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Table I. Background of patients. Control GBF Gender M F ; 20 Height cm ; 165.62.2 167.61.6 Body weight kg ; 57.02.5 58.42.3 Age years ; 40.72.3 42.52.9 First attacked age years ; 31.92.0 34.52.9 Number of recurrence 6.00.9 5.41.4 a Clinical course C C: R 17: 20 12.
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3.1 The Fetal Interventions . 129 3.1.1 Capturing `Real Risks' in Obstetrics . 130 3.1.2 Antepartum Fetal Interventions. 132 3.1.2.1 Ultrasound Screening . 132 3.1.2.2 Amniocentesis . 133 3.1.3 Established Intrapartum Fetal Interventions . 134 3.1.3.1 Intermittent Auscultation . 134 3.1.3.2 Fetal Blood Sampling. 135 3.1.3.3 Fetal Scalp Stimulation . 136 3.1.3.4 Intrauterine Pressure Catheter . 137 3.1.4 New Intrapartum Fetal Interventions . 138 3.1.4.1 Fetal Pulse Oximetry. 138 3.1.4.2 STAN Methodology. 140 3.1.5 Electronic Intrapartum Fetal Interventions . 141 3.1.5.1 Continuous External EFM . 141 3.1.5.2 Intermittent External EFM . 141 3.1.5.3 Internal EFM . 142 3.1.6 Other Intrapartum Interventions. 143 3.1.6.1 Epidural Anaesthesia. 143 3.1.6.2 Vacuum Extraction . 144 3.2 Timing of Application of Different Fetal Interventions . 145 3.3 STUDY THREE: Obstetric Staffs' Risk Perceptions of Fetal Interventions . 146 3.3.1 Setting . 146 3.3.2 Participants. 147 3.3.3 Materials and Method . 147 3.3.3.1 Creating and Validating the Incident Scenarios. 147 3.3.3.2 Description of the Incident Scenarios . 147 3.3.3.3 The Risk Perception Rating Scales . 152 3.3.3.4 `Invasiveness' Hypotheses . 154 3.3.3.5 `Frequency of Use' Hypotheses . 155 3.3.3.6 The Questionnaire Design. 157 3.3.3.7 Participant Feedback . 159 vii and propulsid, for example, drug domperidone.
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Referenz 233 Neurologie, 11. Auflage ; Diaz Espejo CE, Villalobos Chaves F, Sureda Ramis B. Chronic intracranial hypertension secondary to neurobrucellosis. J Neurol 234: 59-61, 1987 Chronic intracranial hypertension in the presence of hydrocephalus and or arachnoiditis is a rare presentation of neurobrucellosis. The present case is exceptional because neither hydrocephalus nor arachnoiditis were present. Brucellosis was diagnosed by serological tests. The patient developed asthenia, anorexia, weight loss, violent headaches, explosive vomiting, bilateral papilloedema, diplopia with paralysis of the abducens nerves, left supranuclear facial paralysis and left hemiparesis. A skull radiograph showed destruction of the sella turcica. Rapid recovery was attained with the use of antibiotics. The pathogenesis of this intracranial hypertension syndrome with destruction of sella turcica is discussed.
