Root,shoot and soil parameters required for process-oriented models of crop growth limited by water or nutrients

A review is given of the prospects for using process-oriented models of water and nutrient uptake in improving integrated agriculture. Government-imposed restrictions on the use of external inputs will increase the likelihood of (temporary) nutrient or water stress in crop production in NW Europe and thus a better understanding is required of shoot-root-soil interactions than presently available. In modelling nutrient and water uptake, three approaches are possible: 1) models-without-roots, based on empirically derived efficiency ratios for uptake of available resources, 2) models evaluating the uptake potential of root systems as actually found in the field and 3) models which also aim at a prediction of root development as influenced by interactions with environmental factors. For the second type of models the major underlying processes are known and research can concentrate on model refinement on the one hand and practical application on the other. The main parameters required for such models are discussed and examples are given of practical applications. For the third type of models quantification of processes known only qualitatively is urgently needed.     

多异瓢虫生物学的研究

多异瓢虫在山东省德州地区一年发生４代,部分个体５代,以成虫在杂草丛内、残枝落叶及土块下越冬。在自然变温下,卵、幼虫、预蛹、蛹、成虫产卵前期和全世代的发育始点和有效积温分别为１８．８±０．５２℃和１５．０日度、１６．９７±０．０３℃和７３．３日度、１５．９７±０．０１℃和１０．２３日度、１５．４７±０．０５℃和２３．０５日度、１７．６±０．０４℃和３４．１日度、１８．２±０．１０℃和１７０．３日度。据Ｈｏｌｉｎｇ圆盘方程测定,１─４龄幼虫和产卵前期成虫日最大捕食棉蚜量依次力６．７头、３６．４头、７７．５头、８１．３头和６８．０头。     

P0 phosphorylation in nerves from normal and diabetic rats: Role of protein kinase C and turnover of phosphate groups

The effects of phorbol ester and forskolin on the net phosphorylation and turnover of P₀ phosphate groups was studied in normal and exprimentally diabetic rats. In sciatic nerve segments isolated from normal rats and incubated with [³²P]-inorganic phosphate, phosphorylation of the major peripheral myelin protein, P₀, was increased 2–5 fold in a time and dose-dependent manner by phorbol 12,13 dibutyrate (PDB). This increase was blocked by the protein kinase inhibitors, H-7 and staurosporine. Both the basal and PDB-stimulated phosphorylation of P₀ were significantly greater in segments of sciatic nerve from streptozotocin-induced diabetic rats. Prolonged exposure of nerve segments to PDB abolished the stimulated phosphorylation of P₀ and immunoblots of nerve proteins revealed a decrease in the content of the protein kinase C -isoform. The adenylate cyclase activator, forskolin, had no affect on the PDB-stimulated phosphorylation of P₀ in normal nerve but decreased phosphorylation in diabetic nerve. To measure turnover of P₀ phosphate groups, nerves were incubated with³²P and incorporated label was then chased in radioactivity-free medium for up to 4 hours. P₀ from normal nerve prelabeled under basal conditions lost 25% of its radioactivity during this time. In contrast, nearly all of the additional phosphate groups prelabeled in the presence of PDB disappeared after 2 hours of chase. P₀ phosphate groups from diabetic nerve displayed similar turnover kinetics. When forskolin was added to the chase medium, the turnover of P₀ phosphate moieties was accelerated in normal, but not in diabetic nerve. These findings clearly establish a prominent role for protein kinase C in P₀ phosphorylation, provide evidence for heterogeneous turnover of P₀ phosphate groups and suggest that cyclic AMP-mediated processes may modulate P₀ phosphorylation. Further, these results indicate that the metabolism of P₀ phosphate moieties is perturbed in nerve from diabetic animals.Special issue dedicated to Dr. Marjoris B. Lees.     

