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M J Carter, Division of Molecular and Genetic Medicine, Royal Hallamshire Hospital, Sheffield, UK A J Lobo, Gastroenterology and Liver Unit, Royal Hallamshire Hospital, Sheffield, UK S P L Travis, Gastroenterology Unit, John Radcliffe Hospital NHS Trust, Oxford, UK Correspondence to: Dr S Travis, Gastroenterology Unit, John Radcliffe Hospital NHS Trust, Oxford OX3 9DU, UK; simon.travis orh.nhs.
RNA isolation and Northern analysis. RNA was isolated from DF-1 cells and from mouse tissue using the RNeasy RNA isolation kit Qiagen ; . Northern blots were prepared as described Sambrook et al., 1989 ; . Probes used for Northern blot analysis were created using digoxigen-11-uridine 5h-triphosphate as described by the manufacturer Roche ; . Primers used to produce probes were : TA-48FR for gfp, TA-64FR for orfX, TA-56FR for SU and TA-60FR for env Table 1!
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[Phenoxybenxomine-Prostheses] Polarographical electrodes hydrogen clearance technique, 904 Polybrene neutralization for monitoring blood heparin levels, 95 Polycythemia progressive neurological deficits in primary, 100 Polycythemia vera arterial complications of, 996 Polymyalgia rheumatica clinical and biopsy findings, 478 Pons blood pressure changes in cerebrovascular diseases, 80 Pontine hematoma successful evacuation of acute, 96 Pontine lesions tracheostomies and stroke, 459 Pontine syndrome lateral inferior, 827 Population studies cerebral atherosclerosis in European populations, 898 cerebrovascular and cardiovascular diseases in Japanese fishing villages, 86 natural history of stroke in Rochester, Minn., 20 primary SAH in Iceland, 764 risk factors in stroke in Mexican patients, 773 TIAs and risk of stroke in elderly, 980 Postganglionic autonomic insufficiency cerebrovascular regulation, 12 Predisposing factors in children with stroke, 873 Preganglionic autonomic insufficiency cerebrovascular regulation, 12 Pregnancy in six patients with Starr-Edwards prostheses, 248 President's Page "Teaching Scholars: The Promise of Better Patient Care" Yu ; , 492 Pressure-flow relationships effects of blood gases on, in canine cerebral circulation, 65 lactate in cerebrospinal fluid and, in canine cerebral circulation, 207 Pressures differential pressures recorded in actue epidural expanding lesions, 347 intracranial. See Intracranial pressures intraocular pressure and common carotid occlusion, 705 perfusion. See Perfusion pressure Prevalence natural history of stroke in Rochester, Minn. 1955-69 ; , 20 Procainamide induced systemic lupus erythematosus, 249 Prognosis relationship of neurological status and angiographical evidence of spasm to prognosis, 973 strokes in children, 890 visual field defects and, 163 Propranolol effects on cerebral circulation, 50 hypertriglyceridemia and, 825 Prostaglandins effect on canine cerebral circulation, 356 effect on carotid arterial blood flow, CSF pressure and intraocular pressure, 706 experimental vasoconstriction of cerebral arteries, 248 inhibition and reversal of vasospasm induced by, 356 role in genesis of cerebral vasospasm 248 Prostheses autogenization of prostheses for small artery replacement 715 Beall valve, platelet survival: relation to low incidence of thromboembolism, 91 heparin-bound aminoethylcellulose as an antithrombogenic surface, 256 mitral valve: follow-up study, 816 Starr-Edwards cloth-covered composite seat, 820 long-term evaluation, 256 pregnancy in six patients with, 248 surface thrombogenicity of, 719 1073.
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NTIPARKINSONIAN drug trials have mainly focused on the substitution of the nigrostriatal dopaminergic deficit and have mainly resulted in improvement of parkinsonian motor symptoms. But insidious deteriorating neurodegeneration also affects other neurotransmitter systems and extranigral anatomical structures in patients with idiopathic Parkinson disease PD ; .1 Thus, the neurodegenerative process causes onset of a wide heterogeneous variety of parkinsonian features, all of which limit quality of life.2 Therefore, compounds with a complex pharmacological profile, which also influences neurotransmission beyond the dopaminergic system, may hypothetically provide an additional therapeutic benefit in patients with PD. Budipine represents such a drug, because it also influences, for instance, GABAergic, norepinephrinergic, serotoninergic, and cholinergic neurotransmission.3-7 Eltze8 provides a review. Previous clinical trials9-12 have demonstrated the therapeutic efficacy of budipine on motor symptoms in subjects with PD who receive an insufficient antiparkinsonian drug regimen. Przuntek and Muller13 provide a review. The objective of this multicenter and procaine.
