Unveiling the Enhancement of Spontaneous Emission at Exceptional Points.

Exceptional points (EPs), singularities of non-Hermitian physics where complex spectral resonances degenerate, are one of the most exotic features of nonequilibrium open systems with unique properties. For instance, the emission rate of quantum emitters placed near resonators with EPs is enhanced (compared to the free-space emission rate) by a factor that scales quadratically with the resonance quality factor. Here, we verify the theory of spontaneous emission at EPs by measuring photoluminescence from photonic-crystal slabs that are embedded with a high-quantum-yield active material. While our experimental results verify the theoretically predicted enhancement, they also highlight the practical limitations on the enhancement due to material loss. Our designed structures can be used in applications that require enhanced and controlled emission, such as quantum sensing and imaging.

1D and 2D arrays of coupled photonic crystal cavities with a site-controlled quantum wire light source.

We investigated experimentally 1D and 2D arrays of coupled L3 photonic crystal cavities. The optical modes of the coupled cavity arrays are fed by a site-controlled quantum wire light source. By performing photoluminescence measurements and relying on near-field calculation of the cavitiy modes, we evidence optical coupling between the cavities as well as supermode delocalization. In particular, for small cavity separations, fabrication induced disorder effects are shown to be negligible compared to optical coupling between cavities.

Propagation and amplification dynamics of 1D polariton condensates.

The dynamics of propagating polariton condensates in one-dimensional microcavities is investigated through time resolved experiments. We find a strong increase in the condensate intensity when it travels through the nonresonantly excited area. This amplification is shown to come from bosonic stimulated relaxation of reservoir excitons into the polariton condensate, allowing for the repopulation of the condensate through nonresonant pumping. Thus, we experimentally demonstrate a polariton amplifier with a large band width, opening the way towards the transport of polaritons with high densities over macroscopic distances.

Backscattering suppression in supersonic 1D polariton condensates.

We investigate the effect of disorder on the propagation of one-dimensional polariton condensates in semiconductor microcavities. We observe a strong suppression of the backscattering produced by the imperfections of the structure when increasing the condensate density. This suppression occurs in the supersonic regime and is simultaneous to the onset of parametric instabilities which enable the "hopping" of the condensate through the disorder. Our results evidence a new mechanism for the strong scattering reduction of polaritons at high speeds.

Design and investigation of surface addressable photonic crystal cavity confined band edge modes for quantum photonic devices.

We propose to use a localized Γ-point slow Bloch mode in a 2D-Photonic Crystal (PC) membrane to realize an efficient surface emitting source. This device can be used as a quantum photonic device, e.g. a single photon source. The physical mechanisms to increase the Q/V factor and to improve the directivity of the PC microcavity rely on a fine tuning of the geometry in the three directions of space. The PC lateral mirrors are first engineered in order to optimize photons confinement. Then, the effect of a Bragg mirror below the 2DPC membrane is investigated in terms of out-of-plane leakages and far field emission pattern. This photonic heterostructure allows for a strong lateral confinement of photons, with a modal volume of a few (λ/n)3 and a Purcell factor up to 80, as calculated by two different numerical methods. We finally discuss the efficiency of the single photon source for different collection set-up.

3D integration of photonic crystal devices: vertical coupling with a silicon waveguide.

Two integrated devices based on the vertical coupling between a photonic crystal microcavity and a silicon (Si) ridge waveguide are presented in this paper. When the resonator is coupled to a single waveguide, light can be spectrally extracted from the waveguide to free space through the far field emission of the resonator. When the resonator is vertically coupled to two waveguides, a vertical add-drop filter can be realized. The dropping efficiency of these devices relies on a careful design of the resonator. In this paper, we use a Fabry-Perot (FP) microcavity composed of two photonic crystal (PhC) slab mirrors. Thanks to the unique dispersion properties of slow Bloch modes (SBM) at the flat extreme of the dispersion curve, it is possible to design a FP cavity exhibiting two quasi-degenerate modes. This specific configuration allows for a coupling efficiency that can theoretically achieve 100%. Using 3D FDTD calculations, we discuss the design of such devices and show that high dropping efficiency can be achieved between the Si waveguides and the PhC microcavity.

Slow Bloch mode confinement in 2D photonic crystals for surface operating devices.

