Background: Atopic dermatitis (AD) can be exacerbated or induced in genetically predisposed individuals by psychological stress, which causes the release of substance P (SP). Therefore, SP may play an etiological role in the mechanisms underlying AD. Methods: Changes in the number of mast cells and SP-containing mast cells in lesional skin, and the serum concentrations of SP and IgE during the development of AD-like disease up to 8 weeks after the start of picryl chloride (PiCl) induction in NC/Nga mice were examined. Results: Clinical signs and symptoms seen in PiCl-treated NC/Nga mice as a model of AD-like disease began with erythema and haemorrhage, followed by oedema, superficial erosion, deep excoriation, scaling and dryness of the skin, as well as retarded growth, and the changes were exacerbated with an increase in the number of PiCl applications. An increase in the number of mast cells and eosinophil infiltration was observed in the lesional skin. The increase in SP-positive mast cells in the dermis in this model was significant from 1 week after the start of induction treatment, compared with intact mice, and SP-positive nerve fibres were observed in the dermis. Conclusion: SP is a crucial mediator of both dermatitis and scratching behaviour in this model.
We examined paclitaxel for anti‐tumor activity against human lung cancer xenografts in nude mice and compared its efficacy with that of cisplatin, currently a key drug for lung cancer chemotherapy. Five non‐small cell lung cancers (A549, NCI‐H23, NCI‐H226, NCI‐H460 and NCI‐H522) and 2 small cell lung cancers (DMS114 and DMS273) were chosen for this study, since these cell lines have been well characterized as regards in vitro and in vivo drug sensitivity. These cells were exposed to graded concentrations of paclitaxel (0.1 to 1000 nM) for 48 h. The 50% growth‐inhibitory concentrations (GI50) for the cell lines ranged from 4 to 24 nM, which are much lower than the achievable peak plasma concentration of paclitaxel. In the in vivo study, 4 cell lines (A549, NCI‐H23, NCI‐H460, DMS‐273) were grown as subcutaneous tumor xenografts in nude mice. Paclitaxel was given intravenously as consecutive daily injections for 5 days at the doses of 24 and 12 mg/kg/day. Against every xenograft, paclitaxel produced a statistically significant tumor growth inhibition compared to the saline control. Paclitaxel at 24 mg/kg/day was more effective than cisplatin at 3 mg/kg/day with the same dosing schedule as above, although the toxicity of paclitaxel was similar to or rather lower than that of cisplatin, in terms of body weight loss. In addition, paclitaxel showed potent activity against 2 other lung cancer xenografts (NCI‐H226 and DMS114). Therefore, paclitaxel showed more effective, wider‐spectrum anti‐tumor activity than cisplatin in this panel of 6 lung cancer xenografts. These findings support the potential utility of paclitaxel in the treatment of human lung cancer
We study a model of dynamic storage allocation in which requests for single units of memory arrive in a Poisson stream at rate λ and are accommodated by the first available location found in a linear scan of memory. Immediately after this first-fit assignment, an occupied location commences an exponential delay with rate parameter μ, after which the location again becomes available. The set of occupied locations (identified by their numbers) at time t forms a random subset S t of {1,2, . . .}. The extent of the fragmentation in S t , i.e. the alternating holes and occupied regions of memory, is measured by (S t ) -|S t |. In equilibrium, the number of occupied locations, |S|, is known to be Poisson distributed with mean ρ = λ/μ. We obtain an explicit formula for the stationary distribution of max (S), the last occupied location, and by independent arguments we show that (E max (S) -E|S|)/E|S| → 0 as the traffic intensity ρ → ∞. Moreover, we verify numerically that for any ρ the expected number of wasted locations in equilibrium is never more than 1/3 the expected number of occupied locations.Our model applies to studies of fragmentation in paged computer systems, and to containerization problems in industrial storage applications. Finally, our model can be regarded as a simple concrete model of interacting particles [Adv. Math., 5 (1970) Abstract. We study a model of dynamic storage allocation in which requests for single units of memory arrive in a Poisson stream at rate A and are accommodated by the first available location found in a linear scan of memory. Immediately after this first-fit assignment, an occupied location commences an exponential delay with rate parameter/z, after which the location again becomes available. The set of occupied locations (identified by their numbers) at time forms a random subset S, of 1, 2, .}. The extent of the fragmentation in S,, i.e. the alternating holes and occupied regions of memory, is measured by max (St) -IStl. In equilibrium, the number of occupied locations, ISI, is known to be Poisson distributed with mean p A//x. We obtain an explicit formula for the stationary distribution of max (S), the last occupied location, and by independent arguments we show that (E max (S) EISI)/EISI-0 as the traffic intensity /9 . Moreover, we verify numerically that for any/9 the expected number of wasted locations in equilibrium is never more than 1 / 2 the expected number of occupied locations.Our model applies to studies of fragmentation in paged computer systems, and to containerization problems in industrial storage applications. Finally, our model can be regarded as a simple concrete model of interacting particles [Adv. Math., 5(1970), pp. 246-290].
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