Effect of Temperature on Pratylenchus penetrans Development

Reproduction and development of Pratylenchus penetrans were studied on genetically transformed ladino clover roots. Solitary females developing on transformed roots in nutrient gellan gum medium (pH 5.5) deposited 1.2, 1.5, 1.6, 1.8, and 2.0 eggs per day at the respective temperatures of 17, 20, 25, 27, and 30 °C. The number of eggs deposited was highly correlated with temperature. A reduction in egg-laying rates at the start of hatching was observed at all temperatures. Juvenile mortality was higher at 17 °C (50.4%), 20 °C (50.3%), and 30 °C (58.4%) than at 25 °C (34.6%) and 27 °C (37.6%). Life-cycle (egg deposition to egg deposition) duration was 46, 38, 28, 26, and 22 days at the respective temperatures. The developmental zero degrees (°C) and the effective accumulative temperatures (degree-days) required for hatching, female emergence, and onset of oviposition (completion of one generation) of P. penetrans were estimated to be 2.7 and 200, 4.2 and 548, and 5.1 and 564, respectively. Pratylenchus penetrans reproduces over a wide range of temperatures.     

Enhanced hippocampus‐dependent memory and reduced anxiety in mice over‐expressing human catalase in mitochondria

Oxidative stress (OS) and reactive oxygen species (ROS) play a modulatory role in synaptic plasticity and signaling pathways. Mitochondria (MT), a major source of ROS because of their involvement in energy metabolism, are important for brain function. MT‐generated ROS are proposed to be responsible for a significant proportion of OS and are associated with developmental abnormalities and aspects of cellular aging. The role of ROS and MT function in cognition of healthy individuals is relatively understudied. In this study, we characterized behavioral and cognitive performance of 5‐ to 6‐month‐old mice over‐expressing mitochondrial catalase (MCAT). MCAT mice showed enhancements in hippocampus‐dependent spatial learning and memory in the water maze and contextual fear conditioning, and reduced measures of anxiety in the elevated zero maze. Catalase activity was elevated in MCAT mice in all brain regions examined. Measures of oxidative stress (glutathione, protein carbonyl content, lipid peroxidation, and 8‐hydroxyguanine) did not significantly differ between the groups. The lack of differences in these markers of oxidative stress suggests that the differences observed in this study may be due to altered redox signaling. Catalase over‐expression might be sufficient to enhance cognition and reduce measures of anxiety even in the absence of alteration in levels of OS.     

The brain‐derived neurotrophic factor VAL68MET polymorphism modulates how developmental ethanol exposure impacts the hippocampus

Prenatal exposure to alcohol causes a wide range of deficits known as fetal alcohol spectrum disorders (FASDs). Many factors determine vulnerability to developmental alcohol exposure including timing and pattern of exposure, nutrition and genetics. Here, we characterized how a prevalent single nucleotide polymorphism in the human brain‐derived neurotrophic factor (BDNF) gene (val66met) modulates FASDs severity. This polymorphism disrupts BDNF's intracellular trafficking and activity‐dependent secretion, and has been linked to increased incidence of neuropsychiatric disorders such as depression and anxiety. We hypothesized that developmental ethanol (EtOH) exposure more severely affects mice carrying this polymorphism. We used transgenic mice homozygous for either valine (BDNF^val/val) or methionine (BDNF^met/met) in residue 68, equivalent to residue 66 in humans. To model EtOH exposure during the second and third trimesters of human pregnancy, we exposed mice to EtOH in vapor chambers during gestational days 12 to 19 and postnatal days 2 to 9. We found that EtOH exposure reduces cell layer volume in the dentate gyrus and the CA1 hippocampal regions of BDNF^met/met but not BDNF^val/val mice during the juvenile period (postnatal day 15). During adulthood, EtOH exposure reduced anxiety‐like behavior and disrupted trace fear conditioning in BDNF^met/met mice, with most effects observed in males. EtOH exposure reduced adult neurogenesis only in the ventral hippocampus of BDNF^val/val male mice. These studies show that the BDNF val66met polymorphism modulates, in a complex manner, the effects of developmental EtOH exposure, and identify a novel genetic risk factor that may regulate FASDs severity in humans.     

