Tandem-repeat internal mapping (TRIM) of the involucrin gene: repeat number and repeat-pattern polymorphism within a coding region in human populations.

We have analyzed the human involucrin gene in 41 British African-Caribbeans and 37 British white Caucasians by tandem-repeat internal mapping and DNA sequencing. A point mutation (i.e., Bc) in the last B repeat unit was found in 98.6% of British white Caucasians and in 52.4% of British African-Caribbeans. The distribution of repeat patterns was also different between the two populations. Nine previously unreported repeat pattern alleles, 4 with and 5 without the Bc repeat, have been found, increasing the range of variation in humans to 15 reported repeat patterns, 6 with and 9 without the Caucasian mutation. Three further sequence variations, each occurring in a single individual, were found. The evolutionary significance of variation in the human involucrin gene is discussed.     

Effects of Interactions BetweenPasteurella haemolyticaandBordetella parapertussisonin vitroPhagocytosis by Lung Macrophages

The aim of the work was to determine the effect of exposing ovine bronchoalveolar macrophages (BAM)in vivotoPasteurella haemolyticaand/orBordetella parapertussison the subsequent uptake and killing ofP. haemolyticaby these cellsin vitro. Exposurein vivotoP. haemolyticadid not affect the uptake ofP. haemolyticaby BAMin vitrobut reduced (P< 0·05) the intracellular killing of bacteria. Exposurein vivotoB. parapertussishad no significant effect on either the uptake of killing ofP. haemolytica in vitro. However, sequential exposurein vivotoB. parapertussisandP. haemolyticareduced both the ingestion (P< 0·05) and killing (P< 0·001) ofP. haemolytica in vitro. These results indicate that exposure toP. haemolyticacompromised the bacterial killing mechanisms of BAM and that synergy betweenB. parapertussisandP. haemolyticareduced the ability of BAM to ingest bacteria.     

Cosmid-derived markers anchoring the bovine genetic map to the physical map

The mapping strategy for the bovine genome described in this paper uses large insert clones as a tool for physical mapping and as a source of highly polymorphic microsatellites for genetic typing, and was one objective of the BovMap Project funded by the European Union (UE). Eight-three cosmid and phage clones were characterized and used to physically anchor the linkage groups defining all the bovine autosomes and the X Chromosome (Chr). By combining physical and genetic mapping, clones described in this paper have led to the identification of the linkage groups corresponding to Chr 9, 12, 16, and 25. In addition, anchored loci from this study were used to orient the linkage groups corresponding to Chr 3, 7, 8, 9, 13, 16, 18, 19, and 28 as identified in previously published maps. Comparison of the estimated size of the physical and linkage maps suggests that the genetic length of the bovine genome may be around 4000 cM. Received: 1 July 1996 / Accepted: 13 September 1996     

Effect of mutations in Shigella flexneri chromosomal and plasmid-encoded lipopolysaccharide genes on invasion and serum resistance

This study shows that both length and distribution of lipopolysaccharide (LPS) are important for Shigella flexneri invasion and virulence. Mutants were generated in the chromosomal LPS synthesis genes rfa , rfb , and rol , and in a plasmid-encoded O-antigen chain-length regulator, cld _pHS-2. LPS analysis showed that mutations in rfb genes and in a candidate rfaL gene either eliminated the entire O-antigen side chains or produced chains of greatly reduced length. Mutation in a previously unidentified gene, rfaX , affected the LPS core region and resulted in reduced amounts of O-antigen. Mutants defective in cld _pHS-2 or rol had different distributions of O-antigen chain lengths. The results of tissue-culture cell invasion and plaque assays, the Serény test, and serum-sensitivity assay suggested roles for the different LPS synthesis genes in bacterial survival and virulence; rfaL, rfaX and rfb loci are required for serum resistance and intercellular spread, but not for invasion; cld _pHS-2 is required for resistance to serum killing and for full inflammation in the Serény test, but not for invasion or intercellular spread, while rol is required for normal invasiveness and plaque formation, but not for serum resistance. Thus, O-antigen synthesis and chain-length regulation genes encoded on both the chromosome and the small plasmid pHS-2 play important roles in S. flexneri invasion and virulence.     

Mapping of the α4 subunit gene (GABRA4) to human chromosome 4 defines an α2—α4—β1—γ1 gene cluster: further evidence that modern GABAA receptor gene clusters are derived from an ancestral cluster

We demonstrated previously that an α₁—β₂—γ₂ gene cluster of the γ-aminobutyric acid (GABA_A) receptor is located on human chromosome 5q34–q35 and that an ancestral α—β—γ gene cluster probably spawned clusters on chromosomes 4, 5, and 15. Here, we report that the α₄ gene (GABRA4) maps to human chromosome 4p14–q12, defining a cluster comprising the α₂, α₄, β₁, and γ₁ genes. The existence of an α₂—α₄—β₁—γ₁ cluster on chromosome 4 and an α₁—α₆—β₂—γ₂ cluster on chromosome 5 provides further evidence that the number of ancestral GABA_A receptor subunit genes has been expanded by duplication within an ancestral gene cluster. Moreover, if duplication of the α gene occurred before duplication of the ancestral gene cluster, then a heretofore undiscovered subtype of α subunit should be located on human chromosome 15q11–q13 within an α₅—α_x—β₃—γ₃ gene cluster at the locus for Angelman and Prader—Willi syndromes.     

