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M Daniel

Publications and source records attributed to M Daniel.

At least 91 records · Page 5Linked to original sources

Ulcerative colitis in Oman. A prospective study of the incidence and disease pattern from 1987 to 1994.

OBJECTIVE: Inflammatory bowel disease has been reported to have varying frequencies in different parts of the world, and there seem to be significant differences in the disease pattern and clinical course in cases of ulcerative colitis (UC). The aim of the present study was to assess the incidence and disease pattern of UC in Oman. METHOD: A prospective study, over a period of 8 years (1987-1994), was performed to study 108 patients found to have UC. RESULTS: The annual incidence of UC was 1.35/100,000. The disease was mainly seen in the middle and upper middle class group, and the majority were nonsmokers or exsmokers. There was no significant difference in the incidence of the disease between nationalities or sexes. Total colitis was seen in 18%, and a significant number had disease extending up to the splenic flexure. Proctitis was seen in 8%. Although, the extent of the disease was similar to reports from the West, these patients had fewer hospital admissions, blood transfusions and none of them suffered local complications such as toxic dilatation, perforation or severe bleeding. Sclerosing cholangitis occurred in 2 patients. Patients were followed up for a maximum period of up to 7 years after diagnosis and none developed dysplasia or cancer. Three patients had surgery mainly for failure of medical treatment. CONCLUSIONS: From this report it seems that UC occurs in Oman at a lower frequency compared to the West. Although, the extent of the disease was similar to Europeans, these patients had less severe disease with fewer complications.

Adolescent↗

Neuroprotective effects of RPR 104632, a novel antagonist at the glycine site of the NMDA receptor, in vitro.

The NMDA antagonist and neuroprotective effects of RPR 104632 (2H-1,2,4-benzothiadiazine-1-dioxide-3-carboxylic acid), a new benzothiadiazine derivative, with affinity for the glycine site of the NMDA receptor-channel complex are described. RPR 104632 antagonized the binding of [3H]5,7-dichlorokynurenic acid to the rat cerebral cortex, with a Ki of 4.9 nM. This effect was stereospecific, since the (-)-isomer was 500-fold more potent than the (+)-isomer. The potent affinity of RPR 104632 for the glycine site was confirmed by the observation that RPR 104632 inhibited [3H]N-[1-(2-thienyl)cyclohexyl]-3,4-piperidine ([3H]TCP) binding in the presence of N-methyl-D-aspartate (NMDA) (IC50 = 55 nM), whereas it had no effect on the competitive NMDA site or on the dissociative anaesthetic site. RPR 104632 inhibited the NMDA-evoked increase in guanosine 3',5'-cyclic monophosphate (cGMP) levels of neonatal rat cerebellar slices (IC50 = 890 nM) in a non-competitive manner and markedly reduced NMDA-induced neurotoxicity in rat hippocampal slices and in cortical primary cell cultures. These results suggest that RPR 104632 is a high-affinity specific antagonist of the glycine site coupled to the NMDA receptor channel with potent neuroprotective properties in vitro.

Aminoquinolines↗

Sevoflurane.

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Anesthetics, Inhalation↗

Digestibilities of energy, protein, fat and nonstarch polysaccharides in a low fiber diet and diets containing coarse or fine whole meal rye are comparable in rats and humans.

