The direct effect of graft compliance mismatch per se on development of host arterial intimal hyperplasia at the anastomotic interface

To study the direct and sole effect of compliance mismatch on anastomotic intimal hyperplasia of the host arterial wall and to minimize possible confounding factors, dogs with a low thrombotic potential were selected as experimental subjects. Externally supported 6 cm x 5 mm Dacron grafts with a compliance value of approximately 1/300 of the host artery were implanted into the carotid arteries with end-to-end anastomoses on one side and end-to-side anastomoses on the other. The control graft was an autogenous carotid artery segment 4 cm in length transplanted into the femoral artery. Eight cases (24 grafts) were studied for 1 year and three (nine grafts) for 6 months. All were patent throughout the study period except for two noncompliant grafts with end-to-end anastomoses; thrombosis was the documented cause of occlusion. For the patent grafts, follow-up arteriograms showed no progressive narrowing of noncompliant anastomoses. Whether compliant or noncompliant, light microscopy studies showed slight intimal thickening within 1 to 2 mm of the anastomotic line, possibly the result of the normal healing response to stitch and surgical trauma. Quantitatively, 22 measurements representing longitudinal and circumferential thickness of the neointima were taken at each of the 40 patent noncompliant and 22 patent compliant control anastomoses. There was no statistically significant difference in anastomotic neointimal thickness in compliant and noncompliant grafts or for the different implantation periods. These data suggest that graft/host artery compliance mismatch does not cause arterial intimal hyperplasia at the anastomotic interface.     

Incidental finding of a microsporidian parasite from an AIDS patient

Light microscopic examination of feces from a human immunodeficiency virus-positive patient with chronic diarrhea, anorexia, and lethargy revealed the presence of numerous refractile bodies resembling microsporidian spores. They were subsequently identified as belonging to the genus Nosema on the basis of their ultrastructural characteristics. However, the microsporidia were enclosed within striated muscle cells, suggesting that they were probably ingested in food; thus, this represented an incidental finding rather than a true infection.     

A solid-phase protein assay: quantitation of protein in the nanogram range

A solid-phase protein assay (SPA) for the determination of protein concentrations in the nanogram range is described. The technique is based on biotinylation of immobilized protein on the solid phase of a microtiter plate and quantitation of the protein-biotin complexes by peroxidase-coupled avidin. Compared to the routinely used Bradford and Lowry protein detection techniques, the described SPA assay is (depending upon the protein assayed) 1000 to 10,000 times more sensitive. Moreover, the SPA assay can be suitable for protein quantitation of samples containing agents which commonly interfere with the routinely used detection techniques. The SPA assay is a valuable addition to the Bradford and the Lowry techniques. Used in combination with an antigen-specific ELISA it gives a reliable ratio of specific versus total protein.     

Oxygen-derived free radicals contribute to baroreceptor dysfunction in atherosclerotic rabbits

The goal of the present study was to determine whether oxygen-derived free radicals contribute to baroreceptor dysfunction in atherosclerosis. Baroreceptor activity was measured from the carotid sinus nerve during pressure ramps in isolated carotid sinuses of anesthetized rabbits. Rabbits fed a 0.5% to 1.0% cholesterol diet for 7.9 +/- 0.4 months (mean +/- SE; range, 5.5 to 10) developed atherosclerotic lesions in the carotid sinuses. Maximum baroreceptor activity measured at 140 mm Hg and the slope of the pressure-activity curve were reduced in atherosclerotic (n = 15) compared with normal (n = 13) rabbits (425 +/- 34 versus 721 +/- 30 spikes per second and 6.2 +/- 0.6 versus 10.8 +/- 0.8 spikes per second per mm Hg, respectively, P < .05). The level of activity was inversely related to plasma cholesterol concentration (r = .86, P < .001) and total cholesterol load (plasma concentration x duration of diet, r = .92). Mean arterial pressure was normal in both groups. Exposure of the carotid sinus to the free-radical scavengers superoxide dismutase (SOD) and catalase significantly increased maximum baroreceptor activity by 25 +/- 4% in atherosclerotic rabbits (n = 6) but caused only small and irreversible changes in activity in normal rabbits (n = 8). Catalase alone but not SOD also increased baroreceptor activity in atherosclerotic rabbits (n = 7). Exposure of the carotid sinus of normal rabbits to exogenous free radicals generated from the reaction between xanthine and xanthine oxidase inhibited baroreceptor activity in a dose-dependent and reversible manner (n = 8, P < .05). The inhibition of activity was attenuated by SOD and catalase but was not attenuated by the inhibitor of hydroxyl radical formation, deferoxamine. Neither restoration of baroreceptor activity in atherosclerotic rabbits by catalase nor inhibition of activity by xanthine/xanthine oxidase could be explained by changes in the carotid pressure-diameter relation or prostacyclin formation. These results indicate that oxidant stress inhibits baroreceptor activity and that endogenous oxyradicals produced in atherosclerotic carotid sinuses contribute to baroreceptor dysfunction.     

