Plasmonic Perfect Absorbers for Biosensing Applications

We present a theoretical modal investigation of plasmonic perfect absorbers (PPAs) based on the localized surface plasmon resonance (LSPR) for biosensing applications. We design the PPA geometry with a layer of periodic metallic nanoparticles on one side of a dielectric substrate and a single metallic layer on the opposite side. The electromagnetic (EM) fields confine partly in the surrounding medium above the substrate and within the substrate itself. We examine the modes of the PPA geometry for a wavelength range of 600–1500 nm. The fundamental mode of the system provides perfect absorption for a wide angle of incidence 0–70°. The second-order mode shows a strong angular dependence with a sharp resonance and exhibits perfect optical absorption when the critical coupling condition for LSPR is achieved. The coupling condition depends on the size, periodicity, dielectric spacer, and the surrounding material of the system. The strong dependence on the surrounding material makes it a promising candidate for biosensing applications. We introduce a novel approach to investigate the angular dependence of the refractive index change for the PPA system. This novel technique contributes the significant attributes of the LSPR sensors, can be used for any required resonance wavelength depending on geometric design, and it also provides sensitivity analogous to the standard surface plasmon resonance (SPR) biosensors.     

Involvement of protein kinases on the upregulation of endothelin receptors in rat basilar and mesenteric arteries

Endothelin(B) (ET(B)) receptors are upregulated in experimental stroke or after 24 hrs of organ culture. This upregulation is manifested both as stronger contraction and as an increase in ET(B) receptor messenger RNA (mRNA) levels. The present study was designed to evaluate the importance of protein kinases (c-Jun N-terminal kinase [JNK], protein kinase C [PKC], and extracellular signal-regulated kinase [ERK1/2]) in ET(B) receptor upregulation after organ culture. Rat basilar and mesenteric arteries were incubated for 24 hrs in Dulbecco's modified Eagle's medium (DMEM) with or without the PKC inhibitor, RO-31-7549; the ERK1/2 inhibitor, SB386023; or the JNK inhibitor, SP600125, added 3, 6, or 12 hrs after initiation of incubation. Subsequently, vessel segments were mounted in myographs and the contractile responses to ET-1 and sarafotoxin 6c were studied. The ET(B) and ET(A) receptor mRNA levels were determined with a real-time polymerase chain reaction (PCR). The cellular localization and protein level of ET(B) receptors were evaluated by immunohistochemistry. The PKC and ERK1/2 inhibitors attenuated the contraction induced by S6c in the basilar arteries more than in the mesenteric arteries. The efficiency of the inhibitors was proportional to the incubation time. Real-time PCR showed a decrease in the ET(B) receptor mRNA levels in arteries treated with PKC or ERK inhibitors. The JNK inhibitor had a significant inhibitory effect on ET(B) receptor upregulation in the basilar arteries. Immunohistochemistry revealed that the ET(B) receptor upregulation occured in the smooth-muscle cells and that it had the same pattern as in the quantitative PCR. Our results show that the PKC, ERK1/2, and JNK are more important for the upregulation of contractile ET(B) receptors in cerebral arteries compared with mesenteric arteries. ERK1/2 seems to be more important for the ET(B) receptor upregulation, as compared with PKC and JNK. The evaluation of the time dependency suggests that the phenomenon can be reversed even after its initiation.     

Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca2+/c-Abl signaling pathway

The importance of H₂O₂ as a cellular signaling molecule has been demonstrated in a number of cell types and pathways. Here we explore a positive feedback mechanism of H₂O₂-mediated regulation of the phagocyte respiratory burst NADPH oxidase (NOX2). H₂O₂ induced a dose-dependent stimulation of superoxide production in human neutrophils, as well as in K562 leukemia cells overexpressing NOX2 system components. Stimulation was abrogated by the addition of catalase, the extracellular Ca²⁺ chelator BAPTA, the T-type Ca²⁺ channel inhibitor mibefradil, the PKCδ inhibitor rottlerin, or the c-Abl nonreceptor tyrosine kinase inhibitor imatinib mesylate or by overexpression of a dominant-negative form of c-Abl. H₂O₂ induced phosphorylation of tyrosine 311 on PKCδ and this activating phosphorylation was blocked by treatment with rottlerin, imatinib mesylate, or BAPTA. Rac GTPase activation in response to H₂O₂ was abrogated by BAPTA, imatinib mesylate, or rottlerin. In conclusion, H₂O₂ stimulates NOX2-mediated superoxide generation in neutrophils and K562/NOX2 cells via a signaling pathway involving Ca²⁺ influx and c-Abl tyrosine kinase acting upstream of PKCδ. This positive feedback regulatory pathway has important implications for amplifying the innate immune response and contributing to oxidative stress in inflammatory disorders.     

Insulin-sparing effect of hydroxychloroquine in diabetic rats is concentration dependent.

