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PubMed2006

U.S. policy on health inequities: the interplay of politics and research.

What is the relationship between scientific research and government action in addressing health inequalities in the United States? What factors increase the impact of scientific research on public policy? To answer these questions, we focus on racial and ethnic disparities in health status and health care in the United States. We first review the history of the disparities issue to elucidate how the continual and persistent interplay between political action and scientific research drives government policy. We then analyze two recent government-sponsored reports about racial and ethnic disparities to understand the strategic consequences of issue framing. We draw lessons about how disparities research can have a greater impact on public policy.

Ethnicity↗
PubMed2003

Interplay between the tumor suppressor p53 and TGF beta signaling shapes embryonic body axes in Xenopus.

The transcription factor p53 has been shown to mediate cellular responses to diverse stresses such as DNA damage. However, the function of p53 in cellular differentiation in response to growth factor stimulations has remained obscure. We present evidence that p53 regulates cellular differentiation by modulating signaling of the TGF beta family of growth factors during early Xenopus embryogenesis. We show that p53 functionally and physically interacts with the activin and bone morphogenetic protein pathways to directly induce the expression of the homeobox genes Xhox3 and Mix.1/2. Furthermore, functional knockdown of p53 in embryos by an antisense morpholino oligonucleotide reveals that p53 is required for the development of dorsal and ventral mesoderm. Our data illustrate a pivotal role of interplay between the p53 and TGF beta pathways in cell fate determination during early vertebrate embryogenesis.

Animals↗
PubMed2005

Resolving embryonic blood cell fate choice in Drosophila: interplay of GCM and RUNX factors.

The differentiation of Drosophila embryonic blood cell progenitors (prohemocytes) into plasmatocytes or crystal cells is controlled by lineage-specific transcription factors. The related proteins Glial cells missing (GCM) and GCM2 control plasmatocyte development, whereas the RUNX factor Lozenge (LZ) is required for crystal cell differentiation. We have investigated the segregation process that leads to the formation of these two cell types, and the interplay between LZ and GCM/GCM2. We show that, surprisingly, gcm is initially expressed in all prohemocytes but is rapidly downregulated in the anterior-most row of prohemocytes, which then initiates lz expression. However, the lz+ progenitors constitute a mixed-lineage population whose fate depends on the relative levels of LZ and GCM/GCM2. Notably, we demonstrate that GCM/GCM2 play a key role in controlling the size of the crystal cell population by inhibiting lz activation and maintenance. Furthermore, we show that prohemocytes are bipotent progenitors, and that downregulation of gcm/gcm2 is required for lz-induced crystal cell formation. These results provide new insight into the mechanisms controlling Drosophila hematopoiesis and establish the basis for an original model for the resolution of the choice of blood cell fate.

Animals↗
PubMed2003

Sexy splicing: regulatory interplays governing sex determination from Drosophila to mammals.

A remarkable array of strategies is used to produce sexual differentiation in different species. Complex gene hierarchies govern sex determination pathways, as exemplified by the classic D. melanogaster paradigm, where an interplay of transcriptional, splicing and translational mechanisms operate. Molecular studies support the hypothesis that genetic sex determination pathways evolved in reverse order, from downstream to upstream genes, in the cascade. The recent identification of a role for the key regulatory factors SRY and WT1(+KTS) in pre-mRNA splicing indicates that important steps in the mammalian sex determination process are likely to operate at the post-transcriptional level.

Animals↗
PubMed2006

Interplay of PIWI/Argonaute protein MIWI and kinesin KIF17b in chromatoid bodies of male germ cells.

Chromatoid bodies are thought to act as male-germ-cell-specific platforms for the storing and processing of haploid transcripts. The molecular mechanisms governing the formation and function of these germ-cell-specific structures have remained elusive. In this study, we show that the kinesin motor protein KIF17b, which is involved in the nucleocytoplasmic transport of RNA and of a transcriptional coactivator, localizes in chromatoid bodies. The chromatoid body moves actively and non-randomly in the cytoplasm of round spermatids, making frequent contacts with the nuclear envelope. The localization of KIF17b thereby offers a potential mechanism for microtubule-dependent mobility of chromatoid bodies, as well as for the transport of the specific components in and out of the chromatoid body. Interestingly, we demonstrate that KIF17b physically interacts with a testis-specific member of the PIWI/Argonaute family, MIWI, a component of chromatoid bodies implicated in RNA metabolism. A functional interplay between KIF17b and MIWI might be needed for the loading of haploid RNAs in the chromatoid body. Importantly, chromatoid bodies from round spermatids of miwi-null mice are not fully compacted and remain as a diffuse chromatoid material, revealing the essential role played by MIWI in the formation of chromatoid bodies. These results shed new light on the function of chromatoid bodies in the post-transcriptional regulation of gene expression in haploid germ cells.

