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"the negro in chicago".
"the negro in chicago".
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1" (monad, 1979)* "live in chicago, vol.
1" (monad, 1979)* "live in chicago, vol.
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» emanuel triumphs in chicago mayoral race (new york times)
» emanuel triumphs in chicago mayoral race (new york times)
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trial air monitoring of pops chemicals at background sites in east asian countries;
the trial air monitoring of pops chemicals at background sites in east asian countries;
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» hastert to make first court appearance in chicago today (washington post)
» hastert to make first court appearance in chicago today (washington post)
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for example, unity temple in chicago is a unitarian universalist congregation designed by frank lloyd wright.
for example, unity temple in chicago is a unitarian universalist congregation designed by frank lloyd wright.
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también apareció en "sexual perversity in chicago" creada por david mamet, en londres.
he also appeared in david mamet's "sexual perversity in chicago" in london.
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a study showing native birds being excluded from up to 80% of nesting sites in canberra, australia.
a study showing native birds being excluded from up to 80% of nesting sites in canberra, australia.
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davey and pielke visited 10 hcn sites in eastern colorado, but did not provide percentages of good or badly sited stations.
davey and pielke visited 10 hcn sites in eastern colorado, but did not provide percentages of good or badly sited stations.
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in demonstrations before the american institute of electrical engineers and at the 1893 columbian exposition in chicago he lit light bulbs from across a stage.
in demonstrations before the american institute of electrical engineers and at the 1893 columbian exposition in chicago he lit light bulbs from across a stage.
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ginny georgantäs (segunda desde la derecha) en el panel del título ix, en la mañana de este sábado pasado en in chicago
ginny georgantäs (second from right) on the title ix panel this past saturday morning in chicago.
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== referencias ==== enlaces externos ==* arkive stills, video]* an rspb guide to cirl bunting sites in devon.
==references====external links==* arkive stills, video]* an rspb guide to cirl bunting sites in devon.
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en 2003 apareció en el teatro de londres west end como bernard en "sexual perversity in chicago", junto con matthew perry y minnie driver.
in 2003, he appeared as bernard in a run of david mamet's play "sexual perversity in chicago", along with matthew perry and minnie driver, in london's west end.
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la iniciativa siria sit-in ha recivido más de 200 envíos
the syrian sit-in initiative has received more than 200 submissions
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(4) the commission shall sit in public meetings.
(4) the commission shall sit in public meetings.
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" (pablo, 1979)* "ain't misbehavin'" (pablo, 1979)* "live in chicago, vol.
" (pablo, 1979)* "ain't misbehavin'" (pablo, 1979)* "live in chicago, vol.
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esas protestas son muy activas públicamente, como por ejemplo las manifestaciones o los sit-in.
wellbeing. this is especially true, of course, if they are highly social, such as marches or sit-ins.
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live in chicago 12.19.98 at the united center, conocido simplemente como live in chicago 12.19.98, es un álbum en vivo de la banda estadounidense dave matthews band, lanzado por el sello rca el 23 de octubre de 2001.
live in chicago 12.19.98 at the united center, also known as simply live in chicago 12.19.98, is a live album by the dave matthews band, released by rca on october 23, 2001.
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holathe na -ca2 exchanger (ncx) links transmembrane movements of ca2 ions to the reciprocal movement of na ions. it normally functions primarily as a ca2 efflux mechanism in excitable tissues such as the heart, but it can also mediate ca2 influx under certain conditions. na and ca2 ions exert complex regulatory effects on ncx activity. ca2 binds to two regulatory sites in the exchanger’s central hydrophilic domain, and this interaction is normally essential for activation of exchange activity. high cytosolic na concentrations, however, can induce a constitutive activity that bypasses the need for allosteric ca2 activation. constitutive ncx activity can also be induced by high levels of phosphatidylinositol- 4,5-bisphosphate (pip2) and by mutations affecting the regulatory calcium binding domains. in addition to promoting constitutive activity, high cytosolic na concentrations also induce an inactivated state of the exchanger (na -dependent inactivation) that becomes dominant when cytosolic ph and pip2 levels fall. na -dependent inactivation may provide a means of protecting cells from ca2 overload due to ncx-mediated ca2 influx during ischemia. na /ca2 exchange (ncx) is a carrier-mediated transport process that translocates ca2 ions across membranes in an obligatory exchange for na ions. in excitable tissues such as heart and nerve, it functions primarily as a plasma membrane ca2 efflux mechanism, although it can also mediate ca2 influx given the appropriate thermodynamic gradients. ncx activity is regulated principally by the ions that comprise the major determinants of the ncx driving forces, i.e., cytosolic na and ca2 . increases in cytosolic na downregulate ncx activity by inducing an inactive state of the exchanger (na -dependent inactivation), whereas increases in cytosolic ca2 upregulate activity (through allosteric ca2 activation). here we will briefly review the history and molecular biology of na /ca2 exchange, describe the major characteristics of na -dependent inactivation and allosteric ca2 activation, and discuss issues related to the possible physiological roles of these regulatory mechanisms. we will focus mainly on the cardiac isoform of the na /ca2 exchanger (ncx1.1). the na /ca2 exchange family of transporters has been the subject of several recent reviews.1-3 a brief history of na /ca2 exchange the existence of a transporter linking oppositely-directed movements of na and ca2 across the plasma membrane was first described 40 years ago by two groups working (independently and respectively) with squid giant axons4 and guinea pig atria.5 it was immediately recognized that this novel transporter could be crucial to the understanding of the inotropic effects of cardiac glycosides. experimental work in the two decades that followed, done mostly with internally dialyzed squid axons or barnacle muscle, did much to establish the basic features of na /ca2 exchange and its regulation by atp and by cytosolic ca2 (see review by blaustein and lederer6). in 1979, the introduction of plasma membrane vesicles for exchange studies provided an important biochemical tool for further characterization of exchange activity. the stoichiometry of the exchanger was demonstrated to be 3na /1ca2 in null-point studies with vesicles where the electrical potential as a driving force for exchange activity was offset by an oppositely directed na -gradient.7 this value is still generally accepted although there have recently been indications from exchange current measurements of higher stoichiometries.8,9 the situation is complicated by the existence of a na -ca2 co-transport mode of the exchanger which provides an electrogenic na -leak current when na plus ca2 exchanges for ca2 alone.10 the use of plasma membrane vesicles also provided a route for the purification and identification of the exchanger protein using detergent solubilization, protein purification and vesicle reconstitution techniques. philipson and his colleagues11 succeeded in cloning the cardiac exchanger (ncx1) in 1990. the philipson group later described additional genes coding for ncx2 and ncx3 (both expressed primarily in brain and skeletal muscle). the cdna for the na /ca2 exchanger in squid axons, in which so much early work was carried out, was cloned in 1998;12 the squid axon exchanger (ncx-sq1) showed 58% identity to mammalian ncx1. electrical currents due to na /ca2 exchange activity were first demonstrated definitively by kimura et al.13 electrophysiological studies of na /ca2 exchange were markedly enhanced by the use of giant membrane patches, initially from cardiac myocytes and later from xenopus oocytes expressing the exchanger.14,15 the giant patch technology allowed the fluid composition on both sides of the membrane to be controlled and provided access to the cytosolic membrane surface for biochemical modification.
