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Continuous treatment

Petroleum sulfonates have traditionally been produced by both batch and continuous treatment of petroleum oils with oleum. These processes have been covered in several reviews (138,139). Natural petroleum sulfonates are coproducts in the manufacture of a variety of refined oils, most notably white (mineral) oils, lube oils, and process oils (plasticizer oils for mbber compounding). The feedstocks are selected primarily on the basis of the desired characteristics of the refined oils which generally contain 15—30% aromatics. [Pg.80]

When the adsorption capacity of a carbon unit is exceeded, there is breakthrough of the contaminant in the treated stream. Eixed beds may be operated in series to allow continuous treatment while spent or exhausted units are replaced with fresh carbon. In series operation, there are two or more units. The majority of the contaminant is removed by the first unit in the series with the downstream units acting as polishing units. When breakthrough occurs in the first or primary unit, it is replaced with fresh carbon and becomes a polishing unit while the next unit in the series takes over and becomes the primary treatment unit. An example of this round-robin operation of a three-carbon bed is shown in Eigure 2. [Pg.160]

Lime and Lime-Soda Processes. The first softening plant in the early 1900s used the lime softening process with fill and draw units. Later, continuous-treatment units, which greatiy increased the amount of water that could be treated in a faciUty of given size, were developed. More than 1000 municipahties soften water. Most are in the Midwest and in Florida. However, concern for the adverse effect of soft water on cardiovascular disease (CVD) may limit the number of plants that introduce softening. [Pg.278]

Pure piperitone was subjected to the action of purified hydrogen, in the presence of a nickel catalyst, for six hours, the temperature ranging between 175° to 180° C. The double bond in piperitone was readily opened out with the formation of menthone, but further action of the hydrogen under these conditions did not reduce the carbonyl group, even after continued treatment for two days. Under correct conditions, however, the reduction to menthol should take place. The ease with which menthone is formed in this way is of special interest, not only in connection with the production of this ketone, but also as a stage in the manufacture of menthol. [Pg.240]

Application of Corrosion Inhibitors. There are basically two main techniques used to apply corrosion inhibitors in drilling operations. In the first method inhibitors are added to the drilling fluid system either by mixing the additives through the rig s chemical hopper or through additions into the mud pit. The treatment can be achieved in two ways, batch treatment or continuous treatment. In some cases it may be necessary to use both types of treatment simultaneously. The second technique of applying is directly coating the corrosion inhibitors on the drillpipe. [Pg.1330]

Continuous Treatment. Continuous treatment involves introducing a corrosion inhibitor on a regular basis to maintain the specified concentrations of inhibitors in the system. Depending on the prevailing conditions and manufacturer s recommendation, the concentration may vary from a few parts per million to 50 ppm or more. [Pg.1331]

Direct Treatment. Although batch and continuous treatment are both quite effective, there is a problem with inhibitor waste. When corrosion inhibitors contact the circulating drilling fluid, they are likely to coat the solids in the fluid system (cuttings or other solids). By applying the corrosion inhibitor directly to drillstem components before they are run in the hole, the corrosion inhibitor is the first thing that contacts the exposed metal surface. There are two methods for this type of corrosion inhibitor treatment. [Pg.1331]

Once the microbiocide is selected, a method of application should be considered. The chemical can be introduced to the system by either batch treatment, continuous treatment or by a combination of both. For batch treatment, NACE provides an equation given below. This equation can be used to determine the concentration of chemical at any time during the eight hour period. The equation is... [Pg.1336]

Stresses the importance of continuing treatment until the entire drug lias evaporated, and misting lias ceased. [Pg.355]

Each of the analyses reported outcomes for patients responding to and continuing treatment after the original 6-week clinical trial that is, after the exclusion of patients withdrawing from the original trial for whatever reason (e.g. poor tolerability, lack of response). This probably introduced bias in favour of haloperidol, since there were significantly more responders to olanzapine. [Pg.31]

Figure 20.6 Schematic representation of the effects of 5-HT reuptake inhibitors on serotonergic neurons, (a) 5-HT is released at the somatodendritic level and by proximal segments of serotonergic axons within the Raphe nuclei and taken up by the 5-HT transporter. In these conditions there is little tonic activation of somatodendritic 5-HTia autoreceptors. At nerve terminals 5-HTib receptors control the 5-HT synthesis and release in a local manner, (b) The blockade of the 5-HT transporter at the level of the Raphe nuclei elevates the concentration of extraneuronal 5-HT to an extent that activates somatodendritic autoreceptors (5-HTia). This leads to neuronal hyperpolarisation, reduction of the discharge rate and reduction of 5-HT release by forebrain terminals, (c) The exposure to an enhanced extracellular 5-HT concentration produced by continuous treatment with SSRIs desensitises Raphe 5-HTia autoreceptors. The reduced 5-HTia function enables serotonergic neurons to recover cell firing and terminal release. Under these conditions, the SSRI-induced blockade of the 5-HT transporter in forebrain nerve terminals results in extracellular 5-HT increases larger than those observed after a single treatment with SSRIs. (Figure and legend taken from Hervas et al. 1999 with permission)... Figure 20.6 Schematic representation of the effects of 5-HT reuptake inhibitors on serotonergic neurons, (a) 5-HT is released at the somatodendritic level and by proximal segments of serotonergic axons within the Raphe nuclei and taken up by the 5-HT transporter. In these conditions there is little tonic activation of somatodendritic 5-HTia autoreceptors. At nerve terminals 5-HTib receptors control the 5-HT synthesis and release in a local manner, (b) The blockade of the 5-HT transporter at the level of the Raphe nuclei elevates the concentration of extraneuronal 5-HT to an extent that activates somatodendritic autoreceptors (5-HTia). This leads to neuronal hyperpolarisation, reduction of the discharge rate and reduction of 5-HT release by forebrain terminals, (c) The exposure to an enhanced extracellular 5-HT concentration produced by continuous treatment with SSRIs desensitises Raphe 5-HTia autoreceptors. The reduced 5-HTia function enables serotonergic neurons to recover cell firing and terminal release. Under these conditions, the SSRI-induced blockade of the 5-HT transporter in forebrain nerve terminals results in extracellular 5-HT increases larger than those observed after a single treatment with SSRIs. (Figure and legend taken from Hervas et al. 1999 with permission)...
Water-soluble corrosion inhibitors are necessary to prevent corrosion of the pipe walls, joints, pumps, and collection stations. An ampholytic, substituted imidazoline has been described for inhibiting corrosion in such systems [297]. This type of corrosion inhibitor is intended for continuous treatment. [Pg.97]

