Randomized clinical trial comparing primary closure with the Limberg flap in the treatment of primary sacrococcygeal pilonidal disease (Br J Surg 2005; 92: 1081-1084).
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Biomedical subjects
Publications and source records attributed to M Cheetham.
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BACKGROUND: Faecal incontinence is a common symptom which causes significant distress and reduction in quality of life. Available treatment options for faecal incontinence include conservative treatments (biofeedback, pelvic floor muscle training, dietary manipulation or drug therapy) or surgical treatments (e.g. sphincter repair, post anal repair, neosphincter). Drug treatment is often given either alone or in combination with other treatment modalities. OBJECTIVES: To assess the effects of drug therapy for the treatment of faecal incontinence. In particular, to assess the effects of individual drugs relative to placebo or other drugs, and to compare drug therapy with other treatment modalities. SEARCH STRATEGY: We searched the Cochrane Incontinence Group trials register (January 2003) and the reference lists of relevant articles. Date of the most recent search: January 2003. SELECTION CRITERIA: All randomised or quasi-randomised controlled trials of the use of pharmacological agents for the treatment of faecal incontinence in adults. DATA COLLECTION AND ANALYSIS: Working independently, reviewers selected studies from the literature, assessed the methodological quality of each trial, and extracted data. MAIN RESULTS: Eleven trials were identified for inclusion in this review. Nine trials were of cross-over design. Seven trials included only people with faecal incontinence related to liquid stool (either chronic diarrhoea or following ileoanal pouch surgery). Three trials (total 58 participants) compared topical phenylephrine gel with placebo. Two trials (56 participants) compared loperamide with placebo. One trial (11 participants) compared loperamide oxide with placebo. One trial (15 participants) compared diphenoxylate plus atropine with placebo. One trial (17 participants) compared sodium valproate with placebo. One trial (30 participants) compared loperamide with codeine with diphenoxylate plus atropine. Two further trials (total 265 participants) assessed the use of lactulose in elderly people.No studies comparing drugs with other treatment modalities were identified. There was limited evidence that antidiarrhoeal drugs and drugs which enhance anal sphincter tone may reduce faecal incontinence in patients with liquid stools. However, the trials were small and of short duration. REVIEWER'S CONCLUSIONS: The small number of trials identified for this review assessed several different drugs in a variety of patient populations. The focus of most of the included trials was on the treatment of diarrhoea, rather than faecal incontinence. There is little evidence to guide clinicians in the selection of drug therapies for faecal incontinence. Larger, well-designed controlled trials, which include clinically important outcome measures, are required.
Glial cells release a variety of molecules that support neuronal function. Because heat shock proteins (Hsps) are important in the survival of neurons subjected to metabolic stress, the possibility that glia can release the inducible form of the 70 kDa Hsp (Hsp70) was examined. Additionally, the ability of neuronal cells to show increased stress tolerance by taking up a mixture of constitutive and inducible forms of Hsp70 (Hsc/Hsp70) added to the extracellular fluid was tested. Human T98G glioma cells and differentiated LA-N-5 neuroblastoma cells were used as model glia and neurons to investigate these points. Hsp70 was analyzed using affinity chromatography, Western blotting, and immunofluorescence microscopy. The glioma cells were shown to export Hsp70 into the culture medium whether under normal conditions or subjected to heat shock. The amount of glial Hsp70 released ranged from 5 to 15 pg per 10(6) cells per day, being greater following heat shock. Neuroblastoma cells took up biotinylated Hsc/Hsp70 within 1 h after it was added to the culture medium and it made them more resistant to heat shock (44 degrees C) and to staurosporine-induced apoptosis. This increased stress tolerance was especially important in neuroblastoma cells induced to differentiate with phorbol ester because those 'mature neurons' showed a 10-fold decline in endogenous Hsp70, which was accompanied by increased susceptibility to heat shock and staurosporine-induced apoptosis. These results suggest that extracellular Hsp70 may provide a means by which glia can affect neuronal function, perhaps enhancing neuronal stress tolerance.
