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Dive into the research topics where Susan E. Robinson is active.

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Featured researches published by Susan E. Robinson.


Journal of Applied Microbiology | 2004

Intermittent and persistent shedding of Escherichia coli O157 in cohorts of naturally infected calves

Susan E. Robinson; E.J. Wright; C. A. Hart; M. Bennett; N. P. French

Aims:  We conducted two short‐term studies of cohorts of naturally infected calves to determine the prevalence and concentrations of Escherichia coli O157 shed in faeces.


Journal of the Royal Society Interface | 2007

Recent network evolution increases the potential for large epidemics in the British cattle population

Susan E. Robinson; M.G Everett; R. M. Christley

Following the foot and mouth disease epidemic in Great Britain (GB) in 2001, livestock movement bans were replaced with mandatory periods of standstill for livestock moving between premises. It was anticipated that these movement restrictions would limit each individuals contact networks, the extent of livestock movements and thus the spread of future disease outbreaks. However, the effect of behaviour changes on the global network in adapting to these restrictions is currently unknown. Here, we take a novel approach using GB cattle movement data to construct week-by-week contact networks between animal holdings (AH) to explore the evolution of the network since this policy was introduced, the first time network theory has been used for this purpose. We show that the number of AH moving cattle as part of the giant strong component (GSC), representing the region of maximal connectivity, has been increasing linearly over time. This is of epidemiological significance as the size of the GSC indicates the number of holdings potentially exposed to disease, thus giving a lower bound of maximum epidemic size. Therefore, despite restriction of cattle movements, emergent behaviour in this self-organizing system has potentially increased the size of infectious disease epidemics within the cattle industry.


Glia | 2008

Opioid Addiction and Pregnancy: Perinatal Exposure to Buprenorphine Affects Myelination in the Developing Brain

Emilse S. Sanchez; John W. Bigbee; Wambura Fobbs; Susan E. Robinson; Carmen Sato-Bigbee

Buprenorphine is a μ‐opioid receptor partial agonist and κ‐opioid receptor antagonist currently on trials for the management of pregnant opioid‐dependent addicts. However, little is known about the effects of buprenorphine on brain development. Oligodendrocytes express opioid receptors in a developmentally regulated manner and thus, it is logical to hypothesize that perinatal exposure to buprenorphine could affect myelination. To investigate this possibility, pregnant rats were implanted with minipumps to deliver buprenorphine at 0.3 or 1 mg/kg/day. Analysis of their pups at different postnatal ages indicated that exposure to 0.3 mg/kg/day buprenorphine caused an accelerated and significant increase in the brain expression of all myelin basic protein (MBP) splicing isoforms. In contrast, treatment with the higher dose caused a developmental delay in MBP expression. Examination of corpus callosum at 26‐days of age indicated that both buprenorphine doses cause a significant increase in the caliber of the myelinated axons. Surprisingly, these axons have a disproportionately thinner myelin sheath, suggesting alterations at the level of axon‐glial interactions. Analysis of myelin associated glycoprotein (MAG) expression and glycosylation indicated that this molecule may play a crucial role in mediating these effects. Co‐immunoprecipitation studies also suggested a mechanism involving a MAG‐dependent activation of the Src‐family tyrosine kinase Fyn. These results support the idea that opioid signaling plays an important role in regulating myelination in vivo and stress the need for further studies investigating potential effects of perinatal buprenorphine exposure on brain development.


Applied and Environmental Microbiology | 2008

Longitudinal study of the molecular epidemiology of Campylobacter jejuni in cattle on dairy farms

Patrick S. L. Kwan; Andrew Birtles; Frederick J. Bolton; N. P. French; Susan E. Robinson; Lynne S. Newbold; Mathew Upton; Andrew J. Fox

ABSTRACT Multilocus sequence typing (MLST), an accurate and phylogenetically robust characterization method for population studies of Campylobacter, was applied to Campylobacter jejuni isolates (n = 297) from the fecal samples of cattle from five dairy farms in Cheshire, United Kingdom, collected throughout 2003. The population dynamics of the C. jejuni strains, as identified by the occurrence of sequence types and clonal complexes, demonstrated variations within and between cattle populations over time. Three clonal lineages have emerged to predominate among the cattle isolates, namely, the ST-61 complex (24.2%), ST-21 complex (23.6%), and ST-42 complex (20.5%). This provided further evidence that the ST-61 clonal complex may present a cattle-adapted C. jejuni genotype. In addition, the ST-42 clonal complex may also represent an important cattle-associated genotype. Strong geographical associations for these genotypes were also found among the farms. This is the first longitudinal study and the largest study to date for C. jejuni involving cattle populations using MLST for accurate strain characterization. This study shows the important associations between cattle and C. jejuni clonal complexes ST-61, ST-21, and ST-42, and it suggests that cattle and/or dairy products are likely to be a source of the human Campylobacter gastroenteritis caused by such genotypes. The reported findings have significant implications for the design of effective intervention strategies for disease control and prevention.


