The median weight loss for both phone and clinic groups at 12 and 26 weeks exceeded the NHLBI guideline of 10% weight loss from baseline. The phone approach may be a viable option to the traditional weight management clinic for both service providers and participants.

Reports of sex differences in crossing-over in animals, published since Haldane in 1922 suggested that crossing-over should be less frequent in the heterogametic sex, have been reviewed and discussed. No general rule is discernible apart from the absence of crossing-over in males of the dipteran genera Drosophila and Phryne and in females of some lepidopteran species, due apparently to failure of chiasma formation in the heterogametic sex. In the majority of animal species examined crossing-over occurs in both sexes. While there is some tendency in mammals for crossover values in females to exceed those in males, it was of greater interest to find that marked sex-differences occur in the same species (data chiefly from the house mouse) in opposite directions in different chromosomes. The influence of factors acting locally in the chromosomes, such as those associated with hetero-chromatin, were indicated as promising subjects for the study of variations associated with sex.

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VER the past several years DUNN and his collaborators have shown that most wild populations of Mus musculus in the United States are polymorphic for variant alleles at the T (Brachy, short tail) locus (DUNN and SUCKLING 1956; DUNN 1957). A mutant t allele at this locus has been identified in each of 16 different populations, and only one population thus far tested has been shown with any degree of certainty to be free of such alleles.This widespread polymorphism has several remarkable features which make it unlike other polymorphic systems so far studied. First, of 16 alleles from wild populations, 13 are unconditional prenatal lethals when homozygous (t", $ 9 4 , 5 y 6 ,

1. Inoculation of suspensions of brain, cord, ganglia or nerves of chickens with neurolymphomatous lesions, into newly hatched chicks, is followed by the development of typical lesions in approximately 25 per cent of cases. 2. In control chickens kept under laboratory conditions the incidence of the disease is about 7 per cent. 3. The disease does not become manifest until at least 2 months after inoculation; symptoms may not appear until after 4 months. 4. The active agent is not destroyed by 50 per cent glycerol in 9 days at ice box temperature.

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A cell-surface component specified by a mutant gene at the T-locus in the mouse has been detected on sperm by serological methods. The gene product thus recognized is not present on other adult cells.At present, there is in mammals no single morphogenetic event of which the mechanisms and controls are really understood. One recurrent theme common to the thinking of most embryologists has been that during the sorting out of cells, which comprises a large part of embryonic development, the surfaces of the cells must come to bear differential displays that can serve as recognition devices.Among many others, two of us (D.B., L.C.D.) have been interested for a long time in using developmental genetics as an approach to the problem of the control of differentiation. Our approach has been to use as analytical tools lethal mutants with marked morphogenetic effects on specific populations of cells in the early embryo, whose effects are therefore readily approachable descriptively. Such mutants should provide delicate ways of detecting factors or events essential to embryogenesis, since their effects may initially be restricted to the abnormality or absence of a single gene product. We have concentrated on genetic and embryological studies of mutant alleles at the complex T-locus in linkage group IX of the mouse. Our efforts and those of others (for review see refs. 1 and 2) have revealed in the region of the T-locus a well defined system of morphological mutants. The abnormalities produced by these mutants in both heterozygous and homozygous condition have led us to suspect that aberrations of the cell surface may be responsible (3). GeneticsThe T-locus is marked by a dominant mutant, T, which in heterozygotes leads to a shortened tail and in homozygotes to lethality midway through embryogenesis. Recessive alleles at the locus are identified by their interaction with T to produce taillessness. Several recessive embryonic lethal alleles of independent origin have been detected and maintained in balanced lethal tailless lines as T/t'. The lethal alleles that have so far been well studied are found by genetic test to fall into six different complementation groups designated Ty to, t9, t'2, t5ll, and tW5. Alleles of any one complementation group have similar homozygous effects on embryonic development and these are different from those of any other group in time and in detail. EmbryologyThe earliest effect of each of the six lethal T-locus alleles can be characterized, in general terms, as an interference with apparent switch points, which occur as ectodermal and primitive streak derivatives diverge along separate pathways. The embryology of the lethal homozygotes suggests an inability of particular groups of cells either to reach their normal location or to maintain their morphological positions or their viability once they have attained their destinations. An extensive discussion of the detailed morphogenetic defects seen in all the homozygous lethal T-locus mutants is not appropriate here. It will suffice to say t...