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C Buchanan

Publications and source records attributed to C Buchanan.

At least 91 records · Page 5Linked to original sources

Measurement of the CP asymmetry amplitude sin2beta with B0 mesons.

We present results on time-dependent CP asymmetries in neutral B decays to several CP eigenstates. The measurements use a data sample of about 88 x 10(6) Upsilon(4S)-->B(-)B decays collected between 1999 and 2002 with the BABAR detector at the PEP-II asymmetric-energy B factory at SLAC. We study events in which one neutral B meson is fully reconstructed in a final state containing a charmonium meson and the other B meson is determined to be either a B(0) or B(-0) from its decay products. The amplitude of the CP asymmetry, which in the standard model is proportional to sin2beta, is derived from the decay-time distributions in such events. We measure sin2beta=0.741+/-0.067(stat)+/-0.034(syst) and |lambda|=0.948+/-0.051(stat)+/-0.030(syst). The magnitude of lambda is consistent with unity, in agreement with the standard model expectation of no direct CP violation in these modes.

Journal Article↗

Measurement of the branching fraction and CP content for the decay B0-->D(*+)D(*-).

We report a measurement of the branching fraction of the decay B0-->D(*+)D(*-) and of the CP-odd component of its final state using the BABAR detector. With data corresponding to an integrated luminosity of 20.4 fb (-1) collected at the Upsilon(4S) resonance during 1999-2000, we have reconstructed 38 candidate signal events in the mode B0-->D(*+)D(*-) with an estimated background of 6.2+/-0.5 events. From these events, we determine the branching fraction to be B(B0-->D(*+)D(*-))=[8.3+/-1.6(stat)+/-1.2(syst)]x10(-4). The measured CP-odd fraction of the final state is 0.22+/-0.18(stat)+/-0.03(syst).

Journal Article↗

Measurement of the B(0) lifetime with partially reconstructed B(0)-->D(-)l(+)nu(l) decays.

The B(0) lifetime was measured with a sample of 23 million BB pairs collected by the BABAR detector at the PEP-II e(+)e(-) storage ring during 1999 and 2000. Events from the semileptonic decay B(0)-->D(*-)l(+)nu(l) have been selected with a partial reconstruction method in which only the charged lepton and the slow pi from the D*--->D(0)pi(-) decay are reconstructed. The result is tau(B(0)) = 1.529+/-0.012(stat)+/-0.029(syst) ps.

Journal Article↗

Search for the rare decays B-->Kl(+)l(-) and B-->K(*)l(+)l(-).

We present results from a search for the flavor-changing neutral current decays B-->Kl(+)l(-) and B-->K(*)l(+)l(-), where l(+)l(-) is either an e(+)e(-) or mu(+)mu(-) pair. The data sample comprises 22.7 x 10(6) Upsilon(4S)-->B(-)B decays collected with the BABAR detector at the PEP-II B Factory. We obtain the 90% C.L. upper limits B(B-->Kl(+)l(-))<0.51 x 10(-6) and B(B-->K(*)l(+)l(-))<3.1 x 10(-6), close to standard model predictions for these branching fractions. We have also obtained limits on the lepton-family-violating decays B-->Ke+/-mu(-/+) and B-->K(*)e(+/-)mu(-/+).

Journal Article↗

Measurement of B0-B-0 flavor oscillations in hadronic B0 decays.

Flavor oscillations of neutral B mesons have been studied in e+e- annihilation data collected with the BABAR detector at center-of-mass energies near the upsilon(4S) resonance. The data sample used for this purpose consists of events in which one B0 meson is reconstructed in a hadronic decay mode, while the flavor of the recoiling B0 is determined with a tagging algorithm that exploits the correlation between the flavor of the heavy quark and the charges of its decay products. From the time development of the observed mixed and unmixed final states, we determine the B0-B-0 oscillation frequency deltamd to be 0.516+/-0.016(stat)+/-0.010(syst) ps-1.

Journal Article↗

Measurement of the B0-B-0 oscillation frequency with inclusive dilepton events.

The B0-B-0 oscillation frequency has been measured with a sample of 23 x 10(6) BB- pairs collected with the BABAR detector at the PEP-II asymmetric B Factory at SLAC. In this sample, we select events in which both B mesons decay semileptonically and use the charge of the leptons to identify the flavor of each B meson. A simultaneous fit to the decay time difference distributions for opposite- and same-sign dilepton events gives deltamd = 0.493+/-0.012(stat)+/-0.009(syst) ps-1.

Journal Article↗

Search for T and CP violation in B0-B-0 mixing with inclusive dilepton events.

We report the results of a search for T and CP violation in B0-B-0 mixing using an inclusive dilepton sample collected by the BABAR experiment at the PEP-II B Factory. The asymmetry between l+l+ and l-l- events allows us to compare the probabilities for B-0-->B0 and B0-->B-0 oscillations and thus probe T and CP invariance. Using a sample of 23 x 10(6) BB- pairs, we measure a same-sign dilepton asymmetry of A(T/CP) = [0.5+/-1.2(stat)+/-1.4(syst)]%. For the modulus of the ratio of complex mixing parameters p and q, we obtain q/p = 0.998+/-0.006(stat)+/-0.007(syst).

