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1. Mouse plagues are a significant problem to agricultural areas of Australia, causing millions of dollars of damage. This study was conducted to determine if rainfall could explain the occurrence of mouse plagues. 2. On average, data on mouse abundance were collected every month, using mark-release-recapture techniques, from the Victorian Mallee cereal-growing region, from February 1983 to October 1994. No data were collected from December 1990 to September 1992. Three plagues of mice occurred during these 12 years. We examined the rate of increase of mouse populations as a function of antecedent rainfall. 3. The highest observed rate of increase per month was during 1986 (r = 1.86). The highest observed rate of decrease per month was during 1984 (r = -2.85). The maximum rate of increase of mouse populations used in the numerical response function was 1.16 month-1. The best estimate for the numerical response function was robs= -6.79 + 7.95 (1-e-1.11V). 4. The numerical response of mouse populations to rainfall was examined against 6-month accumulated rainfall that was lagged by 0, 3 and 6 months. The best fit of the model was to lag rainfall by 3 months. 5. Two systems for the response of mouse populations to rainfall are described. The plague system occurred when mouse populations responded to rainfall: populations increased following high rainfall and decreased following low rainfall. The non-plague system occurred when the exponential rate of increase and rainfall were independent: populations crashed after a plague and were unable to respond to rainfall for at least 2 years thereafter. 6. The two systems suggest that there is `biological memory' that masks the effect of rainfall for a minimum period after a mouse plague. This memory appears to be associated with the time since the last plague, the population response by mice (including shifts in age structure) in the previous year, and the abundance of mice after the spring decline. If rainfall is used to predict mouse plagues to assist in their management, the biology of the system must be known.

Well-known examples of high-amplitude, large-scale fluctuations of small-mammal populations include vole cycles in the boreal zone of Eurasia, lemming cycles in the high-arctic tundra of Eurasia and North America, snowshoe hare cycles in the boreal zone of North America, and outbreaks of house mice in southeastern Australia. We synthesize the recent knowledge of three key aspects of these animals' population cyles: (1) periodicity, amplitude, and spatiotemporal synchrony; (2) reproduction and survival; and (3) underlying mechanisms. Survival rather than reproductive rate appears to drive rates of population increase during these fluctuations. Food limitation may stop increases of cyclic vole, lemming, and hare populations, whereas the decline from peak numbers is caused by predation mortality. In house mice, without coevolved predators, outbreaks may be driven by rainfall, food supply, and disease.

Mice, rats, and other rodents threaten food production and act as reservoirs for disease throughout the world. In Asia alone, the rice loss every year caused by rodents could feed about 200 million people. Damage to crops in Africa and South America is equally dramatic. Rodent control often comes too late, is inefficient, or is considered too expensive. Using the multimammate mouse (Mastomys natalensis) in Tanzania and the house mouse (Mus domesticus) in southeastern Australia as primary case studies, we demonstrate how ecology and economics can be combined to identify management strategies to make rodent control work more efficiently than it does today. Three more rodent--pest systems -- including two from Asia, the rice-field rat (Rattus argentiventer) and Brandt's vole (Microtus brandti), and one from South America, the leaf-eared mouse (Phyllotis darwini) -- are presented within the same bio-economic perspective. For all these species, the ability to relate outbreaks to interannual climatic variability creates the potential to assess the economic benefits of forecasting rodent outbreaks.

Rationale Gamma-butyrolactone (GBL) and 1,4-butanediol (1,4-BD) are prodrugs for gamma-hydroxybutyrate (GHB). Like GHB, GBL and 1,4-BD are drugs of abuse, but their behavioral effects may differ from GHB under some conditions. Objectives The first study compared the behavioral effects of GBL (32–240 mg/kg) and 1,4-BD (32–240 mg/kg) with each other and to effects previously reported for GHB (32–420 mg/kg). A second study determined GHB pharmacokinetics following intragastric administration of GHB, GBL, and 1,4-BD. Methods Operant responding for food, observed behavioral effects, and a fine-motor task occurred at multiple time intervals after administration of drug or vehicle. In a separate pharmacokinetics study, blood samples were collected across multiple time points after administration of GHB, GBL, and 1,4-BD. Results Like GHB, GBL, and 1,4-BD impaired performance on the fine-motor task, but the onset of motor impairment differed across drugs. GBL and 1,4-BD dose dependently decreased the number of food pellets earned, but at lower doses than previously observed for GHB. Similar to GHB, both GBL and 1,4-BD produced sedation, muscle relaxation, gastrointestinal symptoms, and tremors/jerks. Administration of GBL and 1,4-BD produced higher maximum concentrations of GHB with shorter times to maximum concentrations of GHB in plasma when compared to GHB administration. Conclusions GBL and 1,4-BD produced behavioral effects similar to those previously reported with GHB and the time course of effects were related to blood levels of GHB. Given their higher potency and faster onset of effects, the abuse liability of GBL and 1,4-BD may be greater than GHB.

