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These assumptions are: (1) there is negligible metabolism of the inhibitor during the preincubation stage 100 mg lady era with amex women's health center warner robins ga, and (2) there is insignificant enzyme inactivation or direct inhibition during the substrate incubation stage cheap lady era 100mg amex pregnancy estimated due date. In fact order genuine lady era on line best women's health tips, however buy lady era 100 mg without a prescription menopause 34 years old, unless the inhibitor (drug candidate) is removed by dialysis prior to the substrate incubation, there is invariably some metabolism of the inhibitor during the substrate incubation period, and direct inhibition of the enzyme inevitably occurs to some extent because a mechanism-based inhibitor of an enzyme is, by In Vitro Study of Drug-Metabolizing Enzymes 283 definition, a substrate for that enzyme. The ratio of the preincubation time with inhibitor to the incubation time with maker substrate 2. Normalization of data for the spontaneous time-dependent loss in enzyme activity in the absence of inhibitor 5. The substrate incubation time should be short relative to the preincubation time to minimize further inactivation of the enzyme after the preincubation stage. Therefore to maximize the ratio of substrate incubation time to pre- incubation time, the substrate incubation time should be as short as possible (e. In the case of metabolism-dependent inhibitors, the use of a long substrate incubation time can lead to an artifactual overestimation of direct inhibition and a corre- sponding underestimation of mechanism-based inhibition potential because there will be appreciable enzyme inactivation even in the zero-minute preincubation samples. In this case, mibefradil appears to have nearly fourfold greater potency as a direct inhibitor when a long substrate incubation period is used (i. For some metabolism-dependent inhibitors, the blunting effect of long substrate incubation times could be even more pronounced, possibly leading to the erro- neous conclusion that no metabolism-dependent inhibition occurs. After the preincubation stage, the samples should be diluted at least 10-fold (and preferably 25- to 50-fold) prior to the substrate incubation stage to reduce the concentration of inhibitor and thereby minimize its direct inhibitory effects. These very high protein concentrations can dramatically decrease the free (unbound) concentration of drug candidate. Consequently, a correction for protein binding during the preincubation stage is warranted, especially for basic lipophilic 284 Ogilvie et al. However, there are two caveats to this rule: (1) the substrate must be soluble at this concentration and (2) the substrate must remain selective for the enzyme in question. If either solubility or selec- tivity is problematic at a high substrate concentration, then a lower substrate concentration must be used. The use of high substrate concentrations achieves two objectives: (1) it helps to diminish any competitive inhibition that might be In Vitro Study of Drug-Metabolizing Enzymes 285 caused by the remaining drug candidate and (2) it helps to decrease any further inactivation of the enzyme by diminishing the metabolism of the remaining drug candidate. The spontaneous, time-dependent loss in enzyme activity in the absence of inhibitor must be taken into account when analyzing the data from mechanism- based inhibition studies (Fig. To account for this loss, vehicle-control samples should be included and they should match all of the time points for the drug candidate. Normalization of the data can be accomplished by first calculating the decrease in activity over time for each concentration of drug candidate, including 0 mM (i. Further data analysis initially consists of performing linear regression for each line defined by the natural log transformed data at each concentration of drug candidate. If a large dilution factor and saturating concentrations of marker 286 Ogilvie et al. Figure 14 Design and graphical representation of irreversible or quasi-irreversible metabolism-dependent inhibition—determination of kinact and Ki values. The negative slope of the line is equal to kobs, which represents the inactivation rate constant for that particular inhibitor concentration. In this approach, the control activity in the above equation is always the zero-minute