A longitudinal study of pulmonary function in Danish patients with systemic sclerosis

Allergen-specific lymphocyte proliferation was measured by flow cytometry in 16 children with atopic dermatitis (AD). 26 with bronchial asthma (BA) and 13 non-atopic controls. Although the level of mite-S.I.F. (stimulation index measured by flow cytometry) in the younger AD children (2-7 y) was significantly higher than that in the non-atopic subjects (189.6 +/- 70.7 vs 113.9 +/- 11.0, p < 0.02), there was no elevation in the younger BA children (122.6 +/- 23.4). It is therefore likely that the elevated mite-S.I.F. level is related to the development of the allergic cellular inflammation representing the pathology of AD, rather than the IgE-mediated allergic reaction as a mechanism of childhood BA. Because the level of mite-specific IgE antibody in the younger BA children is elevated (93.6 +/- 41.2 PRU/ml), the result also indicates that mite-specific peripheral T lymphocytes do not play a critical role in stimulating the mite-specific IgE synthesis. On the contrary, the older BA children (8-15 y) showed an elevated mite-S.I.F. level (176.0 +/- 54.6) significantly higher than that in the non-atopic subjects (114.6 +/- 13.9, p < 0.05) as well as that in the younger BA children (p < 0.05). Because other investigators have reported that the level of mite-specific lymphocyte proliferation is increased in the adult BA patients, the transition from childhood BA to adult-type BA may start at the age of about 8 y.     

Microvascular function and rheologic changes in hyperdynamic sepsis

OBJECTIVE: To investigate the rheologic changes and circulatory abnormalities at the microvascular level during severe sepsis. DESIGN: Prospective, controlled trial. SETTING: Medical and surgical intensive care units of a university-affiliated hospital. PATIENTS: Nine normal controls and eight adult patients with severe sepsis who met the study entrance criteria. INTERVENTIONS: Forearm blood flow was measured at rest and during reactive hyperemia by air plethysmography. Simultaneous hemodynamic measurements and blood samples for rheologic measurements were taken. MEASUREMENTS AND MAIN RESULTS: Red blood cell deformability index was determined using a simple filtration procedure. Leukocyte aggregation in whole human blood was detected by using a leukergy test. Expression of the neutrophil adhesion molecule CD11b/CD18 was measured using a monoclonal antibody and flow cytometry. All data were taken within 24 hrs of the patient meeting criteria for entrance into the study. Cardiac output, oxygen delivery, and oxygen consumption measurements were consistent with the hyperdynamic phase of severe sepsis. Forearm blood flow was significantly (p < .05) greater in septic patients (21 +/- 3 mL/min) than in controls (12 +/- 2 to 36 +/- 5 mL/min (p < .05), while in the septic patients, forearm blood flow during reactive hyperemia increased from 21 +/- 3 to 32 +/- 4 mL/min. The ratio of forearm blood flow during reactive hyperemia to forearm blood flow at rest was 3.2 +/- 0.1 in the controls and 1.6 +/- 0.1 in the septic patients (p < .01). The red blood cell deformability index in whole blood was significantly (p < .01) decreased in the septic patients compared with the control subjects (0.41 +/- 0.07 vs. 0.98 +/- 0.08 mL/min). This difference remained true when the hematocrit was adjusted to 45% (0.82 +/- 0.06 vs. 1.04 +/- 0.06 mL/min; p < .05). Increased expression of the neutrophil adhesion molecule CD11b/CD18 was observed in septic patients (349 +/- 46 logarithmic fluorescence units) as compared with control subjects (233 +/- 26 logarithmic fluorescence units; p < .05). Leukergy was also significantly (p < .05) increased in septic patients (17.7 +/- 3.8%) as compared with control subjects (8.9 +/- 1.6%). A significant correlation was observed between leukergy and the expression of the neutrophil adhesion molecule CD11b/CD18 in controls and septic patients (r2 = .62; p < .01). Leukergy was also inversely correlated with whole blood red blood cell deformability index (r2 = .28; p < .05). CONCLUSIONS: Reactive hyperemia in the forearm is significantly diminished in patients with sepsis, suggesting impaired microvascular blood flow. Rheologic changes, including impaired red blood cell deformability, increased leukocyte aggregation, and endothelial adherence, may contribute to this abnormality by compromising effective capillary cross-sectional area.     

