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Showing papers by "Yu Huang published in 2006"


Journal ArticleDOI
TL;DR: The cardiovascular effects of berberine suggest its possible clinical usefulness in the treatment of arrhythmias and/or heart failure.
Abstract: Berberine, is an alkaloid from Hydrastis canadensis L., Chinese herb Huanglian, and many other plants. It is widely used in traditional Chinese medicine as an antimicrobial in the treatment of dysentery and infectious diarrhea. This manuscript describes cardiovascular effects of berberine and its derivatives, tetrahydroberberine and 8-oxoberberine. Berberine has positive inotropic, negative chronotropic, antiarrhythmic, and vasodilator properties. Both derivatives of berberine have antiarrhythmic activity. Some of cardiovascular effects of berberine and its derivatives are attributed to the blockade of K + channels (delayed rectifier and K ATP ) and stimulation of Na + -Ca 2+ exchanger. Berberine has been shown to prolong the duration of ventricular action potential. Its vasodilator activity has been attributed to multiple cellular mechanisms. The cardiovascular effects of berberine suggest its possible clinical usefulness in the treatment of arrhythmias and/or heart failure.

242 citations


Journal ArticleDOI
TL;DR: The present communication focuses on the biology of ROS signaling in vascular cells, discusses how oxidative stress contributes to vascular damage, and the therapeutic strategies/biotic factors that can prevent or treat ROS-associated cardiovascular disorders.
Abstract: Reactive oxygen species (ROS) contribute to the pathogenesis of cardiovascular diseases including hypertension, atherosclerosis, cardiac hypertrophy, heart failure and diabetes mellitus. Oxidative stress is resulted from excessive generation of ROS that outstrips the antioxidant system. Various agonists, pathological conditions and therapeutic interventions lead to modulated expression and function of oxidant and antioxidant enzymes, including NAD(P)H oxidase, endothelial nitric oxide synthase, xanthine oxidase, myeloperoxidase, superoxide dismutases, catalase and glutathione peroxidase. ROS formed in vascular wall target a wide range of signaling molecules and cellular pathways in both endothelium and vascular smooth muscle, such as transcription factors, protein tyrosine phosphatase, protein tyrosine kinase, mitogen-activated protein kinase, Ca(2+)-transporting system and protein modification. ROS also have distinct physiological and pathophysiological impacts on vascular cells. ROS contribute to vascular dysfunction and remodeling through oxidative damage by (1) reducing the bioavailability of NO, (2) impairing endothelium-dependent vasodilatation and endothelial cell growth, (3) causing apoptosis or anoikis, (4) stimulating endothelial cell migration, and (5) activating adhesion molecules and inflammatory reaction, leading to endothelial dysfunction, an initial episode progressing toward hypertension and atherosclerosis. Cellular events underlying these processes involve changes in vascular smooth muscle cell growth, apoptosis/anoikis, cell migration, inflammation, and vasoconstriction. The present communication focuses on the biology of ROS signaling in vascular cells, discusses how oxidative stress contributes to vascular damage, and the therapeutic strategies/biotic factors that can prevent or treat ROS-associated cardiovascular disorders.

178 citations


Journal ArticleDOI
TL;DR: The formation mechanism of core-shell spherical structures was proposed and successfully extended this method to prepare microspheres of ceria and ceria-zirconia solid solutions to be easily scaled up for industrial production of microspherical solid solutions photocatalysts and catalysts.
Abstract: A series of Ti1-xZrxO2 solid solutions photocatalysts (x = 0.000, 0.045, 0.090, 0.135, and 0.180) was directly obtained by an ultrasonic spray pyrolysis method. Compared with previous methods for solid solutions, our preparation was very fast. The resulting samples were characterized by X-ray diffraction, scanning electron microscopy, transmission electron microscopy, high-resolution transmission electron microscopy, nitrogen adsorption, and UV−vis diffuse reflectance spectroscopy. The characterizations revealed core−shell spherical structures of the resulting solid solutions. We evaluated photocatalytic activities of the solid solutions on degradation of rhodamine B in aqueous solution under simulated solar light. It was found that Ti0.91Zr0.09O2 solid solution exhibited the highest photocatalytic activity among all the as-prepared samples. Its activity was much higher than that of P25. The formation mechanism of core−shell spherical structures was proposed. Moreover, we successfully extended this method...