Preparation and characterization of flurbiprofen beads by melt solidification technique

Amelt solidification technique has been developed to obtain sustained-release waxy beads of flurbiprofen. Low glass transition temperature (t _g) and shear-induced crystallization of flurbiprofen made it a suitable candidate for melt solidification technique. The process involved emulsification and solidification of flurbiprofen-cetyl alcohol melt at significantly low temperature (5°C). The effect of variables, namely, the amount of cetyl alcohol and the speed of agitation, was studied using 3² factorial design. The technique and the beads were evaluated on the basis of process and desired yield, surface topography, Fourier-transform infrared (FT-IR), differential scanning calorimetry (DSC), particle size distribution, crushing strength, and drug release. Average values for process and desired yields were 97% wt/wt and 26% wt/wt, respectively. No interaction was observed between drug and excipient. Multiple regression analysis was carried out, and response surfaces were obtained. A curvilinear relationship was observed between percentage of desired yield and the amount of cetyl alcohol. Linear decrease in crushing strength was observed with increase in the amount of cetyl alcohol. Drug released from the beads followed zero order kinetics. Burst release was shown to a greater extent in beads containing a lower amount of cetyl alcohol. Response surfaces of time required for certain percentage of drug (t _D%) showed that after critical concentration of about 20% of cetyl alcohol (400 mg/batch), no significant release retardant effect was observed.     

Fully reduced ribonuclease A does not expand at high denaturant concentration or temperature

The dimensions of a denatured protein, fully reduced ribonuclease A (r-RNase A), have been measured using synchrotron-based small angle X-ray scattering. The radius of gyration, 34-35 A, is unchanged from 0-6 M guanidinium chloride and from 20-90 degrees C at pH 2.5, and agrees with the known scaling behavior for a multitude of chemically denatured states. The polypeptide is behaving as a statistical coil in the non-interacting, high-temperature limit.     

Effects of hypomagnetic field on noradrenergic activities in the brainstem of golden hamster

Previous studies found that elimination of the geomagnetic field (GMF) interferes with the normal brain functions, but the underlying mechanism remains unknown. The present study examined the effects of long-term exposures to a near-zero magnetic environment on the noradrenergic activities in the brainstem of golden hamsters. Both the content of norepinephrine (NE) and the density of NE-immunopositive neurons in the tissue decreased significantly after the treatment, and the effects could be progressive with time. These variations may substantially contribute to behavioral and mood disorders reported in other studies when animals are shielded from the GMF.     

A model for activation of the hexadecameric phosphorylase kinase complex deduced from zero‐length oxidative crosslinking

Phosphorylase kinase (PhK) is a hexadecameric (αβγδ)₄ enzyme complex that upon activation by phosphorylation stimulates glycogenolysis. Due to its large size (1.3 MDa), elucidating the structural changes associated with the activation of PhK has been challenging, although phosphoactivation has been linked with an increased tendency of the enzyme's regulatory β‐subunits to self‐associate. Here we report the effect of a peptide mimetic of the phosphoryltable N‐termini of β on the selective, zero‐length, oxidative crosslinking of these regulatory subunits to form β–β dimers in the nonactivated PhK complex. This peptide stimulated β–β dimer formation when not phosphorylated, but was considerably less effective in its phosphorylated form. Because this peptide mimetic of β competes with its counterpart region in the nonactivated enzyme complex in binding to the catalytic γ‐subunit, we were able to formulate a structural model for the phosphoactivation of PhK. In this model, the nonactivated state of PhK is maintained by the interaction between the nonphosphorylated N‐termini of β and the regulatory C‐terminal domains of the γ‐subunits; phosphorylation of β weakens this interaction, leading to activation of the γ‐subunits.