Propagule pressure increase and phylogenetic diversity decrease community's susceptibility to invasion.

BACKGROUND: Invasions pose a large threat to native species, but the question of why some species are more invasive, and some communities more prone to invasions than others, is far from solved. Using 10 different three-species bacterial communities, we tested experimentally if the phylogenetic relationships between an invader and a resident community and the propagule pressure affect invasion probability. RESULTS: We found that greater diversity in phylogenetic distances between the members of resident community and the invader lowered invasion success, and higher propagule pressure increased invasion success whereas phylogenetic distance had no clear effect. In the later stages of invasion, phylogenetic diversity had no effect on invasion success but community identity played a stronger role. CONCLUSIONS: Taken together, our results emphasize that invasion success does not depend only on propagule pressure, but also on the properties of the community members. Our results thus indicate that invasion is a process where both invader and residing community characters act in concert.

Experimental evolution in fluctuating environments: tolerance measurements at constant temperatures incorrectly predict the ability to tolerate fluctuating temperatures.

The ability to predict the consequences of fluctuating environments on species distribution and extinction often relies on determining the tolerances of species or genotypes in different constant environments (i.e. determining tolerance curves). However, very little is known about the suitability of measurements made in constant environments to predict the level of adaptation to rapidly fluctuating environments. To explore this question, we used bacterial clones adapted to constant or fluctuating temperatures and found that measurements across a range of constant temperatures did not indicate any adaptation to fluctuating temperatures. However, adaptation to fluctuating temperatures was only apparent if growth was measured during thermal fluctuation. Thus, tolerance curves based on measurements in constant environments can be misleading in predicting the ability to tolerate fast environmental fluctuations. Such complications could lead to false estimates of the genetic merits of genotypes and extinction risks of species due to climate change-induced thermal fluctuations.

Salt chamber treatment is ineffective in treating eosinophilic inflammation in asthma.

BACKGROUND: We have shown that salt chamber treatment reduces airway hyper-responsiveness as an add-on therapy in adult asthmatics on inhaled corticosteroids. METHODS: We assessed whether this effect is due to the suppression of eosinophilic airway inflammation. Thirty-nine adult asthmatics on inhaled corticosteroids were randomized to receive active salt chamber treatment with low-salt treatment 6.6 mg/m(3) (n = 14), high-salt treatment 10.8 mg/m(3) (n = 15) or placebo 0.3 mg/m(3) (n = 10) 10 times in a 2 weeks' period in a double-blind manner. RESULTS: The level of induced sputum eosinophilic cationic protein µg/l, was 3070 before and 4651 after the low-salt treatment period, on average. In the high-salt treatment group, it was 12 192 µg/l vs 11 803 and in the placebo group 3942 vs 4144, respectively. Salt chamber treatment had no effect on sputum eosinophil or neutrophil cell numbers. CONCLUSIONS: The reduction in hyper-responsiveness observed in the previous study is probably not due to the effect on eosinophilic inflammation.

Birch pollen honey for birch pollen allergy--a randomized controlled pilot study.

BACKGROUND: Only a few randomized controlled trials have been carried out to evaluate various complementary treatments for allergic disorders. This study assessed the effects of the preseasonal use of birch pollen honey (BPH; birch pollen added to honey) or regular honey (RH) on symptoms and medication during birch pollen season. METHODS: Forty-four patients (59% female, mean age 33 years) with physician-diagnosed birch pollen allergy consumed either BPH or RH daily in incremental amounts from November 2008 to March 2009. Seventeen patients (53% female, mean age 36 years) on their usual allergy medication served as the control group. From April to May, patients recorded daily rhinoconjunctival and other symptoms and their use of medication. Fifty patients completed the study. RESULTS: During birch pollen season in 2009, BPH patients reported a 60% lower total symptom score (p < 0.01), twice as many asymptomatic days (p < 0.01), and 70% fewer days with severe symptoms (p < 0.001), and they used 50% less antihistamines (p < 0.001) compared to the control group. The differences between the BPH and RH groups were not significant. However, the BPH patients used less antihistamines than did the RH patients (p < 0.05). CONCLUSIONS: Patients who preseasonally used BPH had significantly better control of their symptoms than did those on conventional medication only, and they had marginally better control compared to those on RH. The results should be regarded as preliminary, but they indicate that BPH could serve as a complementary therapy for birch pollen allergy.

Corticosteroid therapy in intensive care unit patients with PCR-confirmed influenza A(H1N1) infection in Finland.

