Protecting local access telecommunications networks: Toward a minimum-cost solution

The problem of designing fibre-optic networks for local-access telecommunications generates (at least) three non-trivial subproblems. In the first of these subproblems one must determine how many fibre-optic cables (fibres) are required at either end of a street. In the next subproblem a minimum-cost network must be designed to support the fibres. The network must also provide distinct paths from either end of the street to the central exchange(s). Finally, the fibre-optic cables must be placed in protective covers. These covers are available in a number of different sizes, allowing some flexibility when covering each section of the network. In this paper we describe a dynamic programming (DP) formulation for finding a minimum-cost (protective) covering for the network (the third of the subproblems). This problem is a generalised set covering problem with side constraints and is further complicated by the introduction of fixed and variable welding costs. The DP formulation selects covers along each arc (in the network), but cannot exactly model the fixed costs and so does not guarantee optimality. We also describe an integer programming (IP) formulation for assessing the quality of the DP solutions. The cost of the networks constructed by the IP model is less than those designed using the DP model, but the saving is not significant for the problems examined (less than 0.1%). This indicates that the DP model will generally give very good solutions. Furthermore, as the problem dimensions grow, DP gives significantly better solution times than IP.     

K-winner networks.

A special class of mutually inhibitory networks is analyzed, and parameters for reliable K-winner performance are presented. The network dynamics are modeled using interactive activation, and results are compared with the sigmoid model. For equal external inputs, network parameters that select the units with the larger initial activations (the network converges to the nearest stable state) are derived. Conversely, for equal initial activations, networks that select the units with larger external inputs (the network converges to the lowest energy stable state) are derived. When initial activations are mixed with external inputs, anomalous behavior results. These discrepancies are analyzed with several examples. Restrictions on initial states are derived which ensure accurate K-winner performance when unequal external inputs are used.     

Towards deterministic downscaling of SMOS soil moisture using MODIS derived soil evaporative efficiency

A deterministic approach for downscaling ～ 40 km resolution Soil Moisture and Ocean Salinity (SMOS) observations is developed from 1 km resolution MODerate resolution Imaging Spectroradiometer (MODIS) data. To account for the lower soil moisture sensitivity of MODIS surface temperature compared to that of L-band brightness temperature, the disaggregation scale is fixed to 10 times the spatial resolution of MODIS thermal data (10 km). Four different analytic downscaling relationships are derived from MODIS and physically-based model predictions of soil evaporative efficiency. The four downscaling algorithms differ with regards to i) the assumed relationship (linear or nonlinear) between soil evaporative efficiency and near-surface soil moisture, and ii) the scale at which soil parameters are available (40 km or 10 km). The 1 km resolution airborne L-band brightness temperature from the National Airborne Field Experiment 2006 (NAFE'06) are used to generate a time series of eleven clear sky 40 km by 60 km near-surface soil moisture observations to represent SMOS pixels across the three-week experiment. The overall root mean square difference between downscaled and observed soil moisture varies between 1.4% v/v and 1.8% v/v depending on the downscaling algorithm used, with soil moisture values ranging from 0 to 15% v/v. The accuracy and robustness of the downscaling algorithms are discussed in terms of their assumptions and applicability to SMOS.     

Oxygen content of the fixative is important in the interpretation of the ultrastructure of ischaemic myocardium

Isolated rat hearts were subjected to 15, 45, or 60 minutes of global ischaemia and then fixed by perfusion at 37°C with glutaraldehyde containing various amounts of oxygen. This either had been bubbled with 100% oxygen (PO₂ 620 mm Hg) or with 100% nitrogen (PO₂ 40 mm Hg) immediately before use, or it had been routinely prepared and stored exposed to atmospheric oxygen (PO₂ 245 mm Hg). The ultrastructure of myocytes and endothelial cells subjected to 15 minutes of ischaemia was not affected by the treatment of the fixative. However, when the tissue subjected to longer periods of ischaemia was fixed with routinely prepared or oxygen-bubbled glutaraldehyde, ultrastructural changes characteristic of reoxygenation damage were uniformly evident in both the microvasculature and myocytes. These qualitatively distinct changes included mitochondrial swelling, cell swelling, endothelial bleb formation, and narrowing of capillary lumina. These abnormalities were not observed in tissue fixed with nitrogen-bubbled glutaraldehyde. These findings indicate that deliberate steps should be taken to reduce or eliminate dissolved oxygen from the fixatives used to study ischaemic tissues. Otherwise artefactual reoxygenation damage in vitro may occur and make valid ultrastructural interpretation difficult or impossible.     

