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PubMed2000

Cytokine network at the feto-maternal interface.

There is much evidence that cytokines play a very important role in the maintenance of pregnancy by modulating immune and endocrine systems. Placental tissue produces cytokines and hormones that are essential to the regulation of the feto-maternal unit. Decidual lymphocytes express cell surface markers for activation, such as CD69 and HLA-DR, and these cells secrete many cytokines. Recent studies suggested that in pregnant women, cytokines produced by Th2 cells predominate over those produced by Th1 cells, resulting in the maintenance of pregnancy. This review article focuses on the unique cytokine network at the feto-maternal interface in humans. Recently, we demonstrated that Th2 cells were dominant within the decidua in early pregnancy in humans. The Th2-derived cytokines, IL-4 and IL-6, induce the release of hCG from trophoblasts, and the hCG stimulate progesterone production from corpus luteum in pregnancy. Progesterone stimulates the secretion of Th2 and reduces the secretion of Th1 cytokines. Thus, Th2 type cytokines appear to contribute to the maintenance of pregnancy by controlling the immune and endocrine systems and promoting the function of the trophoblasts at the implantation site.

Cytokines↗

PubMed1985

Structure of inclusion complexes of cyclomaltoheptaose (cycloheptaamylose): crystal structure of the 1-adamantanemethanol adduct.

Cyclomaltoheptaose (cycloheptaamylose) has been crystallized with 1-adamantanemethanol as the guest molecule. The complex crystallized in space group C222(1), with unit-cell dimensions a = 19.162 (13), b = 23.965 (17), and c = 32.597 (27) A. The structure was solved by rotation-translation search-methods. The cyclomaltoheptaose exists as a dimer in the crystal by means of extensive hydrogen-bonding across the secondary hydroxyl ends of two cyclomaltoheptaose molecules. The two halves of the dimer are related by a crystallographic two-fold axis. The primary hydroxyl ends of two adjacent cyclomaltoheptaose molecules are also related by a crystallographic two-fold axis, but do not directly hydrogen bond to one another. Instead, they are held in place by a strong hydrogen bond from the hydroxyl group of the 1-adamantanemethanol to a primary hydroxyl group on an adjacent cyclomaltoheptaose molecule. Other stabilizing hydrogen bonds are formed via three water molecules which are situated at the primary hydroxyl interface, and others that form parallel columns stabilizing the crystal structure. A unique feature of this complex is the presence of trapped water in the cavity at the secondary hydroxyl interface. This water is distributed over 3 disordered sites. Its presence blocks one possible site for the 1-adamantanemethanol, which, instead, binds near the primary hydroxyl end, with its hydroxyl group and part of the adamantane moiety protruding from the cyclomaltoheptaose.

Adamantane↗

PubMed2001

Differential dimer activities of the transcription factor Oct-1 by DNA-induced interface swapping.

Two crystal structures of Oct-1 POU domain bound to DNA provide a rationale for differential, conformation-dependent recruitment of transcription cofactors. The POU-homeo and POU-specific subdomains of Oct-1 contain two different nonoverlapping pairs of surface patches that are capable of forming unrelated protein-protein interfaces. Members of the POU factor family contain one or two conserved sequence motifs in the interface that are known to be phosphorylated, as noted for Oct-1 and Pit-1. Modeling of Oct-4 reveals the unique case where the same conserved sequence is located in both interfaces. Our studies provide the basis for two distinct dimeric POU factor arrangements that are dictated by the architecture of each DNA response element. We suggest interface swapping in dimers could be a general mechanism of modulating the activity of transcription factors.

Amino Acid Sequence↗

PubMed2002

Effects of organic matrix proteins on the interfacial structure at the bone-biocompatible nacre interface in vitro.

