The Bioeconomics of Controlling an African Rodent Pest Species

The paper treats the economy of controlling an African pest rodent, the multimammate rat, causing major damage in maize production. An ecological population model is presented and used as a basis for the economic analyses carried out at the village level using data from Tanzania. This model incorporates both density-dependent and density-independent (stochastic) factors. Rodents are controlled by applying poison, and the economic benefits depend on the income from maize production minus the costs for maize production, fertiliser and poison. We analyse how the net present value of maize production is affected by various rodent control strategies, by varying the duration and timing of rodenticide application. Our numerical results suggest that, in association with fertiliser, it is economically beneficial to control the rodent population. In general the most rewarding duration of controlling the rodent population is 3-4 months every year, and especially at the end of the dry season/beginning of rainy season. The paper demonstrates that changing from todays practice of symptomatic treatment when heavy rodent damage is noticed to a practice where the calendar is emphasised, may substantially improve the economic conditions for the maize producing farmers. This main conclusion is quite robust and not much affected by changing prices and costs of the maize production.bio-economics; pest control; multimammate rat; crop production

FGF2 is expressed in human and murine embryonic choroid plexus and affects choroid plexus cell behaviour

<p>Abstract</p> <p>Background</p> <p>Although fibroblast growth factor (Fgf) signalling plays crucial roles in several developing and mature tissues, little information is currently available on expression of Fgf2 during early choroid plexus development and whether Fgf2 directly affects the behaviour of the choroid plexus epithelium (CPe). The purpose of this study was to investigate expression of Fgf2 in rodent and human developing CPe and possible function of Fgf2, using <it>in vitro </it>models. The application of Fgf2 to brain <it>in vivo </it>can affect the whole tissue, making it difficult to assess specific responses of the CPe.</p> <p>Methods</p> <p>Expression of Fgf2 was studied by immunohistochemistry in rodent and human embryonic choroid plexus. Effects of Fgf2 on growth, secretion, aggregation and gene expression was investigated using rodent CPe vesicles, a three-dimensional polarized culture model that closely mimics CPe properties <it>in vivo</it>, and rodent CPe monolayer cultures.</p> <p>Results</p> <p>Fgf2 was present early in development of the choroid plexus both in mouse and human, suggesting the importance of this ligand in Fgf signalling in the developing choroid plexus. Parallel analysis of Fgf2 expression and cell proliferation during CP development suggests that Fgf2 is not involved in CPe proliferation <it>in vivo</it>. Consistent with this observation is the failure of Fgf2 to increase proliferation in the tri-dimensional vesicle culture model. The CPe however, can respond to Fgf2 treatment, as the diameter of CPe vesicles is significantly increased by treatment with this growth factor. We show that this is due to an increase in cell aggregation during vesicle formation rather than increased secretion into the vesicle lumen. Finally, Fgf2 regulates expression of the CPe-associated transcription factors, <it>Foxj1 </it>and <it>E2f5</it>, whereas transthyretin, a marker of secretory activity, is not affected by Fgf2 treatment.</p> <p>Conclusion</p> <p>Fgf2 expression early in the development of both human and rodent choroid plexus, and its ability to modulate behaviour and gene expression in CPe, supports the view that Fgf signalling plays a role in the maintenance of integrity and function of this specialized epithelium, and that this role is conserved between rodents and humans.</p

A review of rodent control programs in New York State

The history of rodent control programs in New York State is reviewed, beginning with state-funded efforts in August 1967. In 1969, Federal rodent control grant funds were used to establish four Model Cities programs. At its peak in 1970, programs were active in 18 counties, eight cities and villages, and in six Model Cities areas. The program encompasses all the major metropolitan areas of the state, serving some nine million persons. As part of the state program, the Rodent Control Evaluation laboratory was established to investigate chemosterilants as a means of rodent control and to develop knowledge of pest rodent biology. Since then, the investigations program has turned to the problem of rodent resistance to anticoagulant rodenticides both in New York and other states in the eastern United States. Initial rat infestations, which ran 24.4 percent statewide in 1969, have been decreased 84 percent by late 1973. Similarly, in the same time period, unapproved refuse storage deficiencies were decreased 55.6 percent and exposed garbage conditions declined 44.7 percent. Rat bites showed a 40 percent decrease during these same years. By all measures, then, the program has been a success. Most programs have relied heavily upon anticoagulant rodenticides in the chemical control or rodent populations. Zinc phosphide, red squill, and norbormide are also used. Harborage removal and environmental improvement are stressed through active cleanups and educational efforts. During the four-year period 1969-1972, some 177,000 tons of rat harborage were removed from 66,000 premises in the state

Traumatic Brain Injury Induces Genome-Wide Transcriptomic, Methylomic, and Network Perturbations in Brain and Blood Predicting Neurological Disorders.

