Landscape Patterns of Sapling Density,Leaf Area,and Aboveground Net Primary Production in Postfire Lodgepole Pine Forests,Yellowstone National Park (USA)

Causes and implications of spatial variability in postfire tree density and understory plant cover for patterns of aboveground net primary production (ANPP) and leaf area index (LAI) were examined in ninety 11-year-old lodgepole pine (Pinus contorta var. latifolia Engelm.) stands across the landscape of Yellowstone National Park (YNP), Wyoming, USA. Field studies and aerial photography were used to address three questions: (1) What is the range and spatial pattern of lodgepole pine sapling density across the burned Yellowstone landscape and what factors best explain this variability? (2) How do ANPP and LAI vary across the landscape and is their variation explained by abiotic factors, sapling density, or both? (3) What is the predicted spatial pattern of ANPP and LAI across the burned Yellowstone landscape? Stand density spanned six orders of magnitude, ranging from zero to 535,000 saplings ha^?1, and it decreased with increasing elevation and with increasing distance from unburned forest (r ²?=?0.37). Postfire densities mapped from 1:30,000 aerial photography revealed that 66% of the burned area had densities less than 5000 saplings ha^?1 and approximately 25% had densities greater than 10,000 saplings ha^?1; stand density varied spatially in a fine-grained mosaic. New allometric equations were developed to predict aboveground biomass, ANPP, and LAI of lodgepole pine saplings and the 25 most common herbaceous and shrub species in the burned forests. These allometrics were then used with field data on sapling size, sapling density, and percent cover of graminoid, forb, and shrub species to compute stand-level ANPP and LAI. Total ANPP averaged 2.8 Mg ha^?1y^?1 but ranged from 0.04 to 15.12 Mg ha^?1y^?1. Total LAI averaged 0.80 m² m^?2 and ranged from 0.01 to 6.87 m² m^?2. Variation in ANPP and LAI was explained by both sapling density and abiotic factors (elevation and soil class) (ANOVA, r ²?=?0.80); abiotic variables explained 51%–54% of this variation. The proportion of total ANPP contributed by herbaceous plants and shrubs declined sharply with increasing sapling density (r ²?=?0.72) and increased with elevation (r ²?=?0.36). However, total herbaceous productivity was always less than 2.7 Mg ha^?1 y^?1, and herbaceous productivity did not compensate for tree production when trees were sparse. When extrapolated to the landscape, 68% of the burned landscape was characterized by ANPP values less than 2.0 Mg ha^?1y^?1, 22% by values ranging from 2 to 4 Mg ha^?1y^?1, and the remaining 10% by values greater than 4 Mg ha^?1y^?1. The spatial patterns of ANPP and LAI were less heterogeneous than patterns of sapling density but still showed fine-grained variation in rates. For some ecosystem processes, postfire spatial heterogeneity within a successional stage may be similar in magnitude to the temporal variation observed through succession.     

Molecular basis of bird respiration: primary hemoglobin structure component from Tufted duck (Aythya fuligula, Anseriformes)--role of alpha99Arg in formation of a complex salt bridge network

The primary structure of the major hemoglobin component, HbA (alpha(A)- and beta-chain), from Tufted duck (Aythya fuligula) is presented. The separation of the globin subunits was achieved by ion exchange chromatography on CM-cellulose in 8 M urea. The amino acid sequence was determined by automatic Edman degradation of native chains as well as tryptic and hydrolytic peptides in a gas-phase sequencer. The automated homology model was generated by the protein structure modeling package WHAT IF using the crystal structure coordinates of Bar-headed goose hemoglobin. The 3D structure prediction enables alpha99Arg and beta101Glu to emerge as a new intersubunit contact site not found in the hemoglobin structure of any other species. alpha99Arg forms a complex salt bridge network involving alpha99Arg-beta101Glu-beta104Arg-beta108Asp. Also the substitution at alpha34 --> Ile, alpha38 --> Gln and beta55 --> Leu serves to stabilize the oxy-structure, leading to higher oxygen affinity.     

Bone typology and growth rate: testing and quantifying 'Amprino's rule' in the mallard (Anas platyrhynchos)

Periosteal bone histology expresses its rate of deposition. This fundamental relationship between bone structure and growth dynamics, first assumed by Amprino many decades ago, was quantified in preliminary studies, but never statistically tested. Moreover, the precise typological characters of bone tissue linked to growth rate remained poorly known. Here, we present the first statistical analysis of 'Amprino's rule', measured on comprehensive growth series of the mallard, Anas platyrhynchos. Growth rates were assessed by fluorescent labelling. Bone typology was described according to Ricqlès' typological classification. Results show that the presence and proportion of primary osteons, two consequences of bone initial porosity at the time of its deposit, are strongly related to bone growth rate. However, no significant relationship between primary osteons orientation and bone growth rate could be detected, at least for osteonal orientations (longitudinal, laminar and reticular) and growth rates values observed in mallard long bones. These results suggest that Amprino's rule holds for some major typological characters of primary compact bone tissues (i.e. primary osteons presence and proportion). However, it is irrelevant to some other characters (i.e. osteonal orientation), the meaning of which remains to be discovered.     