Childhood epilepsy and asthma: comparison of quality of life

We report results from the first data collection on an ongoing longitudinal study aimed at describing the natural history of adaptation to childhood epilepsy and asthma in children and their families. We studied 136 children with epilepsy and 134 children with asthma aged 8-12 years. Data were collected from the children, their mothers, and their school teachers through interviews, school records, and questionnaires. The two samples were compared on four domains of quality of life: physical, psychological, social, and school. Data were analyzed by a 2 x 2 between-subjects multivariate analysis of covariance with type of illness (epilepsy or asthma) as the independent variable and length of time since onset of illness as a covariate. A significant main effect was noted for illness [multivariate F (15, 236) = 11.36, p < 0.001]. Our major finding was that children with epilepsy had a relatively more compromised quality of life in the psychological, social, and school domains. In contrast, children with asthma had a more compromised quality of life in the physical domain. Our findings suggest that attention simply to seizure control in the clinical setting will not address the full range of quality-of-life problems of children with epilepsy.     

Increased incidence of sepsis at birth in neutropenic infants of mothers with preeclampsia

Neutropenia is often found at birth in infants born to mothers with preeclampsia, and is most likely present in utero. To determine whether this neutropenia is associated with an increased incidence of early-onset sepsis, we reviewed the hospital records of 301 low birth weight infants of mothers with preeclampsia. Early-onset sepsis was proved if the result of a culture of blood or cerebrospinal fluid in the first 48 hours of life was positive, or presumed if culture results were negative but two or more clinical signs of sepsis were present and the attending neonatologist believed that an infant was infected and needed at least 7 days of antibiotic therapy. Forty-eight percent of low birth weight infants of mothers with preeclampsia had neutropenia at less than 12 hours of age. Infants with neutropenia had mothers with more severe preeclampsia, were more premature (30 weeks vs 32 weeks), weighed less (1097 gm vs 1615 gm), and were more likely to be small for gestational age. Although maternal and obstetric risk factors for infection were less common in the group with neutropenia, rates of proven or presumed early-onset sepsis were higher (14% vs 2%; p < 0.001). Sepsis was proved in 6% of infants with neutropenia and in none of the infants without neutropenia (p = 0.03). A logistic regression analysis of the relative effects of birth weight, gestational age, and absolute neutrophil count on the incidence of sepsis revealed that only a low absolute neutrophil count correlated significantly with an increased risk of early-onset sepsis in infants with neutropenia.     

IL-2 reduces graft-versus-host disease and preserves a graft-versus-leukemia effect by selectively inhibiting CD4+ T cell activity

We have recently demonstrated, in a fully MHC-mismatched murine bone marrow transplantation model, that administration of a short course of high dose IL-2 markedly diminishes graft-vs-host disease (GVHD) without compromising alloengraftment or the graft-vs-leukemia (GVL) effect of allogeneic T cells. We have now evaluated the mechanism of the dissociation of GVL and GVHD observed in this model. We demonstrate that CD4+ T cells were required to produce severe, acute GVHD in the fully MHC-mismatched plus minor histocompatibility Ag-mismatched A/J-->B10 strain combination. The GVHD-producing activity of A/J CD4+ T cells administered without CD8+ T cells was inhibited by IL-2 treatment. In contrast, CD8+ T cells alone mediated the GVL effect observed in the EL4 leukemia/lymphoma model, and CD4+ cells did not contribute to this effect. This CD8-mediated GVL activity was not inhibited by IL-2 treatment. Because naive A/J CD8+ T cells administered without CD4+ T cells did not produce acute GVHD, we were unable to evaluate the effect of IL-2 in this model. However, when A/J donors were presensitized with B10 skin grafts, CD4-depleted A/J spleen cells were capable of causing acute GVHD in B10 recipients. This CD8-mediated GVHD was not inhibited by treatment with IL-2. However, IL-2 did partially inhibit the GVHD produced by nondepleted presensitized A/J spleen cells, probably due to selective inhibition of the function of presensitized A/J CD4+ T cells. The dissociation of GVHD and GVL against the EL4 leukemia/lymphoma in IL-2-treated mice can therefore be explained by selective inhibition by IL-2 of CD4 activity.     

Temporal changes in PO2 of R3230AC tumors in Fischer-344 rats

It has been hypothesized that abdominal trauma may be one of the factors involved in membranous obstruction of the inferior vena cava. We present two cases of membranous obstruction of the inferior vena cava associated with trauma. One asymptomatic case, associated with an occult myeloproliferative disorder, developed within 3 years of a violent abdominal trauma. The other case, associated with familial plasminogen deficiency, was discovered at surgery 3 days after a road accident with obvious abdominal trauma, since superimposed extensive thrombosis of the inferior vena cava caused acute Budd-Chiari syndrome. We conclude that underlying prothrombotic conditions are probably necessary for the development of membranous obstruction of the inferior vena cava and that minor trauma may contribute to the development of thrombosis through indirect mechanisms.