Cambridge Science Centre

Elephant-shrews or sengis (Macroscelidea, Afrotheria) are grouped into two subfamilies, Rhynchocyoninae with a single genus and four species, and Macroscelidinae represented by three genera and 13 species. Our current understanding of the evolutionary relationships within this group is largely based on a molecular phylogeny that suffers from incomplete species representation. We present the first complete phylogeny (with the exception of the recently described East African Rhynchocyon udzungwensis) for Macroscelidea based on mitochondrial and nuclear markers. Novel cytogenetic characters as well as previously described allozyme variation and various morphological features are evaluated and mapped to the molecular topology. Our analyses indicate that Elephantulus is paraphyletic, and that Petrodromus and Macroscelides should be subsumed in Elephantulus. A relaxed Bayesian dating approach supports the hypothesis that an arid-adapted Macroscelidinae lineage dispersed from east Africa at ∼11.5 MYA via an African arid corridor to south-western Africa. The timing of speciation within the east African Rhynchocyoninae (8–10 MYA) is coincidental with the diversification of some other forest specialists. In turn, divergence within the Macroscelidinae coincides with major aridification events across Africa.

In our paper [1], the name of one of the authors is incorrectly given. Included here also is the biography with the missing IEEE membership information.

An image enhancement procedure was developed to produce high-contrast chromosome paint images. This procedure is well suited for images where brightness-contrast enhancement is subjective. Three examples are given to show that the procedure is very efficient to remove non-specific hybridization signals from the chromosome paint image. Chromosomes of roe deer contain large amounts of centromeric heterochromatic DNA. Echidna chromosomes show specific heterochromatic DNA distributed over several chromosomes. In both cases chromosome identification was hampered by bright heterochromatic regions. The enhancement tool was fully used in cross-species chromosome painting, which is the last example. The three examples show that the procedure is very simple to use and removes background in a controlled and defined manner.

Intrachromosomal duplications play a significant role in human genome pathology and evolution. To better understand the molecular basis of evolutionary chromosome rearrangements, we performed molecular cytogenetic and sequence analyses of the breakpoint region that distinguishes human chromosome 3p12.3 and orangutan chromosome 2. FISH with region-specific BAC clones demonstrated that the breakpoint-flanking sequences are duplicated intrachromosomally on orangutan 2 and human 3q21 as well as at many pericentromeric and subtelomeric sites throughout the genomes. Breakage and rearrangement of the human 3p12.3-homologous region in the orangutan lineage were associated with a partial loss of duplicated sequences in the breakpoint region. Consistent with our FISH mapping results, computational analysis of the human chromosome 3 genomic sequence revealed three 3p12.3-paralogous sequence blocks on human chromosome 3q21 and smaller blocks on the short arm end 3p26→p25. This is consistent with the view that sequences from an ancestral site at 3q21 were duplicated at 3p12.3 in a common ancestor of orangutan and humans. Our results show that evolutionary chromosome rearrangements are associated with microduplications and microdeletions, contributing to the DNA differences between closely related species.

Studies in conventional murine models of HSV infection use immunologically naive animals. These models thus mimic primary infections rather than recurrent infections in humans. We have, therefore, used a newly developed mouse model that more closely mimics recurrent HSV infection in humans. In this model, the mice are infected, and zosteriform HSV-1 infection develops in the presence of a primed immune response using adoptive transfer of immunity (ATI) as we have described previously. Using the ATI mouse model, it has been shown that a more beneficial therapy for recurrent mucocutaneous HSV infection could be achieved by controlling both the viral replication and the inflammatory response to the virus. Topical treatment was initiated in this model at the time of first occurrence of symptoms and was given three times daily for 4 days. Topical treatment with ME-609 (which contains 5% acyclovir and 1% hydrocortisone) in the ATI mouse model was substantially more efficacious than 5% Zovirax cream, 1% hydrocortisone or no treatment, respectively. The beneficial properties of ME-609 were also found to be superior to those of Zovirax cream when tested in the standard guinea pig model, representing a primary HSV infection. ME-609 represents a novel treatment principle of recurrent HSV infections and the present paper summarizes the preclinical and early clinical experience of ME-609.

The ability of famciclovir and valaciclovir to affect the establishment and maintenance of latency in mice with a cutaneous herpes simplex type 1 (HSV-1) infection was examined. Mice were treated via drinking water starting at various times between days 1 and 5 and terminating on day 10 after inoculation. Clinical signs and viral replication in the target tissues were monitored. Three to four months later, trigeminal and dorsal root ganglia were explanted from groups of 16 mice and examined for latent virus by cocultivation. The two compounds differed in their effects on the acute neural infection, and ganglia explanted from famciclovir-treated mice were markedly reduced in their ability to reactivate virus, although neither drug affected latency if treatment was delayed for several months. The difference between the compounds is likely to reflect differences in the metabolism of their respective products, penciclovir and acyclovir, in infected neurons.

The Journal of Pathology and BacteriologyVolume 95, Issue 2 p. 540-546 Short Article A rapidly fatal infection caused by Nocardia caviae in a dog D. A. Kinch, D. A. Kinch Veterinary Investigation Centre, CambridgeSearch for more papers by this author D. A. Kinch, D. A. Kinch Veterinary Investigation Centre, CambridgeSearch for more papers by this author First published: April 1968 https://doi.org/10.1002/path.1700950228Citations: 17AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume95, Issue2April 1968Pages 540-546 RelatedInformation