77 citations


Journal ArticleDOI
TL;DR: Data strongly suggest that the inhibitory action of PKC on TRPC3 is partly mediated through PKG in these PKG‐overexpressing cells, and an important role of PKG is suggested in the PMA‐induced inhibition of TRPC channels in native endothelial cells.
Abstract: There are two known phosphorylation-mediated inactivation mechanisms for TRPC3 channels. Protein kinase G (PKG) inactivates TRPC3 by direct phosphorylation on Thr-11 and Ser-263 of the TRPC3 proteins, and protein kinase C (PKC) inactivates TRPC3 by phosphorylation on Ser-712. In the present study, we explored the relationship between these two inactivation mechanisms of TRPC3. HEK cells were first stably transfected with a PKG-expressing construct and then transiently transfected with a TRPC3-expressing construct. Addition of 1-oleoyl-2-acetyl-sn-glycerol (OAG), a membrane-permeant analog of diacylglycerol (DAG), elicited a TRPC3-mediated [Ca2+]i rise in these cells. This OAG-induced rise in [Ca2+]i could be inhibited by phorbol 12-myristate 13-acetate (PMA), an agonist for PKC, in a dose-dependent manner. Importantly, point mutations at two PKG phosphorylation sites (T11A-S263Q) of TRPC3 markedly reduced the PMA inhibition. Furthermore, inhibition of PKG activity by KT5823 (1 microM) or H8 (10 microM) greatly reduced the PMA inhibition of TRPC3. These data strongly suggest that the inhibitory action of PKC on TRPC3 is partly mediated through PKG in these PKG-overexpressing cells. The importance of this scheme was also tested in vascular endothelial cells, in which PKG plays a pivotal functional role. In these cells, OAG-induced [Ca2+]i rise was inhibited by PMA, which activates PKC, and by 8-BrcGMP and S-nitroso-N-acetylpenicillamine (SNAP), both of which activate PKG. Importantly, the PMA inhibition on OAG-induced [Ca2+]i rise was significantly reduced by PKG inhibitor KT5823 (1 microM) or DT-3 (500 nM), suggesting an important role of PKG in the PMA-induced inhibition of TRPC channels in native endothelial cells.

53 citations


Journal ArticleDOI
TL;DR: The data suggest that bradykinin-induced non-CCE is mediated via the B2-PLC pathway, and that DAG may be involved in this process.
Abstract: Bradykinin is a potent vasoactive nonapeptide. It elicits a rise in cytosolic Ca(2+) (Ca(2+))(i) in endothelial cells, resulting in Ca(2+)-dependent synthesis and release of endothelial vasodilators. In the present study, we investigated the mechanism of bradykinin-induced Ca(2+) influx in primary cultured rat aortic endothelial cells and in a mouse heart microvessel endothelial cell line (H5V). Bradykinin-induced Ca(2+) influx was resolved into capacitative Ca(2+) entry (CCE) and non-CCE. The non-CCE component was inhibited by a B2 receptor antagonist (HOE140; 1 microM) and a phospholipase C (PLC) inhibitor (U73122; 10 microM). The action of bradykinin could be mimicked by 1-oleoyl-2-acetyl-glycerol, an analogue of diacylglycerol (DAG), and by RHC80267, a DAG-lipase inhibitor. Immunoblots showed that TRPC6 was one of the main TRPC channels expressed in endothelial cells. Transfection of H5V cells with two siRNA constructs against TRPC6 both markedly reduced the TRPC6 protein level and, at the same time, decreased the percentage of cells displaying bradykinin-induced non-CCE. siRNA transfection also reduced the magnitude of non-CCE among the cells responding to bradykinin. Taken together, our data suggest that bradykinin-induced non-CCE is mediated via the B2-PLC pathway, and that DAG may be involved in this process. Further, TRPC6 is one of the important channels participating in bradykinin-induced non-CCE in endothelial cells.

