Despite its importance in benefit-cost analyses in the water supply, transportation, and health care sectors, there are relatively few empirical estimates of the value of travel time savings (VTT) in low-income countries, particularly in rural areas. Analysts instead often rely on a textbook “rule of thumb” of valuing time at 50% of prevailing unskilled wage rates, though these benchmarks have little empirical support in these settings. We estimate the value of travel time through the use of a repeated discrete choice stated preference exercise. We asked 325 rural households in Meru County, Kenya to rank two new hypothetical water sources against their current water source. The two new hypothetical sources were described as safe and reliable to use, but varied only in their distance from the household and the price charged per water container. Results from random-parameters logit models imply an average value of travel time of 18 Ksh/hr, and generally support the 50% rule. These models produce the first individual-level VTT estimates reported in a low-income setting, and indicate statistically-significant heterogeneity in VTTs, though the heterogeneity is not well correlated with observables. A latent-class approach identifies four classes of respondents: one class (about one third of respondents) values time very highly (49 Ksh/hr), one poorer group values time hardly at all (less than 1 Ksh/hr), and two groups value time at approximately 9 Ksh/hr.

Even if the foundation, rise and eventual demise of Carthage and its overseas territories in the West Mediterranean occurred in much the same space and time as the glory days of Archaic, Classical and Hellenistic Greece and Rome, there is no doubt that the Phoenicians and their Punic successors (to use the conventional terms) have rarely been regarded as fully signed-up members of the ancient world. Reduced to walk-on cameos as skilled silversmiths, agricultural experts, shrewd traders or military strategists, Phoenician and Punic representations tend to be rather stereotypical (Prag 2010, with earlier bibliography), which perhaps should not come as a surprise, as nearly all these portraits have been sketched by outsiders; they certainly do not add up to a coherent ethnographic or political description.

The behaviour of the X- and Y-borne Sts locus has been studied in male and female mice. There was considerable heterogeneity in STS activity between inbred mouse strains, with a four fold difference in activity between the highest (101/H) and lowest (Ju/Ct) activity strains, which can be interpreted in terms of allelic differences. In all inbred strains male STS levels were higher than those of female STS levels and in the majority of strains tested male STS levels were nearly twice as high as female levels. Reciprocal crosses between C3H/HeH and the STS-deficient substrain, C3H/An, demonstrated that activities of the X- and Y-borne genes in males are essentially the same and this suggested that the lower STS level in females derives from X-inactivation of the locus. The possibility that hormonal differences could instead be responsible for the lower activity in females was ruled out by the findings that (a) castration of males did not reduce their STS levels and (b) sex-reversed males, X / X Sxr, had STS levels typical of females. Final proof that the mouse Sts locus can be subject to the X-inactivation process was provided by the observation that XX females had STS levels that were only slightly (20%) higher than those of XO females. The difference may indicate incomplete inactivation of the locus. Linkage data verifying the location of Sts on the distal end of the X chromosome are provided.

In total, the results of this study show that the murine Sts locus can be subject to the X-inactivation process and this, together with the existence of functional loci of near-equal activities on the X and Y chromosomes, results in an imbalance of STS levels between the sexes. X-inactivation does not therefore serve as a dosage compensation mechanism for the Sts locus in the mouse. All of these findings were made in C3H/HeH mice or in animals carrying C3H/HeH functional Sts alleles, and it is pointed out that the diverse results previously obtained by other investigators may be attributable to their use of different strains and crosses between strains but could also be complicated by technical factors.

An electrophoretically detectable variant of acid α-glucosidase has been found in SM/J mice. This variant is attributable to excess sialylation of the enzyme and is determined by a gene, alpha-glucosidase processing, Aglp, on chromosome 17. In addition, as also reported by Potier, Lu Shun Yan & Womack (1979), SM/J mice are relatively deficient in neuraminidase and it appears that the low level of this enzyme in SM/J is determined by an autosomal codominant gene, neuraminidase-1, Neu-1. Preliminary data indicate that Neu-1 is also on chromosome 17. It seems probable that the several processing genes Apl, Aglp and Map-2 which are all closely linked on chromosome 17 are one and the same, a gene Neu-1 coding for neuraminidase.