control for the solvent, rather than the solvent control at each time point. The incubations were then continued for two minutes to allow for conversion of paclitaxel to 6a-hydroxypaclitaxel. The data are plotted with incubation time on the x axis and enzymatic rates on the y axis. Subsequently, for each inhibitor concentration, the pre- incubation time (x axis) was plotted against the natural log of the percentage of remaining enzyme activity (y axis) (middle graph). The inhibitor concentration was then plotted against the initial rates of inactivation of the enzyme (negative slope of the lines in the middle graph). The ratio of these absorbance maxima is pH-dependent: alkaline con- ditions favor the 455-nm chromophore and acidic conditions favor the 430-nm chromophore. Several methods have been developed to investigate the covalent binding of drug candidates to microsomal protein. The method used in our laboratory relies on the use of radiolabeled compound and is based on the method described by Munns et al. To evaluate the ability of a drug candidate to bind covalently to protein, human liver microsomes (e. Samples are kept on ice for 30 to 120 minutes, and then centrifuged at 920 Â g for 10 minutes at 48C to recover precipitated protein, and the amount of radioactivity in the supernatant fraction (1-mL aliquot) is determined by liquid scintillation counting. A 1-mL aliquot of supernatant fraction may be retained and stored at À808C for potential future analysis. Precipitated protein is removed by centrifugation as above, after which the In Vitro Study of Drug-Metabolizing Enzymes 289 supernatant fraction is analyzed by liquid scintillation counting. The precipitated protein (the protein pellet) is then washed three times with neat methanol to remove traces of unbound drug candidate, with each wash step being followed by centrifugation at 920 Â g for 10 minutes at 48C[andbyanalysisofeachsuper- natant (wash) fraction by liquid scintillation counting]. Following the methanol washes, additional extraction procedures with water or hexane may be performed to evaluate the ability of different solvents to remove unbound radioactivity from the precipitated protein. A second 1-mL aliquot is used to determine the final protein concentration of each sample using a bicinchoninic acid protein assay kit. The gel can be stained with Coomassie Blue to locate pro- teins and then desiccated. Mechanism-based inhibition can complicate attempts to predict the clinical outcome, which is the topic of chapter 11. Therefore, this criterion for possible exclusion from a clinical drug-drug inter- action study is more conservative than the upper limit of the bioequivalence goalpost of 125% (see “Introduction”). In some cases, such as fluvoxamine, the cause of the underestimation is not known (130). With this approach, an investigator would identify the enzyme that is most potently inhibited in vitro (with an [I]/Ki value > 0. Criteria have not yet been developed to guide decision making as to when the next most potently inhibited enzyme does not need to be examined in vivo. Industry perspectives on the rank-order approach have been published, which attempt to define criteria that ultimately prevent false negatives (119,120). The estimated Cmax,u,inlet (estimated unbound steady-state Cmax at the inlet to the liver) can be used in this equation in an attempt to approximate the actual unbound concentration in the liver, as described by Kanamitsu et al. The estimated Cmax,u,inlet is higher than the unbound systemic concentration, but less than the total systemic concentration. This relationship relies on certain assumptions including (1) the conditions of the well-stirred pharmacokinetic model are met, (2) the substrate exhibits linear pharmacokinetics and is metabolized only in the liver, and (3) the complete absorption from the gas- trointestinal tract occurs (123). The rate of enzyme degradation has a dramatic In Vitro Study of Drug-Metabolizing Enzymes 293 impact on the predictions made from this equation. This assumption is made because any in vivo phenomena that can lead to discrepancies between in vitro and in vivo data (e. If these assumptions are true, then clinical drug-drug interaction studies need only be conducted for the enzymes that are most potently inhibited in vitro. To assess whether or not the rank-order of inhibitory potency is the same both in vitro and in vivo, Obach et al.

