Seamen\u27s Club Restaurant, 1982

1982 Menu from the Seamen\u27s Club Restaurant, 375 Fore Street. The tavern (later known as Bull Feeney\u27s) was located in the Charles Q. Clapp Block, built in 1866. 1978 Photograph of the Seamen\u27s Club Restaurant can be seen at this link.https://digitalcommons.portlandlibrary.com/menus/1052/thumbnail.jp

SB43-07/08: Support of The Healthy Montana Kids Plan

SB43-07/08: Support of The Healthy Montana Kids Plan. This resolution passed 14Y-1N on a roll call vote during the April 23, 2008 meeting of the Associated Students of the University of Montana (ASUM)

Exact Thermodynamics of Disordered Impurities in Quantum Spin Chains

Exact results for the thermodynamic properties of ensembles of magnetic impurities with randomly distributed host-impurity couplings in the quantum antiferromagnetic Heisenberg model are presented. Exact calculations are done for arbitrary values of temperature and external magnetic field. We have shown that for strong disorder the quenching of the impurity moments is absent. For weak disorder the screening persists, but with the critical non-Fermi-liquid behaviors of the magnetic susceptibility and specific heat. A comparison with the disordered Kondo effect experiments in dirty metallic alloys is performed.Comment: 4 pages Late

Expanding the 3- O -Sulfate Proteome—Enhanced Binding of Neuropilin-1 to 3- O -Sulfated Heparan Sulfate Modulates Its Activity

Binding of proteins to heparan sulfate is driven predominantly by electrostatic interactions between positively charged amino acid residues in the protein and negatively charged sulfate groups located at various positions along the polysaccharide chain. Although many heparin/heparan-sulfate-binding proteins have been described, few exhibit preferential binding for heparan sulfates containing relatively rare 3-O-sulfated glucosamine residues. To expand the "3-O-sulfate proteome," affinity matrices were created from Chinese hamster ovary (CHO) cell heparan sulfate engineered in vitro with and without 3-O-sulfate groups. Fractionation of different animal sera yielded several proteins that bound specifically to columns containing 3-O-sulfated heparan sulfate modified by two members of the heparan sulfate 3-O-sulfotransferase superfamily, Hs3st1 and Hs3st2. Neuropilin-1 was analyzed in detail because it has been implicated in angiogenesis and axon guidance. We show that 3-O-sulfation enhanced the binding of neuropilin-1 to heparan sulfate immobilized on plastic plates and to heparan sulfate present on cultured cells. Chemoenzymatically synthesized 3-O-sulfated heparan sulfate dodecamers protected neuropilin-1 from thermal denaturation and inhibited neuropilin-1-dependent, semaphorin-3a-induced growth cone collapse of neurons derived from murine dorsal root ganglia. The effect of 3-O-sulfation was cell autonomous and specific to Hs3st2 based on collapse assays of neurons derived from Hs3st1- and Hs3st2-deficient mice. Finally, 3-O-sulfated heparan sulfate enhanced the inhibition of endothelial cell sprouting by exogenous heparan sulfate. These findings demonstrate a reliable method to identify members of the 3-O-sulfate proteome and that 3-O-sulfation of heparan sulfate can modulate axonal growth cone collapse and endothelial cell sprouting

P-Type ATPase TAT-2 Negatively Regulates Monomethyl Branched-Chain Fatty Acid Mediated Function in Post-Embryonic Growth and Development in C. elegans

