Showing papers by "Yu Huang published in 2003"

Single-nanowire electrically driven lasers

Abstract: Electrically driven semiconductor lasers are used in technologies ranging from telecommunications and information storage to medical diagnostics and therapeutics. The success of this class of lasers is due in part to well-developed planar semiconductor growth and processing, which enables reproducible fabrication of integrated, electrically driven devices. Yet this approach to device fabrication is also costly and difficult to integrate directly with other technologies such as silicon microelectronics. To overcome these issues for future applications, there has been considerable interest in using organic molecules, polymers, and inorganic nanostructures for lasers, because these materials can be fashioned into devices by chemical processing. Indeed, amplified stimulated emission and lasing have been reported for optically pumped organic systems and, more recently, inorganic nanocrystals and nanowires. However, electrically driven lasing, which is required in most applications, has met with several difficulties in organic systems, and has not been addressed for assembled nanocrystals or nanowires. Here we investigate the feasibility of achieving electrically driven lasing from individual nanowires. Optical and electrical measurements made on single-crystal cadmium sulphide nanowires show that these structures can function as Fabry-Perot optical cavities with mode spacing inversely related to the nanowire length. Investigations of optical and electrical pumping further indicate a threshold for lasing as characterized by optical modes with instrument-limited linewidths. Electrically driven nanowire lasers, which might be assembled in arrays capable of emitting a wide range of colours, could improve existing applications and suggest new opportunities.

Nanoscale coherent optical components

Abstract: This invention generally relates to nanotechnology and nanoelectronics as well as associated methods and devices. In particular, the invention relates to nanoscale optical components such as electroluminescence devices (e.g., LEDs), amplified stimulated emission devices (e.g., lasers), waveguides, and optical cavities (e.g., resonators). Articles and devices of a size greater than the nanoscale are also included. Such devices can be formed from nanoscale wires such as nanowires or nanotubes. In some cases, the nanoscale wire is a single crystal. In one embodiment, the nanoscale laser is constructed as a Fabry-Perot cavity, and is driven by electrical injection. Any electrical injection source may be used. For example, electrical injection may be accomplished through a crossed wire configuration, an electrode or distributed electrode configuration, or a core/shell configuration. The output wavelength can be controlled, for example, by varying the types of materials used to fabricate the device. One or more such nanoscale lasers may also be integrated with other nanoscale components within a device.

SOC test scheduling using simulated annealing

Abstract: We propose an SOC test scheduling method based on simulated annealing. In our method, the test scheduling is formulated as a two-dimensional bin packing problem (rectangle packing) and a data structure called a sequence pair is used to represent the placement of the rectangles. Simulated annealing is used to find the optimal test schedule by altering an initial sequence pair and changing the width of the core wrapper. We also propose a method of wrapper design for cores without internal scan chains. Experiments are conducted on ITC'02 benchmarks, showing that overall the proposed method provides better solutions compared to earlier methods.

Statistical diagnosis for intermittent scan chain hold-time fault

Abstract: Intermittent scan chain hold-time fault is discussed in this paper and a method to diagnose the faulty site in a scan chain is proposed a s well. Unlike the previous scan chain diagnosis methods that targeted p ermanent faults only, the proposed method targets both permanent faults and intermittent faults. Three ideas are presented in this paper. First an enhanced upper bound on the location o f candidate faulty scan cells is obtained. Second a n ew method to determine a lower bound is proposed. Finally a statistical diagnosis algorithm is proposed to calculate the probabilities of t he bounded set of candidate faulty scan cells. The proposed algorithm is shown to be efficient and effective for large industrial designs with multiple faulty scan chains.

Depletion of Intracellular Ca2+ Stores Sensitizes the Flow-Induced Ca2+ Influx in Rat Endothelial Cells

