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Hyperglycemia in diabetic conditions may cause oxidative stress in pancreatic ß-cells, leading to their dysfunction and insulin resistance within peripheral tissues. Previous studies suggest that American ginseng berry extract may have hypoglycemic effects, as well as offer antioxidant protection. We examined effects of American ginseng berry extract and ginsenoside Re in a pancreatic ß-cell line, MIN-6, to determine if these two properties are related. Cells were exposed to oxidative stress via hydrogen peroxide incubation and oxidative stress was measured by oxidation of 2′,7′-dichlorofluorescin diacetate. These cells showed a concentration-related response to hydrogen peroxide at 100–500 μM. In acute conditions where cells were treated with the extract for 10 min, we observed reduced oxidant injury suggesting direct scavenging effects. Chronic incubation of cells with the extract for 48 hours also demonstrated attenuation of oxidative stress. At high concentrations, Re showed a mild antioxidant effect in MIN-6 cells. Our insulin release observations also showed that the extract may help to increase insulin secretions from the cells. Our data suggest that the observed ability of ginseng to reduce blood glucose levels may be linked to its antioxidant effects on pancreatic ß-cells.

Vascular inflammation is a pivotal factor of a variety of diseases, such as atherosclerosis and tumor progression. The present study was designed to examine the anti-inflammatory effect of ethanol extract of Gastrodia elata rhizome (EGE) in primary cultured human umbilical vein endothelial cells (HUVEC). Pretreatment of cells with EGE attenuated TNF-α-induced increase in expression levels of cell adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin. Real time qRT-PCR also showed that EGE decreased the mRNA expression levels of ICAM-1, VCAM-1, E-selectin as well as macrophage chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). In addition, EGE significantly inhibited TNF-α-induced increase in monocyte adhesion of HUVEC in a dose-dependent manner. Furthermore, EGE significantly inhibited TNF-α-induced intracellular reactive oxygen species (ROS) production and p65 NF-κB activation by preventing IκB-α phosphorylation. In conclusion, the present data suggest that EGE could suppress TNF-α-induced vascular inflammatory process via inhibition of oxidative stress and NF-κB activation in HUVEC.

Mesangial cell proliferation is correlated with the progression of renal failure. The purpose of this study was to determine whether a water extract of Poria cocos Wolf (WPC), a well-known medicinal plant, regulates rat mesangial cell proliferation in the presence of high glucose (HG). HG significantly accelerated [³H]-thymidine incorporation, which was inhibited by WPC (1–50 μg/mL) in a dose-dependent manner. Cell migration and fibronectin mRNA expression data also supported the anti-proliferative effect of WPC. Western blot analysis revealed that pretreatment with WPC decreased the expression of cyclins and cyclin-dependent kinases (CDKs) and promoted the expression of p21^waf1/cip1 and p27^kip1. WPC also suppressed HG-induced p38 mitogen-activated protein kinase (p38 MAPK) and extracellular-signal-regulated kinase 1/2 (ERK 1/2) phosphorylation. Furthermore, WPC inhibited HG-induced production of dichlorofluorescein (DCF)-sensitive intracellular reactive oxygen species (ROS). In conclusion, HG promoted mesangial cell proliferation, and WPC inhibited this activity, at least in part, via induction of cell cycle arrest and activation of anti-oxidant properties. Taken together, these results suggest that P. cocos may be a potent regulator of HG-induced proliferation.

Solena amplexicaulis (Lam.) Gandhi (SA) has been used as a traditional medicine for the treatment of dysentery, multiple abscess, gastralgia, urethritis, and eczema in the minority area of China. This study was aimed to examine the cell proliferation inhibitory activity of the SA extract (SACE) and its mechanism of action in human hepatoma cell line (HepG2) and evaluate its anti-angiogenesis activity in human umbilical vein endothelial cell line (HUVEC). SACE could inhibit the growth of HepG2 cells in a dose- and time-dependent manner. FCM analysis showed that SACE could induce G2/M phase arrest, cell apoptosis, the mitochondrial membrane potential loss (ΔΨm) and increase the production of intracellular ROS of HepG2 cells. After treatment with SACE, topical morphological changes of apoptotic body formation, obvious increase of apoptosis-related protein expressions, such as Bax, cytochrome c, caspase-3, PARP-1, and decrease of Bcl-2, procaspase-9 protein expressions were observed at the same time. Moreover, SACE caused the significant inhibition of endothelial cell migration and tube formation in HUVEC cells. The results suggested that SACE could act as an angiogenesis inhibitor and induce cell apoptosis via a caspase-dependent mitochondrial pathway. Therefore, SACE could be a potent candidate for the prevention and treatment of liver cancer.