The biocompatibility and potential osteoinductivity of nacre have favored its use as a bone-grafting material. The present study is to investigate the interfacial structure at the bone-nacre interface resulting from organic matrix proteins, which emphasizes the mechanism of bone-bonding ability and biocompatibility of the shell tissues such as nacre and biogenic calcite. To understand the interfacial reaction, the zeta potential measurements, provide for a unique method to quantify the actual state of the interface in situ, were used for synthetic and biogenic calcium carbonate suspensions with respect to pH and the organic matrix as an additive. The zeta potentials and surface charge density show that the organic matrix proteins are main charge regulators, resulting in the stabilized tissue properties as compared with synthetic crystals. Also, in forming calcium carbonate crystals with the additives, the conformation of organic matrix has an important role in the understanding of the newly formed interfacial structure. The result provides the primary role of the organic matrix proteins in controlling the formation of interfacial structure and biocompatibility with bone as well as the stability of biogenic tissues. And it gives a new insight into the usefulness of zeta potential measurement to describe the in vivo interaction between the bone and implants.

Adsorption↗

PubMed1999

Transient coexpression of nestin, GFAP, and vascular endothelial growth factor in mature reactive astroglia following neural grafting or brain wounds.

The spatial and temporal immunoexpression of the intermediate filament (IF) protein nestin and its relationship to glial fibrillary acidic protein (GFAP), vascular endothelial growth factor (VEGF), and its receptor flt-1 (VEGF-R1) in reactive astroglia was examined following stab wounds or transplants of fetal CNS tissue into the adult brain. Since developmentally regulated proteins and gene transcripts can be reexpressed in reactive astroglia following certain brain injuries, we analyzed the nestin profile in these experimental paradigms in order to more fully understand the nature of the gliotic "scar." Nestin expression was transiently up-regulated in some but not all astrocytes which often had a different morphology than the typical stout, stellate GFAP (+) cells; the processes of the nestin (+) cells tended to be slender and elongated. In reactive astroglia from the mature brain, nestin expression was robust but generally localized to the wound or graft site, peaked at 7-10 days postoperative, and was absent by 28 days, whereas GFAP (+) astrocytes were far more widespread and persisted for many months. Only nestin was strongly expressed immediately adjacent to early stab wounds, whereas GFAP (+) cells were located further from the wound sites. In contrast, there was marked nestin/GFAP colocalization at the graft/host interface. Semiquantitative analysis combined with confocal microscopy revealed a unique compartmentalization of protein expression; processes from single astrocytes could be entirely nestin (+), GFAP (+), or could show coexpression. At 4, 7, and 14 days postoperative, 41, 58, and 32% of the immunoexpression, respectively, was accounted for by nestin at the graft/host interface, and it was essentially undetectable at 28 days postoperative. In situ hybridization studies showed nestin transcripts within GFAP (+) cells primarily between 4 and 10 days postoperative and absent by 28 days. Many nestin (+) astrocytes, as shown by electron microscopy, were closely related to the vasculature. Therefore we further examined the expression of vascular endothelial growth factor (VEGF), an endothelial cell mitogen associated with angiogenesis. Nestin colocalized with VEGF in some astrocytes (7%) but far more prominently with the VEGF flt-1 receptor (25%). Early astroglial activation may involve several different IF components and possibly a distinct astrocytic population that shows a rapid, transient nestin expression adjacent to injury sites. Expression of the nestin IF phenotype within affected astrocytes in the surgical vicinity may be indicative of a reversion to an immature phenotype that might be less susceptible to attendant hypoxia after injury. Since injured astrocytes are well known to express many bioactive compounds, such transient reexpression of early, developmentally regulated proteins may be a hallmark for the elaboration of growth factors such as VEGF.

Animals↗

PubMed2004

Intimate partner violence and the justice system: an examination of the interface.

Women entering the court system face a challenging experience, in part, because a courtroom can be an intimidating and difficult place for any person, and in part because women victimized by crimes in which the offender is known to them face distinctive difficulties when they seek the court's remedies. The interface is also made more challenging for women as the literature offers disparate findings as to the efficacy of criminal justice responses and civil remedies. This article briefly explores the unique characteristics of intimate partner violence cases that influence the interface of these victims with the court system. Areviewis provided of research on the criminal justice interventions in cases of intimate partner violence; and research on the efficacy of civil protective orders.

Battered Women↗

PubMed2000

A null mutation in HLA-G is not associated with preeclampsia or intrauterine growth retardation.

