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In this paper, it is studied for the first time, the possibility of manufacturing a Bulk Barrier diode in planar technology using simulation. This study is based on simulation results obtained with a 2-D device simulator (S-PISCES). More precisely, the electrical and switching behavior of the proposed devices in planar technology were investigated. The results of this study show that the technological parameters (doping concentrations), as well as the geometrical sizes (middle region width) and the bias conditions (applied voltage), have significant effects on the electrical and switching behavior of the proposed devices. The appropriate choice of these parameters can reduce the switching time in the range of few picoseconds and also dramatically modify the current through the device. The simulation results of devices in planar technology have been compared with those designed in non planar technology. Finally, good agreement among theory and simulations results of the proposed devices observed. [ABSTRACT FROM AUTHOR]

Two-dimensional transitional metal halides have recently attracted significant attention due to their thickness-dependent and electrostatically tunable magnetic properties. However, this class of materials is highly reactive chemically, which leads to irreversible degradation and catastrophic dissolution within seconds in ambient conditions, severely limiting subsequent characterization, processing, and applications. Here, we impart long-term ambient stability to the prototypical transition metal halide CrI 3 by assembling a noncovalent organic buffer layer, perylenetetracarboxylic dianhydride (PTCDA), which templates subsequent atomic layer deposition (ALD) of alumina. X-ray photoelectron spectroscopy demonstrates the necessity of the noncovalent organic buffer layer since the CrI 3 undergoes deleterious surface reactions with the ALD precursors in the absence of PTCDA. This organic-inorganic encapsulation scheme preserves the long-range magnetic ordering in CrI 3 down to the monolayer limit as confirmed by magneto-optical Kerr effect measurements. Furthermore, we demonstrate field-effect transistors, photodetectors, and optothermal measurements of CrI 3 thermal conductivity in ambient conditions.

Objective: Results from three observational methods for assessing effectiveness of long-acting bronchodilator therapies for reducing severe exacerbations of chronic obstructive pulmonary disease (COPD) were compared: intent-to-treat (ITT), as protocol (AP), and an as-treated analysis that utilized a marginal structural model (MSM) incorporating time-varying covariates related to treatment adherence and moderate exacerbations., Study Design and Setting: Severe exacerbation risk was assessed over a 2-year period using claims data for patients aged ≥40 years who initiated long-acting muscarinic antagonist (LAMA), inhaled corticosteroid/long-acting beta-agonist (ICS/LABA), or triple therapy (LAMA + ICS/LABA)., Results: A total of 5475 COPD patients met inclusion criteria. Six months post-initiation, 53.5 % of patients discontinued using any therapy. The ITT analysis found an increased severe exacerbation risk for triple therapy treatment (hazard ratio [HR] 1.24; 95 % confidence interval [CI] 1.00-1.53). No increased risk was found in the AP (HR 1.00; 95 % CI 0.73-1.36), or MSM analyses (HR 1.11; 95 % CI 0.68-1.81). The MSM highlighted important associations among post-index events., Conclusion: Neglecting to adjust for treatment discontinuation may produce biased risk estimates. The MSM approach is a promising tool to compare chronic disease management by illuminating relationships between treatment decisions, adherence, patient choices, and outcomes.

New therapies are required to target hypoxic areas of tumors as these sites are highly resistant to conventional cancer therapies. Monocytes continuously extravasate from the bloodstream into tumors where they differentiate into macrophages and accumulate in hypoxic areas, thereby opening up the possibility of using these cells as vehicles to deliver gene therapy to these otherwise inaccessible sites. We describe a new cell-based method that selectively targets an oncolytic adenovirus to hypoxic areas of prostate tumors. In this approach, macrophages were cotransduced with a hypoxia-regulated E1A/B construct and an E1A-dependent oncolytic adenovirus, whose proliferation is restricted to prostate tumor cells using prostate-specific promoter elements from the TARP, PSA, and PMSA genes. When such cotransduced cells reach an area of extreme hypoxia, the E1A/B proteins are expressed, thereby activating replication of the adenovirus. The virus is subsequently released by the host macrophage and infects neighboring tumor cells. Following systemic injection into mice bearing subcutaneous or orthotopic prostate tumors, cotransduced macrophages migrated into hypoxic tumor areas, upregulated E1A protein, and released multiple copies of adenovirus. The virus then infected neighboring cells but only proliferated and was cytotoxic in prostate tumor cells, resulting in the marked inhibition of tumor growth and reduction of pulmonary metastases. This novel delivery system employs 3 levels of tumor specificity: the natural "homing" of macrophages to hypoxic tumor areas, hypoxia-induced proliferation of the therapeutic adenovirus in host macrophages, and targeted replication of oncolytic virus in prostate tumor cells., (©2011 AACR.)

Destruction of cancer cells by genetically modified viral and nonviral vectors has been the aim of many research programs. The ability to target cytotoxic gene therapies to the cells of interest is an essential prerequisite, and the treatment has always had the potential to provide better and more long-lasting therapy than existing chemotherapies. However, the potency of these infectious agents requires effective testing systems, in which hypotheses can be explored both in vitro and in vivo before the establishment of clinical trials in humans. The real prospect of off-target effects should be eliminated in the preclinical stage, if current prejudices against such therapies are to be overcome. In this review we have set out, using adenoviral vectors as a commonly used example, to discuss some of the key parameters required to develop more effective testing, and to critically assess the current cellular models for the development and testing of prostate cancer biotherapy. Only by developing models that more closely mirror human tissues will we be able to translate literature publications into clinical trials and hence into acceptable alternative treatments for the most commonly diagnosed cancer in humans.

These data on families of pediatric probands with the hyperapoB phenotype confirm and extend our previous findings of familial aggregation of hyperapoB and document further the expression of hyperapoB in the pediatric age group (Sniderman et al, 1985). In agreement with a more recent report (Beaty et al, 1986) the data suggest, but do not prove, the presence of a Mendelian dominant trait for hyperapoB. The observation that most of the parents affected with hyperapoB were normolipidemic clearly suggests a difference between the expression of hyperapoB in these families and FCH. Further studies on the basic biochemical and genetic defect(s) underlying these common disorders associated with CHD will be necessary to provide a better understanding of the pathogenesis of these important lipoprotein disorders. A significant proportion of children referred to a Lipid Clinic for suspected hyperlipidemia or because of a family history of premature CHD may have hyperapoB. We suggest that measurement of plasma LDL B be added to the standard measurements of lipids and lipoproteins made in Lipid Clinics and that further studies be performed on the utility of using the ratio of LDL C/B as a useful clinical tool to differentiate between those patients with hyperapoB and those with more conventional type II hyperlipoproteinemia.

These data confirm the effectiveness of therapeutic diets in children with type II hyperlipoproteinemia in conventional terms. However, the decrease in LDL cholesterol was not accompanied by a significant decrease in LDL B (suggesting only a small change in the number of LDL particles in plasma), and a fall in HDL cholesterol occurred, with no significant improvement in the LDL to HDL cholesterol ratio. These findings indicate that further research is needed to develop diets with more optimal effects. Finally, our hypothesis that such diets may produce an LDL particle of altered composition, needs to be confirmed using additional physical-chemical measurements of the size, composition and molecular weight distribution of LDL in plasma before and after dietary intervention.