Transmission resonances through aperiodic arrays of subwavelength apertures

Resonantly enhanced light transmission through periodic subwavelength aperture arrays perforated in metallic films has generated significant interest because of potential applications in near-field microscopy, photolithography, displays, and thermal emission. The enhanced transmission was originally explained by a mechanism where surface plasmon polaritons (collective electronic excitations in the metal surface) mediate light transmission through the grating. In this picture, structural periodicity is perceived to be crucial in forming the transmission resonances. Here we demonstrate experimentally that, in contrast to the conventional view, sharp transmission resonances can be obtained from aperiodic aperture arrays. Terahertz transmission resonances are observed from several arrays in metallic films that exhibit unusual local n-fold rotational symmetries, where n = 10, 12, 18, 40 and 120. This is accomplished by using quasicrystals with long-range order, as well as a new type of 'quasicrystal approximates' in which the long-range order is somewhat relaxed. We find that strong transmission resonances also form in these aperiodic structures, at frequencies that closely match the discrete Fourier transform vectors in the aperture array structure factor. The shape of these resonances arises from Fano interference of the discrete resonances and the non-resonant transmission band continuum related to the individual holes. Our approach expands potential design parameters for aperture arrays that are aperiodic but contain discrete Fourier transform vectors, and opens new avenues for optoelectronic devices.     

VEGF regulates haematopoietic stem cell survival by an internal autocrine loop mechanism

Vascular endothelial growth factor (VEGF) is a principal regulator of blood vessel formation and haematopoiesis, but the mechanisms by which VEGF differentially regulates these processes have been elusive. Here we describe a regulatory loop by which VEGF controls survival of haematopoietic stem cells (HSCs). We observed a reduction in survival, colony formation and in vivo repopulation rates of HSCs after ablation of the VEGF gene in mice. Intracellularly acting small-molecule inhibitors of VEGF receptor (VEGFR) tyrosine kinase dramatically reduced colony formation of HSCs, thus mimicking deletion of the VEGF gene. However, blocking VEGF by administering a soluble VEGFR-1, which acts extracellularly, induced only minor effects. These findings support the involvement in HSC survival of a VEGF-dependent internal autocrine loop mechanism (that is, the mechanism is resistant to inhibitors that fail to penetrate the intracellular compartment). Not only ligands selective for VEGF and VEGFR-2 but also VEGFR-1 agonists rescued survival and repopulation of VEGF-deficient HSCs, revealing a function for VEGFR-1 signalling during haematopoiesis.     

Cytopathological effects of aristolochic acid on male houseflies causing sterility

Summary Feeding male houseflies with 0.075% aristolochic acid obtained from the plants of the genusAristolochia induced sterility. High condensation of chromosomes, and breakages, have been shown to be responsible for sterility. When onion roots were exposed to aristolochic acid similar chromosomal aberrations were noticed in cells at the tip.Authors are thankful to Prof. Dr G. Rücker (Universität Bonn) for a generous gift of aristolochic acid.     

Enhancement of humoral immune response against human lung elastin peptides

Summary When guinea pigs instead of rabbits were used as the host animals, 8–16 times higher antibody titers against human lung elastin peptides were produced with only 1/20 the amount of antigen per unit body weight. This corresponds to a 200-fold enhancement of the immune response.Presented at the 6th Colloquium of the Federation of European Connective Tissue Clubs, Paris, August 28–30, 1978. The data form part of the Ph.D. thesis submitted by T.V. Darnule to the Department of Biology, New York University. Supported in part by NIH Program Project Grant HL15832 and by a Parker B. Francis Fellowship to T.V. Darnule.     

心肌缺血后处理对急性心肌梗死患者血清CK和CK-MB的影响

目的探讨缺血后处理对急性心肌梗死(AMI)患者血清CK和CK-MB峰值及其动态变化的影响.方法将64例12 h内行直接经皮冠状动脉介入治疗(PCI)的ST段抬高型AMI患者随机分为两组,对照组34例,缺血后处理组30例.对照组给予单纯再灌注治疗,缺血后处理组采用再灌注30 s/再缺血30 s,交替3次后再持续灌注的方法...     