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The two major ways of increasing cardiac performance are by increasing initial muscle length (preload) and/or by increasing contractility cheap lady era on line menstrual cycle phases. An ideal index of contractility order lady era discount menopause dryness, therefore discount lady era online mastercard women's health center vancouver wa, would be one which is not changed by a change in initial muscle length but is altered only by an increase in contractility discount 100mg lady era otc women's health center of jackson wy. The three indices of contractility which we have discussed are (1) maximum rate of force development (max dF/dt), (2) V max, and (3) total force line. At a constant preload in the isometrically contracting muscle, max dF/dt is an excellent index of contractile state when testing the effects of different drugs. However, max dF/dt does change somewhat with changes in preload, so that it is not totally specific for contractile state alone. The same is true for V max which is altered substantially by changes in contractility and slightly by changes in preload. On the other hand, the total force line is more specific for changes only in contractile state. Table 3 has paired some of the analogous terms which are used in isolated heart muscle and in the intact heart. In isolated heart muscle we measure force, whereas in the intact heart we measure intraventricular pressure. Force in the wall of the heart is related to pressure by the Laplace relation, a simplified form of which is shown in the table. The passive length-tension curve of isolated muscle and the passive pressure volume relation of the left ventricle are both exponential curves which resist further lengthening at higher force or pressure. The term preload refers to the initial load stretching isolated heart muscle prior to contraction. In isolated heart muscle, the afterload refers to the additional load above the preload which the muscle has to match in order to shorten. In an analogous way, the aortic pressure represents the pressure that must be developed by the left ventricle before it can open the aortic valve and eject blood. The active length-tension curve has a somewhat similar shape to the ventricular function curve illustrated in Figure 20. These pressures represent the diastolic filling pressure of the left ventricle, and thus are an index of preload. A normal left atrial pressure is generally less than 12 mmHg, so that the heart is normally working on the ascending limb of the left ventricular function curve. The pulmonary capillary wedge pressure is an approximation of the left atrial pressure (and therefore of left ventricular end-diastolic pressure). By definition, the ejection fraction is the stroke volume divided by the end-diastolic volume. In principle, this is conceptually related to a ventricular function curve, as illustrated in Figure 21. By plotting stroke volume versus the end-diastolic volume, different curves of left ventricular performance are illustrated. As left ventricular performance decreases, ejection fraction is reduced and the ventricular function curve is shifted down and to the right (A to B to C). The ejection fraction is one of the most useful single numbers for characterizing left ventricular performance (although it is load-dependent). The ejection fraction is the slope of the dashed line connecting the origin to points A, B, and C on the three different curves. As the curves are progressively shifted down and to the right to a lower level of function, there is a decrease in the ejection fraction. During the process of heart failure, there are three immediate compensatory mechanisms used to maintain cardiovascular compensation. These are (1) dilation (Frank-Starling mechanism), (2) sympathetic stimulation and an increase in circulating catecholamines, and (3) increased heart rate. The effect of two of these mechanisms on the ventricular function curve is shown in Figure 22. During the process of heart failure, the left ventricle has moved from point A on the normal curve down to point B on a depressed and failing curve. Since cardiac output is the product of stroke volume and heart rate, an increase in heart rate will also tend to maintain cardiac output when stroke volume is reduced. Chronic compensatory mechanisms include (1) hypertrophy, which occurs with both volume and pressure overload, and (2) increased extraction of oxygen from the blood. This latter effect increases oxygen delivery to body tissues at a given cardiac output. The patient begins at point A on a normal ventricular function curve and shifts down to point B with the development of heart failure. The responses of the ventricle to volume or pressure overload are shown in Figures 22 and 23. The passive-pressure volume relations of the ventricle are usually altered by pressure or volume overload (Fig. In volume overload such as occurs with aortic or mitral valvular regurgitation, the ventricle tends to dilate and the curve is shifted to the right with an increase in compliance. In pressure overload such as occurs with aortic stenosis, the curve is often shifted to the left. The wall hypertrophies with a reduction in intraventricular volume (decreased compliance). Figure 23: Changes in the passive-pressure volume relation of the ventricle in response to volume overload (increased compliance) and pressure overload (decreased compliance). An important principle relating to the onset of heart failure is that there may be preservation of ventricular function at rest although the reserve of the heart in response to stress or exercise is markedly reduced. In response to an increase in arterial pressure, there is a tendency for stroke volume to be reduced because of the increased afterload. The ventricle, therefore, increases its contractility by responding to increased systemic and local norepinephrine secretion to maintain stroke volume. This results in a shift upward in function as shown by the dashed line (A) to the higher function curve. This represents a normal integrated response to an increase in arterial pressure in a compensated ventricle. The upper control curve of patient B has resting measurements similar to the resting measurements of patient A. In response to the same increase in arterial pressure, however, this patient has little reserve. Therefore, as afterload is increased, there is a reduction in left ventricular performance and cardiac dilation. This results in a marked shift of function down and to the right (dashed line), as illustrated. Thus, although resting measurements of performance were similar in the two patients, patient A had relatively normal ventricular reserve, whereas patient B had a marked reduction in ventricular reserve. Patient B, therefore, would probably also be limited by symptoms of shortness of breath and fatigue during exercise. It appears that some depletion of high energy phosphates may occur in heart failure, although this is probably not the cause of the heart failure. The oxygen consumption of the heart has an important relationship to pressure development and to shortening.