The apparent digestibility of energy, protein, fat and nonstarch polysaccharides (NSP) of a low fiber diet and two high fiber diets containing coarse or fine whole meal rye bread was studied in experiments with humans and rats. Human subjects consumed the experimental diets for 3 wk each in a 3 x 3 cross over design. For the rat diets, duplicate portions of the foods consumed by the human subjects were mixed together, freeze dried and ground. There was a good agreement in the digestibility of energy (humans: 94.7 +/- 0.9, 91.2 +/- 1.2 and 91.6 +/- 1.4%; rats: 95.0 +/- 0.8, 92.5 +/- 1.4 and 91.7 +/- 1.8%) and fat (humans: 95.2 +/- 1.5, 94.4 +/- 1.0 and 94.8 +/- 2.5%, rats: 95.4 +/- 0.9, 94.0 +/- 0.4 and 94.0 +/- 0.4%) for the low fiber diet and the diets containing coarse or fine whole meal bread, respectively. Apparent and true digestibility of protein was consistently lower (P < 0.0001) in humans (apparent digestibility: 90.6 +/- 1.5, 86.2 +/- 1.4 and 86.3 +/- 2.3%; true digestibility: 95.1 +/- 1.5, 90.7 +/- 1.4 and 90.8 +/- 2.2%) than in rats (apparent digestibility: 92.3 +/- 1.1, 89.4 +/- 0.9 and 88.9 +/- 1.0%; true digestibility: 98.3 +/- 1.1, 94.9 +/- 0.9 and 94.2 +/- 1.0%) for all three diets. The digestibility of NSP tended to be lower (P < 0.066) in rats than in humans for the diet containing fine whole meal bread (rats: 59.6 +/- 8.0%, humans: 68.0 +/- 5.2%) and the low fiber diet (rats: 72.1 +/- 10.8%; humans: 80.5 +/- 7.1%), whereas it was similar in both species for the diet containing the coarse whole meal bread (rats: 66.1 +/- 6.0%; humans: 65.8 +/- 9.3%). In spite of some differences in digestibility values, our results suggest that the rat is a suitable model for humans to predict digestibility of nutrients in mixed diets containing cereal fiber sources.

Adult↗

Propofol fails to attenuate the cardiovascular response to rapid increases in desflurane concentration.

BACKGROUND: A rapid increase in desflurane concentration to greater than 1 MAC transiently increases heart rate, arterial blood pressure, and circulating catecholamine concentration. Because propofol decreases sympathetic outflow, it was hypothesized that propofol would blunt these responses. METHODS: To test this hypothesis, five healthy male volunteers were studied three times. After induction of anesthesia with 2 mg.kg-1 propofol, anesthesia was maintained with 4% end-tidal desflurane in oxygen (0.55 MAC) via an endotracheal tube for 32 min. On separate occasions, in random order, either no propofol or 2 mg.kg-1 propofol was administered either 2 or 5 min before increasing end-tidal desflurane concentration from 4% to 8%. RESULTS: Without propofol pretreatment, the increase to 8% desflurane transiently increased heart rate (from 63 +/- 3 beats/min to 108 +/- 5 beats/min, mean +/- SEM; P < 0.01), mean arterial pressure (from 73 +/- 1 mmHg to 118 +/- 6 mmHg; P < 0.01), and epinephrine concentration (from 14 +/- 1 pg.ml-1 to 279 +/- 51 pg.ml-1; P < 0.05). There was no significant change in norepinephrine concentration (from 198 +/- 37 pg.ml-1 to 277 +/- 46 pg.ml-1). The peak plasma epinephrine concentration was attenuated by each propofol pretreatment (158 +/- 35 pg.ml-1, propofol given 2 min before, and 146 + 41 pg.ml-1, propofol given 5 min before; P < 0.05), but neither propofol pretreatment modified the cardiovascular or norepinephrine responses. CONCLUSIONS: Although able to blunt the increase in epinephrine concentration, propofol 2 mg.kg-1 propofol does no attenuate the transient cardiovascular response to a rapid increase in desflurane concentration to greater than 1 MAC.

Adult↗

Sympathetic nervous system does not mediate reflex pupillary dilation during desflurane anesthesia.

BACKGROUND: Pupil size is determined by an interaction between the sympathetic and parasympathetic divisions of the autonomic nervous system. Noxious stimulation dilates the pupil in both unanesthetized and anesthetized humans. In the absence of anesthesia, dilation is primarily mediated by the sympathetic nervous system. In contrast, pupillary dilation in cats given barbiturate or cloralose anesthesia is mediated solely by inhibition of the midbrain parasympathetic nucleus. The mechanism by which noxious stimuli dilate pupils during anesthesia in humans remains unknown. Accordingly, the authors tested the hypothesis that the pupillary dilation in response to noxious stimulation during desflurane anesthesia is primarily a parasympathetic reflex. METHODS: In six volunteers, the alpha-I adrenergic receptors of the iris musculature were blocked by unilateral administration of topical dapiprazole; six other volunteers were given unilateral topical tropicamide to block the muscarinic receptors in the iris. Desflurane anesthesia was subsequently induced in all volunteers. Sympathetic nervous system activation, with reflex dilation of the pupil, was produced by noxious electrical stimulation during 4% and 8% end-tidal desflurane, and by a rapid 4%-to-8% step-up in the desflurane concentration. Pupil diameter and the change in pupil size induced by a light stimulus (light reflex amplitude) were measured with infrared pupillometry. RESULTS: Dapiprazole drops produced a Horner's miosis, but pupils were equally small after induction of anesthesia. Pupillary dilation after noxious stimulation and desflurane step-up was identical in the unblocked and dapiprazole-blocked pupils. After tropicamide administration, the pupil was dilated and the light reflex was completely inhibited. Noxious stimulation nonetheless produced a slight additional dilation. CONCLUSIONS: During desflurane anesthesia, pupillary dilation in response to noxious stimulation or desflurane step-up is not mediated by the sympathetic nervous system (as it is in unanesthetized persons). Although inhibition of the pupillo-constrictor nucleus may be the cause of this dilation, the mechanism remains unknown.

