Pizzaner study: a contribution to the classification of equine herpesviruses. Arch Virol 90: 273-278, 1986 Edington N, Bridges CG, Huckle A: Experimental reactivation of equid herpesvirus 1 EHV-1 ; following administration of corticosteroids. Equine Vet J 17: 369-372, 1985 Edington N, Bridges CG, Pate1 JR: Endothelial cell infection and thrombosis in paralysis caused by equid herpesvirus-1: equine stroke. Arch Virol 90: 111-124, 1986 Greenwood RE, Simpson ARB: Clinical report of a paralytic syndrome affecting stallions, mares, and foals on a Thoroughbred stud farm. Equine Vet J 12: 113-117, 1980 Little PB, Thorsen J: Disseminated necrotizing myeloencephalitis: a herpes-associated neurological disease of horses. Vet Path01 13: 161-171, 1976 Montgomery DL: Astrocytes: form, functions, and roles in disease. Vet Path01 31: 145-167, 1994 O'Callaghan DJ, Gentry GA, Randall CC: The equine herpesviruses. In: The Herpesviruses, ed. Roizman B, vol. 2, pp. 215-318. Plenum Press, New York, NY, 1983 9 Pate1 JR, Edington N, Mumford JA: Variation in cellular tropism between isolates of equine herpesvirus-l in foals. Arch Virol 74: 41-5 1, Rimstad E, Evensen 0: The identification of equid herpesvirus 1 in paraffin-embedded tissues from aborted fetuses by polymerase chain reaction and immunohistochemistry. J Vet Diagn Invest 5: 174-183, 1993 Saxegaard F: Isolation and identification of equine rhinopneumonitis virus 1 equine abortion virus ; from cases of abortion and paralysis. Nord Vet Med l&504-512, 1966 12 Schultheiss PC, Collins JK, Carmen J: Use of an immunoperoxidase technique to detect equine herpesvirus- 1 antigen in formalin-fixed paraffin embedded equine fetal tissues. J Vet Diagn Invest 5: 12-15, 1993 Slater JD, Borchers K, Thackray AM, Field HJ: The trigeminal ganglion is a location for equine herpesvirus 1 latency and reactivation in the horse. J Gen Virol 75: 2007-2016, 1994 Whitewell KE, Blunden AS: Pathological findings in horses dying during an outbreak of the paralytic form of equid herpesvirus type 1 EHV-1 ; infection. Equine Vet J 24: 13-19, 1992 Request reprints from Dr. I? C. Schultheiss, Veterinary Diagnostic Laboratory, Colorado State University, Fort Collins, CO 80526 USA.
Insight into the potential molecular and cellular mechanisms underlying adaptive changes of receptor function can be derived from studies using primary neuronal cultures expressing native GABAARs. Such results have demonstrated that persistent exposure of cultured neurons to positive modulators of the GABA response, such as BZDs, produces uncoupling of allosteric interactions 5, 12-14 ; that is not accompanied by changes in receptor number 5 ; . Prolonged exposure of neurons in culture to steroids such as pregnanolone, as well as barbiturates, also leads to uncoupling 5, 15-17 ; in the absence of regulation of receptor number 5, 15, 16 ; . In contrast to BZD treatment, occupancy of GABAARs by GABA induces a downregulation in receptor number 15, 18, 19 ; , a reduction in the allosteric interactions between GABA and BZD binding sites homologous uncoupling ; , and a reduction in allosteric interactions between BZD and barbiturate recognition sites heterologous uncoupling, 15, 18 ; . Because exposure to BZDs, steroids, and barbiturates, can cause uncoupling of allosteric modulatory sites on the GABAAR without producing down-regulation, it has been postulated that down-regulation and uncoupling are controlled by different mechanisms of action. Down-regulation is most likely the product of a transcriptional repression of GABAAR subunit genes 20, 21 ; that depends on activation of L-type voltage-gated calcium channels 22 ; . Previous studies from our laboratory demonstrate that chronic exposure of neurons to GABA induces down-regulation of receptor number with a t1 2 hours and uncoupling occurs with a similar time course t1 2 24 Uncoupling is unlike down-regulation in that it is independent of voltage-gated calcium channel activation 22 ; . Our initial reports using neurons in primary culture revealed a t1 2 hours for BZD-induced uncoupling but no uncoupling was detected for exposures of 6 hours or less 5 ; . Contrary to this result in neurons, BZD-induced uncoupling in transfected cell lines occurs more rapidly and appears to be independent of transcription. The results from stably transfected Ltk- fibroblast uncoupling a t1 2 min ; and WSS-1 kidney uncoupling t1 2 3 cell lines expressing recombinant GABAARs argue against a mechanism involving transcriptional regulation 23, 24 ; . Similarly, the results obtained using the transiently transfected Sf9 insect cell line support internalization as a mechanism for uncoupling 25 ; . These results appear to demonstrate that BZD-induced uncoupling is the result of a posttranscriptional