ALCOHOL DECREASES INSULIN SENSITIVITY IN HEALTHY SUBJECTS

To study the effect of alcohol on glucose and insulin metabolism,a simultaneous infusion of glucose and insulin was given for150 min to healthy volunteers, once during alcohol and onceduring calorie-free gingerale (control) ingestion. During alcoholintake, the average steady-state (between 100 and 150 min) glucoseof 5.44±0.39 mmol/1. and the average steady-state insulinof 6.3±1.1 ng/ml were significantly higher than those(4.0±0.39 mmol/1. of glucose and 4.4±0.6 ng/mlof insulin) observed during the control state. Despite the highersteady-state insulin concentrations, the glucose metabolismwas significantly less during alcohol ingestion. These findingssuggest alcohol-induced impairment in glucose metabolism iscaused by a decreased tissue sensitivity to insulin.     

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.     

MORTALITY OF JAMAICAN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

A retrospective study of all patients with systemic lupus erythematosus(SLE) who died at the University Hospital of the West Indiesover a 14-year period is presented. The major cause of deathwas infection followed by renal failure. Gram-negative organismswere the major microbiological agents causing infections. Side-effectsof therapy were common, in particular bone marrow depressionand haemorrhage related to anticoagulants. It appears that controllingsevere lupus activity without increasing the risk of life-threateningcomplications remains an important goal in the treatment ofSLE. KEY WORDS: Systemic lupus erythematosus, Mortality, Infection, Anticoagulants, Jamaica     

Sudden and Fatal Malfunction of a Durata Defibrillator Lead due to External Insulation Failure

Defibrillator lead malfunction can be a disastrous complication, leading to loss of protection from sudden cardiac death in a high‐risk patient population. Recognition of lead‐specific risk for failure can assist in development of focused screening or surveillance, as in the case of the Riata lead (St. Jude Medical, St. Paul, MN, USA) or the Sprint Fidelis lead (Medtronic Inc., Minneapolis, MN, USA). A case of defibrillation failure secondary to a Durata lead insulation failure is presented. A brief review of the literature and current St. Jude Medical implantable cardiac defibrillator lead design is presented. Identification of arcing is identified as a potential sign of catastrophic insulation failure.     

Duration of hospitalization in extremely preterm infants

This study reports the age at hospital discharge of 233 survivors and age at death of 209 infants who were born at 23-28 weeks gestation over a 10 year period, 1977-86. The mean duration of hospitalization of survivors was 95 days and was inversely related to maturity at birth; those born at 23-25 weeks remained in hospital on average 1-2 weeks beyond term while those born at 26-28 weeks went home on average at term or 1 week before term. The mean age at death was 12 days: 53% within 1 day, 23% between 2 and 7 days, 15% between 8 and 28 days and 9% between 28 days and 1 year. The proportions of death in the post-neonatal period for infants born at 23-24 weeks, 25-26 weeks and 27-28 weeks were 2, 9 and 16% respectively. There was no significant trend in prolonged hospitalization of survivors or postponement of neonatal deaths to the post-neonatal period over the 1977-86 period. Nevertheless, both neonatal and post-neonatal mortality should continually be monitored in this extremely preterm group.     

Suicidal ideation amongst acutely medically ill and continuing care geriatric inpatients

Suicidal ideation amongst acutely medically ill and continuing care geriatric inpatients has not been examined previously. Data from two pooled depression prevalence studies on acute geriatric wards and one such study on continuing care geriatric wards were re-examined. The Brief Assessment Schedule (BAS) measured depression. It also contains items measuring feelings of life not worth living, suicidal ideation and pessimism. The prevalence of feelings of life not worth living, suicidal ideation and pessimism were 29%, 13% and 50%, respectively, in the acute sample, 33%, 26% and 52%, respectively, in the continuing care sample, and 38%, 29% and 55%, respectively, in the continuing care dementia sub-sample. These three variables were significantly inter-correlated, and they were associated with BAS depression scores and caseness in both the acute and continuing care sample. Feelings of life not worth living, suicidal ideation and pessimism are not uncommon in this population. Findings of this study require replication and implications for further avenues of research are discussed.     

Dendritic Cell Numbers in the Blood of HIV-1 Infected Patients Before and After Changes in Antiretroviral Therapy

Antigen presenting dendritic cells (DCs) can serve as sites for HIV replication and as vehicles for transmission of the virus to T cells. It is known that the numbers of DCs in blood is reduced during HIV-1 infection. Here we monitored the two major subsets of blood DCs in 12 individuals undergoing a change, primarily initiation, of highly active antiretroviral therapy. The numbers of plasmacytoid DCs were reliably higher on therapy, although in the 1–3 month interval we followed, these numbers did not return to those seen in HIV uninfected controls. An increase in plasmacytoid DCs was accompanied by an increase in IFN- production in response to a standard challenge in culture with UV-inactivated herpes simplex virus. The levels of myeloid DCs also demonstrated an increase while on HAART, and these numbers become comparable to the HIV uninfected controls. The numbers of plasmacytoid and myeloid DCs varied inversely with the levels of plasma HIV viremia. These longitudinal studies extend prior work showing that virus infection with HIV leads to a decrease in the number of dendritic cells in blood, and that this can be reversed at least in part by therapy.