The concerns related to particulate matter’s health effects alongside the increasing demands from citizens for more participatory, timely, and diffused air quality monitoring actions have resulted in increasing scientific and industrial interest in low-cost particulate matter sensors (LCPMS). In the present paper, we discuss 50 LCPMS models, a number that is particularly meaningful when compared to the much smaller number of models described in other recent reviews on the same topic. After illustrating the basic definitions related to particulate matter (PM) and its measurements according to international regulations, the device’s operating principle is presented, focusing on a discussion of the several characterization methodologies proposed by various research groups, both in the lab and in the field, along with their possible limitations. We present an extensive review of the LCPMS currently available on the market, their electronic characteristics, and their applications in published literature and from specific tests. Most of the reviewed LCPMS can accurately monitor PM changes in the environment and exhibit good performances with accuracy that, in some conditions, can reach R2 values up to 0.99. However, such results strongly depend on whether the device is calibrated or not (using a reference method) in the operative environment; if not, R2 values lower than 0.5 are observed.
Hypertrophic cardiomyopathy (HCM) is the most frequent genetic cardiovascular disorder worldwide. It is the leading cause of sudden cardiac-related death in young people and a major cause of cardiac failure and death in elderly people. However, HCM frequently goes undiagnosed until the appearance of overt signs and symptoms, thereby delaying prophylactic and therapeutic measures. We screened patients for sarcomeric genes associated with HCM to obtain information that could be useful for an early diagnosis and so limit the severe consequences of silent HCM. We recruited 39 families with HCM from southern Italy and found mutations in 41% of families (12 with familial HCM and 4 with sporadic HCM). The remaining 23 families (59%) were negative for myofilament gene mutations. Of the 12 mutations identified, 8 were novel. Screening of the other family members available revealed that 27 had mutations; 11 of these individuals had no signs or symptoms suggestive of HCM. This study, besides characterizing the spectrum of mutations in another childhood population, and revealing an even greater genetic heterogeneity than formerly recognized, may increase genotype-phenotype correlations, and thus may help to identify asymptomatic candidates for early preventive or therapeutic measures.
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