Artificial Neural Network-based Approach for Plate Segmentation and Character Recognition

A procedure is presented for Plate Segmentation and Character Recognition through artificial neural network (ANN). All the tasks are accomplished using following steps. Violation Detection, Violation Plate localization, and Plate Recognition. The neural network was able to learn the nonlinear relationship between the pixel ratios for each of the nine blocks and a unique character and are able to help us out In resolving Artificial Neural Network-based Approach for Plate Segmentation and Character Recognition proble

A Neural Network-based Approach for the Machine Vision of Character Recognition

In this paper, an attempt is made to develop off-line recognition strategies for the isolated Handwritten English character(A to Z) and (0 to 9). Challenges in handwritten character recognition wholly lie in the variation and distortion of handwritten characters, since different people may use different style of handwritten, and direction to draw the same shape of the characters of their known script. The paper provides a review on the process of character recognition using neural network. Character recognition methods are listed under two main headlines. The Offline methods use the static images properties. The Offline methods are further divided into four methods, which are clustering, Feature Extraction, Pattern Matching and Artificial Neural Network. The Online methods are subdivided into k-NN classifier and direction based algorithm. Character preprocessing is used binarization, thresolding and segmentation method. Neural network based method improves the character recognition. The proposed method is based on the feed forward back propogation method to classify the characters. The ANN is trained using the Back Propogation algorithm. In the proposed system, English nue-merical letter is represented by binary numbers that are assume as input and fed to an ANN. Neural network followed by Back Propagation Algorithm which compromises Training

TO INVESTIGATE THE CONSEQUENCES OF INTERNET ADDICTION DISORDER

ABSTRACT Around the world more than 80% of youth are spending a large amount of time on the internet. Therefore, it becomes essential for us to aware of its impact on adolescent behavior, their psychological well-being and development. In some respects, addictive use of the Internet resembles other so-called "process" addictions, in which a person is addicted to an activity or behavior (including gambling, shopping, or certain sexual behaviors) rather than a substance (mood-altering drugs, tobacco, food, etc.). This study investigated the continuation of Internet addiction and the extent of problems caused by such potential misuse

A quadrafunctional electrocatalyst of nickel/nickel oxide embedded N-graphene for oxygen reduction, oxygen evolution, hydrogen evolution and hydrogen peroxide oxidation reactions

A multifunctional nano-heterostructured electrocatalyst of transition metal/metal oxide (nickel/nickel oxide) embedded on nitrogen-doped graphene is reported. The hybrid composite of N-doped graphene nanosheets with a high atomic percentage of nitrogen (8.2 at%) and embedded with highly distributed nickel/nickel oxide nanoparticles inside the graphene layers is synthesized by a one pot thermal annealing process. The resultant composite demonstrates excellent electrocatalytic activity utilizing the superior electrocatalytic properties of nickel/nickel oxide nanoparticles supported on nitrogen-doped graphene. The hybrid exhibits efficient oxygen reduction reaction (ORR) properties comparable with state-of-the-art electrode Pt/C with a four-electron transfer pathway and superior oxygen evolution reaction (OER) compared to the state-of-the-art electrode for the OER, Ru/C. Alternatively, this composite acts as an excellent electrode material for the hydrogen evolution reaction (HER) both in acidic and alkaline media. Nevertheless, this composite facilitates the hydrogen peroxide oxidation reaction (HPOR) in the presence of hydrogen peroxide, which is crucial for developing reversible fuel cells and fuel cells with liquid oxidant

Acquired differential regulation of caspase-8 in cisplatin-resistant non-small-cell lung cancer

Failure to efficiently induce apoptosis contributes to cisplatin resistance in non-small-cell lung cancer (NSCLC). Although BCL-2-associated X protein (BAX) and BCL-2 antagonist killer (BAK) are critical regulators of the mitochondrial apoptosis pathway, their requirement has not been robustly established in relation to cisplatin. Here, we show that cisplatin can efficiently bypass mitochondrial apoptosis block caused by loss of BAX and BAK, via activation of the extrinsic death receptor pathway in some model cell lines. Apoptosis resistance following cisplatin can only be observed when both extrinsic and intrinsic pathways are blocked, consistent with redundancy between mitochondrial and death receptor pathways in cisplatin-induced apoptosis. In H460 NSCLC cells, caspase-8 cleavage was shown to be induced by cisplatin and is dependent on death receptor 4, death receptor 5, Fas-associated protein with death domain, acid sphingomyelinase and ceramide synthesis. In contrast, cisplatin-resistant cells fail to activate caspase-8 via this pathway despite conserving sensitivity to death ligand-driven activation. Accordingly, caspase-8 activation block acquired during cisplatin resistance, can be bypassed by death receptor agonism

