Crossing mice deficient in eNOS with placental-specific Igf2 knockout mice: a new model of fetal growth restriction.

We tested the hypothesis that crossing two mouse models of fetal growth restriction (FGR) of differing phenotype would induce more severe FGR than either model alone. Female endothelial nitric oxide synthase knockout mice (eNOS(-/-)) were mated with placental-specific Igf2 knockout males (P0). Resultant fetuses were no more growth restricted than those with P0 deletion alone. However, P0 deletion attenuated the reduced placental system A amino acid transporter activity previously observed in eNOS(-/-) mice. Manipulating maternal and fetal genotypes provides a means to compare maternal and fetal regulation of fetal growth.

Defining fetal growth restriction in mice: A standardized and clinically relevant approach.

The increasing number of mouse models of fetal growth restriction (FGR) make it crucial to standardize the way FGR is defined. By constructing growth curves in the placental-specific Igf2 knockout mouse (P0) it was demonstrated that 93% of P0 fetuses fell below the 5th centile of wild-type weights at E18.5, up from 44% at E16.5. This analysis, coupled with anthropomorphic measurements showing evidence of head sparing in P0 fetuses, allows clinical comparisons of FGR in mice through the use of clinically relevant growth curves. We suggest this as a standardized approach to defining FGR in mouse, and other animal models.

[Cutaneous leishmaniasis following military deployment to Iraq]. / Leishmaniose cutanée au cours du déploiement militaire en Irak.

Cutaneous leishmaniasis (CL) is a parasitic disease of the tropics and subtropics, transmitted by bites of infected female phlebotonine sandflies. Although CL lesions are normally self-healing they may be disfiguring or potentially disabling, and in field conditions may become secondarily infected; clinical intervention is appropriate in these circumstances. We describe two soldiers normally stationed in British Forces Germany who following deployment to Iraq presented with Leishmania tropica infection. The primary prevention of CL is discussed, together with the epidemiology of the disease, and its treatment under deployed conditions. Old World CL rarely requires aggressive antimonial terapy. Antiiosis with or without curettage is a simple, safe and effective field treatment.

Hospitalisation due to Lyme disease: case series in British Forces Germany.

Lyme disease is a tick-transmitted infection with disabling sequelae and important occupational health implications for a military workforce. It is likely that some military patients with typical clinical signs remain undiagnosed and untreated. Prompt treatment with an antibiotic is essential, besides targeted education on preventing infection through avoiding exposure to tick bites. We describe four British Forces Germany personnel (two serving military personnel, one adult civilian, one child) who during 2002--2003 required hospital inpatient treatment for Lyme disease. The epidemiology, pathogenesis, clinical features, diagnosis and treatment of the disease are discussed.

Purification and partial characterization of rat factor D.

Rat factor D has been purified to homogeneity (10,559-fold) from serum by chromatography on CM-Sepharose Fast Flow, phenyl-Sepharose CL-4B and Mono S and has been shown to resemble its human and mouse counterparts both in substrate specificity and in its susceptibility to inhibition by the organophosphorous inhibitor di-isopropylfluorophosphate. The rat enzyme, however, is heavily glycosylated and binds to wheat-germ lectin-Sepharose 6MB and 5-hydroxytryptamine-agarose, but not to concanavalin A-Sepharose 4B. All of the carbohydrate chains are N-linked. Enzymic removal of this carbohydrate decreased the Mr by approx. 15,000. The deglycosylated rat enzyme had the same mobility as native human factor D on SDS/PAGE, corresponding to an Mr of 24,500. N-Terminal sequence analysis of the first 30 amino acids of rat factor D highlighted the sequence similarity with human factor D (greater than 76%) and, in particular, with mouse adipsin (greater than 93%).