Hai cercato la traduzione di mode of production da Spagnolo a Inglese

year(s) of production
year(s) of production

remain the same , the higher the cost of production ,
remain the same , the higher the cost of production ,

the annual increase of production was about 50%.
the annual increase of production was about 50%.

* charles forgy, "on the efficient implementation of production systems.
* charles forgy, ""on the efficient implementation of production systems.

no operativo@item:intext mode of network card
down@item:intext mode of network card

* pasinetti, l. , "lectures on the theory of production", macmillan.
* pasinetti, l. , "lectures on the theory of production", macmillan.

increases in the prices of production factors , such shift to the left in aggregate supply .
increases in the prices of production factors , such shift to the left in aggregate supply .

these expectations into higher costs of production , which again meant spending faster and faster .
these expectations into higher costs of production , which again meant spending faster and faster .

ocde (2002): “intraindustry and intra-firm trade and the internationalisation of production”.
oecd (2002): "intraindustry and intra-firm trade and the internationalization of production".

potencia@info: tooltip the operation mode of wi-fi network
strength

(1984) "spatial divisions of labor: social structures and the geography of production".
(1995) "spatial divisions of labor: social structures and the geography of production" 2nd edition.

entre 1946 y 1951, portal fue "controller of production" del programa nuclear británico en el ministerio de abastecimiento.
from 1946 to 1951, portal was controller of production (atomic energy) at the ministry of supply.

(1995) "spatial divisions of labor: social structures and the geography of production" 2nd edition.
(1984) "spatial divisions of labour: social structures and the geography of production".

tempo & mode of early animal evolution: inferences from rocks, hox, & molecular clocks.
tempo & mode of early animal evolution: inferences from rocks, hox, & molecular clocks.

si selecciona esta opción, kdm completará automáticamente los nombres de los usuarios mientras se introducen en la casilla.@option:check mode of the user selection
if this option is ticked, kdm will automatically complete user names while they are typed in the line edit.

"the institutional structure of production," nobel lecture, reprinted in 1992, "american economic review", 82(4), pp.
"the institutional structure of production," nobel lecture, reprinted in 1992, "american economic review", 82(4), pp.

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.