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Abstract Excitatory amino acids, such as glutamate, constitute a major transmitter system in the control of hypothalamic pituitary secretion. Different subtypes of glutamate receptors, such as NMDA N-methyl-D-aspartic acid ; and KA kainate ; receptors, are involved in the control of anterior pituitary secretion. Other receptor subtypes, such as AMPA activated by acid ; and metabotropic receptors, have been identified, although their role in the control of neuroendocrine function remains largely unknown. Recent reports have demonstrated the involvement of AMPA receptors in the control of the steroidinduced luteinizing hormone LH ; surge in female and growth hormone GH ; secretion in male rats. The aim of this study was to assess the potential role of AMPA receptors in the control of GH, prolactin PRL ; , LH and follicle-stimulating hormone FSH ; secretion in prepubertal 23-day-old rats. To this end, prepubertal female rats were injected with AMPA 25 or 5 mg kg i.p. ; or the antagonist of AMPA receptors 1, 2, 3, f ; quinoxaline-7-sulfonamide NBQX; 025 or 050 mg kg i.p. ; . Serum LH and FSH concentrations and hypothalamic LH-releasing hormone LHRH ; content remained unchanged after AMPA or NBQX administration. In contrast, serum PRL levels significantly decreased 15, 30 and 60 min after i.p. administration of AMPA and increased 120 min after NBQX treatment, whereas serum GH levels increased after AMPA treatment and decreased after NBQX administration. Considering that AMPA has been shown to activate a subset of kainate receptors, its effects were compared with those elicited by 25 mg kg KA in prepubertal female rats. At this age, however, KA was unable to reproduce the effects of AMPA on PRL and GH secretion, thus suggesting that the actions observed after AMPA administration were carried out specifically through AMPA receptors. In addition, as the effects of AMPA on LH secretion in adult females have been proved to be steroid-dependent, the effects of AMPA 25 mg kg ; and NBQX 05 mg kg ; were tested in prepubertal animals with different gonadal backgrounds, i.e. intact males, and intact and ovariectomized OVX ; females. The effects of AMPA in prepubertal females appeared to be modulated by ovarian secretion, as the inhibition of PRL secretion disappeared and LH secretion was partially suppressed by AMPA in OVX animals whereas the stimulatory effect on GH release was enhanced by ovariectomy. Furthermore, in male rats, AMPA administration significantly decreased PRL secretion and increased serum GH levels, the amplitude of the GH response being higher than in prepubertal females. To ascertain the pituitary component for the reported actions of AMPA, hemi-pituitaries of male rats were incubated in the presence of AMPA 10 810 6 M ; . The results obtained showed no effect of AMPA on PRL, GH and gonadotropin secretion in vitro. Finally, we investigated the involvement of the dopaminergic DA ; system in the inhibitory action of AMPA on PRL secretion. Pre-treatment of prepubertal female rats with a dopamine receptor antagonist domperidone: 1 mg kg ; resulted in the blockage of AMPA-mediated inhibition of PRL secretion, thus suggesting that this action is probably mediated by an increase in DA activity. In conclusion, we provide evidence for the physiological role of AMPA receptors in the control of PRL and GH secretion in prepubertal rats. In contrast, our data cast doubts on the involvement of AMPA receptors in the regulation of gonadotropin secretion at this age. The effects of AMPA reported herein were not mediated through activation of kainate receptors and were probably exerted at the hypothalamic or suprahypothalamic levels. In addition, we show that ovarian secretion actively modulates the effects of AMPA receptor activation on anterior pituitary secretion in prepubertal female rats.
Absorption In fasting subjects, domperidone is rapidly absorbed after oral administration, with peak plasma concentrations at 30 to minutes. The low absolute bioavailability of oral domperidone approximately 15% ; is due to an extensive first-pass metabolism in the gut wall and liver. Although domperidone's bioavailability is enhanced in normal subjects when taken after a meal, patients with gastro-intestinal complaints should take domperidone 15-30 minutes before a meal. Reduced gastric acidity impairs the absorption of domperidone. Oral bioavailability is decreased by prior concomitant administration of cimetidine and sodium bicarbonate. The time of peak absorption is slightly delayed and the AUC somewhat increased when the oral drug is taken after a meal. Distribution Oral domperidone does not appear to accumulate or induce its own metabolism; a peak plasma level after 90 minutes of 21 ng after two weeks oral administration of 30 mg per day was almost the same as that of 18 ng after the first dose. Dom0eridone is 91 93% bound to plasma proteins. Distribution studies with radiolabelled drug in animals have shown wide tissue distribution, but low brain concentration. Small amounts of drug cross the placenta in rats. Metabolism Domperidon undergoes rapid and extensive hepatic metabolism by hydroxylation and Ndealkylation. In vitro metabolism experiments with diagnostic inhibitors revealed that CYP3A4 is a major form of cytochrome P-450 involved in the N-dealkylation of domperidone, whereas CYP3A4, CYP1A2 and CYP2E1 are involved in domperidone aromatic hydroxylation. Excretion Urinary and faecal excretions amount to 31 and 66% of the oral dose respectively. The proportion of the drug excreted unchanged is small 10% of faecal excretion and approximately 1 % of urinary excretion ; . The plasma half-life after a single oral dose is 7 9 hours in healthy subjects but is prolonged in patients with severe renal insufficiency and danocrine.
