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Surface roughness plays an important role in the control of emissions and friction losses in the cylinder liner–piston ring system as well as securing economically favourable manufacturing. A number of different commercial cylinder liner types have been characterized using traditional two-dimensional stylus and ISO parameters together with the latest three-dimensional characterization. The results highlight the weak and strong correlations between different families of parameters traditionally used for liner surface specifications. The bearing curve based Rxq and Rk parameter families have been evaluated and show systematic and consistent differences when characterizing the same surface features when trying to establish independent characterization of the highly stratified, two-process cylinder liner surfaces. No significant improvement in discrimination results from using ensemble averages. Presentation of correlations in the form of topological diagrams helps to show when parameters with a high intrinsic variability can be effectively replaced by other more robust parameters with which they have a high correlation. Plateau parameters are in general more highly correlated than valley parameters. Three-dimensional parameters show high internal correlations and also correlate highly with some corresponding two-dimensional parameters.

Both X chromosome inactivation and autosomal genomic imprinting generate a functional hemizygosity. Here we consider models that explain the evolution of genomic imprinting and X chromosome inactivation from novel perspectives. Specifically, we suggest th, Addresses: Ohlsson R, Uppsala Univ, Evolut Biol Ctr, Dept Genet & Dev, Norbyvagen 18A, S-75236 Uppsala, Sweden. Uppsala Univ, Evolut Biol Ctr, Dept Genet & Dev, S-75236 Uppsala, Sweden. EPHE, Inst Jacques Monod, F-75005 Paris, France. La Trobe Univ, Dept

CTCF is an evolutionarily conserved zinc finger (ZF) phosphoprotein that binds through combinatorial use of its 11 ZFs to similar to 50 bp target sites that have remarkable sequence variation. Formation of different CTCF-DNA complexes, some of which are m, Addresses: Ohlsson R, Uppsala Univ, Dept Genet & Dev, Evolut Biol Ctr, Norbyvagen 18A, S-75236 Uppsala, Sweden. Uppsala Univ, Dept Genet & Dev, Evolut Biol Ctr, S-75236 Uppsala, Sweden. Univ Giessen, Inst Genet, D-35392 Giessen, Germany. NIAID, Immunopath

We previously described a gene, Ipl (Tssc3), that is expressed selectively from the maternal allele in placenta, yolk sac, and fetal liver and that maps within the imprinted domain of mouse distal Chromosome (Chr) 7/human Chr 11p15.5 (Hum Mol Genet 6, 2021, 1997). Ipl is similar to TDAG51, a gene that is involved in FAS/CD95 expression. Here we describe another gene, Tih1 (TDAG/Ipl homologue 1), with equivalent sequence similarity to Ipl. Structural prediction indicates that the products of these three genes share a central motif resembling a pleckstrin-homology (PH) domain, and TIH1 protein has weak sequence similarity to the PH-domain protein SEC7/CYTOHESIN. Like Ipl, Tih1 is a small gene with a single small intron. Tih1 maps to distal mouse Chr 1 and human Chr 1q31, chromosomal regions that have not shown evidence for imprinting and, in contrast to Ipl, Tih1 is expressed equally from both parental alleles. Ipl, Tih1, and TDAG51 have overlapping but distinct patterns of expression. Tih1 and TDAG51 are expressed in multiple fetal and adult tissues. In contrast, during early mouse development Ipl mRNA and protein are highly specific for two tissues involved in maternal/fetal exchange: visceral endoderm of the yolk sac and labyrinthine trophoblast of the placenta. These findings highlight the dominance of chromosomal context over gene structure in some examples of parental imprinting and extend previous evidence for placenta-specific expression of imprinted genes. The data also define a new subfamily of PH domain genes.

The increasing number of RNA polymease II transcripts without any apparent open reading frame has increased our awareness that gene functions can be selected for without involving a protein product. By using the H19 gene as a point of reference, we highlight here several common features among non-coding genes, such as their antisense position in subchromosomal expression domains which are often genomically imprinted. We also discuss the need to critically examine the translatability of transcripts which are considered non-coding. Finally, we present a model to explain the origin of non-coding genes.

