Self-revealing events and interpersonal evaluations.
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Biomedical subjects
Publications and source records attributed to S C Jones.
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Eighty-five patients with non-organic abdominal pain, were interviewed with the help of a questionnaire. Those who responded to a high fibre diet were excluded from the study. Twenty-seven patients had multiple pains and 58 described a single pain, which was intermittent in 39. A detailed analysis of the symptoms and family history of the latter group suggested that in 19 patients the symptoms might have been caused by abdominal migraine. Six of these 19 had typical migraine-associated symptoms during the attack, characteristic abdominal pain and a family or personal history of classical migraine. Abdominal migraine should be considered in patients with non-organic abdominal pain where symptoms are not typical of irritable bowel syndrome and when organic disease has been excluded.
To investigate the relationship between serum concentrations of interleukin-8 (IL-8) and disease activity in inflammatory bowel disease, serum IL-8 concentrations were measured by enzyme-linked immunosorbent assay (ELISA) in 93 patients. Interleukin-8 levels were compared with plasma interleukin-6 (IL-6) levels in 80 of these patients. Interleukin-8 levels were also measured in ten patients with active Crohn's disease, before and after treatment with a defined formula polymeric diet. Of these patients, 70 out of 93 IL-8 concentrations were below the detection limit of the assay. Levels were higher in patients with active ulcerative colitis (median < 20 pg/mL, 75th centile value = 190) compared with inactive disease (median and 75th centile value < 20; P < 0.05). Interleukin-8 concentrations correlated with a combined score for disease severity and extent (P = 0.01). Thirty-eight per cent (8/20) of patients with active Crohn's disease also had high levels of IL-8 but there was no significant difference between active and inactive disease. There was no correlation between serum IL-8 and plasma IL-6; on the contrary, very few patients had raised blood levels of both cytokines. In the diet treated group, serum IL-8 fell significantly after treatment (median = 37 pg/mL, range < 20-4615 before treatment, median < 20, range < 20-104 after treatment; P = 0.03). The results suggest that although IL-8 may be involved in the inflammatory process in inflammatory bowel disease, it is a poor marker of disease activity.
Focal ischemia was produced in cat brain by occluding the middle cerebral artery. After 60 min of ischemia the rate of glucose utilization, as measured by the uptake of [14C] deoxyglucose ([14C]DG), was correlated with tissue levels of ATP, phosphocreatine, and lactate measured in the same regional samples. Ischemia caused local increases of [14C]DG uptake which were associated with mild to moderate anaerobic perturbations of metabolite levels. Altered metabolite levels also occurred in regions in which the rate of glucose consumption was not markedly different from that of the non-ischemic hemipshere. In addition, there were regions with decreased [14C] DG uptake which invariably were depleted of ATP and phosphocreatine. Thus, suppression of glucose metabolism was restricted to the most severely ischemic areas, where the delivery of glucose may be rate-limiting.
We have developed an autoradiographic technique for the simultaneous measurement of local cerebral blood flow (LCBF) and local cerebral metabolic rate for glucose (LCMRgl) using 123I-iodoantipyrine and 14C-2-deoxyglucose respectively. By exploiting the different half-lives of 123I and 14C, 13.0 hours versus 5730 years, we produce 2 autoradiographic images. The first is predominantly a result of the 123I and the second is predominantly from the 14C. Because of the impracticality of making 123I standards, it was necessary to determine the constant which relates the ability of 123I, with respect to 14C, to expose Kodak SB-54 film, so that the 123I exposure could be quantified using 14C standards. Subtraction equations can then be used to solve for the local 123I and 14C concentrations. The technique was validated in conditions simulating a 12-fold decoupling of flow and metabolism and the standard deviation of error in measuring tracer concentrations was less than 6%. It was then used to measure these parameters in the normal awake rats and values obtained agreed well with published values from single radionuclide studies. The technique is expected to be useful in the simultaneous measurement of LCBF and LCMRgl in various physiologic or pathologic states, including those with significant decoupling of flow and metabolism. In addition, by using other tracers labelled with 123I and 14C, other parameters can be measured concurrently.
Nimodipine is a calcium slow channel blocker with several pharmacologic properties suggesting the potential to favorably modify outcome in focal cerebral ischemia. Thirty adult cats underwent unilateral middle cerebral artery (MCA) occlusion for 4 hours. Seventeen cats were treated with an ipsilateral intracarotid infusion of nimodipine (1 microgram kg-1 min -1) beginning 15 minutes before MCA occlusion and continuing throughout the occlusion period. Eight nimodipine treated cats maintaining MAP greater than 90 mmHg were assigned to a Higher Pressure Nimodipine (HPN) group. The remaining nine treated cats with MAP less than 90 mmHg were assigned to the Lower Pressure Nimodipine (LPN) group. Thirteen cats were untreated, receiving an isovolumetric amount of vehicle through the ipsilateral carotid artery. Local cerebral blood flow (ICBF) was continuously monitored using thermal diffusion probes. The brains, assessed for colloidal carbon perfusion, fluorescein and Evans blue staining, electroencephalographic activity (EEG), and histological changes, revealed no significant differences by any of these methods between the HPN and control animals with the exceptions of: HPN treated cats exhibited a preservation of EEG activity at 15 minutes post-occlusion compared to the untreated cats, and Post-ischemic surface colloidal carbon perfusion was better preserved in the treated cats than in the untreated cats. Mild hypotension, as demonstrated by the LPN group, negated these two positive effects. Prior to MCA occlusion, ICBF was bilaterally significantly increased after nimodipine infusion in the HPN group as compared to vehicle infusion. Intra-arterially infused nimodipine did not reduce infarct size.
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Cerebral cortical blood flow (lCoBF) and metabolic rate for oxygen (lCoMRO2) were studied in eight patients undergoing intracranial aneurysm clipping. The patients were anesthetized with fentanyl 10 micrograms/kg and 70% nitrous oxide combined with 30% oxygen. Hypotension was induced with isoflurane. A thermal diffusion probe was used to measure lCoBF, and arterial and cerebral venous blood samples were obtained for measurement of arterio-cerebral venous O2 content difference. Measurements were made prior to hypotension, during hypotension (to mean arterial pressure approximately 50 mmHg), and posthypotension. Mean lCoBF decreased from 69 +/- 20 mL/100 g/min at normotension to 59 +/- 13 mL/100 g/min during hypotension (P less than .03, NS) and was 61 +/- 18 mL/100 g/min upon return to normotension (all values mean +/- 1 SD). The lCoMRO2 averaged 3.9 +/- 1.6 mL/100 g/min and 3.1 +/- 1.5 mL/100 g/min, respectively (P less than .03, NS) for normotension upsilon hypotension. Values for cerebral venous PO2 and O2 saturation also did not differ significantly between study periods. These results indicate that isoflurane-induced hypotension during fentanyl-nitrous oxide anesthesia allows maintenance of a constant lCoBF and oxygen delivery.
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