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301 Results The intramuscular injection of a standard dose of xylazine 2 mg kg, IM ; in saline group evoked vomiting incidence of 100% and mean latency of 2.8 1.0 min. All cats vomited most of the food they were fed. Dexamethasone completely prevented vomiting induced by xylazine in five of ten cats. On the other hand, pre-treatment with dexamethasone reduced incidence of xylazineinduced vomiting in the other five cats in this group, but did not delay significantly latency of vomiting Table 1 ; . In contrast, metoclopramide and acepromazine did not reduce incidence of xylazine-induced vomiting. The time until the onset of the first emetic episode mean SD ; was 2.8 1.0 minutes when the cats were administered saline. When the cats were administered dexamethasone, metoclopramide, and acepromazine prior to administration of xylazine, the time until the first emetic episodes p 0.05 ; were 6.5 1.7, 6.7 and 6.2 2.0 min, respectively. The number of episodes of emesis was 2.4 0.9 for the saline treatment. Emetic episodes occured only in five cats of the dexamethasone group. The number of episodes of emesis was 1.4 0.5 in five cats displaying emesis in the dexamethasone group p 0.05 ; . In all of the groups, xylazine caused CNS depression which was characterized by recumbency. The time until the onset of sedation was 6.8 2.3 min for saline treatment, and 8.2 1.4, 9.3 minutes for dexamethasone, metoclopramide and acepromazine, respectively. The time until the onset of sedation was found longer in the metoclopramide group, compared to others p 0.05 ; . Dexamethasone and acepromazine at the doses studied, and saline apparently did not alter the recumbency period induced by xylazine. However, pretreatment with metoclopramide delayed the latency period and also prolonged the sedation period p 0.05 ; after administration of xylazine. Discussion It was shown in the present study that a standard dose of xylazine 2 mg kg, IM ; induced vomiting in 100% of the cats, even when pre-treated with saline, metoclopramide 0.4 mg kg, IM ; , or acepromazine 0.1mg kg, IM ; . However, vomiting was induced only in 50% of the cats administered xylazine after pre- treatment with dexamethasone 4 mg kg, IM ; . Moreover, dexamethasone significantly reduced the episodes of vomiting in the remaining cats. These cats displayed only 1.4 0.5 episode of vomiting. These results were similar to the data obtained in a previous study on cats treated with xylazine Ho et al. 2001 ; . In previous studies, antagonist of 1-adrenoceptors prozasin or phenoxybenzamine ; , 1-adrenoceptors propranolol ; , dopaminergic receptors doperidone ; , muscarinic receptors atropine ; , 5-hydroxytryptamine3 receptors, opioid receptors naloxone ; and histamine receptors diphenhydramine ; did not prevent xylazine induced vomiting Hikasa et al. 1989; Lucot 1989; Hikasa et al. 1992a ; . These results suggested that the emetic action of xylazine is mediated by central 2- adrenoceptors in cats. The 2-adrenoceptor antagonist, yohimbine, prevented vomiting induced by xylazine Hikasa et al. 1989; Hikasa et al. 1992b ; . The antagonism of this specific 2-adrenoceptor is effective against xylazine-induced emesis, but it is also capable of antagonizing the sedative effect of xylazine Ho et al. 2001 ; . It was first reported in 1981 that dexamethasone is an effective antiemetic in cancer patients receiving chemotherapy Aapro and Alberts 1981 ; . Since then, several studies have documented that dexamethasone is effective in preventing emesis caused by chemothrerapy in humans Jones et al. 1991; Spector et al. 1998; Wang et al. 1999 ; , cats Rudd et al. 2000 ; , dogs Fukui and Yamamoto, 1999 ; ferrets Hawthorn and C u n 1990; R u d d and N a y 1996 ; , and pigeons T a n al. 2000.