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The discrimination of apoptotic and normal rat thymocytes by forward-angle light scatter in the UV depended on the angle over which the scattered light was collected. To achieve good separation, the light needed to be collected over a narrow angle. It was also observed that apoptotic thymocytes gave less forward light scatter than normal cells, whereas, under identical conditions, apoptotic cells from a murine cell line gave more light scatter than their normal counterparts. We suggest that the forward light scatter of apoptotic cells is affected by several factors, including changes in cell size and in the internal structure of the cell.
Muscle pH and temperature were measured before, and continuously for 30 min after, a 30-s maximal sprint exercise in ten subjects. These measurements were made with a needle-tipped pH electrode and a thermocouple placed in vastus lateralis. Venous blood samples were collected for pH, lactate and catecholamine estimations and measurements were also made of the arterial blood pressure and heart rate. The muscle and venous pH decreased from 7.17 +/- 0.01 (mean +/- SEM) and 7.39 +/- 0.01 to 6.57 +/- 0.04 and 7.04 +/- 0.03, respectively, in response to the exercise. No significant recovery occurred in either pH measurement for 10 min, after which muscle pH increased to 7.03 +/- 0.03 and venous pH to 7.29 +/- 0.01 by 30 min. Muscle temperature increased by 2.1 degrees C with exercise and also failed to return to pre-exercise values by 30 min. Blood lactate concentration increased from 0.75 +/- 0.04 mmol l-1 before exercise to a peak value of 15.76 +/- 0.35 mmol l-1 5 min after completion of the exercise, and then declined slowly to 10.30 +/- 0.61 mmol l-1 by 30 min. Arterial blood pressure increased transiently with exercise but recovered rapidly, whereas the exercise-induced tachycardia was sustained throughout the recovery period. The recovery from the metabolic and cardiovascular responses to maximal sprint exercise in man is incomplete 30 min after cessation of the exercise.
Higher levels of the expression of CR1 and CR3 molecules were detected on the surface of monocytes and neutrophils from maternal and newborn (cord) blood samples than in adult controls. Chemotactic factors such as formyl-methionyl-leucyl-phenylalanine or leukotriene B4 induced an increase of the expression of CR1 and CR3 which was more pronounced on cells from maternal and cord samples than from nonpregnant adult controls. CR1 and CR3 molecules were detected in monocytes and neutrophils from peripheral blood obtained from fetuses more than 14 weeks old and on subpopulations of cells in bone marrow, spleen and thymus.
A T cell subset (T4+,2H4+) has recently been identified, which acts as an inducer of T8+ suppressor cells; however 2H4 molecules have not been detected in thymuses from normal individuals or on the surface of immature thymocyte clones. In the present study, T4+,2H4+ and T8+,2H4+ cells have been found in maternal and new-born blood samples. However, only a small percentage of 2H4+ cells were detected in human fetal thymus, bone marrow, liver and spleen, thus suggesting that T cells acquire these molecules only in circulation and at a late stage of maturation.
To determine the effect of barbiturates on sleep two subjects, after a control period, received 200 mg. of sodium amylobarbitone for 26 nights. All night sleep records taken during this period showed that the barbiturate shortened the delay to sleep, increased the total sleep period, lengthened the delay to rapid eye movement (R.E.M.) sleep, and depressed R.E.M. sleep. After five nights R.E.M. sleep returned to baseline values -that is, showed tolerance. On stopping the drug withdrawal phenomena were seen, even to this small dose of the drug.In a second experiment a subject dependent on 600 mg. of Tuinal was found to have low normal R.E.M. sleep while on drugs. On withdrawal, delay to sleep increased and total sleep time fell. R.E.M. sleep was doubled and the delay to R.E.M. became abnormally short.These findings suggest that hypnotics allow sleep to be "borrowed," and that patients should be supported while they are being withdrawn.