Rodents cause significant damage to lowland irrigated rice crops in the Red River Delta of Vietnam. A four-year study was conducted in 1999-2002 to examine the effectiveness of applying rodent control practices using the principles of ecologically based pest management. Four 100-150 ha study sites adjacent to villages were selected and farmers on two treated sites were asked to follow a set of rodent management practices, while farmers on the untreated sites were asked not to change their typical practices. Farmers on the treated sites were encouraged to use trap-barrier systems (TBS's; 0.065-ha early planted crop surrounded by a plastic fence with multiple capture traps; one TBS for every 10-15 ha), to work together over large areas by destroying burrows in refuge habitats soon after planting (before the rats reestablish in the fields and before the onset of breeding), synchronizing planting and harvesting of the their rice crops, cleaning up weeds and piles of straw, and keeping bund (embankment) size small (<30 cm) to prevent burrowing. A 75% reduction in the use of rodenticides and plastic barrier fences (without traps or an early crop) was achieved on treated sites. The abundance of rodents was low after implementation of the management practices across all sites. There was no evidence for an effect of treatment on the abundance of rodents captured each month using live-capture traps, and no difference in damage between treatments or in yields obtained from the rice crops. Therefore, ecologically based rodent management was equally effective as typical practices for rodent management. Farmers on the treated sites spent considerably less money applying rodent control practices, which was reflected in the comparative increase in the partial benefit : cost of applying ecologically based rodent management from 3:1 on treated sites and untreated sites prior to the implementation of treatments to 17:1 on treated sites in the final year of the project.

Electrospray ionization (ESI) and collisionally induced dissociation (CID) mass spectra were obtained for five tetracyclines and the corresponding compounds in which the labile hydrogens were replaced by deuterium by either gas phase or liquid phase exchange. The number of labile hydrogens, x, could easily be determined from a comparison of ESI spectra obtained with N 2 and with ND 3 as the nebulizer gas. CID mass spectra were obtained for [M + H] + and [M − H] − ions and the exchanged analogs, [M(D x ) + D] + and [M(D x ) − D] −, and produced by ESI using a Sciex API-III plus and a Finnigan LCQ ion trap mass spectrometer. Compositions of product ions and mechanisms of decomposition were determined by comparison of the MS N spectra of the un-deuterated and deuterated species. Protonated tetracyclines dissociate initially by loss of H 2O (D 2O) and NH 3 (ND 3) if there is a tertiary OH at C-6. The loss of H 2O (D 2O) is the lower energy process. Tetracyclines without the tertiary OH at C-6 lose only NH 3 (ND 3) initially. MS N experiments showed easily understandable losses of HDO, HN(CH 3) 2, CH 3 − NCH 2, and CO from fragment ions. The major fragment ions do not come from cleavage reactions of the species protonated at the most basic site. Deprotonated tetracyclines had similar CID spectra, with less fragmentation than those observed for the protonated tetracyclines. The lowest energy decomposition paths for the deprotonated tetracyclines are the competitive loss of NH 3 (ND 3) or HNCO (DNCO). Product ions appear to be formed by charge remote decompositions of species de-protonated at the C-10 phenol.

gamma-Hydroxybuyrate (GHB) is a current drug of abuse that may produce physical dependence. The present study characterized the behavioral effects of chronic GHB in baboons (n = 4), and evaluated whether signs of withdrawal occurred (1) after administration of the GABA-B antagonist CGP36742 during chronic GHB administration (precipitated withdrawal) and (2) following discontinuation of chronic GHB administration (spontaneous withdrawal). Water (vehicle) and then GHB was continuously infused via intragastric (IG) catheters. GHB administration was initiated at 350 mg/kg per day, and the dose was increased by 100 mg/kg over 4 days to 750 mg/kg per day. Food pellets were available 20 h/day under a fixed ratio (FR5 or 10) schedule of reinforcement. Observation sessions and a 2-min fine motor task were conducted during vehicle and GHB administration. CGP36742 (32 and 56 mg/kg, IM) was administered during vehicle and chronic GHB administration. After a total of 32-36 days GHB administration was abruptly discontinued. Blood samples were collected during all interventions and analyzed for GHB content. Chronic GHB decreased food-maintained behavior, disrupted performance of the fine motor task, and produced ataxia, muscle relaxation, tremors and jerks. At the end of GHB administration, plasma levels of GHB ranged from 486 to 2080 micromol/L. Administration of CGP36742 during chronic GHB administration produced increases in aggression, self-directed behaviors, vomit/retch, tremors and/or jerks, which is consistent with a precipitated withdrawal syndrome. Similar signs were observed when GHB administration was discontinued. Seizures were not observed. These data indicate that chronic GHB administration produced physical dependence and that activation of the GABA-B receptor may be important for GHB physical dependence.