Administration, Topical↗

Diabetes and Canada's aboriginal peoples: the need for primary prevention.

The high prevalence of non-insulin-dependent diabetes mellitus (NIDDM) in Canada's native communities corresponds with high diabetes prevalence rates in other populations of indigenous peoples that have undergone changes associated with acculturation. Behavioural risk factors can be particularly amenable to public health action. There exists a need to develop, implement and test in collaboration with native people, interventions aimed at reducing the incidence and impact of NIDDM, by reducing the risk of its onset, and by early detection and treatment. Intervention programmes should be conceived with sensitivity to the overall health, social, economic, educational and cultural environment within a community. Although this review focuses specifically on diabetes in Canada, many of the points relating to the need for primary prevention of the disease will be appropriate in other situations.

Acculturation↗

Sequential emergence of multi-resistant Klebsiella pneumoniae in Bahrain.

During the mid-1980s, nosocomial infections due to aminoglycoside-resistant Klebsiella pneumonia were prevalent in the intensive care unit (ICU) of the Salamanya Medical Centre, Bahrain. In an attempt to control the spread of such organisms, the third-generation cephalosporins were introduced in early 1987. Subsequently there was a marked increase in the incidence of cephalosporin resistance among Klebsiella spp. isolated in the ICU. In 1990, over 60% of Klebsiella isolates were resistant to both cephalosporins and aminoglycosides. Cephalosporin resistance was due to production of extended-spectrum beta-lactamases encoded on the same plasmid as aminoglycoside resistance. The incidence of cephalosporin resistance declined during 1991-1992, which was coincident with severe restrictions on the use of third-generation cephalosporins and the preferential use of ciprofloxacin and imipenem for nosocomial klebsiella infections. Sequential overuse of aminoglycosides and cephalosporins for nosocomial klebsiella infection may select for organisms resistant to both classes of antibiotics.

Aminoglycosides↗

Fentanyl, clonidine, and repeated increases in desflurane concentration, but not nitrous oxide or esmolol, block the transient mydriasis caused by rapid increases in desflurane concentration.

Initial, but not subsequent, inhalation of 8% desflurane produces transient sympathetic stimulation. We hypothesized that initial but not subsequent increases should produce pupil dilation, and that N2O, fentanyl, and clonidine, but not esmolol, should blunt the response. In 10 volunteers, we maintained anesthesia with 4% end-tidal desflurane in oxygen for 32 min, then increased the concentration to 8% for 10 min. In nine of the volunteers, we twice repeated the increase to 8%, separating each increase by a 32-min period at 4%. On separate days, five volunteers received 4%-8% desflurane in 60% N2O; five received fentanyl 1.5 micrograms/kg or 4.5 micrograms/kg intravenously 5 min before 4%-8% desflurane; four received clonidine 4.3 micrograms/kg, orally, 90 min before 4% to 8%; and four received esmolol 0.75 mg/kg, intravenously, 1.5 min before 4%-8%. Without other drugs present, 4%-8% desflurane transiently increased pupil diameter to 5.4 +/- 0.5 mm (mean +/- SD), with subsequent 4%-8% increases producing attenuated responses (2.9 +/- 1.5 and 3.2 +/- 1.8 mm). N2O produced a higher peak (6.2 +/- 0.7 mm). Fentanyl 1.5 micrograms/kg and 4.5 micrograms/kg decreased peak diameter (2.3 +/- 0.9 and 1.6 +/- 0.3 mm), as did clonidine (2.3 +/- 1.7 mm) but not esmolol. We conclude that, concurrent with sympathetic stimulation, an initial rapid increase in desflurane concentration transiently increases pupil diameter, whereas repeated increases produce attenuated responses. N2O augments, fentanyl and clonidine attenuate, and esmolol does not affect the response.