hellothe na -ca2 exchanger (ncx) links transmembrane movements of ca2 ions to the reciprocal movement of na ions. it normally functions primarily as a ca2 efflux mechanism in excitable tissues such as the heart, but it can also mediate ca2 influx under certain conditions. na and ca2 ions exert complex regulatory effects on ncx activity. ca2 binds to two regulatory sites in the exchanger’s central hydrophilic domain, and this interaction is normally essential for activation of exchange activity. high cytosolic na concentrations, however, can induce a constitutive activity that bypasses the need for allosteric ca2 activation. constitutive ncx activity can also be induced by high levels of phosphatidylinositol- 4,5-bisphosphate (pip2) and by mutations affecting the regulatory calcium binding domains. in addition to promoting constitutive activity, high cytosolic na concentrations also induce an inactivated state of the exchanger (na -dependent inactivation) that becomes dominant when cytosolic ph and pip2 levels fall. na -dependent inactivation may provide a means of protecting cells from ca2 overload due to ncx-mediated ca2 influx during ischemia. na /ca2 exchange (ncx) is a carrier-mediated transport process that translocates ca2 ions across membranes in an obligatory exchange for na ions. in excitable tissues such as heart and nerve, it functions primarily as a plasma membrane ca2 efflux mechanism, although it can also mediate ca2 influx given the appropriate thermodynamic gradients. ncx activity is regulated principally by the ions that comprise the major determinants of the ncx driving forces, i.e., cytosolic na and ca2 . increases in cytosolic na downregulate ncx activity by inducing an inactive state of the exchanger (na -dependent inactivation), whereas increases in cytosolic ca2 upregulate activity (through allosteric ca2 activation). here we will briefly review the history and molecular biology of na /ca2 exchange, describe the major characteristics of na -dependent inactivation and allosteric ca2 activation, and discuss issues related to the possible physiological roles of these regulatory mechanisms. we will focus mainly on the cardiac isoform of the na /ca2 exchanger (ncx1.1). the na /ca2 exchange family of transporters has been the subject of several recent reviews.1-3 a brief history of na /ca2 exchange the existence of a transporter linking oppositely-directed movements of na and ca2 across the plasma membrane was first described 40 years ago by two groups working (independently and respectively) with squid giant axons4 and guinea pig atria.5 it was immediately recognized that this novel transporter could be crucial to the understanding of the inotropic effects of cardiac glycosides. experimental work in the two decades that followed, done mostly with internally dialyzed squid axons or barnacle muscle, did much to establish the basic features of na /ca2 exchange and its regulation by atp and by cytosolic ca2 (see review by blaustein and lederer6). in 1979, the introduction of plasma membrane vesicles for exchange studies provided an important biochemical tool for further characterization of exchange activity. the stoichiometry of the exchanger was demonstrated to be 3na /1ca2 in null-point studies with vesicles where the electrical potential as a driving force for exchange activity was offset by an oppositely directed na -gradient.7 this value is still generally accepted although there have recently been indications from exchange current measurements of higher stoichiometries.8,9 the situation is complicated by the existence of a na -ca2 co-transport mode of the exchanger which provides an electrogenic na -leak current when na plus ca2 exchanges for ca2 alone.10 the use of plasma membrane vesicles also provided a route for the purification and identification of the exchanger protein using detergent solubilization, protein purification and vesicle reconstitution techniques. philipson and his colleagues11 succeeded in cloning the cardiac exchanger (ncx1) in 1990. the philipson group later described additional genes coding for ncx2 and ncx3 (both expressed primarily in brain and skeletal muscle). the cdna for the na /ca2 exchanger in squid axons, in which so much early work was carried out, was cloned in 1998;12 the squid axon exchanger (ncx-sq1) showed 58% identity to mammalian ncx1. electrical currents due to na /ca2 exchange activity were first demonstrated definitively by kimura et al.13 electrophysiological studies of na /ca2 exchange were markedly enhanced by the use of giant membrane patches, initially from cardiac myocytes and later from xenopus oocytes expressing the exchanger.14,15 the giant patch technology allowed the fluid composition on both sides of the membrane to be controlled and provided access to the cytosolic membrane surface for biochemical modification.