Biomedical subjects

S Nam

Publications and source records attributed to S Nam.

At least 19 recordsLinked to original sources

PubMed2004

Decoherence in josephson phase qubits from junction resonators.

Although Josephson junction qubits show great promise for quantum computing, the origin of dominant decoherence mechanisms remains unknown. Improving the operation of a Josephson junction based phase qubit has revealed microscopic two-level systems or resonators within the tunnel barrier that cause decoherence. We report spectroscopic data that show a level splitting characteristic of coupling between a two-state qubit and a two-level system. Furthermore, we show Rabi oscillations whose "coherence amplitude" is significantly degraded by the presence of these spurious microwave resonators. The discovery of these resonators impacts the future of Josephson qubits as well as existing Josephson technologies.

Journal Article↗

PubMed2004

Observation of eta'c production in gammagamma fusion at CLEO.

We report on the observation of the eta(')(c)(2(1)S0), the radial excitation of the eta(c)(1(1)S0) ground state of charmonium, in the two-photon fusion reaction gammagamma-->eta(')(c)-->K(0)(S)K+/-pi(-/+) in 13.6 fb(-1) of CLEO II/II.V data and 13.1 fb(-1) of CLEO III data. We obtain M(eta(')(c))=3642.9+/-3.1(stat)+/-1.5(syst) MeV and M(eta(c))=2981.8+/-1.3(stat)+/-1.5(syst) MeV. The corresponding values of hyperfine splittings between 1S0 and 3S1 states are DeltaM(hf)(1S)=115.1+/-2.0 MeV and DeltaM(hf)(2S)=43.1+/-3.4 MeV. Assuming that the eta(c) and eta(')(c) have equal branching fractions to K(S)Kpi, we obtain Gamma(gammagamma)(eta(')(c))=1.3+/-0.6 keV.

Journal Article↗

PubMed2003

Branching fractions of tau leptons to three charged hadrons.

From electron-positron collision data collected with the CLEO detector operating at Cornell Electron Storage Ring near sqrt[s]=10.6 GeV, improved measurements of the branching fractions for tau decays into three explicitly identified hadrons and a neutrino are presented as B(tau(-)-->pi(-)pi(+)pi(-)nu(tau))=(9.13+/-0.05+/-0.46)%, B(tau(-)-->K-pi(+)pi(-)nu(tau))=(3.84+/-0.14+/-0.38) x 10(-3), B(tau(-)-->K-K+pi(-)nu(tau))=(1.55+/-0.06+/-0.09) x 10(-3), and B(tau(-)-->K-K+K-nu(tau))<3.7 x 10(-5) at 90% C.L., where the uncertainties are statistical and systematic, respectively.

Journal Article↗

PubMed2003

Needles to promote ventricular blood into the ischemic myocardium applied in a rat heart transplant model: an acute observation [corrected].

Two needles were designed in order to revascularize an ischemic myocardium in the event of left coronary artery occlusion. This study was conducted by performing the Lee modified Fox-Montorsi heart-lung transplant on 25 San Diego Microsurgical Institute-bred Sprague Dawley rats that were subjected to left coronary artery ligation in each case. Of these 25 rats, a straight-porous (SP) needling procedure was applied to 9 heterotopically transplanted rat hearts, and a distinct horseshoe (HS)-shaped needle application was performed on the remaining 16 heterotopically transplanted rat hearts. This report represents an acute study on the efficiency of these two needles to transmit oxygen-rich blood from the left ventricle into the ischemic myocardium. Doppler readings for male vs. female transplants showed that the control peak (PK) and mean (MN) kHz values are on the average of 0.20 kHz higher in males than in females. However, control heart rate values in both sexes are approximately equal. Ligation of the left coronary artery caused a dramatic decrease of PK and MN kHz values in both sexes, while heart rate showed no significant decrease from the original control values in response to ischemia. Application of the SP needle showed only a slight return of PK and MN values in both sexes, but heart rate values increased to levels higher than the original control values. The HS needling procedure was able to recover approximately 80% of the control PK and MN kHz values in both sexes. Thus, these data indicate that the HS needle can successfully transmit left ventricular blood into the myocardium.

Animals↗

PubMed2003

Consecutive en-bloc liver (30%)-pancreas-duodenum-spleen-stomach transplant in Lewis rats.