Mediation of pathogen resistance by exudation of antimicrobials from roots

Most plant species are resistant to most potential pathogens. It is not known why most plant-microbe interactions do not lead to disease, although recent work indicates that this basic disease resistance is multi-factorial. Here we show that the exudation of root-derived antimicrobial metabolites by Arabidopsis thaliana confers tissue-specific resistance to a wide range of bacterial pathogens. However, a Pseudomonas syringae strain that is both at least partly resistant to these compounds and capable of blocking their synthesis/exudation is able to infect the roots and cause disease. We also show that the ability of this P. syringae strain to block antimicrobial exudation is dependent on the type III secretory system.     

Alternatively activated macrophages produce catecholamines to sustain adaptive thermogenesis

All homeotherms use thermogenesis to maintain their core body temperature, ensuring that cellular functions and physiological processes can continue in cold environments. In the prevailing model of thermogenesis, when the hypothalamus senses cold temperatures it triggers sympathetic discharge, resulting in the release of noradrenaline in brown adipose tissue and white adipose tissue. Acting via the β(3)-adrenergic receptors, noradrenaline induces lipolysis in white adipocytes, whereas it stimulates the expression of thermogenic genes, such as PPAR-γ coactivator 1a (Ppargc1a), uncoupling protein 1 (Ucp1) and acyl-CoA synthetase long-chain family member 1 (Acsl1), in brown adipocytes. However, the precise nature of all the cell types involved in this efferent loop is not well established. Here we report in mice an unexpected requirement for the interleukin-4 (IL-4)-stimulated program of alternative macrophage activation in adaptive thermogenesis. Exposure to cold temperature rapidly promoted alternative activation of adipose tissue macrophages, which secrete catecholamines to induce thermogenic gene expression in brown adipose tissue and lipolysis in white adipose tissue. Absence of alternatively activated macrophages impaired metabolic adaptations to cold, whereas administration of IL-4 increased thermogenic gene expression, fatty acid mobilization and energy expenditure, all in a macrophage-dependent manner. Thus, we have discovered a role for alternatively activated macrophages in the orchestration of an important mammalian stress response, the response to cold.     

Macrophage-specific PPARgamma controls alternative activation and improves insulin resistance

Obesity and insulin resistance, the cardinal features of metabolic syndrome, are closely associated with a state of low-grade inflammation. In adipose tissue chronic overnutrition leads to macrophage infiltration, resulting in local inflammation that potentiates insulin resistance. For instance, transgenic expression of Mcp1 (also known as chemokine ligand 2, Ccl2) in adipose tissue increases macrophage infiltration, inflammation and insulin resistance. Conversely, disruption of Mcp1 or its receptor Ccr2 impairs migration of macrophages into adipose tissue, thereby lowering adipose tissue inflammation and improving insulin sensitivity. These findings together suggest a correlation between macrophage content in adipose tissue and insulin resistance. However, resident macrophages in tissues display tremendous heterogeneity in their activities and functions, primarily reflecting their local metabolic and immune microenvironment. While Mcp1 directs recruitment of pro-inflammatory classically activated macrophages to sites of tissue damage, resident macrophages, such as those present in the adipose tissue of lean mice, display the alternatively activated phenotype. Despite their higher capacity to repair tissue, the precise role of alternatively activated macrophages in obesity-induced insulin resistance remains unknown. Using mice with macrophage-specific deletion of the peroxisome proliferator activated receptor-gamma (PPARgamma), we show here that PPARgamma is required for maturation of alternatively activated macrophages. Disruption of PPARgamma in myeloid cells impairs alternative macrophage activation, and predisposes these animals to development of diet-induced obesity, insulin resistance, and glucose intolerance. Furthermore, gene expression profiling revealed that downregulation of oxidative phosphorylation gene expression in skeletal muscle and liver leads to decreased insulin sensitivity in these tissues. Together, our findings suggest that resident alternatively activated macrophages have a beneficial role in regulating nutrient homeostasis and suggest that macrophage polarization towards the alternative state might be a useful strategy for treating type 2 diabetes.