Dye Transfer Research Articles

Accurate Plane Fat Grafting in Gluteal Augmentation: An Anatomic Study.

The safety of gluteal fat grafting is a global concern in plastic surgery. The goal of this study was to test whether fat grafting to the buttocks with Auto Stop Reach (ASR) technology prevents penetration from the subcutaneous space into the fascia and muscle layers of the buttocks. Fat transfer simulation was performed with blue dye on 8 fresh tissue cadaver buttocks by 3 board-certified plastic surgeons (S.S.K., S.C., B.W.). An open control was utilized to visualize the process in the different anatomic layers, and all of the other procedures were performed blindly, akin to live surgery. After blue dye transfer reached maximum capacity (ranging from 400-800 mL per buttock), dissection of the anatomical layers of the buttocks was performed to determine the plane(s) of injection. Blue dye fat transfer injection to the buttocks did not penetrate the gluteal fascia or muscle layers from the subcutaneous space while using ASR. Auto Stop Reach technology supports the safety of gluteal fat transfer in the subcutaneous space by board-certified plastic surgeons.

Imaging analysis reveals budding of filamentous human metapneumovirus virions and direct transfer of inclusion bodies through intercellular extensions.

Human metapneumovirus is an important respiratory pathogen that causes significant morbidity and mortality, particularly in the very young, the elderly, and the immunosuppressed. However, the molecular details of how this virus spreads to new target cells are unclear. This work provides important new information on the formation of filamentous structures that are consistent with virus particles and adds critical new insight into the structure of extensions between cells that form during infection. In addition, it demonstrates for the first time the movement of viral replication centers through these intercellular extensions, representing a new mode of direct cell-to-cell spread that may be applicable to other viral systems.

Non-thermal plasma degradation of dye wastewater assisted by reverse osmosis process through interfacial mass transfer enhancement

A two-stage system of dye wastewater treatment was proposed, containing reverse osmosis (RO) process and non-thermal plasma (NTP) degradation. The dye wastewater was concentrated by reverse osmosis to enhance the mass transfer of organic dye from the falling film to the reaction interface, promoting dye removal and energy yield of the plasma degradation. The effects of the methylene blue concentration (100–500 mg·L-1), flow rate, and the discharge power of plasma (40–100 W) on the methylene blue removal and the energy yield of the NTP mode were investigated. At the removal of 45%, the energy yield of RONTP mode was 1198.0 mg·kWh−1, which was 2.36 times than NTP mode. 8 degradation intermediates were detected by LC-MS, which mass/charge ratio were in the range of 80–400. This investigation provides a guidance to improve the energy yield of dye wastewater by plasma through mass transfer enhancement.

Experimental study on co-culture of DiI-labeled rat bone marrow mesenchymal stem cells and neonatal rat cardiomyocytes to induce differentiation into cardiomyocyte-like cells.

Myocardial infarction is a serious clinical disease with high mortality and poor prognosis. Cardiomyocytes (CMs) have limited regeneration abilities after ischemic injury. Their growth and differentiation can be enhanced by contact co-culture with stem cells. The aim was to study the contact co-culture of Dil-labeled bone marrow mesenchymal stem cells (BMSCs) and CMs for inducing differentiation of CMs from stem cells for treating myocardial infarction. After contact co-culture, the differentiation of BMSCs into CMs was analyzed qualitatively by detecting myocardial markers (cardiac troponin T and α-smooth muscle actin) using immunofluorescence and quantitatively using flow cytometry. To examine the mechanism, possible gap junctions between BMSCs and CMs were analyzed by detecting gap junction protein connexin 43 (C×43) expression in BMSCs using immunofluorescence. The functionality of gap junctions was analyzed using dye transfer experiments. The results revealed that BMSCs in contact with CMs exhibited myocardial markers and a significant increase in differentiation rate (P <0.05); they also proved the existence and function of gap junctions between BMSCs and CMs. It was shown that contact co-culture can induce Dil-labeled BMSCs to differentiate into CM-like cells and examined the principle of gap junction-mediated signaling pathways involved in inducing stem cells to differentiate into cardiomyocytes.

