Evaluation of computerized analysis of the propagation of human duodenojejunal contractions

Abstract Detection of peristalsis in the human small intestine has been limited in the past by both the available measurement techniques and the complexity of this activity. Recent developments in ambulant recording have provided a means of monitoring the occurrence of intestinal contractions at multiple sites in the small bowel, but the problem of complexity remains. Using digital data recorded from an intra-luminal strain-gauge transducer in the proximal gut, an algorithm was implemented to identify and classify contractile events within the small bowel. By modelling propagated activity the effect of varying transducer spacing and the number of transducers used was assessed. The question of variability of apparent velocity of peristaltic contractions was examined using successive cross-correlation calculations to extract underlying phase differences between samples of 512 minutes of manometric recording over 150 mm of human small bowel. The effective velocity was found to have a median value of 14 mm sec^-1 and an inter quartile range of 12–18 mm see^-1). It is proposed that, in dynamically tracking variations in phase difference between adjacent recording sites, cross-correlation techniques should be used to control the parameters used for the recognition of propagated contractile events and thereby improve the specificity of this process.     

Effects of the Long-Term Depletion of Reduced Glutathione in Mice Administered L-Buthionine-S,R-sulfoximine

Effects of the Long-Term Depletion of Reduced Glutathione inMice Administered L-Buthionine-S,R-sulfoximine. SUN, J. D.,RAGSDALE, S. S., BENSON, J. M., AND HENDERSON, R. F. (1985).Fundam. Appl. Toxicol.. 5,913-919. Previous methods to depletein vivo concentrations of reduced glutathione (GSH) have notbeen able to lower tissue GSH levels for extended periods, havebeen toxic, and can alter the metabolism of xenobiotics. A possiblealternative to lower in vivo concentrations of GSH may be theuse of buthionine-S,R-sulfoximine (BSO) in the drinking waterof laboratory animals to inhibit the biosynthesis of GSH. Ithas been previously reported that 20 mM BSO in the drinkingwater given to mice was able to lower GSH levels in a varietyof tissues after 15 days. In order to more fully characterizethe in vivo depletion of GSH in tissues by ingestion of BSOand determine if this method would be suitable in studies requiringdepressed levels of GSH for extended periods, we added differentamounts of this agent to the drinking water given to mice forvarious times up to 28 days. We found that ingested BSO at thehighest concentrtion used in drinking water (30 mM) was ableto maximally lower GSH concentrations in mouse lungs, lung lavagefluid, liver, kidneys, and blood to 59.0 ? 3.6%, 35.0 ? 5.1%,44.3 ? 1.5%, 69.5 ? 3.9%, and 70.0 ? 6.0% of control mice, respectively,for up to 28 days. These lowered concentrations of tissue GSHreturned to control levels after mice were returned to untreateddrinking water for 7 days. The potential toxicity of such treatmentswas also evaluated. Levels of alkaline phosphatase, lactatedehydrogenase, glucose-6-phosphate dehydrogenase, glutathioneperoxidase, and glutathione reductase in lungs and lung lavagefluid, and total and differential cell counts from lung lavagefluid were not different between control and BSO-treated mice.This showed that BSO treatment did not produce indications oflung injury as measured by these biochemical parameters. Serumaspartyl transferase and -glutamyl transpeptidase activitieswere unaffected by the BSO treatments, indicating normal liverfunctions. Lung and liver cytochrome P-450 concentrations werealso not different between controls and BSO-treated animals.Thus, BSO in the drinking water of mice was able to effectivelylower in vivo levels of GSH without eliciting aCUte toxic responses.     

Management of muscle haematomas in patients with severe haemophilia in an evidence-poor world

Treatment studies in haemophilia focus on joint bleeds; however, some 10-25% of bleeds occur in muscles. This review addresses management of muscle haematoma in severe haemophilia, defines gaps in the published evidence, and presents a combined clinician and physiotherapist perspective of treatment modalities. The following grade 2C recommendations were synthesized: (i) Sport and activity should be based on individual factor levels, bleeding history and physical characteristics, (ii) Musculoskeletal review aids the management of children and adults, (iii) 'Time to full recovery' should be realistic and based on known timelines from the healthy population, (iv) Diagnosis should be carried out by both a clinician and physiotherapist, (v) Severe muscle bleeds should be treated similarly to surgical patients: a 50% trough for 10-14 days followed by high-level prophylaxis, (vi) Protection, rest, ice, compression and elevation should be implemented in the acute stage, and (vii) Physiotherapy and rehabilitation should be divided into: control of haemorrhage (phase 1); restoration of Range of Movement (ROM) and strength (phase 2); functional rehabilitation and return to normal living (phase 3). Recommendations specifically for inhibitor patients include: (i) Minor to moderate bleeds should be managed by home-treatment within 1 h of bleed onset using either one injection of rFVIIa 270 μg kg(-1), or two to three injections of rFVIIa 90 μg kg(-1) (2-3 h intervals), or FEIBA 50-100 U kg(-1) (repeated at 12-hourly intervals, if necessary) and (ii) Severe muscle bleeds should be supervised by the treatment centre and include bypassing agents until clinical improvement is observed.     

Clodronate Treatment in Patients with Malignancy-associated Hypercalcemia

ABSTRACT. Rastad J, Benson L, Johansson H, Knuutila M, Pettersson B, Wallfelt C, Åkerström G, Ljunghall S (Departments of Surgery and Internal Medicine, University Hospital, Uppsala, Sweden). Clodronate treatment in patients with malignancy-associated hypercalcemia. Acta Med Scand 1987; 221:489–94. The possibility of reducing symptomatic hypercalcemia and of maintaining total serum calcium concentrations <2.8 mmol/1 with clodronate (dichloromethylene bisphosphonate) was evaluated in 28 patients with various types of malignant tumors. Four episodes of hypercal-cemic crisis with mean serum calcium concentrations of 4.43 mmol/1 were controlled within 4–6 days of intravenous clodronate (4 mg/kg BW/day). This was accompanied by a moderate increase in serum creatinine values which, however, returned to pretreatment levels after therapy withdrawal in all but one case. Oral clodronate successfully reduced a mean serum calcium concentration of 3.16 mmol/1 in 22 out of 25 patients after 3–12 days (800–3 200 mg/ day). After reversal of the hypercalcemias oral clodronate controlled the serum calcium concentration for up to 42 weeks in six out of 15 patients After discontinuation of initial therapy five of seven recurrent hypercalcemias were successfully treated with oral or intravenous clodronate. Hypocalcemia and subjective side-effects were uncommon. It is concluded that clodronate is a valuable clinical tool in the management of patients with malignancy-associated hypercalcemia.