Two substrains of the inbred mouse strain 101, maintained at Harwell and at Neuherberg, and designated 101/H and 101/E1, differed at five of the eight genetic loci tested and it seems very likely that one of these substrains has been genetically contaminated. The available evidence suggests that 101/E1 is probably the contaminated substrain.

An animal with low erythrocyte triose phosphate isomerase (TPI) activity was found amongst mice trapped on a farm in Leicestershire. The low TPI activity was caused by the segregation of a single co-dominant gene which also affected the Km for glyceraldehyde-3-phosphate and heat stability of the enzyme. We designate the gene Tpi-1, the structural locus for TPI, with the a allele in the common inbred strains and the b allele derived from the wild-caught mouse. Tpi-1 was known to be on chromosome 6 by somatic cell techniques and, as shown in a preliminary report (Peters & Bulfield, 1984), we have confirmed and extended this finding using three chromosome-6 marker genes giving the order: Sig-28-Lc-11-Miwh-16-Tpi-1.

Genetic polymorphisms revealed two distinct substrains of the inbred strain 101. One group included substrains 101*/Rl, 101/H and 101/HOxe; the other group comprised 101/El and 101/Sl. The two groups differed at 5 of the 8 genetic loci tested. The accompanying paper (Evans, Burtenshaw & Adler, 1985) shows that the two groups also differ for several chromosome polymorphisms. We suggest that genetic contamination occurred during the derivation of 101/El from 101/Rl and was already present in 101/El when 101/Sl was produced from this substrain. We further propose that these substrains be renamed 102/El and 102/Sl respectively.

A null allele of the Gpi-1s structural gene, that encodes glucose phosphate isomerase (GPI-1; E.C. 5.3.1.9), arose in a mutation experiment and was designated Gpi-1sa-m1H. The viability of homozygotes has been investigated. No offspring homozygous for the null allele were produced by intercrossing two heterozygotes, so the homozygous condition was presumed to be embryonic lethal. Embryos were produced by crossing Gpi-1sa/null heterozygous females and Gpi-1sb/null heterozygous males. Homozygous null embryos were identified at different stages of development by electrophoresis and staining either for GPI-1 alone or GPI-1 plus phosphoglycerate kinase (PGK) activity. At 6½ and 7½ days post coitum homozygous null embryos were present at approximately the expected 25% frequency (37/165; 22·4% overall) although at 7½ days the homozygous null embryos tended to be small. By 8½ days most homozygous null embryos were developmentally retarded and had not developed significantly further than at 7½ days; some were dead or dying. By 9½ days the homozygous null conceptus was characterised by a small implantation site that contained trophoblast and often a small amount of extraembryonic membrane. Surviving trophoblast tissue was also detectable at 10½ days. Previous studies have shown that oocyte-coded GPI-1 persists only until 5½ or 6½ days. Survival of homozygous null embryos to 7½ or 8½ days and survival of certain extraembryonic tissue to 10½ days suggests that the homozygous null condition may not be cell-lethal although it is certainly embryo-lethal. Mutant cells that are deficient in glycolysis may use the pentose phosphate shunt to bypass the block in glycolysis created by the deficiency of glucose phosphate isomerase, and/or might be rescued by the transport, from the maternal blood, of energy sources other than glucose (such as glutamine). Either strategy may only permit slow cell growth that would not be adequate to support normal embryogenesis. Transport of maternal nutrients would be more efficient to the trophoblast and extraembryonic membranes and this may help to explain why these tissues survive for longer than the embryo itself. The morphological similarity between homozygous nulls and androgenetic conceptuses, where the trophoblast also survives better than the embryo, is discussed.

