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41.
42.
《Journal of labelled compounds & radiopharmaceuticals》2003,46(8):699-713
The first application of a Sonogashira cross‐coupling reaction in 18F chemistry has been developed. The reaction was exemplified by the cross‐coupling of terminal alkynes (ethynylcyclopentyl carbinol 6 , 17α‐ethynyl‐3,17β‐estradiol 7 and 17α‐ethynyl‐3‐methoxy‐3,17β‐estradiol 8 ) with 4‐[18F]fluoroiodobenzene. 4,4′‐Diiododiaryliodonium salts were used as precursors for the synthesis of 4‐[18F]fluoroiodobenzene, enabling the convenient access to 4‐[18F]fluoroiodobenzene in 13–70% yield using conventional heating or microwave activation. The Sonogashira cross‐coupling of 4‐[18F]fluoroiodobenzene with terminal alkynes gave the corresponding 4‐[18F]fluorophenylethynyl‐substituted compounds [18F]‐9 , [18F]‐10 and [18F]‐13 in yields up to 88% within 20 min of starting from 4‐[18F]fluoroiodobenzene. Copyright © 2003 John Wiley & Sons, Ltd. 相似文献
43.
Desipramine (DMI, 15 mg/kg, s.c.) decreased [3H]CGP-12177-labelled cortical β-adrenoceptor density (Bmax) by 30% upon chronic (14 day) treatment. However, even a single dose (in mg/kg) of DMI (15) or the β-adrenoceptor agonist, clenbuterol (20), induced a rapid (24 hour) and significant reduction of β-adrenoceptor Bmax (−15%; p<0.01). Acute treatment with amitryptiline (10), clorgyline (1), fluoxetine (10), nomifensine (10) or maprotiline (20) had no significant effect on [3H]CGP-12177-labelled β-adrenoceptors, suggesting that rapid down-regulation may not be a general property of antidepressant drugs. None of the antidepressants altered the Bmax of [3H]ketanserin-labelled 5-HT2A receptors on acute treatment. These results show that β-adrenoceptor down-regulation by clenbuterol and DMI is not dependent on chronic treatment and may, therefore, be a poor correlate of the gradual onset of therapeutic efficacy seen clinically with antidepressant drugs. 相似文献
44.
1. The effect of strophanthidin on the slow inward current (Isi) and on contractile force were studied in guinea-pig isolated ventricular myocytes and intact papillary muscles, respectively. In myocytes, both low (10 nmol/L) and high (1-10 mumols/L) concentrations had small or no effects in either direction on Isi whereas norepinephrine (10-100 nmol/L) increased it. To determine whether the same results are obtained after decreasing or increasing intracellular calcium or sodium, the same concentrations of strophanthidin were tested in different procedures that are known to (i) increase [Ca]i and decrease [Na]i (high [Ca]o, 3.6-5.4 mmol/L; low [Na]o, 112 mmol/L; (ii) decrease [Ca]i and increase [Na]i (low [Ca]o, 0.45-1 mmol/L; Sr, 1 mmol/L; (iii) decrease [Ca]i and [Na]i (Cd, 0.1-0.2 mmol/L); and (iv) increase [Ca]i and [Na]i (veratridine, 0.2 mumol/L). High [Ca]o and veratridine increased whereas low [Ca]o and Cd decreased Isi. In contrast, during these various procedures, strophanthidin had small and inconsistent effects at a low or high concentration. In intact papillary muscles, low strophanthidin decreased whereas high strophanthidin increased contractile force. It is concluded that strophanthidin has little direct or indirect effect on Isi and that the decrease in force by low and increase in force by high concentrations in intact muscle are probably related to demonstrated decrease and increase, respectively, in intracellular sodium activity. 相似文献
45.