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Ifthisis severe and renal function is impaired 100 mg lady era for sale pregnancy zumba dvd, a dose reduction may be necessary buy cheap lady era online menstruation 3 days late. Prothrombin time If indicated and in * A slightprolongation of prothrombin time occurs at-risk individuals rarely best lady era 100 mg pregnancy pains. Development of signs Throughout treatment * The drug can precipitate in the gallbladder lady era 100 mg menopause diet. Signs of Throughout treatment * The drug may result in the overgrowth of supra-infection or non-susceptibleorganisms--appropriatetherapy superinfection should be commenced; treatment may need to be interrupted. Development of Throughout and up to * Development of severe, persistent diarrhoea diarrhoea 2 months after may be suggestive of Clostridium difficile- treatment associated diarrhoea and colitis (pseudomembranous colitis). Ceftriaxone | Cefuroxime | 139 Additional information Common and serious Immediate: Anaphylaxis and other hypersensitivity reactions have been reported. This assessment is based on the full range of preparation and administration options described in the monograph. Pre-treatment checks Do not give if there is known hypersensitivity to cefuroxime, cephalosporins or previous immediate hypersensitivity reaction to penicillins or any other beta-lactam antibiotic. An oral dose of 1g probenecid may also be given (to slow the rate of tubular secretion of cefuroxime). Dose in renal impairment: adjusted according to creatinine clearance: * CrCl >50mL/minute: dose as in normal renal function. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Withdraw the required dose and add to 50--100mL of compatible infusion fluid (usually NaCl 0. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Amikacin, ciprofloxacin, cisatracurium, clarithromycin, fluconazole, gentamicin, midazolam, pantoprazole, ranitidine, tobramycin, vancomycin. Monitoring Measure Frequency Rationale U&Es Periodically * Transient rises in urea and creatinine may occur. Signs of Throughout * May result in the overgrowth of non-susceptible supra-infection or treatment organisms -- appropriate therapy should be superinfection commenced; treatment may need to be interrupted. Development of Throughout and * Development of severe, persistent diarrhoea may be diarrhoea up to 2 months suggestive of Clostridium difficile-associated after treatment diarrhoea and colitis (pseudomembranous colitis). Patients at-risk individuals with impaired vitamin K synthesis or low vitamin K stores, e. Action in case of In overdose cerebral irritation and seizures may occur (use anticonvulsant overdose therapy if indicated). Counselling Women taking the combined contraceptive pill should be should be advised to take additional precautions during and for 7 days after the course. This assessment is based on the full range of preparation and administration options described in the monograph. Chloram phenicol 1-g dry powder vials * Chloramphenicol sodium succinate is a potent broad-spectrum antibiotic. However, the riskoflife-threatening adverse effects, particularly bone-marrow aplasia, has severely limited the clinical usefulness of chloramphenicol. Chloramphenicol | 143 Pre-treatment checks * Do not give if there is known hypersensitivity and/or toxic reaction to chloramphenicol. To prevent relapse treatment should be continued until apyrexial for 4 days in rickettsial diseases and for 8--10 days in typhoid fever. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Withdraw the required dose and add to a suitable volume of compatible infusion fluid (usually 100mL NaCl 0. Inspect visually for particulate matter or discolor- ation prior to administration and discard if present. Intramuscular injection (not recommended -- absorption can be slow and unpredictable) Preparation and administration 1. Chloramphenicol Every 2--3 days * A trough level is taken just before a dose and should plasma (usually only required be 5--15mg/L. Development of Throughout and up to * Development of severe, persistent diarrhoea may be diarrhoea 2 months after suggestive of Clostridium difficile-associated treatment diarrhoea and colitis (pseudomembranous colitis). Additional information Common and serious Dryness of the mouth, nausea and vomiting, diarrhoea, urticaria. Blood disorders including reversible and irreversible aplastic anaemia (with reports of resulting leukaemia), erythema multiforme. Significant interactions * The following may #chloramphenicol levels or effect: barbiturates, primidone. This assessment is based on the full range of preparation and administration options described in the monograph. Chlorphenam ine aleate (chlorpheniram