The renin angiotensin system (RAS) has been implicated as one mediator of the cardiovascular effects of estrogen. Since changes in angiotensin type 1 (AT(1)) receptor expression are central to modulation of the RAS, we used the noninvasive PET imaging technique to study for the in vivo effects of estrogen on membrane and intracellular AT(1) receptors. Dynamic PET measurements of canine AT(1) (cAT(1)) receptors using the radiolabeled AT(1) receptor antagonist, (11)C-L-159,884, were performed during 2-wk consecutive periods of estrogen deprivation induced by ovariectomy and 17beta-estradiol (E(2)) replacement. Kinetic modeling of time-activity curves in the kidney and adrenal showed lower receptor expression in the estrogen replete state (21% and 30% decrease in Gjedde-Patlak slope, influx constant, respectively). These in vivo findings correlated with in vitro radioligand-binding assays with (125)I-[Sar(1),Ile(8)]angiotensin II showing reduced AT(1) receptor number in the adrenal (35%), glomeruli (30%), myocardium (35%), and liver (21%) in the estrogen-replenished compared with estrogen-depleted animals. Although other endogenous systems are known to regulate AT(1) receptors and could compete with estrogenic actions, these PET studies reveal that estrogen attenuates AT(1) receptor expression in vivo. Thus, estrogen modulation of AT(1) receptors may contribute to the cardiovascular protective effects associated with estrogen.

BackgroundAlendronate is a pyrophosphate analogue of bisphosphonate that has been shown to inhibit osteoclastic bone resorption. Bone formation and remodeling are necessary to establish initial fixation of uncemented implants, especially those coated with a bioactive surface such as hydroxyapatite. Because the process of bone-remodeling that culminates in new-bone formation is thought to be initiated by osteoclastic bone resorption, it is appropriate to test the influence of osteoclast-inhibiting medications on bone apposition to hydroxyapatite-coated implants.MethodsTwelve dogs underwent staged bilateral total hip arthroplasty, with twenty weeks between the first and second operations, with use of a titanium-alloy femoral stem that had a proximal macrotextured surface and a plasma-sprayed hydroxyapatite coating. Six of the dogs received oral alendronate therapy from the time of the surgery until they were killed; the other six dogs were untreated controls. The animals were killed four weeks after the second operation. Sections from matched implant sites (proximal, middle, and distal) were histologically analyzed. The linear extent of bone apposition, the linear extent and the thickness of the hydroxyapatite coating, and the total amount of cortical and trabecular bone were measured with the use of an interactive image analysis system.ResultsThere were no significant differences in radiographic or histologic findings between the two groups at either four or twenty-four weeks. Although the extent of the hydroxyapatite coating decreased significantly with time in both groups (p < 0.01), we identified no significant influence of alendronate on the extent of bone apposition, the extent or thickness of the hydroxyapatite coating, or the cortical or trabecular bone area around the implants.ConclusionsMany patients who are receiving alendronate for osteoporosis or other disorders may also be candidates for cementless total joint arthroplasty. Although bone formation is generally thought to be initiated by and coupled with bone resorption, our results suggest that alendronate has no discernible effect on the initial fixation of or the short-term bone-remodeling around hydroxyapatite-coated femoral total joint implants.

IRON is essential to the growth of organisms, and iron derived from the atmosphere may be the limiting nutrient for primary productivity in some oceanic regions 1–6 . Aeolian mineral dust is the chief source of marine iron in many areas 1–3,5,7 , but there is little information on the chemical form of the iron in this dust. Here we report that Fe(n) contributed 56±32% of the total iron in marine aerosol samples collected over the central North Pacific and 49 + 15% at Barbados. We suggest that the key reaction that produces Fe(n), and hence increases the solubility of marine aerosol iron in sea water, is [Fe(in)(OH)(H 2 O) 5 ] 2+ + H 2 O^ [Fe(n)(H 2 O) 6 ] 2+ + OH- (refs 8–10). The presence of Fe(n) in remote marine aerosols suggests that the OH radical has been produced in these heterogeneous reactions. From consideration of both the marine biological production of dimethylsulphide and the subsequent oxidation of reduced forms of sulphur in the atmosphere, we propose that the iron and sulphur cycles in both the atmosphere and the ocean may be closely coupled.