48 citations


Journal ArticleDOI
TL;DR: Flow‐induced dilatation in rat mesenteric arteries can be markedly enhanced by prior depletion of intracellular Ca2+ stores, consistent with a role for H2O2 as the vasodilator involved.
Abstract: The effect of depleting intracellular Ca2+ stores on flow-induced vascular dilatation and the mechanism responsible for the vasodilatation were examined in rat isolated small mesenteric arteries. The arteries were pressurized to 50 mmHg and preconstricted with phenylephrine. Intraluminal flow reversed the effect of phenylephrine, resulting in vasodilatation. Flow dilatation consisted of an initial transient peak followed by a sustained plateau phase. The magnitude of dilatation was markedly reduced by removing Ca2+ from the intraluminal flow medium. Depletion of intracellular Ca2+ stores with either cyclopiazonic acid (CPA, 2 μM) or 1,4-dihydroxy-2,5-di-tert-butylbenzene (BHQ, 10 μM) significantly augmented the magnitude of flow dilatation. Flow-induced endothelial cell Ca2+ influx was also markedly enhanced in arteries pretreated with CPA or BHQ. Flow-induced dilatation was insensitive to Nw-nitro-L-arginine methyl ester (100 μM) plus indomethacin (3 μM) or to oxyhemoglobin (3 μM), but was markedly reduced by 30 mM extracellular K+ or 2 mM tetrabutylammonium (TBA), suggesting an involvement of EDHF. Catalase at 1200 U ml−1 abolished the flow-induced dilatation, while the application of exogenous H2O2 (90–220 μM) induced relaxation in phenylephrine-preconstricted arteries. Relaxation to exogenous H2O2 was blocked in the presence of 30 mM extracellular K+, and H2O2 (90 μM) hyperpolarized the smooth muscle cells, indicating that H2O2 can act as an EDHF. In conclusion, flow-induced dilatation in rat mesenteric arteries can be markedly enhanced by prior depletion of intracellular Ca2+ stores. Furthermore, these data are consistent with a role for H2O2 as the vasodilator involved. British Journal of Pharmacology (2006) 147, 506–515. doi:10.1038/sj.bjp.0706639

41 citations


Proceedings ArticleDOI
01 Oct 2006
TL;DR: Experimental results illustrate that per-pin based failure logging and diagnosis algorithms enable scan chain diagnosis in volume production environment.
Abstract: This paper discusses the challenges associated with diagnosing chain integrity and system logic failures in the production test environment with limited failure information. The following three methods were proposed to enhance diagnosis resolution in this scenario: (1) static pattern re-ordering (2) dynamic pattern re-ordering (3) per-pin based diagnosis. Experimental results illustrate that per-pin based failure logging and diagnosis algorithms enable scan chain diagnosis in volume production environment. Successful application of per-pin based chain diagnosis is demonstrated with an industrial case