OBJECTIVE: To evaluate the incidence, treatment, and outcome of influenza A(H1N1) in Finnish intensive care units (ICUs) with special reference to corticosteroid treatment. METHODS: During the H1N1 outbreak in Finland between 11 October and 31 December 2009, we prospectively evaluated all consecutive ICU patients with high suspicion of or confirmed pandemic influenza A(H1N1) infection. We assessed severity of acute disease and daily organ dysfunction. Ventilatory support and other concomitant treatments were evaluated and recorded daily throughout the ICU stay. The primary outcome was hospital mortality. RESULTS: During the 3-month period altogether 132 ICU patients were tested polymerase chain reaction-positive for influenza A(H1N1). Of these patients, 78% needed non-invasive or invasive ventilatory support. The median (interquartile) length of ICU stay was 4 [2-12] days. Hospital mortality was 10 of 132 [8%, 95% confidence interval (CI) 3-12%]. Corticosteroids were administered to 72 (55%) patients, but rescue therapies except prone positioning were infrequently used. Simplified Acute Physiology Score II and Sequential Organ Failure Assessment scores in patients with and without corticosteroid treatment were 31 [24-36] and 6 [2-8] vs. 22 [5-30] and 3 [2-6], respectively. The crude hospital mortality was not different in patients with corticosteroid treatment compared to those without: 8 of 72 (11%, 95% CI 4-19%) vs. 2 of 60 (3%, 95% CI 0-8%) (P = 0.11). CONCLUSIONS: The majority of H1N1 patients in ICUs received ventilatory support. Corticosteroids were administered to more than half of the patients. Despite being more severely ill, patients given corticosteroids had comparable hospital outcome with patients not given corticosteroids.

Duration of clinical reactivity in cow's milk allergy is associated with levels of specific immunoglobulin G4 and immunoglobulin A antibodies to beta-lactoglobulin.

BACKGROUND: The development of tolerance in IgE-mediated allergies has been associated with lower cow's milk (CM)-specific IgE levels, increasing levels of specific IgG4 and, more contestably, IgA. OBJECTIVE: We investigated whether specific antibody responses to CM proteins differ over time between patients who recovered from cow's milk allergy (CMA) by the age of 3 years and those who developed tolerance only after the age of 8 years. METHODS: The study population comprised of 83 patients with IgE-mediated CMA. They belonged to a cohort of 6209 healthy, full-term infants followed prospectively for the emergence of CMA. Serum samples were available at diagnosis (median age 7 months), 1 year later (median 19 months) and at follow-up (median 8.5 years). Age-matched control subjects with no history of CMA (n=76) participated in the follow-up. Serum levels of IgE antibodies to CM were measured using UniCAP. Levels of IgA, IgG1 and IgG4 antibodies to beta-lactoglobulin and alpha-casein were measured using ELISA. RESULTS: Patients with persistent CMA at the age of 8 years (n=18 at diagnosis, n=16 at later time-points) had higher CM-specific IgE levels at all three time-points (P<0.001) compared with patients who became tolerant by 3 years (n=55 at diagnosis, n=54 a year later, n=40 at follow-up). They had lower serum IgA levels to beta-lactoglobulin at diagnosis (P=0.01), and lower IgG4 levels to beta-lactoglobulin (P=0.04) and alpha-casein (P=0.05) at follow-up. CONCLUSION: High CM-specific IgE levels predict the persistence of CMA. Development of tolerance is associated with elevated levels of beta-lactoglobulin-specific serum IgA at the time of diagnosis, and later increasing specific IgG4 levels to beta-lactoglobulin and alpha-casein.

Cow's milk allergy as a predictor of bronchial hyperresponsiveness and airway inflammation at school age.

