Many effluents are released into water bodies or into the atmosphere, and dilution is relied on to minimize the toxic effects of the pollutants on the environment. Dilution occurs due to entrainment and subsequent mixing of the "clean" (or cleaner) ambient fluid and the effluent stream. In the near field, dilution occurs due to momentum or buoyancy driven entrainment into the effluent stream, which is proportional to a characteristic velocity of the jet or plume.Whereas in the far field, dilution occurs due to turbulent diffusion at a rate dependent on the level of turbulence in the receiving fluid. In order to predict the expected dilution of an effluent stream, it is necessary to answer the question, at what point does the dilution mechanism change and how does it affect dilution rates. An experimental study examining the velocity and concentration decay of plane jets released into shallow coflows with increasing levels of external turbulence, indicated that levels of external turbulence just large enough to disrupt the jet structure reduced dilution rates significantly. This indicates that models, in which the jet dilution and turbulent diffusion are superimposed, will not always give a conservative estimate of effluent dilution.

BackgroundMolecular hydrogen has been shown to have antioxidant effect and have been used to prevent oxidative stress-related diseases. The goal of this study was to explore if hydrogen-rich saline (HRS) plays a cardioprotective effect on abdominal aortic constriction (AAC) induced cardiac hypertrophy in rats. 60adult Sprague–Dawley rats received surgically the AAC for 6-week. After the surgery, the rats were randomly divided into 4 groups (15 for each):1: sham-operated (sham); 2: AAC-model; 3: AAC + Low HRS (LHRS); and 4: AAC + High HRS (HHRS). The rats in sham and AAC-model groups were treated with normal saline intraperitoneally, while rats in LHRS and HHRS groups were intraperitoneally treated with 3 or 6 mL/kg HRS daily, respectively, for 6-week.ResultsThe ratios of HW/BW and LVW/BW were shown in an order of Model > LHRS > HHRS > SHAM groups. The cardiac hypertrophy was also manifested with increased expressions of atrial natriuretic peptide (ANP), brain natriuretic peptides (BNP) and fibrosis of cardiac tissues in AAC-model group, which could likewise be restrained in LHRS and HHRS groups. Moreover, the JAK-STAT (Janus Kinase-Signal transducers and activators of transcription) signaling molecule expressions were decreased with HRS treatment.ConclusionsOur results showed a protective effect of HRS on pressure overload-induced cardiac hypertrophy in rats, which may be associated to a decreasing in JAK-STAT signaling pathway.

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