Frequency estimation in multipath rayleigh-sparse-fading channels

Maximum-likelihood (ML) data-aided frequency estimation in multipath Rayleigh-fading channels with sparse impulse responses is investigated. We solve this problem under the assumption that the autocorrelation matrix of the pilot signal can be approximated by a diagonal matrix, the fading of different path amplitudes are independent from each other, and the additive noise is white and Gaussian. The ML frequency estimator is shown to be based on combining nonlinearly transformed path periodograms. We have derived the nonlinear function for the two cases: known and unknown fading variances. The new frequency estimators lead, in particular cases, to known ML frequency estimators for nonsparse multipath fading channels. The use of a priori information about the mean number of paths in the channel allows a significant improvement of the accuracy performance. Exploiting the sparseness of the channel impulse response is shown to significantly reduce the threshold signal-to-noise ratio at which the frequency error departs from the Cramer-Rao lower bound. However, precise knowledge of the channel sparseness is not required in order to realize this improvement

Optimizing an array of antennas for cellular coverage from a high altitude platform

In a wireless communications network served by a high altitude platform (HAP) the cochannel interference is a function of the antenna beamwidth, angular separation and. sidelobe level. At the millimeter wave frequencies proposed for HAPs, an array of aperture type antennas on the platform is a practicable solution for serving the cells. We present a method for predicting cochannel interference based on curve-fit approximations for radiation patterns of elliptic beams which illuminate cell edges with optimum power, and a means of estimating optimum beamwidths for each cell of a regular hexagonal layout. The method is then applied to a 121 cell architecture. Where sidelobes are modeled As a flat floor at 40-dB below peak directivity, a cell cluster size of four yields carrier-to-interference ratios (CIRs), which vary from 15 dB at cell edges to 27 dB at cell centers. On adopting a cluster size of seven, these figures increase, respectively, to 19 and 30 dB. On reducing the sidelobe level, the. improvement in CIR can be quantified. The method also readily allows for regions of overlapping channel coverage to be shown

Avalanche multiplication and breakdown in AlxGa1-xAs (x < 0-9)

Measurements carried out on thick Al/sub x/Ga/sub 1-x/As (x 0.63

Excess noise characteristics of Al0.8Ga0.2As avalanche photodiodes

The avalanche noise characteristics of Al0.8Ga0.2 As have been measured in a range of p-i-n and n-i-p diodes with i-region widths ω varying from 1.02 to 0.02 μm. While thick bulk diodes exhibit low excess noise from electron initiated multiplication, owing to the large α/β ratio (1/k), the excess noise of diodes with ω < 0.31 μm were found to be greatly reduced by the effects of dead space. The thinnest diodes exhibit very low excess noise, corresponding to k = 0.08, up to a multiplication value of 90. In contrast to most III-V materials, it was found that both thick and thin Al0.8Ga0.2As multiplication layers can give very low excess noise and that electrons must initiate multiplication to minimize excess noise, even in thin structure

Modification of tumour blood flow using the hypertensive agent, angiotensin II

The effects of different doses of angiotensin II (0.02 to 0.5 microgram kg-1 min-1 on mean arterial blood pressure, tissue blood flow and tissue vascular resistance were investigated in BD9 rats. Blood flow was measured using the uptake of 125I- or 14C-labelled iodoantipyrine (125I-IAP and 14C-IAP). Spatial heterogeneity of blood flow within tumours, before and after angiotensin II infusion, was also measured using 14C-IAP and an autoradiographic procedure. Mean arterial blood pressure rose steeply with angiotensin II dose. Blood flow to skeletal muscle, skin overlying the tumour, contralateral skin, small intestine and kidney tended to decline in a dose-dependent manner. Blood flow to the tumour was also reduced (to 80% of control values) but there was no dose response. Blood flow to the heart was slightly increased and blood flow to the brain was unaffected by angiotensin II. Vascular resistance, in all tissues, was increased by angiotensin II infusion. The increase in tumour tissue was similar to that found in skeletal muscle and small intestine and is likely to be caused by a direct vasoconstricting effect of the drug rather than autoregulation of tumour blood flow in the face of an increase in perfusion pressure. The reduction in overall blood flow at the highest perfusion pressure was due to a preferential effect of angiotensin II at the tumour periphery. These results show that some tumours, at least, can respond directly to the effects of vasoactive agents

The response of tumour vasculature to angiotensin II revealed by its systemic and local administration to 'tissue-isolated' tumours.

