A note on the heat-transfer to nonspherical particles from plasma

Heat transfer from plasma to a nonspherical partical in the free-molecular regime is studied in the present paper under thin plasma sheath condition. Analytical expressions for the floating potential charge and heat fluxes of an ellipsoid particle of revolution are derived and curves are given for key parameters for arbitrary plasma flow direction. On the basis of these results, an equivalent sphere with the same surface area as the nonspherical particle is suggested to be used for calculating the total heat flux of nonspherical particle in engineering application with acceptable accuracy. Furthermore, the effects of particle rotation, which occurs in most aerosol systems, on the heat transfer are also discussed.

Basic equations for suspension flows with interphase mass-transfer

In the case of suspension flows, the rate of interphase momentum transfer M(k) and that of interphase energy transfer E(k), which were expressed as a sum of infinite discontinuities by Ishii, have been reduced to the sum of several terms which have concise physical significance. M(k) is composed of the following terms: (i) the momentum carried by the interphase mass transfer; (ii) the interphase drag force due to the relative motion between phases; (iii) the interphase force produced by the concentration gradient of the dispersed phase in a pressure field. And E(k) is composed of the following four terms, that is, the energy carried by the interphase mass transfer, the work produced by the interphase forces of the second and third parts above, and the heat transfer between phases. It is concluded from the results that (i) the term, (-alpha-k-nabla-p), which is related to the pressure gradient in the momentum equation, can be derived from the basic conservation laws without introducing the "shared-pressure presumption"; (ii) the mean velocity of the action point of the interphase drag is the mean velocity of the interface displacement, upsilonBAR-i. It is approximately equal to the mean velocity of the dispersed phase, upsilonBAR-d. Hence the work terms produced by the drag forces are f(dc) . upsilonBAR-d, and f(cd) . upsilonBAR-d, respectively, with upsilonBAR-i not being replaced by the mean velocity of the continuous phase, upsilonBAR-c; (iii) by analogy, the terms of the momentum transfer due to phase change are upsilonBAR-d-GAMMA-c, and upsilonBAR-d-GAMMA-d, respectively; (iv) since the transformation between explicit heat and latent heat occurs in the process of phase change, the algebraic sum of the heat transfer between phases is not equal to zero. Q(ic) and Q(id) are composed of the explicit heat and latent heat, so that the sum Q(ic) + Q(id)) is equal to zero.

A short in-frame deletion in NTRK1 tyrosine kinase domain caused by a novel splice site mutation in a patient with congenital insensitivity to pain with anhidrosis

Background: Congenital insensitivity to pain with anhidrosis (CIPA) is a rare autosomal recessive genetic disease characterized by the lack of reaction to noxious stimuli and anhidrosis. It is caused by mutations in the NTRK1 gene, which encodes the high affinity tyrosine kinase receptor I for Neurotrophic Growth Factor (NGF). -- Case Presentation: We present the case of a female patient diagnosed with CIPA at the age of 8 months. The patient is currently 6 years old and her psychomotor development conforms to her age (RMN, SPECT and psychological study are in the range of normality). PCR amplification of DNA, followed by direct sequencing, was used to investigate the presence of NTRK1 gene mutations. Reverse transcriptase (RT)-PCR amplification of RNA, followed by cloning and sequencing of isolated RT-PCR products was used to characterize the effect of the mutations on NTRK1 mRNA splicing. The clinical diagnosis of CIPA was confirmed by the detection of two splice-site mutations in NTRK1, revealing that the patient was a compound heterozygote at this gene. One of these alterations, c.574+1G > A, is located at the splice donor site of intron 5. We also found a second mutation, c.2206-2 A > G, not previously reported in the literature, which is located at the splice acceptor site of intron 16. Each parent was confirmed to be a carrier for one of the mutations by DNA sequencing analysis. It has been proposed that the c.574+1G > A mutation would cause exon 5 skipping during NTRK1 mRNA splicing. We could confirm this prediction and, more importantly, we provide evidence that the novel c.2206-2A > G mutation also disrupts normal NTRK1 splicing, leading to the use of an alternative splice acceptor site within exon 17. As a consequence, this mutation would result in the production of a mutant NTRK1 protein with a seven aminoacid in-frame deletion in its tyrosine kinase domain. --Conclusions: We present the first description of a CIPA-associated NTRK1 mutation causing a short interstitial deletion in the tyrosine kinase domain of the receptor. The possible phenotypical implications of this mutation are discussed.