Modulation of the expression of genes of the major histocompatibility complex (MHC) in tissues at the maternal-fetal interface almost certainly plays a role in successful development of the semi-allogeneic fetus. While expression of the classical class I genes (HLA-A, B, C) is low to non-existent at this site, the non-classical molecule, HLA-G, is expressed uniquely in fetal cells at the maternal-fetal interface. The recent demonstration that homozygotes for a deletion mutation in exon 3 (1597DeltaC) of HLA-G do not express the full-length HLA-G1 isoforms indicates a potential reduction in expression of this isoform in heterozygotes. If the full-length isoform of HLA-G (i.e. HLA-G1) contributes to proper invasion of maternal spiral arteries by extravillous cytotrophoblast, then 1597DeltaC heterozygotes could be at increased risk for disorders of trophoblast invasion. Two populations, infants with intrauterine growth retardation (IUGR) and infants of preeclamptic (PE) mothers, were genotyped for the 1597DeltaC polymorphism. The frequency of 1597DeltaC in these samples was not significantly different from healthy controls, suggesting that heterozygotes for this deletion mutation are not at significantly increased risk for PE or IUGR (P = 0.727 and 0.803, respectively).

Adolescent↗

PubMed2003

Nonlinear evolution of an interface in the Richtmyer-Meshkov instability.

The linear theory of the Richtmyer-Meshkov instability derived by Wouchuk and Nishihara [Phys. Plasmas 4, 3761 (1997)] indicates that the instability is driven by the nonuniform velocity shear left by transmitted and reflected rippled shocks at a corrugated interface. In this work, the nonlinear evolution of the interface has been investigated as a self-interaction of a nonuniform vortex sheet with a density jump. The theory developed shows the importance of the finite density jump and the finite initial corrugation amplitude of the interface. By introducing Lagrangian markers on the interface with proper kinematic boundary conditions, it is shown that stretching and shrinking of the interface occur locally even in the tangential direction. This causes deformation of bubble and spike profiles depending on the Atwood number. The vorticity on the interface for a finite density jump is not conserved in the nonlinear regime. Our results suggest that the spiral structure of the spike is due to local increase and decrease of the vorticity on the interface. Nonlinear analysis shows that the large initial amplitude of the corrugation results in rapid increase of the vorticity, which may also explain the fast roll up motion of the spiral for large amplitudes. With the use of the asymptotic linear growth rate, the nonlinear evolution of the instability is uniquely determined from the initial corrugation amplitude of the interface, the Atwood number, and the incident shock intensity. There is no need to use an impulsive formulation. The analytical nonlinear growth agrees well with the experiment [Dimonte et al., Phys. Plasmas 3, 614 (1996)]. The theory reveals nonlinear properties of the instability, such as the time evolution of the interface profiles and the vorticity on the interface, and also their dependence on the Atwood number and the corrugation amplitude.

Journal Article↗

PubMed2002

Functionally orthogonal ligand-receptor pairs for the selective regulation of gene expression generated by manipulation of charged residues at the ligand-receptor interface of ER alpha and ER beta.

The reengineering of protein-small molecule interfaces represents a powerful tool of chemical biology. For many applications it is necessary to engineer receptors so that they do not interact with their endogenous ligands but are highly responsive to designed ligand analogues, which in turn do not interact with endogenous proteins. The chemical design strategy used to reengineer protein-small molecule interfaces is particularly challenging for interfaces involving relatively plastic receptor binding sites and therefore presents a unique challenge in molecular design. In this study we explore the scope and limitations of a new strategy for manipulating polar/charged residues across the ligand receptor interface of estradiol (E2) and the estrogen receptor (ER). Carboxylate-functionalized E2 analogues can activate ER alpha(Glu353-->Ala) and ER beta(Glu305-->Ala) with very large selectivites, demonstrating that this design strategy is extendable to other members of the steroid hormone receptor family. Neutral E2 analogues were found to complement ER alpha(E353A) with similar potencies but with generally lower selectivities. This suggests that the high selectivity observed with ligand-receptor pairs generated by exchanging charged residues across ligand-receptor interfaces is only due in part to their complementary shapes and that appropriate introduction of charged functionality on the ligand can provide substantial enhancement of selectivity by decreasing the engineered ligands affinity for the endogenous receptor. Attempts to modify the cationic residues by complementing Arg394-->Ala or Arg394-->Glu were not successful.

