Cavitation/NPSH (Field Problems)

Discussion GroupUnexpected cavitation erosion Key parameters to consider for Root Cause Analysis when experiencing cavitation damage NPSHR, NPSHA, NPSH margin Performance loss due to insufficient NPSHA (margin) NPSH 40,000 hours Cavitation erosion rate and impeller life assessment Impact of dissolved and/or entrained gas Pumping hot water or hydrocarbons Reliability of operating with low NPSHA on hydrocarbons High cavitation-resistant materials Common types of pump cavitation, including: sheet cavitation, suction recirculation induced vortex cavitation, corner (vortex) cavitation, and tip vortex cavitation Suction specific speed Field cases (suggested by audience) : Quick fix and ultimate solutio

Data on cardiovascular and pulmonary diseases among smokers of menthol and non-menthol cigarettes compiled from the National Health and Nutrition Examination Survey (NHANES), 1999–2012

This Data in Brief contains results from three different survey logistic regression models comparing risks of self-reported diagnoses of cardiovascular and pulmonary diseases among smokers of menthol and non-menthol cigarettes. Analyses employ data from National Health and Nutrition Examination Survey (NHANES) cycles administered between 1999 and 2012, combined and in subsets. Raw data may be downloaded from the National Center for Health Statistics. Results were not much affected by which covariates were included in the models, but depended strongly on the NHANES cycles included in the analysis. All three models returned elevated risk estimates for three endpoints when they were run in individual NHANES cycles (congestive heart failure in 2001–02; hypertension in 2003–04; and chronic obstructive pulmonary disease in 2005–06), and all three models returned null results for these endpoints when data from 1999–2012 were combined

<em>C. elegans</em> BLOC-1 Functions in Trafficking to Lysosome-Related Gut Granules

<div><p>The human disease Hermansky-Pudlak syndrome results from defective biogenesis of lysosome-related organelles (LROs) and can be caused by mutations in subunits of the BLOC-1 complex. Here we show that <em>C. elegans glo-2</em> and <em>snpn-1</em>, despite relatively low levels of amino acid identity, encode Pallidin and Snapin BLOC-1 subunit homologues, respectively. BLOC-1 subunit interactions involving Pallidin and Snapin were conserved for GLO-2 and SNPN-1. Mutations in <em>glo-2</em> and <em>snpn-1</em>,or RNAi targeting 5 other BLOC-1 subunit homologues in a genetic background sensitized for <em>glo-2</em> function, led to defects in the biogenesis of lysosome-related gut granules. These results indicate that the BLOC-1 complex is conserved in <em>C. elegans</em>. To address the function of <em>C. elegans</em> BLOC-1, we assessed the intracellular sorting of CDF-2::GFP, LMP-1, and PGP-2 to gut granules. We validated their utility by analyzing their mislocalization in intestinal cells lacking the function of AP-3, which participates in an evolutionarily conserved sorting pathway to LROs. BLOC-1(−) intestinal cells missorted gut granule cargo to the plasma membrane and conventional lysosomes and did not have obviously altered function or morphology of organelles composing the conventional lysosome protein sorting pathway. Double mutant analysis and comparison of AP-3(−) and BLOC-1(−) phenotypes revealed that BLOC-1 has some functions independent of the AP-3 adaptor complex in trafficking to gut granules. We discuss similarities and differences of BLOC-1 activity in the biogenesis of gut granules as compared to mammalian melanosomes, where BLOC-1 has been most extensively studied for its role in sorting to LROs. Our work opens up the opportunity to address the function of this poorly understood complex in cell and organismal physiology using the genetic approaches available in <em>C. elegans</em>.</p> </div

<i>C. elegans</i> BLOC-1 subunits.

<p>The gene name of each <i>C. elegans</i> BLOC-1 subunit and its human and <i>D. melanogaster</i> orthologues are listed. The amino acid identity of the <i>C. elegans</i> protein with each orthologue was derived from pairwise sequence alignments with the full length <i>C. elegans</i> protein.</p

Analysis of CDF-2::GFP trafficking.

<p>In wild type, CDF-2::GFP (black arrows) colocalized with PGP-2 on gut granules (A–C) and CDF-2::GFP (black arrows) was not associated with F11E6.1::mCherry containing conventional lysosomes (white arrows) (G–I). (D–F) CDF-2::GFP was associated with PGP-2 containing gut granules (black arrows) and apical compartments (white arrows) in an AP-3 mutant. (J–L) PGP-2 was lacking and CDF-2::GFP was localized to conventional lysosomes (black arrows) and the plasma membrane (white arrowhead) in <i>glo-2(zu455)</i>. In all panels, black arrowheads flank the intestine of 1.5-fold stage embryos.</p

Gut granule formation in adults.

<p>In wild-type adults, autofluorescent gut granules accumulated markers of acidification (A–B), hydrophobicity (C–D), terminal endocytic compartments (E–F) and contained PGP-2::GFP (G–H). <i>glo-2(zu455)</i> adults had substantially reduced numbers of autofluorescent compartments (I). The majority of these organelles were stained with LysoTracker Red (I-J), Nile Red (K–L) and contained PGP-2::GFP (O–P). (M–N) In contrast, few of the autofluorescent compartments accumulated TRITC-Dextran and those that did localized the marker to a subdomain within the organelle. In all panels, white arrows identify autofluorescent compartments that contained the gut granule marker. The black arrows denote the location of the intestinal lumen.</p