Modeling the temperature response of nitrification

To model nitrification rates in soils, it is necessary to have equations that accurately describe the effect of environmental variables on nitrification rates. A variety of equations have been used previously to describe the effect of temperature on rates of microbial processes. It is not clear which of these best describes the influence of temperature on nitrification rates in soil. I compared five equations for describing the effects of temperature on nitrification in two soils with very different temperature optima from a California oak woodland-annual grassland. The most appropriate equation depended on the range of temperatures being evaluated. A generalized Poisson density function best described temperature effects on nitrification rates in both soils over the range of 5 to 50 °C; however, the Arrhenius equation best described temperature effects over the narrower range of soil temperatures that normally occurs in the ecosystem (5 to 28 °C). Temperature optima for nitrification in most of the soils were greater than even the highest soil temperatures recorded at the sites. A model accounting for increased maintenance energy requirements at higher temperatures demonstrates how net energy production, rather than the gross energy production from nitrification, is maximized during adaptation by nitrifier populations to soil temperatures.     

USE OF A PETHIDINE AND MIDAZOLAM COMBINATION FOR THE REVERSIBLE SEDATION OF CRABEATER SEALS (LOBODON CARCINOPHAGUS)

Between October and December of 1996–1999, off eastern Antarctica (60°-150°E), we darted 31 crabeater seals with midazolam and pethidine at estimated dose rates of 0.15–0.4 mg/kg and 1–3 mg/kg, respectively. Maximum sedation was reached at 23 ± 9 min (n = 18) and first signs of recovery were noted at 54 ± 24 min (n = 4). Seals greater than 250 kg body-mass were sedated by administration of approximately 90–100 mg midazolam and 600 mg pethidine, but the degree of sedation was unpredictable and did not permit invasive procedures in some cases. Behavior of the seal and adjacent conspecifics affected the success of procedures and our ability to monitor vital signs. Naloxone and flumazenil reversed sedation, making this combination attractive for use in animals adjacent to water. Additional ketamine was administered to two seals, resulting in improved restraint.     

EFFECTS OF METAL AND PETROLEUM HYDROCARBON CONTAMINATION ON BENTHIC DIATOM COMMUNITIES NEAR CASEY STATION,ANTARCTICA: AN EXPERIMENTAL APPROACH1

The effects of metals and petroleum hydrocarbons on benthic marine diatom communities were assessed using a manipulative field experiment at Casey Station, Antarctica. Uncontaminated, metal contaminated, and petroleum hydrocarbon contaminated sediments were deployed for 11 weeks during the 1999 austral summer. The treatments were deployed at three different locations: Brown Bay, which has elevated levels of anthropogenic contaminants, and two uncontaminated reference locations, O'Brien Bay and Sparkes Bay, the latter of which has naturally occurring high concentrations of some heavy metals. At each location, significant differences between the composition of diatom communities recruiting to control and petroleum hydrocarbon contaminated treatments were observed. Navicula directa (Smith) Ralfs occurred at lower abundances in the petroleum hydrocarbon contaminated treatments than in the control treatments. In contrast, Navicula cancellata Donkin occurred at higher relative abundances in both contaminated treatments relative to the control treatment. Interactions between treatment and location were also observed for several species, including Navicula glaciei Van Heurck. Significant differences in the overall community composition of diatom communities between control and metal contaminated treatments and metal contaminated and petroleum hydrocarbon contaminated treatments were only observed within Brown Bay. The location of deployment also had a significant influence on the composition of diatom communities. Brown Bay had higher abundances of Achnanthes brevipes Agardh but lower abundances of Navicula aff. cincta (Ehrenberg) Van Heurck than either reference locations. This experiment demonstrated that benthic diatom communities are sensitive to sediment contamination and would be suitable for future monitoring work within this and other areas of Antarctica.     

Solution structure of the Tn3 resolvase-crossover site synaptic complex

Tn3 resolvase is a site-specific DNA recombinase, which catalyzes strand exchange in a synaptic complex containing twelve resolvase subunits and two res sites. Hyperactive mutants of resolvase can form a simpler complex (X synapse) containing a resolvase tetramer and two shorter DNA segments at which strand exchange takes place (site I). We have solved the low-resolution solution structure of the purified, catalytically competent X synapse from small-angle neutron and X-ray scattering data, using methods in which the data are fitted with models constructed by rigid body transformations of a published crystallographic structure of a resolvase dimer bound to site I. Our analysis reveals that the two site I fragments are on the outside of a resolvase tetramer core and provides some information on the quaternary structure of the tetramer. We discuss implications of our structure for the architecture of the natural synaptic complex and the mechanism of strand exchange.     

Mammalian Fbh1 is important to restore normal mitotic progression following decatenation stress

We have addressed the role of the F-box helicase 1 (Fbh1) protein during genome maintenance in mammalian cells. For this, we generated two mouse embryonic stem cell lines deficient for Fbh1: one with a homozygous deletion of the N-terminal F-box domain (Fbh1^f/f), and the other with a homozygous disruption (Fbh1^?/?). Consistent with previous reports of Fbh1-deficiency in vertebrate cells, we found that Fbh1^?/? cells show a moderate increase in Rad51 localization to DNA damage, but no clear defect in chromosome break repair. In contrast, we found that Fbh1^f/f cells show a decrease in Rad51 localization to DNA damage and increased cytoplasmic localization of Rad51. However, these Fbh1^f/f cells show no clear defects in chromosome break repair. Since some Rad51 partners and F-box-associated proteins (Skp1-Cul1) have been implicated in progression through mitosis, we considered whether Fbh1 might play a role in this process. To test this hypothesis, we disrupted mitosis using catalytic topoisomerase II inhibitors (bisdioxopiperazines), which inhibit chromosome decatenation. We found that both Fbh1^f/f and Fbh1^?/? cells show hypersensitivity to topoisomerase II catalytic inhibitors, even though the degree of decatenation stress was not affected. Furthermore, following topoisomerase II catalytic inhibition, both Fbh1-deficient cell lines show substantial defects in anaphase separation of chromosomes. These results indicate that Fbh1 is important for restoration of normal mitotic progression following decatenation stress.     

