Propagation of Surface Plasmons in Ordered and Disordered Chains of Metal Nanospheres

We report a numerical investigation of surface plasmon (SP) propagation in ordered and disordered linear chains of metal nanospheres. In our simulations, SPs are excited at one end of a chain by a near-field tip. We then find numerically the SP amplitude as a function of propagation distance. Two types of SPs are discovered. The first SP, which we call the ordinary or quasistatic, is mediated by short-range, near-field electromagnetic interaction in the chain. This excitation is strongly affected by Ohmic losses in the metal and by disorder in the chain. These two effects result in spatial decay of the quasistatic SP by means of absorptive and radiative losses, respectively. The second SP is mediated by longer range, far-field interaction of nanospheres. We refer to this SP as the extraordinary or non-quasistatic. The non-quasistatic SP can not be effectively excited by a near-field probe due to the small integral weight of the associated spectral line. Because of that, at small propagation distances, this SP is dominated by the quasistatic SP. However, the non-quasistatic SP is affected by Ohmic and radiative losses to a much smaller extent than the quasistatic one. Because of that, the non-quasistatic SP becomes dominant sufficiently far from the exciting tip and can propagate with little further losses of energy to remarkable distances. The unique physical properties of the non-quasistatic SP can be utilized in all-optical integrated photonic systems

Effects of Size Polydispersity on the Extinction Spectra of Colloidal Nanoparticle Aggregates

We investigate the effect of particle polydispersity on the optical extinction spectra of colloidal aggregates of spherical metallic (silver) nanoparticles, taking into account the realistic interparticle gaps caused by layers of stabilizing polymer adsorbed on the metal surface (adlayers). The spectra of computer-generated aggregates are computed using two different methods. The coupled-multipole method is used in the quasistatic approximation and the coupled-dipole method beyond the quasistatics. The latter approach is applicable if the interparticle gaps are sufficiently wide relative to the particle radii. Simulations are performed for two different particle size distribution functions (bimodal and Gaussian), varying the number of particles per aggregate, and different distribution functions of the interparticle gap width. The strong influence of the latter factor on the spectra is demonstrated and investigated in detail

Renin-angiotensin-aldosterone system in ISIAH rats with stressinduced arterial hypertension

Because the renin-angiotensin system (RAS) has a wide range of opportunities in the regulation of fluid and electrolyte balance and arterial pressure, it is currently hypothesized that alterations in systemic circulating or local tissue RAS are some of the most important pathogenetic factors in the development of essential hypertension. The aim of the study was to investigate circulating and local tissue RAS activities in ISIAH rats with stress-induced arterial hypertension. We estimated the serum levels of renin, the angiotensin-converting enzyme, angiotensin II and aldosterone by an enzymelinked immunosorbent assay, and mRNA expression of RAS genes in kidney, adrenals and brain tissues was measured by the real-time polymerase chain reaction. The mRNA expression of the renin gene (Ren) in the ISIAH rats was significantly decreased as compared to the normotensive WAG rats, but plasma renin concentrations had no difference. At the same time, the serum levels of angiotensin II and aldosterone in the ISIAH rats were enhanced, which suggests the existence of an ectopic site of angiotensin synthesis. Expression of RAS genes in the adrenals of hypertensive rats was unchanged. By contrast, a significant increase of RAS genes expression was found in the brain tissues. The mRNA of the Ren gene was increased in the hypothalamus, and the mRNA of Ace gene was increased in the brain stem of the ISIAH rats. This may be indicative of a local increase of RAS activity in the brain tissues of ISIAH rats. Nevertheless, the results of the study define ISIAH rat strain as a model of human low-renin hypertension

GC-based chemoprofile of lipophilic compounds in Altaian Ganoderma lucidum sample

The presented data contains information about component composition of lipophilic compounds in Ganoderma lucidum fungal body sample obtained using gas chromatography and subsequent mass spectrometry

Menadione Suppresses Benzo(a)pyrene-Induced Activation of Cytochromes P450 1A : Insights into a Possible Molecular Mechanism