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Gully. Lengths were measured directly from the MOC images and therefore along-slope lengths may be slightly longer than reported here since these features are found on sloped terrain. The length of the alcoves was measured from the alcove head to the alcove base. Channel lengths were measured from the alcove base to the beginning of the debris apron or until the channel ended if there was no clear debris apron. The horizontal extent of the debris apron was measured from the head of the apron to the debris apron end. The range of gully orientations was measured for each gully system within an image. Gully orientations were measured from the map projected MOC images along the gully axis formed by the alcove-channel-debris apron structure with respect to the geographic pole. We estimate that elevations derived from MOLA data and lengths derived from MOC data are both typically accurate to 10 m. The vertical accuracy of MOLA is 1.5 m Zuber et al., 1992 ; and elevation maps were created at 50 m contour intervals; smaller contour intervals proved impractical due to the high density of contours obscuring the gully slopes. The horizontal accuracy of MOLA is 100 m which is smaller than the 160 m diameter MOLA footprint Zuber et al., 1992; Kirk et al., 2001b ; . Hence, our elevation uncertainty is mainly an artifact of our contour map interpolation. Horizontal length uncertainties are governed by the lowest image resolution of 10 m pixel. TES thermal inertia and albedo measurements are valuable in characterizing the surface and subsurface temperature environment, and were extracted from 1 20 resolution binned maps Mellon et al., 2000, 2002 ; for each MOC image containing gullies. TES resolution is significantly lower than the scale of individual gullies; a single TES footprint is about the same as the width of an entire MOC image. Thermal inertia and albedo values are therefore representative of the general terrain surrounding the gully systems and procarbazine.
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Oxygen Indication: 1 ; Hypoxemia and or respiratory distress 2 ; Carbon monoxide poisoning 3 ; Shock Dosage: 100% by nonrebreather mask initially or endotracheal tube; wean as tolerated. Note: The administration of supplemental oxygen should be considered during EVERY pediatric emergency. Pancuronium Indication: 1 ; Neuromuscular blockade to facilitate mechanical ventilation 2 ; Emergency intubation Dosage: IV: 0.1 mg kg Note: This drug does not alter the level of consciousness or provide analgesia or amnesia. Note: This agent can be used when succinylcholine is contraindicated. Pancuronium is a long-acting neuromuscular blocker that requires ventilatory assistance for at least 1 hour. Satisfactory conditions for endotracheal intubation will generally occur 2 to 3 minutes after administration. WARNING: Ventilatory support will be necessary. Personnel with skills in advanced airway management must be present and prepared to respond when this agent is administered. Age-appropriate equipment for suctioning, oxygenation, intubation, and ventilation should be immediately available. Phenobarbital Indication: Status epilepticus Dosage: IV: 20 mg kg. Maximum dose, 1000 mg. Repeat dose once if necessary for clinical effect after 15 minutes. WARNING: There is an increased incidence of apnea when combined with other sedative agents. Be prepared to provide respiratory support. Monitor oxygen satura Phenylephrine Indication: Infundibular spasm "Tet Spell" ; Dosage: 5 to 20 push then followed by infusion at 0.1 to 5.0 g kg min. WARNING: Blood pressure must be carefully followed and dose titrated to effect. Phenytoin Indication: Status epilepticus Dosage: IV: 10 to 20 mg kg initial dose. Maximum initial dose, 1000 mg. Maximum rate of administration, 50 mg min or 1 mg kg min, whichever is less. Note: The lower dose is indicated in neonates because of increased risk of toxicity due to decreased protein binding. Should be diluted in normal saline to avoid precipitation. WARNING: Rate of infusion should not exceed 0.1 mL of undiluted preparation per kg min. Heart rate should be monitored and the rate of infusion reduced if the heart rate decreases by 10 beats minute. Procainamide Indication: Wide complex tachycardia Dosage: IV: Start at 3 to mg kg dose over 5 minutes not to exceed 100 mg to a titrated maximum of 15 mg kg loading dose. Maintenance dose, 20 to 80 g min 0.02 to 0.08 mg kg min maximum, 2 g 24 h. WARNING: If 50% QRS widening or hypotension occurs during loading dose, the remainder of the loading dose is held, and the maintenance dose is delayed until these signs have resolved. Propranolol Indication: Infundibular spasm "Tet Spell" ; Dosage: IV: 0.01 to 0.02 mg kg per dose infused over 10 min in 5% dextrose in water. Maximum initial dose, 1.0 mg Note: Oxygen should be administered first. Morphine is also an effective treatment for infundibular spasms. Phenylephrine is another adjunct for reversal of infundibular spasm. Use is contraindicated in congestive heart failure. Avoid in patients with a history of bronchospasm. Prostaglandin E1 Indication: Possible ductal-dependent cardiac malformation in the neonatal period Dosage: 0.05 to 0.10 g kg min as an infusion in 5% dextrose in water. Note: Preparation of infusion solution: 250 g in 80 D5W infuse at 1 mL 0.05 g kg min. WARNING: Apnea, hyperthermia, and seizures may occur. Be prepared to provide respiratory support. Monitor oxygen saturation.