Enzymatic synthesis of tea theaflavin derivatives and their anti-inflammatory and cytotoxic activities

Derivatives based on a benzotropolone skeleton (9-26) have been prepared by the enzymatic coupling (horseradish peroxidase/H2O2) of selected pairs of compounds (1-8), one with a vic-trihydroxyphenyl moiety, and the other with an ortho-dihydroxyphenyl structure. Some of these compounds have been found to inhibit TPA-induced mice ear edema, nitric oxide (NO) synthesis, and arachidonic acid release by LPS-stimulated RAW 264.7 cells. Their cytotoxic activities against KYSE 150 and 510 human esophageal squamous cell carcinoma and HT 29 human colon cancer cells were also evaluated.     

The effects of sleep deprivation and time of day on cognitive performance

The extent to which the diurnal fluctuations of different cognitive processes could be affected by sleep loss may be explored to predict performance decrements observed in the real world. Twenty healthy male subjects voluntarily took part in 8 test sessions at 06:00, 10:00, 14:00, and 18:00 h, following either a night with or without sleep in random order. Measurements included oral temperature, simple reaction time, sign cancelation, Go/NoGo, and the Purdue pegboard test. The results indicate that simple reaction time and motor coordination had morning–afternoon variations closely following the rhythms of temperature and vigilance. Inhibitory attention (Go/NoGo) presented no morning–afternoon variations. Sleep deprivation may affect the profiles of cognitive performance depending on the processes solicited. Sustained and inhibitory attention are particularly affected in the morning (after 24 and 28 waking hours), while a complex task (visuo-motor coordination) would be affected after 32 waking hours only.     

Acute stress induces contrasting changes in AMPA receptor subunit phosphorylation within the prefrontal cortex, amygdala and hippocampus

Exposure to stress causes differential neural modifications in various limbic regions, namely the prefrontal cortex, hippocampus and amygdala. We investigated whether α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) phosphorylation is involved with these stress effects. Using an acute inescapable stress protocol with rats, we found opposite effects on AMPA receptor phosphorylation in the medial prefrontal cortex (mPFC) and dorsal hippocampus (DH) compared to the amygdala and ventral hippocampus (VH). After stress, the phosphorylation of Ser831-GluA1 was markedly decreased in the mPFC and DH, whereas the phosphorylation of Ser845-GluA1 was increased in the amygdala and VH. Stress also modulated the GluA2 subunit with a decrease in the phosphorylation of both Tyr876-GluA2 and Ser880-GluA2 residues in the amygdala, and an increase in the phosphorylation of Ser880-GluA2 in the mPFC. These results demonstrate that exposure to acute stress causes subunit-specific and region-specific changes in glutamatergic transmission, which likely lead to the reduced synaptic efficacy in the mPFC and DH and augmented activity in the amygdala and VH. In addition, these findings suggest that modifications of glutamate receptor phosphorylation could mediate the disruptive effects of stress on cognition. They also provide a means to reconcile the contrasting effects that stress has on synaptic plasticity in these regions. Taken together, the results provide support for a brain region-oriented approach to therapeutics.     

Effect of heat stress on glucose kinetics during exercise

Hargreaves, Mark, Damien Angus, Kirsten Howlett, Nelly MarmyConus, and Mark Febbraio. Effect of heat stress on glucose kinetics during exercise. J. Appl.Physiol. 81(4): 1594-1597, 1996.To identify themechanism underlying the exaggerated hyperglycemia during exercise inthe heat, six trained men were studied during 40 min of cyclingexercise at a workload requiring 65% peak pulmonary oxygen uptake(O_{2 peak}) on twooccasions at least 1 wk apart. On one occasion, the ambient temperaturewas 20°C [control (Con)], whereas on the other, it was40°C [high temperature (HT)]. Rates ofglucose appearance and disappearance were measured by using a primedcontinuous infusion of[6,6-²H]glucose. Nodifferences in oxygen uptake during exercise were observed betweentrials. After 40 min of exercise, heart rate, rectal temperature,respiratory exchange ratio, and plasma lactate were all higher in HTcompared with Con (P < 0.05). Plasmaglucose levels were similar at rest (Con, 4.54 ± 0.19 mmol/l; HT,4.81 ± 0.19 mmol/l) but increased to a greater extent duringexercise in HT (6.96 ± 0.16) compared with Con (5.45 ± 0.18;P < 0.05). This was the result of ahigher glucose rate of appearance in HT during the last 30 min ofexercise. In contrast, the glucose rate of disappearance and metabolicclearance rate were not different at any time point during exercise.Plasma catecholamines were higher after 10 and 40 min of exercise in HTcompared with Con (P < 0.05),whereas plasma glucagon, cortisol, and growth hormone were higher in HTafter 40 min. These results indicate that the hyperglycemia observedduring exercise in the heat is caused by an increase in liver glucoseoutput without any change in whole body glucoseutilization.