evolutionary niche in preserving genomic integrity without requiring exactly identical molecular mechanisms