Atopic dermatitis severity during exposure to air pollutants and weather changes with an Artificial Neural Network (ANN) analysis.

BACKGROUND: Epidemiological studies have shown an association between global warming, air pollution, and allergic diseases. Several air pollutants, including volatile organic compounds, formaldehyde, toluene, nitrogen dioxide (NO2 ), and particulate matter, act as risk factors for the development or aggravation of atopic dermatitis (AD). We evaluated the impact of air pollutants and weather changes on AD patients. MATERIALS AND METHODS: Sixty AD patients ≥5 years of age (mean age: 23.5 ± 12.5 years), living in the Campania Region (Southern Italy), were followed for 18 months. The primary outcome was the effect of atmospheric and climatic factors on signs and symptoms of AD, assessed using the SCORAD (SCORing Atopic Dermatitis) index. We measured mean daily temperature (TOD), outdoor relative humidity (RH), diurnal temperature range (DTR), precipitation, particulate with aerodynamic diameter ≤ 10 µm (PM10 ), NO2 , tropospheric ozone (O3 ), and total pollen count (TPC). A multivariate logistic regression analysis was used to examine the associations of AD signs and symptoms with these factors. An artificial neural network (ANN) analysis investigated the relationships between weather changes, environmental pollutants, and AD severity. RESULTS: The severity of AD symptoms was positively correlated with outdoor temperatures (TOD, DTR), RH, precipitation, PM10 , NO2 , O3 , and TPC. The ANN analysis also showed a good discrimination performance (75.46%) in predicting disease severity based on environmental pollution data, but weather-related factors were less predictive. CONCLUSION: The results of the present study provide evidence that weather changes and air pollutions have a significant impact on skin reactivity and symptoms in AD patients, increasing the severity of the dermatitis. The knowledge of the single variables proportion on AD severity symptoms is important to propose alerts for exacerbations in patients with AD of each age. This finding represents a good starting point for further future research in an area of increasingly growing interest.

Urban air pollution and climate change: "The Decalogue: Allergy Safe Tree" for allergic and respiratory diseases care.

BACKGROUND: According to the World Health Organization, air pollution is closely associated with climate change and, in particular, with global warming. In addition to melting of ice and snow, rising sea level, and flooding of coastal areas, global warming is leading to a tropicalization of temperate marine ecosystems. Moreover, the effects of air pollution on airway and lung diseases are well documented as reported by the World Allergy Organization. METHODS: Scientific literature was searched for studies investigating the effect of the interaction between air pollution and climate change on allergic and respiratory diseases. RESULTS: Since 1990s, a multitude of articles and reviews have been published on this topic, with many studies confirming that the warming of our planet is caused by the "greenhouse effect" as a result of increased emission of "greenhouse" gases. Air pollution is also closely linked to global warming: the emission of hydrocarbon combustion products leads to increased concentrations of biological allergens such as pollens, generating a mixture of these particles called particulate matter (PM). The concept is that global warming is linked to the emission of hydrocarbon combustion products, since both carbon dioxide and heat increase pollen emission into the atmosphere, and all these particles make up PM10. However, the understanding of the mechanisms by which PM affects human health is still limited. Therefore, several studies are trying to determine the causes of global warming. There is also evidence that increased concentrations of air pollutants and pollens can activate inflammatory mediators in the airways. Our Task Force has prepared a Decalogue of rules addressing public administrators, which aims to limit the amount of allergenic pollen in the air without sacrificing public green areas. CONCLUSIONS: Several studies underscore the significant risks of global warming on human health due to increasing levels of air pollution. The impact of climate change on respiratory diseases appears well documented. The last decades have seen a rise in the concentrations of pollens and pollutants in the air. This rise parallels the increase in the number of people presenting with allergic symptoms (e.g., allergic rhinitis, conjunctivitis, and asthma), who often require emergency medical care. Our hope is that scientists from different disciplines will work together with institutions, pharmaceutical companies and lay organizations to limit the adverse health effects of air pollution and global warming.

Serological and molecular identification of Legionella spp. isolated from water and surrounding air samples in Italian healthcare facilities.