PDGFB is a growth factor which is vital for the completion of normal prenatal development. In this study, we report the phenotypic analysis of placentas from mouse conceptuses that lack a functional PDGFB or PDGFRbeta gene. Placentas of both types of mutant exhibit changes in the labyrinthine layer, including dilated embryonic blood vessels and reduced numbers of both pericytes and trophoblasts. These changes are seen from embryonic day (E) 13.5, which coincides with the upregulation of PDGFB mRNA levels in normal placentas. By E17, modifications in shape, size, and number of the fetal blood vessels in the mutant placentas cause an abnormal ratio of the surface areas between the fetal and the maternal blood vessels in the labyrinthine layer. Our data suggest that PDGFB acts locally to contribute to the development of the labyrinthine layer of the fetal placenta and the formation of a proper nutrient-waste exchange system during fetal development. We point out that the roles of PDGFB/Rbeta signaling in the placenta may be analogous to those in the developing kidney, by controlling pericytes in the labyrinthine layer and mesangial cells in the kidney.

PDGFB is a growth factor which is vital for the completion of normal prenatal development. In this study, we report the phenotypic analysis of placentas from mouse conceptuses that lack a functional PDGFB or PDGFRbeta gene. Placentas of both types of mutant exhibit changes in the labyrinthine layer, including dilated embryonic blood vessels and reduced numbers of both pericytes and trophoblasts. These changes are seen from embryonic day (E) 13.5, which coincides with the upregulation of PDGFB mRNA levels in normal placentas. By E17, modifications in shape, size, and number of the fetal blood vessels in the mutant placentas cause an abnormal ratio of the surface areas between the fetal and the maternal blood vessels in the labyrinthine layer. Our data suggest that PDGFB acts locally to contribute to the development of the labyrinthine layer of the fetal placenta and the formation of a proper nutrient-waste exchange system during fetal development. We point out that the roles of PDGFB/Rbeta signaling in the placenta may be analogous to those in the developing kidney, by controlling pericytes in the labyrinthine layer and mesangial cells in the kidney.

Nuclear receptors regulate metabolic pathways in response to changes in the environment by appropriate alterations in gene expression of key metabolic enzymes, Here, a computational search approach based on iteratively built hidden Markov models of nuclea, Addresses: Berkenstam A, Pharmacia & Upjohn Inc, Dept Mol Biol & Genomics, S-11287 Stockholm, Sweden. Pharmacia & Upjohn Inc, Dept Mol Biol & Genomics, S-11287 Stockholm, Sweden. Pharmacia & Upjohn Inc, Dept Biochem & Cell Biol, S-11287 Stockholm, Sweden.

Addresses: Ohlsson R, Uppsala Univ, Dept Anim Dev & Genet, Norbyvagen 18A, S-75236 Uppsala, Sweden. Uppsala Univ, Dept Anim Dev & Genet, S-75236 Uppsala, Sweden. Columbia Univ, Coll Phys & Surg, Dept Pathol, New York, NY 10032 USA. Temple Univ, Sch Med, F

Genetic evidence shows that the parent of origin-dependent expression patterns of the Igf2 and H19 genes is coordinated in mouse, such that H19 controls the activity of Igf2 in cis. Equally compelling evidence for a similar situation in humans is absent, although the frequently observed activation of the maternal IGF2 allele (ie., loss of imprinting) in Wilms' tumors has been attributed to the silencing of the maternal H19 locus. We show here that loss of H19 activity is generally a preneoplastic event, which may be linked with an overgrowth lesion that has been proposed to be permissive for tumor formation. Although our results document one instance in which a postneoplastic loss of H19 activity correlates with loss of IGF2 imprinting at the cellular level, it appears that inactivation of H19 is more generally independent of loss of imprinting of IGF2, at least in our specimens. Our results imply that inactivation of H19 correlates with blastema overgrowth and can be independent of a regulatory role with respect to IGF2 imprinting status in cis.

Members of the nuclear hormone receptor gene family of transcription factors have been shown to be expressed in characteristic patterns during mouse organogenesis and postnatal development. Using an RT-PCR based screening assay, we have identified nuclear, Addresses: KAROLINSKA INST, DEPT MED NUTR, NOVUM F60, S-14186 HUDDINGE, SWEDEN. UPPSALA UNIV, DEPT ANIM DEV & GENET, S-75236 UPPSALA, SWEDEN. KAROBIO AB, S-14186 HUDDINGE, SWEDEN.