It is well-known that 30% of the remaining liver mass, following partial hepatectomy, regenerates to full original mass within 2 weeks in rats. In order to carry the transplanted rat liver to repeated transplantation, a technique of combining 30% of the liver with the pancreaticoduodenum and spleen transplantation is performed in this consecutive organ transplantation study. Our laboratory observed several 37-month-old transplanted rats by carrying through 2-3 generations, and histological disclosure were made. Because the partial liver transplants did not regenerate after the transplantation with other splanchnic organs, this technique is not so difficult though subsequent surgical maneuvers are needed and the liver histology proved entirely normal in every aspect when followed beyond the rat's life span of 24 months.

Animals↗

PubMed2003

Observations of rat ovarian-splenic consecutive transplants.

We examined the results after implantation of ovarian follicles by various modes in a total of 82 cases. One or five ovarian follicles were implanted into spleens in castrated female rats. In 20 cases among these, each five follicles were implanted into native and transplanted spleens after spleen transplantation (double implantation of the ovary). Through consecutive spleen transplantation, we observed the results beyond the rat's life span for a limited period. In many cases, we found a more aggressive form of malignant tumor, i.e., dysgerminoma. We present the results and discuss the modes of implantations and possible pathogenetic mechanisms of tumor formation.

Animals↗

PubMed2002

Measurements of inclusive B-->psi production.

Using the combined CLEO II and CLEO II.V data sets of 9.1 fb(-1) at the Upsilon(4S), we measure properties of psi mesons produced directly from decays of the B meson, where "B" denotes an admixture of B+, B-, B0, and B;(0), and "psi" denotes either J/psi(1S) or psi(2S). We report first measurements of psi polarization in B-->psi(direct)X: alpha(psi(1S))=-0.30(+0.07)(-0.06)+/-0.04 and alpha(psi(2S))=-0.45(+0.22)(-0.19)+/-0.04. We also report improved measurements of the momentum distributions of psi produced directly from B decays, correcting for measurement smearing. Finally, we report measurements of the inclusive branching fraction for B-->psiX and B-->chi(c1)X.

Journal Article↗

PubMed2002

Dalitz analysis of D0-->K(0)(S)pi(+)pi(-).

In e(+)e(-) collisions using the CLEO detector, we have studied the decay of the D0 to the final state K(0)(S)pi(+)pi(-) with the initial flavor of the D0 tagged by the decay D(*+)-->D0pi(+). We use the Dalitz technique to measure the resonant substructure in this final state and clearly observe ten different contributions by fitting for their amplitudes and relative phases. We observe a K(*)(892)(+)pi(-) component which arises from doubly Cabibbo suppressed decays or D0-D0; mixing.

Journal Article↗

PubMed2002

Observation of B-->K(0)(S)pi(+)pi(-) and Evidence for B-->K(*+/-)pi(-/+).

We report on a search for charmless hadronic B decays to the three-body final states K(0)(S)h(+)pi(-), K(+)h(-)pi(0), K(0)(S)h(+)pi(0) (h(+/-) denotes a charged pion or kaon), and their charge conjugates, using 13.5 fb(-1) of integrated luminosity produced near sqrt[s]=10.6 GeV, and collected with the CLEO detector. We observe the decay B-->K0pi(+)pi(-) with a branching fraction (50(+10)(-9)(stat.)+/-7(syst.))x10(-6) and the decay B-->K(*+)(892)pi(-) with a branching fraction (16(+6)(-5)(stat.)+/-2(syst.))x10(-6).

Journal Article↗

PubMed2002

Measurement of B(D+-->K(*0)l(+)nu(l)).

Using 13.53 fb(-1) of CLEO data, we have measured the ratios of the branching fractions R(+)(e),R(+)(mu) and the combined branching fraction ratio R(+)(l), defined by R(+)(l)=[B(D+-->K(*0)l(+)nu(l))]/[B(D+-->K-pi(+)pi(+))]. We find R(+)(e)=0.74+/-0.04+/-0.05, R(+)(mu)=0.72+/-0.10+/-0.05, and R(+)(l)=0.74+/-0.04+/-0.05, where the first and second errors are statistical and systematic, respectively. The known branching fraction B(D+-->K-pi(+)pi(+)) leads to B(D+-->K(*0)e(+)nu(e))=(6.7+/-0.4+/-0.5+/-0.4)%, B(D+-->K(*0)mu(+)nu(mu))=(6.5+/-0.9+/-0.5+/-0.4)%, and B(D+-->K(*0)l(+)nu(l))=(6.7+/-0.4+/-0.5+/-0.4)%, where the third error is due to the uncertainty in B(D+-->K-pi(+)pi(+)).