Development of dissolvable dye transfer inhibitor for household laundry

Development of dissolvable dye transfer inhibitor for household laundry

Controlling Three-Color Förster Resonance Energy Transfer in an Optical Fabry–Pérot Microcavity at Low Mode Order

We study three-color Förster resonance energy transfer (triple FRET) between three spectrally distinct fluorescent dyes, a donor and two acceptors, which are embedded in a single polystyrene nanosphere. The presence of triple FRET energy transfer is confirmed by selective acceptor photobleaching. We show that the fluorescence lifetimes of the three dyes are selectively controlled using the Purcell effect by modulating the radiative rates and relative fluorescence intensities when the nanospheres are embedded in an optical Fabry–Pérot microcavity. The strongest fluorescence intensity enhancement for the second acceptor can be observed as a signature of the FRET process by tuning the microcavity mode to suppress the intermediate dye emission and transfer more energy from donor to the second acceptor. Additionally, we show that the triple FRET process can be modeled by coupled rate equations, which allow to estimate the energy transfer rates between donor and acceptors. This fundamental study has the potential to extend the classical FRET approach for investigating complex systems, e.g., optical energy switching, photovoltaic devices, light-harvesting systems, or in general interactions between more than two constituents.

Somatic mutations of CADM1 in aldosterone-producing adenomas and gap junction-dependent regulation of aldosterone production

Aldosterone-producing adenomas (APAs) are the commonest curable cause of hypertension. Most have gain-of-function somatic mutations of ion channels or transporters. Herein we report the discovery, replication and phenotype of mutations in the neuronal cell adhesion gene CADM1. Independent whole exome sequencing of 40 and 81 APAs found intramembranous p.Val380Asp or p.Gly379Asp variants in two patients whose hypertension and periodic primary aldosteronism were cured by adrenalectomy. Replication identified two more APAs with each variant (total, n = 6). The most upregulated gene (10- to 25-fold) in human adrenocortical H295R cells transduced with the mutations (compared to wildtype) was CYP11B2 (aldosterone synthase), and biological rhythms were the most differentially expressed process. CADM1 knockdown or mutation inhibited gap junction (GJ)-permeable dye transfer. GJ blockade by Gap27 increased CYP11B2 similarly to CADM1 mutation. Human adrenal zona glomerulosa (ZG) expression of GJA1 (the main GJ protein) was patchy, and annular GJs (sequelae of GJ communication) were less prominent in CYP11B2-positive micronodules than adjacent ZG. Somatic mutations of CADM1 cause reversible hypertension and reveal a role for GJ communication in suppressing physiological aldosterone production.

Betacellulin regulates gap junction intercellular communication by inducing the phosphorylation of connexin 43 in human granulosa-lutein cells

BackgroundThe gap junction protein, connexin 43 (Cx43) is highly expressed in human granulosa-lutein (hGL) cells. The phosphorylation of certain amino acid residues in the Cx43 protein has been shown to be related to a decline in gap junction intercellular communication (GJIC), which subsequently affects oocyte meiotic resumption. As a member of the epidermal growth factor (EGF) family, betacellulin (BTC) mediates luteinizing hormone (LH)-induced oocyte maturation and cumulus cell expansion in mammalian follicles. Whether BTC can regulate Cx43 phosphorylation, which further reduces Cx43-coupled GJIC activity in hGL cells remains to be determined.MethodsImmortalized human granulosa cells (SVOG cells) and primary human granulosa-lutein cells obtained from women undergoing in vitro fertilization in an academic research center were used as the study models. The expression levels of Cx43 and phosphorylated Cx43 were examined following cell incubation with BTC at different time points. Several kinase inhibitors (sotrastaurin, AG1478, and U0126) and small interfering RNAs targeting EGF receptor (EGFR) and receptor tyrosine-protein kinase 4 (ErbB4) were used to verify the specificity of the effects and to investigate the molecular mechanisms. Real-time-quantitative PCR and western blot analysis were used to detect the specific mRNA and protein levels, respectively. GJIC between SVOG cells were evaluated using a scrape loading and dye transfer assay. Results were analyzed by one-way analysis of variance.ResultsThe results showed that BTC induced the rapid phosphorylation of Cx43 at serine368 without altering the expression of Cx43 in primary and immortalized hGL cells. Additionally, using a dual inhibition approach (kinase inhibitors and siRNA-based expression knockdown), we demonstrated that this effect was mainly mediated by the EGFR but not the ErbB4 receptor. Furthermore, using a protein kinase C (PKC) kinase assay and a scrape-loading and dye transfer assay, we revealed that PKC signaling is the downstream signaling pathway that mediates the increase in Cx43 phosphorylation and subsequent decrease in GJIC activity in response to BTC treatment in hGL cells.ConclusionsBTC promptly induced the phosphorylation of connexin 43 at Ser368, leading to decreased GJIC activity in hGL cells. The BTC-induced cellular activities were most likely driven by the EGFR-mediated PKC-dependent signaling pathway. Our findings shed light on the detailed molecular mechanisms by which BTC regulates the process of oocyte meiotic resumption.

