First pass

Both vacuum operation and the use of refrigeration incur capital and operating cost penalties and increase the complexity of the design. They should be avoided if possible. For a first pass through... 

It is thus recommended that in a first pass through a design, thermal coupling should not be considered. Rather, simple columns should be used until a first overall design has been established. Only when the full heat-integration context has been understood should thermal coupling be considered. 

The relative separation is scaled by a, the distance at which the Leimard-Jones first passes tlirough zero. The energy is scaled by the well depth, s. 

IlyperChem assumes that it is easiest for yon to just use subset selection to select that portion oT the molecular system that is to be treated quantum mechanically. You can then extend the initial selection to form a convenient and universally acceptable boundary. Thus, you make a simple selection of atoms for the first pass at selecting the quantum mechanical portion. The selected atoms are quantum atomsand the iinselecied atoms are classical atoms. 

The oxygen used in the combustion is supplied by a small cylinder (120 Atm.) fitted with a pressure reduction valve, pressure gauge (to avoid the risk of the cylinder becoming exhausted during an actual determination) and fine control knob. It is important that the valve is kept free from oil or grease of any kind. In order to ensure the complete purity of the oxygen it is first passed through a purification train. 

W. P. Me3.de, A First Pass at Computing the Cost of Fire in a Modem Society, The Herndon Group, Inc., Chapel Hill, N.C., 1991. 

Medroxyprog esteroneAcetate. Accurate pharmacokinetic and metaboHsm studies on MPA have been difficult because the radioimmunoassays employed caimot differentiate between MPA and its metaboHtes (346). Comparison of MPA plasma levels assayed by hplc and radioimmunoassay show that radioimmunoassay may overestimate intact MPA concentrations by about fivefold (347). However, values of the mean elimination half-life of MPA were similar, being 33.8 and 39.7 h when measured by hplc and radioimmunoassay, respectively (347). Approximately 94% of MPA in the blood is bound to albumin (348). When taken orally, MPA is rapidly absorbed with Htde or no first-pass metaboHsm (13). Peak semm levels ate reached after 3 h. Steady state occurs after three days of daily adininistration (349). The pharmacokinetics of MPA when adininistered in a depot formulation have been described (350). 

Retention and drainage additives are vital to the use of recycled fibers. Papermakers consider recycled fibers to behave like virgin fines, while recycled fines behave like filler. Drainage on the paper machine can be impeded and first-pass retention reduced by the use of recycled fiber (9). Additionally, the negative impact of contaminants found in recycled fibers can be minimized by the appropriate use of dispersants and other pitch-control additives. 

The process of pulverized cuUet reduction yields a product having near-batch equivalent sizing (—12 mesh (<1.7 mm mm)) and in a furnace-ready condition. Foil-backed paper, lead and other metals, and some tableware ceramics can be removed in an oversized scalping operation after the first pass through the system. Other contaminants are reduced to a fine particle size that can be assimilated into the glass composition during melting. 

SO2 gas is catalyticaHy oxidized to SO in a fixed bed reactor (converter) which operates adiabaticaHy in each catalyst pass. The heat of reaction raises the process gas temperature in the first pass to approximately 600°C (see Table 7). The temperature of hot gas exiting the first pass is then lowered to the desired second pass inlet temperature (430—450°C) by removing the heat of reaction in a steam superheater or second boiler. 

In converter passes downstream of the first pass, exit temperatures are limited by thermodynamic equiUbrium to around 500°C or less. To obtain optimum conversion, the heats of reaction from succeeding converter passes are removed by superheaters or air dilution. The temperature rise of the process gas is almost direcdy proportional to the SO2 converted in each pass, even though SO2 and O2 concentrations can vary widely. 

One concern in conventional processing is the achievement of uniform reagent appUcation and uniform cross-linking (18). An area in which adequate treatment of aU fibers is necessary is in flame-retardant finishing. One means of obtaining thorough treatment has been the use of vacuum impregnation, in which the fabric is first passed over a vacuum slot to remove air from the fabric interstices, foUowed by exposure to the phosphoms flame-retardant solution in the precondensate ammonia system (19). 

Procainamide may be adininistered by iv, intramuscular (im), or po routes. After po dosing, 75—90% of the dmg is absorbed from the GI tract. About 25% of the amount absorbed undergoes first-pass metaboHsm in the fiver. The primary metabolite is A/-acetylprocainamide (NAPA) which has almost the same antiarrhythmic activity as procainamide. This is significant because the plasma concentration of NAPA relative to that of procainamide is 0.5—2.5. In terms of dmg metabolism there are two groups of patients those that rapidly acetylate and those that slowly acetylate procainamide. About 15—20% of the dmg is bound to plasma proteins. Peak plasma concentrations are achieved in 60—90 min. Therapeutic plasma concentrations are 4—10 lg/mL. Plasma half-lives of procainamide and NAPA, which are excreted mainly by the kidneys, are 2.5—4.5 and 6 h, respectively. About 50—60% is excreted as unchanged procainamide (1,2). 

Mexifitene is well absorbed from the GI tract and less than 10% undergoes first-pass hepatic metabolism. In plasma, 60—70% of the dmg is protein bound and peak plasma concentrations are achieved in 2—3 h. Therapeutic plasma concentrations are 0.5—2.0 lg/mL. The plasma half-life of mexifitene is 10—12 h in patients having normal renal and hepatic function. Toxic effects are noted at plasma concentrations of 1.5—3.0 lg/mL, although side effects have been noted at therapeutic concentrations. The metabolite, /V-methy1mexi1itene, has some antiarrhythmic activity. About 85% of the dmg is metabolized to inactive metabolites. The kidneys excrete about 10% of the dmg unchanged, the rest as metabolites. Excretion can also occur in the bile and in breast milk (1,2). 

