Imaging radar polarimetry from wave synthesis

It was shown that it is possible to measure the complete scattering matrix of an object using data acquired on a single aircraft pass, and can combine the signals later in the data processor to generate radar images corresponding to any desired combination of transmit and receive polarization. Various scattering models predict different dependence on polarization state of received power from an object. The imaging polarimeter permits determination of this dependence, which is called the polarization signature, of each point in a radar image. Comparison of the theoretical predictions and observational data yield identification of possible scattering mechanisms for each area of interest. It was found that backscatter from the ocean is highly polarized and well-modeled by Bragg scattering, while scattering from trees in a city park possesses a considerable unpolarized component. Urban regions exhibit the characteristics expected from dihedral corner reflectors and their polarization signatures are quite different from the one-bounce Bragg model

Radar-aeolian roughness project

The objective is to establish an empirical relationship between measurements of radar, aeolian, and surface roughness on a variety of natural surfaces and to understand the underlying physical causes. This relationship will form the basis for developing a predictive equation to derive aeolian roughness from radar backscatter. Results are given from investigations carried out in 1989 on the principal elements of the project, with separate sections on field studies, radar data analysis, laboratory simulations, and development of theory for planetary applications

A temperature sensitive variant of p53 drives p53-dependent MicroRNA expression without evidence of widespread post-transcriptional gene silencing

The p53 tumour suppressor is a transcription factor that can regulate the expression of numerous ge

The p53 protein induces stable miRNAs that have the potential to modify subsequent p53 responses

The p53 tumour suppressor is a transcription factor that can increase the expression of mRNAs and microRNAs (miRNAs). HT29-tsp53 cells expressing a temperature sensitive variant of p53 have provided a useful model to rapidly and reversibly control p53 activity. In this model, the majority of p53-responsive mRNAs were upregulated rapidly but they were short-lived leading to rapid decay of the p53 response at the restrictive temperature. Here we used oligonucleotide microarrays and reverse transcriptase PCR to show that p53-induced miRNAs exhibited a distinct temporal pattern of expression. Whereas p53-induced miRNAs like miR-143-3p, miR-145-5p, miR-34a-5p and miR-139-5p increased as fast as mRNAs, they were extremely stable persisting long after p53 induced mRNAs and even their corresponding primary miRNAs had decayed to baseline levels. Three p53-induced mRNAs (MDM2, BTG2 and CDKN1A) are experimentally verified targets of one or more of these specific miRNAs so we hypothesized that the sustained expression of p53-induced miRNAs could be explained by a post-transcriptional feedback loop. Activation of consecutive p53 responses separated by a period of recovery led to the selective attenuation of a subset of p53 regulated mRNAs corresponding to those targeted by one or more of the p53-responsive miRNAs. Our results indicate that the long term expression of p53 responsive miRNAs leads to an excess of miRNAs during the second response and this likely prevents the induction of MDM2, BTG2 and CDKN1A mRNA and/or protein. These observations are likely to have important implications for daily cancer therapies that activate p53 in normal tissues and/or tumour cells

The expression of CDK4 and CDK6 at the permissive temperature.

<p>(A) Total RNA was isolated from control (open symbols) and HT29tsp53 (closed symbols) cells at the indicated time and the expression of a variety of mRNAs was determined. Expression in each sample was normalized to the expression of the same transcript in samples collected immediately before the temperature shift. (Each point represents the mean (± SEM) determined from a minimum of 3 independent experiments. (B) Signal intensity of individual probesets from microarray analysis at the restrictive temperature (X axis) is compared to the signal intensity at the permissive temperature (y axis). The mean fold change (± SEM and n) for each transcript is inset in the corresponding panel. (C) Immunoblot analysis of the indicated protein derived from whole cell lysates collected at the indicated time at the permissive temperature. Similar results were obtained in 3 independent experiments. In A, B and C, CDKN1A (p21 ^<b>WAF</b>) and/or MDM2 serve as positive controls for the activation of the p53 transcriptional response.</p

The p53-dependent induction of miRNAs.

<p>(A) Small RNAs were collected from HT29-tsp53 cells following incubation for 16 hours at the permissive temperature. RNA samples obtained from 2 independent experiments were labelled and hybridized to oligonucleotide microarrays. Individual miRNAs meeting our statistical cut off (P ≤ 0.01) are presented. Values reflect fold change in expression at the permissive compared to the restrictive temperature. The miRNAs are arranged in order of expression from most highly induced on the left to least well-induced on the right. Open bars denote passenger strand miRNAs while solid bars represent guide strand miRNAs. ‘*’ indicates that the increased expression of the miRNA was confirmed by qRT-PCR. The ‘X’ denotes the only miRNA that we could not confirm by qRT-PCR. (B) qRT-PCR was performed using similar samples derived from vector control (HT29-neo) and HT29-tsp53 cells. Each value in (B) represents the mean (± SEM) determined from a minimum of 3 independent experiments.</p

List of miRNAs induced at the permissive temperature grouped by locus.

<p>List of miRNAs induced at the permissive temperature grouped by locus.</p