Universal fine-structure eraser for quantum dots.

We analyze the degree of entanglement measurable from a quantum dot via the biexciton-exciton cascade as a function of the exciton fine-structure splitting and the detection time resolution. We show that the time-energy uncertainty relation provides means to measure a high entanglement even in presence of a finite fine-structure splitting when a detection system with high temporal resolution is employed. Still, in many applications it would be beneficial if the fine-structure splitting could be compensated to zero. To solve this problem, we propose an all-optical approach with rotating waveplates to erase this fine-structure splitting completely which should allow obtaining a high degree of entanglement with near-unity efficiency. Our optical approach is possible with current technology and is also compatible with any quantum dot showing fine-structure splitting. This bears the advantage that for example the fine-structure splitting of quantum dots in nanowires and micropillars can be directly compensated without the need for further sample processing.

Fibroblast growth factor receptor-1 expression is associated with neointimal formation in vitro.

Neointimal formation was studied in a porcine aortic organ culture model that exhibits intimal smooth muscle cell accumulation after a brief time in culture. This in vitro model is dependent upon an intact endothelium, as removal of the endothelium at the time of harvesting results in the failure to develop a neointima. We previously showed that conditioned media from intact cultures induce neointimal formation in denuded aortic explants, and we speculated that basic fibroblast growth factor was the endothelial-derived factor in conditioned media promoting neointimal formation. However, the concentration of basic fibroblast growth factor in conditioned media from both intact and denuded explants, measured by an enzyme-linked immunosorbent assay, was not significantly different and, in fact, steadily decreased over the first 7 days of culture. Furthermore, the amount and intensity of immunoreactive basic fibroblast growth factor in tissue sections, also similar in both groups, decreased over the same time course. Nonetheless, exogenous basic fibroblast growth factor (1 ng/ml) induced neointimal formation in intact explants but was unable to do so in denuded explants. Western blot analysis of intimal lysates prepared from both intact and denuded explants showed a time-dependent increase in fibroblast growth factor receptor-1 expression over the first 7 days of culture, with higher levels seen in intimal lysates from intact explants at each time point examined. Immunoreactive fibroblast growth factor receptor-1 was detected in both endothelial cells and intimal smooth muscle cells of intact explant sections. These data indicate that, in the presence of the endothelium, neointimal formation may in part be mediated by upregulation of fibroblast growth factor receptor-1 in the intimal cells of porcine aortic explants.

Increased elastin-degrading activity and neointimal formation in porcine aortic organ culture. Reduction of both features with a serine proteinase inhibitor.

We investigated the association between tissue elastolytic activity and the development of neointimal formation using a previously described porcine aortic organ culture. Neointimal formation is associated with the presence of intact endothelium (nondenuded cultures) but is markedly reduced if endothelial cells are removed (denuded cultures). In nondenuded organ cultures, elastolytic activity assessed by using [3H]elastin increased sixfold at day 3 after initiation of the culture (P < .01), a time earlier than the previously published increase in intimal smooth muscle cells (ISMCs). Elastolytic activity did not increase from day 3 to day 7 despite doubling of ISMCs but did double by day 14 (P < .01) and remained elevated to day 28, correlating with increases in ISMCs. In denuded organ cultures, elastolytic activity was much lower than in nondenuded organ cultures at day 3 (P < .05) but increased fivefold in the presence of nondenuded organ culture conditioned medium (P < .01). Addition of alpha 1-proteinase inhibitor for 14 days caused a 60% decrease in elastolytic activity in nondenuded organ cultures and a 27% reduction in ISMCs compared with untreated controls (P < .05 for both). The elastolytic activity, resolved as lytic bands on an elastin substrate gel, reflected candidate enzymes, one at 76 kD and perhaps a doublet at 43 and 50 kD. Our study suggests that endothelial cells release a soluble agent that enhances elastin-degrading activity in the aorta and may at least partially account for the initiation of neointimal formation.

Cholesterol-fed and casein-fed rabbit models of atherosclerosis. Part 2: Differing morphological severity of atherogenesis despite matched plasma cholesterol levels.