A new case of false aneurysm of the superior mesenteric artery

The sensitizing capacity of brewer's yeast (Saccharomyces cerevisiae) was studied with the skin prick test method in 449 subjects, including 226 atopic dermatitis (AD) patients, 50 patients with allergic rhinitis (AR) and/or asthma (A), and 173 nonatopic controls. A positive SPT reaction (> or = + +) was seen in 94% of patients with severe AD, in 76% with moderate AD, and in 25% with mild AD or no history of AD. Patients with AR and/or A and nonatopic controls displayed a positive reaction in only 8 and 2% of cases, respectively. There was also a parallel skin prick test reactivity with other yeasts including Pityrosporum ovale and Candida albicans, suggesting cross-reactivity. Parallel skin reactivity was observed also with molds and animal dander but not with pollen or house-dust mite. A significant correlation was also found between total serum IgE level and skin prick test (SPT) results with S. cerevisiae.     

Use of a novel electronic data collection system in multicenter studies of irritable bowel syndrome

To evaluate whether atherosclerosis may be associated with altered leucocyte rheology, we assessed leucocyte count (by Coulter counter), aggregation (by means of the leukergy test) and expression of adhesion molecules integrin LFA-1 and CD 44 (by means of immunofluorescence staining and flow cytometry) in 9 patients with carotid plus lower limb artery atherosclerosis (group A), 14 patients with carotid atherosclerosis only (group B) and 23 controls without atherosclerosis (group C). The level of LFA-1 (calculated as mean fluorescence channels-MFCs) on neutrophils, lymphocytes and monocytes was significantly higher (p < 0.05) in group A and B patients than in controls (group A-mean +/- SE: 383.77 +/- 9.42 vs 295.45 +/- 5.76; 474.22 +/- 8.86 vs 388.35 +/- 7.84; 457.66 +/- 12.03 vs 396.25 +/- 4.37. Group B: 322.42 +/- 6.36 vs 295.45 +/- 5.76; 421.42 +/- 7.21 vs 388.35 +/- 7.84; 415.71 +/- 7.73 vs 396.25 +/- 4.37, respectively); furthermore, the MFC of LFA-1 on neutrophils was significantly different (p < 0.05) between group A and B patients. The percentage of aggregated leucocytes was significantly higher (p < 0.05) in group A patients (4.46 +/- 1.07) than those in groups B (1.75 +/- 0.38) and C (1.43 +/- 0.25), whereas no significant difference was detected between groups B and C. Leucocyte number and expression of CD44 were not significantly different among the 3 groups. In conclusion, changes in leucocyte rheology are present in patients with atherosclerosis and may contribute to chronic ischaemia.     

Insulin-like growth factor I is an independent coregulatory modulator of natural killer (NK) cell activity

