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We use density functional theory to examine the stability of defects in p-ZnSe that are formed by a transition of the nitrogen acceptor to the interstitial site. We find that the threefold positive complex of the interstitial nitrogen with the remaining vacancy is considerably more stable than the nitrogen acceptor. The formation of the complex is, however, limited by a kinetic barrier of 1.8 eV for the site transition, and the fact that the charge of the defect must change. The energetic position of the defect in the energy gap is about 2 eV above the valence band edge. This is in agreement with optical degradation experiments which show the formation of a deep defect in the p-doped waveguide with a transition energy of about 2.1 eV and the diffusion of a positively charged species. ͓S0163-1829͑99͒52548-4͔ RAPID COMMUNICATIONS R16 274PRB 60 GUNDEL, ALBERT, NÜ RNBERGER, AND FASCHINGER

We present results of optical degradation experiments on blue-green ZnSe-based diode laser structures. A micro-focused wavelength selectable laser is used for degradation and the luminescence from the degrading region is simultaneously recorded. The degradation speed at a given optical power density depends strongly on the doping of the structure and on the photon energy: undoped structures do not degrade, while the threshold photon energy to induce degradation depends on the degree of compensation in the p-doped layers. However, at high photon energies, an improvement in compensation does not slow down the degradation process, leading to the suggestion that the nitrogen acceptor itself is unstable under these conditions.

Recombinant human ciliary neurotrophic factor (rh-CNTF) was reported to attenuate skeletal muscle wasting in rats after unilateral transection of the sciatic nerve (M. E. Helgren, S. P. Squinto, H. L. Davis, D. J. Parry, T. G. Bolton, C. S. Heck, Y. Zhu, G. D. Yancopoulos, R. M. Lindsay, and P. S. DiStefano. Cell 76: 493-504, 1994). Under the experimental conditions reported herein, the absolute masses of the denervated gastrocnemius and soleus muscles were not increased in mature or immature rats of either sex by treatment with rhCNTF. At the highest doses of rhCNTF (1 and 0.1 mg/kg), increases in the ratio of the masses of the denervated to the contralateral innervated gastrocnemius and soleus muscles could be attributed entirely to a muscle-wasting effect on the contralateral innervated muscle rather than any muscle-sparing effect on the denervated muscle. The muscle-wasting effects of rhCNTF were associated with reductions in body weight gain and reduced food intake. Pair-fed rats lost less body weight and skeletal muscle mass than rhCNTF-injected freely fed rats but experienced significantly greater loss of visceral mass. Male rats displayed greater loss of body weight and skeletal muscle mass than female rats. Recombinant inhibitors of the cachectic cytokines, tumor necrosis factor and interleukin-1, did not significantly alter the wasting effects of rhCNTF. These findings demonstrate that, in contrast to its well-characterized trophic effects on cells of the nervous system, rhCNTF causes atrophy of skeletal muscle by mechanisms involving both anorexia and cachexia based on the results of pair-feeding experiments.