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Cardiac toxicity — although some of the cardiac side effects of procainamide can be seen at therapeutic levels, a variety of more serious and potentially lethal effects are more common at toxic plasma levels above 30 mg l for procainamide plus its major metabolite n-acetylprocainamide versus a therapeutic range of 4 to mg l for procainamide alone.
Acquired long QT syndrome LQTS ; is induced by various pharmacological agents that prolong ventricular repolarization. Quinidine Bauman et al., 1984; Jenzer and Hagemeijer, 1976; Roden et al., 1986 ; , disopyramide Kurita et al., 1997 ; and procainamide Singh et al., 1995 ; which are class Ia antiarrhythmic agents, and sotalol Singh et al., 1995 ; , dofetilide Torp-Pedersen et al., 1999 ; and amiodarone Skanes et al., 1997 ; , which are class III antiarrhythmics, prolong ventricular repolarization as part of their anticipated pharmacological ac1 To whom correspondence should be addressed. Fax: E-mail: Yamamoto Keiji takeda.co.jp and prohibit.
Wild-type, db m, and db db mice stock number 000697 ; were purchased from Jackson Laboratories Bar Harbor, ME ; . As noted in the Jackson Laboratories database : jaxmice.jax jaxmice-cgi jaxmicedb ; , the nomenclature of these db db mice has changed. They are now identified as B6.Cg-m Leprdb J or Leprdb, but they formerly were designated as C57BL 6J-m Leprdb. The heterozygote Leprdb ; will be referred to as db and the wild type Lepr ; as WT. The three groups were allowed free access to chow and water. The db db mice, at 8 10 wk age, manifested hyperglycemia and glycosuria, as well as striking weight gain db db mice at 10 wk weigh about 45 g, with blood glucose 14 mM ; vs. the WT and db m mice weighing about 33 and 25 g, respectively, with blood glucose 6 mM.
NAPA renal clearance to creatinine clearance decreased by 10% range: 2 to 21% ; . Cotreatment with the fluoroquinolone antibiotics did not significantly change the pharmacodynamic parameters of electrocardiogram intervals, heart rate, or blood pressure compared to the control values. When potential drug interactions are addressed in patient care settings, clinicians often fail to recognize that significant renal drug interactions occur. The organic anion transport OAT ; and organic cation transport OCT ; systems are two of the major families of renal drug transport systems in humans. Procainamide and NAPA are organic cations, are transported by OCT in the kidney, and undergo significant active secretion in the proximal tubule 7, 12, 17 ; . Typically, the renal clearances of these two drugs are approximately two to three times the concurrent glomerular filtration rate in humans 4, 5, 18 ; . Procainamide is a substrate for human OCT1, OCT2, and OCT3 transporters 12 ; . The pattern of drug interactions with procainamide and NAPA are consistent with this mechanism of renal drug excretion. For example, both cimetidine and trimethoprim can cause clinically significant drug interactions with procainamide 4, 8, 10, ; . Interestingly, levofloxacin and ciprofloxacin are zwitterions, and so they potentially could be transported by either the OCT or the OAT system. Both undergo significant active secretion in the proximal renal tubule 14 ; . At present, the transport systems involved in the renal disposition of these drugs are not completely understood. Levofloxacin has been reported to be a substrate for rat OCT2 and OAT-K2 7 ; . Renal drug transport of levofloxacin is inhibited by both cimetidine and tetraethylammonium, suggesting that OCT is involved in its elimination 21 ; . Ciprofloxacin renal drug transport is inhibited by azlocillin and famotidine, implying that both the OAT and OCT systems are concerned with its elimination 1, 2 ; . Ofloxacin has been reported to interact with procainamide in humans, and so the potential for a drug interaction with levofloxacin exists 15 ; . When nine healthy adults were administered ofloxacin 400 mg orally twice daily for five doses ; and and prolixin.
