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We evaluate road and lane estimation performance in the bird's-eye-view space. For the classical pixel-based evaluation we use established measures as discussed in our ITSC 2013 publication. MaxF: Maximum F1-measure, AP: Average precision as used in PASCAL VOC challenges, PRE: Precision, REC: Recall, FPR: False Positive Rate, FNR: False Negative Rate (the four latter measures are evaluated at the working point MaxF), F1: F1 score, HR: Hit rate. For the novel behavior-based evaluation a corridor with the vehicle width (2.2m) is fitted to the lane estimation processing result and evaluation is performed for 3 different distance values: 20 m, 30 m, and 40 m. We refer to our ITSC 2013 publication for more details. IMPORTANT NOTE: On 09.02.2015 we have improved the accuracy of the ground truth and re-calculated the results for all methods. Please download the devkit and the dataset with the improved ground truth for training again, if you have downloaded the files prior to 09.02.2015. Please consider reporting these new number for all future submissions. The last leaderboards right before the changes can be found here!

"Kept you waiting, huh?"This is a project that started at the beginning of November. My initial idea was to make complete models for the HECU and it ended up becoming a revitalization project of all the NPCs of the first 4 Half LIfe.This project does not follow any particular style or order. It is a totally idealized work with a personal version, giving it consistencies between models, and individual views of some models.There are not many more to say, only that this is my last pack that I will do for Half Life and its expansions.I hope you enjoy it and that many people continue to keep this beautiful community of moders active.As a final message, VIVA ARGENTINA CARAJOO.Other addons I recommend using this one

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In this short review we outline the morphology and biochemistry of normal discs and the changes that arise during degeneration. We review recent advances in our understanding of the aetiology of this disorder and discuss new approaches to treatment.

A schematic view of a spinal segment and the intervertebral disc. The figure shows the organization of the disc with the nucleus pulposus (NP) surrounded by the lamellae of the annulus fibrosus (AF) and separated from the vertebral bodies (VB) by the cartilaginous end-plate (CEP). The figure also shows the relationship between the intervertebral disc and the spinal cord (SC), the nerve root (NR), and the apophyseal joints (AJ).

There is frequently cleft formation with fissures forming within the disc, particularly in the nucleus. Nerves and blood vessels are increasingly found with degeneration [15]. Cell proliferation occurs, leading to cluster formation, particularly in the nucleus [19, 20]. Cell death also occurs, with the presence of cells with necrotic and apoptotic appearance [21, 22]. These mechanisms are apparently very common; it has been reported that more than 50% of cells in adult discs are necrotic [21]. The morphological changes associated with disc degeneration were comprehensively reviewed recently by Boos et al. [5], who demonstrated an age-associated change in morphology, with discs from individuals as young as 2 years of age having some very mild cleft formation and granular changes to the nucleus. With increasing age comes an increased incidence of degenerative changes, including cell death, cell proliferation, mucous degeneration, granular change and concentric tears. It is difficult to differentiate changes that occur solely due to ageing from those that might be considered 'pathological'.

Abnormal mechanical loads are also thought to provide a pathway to disc degeneration. For many decades it was suggested that a major cause of back problems is injury, often work-related, which causes structural damage. It is believed that such an injury initiates a pathway that leads to disc degeneration and finally to clinical symptoms and back pain [83]. Animal models have supported this finding. Although intense exercise does not appear to affect discs adversely [84] and discs are reported to respond to some long-term loading regimens by increasing proteoglycan content [85], experimental overloading [86] or injury to the disc [63, 87] can induce degenerative changes. Further support for the role of abnormal mechanical forces in disc degeneration comes from findings that disc levels adjacent to a fused segment degenerate rapidly (for review [88]).

The aim of these therapies is to achieve cellular repair of the degenerated disc matrix. One approach has been to stimulate the disc cells to produce more matrix. Growth factors can increase rates of matrix synthesis by up to fivefold [123, 124]. In contrast, cytokines lead to matrix loss because they inhibit matrix synthesis while stimulating production of agents that are involved in tissue breakdown [125]. These proteins have thus provided targets for genetic engineering. Direct injection of growth factors or cytokine inhibitors has proved unsuccessful because their effectiveness in the disc is short-lived. Hence gene-therapy is now under investigation; it has the potential to maintain high levels of the relevant growth factor or inhibitor in the tissue. In gene therapy, the gene of interest (e.g. one responsible for producing a growth factor such as transforming growth factor-β or inhibiting interleukin-1) is introduced into target cells, which then continue to produce the relevant protein (for review [126]). This approach has been shown to be technically feasible in the disc, with gene transfer increasing transforming growth factor-β production by disc cells in a rabbit nearly sixfold [127]. However, this therapy is still far from clinical use. Apart from the technical problems of delivery of the genes into human disc cells, the correct choice of therapeutic genes requires an improved understanding of the pathogenesis of degeneration. In addition, the cell density in normal human discs is low, and many of the cells in degenerate discs are dead [21]; stimulation of the remaining cells may be insufficient to repair the matrix.

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