Administration, Inhalation↗

Cardiovascular stimulation induced by rapid increases in desflurane concentration in humans results from activation of tracheopulmonary and systemic receptors.

BACKGROUND: It was hypothesized that stimulation of rapidly adapting airway receptors produces the transient (2-4 min) circulatory responses to rapid increases in desflurane concentrations greater than 6%. Accordingly, it was reasoned that increasing the concentration of desflurane in one lung, without altering the concentration of desflurane in systemic blood, should cause cardiovascular stimulation, whereas once the airway receptors had adapted to the stimulation, an initial increase in the systemic concentration of desflurane should have little effect. METHODS: After placement of a double-lumen endotracheal tube in four volunteers and establishment of a steady-state level of 4% desflurane in both lungs, the desflurane concentration was rapidly increased from 4% to 8% in one lung while decreasing it in the other, thereby obviating any increase in the systemic desflurane blood concentration (confirmed by analysis). After returning the desflurane end-tidal concentration to 4% in both lungs, this process was repeated for the contralateral lung thereby having exposed both lungs to 8% desflurane without increasing the systemic desflurane concentration. After returning desflurane concentration to 4%, it was increased in both lungs simultaneously to 8% and consequently in blood to 8% of an atm. RESULTS: Rapid increases in desflurane concentrations in either lung, but not blood, significantly increased heart rate (17 +/- 5 beats/min, mean +/- SE, P < 0.05) and mean arterial blood pressure (15 +/- 5 mmHg, P < 0.05), but a greater increase in heart rate (43 +/- 5 beats/min, P < 0.05) and mean arterial blood pressure (46 +/- 11 mmHg, P < 0.05) occurred when both lungs were exposed simultaneously to rapidly increased desflurane concentration for the second time within 90 min. This result did not differ from the increase occurring on another day when both lungs and blood were exposed for the first time that day to 8% desflurane (heart rate 40 +/- 7 beats/min, P = 0.8; mean arterial blood pressure 40 +/- 3 mmHg, P = 0.5). CONCLUSIONS: It was concluded that at least two sites respond to a rapid increase in desflurane concentrations greater than 6%: one site in the airways and/or lungs, and at least one other in a highly perfused tissue(s). The systemic site contributes more importantly.

Adult↗

Epidural diamorphine. A comparison of bolus and infusion administration in labour.

In a randomly allocated double blind study of 54 primigravidae, we examined the relative efficacy of the addition of diamorphine 3 mg to either an initial bolus or an infusion of bupivacaine. Both groups received an initial bolus of 10 ml of bupivacaine 0.25% followed by an infusion of bupivacaine 0.1% at 10 ml.h-1. Group 1 received diamorphine 3 mg in the bolus and group 2 received diamorphine 3 mg in the initial 100 ml of infusion solution. Both groups had comparable total bupivacaine requirements. Analgesia, assessed by visual analogue scores, was superior at 7h in group 2, but was similar at all other times. Sedation scores were significantly lower in group 2 for the first 3h and the incidence of nausea was significantly lower in group 2. The addition of diamorphine, whether as a bolus or added to an infusion of bupivacaine, results in similar quality of analgesia, but there is a reduction in side effects when diamorphine is administered in an infusion.

Adult↗

Maternal position during induction of spinal anaesthesia for caesarean section. A comparison of right lateral and sitting positions.

Forty women presenting for elective Caesarean section under spinal anaesthesia were randomly assigned to have anaesthesia induced in either the sitting or right lateral positions; 2.5 ml 0.5% hyperbaric bupivacaine was injected over 10 s before the mother was placed in a supine position with a 20 degree lateral tilt. The onset time and height of the subsequent analgesic and anaesthetic block was measured. It took longer to site spinal needles in the lateral position (240 vs 115 s, p < 0.001). There was a faster onset of sensory block to the sixth thoracic dermatomal level (8 vs 10 min, p < 0.001), in the lateral group, although onset time to T4 was comparable. There was no difference in maximum block height or degree of motor block. Mothers in the lateral group required more ephedrine in the first 10 m after siting the spinal (13.5 vs 10.5 mg, p < 0.05).

Adult↗