Patterns of intraspecific variation inAntennaria alborosea,A. corymbosa,A. marginata,A. microphylla,A. parvifolia,andA. umbrinella (Asteraceae:Inuleae)

Patterns of intraspecific variation were examined inAntennaria alborosea A. E. Porsild,A. corymbosa E. Nels,A. marginata Greene,A. microphylla Rydb.,A. parvifolia Nutt., andA. umbrinella Rydb. AlthoughA. alborosea was initially considered arctic in distribution, it became apparent that a southern montane element also exists. Our results suggest that morphological differences between arctic and southern montane specimens represent clinal variation. The additional morphological data for specimens that occur more than 1,500 km south of the species' range as it was initially described result in a better understanding of this once presumed arctic taxon. Morphological variation in the dioecious speciesA. corymbosa, A. marginata, A. microphylla, A. parvifolia, andA. umbrinella was greater between the genders than was geographic variation within each gender. These results demonstrate that both pistillate and staminate specimens must be examined in dioecious species ofAntennaria if morphological variation in the respective species is to be fully understood. Character size or number of broadly distributed species (A. microphylla andA. parvifolia) generally decreased with increasing longitude, whereas characters of species with more restricted distributions (A. alborosea, A. corymbosa, andA. marginata) generally increased in size or number with increasing latitude or longitude.Antennaria umbrinella was an exception in this respect.     

The "cricket bat" flap: a one-stage free forearm flap phalloplasty

Total and subtotal penile reconstruction represents a major surgical challenge. We present a new method and two illustrative cases using a modified design of the radial forearm free-tissue transfer: the "cricket bat" flap.     

Natural killer cell activity in murine muscular dystrophy. III. NK-sensitive myoblast cells and lack of NK activity in beige/dystrophic hybrid mice

The NK-susceptibility of dystrophic mouse myoblast cells was investigated. Spleen cells from 8- to 10-week-old normal (+/+) and dystrophic (dy2J/dy2J) male C57BL/6J mice were fractionated on Percoll density gradients and the cells at each density interface were incubated with either 51Cr-labeled YAC-1 or myoblast cells in a 6 hr 51Cr-release assay. Myoblast target cells were obtained from either heterozygous (+/dy2J) or homozygous (dy2J/dy2J) muscle cultures or a transformed tetraploid myoblast line (M14D2). The data indicate that the interface between the 50 and 60% (1.060-1.075 g/ml) Percoll density fractions of spleen cells from either normal or dystrophic mice contains the largest proportion of asialo GM-1 positive and NK-1 positive cells displaying NK activity. Myoblast cells from either heterozygous (phenotypically normal) or homozygous dystrophic mice were not significantly different in susceptibility to NK-mediated lysis by Percoll enriched normal or dystrophic mouse NK cells. However, dystrophic mouse spleen cells had the highest NK activity against both myoblast targets as compared with normal mouse spleen cells. The transformed myoblast cell line, M14D2, was significantly less susceptible to NK-mediated lysis by dystrophic mouse spleen cells when compared with freshly cultured myoblast target cells. Target cell binding studies revealed that conjugate forming cells from the 50% Percoll density interface of dystrophic mouse spleen cells were approximately twofold greater than that of normal mouse spleen cells against either heterozygous or homozygous dystrophic mouse myoblast targets. Cold target inhibition studies revealed that the natural killing of dystrophic mouse myoblast cells was due to a YAC-1 reactive NK cell. Breeding experiments between C57BL/6J homozygous "beige" (bgJ/bgJ) mutant mice and dystrophic (dy2J/dy2J) mice produced beige/dystrophic hybrid mice which displayed clinical symptoms of the dystrophy process by 3 to 4 weeks of age. Spleen cells from these hybrid mice showed no significant differences in NK activity against YAC-1 target cells when compared with homozygous beige mice. Taken together, these results demonstrate the first reported evidence that murine myoblasts are susceptible to NK-mediated lysis. In addition, the data indicate that although dystrophic mouse NK cells recognize myoblast cells as targets, the NK cell studies with the beige/dystrophic hybrid mice do not indicate a direct in vivo role for NK cells in the dystrophy process.     

Chromosome numbers of goldenrods,Euthamia and Solidago (Compositae: Astereae). II. Additional counts with comments on cytogeography

Chromosome number determinations were made from 407 wild or transplanted individuals and seedlings representing 65 taxa and hybrids inEuthamia andSolidago. The following are first reports:Euthamia remota, 2n=9II;Solidago leavenworthii, 2n=54;S. mollis, 2n=36;S. mollis var.angustata, 2n=36;S. rigida var.glabrata, 2n=9II;S. sempervirens var.azorica, 2n=9II; andS. sparsiflora, 2n=54. Most species have been sampled only a few times or are consistently of one cytotype. Sufficient counts have been made to indicate some general patterns of cytotype distribution in the following species complexes:S. gigantea, S. canadensis, S. flexicaulis, S. rugosa, andS. uliginosa.     

Enhanced natural killer (NK) cell activity and NK-sensitive thymic cells in murine muscular dystrophy

Studies have shown that there is an abnormality in the thymus of dystrophic mice with respect to age-dependent thymus weight changes and altered morphology (T. DeKretser and B. Livett, Nature (London), 263, 682, 1976). Recently, others have shown that natural killer (NK) cells can lyse cells of a large, immature, rapidly dividing cell subpopulation within the thymus of normal young (3 weeks of age) mice (M. Hansson, K. Karre, R. Kiessling, J. Roder, B. Anderson, and P. Hayry, J. Immunol., 123, 765, 1979). The NK susceptibility of dystrophic mouse thymocytes as targets was therefore studied. Spleen cells from normal (+/+) and dystrophic ($\text{dy}{}^{\mathrm{2J}}\text{dy}{}^{\mathrm{2J}}$) male C57BL/6J mice 8–10 weeks old were passed over nylon wool and the nonadherent cells were incubated with ⁵¹Cr-labeled YAC-1 lymphoma target cells or thymocytes in a ⁵¹Cr-release assay. Spleen cells from dystrophic mice killed twofold more YAC-1 target cells than did spleen cells from normal mice. Thymocytes from 3- to 4-week-old dystrophic mice were three to four times more susceptible to NK lysis by dystrophic mouse spleen cells as compared with normal mouse spleen cells. Spleen cells from dystrophic mice had the same NK activity against dystrophic and normal mouse thymocytes as targets. Normal mouse spleen cells killed three- to fourfold more dystrophic mouse thymocytes than that of normal mouse thymocytes as targets. Target cellbinding studies revealed that conjugate-forming cells from nylon nonadherent dystrophic mouse spleen cells were found to be two- to fourfold greater than for normal mouse spleen cells using YAC-1 tumor cells as targets. The number of lymphocytes bound per YAC-1 target cell ranged from 2 to 5 for dystrophic mouse spleen cells as compared with 1 to 2 for the normal control group. Using both normal and dystrophic mouse thymocytes as targets, the conjugate-forming cells from dystrophic mouse spleen cells were also found to be twofold greater than in the normal control group. Cold target inhibition studies revealed that the natural killing of dystrophic mouse thymocytes was due to a YAC-1-reactive NK cell. Effector cell depletion studies using monoclonal anti-Thy-1.2 plus complement treatment and plastic petri dish adherence also revealed that the natural killing of dystrophic mouse thymocytes was not due to either T lymphocytes or macrophages. Taken together, these results show an increase in NK-sensitive thymocyte targets in dystrophic mice, in combination with an increase in splenic NK activity.