Abeta peptides can enter the brain through a defective blood-brain barrier and bind selectively to neurons.

We have investigated the possibility that soluble, blood-borne amyloid beta (Abeta) peptides can cross a defective blood-brain barrier (BBB) and interact with neurons in the brain. Immunohistochemical analyses revealed extravasated plasma components, including Abeta42 in 19 of 21 AD brains, but in only 3 of 13 age-matched control brains, suggesting that a defective BBB is common in AD. To more directly test whether blood-borne Abeta peptides can cross a defective BBB, we tracked the fate of fluorescein isothiocyanate (FITC)-labeled Abeta42 and Abeta40 introduced via tail vein injection into mice with a BBB rendered permeable by treatment with pertussis toxin. Both Abeta40 and Abeta42 readily crossed the permeabilized BBB and bound selectively to certain neuronal subtypes, but not glial cells. By 48 h post-injection, Abeta42-positive neurons were widespread in the brain. In the cerebral cortex, small fluorescent, Abeta42-positive granules were found in the perinuclear cytoplasm of pyramidal neurons, suggesting that these cells can internalize exogenous Abeta42. An intact BBB (saline-injected controls) blocked entry of blood-borne Abeta peptides into the brain. The neuronal subtype selectivity of Abeta42 and Abeta40 was most evident in mouse brains subjected to direct intracranial stereotaxic injection into the hippocampal region, thereby bypassing the BBB. Abeta40 was found to preferentially bind to a distinct subset of neurons positioned at the inner face of the dentate gyrus, whereas Abeta42 bound selectively to the population of large neurons in the hilus region of the dentate gyrus. Our results suggest that the blood may serve as a major, chronic source of soluble, exogenous Abeta peptides that can bind selectively to certain subtypes of neurons and accumulate within these cells

Brain-reactive autoantibodies prevalent in human sera increase intraneuronal amyloid-β(1-42) deposition.

Previous studies have reported immunoglobulin-positive neurons in Alzheimer\u27s disease (AD) brains, an observation indicative of blood-brain barrier (BBB) breakdown. Recently, we demonstrated the nearly ubiquitous presence of brain-reactive autoantibodies in human sera. The significance of these observations to AD pathology is unknown. Here, we show that IgG-immunopositive neurons are abundant in brain regions exhibiting AD pathology, including intraneuronal amyloid-β(42) (Aβ(42)) and amyloid plaques, and confirm by western analysis that brain-reactive autoantibodies are nearly ubiquitous in human serum. To investigate a possible interrelationship between neuronal antibody binding and Aβ pathology, we tested the effects of human serum autoantibodies on the intraneuronal deposition of soluble Aβ(42) peptide in adult mouse neurons in vitro (organotypic brain slice cultures). Binding of human autoantibodies to mouse neurons dramatically increased the rate and extent of intraneuronal Aβ(42) accumulation in the mouse cerebral cortex and hippocampus. Additionally, individual sera exhibited variable potency related to their capacity to enhance intraneuronal Aβ(42) peptide accumulation and immunolabel neurons in AD brain sections. Replacement of human sera with antibodies targeting abundant neuronal surface proteins resulted in a comparable enhancement of Aβ(42) accumulation in mouse neurons. Overall, results suggest that brain-reactive autoantibodies are ubiquitous in the blood and that a defective BBB allows these antibodies to access the brain interstitium, bind to neuronal surfaces and enhance intraneuronal deposition of Aβ(42) in AD brains. Thus, in the context of BBB compromise, brain-reactive autoantibodies may be an important risk factor for the initiation and/or progression of AD as well as other neurodegenerative diseases