We aimed to investigate the natural killer (NK) cell activity in hGH-deficient adults and to analyze the effect of insulin-like growth factor (IGF)-I in vivo and in vitro on NK cell activity. NK cell activity was measured in a 4-h nonisotopic assay with europium-labeled and cryopreserved K-562 cells. NK-cell numbers were measured after incubation with murine monoclonal CD3 and CD16 antibodies by flow cytometry analysis. In a cross-sectional study, the basal and interferon-beta (IFN-beta) stimulated (1000 IU/ml) NK cell activity of 15 hGH-deficient patients and 15 age- and sex-matched controls was measured. The percentages and absolute numbers of CD3-/16+ NK-cells were not significantly different in the patient vs. control group. The basal and IFN-beta stimulated NK cell activity however was significantly decreased in the patient vs. control group at all effector/target (E/T) cell ratios from 12.5-100 (e.g. 17 +/- 3 vs. 28 +/- 3% lysis without IFN-beta, P < 0.05, and 42 +/- 4 vs. 57 +/- 4% lysis with IFN-beta, P < 0.05; both at E/T 50). IGF-I levels of patients and controls showed a significant positive correlation with NK cell activity (r = 0.37; P < 0.05). In an IGF-I in vitro study (IGF-I in vitro 250-1250 microg/L), the basal and IFN-beta stimulated NK cell activity of 13 hGH-deficient patients and of 18 normal subjects was significantly enhanced by IGF-I in vitro (e.g. GH-deficient patients: 9 +/- 2 vs. 10 +/- 2% lysis without IFN-beta, P < 0.05 and 25 +/- 4 vs. 30 +/- 4% lysis with IFN-beta, P < 0.005; and normal subjects: 15 +/- 3 vs. 23 +/- 3% lysis without IFN-beta, P < 0.001 and 35 +/- 4 vs. 44 +/- 5% lysis with IFN-beta, P < 0.001; both at IGF-I 500 microg/L). In summary, in our cross-sectional study, adult GH-deficient patients showed a significantly lower basal and IFN-beta stimulated NK cell activity than matched controls, despite equal NK cell numbers. IGF-I levels of patients and controls showed a weak positive correlation with NK cell activity. In an in vitro study, IGF-I significantly enhanced basal and IFN-beta stimulated NK cell activity of hGH-deficient patients and also of normal subjects. The decreased NK cell activity in GH-deficient patients may be caused at least in part by low serum IGF-I levels. IGF-I appears to be an independent coregulatory modulator of NK cell activity.     

Color Doppler imaging and plasma levels of endothelin-1 in low-tension glaucoma

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelin cells There are reports in the literature that ET-1 plasma levels are raised in low tension glaucoma (LTG). ET-1 plasma concentration and Color Doppler Imaging (CDI) evaluation in ophthalmic and posterior ciliary arteries were measured in 15 LTG patients and in 15 healthy subjects. The blood flow index recorded for the ophthalmic artery in normal subjects was a PSV of 36.646 +/- 6.611 cm/sec with RI of 0.717 +/- 0.019 while in the LTG patients it was 32.961 +/- 3.045 cm/sec (p < 0.003) with RI of 0.789 +/- 0.018 (p < 0.001). For the posterior ciliary arteries in the same two groups, we obtained a PSV of 13.878 +/- 4.149 cm/sec vs 8.720 +/- 1.645 cm/sec (p < 0.001) and an RI of 0.679 +/- 0.039 vs 0.722 +/- 0.024 (p < 0.001). The plasma ET-1 level in normal subjects was 1.720 +/- 0.174 pg while in LTG patients it was 2.947 +/- 0.217 pg (p < 0.001). On the basis of our experience, we think that GON and the visual field damage found in LTG can be attributed to an alteration in the endothelial self-regulating sections and consequent vascular insufficiency, particularly pronounced in the posterior ciliary arteries which, since it is these that provide the blood supply to the optic nerve head, leads to irreversible functional damage.     

Fusion variations of pancreatic ducts in patients with anomalous arrangement of pancreaticobiliary ductal system

Portal vein flow was recorded by color Doppler sonography in 31 patients with chronic heart failure and 18 control subjects. Compared with patients showing a forward flow (Group A), those with reversed portal vein flow (Group B) had higher prevalence of tricuspid regurgitation (75% vs. 43%), hepatic congestion (100% vs. 30%) and ascites (50% vs. 18%), and showed higher right atrial pressure (25.3 +/- 3.01 mmHg vs. 11.8 +/- 5.75 mmHg, p < 0.01). In controls, portal vein pulsatility ratio was 0.66 +/- 0.08, in Group A it was 0.46 +/- 0.28 (p < 0.01), in Group B -0.60 +/- 0.19 (p < 0.01). Portal vein pulsatility ratio negatively correlated with right atrial pressure (r = -0.87; p < 0.01). In Group A, hepatic congestion, ascites and tricuspid regurgitation were associated with a higher portal vein pulsatility. This study indicates that portal vein pulsatility ratio reflects the level of impairment of the right heart.     