Seven imprinted genes are currently known in the mouse but none have been identified yet in the distal imprinting region of mouse Chromosome (Chr) 2, a region which shows striking linkage conservation with human chromosome 20q13. Both maternal duplication/paternal deficiency and its reciprocal for distal Chr 2 lead to mice with abnormal body shapes and behavioural abnormalities. We have tested a number of candidate genes, that are either likely or known to lie within the distal imprinting region, for monoallelic expression. These included 3 genes (Cebpb, E2f1 and Tcf4) that express transcription factors, 2 genes (Cyp24 and Pck1) that are involved in growth, 5 genes (Acra4, Edn3, Kcnb1, Mc3r and Ntsr) where a defect could lead to neurological and probably behavioural problems, and 3 genes (Cd40, Plcg1 and Rcad) that are less obvious candidates but sequence information was available for designing primers to test their expression. On/off expression of each gene was tested by reverse transcription–polymerase chain reaction (RT–PCR) analysis of RNA extracted from tissues of mice with maternal duplication/paternal deficiency and its reciprocal for the distal region of Chr 2. None of the 13 genes is monoallelically expressed in the appropriate tissues before and shortly after birth which suggests that these genes are not imprinted later in development. This study has narrowed down the search for imprinted genes, and valuable information on which genes have been tested for on/off expression is provided. Since there is considerable evidence of conservation of imprinting between mouse and human, we would predict that the 13 genes are not imprinted in human. Five of the genes: E2f1, Tcf4, Kcnb1, Cd40 and Rcad, have not yet been mapped in human. However, because of the striking linkage conservation observed between mouse Chr 2 and human chromosome 20, we would expect these genes to map on human chromosome 20q13.

A male mouse with irregular white spotting, typical of piebald, s, arose during an experiment designed to search for mutations induced in spermatogonial cells by ethylnitrosourea (ENU). On being examined cytologically it was found to carry 40 chromosomes but was effectively XXY since one of the two X chromosomes present was distally fused to a Y chromosome. In common with the previously described XXY mice, all of which carried 41 chromosomes, the mouse was sterile with a total absence of germ cells. Because of this, it was not possible to determine if the white spotting was inherited. The spotting could not be related to any observable abnormality of chromosomes known to carry spotting genes, nor could it be linked in any way with the X and Y fusion. It was concluded from the cytological considerations and the time interval (6 months) that had elapsed between mutagen treatment and birth of the offspring, that whereas the spotting was probably the result of ENU damage in a spermatogonial stem cell, the XY fusion was probably a later and spontaneous event.

An Aboriginal man done to death on the dunes 4000 years ago was recently discovered during excavations beneath a bus shelter in Narrabeen on Sydney's northern beaches. The presence of backed microliths and the evidence for trauma in the bones showed that he had been killed with stone-tipped spears. Now we know how these backed points were used. A punishment ritual is implied by analogies with contact-period observations made in the eighteenth century AD.

Previous studies have shown that the distal region on mouse chromosome (Chr) 2 is subject to imprinting as mice with maternal duplication/paternal deficiency (MatDp.dist2) and the reciprocal (PatDp.dist2) for this region exhibit phenotypic anomalies at birth and die neonatally. We show here that imprinting effects are detectable in utero. Notably PatDp.dist2 embryos show an increase in wet weight compared with normal, which peaks at 16·5 d post coitum (dpc), and diminishes by birth, whereas the wet weight of placenta is slightly reduced in the latter half of gestation. Newborns have increased length of the long bones. By contrast, the wet weight of MatDp.dist2 embryos decreases during the second half of gestation. Measurements of dry weights of embryos at 16·5 dpc have indicated that there is no difference in either PatDp.dist2 or MatDp.dist2 compared with normal so that the wet weight differences are due to fluid retention in PatDp.dist2 but fluid loss in MatDp.dist2. In PatDp.dist2 embryos excess fluid is particularly prominent in the subcuticular skin layer, whereas by birth fluid is evident around the neck and tongue. At 16·5 dpc the PatDp.dist2 embryos are severely oedematous, as the average fluid content per unit dry weight per embryo was increased by 40%, whereas the MatDp.dist2 embryos are dehydrated as the average water content per unit dry weight per embryo was reduced by 6%. A preliminary conclusion is that there is neither growth enhancement in PatDp.dist2 nor growth retardation in MatDp.dist2 offspring.