Abstract: Hemodynamic shear stress elicits a rise in endothelial [Ca 2+ ] i , which may serve as a key second messenger to regulate many flow-associated physiological and biochemical processes. In the present study, we used Mn 2+ quenching of fluorescent dye Fluo3 as an assay to investigate the Ca 2+ influx of rat aortic endothelial cells in response to flow. We found that the Ca 2+ signaling in response to flow could be greatly influenced by the status of intracellular Ca 2+ stores. Depletion of intracellular Ca 2+ stores by thapsigargin (4 μmol/L) or cyclopiazonic acid (10 μmol/L) drastically sensitized the Ca 2+ influx in response to flow. Ca 2+ -mobilizing agonist bradykinin (100 nmol/L) or ATP (100 μmol/L) had similar sensitizing effect. The effect of bradykinin or ATP was blocked by Xestospongin C and U73122, suggesting that the sensitization was related to the IP 3 -mediated store depletion. On the other hand, the Mn 2+ quenching in response to flow was greatly reduced by ochratoxin A (100 nmol/L), an agent that could increase the filling state of intracellular Ca 2+ stores. In addition, we found that depletion-sensitized Ca 2+ influx in response to flow was mediated by a PKG-inhibitable cation channel and that the influx was affected by membrane potential and K + channel activity. In conclusion, the present study argues for a critical role of intracellular Ca 2+ status in determining the Ca 2+ signaling in response to flow and it provides a general mechanistic explanation for the stimulatory role of blood-borne agonists on flow-induced Ca 2+ influx.

Roles of cyclic AMP and Ca2+-activated K+ channels in endothelium-independent relaxation by urocortin in the rat coronary artery.

Abstract: Objective: Urocortin possesses cardioprotective properties against the damaging effects of ischemia/reperfusion injury. Our previous study demonstrated that urocortin can induce both endothelium-dependent and -independent coronary relaxation. However, the mechanisms thereby urocortin triggers endothelium-independent relaxation have not been investigated. The present study aimed to examine the role of cyclic AMP and Ca2+-activated K+ channels in the relaxant response to urocortin in the isolated endothelium-denuded rat left anterior descending coronary arteries. Methods: Changes in vessel tension were measured by using a force transducer built in a Multi Myograph System. Results: In 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F2α (U46619)-contracted rings, urocortin-induced relaxation (p D 2: 8.40±0.04) was significantly reduced by cyclic AMP-dependent protein kinase (PKA) inhibitors, Rp-cAMPS triethylamine (Rp-cAMPS) and KT 5720. Treatment with the large-conductance Ca2+-activated K+ channel blockers, iberiotoxin or tetraethylammonium ions (TEA+) attenuated urocortin-induced relaxation; this effect was abolished in the presence of 200 nmol/l KT 5720. In contrast, apamin (small-conductance Ca2+-activated K+ channel blocker), glibenclamide (ATP-sensitive K+ channel blocker), or BaCl2 (inwardly rectifier K+ channel blocker) had no effect. Urocortin-induced relaxation was reduced in rings contracted with increasing concentrations of extracellular K+ (35 and 50 mmol/l). Treatment with TEA+ or Rp-cAMPS inhibited the relaxant effect of urocortin in 35 mmol/l K+-contracted rings. Combined treatment with TEA+ and Rp-cAMPS had no additional effect. Similarly, forskolin produced significantly less relaxant response in 50 mmol/l K+-contracted than U46619-contracted rings. Forskolin-induced relaxation was attenuated by pretreatment with 3 mmol/l TEA+. Conclusion: Urocortin relaxed the rat coronary artery in substantial part via activation of the vascular Ca2+-activated K+ channels and this effect appears to be primarily mediated through PKA-dependent intracellular mechanisms.

Epimerisation of tea polyphenols in tea drinks

Abstract: The present study was carried out to quantify green tea epicatechin (GTE) derivatives and to investigate the origin of epicatechin epimers present in 18 selected canned or bottled tea drinks The major GTEs present in tea are (−)-epigallocatechin gallate (EGCG), (−)-epigallocatechin (EGC), (−)-epicatechin gallate (ECG) and (−)-epicatechin (EC) HPLC analysis showed that the content of total GTEs was lower (164–2683 mg l−1) in the canned and bottled tea drinks than in tea traditionally prepared as a beverage in a cup or teapot (3–5 g l−1) The major finding was that they contained higher levels of epicatechin epimers, namely (−)-gallocatechin gallate (GCG), (−)-gallocatechin (GC), catechin gallate (CG) and (−)-catechin (C), than of GTEs, ranging from 76 to 3318 mg l−1 To investigate the origin of these epimers, GTEs were extracted from longjing green tea and autoclaved at various temperatures for 10–60 min It was found that at least 50% of GTEs were epimerised to their corresponding epimers when autoclaved at 120 °C for 20 min It is concluded that epicatechin epimers in tea drinks are not originally present in green tea leaf but are instead derived from thermal conversion of GTEs Copyright © 2003 Society of Chemical Industry