2D photonic crystal (2DPC) structures consisting in 2D silicon nanopillar arrays in silica are investigated. The main motivation of this work lies in that 2D rod arrays should be easily combined with refractive structures (e. g. micro-wire waveguides), unlike 2DPC consisting in hole lattices. Such an association is expected to lead to both new functionalities and larger scale integration. In this paper, we study the loss mechanism for non degenerated Bloch modes located at Gamma-point in a 2DPC slab constituted by a square lattice of silicon rods in silica. For such modes, we show that the quality factor is mainly governed by the lateral losses. To further inhibit the lateral losses, a photonic heterostructure is used. 3D FDTD calculations show that quality factors of 4000 are achieved. To reduce the vertical losses, the 2DPC heterostructure is associated with a vertical Bragg mirror, thus resulting in very high quality factors (>40000).

Increased faecal serine protease activity in diarrhoeic IBS patients: a colonic lumenal factor impairing colonic permeability and sensitivity.

OBJECTIVES: Diarrhoea-predominant irritable bowel syndrome (IBS-D) is characterised by elevated colonic lumenal serine protease activity. The aims of this study were (1) to investigate the origin of this elevated serine protease activity, (2) to evaluate if it may be sufficient to trigger alterations in colonic paracellular permeability (CPP) and sensitivity, and (3) to examine the role of the proteinase-activated receptor-2 (PAR-2) activation and signalling cascade in this process. PATIENTS AND METHODS: Faecal enzymatic activities were assayed in healthy subjects and patients with IBS, ulcerative colitis and acute infectious diarrhoea. Following mucosal exposure to supernatants from control subjects and IBS-D patients, electromyographic response to colorectal balloon distension was recorded in wild-type and PAR-2(-/-) mice, and CPP was evaluated on colonic strips in Ussing chambers. Zonula occludens-1 (ZO-1) and phosphorylated myosin light chain were detected by immunohistochemistry. RESULTS: The threefold increase in faecal serine protease activity seen in IBS-D patients compared with constipation-predominant IBS (IBS-C) or infectious diarrhoea is of neither epithelial nor inflammatory cell origin, nor is it coupled with antiprotease activity of endogenous origin. Mucosal application of faecal supernatants from IBS-D patients in mice evoked allodynia and increased CPP by 92%, both of which effects were prevented by serine protease inhibitors and dependent on PAR-2 expression. In mice, colonic exposure to supernatants from IBS-D patients resulted in a rapid increase in the phosphorylation of myosin light chain and delayed redistribution of ZO-1 in colonocytes. CONCLUSIONS: Elevated colonic lumenal serine protease activity of IBS-D patients evokes a PAR-2-mediated colonic epithelial barrier dysfunction and subsequent allodynia in mice, suggesting a novel organic background in the pathogenesis of IBS.

Colonic luminal proteases activate colonocyte proteinase-activated receptor-2 and regulate paracellular permeability in mice.

Luminal activation of protease-activated receptors-2 (PAR(2)) on colonocytes by trypsin or PAR(2)-activating peptide increases colonic paracellular permeability (CPP). The aim of this study was to evaluate the role of proteases from endogenous and bacterial origin in the modulation of CPP and colonocyte PAR(2) expression in mice. CPP was assessed with (51)Cr-EDTA after intracolonic administration of different protease inhibitors. After 12 days of oral antibiotic treatment, measurements of colonic luminal serine protease activity (CLSPA), CPP, mucosal mouse mast cell proteinase-1 (MMCP-1) content, immunochemistry of PAR(2) and assessment of effects of PAR(2) agonist (SLIGRL) and mast cell degranulator (C48/80) on CPP in Ussing chambers were performed. Immunochemistry was repeated after intracolonic trypsin administration. Colonic infusion of protease inhibitors significantly reduced CPP. In antibiotic-treated mice, CLSPA was reduced coupled with a decrease in PAR(2) expression, but with no change in CPP and MMCP-1 content. Trypsin administration restored PAR(2) expression. The increase in CPP induced by SLIGRL and C48/80 was reduced after antibiotic treatment. Protease activity of colonic content plays an important role in the regulation of mucosal barrier through activation of PAR(2).

Phenotypic changes in colonocytes following acute stress or activation of mast cells in mice: implications for delayed epithelial barrier dysfunction.