ine aleate) 10mg/mL solution in 1-mL ampoules * Chlorphenamine maleate is a sedating antihistamine that causes a moderate degree of sedation; it also has antimuscarinic activity. Pre-treatment checks * Avoid in patients taking monoamine oxidase inhibitors up to 14 days previously because of "risk of extrapyramidal side-effects. Chlorphenamine maleate | 147 Intramuscular injection Preparation and administration 1. Technical information Incompatible with Noradrenaline (norepinephrine) Compatible with Flush: NaCl 0. Other: Drowsiness, headache, psychomotor impairment, urinary retention, dry mouth, blurred vision Pharmacokinetics In adults with normal renal and hepatic function, the half-life of chlorphenamine ranges from 2 to 43 hours. This assessment is based on the full range of preparation and administration options described in the monograph. Chlorprom azine hydrochloride 25mg/mL solution in 2-mL ampoules * Chlorpromazine hydrochloride is a phenothiazine antipsychotic with a wide range of actions. It is a dopamine inhibitor; it has antiemetic activity; it has muscle relaxant properties; and it inhibits the heat-regulating centre. It has been used to facilitate the induction of hypothermia because it prevents shivering and causes vasodilatation. Chlorpromazine hydrochloride | 149 Intramuscular injection Preparation and administration See Special handling below. Ifirritationattheinjection site is a problem the injection may be diluted with NaCl 0. Intermittent intravenous infusion Preparation and administration See Special handling below. Inspect visually for particulate matter or discoloration prior to administration and discard if present. Technical information Incompatible with Amphotericin, aztreonam, furosemide, linezolid, piperacillin with tazobactam, remifentanil, tigecycline. A slight yellowish discoloration does notindicatelossofpotency --markedly discolouredsolutions should notbe used. Special handling Handle solutions with care to avoid risk of contact sensitisation. Injection site Post administration * May be painful and may cause nodule formation.

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Vitamin E The photoprotective effect of vitamin E (α–tocopherol) and its acetyl ester have been studied extensively (see Table 7) safe 100 mg lady era women's health clinic bowling green ky. However discount lady era 100mg on line pregnancy month by month, most studies used animal models buy lady era 100mg overnight delivery womens health nurse practitioner programs, while only few studies exist demonstrating photoprotection by topical application of vitamin E in humans (126 order lady era 100mg line pregnancy 9th week,127,138,139). However, their photoprotective effects appeared to be less pronounced as compared to vitamin E; moreover, some studies failed to detect photoprotection provided by vitamin E esters (125,138,143). Since the free aro- matic hydroxyl group is responsible for the antioxidant properties of vitamin E, vitamin E esters need to be hydrolyzed during skin absorption to show activity. A skin bioavailability study demonstrated that vitamin E and vitamin E acetate behave similarly with regard to penetration of rat epidermis (132). The authors concluded that the aromatic hydroxyl group in vitamin E is not dissoci- ated in the skin penetration limiting layer, the stratum corneum. Consequently, the difference between physicochemical parameters determining skin transport for vitamin E and its esters seem negligible. Notably, the bioconversion of vita- min E acetate to its active antioxidative form, α–tocopherol, was found to be slow and to occur only to a minor extent in vivo (132,147). Hence, the less pronounced or missing photoprotective effects of topically applied vitamin E acetate after a single application might be explained by a limited bioavailability of the ester-cleaved form during oxidative stress at the site of action (e. As was further shown by the same authors, photoprotection was obtained only after several topical applications of vitamin E acetate. A human study further demonstrated that topically applied α–tocopherol acetate, though substan- tially absorbed into skin, is not significantly metabolized to the hydrolyzed form, even after long-term administration (147). In addition to the antioxidative properties of vitamin E, further photoprotec- tive mechanisms have been discussed. Recent studies on vitamin E using a lipo- some dispersion model to estimate the photooxidation of biomolecules (148), or 168 Thiele et al. Additionally, interactions of vitamin E with the metabolism of arachidonic acid have been described. Vitamin E was shown to modulate the activity of cyclo- oxygenase and to depress the biosynthesis rate of