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Disaster Recovery Tags > Tag based links for Loss

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  1. Estrogen deficiency, T cells and bone loss.: Cellular immunology, Vol. 252, No. 1-2. (r 2008), pp. 68-80.Estrogen plays a fundamental role in the maintenance of skeletal homeostasis. Although estrogen is established to have direct effects on bone cells, animal studies have identified additional regulatory effects of estrogen centered at the level of the adaptive immune response. Furthermore, a potential role for reactive oxygen species has now been identified in both humans and animals. One of the major challenges has been to integrate a multitude of redundant pathways and cytokines, that all appear capable of playing a relevant role, into a global model of postmenopausal osteoporosis. This review presents our current understanding of the process of estrogen deficiency mediated bone destruction and explores some of the most recent findings and hypotheses to explain estrogen action in bone.R Pacifici

    Source: Cellular immunology, Vol. 252, No. 1-2. (r 2008), pp. 68-80.

  2. Estrogen deficiency increases osteoclastogen esis up-regulating T cells activity: a key mechanism in osteoporosis.: Bone, Vol. 43, No. 1. (July 2008), pp. 92-100.Compell ing evidences suggest that increased production of osteoclastogen ic cytokines by activated T cells plays a relevant role in the bone loss induced by estrogen deficiency in the mouse. However, little information is available on the role of T cells in post-menopausa l bone loss in humans. To investigate this issue we have assessed the production of cytokines involved in osteoclastogen esis (RANKL, TNFalpha and OPG), in vitro osteoclast (OC) formation in pre and post-menopausa l women, the latter with or without osteoporosis. We evaluated also OC precursors in peripheral blood and the ability of peripheral blood mononuclear cells to produce TNFalpha in both basal and stimulated condition by flow cytometry in these subjects. Our data demonstrate that estrogen deficiency enhances the production of the pro-osteoclast ogenetic cytokines TNFalpha and RANKL and increases the number of circulating OC precursors. Furthermore, we show that T cells and monocytes from women with osteoporosis exhibit a higher production of TNFalpha than those from the other two groups. Our findings suggest that estrogen deficiency stimulates OC formation both by increasing the production of TNFalpha and RANKL and increasing the number of OC precursors. Women with post-menopausa l osteoporosis have a higher T cell activity than healthy post-menopausa l subjects; T cells thus contribute to the bone loss induced by estrogen deficiency in humans as they do in the mouse.P D'Amelio, A Grimaldi, S Di Bella, SZ Brianza, MA Cristofaro, C Tamone, G Giribaldi, D Ulliers, GP Pescarmona, G Isaia

    Source: Bone, Vol. 43, No. 1. (July 2008), pp. 92-100.

  3. T cells: unexpected players in the bone loss induced by estrogen deficiency and in basal bone homeostasis.: Annals of the New York Academy of Sciences, Vol. 1116 (November 2007), pp. 360-375.The bone-immune interface has become a subject of intense interest in recent years. It has long been recognized that infection, inflammation, and autoimmune disorders are associated with systemic and local bone loss. Yet, it is only recently that T lymphocytes and their products have been recognized as key regulators of osteoclast formation, life span, and activity. Similarly, sex steroids and aging have been known to regulate the immune system and T cells for decades. In spite of the abundance of clinical and physiological clues, it is only in the last few years that investigators have linked immune cells to the etiology of postmenopausal and senile osteoporosis, as well as to the bone loss caused by a variety of endocrine conditions. As surprising is new evidence showing that in contrast to their bone destructive effects under certain pathological conditions, T cells are highly protective of basal bone homeostasis, through complex regulatory effects on osteoprotegeri n (OPG) production by B cells, involving CD40 to CD40 Ligand (CD40L) costimulation. This article examines the experimental evidence suggesting that estrogen prevents bone loss by regulating T cell function, and that T cell costimulation with B cells is critical for OPG production and maintenance of basal bone homeostasis.MN Weitzmann, R Pacifici

    Source: Annals of the New York Academy of Sciences, Vol. 1116 (November 2007), pp. 360-375.

  4. End-to-end packet delay and loss behavior in the internet: SIGCOMM Comput. Commun. Rev., Vol. 23, No. 4. (October 1993), pp. 289-298.Jean-C hrysotome Bolot

    Source: SIGCOMM Comput. Commun. Rev., Vol. 23, No. 4. (October 1993), pp. 289-298.