Journal Article↗

PubMed2002

Observation of the decay Omega(0)(c)-->Omega(-)e(+)nu(e).

Using the CLEO detector at the Cornell Electron Storage Ring we have observed the Omega(0)(c) (css ground state) in the decay Omega(0)(c)-->Omega(-)e(+)nu(e). We find a signal of 11.4+/-3.8(stat) events. The probability that we have observed a background fluctuation is 7.6x10(-5). We measure B(Omega(0)(c)-->Omega(-)e(+)nu(e)).sigma(e(+)e(-)-->Omega(0)(c)X)=(42.2+/-14.1(stat)+/-5.7(syst)) fb and R=[Gamma(Omega(0)(c)-->Omega(-)pi(+))]/[Gamma(Omega(0)(c)-->Omega(-)enu(e))]=00.41+/-0.19(stat)+/-0.04(syst). This is the first statistically significant observation of an individual decay mode of the Omega(0)(c) in e(+)e(-) annihilation and the first example of a baryon decaying via beta emission, where no quarks from the first generation participate in the reaction.

Journal Article↗

PubMed2002

Rabi oscillations in a large Josephson-junction qubit.

We have designed and operated a circuit based on a large-area current-biased Josephson junction whose two lowest energy quantum levels are used to implement a solid-state qubit. The circuit allows measurement of the qubit states with a fidelity of 85% while providing sufficient decoupling from external sources of relaxation and decoherence to allow coherent manipulation of the qubit state, as demonstrated by the observation of Rabi oscillations. This qubit circuit is the basis of a scalable quantum computer.

Journal Article↗

PubMed2002

The pre-operative identification of low-risk endometrialcancer: an audit of women treated in the South Island of New Zealand 1998-2000.

OBJECTIVE: To determine whether pre-operative investigations identify a group of patients with low-risk endometrial cancer, who do not require tertiary referral for surgical staging or pelvic radiotherapy. DESIGN: Retrospective chart review. SETTING: South Island of New Zealand gynaecological oncology services. SAMPLE: One hundred and forty consecutive patients with newly diagnosed endometrial cancer from 1988 to 2000. METHODS: The results of preoperative investigations were compared with the final pathology. MAIN OUTCOME MEASURES: Correlation of preoperative investigations with low risk disease. For the purpose of the study, women with grade 1 or 2 endometrioid tumours confined to the uterine body and less than 50% myometrial invasion were considered to have low risk disease. RESULTS: In total, 50 women had low risk disease. Only 53% of patients with grade 1 tumours on initial biopsy had low risk disease. Women who had a grade 1 tumour at biopsy and, an ultrasound report with an endometrial thickness of less than 20 mm, and no evidence of myometrial invasion, cervical involvement or adnexal metastasis had a 76% chance of having low risk disease. CONCLUSION: We were unable to accurately define the low risk group from pre-operative assessment.

Curettage↗

PubMed2001

CEP1612, a dipeptidyl proteasome inhibitor, induces p21WAF1 and p27KIP1 expression and apoptosis and inhibits the growth of the human lung adenocarcinoma A-549 in nude mice.

The ubiquitin proteasome system is responsible for the proteolysis of important cell cycle and apoptosis-regulatory proteins. In this paper we report that the dipeptidyl proteasome inhibitor, phthalimide-(CH2)8CH-(cyclopentyl) CO-Arg(NO2)-Leu-H (CEP1612), induces apoptosis and inhibits tumor growth of the human lung cancer cell line A-549 in an in vivo model. In cultured A-549 cells, CEP1612 treatment results in accumulation of two proteasome natural substrates, the cyclin-dependent kinase inhibitors p21WAF1 and p27KIP1, indicating its ability to inhibit proteasome activity in intact cells. Furthermore, CEP1612 induces apoptosis as evident by caspase-3 activation and poly(ADP-ribose) polymerase cleavage. Treatment of A-549 tumor-bearing nude mice with CEP1612 (10 mg/kg/day, i.p. for 31 days) resulted in massive induction of apoptosis and significant (68%; P < 0.05) tumor growth inhibition, as shown by terminal deoxynucleotidyltransferase-mediated UTP end labeling. Furthermore, immunostaining of tumor specimens demonstrated in vivo accumulation of p21WAF1 and p27KIP1 after CEP1612 treatment. The results suggest that CEP1612 is a promising candidate for further development as an anticancer drug and demonstrate the feasibility of using proteasome inhibitors as novel antitumor agents.