Bird species turnover and stochastic extinction in woodland fragments

Year-to-year turnover in bird species composition was recorded across, the whole size range (0 02-30 ha) of 146 woods studied The mean number of resident breeding species both lost and gained per wood between consecutive breeding seasons was 2 (range 0-8) No relationship was found between this absolute turnover rate and woodland area, or any other of 24 predictor variables (describing woodland structure, isolation, connectedness and surrounding land use) Extriction and colonisation rates (in terms of numbers of species lost and gained) were also unrelated to woodland area In all sizes of woods, the species most likely to show local extinctions and colonisations were those with small populations within those woods, but the identity of the species concerned changed as woodland area increased In the smallest woods, the majority of turnover involved common species, such as wren and dunnock, which occurred in only small numbers in these small woods As woodland area increased, these species attained sufficient numbers to usually avoid stochastic extinction The majority of turnover was then due to more specialist (and less numerous) woodland species, such as great-spotted woodpecker and marsh tit, which were usually lacking in small woods In Britain, much existing broadleaved woodland falls within the size range studied Thus the numbers of many bird species are liable to be small enough for yearly turnover in woodland bird communities to be appreciable, and for the long-term persistence of individual species in particular woods to depend on dispersal     

Reduced cell proliferation in fetal lung after maternal administration of pilocarpine: a scintillation autoradiographic study.

Fetuses were obtained on the 28th gestational day from pregnant New Zealand white rabbits treated daily, on the 24th through the 27th gestational day, with pilocarpine HCl, 5 mg/kg in saline, or saline alone. Lung fragments from these fetuses were incubated for two hours in medium containing 3H-thymidine. Scintillation autoradiography of 1-micrometer-thick sections of these fetal lungs revealed that the lung tissue from pilocarpine-treated fetuses had significantly lower labelled cell indices for both alveolar epithelial cells and interstitial cells. These results indicate that pilocarpine treatment promotes differentiation of immature cells in the fetal lung at the expense of cell proliferation.     

Mycoplasma pneumoniae infection and arthritis in man.

Seven patients developed arthritis after Mycoplasma pneumoniae infection. Their joint symptoms persisted for up to one year. One patient developed an articular erosion and in another rheumatoid factor was present in serum transiently. Mycoplasma infection often causes ill-defined arthralgias and myalgias, but the migratory polyarthropathy of middle-sized joints that occurred in these patients is much less common. The prognosis seems to be good.     

The indirect negative inotropic effects of the P1-receptor agonist, L-phenylisopropyladenosine, in guinea-pig isolated cardiac preparations: comparison with cromakalim.

The possible mechanisms of the indirect negative inotropic responses to the P1-receptor agonist, L-phenylisopropyladenosine (L-PIA) were evaluated in electrically paced (2 Hz, 5 ms pulse width, voltage 50% above threshold) left atria and papillary muscles of guinea pigs. The responses were compared in naive tissues (direct effects) or after prestimulation with submaximal concentrations of either cAMP-dependent positive inotropes (isoprenaline or forskolin) or the cAMP-independent inotrope Bay K 8644. Cumulative concentration-response curves were obtained in naive or prestimulated preparations for L-PIA or the potassium channel activator, cromakalim, for comparison. L-PIA and cromakalim exerted negative inotropy in naive atrial tissues, whereas only cromakalim was active in naive papillary muscles. In atria prestimulated with isoprenaline (31 nM) or forskolin (1.4 microM), the negative inotropy of L-PIA was enhanced compared with naive tissues. In contrast, prestimulation with Bay K 8644 (1 microM) exerted a significant functional antagonism of the response to L-PIA. In the case of cromakalim, prestimulation with isoprenaline exerted a functional antagonistic effect. In papillary muscles, an indirect negative inotropic effect of L-PIA was only seen in tissues prestimulated with the cAMP-dependent inotropes isoprenaline (31 nM) or forskolin (2.4 microM), and not in naive tissues or those prestimulated by Bay K 8644 (333 nM). As with atria, prestimulation with isoprenaline exerted a functional antagonistic effect on the response to cromakalim. These results suggest that the P1-receptor agonist, L-PIA, exerts its indirect negative inotropic effects in left atria by two mechanisms.2+ with cAMP-dependent positive inotropes.(ABSTRACT TRUNCATED AT 250 WORDS)