CommentsComments «e sh«t papers which comment on papers of other authors preuiously published tn the phys&eai Revievr Comment should state clearly to which paper it refers and must be accompanied by a brief abstract. The same publication schedule as for regular articles is followed, and page proofs are sent to authors.In their recent paper [Phys. Rev. A 35, 4122 (1987)]Castrigiano and Kokiantonis claim to present an exact calculati. on of the partition function for a quantum oscillator interacting with the blackbody radiation field. In this Comment it is shown that their result is in fact wrong, due essentially to their neglect at the outset of the A term in the Hamiltonian. It is further shown how their error can be repaired to give the correct result given by us in an earlier publication [Phys. Rev. Lett. 55, 2273(1985].In their paper' Castrigiano and Kokiantonis claim to present an exact calculation of the partition function and, hence, the free energy of a quantum harmonic oscillator interacting with the radiation field. We wish to point out here that their calculation is wrong and that when the error is repaired a calculation such as theirs gives the correct result.The point is this. They begin with the correct Hamiltonian for a three-dimensional charged oscillator of (bare) mass m and spring constant K interacting via dipole coupling with the radiation 6eld 0= ' p--'A +-, 'K:'+H, .' 2@i tonian (1), takes the form "2 2&e 2VX Finally they interchange the meaning of coordinate and momentum with the canonical transformation: r~p, p~-r. The result is the Hamiltonian H"= -Kp + r -=1 2 1 2 2 2@i ' ]/2 2~e r + gAco a& + ei, fico V where the vector potential in dipole approximation is ' 1/2 2vTRc A= g e"(a"+ai", ), co V (2) ' 1/2 2me r X &g + eg + %co V and the radiation field Hamiltonian is H"d --g fico(a& az +-, ') . k, cr But at the outset they drop the term e A /2m' Then, at a later stage, they add a term [the "counterterm" appearing in the text following Eq. (10)] that, when expressed in terms of the variables of the original HamilThis Harniltonian does not correspond to the oscillator coupled to the radiation field. In fact, it corresponds to a Drude model with a frequency-independent friction constant equal to 2Ke /3mc . This, then, is their error: they calculate from the outset with the wrong Hamiltonian. Indeed, the "main result" of Castrigiano and Kokiantonis, their Eq. (11), is equivalent with the expression for the free energy for such a Drude model given in Ref. 2, Eq. (25). Thus their path-integral calculation is correct; it is their physics which is wrong. Here we should 37 3609 O~1988 The Axnerican Physical Society
Autotransplantation of islets of Langerhans has resulted in long-term normoglycemia in pancreatectomized dogs. This canine model is useful in evaluating both the progress of islet transplantation and the effect of a reduced islet mass upon the determinants of glucose tolerance: i.e., insulin secretion, insulin sensitivity, and glucose effectiveness. To determine the effect of a reduced islet mass on these factors, we measured the acute insulin response to arginine (AIRa) and glucose (AIRg), the slope of glycemic potentiation of AIRa (SP), insulin sensitivity (Sl), and glucose effectiveness (SG) in control (CN), diabetic (DM), and pancreatectomized dogs rendered normoglycemic with transplanted autografts of islets of Langerhans (TX). Normal fasting plasma glucose (FPG) (TX 4.7 +/- 0.2 mM; CN 4.9 +/- 0.1 mM; P greater than 0.05) was maintained despite a markedly reduced insulin secretion in TX (AIRa 24%, AIRg 15%, and SP 11% of CN). All measures of insulin secretion were significantly correlated (SP vs. AIRg, r = 0.80, P less than 0.0001; AIRa vs. AIRg, r = 0.92, P less than 0.0001) across all animals, but none of the measures of secretion were significantly correlated with either the number of islets transplanted or time posttransplant (P greater than 0.10). Insulin sensitivity was normal in islet autografted dogs (TX: 136 +/- 12 min-1/(nmol/ml); CN: 101 +/- 11 min-1/(nmol/ml), P greater than 0.05) but SG was reduced (TX: 1.93 +/- 0.28 x 100 min-1; CN: 3.53 +/- 0.35 x 100 min-1, P less than 0.05), as determined by the minimal-model method. In diabetic animals (FPG = 16.1 +/- 1.3 mM), insulin secretion was negligible by all measures (P greater than 0.05), and was associated with insulin resistance (Sl = 28 +/- 8 min-1/(nmol/ml)) and reduced SG (1.72 +/- 0.11 x 100 min-1). These studies indicate that across a range of insulin secretion in dogs, the secretagogues arginine and glucose provide similar estimates of beta-cell function. This markedly reduced beta-cell function does not result in insulin resistance when fasting normoglycemia is maintained, but is associated with a decrease in glucose action at basal insulin.
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