Photonic Burst Research Articles

Optimum drift velocity for single molecule fluorescence bursts in micro/nano-fluidic channels

Photonic burst histograms can be used to identify single protein molecules in micro/nano-fluidic channels provided the width of the histogram is narrow. Photonic shot noise and residence time fluctuations, caused by longitudinal diffusion, are the major sources of the histogram width. This Communication is a sequel to an earlier Letter of ours [L. L. Kish et al., Appl. Phys. Lett. 99, 143121 (2011)] and demonstrates that, for a given diffusion coefficient, an increase of the drift velocity enhances the relative shot noise and decreases the relative residence time fluctuations. This leads to an optimum drift velocity which minimizes the histogram width and maximizes the ability to identify single molecules, which is an important result for applications.

Versatile optical code-based MPLS for circuit, burst, and packet switchings

We will present versatile optical code (OC)-based photonic MPLS, so-called OC-MPLS which ranges from circuit switching, burst switching, to packet switching. OC-label is an identifier attached to the data, of which information is mapped onto an optical code, a sequence of optical pulses. The OC-label recognition is performed by the optical correlation between an incoming OC-label and the OC-label entries. Unique to the OC-label processing is that it is analog operation entirely in optical domain, and no optical logic operation is involved, therefore, the processing speed is only limited by the propagation delay in the optical correlator, which is a passive optical device. This is a key to the ultrahigh-speed processing capability. Circuit switching of OC-label switched path (OC-LSP) is characterized by the finer data granularity than the wavelength path of GMPS, resulting in a better bandwidth efficiency. In a one-way reservation protocol of photonic burst switching, the OC-labeled control packet improves the throughput by nearly cutting the offset time between the control packet and the following data burst. OC-labeled header of the packet can enables the ultrafast routing in photonic packet switching. To exploit the ultrafast routing capability, a new packet switch architecture is investigated, in which the longest-prefix match algorithm as well as WDM buffering into the fiber delay lines are introduced.

Photonic burst switching (pbs) architecture for hop and span-constrained optical networks

The paper presents a new architecture, called photonic burst switching (PBS), with variable time slot provisioning, supporting high-speed bursty data transmission within hop and span-constrained networks. First, the edge and switching node architecture for in-band and out-of-band signaling is defined with optical switch fabric performance parameters. Second, the edge router regions of operation for burst assembly are studied via simulations. Third, we introduce: (i) a GMPLS-based PBS software architecture in terms of control and data plane operations that is extended to enable the PBS optical interfaces with software building blocks for edge and switching nodes; (ii) an adaptive PBS MAC layer functionality and framing of multiple generic payloads. The integration of the proposed PBS network architecture with low-cost optical switching fabrics and GMPLS-based software architecture should provide the means for robust and efficient optical transport of bandwidth-demanding applications within enterprise networks.

The antithrombotic factor singlet oxygen/light (1O2/h nu).

Activated phagocytes (especially polymorphonuclear granulocytes (PMNs)) by respiratory oxidative/photonic burst (activation of NADPH-oxidase and myeloper-oxidase) generate large amounts of oxidants of the hypochlorite-/chloramine-type, which are physiologic sources for singlet oxygen (1O2), a nonradical-excited (photon (h nu) emitting) oxygen species [Weiss SJ, NEJM 1989;320:365-376]. In vitro experiments show that 1O2 (1) inhibits coagulation by inactivation of thrombocytes, fibrinogen, factor V, factor VIII, and factor X and (2) activates fibrinolysis by inactivation of the main fibrinolysis inhibitors plasminogen activator inhibitor (PAI)-1 and alpha-2-antiplasmin, and by activation of single-chain urokinase by plasmin and oxidized fibrin. Additionally, this work suggests that 1O2/h nu acts antithrombotically, inducing selective thrombolysis in vivo (i.e., thrombolysis induced by 0.1 to 0.5 mmol/l chloramine within 30 to 60 minutes without changes of the plasmatic hemostasis system). 1O2 might activate flowing to (on the endothelium) rolling PMN, increasing their chance to get in contact with fibrin/platelet aggregates deposited on the endothelial layer. Via 1O2 generation, the thrombus-activated phagocytes might call for (acute, physiologic) inflammation/fibrinolysis amplification, resulting in the "moving front" of PMN, which infiltrates and destroys the thrombus. 1O2 seems to (partially) participate in the reactivity of nitric oxide, another prooxidative agent. The inhibition of physiologic amounts of 1O2 by blood cholesterol might be involved in the pathogenesis of atherothrombosis. Consequently, it is suggested that activated PMNs modulate hemostasis, shifting it into an antithrombotic state; this cellular part of fibrinolysis seems to be of greater physiologic importance than the plasmatic one. Impaired PMN function (e.g., as occurring in patients with antineutrophil cytoplasmic antibodies or under cytostatic treatments) often results in serious thrombotic complications. Light is the only signal whose origin can be immediately recognized by a fast moving cell in the (dark) blood stream. The cell signal action of 1O2/h nu (e.g., released by chloramines such as taurine-chloramine or vancomycin, by fiberoptic, by photodynamic therapy, or by so-called redox-cycling drugs such as quinones or tetracyclines) might be a new and physiologic principle for pharmacologic intervention in atherothrombosis.