  5. A Performance Study of Loss Detection/Reco very in Real-world TCP Implementation s: Network Protocols, 2007. ICNP 2007. IEEE International Conference on (2007), pp. 256-265.TCP is the dominant transport protocol used in the Internet and its performance fundamentally governs the performance of Internet applications. It is well-known that packet losses can adversely affect the connection duration of TCP connections - however, what is not fully understood is how well does the TCP design deal with losses. In this paper, we systematically evaluate the impact of design parameters associated with TCP's loss detection/reco very mechanisms on the performance of real-world TCP connections. For this, we rely on an analysis tool that partially emulates the sender-side TCP implementation s of 5 prominent OSes for passively analyzing the traces of TCP connections. Our study conducts passive analysis of more than 2.8 million real Internet TCP connections. We find that the recommended as well as widely-impleme nted settings of TCP parameters are not optimal for a significant fraction of Internet connections.S Rewaskar, J Kaur, FD Smith

    Source: Network Protocols, 2007. ICNP 2007. IEEE International Conference on (2007), pp. 256-265.

  6. Loss as a lifelong regenerative learning process: Psychodynamic Counselling, Vol. 7, No. 4. (1 November 2001), pp. 413-430.Griffi n, David

    Source: Psychodynamic Counselling, Vol. 7, No. 4. (1 November 2001), pp. 413-430.

  7. Attachment, loss, and complicated grief.: Developmental Psychobiology, Vol. 47, No. 3. (November 2005), pp. 253-267.Bereav ement is a highly disruptive experience that is usually followed by a painful but time-limited period of acute grief. An unfortunate minority of individuals experience prolonged and impairing complicated grief, an identifiable syndrome that differs from usual grief, major depression, and other DSM IV diagnostic entities. Underlying processes guiding symptoms are not well understood for either usual or complicated grief. We propose a provisional model of bereavement, guided by Myron Hofer's question "What exactly is lost when a loved one dies?" We integrate insights about biobehavioral regulation from Hofer's animal studies of infant separation, research on adult human attachment, and new ideas from bereavement research. In this model, death of an attachment figure produces a state of traumatic loss and symptoms of acute grief. These symptoms usually resolve following revision of the internalized representation of the deceased to incorporate the reality of the death. Failure to accomplish this integration results in the syndrome of complicated grief.K Shear, H Shair

    Source: Developmental Psychobiology, Vol. 47, No. 3. (November 2005), pp. 253-267.

  8. Adaptive Evolution of Eye Degeneration in the Mexican Blind Cavefish: Journal of Heredity, Vol. 96, No. 3. (May 2005), pp. 185-196.WR Jeffery

    Source: Journal of Heredity, Vol. 96, No. 3. (May 2005), pp. 185-196.

  9. Relevance of sub-surface chip layers for the lifetime of magnetically trapped atoms: The European Physical Journal D - Atomic, Molecular, Optical and Plasma Physics, Vol. 35, No. 1. (2005), pp. 97-104.We investigate the lifetime of magnetically trapped atoms above a planar, layered atom chip structure. Numerical calculations of the thermal magnetic noise spectrum are performed, based on the exact magnetic Green function and multi layer reflection coefficients. We have performed lifetime measurements where the center of a side guide trap is laterally shifted with respect to the current carrying wire using additional bias fields. Comparing the experiment to theory, we find a fair agreement and demonstrate that for a chip whose topmost layer is metallic, the magnetic noise depends essentially on the thickness of that layer, as long as the layers below have a much smaller conductivity; essentially the same magnetic noise would be obtained with a metallic membrane suspended in vacuum. Based on our theory we give general scaling laws of how to reduce the effect of surface magnetic noise on the trapped atoms.B Zhang, C Henkel, E Haller, S Wildermuth, S Hofferberth, P Krüger, J Schmiedmayer

    Source: The European Physical Journal D - Atomic, Molecular, Optical and Plasma Physics, Vol. 35, No. 1. (2005), pp. 97-104.

  10. Reduction of magnetic noise in atom chips by material optimization: The European Physical Journal D - Atomic, Molecular, Optical and Plasma Physics, Vol. 35, No. 1. (2005), pp. 87-95.We discuss the influence of the material type in metal wires to the electromagneti c fluctuations in magnetic microtraps close to the surface of an atom chip. We show that significant reduction of the magnetic noise can be achieved by replacing the pure noble metal wires with their dilute alloys. The alloy composition provides an additional degree of freedom which enables a controlled reduction of both magnetic noise and resistivity if the atom chip is cooled. In addition, we provide a careful re-analysis of the magnetically induced trap loss observed by Yu-Ju Lin et al. [Phys. Rev. Lett. 92, 050404 (2004)] and find good agreement with an improved theory.V Dikovsky, Y Japha, C Henkel, R Folman

    Source: The European Physical Journal D - Atomic, Molecular, Optical and Plasma Physics, Vol. 35, No. 1. (2005), pp. 87-95.

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