Following injection of an appropriate certain time, a proportion, p, of the 2N radioactive DNA precursor, suppose that labeled cells has transferred out of the after mitosis of the labeled cells in the basal layer. I f the transfer of the labeled basal layer of the esophagus, there are N cells is a random event, then the probabilpairs of labeled daughter cells or 2N ity that such a cell will transfer is p and labeled cells. Suppose further that at a the probability that it will not is 1 -p.
__ -With one degree of freedom, the x-squares for the 24-hour map, 2.44, and for the 48-hour map, 1.89. give a P value between 0.20 ( P = 1.64) and 0.10 ( P = 2.76). Hence, the differences between observed and expected numbers of pairs are not significant.
A one-dimensional preliminary design impedance prediction model is derived for Helmholtz resonators constructed with circular ori ces. The model addresses only the effects of resonator geometry and incident sound-pressure amplitude. The effects of grazing ow are not included. An experimental program was conducted to calibrate unknown empirical parameters derived in the model. The model was shown to predict, reasonably accurately, impedance data published in the open literature for resonators constructed with single and multiple ori ces over a wide range of sound-pressure amplitudes and frequencies. The model provides a rapid means of calculating resonator impedance as a function of resonator geometry, incident sound-pressure amplitude, and frequency.
Nomenclaturece inertia length de ned by Eq. (19) d N = multiple-ori ce diameter de ned by Eq. (34) d o = single-ori ce diameter F = sound frequency H = ori ce nonlinear inertial length de ned by Eq. (20) and Fig. 1 K ac = acoustic viscous loss parameter de ned by Eq. (22) K ss = steady-state viscous loss parameter de ned by Eq. (21) k = sound wave number !=c 0 L c = cavity depth N = number of ori ces P c = peak cavity sound pressure de ned by Eq. (7) P pk = p 2P 0 P 0 = peak driving sound pressure acting on control volume upper surface S o R = real part of resonator impedance R fd = steady-state fully developed laminar resistive loss de ned by Eq. (16) R L = linear resistive loss de ned by Eq. (15) r o = ori ce radius S BL = ori ce boundary-layer area, S BL D S o ¡ S inv de ned in Fig. 1 S c= cavity cross-sectionalarea S inv = ori ce inviscid area de ned in Fig. 1 S N = multiple ori ce center-to-center spacing S o = ori ce area S w = ori ce wetted area t = time u BL = acoustic velocity passing through S BL de ned in Fig. 1 u inv = acoustic velocity passing through S inv de ned in Fig. 1 u o = ori ce peak acoustic velocity hu o i rms = rms amplitude averaged over each half-cycle V non = nondimensional acoustic particle velocity de ned by Eq. (23) X = imaginary part of resonator impedance ± = ori ce instantaneous boundary-layer thickness µ p = phase angle between P 0 and u o de ned by Eq. (5) · vis = ori ce viscous loss parameter de ned by Eq. (10) = sound wavelength ¹ = uid viscosity º = uid kinematic viscosity ½ 0 = uid density ¾= ori ce open area ratio, S o =S c ¿ = ori ce thickness ¿ w = acoustic shear stress acting on ori ce wetted area de ned by Eq. (8) ! = sound radian frequency (D 2¼ F) Subscripts c = cavity L = linear NL = nonlinear res = resonance
Mice exposed prenatally to diethylstilbestrol (DES-exposed mice) can transmit a carcinogenic influence to the next generation (DES-lineage mice) when mated to control mice. The persistence of this effect was studied one generation further (DES-lineage-2 mice) by mating DES-lineage female mice to control males. The interaction of maternal dietary fat levels with DES was also tested by feeding high and low levels of dietary fat during the pregnancies that produced the final two generations. DES-lineage-2 mice, exposed to low or high fat maternal diets, had significantly more tumors than control mice with corresponding dietary fat exposure. The frequency of tumors in DES-lineage-2 mice was not significantly lower than in DES-lineage mice from a previous experiment. Thus, the multigenerational effect of DES is relatively intense in mice. If this type of carcinogenesis can occur in the human population, it poses a major threat to future generations.
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