2,4-(hydroxyphenyl)-ethanol, an antioxidative agent produced by Candida spp., impairs neutrophilic yeast killing in vitro

Culture supernatants of Candida albicans were examined for factors with inhibitory activity against the chemiluminescence of human neutrophils. By high resolution gel chromatography, a low-molecular-mass chemiluminescence inhibitor was isolated. The compound was identified as 2,4-(hydroxyphenyl)-ethanol. Half-maximum inhibition (IC50) of the chemiluminescence response of neutrophils phagocytizing opsonized zymosan or C. albicans occurred at 38.1 +/- 2.3 microM and 19.9 +/- 8.3 microM, respectively. As shown by flow cytometry, the compound protected C. albicans against phagocytic killing (IC50 = 73.8 +/- 16.9 microM). Substantially higher concentrations of the inhibitor were produced by C. albicans and C. tropicalis than by C. parapsilosis and C. glabrata, suggesting a potential role in pathogenicity ranking.     

Decreased melatonin levels in postmortem cerebrospinal fluid in relation to aging, Alzheimer's disease, and apolipoprotein E-epsilon4/4 genotype

Sleep disruption, nightly restlessness, sundowning, and other circadian disturbances are frequently seen in Alzheimer's disease (AD) patients. Changes in the suprachiasmatic nucleus and pineal gland are thought to be the biological basis for these behavioral disturbances. Melatonin is the main endocrine message for circadian rhythmicity from the pineal. To determine whether melatonin production was affected in AD, melatonin levels were determined in the cerebrospinal fluid (CSF) of 85 patients with AD (mean age, 75 +/- 1.1 yr) and in 82 age-matched controls (mean age, 76 +/- 1.4 yr). Ventricular postmortem CSF was collected from clinically and neuropathologically well defined AD patients and from control subjects without primary neurological or psychiatric disease. In old control subjects (>80 yr of age), CSF melatonin levels were half of those in control subjects of 41-80 yr of age [176 +/- 58 (n = 29) and 330 +/- 66 (n = 53) pg/mL, respectively; P = 0.016]. We did not find a diurnal rhythm in CSF melatonin levels in control subjects. In AD patients the CSF melatonin levels were only one fifth (55 +/- 7 pg/mL) of those in control subjects (273 +/- 47 pg/mL; P = 0.0001). There was no difference in the CSF melatonin levels between the presenile (42 +/- 11 pg/mL; n = 21) and the senile (59 +/- 8 pg/mL; n = 64; P = 0.35) AD patients. The melatonin level in AD patients expressing apolipoprotein E-epsilon3/4 (71 +/- 11 pg/mL) was significantly higher than that in patients expressing apolipoprotein E-epsilon4/4 (32 +/- 8 pg/ml; P = 0.02). In the AD patients no significant correlation was observed between age of onset or duration of AD and CSF melatonin levels. In the present study, a dramatic decrease in the CSF melatonin levels was found in old control subjects and even more so in AD patients. Whether supplementation of melatonin may indeed improve behavioral disturbances in AD patients should be investigated.     

Mannan-binding lectin in human serum, cerebrospinal fluid and brain tissue and its role in Alzheimer's disease

Mannan-Binding lectin (MBL) is a serum lectin which can activate the classical complement pathway. Complement proteins of the classical pathway have been found in the brains of patients with Alzheimer's disease (AD) in association with AD brain pathology. To investigate the role for MBL in AD we have looked for its presence in the brain by immunohistochemistry and determined the levels of MBL in paired samples of cerebrospinal fluid and serum from AD patients and controls. MBL was detected in association with blood vessels in the brain tissue of both AD patients and control subjects. There was no apparent difference in the distribution of MBL in the brain tissue between the two groups. The mean concentration of MBL in the CSF was 44% lower in AD patients than in controls (AD 154 +/- 35 pg/ml, n = 19; non-AD 276 +/- 50 pg/ml, n = 15, p < 0.05). The levels of MBL in serum were not significantly different in the two groups. Thus, this study shows that MBL is associated with blood vessels in the brains of both AD and control subjects. Moreover, CSF levels of MBL appear to be lower in AD patients than in control subjects which may indicate a higher degree of MBL consumption connected with complement activation in the AD patients.     