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When used in conjunction with a low-calorie diet, data show that 77% of sibutramine-administered patients achieve a medically beneficial weight loss AQ ref of at least 5%. Importantly, continuation of therapy can sustain these weight losses for at least 2 years. Further, a recent meta-analysis has shown required that, in sibutramine-administered obese patients, subjects who achieved weight losses of over 4 kg in the first 3 months of treatment were more likely to achieve long-term weight loss maintenance if therapy was continued. This in turn, led to marked improvements in metabolic factors such as lipid profile, insulin sensitivity and hypertension and
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[3H]domperidone or [14C]phenytoin not shown ; . Even after a relatively short distribution period chosen to minimize the degree of metabolism, no substantial difference could be found 30 min, data not shown ; . As domperidon3 is a very good P-GP substrate in vitro, we think that this lack of apparent difference may be explained by the rapid metabolism of [3H]domperidone in the mouse. For instance, in male rats domperidone is rapidly metabolized, with plasma levels of labeled metabolites surpassing the level of unchanged drug 3 min after injection 22 ; . Clear support for a role of mdr1a P-GP in the pharmacological handling of domperidone came from an oral toxicity test of domperidone in mdr1a ; and ; mice. When dosages of 5, 10, 20, or 80 mg kg of domperidone were administered, the mdr1a ; mice at 20, 40, and 80 mg kg demonstrated a transient period of extreme passivity, crouched posture, and total lack of spontaneous movement or exploratory behavior, even when handled. This lasted from about 30 min to 2 h after administration, after which most mice gradually recovered one mouse at 80 mg kg maintained a crouched posture and died after 1.5 d ; . Effects were more intense and.
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The types of prescribing errors identified at the different stages are shown in Table 28. Errors grouped as "need for the drug" occurred more frequently on admission and discharge, in comparison with the other stages 2 325.1, df 3, p 0.0001 ; . This was most commonly due to drugs at admission not having been prescribed on the prescription chart, or drugs being left off discharge prescriptions. Errors grouped as "select dosage regimen" were significantly more common on admission and when rewriting prescription charts 2 55.6, df 3, p 0.0001 ; . On discharge prescriptions, for example, there were comparatively few prescriptions where a maximum dose was not cited; this occurred commonly for the other stages. Errors grouped as "administration of drug" were significantly less likely to occur during the hospital admission than at any other time 2 126.7, df 3, p 0.0001 ; . Again, on 87 and
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Twenty studies were identified that assessed the effect of EPO therapy on intermediate outcomes, including blood pressure effects, deterioration of kidney function, left ventricular geometry, kidney hemodynamics, levels of vasoactive substances, and nutritional status and quality of life. Of these, eight were randomized controlled trials, 26, 28-34 three were cohort studies, 35-37 and nine were before after studies.1, 38-45 Effects on hematopoietic outcomes or direct assessment of drug efficacy were not considered, but a number of studies that focused on such efficacy outcomes did provide evidence of EPO effects on other outcomes and were therefore considered. These are summarized in Evidence Table 1. No studies were identified that assessed mortality.
TABLE 1: Parameters Obtained From Density Measurements and Heckel And Kawakita Plots Heckel Plots Starch Binder conc. % w w ; 0.0 2.5 5.0 7.5 Corn Starch 2.5 5.0 7.5 Do 0.276 0.346 0.387 Py MN m2 ; 95.56 114.21 111.12 DA 0.863 0.772 0.802 DB 0.587 0.426 0.415 Kawakita Plots Pk MN m ; 3.212 2.661 2.583 Di 0.424 0.410 0.403.
