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Biomedical subjects

E C Burke

Publications and source records attributed to E C Burke.

At least 37 records · Page 2Linked to original sources
PubMed1991

Wound healing after anorectal surgery in human immunodeficiency virus-infected patients.

Medical records of 52 human immunodeficiency virus (HIV)-infected patients who underwent a total of 80 anorectal operations from January 1985 to January 1990 were retrospectively reviewed to determined whether anorectal surgical wounds healed in HIV-infected patients and the mean survival time of these patients after surgery. Twenty-four operations were performed in asymptomatic HIV-infected patients, 19 in HIV-infected patients with persistent lymphadenopathy, and 37 in patients with acquired immunodeficiency syndrome. Wounds healed in 49 patients (94%). The mortality rate 30 days after surgery was 2%. There were no major complications. The mean survival time of HIV-infected patients after surgery was 15 months. We conclude that anorectal surgical wounds heal in most HIV-infected patients and that the survival time after surgery of HIV-infected patients with anorectal disease justifies appropriate surgical treatment.

Abscess↗
PubMed1991

Demonstration of local immunosuppression with methylprednisolone in the sponge matrix allograft model.

This study evaluated the effect of locally delivered methylprednisolone on the systemic and local immune response in the sponge matrix allograft model. Polyurethane sponges were coated with peritoneal exudate cells from DBA/2 (H-2d) or C57Bl/6 mice (H-2b) and placed subcutaneously in C57BL/6 recipients 24 hr later. Each mouse received both a syngeneic and an allogeneic sponge graft. Local immunosuppression was effected by placement on day 0 of cellulose/matrix pellets containing a preparation of increasing quantity of controlled release MP or by daily intrasponge injection of MP. Local immunosuppression was demonstrated by decreased cytotoxicity on day 12 in the allogeneic sponge receiving MP directly, as compared with the groups that received MP in the opposite syngeneic sponge or no MP. This effect was noted at a specific MP dose (0.5 mg/kg/day). Absolute numbers of precursor cytolytic cells and mature cytolytic cells (determined by limiting dilution analyses) infiltrating the allografts were also decreased in the sponges receiving MP directly, relative to the groups receiving MP in the opposite syngeneic sponge. Maintenance of systemic (in contrast to local) immunity was also demonstrated. Animals treated with local MP into a simultaneously placed syngeneic sponge or in whom no MP was delivered became sensitized to a synchronous DBA/2 sponge and rejected a subsequent DBA/2 skin graft in second-set fashion. Conversely, animals that received local MP into their synchronous DBA/2 sponge rejected a subsequent DBA/2 skin graft or a third-party graft with first-set kinetics. The presence of local MP at the initial graft site prevented the animals from becoming sensitized to the presented alloantigen but did not keep the animal from developing a rejection response to a third-party skin graft with first-set kinetics. It appears that delivery of MP locally to the site of antigen is an effective method to modulate alloreactivity. In addition, the sponge matrix allograft appears to be a useful model for studying local immunosuppression.

Animals↗
PubMed1990

In vitro cardiac function in early sepsis.

The involvement of the myocardium in the injury resulting from bacteremia has been somewhat controversial. Recently, some investigators have suggested that the transition from an early stage of sepsis, in which the cardiovascular system is stable and mortality is relatively low, to the late or preterminal stage of sepsis is a result of cardiac dysfunction. Here, however, data are presented to show that contractile defects and loss of myocardial reserve occur even early during a septic episode, i.e., at a time when cardiac output is elevated or normal. Efforts to determine the mechanism of the cardiac dysfunction are described. These entail studies of whole heart performance under conditions of varying the calcium availability for contraction and assessment of subcellular organelle function. The data indicate that calcium dyshomeostasis may at least partially contribute to the cardiac dysfunction of sepsis. The in vivo adequacy of cardiac function probably results from the capacity of the myocardium in early sepsis to respond to catecholamine support of chronotropy and inotropy.

Animals↗
PubMed1988

Long-term prognosis for children with nephrotic syndrome.

Follow-up survival and health information were obtained, after a median of 27.5 years, from 132 patients who had been seen originally as children with nephrotic syndrome between 1951 and 1967. Ninety seven patients were alive. Recurring edema or proteinuria, or both, persisted in 15 percent of those still alive. Eight of 11 parous women reported relapses during pregnancy. There was no apparent increase in malignancies, atopic diseases, clinical defects in cell-mediated immunity, or cardiovascular diseases. Twenty two patients (17%) died of renal causes between 3 months and 8 years after the onset of nephrotic syndrome. Steroid resistance was the presenting feature universally predictive of a poor outcome; nine of the 11 such patients died and the other two are now receiving hemodialysis. Hematuria was present initially in 41 percent of the patients who died of renal causes, compared with 14 percent of those still alive. Hypertension was noted on the first examination in 22 percent of those who died of renal causes, compared with 10 percent of those alive.

Adolescent↗
PubMed1987

Myocardial dysfunction in sepsis.

A synthesis of the postulated sequence of events for development of the inappropriate response of the myocardium to a demand for increased cardiac index is schematically represented in Fig. 10. In sepsis, bacteremia and/or the release of endotoxin activate the macrophages which release a spectrum of mediators. Some of these mediators (and possibly also endotoxin itself) have a negative influence on myocardial contractile function either directly and/or through altering cellular calcium flux. This results in impaired myocardial function manifested initially by decreased stroke volume. Subsequently, stroke volume will be either partially or completely restored to normal through the action of circulating catecholamines, the concentration of which is markedly elevated due to the presence of endotoxin and/or macrophage-produced mediators. Endotoxin and/or these mediators also act on the SA node increasing its sensitivity to beta-adrenergic stimulation. This will result in elevated heart rates. The latter, combined with the restored stroke volume, will yield an increased cardiac index which is the hallmark of the hyperdynamic phase of sepsis. In the cecal ligation and puncture model of sepsis, where cardiac index is maintained at the original level, the partially restored stroke volume and the elevated heart rate will combine to maintain cardiac index. Although this mechanism of increasing cardiac index through tachycardia is not energy efficient, the myocardium is able to cope with these changes and also to maintain its high energy phosphate concentrations, since the utilization of the three major myocardial substrates (fatty acids, lactate and glucose) is not affected by sepsis. Although this putative sequence of events is consistent with the observed experimental findings, further work is needed to substantiate its applicability to the etiology of myocardial dysfunction in man during sepsis.

Animals↗