Platelet-activating factor and granulocyte-mediated oxidative stress. Strategy for in vivo oxyradical visualization.

Platelet-activating factor (PAF) and leukotriene B4 are potent lipid mediators of endothelium-granulocyte interaction which results in granulocyte-dependent increased microvascular permeability. The specific mechanism by which PAF induces granulocyte-mediated endothelial injury has not been fully investigated. Digital imaging photonic intensified microscopy has revealed that PAF effectively induces granulocyte-mediated oxidative stress on microvascular beds. The method has made it possible to visualize luminol-dependent photonic burst released from PAF-treated microvascular beds in the rat mesentery. The photonic activities clearly corresponded to the localization of sticking granulocytes in post-capillary venules. By contrast, no significant chemilumigenic response could be detected in the leukotriene B4-induced activation of endothelium-granulocyte interaction in vivo. The present findings suggest that oxygen radicals are not prerequisites for granulocyte adhesion in the microcirculation and provide evidence for a dissociation of in vivo granulocyte function between leukotactic and oxidative activation in leukotriene B4-induced microvascular changes.

炎症メディエーターによる血管内皮―か粒球相互反応活性化と活性酸素放出反応の生体内撮像 ＰＡＦおよびｌｅｕｋｏｔｒｉｅｎｅ Ｂ４の作用

Oxyradicaldependent chemiluminescence from granulocytes was visualized in rat mesenteric microvascular beds treated with platelet-activating factor (PAF), leukotriene B4 (LTB4) and bacterial chemotactic peptide (FMLP) by means of digital imaging photonic intensified microscopy. The topical application of PAF-acether (100 nM) caused remarkable granulocyte adherence on venular endothelial walls and the subsequent activation of a luminol-dependent photonic burst. Chemilumigenic sites clearly corresponded to the spatial distribution of sticking cells in post-capillary venules. LTB4 and FMLP, however, did not induce any significant photonic burst at concentrations which caused adherent changes between endothelial cells and granulocytes.These findings suggest that PAF may play a role in granulocyte-mediated oxidative stress on venular endothelial cells during acute inflammatory processes, and also provide the first evidence of an intravital oxidative burst of granulocytes in microcirculatory disturbances.

In vivo visualization of oxyradical-dependent photoemission during endothelium-granulocyte interaction in microvascular beds treated with platelet-activating factor.

Oxyradical-dependent chemiluminescence from granulocytes sticking to venular endothelium was successfully visualized in rat mesenteric microvascular beds treated with platelet-activating factor (PAF). Intravital photonic image intensifier microscopy revealed that topical application of PAF-acether (100 nM) caused remarkable granulocyte adherence on endothelial walls and the subsequent activation of a luminol-dependent photonic burst. Chemilumigenic sites clearly corresponded to the spatial distribution of sticking cells in post-capillary venules. The present findings thus serve as the first demonstration of an intravital oxidative burst of granulocytes on venular endothelium in PAF-induced microcirculatory disturbances.

Effects of serine protease inhibitors on oxyradical burst from phagocytizing neutrophils--analysis by chemiluminescence counting and its microscopic imaging.

Reaction difference of oxyradical generation and luminol-dependent photoemission of zymosan- and phorbol ester-treated neutrophils were investigated using a conventional photomultiplier and ultrasensitive photonic imaging technique. Zymosan-treated cells released a concentrated photonic burst corresponding to the cellular distribution. In contrast, phorbol ester-treated cells produced a negligible level of photoemission, and the additional application of Ca2+ ionophore enhanced the photonic burst, which was gradually spread out into extracellular space. Serine protease inhibitors did not attenuate PMA-induced chemiluminescence but did attenuate zymosan-induced chemiluminescence. This suggests the involvement of serine protease in the respiratory burst of phagocytizing neutrophils.

Luminol-dependent photoemission from single neutrophil stimulated by phorbol ester and calcium ionophore — role of degranulation and myeloperoxidase

Luminol-dependent photonic burst from phorbol ester-treated single neutrophil was visually investigated by using an ultrasensitive photonic image intensifier microscope. Neutrophils stimulated by phorbol myristate acetate (0.1 microgram/ml) alone produced a negligible level of photonic activities in the presence of luminol (10 micrograms/ml). The additional application of 0.1 microM Ca2+ ionophore A23187 induced explosive changes of photonic burst corresponding to the distribution of neutrophils, and these photonic activities were gradually spread to extracellular space. Sodium azide, which prevents myeloperoxidase activity, inhibited Ca2+ ionophore-induced photonic burst from phorbol ester-treated neutrophil. These findings suggest a prerequisite role of degranulation and myeloperoxidase release in luminol-dependent photoemission from stimulated neutrophils.

Real-time visualization of oxyradical burst from single neutrophil by using ultrasensitive video intensifier microscopy.

Dynamics of oxyradical burst from single human neutrophils stimulated by opsonized zymosan was visualized by using an ultrasensitive video intensifier microscopy in the presence of chemiluminescence probe. Luminol-dependent photonic burst activities were clearly corresponding to the distribution of zymosan-treated neutrophils. Heterogeneity of photon-bursting period and the maximum photonic intensity among reactive cells was demonstrated. This may reflect functional heterogeneity of the ability to release oxyradicals among neutrophils.