BACKGROUND AND AIMS: Stressful life events are known to modulate the development or relapse of disease in both inflammatory bowel disease and irritable bowel disease patients but underlying mechanisms remain unclear. Stress is known to effect mast cells, interferon gamma (IFN-gamma), and myosin light chain phosphorylation to trigger colonic epithelial barrier dysfunction. The aim of this study was to investigate whether acute stress induced or chemical mast cell activation impaired expression and function of epithelial tight junctions, and altered colonocyte differentiation in mice. METHODS: Colonic paracellular permeability was assessed as the in vivo lumen to blood ratio of 51Cr-EDTA in different groups of mice (controls, stressed, mast cell degranulator BrX-537A treated), pretreated or not with the mast cell stabiliser doxantrazole. Involvement of mast cells and IFN-gamma was evaluated in wild-type and IFN-gamma deficient mice. Tight junction alteration was assessed by histology, transmission electron microscopy, and real time reverse transcription-polymerase chain reaction. Colonocyte differentiation was determined by protein kinase C zeta (PKCzeta) immunofluorescence and western blotting, and alkaline phosphatase activity assay. RESULTS: Acute stress induced a three day delayed increase in colonic paracellular permeability which involved mast cell degranulation and overproduction of IFN-gamma. The colonic epithelial barrier was morphologically altered and expression of mRNA encoding tight junction proteins ZO-2 and occludin was decreased. Moreover, three days after acute stress, colonocyte differentiation was reduced, as shown by decreased expression of both PKCzeta isotype and alkaline phosphatase. CONCLUSION: These data highlight new mechanisms whereby an acute stress acts on the gastrointestinal tract by inducing alterations in colonocyte differentiation and decreased expression of mRNA encoding tight junction proteins. Thus phenotypic changes in colonocytes could pave the way for stress related intestinal disorders.

Neonatal maternal deprivation triggers long term alterations in colonic epithelial barrier and mucosal immunity in rats.

BACKGROUND: Stressful events in the early period of life (for example, maternal deprivation) have been shown to modify adult immune and gastrointestinal tract functions. The present study aimed to establish whether maternal deprivation affects colonic epithelial barrier and the development of an experimental colitis in adult rats. METHODS: Male Wistar rat pups were separated during postnatal days 2-14 or left undisturbed with their dam. At 12 weeks of age, we assessed colonic paracellular permeability, bacterial translocation, myeloperoxidase (MPO) activity, mucosal mast cell density, cytokine (interleukin (IL)-1 beta, IL-2, IL-4, IL-10, and interferon gamma (IFN-gamma)) mRNA expression, and macroscopic damage. Total gut permeability, MPO activity, and macroscopic damage were also assessed four days after intracolonic administration of 2,4,6-trinitrobenzenesulphonic acid (TNBS). RESULTS: Maternal deprivation triggered a significant increase in colonic permeability associated with bacterial translocation into the mesenteric lymph nodes, liver, and spleen. These alterations were associated with some macroscopic damage and an increase in colonic MPO activity, mucosal mast cell density, and cytokine mRNA expression. Intracolonic infusion of TNBS induced a significantly higher inflammatory reaction in separated animals, as judged by enhanced MPO colonic levels, total gut permeability, and macroscopic lesions. CONCLUSIONS: Maternal deprivation promotes long term alterations in the colonic epithelial barrier associated with an exaggerated immune response to an external immune stimulus. This suggests a role for early psychological factors in the regulation of colonic mucosal barrier in later life.

Short-chain fatty acids induce cytoskeletal and extracellular protein modifications associated with modulation of proliferation on primary culture of rat intestinal smooth muscle cells.

Short-chain fatty acids are the main end products of bacterial fermentation of carbohydrates. Their role on the metabolism and biology of colonocytes is now well characterized. However, the functional consequences of their presence on intestinal smooth muscle cells remain poorly studied. We aimed to assess the effect of different short-chain fatty acids on ileal and colonic smooth muscle cells in primary culture and on A7R5 line. Butyrate (above 0.1 mM) inhibited A7R5 cell proliferation, while at low concentration (0.05 to 0.5 mM) butyrate significantly stimulated the proliferation of ileal and colonic myocytes in primary culture. An inhibition was observed at higher concentrations. Collagenous and noncollagenous protein synthesis was stimulated by butyrate. Moreover, butyrate stimulated actin and myosin expression. Thus, butyrate, which is produced by dietary fiber fermentation, may affect intestinal muscles by directly acting at the molecular level on myocytes.