Genomic imprinting, which results in the mono-allelic expression of certain genes in a parent of origin-dependent manner, represents a specialized form of gene regulation which may be vitally important for mammalian development. The mechanisms which underlie imprinting and the molecular nature of the imprint itself remain elusive but most likely include epigenetic modifications of DNA, such as methylation and chromatin structure changes. It is clear, however, that many of the known imprinted genes play important developmental roles and that changes in the functional imprinting of some of these genes may have important pathological consequences, including placental abnormalities., Addresses: Franklin GC, UPPSALA UNIV, DEPT ANIM DEV & GENET, NORBYVAGEN 18A, S-75236 UPPSALA, SWEDEN.

Precursory studies of H19 transcription during human foetal development have demonstrated maternally derived monoallelic expression, Analyses in extra-embryonic tissues, however, have been more equivocal, with discernible levels of expression of the pater, Addresses: Adam GIR, UPPSALA UNIV, DEPT ANIM DEV & GENET, NORBYVAGEN 18, S-75236 UPPSALA, SWEDEN. KAROLINSKA HOSP, DEPT OBSTET & GYNAECOL, S-17176 STOCKHOLM, SWEDEN.

We have studied the promoter utilization and parental imprinting status of human IGF2 in three genetically informative hepatoblastomas from patients ranging in age from 9 months to 3 years, In all three cases, there is a downregulation of promoter P1 in t, Addresses: KAROLINSKA HOSP, DEPT CLIN NEUROSCI, EXPTL ALCOHOL & DRUG ADDICT RES SECT, S-17176 STOCKHOLM, SWEDEN. UNIV UPPSALA, DEPT ANIM DEV & GENET, S-75236 UPPSALA, SWEDEN. KAROLINSKA HOSP, DEPT PATHOL, DIV PEDIAT, S-17176 STOCKHOLM, SWEDEN.

The observation that a number of autosomal genes are expressed in a parent of origin-dependent monoallelic manner has fuelled a frantic research effort into the underlying mechanisms and biological functions of this phenomenon, termed genomic or parental, Addresses: Ohlsson R, UPPSALA UNIV, DEPT ANIM DEV & GENET, NORBYVAGEN 18A, S-75236 UPPSALA, SWEDEN.

IGF2 has been shown to be expressed preferentially from the paternally derived allele, although the maternal allele can be found active during both prenatal and postnatal development as well as in neoplastic tumours in humans. We addressed here whether or not the biallelic expression patterns that can be seen during postnatal human liver development reflected a coordinated change in the activities of the four promoters of human IGF2. We show here that the P2, P3 and P4 promoters, but not the P1 promoter, display monoallelic activity in embryonic, neonatal and younger infant liver specimens. The P2, P3 and P4 promoters can, however, be found active either monoallelically or biallelically or even monoallelically on opposite parental alleles in older infant and adult liver specimens. In contrast, H19, which is closely linked to IGF2, is monoallelically expressed in all postnatal liver samples analysed. We conclude that the functional imprinting status of IGF2 during postnatal liver development appears to be promoter/enhancer-specific and either partly or completely independent of H19., Addresses: KAROLINSKA HOSP, EXPTL ALCOHOL & DRUG ADDICT RES SECT, DEPT CLIN NEUROSCI, S-17176 STOCKHOLM, SWEDEN. UNIV UPPSALA, DEPT ANIM DEV & GENET, S-75236 UPPSALA, SWEDEN.

The paternal allele of the H19 gene has been shown to be transcriptionally inactive in the developing human embryo. Using reverse transcription PCR and RNase protection assays, we demonstrate that expression of H19 is predominantly, but not exclusively, f, Addresses: UPPSALA UNIV, DEPT ANIM DEV & GENET, S-75236 UPPSALA, SWEDEN. CHARING CROSS & WESTMINSTER MED SCH, DEPT MED ONCOL & BIOCHEM, CANC RES CAMPAIGN LABS, LONDON W6 8RP, ENGLAND. KAROLINSKA HOSP, DEPT OBSTET & GYNECOL, S-17176 STOCKHOLM, SWEDEN.