Efficient diagnosis for multiple intermittent scan chain hold-time faults

Abstract: When VLSI design and process enter the stage of ultra deep submicron (UDSM), process variations, signal integrity (SI) and design integrity (DI) issues can no longer be ignored These factors introduce some new problems in VLSI design, test and diagnosis, which increase lime-to-market, time-to-volume and cost for silicon debug Intermittent scan chain hold-time fault is one of such problems we encountered in practice The fault sites have to be located to speedup silicon debug and improve yield Recent study of the problem proposed a statistical algorithm to diagnose the faulty scan chains if only one fault per chain Based on the previous work, in this paper, an efficient diagnosis algorithm is proposed to diagnose faulty scan chains with multiple faults per chain The presented experimental results on industrial designs show that the proposed algorithm achieves good diagnosis resolution in reasonable time

Expression of olfactory-type cyclic nucleotide-gated channel (CNGA2) in vascular tissues

Abstract: Cyclic nucleotide-gated (CNG) ion channels are Ca2+-permeable nonselective cation channels that are directly gated by the binding of cAMP or cGMP. Previous studies have identified the expression of CNGA1 channels in vascular endothelial cells. The opening of CNG channels is expected to result in a rise in endothelial cytosolic Ca2+, which may trigger multiple physiological changes. In the present study, we extensively studied the expression pattern of the functional subunit of olfactory-type CNG channels (CNGA2) in vascular tissues. Northern blot analysis detected a transcript of approximately 2.6 kb in mRNA isolated from rat aorta. RT-PCR amplified a 582-bp CNGA2 fragment from RNA samples isolated from rat aorta, bovine endothelia cell CCL-209, and rat smooth muscle cell A7r5. Furthermore, in situ hybridization and immunohistochemistry revealed that CNGA2 mRNA and proteins were expressed in the endothelium and smooth muscle layers of human coronary and cerebral arteries. In conclusion, our study indicates that CNGA2 channels are widely expressed in vascular tissues across different species. These results suggest a potential ubiquitous role of CNGA2 channels in mediating Ca2+ influx in vascular cells.

Contribution of K+ channels to relaxation induced by 17beta-estradiol but not by progesterone in isolated rat mesenteric artery rings.

Abstract: 17β-Estradiol and progesterone were found to relax various vascular beds through multiple mechanisms. However, the exact ionic mechanisms underlying the acute relaxant responses to both hormones are incompletely understood. This study was aimed to examine the possible role of K + channel activation in the relaxation induced by both hormones in isolated rat mesenteric artery rings. Isometric tension of each ring was measured with Grass force displacement transducers. In rat endothelium-denuded rings preconstricted by 9,11-dideoxy-11α,9α-epoxy-methanoprostaglandin F 2α (U46619), the relaxation induced by 17(3-estradiol was partially inhibited by tetrapentylammonium, 4-aminopyridine, iberiotoxin, BaCl 2 , and tertiapin-Q but not by tetraethylammonium, charybdotoxin, apamin, or glibenclamide. In contrast, these putative K + channel blockers, except for glibenclamide, did not affect the relaxant response to progesterone. In 4 x 10 -2 M K + -preconstricted rings, the K + channel blockers lost their inhibitory effects on 17β-estradiol-induced relaxation. Endothelium did not seem to be involved in the effects of K + channel blockers on 17β-estradiol-mediated relaxation. Nifedipine-induced relaxation was not inhibited but was instead enhanced by tetrapen-tylammonium, iberiotoxin, 4-aminopyridine, and BaCl 2 . The above results indicate that in rat mesenteric artery rings, nonselective activation of K + channels contributes partially to the relaxation induced by 17β-estradiol. These K + channels involved in the estrogen response appeared to be sensitive to inhibition by K Ca , K V , and K IR channel blockers. Lack of effect of K + channel blockers on progesterone-induced relaxation suggests that these K + channels play little or no role. The present findings provide pharmacological evidence for an additional mechanism contributing to acute vasorelaxation induced by 17β-estradiol.

An expression study of hormone receptors in spontaneously developed, carcinogen-induced and hormone-induced mammary tumors in female Noble rats.