EoUowing po administration moricizine is completely absorbed from the GI tract. The dmg undergoes considerable first-pass hepatic metabolism so that only 30—40% of the dose is bioavailable. Moricizine is extensively (95%) bound to plasma protein, mainly albumin and a -acid glycoprotein. The time to peak plasma concentrations is 0.42—3.90 h. Therapeutic concentrations are 0.06—3.00 ]l/niL. Using radiolabeled moricizine, more than 30 metabolites have been noted but only 12 have been identified. Eight appear in urine. The sulfoxide metabolite is equipotent to the parent compound as an antiarrhythmic. Elimination half-life is 2—6 h for the unchanged dmg and known metabolites, and 84 h for total radioactivity of the labeled dmg (1,2). 

Tocainide is rapidly and well absorbed from the GI tract and undergoes very fitde hepatic first-pass metabolism. Unlike lidocaine which is - 30% bioavailable, tocainide s availability approaches 100% of the administered dose. Eood delays absorption and decreases plasma levels but does not affect bio availability. Less than 10% of the dmg is bound to plasma proteins. Therapeutic plasma concentrations are 3—9 jig/mL. Toxic plasma levels are >10 fig/mL. Peak plasma concentrations are achieved in 0.5—2 h. About 30—40% of tocainide is metabolized in the fiver by deamination and glucuronidation to inactive metabolites. The metabolism is stereoselective and the steady-state plasma concentration of the (3)-(—) enantiomer is about four times that of the (R)-(+) enantiomer. About 50% of the tocainide dose is efirninated by the kidneys unchanged, and the rest is efirninated as metabolites. The elimination half-life of tocainide is about 15 h, and is prolonged in patients with renal disease (1,2,23). 

About 97% of po dose is absorbed from the GI tract. The dmg undergoes extensive first-pass hepatic metaboHsm and only 12% of the po dose is bioavailable. More than 95% is protein bound and peak plasma concentrations are achieved in 2—3 h. Therapeutic plasma concentrations are 0.064—1.044 lg/mL. The dmg is metabolized in the Hver to 5-hyroxypropafenone, which has some antiarrhythmic activity, and to inactive hydroxymethoxy propafenone, glucuronides, and sulfate conjugates. Less than 1% of the po dose is excreted by the kidney unchanged. The elimination half-life is 2—12 h (32). 

Absorption is complete and bioavailabihty is about 100% at steady state during continuous po dosing. There is extensive hepatic first-pass metabohsm to norlorcainide and hydroxylated metaboUtes. Nodorcainide is equipotent and equieffective to lorcainide in antiarrhythmic activity. 

Acebutolol is well absorbed from the GI tract. It undergoes extensive hepatic first-pass metabohsm. BioavailabiUty of the parent compound is about 40%. The principal metaboflte, A/-acetylacebutolol, has antiarrhythmic activity and appears to be more cardioselective. Binding to plasma proteins is only 26%. Peak plasma concentrations of acebutolol are achieved in 2.5 h, 3.5 h for A/-acetylacebutolol. The elimination half-Hves of acebutolol and its metabohte are 3—4 and 8—13 h, respectively. The compounds are excreted by the kidneys (30—40%) and by the Hver into the bile (50—60%). About 40% of the amount excreted in the urine is unchanged acebutolol, the rest as metabofltes (32). 

After po dosing, verapamil s absorption is rapid and almost complete (>90%). There is extensive first-pass hepatic metabolism and only 10—35% of the po dose is bioavahable. About 90% of the dmg is bound to plasma proteins. Peak plasma concentrations are achieved in 1—2 h, although effects on AV nodal conduction may be apparent in 30 min (1—2 min after iv adrninistration). Therapeutic plasma concentrations are 0.125—0.400 p.g/mL. Verapamil is metabolized in the liver and 12 metabolites have been identified. The principal metabolite, norverapamil, has about 20% of the antiarrhythmic activity of verapamil (3). The plasma half-life after iv infusion is 2—5 h whereas after repeated po doses it is 4.5—12 h. In patients with liver disease the elimination half-life may be increased to 13 h. Approximately 50% of a po dose is excreted as metabolites in the urine in 24 h and 70% within five days. About 16% is excreted in the feces and about 3—4% is excreted as unchanged dmg (1,2). 

Isosorbide is rapidly absorbed and undergoes rapid first-pass metaboHsm by the Hver. The bioavaUabUity of the subHngual and chewable tablets is 59% and 22%, respectively, for the regular tablet. Isosorbide is metabolized to isosorbide-2-mononitrate and isosorbide-5-mononitrate, both of which have pharmacologic activity. The elimination half-Hves of subHngual and po isosorbide dinitrate ate 1 and 4 h, respectively. Those of the 2- and 5-mononitrate metaboHtes are 1.5—3.1 h and 4—5.6 h, respectively. The two metaboHtes prolong the elimination half-life of the dinitrate. Adverse effects with isosorbide are similar to those described for nitroglycerin (99). 

Erythrityl is readily absorbed from the GI tract. It undergoes extensive first-pass metaboHsm ia the Hver by glutathione organic nitrate reductase. Time to onset of effect is 5—10 min by subHngual adrninistration and 20—30 min when swallowed. The duration of effects for the two routes ate up to 3 and 6 h, respectively. Adverse effects are similar to those described for nitroglycerin (99). 

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