Cells, Cultured↗

PubMed2000

Interfacial control of lid opening in Thermomyces lanuginosa lipase.

Small unilamelar vesicles of anionic phospholipids (SUV), such as 1-palmitoyl-2-oleoylglycero-sn-3-phosphoglycerol (POPG), provide an interface where Thermomyces lanuginosa triglyceride lipase (TlL) binds and adopts a catalytically active conformation for the hydrolysis of substrate partitioned in the interface, such as tributyrin or p-nitrophenylbutyrate, with an increase in catalytic rate of more than 100-fold for the same concentration of substrate [Berg et al. (1998) Biochemistry 37, 6615-6627.]. This interfacial activation is not seen with large unilamelar vesicles (LUV) of the same composition, or with vesicles of zwitterionic phospholipids such as 1-palmitoyl-2-oleoylglycero-sn-3-phosphocholine (POPC), independently of the vesicle size. Tryptophan fluorescence experiments show that lipase binds to all those types of vesicles with similar affinity, but it adopts different forms that can be correlated with the enzyme catalytic activity. The spectral change on binding to anionic SUV corresponds to the catalytically active, or "open" form of the enzyme, and it is not modified in the presence of substrate partitioned in the vesicles, as demonstrated with inactive mutants. This indicates that the displacement of the lid characteristic of lipase interfacial activation is induced by the anionic phospholipid interface without blocking the accessibility of the active site to the substrate. Experiments with a mutant containing only Trp89 in the lid show that most of the spectral changes on binding to POPG-SUVs take place in the lid region that covers the active site; an increase in Trp anisotropy indicates that the lid becomes less flexible in the active form, and quenching experiments show that it is significantly buried from the aqueous phase. On the other hand, results with a mutant where Trp89 is changed to Leu show that the environment of the structural tryptophans in positions 117, 221, and 260 is somehow altered on binding, although their mobility and solvent accessibility remains the same as in the inactive form in solution. The form of TlL bound to POPC-SUV or -LUV vesicles as well as to LUV vesicles of POPG has the same spectral signatures and corresponds to an inactive or "closed" form of the enzyme. In these interfaces, the lid is highly flexible, and Trp89 remains accessible to solvent. Resonance energy transfer experiments show that the orientation of TlL in the interface is different in the active and inactive forms. A model of interaction consistent with these data and the available X-ray structures is proposed. This is a unique system where the composition and physical properties of the lipid interface control the enzyme activity.

Binding Sites↗

PubMed2005

Nucleocytoplasmic distribution of opioid growth factor and its receptor in tongue epithelium.

The subcellular distributions of the opioid growth factor (OGF), [Met(5)]-enkephalin, and opioid growth factor receptor (OGFr) in the epithelium of the rat tongue were determined in order to reveal structure-function relationships. Laser scanning confocal microscopic analysis showed that both OGF and OGFr were colocalized in the paranuclear cytoplasm and in the nuclei of keratinocytes in the stratum basale. Using immunoelectron microscopy and postembedding techniques, double labeling experiments disclosed that complexes of OGF-OGFr were colocalized on the outer nuclear envelope, in the paranuclear cytoplasm, perpendicular to the nuclear envelope in a putative nuclear pore complex, and in the nucleus adjacent to heterochromatin. Anti-OGF IgG alone was detected in the cytoplasm, and anti-OGFr IgG alone was associated with the outer nuclear envelope. Study of chronic treatment with the opioid antagonist, naltrexone (NTX), which blocks opioid-receptor binding, revealed the presence of OGFr immunoreactivity alone in the cytoplasm and the nucleus; some OGF-OGFr complexes were also observed. Colocalization of OGFr and karyopherin (importin) beta was recorded in the cytoplasm and nucleus. These results in tongue epithelium are the first to suggest that OGFr resides on the outer nuclear envelope, where OGF interacts with OGFr; that the OGF-OGFr complex translocates between cytoplasm and nucleus at the nuclear pore; and that the nuclear localization signal of OGFr interacts with karyopherin beta for nuclear transport. These novel data also indicate that signal transduction for cell proliferation appears to involve an OGF-OGFr complex that interfaces with chromatin in the nucleus. Moreover, the unique finding that OGFr was found in the cytoplasm and nucleus in NTX-treated specimens may suggest that NTX-OGFr complexes have the same pathway as OGF-OGFr.