prostaglandin E2, possibly by inhibiting the release of arachidonic acid by phospholipase A2 (33,149). Interac- tions with the eicosanoid system may result in an anti-inflammatory effect and thus complement antioxidative photoprotection in skin. Vitamin C Few studies have reported photoprotective effects for vitamin C (see Table 8). Using a porcine skin model, Darr and associates proposed that topically applied vitamin C is only effective when formulated at high concentration in an appro- priate vehicle (150). Vitamin C is highly unstable and is only poorly absorbed into the skin, possibly explaining its modest photoprotective effect when applied topically (151). Hence, more lipophilic and more stable vitamin C esters, such as its palmitatyl, succinyl, or phosphoryl ester (151–153), might be promising derivatives providing increased photoprotection, as compared to vitamin C. As described for vitamin E esters, such compounds must be hydrolyzed to vitamin C to be effective as antioxidants. Other Antioxidants Besides vitamin E and vitamin C, several other compounds with antioxidative potential have been suggested to lower photodamage when topically applied (see Table 9). Thiols, such as N-acetyl- cysteine and derivatives, are another important group of potent radical scavengers (161,162). A photoprotective effect for the redox couple α-lipoate/dihydrolipoate (also referred to as ‘‘α-lipoic acid’’) has been proposed for skin (168). Dihydro- lipoate, the reduced form of lipoic acid, is a reductant with a more negative redox potential ( 0. It was demon- strated in hairless mice that α-lipoate readily penetrates skin and thereafter is reduced to its more potent antioxidant form, dihydrolipoate (169). Besides melatonin’s antioxidant (171) and dose- dependent sunscreening properties (127,170), it may also act in an immuno- modulatory way (172,173). Photoprotective effects were also reported for topical application of several other substances with antioxidant properties. Antioxidant Combinations The cutaneous antioxidant system is complex and far from being completely understood. As pointed out above, the system is interlinked and operates as an antioxidant network (Fig. Thus, an enhanced photoprotective effect may be obtained by applying appropriate combinations of antioxidants (see Table 10). As was shown in a human study, application of vitamin C or vitamin E alone resulted in modestly decreased erythema reaction (127). However, a much more pronounced effect was obtained by combining these two vitamins. Notably, the most dramatic improvement resulted from the coformulation of melatonin to- Antioxidant Defense Systems in Skin 173 174 Thiele et al. Studying the effect of distinct mixtures of topically applied antioxidants in photodermatoses, Hadshiew and associates demonstrated that the development and severity of polymorphous light eruption were significantly reduced by administration of a combination consisting of α- glycosylrutin, ferulic acid, and tocopheryl acetate (178). Iron participates as a catalyst in the formation of the highly damaging hydroxyl radical (15). Hence, topical application of certain iron chela- tors such as 2-furildioxime were demonstrated to be efficient in providing photo- protection alone (182) or in combination with sunscreens (183). The authors postulated that the cysteine-rich metallothionein may act as a radical scavenger. Applying topical selenium in the form of l-selenomethionine proved to reduce acute and/or chronic skin damage in mice (185) as well as in humans (186). Topical applica- tion of l-selenomethionine led to increased skin selenium levels, whereas free selenium was apparently not absorbed (187,188). More successful in preventing such damage were appropriate combinations of antioxidants resulting in a sustained antioxidant ca- pacity of the skin, possibly due to antioxidant synergisms. Therefore, efficient sunscreens are indis- pensable in the effective prevention of skin photodamage. However, antioxidants, in combination with sunscreens (128) or anti-inflammatory agents (135), seem to be highly effective adjuncts increasing the safety and the efficacy of photopro- tective products. This work was supported by a postdoctoral fellowship from the Deutsche Forschungsgemeinschaft (Th 620/1- 1). Ozone exposure depletes vitamin E and induces lipid peroxidation in murine stratum corneum. In vivo exposure to ozone depletes vitamins C and E and induces lipid peroxidation in epidermal layers of murine skin. Macromolecular carbonyls in human stratum corneum: a biomarker for environmental oxidant exposure? Regeneration of vitamin E from alpha chromanoxyl radical by glutathione and vitamin C.

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