A biologically inspired spiking model of visual processing for image feature detection

To enable fast reliable feature matching or tracking in scenes, features need to be discrete and meaningful, and hence edge or corner features, commonly called interest points are often used for this purpose. Experimental research has illustrated that biological vision systems use neuronal circuits to extract particular features such as edges or corners from visual scenes. Inspired by this biological behaviour, this paper proposes a biologically inspired spiking neural network for the purpose of image feature extraction. Standard digital images are processed and converted to spikes in a manner similar to the processing that transforms light into spikes in the retina. Using a hierarchical spiking network, various types of biologically inspired receptive fields are used to extract progressively complex image features. The performance of the network is assessed by examining the repeatability of extracted features with visual results presented using both synthetic and real images

Biologically inspired intensity and depth image edge extraction

In recent years artificial vision research has moved from focusing on the use of only intensity images to include using depth images, or RGB-D combinations due to the recent development of low cost depth cameras. However, depth images require a lot of storage and processing requirements. In addition, it is challenging to extract relevant features from depth images in real-time. Researchers have sought inspiration from biology in order to overcome these challenges resulting in biologically inspired feature extraction methods. By taking inspiration from nature it may be possible to reduce redundancy, extract relevant features, and process an image efficiently by emulating biological visual processes. In this paper, we present a depth and intensity image feature extraction approach that has been inspired by biological vision systems. Through the use of biologically inspired spiking neural networks we emulate functional computational aspects of biological visual systems. Results demonstrate that the proposed bio-inspired artificial vision system has increased performance over existing computer vision feature extraction approaches

Biddy : Fox Trot Song

https://digitalcommons.library.umaine.edu/mmb-vp/1101/thumbnail.jp

Love Me

https://digitalcommons.library.umaine.edu/mmb-vp/3646/thumbnail.jp

G84-702 Root and Soil Analayses for Nematodes in Corn

This NebGuide describes how to interpret laboratory results of samples submitted for nematode analysis and discusses ten species that are potentially damaging to corn. Several kinds of plant parasitic nematodes (small, soil-inhabiting roundworms) are associated with root injury, poor plant color, stunted growth, and reduced grain yields in field corn. Symptoms caused by these pests are often confused with root rot diseases, nutritional deficiencies or climatic stresses. Special laboratory analyses are, therefore, necessary to determine if nematodes are the primary cause of reduced corn performance. Since corn growers may be unfamiliar with nematode diseases, the following discussion of laboratory reports may be helpful

Lull Me To Sleep : That Slumber Melody

https://digitalcommons.library.umaine.edu/mmb-vp/2050/thumbnail.jp

My Cairo Love: An Egyptian Serenade

https://digitalcommons.library.umaine.edu/mmb-vp/3298/thumbnail.jp

One Sweet Day

https://digitalcommons.library.umaine.edu/mmb-vp/2335/thumbnail.jp

Pharmacological Preconditioning with GYKI 52466: A Prophylactic Approach to Neuroprotection.

Some toxins and drugs can trigger lasting neuroprotective mechanisms that enable neurons to resist a subsequent severe insult. This "pharmacological preconditioning" has far-reaching implications for conditions in which blood flow to the brain is interrupted. We have previously shown that in vitro preconditioning with the AMPA receptor antagonist GYKI 52466 induces tolerance to kainic acid (KA) toxicity in hippocampus. This effect persists well after washout of the drug and may be mediated via inverse agonism of G-protein coupled receptors (GPCRs). Given the amplifying nature of metabotropic modulation, we hypothesized that GYKI 52466 may be effective in reducing seizure severity at doses well below those normally associated with adverse side effects. Here we report that pharmacological preconditioning with low-dose GYKI imparts a significant protection against KA-induced seizures in vivo. GYKI (3 mg/kg, s.c.), 90-180 min prior to high-dose KA, markedly reduced seizure scores, virtually abolished all level 3 and level 4 seizures, and completely suppressed KA-induced hippocampal c-FOS expression. In addition, preconditioned animals exhibited significant reductions in high frequency/high amplitude spiking and ECoG power in the delta, theta, alpha, and beta bands during KA. Adverse behaviors often associated with higher doses of GYKI were not evident during preconditioning. The fact that GYKI is effective at doses well-below, and at pre-administration intervals well-beyond previous studies, suggests that a classical blockade of ionotropic AMPA receptors does not underlie anticonvulsant effects. Low-dose GYKI preconditioning may represent a novel, prophylactic strategy for neuroprotection in a field almost completely devoid of effective pharmaceuticals

In vitro and in vivo studies of the trypanocidal properties of WRR-483 against Trypanosoma cruzi.

BackgroundCruzain, the major cysteine protease of Trypanosoma cruzi, is an essential enzyme for the parasite life cycle and has been validated as a viable target to treat Chagas' disease. As a proof-of-concept, K11777, a potent inhibitor of cruzain, was found to effectively eliminate T. cruzi infection and is currently a clinical candidate for treatment of Chagas' disease.Methodology/principal findingsWRR-483, an analog of K11777, was synthesized and evaluated as an inhibitor of cruzain and against T. cruzi proliferation in cell culture. This compound demonstrates good potency against cruzain with sensitivity to pH conditions and high efficacy in the cell culture assay. Furthermore, WRR-483 also eradicates parasite infection in a mouse model of acute Chagas' disease. To determine the atomic-level details of the inhibitor interacting with cruzain, a 1.5 A crystal structure of the protease in complex with WRR-483 was solved. The structure illustrates that WRR-483 binds covalently to the active site cysteine of the protease in a similar manner as other vinyl sulfone-based inhibitors. Details of the critical interactions within the specificity binding pocket are also reported.ConclusionsWe demonstrate that WRR-483 is an effective cysteine protease inhibitor with trypanocidal activity in cell culture and animal model with comparable efficacy to K11777. Crystallographic evidence confirms that the mode of action is by targeting the active site of cruzain. Taken together, these results suggest that WRR-483 has potential to be developed as a treatment for Chagas' disease