Eutrophication has become increasingly serious and noxious algal blooms have been of more frequent occurrence in the Yangtze River Estuary and in the adjacent East China Sea. In 2003 and 2004, four cruises were undertaken in three zones in the estuary and in the adjacent sea to investigate nitrate (NO 3 -N), ammonium (NH 4 -N), nitrite (NO 2 -N), soluble reactive phosphorus (SRP), dissolved reactive silica (DRSi), dissolved oxygen (DO), phytoplankton chlorophyll a (Chl a) and suspended particulate matter (SPM). The highest concentrations of DIN (NO 3 -N+NH 4 -N+NO 2 -N), SRP and DRSi were 131.6, 1.2 and 155.6 lM, respectively. The maximum Chl a concentration was 19.5 mg m )3 in spring. An analysis of historical and recent data revealed that in the last 40 years, nitrate and SRP concentrations increased from 11 to 97 lM and from 0.4 to 0.95 lM, respectively. From 1963 to 2004, N:P ratios also increased from 30-40 up to 150. In parallel with the N and P enrichment, a significant increase of Chl a was detected, Chl a maximum being 20 mg m )3 , nearly four times higher than in the 1980s. In 2004, the mean DO concentration in bottom waters was 4.35 mg l )1 , much lower than in the 1980s. In comparison with other estuaries, the Yangtze River Estuary was characterized by high DIN and DRSi concentrations, with low SRP concentrations. Despite the higher nutrient concentrations, Chl a concentrations were lower in the inner estuary (Zones 1 and 2) than in the adjacent sea (Zone 3). Based on nutrient availability, SPM and hydrodynamics, we assumed that in Zones 1 and 2 phytoplankton growth was suppressed by high turbidity, large tidal amplitude and short residence time. Furthermore, in Zone 3 water stratification was also an important factor that resulted in a greater phytoplankton biomass and lower DO concentrations. Due to hydrodynamics and turbidity, the open sea was unexpectedly more sensitive to nutrient enrichment and related eutrophication processes.

Stable isotopes of N provide a new approach to the study of algal production in the ocean, yet know!edge of the isctopc fractionation (c) in various oceanic regime5 is i d~k i~~y .tiere w e report large and rapid changes in isotope composit~on (6'") of 2 coastal diatoms and 2 clones (open and coastal) of a coccolithophore grown in the simultaneous presence of nitrate, ammonium and urea under varylng conditions of N availability (i.e. N-sufficiency and N-starvation followed by N-resupply) and hence different physiological states. Du.ring N-sufficiency, the SI5N of particulate organic N (PON) was well reproduced, uslng a model derived from Rayleigh distillation theory, with constant E similar to that for growth on each individual N source. However, following N-resupply, the variations in S15NpoU could be well explained only in the case of the open ocean Emiliania huxleyi, with E similar to N-sufficient conditions. It was concluded that the mechanism of isotope fractionation changed rapidly with N availability for the 3 coastal clones. However, in the case of E. huxleyi isolated from the Subarctic Pacific Ocean, no evidence of a change in mechanism was found, suggesting that perhaps open ocean species can quickly recover from N-depleted conditions.

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BACKGROUND: The etiology of postoperative cognitive decline (POCD) remains to be determined. Anesthetic isoflurane, but not desflurane, may induce neurotoxicity. However, the functional consequences of these effects have not been assessed. We therefore performed a pilot study to determine the effects of isoflurane and desflurane on cognitive function in humans. METHODS: The subjects included patients who had lower extremity or abdominal surgery under spinal anesthesia alone (S, n = 15), spinal plus desflurane anesthesia (SD, n = 15), or spinal plus isoflurane anesthesia (SI, n = 15) by randomization. Each of the subjects received cognitive tests immediately before and 1 week after anesthesia and surgery administered by an investigator who was blinded to the anesthesia regimen. POCD was defined using the scores from each of these tests. RESULTS: We studied 45 subjects, 24 males and 21 females. The mean age of the subjects was 69.0 ± 1.9 years. There was no significant difference in age and other characteristics among the treatment arms. The mean number of cognitive function declines in the S, SD, and SI groups was 1.13, 1.07, and 1.40, respectively. POCD incidence after SI (27%), but not SD (0%), anesthesia was higher than that after S (0%), P = 0.028 (3-way comparison). CONCLUSION: These findings from our pilot study suggest that isoflurane and desflurane may have different effects on postoperative cognitive function, and additional studies with a larger sample size and longer times of follow-up testing are needed.

Background Some anesthetics have been suggested to induce neurotoxicity including promotion of Alzheimer’s disease neuropathogenesis. Nitrous oxide and isoflurane are common anesthetics. Here, we set out to assess effects of nitrous oxide and/or isoflurane on apoptosis and β-amyloid (Aβ) levels in H4 human neuroglioma cells and primary neurons from naïve mice. Methods The cells or neurons were exposed to 70% nitrous oxide and/or 1% isoflurane for six hours. The cells or neurons and conditioned media were harvested at the end of the treatment. Caspase-3 activation, apoptosis, processing of amyloid precursor protein, and Aβ levels were determined. Results Treatment with a combination of 70% nitrous oxide and 1% isoflurane for six hours induced caspase-3 activation and apoptosis in H4 naïve cells and primary neurons from naïve mice. The 70% nitrous oxide plus 1% isoflurane, but neither alone, for six hours induced caspase-3 activation and apoptosis, and increased levels of β-site amyloid precursor protein-cleaving enzyme and Aβ in H4-amyloid precursor protein cells. In addition, the nitrous oxide plus isoflurane-induced Aβ generation was reduced by a broad caspase inhibitor Z-VAD. Finally, the nitrous oxide plus isoflurane-induced caspase-3 activation was attenuated by γ-secretase inhibitor L-685,458, but potentiated by exogenously added Aβ. Conclusion These results suggest that common anesthetics nitrous oxide plus isoflurane may promote neurotoxicity by inducing apoptosis and increasing Aβ levels. The generated Aβ may further potentiate apoptosis to form another round of apoptosis and Aβ generation. More studies, especially the in vivo confirmation of these in vitro findings, are needed.

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Accumulation and deposition of b-amyloid protein (Ab) are the hallmark features of Alzheimer's disease. The inhalation anesthetic isoflurane has been shown to induce caspase activation and increase Ab accumulation. In addition, recent studies suggest that isoflurane may directly promote the formation of cytotoxic soluble Ab oligomers, which are thought to be the key pathological species in AD. In contrast, propofol, the most commonly used intravenous anesthetic, has been reported to have neuroprotective effects. We therefore set out to compare the effects of isoflurane and propofol alone and in combination on caspase-3 activation and Ab oligomerization in vitro and in vivo. Naïve and stably-transfected H4 human neuroglioma cells that express human amyloid precursor protein, the precursor for Ab; neonatal mice; and conditioned cell culture media containing secreted human Ab40 or Ab42 were treated with isoflurane and/or propofol. Here we show for the first time that propofol can attenuate isoflurane-induced caspase-3 activation in cultured cells and in the brain tissues of neonatal mice. Furthermore, propofol-mediated caspase inhibition occurred when there were elevated levels of Ab. Finally, isoflurane alone induces Ab42, but not Ab40, oligomerization, and propofol can inhibit the isoflurane-mediated oligomerization of Ab42. These data suggest that propofol may mitigate the caspase-3 activation by attenuating the isoflurane-induced Ab42 oligomerization. Our findings provide novel insights into the possible mechanisms of isofluraneinduced neurotoxicity that may aid in the development of strategies to minimize potential adverse effects associated with the administration of anesthetics to patients.