Animals↗
PubMed2001

The interplay between cyclin-B-Cdc2 kinase (MPF) and MAP kinase during maturation of oocytes.

Throughout oocyte maturation, and subsequently during the first mitotic cell cycle, the MAP kinase cascade and cyclin-B-Cdc2 kinase are associated with the control of cell cycle progression. Many roles have been directly or indirectly attributed to MAP kinase and its influence on cyclin-B-Cdc2 kinase in different model systems; yet a principle theme does not emerge from the published literature, some of which is apparently contradictory. Interplay between these two kinases affects the major events of meiotic maturation throughout the animal kingdom, including the suppression of DNA replication, the segregation of meiotic chromosomes, and the prevention of parthenogenetic activation. Central to many of these events appears to be the control by MAP kinase of cyclin translation and degradation.

Animals↗
PubMed2006

Interplay of nonlinearity and gain shaping in femtosecond fiber amplifiers.

A study of chirped-pulse amplification in the presence of large nonlinear phase shifts (as large as approximately 12pi) and finite gain bandwidth is presented. Numerical simulations that include the effect of nonlinearity, group-velocity dispersion, higher-order dispersion, and finite gain bandwidth predict the spectral signature of the interplay of nonlinearity with gain shaping. Experimental results obtained for up to approximately 0.4 microJ pulse energies from a Yb fiber amplifier agree with the numerical calculations.

Journal Article↗
PubMed2006

The interplay between PolyQ and protein context delays aggregation by forming a reservoir of protofibrils.

Polyglutamine (polyQ) diseases are inherited neurodegenerative disorders caused by the expansion of CAG codon repeats, which code for polyQ in the corresponding gene products. These diseases are associated with the presence of amyloid-like protein aggregates, induced by polyQ expansion. It has been suggested that the soluble aggregates rather than the mature fibrillar aggregates are the toxic species, and that the aggregation properties of polyQ can be strongly modulated by the surrounding protein context. To assess the importance of the protein carrier in polyQ aggregation, we have studied the misfolding pathway and the kinetics of aggregation of polyQ of lengths above (Q41) and below (Q22) the pathological threshold fused to the well-characterized protein carrier glutathione S-transferase (GST). This protein, chosen as a model system, is per se able to misfold and aggregate irreversibly, thus mimicking the behaviour of domains of naturally occurring polyQ proteins. We prove that, while it is generally accepted that the aggregation kinetics of polyQ depend on its length and are faster for longer polyQ tracts, the presence of GST alters the polyQ aggregation pathway and reverses this trend. Aggregation occurs through formation of a reservoir of soluble intermediates whose populations and kinetic stabilities increase with polyQ length. Our results provide a new model that explains the toxicity of expanded polyQ proteins, in which the interplay between polyQ regions and other aggregation-prone domains plays a key role in determining the aggregation pathway.

Carrier Proteins↗
PubMed2006

New perspectives on host-parasite interplay by comparative transcriptomic and proteomic analyses of Schistosoma japonicum.

Schistosomiasis remains a serious public health problem with an estimated 200 million people infected in 76 countries. Here we isolated ~ 8,400 potential protein-encoding cDNA contigs from Schistosoma japonicum after sequencing circa 84,000 expressed sequence tags. In tandem, we undertook a high-throughput proteomics approach to characterize the protein expression profiles of a number of developmental stages (cercariae, hepatic schistosomula, female and male adults, eggs, and miracidia) and tissues at the host-parasite interface (eggshell and tegument) by interrogating the protein database deduced from the contigs. Comparative analysis of these transcriptomic and proteomic data, the latter including 3,260 proteins with putative identities, revealed differential expression of genes among the various developmental stages and sexes of S. japonicum and localization of putative secretory and membrane antigens, enzymes, and other gene products on the adult tegument and eggshell, many of which displayed genetic polymorphisms. Numerous S. japonicum genes exhibited high levels of identity with those of their mammalian hosts, whereas many others appeared to be conserved only across the genus Schistosoma or Phylum Platyhelminthes. These findings are expected to provide new insights into the pathophysiology of schistosomiasis and for the development of improved interventions for disease control and will facilitate a more fundamental understanding of schistosome biology, evolution, and the host-parasite interplay.

Amino Acid Sequence↗
PubMed2005

Respiratory syncytial virus and T cells: interplay between the virus and the host adaptive immune system.