Adenocarcinoma↗

PubMed2001

Ester bond-containing tea polyphenols potently inhibit proteasome activity in vitro and in vivo.

It has been discovered that proteasome inhibitors are able to induce tumor growth arrest or cell death and that tea consumption is correlated with cancer prevention. Here, we show that ester bond-containing tea polyphenols, such as (-)-epigallocatechin-3-gallate (EGCG), potently and specifically inhibit the chymotrypsin-like activity of the proteasome in vitro (IC(50) = 86-194 nm) and in vivo (1-10 microm) at the concentrations found in the serum of green tea drinkers. Atomic orbital energy analyses and high performance liquid chromatography suggest that the carbon of the polyphenol ester bond is essential for targeting, thereby inhibiting the proteasome in cancer cells. This inhibition of the proteasome by EGCG in several tumor and transformed cell lines results in the accumulation of two natural proteasome substrates, p27(Kip1) and IkappaB-alpha, an inhibitor of transcription factor NF-kappaB, followed by growth arrest in the G(1) phase of the cell cycle. Furthermore, compared with their simian virus-transformed counterpart, the parental normal human fibroblasts were much more resistant to EGCG-induced p27(Kip1) protein accumulation and G(1) arrest. Our study suggests that the proteasome is a cancer-related molecular target of tea polyphenols and that inhibition of the proteasome activity by ester bond-containing polyphenols may contribute to the cancer-preventative effect of tea.

Calpain↗

PubMed2001

Syngeneic consecutive rat spleen transplantation bearing infantile testis.

Seventy-seven Lewis adult rats received autologous testicular implants in the spleen. These spleens were retransplanted in a consecutive transplant fashion as we described earlier. Some were observed as long as 26 to 27 months. Although earlier splenic-testicular transplants showed benign granulosa cell tumors, some of the long-term follow-ups showed a seminoma-like transformation.

Animals↗

PubMed2001

Substituent effects on azo dye oxidation by the FeIII-EDTA-H2O2 system.

The effect of substituents on the oxidation of azo dyes in the FeIII-EDTA-H2O2 system was examined at pH 7. 4-(4'-sulfophenylazo)phenol and 2-(4'-sulfophenylazo)phenol, with methyl, methoxy, and halo substituents on the phenolic ring, were used as model systems. Oxidation of the naphthol dyes Orange I and Orange II were also examined. All of the dyes tested were decolorized in the FeIII-EDTA-H2O2 system, but the degree of decolorization varied over a factor of 10. Dyes substituted with one or two halogens were oxidized to a greater extent than the corresponding methyl- or methoxy-substituted dyes. One explanation for the effect of halogen substituents is that they make the phenolic moieties more acidic, which favors the phenolate anion, which is more readily attacked by *OH. This explanation is supported by the observed correlation between charge density of the phenolate anion and the degree of decolorization. Based on an analysis of products formed from Orange II, a probable mechanism for decolorization of phenolic azo dyes by *OH is proposed. In addition, the optimal levels of H2O2 needed for the process have been examined. It appears that high levels of H2O2 could reduce decolorization by scavenging the *OH.

Azo Compounds↗

PubMed2001

Tannic acid potently inhibits tumor cell proteasome activity, increases p27 and Bax expression, and induces G1 arrest and apoptosis.

Animal studies have demonstrated that a dietary polyphenol known as tannic acid (TA) exhibits anticarcinogenic activity in chemically induced cancers, although the involved molecular target remains unknown. In addition, proteasome inhibitors have been shown to suppress human tumor growth in nude mice. Most recently, we have reported that ester-bond-containing tea polyphenols are potent proteasome inhibitors in vitro and in vivo. We have hypothesized that TA, which contains multiple similar gallate moieties linked by ester bonds, should inhibit the proteasome activity. Here, we report that indeed TA potently and specifically inhibits the chymotrypsin-like activity of purified 20S proteasome (IC(50) = 0.06 microg/ml), 26S proteasome of Jurkat T-cell extracts, and 26S proteasome of living Jurkat cells. Inhibition of the proteasome by TA in Jurkat cells results in accumulation of two natural proteasome substrates, the cyclin-dependent kinase inhibitor p27(Kip1) and the proapoptotic protein Bax, followed by growth arrest in G1 and induction of apoptotic cell death. Our present study suggests that TA targets and inhibits the proteasome in tumor cells, which may contribute to the previously observed anticarcinogenic activity of TA.

Apoptosis↗