The impact of aromatic π-spacers and internal acceptors in triphenylamine dyes for DSSCs: A DFT approach

In present work, the influence of internal acceptors and π-spacers on optoelectronic properties for dye-sensitized solar cells (DSSCs) is investigated. The dyes consist of various internal acceptors (A), a triphenylamine donor and π-spacers combined with cyanoacrylic acid acceptor. Density functional theory (DFT) was employed to inspect the dye geometries, charge transport characteristics and electronic excitations. The frontier molecular orbitals (FMOs), highest occupied molecular orbital, lowest unoccupied molecular orbital and HOMO-LUMO energy gap are assisted in the determination of suitable energy levels for electron transfer, electron injection and regeneration of dye. The required photovoltaic parameters like JSC, ΔGreg, ΔGinj, LHE and other associated parameters are presented. The results demonstrate that altering the π-bridge and adding an internal acceptor to the D-π-A scaffold changes the photovoltaic properties and absorption energies. Therefore, the key objective of the current effort is to launch a theoretical groundwork for suitable operational alterations and scheme in creating successful DSSCs.

Enhanced dye adsorption with conductive polyaniline doped chitosan nanofibrous membranes

Polyaniline is widely used in the field of electrochemistry due to its excellent electrical conductivity. However, its effectiveness and mechanism of enhancing adsorption property are unclear. Herein, chitosan/polyaniline nanofibrous composite membranes with average diameter ranging from 200 to 300 nm were fabricated by electrospinning technology. The as-prepared nanofibrous membranes exhibited significantly improved adsorption capacity of 814.9 mg/g and 618.0 mg/g towards acid blue 113 and reactive orange dyes, which were 121.8 % and 99.4 % higher than that of pure chitosan membrane. The doped polyaniline promoted the dye transfer rate and capacity due to the enhanced conductivity of the composite membrane. Kinetic data showed that chemisorption was the rate-limiting step, and thermodynamic data indicated the adsorption of the two anionic dyes was spontaneous monolayer adsorption. This study provides a feasible strategy to introduce conductive polymer into adsorbent to construct high performance adsorbents for wastewater treatment.

Analgesics can affect the sensitivity of temozolomide to glioma chemotherapy through gap junction.

This study investigated the effect of frequently used analgesics in cancer pain management (flurbiprofen (FLU), tramadol (TRA), and morphine (MOR)) and a novel α2-adrenergic agonist (dexmedetomidine, DEX) on temozolomide (TMZ) sensitivity in glioma cells. Cell counting kit-8 and colony-formation assays were performed to analyze the viability of U87 and SHG-44 cell lines. A high and low cell density of colony method, pharmacological methods, and connexin43 mimetic peptide GAP27 were used to manipulate the function of gap junctions; "Parachute" dye coupling and western blot were employed to determine junctional channel transfer ability and connexin expression. The results showed that DEX (in the concentration range of 0.1 to 5.0ng/ml) and TRA (in the concentration range of 1.0 to 10.0µg/ml) reduced the TMZ cytotoxicity in a concentration-dependent manner but was only observed with high cell density (having formed gap junction). The cell viability percentage was 71.3 to 86.8% when DEX was applied at 5.0ng/ml, while tramadol showed 69.6 to 83.7% viability at 5.0μg/ml in U87 cells. Similarly, 5.0ng/ml of DEX resulted in 62.6 to 80.5%, and 5.0μg/ml TRA showed 63.5 to 77.3% viability in SHG-44 cells. Further investigating the impact of analgesics on gap junctions, only DEX and TRA were found to decrease channel dye transfer through connexin phosphorylation and ERK pathway, while no such effect was observed for FLU and MOR. Analgesics that can affect junctional communication may compromise the effectiveness of TMZ when used simultaneously.

