Characterization of apoptosis in intestinal ischaemia-reperfusion injury — a light and electron microscopic study.

Intestinal ischaemia-reperfusion (IR) injury has largely been attributed to cellular necrosis. Apoptosis, a distinct form of cell death has been observed following IR to the brain, heart, adrenals and the kidneys. In order to characterize the role of apoptosis in intestinal IR, small bowel grafts were stored in saline ( n  = 6) or modified University of Wisconsin solution ( n  = 6) at 4 °C for 12 h and reperfused for 6 h in syngeneic rats. Samples of normal, stored and reperfused intestines at 1, 3 and 6 h were analysed by light and electron microscopy. Following reperfusion, there was crypt and villous epithelial apoptosis, loss of crypt and villous structures, and an increase in mucosal inflammatory cell infiltration. Ongoing apoptosis was maximum at 1 h, its degree decreasing with increasing reperfusion intervals. Large numbers of apoptotic bodies dominated the picture from 3 h of reperfusion. This study has demonstrated the induction of apoptosis by intestinal IR injury, which begins within an hour of reperfusion and is probably responsible for the observed crypt and villous loss. This has potential therapeutic implications as, opposed to necrosis, apoptosis is an active process with genetic regulators and biochemical effectors, which can be specifically targeted to prevent or alleviate IR injury.     

Recombinant factor VIIa in the management of a pseudotumour in acquired haemophilia

Bleeding in nonhaemophilic patients with high-titre factor VIII autoantibodies is often severe, life-threatening and refractory to treatment with factor VIII concentrates. In this report, we describe an elderly woman who required surgical excision of a large haemophilic pseudotumour adjacent to the left gluteal muscle. The Bethesda titre of 11 U precluded treatment with human factor VIII, and the patient had an anaphylactic reaction to porcine factor VIII. However, haemostasis was successfully achieved with recombinant factor VIIa and the pseudotumour was removed. The patient was treated with repeated cycles of cyclophosphamide, vincristine, and prednisone. The Bethesda titre eventually declined to 0.7 U and the factor VIII rose to 20%. During an 18-month follow-up period there has been no recurrence of bleeding or of the pseudotumour.     

Epidemiology of solar keratoses

Solar keratoses (SKs) or actinic keratoses are common dysplastic epidermal lesions which occur in pale-skinned individuals who are chronically exposed to intense sunlight. Together with basal cell carcinomas and sqamous cell carcinomas, they constitute a major public health problem in such individuals. Reported SK prevalence rates range from 11 to 25% in various northern hemisphere populations, and amongst Australian adults the range is from 40 to 60%. In the only study to date reporting SK incidence data, 60% of subjects aged 40 years and over with SKs at baseline developed new lesions during 12 months of follow-up, compared with only 19% of those who were lesion-free on the first examination. Because existing epidemiological data on SKs are sparse, very little is known of their natural history, their role in carcinogenesis, or their preventability. In this review, current knowledge about the aetiology, diagnosis, and occurrence of SKs is discussed, as is the need for prospective studies in unselected communities. With accurate baseline data, public health authorities should be in a better position to determine the best preventive strategies, and to evaluate the effectiveness of these programmes.     

Continuous monitoring of depth of sedation by EEG spectral analysis in patients requiring mechanical ventilation

Twenty-three patients undergoing intensive therapy had continuousEEG recording in an attempt to assess depth of sedation usingspectral analysis. Median power frequency (MPF) and spectraledge frequency (SEF) were calculated and correlated with theclinical sedation score and blood concentration of sedativedrug. Fifteen patients received isoflurane and eight midazolam.There was no correlation between MPF or SEF and sedation scoreor blood concentration of drug. These results suggest that nosimple measure of the EEG is likely to correlate with depthof sedation in critically ill patients.