40 citations


Journal ArticleDOI
TL;DR: The results suggest that TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating the Ca2+ influx into endothelial cells.
Abstract: To test the possible involvement of TRPC3 in agonist-induced relaxation and flow-induced vasodilation in rat small mesenteric arteries. Male Sprague-Dawley rats were used in the present study. After 72 h-treatment of antisense oligo via tail vein injection, isometric tension and isobaric diameter measurement were carried out with isolated mesenteric artery segments by using either a Pressure Myograph or a Multi Myograph system. Endothelial [Ca2+]i changes were measured with a MetaFluor imaging system in response to flow or to 30 nmol/L bradykinin. Immunohistochemical study showed that the 72 h-treatment of antisense oligo via tail vein injection markedly decreased the TRPC3 expression in mesenteric arteries, indicating the effectiveness of the antisense oligo. Isometric tension and isobaric diameter measurement showed that, although the antisense oligo treatment did not affect histamine-, ATP-, and CPA-induced relaxation, it did reduce the magnitude of flow-induced vasodilation by approximately 13% and decreased bradykinin-induced vascular relaxation with its EC50 value raised by nearly 3-fold. Endothelial [Ca2+]i measurement revealed that treatment of the arteries with antisense oligos significantly attenuated the magnitude of endothelial [Ca2+]i rise in response to flow and to 30 nmol/L bradykinin. The results suggest that TRPC3 is involved in flow- and bradykinin-induced vasodilation in rat small mesenteric arteries probably by mediating the Ca2+ influx into endothelial cells.

35 citations


Journal ArticleDOI
TL;DR: The present results indicate that in addition to nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF, sensitive to charybdotoxin plus apamin, ouabain, and BaCl2), the endothelia of rat femoral artery can release H2O2 in response to acetylcholine, which was sensitive to L-NAME.

34 citations


Journal ArticleDOI
TL;DR: It is suggested that chronic oral administration of raloxifene to aging ovariectomized female rats augmented the bioavailability of endothelial nitric oxide in isolated aortic rings without altering eNOS protein levels.

33 citations


Patent
19 Dec 2006
TL;DR: In this article, a set of particles is provided for use in estimating a location of a state of a dynamic system (1010), and a local-mode seeking mechanism is applied to move one or more particles in the set of particle nodes.
Abstract: According to an implementation, a set of particles is provided for use in estimating a location of a state of a dynamic system (1010). A local-mode seeking mechanism is applied to move one or more particles in the set of particles (1020), and the number of particles in the set of particles is modified (1030). The location of the state of the dynamic system is estimated using particles in the set of particles (1040). Another implementation provides dynamic state estimation using a particle filter (565) for which the particle locations are modified using a local-mode seeking algorithm based on a mean-shift analysis (610) and for which the number of particles is adjusted using a Kullback-Leibler-distance sampling process (830-860). The mean-shift analysis may reduce degeneracy in the particles, and the sampling process may reduce the computational complexity of the particle filter. The implementation may be useful with non-linear and non-Gaussian systems.

