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Immune interferon inhibits proliferation and induces 2'-5'-oligoadenylate synthetase gene expression in human vascular smooth muscle cells.
Proliferation of vascular smooth muscle cells (SMC) contributes to formation of the complicated human atherosclerotic plaque. These lesions also contain macrophages, known to secrete SMC mitogens, and T lymphocytes. Many of the SMC in the lesions express class II major histocompatibility antigens, an indication that activated T cells secrete immune IFN-gamma locally in the plaque. We therefore studied the effect of IFN-gamma on the proliferation of cultured SMC derived from adult human blood vessels. IFN-gamma (1,000 U/ml) reduced [3H]thymidine (TdR) incorporation into DNA by SMC stimulated with the well-defined mitogens IL 1 (from 15.3 +/- 0.7 to 6.2 +/- 0.7 dpm X 10(-3)/24 h) or platelet-derived growth factor (PDGF) (from 18.5 +/- 1.0 to 7.3 +/- 0.7 dpm X 10(-3)/24 h). Kinetic and nuclear labeling studies indicated that this effect of IFN-gamma was not due to altered thymidine transport or specific radioactivity of TdR in the cell. In longer term experiments (4-16 d) IFN-gamma prevented net DNA accumulation by SMC cultures stimulated by PDGF. IFN-gamma also delayed (from 30 to 60 min) the time to peak level of c-fos RNA in IL 1-treated SMC. It is unlikely that cytotoxicity caused these effects of IFN-gamma, as the inhibition of growth was reversible and we detected no cell death in SMC cultures exposed to this cytokine. Activation of 2'-5' oligoadenylate synthetase gene expression may mediate certain antiproliferative and antiviral effects of interferons. Both IFN-gamma and type I IFNs (IFN-alpha or IFN-beta) induced 2'-5' oligoadenylate synthetase mRNA and enzyme activity in SMC cultures, but with concentration dependence and time course that may not account for all of IFN-gamma's cytostatic effect on SMC. The accumulation of SMC in human atherosclerotic lesions is a long-term process that must involve altered balance between growth stimulatory and inhibitory factors. The cytostatic effect of IFN-gamma on human SMC demonstrated here may influence this balance during human atherogenesis, because T cells present in the complicated atherosclerotic plaque likely produce this cytokine
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Interleukin 1: a mitogen for human vascular smooth muscle cells that induces the release of growth-inhibitory prostanoids.
There is much interest in defining the signals that initiate abnormal proliferation of cells in a variety of states characterized by the presence of mononuclear phagocytes. Since IL-1 is a major secretory product of activated human monocytes we examined whether this cytokine can stimulate the growth of human vascular smooth muscle cells (SMC). Neither recombinant IL-1 (rIL-1) alpha (less than or equal to 5.0 ng/ml) nor beta (less than or equal to 100 ng/ml) stimulated SMC growth during 2-d incubations under usual conditions. IL-1 did stimulate SMC to produce prostanoids such as PGE1 or PGE2 that can inhibit SMC proliferation. When prostaglandin synthesis was inhibited by indomethacin or aspirin both rIL-1 alpha and beta (greater than or equal to 1 ng/ml) markedly increased SMC growth. In longer-term experiments (7-28 d) rIL-1 stimulated the growth of SMC even in the absence of cyclooxygenase inhibitors. The addition of exogenous PGE1 or PGE2 (but not PGF1 alpha, PGF2 alpha, PGI2) to indomethacin-treated SMC blocked their mitogenic response to rIL-1. Antibody to IL-1 (but not to platelet-derived growth factor [PDGF]) abolished the mitogenic response of SMC to rIL-1. Exposure of SMC to rIL-1 or PDGF caused rapid (maximal at 1 h) and transient (baseline by 3 h) expression of the c-fos proto-oncogene, determined by Northern analysis. We conclude that IL-1 is a potent mitogen for human SMC. Endogenous prostanoid production simultaneously induced by IL-1 appears to antagonize this growth-promoting effect in the short term (2 d) but not during more prolonged exposures. IL-1 produced by activated monocytes at sites of tissue inflammation or injury may thus mediate both positive and negative effects on SMC proliferation that are temporally distinct
Bell inequality for pairs of particle-number-superselection-rule restricted states
Proposals for Bell inequality tests on systems restricted by superselection
rules often require operations that are difficult to implement in practice. In
this paper, we derive a new Bell inequality, where pairs of states are used to
by-pass the superselection rule. In particular, we focus on mode entanglement
of an arbitrary number of massive particles and show that our Bell inequality
detects the entanglement in the pair when other inequalities fail. However, as
the number of particles in the system increases, the violation of our Bell