Respiratory syncytial virus (RSV) is a major cause of morbidity in young infants and is increasingly recognized as an important cause of serious illness/morbidity in the elderly. This agent has also been implicated both in the etiopathogenesis of asthma/airway hyperreactivity and in the exacerbation of wheezing episodes in individuals with asthma. This review deals with our current knowledge of the host adaptive immune response to RSV, focusing on the interaction of the virus with T lymphocytes. Current information on the impact of RSV infection on the function of responding CD4 (+) and, in particular, CD8 (+) T lymphocytes will be reviewed; and the potential implications of this virus/immune cell interaction on the development of RSV-induced disease in the respiratory tract will be discussed. In addition, the long-standing conundrum concerning the development of an effective vaccine against RSV will be discussed in the context of the vaccine-induced enhanced disease during RSV infection and the interplay between the virus and immune/memory T cells in the development of pulmonary injury in vaccinated individuals after the RSV infection.

CD4-Positive T-Lymphocytes↗
PubMedDate not supplied

Cultured lung cells: interplay effects of beta-mimetics, prostaglandins and corticosteroids in the biosynthesis of dipalmitoyl lecithin.

Cell lines derived from type II lung cells were used to study interplays of substances affecting incorporation of labeled precursors [1(-14)C]palmitate and [methyl-3H]choline into phosphatidyl choline. Ethanol stimulated markedly biosynthesis of dipalmitoyl phosphatidyl choline in cloned rabbit lung cells; the stimulating action of ethanol was reduced very much by cortisol and less by ritodrine. In the presence of 0.1 microM isoproterenol, two prostaglandins, E2 and F2alpha, caused marked depressions in the incorporation of both precursors by cell line A 549 derived from human lung adenocarcinoma. One concluded that among the agents studied, ethanol and cortisol are potent antagonists, and so were also the prostaglandins and isoproterenol.

Animals↗
PubMed2003

Verdi's Rigoletto: the dialectic interplay of the psychic positions in seemingly 'mindless' violence.

In this paper the author demonstrates the interplay of the psychic positions (paranoid-schizoid and depressive, alongside more primitive mental states) as they may appear in experiences of overwhelming anxieties relating to fragmentation and disintegration. These are examined in relation to the appearance of what has been described in the literature as 'mindless' violence. The vehicle for this demonstration is Verdi's opera Rigoletto, which the author examines using Fonagy and Target's model for the understanding of mindless violence. The opera is 'read' as a case study of the protagonist, using the drama as a reflection of Rigoletto's internal object representations. The author attempts to extend Fonagy and Target's model to include primitive mental states, in order to understand 'mindless' violence as a result of collapse of the dialectical relationship of the psychic positions, leading to the violent act as a desperate attempt at re-establishing a sense of self. From this perspective, the moment of the violent act may be seen as use of an autistic object and as supplying of autistic shape. The violence is ultimately directed against the already fragmenting self, especially cherished parts of it, however it may enable acknowledgement of repudiated, unmentalised emotions previously experienced as a void.

Depression↗
PubMed2006

Interplay of ryanodine receptor distribution and calcium dynamics.

Spontaneously generated calcium (Ca2+) waves can trigger arrhythmias in ventricular and atrial myocytes. Yet, Ca2+ waves also serve the physiological function of mediating global Ca2+ increase and muscle contraction in atrial myocytes. We examine the factors that influence Ca2+ wave initiation by mathematical modeling and large-scale computational (supercomputer) simulations. An important finding is the existence of a strong coupling between the ryanodine receptor distribution and Ca2+ dynamics. Even modest changes in the ryanodine receptor spacing profoundly affect the probability of Ca2+ wave initiation. As a consequence of this finding, we suggest that there is information flow from the contractile system to the Ca2+ control system and this dynamical interplay could contribute to the increased incidence of arrhythmias during heart failure.

Calcium↗
PubMed2006

The interplay of cell-cell and cell-matrix interactions in the invasive properties of brain tumors.

Impairment of tissue cohesion and the reorganization of the extracellular matrix are crucial events during the progression toward invasive cell phenotype. We studied the in vitro invasion patterns of nine brain tumor cell lines in three-dimensional collagen gels. Cell-cell and cell-matrix interactions were quantified and correlated with the expression level of specific molecules: N-cadherin, matrix metalloproteinases, and their inhibitor. Pattern evolution was studied as a function of time and collagen concentration. Cells with low metalloproteinase expression or high tissue cohesion showed limited invasive potential. Higher metalloproteinase expression and intermediate tissue cohesion resulted in configurations with hypercellular zones surrounding regions mostly devoid of cells and with digested collagen, akin to pseudopalisades in surgically removed malignant astrocytoma specimens. In physical terms, these configurations arise as the result of competition between cell-cell and cell-matrix interactions. Our findings suggest specific ways to characterize, control, or engineer cell migratory patterns and hint at the importance of the interplay between biophysical and biomolecular factors in the characterization of invasive cell behavior and, more generally, in epithelial-mesenchymal transitions.