A tissue-isolated preparation of the P22 rat carcinosarcoma was used to investigate the tumour vascular response to angiotensin II (ATII). In particular, the relative importance of systemic and local tumour factors was assessed by comparing tumour vascular resistance during systemic administration of ATII and during administration directly into the tumour-supplying artery. The effect of hypervolaemia on tumour vascular resistance was determined as well as the effect of ATII on oxygen metabolism. Tumour vascular resistance was increased by ATII in a dose-dependent manner. The response was biphasic with an initial peak in resistance followed by a lower plateau phase. Systemic administration of ATII was more effective in increasing tumour vascular resistance than direct administration. This suggests that systemic administration is not causing any reopening of previously collapsed tumour blood vessels. Further evidence for this is that hypervolaemia caused no reduction in tumour vascular resistance and that there was no difference in oxygen extraction by tumours between groups treated with systemically and directly administered ATII. A heterogeneous distribution of ATII receptors in the P22 tumour is a more likely explanation for the known heterogeneity of blood flow response to ATII

Nonlocal effects in thin 4H-SiC UV avalanche photodiodes

The avalanche multiplication and excess noise characteristics of 4H-SiC avalanche photodiodes with i-region widths of 0.105 and 0.285 mum have been investigated using 230-365-nm light, while the responsivities of the photodiodes at unity gain were examined for wavelengths up to 375 nm. Peak unity gain responsivities of more than 130 mA/W at 265 nm, equivalent to quantum efficiencies of more than 60%, were obtained for both structures. The measured avalanche characteristics show, that beta > alpha and that the beta/alpha ratio remains large even in thin 4H-SiC avalanche regions. Very low excess noise, corresponding to k(eff) < 0.15 in the local noise model, where k(eff) = alpha/beta(beta/alpha) for hole (electron) injection, was measured with 365-nm light in both structures. Modeling the experimental results using a simple quantum efficiency model and a nonlocal description yields effective ionization threshold energies of 12 and 8 eV for electrons and holes, respectively, and suggests that the dead space in 4H-SiC is soft. Although dead space is important, pure hole injection is still required to ensure low excess noise in thin 4H-SiC APDs owing to beta/alpha ratios that remain large, even at very high fields

PyMT-Maclow: A novel, inducible, murine model for determining the role of CD68 positive cells in breast tumor development

CD68+ tumor-associated macrophages (TAMs) are pro-tumorigenic, pro-angiogenic and are associated with decreased survival rates in patients with cancer, including breast cancer. Non-specific models of macrophage ablation reduce the number of TAMs and limit the development of mammary tumors. However, the lack of specificity and side effects associated with these models compromise their reliability. We hypothesized that specific and controlled macrophage depletion would provide precise data on the effects of reducing TAM numbers on tumor development. In this study, the MacLow mouse model of doxycycline-inducible and selective CD68+ macrophage depletion was crossed with the murine mammary tumor virus (MMTV)-Polyoma virus middle T antigen (PyMT) mouse model of spontaneous ductal breast adenocarcinoma to generate the PyMT-MacLow line. In doxycycline-treated PyMT-MacLow mice, macrophage numbers were decreased in areas surrounding tumors by 43%. Reducing the number of macrophages by this level delayed tumor progression, generated less proliferative tumors, decreased the vascularization of carcinomas and down-regulated the expression of many pro-angiogenic genes. These results demonstrate that depleting CD68+ macrophages in an inducible and selective manner delays the development of mammary tumors and that the PyMT-MacLow model is a useful and unique tool for studying the role of TAMs in breast cancer