Decreased fecal bile acid output in patients with coronary atherosclerosis

In most patients with atherosclerosis, the underlying metabolic derangement remains undefined. Animal experiments have suggested that the ability to produce and excrete large amounts of bile acids may be an adaptation mechanism to cholesterol overload protecting against the atherogenic effects of cholesterol. However, there are very few data on bile acid excretion in human atherosclerosis. In the present study, we have investigated fecal bile acid secretion in subjects with and without coronary artery disease. The target group consisted of 30 patients with proven coronary artery disease and the control group consisted of 27 matched subjects without clinical or laboratory evidence of coronary atherosclerosis. Fecal bile acids were measured by gas-liquid chromatography from 24-hr stool collections under a controlled diet. The patients excreted significantly less bile acids than the controls (325+/-135 vs. 592+/-223 mg/day, respectively, p < 0.0001). The difference was primarily due to a reduced excretion of secondary bile acids. Less than 50% of deoxycholate was excreted by patients (180+/-81 mg/day) as compared to controls (367+/-168 mg/day, p < 0.0002), while lithocholic acid excretion was 111+/-62 mg/day in patients vs. 190 +/-70 mg/day in controls (p < 0.005). The fecal output of the two primary bile acids, cholic and chenodeoxycholic acid, did not differ significantly between patients and controls. The fecal output of total bile acids correlated with that of both secondary bile acids in patients as well as in controls. These findings suggest that patients with coronary heart disease are unable to excrete adequate amounts of bile acids to rid themselves of excess cholesterol, even if they are able to maintain a plasma cholesterol level comparable to that of healthy controls.     

Doppler analysis of pulmonary venous flow profiles in orthotopic heart transplant recipients: a comparison with mitral flow profiles and atrial function

Previous Doppler studies of transmitral flow profiles in heart transplant recipients suggested left ventricular (LV) diastolic dysfunction. The influence of left atrial filling and emptying on mitral Doppler profiles in heart transplant recipients has not been studied systematically. In the present study, pulmonary venous flow profiles, mitral flow profiles, left atrial area change and mitral annulus motion were analyzed in 20 orthotopic heart transplant recipient and 20 control subjects by transthoracic and transesophageal echocardiography and Doppler. Mitral flow profiles revealed a "restrictive" pattern with a high early-to-late diastolic flow velocity ratio in transplant patients (2.16 +/- 0.52 vs. 1.30 +/- 0.25, p < 0.0001), which was mainly due to a reduced late diastolic maximum mitral flow velocity (32.6 +/- 8.3 vs. 51.6 +/- 12.4 cm/s, p < 0.0001). Left atrial area change (35.9 +/- 13.9 vs. 58.1 +/- 17.0%, p < 0.0006) and mitral annulus motion (9.2 +/- 3.3 vs. 12.2 +/- 2.0%, p < 0.05) were reduced in transplant recipients, compared to controls. Pulmonary venous flow parameters in transplant recipients were markedly altered during systole, when pulmonary venous flow parameters are influenced primarily by atrial function rather than by diastolic LV properties: peak systolic flow velocity (45.5 +/- 8.2 vs. 62.3 +/- 14.0 cm/s, p < 0.001), maximum flow velocity ratio (0.87 +/- 0.19 vs. 1.45 +/- 0.33), time velocity integral of pulmonary venous flow during systole (9.3 +/- 2.3 vs. 17.1 +/- 4.0 cm, p < 0.001) and the systolic fraction of the time velocity integral (52.6 +/- 10.8 vs. 68.5 +/- 6.8%, p < 0.001) were lower in heart transplant recipients than in controls. These findings are compatible with atrial dysfunction and reduced mitral annulus motion. The results of this study indicate that LV diastolic dysfunction is not the only possible cause of altered transmitral Doppler profiles in heart transplant recipients. Atrial abnormalities represent a major contributing factor to altered mitral and pulmonary venous flow patterns. Analysis of transmitral Doppler profiles alone are therefore not adequate for analysis of diastolic LV function in heart transplant recipients.     