Nal tract. Pharmacol Ther 1996; 69: 103-115 Meissner W, Schmidt U, Hartmann M, Kath R, Reinhart K. Oral naloxone reverses opioid-associated constipation. Pain 2000; 84: 105-109 Cheskin LJ, Chami TN, Johnson RE, Jaffe JH. Assessment of nalmefene glucuronide as a selective gut opioid antagonist. Drug Alcohol Depend 1995; 39: 151-154 Culpepper-Morgan JA, Inturrisi CE, Portenoy RK, Foley K, Houde RW, Marsh F, Kreek MJ. Treatment of opioid-induced constipation with oral naloxone: a pilot study. Clin Pharmacol Ther 1992; 52: 90-95 Yuan CS, Foss JF, O'Connor M, Toledano A, Roizen MF, Moss J. Methylnaltrexone prevents morphine-induced delay in oral-cecal transit time without affecting analgesia: a double-blind randomized placebo-controlled trial. Clin Pharmacol Ther 1996; 59: 469-475 Schmidt WK. Alvimopan * ADL 8-2698 ; is a novel peripheral opioid antagonist. J Surg 2001; 182 5A Suppl ; : 27S-38S Barquist E, Bonaz B, Martinez V, Rivier J, Zinner MJ, Tache Y. Neuronal pathways involved in abdominal surgery-induced gastric ileus in rats. J Physiol 1996; 270 4 Pt 2 ; R888-R894 Matsuda H, Li Y, Yamahara J, Yoshikawa M. Inhibition of gastric emptying by triterpene saponin, momordin, in mice: roles of blood glucose, capsaicin-sensitive sensory nerves, and central nervous system. J Pharmacol Exp Ther 1999; 289: 729-734 Fickel J, Bagnol D, Watson SJ, Akil H. Opioid receptor expression in the rat gastrointestinal tract: a quantitative study with comparison to the brain. Brain Res Mol Brain Res 1997; 46: 1-8 Rowbotham DJ, Nimmo WS. Effect of cisapride on morphineinduced delay in gastric emptying. Br J Anaesth 1987; 59: 536-539 Bianchi G, Ferretti P, Recchia M, Rocchetti M, Tavani A, Manara L. Morphine tissue levels and reduction of gastrointestinal transit in rats. Correlation supports primary action site in the gut. Gastroenterology 1983; 85: 852-858 Patil CK, Kulkarni SK. Effect of physostigmine and cisapride on morphine-induced delayed gastric transit in mice. Ind J Pharmacol 2000; 32: 321-323 Brogden RN, Carmine AA, Heel RC, Speight TM, Avery GS. Domperidone. A review of its pharmacological activity, pharmacokinetics and therapeutic efficacy in the symptomatic treatment of chronic dyspepsia and as an antiemetic. Drugs 1982; 24: 360-400 Pandolfino JE, Howden CW, Kahrilas PJ. Motility-modifying agents and management of disorders of gastrointestinal motility. Gastroenterology 2000; 118: S32-S47 Harrington RA, Hamilton CW, Brogden RN, Linkewich JA, Romankiewicz JA, Heel RC. Metoclopramide. An updated review of its pharmacological properties and clinical use. Drugs 1983; 25: 451-494 Murphy DB, Sutton JA, Prescott LF, Murphy MB. Opioid-induced delay in gastric emptying: a peripheral mechanism in humans. Anesthesiology 1997; 87: 765-770 Wong CL. Central and peripheral inhibitory effects of morphine on intestinal transit in mice. Exp Clin Pharmacol 1986; 8: 479-483 Pasricha PJ. Prokinetic agents, antiemetics and agents used in irritable bowel syndrome. In Hardman JG, Limbard LE, eds The pharmacological basis of therapeutics. McGraw-Hill, New York, 2001: 1021-1036 Pol O, Ferrer I, Puig MM. Diarrhea associated with intestinal inflammation increases the potency of mu and delta opioids on the inhibition of gastrointestinal transit in mice. J Pharmacol Exp Ther 1994; 270: 386-391 Benson MJ, Roberts JP, Wingate DL, Rogers J, Deeks JJ, Castillo FD, Williams NS. Small bowel motility following major intraabdominal surgery: the effects of opiates and rectal cisapride. Gastroenterology 1994; 106: 924-936 Kluger MT, Plummer JL, Owen H. The influence of rectal cisapride on morphine-induced gastric stasis. Anaesth Intensive Care 1991; 19: 346-350 De Winter BY, Boeckxstaens GE, De Man JG, Moreels TG, Schuurkes JA, Peeters TL, Herman AG, Pelckmans PA. Effect of different prokinetic agents and a novel enterokinetic agent on postoperative ileus in rats. Gut 1999; 45: 713-718.