Evaluation of the neurotoxic activity of typical and atypical neuroleptics: relevance to iatrogenic extrapyramidal symptoms

Typical neuroleptic therapy often results in extrapyramidal symptoms (EPS) and tardive dyskinesia (TD). Recent reports reveal neurotoxic activity in some neuroleptics. We hypothesized that neurotoxicity might be implicated in EPS. This study aims to evaluate the neurotoxic activity of typical and atypical neuroleptics and to determine the possible role of neurotoxicity in neuroleptic-induced EPS. Perphenazine, haloperidol, clozapine, sulpiride, and risperidone (10–100 M) were administered, either alone or combined with dopamine, to primary mouse neuronal or intact brain culture and to a human neuroblastoma (NB) cell line (SK-N-SH). Cell viability (measured by neutral red and alamar blue), DNA fragmentation (flow cytometry–NB) were determined. Neuroblastoma: perphenazine, clozapine, and haloperidol (100 M) decreased viability by 87, 43, and 34% respectively. Sulpiride and risperidone were not toxic. At 10 M, toxicity decreased markedly. Dopamine (125 M) potentiated the perphenazine-induced toxicity. Flow cytometry of NB cells treated with perphenazine (2.5–40 M) showed an increase (perphenazine 20 M, 40 M, 48 h) in fragmented DNA (74.7% and 95.0% vs. 8.7% in controls). Lower concentrations increased the G1 phase and decreased S phase in the cell cycle. In primary neurons, perphenazine, haloperidol, and clozapine, but not risperidone and sulpiride, induced a significant neurotoxic effect, which, in intact brain culture, was absent (haloperidol and clozapine) or lowered (perphenazine). Dopamine (0.5 mM) did not modify the effect of the drugs in the primary cultures. Neuroleptics possess differential neurotoxic activity with higher sensitivity of neoplasm tissue (NB compared to primary cultures). The order of toxicity was perphenazine > haloperidol = clozapine; sulpiride and risperidone were not toxic. Neurotoxicity is independent of dopamine and is associated with cell cycle arrest and apoptosis. With the exception of clozapine, neurotoxicity seems relevant to neuroleptic-induced EPS and TD.     

Opposite Effects of Lithium on Proximal and Distal Caspases of Immature and Mature Primary Neurons Correlate with Earlier Paradoxical Actions on Viability

To provide an explanation for earlier paradoxical findings of lithium on survival of mature and immature neurons, this study monitors changes in cytosolic caspases in rat cerebellar granule cells (CGC) grown 2–7 days in vitro (DIV), or in murine E-17 cortical neurons. Data show Li⁺ protects mature 7-DIV CGC parallel to a decrease in proximal and distal caspases but increases levels for immature 2-DIV-CGC or E-17 cortical neurons. Caspases mirror viability based on morphological analyses (dye uptake, phase-contrast, DNA fragmentation), and suggest protection occurs by suppressing activation of a cascade resulting in distal effectors that destroy proteins essential for neuronal survival. Protection was dose-dependent with EC₅₀ 3.0 mM and extended to 64 h in K⁺-serum deprived apoptotic media. Neuronal extracts contain a spectrum of proximal (-2, -8, -9) and distal (-3, -6) caspases sensitive to Li⁺ on assay with preferred peptide substrates and by immunobloting. The lack of direct effect on activated cytosols indicates Li⁺ acts upstream only on intact cells, at sites for recruitment of pivotal procaspases. Alterations of procaspase-9 p46 and membrane-bound cytochrome c (Apaf-1) point to interaction with an intrinsic Mt-mediated pathway as one of the targets. The opposite effects on caspases and viability of immature or embryological neurons point to existence of alternative pathways that alter during neurite outgrowth suggesting the use of Li⁺ as a probe to unravel events relevant to neurogenesis.     

慢性电刺激诱发大鼠癫痫模型中核磁共振检测信号异常的非对称性与特征性行为发作的关系

本文旨在探讨内嗅皮质（EC）－海马环路在颞叶癫痫发生中的作用,慢性强直电刺激大鼠石背海马（DH－PC）或右中部颞叶新皮质（MTNC）,每日一次（60Hz,2s,0.4-0.6mA),加续7－10d,刺激DHPC（57.4%,8/14只）或MTNC（71．42％,10／14只）均能引起电极对侧出现非对称性脑区核磁共振（T2－WI）信号增强,组织学切片证实与扩大的侧脑室吻合,可能涉及脑帝质结构的损伤,DHPC刺激组大鼠对侧脑扣内务 伴有高频原发性湿狗样抖（WEDS）,MTNC刺激组大鼠对侧脑损伤伴有低频原发性WEDS,后者在第2个刺激日开始出现,持续到第10天以后,所有假电极组无脑区T2-WI稚号和行为改变,我们推测,刺激HPC或MTNC所致癫痫性早期脑损伤具有同一种机制,涉及EC－HPC环路,刺激MTNC时,可能由于EC潜在门控作用,削弱了进出EC－HPC环路通往新皮质的信息流,致使脑损伤明显时行为发作频度低,另外,非对称非脑扣内务 提示了颞叶癫痫的致痫灶的对侧易感特征。     

Poly(ADP-ribose) polymerase cleavage during apoptosis: when and where?