Platelet-derived growth factor PDGF-AA upregulates connexin 43 expression and promotes gap junction formations in osteoblast cells through p-Akt signaling

Gap junctions, which are mainly composed of connexin units, play an indispensable role in cell morphogenesis, proliferation, migration, adhesion and differentiation of osteoblast lineage cells, and thus mediate bone development, homeostasis and disease occurrence. Platelet-derived growth factor-AA (PDGF-AA) is proved to have a great influence on osteoblast cell lines and is widely applied in the field of bone defect and wound healing. However, the role of PDGF-AA on gap junction formation in the osteoblast lineage remains elusive. In the current study, we aimed to investigate the impact of PDGF-AA on gap junction formation and cell-to-cell communication in the osteoblast lineage and explore its underlying biomechanism. We first found that PDGF-AA promoted cell proliferation and thus increased gap junction formations in living primary osteoblasts and MC3T3-E1 cells through scrape loading and dye transfer (SL/DT) assay. We then confirmed that PDGF-AA enhanced gap junction formations through up-regulation of connexin 43 (Cx43). We next detected the activation of p-Akt signaling in primary osteoblasts and MC3T3-E1 cells that were induced by PDGF-AA. Through inhibitory experiments, we further confirmed that PDGF-AA-mediated gap junction formation occurred via the activation of PI3K/Akt signaling. Taking together, our results provided evidences that PDGF-AA promoted gap junction formation in the osteoblast lineage through p-Akt signaling, which helped to understand the role of PDGF-AA in bone regeneration and diseases.

Hyperglycaemia-induced impairment of the autorhythmicity and gap junction activity of mouse embryonic stem cell-derived cardiomyocyte-like cells.

Diabetes mellitus with hyperglycaemia is a major risk factor for malignant cardiac dysrhythmias. However, the underlying mechanisms remain unclear, especially during the embryonic developmental phase of the heart. This study investigated the effect of hyperglycaemia on the pulsatile activity of stem cell-derived cardiomyocytes. Mouse embryonic stem cells (mESCs) were differentiated into cardiac-like cells through embryoid body (EB) formation, in either baseline glucose or high glucose conditions. Action potentials (APs) were recorded using a voltage-sensitive fluorescent dye and gap junction activity was evaluated using scrape-loading lucifer yellow dye transfer assay. Molecular components were detected using immunocytochemistry and immunoblot analyses. High glucose decreased the spontaneous beating rate of EBs and shortened the duration of onset of quinidine-induced asystole. Furthermore, it altered AP amplitude, but not AP duration, and had no impact on neither the expression of the hyperpolarisation-activated cyclic nucleotide-gated isoform 4 (HCN4) channel nor on the EB beating rate response to ivabradine nor isoprenaline. High glucose also decreased both the intercellular spread of lucifer yellow within an EB and the expression of the cardiac gap junction protein connexin43 as well as upregulated the expression of transforming growth factor beta1 (TGF-β1) and phosphorylated Smad3. High glucose suppressed the autorhythmicity and gap junction conduction of mESC-derived cardiomyocytes, via mechanisms probably involving TGF-β1/Smad3 signalling. The results allude to glucotoxicity related proarrhythmic effects, with potential clinical implications in foetal diabetic cardiac disease.

Application of electrochemistry technology to effectively inhibit dye pollution and unfixed dye transfer in a washing microenvironment

Application of electrochemistry technology to effectively inhibit dye pollution and unfixed dye transfer in a washing microenvironment

The Role of Mitochondrial RNA from B-Precursor Acute Lymphoblastic Leukaemia Cells in Generating a Chemoprotective Bone Marrow Niche

