Publication date: Available online 10 November 2018
Source: Revista Española de Medicina Nuclear e Imagen Molecular
Author(s): Nese Torun, Emine Tuba Canbolat
from Imaging via a.sfakia on Inoreader https://ift.tt/2DgzCNN
ENT-MD Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete Greece,00306932607174,00302841026182,alsfakia@gmail.com
Publication date: Available online 10 November 2018
Source: Revista Española de Medicina Nuclear e Imagen Molecular
Author(s): Nese Torun, Emine Tuba Canbolat
The incidence of oral cancers associated with human papillomavirus (HPV) has been increasing in recent years. Therefore, it is necessary to elucidate HPV prevalence in oral cells and exposure to risk factors in various age groups.
Oral rinse samples from healthy individuals in northern Thailand were investigated for HPV prevalence and genotyped using the polymerase chain reaction (GP5+/6+ primers) and DNA sequencing of the PCR products.
Samples were collected from 594 participants between 4 and 60 years of age. HPV was detected in 3.7% of samples: there was no gender difference. The prevalence of HPV positive cases was 8.6% in the 31 ‐50 age group. HPV prevalence increased with age and was the highest (9.2%) in the 41‐50 age group, but decreased (to 3%) in the 51‐60 age group. Risk factors significantly associated with HPV‐positive cases included alcohol consumption, coffee drinking, sexual activity and having children. HPV 16 and 18 were common genotypes, especially in the 31‐50 age group, and were associated with having sexual activity [odds ratio 19.0 (95% CI: 2.5‐142.5)]. At follow‐up of some individuals in the 4‐10 age group, a 9‐year‐old child was found to be positive for HPV18.
These results suggest that HPV can be acquired at a young age and the prevalence peaks in the middle age class among healthy individuals in northern Thailand, especially in the 31‐50 age group.
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Previous research has emphasized the importance of eosinophils in allergic asthma, while paying less attention to neutrophils. The known functionality of neutrophils in the inflammatory process has recently changed and knowledge about subsets of neutrophils, as characterized by their expression of CD16 and CD62L, has surfaced. Their specific roles in asthma are still unknown.
To study the functional differences between subsets of neutrophils by characterising the impact of individual subsets on airway smooth muscle reactivity.
The direct effect of neutrophils on airway hyper‐responsiveness was assessed by co‐culturing different subsets of neutrophils (produced by LPS in vitro stimulation) with human isolated small airways or murine tracheae with subsequent evaluation of smooth muscle reactivity to bradykinin in myographs. Supernatants and tissue were saved for ELISA and immunohistochemistry.
The CD16highCD62Ldim neutrophils were found to enhance the response to bradykinin in both human isolated small airways and murine tracheae. No such effects were obtained for the other subsets. The response is due to an upregulation of bradykinin receptor 2 through release of TNFα from the neutrophil.
The present study introduces a new concept regarding the role of neutrophils and defines a novel direct link between a specific activated neutrophil subset and airway smooth muscle, establishing neutrophils as important players in the development of asthmatic airway hyperactivity.
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Blood eosinophils are used to determine eligibility for agents targeting IL‐5 in patients with uncontrolled asthma. However, little is known about the variability of blood eosinophil measures in these patients before treatment initiation.
To characterize variability and patterns of variability of blood eosinophil levels in a real‐world clinic for severe asthmatics.
Retrospective review of blood eosinophils measured over a 5‐year period in patients enrolled in an urban clinic. Repeated measures of blood eosinophil levels in individuals were evaluated and cluster analysis was performed to characterize patients by eosinophil patterns. Clinical characteristics associated with eosinophil levels and patterns of variability were analyzed.
Patients treated in the Bellevue Hospital Asthma Clinic within a 3‐month period were identified (n = 219). Blood eosinophil measures were obtained over the previous 5 years. Only 6% (n= 13) of patients had levels that were consistently above 300 cells/ÎĽL. Nearly 50% (n = 104) had eosinophil levels that traversed the threshold of 300 cells/ÎĽL. In contrast, 102 (46%) had levels that never reached the threshold of 300 cells/ÎĽL. Cluster analyses revealed three clusters with differing patterns of levels and variability. There was a suggestion of decreased clinical control and increased atopy in the cluster with the greatest variability in blood eosinophil measures.
In an urban clinic for patients referred for uncontrolled asthma, blood measures of eosinophils were variable and showed differing patterns of variability. These data reinforce the need to perform repeated eosinophil blood measures for appropriate designation for therapeutic intervention.
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The pathogenesis and pathophysiology of eosinophilia‐related chronic cough such as non‐asthmatic eosinophilic bronchitis and cough variant asthma are still not clear.
This study is to examine the potential role of traffic‐related air pollution (TRAP) in eosinophilic inflammation and cough responses.