Proceedings of the Royal Society of London B: Biological Sciences | 2008

Epidemiological consequences of an incursion of highly pathogenic H5N1 avian influenza into the British poultry flock

Kieran J. Sharkey; Roger G. Bowers; K. L. Morgan; Susan E. Robinson; R. M. Christley

Highly pathogenic avian influenza and in particular the H5N1 strain has resulted in the culling of millions of birds and continues to pose a threat to poultry industries worldwide. The recent outbreak of H5N1 in the UK highlights the need for detailed assessment of the consequences of an incursion and of the efficacy of control strategies. Here, we present results from a model of H5N1 propagation within the British poultry industry. We find that although the majority of randomly seeded incursions do not spread beyond the initial infected premises, there is significant potential for widespread infection. The efficacy of the European Union strategy for disease control is evaluated and our simulations emphasize the pivotal role of duck farms in spreading H5N1.


Neurotoxicology and Teratology | 1987

Neonatal administration of delta-9-tetrahydrocannabinol (THC) alters the neurochemical response to stress in the adult Fischer-344 rat.

David J. Mokler; Susan E. Robinson; James H. Johnson; John S. Hong; John A. Rosecrans

Fischer-344 rat pups were injected with either 10 mg/kg delta 9-tetrahydrocannabinol (THC) or vehicle on postnatal days 4,6 and 8. Pups were then allowed to mature. On day 129 of age rats were exposed to a stress paradigm which consisted of inescapable electric foot-shock administered at 1 mA for 15 sec daily for 8 days. Analgesia induced by foot-shock was measured by tail withdrawal from 55 degree C water. On the 9th day rats were exposed to the shock environment only. Fifteen minutes following measurement of tail withdrawal, animals were sacrificed. Plasma corticosterone and prolactin were measured. Levels of norepinephrine, dopamine and 5-hydroxytryptamine and metabolites were determined in frontal cortex, hippocampus and hypothalamus. Neonatal exposure to THC produced an increase in baseline tail withdrawal latency. No effect of THC exposure was seen on acute stress-induced analgesia. Rats exposed to THC required a greater number of conditioning trials to develop conditioned analgesia than animals treated neonatally with vehicle. The conditioned stress increased plasma corticosterone without affecting prolactin. Stress increased hypothalamic 5HT and 5HIAA while decreasing 5HT turnover in this area. Dopamine and DOPAC levels in the hypothalamus and frontal cortex were increased by stress; dopamine turnover in the frontal cortex was elevated by stress. Neonatal THC and stress elevated norepinephrine above control levels in the hypothalamus, while increasing 5HT in the hippocampus and frontal cortex. The stress-induced increase in DOPAC in the frontal cortex was decreased by THC exposure. These data suggest that long-term neurochemical changes may occur with neonatal administration of THC.(ABSTRACT TRUNCATED AT 250 WORDS)


Biochemical Pharmacology | 2009

Enhanced nicotine reward in adulthood after exposure to nicotine during early adolescence in mice

Dena Kota; Susan E. Robinson; M. Imad Damaj

Approximately one million adolescents begin smoking cigarettes every year. Studies show that adolescents may be particularly vulnerable to various aspects of nicotine dependence. Work on rodents demonstrates parallel findings showing that adolescence is a time of changed sensitivity to both rewarding and aversive effects of nicotine. However, it is unclear if these effects are long-lasting and whether they contribute to a lifetime of nicotine addiction. In this study we have characterized the effects of adolescent nicotine exposure on the rewarding properties of nicotine in adulthood using the CPP model. Specifically, we have addressed whether the phase of adolescence (early, middle, or late adolescence) plays a role in the susceptibility to the enhanced rewarding effects of nicotine. Furthermore, we have investigated the long-term effects of adolescent nicotine exposure on nicotine reward in adulthood and have correlated these behavioral adaptations with possible molecular mechanisms. We observed that early adolescence in the mouse is a unique phase for elevated sensitivity to nicotine reward using a CPP model. In addition, exposure to nicotine during this phase, but not during late adolescence or adulthood, resulted in a lasting enhancement of reward in adulthood. Finally, we have shown that early adolescent nicotine exposure significantly elevates nAChR function in adulthood. Overall, we demonstrate that early adolescence represents a period of development, distinct from middle and late adolescence, during which nicotine exposure can cause persistent changes in behavior and molecular adaptations.