Oxidative reactions that are catalyzed by cytochromes P450 1A (CYP1A) lead to formation of carcinogenic derivatives of arylamines and polycyclic aromatic hydrocarbons (PAHs), such as the widespread environmental pollutant benzo(a) pyrene (BP). These compounds upregulate CYP1A at the transcriptional level via an arylhydrocarbon receptor (AhR)-dependent signaling pathway. Because of the involvement of AhR-dependent genes in chemically induced carcinogenesis, suppression of this signaling pathway could prevent tumor formation and/or progression. Here we show that menadione (a water-soluble analog of vitamin K-3) inhibits BP-induced expression and enzymatic activity of both CYP1A1 and CYP1A2 in vivo (in the rat liver) and BP-induced activity of CYP1A1 in vitro. Coadministration of BP and menadione reduced DNA-binding activity of AhR and increased DNA-binding activity of transcription factors Oct-1 and CCAAT/enhancer binding protein (C/EBP), which are known to be involved in negative regulation of AhR-dependent genes, in vivo. Expression of another factor involved in downregulation of CYP1A-pAhR repressor (AhRR)-was lower in the liver of the rats treated with BP and menadione, indicating that the inhibitory effect of menadione on CYP1A is not mediated by this protein. Furthermore, menadione was well tolerated by the animals: no signs of acute toxicity were detected by visual examination or by assessment of weight gain dynamics or liver function. Taken together, our results suggest that menadione can be used in further studies on animal models of chemically induced carcinogenesis because menadione may suppress tumor formation and possibly progression.Peer reviewe

10 simple rules to create a serious game, illustrated with examples from structural biology

Serious scientific games are games whose purpose is not only fun. In the field of science, the serious goals include crucial activities for scientists: outreach, teaching and research. The number of serious games is increasing rapidly, in particular citizen science games, games that allow people to produce and/or analyze scientific data. Interestingly, it is possible to build a set of rules providing a guideline to create or improve serious games. We present arguments gathered from our own experience ( Phylo , DocMolecules , HiRE-RNA contest and Pangu) as well as examples from the growing literature on scientific serious games

Role of apoptosis genes in aggression revealed using combined analysis of ANDSystem gene networks, expression and genomic data in grey rats with aggressive behavior

Aggressive behavior in animals plays an important role in protecting the territory, offspring, establishing social hierarchical relations, etc. Increased aggression is observed in a number of diseases ( schizophrenia, bipolar disorder, brain degenerative disorders). Neuronal apoptosis is crucial in the maintenance of developmental processes during neurogenesis. Alterations in neuronal apoptosis are observed in aging and neuropathologies accompanied by changes in psycho­emo­ tional state (epilepsy, Alzheimer’s disease, neurotrauma). The expression of key neuronal apoptosis genes (Casp3, Bax and Bcl-xl) in the brain of highly aggressive rats is significantly altered. The aim of this work was to analyze associative networks that describe genetic interactions between genes/proteins involved in neuronal apoptosis, differentially expressed genes and genes with polymorphisms in grey rats with aggressive behavior. Analysis revealed 819 differentially expressed genes in the hypothalamus, ventral tegmental region and periaqueductus Sylvii grey matter in grey rats with aggressive and tame behavior. The Stx1a, Mbp and Th genes have the highest index of betweenness centrality in the associative network of differentially expressed genes. Genome analysis revealed 137 polymorphic genes. Three of them (Lig4, Parp1 and Pigt) were involved in neuronal apoptosis. It was shown that polymorphic and differentially expressed genes were statistically significantly overrepresented among ge nes interacting with neuronal apoptosis genes (p value < 0.01). Three molecular­genetic chains describing connections between polymorphic and neuronal apoptosis genes mediated by differentially expressed genes were reconstructed. Chains included the polymorphic genes Tsc1, Adamts4 and Lgals3, differentially expressed genes Ezr, Acan, Th and 19 neuronal apoptosis genes. It was shown that neuronal apoptosis is closely related to aggressive behavior in animals

Natural Killer Lysis Receptor (NKLR)/NKLR-Ligand Matching as a Novel Approach for Enhancing Anti-Tumor Activity of Allogeneic NK Cells