Butyrate inhibits inflammatory responses through NFkappaB inhibition: implications for Crohn's disease.

BACKGROUND/AIM: Proinflammatory cytokines are key factors in the pathogenesis of Crohn's disease (CD). Activation of nuclear factor kappa B (NFkappaB), which is involved in their gene transcription, is increased in the intestinal mucosa of CD patients. As butyrate enemas may be beneficial in treating colonic inflammation, we investigated if butyrate promotes this effect by acting on proinflammatory cytokine expression. METHODS: Intestinal biopsy specimens, isolated lamina propria cells (LPMC), and peripheral blood mononuclear cells (PBMC) were cultured with or without butyrate for assessment of secretion of tumour necrosis factor (TNF) and mRNA levels. NFkappaB p65 activation was determined by immunofluorescence and gene reporter experiments. Levels of NFkappaB inhibitory protein (IkappaBalpha) were analysed by western blotting. The in vivo efficacy of butyrate was assessed in rats with trinitrobenzene sulphonic acid (TNBS) induced colitis. RESULTS: Butyrate decreased TNF production and proinflammatory cytokine mRNA expression by intestinal biopsies and LPMC from CD patients. Butyrate abolished lipopolysaccharide (LPS) induced expression of cytokines by PBMC and transmigration of NFkappaB from the cytoplasm to the nucleus. LPS induced NFkappaB transcriptional activity was decreased by butyrate while IkappaBalpha levels were stable. Butyrate treatment also improved TNBS induced colitis. CONCLUSIONS: Butyrate decreases proinflammatory cytokine expression via inhibition of NFkappaB activation and IkappaBalpha degradation. These anti-inflammatory properties provide a rationale for assessing butyrate in the treatment of CD.

Pathways and receptors involved in peptide YY induced contraction of rat proximal colonic muscle in vitro.

BACKGROUND: Peptide YY (PYY) is involved in the regulation of several gut functions, including secretion and motility. It exerts its effects through a family of six receptors, commonly named the Y receptor family. AIMS: To characterise the effects of PYY on strips of rat proximal colon in vitro, and to determine the pathways and receptors involved. METHODS: Contractions of strips removed from the muscle layer of rat proximal colon were recorded under isometric conditions, using PYY, Y receptor agonists and antagonists, and nerve blockers. Reverse transcription-polymerase chain reaction was also performed to detect the presence of mRNA coding for Y receptors. Finally, smooth muscle cells were isolated to estimate the cell length and intracellular Ca(2+) concentration in the presence and absence of PYY. RESULTS: PYY, neuropeptide Y (NPY), pancreatic polypeptide (PP) and [Leu31,Pro34]NPY induced a dose dependent contraction of strips from proximal colon. Tetrodotoxin partially inhibited the PYY and NPY induced contractions, and strongly inhibited the PP induced contraction. Specific antagonists showed the involvement of cholinergic nicotinic receptors and NK1 receptor. BIBP 3226, a specific Y1 antagonist, did not modify the colonic smooth muscle response to PYY, whereas blocking L-type Ca(2+) channels with D-600 abolished its effects. Moreover, PYY induced an increase in intracellular Ca(2+) concentration, associated with a reduction in cell length. mRNA encoding Y1 and Y4 receptors were detected in the muscle strips. CONCLUSIONS: These findings suggest that PYY stimulates colonic contractile activity in vitro through (a) a nervous Y4 dependent pathway and (b) a pathway involving a potential new receptor on myocytes.

Short-chain fatty acids modify colonic motility through nerves and polypeptide YY release in the rat.

Short-chain fatty acids (SCFAs) are recognized as the major anions of the large intestinal content in humans, but their effect on colonic motility is controversial. This study explores the colonic motor effect of SCFAs and their mechanisms in the rat. Colonic motility (electromyography) and transit time (plastic markers) were measured in conscious rats while SCFAs were infused into the colon, either alone or after administration of neural antagonists or immunoneutralization of circulating polypeptide YY (PYY). SCFA-induced PYY release was measured by RIA and then simulated by infusing exogenous PYY. Intracolonic infusion of 0.4 mmol/h SCFAs had no effect, whereas 2 mmol/h SCFAs reduced colonic motility (36 +/- 3 vs. 57 +/- 4 spike bursts/h with saline, P < 0.05) by decreasing the ratio of nonpropulsive to propulsive activity. This resulted in an increased transit rate (P < 0.01). Neither alpha-adrenoceptor blockade nor nitric oxide synthase inhibition prevented SCFA-induced motility reduction. Intraluminal procaine infusion suppressed the SCFA effect, indicating that a local neural mechanism was involved. SCFA colonic infusion stimulated PYY release in blood. Immunoneutralization of circulating PYY abolished the effect of SCFAs on colonic motility, whereas exogenous PYY infusion partly reproduced this effect. SCFAs modify colonic motor patterns in the rat and increase transit rate; local nerve fibers and PYY are involved in this effect.

