Phase and group velocity tracing analysis of projected wave packet motion along oblique radar beams ? qualitative analysis of QP echoes

International audienceThe wave packets of atmospheric gravity waves were numerically generated, with a given characteristic wave period, horizontal wave length and projection mean wind along the horizontal wave vector. Their projection phase and group velocities along the oblique radar beam (vpr and vgr), with different zenith angle ? and azimuth angle ?, were analyzed by the method of phase- and group-velocity tracing. The results were consistent with the theoretical calculations derived by the dispersion relation, reconfirming the accuracy of the method of analysis. The RTI plot of the numerical wave packets were similar to the striation patterns of the QP echoes from the FAI irregularity region. We propose that the striation range rate of the QP echo is equal to the radial phase velocity vpr, and the slope of the energy line across the neighboring striations is equal to the radial group velocity vgr of the wave packet; the horizontal distance between two neighboring striations is equal to the characteristic wave period ?. Then, one can inversely calculate all the properties of the gravity wave responsible for the appearance of the QP echoes. We found that the possibility of some QP echoes being generated by the gravity waves originated from lower altitudes cannot be ruled out

Consequences of Aberrant Insulin Regulation in the Brain: Can Treating Diabetes be Effective for Alzheimer’s Disease

There is an urgent need for new ways to treat Alzheimer’s disease (AD), the most common cause of dementia in the elderly. Current therapies are modestly effective at treating the symptoms, and do not significantly alter the course of the disease. Over the years, a range of epidemiological and experimental studies have demonstrated interactions between diabetes mellitus and AD. As both diseases are leading causes of morbidity and mortality in the elderly and are frequent co-morbid conditions, it has raised the possibility that treating diabetes might be effective in slowing AD. This is currently being attempted with drugs such as the insulin sensitizer rosiglitazone. These two diseases share many clinical and biochemical features, such as elevated oxidative stress, vascular dysfunction, amyloidogenesis and impaired glucose metabolism suggesting common pathogenic mechanisms. The main thrust of this review will be to explore the evidence from a pathological point of view to determine whether diabetes can cause or exacerbate AD. This was supported by a number of animal models of AD that have been shown to have enhanced pathology when diabetic conditions were induced. The one drawback in linking diabetes and insulin to AD has been the postmortem studies of diabetic brains demonstrating that AD pathology was not increased; in fact decreased pathology has often been reported. In addition, diabetes induces its own distinct features of neuropathology different from AD. There are common pathological features to be considered including vascular abnormalities, a major feature arising from diabetes; there is increasing evidence that vascular abnormalities can contribute to AD. The most important common mechanism between insulin-resistant (type II) diabetes and AD could be impaired insulin signaling; a form of toxic amyloid can damage neuronal insulin receptors and affect insulin signaling and cell survival. It has even been suggested that AD could be considered as “type 3 diabetes” since insulin can be produced in brain. Another common feature of diabetes and AD are increased advanced glycation endproduct-modified proteins are found in diabetes and in the AD brain; the receptor for advanced glycation endproducts plays a prominent role in both diseases. In addition, a major role for insulin degrading enzyme in the degradation of Aβ peptide has been identified. Although clinical trials of certain types of diabetic medications for treatment of AD have been conducted, further understanding the common pathological processes of diabetes and AD are needed to determine whether these diseases share common therapeutic targets