Epidemiological studies show increased particulate matter (PM${}_{2.5}$) particles in ambient air are correlated with increased myocardial infarctions. Given the close association of capillaries and alveoli, the dysfunction is caused when inhaled PM${}_{2.5}$ particles come in close proximity to capillary endothelial cells. We previously suggested that the inhalation of PM${}_{2.5}$ diesel exhaust particles (DEP) induces oxidative stress and upregulates the Nrf2/HO-1 pathway, inducing vascular permeability factor VEGFA secretion, which results in cell-cell adherens junction disruption and PM${}_{2.5}$ transmigratation into circulation. Here, we minimized the level that PM${}_{2.5}$ traveled in the bloodstream by pre-supplementing with a traditional Chinese medicine (TCM) Ganoderma tsugae DMSO extract (GTDE) prior to PM${}_{2.5}$ exposure. Our results show that PM${}_{2.5}$ caused alterations in enzyme activities and cellular anti-oxidant balance. We found decreased glutathione levels, a reduced cellular redox ratio, increased ROS generation and cytotoxicity in the cellular fractions. The oxidative stress caused DNA damage and apoptosis, likely causing downstream molecular events that trigger vasculature permeabilization and, eventually, cardiovascular disorders. Our results show long-term GTDE treatment increased endogenous glutathione level, while PM${}_{2.5}$-reduced glutathione levels and the cellular redox ratio. GTDE was protective against the genotoxic and apoptotic effects initiated by PM${}_{2.5}$ oxidative stress. Vascular permeability revealed that PM${}_{2.5}$ only accumulated on the surface of cells after GTDE treatment; no penetration was detected. After two weeks of GTDE treatment, VEGFA secretion was significantly reduced in human umbilical vein endothelial cells (HUVEC) and endothelial cell migration was blocked. Our results suggest GTDE prevents PM${}_{2.5}$ transmigration into the bloodstream, and the resultant dysfunction, by inhibiting oxidative stress production and endothelial permeability.

Carnosol is an anti-oxidant and anti-inflammatory compound from rosemary. In this paper, we investigated antitumor activity of carnosol against human osteosarcoma cells. We found the viability of human osteosarcoma MG-63 cells was significantly decreased in the presence of carnosol (cell viabilities: 17.2% for 20μg/ml of CS vs. 100% for control, $p<0.05$). Carnosol induced apoptosis and cell cycle arrest in a dose-dependent manner in MG-63 cells. Furthermore, carnosol exposure increased the levels of reactive oxygen species (ROS). The pre-treatment of NAC, the ROS scavenger, blocked the inhibition of cell viability in the carnosol treatment, indicating that ROS is important in the antiproliferation effect. Moreover, we demonstrated that carnosol significantly induced autophagy and co-administration of autophagy inhibitor reduced the antiproliferating effect of carnosol. This result exhibited the cytotoxic effect of autophagy induced by carnosol in MG-63 cells. Interestingly, the treatment of NAC decreased carnosol-induced autophagy. Collectively, these data indicate that carnosol suppresses the viability of human osteosarcoma MG-63 cells by upregulation of apoptosis and autophagy, which are both mediated by ROS. Thus, carnosol might serve as a potential therapeutic agent against osteosarcoma.

Oxidative stress has been implicated in the pathogenesis of atherosclerotic cardiovascular diseases. Dietary supplementation of anti-oxidants has been reported to have beneficial effects on the prevention of atherogenic diseases. Luteolin (a natural flavonoid) has been shown to possess antimutagenic, antitumorigenic, anti-oxidant and anti-inflammatory properties. However, the effects and underlying molecular mechanisms of luteolin on cardiovascular systems are poorly explored. Therefore, the aim of the present study was to test whether luteolin could protect against oxidative stress-induced endothelial cell injury and explore the underlying mechanisms. In this study, human umbilical vein endothelial cells (HUVECs) were pre-treated with luteolin followed by hydrogen peroxide induction (H₂O₂). Our results showed that luteolin protected against H₂O₂-induced oxidative stress and ameliorated ROS and superoxide generation. In addition, we found that luteolin treatment inhibited the H₂O₂-induced membrane assembly of NADPH oxidase subunits, which was further confirmed by specifically inhibiting NADPH oxidase using DPI treatment. Furthermore, pAMPK protein expression was enhanced and p-PKC isoforms were significantly down-regulated by luteolin treatment in a dose-dependent manner, and a similar effect was observed upon DPI treatment. However, co-treatment with the specific inhibitor of AMPK (Compound C) restored p-PKC levels suggesting the role of AMPK signaling in regulating p-PKC expression under oxidative stress condition in HUVECs. Finally, we confirmed using siRNAs and specific inhibitor and/or activator of AMPK (AICAR) that luteolin treatment induced AMPK is a key player and regulator of activated expression of PKC isoforms and thereby confers protection against H₂O₂-induced oxidative stress in HUVECs.