Abstract: The Noble (Nb) rat model has been used in the study of hormonal carcinogenesis of mammary and prostate glands, as this rat strain is susceptible to tumor induction in these glands by hormonal treatments. Recently, we demonstrated that this rat strain can develop spontaneously mammary tumors at high incidence in aged animals and also show high sensitivity to chemical carcinogens (DMBA and MNU) and combined treatments with sex hormones in mammary tumor induction. In the present study, we examined and compared the expression of hormone receptors [including estrogen receptors (ERalpha and ERbeta), androgen receptor (AR), progesterone receptor (PR), prolactin receptor (PRLR)] and prolactin (PRL) by immunohistochemistry, Western blotting and RT-PCR in spontaneous mammary tumors, and mammary tumors induced by sex hormones (T+E2 and T+DES for 8-10 months) and DMBA in Nb rat model. Immunohistochemistry and Western blotting showed that both the spontaneously developed and hormone-induced carcinomas exhibited strong immunoreactivity of ERalpha, ERbeta, AR, PR and PRLR, while the spontaneous fibroadenomas showed weak to moderate immunoreactivity of ERalpha and PRLR, whereas the DMBA-induced carcinomas exhibited weak to moderate immunoreactivity of ERalpha, AR, PR and PRLR, and sporadic weak ERbeta immunoreactivity. RT-PCR analyses showed that mRNA expression pattern of these markers resembled that of proteins. In addition, weak mRNA expression of PRL was detected in spontaneous carcinomas and carcinomas induced by DMBA and hormones, suggesting that PRL could be produced locally within the tumors. The results showed that the expression status of hormone receptors and PRL was different in spontaneous mammary tumors and tumors induced by carcinogen or hormones, suggesting that the extent of involvement of steroid hormones and their receptors in the spontaneous, carcinogen- or hormone-induced mammary carcinogenesis might be different.

Bioassay of endothelium-derived hyperpolarizing factor with abolishment of nitric oxide and the role of gap junctions in the porcine coronary circulation

Abstract: Previous bioassays of endothelium-derived hyperpolarizing factor (EDHF) were partially related to the residual nitric oxide (NO) resistant to NO synthase inhibitors. Further, the role of gap junctions in EDHF is controversial. We performed a bioassay of EDHF with abolishment of NO production by using the NOS inhibitor N G -nitro-L-arginine (L-NNA) plus the NO scavenger hemoglobin (Hb) and examined the role of gap junctions/K + channels related to EDHF in porcine coronary large and microarteries in an organ chamber/myograph. Bradykinin (BK)-induced EDHF-mediated relaxation and hyperpolarization (by a microelectrode) were studied with indomethacin (7 μM), L-NNA(300 μM), and Hb (20 μM). NO concentrations ([NO]) were measured electrochemically. In large coronary arteries, BK increased [NO] (9.3±1.7 nM vs. 166.7±18.3 nM, P<0.01) that was significantly reduced by L-NNA (49.3±7.8 nM, P<0.01) and eliminated by Hb, and hyperpolarized the downstream endothelium-denuded artery by 9.0±1.4 mV (P<0.01) that was reduced but not abolished by L-NNA and Hb (5.6±0.7 mV, P<0.01). In microarteries, elimination of NO decreased but did not abolish the hyperpolarization (-63.8±1.5 mV vs. -56.9+1.6 mV, P=0.01) and relaxation (70.2±5.7% vs. 42.3±4.4%, P<0.01). Charybdotoxin (0.1 μM) and apamin (0.5 μM), but neither glybenclimide (3 μM) nor gap junction inhibitors (18α-glycyrrhetinic acid, 1-heptanol, and gap 27) reduced the EDHF-mediated response. We conclude that in porcine coronary arteries, with the abolishment of NO by NOS inhibitors plus the NO scavenger Hb, the non-NO EDHF exists and is transferable from an endothelium-intact artery to an endothelium-denuded artery. Compared with the significant involvement of calcium-activated K + channels, the gap junctions may only play a minimal role in the EDHF-mediated response even in the microcirculation of the porcine coronary artery.

Soy leaf lowers the ratio of non-HDL to HDL cholesterol in hamsters.

