Systemic eosinophil response induced by respiratory syncytial virus.

Respiratory syncytial virus (RSV) is a common cause of lower respiratory tract disease (LRTD) in infants. Eosinophils have been suggested to play a role in the disease pathogenesis of LRTD. Inflammation can induce functional and morphological alterations of peripheral blood granulocytes. In patients with RSV LRTD, we aimed to investigate the eosinophil activation status by analysing surface markers. In vitro stimulation of eosinophils with cytokines leads to up-regulation of CD11b and priming markers recognized by the recently developed priming markers A17 and A27, whereas interleukin (IL)-5Ralpha is being down-regulated. In 51 patients and 10 controls we examined the expression of these surface markers on eosinophils in moderate to severe RSV-induced LRTD patients at the time of admission and 6 weeks later during the convalescence phase. RSV-patients were characterized by a higher eosinophil CD11b expression compared to controls. Although basal A17 and A27 expression was not increased, we observed a significantly higher expression of these priming epitopes on N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulated cells of RSV patients compared with cells of controls, indicative of prior in vivo priming. Furthermore, IL-5Ralpha expression was down-regulated on peripheral blood eosinophils of these patients. Follow-up blood samples showed normalization of all markers but CD11b, which was persistently increased. Utilizing cellular markers, we observed that peripheral blood eosinophils from infants with RSV LRTD are in a more activated state compared to eosinophils of controls, which normalizes only partially during convalescence.

Taste perception with age: generic or specific losses in threshold sensitivity to the five basic tastes?

Detection thresholds for NaCl, KCl, sucrose, aspartame, acetic acid, citric acid, caffeine, quinine HCl, monosodium glutamate (MSG) and inosine 5'-monophosphate (IMP) were assessed in 21 young (19-33 years) and 21 elderly (60-75 years) persons by taking the average of six ascending two-alternative forced choice tests. A significant overall effect was found for age, but not for gender. However, an interaction effect of age and gender was found. The older men were less sensitive than the young men and women for acetic acid, sucrose, citric acid, sodium and potassium chloride and IMP. To detect the compound dissolved in water they needed a 1.32 (aspartame) to 5.70 times (IMP) higher concentration than the younger subjects. A significant decline in thresholds with replication was shown. The age effect found could be attributed predominantly to a generic taste loss.

Thyrotropin (TSH) receptor modulation by specific TSH receptor antibodies in Graves' disease.

In Graves' disease (GD), an antireceptor autoantibody disease, individual variability in the pathogenic interaction between TSH receptors and autoantibodies has been reported. This variability can be due to allotypic (person to person) variability in the receptors or differences in autoantibody amount or specificity. This fundamental issue was investigated by evaluating immunoglobulin G (Ig)-induced TSH receptor modulation in thyroid tissue from 19 patients with GD. TSH receptor modulation by Graves' Ig was defined as the appearance of 1 class of high affinity binding sites, instead of the usual 2 classes of binding sites. Ig-induced modulation of receptors occurred in 9 of 19 (47%) experiments with autologous (patient's own) tissues and correlated with the presence of TSH receptor antibodies, measured as TSH binding inhibitor Igs. Of these 9 receptor-modulating Graves' Ig preparations, 7 (78%) also had a receptor-modulating effect in other patient's (homologous) thyroid tissue. Nine of the 10 Graves' Ig preparations that were negative for TSH receptor-modulating activity in autologous thyroid tissue were tested with other patients' thyroid tissues; 7 (78%) were negative, and all were TSH binding inhibitor Ig negative. We conclude that variability in the occurrence of TSH receptor modulation was associated with the presence or absence of TSH-binding inhibitor Ig. No evidence for allotypic differences in TSH receptors in GD was found.

Surgical treatment of renovascular hypertension caused by arteriosclerosis. II. Influence of preoperative risk factors and postoperative blood pressure response on late patient survival.

This study assesses the late survival of 103 patients with renovascular hypertension caused by arteriosclerosis who underwent reconstructive surgery during the period of 1959 through 1982. It provides a detailed analysis of the influence of preoperative factors and the postoperative blood pressure response to fatal and nonfatal cardiovascular events during follow-up. All patients suffered from severe hypertension. Arteriosclerosis was limited to the renal arteries in 52% of the patients, while 48% showed overt extrarenal arteriosclerosis. Hypertensive target organ damage was present in 68% of the patients. At a mean of 8.5 months postoperatively, 80% of the patients showed beneficial and 20% showed unsatisfactory blood pressure responses. These results were not related to the presence or absence of extrarenal arteriosclerosis. Overall, late (10 years) patient survival was significantly lower than the expected survival of a reference population (79% versus 92%; p less than 0.0001). Late patient survival was not influenced by the absence or presence of extrarenal arteriosclerosis (82% versus 82%) or target organ damage (83% versus 82%), but late survival was significantly better with beneficial (87%) than with unsatisfactory blood pressure responses (67%). This effect was especially conspicuous in the presence of extrarenal arteriosclerosis (88% versus 57%; p = 0.04) but not in its absence (86% versus 74%; p = 0.41). In terms of long-term survival, these findings clearly demonstrate the favorable effect of successful surgical treatment of patients with renovascular hypertension caused by arteriosclerosis. Moreover, they illustrate that the mere presence of preoperative extrarenal arteriosclerosis or target organ damage is not sufficient argument against surgical therapy.