Multi-Task Learning of Object States and State-Modifying Actions From Web Videos.

We aim to learn to temporally localize object state changes and the corresponding state-modifying actions by observing people interacting with objects in long uncurated web videos. We introduce three principal contributions. First, we develop a self-supervised model for jointly learning state-modifying actions together with the corresponding object states from an uncurated set of videos from the Internet.

[Mathematical simulation of biomechanical background of osteophyte formation in cervical vertebra].

Purpose Of The Study: The aim of this study was to simulate different types of cervical vertebra loading and to find out whether mechanical stress would concentrate in regions known in clinical practice as predilection sites for osteophyte formation. The objective was to develop a theoretical model that would elucidate clinical observations concerning the predilection site of bone remodelling in view of the physiological changes inside the cervical vertebral body.

Material And Methods: A real 3D-geometry of the fourth cervical vertebra had been made by the commercially available system ATOS II.

The induction of HIF-1 reduces astrocyte activation by amyloid beta peptide.

Reduced glucose metabolism and astrocyte activation in selective areas of the brain are pathological features of Alzheimer's disease (AD). The underlying mechanisms of low energy metabolism and a molecular basis for preventing astrocyte activation are not, however, known. Here we show that amyloid beta peptide (Abeta)-dependent astrocyte activation leads to a long-term decrease in hypoxia-inducible factor (HIF)-1alpha expression and a reduction in the rate of glycolysis.

The regulation of glucose metabolism by HIF-1 mediates a neuroprotective response to amyloid beta peptide.

It is frequently argued that both amyloid beta (Abeta) and oxidative stress are involved in the pathogenesis of Alzheimer's disease (AD). We show here that clonal nerve cell lines and primary cortical neurons that are resistant to Abeta toxicity have an enhanced flux of glucose through both the glycolytic pathway and the hexose monophosphate shunt. AD brain also has increased enzymatic activities in both pathways relative to age-matched controls.

Tuberous sclerosis causing mutants of the TSC2 gene product affect proliferation and p27 expression.

The autosomal dominant disease tuberous sclerosis (TSC) is caused by mutations in either TSC1 on chromosome 9q34, encoding hamartin, or TSC2 on chromosome 16p13.3, encoding tuberin. TSC is characterized by hamartomas that occur in many organs of affected patients and these have been considered to likely result from defects in proliferation control.