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  • 1
    Book
    Book
    Wiesbaden : Vieweg + Teubner
    Type of Medium: Book
    Pages: IX, 298 S. , Ill., graph. Darst.
    Edition: 3., überarb. und erw. Aufl.
    ISBN: 9783834807199 , 3834807192 , 9783834897275
    Series Statement: Studium : Wirtschaftsinformatik
    DDC: 658.4038
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    Language: German
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  • 2
    Online Resource
    Online Resource
    London ; : Routledge,
    Keywords: Industrial policy ; Local government ; Regional planning ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (131 pages) : , illustrations.
    ISBN: 9780429554872 (e-book)
    Series Statement: Routledge Studies in Latin American Development
    DDC: 338.972
    Parallel Title: Print version: Tijerina, Walid. Industrial development in Mexico : policy transformation from below.
    Language: English
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  • 3
    Online Resource
    Online Resource
    Wiesbaden : Vieweg
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource
    Edition: 2., erg. Aufl.
    ISBN: 9783834802750 , 3834802751 , 9783834890566
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    Language: German
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  • 4
    Online Resource
    Online Resource
    Wiesbaden : Vieweg + Teubner
    Type of Medium: Online Resource
    Pages: 1 Online-Ressource (IX, 298 S.) , Ill., graph. Darst.
    Edition: 3., überarb. und erw. Aufl.
    ISBN: 9783834807199 , 9783834897275
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    Language: German
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Prospects 18 (1988), S. 239-247 
    ISSN: 1573-9090
    Source: Springer Online Journal Archives 1860-2000
    Topics: Education
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 12 (1995), S. 609-614 
    ISSN: 1573-904X
    Keywords: diltiazem ; metabolism ; liver ; extrahepatic tissues
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Diltiazem (DTZ) is a calcium channel blocker widely used in the treatment of angina and hypertension. DTZ undergoes extensive metabolism yielding several metabolites, some of which are active like N-desmethyldiltiazem (MA), desacetyldiltiazem (M1) and N-desmethyl,desacetyldiltiazem (M2). Due to the nature of its biotransformation, several organs should have the ability to metabolize DTZ, however it is still assumed that the liver is the only organ implicated in its elimination. In this study, the fate of DTZ, MA and M1 was assessed in several organs that could contribute to their biotransformation. To this purpose, DTZ (48.2 µM) was incubated in the 10,000 × g supernatant of homogenates of rabbit tissues for 60 min at 37°C. Multiple samples were withdrawn, and DTZ and its metabolites were assayed by HPLC. The elimination rate constant of DTZ in 10,000 × g supernatants varied between the organs: liver 334 ± 45, proximal small intestine 69 ± 11, distal small intestine 25 ± 3, lungs 15 ± 6 and kidneys 8 ± 6 (10−4 min−1). The metabolism of DTZ in the liver generated large amounts of MA but no M1, and in the small intestine, modest amounts of both metabolites. When MA (50.0 µM) or M1 (53.7 µM) were incubated in liver homogenates, the estimated elimination rate constant were 166 ± 23 and 468 ± 53 (10−4 min−1), respectively. The rate of degradation of the metabolites in the small intestine was much slower. These results demonstrate that, in vitro, DTZ is metabolized by several organs, the liver accounting for 75% of the total activity, and that MA is the major metabolite generated.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 13 (1996), S. 124-128 
    ISSN: 1573-904X
    Keywords: diltiazem ; first-pass metabolism ; intestine ; liver ; lungs
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. The aim of this study was to assess in vivo which organs contribute to the first-pass metabolism of diltiazem. Methods. Anaesthetized rabbits received diltiazem into the thoracic aorta (TA) (1 mg/kg), jugular vein (JV) (2 mg/kg), portal vein (PV) (4 mg/kg) or small intestine (SI) (5 mg/kg). Serial blood samples were withdrawn from the abdominal aorta to assay diltiazem, N-demethyl-diltiazem (MA) and deacetyldiltiazem (M1). Results. The area under diltiazem plasma concentration curve/time (AUC0−∞) normalized by the dose was AUCTA ≈ AUCJV 〉 AUCPV 〉 AUCSI. Intestinal and hepatic diltiazem availability was 43 and 33%, respectively. The systemic availability of oral diltiazem was 12%. Diltiazem given into the SI and PV generated primarily MA, and injected into the JV and TA produced mainly Ml. Conclusions. In rabbits, the intestine and the liver contribute to the first-pass metabolism of diltiazem, and the amount and species of metabolites generated depend upon the route of administration of diltiazem.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    ISSN: 1573-742X