Autophagy is a process of active programmed cell death, where a dying cell induces autophagosomes and subsequently regulated by degradative machinery. The aim of this study was to investigate the mechanism behind induction of autophagic cell death by Naringin flavonoid in AGS cancer cells. Growth inhibition of AGS cells showed downregulation of PI3K/Akt/mTOR signaling by Naringin treatment. Transmission electron microscopy observation showed swollen mitochondria and lysosome near peri-nuclear zone fused with autophagic vacuoles. Rapamycin pre-treatment with Naringin showed significant decrease in mTOR phosphorylation and increase in LC3B activation in AGS cells. Decrease in mTOR phosphorylation is associated with lysosomal function activation was observed by time-dependent treatment of Naringin. Induction of lysosomal membrane permeabilization (LMP) was observed by LAMP1 activation leading lysosomal cell death by releasing Cathepsin D from lysosomal lumen to cytosol. Naringin treated AGS cells showed up-regulating BH3 domain Bad, down-regulating Bcl-xL, and Bad phosphorylation and significant mitochondrial fluorescence intensity expression. Significant localization of mitochondria and LC3B activation was examined by person coefficient correlation. Activation of ERK1/2-p38 MAPKs and production of intracellular ROS has been observed over Naringin treatment. It has also been elucidated that pre-treatment with NAC inhibited mitochondria-LC3B colocalization, where ROS acted as upstream of ERK1/2-p38 MAPKs activation. Lysosomal cell death involvement has been evaluated by BAF A1 pre-treatment, inhibiting LAMP1, Cathepsin D, ROS, and blocking autophagolysosome in AGS cell death. Taken together, these findings show that, Naringin induced autophagy cell death involves LMP mediated lysosomal damage and BH3 protein Bad activation in AGS cancer cells.

Herpes simplex virus type 1 (HSV-1) is ubiquitous in many populations despite the use of acyclovir or related nucleoside analogs for treating infection. Drug resistance impairs the treatment of HSV-infected individuals who have immune deficits, underscoring the need for new safe and effective antiviral agents. Mori ramulus (the young twig of Morus alba L.) has long been used to treat diseases in Korea, Japan, and China. Recent studies have reported multiple pharmacological activities of Mori ramulus and its constituent morusin, but their effects on HSV-1 remain unknown. Here, we found that treatment with Mori ramulus ethanol extract (MRE) significantly reduced the replication of fluorescently labeled HSV-1 in Vero cells and inhibited the expression of HSV-1 envelope glycoprotein D (gD) and tegument protein VP16. MRE, furthermore, blocked HSV-1-induced production of reactive oxygen species (ROS), and this mediated the inhibition of viral replication. We identified morusin as the active antiviral component of MRE and found that morusin post-treatment was sufficient to inhibit viral gD and VP16 in addition to HSV-1-induced ROS production. Therefore, the inhibition of HSV-1-induced ROS may explain the antiviral activity of MRE against HSV-1. MRE or its component morusin may be potentially developed for anti-HSV-1 agents.