Hold or adjust warfarin dose as necessary. Discontinue UFH, LMWH, or fondaparinux if INR is greater than 2 on two consecutive occasions. If the patient requires continued treatment with UFH, measure aPTT, and adjust dose if necessary. [Pg.159]

Patients who develop resistance to lamivudine have significant improvement in histology while receiving entecavir, but higher doses (1 mg daily) are required. Additionally, 19% of lamivudine-resistant patients had undetectable HBV DNA levels compared to 1% of those who continued treatment with lamivudine.36 At present, no resistance has been associated with entecavir in patients treated for 1 year, but the data beyond 1 year of therapy are unknown. Entecavir resistance has only been seen in patients who already had lamivudine resistance.37... [Pg.355]

Patients are considered responders if at least a 1-log drop in viral count and normalization of ALT levels occur. Continue treatment. [Pg.357]

Continue treatment for at least another 36 weeks (48 weeks total) if the HCV RNA level becomes negative or decreases by at least 2 logs. [Pg.357]

In patients infected with non-genotype 1 HCV disease, check the HCV RNA level at the end of treatment (24 weeks). If HCV RNA is undetectable, continue treatment for another 24 weeks. Repeat the HCV RNA 24 weeks after completion of therapy to determine SVR.41... [Pg.358]

Many issues surrounding neutralizing antibodies remain such as standardization of the neutralizing antibody assay, testing recommendations, and treatment recommendations for positive tests 41 Neutralizing antibodies may disappear even with continued treatment. Neutralizing antibodies exhibit cross-reactivity with the other beta interferons.41... [Pg.438]

Treat behavioral and psychiatric issues as they arise. Consider the patient s choices of nonpharmacologic and pharmacologic options before recommending a treatment. Discontinue the pharmacologic treatments periodically to re-evaluate the need for continued treatment. [Pg.522]

Patients with GAD should be treated to remission of symptoms. While data are lacking on the optimal duration of pharmacotherapy, most guidelines recommend continuing treatment for an additional 3 to 10 months.25-28 An algorithm for the pharmacologic management of GAD is shown in Fig. 37-2. [Pg.610]

Bromocriptine directly binds to the D2 receptors on the lac-totroph cells to exert its effect. Bromocriptine normalizes prolactin level, restores menstrual cycles, and reduces tumor size in approximately 90% of patients.49 Adverse effects such as nausea, dizziness, and orthostatic hypotension often limit 5% to 10% of patients from continuing treatment. Thus, start bromocriptine at a low dose (e.g., 0.625-1.25 mg) at bedtime... [Pg.717]

If the prolactin level remains normal for 2 years, reassess the need to continue treatment. Make sure that the patient is taking the lowest effective dose for management of hyperprolactinemia. [Pg.719]

It has been suggested that a loading dose (twice the usual single dose) of the NSAID be taken, followed by the usually recommended dose until symptoms resolve.28 An alternate recommendation is to begin the NSAID at the onset of menses or perhaps even the day prior and to continue treatment around the clock instead of waiting until the onset of symptoms. For patients in whom NSAID use is contraindicated, the agents discussed below should be considered. The use of acetaminophen has been proven inferior to the use of NSAIDs for the treatment of this disorder.17... [Pg.761]

Assess any repeat blood cultures and vital signs to determine continued treatment effectiveness. [Pg.1103]


See other pages where Continuous treatment is mentioned: [Pg.494]    [Pg.209]    [Pg.179]    [Pg.179]    [Pg.179]    [Pg.197]    [Pg.1156]    [Pg.4]    [Pg.10]    [Pg.205]    [Pg.598]    [Pg.131]    [Pg.350]    [Pg.323]    [Pg.325]    [Pg.167]    [Pg.270]    [Pg.580]    [Pg.611]    [Pg.616]    [Pg.717]    [Pg.796]    [Pg.801]    [Pg.962]    [Pg.36]    [Pg.99]   
See also in sourсe #XX -- [ Pg.18 ]

See also in sourсe #XX -- [ Pg.25 ]




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