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Fig. 8. a ; Fourier-deconvoluted and fitted infrared spectra in the amide I region solid lines ; with individual Gaussian components broken lines ; of cAb-R2 and cAb-HuL6 inset ; . IR spectra were recorded at atmospheric pressure 0.1 MPa ; and 25C, using protein concentrations of about 50 mg mL-1 3.6 mM ; in 1 13C-urea and 10 mM TrisDCl, pD 7.6; b ; Pressure-induced unfolding curves of cAb-R2 followed by IR measurements. The absorbance at 1636 cm-1, the wavenumber corresponding to the maximum in absorbance inset 1 ; , and the amide I bandwidth inset 2 ; were used to monitor VHH unfolding. The solid lines represent the best fits of the data to Equation 3, as calculated from the parameters in Table 4. In each case, the value of the refolded state is indicated open circles c ; FTIR spectra of cAb-R2 and cAb-HuL6 under native 0.1 MPa; continuous line ; , unfolding 1060 MPa, dotted line ; and refolding 0.1 MPa; broken line ; conditions.
Heim, VerlagChemice, 1980, pp 445-459. students, residents, and attending physicians about opiate abuse. J Med Educ 59: 501"507, 31. FoleyKM: Painsyndromesin patientswith cancer, in Bonica JJ, Ventafridda V eds ; : Ad 1984. 15. Charap AD: The knowledge, attitudes and vances in Pain Research and Therapy, vol 2, experienceof medicalpersonneltreatingpain in 1978. 16. Marks RM, Sachar EJ: Undertreatmentof and propantheline.
60. J. H. Cavanaugh, E. P. Winters, A. Cohen, C. S. Locke, and R. Braeckman: Lack of effect of lansoprazole on steady state warfarin metabolism. Gastroenterology 100 Suppl. ; , A40 abstr. ; 1991 ; . 61. W. A. Simon, C. Budingen, S. Fahr, B. Kinder, and M. Koske: The H , K -ATPase inhibitor pantoprazole BY1023 SK&F96022 ; interacts less with cytochrome P450 than omeprazole and lansoprazole. Biochem. Pharmacol. 42, 347355 1991 ; . 62. J. R. Halpert, F. P. Guengerich, J. R. Bend, and M. A. Correia: Contemporary issues in toxicology: selective inhibitors of cytochromes P450. Toxicol. Appl. Pharmacol. 125, 163175 1994 ; . 63. J. O. Miners, M. E. Veronese, and D. J. Birkett: In vitro approaches for the prediction of human drug metabolism. Ann. Rept. Med. Chem. 29, 307316 1994 ; . ` 64. M. Bourrie, V. Meunier, Y. Berger, and G. Fabre: Cytochrome P450 isoform inhibitors as a tool for the investigation of metabolic reactions catalyzed by human liver microsomes. J. Pharmacol. Exp. Ther. 277, 321332 1996 ; . 65. A. D. Rodrigues: Use of in vitro human metabolism studies in drug development. An industrial perspective. Biochem. Pharmacol. 48, 21472156 1994 and procainamide.
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1. Beutler E, Felitti VJ, Koziol JA, Ho NJ, Gelbart T. Penetrance of the 845G3A C282Y ; HFE hereditary hemochromatosis mutation. Lancet. 2002; 359: 211218. Fargion S, Valenti L, Dongiovanni P, et al. Tumor necrosis factor alpha promoter polymorphisms influence the phenotypic expression of hereditary hemochromatosis. Blood. 2001; 97: 3707-3712. George DK, Ramm GA, Walker NI, Powell LW, Crawford DHG. Elevated serum type IV collagen: a sensitive indicator of the presence of cirrhosis in haemochromatosis. J Hepatol. 1999; 31: 47-52 and protopic
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