Animals↗

PubMed2006

Expression of the class A macrophage scavenger receptor on specific subpopulations of murine dendritic cells limits their endotoxin response.

Dendritic cells (DC) function at the interface of innate and acquired immunity and are uniquely sensitive to specific stimuli. Pattern recognition receptors (PRR) on these cells are critically important because of their ability to recognise and initiate responses to conserved microbial-associated molecular signatures. With the exception of Toll-like receptors (TLR), we know relatively little about the specific distribution of other PRR amongst populations of DC. Here, we describe the expression of the murine class A macrophage scavenger receptor (SR-A) and show that it is restricted to specific subpopulations of bone marrow-derived and splenic DC. Importantly, we demonstrate that the receptor significantly alters the response of DC to endotoxin. In contrast to the activities of other PRR that have so far been examined, uniquely SR-A limits the maturation response; SR-A-/- cells display enhanced CD40 expression and TNF-alpha production. We discuss the potential contributions of SR-A to DC biology in the context of the known multiple activities of this receptor.

Animals↗

PubMed1994

Normal and abnormal development of the blood-brain barrier.

The blood-brain barrier is responsible for the maintenance of the neuronal microenvironment. This is accomplished by isolation of the brain from the blood by the tight junctions that join endothelial cells in cerebral microvessels, and by selective transport and metabolism of substances from blood or brain by the endothelial cells. This review describes the growth and maturation of the brain vasculature, and the development of the special properties of the endothelia at the blood-brain interface. Evidence suggests that the development of the unique properties of the brain microvasculature is a consequence of tissue-specific interactions between endothelial cells of extraneural origin and developing brain cells. The cellular and molecular mechanisms that control these processes are as yet unknown but this review will include experimental studies which have used in vivo and in vitro systems to investigate what factors may be involved, and some pathological conditions in which abnormal barrier development is thought to be an important aspect of the disease process.

Animals↗

PubMed2001

Crystal structure of an isolated V(alpha) domain of the 2C T-cell receptor.

The T-cell receptor (TCR) is a heterodimeric cell-surface protein consisting of two chains, alpha and beta, each of which is composed of a variable (V) and a constant (C) domain. Crystals of the isolated V(alpha) domain of the murine TCR 2C were grown by serendipity from a solution containing the extracellular domains of the intact TCR 2C and CD3 gamma epsilon-chains. The V(alpha) crystal structure shows how crystal packing can substitute for another V(alpha) domain in a different fashion from that observed in V(alpha)/V(alpha) homodimer and V(alpha)/V(beta) heterodimer structures. Significant conformational changes occur in the CDR3 and beta(3)beta(4) loops that normally form part of the dimer interface. The monomeric V(alpha) domain provides the unique opportunity to study the effect of dimerization on the conformation of the unliganded complementarity-determining regions (CDR) of a TCR. This structure of an individual V(alpha) module has implications for stability and bioengineering of isolated antibody and immunoglobulin domains.

Animals↗

PubMed2002

Control of melatonin synthesis in the mammalian pineal gland: the critical role of serotonin acetylation.