BACKGROUND: Legionella is an intracellular microorganism living in natural and artificial aquatic environments. Although its transmission to humans is linked to the inhalation of contaminated aerosols, there is no validated air sampling method for the control and prevention of the disease. The aim of the present study was to provide more information on the distribution of Legionella spp. in indoor environments and to determine whether the same Legionella strains are isolated from air and water samples. METHODS: Ten healthcare facilities located in seven regions of Italy were enrolled. The serological typing of Legionella spp. from water samples and the surrounding air by active and passive sampling was assessed using polyvalent and monovalent antisera. Subsequently, the strains identified as Legionella pneumophila (Lpn) underwent molecular typing by sequence-based typing (SBT) using seven genes (flaA, pilE, asd, mip, mompS, proA, and neuA). The allelic profile number was assigned using the European Working Group for Legionella Infections-SBT database. RESULTS: Lpn serogroup 6 was the most prevalent serogroup; it was found simultaneously in the air and water samples of three different healthcare facilities. In the remaining seven hospitals, Lpn serogroups 1, 6, 7, 9, and 12 were isolated exclusively from water samples. The molecular investigation showed that Lpn strains in the water and air samples of each positive healthcare facility had the same allelic profile. Strains, identified as sequence types (STs) 728 and ST 1638+ST 1324, were isolated in two respective healthcare facilities, and a new strain, identified as ST 1989, was obtained in one healthcare facility. CONCLUSION: The application of the SBT method allowed to verify the homology among Legionella strains from water samples and the surrounding air. The results showed that the same Lpn strains were present in the air and water samples, and a new Legionella strain was identified.

[Legionella spp. contamination in indoor air: preliminary results of an Italian multicenter study]. / La contaminazione indoor da Legionella spp: risultati preliminari di una indagine multicentrica italiana.

OBJECTIVE: To propose a standardized protocol for the evaluation of Legionella contamination in air. DESIGN: A bathroom having a Legionella contamination in water >1,000 cfu/l was selected in 10 different healthcare facilities. Air contamination was assessed by active (Surface Air System, SAS) and passive (Index of Microbial Air, IMA) sampling for 8 hours, about 1 m away from the floor and 50 cm from the tap water. Two hundred liters of air were sampled by SAS every 12 min, after flushing water for 2 min. The IMA value was calculated as the mean value of colony forming units/16 plates exposed during sampling (2 plates/hour). Water contamination was evaluated at T0, after 4 and 8 hours, according to the standard methods. RESULTS: Air contamination by Legionella was found in three healthcare facilities (one with active and two with passive sampling), showing a concomitant tap water contamination (median=40,000; range 1,100-43,000 cfu/l). The remaining seven hospitals isolated Legionella spp. exclusively from water samples (median=8,000; range 1,200-70,000 cfu/l). CONCLUSIONS: Our data suggest that environmental Legionella contamination cannot be assessed only through the air sampling, even in the presence of an important water contamination.

Hymenoptera Venom Immunotherapy: Tolerance and Efficacy of an Ultrarush Protocol versus a Rush and a Slow Conventional Protocol.

Background and Objective. Various venom immunotherapy (VIT) protocols are available for Hymenoptera allergy. Although adverse reactions (ADRs) to VIT are widely reported, controlled trials are still needed. We conducted a randomized prospective study to evaluate ADRs and the efficacy of three VIT regimens. Methods. 76 patients with Hymenoptera allergy, aged 16-76 years, were randomized to receive an ultrarush protocol (group A: 27 patients), a rush protocol (group B: 25), or a slow protocol (group C: 24). Aqueous venom extract was used in incremental phase and an adsorbed depot in maintenance phase. ADRs and accidental Hymenoptera stings during VIT were used to evaluate efficacy. Results. During incremental treatment, ADRs occurred in 1.99%, 3.7%, and 3.9% of patients in groups A, B, and C, and in 0.99%, 1.46%, and 2.7%, respectively, during maintenance. ADRs were significantly fewer in group A (incremental + maintenance phase) than in group C (1.29% versus 3.2%; P = 0.013). Reactions to accidental Hymenoptera stings did not differ among groups (1.1%, 1.2%, and 1.1%). Conclusion. Ultrarush was as effective as the rush and slow protocols and was associated with a low incidence of reactions to stings. This study indicates that ultrarush VIT is a valid therapeutic option for Hymenoptera allergy.