Abstract: The present study was to examine effect of soy leaf powder (SLP) and soy leaf ethanol extract (SLEE) on serum lipoproteins in hamsters. The control group was fed a semisynthetic diet containing 0.1% cholesterol, while the tested groups were maintained on the same diet but supplemented with 3% SLP or the equivalent amount of SLEE derived from 3% SLP for 4 weeks. SLP supplementation led to a trend of lowering serum total cholesterol (TC) and nonhigh density lipoprotein cholesterol (non-HDL-C), with HDL-C being unaffected, whereas incorporation of SLEE into the diet led to an elevated level of HDL-C and a lower level of non-HDL-C with TC being unchanged. Both SLP and SLEE supplementation caused favorably a decrease in the ratio of non-HDL-C to HDL-C. The present results demonstrate that not only soybean seeds but also soy leaves are cardioprotective, by favorably modulating serum lipid profile.

Nanowires as Building Blocks for Nanoscale Science and Technology

Abstract: The field of nanotechnology represents an exciting and rapidly expanding research area that crosses the borders between the physical, life and engineering sciences [1, 2]. Much of the excitement in this area of research has arisen from recognition that new phenomena and unprecedented integration density are possible with nanometer scale structures. Correspondingly, these ideas have driven scientists to develop methods for making nanostructures. In general, there are two philosophically distinct approaches for creating small objects, which can be characterized as top-down and bottom-up. In the top-down approach, small features are patterned in bulk materials by a combination of lithography, etching and deposition to form functional devices. The top-down approach has been exceedingly successful in many venues with microelectronics being perhaps the best example today. While developments continue to push the resolution limits of the top-down approach, these improvements in resolution are associated with a near exponential increase in cost associated with each new level manufacturing facility. This economic limitation and other scientific issues with the top-down approach have motivated efforts worldwide to search for new strategies to meet the demand for nanoscale structures today and in the future [3–5].

Contribution of Na+ -Ca2+ exchanger to pinacidil-induced relaxation in the rat mesenteric artery.

