No consensus about the antigenicity of monocomponent insulin has yet been reached. We have therefore administered different insulin preparations to rabbits and rats to determine IgG and IgE antibody production. The preparations used were porcine monocomponent insulin, conventional bovine and porcine insulin powders, porcine b-component and synthesized porcine mono-desamido-insulin and hexa-desamido-insulin. In rabbits, porcine b-component was the most antigenic preparation, followed by conventional bovine and porcine insulins. No antibody production was observed with the other preparations. In rats the 60 h passive cutaneous anaphylaxis test showed virtually no insulin IgE antibody production in response to porcine monocomponent insulin. However, if porcine b-component or porcine hexa-desamido-insulin was employed both for sensitisation and as the challenging antigen, positive skin reactions were observed with demonstration of insulin IgE antibodies. Our results confirm the low antigenicity of the pharmaceutical preparation of porcine monocomponent insulin and suggest that porcine hexa-desamido-insulin and porcine b-component administration may result in the production of reagin-type antibodies.

Spores of Bacillus cereus T

Craniofacial and cervical spinal hyperostoses are rarely seen in the absence of other abnormalities. Only seven patients with isolated cranial hyperostoses have been reported, and only a single patient with both calvarial and cervical vertebral hyperostoses. We report on an adult with late-onset right-sided asymmetrical hyperostoses of the cranium, mandible, and cervical vertebrae in the absence of an AKT1 mutation. At presentation, the patient displayed neither generalized overgrowth nor dysregulated adipose tissue. Standard polymerase chain reaction and Sanger sequencing of DNA extracted from formalin-fixed paraffin-embedded frontal bone and mandibular angular bone was negative for an AKT1 mutation. Though the patient's clinical manifestations did not fulfill the consensus diagnostic criteria of Proteus syndrome, the mosaic distribution of lesions, the sporadic occurrence, and the patient's progressive course were consistent with a somatic mosaicism similar to that syndrome. Hence, the patient's phenotype may have been caused by a very late mesodermal somatic mutation during embryogenesis.

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