Evidence for superantigen involvement in insulin-dependent diabetes mellitus aetiology

Insulin-dependent diabetes mellitus (IDDM) is a T-cell-mediated autoimmune disease whose onset is believed to be triggered by unknown environmental factors acting on a predisposing genetic background. Islet-infiltrating T (IIT) cells from two IDDM patients, who had died at the onset of the disease from brain swelling as a complication of ketoacidosis, were analysed. The results provided evidence for the involvement of a pancreatic islet cell membrane-bound superantigen as a diabetes aetiopathogenetic factor. There was a selective expansion of a T-cell receptor (TCR) variable segment of the beta-chain (V beta 7) in these IIT cells in association with unselected V alpha-chain segments; extensive junctional diversity of the TCR V beta 7 chains; and evidence of positive selection, after exposure to diabetic islet cell membrane preparations, of V beta 7+ T-cell clones among peripheral blood lymphocytes from non-diabetic individuals.     

Renal length in sickle cell disease: observations from a cohort study

Renal length has been measured by ultrasound in 237 subjects with homozygous sickle cell (SS) disease, 147 with sickle cell-hemoglobin C (SC) disease, and in 78 age-matched controls with a normal hemoglobin (AA) genotype. As expected, renal length increased with age in all genotypes but mean length was significantly greater in SS disease compared with SC disease (mean difference 4.3 mm after adjustment for height) and significantly greater in both genotypes than in AA controls (SS/AA difference 9.2 mm, SC/AA difference 5.0 mm after adjustment for height). Examination of relationships between renal length and some hematological indices (hemoglobin, fetal hemoglobin, reticulocyte counts, alpha thalassemia status) in SS or SC disease showed only a significant negative correlation with hemoglobin and positive correlation with reticulocyte count in SS disease. Further analysis suggested that the stronger relationship was between renal length and high reticulocyte count. The mechanism of renal enlargement is unknown although glomerular hypertrophy and increased renal blood volume are likely contributors.     

Arterial reactivity is enhanced in genetic males taking high dose estrogens

OBJECTIVES: We sought to assess whether high dose estrogen treatment is associated with enhanced arterial reactivity in genetic males. BACKGROUND: Although estrogens have been shown to enhance arterial reactivity in women, and are thereby thought to confer cardiovascular benefit, the vascular effects of long-term estrogen therapy in genetic males is unknown. METHODS: We studied the arterial physiology of 30 genetic males--15 male to female transsexuals receiving long-term high dose estrogen therapy and 15 healthy male control subjects matched for age, smoking history and vessel size. Using external vascular ultrasound, brachial artery diameter was measured at rest, after flow increase (causing endothelium-dependent dilation [EDD]) and after nitroglycerin (GTN), an endothelium-independent dilator. Blood pressure, cholesterol and testosterone levels were also measured in each subject. RESULTS: Total testosterone and free testosterone index levels were lower in the transsexuals compared with the control subjects (p < 0.001). In contrast, EDD was significantly higher in the transsexuals than in the control males (mean [+/-SD] 7.1 +/- 3.1% vs. 3.2 +/- 2.8%, p = 0.001), as was the GTN response (21.2 +/- 6.7% vs. 14.6 +/- 3.3%, p = 0.002). Total and high density lipoprotein cholesterol, blood pressure levels and baseline vessel size were similar in the two groups. On multivariate analysis, enhanced EDD was associated independently with estrogen therapy (p = 0.02) and with low total cholesterol (p = 0.04). An enhanced GTN response was also significantly associated with estrogen therapy (p = 0.03). CONCLUSIONS: Long-term treatment with high dose estrogens is associated with enhanced arterial reactivity in genetic males, which may be due to the effects of estrogen excess or androgen deprivation, or both.