The complexity of the traumatic brain injury (TBI) pathology, particularly concussive injury, is a serious obstacle for diagnosis, treatment, and long-term prognosis. Here we utilize modern systems biology in a rodent model of concussive injury to gain a thorough view of the impact of TBI on fundamental aspects of gene regulation, which have the potential to drive or alter the course of the TBI pathology. TBI perturbed epigenomic programming, transcriptional activities (expression level and alternative splicing), and the organization of genes in networks centered around genes such as Anax2, Ogn, and Fmod. Transcriptomic signatures in the hippocampus are involved in neuronal signaling, metabolism, inflammation, and blood function, and they overlap with those in leukocytes from peripheral blood. The homology between genomic signatures from blood and brain elicited by TBI provides proof of concept information for development of biomarkers of TBI based on composite genomic patterns. By intersecting with human genome-wide association studies, many TBI signature genes and network regulators identified in our rodent model were causally associated with brain disorders with relevant link to TBI. The overall results show that concussive brain injury reprograms genes which could lead to predisposition to neurological and psychiatric disorders, and that genomic information from peripheral leukocytes has the potential to predict TBI pathogenesis in the brain

Digestive anatomy and impact of dietary fibre on performances of the growing grasscutter (Thryonomys swinderianus)

The grasscutter is a rodent herbivore recently domesticated in several countries of sub-Saharan Africa for meat production. However, the development of this production to a rational and more productive model needs a better knowledge of the digestive physiology of this animal. This work aimed to study the digestive anatomy of the growing grasscutter and determine the impact of dietary fibre on growth rate and health

Point: From animal models to prevention of colon cancer. Systematic review of chemoprevention in min mice and choice of the model system.

The Apc(Min/+) mouse model and the azoxymethane (AOM) rat model are the main animal models used to study the effect of dietary agents on colorectal cancer. We reviewed recently the potency of chemopreventive agents in the AOM rat model (D. E. Corpet and S. Tache, Nutr. Cancer, 43: 1-21, 2002). Here we add the results of a systematic review of the effect of dietary and chemopreventive agents on the tumor yield in Min mice. The review is based on the results of 179 studies from 71 articles and is displayed also on the internet http://corpet.net/min.(2) We compared the efficacy of agents in the Min mouse model and the AOM rat model, and found that they were correlated (r = 0.66; P < 0.001), although some agents that afford strong protection in the AOM rat and the Min mouse small bowel increase the tumor yield in the large bowel of mutant mice. The agents included piroxicam, sulindac, celecoxib, difluoromethylornithine, and polyethylene glycol. The reason for this discrepancy is not known. We also compare the results of rodent studies with those of clinical intervention studies of polyp recurrence. We found that the effect of most of the agents tested was consistent across the animal and clinical models. Our point is thus: rodent models can provide guidance in the selection of prevention approaches to human colon cancer, in particular they suggest that polyethylene glycol, hesperidin, protease inhibitor, sphingomyelin, physical exercise, epidermal growth factor receptor kinase inhibitor, (+)-catechin, resveratrol, fish oil, curcumin, caffeate, and thiosulfonate are likely important preventive agents

\u3cem\u3eN\u3c/em\u3e-acetylcysteine Decreases Binge Eating in a Rodent Model

Binge-eating behavior involves rapid consumption of highly palatable foods leading to increased weight gain. Feeding in binge disorders resembles other compulsive behaviors, many of which are responsive to N-acetylcysteine (NAC), which is a cysteine prodrug often used to promote non-vesicular glutamate release by a cystine–glutamate antiporter. To examine the potential for NAC to alter a form of compulsive eating, we examined the impact of NAC on binge eating in a rodent model. Specifically, we monitored consumption of standard chow and a high-fat, high carbohydrate western diet (WD) in a rodent limited-access binge paradigm. Before each session, rats received either a systemic or intraventricular injection of NAC. Both systemic and central administration of NAC resulted in significant reductions of binge eating the WD without decreasing standard chow consumption. The reduction in WD was not attributable to general malaise as NAC did not produce condition taste aversion. These results are consistent with the clinical evidence of NAC to reduce or reverse compulsive behaviors, such as, drug addiction, skin picking and hair pulling

Impulsivity in rodents with a genetic predisposition for excessive alcohol consumption is associated with a lack of a prospective strategy

Increasing evidence supports the hypothesis that impulsive decision-making is a heritable risk factor for an alcohol use disorder (AUD). Clearly identifying a link between impulsivity and AUD risk, however, is complicated by the fact that both AUDs and impulsivity are heterogeneous constructs. Understanding the link between the two requires identifying the underlying cognitive factors that lead to impulsive choices. Rodent models have established that a family history of excessive drinking can lead to the expression of a transgenerational impulsive phenotype, suggesting heritable alterations in the decision-making process. In the present study, we explored the cognitive processes underlying impulsive choice in a validated, selectively bred rodent model of excessive drinking-the alcohol-preferring ("P") rat. Impulsivity was measured via delay discounting (DD), and P rats exhibited an impulsive phenotype as compared to their outbred foundation strain-Wistar rats. Steeper discounting in P rats was associated with a lack of a prospective behavioral strategy, which was observed in Wistar rats and was directly related to DD. To further explore the underlying cognitive factors mediating these observations, a drift diffusion model of DD was constructed. These simulations supported the hypothesis that prospective memory of the delayed reward guided choice decisions, slowed discounting, and optimized the fit of the model to the experimental data. Collectively, these data suggest that a deficit in forming or maintaining a prospective behavioral plan is a critical intermediary to delaying reward, and by extension, may underlie the inability to delay reward in those with increased AUD risk