regulatory mechanism. Here we have examined the relationship between GABAAR activation and the subsequent establishment of uncoupling in neocortical neurons. Delayed-onset uncoupling was found to be a transcription-dependent form of receptor regulation that occurs through a two-step mechanism: a rapid initiation process taking several minutes and requiring GABAAR activation, followed by a delayed-onset transduction process independent of the presence of agonist. Materials and Methods Cell cultures - Primary cultures were prepared from 18-day-old rat embryos Sprague Dawley ; . Whole brains were quickly removed and placed in ice-cold Ca2 + Mg2 + free CMF ; buffer. Cerebral cortexes were dissected under a microscope and placed in 5 ml ice-cold CMF. Tissue was finely minced, triturated with a serological pipette and centrifuged for 5 minutes at 500 g. The resulting pellet was resuspended in 5 ml plating medium Neurobasal medium plus B27 serum-free supplement, Life Technologies, 10% fetal bovine serum, 100 U ml penicillin, 0.1 mg ml streptomycin and 2 mM glutamine ; and triturated again with a serological pipette. This cell suspension was added to a final volume of plating medium and plated at a density of 3 4 cortex per 100 mm tissue culture dish coated with poly-Llysine 0.1 mg ml ; . Cultures were incubated at 37C in 5% CO2, and after 1 hour, the medium was aspirated and replaced with serum-free medium. Drug treatment - Cultures, 2-3 x 100 mm dishes treatment group, containing 14 ml of medium were treated on day 7 as follow: 7 ml of medium conditioned medium ; was removed and kept in the incubator, a small volume 70 l ; of.

Recurrent gastrointestinal symptoms among children with autism compared with normal controls No temporal association between MMR vaccination and the onset of gastrointestinal symptoms in children with autism The authors acknowledged that they could not exclude the possibility that some children in the study had sub-clinical gastrointestinal symptoms before their presentation with autistic behaviour. However, they commented that the children described by Wakefield and colleagues had symptomatic gastrointestinal disease. The authors also could not exclude the possibility that severe gastrointestinal disease might be associated with the development of autism in certain individuals. However, they thought that this was likely to be uncommon. Comment: the authors themselves acknowledge the shortcomings of their methodology. Further criticisms are that child health records are unlikely to fully reflect a novel gastrointestinal condition that is subtly different to Crohn's Disease or ulcerative colitis. No children were examined. The study apparently failed to distinguish between late-onset regressive-type autism and autism from infancy or birth. Conclusion: this study does not disprove a link between MMR and certain sub-types of autism. 203. Study by Madsen, Hviid, Vestergaard, Schendel, Wohlfarht, Thorsen, Olsen and Melbye, A Population-Based Study of Measles-Mumps Rubella Vaccination and Autism, New England Journal of Medicine, November 2002, 347: 1478-1482. This study paper, again, not to be confused with the Pediatrics paper reviewed above, also attracted a great deal of attention, largely uncritical, when it was published towards the end of 2002, mainly because of its claimed size and, of course, its conclusion that there was no evidence of any MMR autism link. The paper featured: A retrospective cohort study of all children born in Denmark from January 1991 through till December 1998 MMR vaccination data obtained from the Danish National Board of Health. Information on the children's autism status was obtained from the Danish Psychiatric Central Register, which contains information on all diagnoses received by patients in psychiatric hospitals and outpatient clinics in Denmark Of the 537, 000 children in the cohort, 441, 000 had received MMR. The study identified 316 children with a diagnosis of autistic disorder and a further 442 with a diagnosis of other autistic-spectrum disorder total 758 ; . Note: 758 cases amongst 537, 000 children represents a rate of 1 in 709, or 14 per 10, 000 ; . After comparing autism amongst vaccinated and unvaccinated children, the study concluded that there was no association between the age at the time of vaccination, the time since vaccination, or the date of vaccination and the development of autistic disorder. After initial uncritical review by the press, this study received a very thorough analysis by the parents, notably Dawn Richardson of the US parents' group PROVE and Sally Bernard of the group Safe Minds. Richardson's and Bernard's key criticisms were and procarbazine.

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