Preconditioning has a powerful protective potential against myocardial ischemia-reperfusion injury (I/R). Our prior work demonstrated that baicalein, a flavonoid derived from the root of Scatellaria baicalensis Georgi (also known as Huangqin), confers this preconditioning protection. This study further explored the mechanisms of baicalein preconditioning (BC-PC) in mouse cardiomyocytes. Cells were treated with baicalein (10 μM) for a brief period of time (10 min) prior to simulated ischemia 90 min/reperfusion for 180 min. Baicalein triggered an induction of a small amount of mitochondrial reactive oxygen species (ROS) prior to the initiation of ischemia, assessed by 6-carboxy-2^′, 7^′-dichlorodihydrofluorescein diacetate (6-carboxy-H₂DCFDA). It also significantly increased cell viability measured by propidium iodide (PI) and lactate dehydrogenase and preserved mitochondrial membrane potential assessed by TMRM fluorescence intensity. Myxothiazol, a mitochondrial electron transport chain complex III inhibitor, partially blocked ROS generation induced by BC-PC and reduced cell viability. BC-PC increased phosphorylation of Akt (Thr308 and Ser473) and eNOS Ser1177, and nitric oxide (NO) production measured using 4,5-diaminofluorescein diacetate (DAF-2 DA, 1 μM). Akt inhibitor API-2 abolished Akt phosphorylation and reduced DAF-2 production and cell viability. In addition, BC-PC decreased phosphorylation of pyruvate dehydrogenase (PDH) reflecting upregulated PDH activity, and increased ATP production at 30 min during reperfusion. Taken together, baicalein preconditioning-induced cardioprotection involves pro-oxidant generation, activates survival signaling Akt/eNOS/NO, and improves metabolic recovery after I/R injury. Our work provides new perspectives on the effect of baicalein on cardiac preconditioning against I/R injury.

Isoproterenol (ISO) is widely used to treat bronchial asthma, cardiogenic or septic shock, complete atrioventricular block, and cardiac arrest. However, it can also cause myocardial damage owing to infarct-like necrosis. Curdione, an extract of the Chinese herb Rhizoma Curcumae, has a variety of pharmacological activities, including cardioprotective effects. In this study, we investigated the protective effects of curdione and its underlying mechanisms in an ISO-induced myocardial injury model. Our results showed that curdione attenuated ISO-induced H9c2 cell proliferation inhibition and lactic dehydrogenase (LDH) release. Curdione ameliorated morphological damage and reduced the ISO-induced elevation of serum creatine kinase-MB isoenzyme (CK-MB) and LDH. Furthermore, curdione inhibited ISO-induced cell apoptosis, modulated the expression of Bcl-2 and Bax proteins, repealed the accumulation of ISO-induced reactive oxygen species (ROS), prevented mitochondrial dysfunction, and activated the Nrf2/SOD1/HO-1 signaling pathway. The above results show that curdione exerts a protective effect against ISO-induced myocardial damage by inhibiting apoptosis and oxidative stress, suggesting that curdione is a potential therapeutic strategy to prevent ISO-induced myocardial damage.

Emodin is a natural compound found in several traditional Chinese medicines, including Rheum palmatum and Polygonum cuspidatum. Recent studies have shown that emodin exhibits potent anticancer effects against a variety of cancer types, including liver, breast, lung, and colon cancer. Emodin’s anticancer effects are mediated through several mechanisms, including inhibition of cell proliferation, induction of apoptosis, and suppression of tumor angiogenesis and metastasis. In this review, we provide an overview of recent research progress and new perspectives on emodin’s anticancer effect. We summarize the current understanding of the molecular mechanisms underlying emodin’s anticancer activity, including its effects on signaling pathways such as the PI3K/Akt, MAPK, and NF-$\kappa$B pathways. We also discuss the potential of emodin as a therapeutic agent for cancer treatment, including its use in combination with conventional chemotherapeutic drugs and as a sensitizer for radiotherapy. Furthermore, we highlight recent advances in the development of emodin derivatives and their potential as novel anticancer agents. Finally, we discuss the challenges and opportunities for the translation of emodin’s anticancer properties into clinical applications, including the need for further preclinical and clinical studies to evaluate its safety and efficacy. In conclusion, emodin represents a promising natural compound with potent anticancer properties, and its potential as a therapeutic agent for cancer treatment warrants further investigation. This review provides a comprehensive overview of the current research progress and new perspectives on emodin’s anticancer effects, which may facilitate the development of novel therapeutic strategies for cancer treatment.

