Ataxia-Telangiectasia

Ataxia-telangiectasia is a syndrome of progressive cerebellar ataxia and other neurological manifestations associated with conjunctival and cutaneous telangiectases and with recurrent sino-pulmonary infections. Immunological and endocrine abnormalities occur. Two girls with this disease are described. The first had only minor respiratory infections; her serum proteins and immunity responses appeared normal. The second had recurrent pulmonary infections and bronchiectasis; she also exhibited sclerodermatous changes, poor development of secondary sexual characteristics with low urinary excretion of 17-ketosteroids, and lymphopenia. Autopsy at 17 years showed bilateral ovarian dysgerminomata and excessive cutaneous collagen as well as atrophy, and perhaps hypoplasia, of adrenals, thymus, spleen and lymphoid tissue (after steroid therapy). The cerebellum exhibited cortical degeneration. Both lungs were fibrotic with old and recent bronchopneumonia and bronchiectasis. The left lung was studied by injection of a latex preparation; no arteriovenous aneurysms were found, but the smaller pulmonary vessels showed some unusual morphological characteristics.     

Non-stable resistance to demeton-methyl in a strain of Myzus persicae

The progeny of one viviparous aptera from a strain of Myzus persicae which appeared to have become resistant to organophosphorus insecticides, were bred asexually in an environment free from these materials. At approximately the 7th generation, the clone when compared with a susceptible strain had a 25-fold resistance to demeton-methyl. With subsequent generations the resistance gradually declined and within 30 generations from its establishment the clone was no longer resistant.

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Zusammenfassung Die Nachkommen einer viviparen Aptera von Myzus persicae, die offenbar resistent gegen organische Phosphorverbindungen geworden waren, wurden in einer insektizidfreien Umwelt geschlechtslos vermehrt. Ungefähr in der siebenten Generation, wenn der Klon mit einem normalen Stamm verglichen wurde, hatte er eine 25-fache Resistenz gegen Demeton-methyl. Mit weiteren Generationen nahm die Resistenz allmählich ab und 30 Generationen nach seiner Gründung war der Klon überhaupt nicht mehr resistent.