The relationship of scoring systems and mortality in the surgical intensive care unit

To determine the relationship between severity of illness and mortality, therapeutic intervention score (TISS) and acute physiology score (APS) were determined on admission to the Surgical Intensive Care Unit (SICU). Patients were divided into survivors and nonsurvivors and differences were compared by chi-square analysis. The 1524 patients admitted to the SICU during a 12-month period had a mean TISS of 3.03 and a mean APS of 13. The average length of stay (LOS) was 3.75 days. Of the 1524 patients, 97 (6.4%) died. The number of nonsurvivors increased with higher TISS and APS scores (P less than 0.001). There were no deaths in the TISS Category 1 patients or in the APS 0-5 group. Mortality rates dramatically increased with APS greater than 20 (P less than 0.001). There were 1286 patients with APS less than 20, and 24 (2%) of these patients died, whereas 73 (31%) of 238 patients with APS greater than 20 died. Nonsurvivors had a mean TISS of 3.6, mean APS of 27, and LOS of 4.88 days, all of which totals were higher than the survivors' totals. In this study population, risk of death was one in three if the APS was greater than 20. These data indicate that TISS and APS scores are effective means of assessing mortality risk in SICU patients.     

The physically disabled physician

This article reviews the available literature on physically disabled physicians and discusses the attitudinal, environmental, and political barriers they may encounter. Information on 215 physicians and 92 medical students with a wide range of disabilities was analyzed. Currently available personal and technological resources are outlined and special issues pertaining to medical education are highlighted. Greater awareness and acceptance by medical peers are essential for professional success.     

Revascularization of the renal artery in renovascular hypertension with progressive renal insufficiency

Sixteen patients underwent surgical treatment for severe renovascular hypertension with rapidly progressive renal failure. These patients were assessed preoperatively with the measurement of serum creatinine and blood-urea levels (means 271 +/- 204 mumol/l and 15.6 +/- 10.3 mmol/l respectively), and renal clearances. 5 patients underwent aorto-renal bypass (bilateral in one case) and 11 patients were treated by autotransplantation of the kidney. Operative mortality was 6.2%. Early results were assessed at 1 and 6 months postoperatively. Renal function was normal in 8 patients, improved in 5 (p less than 0.05), unchanged in 1 and worse in 1 by aorto-renal bypass thrombosis. At long-term with a minimum follow-up of 12 months (mean 31 +/- 12 months), the initial improvement in renal function remained steady in 12 patients whilst 1 patient has gone on to hemodialysis. At middle and long-term, 81% of the patients were normotensive without medication or had improved blood pressure (p less than 0.001). These good results confirm the reversibility of renal ischemic lesions and support an aggressive attitude towards the use of revascularization in the surgical treatment of such patients with renovascular hypertension and renal failure.     

Monoclonal antibody production to human and bovine 2′:3′-cyclic nucleotide 3′-phosphodiesterase (CNPase): high-specificity recognition in whole brain acetone powders and conservation of sequence between CNP1 and CNP2

Monoclonal antibodies against human and bovine 2′:3′-cyclic nucleotide 3′-phosphodiesterase (CNPase) were generated by fusing FOX-NY myeloma cells with spleen cells from RBF/Dn mice previously immunized with the purified brain antigens. The enzyme isolated from bovine brain was quite basic, with an isoelectric point of 9.71 and both the bovine and human enzymes consisted of a closely spaced doublet at approximately 44 and 46 kDa on SDS-PAGE. Six monoclonals were identified as strongly recognizing the enzyme on both ELISA plates and on immunoblots of whole brain protein. Four monoclonals very weakly cross-reacted with guinea pig myelin basic protein. In contrast with two previous reports, some of our monoclonal antibodies did immunostain 2 or 3 protein bands in peripheral nerve, two bands closely corresponding to those immunostained in central nervous system (CNS) myelin, the Wolfgram protein fraction and in acetone powders of whole brain. Each of the 6 monoclonals reacting strongly on immunoblots recognized the enzyme in from 2 to 5 of the species examined (human, bovine, rat, mouse and rabbit). In addition, all 6 monoclonals that immunostained the enzyme in whole brain, myelin and Wolfgram protein immunoblots recognized both CNP1 (44 kDa) and CNP2 (46 kDa). The two closely spaced protein bands observed on SDS-PAGE and previously stained on immunoblots of CNS CNPase using polyvalent rabbit anti-bovine CNPase antisera, and now different monoclonal antibodies, appear to be immunologically related and to contain highly conserved sequences.     

Glucocorticoid effects on phenylethanolamine N-methyltransferase (PNMT) in explants of embryonic rat medulla oblongata

Although glucocorticoid hormones have important roles in the development of neurotransmitter systems in cells derived from the neural crest, it is not known whether they have parallel effects on neuronal development in the brain. To address this issue, we have established an in vitro system of fetal medulla oblongata (MO) to follow development of the epinephrine-synthesizing enzyme, phenylethanolamine N-methyltransferase (PNMT). Embryonic MO was explanted from E13 or E18 embryos and maintained for up to 3 weeks. Successful culture of adrenergic neurons was possible only in explants taken from young embryos, since E18 explants failed to develop. In E13 explants, immunoreactivity to both PNMT and tyrosine hydroxylase, the rate limiting enzyme in catecholamine synthesis, was observed. PNMT catalytic activity which was barely detectable at the time of explanation increased markedly during the first week in vitro. To study the effects of glucocorticoids on PNMT development in central neurons, MO explants were grown in glucocorticoid deficient medium in which rat serum from adrenalectomized rats was substituted for human placental serum. Addition of natural glucocorticoids, cortisol or corticosterone, or the mineralcorticoid, deoxycorticosterone, during the third culture week had no effect on PNMT activity. Dexamethasone (DEX), a synthetic glucocorticoid, also had no effect on PNMT during the first or second weeks in culture. However, addition of DEX during the third culture week resulted in a doubling of PNMT activity. However, attempts to block the DEX effect during the third week or to block the increase in PNMT activity during the first week in control cultures with the glucocorticoid receptor antagonist, dexamethasone 21-mesylate, were unsuccessful. These results suggest that PNMT in central neurons does not require glucocorticoids for ontogeny during the embryonic period. This is in contrast to PNMT in adrenal medulla which requires glucocorticoids for normal development during both the embryonic and postnatal periods. More generally, these studies suggest that development of the same neurotransmitter phenotype in brain and periphery may be differentially regulated.     

Effect of dithranol therapy on membrane, basement membrane and nuclear markers in psoriasis lesions

We investigated the effects of anti-psoriatic therapy with dithranol (1/20-1%) in salicylic acid (0.5%) in white petrolatum on lesional skin. FITC-labeled lectins and pemphigus vulgaris antibodies (PV) served as analytical means to study the glycocalyx. Antibodies of bullous pemphigoid (BP) were used as basal membrane markers. Nuclear antigens were recorded according to the binding of speckled, anti-nuclear antibodies (ANA) as well as antibodies to dsDNA. With some lectins, dithranol therapy resulted in pronounced fluorescence of the lower parts of the basal cells. ConA was fixed by the basal cell layer. To a lesser degree, ANA were fixed by nuclei of keratinocytes. PV antibodies were not fixed at all.