NK cells are key players in anti tumor immune response, which can be employed in cell-based therapeutic modalities. One of the suggested ways to amplify their anti tumor effect, especially in the field of stem cell transplantation, is by selecting donor/recipient mismatches in specific HLA, to reduce the inhibitory effect of killer Ig-like receptors (KIRs). Here we suggest an alternative approach for augmentation of anti tumor effect of allogeneic NK cells, which is founded on profile matching of donor NK lysis receptors (NKLR) phenotype with tumor lysis-ligands.We show that an NKLR-mediated killing directly correlates with the NKLR expression intensity on NK cells. Considerable donor variability in the expression of CD16, NKp46, NKG2D and NKp30 on circulating NK cells, combined with the stability of phenotype in several independently performed tests over two months, indicates that NKLR-guided selection of donors is feasible. As a proof of concept, we show that melanoma cells are dominantly recognized by three NKLRs: NKG2D, NKp30 and NKp44. Notably, the expression of NKp30 on circulating NK cells among metastatic melanoma patients was significantly decreased, which diminishes their ability to kill melanoma cells. Ex vivo expansion of NK cells results not only in increased amount of cells but also in a consistently superior and predictable expression of NKG2D, NKp30 and NKp44. Moreover, expanded NK cultures with high expression of NKG2D or NKp30 were mostly derived from the corresponding NKG2D(high) or NK30(high) donors. These NK cultures subsequently displayed an improved cytotoxic activity against melanoma in a HLA/KIR-ligand mismatched setup, which was NKLR-dependent, as demonstrated with blocking anti-NKG2D antibodies.NKLR/NKLR-ligand matching reproducibly elicits enhanced NK anti-tumor response. Common NKLR recognition patterns of tumors, as demonstrated here in melanoma, would allow implementation of this approach in solid malignancies and potentially in hematological malignancies, either independently or in adjunction to other modalities

Ceacam1 separates graft-versus-host-disease from graft-versus-tumor activity after experimental allogeneic bone marrow transplantation.

BACKGROUND: Allogeneic bone marrow transplantation (allo-BMT) is a potentially curative therapy for a variety of hematologic diseases, but benefits, including graft-versus-tumor (GVT) activity are limited by graft-versus-host-disease (GVHD). Carcinoembryonic antigen related cell adhesion molecule 1 (Ceacam1) is a transmembrane glycoprotein found on epithelium, T cells, and many tumors. It regulates a variety of physiologic and pathological processes such as tumor biology, leukocyte activation, and energy homeostasis. Previous studies suggest that Ceacam1 negatively regulates inflammation in inflammatory bowel disease models. METHODS: We studied Ceacam1 as a regulator of GVHD and GVT after allogeneic bone marrow transplantation (allo-BMT) in mouse models. In vivo, Ceacam1(-/-) T cells caused increased GVHD mortality and GVHD of the colon, and greater numbers of donor T cells were positive for activation markers (CD25(hi), CD62L(lo)). Additionally, Ceacam1(-/-) CD8 T cells had greater expression of the gut-trafficking integrin α(4)β(7), though both CD4 and CD8 T cells were found increased numbers in the gut post-transplant. Ceacam1(-/-) recipients also experienced increased GVHD mortality and GVHD of the colon, and alloreactive T cells displayed increased activation. Additionally, Ceacam1(-/-) mice had increased mortality and decreased numbers of regenerating small intestinal crypts upon radiation exposure. Conversely, Ceacam1-overexpressing T cells caused attenuated target-organ and systemic GVHD, which correlated with decreased donor T cell numbers in target tissues, and mortality. Finally, graft-versus-tumor survival in a Ceacam1(+) lymphoma model was improved in animals receiving Ceacam1(-/-) vs. control T cells. CONCLUSIONS: We conclude that Ceacam1 regulates T cell activation, GVHD target organ damage, and numbers of donor T cells in lymphoid organs and GVHD target tissues. In recipients of allo-BMT, Ceacam1 may also regulate tissue radiosensitivity. Because of its expression on both the donor graft and host tissues, this suggests that targeting Ceacam1 may represent a potent strategy for the regulation of GVHD and GVT after allogeneic transplantation