Journal of Applied Microbiology | 2004

Development and application of a spiral plating method for the enumeration of Escherichia coli O157 in bovine faeces

Susan E. Robinson; E.J. Wright; Nicola Williams; C. A. Hart; N. P. French

Aim:  To develop and validate a direct plating method applicable to epidemiological studies for enumerating Escherichia coli O157 in cattle faeces.


Pharmacology, Biochemistry and Behavior | 2005

Differential behavioral responses to nicotine in Lewis and Fischer-344 rats.

Scott D. Philibin; Robert E. Vann; Stephen A. Varvel; Herbert E. Covington; John A. Rosecrans; John R. James; Susan E. Robinson

Individual and strain variability in the effects of nicotine suggests the involvement of a genetic component in nicotinic cholinergic receptor (nAChR) function, which may help explain nicotines variable behavioral and pharmacological effects in different individuals. The present study evaluated differential responses to the discriminative stimulus (DS) and rewarding properties of nicotine in Lewis (LEW) and Fischer-344 (F-344) rats. Drug discrimination (DD) data suggest that the LEW rat is more sensitive to nicotine as LEW rats acquired the nicotine discrimination at a dose of 0.4 mg/kg, whereas F-344 rats acquired the dose of 0.9 mg/kg (all nicotine doses expressed as free base). Similarly, LEW rats exhibited nicotine-conditioned place preference (CPP) at 0.6 mg/kg, whereas the F-344 rats did not. Subsequent testing with a higher dose (0.9 mg/kg) failed to maintain the nicotine-CPP in the LEW rats. Conversely, nicotine-place preference in the F-344 rats was not changed at the higher dose. Taken together, these results suggest potential differences of sensitivities in LEW and F-344 rats to the rewarding and discriminative stimulus (DS) properties of nicotine. These findings support previous research by demonstrating that the F-344 rat is less sensitive to nicotine compared to the LEW rat.


Journal of Pharmacology and Experimental Therapeutics | 2006

Perinatal Nicotine Exposure Eliminates Peak in Nicotinic Acetylcholine Receptor Response in Adolescent Rats

Angela F. Britton; Robert E. Vann; Susan E. Robinson

Maternal smoking is a risk factor associated with nicotine abuse, so the effect of perinatal nicotine exposure was studied on the responsiveness to nicotine across adolescence in the rat. Pregnant Sprague-Dawley rats were implanted with s.c. Alzet osmotic minipumps delivering nicotine (l-nicotine hydrogen tartrate, 2 mg/kg/day free base) or vehicle (0.9% saline) on gestational day 7. There was no effect of nicotine on dam weight gain, food consumption, or water consumption or on the number of live pups or weights at the time of birth. Pups were cross-fostered to obtain the following prenatal/postnatal exposure groups: control/control, nicotine/nicotine, nicotine/control, and control/nicotine. On postnatal days 28, 35, 49, and 63, nicotine-stimulated 86Rb+ efflux was measured in synaptosomes prepared from the frontal cortex, hippocampus, striatum (STR), and thalamus (THL), using a previously developed method. Significant effects of treatment and concentration were detected in all four brain regions, and significant effects of age were observed in the STR and THL. Significant interactions of age and treatment were observed in each of the four brain regions. Nicotine-stimulated 86Rb+ efflux peaked during adolescence in control rats. However, perinatal exposure to nicotine eliminated this peak during adolescence. These results are consistent with recent behavioral and receptor binding results from other laboratories and are the first direct evidence at the cellular level that the nicotinic acetylcholine receptor response varies during adolescence and is affected by perinatal nicotine exposure.

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John A. Rosecrans

Virginia Commonwealth University

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Robert E. Vann

Virginia Commonwealth University

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John R. James

Virginia Commonwealth University

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Scott D. Philibin

Virginia Commonwealth University

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Carmen Sato-Bigbee

Virginia Commonwealth University

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Bruce G. Lyeth

Virginia Commonwealth University

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C. A. Hart

University of Liverpool

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