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Arabic License Plate Recognition System
Agaian,Sos:
Saleh,Hani:In this paper, a new low cost Arabic vehicle license plate recognition (LPR) method is proposed which is easily extendable to other plates. A novel LP segmentation technique with three sets of feature vectors was used with template matching to form the two main modules: license plate localization module and LPR module. This method was tested on more than 238 vehicle images taken from various scenes with different fonts and backgrounds from two Arab countries. The segmentation accuracy of the implemented system was 97.5% with a recognition accuracy of 99% for fairly distorted images. The presented model shows that despite the negative impact of shadows, cracks, dirt, and character separations, the system demonstrated an overall success rate of 92% for plate localization, 95% for plates segmentation, 92% for country and city recognition, and 99% for number segmentation and recognition. Combining all rates led to an overall system accuracy of 93%. Compared to many state-of-the-art LPR systems, this newly developed system uses 3 small training sets which cut the run times of the proposed solution to less than 5 seconds using the MATLAB R2008A running on a Compaq 8510W with 4G RAM. The results are comparable, and in some cases better with restricted conditions such as skew place, plate size, illumination and backgroun
Youth civic and political participation and citizenship education in the Mediterranean: Lessons from the Arab Spring
Psycholog
The Illiteracy of Arabs before Islam : a refutation of a prevailing conception
Oriental Philosoph
Investigation of momentum and kinetic energy correction coefficients in asymmetric compound cross section flumes
Civil Engineerin
Fuzzy Record to Record Travel Algorithm in Solving Rough Set Attribute Reduction
Artificial Intelligence and Related Technologies
Abdullah,Salwani
les acteurs de la broderie, qui brode quoi et pour qui
Les costumes palestiniens d’aujourd’hui proposent
différentes interprétations de la société et des
rapports qui s’y développent, sous le couvert d’une
analogie avec le monde sensible, qui le fait souvent
prendre pour un témoin fidèle. Par ailleurs, l’expression
vestimentaire n’a pas échappé à l’adhésion à une
nouvelle identité qui se fonde sur un discours historique nationaliste codifié, avec ses mythes, sa rhétorique, ses épisodes et ses personnages symboliques, ses hymnes, ses drapeaux, ses chants, son apolitisme de la mémoire, mais aussi ses représentations esthé- tiques. C’est à celles-ci que nous nous intéressons ici à travers les costumes palestinien
Short-term treatment with tolfenamic acid improves cognitive functions in Alzheimer’s disease mice
Tolfenamic acid lowers the levels of the amyloid precursor protein (APP) and amyloid beta (Ab) when administered to C57BL/6 mice by lowering their transcriptional regulator specificity protein 1 (SP1). To
determine whether changes upstream in the amyloidogenic pathway that forms Ab plaques would improve cognitive outcomes, we administered tolfenamic acid for 34 days to hemizygous R1.40 transgenic mice. After the characterization of cognitive deficits in these mice, assessment of spatial learning and memory functions revealed that treatment with tolfenamic acid attenuated long-term memory and
working memory deficits, determined using Morris water maze and the Y-maze. These improvements occurred within a shorter period of exposure than that seen with clinically approved drugs. Cognitive
enhancement was accompanied by reduction in the levels of the SP1 protein (but not messenger RNA [mRNA]), followed by lowering both the mRNA and the protein levels of APP and subsequent Ab levels.
These findings provide evidence that tolfenamic acid can disrupt the pathologic processes associated with Alzheimer’s disease (AD) and are relevant to its scheduled biomarker study in AD patients
Pharmacodynamic mechanisms of tolfenamic acid induced SP1 degradation relative to Alzheimer's disease pathology
Alzheimer’s disease (AD) continues to disrupt the lives of millions of patients and
caregivers around the world. The few drugs currently used for AD have modest effects
on the symptoms and do not prevent the progression of the disease into total memory
loss and death. With the increase in the number of AD cases and the high social and
economical costs of the disease, there is a great need to find disease-modifying
therapeutics that target the core pathology of the disease as well as improve the
symptoms and the patients’ everyday quality of life. Two types of pathological
aggregates are found in AD. The senile plaques are composed of amyloid beta (Aβ),
which is cleaved off the amyloid precursor protein (APP) by beta-site APP cleaving
enzyme (BACE) and γ-secretase. The other deposits are the neurofibrillary tangles
(NFTs), which are mainly composed of hyperphosphorylated tau. These aggregates
and factors involved in the production or clearance of Aβ, as well as the
phosphorylation of tau are being investigated for potential AD treatments but so far no
successful drug candidate has been found. The transcription factor specificity protein 1
(Sp1) has been linked to pathological intermediates in AD. Sp1 regulates the
transcription of APP, BACE1, tau and its cyclin dependent kinase-5 (CDK5)
activators p39 and p35. Previous experiments from our lab have shown that AD like
pathology develops later in vitro and in vivo following early lead (Pb) exposure
including elevated levels of SP1, APP, Aβ, tau and CDK5 as well as cognitive decline
in mice. Studies from our lab demonstrated that decreasing Sp1 protein (SP1) levels
following oral administration of tolfenamic acid to mice was able to reduce APP and
Aβ levels and improve cognition. In this dissertation, we first provided an introduction
to AD with a review on the role of epigenetics in the disease and the various means by
which transcriptional pathways can provide therapeutic alternatives for AD. We then
examined the ability of tolfenamic acid to affect the expression of AD targets that are
regulated by Sp1 including tau, phosphorylated tau, CDK5 and BACE1 in mice by
using Western blot, real time PCR and enzyme activity assays. In addition, we studied
the ability of tolfenamic acid to prevent the increase in SP1, APP and Aβ in
differentiated neuroblastoma cells that was triggered by prior exposure to Pb. After
treatment of cells with Pb, tolfenamic acid or both, we used real time PCR, ELISA and
Western blot analyses to examine the effects of both agents on AD related
intermediates compared to control. In addition to providing a summary of the current
knowledge on epigenetic therapeutic targets for AD, the major findings of this
dissertation provide proof that tolfenamic acid was able to decrease the transcription
and translation of proteins involved in AD like tau, BACE1 and CDK5 as well as the
phosphorylation of tau in mice. Moreover, in differentiated neuroblastoma cells,
tolfenamic acid decreased the expression of SP1, APP gene and Aβ which was
previously upregulated by Pb. Hence, tolfenamic acid represents a novel oral drug
candidate that can be beneficial for AD by affecting both the amyloid and tangle
pathology of the disease through a unique transcription driven mechanis