Treatment resistant cells in precursor B-cell Acute Lymphoblastic Leukaemia (B-ALL) likely reside in a protective bone marrow niche with nestin-expressing mesenchymal stromal cells (MSC) (Duan et al Cancer Cell 2014). Previous work from our laboratory demonstrated that an 'activated MSC' niche, in which MSC have acquired features of cancer associated fibroblasts (CAF), develops in response to reactive oxygen species (ROS)-inducing chemotherapy. Mitochondria are actively transferred along tunneling nanotubes from activated MSC to B-ALL cells and can 'rescue' the cells from chemotherapy (Burt, et al Blood 2019). However, work from other groups suggests that chemoresistant ALL sub-clones exist prior to chemotherapy exposure, carrying a gene expression signature enriched for stemness, mitochondrial metabolism, stress responses and chromatin remodelling (Dobson et al Cancer Discovery 2020). We hypothesised that B-ALL cells may themselves directly activate bone marrow stromal cells and induce niche-formation prior to treatment, leading to ab-inito chemoresistance. To test this hypothesis, we first used our previously-described, in vitro niche model wherein either the HS27a MSC cell line or healthy donor MSCs were co-cultured with either B-ALL cell lines or primary patient B-ALL cells. Three of the five B-ALL cell lines and three of the four primary B-ALL samples that were tested induced activation of the MSCs, as characterised by cytomorphological changes identified by confocal microscopy, up-regulation of CAF-relevant gene expression and increased IL6, IL8 and CCL2 protein secretion. The ability of the B-ALL cell lines to activate MSC correlated directly with the intrinsic ROS level of the cell as determined by CellROX assay. Mitochondrial transfer from the cell-activated MSC to B-ALL cells, as measured by mitotracker dye transfer, occurred exactly as we had seen when we had used chemotherapy to activate the stroma. In vivo, the MSC-activating ALL cell lines also activated murine MSCs when established as xenografts in NOD-SCID gamma (NSG) mice. Immunohistochemistry of NSG murine femora revealed a very significant expansion in nestin+ cells after exposure to niche-induing ALL cells compared to non-niche-inducing controls. We aimed to determine the mechanism behind the B-ALL induced MSC activation. We determined that it was contact-independent, arising from exposure of MSC to ALL cells in transwell but also from exposure to B-ALL cell conditioned media alone. RNA sequencing of MSC after treatment with conditioned medium from activating B-ALL cells compared with non-activating controls unexpectedly showed that most highly upregulated pathways in the MSC-activating scenario were those involved in RNA sensing. Thus, we sought evidence for the role of mitochondrial dsRNA, as it had been recently shown to activate the anti-viral signalling pathway (Dhir et al, Nature 2018). Using the J2 anti-double stranded (ds) RNA monoclonal antibody in both confocal and flow cytometric assays, we observed very significantly higher levels of dsRNA in MSC which had been exposed to stromal-activating B-ALL cell conditioned medium than in non-activating B-ALL or MSC alone controls (see panel for image). We used the small molecule VBIT4, a voltage-dependent anion channel oligomerization inhibitor that decreases mitochondrial nucleic acid release to block this phenomenon in B-ALL cells. We quantified expression of a selection of stromal cell activation marker genes as well as genes in the RNA sensing pathway after treatment with VBIT4-exposed B-ALL cell CM or non-treated control. We observed a 2 to 4-fold reduction in expression of IL6 and CCL2 after VBIT4 exposure, compared to control. In the stromal cell RNA sensing pathway, there was a 15-fold reduction in expression of RIG-I and a 2 to 4-fold reduction in the interferon pathway genes MX2, IFIH1, MAVS and OAS1. Experiments to determine whether knock down of components of the antiviral sensing pathway also abrogates stromal activation and further murine experiments are ongoing. We propose a model in which ROS-induced mitochondrial dysfunction leads to release of dsRNA which in turn activates bone marrow stromal cells leading to protective niche formation and chemoprotection of acute lymphoblastic leukaemia cells despite lack of prior exposure to cytotoxic agents. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Exploration of connexin-43 modulating, multifunctional silver nanocluster-hydrogel system for theranostic management of cancer

Connexin (Cx), a gap junction protein plays an important role in cancer pathophysiology. The enhancement of Cx43, an isoform of Cx, has been reported to improve survival of patients with breast cancer. Since Cxs are expressed in various tissues and organs, their localized modulation is necessary to achieve therapeutic benefits without any side-effects. Therapy combined with diagnostics, i.e. theranostics, is becoming an important facet of cancer management. Thus, considering these two critical aspects, the present study deals with synthesis, bio-imaging, and anti-proliferative effects of a multi-functional chitosan hydrogel incorporating highly fluorescent silver nanoclusters and 4-phenylbutyrate, a histone deacetylase inhibitor for enhancing Cx43 expression. While the remarkable fluorescence of silver nanoclusters enabled cellular uptake and imaging, 4-phenylbutyrate released from the hydrogel specifically upregulated Cx43 expression and induced apoptosis in breast cancer cells. Moreover, the 4-phenylbutyrate released, successfully established gap junction communication between cancer cells as assessed by dye transfer assay. Thus, the current module not only holds potential in cancer theranostics but also for Cx-based cancer therapeutics.

Apelin-13 Increases Functional Connexin-43 through Autophagy Inhibition via AKT/mTOR Pathway in the Non-Myocytic Cell Population of the Heart.