Anti-nausea Treatment i ; ii ; iii ; Domperidoje also available over the counter as Motilium ; Metaclopramide prescription only ; Non-prescription medications are also available for problems with the digestive system e.g. Gaviscon. It may be helpful to take these along with painkillers. It is a good idea to see your doctor.
We speculated that the widened redox potential afforded by oxygen was so important for the evolution of biocomplexity that it must also form the basis for complex diseases. As an extension of this idea we hypothesized that artificial selection for low and high aerobic capacity would yield lines that contrasted for health risks associated with complex diseases. Eleven generations of selection produced lines that differed by 347% in running capacity. The low line demonstrated risk factors including higher visceral adiposity, blood pressure, insulin, free fatty acids, and triglycerides. The high line was superior for VO2max, economy of running, heart function, adaptation to exercise, and nitric oxide-induced vascular dilation. Consistent with these divides in subordinate likely-determinant phenotypes, the low line demonstrated lower abundance in soleus skeletal muscle for six proteins associated with mitochondrial energy transduction and cisapride.
Introduction Much of our Vitamin D is produced by the action of ultraviolet light on skin. Submariners are shielded from sunlight for prolonged periods during patrols, and a reduction in Vitamin D can be demonstrated. Vitamin D deficiency is associated with many infective, inflammatory and malignant diseases. An association between these states and raised matrix metalloproteinase 9 MMP9 ; has been observed in certain ethnic groups. Studies of mortality in submariners show no excess due to cardiovascular, respiratory, or malignant disease. However, submariners may be at increased risk of MMP9 moderated disease due to repeated, prolonged ultraviolet deprivation. Method 49 submariners deploying on patrol following winter ashore, and 43 shore side controls, gave informed consent for blood sampling for Vitamin D and MMP9. Samples were collected from both groups immediately before the patrol and again in the final week. Initial and final questionnaires were used to identify confounding factors. Early and late samples were batched in pairs for assay. Changes in Vitamin D and MMP9 concentrations were assessed. Results Vitamin D levels rose in the control group and fell in the submariners. Pre patrol MMP9 levels were similar in the two groups. In the later samples mean MMP9 doubled in submariners and did not rise in controls. Conclusions MMP9 levels rise in a screened healthy population during a submarine patrol. Further studies will indicate whether ultraviolet replacement or dietary supplementation prevents this rise.
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Figure 3 Frequency-independent human ether-a-go-go-related gene channel inhibition. a ; Representative current traces during pulse trains of indicated frequencies in the presence of domperidone 3 mM ; . The voltage protocol is the same as in Figure 2. Normalized peak current values are plotted vs pulse number for b ; domperidone; c ; bepridil 3 mM ; , E-4031 10 mM, every 10th pulse is shown ; and terfenadine 1 mM, every 10th current is shown ; . Lines represent fits to single exponential functions Ipeak A exp N Nconst ; Iss ; . The steepness parameters Nconst and steady-state levels are given in Table 1.
Figure 2. Effect of endophyte-infected fescue and domperidone treatment on serum progesterone levels in gravid mares. First detectable differences P .05 ; from pre-treatment levels are indicated by stars. Unless otherwise indicated, data points represent four mares per treatment dagger indicates number of mares in EF group ; . Mares which were not prepared for parturition seven days after the calculated date of parturition as determined by veterinary examination ; were relocated to endophyte-free pasture from Redmond, 1994.
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