Thymosin beta-10 protein synthesis suppression reduces the growth of human thyroid carcinoma cells in semisolid medium.

Beta-thymosins are structurally related, highly conserved acidic polypeptides, originally isolated from calf thymus. We have recently shown that the TB10 gene is overexpressed in human thyroid carcinoma cell lines and tissues, particularly in undifferentiated thyroid carcinomas, but expressed at an undetectable level in normal thyroid cells. The precise role of thymosin beta-10 (TB10) activity in maintaining the malignant phenotype of thyroid cell lines is unknown. To investigate TB10 function and relevance in a model system we used an antisense methodology to suppress TB10 protein synthesis in two human thyroid carcinoma cell lines (NPA and ARO). The growth in soft agar of NPA and ARO cells carrying a TB10 construct in an antisense orientation was significantly reduced. Conversely, anchorage-dependent growth was unchanged in NPA and ARO cells carrying the TB10 construct in a sense orientation or carrying the backbone vector. TB10 expression also affected actin organization. In fact, stress fibers were long and thick in ARO cells in which TB10 expression was suppressed by the antisense construct. Conversely, they were scarce and short in the vector-transfected ARO cells. These data suggest that TB10 plays a critical role in the regulation of anchorage-independent growth and assembly of actin filaments.

Assessment of RET/PTC oncogene activation and clonality in thyroid nodules with incomplete morphological evidence of papillary carcinoma: a search for the early precursors of papillary cancer.

Noninvasive thyroid nodules that exhibit borderline morphological signs of papillary cancer are difficult to diagnose and we do not know if they represent papillary carcinoma precursor lesions. Forty-six such nodules were analyzed for RET activation by immunohistochemistry and, in selected cases, by reverse transcriptase-polymerase chain reaction performed on RNA extracted after laser capture microdissection (LCM) of the tumor foci with and without papillary carcinoma features and positive RET immunoreactivity. RET immunoreactivity was identified, at least focally, in 30 of 46 (65.2%) of the nodules where it closely paralleled the morphological changes. Enough RNA was obtained after LCM in seven samples. RET/PTC1 or RET/PTC3 were detected in microscopic foci with papillary carcinoma features in most of the thyroid nodules (five of seven cases). No RET/PTC1 or RET/PTC3 rearrangements were detected in areas of the same tumors that lacked the cytological alterations. Analysis of clonality in the same nodules selected for LCM demonstrated that two were monoclonal and six were polyclonal. We conclude that RET activation closely parallels the morphological changes, that it is restricted to those areas of the tumor with the cytological alterations and that it is detectable in both mono- and polyclonal tumors. Although the finding of microscopic foci indicative of papillary carcinoma in a hyperplastic or adenomatous nodule does not justify the interpretation of the entire lesion as papillary carcinoma, it is possible that such foci may precede the development of invasive papillary cancer.

The RET/PTC oncogene is frequently activated in oncocytic thyroid tumors (Hurthle cell adenomas and carcinomas), but not in oncocytic hyperplastic lesions.

Hurthle cell adenomas and carcinomas, characterized by the presence of oncocytic cells, are unusual thyroid neoplasms, the treatment of which is still controversial. We analyzed specimens from 49 patients with oncocytic cell nodular lesions including 20 adenomas, 19 carcinomas, and 10 hyperplasias for RET/PTC (papillary thyroid carcinoma) activation, which is the most frequent genetic alteration in PTCs. RET/PTC activation was detected in a significant number of cases of Hurthle cell adenomas and carcinomas, but in 0 of 10 patients with hyperplastic nodules. In particular, the RET/PTC1 isoform was found in 7 of 12 adenomas and 4 of 7 carcinomas. These results would indicate that RET/PTC is a genetic event common to papillary carcinomas and to Hurthle cell neoplasias.