    Keywords: coronary ischemic syndromes ; heparin ; anticoagulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The optimal heparin dosing schedule to achieve rapid and therapeutic anticoagulation has not been established. The objective of this study is to determine whether an intravenous heparin dosing nomogram based on body weight achieves adequate anticoagulation more rapidly than a standard-care nomogram. Sixty-four patients requiring intravenous heparin treatment for acute coronary syndromes, but who did not receive thrombolytic therapy, were randomized to a standard-care nomogram in which heparin was given as a 5000 unit IV bolus followed by 1000 U/hr, or a weight adjusted nomogram in which heparin was given as an 80 U/ kg IV bolus and 18 U/kg/hr. Activated partial thromboplastin time (APTT) values were checked at 6,12,18, 24, and 48 hours and adjusted either by 100–200 U/hr (standard-care nomogram) or by 2–4 U/kg/hr (weight-based nomogram). Activated partial thromboplastin times were measured using a widely generalizable laboratory method. The primary goal was to achieve and maintain the APTT between 60 and 90 seconds. The median APTT values were higher in the weight adjusted group compared with the standard-care group at 6, 12, 18, 24, and 48 hours: 150 versus 83 (p=0.001), 100 versus 79 (p=0.09), 66 versus 61 (p=0.005), 63 versus 56 (p = 0.09), and 64 versus 56 (p=0.11). At 18 hours only 11% of patients in the weight-adjusted group had an APTT 〈61 compared with 26% in the standard-care nomogram (p=0.007). No major bleeding complications were noted in either group. A weight-adjusted heparin nomogram offers improved anticoagulation in the first 24 hours after heparin initiation compared with a standard-care nomogram in patients with acute coronary artery syndromes.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 12 (1995), S. 1722-1726 
    ISSN: 1573-904X
    Keywords: diltiazem ; metabolism ; intestine ; rabbits
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Purpose. Since the ability of the small intestine to biotransform a drug may decrease in distal segments of the intestine, this study aimed to assess whether the site of administration in the small intestine could affect the systemic bioavailability of diltiazem and its two active metabolites, N-desmethyldiltiazem (MA) and desacetyldiltiazem (Ml). Methods. Five mg/kg of diltiazem were administered into the lumen of the proximal (0–30 cm, n = 9) or the distal (150–180 cm) small intestine (n = 7) of anesthetized New Zealand rabbits. Blood samples were drawn from the femoral artery for 6 hours, and diltiazem, MA and M1 were assayed by HPLC. Results. The area under the curve (AUC0 → ∞)of diltiazem administered into the distal small intestine was larger than that estimated when diltiazem was given in the proximal segment (14.20 ± 2.82 vs 8.14 ± 0.88 µg.min/ml, p 〈 0.05), due to a lower diltiazem oral clearance (440 ± 78 vs 660 ± 55 ml/min/kg, p 〈 0.05). The AUC0 → 360 of MA was not affected by the site of diltiazem administration, but the AUC0 →360 of M1 was increased when diltiazem was administered in the distal segment of the small intestine. When administered into the distal segment of the intestine, the molar sum of diltiazem and its active metabolites was 48% greater than when delivered into the 0–30 cm segment of the small intestine; as a consequence, absorption of diltiazem in distal segments of the small intestine may enhance its pharmacological response. Conclusions. The site of absorption into the intestine modulates the bioavailability of diltiazem and its two active metabolites.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Pharmaceutical research 8 (1991), S. 1470-1476 
    ISSN: 1573-904X
    Keywords: antipyrine ; metabolites ; rabbit ; oxidation ; conjugation ; pharmacokinetics
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology
    Notes: Abstract Antipyrine (AP) is a commonly used probe of oxidative metabolism. Indirect evidence demonstrates formation rate limited disposition of its metabolites. Kinetic studies using antipyrine and its major metabolites 3-hydroxymethylantipyrine (HMA), norantipyrine (NORA), and 4-hydroxyantipyrine (OHA) were completed to investigate the metabolic fate of preformed antipyrine metabolite and to demonstrate directly formation rate-limited metabolite disposition in vivo. Bolus injections of antipyrine and preformed metabolites (40-50 mg/kg) were administered to male, New Zealand white rabbits. Plasma and urine were analyzed using HPLC. These studies demonstrate that HMA, NORA, and OHA are formation rate limited in the rabbit. NORA appears to undergo further extensive oxidative and conjugative metabolism. Unknown additional peaks were detected in urine after NORA dosing but not after HMA or OHA administration. Mass spectroscopy of the unknown HPLC eluents identified potential structures of these NORA metabolites.
    Type of Medium: Electronic Resource
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