27 research outputs found

    Study of Arthropod Communities in a Virginia Tobacco Agro-Ecosystem

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    The cultivation of tobacco is one of users of agro-chemical substances such as insecticides, herbi-cides, defoliants, and fertilizers among other food crops and plants with high economical value. The use of these chemicals may bring negative effects regarding the richness and abundance of arthropods. The study of arthropod community in the Virginia tobacco ecosystem was carried out in Central Lombok, West Nusa Tenggara Province, during the 2010 plantation year. It was aimed at finding the composition, structure, and dynamic of the arthropod diversity around the tobacco field. Samples were obtained by using trapping techniques (pitfall traps, yellow-pan traps, and sweep net). The number of arthropods found in Virginia tobacco field are 69, consisting of 65 species of insects (belonging to 46 families and 8 orders) and 4 species of spiders (belonging to 4 families). The majority of insects found was Hymenoptera, dominated by bees. Based on the ecological functions, the major group of arthro-pods documented was phytophagous (20 species), mostly Coleoptera and Orthoptera. Yet, the number of predators was relatively more abundant than that of the phytophagous. The number of kinds of ar-thropods commonly interacting around the field fluctuated during the growing period, while in the cultivation period the number decreased. The diversity of the species (H) and the ratio of abundance of the natural enemies and phytophagous in the field was high

    The role of different strain backgrounds in bacterial endotoxin-mediated sensitization to neonatal hypoxic-ischemic brain damage

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    Genetic background is known to influence the outcome in mouse models of human disease, and previous experimental studies have shown strain variability in the neonatal mouse model of hypoxia-ischemia. To further map out this variability, we compared five commonly used mouse strains: C57BL/6, 129SVJ, BALB/c, CD1 and FVB in a pure hypoxic-ischemic setup and following pre-sensitization with lipopolysaccharide (LPS). Postnatal day 7 pups were subjected to unilateral carotid artery occlusion followed by continuous 30 min 8% oxygen exposure at 36 °C. Twelve hours prior, a third of the pups received a single intraperitoneal LPS (0.6 μg/g) or a saline (vehicle) administration, respectively; a further third underwent hypoxia-ischemia alone without preceding injection. Both C57BL/6 and 129SVJ strains showed minimal response to 30min hypoxia-ischemia alone, BALB/c demonstrated a moderate response, and both CD1 and FVB revealed the highest brain damage. LPS pre-sensitization led to substantial increase in overall brain infarction, microglial and astrocyte response and cell death in four of the five strains, with exception of BALB/c that only showed a significant effect with terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). Saline administration prior to hypoxia-ischemia resulted in an increase in inflammatory-associated markers, particularly in the astroglial activation of C57BL/6 mice, and in combined microglial activation and neuronal cell loss in FVB mice. Finally, two of the four strongly affected strains--C57BL/6 and CD1--revealed pronounced contralateral astrogliosis with a neuroanatomical localization similar to that observed on the occluded hemisphere. Overall, the current findings demonstrate strain differences in response to hypoxia-ischemia alone, to stress associated with vehicle injection, and to LPS-mediated pre-sensitization, which partially explains the high variability seen in the neonatal mouse models of hypoxia-ischemia. These results can be useful in future studies of fetal/neonatal response to inflammation and reduced oxygen-blood supply

    Ant Colony Optimization for Routing and Tasking Problems for Teams of UAVs

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    Lung point in the absence of pneumothorax

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    Lung point in the absence of pneumothorax

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    O-079 Regulation of Implantation by Interaction between the Type-1 IGF Receptor (IGF1R) and MiR-145

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    INTRODUCTION: Fetal heart rate variability (fHRV) is an indirect index of fetal wellbeing and autonomous nervous system (ANS) integrity. Fetal monitoring methods in labor are widely based on fHRV analysis but fail in early detection of hypoxia and acidemia. We explored the relation among two measures of ANS regulation, fHR Average Acceleration and Deceleration Capacities (AAC and ADC), computed by Phase-Rectified Signal Averaging (PRSA) method, and biomarkers of fetal acidemia, i.e. pH, Lactate (L) and Base Excess (BE). METHODS: In an in-vivo near-term fetal sheep model (n=9) repetitive umbilical cord occlusions (UCO) were applied for 1 min every 2.5 min as follows: mild partial UCO for 1 h; moderate partial UCO for 1h; and complete UCO x 1-2 h, until arterial pH<7.00. Arterial blood samples were collected at baseline, every 20 min during the UCO series, and at 1 h of recovery. Fetal ECG was recorded. AAC/ADC were computed for each phase of the protocol. Pearson correlation coefficient (r) was determined between AAC/ADC and biomarkers at T=3 (T determines the periodicities detected by PRSA). RESULTS: A significant correlation between AAC/ADC and biomarkers was found (0.45<|r|<0.8, p<0.05). The largest correlation was found between ADC and pH (r=-0.79; p<0.05). The table shows the r values between AAC/ADC and biomarkers. pH L BE ADC -0.79 * 0.55 * -0.72 * AAC 0.75 * -0.57 * 0.69 * Table 1: r between AAC/ADC and biomarkers (* p<0.05). CONCLUSIONS: This is the first in vivo evaluation of the correlation between AAC/ADC and acid-base status biomarkers computed by PRSA analysis of fHR. Our findings suggest that worsening acid-base status has an impact on AAC and ADC of fHR. This finding puts the grounds for future clinical studies

    Peptidylarginine deiminases (PADs): novel drug targets for prevention of neuronal damage following hypoxic ischemic insult (HI) in neonates

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    Neonatal hypoxic ischaemic (HI) injury frequently causes neural impairment in surviving infants. Our knowledge of the underlying molecular mechanisms is still limited. Protein deimination is a post-translational modification caused by Ca(+2) -regulated peptidylarginine deiminases (PADs), a group of five isozymes that display tissue-specific expression and different preference for target proteins. Protein deimination results in altered protein conformation and function of target proteins, and is associated with neurodegenerative diseases, gene regulation and autoimmunity. In this study, we used the neonatal HI and HI/infection [lipopolysaccharide (LPS) stimulation] murine models to investigate changes in protein deimination. Brains showed increases in deiminated proteins, cell death, activated microglia and neuronal loss in affected brain areas at 48 h after hypoxic ischaemic insult. Upon treatment with the pan-PAD inhibitor Cl-amidine, a significant reduction was seen in microglial activation, cell death and infarct size compared with control saline or LPS-treated animals. Deimination of histone 3, a target protein of the PAD4 isozyme, was increased in hippocampus and cortex specifically upon LPS stimulation and markedly reduced following Cl-amidine treatment. Here, we demonstrate a novel role for PAD enzymes in neural impairment in neonatal HI Encephalopathy, highlighting their role as promising new candidates for drug-directed intervention in neurotrauma. Hypoxic Ischaemic Insult (HI) results in activation of peptidylarginine deiminases (PADs) because of calcium dysregulation. Target proteins undergo irreversible changes of protein bound arginine to citrulline, resulting in protein misfolding. Infection in synergy with HI causes up-regulation of TNFα, nuclear translocation of PAD4 and change in gene regulation as a result of histone deimination. Pharmacological PAD inhibition significantly reduced HI brain damage

    Sub-pA Delta-Sigma Current Amplifier for Single Molecule Nanosensors

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    A current-readout front-end for nanosensors based on a ΔΣ converter approach features an input-equivalent noise of 5fA/√Hz in a 1kHz bandwidth.The front-end detects ion-channel activity caused by single-molecule interactions. The device occupies 0.5mm2 in 0.35μm 2P4M CMOS and consumes less than 23mW
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