Outcomes of different radioprotective precautions in children undergoing dental radiography: a systematic review.

PURPOSE: To evaluate the effectiveness of all radioprotective measures in underage patients who undergo a dental radiodiagnostic examination. METHODS: A systematic review was performed including randomised controlled trials (RCTs), or cluster trials, cohort studies, cross-sectional studies, case-control studies and comparative in vitro research. These studies examined the healthy underage human population (below 18 years) undergoing a dental radiodiagnostic examination. All radioprotective measures were included except for justification as an intervention. The primary outcomes were in vivo mortality and morbidity. Some surrogate or indirect outcomes such as in vitro effective dose and organ absorbed doses were also accepted. Secondary outcomes with regards to image quality and therapeutic value were also analysed. RESULTS: Eighteen papers were eligible for implementation. Fifteen studies underwent narrative synthesis. Regression analysis was performed on three studies. CONCLUSION: The following radioprotective measures can reduce the exposure dose. For lateral cephalometry: collimation, filtration, the fastest receptor type and circumstantial thyroid shielding. For oblique lateral radiographs: the shortest exposure time, a smaller horizontal angulation, a longer focus to skin distance. For intraoral radiography: rectangular collimation, the fastest image receptor speed and thyroid shielding when the thyroid gland is in line of or very close to the primary beam. For panoramic radiographs: collimation, the fastest receptor type and the use of automatic exposure control (AEC) or manual adjustment of intensity. For cone-beam computed tomography: collimation, the largest voxels size in relation to the treatment need, change in image settings such as ultra-low dose settings, shorter exposure time, a lower amount of projections, lower beam intensity, reduction of the potential, use of a thyroid shield except in two situations and the use of AEC. All of the changes in exposure parameters should be performed while maintaining a sufficient therapeutic value on an individual and indication-based level.

Worldwide policies on haemochromatosis and blood donation: a survey among blood services.

BACKGROUND AND OBJECTIVES: Haemochromatosis (HC) is a disorder of iron metabolism, requiring frequent phlebotomy to normalize high serum iron levels. There is currently no consensus relating to the eligibility of these patients to donate blood for transfusion. To gain a better understanding of the policies worldwide, a survey amongst blood services was performed. MATERIALS AND METHODS: A web-based questionnaire was developed and distributed among 44 blood services in 41 countries to identify the different policies relating to patients with HC and blood donation. RESULTS: Respondents from 35 blood services (80%) of 33 countries completed the questionnaire. In 24 blood services among them (69%), individuals with genetic susceptibility for HC and/or patients with HC are accepted as blood donors. In approximately one-third of these blood centres (33%), genetic carriers/patients are allowed to donate blood more frequently than regular donors. Prescription from/approval by the patient's treating physician and/or a donor physician is required in the majority of the blood services (87%). Similar policies were identified in a few countries; however, in general, the policies regarding blood donation from patients with HC remain widely variable. CONCLUSION: The results of our survey demonstrate large differences in the blood donation policies regarding carriers/patients with HC illustrating the need for uniform evidence-based and cost-effective policies which could benefit both HC patients and the blood supply around the world.

COPD is associated with reduced pulmonary interstitial expression of pentraxin-3.

Pentraxin (PTX)3 is involved in antimicrobial defence, apoptotic cell clearance and extracellular matrix stability. As these processes are altered in chronic obstructive pulmonary disease (COPD), we aimed to investigate PTX3 expression in patients with this disease. PTX3 expression was quantified by immunohistochemical staining of lung tissue from never-smokers, smokers without COPD, and in patients with COPD of Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage I, II and III-IV. mRNA expression was examined in total lung tissue by quantitative RT-PCR. PTX3 concentration was measured in induced sputum and plasma by ELISA. PTX3 is mainly localised in the interstitium of the small airways and alveolar walls. There were no significant differences in pulmonary, sputum and plasma PTX3 expression between study groups. However, PTX3 expression in small airways correlated significantly with forced expiratory volume in 1 s (r = 0.35, p = 0.004). In the alveolar walls, PTX3 expression correlated significantly with carbon monoxide transfer coefficient (r = 0.28, p = 0.04). In sputum, PTX3 levels were highly correlated with the number of neutrophils. Finally, systemic levels of PTX3 tended to be lower in severe COPD compared with mild COPD. In COPD, airflow limitation and reduced transfer coefficient for carbon monoxide are associated with lower pulmonary interstitial expression of PTX3.

Role of IL-1α and the Nlrp3/caspase-1/IL-1ß axis in cigarette smoke-induced pulmonary inflammation and COPD.

Cigarette smoke (CS), the primary risk factor of chronic obstructive pulmonary disease (COPD), leads to pulmonary inflammation through interleukin-1 receptor (IL-1R)I signalling, as determined using COPD mouse models. It is unclear whether interleukin (IL)-1α or IL-1ß, activated by the Nlrp3/caspase-1 axis, is the predominant ligand for IL-1RI in CS-induced responses. We exposed wild-type mice (treated with anti-IL-1α or anti-IL-1ß antibodies), and IL-1RI knockout (KO), Nlrp3 KO and caspase-1 KO mice to CS for 3 days or 4 weeks and evaluated pulmonary inflammation. Additionally, we measured the levels of IL-1α and IL-1ß mRNA (in total lung tissue by RT-PCR) and protein (in induced sputum by ELISA) of never-smokers, smokers without COPD and patients with COPD. In CS-exposed mice, pulmonary inflammation was dependent on IL-1RI and could be significantly attenuated by neutralising IL-1α or IL-1ß. Interestingly, CS-induced inflammation occurred independently of IL-1ß activation by the Nlrp3/caspase-1 axis. In human subjects, IL-1α and IL-1ß were significantly increased in total lung tissue and induced sputum of patients with COPD, respectively, compared with never-smokers. These results suggest that not only IL-1ß but also IL-1α should be considered as an important mediator in CS-induced inflammation and COPD.