VOC amounts in ambient areas of a high-technology science park in Taiwan: their reciprocal correlations and impact on inhabitants

This study presents bihourly, seasonal, and yearly concentration changes in volatile organic compounds (VOCs) in the inlet and effluent water of the wastewater treatment plant (WWTP) of a high-technology science park (HTIP) in Taiwan, with the VOC amounts at different sites correlated geologically. This research adopted a combination of two systems, solid-phase microextraction with a gas chromatography/flame ionization detector and an assembly of purge and trap coupled with gas chromatography/mass spectrometry, to monitor polar and nonpolar VOCs in wastewater. This paper investigated the total VOCs, acetone, isopropyl alcohol (IPA), and dimethylsulfide (DMS) concentrations in real water samples collected in the ambient area of the HTIP. The major contents of VOCs measured in the effluent of the WWTP in the HTIP and the surrounding river region were DMS (14-176 ppb), acetone (5-95 ppb), and IPA (15-316 ppb). In comparison with the total VOCs in the inlet wastewater of the WWTP, no corresponding relationship for total VOC concentration in the wastewater was observed between the inlet water and effluent water of the WWTP. The peak VOC concentrations appeared in the third season, and the correlation of different VOC amounts reflects the production situation of the factories. In addition, VOC concentrations at different sites indicate that the Ke-Ya River is seemingly an effective channel for transporting wastewater to its final destination. The data are good indications for the management of environmental pollution near the HTIP

Relevance of nitric oxide for myocardial remodeling.

Endogenous myocardial nitric oxide (NO) may modulate the transition from adaptive to maladaptive remodeling leading to heart failure. In rodent models of pressure overload or myocardial infarction, the three NO synthase (NOS) isoforms were shown to play a neutral, protective, or even adverse role in myocardial remodeling, depending on the quantity of NO produced, the location of each NOS and their regulators, the prevailing oxidant stress and resultant NO/oxidant balance, as well as NOS coupling/dimerization. Beside neuronal NOS and--in specific conditions--inducible NOS isoforms, endothelial NOS (eNOS) exerts cardioprotective effects on pressure-overload, ischemia/reperfusion, and myocardial infarction-induced myocardial remodeling, provided the enzyme remains in a coupled state. Besides its effects on excitation-contraction coupling in response to stretch, eNOS acts as an "endogenous beta-blocker" by restoring the sympathovagal balance, opposing excessive hypertrophy as well as promoting vasodilatation and neoangiogenesis, thereby contributing to tissue repair. As eNOS was also shown to mediate the beneficial effects of cardiovascular drugs commonly used in patients with heart failure, strategies to increase its expression and/or coupled catalytic activity in the myocardium offer new therapeutic avenues for the treatment of this disease