K. Mörike M. Koch Peter Fritz Wolfgang Urban Michel Eichelbaum 《Archives of toxicology》1996,70(5):300-305
In the pathogenesis of isoniazid-induced hepatic injury, cytochrome P450-dependent metabolic activation of the metabolite,
acetylhydrazine (AcHz), is the crucial step. Exhalation of [14C]-carbon dioxide has previously been used to quantify indirectly this pathway. In contrast, according to the current concept
of AcHz bioactivation, molecular nitrogen is produced directly, but has not yet been identified. Here, we measured [15N]-nitrogen and 14CO2 exhalation, after the administration of [15N2]-[14C]-AcHz, in rats. Laser magnetic resonance (LMR) spectroscopy, a new sensitive and specific technique for the measurement
of 15N and 14N in gas samples, was used. To demonstrate the involvement of cytochrome P450, rats were treated with phenobarbital (PB) or
PB + cobalt(II) chloride (CoCl2) (n=3 in each group). Time-dependent 15N2 exhalation differed significantly between treatment groups (p<0.001). At 240 min, cumulative exhalation of 15N was 1.92±0.43% (mean±SE) of the dose in the control group, 2.53±0.23% in the PB group, and 1.00±0.15% in the PB+CoCl2 group (p<0.05 compared to controls, p<0.01 compared to PB). Cumulative exhalation of 14CO2 in 24 h ranged from 15.1 to 21.9%, with no significant difference between treatment groups. In conclusion, N2 is a metabolite of AcHz. N2 formation reflects the cytochrome P450-mediated activation of AcHz and can be used as an index of this pathway. Generally,
LMR spectroscopy is valuable for monitoring any N2-liberating process in vivo.
Received: 14 March 1995/Accepted: 15 August 1995 相似文献
46.
D. G. Kim C.-Y. Kim S. H. Paek D. S. Lee J.-K. Chung H.-W. Jung B.-K. Cho 《Acta neurochirurgica》1998,140(7):665-674
Summary
Background To determine its roles in the diagnosis and the systemic evaluation of metastatic brain tumours, whole-body positron emission
tomography (PET) using [18F]FDG was performed in 20 consecutive patients.
Methods
All patients were thought to be suffering or needing to be differentiated from metastatic brain tumours. Nine patients had
multiple brain lesions; six were older and showed a rim-enhancing lesion with surrounding oedema; seven had homogeneously
enhancing periventricular lesion(s) on computed tomography (CT) and/or magnetic resonance (MR) imaging, thought to be central
nervous system lymphomas. Two patients had skull mass(es) and two patients had a solid mass suspected to be, respectively,
a haemorrhagic metastasis and a metastatic malignant melanoma. All of them received whole-body [18F]FDG PET and conventional systemic work-up for metastasis in order to compare the results of the two methods.
Results
Metastatic brain tumours were diagnosed on whole-body [18F]FDG PET in eleven patients who had extracranial and intracranial hypermetabolic lesions. In nine of these, a conventional
work-up also detected primary lesions which on whole-body [18F]FDG PET were seen to be hypermetabolic foci. Systemic lymph node metastases were detected by whole-body [18F]FDG PET only in two patients and histological diagnosis was possible by biopsy of lymph nodes rather than of brain lesions.
In the remaining nine patients who had only intracranial hypermetabolic foci, histological diagnosis was made by craniotomy
or stereotactic biopsy. It was confirmed that seven of nine patients were suffering from a primary brain tumour and two from
metastatic carcinoma. None of the nine showed evidence of systemic cancer on conventional work-up. Histological diagnoses
of the primary brain tumours were four cases of primary central nervous system lymphoma and one each of multifocal glioblastoma,
Ewing's sarcoma, and cavernous angioma.
Patients felt no discomfort during the whole-body [18F]FDG PET procedure and there were no complications. The false negative rate in [18F]FDG PET and in conventional work-up was 15.4% and 30.7% respectively. There were no false positives on either [18F]FDG PET or conventional work-up.
Conclusion
It is suggested that whole-body [18F]FDG PET is a safe, reliable, and convenient method for the diagnosis and systemic evaluation of patients thought to be suffering
or needing to be differentiated from a metastatic brain tumour. 相似文献
47.
H. Kushida T. Hiramoto H. Satoh M. Endoh 《Naunyn-Schmiedeberg's archives of pharmacology》1988,337(2):169-176
Summary The phorbol ester 12-O-tetradecanoyl phorbol-13-acetate (TPA) was used to examine the hypothesis that phosphoinositide turnover is involved in the regulation of myocardial contractility mediated by stimulation of alpha-adrenoceptors in the mammalian cardiac muscle. Exposure of the isolated rabbit papillary muscle electrically driven at a rate of 1 Hz at a temperature of 37°C to TPA in concentrations of 10–1000 nmol/l for 30 min did not affect the basal force of contraction. The concentration-response curve for the positive inotropic effect of (–)-phenylephrine mediated by stimulation of alpha-adrenoceptors in the presence of (±)-bupranolol (100 nmol/1) was shifted to the right and downward by TPA in concentrations of 30–1000 nmol/l, while the effect of (–)-phenylephrine mediated by stimulation of beta-adrenoceptors in the presence of prazosin (100 nmol/l) was not decreased, but slightly enhanced by exposure of the muscle to relatively low concentrations of TPA (10–100 nmol/l). Incubation of the membrane fraction isolated from the rabbit ventricular muscle with TPA in vitro under the same condition as employed in the physiological experiments decreased the specific binding of [3H]prazosin but not that of [3H]CGP-12177, while the non-tumor promoting phorbol ester, PDD, was ineffective. These results indicate that activation of protein kinase C by TPA does not mimic the positive inotropic effect of catecholamines mediated by activation of myocardial alpha-adrenoceptors. on the other hand, the specific interaction of alpha-adrenoceptor-mediated processes with TPA in the rabbit papillary muscle is in line with the view that the facilitation of phosphoinositide turnover and subsequent activation of protein kinase C may play a certain role in the coupling of alpha-adrenoceptor occupation by agonists to the process leading to the positive inotropic action.