Prognostic value of Doppler transmitral flow velocity patterns in acute myocardial infarction

Doppler transmitral flow patterns are partially dependent on age. We investigated the correlations between the age-adjusted transmitral flow patterns, hemodynamic indexes, and the coronary and clinical outcome in 206 patients with acute myocardial infarction (AMI) and 102 normal control subjects. The peak flow velocity at atrial contraction was significantly lower in 50 of the 206 patients (24%) (low-A group) than in the 102 normal controls. Pulmonary capillary wedge pressure was significantly higher in the low-A group than in the remaining 156 patients with AMI (20 +/- 7 vs 11 +/- 5 mm Hg, p <0.001), and the cardiac index and left ventricular ejection fraction were significantly lower (2.2 +/- 0.6 vs 2.9 +/- 0.7 L/min/m2, p <0.001; 38 +/- 15% vs 52 +/- 13%, p <0.001). The incidence of cardiogenic shock was significantly higher in the low-A group than in the other patients with AMI (42% vs 19%, p <0.001). Regression analysis demonstrated a significant association between decreased atrial filling velocity and increased in-hospital mortality as well as the incidence of heart failure in AMI (p <0.001). The 5-year mortality rate was also significantly higher in the low-A group (p <0.001). The age-adjusted transmitral flow pattern in AMI can identify patients with left ventricular dysfunction, which can lead to a poor prognosis.     

Estimation of the pulmonary capillary wedge pressure from transesophageal pulsed Doppler echocardiography of pulmonary venous flow: influence of the respiratory cycle during mechanical ventilation

AIM: Endothelial Dysfunction (ED) is an early functional marker and Intima-Media-Thickness (IMT) an early morphological parameter of atherogenesis. Is there a simple, non-invasive routine method for the identification of atherosclerosis including the detection of the early functional endothelial impairment seen for example in Type 2 diabetic patients? METHODS: Using high resolution ultrasound we studied peripheral endothelial function expressed as flow-associated dilation (FAD %) and endothelial independent vasodilation after administration of 400 micrograms glycerol trinitrate (postnitro %) of the brachial artery as well as IMT of the common carotid artery in 25 Type 2 diabetic patients and their matched controls. RESULTS: (mean +/- SD): The diabetic patients showed a remarkable ED (FAD%: 3.8 +/- 3.3 vs. 6.9 +/- 4.4%, p = 0.01) and an already increased IMT (0.72 +/- 0.14 vs. 0.62 +/- 0.10 mm, p < 0.01). The similar postnitro % in diabetic patients and controls suggests normal dilating capacity of the studied vessels in the diabetic patients (postnitro %: 14.3 +/- 9.4 vs. 14.9 +/- 8.5%, p = ns). CONCLUSION: With a combination of these three sonomorphological parameters it is possible to document the stage of atherosclerosis including endothelial dysfunction in Type 2 diabetic patients.     

Cardiac and skeletal muscle insulin resistance in patients with coronary heart disease. A study with positron emission tomography

