The present study provides the first convincing explanation of the mode of action of the medical device NYDA, a special dimeticone (CAS 9006-65-9) formula containing 92% of two dimeticones with different viscosities specifically designed for the physical treatment of head lice infestations (pediculosis capitis) by suffocation. Both, lice (Pediculus humanus) and house crickets (Acheta domestica) treated with this anti-head lice product are knocked out to the status "of no major vital signs" within less than 1 min that in consequence is accompanied irreversibly with the death of the respective insects. Scanning electron microscopical investigations have revealed that the cuticle is coated by a thin closed layer of the dimeticone formula that also enters the stigmata. In vivo observations and dissections of Acheta domestica have shown that application of the medical device to the thoracic stigmata invariably leads to rapid death; this is strongly correlated with the influx of the special dimeticone formula into the head trachea, whereby the solution effectively blocks the oxygen supply of the central nervous system. Dissections after application of the stained product show that it also enters the finest tracheal branches. Analogous in vivo observations in Pediculus humanus have confirmed the correlation between the disappearance of major vital signs and the displacement of air by the dimeticone formula in the tracheal system of the head. For both insect species, statistical data are provided for the chronological sequence of the filling of the tracheal system in relation to the respective vitality conditions of the Insects. On average, the special dimeticone formula reaches the insect's head tracheae within 0.5 min in house crickets and in less than 1 min in lice with a complete filling of the entire head tracheal system of lice within 3.5 min. In addition, a timed sequence of images illustrates this process for lice. The experiments clearly reveal the exclusive and pure physical mode of action of the tested dimeticone formula.
Since 1955 snails of the Euglandina rosea species complex and Platydemus manokwari flatworms were widely introduced in attempted biological control of giant African snails (Lissachatina fulica) but have been implicated in the mass extinction of Pacific island snails. We review the histories of the 60 introductions and their impacts on L. fulica and native snails. Since 1993 there have been unofficial releases of Euglandina within island groups. Only three official P. manokwari releases took place, but new populations are being recorded at an increasing rate, probably because of accidental introduction. Claims that these predators controlled L. fulica cannot be substantiated; in some cases pest snail declines coincided with predator arrival but concomitant declines occurred elsewhere in the absence of the predator and the declines in some cases were only temporary. In the Hawaiian Islands, although there had been some earlier declines of native snails, the Euglandina impacts on native snails are clear with rapid decline of many endemic Hawaiian Achatinellinae following predator arrival. In the Society Islands, Partulidae tree snail populations remained stable until Euglandina introduction, when declines were extremely rapid with an exact correspondence between predator arrival and tree snail decline. Platydemus manokwari invasion coincides with native snail declines on some islands, notably the Ogasawara Islands of Japan, and its invasion of Florida has led to mass mortality of Liguus spp. tree snails. We conclude that Euglandina and P. manokwari are not effective biocontrol agents, but do have major negative effects on native snail faunas. These predatory snails and flatworms are generalist predators and as such are not suitable for biological control.
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