To study the effect of hydroxychloroquine (HCQ) on glucose and insulin homeostasis, healthy rats were dosed with 160 mg x kg (-1) x day(-1) of HCQ orally, and streptozocin-induced diabetic rats received 80, 120, and 160 mg x kg(-1) x day(-1) of HCQ, while controls received normal saline. Ten days after treatment with HCQ, healthy animals were challenged intravenously with insulin or glucose, while diabetic rats were given only an i.v. injection of insulin. In healthy rats, the areas within and under the glucose concentration - time curve following insulin and glucose challenge were estimated. In diabetic animals, the areas under the curve for both the percent change in serum glucose from baseline (AUG) and the percent change in serum insulin from baseline (AUI) were used as pharmacodynamic end points. In healthy rats, HCQ did not influence fasting serum glucose concentrations or glycemic profiles following i.v. administration of glucose or insulin. In diabetic rats, AUG and AUI were increased dependent on blood HCQ concentrations. The normal homeostatic mechanisms responsible for insulin-glucose regulation may compensate for possible HCQ-induced reduction of insulin metabolism in healthy rats. The HCQ dose- or concentration-effect relationships for glucose and insulin were linear over the range of HCQ concentrations tested. It is concluded that HCQ significantly elevated insulin blood concentration resulting in reduced glucose levels in a concentration-dependent fashion in diabetic rats. HCQ may have therapeutic potential in the treatment of type I and type II diabetes.     

Spring Time and Autumn Time Toxic Effects of Copper (II), 3-(2-Furyl) Prop-2-Enal Semicarbazone and [CuCl2(FASC)2] Complex in Mice

In vitro, 3-(2-furyl) prop-2-enal semicarbazone-copper (II) complex [CuCl₂(FASC)₂] presents antimitotic effects. In this work we studied the in vivo seasonal toxic effects in male Swiss mice of CuCl₂, and FASC and the [CuCl₂(FASC)₂] complex. In spring, one injection of CuCl₂8.10^-2 mmol killed 16% of animals after 24 h. Cupric chloride lethal dose was up to 64.10^-2 mmol with 100% mice dead after 24 h. FASC was well tolerated from 0.65 to 1.3 mmol. The complex was 100% lethal with 48.10^?2 mmol. In autumn, mice were more sensitive to CuCl₂ and to the complex with lethal doses up to 32.10^-2 mmol and 8.10^-2 mmol, respectively. On the other hand, FASC was well tolerated. It is concluded that the in vivo toxic effects of CuCl₂ and [CuCl₂(FASC)₂] complex are quite different in spring and autumn.     

Internet congestion control using nature population control tactics

In this paper we present a novel bio-inspired approach for congestion control in communication networks. This scheme is based on inspiration by natural population interactions: predator–prey and competition. We show that the relations of those Internet entities that are involved in congestion control mechanisms are similar to predator–prey and competition interactions. In order to apply these population control mechanisms to the Internet congestion control scheme, we combine the mathematical models of these interactions and obtain a hybrid mathematical model. The simulation results show that using appropriately defined parameters, this model leads to a scalable, stable, fair, and high-performance congestion control algorithm.     

Effect of fetal hypothyroidism on MyomiR network and its target gene expression profiles in heart of offspring rats

Currently, azoospermia is one of the most common diseases of male infertility. Stem cell research is the new hope for novel therapy with a higher degree of safety and lower cost. This study aimed to investigate the effect of umbilical cord blood-derived stem cells (” and mesenchymal “UCB-MSCs”) and mono-cell layer implanted into the induced azoospermic mice testis. Stem cells were isolated from umbilical cord blood and CD34+ve cells were separated from negative one by Mini MACs column. At 5th week after single injection of busulfan, stained mesenchymal (CD34-ve), hematopoietic stem cells (CD34+ve) and their conjugate (mono-cell layer) were injected locally into testis. At the end of the study, MSCs group showed that mRNA levels of genes related to meiosis (Vasa, SCP3, and PgK2) were increased with significant decrease of FSH and LH levels, compared to control group. Histologically, most of the tubules restored normal architecture. In contrast, HSCs and mono-cell layer groups showed statically insignificant change of FSH, LH, and gene expression, compared to control group. Histologically, distorted seminiferous tubules, with reduction in sperm content, and interstitial mononuclear cellular infiltration were seen. There was significant increase in the optical density of PCNA immune reaction in MSCs group than azoospermia, HSCs, and mono-cell layer, while there was non-significant difference between MSCs and control group. The present study suggested that injection of MSCs into chemotherapeutic-induced azoospermia in mice improved testicular failure; histologically and functionally, by restoration of spermatogenic gene expression while HSC and mono-cell layer showed no effect on spermatogenesis added to that mono-cell layer may induce testicular tissue damage.