On freeze-fracture replicas, gap junctions are frequently colocalized with tight junctions. In this study, to elucidate the relationship between gap- and tight-junction proteins, we investigated the localization of gap-junction proteins Cx32 and Cx26 and tight-junction proteins occludin, claudin-1, ZO-1, and ZO-2 in primary cultured rat hepatocytes, using confocal laser microscopy. In hepatocytes cultured in 2% DMSO and 10(-7) M glucagon medium, Cx32- but not Cx26-immunoreactive lines were observed on the most subapical plasma membrane at cell borders, while on the basolateral membrane both Cx32- and Cx26-positive spots were colocalized. Occludin-, claudin-1-, ZO-1-, and ZO-2-immunoreactive lines were also linearly observed on the most subapical plasma membrane and were colocalized with only Cx32-immunoreactive lines. In freeze-fracture analysis, many small gap-junction plaques were observed within a well-developed tight-junction strand network. The fence function of tight junctions in the cells, as examined by diffusion of labeled sphingomyelin, was well maintained. We also carried out Western blotting for Cx32 following immunoprecipitation with anti-occludin, anti-claudin-1, or anti-ZO-1 antibodies. Cx32 was detectable in all immunoprecipitates. These results suggest that Cx32 gap junctions, but not those with Cx26, are closely coordinated with the expression and function of tight junctions in hepatocytes and that Cx32 gap-junction formation may affect cell polarity through modification of tight-junction expression.     

Detection of the presenilin 1 COOH-terminal fragment in the extracellular compartment: a release enhanced by apoptosis

Mutations in gene encoding presenilin 1 (PS1) are responsible for the majority of familial Alzheimer's disease (FAD) cases. We studied PS1 localization in HEK293 cells and in primary neurons obtained from rat cortex and hippocampus. We first demonstrated that PS1-CTF, but neither PS1-FL nor PS1-NTF, is released into the medium as a soluble and membrane-associated form. After induction of apoptosis with staurosporine (Sts), we observed a dramatic increase in the level of PS1-CTF in the medium, both in HEK293 and in primary neurons. Immunocytochemical analysis suggested that the release of PS1-CTF might occur via membrane shedding. Abeta(1-42) treatment reduced PS1-CTF extracellular levels. This decrease was strongly associated to an impaired secretion of sAPP fragments, thus suggesting a role of PS1-CTF in the control of trafficking and generation of APP fragments.     

Relaxation of variable chlorophyll fluorescence after illumination of dark-adapted barley leaves as influenced by the redox states of electron carriers

Kinetics of the dark relaxation of variable chlorophyll fluorescence, Fv, were studied after brief illumination of dark-adapted barley leaves in order to understand the rapid reversibility of pulse-induced fluorescence increases, which is observed even when fast linear electron transport to an external electron acceptor is not possible. Four kinetically distinct components were observed which reveal complexity in the oxidation of the reduced primary quinone acceptor of Photosystem II, Q_A ⁻: the slowest component accounted for 4–5% of maximal Fv and had a life-time of several seconds. It is suggested to represent a minor population of inactive Photosystem II centers. The other three components displayed first-order kinetics with half-time of 6–8 ms (`fast' component), 60–80 ms (`middle' component) and 650–680 ms (`slow' component). The fast component dominated Fv when methyl viologen or far-red light accelerated oxidation of plastohydroquinone. It shows rapid oxidation of Q_A ⁻ during electron flow to plastoquinone commensurate with maximum linear electron flow through the electron transport chain. The other two components were observed under conditions of restricted electron flow and excessive reduction of electron carriers. Unexpectedly, the slow component, which is interpreted to reflect the recombination between Q_A ⁻ and an intermediate on the oxidizing side of Photosystem II, saturated already at low irradiances of actinic light when plastoquinone was not yet strongly reduced suggesting that dark-adaptation of leaves results not only in the loss of activity of light-regulated enzymes of the carbon cycle but affects also electron flow from Q_A ⁻ to plastoquinone. KCN poisoning or high temperature treatment of leaves produced a nonexponential pattern of slow Fv relaxation. This effect was largely (heat treatment) or even completely (KCN) abolished by far-red light. This revised version was published online in August 2006 with corrections to the Cover Date.