Non-genomic inhibition of human P2X7 purinoceptor by 17beta-oestradiol.

1. Effects of oestrogen on the current evoked by ATP and benzoylbenzoyl ATP (BzATP) in CV-1 monkey kidney cells transformed by SV 40 (COS cells) expressing the human P2X7 (hP2X7) purinoceptor were studied using standard patch-clamp techniques. 2. 17beta-Oestradiol rapidly and reversibly inhibited the whole-cell hP2X7 receptor cation current. This inhibitory action resulted in a rightward shift of the dose-response curve to ATP and BzATP in the presence of physiological as well as low divalent cation concentrations. 3. The inhibitory effect of 17beta-oestradiol on the BzATP- or ATP-induced cation current was concentration dependent. The half-maximal inhibition was obtained with 3 microM 17beta-oestradiol. Progesterone and 17alpha-oestradiol had almost no effect on the hP2X7 receptor cation current. 4. The inhibition of the hP2X7 receptor cation current by 17beta-oestradiol did not depend on the membrane potential. 17beta-Oestradiol added to the extracellular side of outside-out patches inhibited BzATP-activated single-channel currents. 5. Activation of the hP2X7 receptor in both COS and U937 (human macrophage) cells did not induce the formation of large non-specific pores. 6. Since COS cells do not express endogenous nuclear oestrogen receptor, this study shows that, at pharmacological concentrations, 17beta-oestradiol inhibited the hP2X7 receptor cation channel in a non-genomic manner.

alpha-Linolenic acid- and docosahexaenoic acid-enriched eggs from hens fed flaxseed: influence on blood lipids and platelet phospholipid fatty acids in humans.

This study was undertaken to examine the effects that consumption of eggs from hens fed diets containing flaxseed would have on plasma and platelet lipids of male volunteers. Feeding diets containing 0%, 10%, and 20% ground flaxseed to Leghorn pullets provided a marked progressive increase in n-3 fatty acid content as alpha-linolenic acid (alpha-LNA) (28, 261, and 527 mg/egg) and docosahexaenoic acid (DHA) (51, 81, and 87 mg/egg) but no alteration in the cholesterol concentration of the egg yolk. Twenty-eight male volunteers, divided into three groups, were fed four eggs per day for 2 wk according to a cyclic Latin-square design. No statistically significant changes were observed in total cholesterol, high-density-lipoprotein cholesterol, or plasma triglyceride concentrations. Significant increases in total n-3 fatty acids and in DHA content (which rose from 1.5 to 2.0% by wt or 33% overall), and a significant decrease in ratio of n-6 to n-3 fatty acids were found in platelet phospholipids of subjects consuming eggs from flaxseed-fed hens. Health and Welfare Canada in 1990 set recommended intakes for dietary n-3 fatty acids and for the ratio of n-6 to n-3 fatty acids, which are not being met currently by the overall population. Eggs modified by the inclusion of flaxseed in the laying hens' diet could provide an important nutritional source of n-3 fatty acid.

Conversational skills of individuals with fragile-X syndrome: a comparison with autism and Down syndrome.

The conversational skills of 18 individuals with fragile-X syndrome (FXS) were compared with those of two other matched groups with autism and Down syndrome. The FXS group used more eliciting forms in conversation than those with Down syndrome, and also used partial self-repetition more often than the other two groups. The Down syndrome group had more speech dysfluencies than those with autism, but not more than those with FXS. The autistic group used more inappropriate phrases. Qualitative analysis of behavioral phenotype may reveal differences in communicative organization among subgroups whose retardation is based on different genotypes. In addition, analysis of verbal strategies during conversation suggests important differences between individuals with FXS and autism.