The use of NPs in the health care field is increasing. Before their biological application, investigating the toxicities of both n-type ZnO nanoparticles (NPs) and nitrogen-doped (“p-type”) NPs is important. Using L929 cells, the cell viability, oxidative stress, apoptosis induction, inflammatory responses, and cellular uptake were assayed 24h after the addition of n-type ZnO NPs and nitrogen-doped NPs (which act as p-type) (25$\mu$g/mL). The ZnO NPs were fabricated using a gas evaporation method. Increased H₂O₂ generation and decreased levels of glutathione were more evident in with n-type than in those treated with nitrogen-doped (“p-type”) ZnO NPs. Caspase-3/-7 activity was higher in cells treated with n-type ZnO NPs than in those treated with nitrogen-doped (“p-type”) NPs. Elevated levels of TNF-$\alpha$ and IL-1$\beta$ were observed in cell culture supernatants: IL-1$\beta$ levels were higher in n-type ZnO NPs than nitrogen-doped (“p-type”) NPs. The cellular Zn uptake of n-type ZnO NPs was higher than nitrogen-doped (“p-type”) NPs. These findings show that n-type ZnO NPs have higher cytotoxicity than nitrogen-doped (“p-type”) ZnO NPs. This may be due to a reductive effect of n-type ZnO NPs that induces higher free radical production, reactive oxygen species (ROS) generation, and cellular uptake of this type of ZnO NPs.

Due to their special and growing medical recent interest, the fullerenes started to be a very studied class of chemical compounds. In order to improve their water solubility and to reduce their cytotoxic characteristics, the fullerenes have been coupled in a system fullerene/PVP/porphyrin (C60/PVP/TPP) and its application in photodynamic therapy will be evaluated in this paper. The oxidative stress effects on photodynamic therapy with systems fullerene/poly-N-vinylpirrolidone/5,10,15,20-tetrakis(4-phenyl)porphyrin (C60/PVP/TPP) were tested on Wistar rats sub-cutaneously inoculated with Walker 256 carcinoma. The animals were irradiated with red light (λ = 685 nm; D = 50 J/cm²; 15 minutes) 24 h after intra-peritoneal administration of 10 mg/kg body weight of the system C60/PVP/TPP. After photodynamic therapy, the free radicals in tumors have been indirectly evaluated by lipid peroxides level (measured as thiobarbituric reactive substances) and protein carbonyls (indices of oxidative effects produced on susceptible biomolecules), both of them increasing in tumor tissues of animals 24 h after treatment. The levels of thiol groups and total antioxidant capacity have been determined in tumors, too, their decreasing values being the effect of the strong tumoral oxidative process.

Photodynamic therapy (PDT) is a non-invasive method for cancer treatment that relies on the generation of excess reactive oxygen species (ROS), upon excitation of photosensitizer (PS), to eradicate tumor cells. However, the overexpress of endogenous antioxidants in tumor cells will eliminate the ROS and restrict the therapeutic efficacy of PDT. Herein, a novel type of PS was developed by conjugating cinnamaldehyde (CA), a kind of oxidative stress amplified agent, with porpholactam through a hydrazone bond. The new PS retains the photophysical properties of porpholactam, which displays high singlet oxygen quantum yield for the PDT function. The results of in vitro experiments performed including ROS assay and the cytotoxicity in cancer cells suggest that the rational design of the novel porpholactam-CA derivatives result in enhanced ROS generation upon irradiation, providing a possible approach to achieve enhanced therapeutic effects in PDT.

Photodynamic therapy is used to treat a variety of cancers. In this paper, water-soluble porphyrin photosensitizers (H₂P1$\sim$H₂P3) for photodynamic therapy were synthesized, containing three groups -CH₃, -CN, and -CF₃. Density functional theory is used to optimize the structure of H₂P1-H₂P3 and calculate the $\mathrm{\Delta }$E value. The smaller the value of $\mathrm{\Delta }$E, the more favorable the electron transfer and thus the higher activity of the porphyrin photosensitizers. Due to the electron-withdrawing groups of -CN and -CF₃, H₂P2 and H₂P3 have lower $\mathrm{\Delta }$E values, higher reactive oxygen species yields compared with H₂P1. The H₂P2 porphyrin photosensitizers showed positive photodynamic therapeutic activity against hepatocellular carcinoma cells (HepG2) and good compatibility with human umbilical vein endothelial cells (HUVECs) by cellular anticancer activity assay. The anti-cancer mechanism of PSs was explained by living and dead cell staining experiment and intracellular reactive oxygen species experiment. PSs produced reactive oxygen species (ROS) in cancer cells under light irradiation, which induced cancer cell apoptosis.

