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81.
Cryptococcus neoformans was grown first to OD 4 under moderate aeration, then diluted 2.5 times with fresh medium, and grown under limited aeration for 5 h. Oxygen concentration decreased from 5-6 mg l(-1) to 1.5 mg l(-1) 1 h after the shift to limited aeration, and remained at a similar level thereafter. In all the eleven strains examined the shift caused unbudded G(2)-arrest in more than half of the cells. In three strains more than 80% of the cells were arrested in unbudded G(2), and, therefore they were selected for synchrony experiments. After being shifted to extensive aeration again, the cells resumed growth by synchronous budding, followed by synchronous nuclear division. This method has turned out to be a good tool to prepare synchronized culture in C. neoformans, especially when a large amount of synchronized cells is needed. This is worthy of attention, since synchronous cultures after release from G(2)-arrest have not been reported yet in any yeast species. 相似文献
82.
Nutrient enrichment and fisheries exploitation: interactive effects on estuarine living resources and their management 总被引:2,自引:1,他引:2
D. L. Breitburg J. K. Craig R. S. Fulford K. A. Rose W. R. Boynton D. C. Brady B. J. Ciotti R. J. Diaz K. D. Friedland J. D. Hagy III D. R. Hart A. H. Hines E. D. Houde S. E. Kolesar S. W. Nixon J. A. Rice D. H. Secor T. E. Targett 《Hydrobiologia》2009,629(1):31-47
Both fisheries exploitation and increased nutrient loadings strongly affect fish and shellfish abundance and production in
estuaries. These stressors do not act independently; instead, they jointly influence food webs, and each affects the sensitivity
of species and ecosystems to the other. Nutrient enrichment and the habitat degradation it sometimes causes can affect sustainable
yields of fisheries, and fisheries exploitation can affect the ability of estuarine systems to process nutrients. The total
biomass of fisheries landings in estuaries and semi-enclosed seas tends to increase with nitrogen loadings in spite of hypoxia,
but hypoxia and other negative effects of nutrient over-enrichment cause declines in individual species and in parts of systems
most severely affected. More thoroughly integrated management of nutrients and fisheries will permit more effective management
responses to systems affected by both stressors, including the application of fisheries regulations to rebuild stocks negatively
affected by eutrophication. Reducing fishing mortality may lead to the recovery of depressed populations even when eutrophication
contributes to population declines if actions are taken while the population retains sufficient reproductive potential. New
advances in modeling, statistics, and technology promise to provide the information needed to improve the understanding and
management of systems subject to both nutrient enrichment and fisheries exploitation.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users.
Guest editors: J. H. Andersen & D. J. Conley
Eutrophication in Coastal Ecosystems: Selected papers from the Second International Symposium on Research and Management of
Eutrophication in Coastal Ecosystems, 20–23 June 2006, Nyborg, Denmark 相似文献
83.
Hypoxia-inducible factor 1 (HIF-1) is a key regulator of tumor development. Recently, the tumor microenvironment, with the presence of tumor-associated macrophages (TAMs), has gained considerable interest. The mechanisms of macrophage/TAM migration as well as the role of HIF-1 in macrophages for tumor progression are still under debate. We present evidence that under normoxic conditions, nitric oxide (NO) promotes macrophage migration. The response was impaired in macrophages from leukocyte conditional HIF-1α−/− mice. NO production and cell migration in response to cytokines were attenuated in macrophages from iNOS−/− mice, suggesting that iNOS-derived NO transmits cytokine signaling toward cell migration. We further identified the small GTPases Cdc42 and Rac1 as effectors of the NO–HIF axis to drive macrophage migration by modulating the actin cytoskeleton. Our observations strengthen the role of HIF-1 in macrophages as a target of NO in facilitating functional responses such as migration. 相似文献
84.
MicroRNA(miRNA)是一类包含21-25个核苷酸的单链非编码小RNA.研究表明,miR-210可直接抑制线粒体内铁硫蛋白(Fe-S)的支架蛋白ISCUl/2的表达从而抑制线粒体代谢;miR-210对DNA损伤修复基因-RAD家族有抑制作用,减弱了DNA修复能力;miR-210可以通过调节E2F3、纤维母细胞生长因子受体1(FGFRL1)、同源域基因A1(HOXA1)等阻止细胞增殖,调控细胞周期;缺氧刺激可上调miR-210表达,这对促进血管再生有重要作用.miR-210的表达受缺氧诱导,调控缺氧反应相关基因的表达,提示miR-210有可能成为诊治包括缺血性损伤、肿瘤在内等多种疾病的新靶点. 相似文献
85.