Adult↗
PubMed1999

Interplay between chromatin modifying and remodeling complexes in transcriptional regulation.

The question of a possible functional relationship between different chromatin-altering enzymatic activities is of great interest. Several remarkable parallels have been revealed regarding the action of the remodeling complex SWI/SNF and the histone acetylation complex SAGA during transcriptional activation in S. cerevisiae. Many promoters, but not all, that require one complex require the other as well. Mutations that disrupt both complexes cause much more severe phenotypes than single mutations. Both types of complexes are recruited to specific promoters by interaction with DNA-bound acidic activators, resulting in targeted acetylation and transcriptional activation. Taken together the data argue for independent mechanisms, but similar recruitment and functional interplay between these two types of chromatin-altering activities.

Animals↗
PubMed2007

Homology-directed repair is required for the development of radioresistance during S phase: interplay between double-strand break repair and checkpoint response.

The S-phase-dependent radioresistance to killing uniformly seen in eukaryotic cells is absent in radiosensitive mutants with defects in genes involved in the repair of DNA double-strand breaks (DSBs) by homologous recombination (homologous recombination repair: HRR). This implicates, for the first time, a concrete DNA repair process in the radiosensitivity of a specific cell cycle phase. The cell cycle-dependent fluctuations in radiosensitivity reflect a fundamental and well-documented radiobiological phenomenon that still awaits a detailed molecular characterization. The underlying mechanisms are likely to combine aspects of DNA repair and cell cycle regulation. Advances in both fields allow a first dissection in the cell cycle of the molecular interplay between DSB repair and DNA damage checkpoint response and its contribution to cell survival. Here we review the available literature on the topic, speculate on the ramifications of this information for our understanding of cellular responses to DNA damage, and discuss future directions in research. An effort is made to integrate relevant phenomena of radiation action, such as low-dose radiosensitivity and the G(2) assay in this scheme.

Animals↗
PubMed2006

Gene-gene and gene-environment interplay represent specific susceptibility for different types of ischaemic stroke and leukoaraiosis.

Stroke is a very frequent entity. It is the third leading cause of death and the leading cause of adult disability in the developed world. At a population level, the common sporadic form of ischaemic stroke is underpinned by both environmental and genetic risk factors. Typically, in clinical practice, environmental risk factors such as hypertension, diabetes mellitus, smoking, alcohol consumption, and other factors, are usually considered to be more important than genetic factors. However, it is the interplay of both environmental and common genetic factors [such as the Leiden V, methylenetetrahydrofolate reductase C677T, apolipopotein E 4, endothelial nitric oxide synthase G894T, angiotensin-converting enzyme I/D and angiotensin II type 1 receptor A1166C mutations and polymorphisms] that leads to the development of ischaemic stroke. Indeed, a complex network of interactions between genetic factors and clinical risk factors can be supposed. This review evaluates the possible roles of gene-gene and gene-environment interactions concerning the above genetic factors in the evolution of ischaemic stroke and leukoaraiosis. A knowledge of the specific genetic patterns which are associated with a significant risk of ischaemic stroke or leukoaraiosis may also draw attention to a large population at an increased risk of circulatory disorders. This may facilitate the choice of more effective and specific prevention on the basis of the genotype.

Apolipoprotein E4↗
PubMed2006

Role for GABA and Glu plasma membrane transporters in the interplay of inhibitory and excitatory neurotransmission.

Neurotransmitter plasma membrane transporters do have much more to perform than simply terminating synaptic transmission and replenishing neurotransmitter pools. Findings in the past decade have evidenced their function in maintaining physiological synaptic excitability, and their actions in critical or pathological conditions, also. Conclusively these findings indicated a previously unrecognized role for neurotransmitter plasma membrane transporters in both, synaptic and nonsynaptic signaling. Major inhibitory and excitatory neurotransmitters within the brain, GABA and Glu, have long been considered to operate through independent systems (GABAergic or Gluergic), each of them characterized by its own localization, function and dedicated GABAergic or Gluergic cell phenotypes. Recent advances, however, have challenged this long-standing paradigm. Localization of GABA in Gluergic terminals and Glu in GABAergic cells were reported. Specific plasma membrane transporters for GABA and Glu are also co-localized in different brain areas. Although, their role in regulating each other's signal is still far from being understood, emerging lines of evidence on interplaying GABAergic and Gluergic processes through plasma membrane transporters opens up a new avenue in the field of more specific therapeutic intervention.

Amino Acid Transport System X-AG↗