inequality decreases due to the restriction in the measurement space caused by
the superselection rule. This Bell test can be implemented using techniques
that are routinely used in current experiments.Comment: 9 pages, 6 figures; v2 is the published versio
First determination of the content of and updated determination of the contents of and
Quantum-correlated decays collected by the CLEO-c
experiment are used to perform a first measurement of , the
fractional -even content of the self-conjugate decay , obtaining a value of . An important
input to the measurement comes from the use of
and decays to tag the signal mode. This same
technique is applied to the channels and , yielding and
, where the first uncertainty is
statistical and the second systematic. These measurements are consistent with
those of an earlier analysis, based on -eigenstate tags, and can be
combined to give values of and
. The results will enable the three modes to
be included in a model-independent manner in measurements of the unitarity
triangle angle using decays, and in time-dependent
studies of violation and mixing in the system.Comment: Minor revisions following journal acceptanc
¿El tamaño y la orientación del grupo intruso afecta a la distancia de iniciación al vuelo en aves?
Wildlife managers use flight initiation distance (FID), the distance animals flee an approaching predator, to determine set back distances to minimize human impacts on wildlife. FID is typically estimated by a single person; this study examined the effects of intruder number and orientation on FID. Three different group size treatments (solitary person, two people side–by–side, two people one–behind–the–other) were applied to Pied Currawongs (Strepera graculina) and to Crimson Rosellas (Platycerus elegans). Rosellas flushed at significantly greater distances when approached by two people compared to a single person. This effect was not seen in currawongs. Intruder orientation did not influence the FID of either species. Results suggest that intruder number should be better integrated into estimates of set back distance to manage human visitation around sensitive species.Los gestores de la fauna utilizan la distancia de iniciación al vuelo (FID), la distancia a la que los animales huyen cuando se les acerca un depredador, para determinar las distancias de respuesta a fin de minimizar el impacto humano en la fauna. La FID es estimada típicamente por una sola persona; este estudio examinó los efectos del número y de la orientación del intruso en la FID. Se aplicaron tres tratamientos distintos de tamaño del grupo (persona solitaria, dos personas una al lado de la otra, dos personas una detras de la otra) a currawongs cálidos (Strepera graculina) y a pericos elegantes (Platycerus elegans). Los pericos elegantes huían a distancias perceptiblemente mayores cuando se le acercaban dos personas que cuando se le acercaba una sola. Este efecto no fue observado en los currawongs pálidos. La orientación del intruso no influenció en la FID de ninguna especie. Los resultados sugieren que el número de intrusos debería ser considerado en las estimaciones de las distancias de respuesta, para poder gestionar las visitas de personas cerca de especies sensibles
1862-08-21 Lieutenant J.S. Libby recommends brother Henry for lieutenant
https://digitalmaine.com/cw_me_16th_regiment_corr/1080/thumbnail.jp
Automatic Quantification of Epidermis Curvature in H&E Stained Microscopic Skin Image of Mice
Changes in the curvature of the epidermis layer is often associated with many skin disorders, such as ichthyoses and generic effects of ageing. Therefore, methods to quantify changes in the curvature are of a scientific and clinical interest. Manual methods to determine curvature are both laborious and intractable to large scale investigations. This paper proposes an automatic algorithm to quantify curvature of microscope images of H&E-stained murine skin. The algorithm can be divided into three key stages. First, skin layers segmentation based on colour deconvolution to separate the original image into three channels of different representations to facilitate segmenting the image into multiple layers, namely epidermis, dermis and subcutaneous layers. The algorithm then further segments the epidermis layer into cornified and basal sub-layers. Secondly, it quantifies the curvature of the epidermis layer by measuring the difference between the epidermis edge and a straight line (theoretical reference line) connecting the two far sides of the epidermis edge. Finally, the curvature measurements extracted from a large number of images of mutant mice are used to identify a list of genes responsible for changes in the epidermis curvature. A dataset of 5714 H&E microscopic images of mutant and wild type mice were used to evaluate the effectiveness of the algorithm
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