Abstract: Pinacidil relaxes blood vessels through opening the KATP channels with a resultant membrane hyperpolarization and inhibition of Ca2+ influx. The aim of this study was to examine the mechanisms thereby pinacidil induces K+ channel-independent relaxation in isolated endothelium-denuded rat mesenteric artery. Pinacidil-induced relaxation was inhibited by glibenclamide (1–10 μM) in phenylephrine-preconstricted rings, but was unaffected by glibenclamide after inhibition of K+ channels and VGCCs. Pinacidil-induced K+ channel-independent relaxation remained unchanged after treatment with cyclopiazonic acid (10 μM), thapsigargin (1 μM), ouabain (100 μM), propranolol (10 μM), Rp-cAMPS triethylamine (30 μM), L-NNA (100 μM), or ODQ (10 μM). Pinacidil induced more relaxant effect in the presence of nifedipine than in the presence of 60 mM K+ plus nifedipine. Pretreatment with Na+-Ca2+ exchanger inhibitors, nickel (30–300 μM) or benzamil (20 μM) attenuated pinacidil-induced relaxation in normal or in nifedipine-containing solution. Pinacidil (1 μM) produced less relaxant effect with decreasing extracellular Na+ concentration. Na+-free condition abolished the inhibitory effect of benzamil. Both nickel and benzamil inhibited pinacidil-induced relaxation in the presence of glibenclamide (10 μM). Nickel (300 μM) did not affect the relaxant response to sodium nitroprusside. Pinacidil relaxed the rings preconstricted by active phorbol and U46619 with similar potency. The present results indicate that stimulation of the forward mode Na+-Ca2+ exchange pathway is in part responsible for pinacidil-induced K+ channel-independent vasorelaxation. Pinacidil also induces K+ channel-dependent but VGCCs-independent relaxation. The PKC-mediated cellular pathway may be a target site for pinacidil only in higher concentrations. Keywords: Pinacidil, Na+-Ca2+ exchanger, relaxation, smooth muscle, artery, rat Introduction Pinacidil, an antihypertensive drug, lowers blood pressure via direct vasodilation (Ahnfelt-Ronne, 1988; Friedel & Brogden, 1990; Quast, 1992). Many in vitro studies have demonstrated that direct activation of the K+ channel is the primary mechanism for pinacidil-induced vasodilation. Pinacidil was more effective in inhibiting the contraction induced by noradrenaline than by elevated extracellular K+ (Videbaek et al., 1988). Pinacidil stimulated an increase in outward K+ current and hyperpolarized the cell membrane, which were sensitive to glibenclamide (Itoh et al., 1992); and pinacidil-induced vasorelaxation was also inhibited by glibenclamide and other KATP channel blockers (Standen et al., 1989). Pinacidil inhibited noradrenaline-induced inositol 1,4,5- trisphosphate (IP3) production and Ca2+ release resulting from membrane hyperpolarization in rabbit mesenteric arteries and this effect was antagonized by glibenclamide (Itoh et al., 1992). On the other hand, large-conductance Ca2+-activated K+ channels were activated by pinacidil at 100 μM in smooth muscle cells of the rat cerebral arteries (Stockbridge et al., 1991). The glibenclamide-insensitive voltage-dependent K+ current activated by pinacidil (1–20 μM) was sensitive to iberiotoxin in human coronary vascular smooth muscle cells (Bychkov et al., 1997). The K+ channel-independent vascular effects were also reported for pinacidil when its concentration used was higher than 1 μM. For example, pinacidil-induced K+ channel-independent relaxant effect may be due to a stimulatory effect on plasmalemmal Ca2+ extrusion mechanism (Meisheri et al., 1991). The IC50 of K+ channel-independent relaxation was ∼59 μM for the porcine coronary artery (Gollasch et al., 1995) and ∼50 μM for the human internal mammary artery (Gojkovic Bukarica et al., 1997). Even though dissociation of K+ channel opening and vasorelaxation by the K+ channel openers exists in several kinds of arteries from different species, including human resistance arteries (Quast, 1993), no specific mechanism has been provided to explain the K+ channel-independent component of the pinacidil-induced relaxation. The possible mechanisms may include stimulation of Na+-K+ pump or the forward mode of Na+-Ca2+ exchanger, promotion of intracellular Ca2+ uptake into the endoplasmic reticulum, direct inhibition of plasmalemmal Ca2+ channels, activation of cyclic nucleotide-dependent signalling pathway or protein kinase C-mediated contraction. The present study therefore attempts to investigate some cellular mechanisms that may underlie a K+ channel-independent vasorelaxant response to pinacidil with various pharmacological interventions in the isolated endothelium-denuded rat mesenteric arteries.

Static pin mapping and SOC test scheduling for cores with multiple test sets

Abstract: An algorithm for mapping core terminals to system-on-a-chip (SOC) I/O pins and scheduling tests in order to achieve cost-efficient concurrent test for core-based designs is presented in this paper. In this work "static" pin mapping and test scheduling for concurrent testing are studied for the case of multiple test sets for each core. The problem is formulated as a constrained two-dimensional bin-packing problem. A heuristic algorithm is then proposed to determine a solution. The objectives driving this solution are geared towards reducing the total test application time of SOC and satisfying the test constraints such as limited number of SOC pins and maximum peak power dissipation specified by core integrators. Experimental results demonstrate the effectiveness of the proposed method.

Isomeric distribution of conjugated linoleic acids (CLA) in the tissues of layer hens fed a CLA diet.

Abstract: The isomeric distribution of conjugated linoleic acids (CLA) in the tissue lipids of hens in relation to that in the diet was examined. Silver-ion high-performance liquid chromatography was used to quantify individual CLA isomers in total tissue lipids, phospholipids, and triacylglycerols. It was found that the deposition of CLA isomers in hen tissues was selective. All tissues including serum, liver, heart, kidney, abdominal fat, and leg and breast muscles had lesser amounts of total cis/trans isomers ranging from 75.87 to 89.13% of total CLA, which was in contrast to the value of 92% of total CLA in the dietary lipids. Total trans/trans isomers in all tissue lipids ranging from 6.11 to 18.02% of total CLA were greater than that in the diet (4.19%). Among the individual trans/trans isomers, all tissues except for adipose tissue and brain incorporated greater amounts of t-12,t-14-18:2, t-11,t-13-18:2,t-10,t-12-18:2, t-9,t-11-18:2, and t-18,t-10-18:2 compared with the values of the diet. Within the cis/trans group, lesser amounts of c-10,t-12/t-10,c-12-18:2 were found to incorporate into all tissues compared with the value of the diet. Serum and liver had higher percentages of c-9,t-11/t-9,c-11, whereas the other tissues had similar levels of this isomer compared with that of the diet. It was also observed that supplementation of CLA in the diet of layer hens decreased the concentration of docosahexaenoic acid (22:6n-3) in all of the tissue lipids. It is concluded that dietary CLA can transfer to the tissue but that incorporation of CLA isomers into the tissue is selective in hens.