The large daily rhythm in circulating melatonin levels is a highly conserved feature of vertebrate physiology: high values always occur at night. The dynamics of the rhythm are controlled by the next-to-last enzyme in melatonin synthesis (serotonin --> N-acetylserotonin --> melatonin), arylalkylamine N-acetyltransferase (AANAT), the "melatonin rhythm enzyme". In vertebrate biology, AANAT plays a unique time-keeping role as the molecular interface between the environment and the hormonal signal of time, melatonin. This chapter describes the mammalian AANAT regulatory system, which includes the retina, neural structures, transsynaptic processes, and molecular events. In addition, special attention is paid to the functional characteristics of the systems which insure that the nocturnal increase in melatonin is an accurate and reliable indicator of the duration of the night, and why the melatonin rhythm is the most reliable output signal of the Mind's Clock.

Acetylation↗

PubMed1996

Expression of membrane form of the pregnancy associated protein TJ6 on decidual lymphocytes in the first trimester of pregnancy.

TJ6, a newly described protein produced locally in the uterine decidua during pregnancy, may be involved in maintaining a unique immunological environment at the maternal-fetal interface. The aim of this study was to determine whether TJ6 is expressed as membrane form on decidual lymphocytes (DL), to define the phenotypes of TJ6m (membrane form TJ6) expressing cells and to analyze the fluorescence intensity of TJ6m expression. Peripheral blood lymphocytes (PBL) and DL were obtained from first trimester pregnancies undergoing elective termination and immunophenotyped for TJ6m and other cell surface antigens (CD3, CD8, CD19, CD56, CD16) by flow cytometry. This is the first study showing that TJ6 molecules are present on decidual lymphocytes in human pregnancy. TJ6m expression on PBL was not different from that of DL. However, a significantly higher percentage of double positive (TJ6m+CD3+, TJ6m+,CD8+,TJ6m+CD19+) cells were found in PBL when compared to DL. The average fluorescence intensity (AFI) for the TJ6m marker among cells with CD8+, CD19+ and CD56+ double positive was significantly higher in DL as compared with those of PBL. The AFI for granularity of double positive DL was significantly higher than observed in PBL.

Antigens, CD↗

PubMed1992

A universal data acquisition program for use with anesthetic monitors and Windows 3.0.

A method is described whereby a single program can acquire data from any patient monitor which has a data output facility. No changes are necessary to the program for different monitors. It provides a method of standardizing data transfer between computers and monitors. The program runs in the Microsoft Windows 3.0 operating system. It utilizes Dynamic Link Libraries (DLL) which enable the operating system to communicate with monitors. Each kind of monitor will use a unique DLL in order to provide a standard interface to the Windows 3.0 operating system.

Anesthesiology↗

PubMed2004

Strengthening mechanisms of bone bonding to crystalline hydroxyapatite in vivo.

The formation and strengthening mechanisms of bone bonding of crystalline hydroxyapatite (HA) has been investigated using high-resolution transmission electron microscope (HRTEM) and energy-dispersive X-ray (EDX) analysis. A series of results were obtained: (i) a layer of amorphous HA, which has almost the same chemistry as the implanted HA, was formed on the surface of crystalline HA particles prior to dissolution; (ii) at 3 months a bone-like tissue formed a bonding zone between mature bone and the HA implant, composed of nanocrystalline and amorphous apatite; and (iii) at 6 months, mature bone was in direct contact with HA particles, and collagen fibres were perpendicularly inserted into the surface layer of implanted HA crystals. Findings (i) and (ii) indicated the following dissolution-precipitation process. (i) The crystalline HA transforms into amorphous HA; (ii) the amorphous HA dissolves into the surrounding solution, resulting in over-saturation; and (iii) the nanocrystallites are precipitated from the over-saturated solution in the presence of collagen fibres. A preliminary analysis indicated several conclusions: (i) the transition from crystalline to amorphous HA might be the controlling step in the bone bonding of crystalline HA; (ii) biological interdigitation (or incorporation) of collagen fibres with HA and chemical bonding of a apatite layer were both necessary to strengthen and toughen a bone bond, not only for the bonding between bone and HA at 6 months, but also for the bonding zone at 3 months, which would otherwise be very fragile due to the inherited brittleness of polycrystalline ceramics; and (iii) perpendicular interdigitation is an effective way for collagen fibres to impart their unique combination of flexibility and strength to the interface which they are keying.

Adhesiveness↗