Kim MH Kim MO Heo JS Kim JS Han HJ 《Apoptosis : an international journal on programmed cell death》2008,13(2):295-304
This study examined the effect of acetylcholine (ACh) on the hypoxia-induced apoptosis of mouse embryonic stem (ES) cells.
Hypoxia (60 h) decreased both the cell viability and level of [3H] thymidine incorporation, which were prevented by a pretreatment with ACh. However, the atropine (ACh receptor [AChR] inhibitor)
treatment blocked the protective effect of ACh. Hypoxia (90 min) increased the intracellular level of reactive oxygen species
(ROS). On the other hand, ACh inhibited the hypoxia-induced increase in ROS, which was blocked by an atropine treatment. Subsequently,
the hypoxia-induced ROS increased the level of p38 mitogen activated protein kinase (MAPK) and Jun-N-terminal kinase (JNK)
phosphorylation, which were inhibited by the ACh pretreatment. Moreover, hypoxic exposure (90 min) increased the level of
nuclear factor-κB (NF-κB) phosphorylation, which was blocked by a pretreatment with SB 203580 (p38 MAPK inhibitor) or SP 600125
(JNK inhibitor). However, hypoxia (60 h) decreased the protein levels of Bcl-2 and c-IAPs (cellular inhibitor of apoptosis
proteins) but increased the level of caspase-3 activation. All these effects were inhibited by a pretreatment with ACh. In
conclusion, ACh prevented the hypoxia-induced apoptosis of mouse ES cells by inhibiting the ROS-mediated p38 MAPK and JNK
activation as well as the regulation of Bcl-2, c-IAPs, and caspase-3.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
86.
Münch C Zhu BG Mink A Seefried U Riepe MW Ludolph AC Meyer T 《Neurochemical research》2008,33(6):1005-1010
Hypoxia is one of the major common components of vascular risk factors for pathogenesis of Alzheimer’s disease. This study
investigated the possible relationship between hypoxia and alternative splicing of the excitatory amino acid transporter 2
(EAAT2) in a transgenic model for Alzheimer’s disease. We used an APP23 mouse model prior to amyloid deposition and subjected
it to chemical hypoxia treatment as induced by 3-nitropropionic acid. One hour after administration of 3-nitropropionic acid
changes in the expression of the 5′-splice forms mEAAT2/5UT3, mEAAT2/5UT4, and mEAAT2/5UT5 were found in the frontal cortex,
hippocampus and cerebellum of the APP23 model. In untreated APP23 animals the expression of EAAT2 splice variants was unchanged.
Our results demonstrate that hypoxia facilitates alternative splicing of EAAT2 in the APP23 model. This may be a molecular
mechanism linking vascular factors to early pathophysiology of Alzheimer’s disease. 相似文献
87.
Rakhee S. Gupte Dhawjbahadur K. Rawat Sukrutha Chettimada Donna L. Cioffi Michael S. Wolin William T. Gerthoffer Ivan F. McMurtry Sachin A. Gupte 《The Journal of biological chemistry》2010,285(25):19561-19571
Hypoxic pulmonary vasoconstriction (HPV) is a physiological response to a decrease in airway O2 tension, but the underlying mechanism is incompletely understood. We studied the contribution of glucose-6-phosphate dehydrogenase (Glc-6-PD), an important regulator of NADPH redox and production of reactive oxygen species, to the development of HPV. We found that hypoxia (95% N2, 5% CO2) increased contraction of bovine pulmonary artery (PA) precontracted with KCl or serotonin. Depletion of extracellular glucose reduced NADPH, NADH, and HPV, substantiating the idea that glucose metabolism and Glc-6-PD play roles in the response of PA to hypoxia. Our data also show that inhibition of glycolysis and mitochondrial respiration (indicated by an increase in NAD+ and decrease in the ATP-to-ADP ratio) by hypoxia, or by inhibitors of pyruvate dehydrogenase or electron transport chain complexes I or III, increased generation of reactive oxygen species, which in turn activated Glc-6-PD. Inhibition of Glc-6-PD decreased Ca2+ sensitivity to the myofilaments and diminished Ca2+-independent and -dependent myosin light chain phosphorylation otherwise increased by hypoxia. Silencing Glc-6-PD expression in PA using a targeted small interfering RNA abolished HPV and decreased extracellular Ca2+-dependent PA contraction increased by hypoxia. Similarly, Glc-6-PD expression and activity were significantly reduced in lungs from Glc-6-PDmut(−/−) mice, and there was a corresponding reduction in HPV. Finally, regression analysis relating Glc-6-PD activity and the NADPH-to-NADP+ ratio to the HPV response clearly indicated a positive linear relationship between Glc-6-PD activity and HPV. Based on these findings, we propose that Glc-6-PD and NADPH redox are crucially involved in the mechanism of HPV and, in turn, may play a key role in increasing pulmonary arterial pressure, which is involved in the development of pulmonary hypertension. 相似文献
88.
