Long-term trends in riverine nutrient availability have rarely been linked to both phytoplankton composition and functioning. To explore how the changing availability of N and P affects not only phytoplankton abundance and composition but also the resource use efficiency of N, P, and CO, a 25-year time series of water quality in the lower Han River, Korea, was combined with additional measurements of riverine dissolved organic carbon (DOC) and CO. Despite persistent eutrophication, recent decreases in P relative to N have been steep in the lowest reach, increasing the annual mean mass ratio of N to P (N/P) from 24 (1994-2015) to 65 (2016-2018).
View Article and Find Full Text PDFAlthough eutrophic urban rivers receiving loads of wastewater represent an important anthropogenic source of NO, little is known as to how temperature and other environmental factors affect temporal variations in NO emissions from wastewater treatment plants (WWTPs) and downstream rivers. Two-year monitoring at a WWTP and five river sites was complemented with available water quality data, laboratory incubations, and stable isotopes in NO and NO to explore how wastewater effluents interact with seasonal changes in environmental conditions to affect downstream metabolic processes and NO emissions from the lower Han River traversing the megacity Seoul. Water quality data from four WWTPs revealed significant inverse relationships between water temperature and the concentrations or fluxes of total N (TN) in effluents.
View Article and Find Full Text PDFObjectives: The purpose of this study was to carry out systematic review of the literature and meta-analysis to evaluate the diagnostic utility of cerebrospinal fluid (CSF) levels of the 42 amino acid form of amyloid-beta (Aβ1-42) as a biomarker for differentiating Alzheimer's disease (AD) from non-AD dementia.
Methods: Design. Systematic literature review was used to evaluate the effectiveness of the Aβ for the diagnosis of AD.
Previously, we suggested that tetrahydrobiopterin (BH4), an obligatory cofactor for dopamine synthesis, as an intrinsic contributor to dopaminergic neuron vulnerability. The BH4 toxicity is observed in dopamine-producing cells, including Cath.a cells, but not in non-dopaminergic cells.
View Article and Find Full Text PDFParkinson's disease (PD) is a neurodegenerative disorder associated with selective loss of dopaminergic neurons in the substantia nigra. Because oxidative stress caused by dopamine oxidation to dopamine quinone is suggested as a major factor contributing to the pathogenesis of PD, the induction of the enzyme that catalyzes the reduction of quinones, NAD(P)H quinone oxidoreductase1 (NQO1), could be a desirable therapeutic strategy to protect cells from oxidative damage. The dopamine agonist bromocriptine is used clinically for PD therapy.
View Article and Find Full Text PDFArch Pharm Res
December 2007
Because oxidative stress is involved in the pathogenesis of various chronic diseases and the aging process, antioxidants that can increase the intrinsic antioxidant potency are proposed as desirable therapeutic agents to counteract oxidative stress-related diseases. NF-E2-related factor-2 (Nrf2) is a transcription factor that regulates important antioxidant and phase II detoxification genes, and therefore, the molecule that regulates nuclear translocation of Nrf2 and the induction of antioxidative proteins is thought to be a promising candidate as a cytoprotective agent for oxidative stress. In the present study, we show that isoorientin (luteolin 6-C-beta-D-glucoside) obtained from the leaves of Sasa borealis upregulates and activates Nrf2, and has protective ability against oxidative damage caused by reactive oxygen intermediates in HepG2 cells.
View Article and Find Full Text PDFSasa borealis (Poaceae) is a perennial medicinal plant which is a major source of bamboo leaves in Korea. The n-BuOH extract of S. borealis leaves exhibited significant antioxidant activity against the 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and a cytoprotective effect against oxidative damage in HepG2 cells.
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