BACKGROUND: Cow's milk allergy (CMA) has been found to be associated with an increased incidence of asthma at school age. However, prospective population-based studies of CMA and the development of airway inflammation and bronchial hyperresponsivess (BHR) are lacking. OBJECTIVE: The aims of this study was to evaluate CMA as a risk factor for BHR and airway inflammation presented later in childhood. METHODS: We followed prospectively 118 children with CMA and invited them to a clinical visit at a mean age of 8.6 years including the measurement of exhaled nitric oxide (FE(NO) ) and bronchial challenge with histamine. Ninety-four patients and 80 control subjects from the same cohort participated. RESULTS: At school age, children with a history of CMA had higher FE(NO) levels (P=0.0009) and more pronounced responsiveness to histamine (P=0.027) than their controls. Stratified analysis showed a significant difference only in IgE-positive CMA. Multinomial logistic regression analysis showed that IgE-positive CMA [odds ratio (OR) 3.51; 95% confidence intervals (CI) 1.56-7.90; P=0.002] and a history of wheeze during the first year of life (OR 2.81; 95% CI 1.16-6.84; P=0.023) were independent explanatory factors for increased FE(NO) , and IgE-positive CMA (OR 3.37; 95% CI 1.03-10.97; P=0.044) and parental smoking (OR 3.41; 95% CI 1.14-10.22; P=0.028) for increased BHR, whereas for IgE-negative CMA, no associations with FE(NO) or BHR were found. In the CMA group, those exposed to CM very early at the maternity hospital, had less BHR (P=0.002). CONCLUSIONS: Compared with their controls, children with a history of IgE-positive CMA show signs of airway inflammation, expressed as higher FE(NO) , and more pronounced bronchial responsiveness to histamine at school age. In contrast to IgE-negative CMA, IgE-positive CMA is a significant predictor of increased FE(NO) and BHR at school age. Very early exposure to CM was associated with less BHR.

Evaluation of QT interval duration and dispersion and proposed clinical criteria in diagnosis of long QT syndrome in patients with a genetically uniform type of LQT1.

OBJECTIVES: This study investigated the ability of QT duration, QT dispersion (QTD) and clinical diagnostic criteria to correctly identify genetically documented LQT1 type long QT syndrome (LQTS) patients, and to separate symptomatic and asymptomatic LQT1 patients. BACKGROUND: Ventricular repolarization has played an essential role both in diagnosis and risk assessment of LQTS. Today, molecular genetic techniques permit unequivocal identification of many LQTS patients. METHODS: QT interval and QTD in 12 symptomatic and 18 asymptomatic LQT1 patients and their 43 healthy relatives were evaluated. The sensitivity and specificity of upper normal limits of QT interval, two QT interval adjustment methods (Bazett's and Fridericia's formulas), and the proposed clinical criteria for LQTS were assessed. Occurrence of a mutant (D188N) KVLQT1 gene was considered as the basis of classification into affected and nonaffected individuals. RESULTS: Diagnostic sensitivity and specificity values were 90% and 88% using Bazett's formula, and 80% and 100% using Fridericia's cubic root formula or upper normal limits for QT interval. Suggested diagnostic criteria for LQTS reached 100% specificity, but 47% of the DNA-documented LQT1 patients were classified into the category of low or intermediate probability of LQTS. QT interval and heart rate did not differ between symptomatic (464 +/- 47 ms, 70 +/- 9 min(-1)) and asymptomatic 460 +/- 41 ms, 65 +/- 13 min(-1)) LQT1 patients. QTD was increased in symptomatic LQT1 patients compared to unaffected relatives (66 +/- 48 vs. 37 +/- 15 ms, p = 0.02), but symptomatic patients LQT1 did not differ from asymptomatic (45 +/- 19 ms). CONCLUSIONS: Not all LQT1 patients can be distinguished from healthy relatives by assessment of QT duration or clinical criteria. Presence of LQT1 gene can carry the risk of cardiac events even with no or only marginal prolongation of QT interval.

Systemic suppression of human peripheral blood phagocytic leukocytes after whole-body UVB irradiation.

We examined systemic effects of whole-body UVB irradiation on human peripheral blood phagocytes. We found that 24 h after a single erythemal dose of UVB radiation two phagocyte functions, adhesion and phagocytosis, were reduced by 50%. This functional suppression was accompanied by a significant decrease in the expression of complement receptors (CR1 and CR3) and IgG Fc receptors (FcRII and FcRIII). The greatest reduction (47%) was observed in CR3, which is important for both adhesion and phagocytosis. A kinetic analysis showed that both CR1 and CR3 levels started to decrease 15 min after the UVB exposure, reaching the lowest levels at 4.5- and 24-h time points, respectively. The down-modulation of CRs after whole-body UVB exposure was not due to a defective receptor synthesis or translocation from internal stores to plasma membrane because the maximal CR levels in stimulated cells were not affected by UVB. No change in the serum soluble ICAM-1 was detected after UVB, which rules out CD1 1b epitope masking by sICAM-1. UVB did not release low-receptor-density myeloid progenitor cells from storage pools into circulation. Interleukin 10, a mediator of UVB-induced immunosuppression, was unable to modulate CR expression in vitro. When seven suberythemal whole-body UVB exposures were given repeatedly within 2 weeks, a significant decrease in CR expression was seen, which was greatest after three irradiations. Our data suggest that an exposure to UVB has systemic effects in humans which, possibly due to the down-modulation of preexisting cell-surface receptors, suppress some important functions of circulating phagocytic cells.

