The determinants of sexual segregation in the scalloped hammerhead shark,Sphyrna lewini

Synopsis Female scalloped hammerhead sharks move offshore at a smaller size than do males to form schools composed primarily of intermediate size female sharks. This movement results in smaller females feeding more on pelagic prey than do males and with greater predatory success. It is contended that this change in habitat causes females to grow more rapidly to reproductive size. Intermediate size females grow at a more rapid rate than males. Female scalloped hammerhead sharks mature at a size larger than males. For many elasmobranch species, females: (1) occupy a different habitat, (2) grow more rapidly prior to maturity and continue growth following maturation, (3) feed on different prey with increased feeding success, and (4) reproduce at a size larger than males. It is suggested that female segregation increases fitness, resulting in more rapid growth for the former sex. The females reach maturity at the larger size necessary to support embryonic young, yet similar age to males, matching the female reproductive lifetime to that of males.     

Patterns of polymorphism and linkage disequilibrium for cystic fibrosis

Four polymorphic markers that map within 80 kb of an HTF island which is genetically very close to the cystic fibrosis locus have been identified. We have analyzed the linkage disequilibrium between each of these markers and the cystic fibrosis mutation in 89 families from four European countries, Denmark, Finland, Spain, and Great Britain. Strong linkage disequilibrium between three polymorphic sites and cystic fibrosis was observed. The markers on the J3.11 (D7S8) side of the HTF island show stronger disequilibrium than those on the met side. Linkage disequilibrium between markers and disease alters the probability that a person of a given haplotype is a carrier in some populations and helps to identify regions of a sequence that are most likely to contain the cystic fibrosis mutation.     

Localization of 27 DNA markers to the region of human chromosome 22q11-pter deleted in patients with the DiGeorge syndrome and duplicated in the der22 syndrome

DiGeorge syndrome is a human developmental field defect with the pathological features of an abnormality of embryogenesis at 4 to 6 weeks of gestation. Cytogenetic analyses of patients have revealed a number of instances of monosomy 22q11-pter in this condition. We have analyzed 52 DNA markers that map to 22q11-pter and have found 27 that are deleted in DiGeorge syndrome patients with known monosomy for part of this region and that are duplicated in patients with the der22 syndrome. The set of clones mapping to the DiGeorge region was further assigned to a proximal or a distal location within the deletion.     

Survey of general practitioners' attitudes to AIDS in the North West Thames and East Anglian regions

As the numbers of people suffering from human immunodeficiency virus infection and the acquired immune deficiency syndrome (AIDS) increase, so will the contribution to care required from general practice. A postal questionnaire survey was therefore carried out among general practitioners in the North West Thames and East Anglian regions to determine their attitudes to AIDS and the issues it raises for them. One hundred and thirty seven questionnaires were returned (response rate 57%) and four factors underlying the doctors'' attitudes identified; these concerned disease control, general practitioner care, patient support, and perception of seriousness. There were wide divergencies of attitude among the general practitioners, younger doctors being more in line with specialist thinking on AIDS than older colleagues, and evidence of important gaps between policies advocated by AIDS specialists and bodies of opinion in general practice.Attitudes to AIDS in general practice may partly be a function of personal experience; further study is required.     

The structural gene for human coagulation factor X is located on chromosome 13q34

The gene coding for coagulation factor X was studied in a family segregating chromosomal abnormalities involving chromosomes 13 and 6. An individual monosomic for 13q34 was deficient in levels of clotting factors VII and X, while her brother, who is trisomic for 13q34, had elevated levels. DNA dosage studies with a cloned human factor X gene demonstrated that the low levels of factor X expression in the individual with the chromosome 13q34 deletion were due to the absence of one copy of the factor X structural gene. This confirms the assignment of the human gene coding for factor X to 13q34.     

Molecular genetic study of the frequency of monosomy 22q11 in DiGeorge syndrome

It is well established that DiGeorge syndrome (DGS) may be associated with monosomy of 22q11-pter. More recently, DNA probes have been used to detect hemizygosity for this region in patients with no visible karyotypic abnormality. However, DGS has also been described in cases where the cytogenetic abnormality does not involve 22q11; for instance, four cases of 10p- have been reported. In this study we have prospectively analyzed patients, by using DNA markers from 22q11, to assess the frequency of 22q11 rearrangements in DGS. Twenty-one of 22 cases had demonstrable hemizygosity for 22q11. Cytogenetic analysis had identified interstitial deletion in 6 of 16 cases tested; in 6 other cases no karyotype was available. When these results are combined with those from our previous studies, 33 of 35 DGS patients had chromosome 22q11 deletions detectable by DNA probes.     

Cover crops do not increase soil organic carbon stocks as much as has been claimed: What is the way forward?

When compared to virgin land (forest and grassland), croplands store significantly lower amounts of organic carbon (OC), mainly as a result of soil tillage, and decreased plant inputs to the soil over the whole year. Doubts have been expressed over how much reduced and zero tillage agriculture can increase OC in soils when the whole soil profile is considered. Consequently, cover-crops that are grown in-between crops instead of leaving soils bare appear as the “last man standing” in our quest to enhance cropland OC stocks. Despite the claim by numerous meta-analyses of a mean carbon sequestration rate by cover crops to be as high as 0.32 ± 0.08 ton C ha⁻¹ year⁻¹, the present analysis showed that all of the 37 existing field studies worldwide only sampled to a depth of 30 cm or less and did not compare treatments on the basis of equivalent soil mass. Thirteen studies presented information on OC content only and not on OC stocks, had inappropriate controls (n = 14), had durations of 3 years or lower (n = 5), considered only one to two data points per treatment (n = 4), or used cover crops as cash crops (i.e., grown longer that in-between two crops) instead of catch crops (n = 2), which in all cases constitutes shortcomings. Of the remaining six trials, four showed non-significant trends, one study displayed a negative impact of cover crops, and one study displayed a positive impact, resulting in a mean OC storage of 0.03 ton ha⁻¹ year⁻¹. Models and policies should urgently adapt to such new figure. Finally, more is to be done not only to improve the design of cover-crop studies for reaching sound conclusions but also to understand the underlying reasons of the low efficiency of cover crops for improved carbon sequestration into soils, with possible strategies being suggested.     

Cloning and comparative mapping of a gene from the commonly deleted region of DiGeorge and Velocardiofacial syndromes conserved in C. elegans

We have identified and cloned a gene, ES2, encoding a putative 476 amino acid protein with a predicted M _r of 52,568. The gene is localized within the DiGeorge/Velocardiofacial syndrome locus on 22q11.2 and is deleted in all the patients in which a deletion within 22q11 could be demonstrated, with the exception of one patient. ES2 is expressed in all the tissues studied. Sequence comparison showed identity with five ESTs and at the amino acid level the sequence was highly similar to, and collinear with, a hypothetical C. elegans protein of unknown function. Mutation analysis was performed in 16 patients without deletion, but no mutation has been found. The cDNA sequence is conserved in mouse and is localized on MMU16B1-B3, known to contain a syntenic group in common with HSA 22q11.2. Received: 25 March 1996 / Accepted: 15 May 1996