Journal ArticleDOI
TL;DR: The present results demonstrate that cilnidipine can produce endothelium‐dependent relaxation in porcine coronary arteries in vitro in addition to blocking Ca2+ channels, and suggests the usefulness of cilNdipine in the treatment of cardiovascular diseases associated with diminished NO release, such as atherosclerosis.
Abstract: Cilnidipine is a dual blocker of L-type voltage-gated Ca2+ channels in vascular smooth muscle and N-type Ca2+ channels in sympathetic nerve terminals that supply blood vessels. However, the clinical benefits of cilnidipine and underlying mechanisms are incompletely understood. This study was designed to compare the time course of relaxant responses to cilnidipine and nifedipine, and to examine the role of endothelial NO and [Ca2+]i in the vasorelaxation. Porcine left circumflex coronary arteries were isolated and isometric tension was measured with Grass force transducers. Endothelial [Ca2+]i in intact arteries was determined by a calcium fluorescence imaging technique. The free radical scavenging capacity was also assayed. Cilnidipine and nifedipine induced concentration-dependent relaxations in high KCl-precontracted artery rings, while the former-induced relaxation was slower as compared to the latter. Treatment with L-NAME or ODQ reduced relaxations to cilnidipine or nifedipine to the same extent as in rings without endothelium. Indomethacin or ω-conotoxin had no effects. L-Arginine antagonized the effect of L-NAME on cilnidipine-induced relaxations. Cilnidipine did not affect sodium nitroprusside-induced relaxation in rings with and without endothelium. Cilnidipine and nifedipine caused extracellular Ca2+-dependent increases in endothelial [Ca2+]i in intact arteries and cilnidipine's action had a slower onset, similar to that of cilnidipine-induced relaxation. Neither cilnidipine nor nifedipine exhibited a free radical scavenging property. The present results demonstrate that cilnidipine can produce endothelium-dependent relaxation in porcine coronary arteries in vitro in addition to blocking Ca2+ channels. Like short-acting nifedipine, cilnidipine-dependent relaxation, albeit to a slower onset, is partly mediated by endothelial NO but not by prostacyclin. The increased release or bioavailability of NO may causally result from elevated endothelial [Ca2+]i in arteries. The Ca2+ channel-independent effect suggests the usefulness of cilnidipine in the treatment of cardiovascular diseases associated with diminished NO release, such as atherosclerosis. Keywords: Ca2+ channel, cilnidipine, nitric oxide, intracellular calcium, arteries Introduction Dihydropyridine (DHP) Ca2+ antagonists, including nifedipine, are frequently used in the treatment of hypertension, stable angina pectoris and cerebrovascular disease by blocking L-type voltage-gated Ca2+ channels. These therapeutic agents relax coronary arteries, cause peripheral vasodilatation, and decrease left ventricular contraction, thereby reducing the myocardial oxygen demand. The clinical studies and meta-analysis, however, have questioned the long-term safety of nifedipine regimen that actually increases the risk of myocardial infarction and mortality in patients with coronary artery disease (Furberg et al., 1995; Psaty et al., 1995; Stason et al., 1999). The deleterious mechanism for this fatal adverse effect of nifedipine is unclear. Rapid hypotensive action of short-acting DHPs causes an elevation in vascular sympathetic tone and reflex tachycardia. The increased release of noradrenaline may represent a coronary risk factor in hypertensive patients (Julius, 1993). In contrast to nifedipine, a short-acting first generation DHP that exclusively blocks L-type Ca2+ channels, cilnidipine is a new, long-acting second generation DHP that blocks both L- and N-type Ca2+ channels. Cilnidipine is a slow-onset vasodilator and antihypertensive drug as revealed in clinical and animal studies (Yoshimoto et al., 1991; Tominaga et al., 1997). Cilnidipine blocks L-type Ca2+ channels in vascular smooth muscle at concentrations that do not inhibit protein kinase C (Lohn et al., 2002), while nifedipine is a potent inhibitor of protein kinase C (Hempel et al., 1999). Besides, cilnidipine also inhibits T-type Ca2+ currents in guinea-pig ventricular myocytes (Takeda et al., 2004). Cilnidipine attenuates vascular sympathetic neurotransmission (Hosono et al., 1995) probably by blocking the N-type Ca2+ channels (Fujii et al., 1997). With this unique dual L/N-type blocking property, cilnidipine may have clinical advantages over nifedipine with respect to cardiovascular protection. Indeed, cilnidipine effectively lowers blood pressure with much less influence on heart rate and sympathetic nerve activity than nifedipine in hypertensive patients (Minami et al., 1998; 2000). Cilnidipine is also demonstrated to reduce blood pressure in animal studies (Nakajima et al., 2002; Varagic et al., 2002). The endothelium regulates the vascular tone and blood pressure. Endothelial dysfunction characterized by impaired endothelium-dependent vasodilatation has been described in both human and animal hypertension (Mombouli & Vanhoutte, 1999). Some DHPs exhibit Ca2+ channel-independent vascular effects leading to improved endothelial function (Taddei et al., 1997; Krenek et al., 2001). Recent in vitro studies have shown that nifedipine enhances NO release via the upregulation of eNOS expression (Ding & Vaziri, 2000) and possesses antioxidant or free radical scavenging effects (Lesnik et al., 1997). As compared with nifedipine, it is, however, unknown whether cilnidipine exerts similar benefits on the endothelium by releasing relaxing substances. The present study tested the hypothesis that cilnidipine produces endothelium-dependent relaxation in porcine coronary arteries in vitro in addition to its known Ca2+ channel-blocking property. Specifically, this study examined (i) whether cilnidipine induces endothelium-dependent relaxation and what endothelium-derived vasoactive factors are involved, (ii) whether cilnidipine stimulates an increase in endothelial [Ca2+]i in situ in freshly isolated arteries, and (iii) whether cilnidipine possesses a free radical-scavenging activity. For comparison, we studied the arterial effects of nifedipine, the clinically relevant prototype of DHP Ca2+ antagonists in the same preparations.

