Effects of nitrate on phosphorus release from lake sediments.

Phosphorus (P) release from sediment is a key process affecting the effectiveness of eutrophication mitigation. We hypothesized that high nitrate (NO3-) input may have dual effect on sediment P release: reduce the sediment P release by improving the oxidation of sediment or promote P release by stimulating the growth of phytoplankton and increase the decomposition rates and oxygen consumption at the sediment water interface. To test the effect of different NO3- concentrations, we conducted a three-month experiment in 15 cement tanks (1 m3), with five targeted concentrations of NO3-: control, 2 mg L-1, 5 mg L-1, 10 mg L-1, and 15 mg L-1. The results showed that: i) when NO3- was maintained at high levels: NO3-≥5-7 mg L-1 (range of median values), there was no effect of NO3- on net P release from the sediment, likely because the positive effects of NO3- (increasing oxidation) was counteracted by a promotion of phytoplankton growth. ii) after NO3- addition was terminated NO3- dropped sharply to a low level (NO3-≤0.4 mg L-1), followed by a minor P release in the low N treatments but a significant P release in the high N treatments, which likely reflect that the inhibition effect of NO3- on P release decreased, while the promotion effects at high NO3- concentrations continued. The results thus supported our hypotheses of a dual effect on sediment P release and suggest dose-dependent effect of NO3- loading on stimulating P release from the sediment, being clear at high NO3- exceeding 5-7 mg L-1.

High ammonium loading can increase alkaline phosphatase activity and promote sediment phosphorus release: A two-month mesocosm experiment.

In aquatic ecosystems, ammonium is one of the dominant substances in the effluent discharge from wastewater treatment plants and its impact has been widely explored as it is thought, in its toxic form (NH3), to cause stress on organisms. Little is, however, known about its potential effect on the release of phosphorus (P) from the sediment. In a two-month mesocosm (150 L) experiment, we tested if high loading of ammonium promotes sediment P release and investigated the dominant underlying mechanisms. A gradient of five target ammonium loading levels was used by adding NH4Cl fertilizer: no addition/control (N0), 3 (N1), 5 (N2), 10 (N3), and 21 (N4) mg NH4Cl L-1 (NH4Cl expressed as nitrogen). We found that: 1) significant sediment P release for N3 and N4 but minor release or retention for N0, N1, and N2 were detected both by the total phosphorus concentration (TP) in the overlying water and in situ measurements of diffusive gradients in thin-films (DGT) at the sediment-water interface; 2) overall, TP correlated significantly and positively with total nitrogen (TN) concentrations in the water. Further correlation and path analyses suggested that stimulated alkaline phosphatase activity (APA) was likely the dominant mechanisms behind the ammonium-induced sediment P release and decreased dissolved oxygen (DO) levels (an approximate reduction from 9.2 to 6.6 mg O2 L-1) was likely a contributing factor, particularly in the beginning of the experiment.

Effects of high nitrogen concentrations on the growth of submersed macrophytes at moderate phosphorus concentrations.

Eutrophication of lakes leading to loss of submersed macrophytes and higher turbidity is a worldwide phenomenon, attributed to excessive loading of phosphorus (P). However, recently, the role of nitrogen (N) for macrophyte recession has received increasing attention. Due to the close relationship between N and P loading, disentanglement of the specific effects of these two nutrients is often difficult, and some controversy still exists as to the effects of N. We studied the effects of N on submersed macrophytes represented by Vallisneria natans (Lour.) Hara in pots positioned at three depths (0.4 m, 0.8 m, and 1.2 m to form a gradient of underwater light conditions) in 10 large ponds having moderate concentrations of P (TP 0.03 ± 0.04 mg L(-1)) and five targeted concentrations of total nitrogen (TN) (0.5, 2, 10, 20, and 100 mg L(-1)), there were two ponds for each treatment. To study the potential shading effects of other primary producers, we also measured the biomass of phytoplankton (ChlaPhyt) and periphyton (ChlaPeri) expressed as chlorophyll a. We found that leaf length, leaf mass, and root length of macrophytes declined with increasing concentrations of TN and ammonium, while shoot number and root mass did not. All the measured growth indices of macrophytes declined significantly with ChlaPhyt, while none were significantly related to ChlaPeri. Neither ChlaPhyt nor ChlaPeri were, however, significantly negatively related to the various N concentrations. Our results indicate that shading by phytoplankton unrelated to the variation in N loading and perhaps toxic stress exerted by high nitrogen were responsible for the decline in macrophyte growth.

Treatment with Huperzine A improves cognition in vascular dementia patients.

UNLABELLED: In the present study, we tested the efficacy and safety of Huperzine A in treatment of mild to moderate vascular dementia (VaD). This was a randomized, double-blinded, placebo-controlled study with 78 patients with mild to moderate VaD. The participants were randomized to receive either vitamin C (100-mg bid) as placebo (n = 39) or Huperzine A (0.1-mg bid) (n = 39) for 12 consecutive weeks. The mini-mental state examination (MMSE), clinical dementia rating (CDR), and activities of daily living (ADL) scores were used for the assessment of cognition. The assessments were made prior to treatment, and 4, 8, and 12 weeks of the treatment. The adverse effects of the treatment were also recorded. After 12 weeks of treatment, the MMSE, CDR, and ADL scores significantly improved in the Huperzine A group (P < 0.01 for all comparisons), whereas the placebo group did not show any such improvement (P > 0.05 for all comparisons). No serious adverse events were recorded during the treatment. CONCLUSION: Huperzine A can significantly improve the cognitive function in patients with mild to moderate vascular dementia. Further, the medicament is safe.