Choosing the right photosensitizers (PSs) as well as the right light source is very critical in antimicrobial photodynamic therapy (aPDT). Some light sources, such as ultraviolet, have high cytotoxicity and poor penetration and some PSs are hydrophobic with low solubility in water, and easy aggregation. To address these issues, we modified TiO₂ nanoparticles with urea and TCPP (TCPP=tetra(4-carboxyphenyl) porphyrin) as a PS and prepared N-doped-TiO₂ (NT), TCPP/TiO₂ (PT), and TCPP/N-doped-TiO₂ (PNT). Urea is a safe compound used here as a source of nitrogen (N). Nitrogen doping produces a localized N state within the TiO₂ bandgap which broadens the absorption in the visible light region. Both urea and TCPP shifted the bandgap of TiO₂ to the visible area and enabled the photodegradation of methylene blue after 30 min of aging under visible light. ¹O₂ production was monitored by the rapid and irreversible conversion of anthracene to its corresponding endoperoxide. Meanwhile, different scavengers such as p-benzoquinone (p-BQ) and tert-butanol (t-BuOH) were employed in a photocatalytic process to specify the existence of superoxide and hydroxyl radical species, respectively. PNT showed a promising photobactericidal activity and reached 100% of inhibition activity against both types of bacteria after 120 and 180 min, respectively under LED lamp (15 W) irradiation. The interaction between PNT and bacteria was also examined by FESEM.

Graphene oxide (GO), a 2D nanomaterial, is a promising material for medical application, thanks to its water solubility, antibacterial activity and relatively low cytotoxicity. However, many factors, such as lateral dimension, purity and surface chemistry, may influence its antibacterial activity, its exact mechanism is still unknown. In this work, E. coli was used as model bacterium to determine the antibacterial activity of well-dispersed GO which was obtained by a modified Hummer method and dialyzed to remove the salts and acid used in the oxidation process. After co-culture with GO for 2h, up to 90% E. coli cells were inactivated when GO concentration at 8$\mu$g/mL. The direct interaction was not detected in FE-SEM images and the results of $\zeta$ potential showed that the interaction between GO and E. coli are repulsive$.$ Our results showed that GO can produce ROS and inactivate SOD and CAT enzymes in low concentration after co-cultured with E. coli which explained the antibacterial activity of GO in aqueous solution. Meanwhile, GO, with high purity, showed low cytotoxicity towards mammalian cells and did not cause any observable hemoglobin after co-cultured with blood cells. The data presented here prove that GO is effectively inhibit E. coli through inactivating SOD, CAT enzymes and the oxidative stress produced by ROS. Furthermore, the good biocompatibility promised its future application.

The accelerating fatality rate of breast cancer patients has led to the idea of unconventional therapeutic approach in this work. Here, we report the facile, eco-benign and economically advantageous route for producing iron oxide nanoparticles employing triphala extract (TR-IONPs). MTT assay was used to assess the in-vitro anticancer effectiveness of TR-IONPs against the multi-drug-resistant breast malignant cell (MCF-7). TR-IONPs revealed a concentration-dependent effect on MCF-7 viability, with an IC${}_{50}$ value of 6.8$\mu$g/mL for a 24-h treatment. Thus, the cytotoxic ability was established at a much lower half-maximal inhibitory concentration. As the TR-IONPs did not show remarkable toxicity toward L929 fibroblast cells, they can be trusted as a biocompatible material for real-time biomedical applications. Apoptotic death of MCF-7 cells caused by the release of Reactive Oxygen Species (ROS) was affirmed by DCFH-DA staining, DNA fragmentation assay and cell cycle analysis. Through Kirby–Bauer Disk Diffusion assay, TR-IONPs were found to hold potent antibacterial efficacy against S. aureus, E. coli and P. aeruginosa bacterial pathogens. With the demonstrated favorable results, TR-IONPs may serve as a reliable multi-functional material in the field of nanobiotechnology.

This paper describes an industrial robotics application, named Gilbreth, for autonomously picking up objects of different types from a moving conveyor belt and sorting the objects into bins according to their type. The environment, which consists of a moving conveyor belt, a break beam sensor, a 3D camera Kinect sensor, a UR10 industrial robot arm with a vacuum gripper, and different object types such as pulleys, disks, gears, and piston rods, is inspired by the NIST ARIAC competition. A first version of the Gilbreth application is implemented leveraging a number of Robot Operating System (ROS) and ROS-Industrial (ROS-I) packages. The Gazebo package is used to simulate the environment, and six external ROS nodes have been implemented to execute the required functions. Experimental measurements of CPU usage and processing times of the ROS nodes are discussed. In particular, the object recognition ROS package requires the highest processing times and offers an opportunity for designing an iterative method with the aim to fasten completion time. Its processing time is found to be on par with the time required by the robot arm to execute its movement between four poses: pick approach, pick, pick retreat and place.