Non‐sensitized guinea pigs were exposed to TRAP in an urban traffic tunnel or kept in a filtered air environment for 7 or 14 days. Reflexive cough was measured using citric acid and allyl isothiocyanate (AITC) challenges, respectively. Spontaneous cough counting was determined using audio recording and a waveform analysis. Airway inflammation was evaluated using differential cells in bronchoalveolar lavage fluid (BALF) and lung histopathology. To further elucidate the relationship between airway inflammation and cough hypersensitivity, a subgroup of those exposed for 14 days received a dexamethasone treatment.
Compared to reflexive cough count (mean (95% confidence interval) in 10 min) provoked by the AITC challenge for the unexposed animals (3.1 (1.7‐4.5)), those were increased significantly following both the 7‐day (12.0 (6.8‐17.2), p<0.01) and the 14‐day (12.0 (6.4‐17.6), p<0.01) TRAP exposure. The effect provoked by the citric acid challenge was more profound following the 14‐day exposure (26.0 (19.5‐32.5) vs. 3.8 (1.5‐6.0) for the control, p<0.001). TRAP exposures enhanced spontaneous cough events, caused a significant increase of eosinophils and neutrophils in BALF, and resulted in a dramatic eosinophilic infiltration in submucosal layer of trachea and bronchus, which can be inhibited significantly by dexamethasone treatment.
TRAP exposures induced cough hypersensitivity and non‐allergic eosinophilic inflammation of airways in guinea pigs. This study highlights the potential mechanisms of eosinophilia‐related chronic cough that can be induced by traffic‐related air pollution.
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Previous reports indicate that patients with chronic spontaneous urticaria (CSU) are undertreated and that physicians show poor adherence to guideline recommendations. Awareness of CSU has improved in recent years, but it remains unclear if this has improved the management of these patients in clinical practice.
To describe disease burden, quality of life (QoL), and treatment patterns of patients with H1‐antihistamine‐refractory CSU in Germany.
AWARE (A World‐wide Antihistamine‐Refractory chronic urticaria patient Evaluation) is a global prospective, non‐interventional study of chronic urticaria in the real‐world setting, supported by the manufacturer of omalizumab. Patients (18–75 years) were included who had H1‐antihistamine‐refractory CSU for ≥2 months. Disease characteristics, pharmacological treatments, and QoL (dermatology life quality index [DLQI], chronic urticaria QoL questionnaire, and angioedema QoL questionnaire) are reported for patients enrolled in Germany.
After 1 year in AWARE, CSU remained uncontrolled (urticaria control test [UCT] score <12) in 432 of 1032 (42.2%) patients. QoL impairment remained high after one year, with 28.2% of patients reporting that CSU had a moderate/very large/extremely large effect on the DLQI. Most patients did not receive guideline‐recommended treatments at the end of the one‐year observation period. Changes in treatments were most evident at the first patient visit, with an increase in patients receiving omalizumab vs. prior therapy from 8.5% to 21.4%, and a decrease in those receiving no treatment from 29.9% to 12.8%. These changes were associated with reduced hives, angioedema, UCT scores, and QoL scores at Month 3, but only modest improvements thereafter. Of 528 patients with uncontrolled CSU and who were eligible for treatment escalation, only 3% received up‐dosing of H1‐antihistamines and only 5% were initiated on omalizumab during one year of treatment.
This study highlights a significant discrepancy between recommendations for managing CSU in international guidelines, and in real‐world clinical practice in Germany.
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Publication date: Available online 10 November 2018
Source: Allergology International
Author(s): Takashi Ito, Koichi Hirose, Hiroshi Nakajima
Asthma is the most prevalent allergic disease of the airway, which is characterized by eosinophilic inflammation, mucus hyperproduction, and airway hyper-responsiveness. Although these pathognomonic features are mainly mediated by antigen-specific Th2 cells and their cytokines, such as IL-4, IL-5, and IL-13, recent studies have revealed that other inflammatory cells, including Th17 cells and innate lymphoid cells (ILCs), also play a critical role in the pathogenesis of asthma. IL-22, one of the cytokines produced by Th17 cells and type 3 ILCs, has distinct functional properties, as IL-22 exclusively acts on non-hematopoietic cells including epithelial cells of mucosal surface and exhibits a broad range of action in regeneration and host protection. In accordance with the fact that lung epithelial cells play a critical role in the pathogenesis of asthma, we and other groups have shown that IL-22 is involved in the regulation of allergic airway inflammation. In this review, we discuss recent advances in the biology of IL-22 and its involvement in the pathogenesis of allergic airway inflammation.
International Journal of Environmental Research and Public Health IJERPH, Vol. 17, Pages 6976: Overcoming Barriers to Agriculture Green T...