Optimality and strong stability of control systems

Optimality and strong stability of control syste

Gritchenko

Retrospective Exhibit of the artwork of Alexis Gritchenko, February 27- March 5, 1972https://digitalcommons.lasalle.edu/exhibition_catalogues/1005/thumbnail.jp

Lyapunov Control on Quantum Open System in Decoherence-free Subspaces

A scheme to drive and manipulate a finite-dimensional quantum system in the decoherence-free subspaces(DFS) by Lyapunov control is proposed. Control fields are established by Lyapunov function. This proposal can drive the open quantum system into the DFS and manipulate it to any desired eigenstate of the free Hamiltonian. An example which consists of a four-level system with three long-lived states driven by two lasers is presented to exemplify the scheme. We have performed numerical simulations for the dynamics of the four-level system, which show that the scheme works good.Comment: 5 pages, 6 figure

Gene induction during differentiation of human monocytes into dendritic cells: an integrated study at the RNA and protein levels

Changes in gene expression occurring during differentiation of human monocytes into dendritic cells were studied at the RNA and protein levels. These studies showed the induction of several gene classes corresponding to various biological functions. These functions encompass antigen processing and presentation, cytoskeleton, cell signalling and signal transduction, but also an increase in mitochondrial function and in the protein synthesis machinery, including some, but not all, chaperones. These changes put in perspective the events occurring during this differentiation process. On a more technical point, it appears that the studies carried out at the RNA and protein levels are highly complementary.Comment: website publisher: http://www.springerlink.com/content/ha0d2c351qhjhjdm

Research in the general area of non-linear dynamical systems Final report, 8 Jun. 1965 - 8 Jun. 1967

Nonlinear dynamical systems research on systems stability, invariance principles, Liapunov functions, and Volterra and functional integral equation

Collapse in the nonlocal nonlinear Schr\"odinger equation

We discuss spatial dynamics and collapse scenarios of localized waves governed by the nonlinear Schr\"{o}dinger equation with nonlocal nonlinearity. Firstly, we prove that for arbitrary nonsingular attractive nonlocal nonlinear interaction in arbitrary dimension collapse does not occur. Then we study in detail the effect of singular nonlocal kernels in arbitrary dimension using both, Lyapunoff's method and virial identities. We find that for for a one-dimensional case, i.e. for $n=1$, collapse cannot happen for nonlocal nonlinearity. On the other hand, for spatial dimension $n\geq2$ and singular kernel $\sim 1/r^\alpha$, no collapse takes place if $\alpha<2$, whereas collapse is possible if $\alpha\ge2$. Self-similar solutions allow us to find an expression for the critical distance (or time) at which collapse should occur in the particular case of $\sim 1/r^2$ kernels. Moreover, different evolution scenarios for the three dimensional physically relevant case of Bose Einstein condensate are studied numerically for both, the ground state and a higher order toroidal state with and without an additional local repulsive nonlinear interaction. In particular, we show that presence of an additional local repulsive term can prevent collapse in those cases

Platelet FcγRIIA-induced serotonin release exacerbates the severity of Transfusion-Related Acute Lung Injury in mice

Transfusion-related acute lung injury (TRALI) remains a major cause of transfusion-related fatalities. The mechanism of human antibody-mediated TRALI, especially the involvement of the Fcγ receptors, is not clearly established. Contrary to mice, human platelets are unique in their expression of the FcγRIIA/CD32A receptor, suggesting that our understanding of the pathogenesis of antibody-mediated TRALI is partial, as the current murine models incompletely recapitulate the human immunology. We evaluated the role of FcγRIIA/CD32A in TRALI using a humanized mouse model expressing the FcγRIIA/CD32A receptor. When challenged with a recombinant chimeric human immunoglobulin G1/mouse anti–major histocompatibility complex class I monoclonal antibody, these mice exhibited exacerbated alveolar edema and higher mortality compared with wild-type (WT) mice. Unlike in WT mice, monocytes/macrophages in CD32A(+) mice were accessory for TRALI initiation, indicating the decisive contribution of another cell type. Platelet activation was dramatically increased in CD32A(+) animals, resulting in their increased consumption and massive release of their granule contents. Platelet depletion prevented the exacerbation of TRALI in CD32A(+) mice but did not affect TRALI in WT animals. By blocking platelet serotonin uptake with fluoxetine, we showed that the severity of TRALI in CD32A(+) mice resulted from the serotonin released by the activated platelets. Furthermore, inhibition of 5-hydroxytryptamine 2A serotonin receptor with sarpogrelate, before or after the induction of TRALI, abolished the aggravation of lung edema in CD32A(+) mice. Our findings show that platelet FcγRIIA/CD32A activation exacerbates antibody-mediated TRALI and provide a rationale for designing prophylactic and therapeutic strategies targeting the serotonin pathway to attenuate TRALI in patients

Phenotypic Studies of Natural Killer Cell Subsets in Human Transporter Associated with Antigen Processing Deficiency

Peripheral blood natural killer (NK) cells from patients with transporter associated with antigen processing (TAP) deficiency are hyporesponsive. The mechanism of this defect is unknown, but the phenotype of TAP-deficient NK cells is almost normal. However, we noticed a high percentage of CD56bright cells among total NK cells from two patients. We further investigated TAP-deficient NK cells in these patients and compared them to NK cells from two other TAP-deficient patients with no clinical symptoms and to individuals with chronic inflammatory diseases other than TAP deficiency (chronic lung diseases or vasculitis). Peripheral blood mononuclear cells isolated from venous blood were stained with fluorochrome-conjugated antibodies and the phenotype of NK cells was analyzed by flow cytometry. In addition, 51Chromium release assays were performed to assess the cytotoxic activity of NK cells. In the symptomatic patients, CD56bright NK cells represented 28% and 45%, respectively, of all NK cells (higher than in healthy donors). The patients also displayed a higher percentage of CD56dimCD16− NK cells than controls. Interestingly, this unusual NK cell subtype distribution was not found in the two asymptomatic TAP-deficient cases, but was instead present in several of the other patients. Over-expression of the inhibitory receptor CD94/NKG2A by TAP-deficient NK cells was confirmed and extended to the inhibitory receptor ILT2 (CD85j). These inhibitory receptors were not involved in regulating the cytotoxicity of TAP-deficient NK cells. We conclude that expansion of the CD56bright NK cell subtype in peripheral blood is not a hallmark of TAP deficiency, but can be found in other diseases as well. This might reflect a reaction of the immune system to pathologic conditions. It could be interesting to investigate the relative distribution of NK cell subsets in various respiratory and autoimmune diseases