Air-transmissible pathogenic viruses, such as influenza viruses and coronaviruses, are some of the most fatal strains and spread rapidly by air, necessitating quick and stable measurements from sample air volumes to prevent further spread of diseases and to take appropriate steps rapidly. Measurements of airborne viruses generally require their collection into liquids or onto solid surfaces, with subsequent hydrosolization and then analysis using the growth method, nucleic-acid-based techniques, or immunoassays. Measurements can also be performed in real time without sampling, where species-specific determination is generally disabled. In this review, we introduce some recent advancements in the measurement of pathogenic airborne viruses. Air sampling and measurement technologies for viral aerosols are reviewed, with special focus on the effects of air sampling on damage to the sampled viruses and their measurements. Measurement of pathogenic airborne viruses is an interdisciplinary research area that requires understanding of both aerosol technology and biotechnology to effectively address the issues. Hence, this review is expected to provide some useful guidelines regarding appropriate air sampling and virus detection methods for particular applications.

Smoking is one of the most serious but preventable causes of cardiovascular disease (CVD). Key aspects of pathological process associated with smoking include endothelial dysfunction, a prothrombotic state, inflammation, altered lipid metabolism, and hypoxia. Multiple molecular events are involved in smokinginduced CVD. However, the dysregulations of reactive oxygen species (ROS) generation and metabolism mainly contribute to the development of diverse CVDs, and NADPH oxidase (NOX) has been established as a source of ROS responsible for the pathogenesis of CVD. NOX activation and resultant ROS production by cigarette smoke (CS) treatment have been widely observed in isolated blood vessels and cultured vascular cells, including endothelial and smooth muscle cells. NOX-mediated oxidative stress has also been demonstrated in animal studies. Of the various NOX isoforms, NOX2 has been reported to mediate ROS generation by CS, but other isoforms were not tested thoroughly. Of the many CS constituents, nicotine, methyl vinyl ketone, and α,β-unsaturated aldehydes, such as, acrolein and crotonaldehyde, appear to be primarily responsible for NOX-mediated cytotoxicity, but additional validation will be needed. Human epidemiological studies have reported relationships between polymorphisms in the CYBA gene encoding p22phox, a catalytic subunit of NOX and susceptibility to smoking-related CVDs. In particular, G allele carriers of A640G and -930A/G polymorphisms were found to be vulnerable to smoking-induced cardiovascular toxicity, but results for C242T studies are conflicting. On the whole, evidence implicates the etiological role of NOX in smoking-induced CVD, but the clinical relevance of NOX activation by smoking and its contribution to CVD require further validation in human studies. A detailed understanding of the role of NOX would be helpful to assess the risk of smoking to human health, to define high-risk subgroups, and to develop strategies to prevent or treat smoking-induced CVD.

BackgroundContralateral acupuncture (CAT) involves inserting needles in the meridian on the side opposite the disease location and is often used in post-stroke rehabilitation. The aim of this systematic review is to summarize and critically evaluate the evidence for and against the effectiveness of CAT for post-stroke rehabilitation as compared to ipsilateral acupuncture (IAT).MethodsSeventeen databases were searched from their inceptions through June 2010. Prospective clinical trials were included if CAT was tested as the sole treatment or as an adjunct to other treatments for post-stroke rehabilitation and compared to IAT.ResultsEight randomized clinical trials (RCTs) met our inclusion criteria. Four of them reported favorable effects of CAT compared to IAT for at least one outcome. A meta-analysis showed superior effects of CAT compared to IAT on recovery rate (n = 361; risk ratio (RR), 1.12; 95% confidence intervals (CIs), 1.04 to 1.22, P = 0.005). Subgroup analysis also showed favorable effects of using CAT on patients with cerebral infarction (n = 261; RR, 1.15; 95% CIs, 1.04 to 1.27, P = 0.006). Further analysis including patients with cerebral infarction and intracranial hemorrhage, however, failed to show these advantages (n = 100; RR, 1.11; 95% CIs, 0.85 to 1.46, P = 0.43).ConclusionThe results of our systematic review and meta-analysis suggest that there is limited evidence for CAT being superior to IAT in the treatment of cerebral infarction. The total number of RCTs included in our analysis was low, however, and the RCTs included had a high risk of bias. Future RCTs appear to be warranted.

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