Purpose of review Health agencies recommend transmission-based precautions, including contact, droplet and airborne precautions, to mitigate transmission of respiratory viruses in healthcare settings. There is particular controversy over the importance of aerosol transmission and whether airborne precautions should be recommended for some respiratory viruses. Here, we review the current recommendations of transmission-based precautions and the latest evidence on the aerosol transmission of respiratory viruses. Recent findings Viral nucleic acids, and in some instances viable viruses, have been detected in aerosols in the air in healthcare settings for some respiratory viruses such as seasonal and avian influenza viruses, Middle East respiratory syndrome-coronavirus and respiratory syncytial virus. However, current evidences are yet to demonstrate that these viruses can effectively spread via airborne route between individuals, or whether preventive measures in airborne precautions would be effective. Summary Studies that use transmission events as outcome to demonstrate human-to-human transmission over the aerosol route or quantitative measurement of infectious respiratory viruses in the air are needed to evaluate the infectiousness of respiratory viruses over the aerosol route. When a respiratory virus in concern only leads to disease with low severity, airborne precautions are not likely to be justified.

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To investigate the clinical significance of circulating matrix metalloproteinases (MMPs) and their tissue inhibitos (TIMPs) in patients with premature coronary atheroscrelosis, we studied 53 consecutive male patients with angiographically defined premature (<65 years) and stable coronary artery disease. Plasma levels of MMP-2, MMP-3, MMP-9, TIMP-1, and TIMP-2 were determined in peripheral blood by a sandwich enzyme immunoassay, and the results were compared with those from 133 age-matched control males. There were significant differences in all the MMPs and TIMPs (p<0.001) between patients and controls. In the patient group, the levels of MMP-9 (mean +/- SD (ng/ml) 27.2 +/- 15.2/21.8 +/- 15.2) and TIMP-1 (130.4 +/- 55.7/94.5 +/- 26.3) were significantly higher, and the levels of MMP-2 (632.5 +/- 191.6/727.6 +/- 171.4), MMP-3 (53.1 +/- 31.2/79.6 +/- 29.9), and TIMP-2 (24.7 +/- 15.2/35.4 +/- 16.4) were significantly lower than those of controls. We found significant positive correlation between plasma MMP-9 levels and low-density lipoprotein (LDL)-cholesterol levels (Rs = 0.168, p = 0.022), and significant negative correlation between plasma MMP-9 levels and high-density lipoprotein (HDL)-cholesterol levels (Rs = -0.164, p = 0.026) by Spearman rank correlation test. In contrast, plasma MMP-2 (Rs = 0.181, p = 0.014) and MMP-3 (Rs = 0.260, p = 0.0004) levels were positively correlated with HDL-cholesterol levels. TIMP-2 levels were negatively correlated with total cholesterol (Rs = -0.197, p = 0.007) and LDL-cholesterol (Rs = -0.168, p=0.022) levels. These results suggest that the circulating levels of MMPs and TIMPs are altered in patients with premature coronary atherosclerosis and that plasma lipoprotein cholesterol levels correlate with these, possibly as a result of the lipoprotein-vessel wall interactions.

The effects of in vivo modulation of HDL phospholipid (PL) on scavenger receptor class BI (SR-BI)-and ATP binding cassette transporter 1 (ABCA1)-mediated efflux were examined by overexpressing either endothelial lipase (EL) or phosphatidylserine phospholipase (PS-PLA 1 ) in human apolipoprotein A-I (apoA-I) transgenic mice. Overexpression of EL led to large reductions in the serum PL/apoA-I ratio ( ؊ 60%), total cholesterol (TC; ؊ 89%), and HDL cholesterol ( ؊ 91%). Relative to the serum before overexpression of EL, the efflux potential of the serum via SR-BI decreased by 90% and ABCA1-mediated efflux increased by 63%. In contrast to overexpression of EL, overexpression of PS-PLA 1 led to increases in the PL/apoA-I ratio (88%), TC (78%), HDL cholesterol (57%), and HDL size. The efflux potential of the serum increased by 60% via SR-BI and decreased by 57% via ABCA1. There were significant positive correlations between SR-BI-mediated efflux and a number of serum parameters, including PL/apoA-I ratio, PL, TC, free cholesterol (FC), and HDL cholesterol. In striking contrast, the same correlations were seen with ABCA1-mediated efflux, but the relationships were inverse. In summary, in vivo modulation of HDL PL content affects ABCA1-and SR-BI-mediated efflux in a reciprocal manner. These findings indicate that the type of lipase acting on HDL in vivo will determine which FC efflux pathway the HDL serves. Additionally, the extent of lipolysis will determine the efficiency of FC removal via this pathway. HDL cholesterol levels are inversely correlated with the incidence of coronary artery disease (1-4). One mechanism by which HDL is thought to protect against atherosclerosis is by the removal of excess free cholesterol (FC) from peripheral cells and subsequent delivery to the liver for excretion (5-7). There are three known mechanisms by which HDL and/or its apolipoproteins can remove FC from cells. Aqueous diffusion is a relatively inefficient efflux mechanism that occurs with all cell types (8). In recent years, two proteins have been discovered that mediate efficient cholesterol efflux. The scavenger receptor class BI (SR-BI) facilitates the bidirectional flux of FC between cells and HDL (9, 10), and the ATP binding cassette transporter 1 (ABCA1) (11-13) mediates the unidirectional efflux of cellular FC and phospholipid (PL) to lipid-poor apolipoprotein A-I (apoA-I) and other exchangeable apolipoproteins. A number of studies suggest that both mechanisms of efflux may operate in atherosclerotic lesions (14-16).The goal of the present study was to determine the effects of in vivo modulation of HDL PL on both ABCA1-and SR-BI-mediated FC efflux. The importance of studying the role of HDL PL in the flux of FC between cells and HDL is supported by a number of previous observations. The efflux of cholesterol from cells to serum is correlated with HDL PL content (17, 18). Importantly, it has been demonstrated that patients with coronary artery disease have low HDL PL levels (19). Past studies have used in vitro mani...

Sitosterolemia is a rare inherited disease characterized by increased levels of plant sterols, such as sitosterol. The cause of this disease is ATP-binding cassette (ABC) subfamily G member 5 or member 8 (ABCG5 or ABCG8, respectively) gene mutations. Recent advances in genetics have revealed that the prevalence of subjects with deleterious mutations in ABCG5 and/or ABCG8 genes could be more than 1 in ∼200,000 individuals among the general population. Furthermore, accumulated evidence, including infantile cases exhibiting progression/regression of systemic xanthomas associated with LDL cholesterol levels, have shown that the elevation of LDL cholesterol seems to be the major cause of development of atherosclerosis and not the elevation of sitosterol. Regarding therapies, LDL apheresis, as well as proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, could be useful for sitosterolemia, in addition to ezetimibe and/or colestimide. In this study, we provide the current understanding and future perspectives of sitosterolemia, which is currently considered an extremely rare disorder but is expected to be much more prevalent in clinical settings.

M. Impact of anti-apoptotic and anti-oxidative effects of bone marrow mesenchymal stem cells with transient overexpression of heme oxygenase-1 on myocardial ischemia. Am

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