Soils,a sink for N2O? A review

Soils are the main sources of the greenhouse gas nitrous oxide (N₂O). The N₂O emission at the soil surface is the result of production and consumption processes. So far, research has concentrated on net N₂O production. However, in the literature, there are numerous reports of net negative fluxes of N₂O, (i.e. fluxes from the atmosphere to the soil). Such fluxes are frequent and substantial and cannot simply be dismissed as experimental noise.
Net N₂O consumption has been measured under various conditions from the tropics to temperate areas, in natural and agricultural systems. Low mineral N and large moisture contents have sometimes been found to favour N₂O consumption. This fits in with denitrification as the responsible process, reducing N₂O to N₂. However, it has also been reported that nitrifiers consume N₂O in nitrifier denitrification. A contribution of various processes could explain the wide range of conditions found to allow N₂O consumption, ranging from low to high temperatures, wet to dry soils, and fertilized to unfertilized plots. Generally, conditions interfering with N₂O diffusion in the soil seem to enhance N₂O consumption. However, the factors regulating N₂O consumption are not yet well understood and merit further study.
Frequent literature reports of net N₂O consumption suggest that a soil sink could help account for the current imbalance in estimated global budgets of N₂O. Therefore, a systematic investigation into N₂O consumption is necessary. This should concentrate on the organisms, reactions, and environmental factors involved.     

人谷胱甘肽S-转移酶pi(GSTp)中半胱氨酸对其在细胞氧化应激下功能的影响

利用PCR定点突变技术构建人GSTp三种半胱氨酸突变体C~(47/101)、C~(14/47/101)和C~(14/47/101/169)。将CSTp 野生型和突变体表达质粒转染293细胞,以CDNB 为底物测定胞内GST 的转移酶活性,结果显示各类突变体均明显抑制了细胞内源性CST 的催化活性,具有显著的负显性(dominant nega-tive)突变体的功能;将CSTp 野生型和突变体与c-Jun、NF-kB 和p53的报告基因载体共转染,通过萤光素酶活性测定发现突变体C~(14/47/101)和C~(14/47/101/169)能明显激活c-Jun 和p21的转录活性;Western印迹分析显示突变体均能上调细胞内p21蛋白的水平,细胞存活率的测定表明GSTp 突变体能增强293细胞对H_2O_2刺激的敏感性;实验结果表明半胱氨酸残基对于维持GSTp 在对抗细胞氧化应激过程中的保护作用至关重要。     

False belief reasoning in the brain: An ERP study

Understanding others mind and interpersonal interaction are the cognitive basis of successful social interactions. People's mental states and behaviors rely on their holding beliefs for self and others. To investigate the neural substrates of false belief reasoning, the 32 channels event-related potentials (ERP) of 14 normal adults were measured while they understood false-belief and true belief used de-ceptive appearance task. After onset of the false-belief or true-belief questions, N100, P200 and late negative component (LNC) were elicited at centro-frontal sites. Compared with true belief, false belief reasoning elicited significant declined LNC in the time window from 400 to 800 ms. The source analysis of difference wave (False minus True) showed a dipole located in the middle cingulated cortex. These findings show that false belief reasoning probably included inhibitive process.     

Quantification of F-ring isoprostane-like compounds (F4-neuroprostanes) derived from docosahexaenoic acid in vivo in humans by a stable isotope dilution mass spectrometric assay

Lipid peroxidation has been implicated in the pathophysiological sequelae of human neurodegenerative disorders. It is recognized that quantification of lipid peroxidation is best assessed in vivo by measuring a series of prostaglandin (PG) F2-like compounds termed F2-isoprostanes (IsoPs) in tissues in which arachidonic acid is abundant. Unlike other organs, the major polyunsaturated fatty acid (PUFA) in the brain is docosahexaenoic acid (DHA, C22:6 omega-6), and this fatty acid is particularly enriched in neurons. We have previously reported that DHA undergoes oxidation in vitro and in vivo resulting in the formation of a series of F2-IsoP-like compounds termed F4-neuroprostanes (F4-NPs). We recently chemically synthesized one F4-NP, 17-F4c-NP, converted it to an 18O-labeled derivative, and utilized it as an internal standard to develop an assay to quantify endogenous production of F4-NPs by gas chromatography (GC)/negative ion chemical ionization (NICI) mass spectrometry (MS). The assay is highly precise and accurate. The lower limit of sensitivity is approximately 10 pg. Levels of F4-NPs in brain tissue from rodents were 8.7 +/- 2.0 ng/g wet weight (mean +/- S.D.). Levels of the F4-NPs in brains from normal humans were found to be 4.9 +/- 0.6 ng/g (mean +/- S.D.) and were 2.1-fold higher in affected regions of brains from humans with Alzheimer's disease (P = 0.02). Thus, this assay provides a sensitive and accurate method to assess oxidation of DHA in animal and human tissues and will allow for the further elucidation of the role of oxidative injury to the central nervous system in association with human neurodegenerative disorders.     

