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cukup sekian penjelasan dari saya
enough of my explanation
Ultimo aggiornamento 2020-08-27
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cukup sekian dari saya dan terima kasih
that's all and thank you
Ultimo aggiornamento 2020-11-01
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terima kasih pak
hello everyone, welcome to blockchain island
Ultimo aggiornamento 2021-12-20
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terima kasih banyak
i'm so sorry.
Ultimo aggiornamento 2022-08-30
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terima kasih banyak.
thanks a lot.
Ultimo aggiornamento 2016-03-25
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terima kasih atas doa nya
thank you for your prayers and support
Ultimo aggiornamento 2022-03-06
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terima kasih suami terbaikku
thank kashi my best husband
Ultimo aggiornamento 2023-01-19
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terima kasih atas kepercayaan anda.
thank you for your trust and cooperation.
Ultimo aggiornamento 2023-01-01
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terima kasih atas jasa-jasanya
keep inspiring
Ultimo aggiornamento 2020-06-21
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sekian dari saya,saya akhiri wassalam
from the psp b class, here
Ultimo aggiornamento 2020-12-10
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terima kasih tuhan 11 years old
terima kasih tuhan 11 years old
Ultimo aggiornamento 2024-03-04
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terima kasih untuk sahabat ku anandamp
thank you for my friend anandamp
Ultimo aggiornamento 2020-10-16
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peluk jauh dari saya
hug away from me
Ultimo aggiornamento 2024-04-14
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kamu lebih muda dari saya
google transleter
Ultimo aggiornamento 2014-12-29
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masih ada yang ditutupi dari saya
the most potent suppressors of gastric acid secretion are inhibitors of the gastric h+,k+-atpase (proton pump) (figure 36–2a). in typical doses, these drugs diminish the daily production of acid (basal and stimulated) by 80% to 95%. five proton pump inhibitors are available for clinical use: omeprazole (prilosec, rapinex, zegerid) and its s-isomer, esomeprazole (nexium), lansoprazole (prevacid), rabeprazole (aciphex), and pantoprazole (protonix). these drugs have different substitutions on their pyridine and/or benzimidazole groups but are remarkably similar in their pharmacological properties (see appendix ii). omeprazole is a racemic mixture of r- and s-isomers; the s-isomer, esomeprazole (s-omeprazole), is eliminated less rapidly than r-omeprazole, which theoretically provides a therapeutic advantage because of the increased half-life. despite claims to the contrary, all proton pump inhibitors have equivalent efficacy at comparable doses. proton pump inhibitors are prodrugs that require activation in an acid environment. after absorption into the systemic circulation, the prodrug diffuses into the parietal cells of the stomach and accumulates in the acidic secretory canaliculi. here, it is activated by proton-catalyzed formation of a tetracyclic sulfenamide (figure 36–2), trapping the drug so that it cannot diffuse back across the canalicular membrane. the activated form then binds covalently with sulfhydryl groups of cysteines in the h+,k+-atpase, irreversibly inactivating the pump molecule. acid secretion resumes only after new pump molecules are synthesized and inserted into the luminal membrane, providing a prolonged (up to 24- to 48-hour) suppression of acid secretion, despite the much shorter plasma half-lives (0.5 to 2 hours) of the parent compounds. because they block the final step in acid production, the proton pump inhibitors are effective in acid suppression regardless of other stimulating factors. the most potent suppressors of gastric acid secretion are inhibitors of the gastric h+,k+-atpase (proton pump) (figure 36–2a). in typical doses, these drugs diminish the daily production of acid (basal and stimulated) by 80% to 95%. five proton pump inhibitors are available for clinical use: omeprazole (prilosec, rapinex, zegerid) and its s-isomer, esomeprazole (nexium), lansoprazole (prevacid), rabeprazole (aciphex), and pantoprazole (protonix). these drugs have different substitutions on their pyridine and/or benzimidazole groups but are remarkably similar in their pharmacological properties (see appendix ii). omeprazole is a racemic mixture of r- and s-isomers; the s-isomer, esomeprazole (s-omeprazole), is eliminated less rapidly than r-omeprazole, which theoretically provides a therapeutic advantage because of the increased half-life. despite claims to the contrary, all proton pump inhibitors have equivalent efficacy at comparable doses. proton pump inhibitors are prodrugs that require activation in an acid environment. after absorption into the systemic circulation, the prodrug diffuses into the parietal cells of the stomach and accumulates in the acidic secretory canaliculi. here, it is activated by proton-catalyzed formation of a tetracyclic sulfenamide (figure 36–2), trapping the drug so that it cannot diffuse back across the canalicular membrane. the activated form then binds covalently with sulfhydryl groups of cysteines in the h+,k+-atpase, irreversibly inactivating the pump molecule. acid secretion resumes only after new pump molecules are synthesized and inserted into the luminal membrane, providing a prolonged (up to 24- to 48-hour) suppression of acid secretion, despite the much shorter plasma half-lives (0.5 to 2 hours) of the parent compounds. because they block the final step in acid production, the proton pump inhibitors are effective in acid suppression regardless of other stimulating factors.
Ultimo aggiornamento 2014-04-24
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