Send offprint requests to M. Endoh 相似文献
48.
Miwa Baba Ryozo Oishi Kiyomi Saeki 《Naunyn-Schmiedeberg's archives of pharmacology》1988,337(4):423-428
Summary The effects of opioids on the permeability of the blood-brain barrier (BBB) were examined in mice with sodium fluorescein as an indicator of the permeability. The brain was perfused with saline 30 min after injection of sodium fluorescein (40 mg/kg, i. v.) and examined by fluorometry. Morphine hydrochloride (0.3–10 mg/kg, s. c.) markedly increased the brain level of sodium fluorescein dose-dependently without influencing the plasma level, when administered 20 min before sodium fluorescein injection. Intracerebroventricularly (i. c. v.) injected morphine hydrochloride (0.5 and 1.0 Erg) increased the brain sodium fluorescein level. Buprenorphine (0.1 and 0.5 mg/kg, s. c.) was also effective. However, pentazocine, ethylketazocine, U-50488H and SKF-10047 had no significant influence. The i.c.v. administration of [D-Ala2, McPhe4, Gly(ol)5]enkephalin (0.1 g) and [D-Ala2, D-Leu5]enkephalin (0.5 g) but not of [D-Thr2, Leu5]enkephalin-Thr increased the brain level of sodium fluorescein significantly. A small dose of naloxone (i. p.) significantly inhibited the effects of morphine, buprenorphine, [D-Ala2, McPhe4, Gly(ol)5]enkephalin and [D-Ala3, D-Leu5]enkephalin. ICI-174864 co-administered i. c. v. with [D-Ala2, D-Leu5]enkephalin was ineffective in antagonizing the effect of the latter. These findings suggest that the stimulation of µ opioid receptors results in an increase in BBB permeability to sodium fluorescein.
Send offprint requests to K. Saeki 相似文献
49.
S. C. Cheetham R. W. Horton 《Journal of neural transmission (Vienna, Austria : 1996)》1989,78(1):53-59
Summary The effects of different membrane preparations and assay conditions on [3H]5-HT binding to post-mortem human cortical tissue was studied. Optimal binding necessitated thorough removal of endogenous 5-HT and this was achieved either by hypotonic lysis or by preincubation of the membranes at 37C. Calcium chloride (4 mM) increased specific [3H]5-HT binding. The further addition of ascorbic acid (5.7 mM) or ascorbic acid and clorgyline (10 M) reduced specific [3H]5-HT binding. 相似文献
50.
P. W. L. Tas H. G. Kress K. Koschel 《Journal of neural transmission (Vienna, Austria : 1996)》1989,76(2):99-107
Summary We have studied the ion flux through the sodium channels of low passage number (<50p.) and high passage number (>150p.) neuroblastoma x glioma hybrid cells using [14C] guanidinium and specific neurotoxins to induce channel opening and closing. The sodium channels of low passage number hybrid cells could be opened by veratridine alone, suggesting the presence of voltage dependent channels in agreement with electrophysiological studies reported in the literature. The sodium channels of the high passage number hybrid cells, however, needed the synergistic action of veratridine and scorpion toxin for activation suggesting that these channels are silent. The [14C] guanidinium ion flux through the sodium channels of the high passage number hybrid cells was inhibited by significantly lower concentrations of the volatile anesthetics (halothane, isoflurane and enflurane) and the lcoal anesthetics (tetracaine and bupivacaine) than the comparable flux through the sodium channels of the low passage number hybrid cells.Dedicated to Prof. Dr. E. Wecker on the occasion of his 65th birthday. 相似文献