Patients with coronary artery disease or heart failure have been shown to be insulin resistant. Whether in these patients heart muscle participates in the insulin resistance, and whether reduced blood flow is a mechanism for such resistance is not known. We measured heart and skeletal muscle blood flow and glucose uptake during euglycemic hyperinsulinemia (insulin clamp) in 15 male patients with angiographically proven coronary artery disease and chronic regional wall motion abnormalities. Six age- and weight-matched healthy subjects served as controls. Regional glucose uptake was measured by positron emission tomography using [18F]2-fluoro-2-deoxy-D-glucose (FDG), blood flow was measured by the H2(15)O method. Myocardial glucose utilization was measured in regions with normal perfusion and wall motion as assessed by radionuclide ventriculography. Whole-body glucose uptake was 37+/-4 micromol x min(-1) x kg(-1) in controls and 14+/-2 mciromol x min(-1) x kg(-1) in patients (P = 0.001). Myocardial blood flow (1.09+/-0.06 vs. 0.97+/-0.04 ml x min(-1) x g(-1), controls vs. patients) and skeletal muscle (arm) blood flow (0.046+/-0.012 vs. 0.043+/-0.006 ml x min(-1) x g(-1)) were similar in the two groups (P = NS for both). In contrast, in patients both myocardial (0.38+/-0.03 vs. 0.70+/-0.03 micromol x min(-1) x g(-1), P = 0.0005) and muscle glucose uptake (0.026+/-0.004 vs. 0.056+/-0.006 micromol x min(-1) x g(-1), P = 0.005) were markedly reduced in comparison with controls. In the whole dataset, a direct relationship existed between insulin-stimulated glucose uptake in heart and skeletal muscle. Patients with a history of myocardial infarction and a low ejection fraction are insulin resistant. This insulin resistance affects both the myocardium and skeletal muscle and is independent of blood flow.     

Credibility of treatment in controlled trials of acupuncture

Total body water (TBW) was measured by deuterium oxide dilution (D2O) and predicted by bioelectric impedance analysis (BIA) (Deurenberg, Schouten, Andreoli and De Lorenzo 1993) in 21 subjects with Schistosoma mansoni infection and 17 healthy controls of similar age (32.8 +/- 13.7 years, n=38). Patients were selected to have no visible fluid retention and no cardiac or renal abnormalities. Body hydration (TBW per kg of body weight) was significantly higher in patients with schistosomiasis than in controls (62.9 +/- 3.6 vs 57.4 +/- 4.3%, p < 0.0005). A significant correlation was found between albumin levels and TBW% on the pooled sample (n=38; r=0.660, p < 0.0001). This relationship was not influenced by the presence of disease, as determined by ANCOVA. Values of TBW predicted by BIA were highly correlated and not significantly different (p=n.s., ANOVA) from those measured by D2O in both controls and patients (r=0.854, p < 0.001, SEE = 2.3 1, CV=5.9% and r=0.848, p < 0.001, SEE=4.0 1, CV=9.3%, respectively). The bias (TBW by BIA - TBW by D2O) was of 0.9 +/- 3.7 in controls and of -1.3 +/- 4.2 1 in patients. This bias was significantly correlated to TBW% in patients (r=0.575, p < 0.05) but not in controls (p=n.s.). It is concluded that subjects with schistosomiasis show an apparent subclinical increase in body hydration which could affect the prediction of TBW from BIA.     

QT interval dispersion in healthy subjects and survivors of sudden cardiac death: circadian variation in a twenty-four-hour assessment

Twenty-four-hour acquisition of QT dispersion (QTd) from the Holter and the circadian variation of QTd were evaluated in 20 survivors of sudden cardiac death (SCD), in 20 healthy subjects, and in 14 control patients without a history of cardiac arrest who were age, sex, diagnosis and therapy matched to 14 SCD patients. Computer-assisted QT measurements were performed on 24-hour Holter recordings; each recording was divided into 288 5-minute segments and templates representing the average QRST were generated. QTd was calculated as the difference between QT intervals in leads V1 and V5 for each template on Holter. The 24-hour mean QTd was significantly greater in SCD patients (40 +/- 28 ms) than in healthy subjects (20 +/- 10 ms) and control patients (15 +/- 5 ms) (p <0.05). There was a circadian variation in QTd with greater values at night (0 to 6 A.M.) than at daytime (10 A.M. to 4 P.M.) in healthy subjects (25 +/- 13 vs 15 +/- 8 ms, p <0.001) and control patients (18 +/- 10 vs 12 +/- 4 ms p <0.05), whereas in SCD patients there was no significant difference between night and day values (45 +/- 31 vs 37 +/- 28 ms, p = NS). It is concluded that QTd measured by Holter was greater in SCD patients than in healthy subjects and matched control patients during the entire day. QTd has a clear circadian variation in normal subjects, whereas this variation is blunted in SCD patients. QTd measured on Holter differentiates survivors of cardiac arrest and may be a useful tool for risk stratification.     