Evidence for Disaggregation of Oligomeric Goα Induced by Guanosine-5"-3-O-(thio)triphosphate Activation

Abstract: Myristoylated Goα was expressed in and highly purified from Escherichia coli strain JM109 cotransformed with pQE60 (Goα) and pBB131 (N-myristoyltransferase, NMT). Non-denaturing gel electrophoresis and gel filtration analysis revealed that the Goα, in its GDP-bound form, could form oligomers involving dimer, trimer, tetramer, pentamer, or hexamer and guanosine 5"-3-O-(thio)triphosphate (GTPγS) activation induced disaggregation of the Goα oligomers to monomers. The Goα was crosslinked by a cross-linker, N,N"-1,4-phenylenedimaleimide (p-PDM), yielding multiple crosslinked products. In contrast, no obvious cross-linking occurred when Goα was pretreated with GTPγS. Immunoblot analysis also demonstrated oligomerization of the purified Goα proteins and its disaggregation triggered by GTPγS. These results provided direct evidence for the “disaggregation–coupling” theory and the disaggregation action of GTPγS may further elucidate the regulatory role of GDP/GTP exchange in G protein-coupled signal transduction pathways.

Spontaneous mammary tumors in aging Noble rats.

Abstract: Noble (Nb) rat strain has been used for the study of hormonal carcinogenesis of mammary and prostate glands, for its susceptibility to develop premalignant lesions as well as carcinomas in these organs by sex hormones. However, background information on the spontaneously developed mammary tumors in this rat strain is scarce. We report on the incidence rate, latency period and histopathology of mammary tumors spontaneously developed in the senile intact and untreated Nb rats compared with those induced by either combined treatments with sex steroids or 7,12-dimethylbenz[a]anthracene (DMBA) in the same rat strain. We observed that the incidence rate of spontaneous mammary tumors was 45% in female Nb rats and 3% in the males. The average age of the female Nb rats to develop palpable tumors was 14 months and rarely detected in animals less than 12 months old. It was also noted that the incidence rate of the spontaneous mammary tumors was similar to those induced by combined treatments with sex steroids for 8-10 months (46.7% for T+E 2 and 55.6% for T+DES) but less than those by DMBA treatment in 8 months (over 80%). Histologically, majority of the spontaneous mammary tumors were fibroadenomas, which comprised 70% of all collected tumors and about 20% were carcinomas whereas tumors induced by steroid hormones and DMBA were all carcinomas. Distant metastases of spontaneous mammary carcinomas to lung, liver and lymph nodes were also noted, but rarely.

Composants optiques coherents nanometriques

Abstract: L'invention concerne en general la nanotechnologie et la nanoelectronique, ainsi que des procedes et des dispositifs associes. Elle concerne en particulier des composants optiques nanometriques tels que des dispositifs electroluminescents (par exemple des DEL), des dispositifs d'emission stimulees amplifiees (par exemple des lasers), des guides d'ondes et des cavites optiques (par exemple des resonateurs). Elle concerne en outre des articles et des dispositifs d'une taille superieure a la taille nanometrique. De tels dispositifs peuvent etre formes a partir de fils nanometriques tels que des nanofils ou des nanotubes. Dans certains cas, le fil nanometrique est un simple cristal. Dans un mode de realisation, le laser nanometrique est construit sous forme d'une cavite Fabry-Perot et il est excite par une injection electrique. N'importe quelle source d'injection electrique peut etre utilisee. Par exemple, l'injection electrique peut etre realisee au moyen d'un systeme a fils croises, d'un systeme a electrodes ou a electrodes reparties, ou d'un systeme noyau/coquille. On peut maitriser la longueur d'onde de sortie, par exemple en utilisant differents types de materiaux pour fabriquer le dispositif. Au moins un tel laser nanometrique peut egalement etre integre a d'autres composants nanometriques, dans un dispositif.