Monomethyl branched-chain fatty acids (mmBCFAs) are essential for Caenorhabditis elegans growth and development. To identify factors acting downstream of mmBCFAs for their function in growth regulation, we conducted a genetic screen for suppressors of the L1 arrest that occurs in animals depleted of the 17-carbon mmBCFA C17ISO. Three of the suppressor mutations defined an unexpected player, the P-type ATPase TAT-2, which belongs to the flippase family of proteins that are implicated in mediating phospholipid bilayer asymmetry. We provide evidence that TAT-2, but not other TAT genes, has a specific role in antagonizing the regulatory activity of mmBCFAs in intestinal cells. Interestingly, we found that mutations in tat-2 also suppress the lethality caused by inhibition of the first step in sphingolipid biosynthesis. We further showed that the fatty acid side-chains of glycosylceramides contain 20%–30% mmBCFAs and that this fraction is greatly diminished in the absence of mmBCFA biosynthesis. These results suggest a model in which a C17ISO-containing sphingolipid may mediate the regulatory functions of mmBCFAs and is negatively regulated by TAT-2 in intestinal cells. This work indicates a novel connection between a P-type ATPase and the critical regulatory function of a specific fatty acid

Mitochondrial Oxidative Stress Alters a Pathway in Caenorhabditis elegans Strongly Resembling That of Bile Acid Biosynthesis and Secretion in Vertebrates

Mammalian bile acids (BAs) are oxidized metabolites of cholesterol whose amphiphilic properties serve in lipid and cholesterol uptake. BAs also act as hormone-like substances that regulate metabolism. The Caenorhabditis elegans clk-1 mutants sustain elevated mitochondrial oxidative stress and display a slow defecation phenotype that is sensitive to the level of dietary cholesterol. We found that: 1) The defecation phenotype of clk-1 mutants is suppressed by mutations in tat-2 identified in a previous unbiased screen for suppressors of clk-1. TAT-2 is homologous to ATP8B1, a flippase required for normal BA secretion in mammals. 2) The phenotype is suppressed by cholestyramine, a resin that binds BAs. 3) The phenotype is suppressed by the knock-down of C. elegans homologues of BA–biosynthetic enzymes. 4) The phenotype is enhanced by treatment with BAs. 5) Lipid extracts from C. elegans contain an activity that mimics the effect of BAs on clk-1, and the activity is more abundant in clk-1 extracts. 6) clk-1 and clk-1;tat-2 double mutants show altered cholesterol content. 7) The clk-1 phenotype is enhanced by high dietary cholesterol and this requires TAT-2. 8) Suppression of clk-1 by tat-2 is rescued by BAs, and this requires dietary cholesterol. 9) The clk-1 phenotype, including the level of activity in lipid extracts, is suppressed by antioxidants and enhanced by depletion of mitochondrial superoxide dismutases. These observations suggest that C. elegans synthesizes and secretes molecules with properties and functions resembling those of BAs. These molecules act in cholesterol uptake, and their level of synthesis is up-regulated by mitochondrial oxidative stress. Future investigations should reveal whether these molecules are in fact BAs, which would suggest the unexplored possibility that the elevated oxidative stress that characterizes the metabolic syndrome might participate in disease processes by affecting the regulation of metabolism by BAs

Pulsed power performance of PBFA Z

PBFA Z is a new 60-TW/5-MJ electrical driver located at Sandia National Laboratories. The authors use PBFA Z to drive z pinches. The pulsed power design of PBFA Z is based on conventional single-pulse Marx generator, water-line pulse-forming technology used on the earlier Saturn and PBFA II accelerators. PBFA Z stores 11.4 MJ in its 36 Marx generators, couples 5 MJ in a 60-TW/105-ns pulse to the output water transmission lines, and delivers 3.0 MJ and 50 TW of electrical energy to the z-pinch load. Depending on the initial load inductance and the implosion time, the authors attain peak currents of 16-20 MA with a rise time of 105 ns. Current is fed to the z-pinch load through self magnetically-insulated transmission lines (MITLs). Peak electric fields in the MITLs exceed 2 MV/cm. The current from the four independent conical-disk MITLs is combined together in a double post-hole vacuum convolute with an efficiency greater than 95%. The authors achieved x-ray powers of 200 TW and x-ray energies of 1.9 MJ from tungsten wire-array z-pinch loads

Mercantile Navy List, 1904 p. 0707-0860

The official registry of merchant vessels operating under the British flag