Management of Isolated Blunt Duodenal Injury

Five cases of duodenal injuries were treated in our hospital between January 1, 1975 and June 18, 1979. They belonged to the Class II and early Class III of duodenal injuries. They were treated with simple closure of the perforation in a single or double layer with external drainage. Only in one case were gastrojejunostomy and bilateral vagotomy added because the patient had a history of ulcer disease. The delay in operative treatment ranged between five and 48 hours. All responded well to the surgical treatment. In the instance of the longest operative delay, a purulent drainage occurred and it responded promptly to a selective antibiotic therapy. The average hospitalization stay was nine days for the patients operated upon early, whereas it was 15 days for the two delayed cases. No mortality was recorded.     

Telemedicine and distributed medical intelligence.

Recent trends in health care informatics and telemedicine indicate that systems are being developed with a primary focus on technology and business, not on the process of medicine itself. The authors present a new model of health care information, distributed medical intelligence, which promotes the development of an integrative medical communication system addressing the process of providing expert medical knowledge to the point of need. The model incorporates audio, video, high-resolution still images, and virtual reality applications into an integrated medical communications network. Three components of the model (care portals, Docking Station, and the bridge) are described. The implementation of this model at the East Carolina University School of Medicine is also outlined.     

Fetal and neonatal IL-13 production during pregnancy and at birth and subsequent development of atopic symptoms

BACKGROUND: Cytokine production at the materno-fetal interface may influence the development of atopy-predisposing immune responses. Because IL-13 possesses IL-4-like activity and may regulate the immune responses observed in atopy, it may contribute to the expression of the atopic phenotype initiated during intrauterine life. OBJECTIVE: We sought to examine IL-13 expression by fetal and neonatal cells and the placenta. METHODS: The production of IL-13 by neonatal and fetal T cells was examined by culturing the cells in the presence or absence of PHA. Production of IL-13 at term was considered in the context of the later development of atopic disease in the child. IL-13 expression in the placenta was assessed by using immunohistochemistry. RESULTS: IL-13 immunoreactivity within the placenta was restricted to 16 to 27 weeks' gestation (6/6 positive vs 0/10 at >27 weeks' gestation). In contrast, spontaneous release of IL-13 by fetal mononuclear cells was first observed from 27 weeks' gestation but was undetectable after 37 weeks' gestation. PHA-stimulated mononuclear cells showed increased IL-13 levels in 80% of samples. Term babies (>37 weeks' gestation) with a parental history of atopy with atopic symptoms by 3 years of age produced significantly lower concentrations of PHA-induced IL-13 when compared with babies with no parental history of atopy (P =.034). CONCLUSION: Thus babies at risk of atopic disease in infancy display defective IL-13 production at birth. This may represent an inherent immaturity in the development of T cell-cytokine responses in babies at genetic risk for atopy or could be a consequence of downregulation of responses by other factors. Normal pregnancy, irrespective of atopic status, is associated with the production of appreciable quantities of IL-13 initially by the placenta and subsequently by the fetus. The regulation of this production and its consequences for the mother and fetus remains to be elaborated.     

Testicular metastasis of primary cecal carcinoid tumor

Testicular carcinoids are rare and the majority are of primary testicular origin. Testicular carcinoids can also be secondary from extra-testicular primary tumors, but the incidence is even less common. The case described here is a patient who initially had an infiltrating cecal carcinoid with hepatic metastasis. Following surgery, he was managed with octreotide and had close monitoring of the levels of serum serotonin and its urinary metabolite. He experienced a fairly indolent clinical course and 5 years after excision of the primary cecal carcinoid, his hepatic lesion has virtually been unchanged. However, he developed a secondary testicular metastasis. He has otherwise remained well, without evidence of metastases elsewhere on imaging studies.     