One-month-old male New Zealand White rabbits were fed either a cholesterol-free casein diet (n = 10) or low-level cholesterol-supplemented chow (n = 10) for 24 weeks, during which total plasma cholesterol levels were matched. After perfusion fixation, aortic tissue samples were taken from six predetermined locations and embedded in epoxy resin for examination by light and electron microscopy. Frozen sections were also obtained for histochemical demonstration of collagen and elastin. Lesion morphology was classified in toluidine blue-stained, semithin epoxy sections as early fatty streaks (round foam cells with little intervening extracellular matrix); advanced fatty streaks (foam cells with extracellular lipid); fibrous plaques (spindle-shaped cells within extracellular matrix); or atheromatous lesions (presence of an atheromatous core). In representative specimens, electron microscopy showed that the ultrastructure of round foam cells was consistent with macrophage derivation, whereas most spindle-shaped cells were clearly smooth muscle cells. Fibrous plaques were more common in the distal than the proximal aorta. Lesions in the casein-fed animals were essentially equally distributed among the four morphological categories, whereas lesions in the cholesterol-fed rabbits were predominantly of the atheromatous type. Thus, cholesterol-fed rabbits had, in general, more advanced lesions than casein-fed rabbits with matched total plasma cholesterol levels. Moreover, the feeding of a low-level cholesterol diet (0.125% to 0.5% by weight) to rabbits for a relatively short time (6 months) led to the development of advanced lesions similar to those seen in humans.

Cholesterol-fed and casein-fed rabbit models of atherosclerosis. Part 1: Differing lesion area and volume despite equal plasma cholesterol levels.

One-month-old male New Zealand White rabbits were fed either a cholesterol-free casein diet (CAS; n = 10); low-level cholesterol-supplemented (0.125% to 0.5% by weight) chow (CH; n = 10); or standard laboratory rabbit chow (n = 3) for 24 weeks, during which total plasma cholesterol (TPC) levels were matched for the two experimental groups (TPCCAS = 475 +/- 39 mg/dL; TPCCH = 515 +/- 70 mg/dL). The percentage of cholesterol partitioned into each of the lipoprotein fractions except high-density lipoprotein (HDL) was significantly different for the experimental groups: casein-fed rabbits had a primarily low-density lipoprotein (LDL) hypercholesterolemia while cholesterol-fed rabbits had approximately equal levels of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and LDL cholesterol. Despite matched TPC, lesions in CH animals covered twice the luminal surface area (as detected by oil red O staining; P < .05) and had three times the total volume compared with lesions in the CAS group (P < .05). Lesion volume was positively correlated with TPC and IDL and LDL cholesterol for the CAS group and with TPC and IDL cholesterol for the CH group. When the experimental groups were combined, TPC and VLDL and IDL cholesterol were positively correlated with the lesion volume. Probability of occurrence maps revealed, however, that both groups were virtually identical with respect to the topographic distribution of lesions in the thoracic and abdominal aortas. The data suggested that the differential partitioning of cholesterol into the lipoprotein fractions seen in CAS and CH rabbits influenced lesion area and volume but not topographic distribution.

Effects of injection mechanics, pH of infusate and 6-hydroxydopamine on cerebromicrovascular permeability in rats.

The effects of altering the rate, manner and vehicle used for intracerebral injection upon microvascular permeability were studied in Sprague-Dawley rats employing horseradish peroxidase histochemistry. The volume of vehicle delivered and the site of intracerebral injection were kept constant. In comparison to continuous infusion, vascular permeability was significantly greater following manual (intermittent) injections; however, no differences were found when the infusion rate was decreased 10-fold. Use of a buffered vehicle (Hanks' balanced salt solution) with pH adjusted to 7.4, in contrast to the more commonly used non-buffered vehicle (saline-ascorbate), resulted in significant reductions in permeability. The apparent influence of the agent 6-hydroxydopamine (6-OHDA) on changes in vascular permeability was found to vary depending on the type and pH of the vehicle used for injection. Significantly greater permeability resulted with saline-ascorbate (pH 3.1) as the vehicle when compared to Hanks' balanced salt solution (pH 7.4). Changes in vascular permeability can therefore be produced by varying mechanical and vehicular factors which, in the case of 6-OHDA, far outweigh previously reported permeability changes specifically attributed to this neurotoxin.