Time-resolved fluorometric assay for leukocyte adhesion using a fluorescence enhancing ligand.

A new 96-well microtiter plate, time-resolved fluorometric assay was developed to measure leukocyte adhesion in vitro. The assay is based on loading leukocytes with a fluorescence enhancing ligand 2,2':6', 2"-terpyridine-6,6"-dicarboxylic acid (TDA), which in its acetoxymethyl ester form readily diffuses through the cell membrane. After hydrolysis by nonspecific intracellular esterases, the impermeable TDA accumulates inside the cells. When the TDA-labeled adherent leukocytes are lysed, the ligand is released and reacts with europium present in the lysis solution to produce a highly fluorescent and stable chelate. The fluorescence signal can be measured by time-resolved fluorometry and correlates directly with the number of adherent cells. In this study, we have optimized both the TDA-labeling and adhesion assay conditions in isolated human neutrophils. Furthermore, we have compared the assay with a traditional microscopic counting method. This time-resolved fluorometric assay provides a rapid, reproducible and convenient method for the routine analysis of leukocyte adhesion.

Breast-feeding and the development of cows' milk protein allergy.

Early feeding with cows' milk (CM) may cause cows' milk allergy (CMA). Breast milk contains many immune factors which compensate for the undeveloped defence mechanisms of the gut of the newborn infant. We studied the effect of supplementary CM feeding at the maternity hospital on the subsequent incidence of CMA, the effects of formula and breast feeding on the subsequent immunologic types of CMA, and the importance of immune factors present in colostrum in the immune responses of infants with CMA. In a cohort of 6209 infants, 824 were exclusively breast-fed and 87% required supplementary milk while in the maternity hospital: 1789 received CM formula, 1859 pasteurized human milk, and 1737 whey hydrolysate formula. The cumulative incidence of CMA, verified by a CM elimination-challenge test, was 2.4% in the CM, 1.7% in the pasteurized human milk and 1.5% in the whey hydrolysate group. Among these infants, exposure to CM at hospital and a positive atopic heredity increased the risk of CMA. Of the exclusively breast-fed infants, 2.1% had CMA. Risk factors for the development of IgE-mediated CMA were: exposure to CM at hospital, breast-feeding during the first 8 weeks at home either exclusively or combined with infrequent exposure to small amounts of CM and long breast-feeding. The content of transforming growth factor-beta1 (TGF-beta1) in colostrum from mothers of infants with IgE-mediated CMA was lower than from mothers of infants with non-IgE-mediated CMA. In infants with CMA, TGF-beta1 in colostrum negatively correlated with the result of skin prick test and the stimulation of peripheral blood mononuclear cells to CM, but positively with infants' IgA and IgG antibodies to CM proteins. Feeding of CM formula at maternity hospital increases the risk of CMA, but exclusive breast-feeding does not eliminate the risk. Prolonged breast-feeding exclusively or combined with infrequent exposure to small amounts of CM during the first 8 weeks induces the development of IgE-mediated CMA. Colostral TGF-beta1 may inhibit IgE- and cell mediated reactions and promote IgG-IgA antibody production to CM in infants prone to developing CMA.

Design and development of the THYROID system.

This paper discusses the design and development of our decision support system for thyroid function diagnostics, named Thyroid. The objective of our work has been to develop a decision support system for practical use. The Thyroid system has been designed to utilize the existing laboratory test results of the patient. The task of the system is to produce interpretative reports for the clinicians. The system is integrated with the laboratory information system of University Central Hospital of Turku. It has been under clinical testing for more than 2 years with over 1600 actual cases. The system has produced promising results and it has also shown the limitations of the knowledge-based systems in this infrastructure environment.

Etiology of toe-web disease in Al-Ain, United Arab Emirates: bacteriological and mycological studies.

We examined and sampled 45 patients with toe-web intertrigo for bacteriological and mycological studies. Prominent isolated pathogens were the genus Candida (57.7%), genus Aspergillus (28.8%), Pseudomonas aeruginosa (26.7%) and coliforms (24.4%). Dermatophytes scored 4.4% (Trichophyton rubrum). There were 43 patents (95.5%) who presented with marked hyperkeratosis and maceration of the toe-webs involved. The tradition of the Emirati population of sitting cross-legged may, over time, induce in the toe-webs of overweight individuals a macerated pressure-reaction hyperkeratosis that is colonized by environmental germs. T. rubrum and T. mentagrophytes are uncommon in the Al-Ain environment and this may explain the rarity of dermatophytes in toe-web intertrigo in our study.