Günther A Manaenko A Franke H Wagner A Schneider D Berrouschot J Reinhardt R 《Neurochemistry international》2004,45(8):1125-1132
Hyperbaric oxygen treatment has been suggested as able to reduce hypoxia induced neuronal damage. The aim of the study was to compare the impact of different reoxygenation strategies on early metabolical (purine nucleotide content determined by HPLC) and morphological changes (index of cell injury after celestine blue/acid fuchsin staining) of hypoxically damaged rat neocortical brain slices. For this purpose slices (300 μm and 900 μm) were subjected to either 5 or 30 min of hypoxia by gassing the incubation medium with nitrogen. During the following reoxygenation period treatment groups were administered either 100% oxygen (O) or room air (A) at normobaric (1 atm absolute, NB-O; NB-A) or hyperbaric (2.5 atm absolute, HB-O; HB-A) conditions. After 5 min of hypoxia, both HB-O and NB-O led to a complete nucleotide status restoration (ATP/ADP; GTP/GDP) in 300 μm slices. However, reoxygenation after 30 min of hypoxia was less effective, irrespective of the oxygen pressure. Furthermore, administering hyperbaric room air resulted in no significant posthypoxic nucleotide recovery. In 900 μm slices, both control incubation as well as 30 min of hypoxia resulted in significantly lower trinucleotide and higher dinucleotide levels compared to 300 μm slices. While there was no significant difference between HB-O and NB-O on the nucleotide status, morphological evaluation revealed a better recovery of the index of cell injury (profoundly injured/intact cell-ratio) in the HB-O group. Conclusively, the posthypoxic recovery of metabolical characteristics was dependent on the duration of hypoxia and slice thickness, but not on the reoxygenation pressure. A clear restorative effect on purine nucleotides was found only in early-administered HB-O as well as NB-O in contrast to room air treated slices. However, these pressure independent metabolic changes were morphologically accompanied by a significantly improved index of cell injury, indicating a possible neuroprotective role of HB-O in early posthypoxic reoxygenation. 相似文献
89.
90.
Understanding the cellular response to hypoxia may help elucidate the role of altered oxidation in neuronal death or abnormal cell function. In PC12 cells, 30 min of chemical hypoxia (i.e., KCN) reduced ATP concentrations by 92%, but diminished viability by only 10%. Ten minutes of hypoxia increased cytosolic free calcium ([Ca2+]i) 2.5-fold above control, but after 30 min of hypoxia, [Ca2+]i was slightly below that of nonhypoxic cells. Short periods of hypoxia also exaggerated the K(+)-induced elevation of [Ca2+]i, but by 30 min these ATP-depleted cells reestablished a calcium gradient that was equal to nonhypoxic, K(+)-depolarized cells. Thus, 30 min of severe ATP depletion left [Ca2+]i and viability relatively unaffected. Nerve growth factor caused slight, but significant, improvements in ATP and viability of hypoxic cells, but had no effect on [Ca2+]i. Although [Ca2+]i was equivalent in control and hypoxic cells after 30 or 60 min, hypoxia abolished the K(+)-stimulated elevation of [Ca2+]i. The nerve growth factor induction of c-fos, an indicator of the genomic response, was diminished by approximately 80%. Thus, hypoxic PC12 cells with greatly reduced ATP stores maintained normal [Ca2+]i, but their ability to respond to external stimulation was impaired. Further, the reduced oxidation that occurs in the brain in a variety of pathological conditions may interfere with the cellular response to stimulation and growth factors. 相似文献