Use of alkaline phosphatase to correct the underestimation of fosphenytoin concentration in serum measured by phenytoin immunoassays

The pharmacologic activity of fosphenytoin, a new phosphate ester pro-drug of phenytoin, is due to in vivo conversion to phenytoin. Fosphenytoin concentrations cannot be accurately estimated by phenytoin immunoassays (fluorescence polarization and chemiluminescence) owing to the nonlinear relation between fosphenytoin concentration and the observed cross-reactivity. The problem of slow conversion of fosphenytoin to phenytoin in serum in vitro can be circumvented by rapidly converting fosphenytoin to phenytoin in vitro by alkaline phosphatase. Drug-free serum, heparin, EDTA, or citrated plasma were supplemented with 2 concentrations of fosphenytoin. Then to 1-mL aliquots of specimen, no enzyme (control), 10 microL, or 25 microL of enzyme solution was added. The specimens were incubated, and phenytoin concentrations were measured by fluorescence polarization and chemiluminescent assays. In the absence of enzyme, we observed little conversion of fosphenytoin to phenytoin, but in the presence of only 10 microL of enzyme, the conversion of fosphenytoin to phenytoin was complete in 5 minutes. We also observed complete conversion of fosphenytoin to phenytoin by alkaline phosphatase in heparin, EDTA, and citrated plasma. If clinically indicated, the phenytoin concentration can be measured before and after addition of enzyme to roughly estimate the rate of conversion.     

Stimulus-dependent leukotriene release from human basophils: a comparative study of C5a and Fmet-leu-phe

Previous studies of human basophil mediator release have noted that the bacterial peptide fmet-leu-phe and the anaphylatoxin C5a induce comparable levels of histamine release while only fmet peptide induces leukotriene release. Since 5-lipoxygenase metabolism of arachidonic acid is calcium dependent, we examined the characteristics of the human basophil [Ca++]i response which follows its activation by either fmet peptide or C5a. While the peak [Ca++]i response was essentially identical for these two stimuli, fmet peptide induced a prolonged increase in [Ca++]i while C5a stimulated only a transient increase in [Ca++]i that was essentially over within 2 minutes of adding the stimulus. Simultaneous addition of EDTA with fmet peptide revealed the two phases of the [Ca++]i response and demonstrated that leukotriene release was dependent on an elevated [Ca++]i level in the 2-5 minutes following challenge. Enhancement of leukotriene release induced by C5a by agents such as staurosporine and interleukin-3 also produced a [Ca++]i kinetic curve which resembled fmet peptide. Single cell studies of the [Ca++]i response could detect no subpopulations of cells which responded preferentially to fmet peptide or C5a, eliminating the possibility that the ability of fmet peptide to induce leukotriene was a result of its action on a functionally distinct population of basophils.     

Action of some foreign cations and anions on the chloride permeability of frog muscle

1. Evidence for the existence in skeletal muscle of a specific cation binding system capable of lowering the chloride permeability was obtained by testing the effect of several metal ion species upon the efflux of (36)Cl from frog muscles equilibrated in high-KCl solution.2. Cu(2+), Zn(2+) and UO(2) (2+) ions, when present in concentrations of approximately 10(-4)M in inactive wash solution at pH 7.4 slowed the efflux of (36)Cl to half its original value. At pH 5.0, when the chloride permeability was already low as a consequence of hydrogen ion binding, these metal ions had little further effect.3. Presence of Ni(2+), Co(2+), Pb(2+), Ce(3+) and La(3+) in 10(-4)M or higher concentrations had no detectable influence on the (36)Cl efflux. Wide variations in Ca(2+) concentration were similarly ineffective.4. The influence of more adsorbable anions on the chloride permeability was examined at different pH values. Extracellular iodide greatly slowed the rapid efflux of (36)Cl into alkaline solution. In acid solutions, when the chloride permeability was already low, the effect of iodide was less pronounced, but still demonstrable. The chloride permeability was consequently increased to a lesser extent by a rise in pH in the presence of iodide.5. The efflux of iodide and bromide was measured at different pH values under conditions of self exchange. In alkaline solution the permeabilities to iodide and bromide were considerably lower than that to chloride. In acid solution the membrane differentiated less between anion species of different adsorbability.