Studies have shown a link between the downregulation of connexin 43 (Cx43), the predominant isoform in cardiac gap junctions, and high susceptibility to cardiac arrhythmias and cardiomyocyte death. Non-myocytic cells (NMCs), the most abundant component of the heart, exert multiple cardiac functions and represent an important therapeutic target for diseased cardiac tissue. A few studies have investigated the effect of Apelin-13, an endogenous peptide with a key role in various cardiovascular functions, on Cx43 expression in cardiomyocytes. However, it remained unknown whether Apelin-13 influences Cx43 expression in NMCs. Here, we found that in NMCs, Cx43 protein expression increased after Apelin-13 treatment (100 nM for 48 h). Furthermore, dye transfer assays proved that Apelin-13-treated NMCs had a greater ability to communicate with surrounding cardiomyocytes, and this effect was abrogated by carbenoxolone, a gap junction inhibitor. Interestingly, we showed that Apelin-13 increased Cx43 through autophagy inhibition, as proved by the upregulation of p62 and LC3I, acting as 3-MA, a well-known autophagy inhibitor. In addition, Apelin-13-induced AKT and mTOR phosphorylation was abolished by LY294002 and rapamycin inhibitors resulting in Cx43 increased suppression. These results open the possibility of targeting gap junctions in NMCs with Apelin-13 as an exciting therapeutic approach with great potential.

Pollinator sharing between reproductively isolated genetic lineages of Silene nutans.

High reciprocal pollination specialization leading to pollinator isolation can prevent interspecific pollen transfer and competition for pollinators. Sharing pollinators may induce mating costs, but it may also increase pollination services and pollen dispersal and offer more resources to pollinators, which may be important in case of habitat fragmentation leading to pollination disruption. We estimated pollen dispersal and pollinator isolation or sharing between two reproductively isolated genetic lineages of Silene nutans (Caryophyllaceae), which are rare and occur in parapatry in southern Belgium, forming two edaphic ecotypes. As inter-ecotypic crosses may lead to pollen wastage and inviable progeny, pollinator isolation might have evolved between ecotypes. Silene nutans is mainly pollinated by nocturnal moths, including nursery pollinators, which pollinate and lay their eggs in flowers, and whose caterpillars feed on flowers and seeds. Pollinator assemblages of the two ecotypes are largely unknown and inter-ecotypic pollen flows have never been investigated. Fluorescent powdered dyes were used as pollen analogues to quantify intra- and inter-ecotypic pollen transfers and seeds were germinated to detect chlorotic seedlings resulting from inter-ecotypic pollination. Nocturnal pollinators were observed using infrared cameras on the field, and seed-eating caterpillars were collected and reared to identify nursery pollinator species. No pollinator isolation was found: we detected long-distance (up to 5km) inter-ecotypic dye transfers and chlorotic seedlings, indicating inter-ecotypic fertilization events. The rare moth Hadena albimacula, a nursery pollinator specialized on S. nutans, was found on both ecotypes, as well as adults visiting flowers (cameras recordings) as seed-eating caterpillars. However, S. nutans populations harbor different abundance and diversity of seed predator communities, including other rare nursery pollinators, suggesting a need for distinct conservation strategies. Our findings demonstrate the efficiency of moths, especially of nursery pollinators, to disperse pollen over long distances in natural landscapes, so to ensure gene flow and population sustainability of the host plant. Seed-predator specificities between the two reproductively isolated genetic lineages of S. nutans, and pollinator sharing instead of pollinator isolation when plants occur in parapatry, suggest that conservation of the host plant is also essential for sustaining (rare) pollinator and seed predator communities.

CONSIDERING PLEURAL FLUID GLUCOSE LEVELS COULD PREVENT UNNECESSARY PROCEDURES

CONSIDERING PLEURAL FLUID GLUCOSE LEVELS COULD PREVENT UNNECESSARY PROCEDURES

Synthesis and Spectral Characteristics of RhB and Rh6G Dyes and their Mixture in Solid Matrix

The absorption and fluorescence spectra of RhB dye and Rh6G in solvent and doped in silica glass with different concentrations have been carried out in the spectral range of 450-750 nm. The fluorescence spectra have been recorded with two excitation wavelength 370 and 450 nm. CdS nanoparticles (NPs) were prepared by sol-gel method in order to investigate their optical behaviors as efficient Förster resonance energy transfer (FRET). Pure RhB and RhB dye doped in Silica glass with different concentrations were tested as acceptor from the CdS nanoparticles. In this paper, we study FRET behavior of CdS NPs with RhB dye and energy transfer between RhB dye and Rh6G dye.