A missense mutation (Asp250----Asn) in exon 6 of the human lipoprotein lipase gene causes chylomicronemia in patients of different ancestries.

We have previously reported two common lipoprotein lipase (LPL) gene mutations underlying LPL deficiency in the majority of 37 French Canadians (Monsalve et al., 1990. J. Clin. Invest. 86: 728-734; Ma et al., 1991. N. Engl. J. Med. 324: 1761-1766). By examining the 10 coding exons of the LPL gene in another French Canadian patient, we have identified a third missense mutation that is found in two of the three remaining patients for whom mutations are undefined. This is a G to A transition in exon 6 that results in a substitution of asparagine for aspartic acid at residue 250. Using in vitro site-directed mutagenesis, we have confirmed that this mutation causes a catalytically defective LPL protein. In addition, the Asp250----Asn mutation was also found on the same haplotype in an LPL-deficient patient of Dutch ancestry, suggesting a common origin. This mutation alters a TaqI restriction site in exon 6 and will allow for rapid screening in patients with LPL deficiency.     

Age-specific differences in the winter foraging strategies of rooks Corvus frugilegus

Summary Foraging efficiency and intraspecific competition were compared between wild adult and immature rooks Corvus frugilegus with respect to flock size. Behavioural time budgets, and observations of prey selection and prey energetic values revealed that adult rooks in large flocks (> 50 individuals) consumed smaller, less profitable prey, but allocated more time to feeding and fed at a faster rate and with greater success than adults in small flocks. By contrast, immature rooks in flocks of more than 30 individuals allocated proportionally less time to feeding, fed at a lower rate and fed with no increase in success rate than when foraging in smaller flocks. Agonistic encounters and the avoidance of adults by immature rooks appeared responsible for such inefficient foraging. Hence immature rooks showed a preference for smaller flocks (< 50 individuals) with low adult: immature ratios while adults preferred larger flocks (> 50 individuals). We discuss the possible influence of competitive disadvantages on immature rook distribution, flock composition and post-natal dispersal.     

Prediction of F3 row performance from F2 individual plant data in oats

Summary Parameters estimated from a Gardner-Eberhart analysis of the F₂ generation of a six-parent diallel in oats (Avena sativa L.) were used to compare methods for predicting the performance of F₃ row plots. The prediction methods were: (1) individual F₂ plant performance (F2I), (2) parent average plus F₂ plot deviations (PF2), (3) parent average plus weighted F₂ plot deviations (PF2P), (4) best linear unbiased prediction (BLUP) of parent average plus F₂ plot deviations (BPF2), and (5) BLUP plus weighted F₂ deviations (BF2). The F₂ single-plant traits used for prediction were biological yield to predict F₃ biological yield, whole plant and primary tiller grain yield for prediction of F₃ grain yield, and whole plant and primary tiller harvest index (HI) to predict F₃ HI. Prediction methods were evaluated by correlations between predicted and observed F₃ performance. Prediction methods and traits for which correlations were greater than for F2I included: BF2 for biological yield, PF2, PF2P and BF2 for whole plant grain yield, PF2, BPF2, and BF2 for primary tiller grain yield. None had a correlation significantly greater than F2I for either measure of HI, where heritability was large. PF2 is the recommended method for traits with low heritability because of its simplicity and because it had the largest or nearly the largest correlation for each of the yield traits. F2I is the recommended method for traits with larger heritability.Contribution No. 8821 of the U.S. Regional Pasture Research LaboratoryDeceased     

The AXB and BXA set of recombinant inbred mouse strains

The recombinant inbred (RI) set of strains, AXB and BXA, derived from C57BL/6J and A/J, originally constructed and maintained at the University of California/San Diego, have been imported into The Jackson Laboratory and are now in the 29th to 59th generation of brother-sister matings. Genetic quality control testing with 45 proviral and 11 biochemical markers previously typed in this RI set indicated that five strains had been genetically contaminated sometime in the past, so these strains have been discarded. The correct and complete strain distribution patterns for 56 genetic markers are reported for the remaining RI strain set, which consists of 31 living strains and 8 extinct strains for which DNA is available. Two additional strains, AXB 12 and BXA 17, are living and may be added to the set pending further tests of genetic purity. The progenitors of this RI set differ in susceptibility to 27 infectious diseases as well as atherosclerosis, obesity, diabetes, cancer, cleft palate, and hydrocephalus. Thus, the AXB and BXA set of RI strains will be useful in the genetic analysis of several complex diseases.     

Membrane transport proteins: implications of sequence comparisons.

Analyses of the sequences and structures of many transport proteins that differ in substrate specificity, direction of transport and mechanism of transport suggest that they form a family of related proteins. Their sequence similarities imply a common mechanism of action. This hypothesis provides an objective basis for examining their mechanisms of action and relationships to other transporters.     

What happens to homeless mentally ill people? Follow up of residents of Oxford hostels for the homeless.

OBJECTIVES--To follow up severely mentally ill residents of hostels for the homeless to determine their social and psychiatric outcome. DESIGN--Follow up at 18 months of hostel residents previously assessed with psychiatric and behavioural measures. SETTING--Two Oxford hostels for the homeless. SUBJECTS--48 hostel residents previously identified as disabled by mental illness. MAIN OUTCOME MEASURES--Current housing, admissions to psychiatric hospital, violent or antisocial behaviour, and score on standardised behavioural rating. RESULTS--45 of the 48 residents were traced. 27 had remained in the hostels; only 10 had been rehoused, mainly in bedsits or with their families. 16 had a poor outcome as judged by death (four subjects), lengthy hospital readmission (two), marked deterioration in behaviour (six), sleeping rough (one), or disappearance (three). CONCLUSION--More effort is needed to provide suitable housing for homeless mentally ill people.     

The GTPase stimulatory activities of the neurofibromatosis type 1 and the yeast IRA2 proteins are inhibited by arachidonic acid.

Three proteins, GTPase activating protein (GAP), neurofibromatosis 1 (NF1) and the yeast inhibitory regulator of the RAS-cAMP pathway (IRA2), have the ability to stimulate the GTPase activity of Ras proteins from higher animals or yeast. Previous studies indicate that certain lipids are able to inhibit this activity associated with the mammalian GAP protein. Inhibition of GAP would be expected to biologically activate Ras protein. In these studies arachidonic acid is shown also to inhibit the activity of the catalytic fragments of the other two proteins, mammalian NF1 and the yeast IRA2 proteins. In addition, phosphatidic acid (containing arachidonic and stearic acid) was inhibitory for the catalytic fragment of NF1 protein, but did not inhibit the catalytic fragments of GAP or IRA2 proteins. These observations emphasize the biochemical similarity of these proteins and provide support for the suggestion that lipids might play an important role in their biological control, and therefore also in the control of Ras activity and cellular proliferation.