Journal ArticleDOI
TL;DR: Experiments were designed to determine the mechanism of the relaxation induced by tamoxifen in porcine coronary arteries at the tissue, cellular and molecular levels.
Abstract: Background and purpose: Experiments were designed to determine the mechanism of the relaxation induced by tamoxifen in porcine coronary arteries at the tissue, cellular and molecular levels. Experimental approach: Porcine left circumflex coronary arteries were isolated and isometric tension was measured. [Ca2+]i in native endothelial cells of intact arteries was determined by a calcium fluorescence imaging technique and eNOS ser1177 phosphorylation was assayed by Western blotting. Key results: Tamoxifen induced an endothelium-dependent relaxation that was antagonized by ICI 182,780 and abolished by NG-nitro-L-arginine methyl ester (L-NAME) or 1H-[1,2,4]oxadizolo[4,3-a]quinoxalin-1-one (ODQ). L-Arginine reversed the effect of L-NAME while indomethacin was without effect. Tamoxifen-induced relaxation was attenuated by charybdotoxin (CTX) plus apamin, ouabain or by incubation in a K+-free solution. Moreover, tamoxifen triggered extracellular Ca2+-dependent increases in endothelial [Ca2+]i and this effect was abolished by ICI 182,780. Endothelium-independent relaxation to sodium nitroprusside was also inhibited by ouabain or in a K+-free solution. Furthermore, tamoxifen increased endothelial nitric oxide synthase (eNOS) phosphorylation at Ser-1177 and ICI 182,780 prevented this effect. Conclusions and Implications: The present results suggest that tamoxifen mainly induces endothelium-dependent relaxation and that endothelial nitric oxide (NO) is the primary mediator of this effect. NO-dependent responses may result from elevated [Ca2+]i in endothelial cells; an effect abolished by ICI 182,780. NO activates Na+/K+-ATPase in vascular smooth muscle, leading to relaxation. These results suggest that tamoxifen is able to modulate eNOS phosphorylation directly. British Journal of Pharmacology (2006) 149, 703–711. doi:10.1038/sj.bjp.0706921

Proceedings ArticleDOI
Yu Huang1
27 Mar 2006
TL;DR: It is illustrated that the traditional N-detect ATPG is unoptimized in terms of the size of the generated pattern set in order to obtain sub-optimal solutions efficiently.
Abstract: In this paper, we illustrate that the traditional N-detect ATPG is unoptimized in terms of the size of the generated pattern set. The optimization problem is formulated as a minimum covering problem. Integer linear programming (ILP) is applied to obtain an N-detection ATPG pattern set with the minimum number of patterns. A heuristic method is also proposed to obtain sub-optimal solutions efficiently. Experimental results demonstrate that by using the proposed method, the number of N-detection patterns can be reduced by about 18% for N=3 and about 13% for N=5 without compromising N-detection objective.

Journal ArticleDOI
TL;DR: Both NO and EDHF play an important role in regulation of porcine pulmonary arterial and venous tones and the more significant role of NO and EdHF is revealed in pulmonary arteries than in veins.

Journal ArticleDOI
TL;DR: In this article, a multi-step inverse method is used together with RSM to check various intermediate surfaces to search for the optimal shape parameters, and the result is validated using commercial software DYNAFORM ®.