Fungicidal effect of tyrothricin on Candida albicans

Tyrothricin, a polypeptide antibiotic, is active against yeast cells. Tyrothricin was rapidly fungicidal towards Candida albicans. Concentration of four times the minimum inhibitory (25 mg l-1) reduced the yeast numbers by more than 3 log10 within 1 h. Similar results were obtained in a flow cytometric antifungal activity assay using the new two-colour probe for yeast viability, FUN-1, which measures impairment of metabolic activity. The respiratory activity of Candida albicans, measured in a XTT kinetic assay, was significantly reduced in comparison with controls by 3.12 mg l-1 of the substance. Because fungicidal concentrations of tyrothricin are locally achievable in patients, an evaluation of the local effect of tyrothricin in patients suffering from mucosal infections with Candida species should be considered.     

Clinical evaluation of urinary leukotriene E4 levels in asymptomatic bronchial asthma

To evaluate the significance of peptide leukotrienes (LTC4, D4, E4) in asymptomatic asthmatic patients, we measured urinary LTE4 levels which is thought to reflect in vivo production of peptide LTs. Urinary LTE4, was extracted using C18 solid phase column and measured by radioimmunoassay. There was no significant difference in urinary LTE4 levels among asthmatics with different severity or between atopic and non-atopic asthmatics. Urinary LTE4 levels were significantly elevated in asthmatics compared with normal controls (p < 0.05). When compared with normal controls, urinary LTE4 levels were significantly elevated in moderate to severe asthma (p < 0.05), and non-atopic asthmatics (p < 0.001). Urinary LTE4 levels were significantly elevated in aspirin-sensitive asthmatics compared with aspirin-tolerant asthmatics (p < 0.05). There was no significant difference in urinary LTE4 levels among aspirin-sensitive asthmatics with different severity. These results suggest that increased production of peptide LTs is a characteristic in aspirin-sensitive asthma, and that the severity and type of asthma and the presence of aspirin-sensitive asthma should be taken into consideration in the analysis of urinary LTE4 levels.     

Membrane modifications of red blood cells in Alzheimer's disease

Red blood cells (RBC) from 24 Alzheimer's disease (AD) patients, 18 age- and sex-matched nondemented (ND) patients, hospitalized in the same facility for orthopedic problems, and 18 healthy volunteers aged 30-52 years were studied in order to gain insight into the nature of RBC membrane modifications in AD. Significant differences were found between RBC from AD and ND patients or young controls respectively for annexin V-binding (45.5 +/- 18.0% vs 27.1 +/- 14.7 and 2.7 +/- 1.9, p = .003), fraction of glycerol resistant cells (30.8 +/- 11.1% vs 19.6 +/- 6.4 and 10.2 +/- 3.1, p = .026), cell electrophoretic mobility in polymer (1.028 +/- 0.022 microns sec-1 V-1 cm vs 1.046 +/- 0.022 and 1.053 +/- 0.021, p = .02) and only limited significance for the filterability (1.46 +/- 0.12 msec vs 1.58 +/- 0.11 and 1.54 +/- 0.11, p = 0.1). A logistic analysis, using simultaneously several features as independent variables, suggested the combined use of annexinV- binding, glycerol resistance, and cell filterability which allowed the assignment of 95% of patients from this cohort to the right group. A prospective analysis of a larger cohort is required for the estimation of the diagnostic value of this test battery. In addition, the high level of annexin binding is characteristic of a disruption of the phospholipid asymmetry in aged or damaged cells, while the high glycerol resistance combined with low electrophoretic mobility an rigidity characterize young RBC, thus indicating an enhanced turnover of RBC in Alzheimer's disease.