城市不同植被配置类型空气负离子效应评价

通过对南宁城区、城郊绿地及农田开发区进行负离子含量的测定,找出不同植被配置类型空气负离子效应的差别。结果表明,就空气负离子而言,城郊大规模绿地的空气质量〉农田开发区〉城区;植被配置的复层结构（乔灌草）〉简单植被配置结构（乔灌、乔草、灌草）〉单一配置结构（草坪、稀乔、稀灌草）。溪流和瀑布对增加负离子浓度的作用显著。随着海拔和郁闭度的增加,空气负离子含量有上升的趋势。空气负离子含量随季节有一定的波动。     

Acid phosphatase from maize scutellum: Negative cooperativity suppression by glucose

Acid phosphatase purified from maize scutellum, upon acylation with succinic anhydride, still shows negative co-operativity for the hydrolysis of glucose-6-phosphate at pH 5.4. This phenomenon is abolished by glucose, for both native and succinylated enzymes, through stimulation of the initial velocities at sub-optimal substrate concentrations. However, negative co-operativity for the enzymatic hydrolysis of p-nitrophenylphosphate at pH 5.4 is suppressed only at high concentrations of glucose. Furthermore, the hydrolysis of p-nitrophenylphosphate is noncompetitively inhibited (low affinity form of the enzyme molecule) by glucose, which suggests the existence of different substrate binding sites.     

Notes on the almost unknown genus Jeotgalicoccus

Aims: To facilitate isolation and differentiation of the almost entirely unknown Jeotgalicoccus spp. Methods and Results: Jeotgalicoccus spp. have been found in dust samples using SSCP‐PCR analysis. As the cultivation of strains is necessary for further studies on virulence, pathogenicity or metabolism, we developed a method for cultural isolation and further differentiation of Jeotgalicoccus spp. We found that J. halotolerans, J. psychrophilus, J. marinus, as well as the related species Salinicoccus roseus grow on Baird Parker (BP) agar as black colonies without clear zones. J. pinnipedialis and S. jeotgali grow only weakly on BP agar without forming clearly delineated colonies. On BP agar, the colony‐forming Jeotgalicoccus and Salinicoccus spp. are not distinguishable from coagulase‐negative Staphylococcus spp. (CNS). However, unlike CNS, all of the above mentioned species are unreactive in the OF test. SSCP‐PCR was able to differentiate between all investigated Jeotgalicoccus and Salinicoccus spp., as all species had different band positions. Conclusions: Jeotgalicoccus spp. and Salinicoccus spp. may be widely distributed in the environment, but, until now, overlooked or confused with staphylococci. Further epidemiological studies, which are required to prove this hypothesis, are facilitated by the observations of our study. Significance and Impact: This not yet published information enables researchers to carry out epidemiological studies on Jeotgalicoccus spp. in a very cheap and easy way.     

Autoreceptors do not regulate routinely neurotransmitter release: focus on adrenergic systems

The theory that neurotransmitter release is regulated locally at the individual terminals of neurons has achieved a rapid and seemingly secure status in our understanding of neuronal function both in the periphery and in the central nervous system. This concept of negative feedback control through the monitoring of the perineuronal concentration of previously released transmitter has been extended to a multiplicity of transmitters and utilized to explain the mechanisms of action of diverse classes of drugs, ranging from antihypertensives to antidepressants. It is my view that negative feedback by terminal and by somadendritic receptors cannot account for the existing body of experimental work. Analyses of the profiles of action of agonists and antagonists, and of the per pulse release of transmitter in the absence of drugs in a variety if peripheral organ systems, as well as in superfused brain slices, demonstrates the need for alternate interpretations of the available data. Evidence is provided that the actions of agonists to inhibit transmitter release and that of antagonists to enhance release occur at different cellular loci and that the purported unitary action of these two classes that is so central to the validity of presynaptic theory is unsupportable.