Journal ArticleDOI
TL;DR: It was concluded that both soybean and kudzu phytoestrogens could modify favorably lipoprotein profiles in ovariectomized and castrated hamsters.
Abstract: The present study compared the hypolipidemic activity of kudzu phytoestrogens with that of soybean phytoestrogen in estrogen- and androgen-deficient hamsters. In the first experiment, ovariectomized hamsters (n = 37) were randomly divided into four groups (n = 9−10 each group). The first group was the control group, whereas the second group had the time-releasing estradiol-17β subcutaneous (pellet) implants as a positive control. The third and fourth groups were orally administered soybean or kudzu phytoestrogen extracts (30 mg/kg of body weight) per day. In the second experiments, the first group of male hamsters (n = 9) received a sham operation, whereas the other three groups of male hamsters (n = 9 each) were castrated. The castrated control group received orally distilled water, whereas the second and third castrated groups were orally given 30 mg/kg soybean or kudzu phytoestrogen extracts. The results for the first experiment showed that the ovariectomized hamsters orally given soybean and kudzu phy...

Journal ArticleDOI
TL;DR: In this article, measurements of the beat frequencies between vibrational modes of dipicolinic acid (DPA) and a series of other molecules (interferents) are presented.
Abstract: Measurements of the beat frequencies between vibrational modes of dipicolinic acid (DPA) and a series of other molecules (interferents) are presented. The results were obtained from femtosecond time-resolved coherent Raman scattering, and the vibrational level spacings were determined from a Fourier transform of the signal versus probe pulse delay. The entire spectrum of the generated signal is recorded in order to demonstrate multimode excitation and to explain the variety of qualitatively different traces that can be obtained for the same molecule. Since the spectral signature of DPA is unique enough to be used for identification purposes, this technique has the potential to detect hazardous bacterial species, such as anthrax spores.

Journal ArticleDOI
TL;DR: Based on high homology of ERRs with ERs, it is hypothesized that ERRs might functionally cross talk withERs or independently in prostatic cells.
Abstract: BACKGROUND Based on high homology of ERRs with ERs, we hypothesize that ERRs might functionally cross talk with ERs or independently in prostatic cells. METHODS We examined the ERRγ expressions in rat prostates and Nb rat prostate cancer model, and its growth regulation in stable transfectants of prostatic cells. RESULTS We cloned the ERRγ cDNA from rat prostate by RACE-PCR. Its expression was confirmed by Northern and immunoblottings. Real-time RT-PCR showed that its expression in castrated prostates was androgen-dependent. ERRγ was expressed in prostatic epithelial cells, but showed reduced expressions in neoplastic prostates. Transfections confirmed that ERRγ was expressed in prostatic cells as nuclear protein and transcriptionally active without estradiol. Its overexpression in ERRγ-stable transfectants of NbE-1 and MAT-Lu cells inhibited their in vitro proliferation, anchorage-independent growth in soft-agar and tumorigenicity in nude mice. CONCLUSIONS Our studies show that ERRγ is functionally expressed in rat prostate and may play anti-proliferative actions in prostatic cells. Its co-expression with ERs suggests that besides ERs, ligand-independent ERRγ is also involved in prostatic growth and functions. Prostate 66: 1600–1619, 2006. © 2006 Wiley-Liss, Inc.

Proceedings ArticleDOI
06 Mar 2006
TL;DR: This paper proposes a different software based method that does not require any extra effort manipulating test parameters and attempts to diagnose with stuck-at-0 fault model at scan enable defects.
Abstract: In this paper, we propose a different software based method that does not require any extra effort manipulating test parameters. First, we assume the defects are on scan chains and use previously published chain diagnosis algorithms presented in Y. Huang et al. (2005) to identify the suspect scan cells. Secondly, if there is at least one faulty chain that is modeled with stuck-at-X fault, we attempt to diagnose with stuck-at-0 fault model at scan enable. As we mentioned earlier that the shift operation is incorrect when the scan cell value is obtained from the system logic for each shift cycle, it is very likely we see both stuck-at-1 and stuck-at-0 at scan cells. So stuck-at-X fault model at scan cells is a sign of the stuck-at-0 fault model for scan enable defects