Journal Article↗

An open-label acceptability study of Norditropin SimpleXx--a new liquid growth hormone formulation.

A new liquid formulation of hGH (Norditropin SimpleXx) has been developed to avoid the need for reconstitution before administration. In addition, the liquid GH formulation has been combined with an advanced pen delivery system, either with or without a needle auto-insertion mechanism. This study was designed to assess the acceptability of the new system compared with the patient's previous system. A total of 103 children with GH deficiency received a daily injection of Norditropin liquid GH for 12 weeks with a choice of a pen/auto-insertion system. Acceptability was determined by nurse-supervised questionnaires administered to the patients and parents. Following treatment, 94% of patients preferred the Norditropin liquid GH system. This preference was irrespective of the previous system in use, patient age or length of GH therapy. More patients found it the less painful system (50% vs 13%), 92% of patients found it more convenient, and the formulation was well tolerated. In conclusion, Norditropin liquid GH was very well accepted and preferred by the majority of patients. It avoided reconstitution which had been a major cause of dissatisfaction with the patients' previous systems, and resulted in greater convenience and reduced levels of pain associated with injection.

Adolescent↗

A chimeric MIP-1alpha/RANTES protein demonstrates the use of different regions of the RANTES protein to bind and activate its receptors.

Human RANTES (CCL5) and MIP-1alpha (CCL3) bind and activate several CC chemokine receptors. RANTES is a high-affinity ligand for CCR1 and CCR5, and it binds CCR3 with moderate affinity and CCR4 with low affinity. MIP-1alpha has similar binding characteristics to RANTES except that it does not bind to CCR3. Here we have generated a chimera of human MIP-1alpha and RANTES, called MIP/RANTES, consisting of the eight amino terminal residues of MIP-1alpha preceding the CC motif, and the remainder of the sequence is RANTES. The chimera is able to induce chemotaxis of human monocytes. MIP/RANTES has >100-fold reduction in binding to CCR1 and does not bind to CCR3 but retains full, functional binding to CCR5. It has equivalent affinity for CCR5 to MIP-1alpha and RANTES, binding with an IC(50) of 1.12 nM, and is able to mobilize calcium and induce endocytosis of CCR5 in PBMC in a manner equi-potent to RANTES. It also retains the ability to inhibit R5 using HIV-1 strains. Therefore, we conclude that the amino terminus of RANTES is not involved in CCR5 binding, but it is essential for CCR1 and CCR3.

Amino Acid Sequence↗

New limit on CPT violation

A search for antiproton decay has been made at the Fermilab Antiproton Accumulator. Limits are placed on fifteen antiproton decay modes. The results are used to place limits on the characteristic mass scale m(X) that could be associated with CPT violation accompanied by baryon number violation.

Journal Article↗

Cranial computed tomography in the emergency evaluation of adult patients without a recent history of head trauma: a prospective analysis.

OBJECTIVES: To examine the pattern of nontrauma cranial CT use in an urban ED, to identify the rate of significant CT abnormalities in this setting, and to develop criteria for restricting the ordering of CT scans. METHODS: A prospective, observational study of a case series of adults who underwent cranial CT scanning for nontraumatic cases was performed at the EDs of an urban teaching hospital and an affiliated community hospital with a combined annual census of 110,000. Clinically significant CT scans were defined as: 1) acute stroke, 2) CNS malignancy, 3) acute hydrocephalus, 4) intracranial bleeding, or 5) intracranial infection. X2 recursive partitioning was used to derive a decision rule to restrict ordering of CT scans. RESULTS: Only 61 (8%) of 806 CT scans revealed clinically significant abnormalities. The presence of any of the following: age > or = 60 years, focal neurologic deficit, headache with vomiting, or altered mental status, was 100% sensitive (95% CI: 94-100%) and 31% specific (95% CI: 28-33%) in detecting clinically significant CT scans. This set of features had positive and negative predictive values of 11% (95% CI: 8-13%) and 100% (95% CI: 98-100%), respectively. If these criteria had been used to restrict cranial CT use, 229 fewer patients (28%) would have had CT scans obtained and no clinically significant abnormalities would have been missed. CONCLUSION: Clinically significant CT abnormalities were uncommon in this study population, suggesting that current criteria for ordering nontrauma cranial CT scans may be too liberal. In this study, a set of clinical criteria was derived that may be useful at separating patients into high- and low-risk categories for clinically significant cranial CT abnormalities. Before these results are applied clinically, these criteria should be validated in larger, prospective studies.

Adult↗

Effects of long-term growth hormone releasing hormone 1-29 in significantly short children.

Seven children with significant idiopathic short stature (SISS) whose heights were significantly below the third percentile (SD score for height -2.5 to -3.5) and who had normal levels of growth hormone (GH) were treated with growth hormone releasing hormone (GH-RH) in a dose of 30 micrograms/kg/day. Therapy was discontinued if patients failed to increase their rates of growth by more than 2.0 cm/year over their pre-therapy growth rate. Treatment was discontinued in two of the patients after 12 months but was continued in the other five for 24 months. These data demonstrate that some patients with SISS grow well during the first 2 years of treatment with GH-RH.

Child↗

Critically ill patients have high basal growth hormone levels with attenuated oscillatory activity associated with low levels of insulin-like growth factor-I.

OBJECTIVE: The aim was to study the relationship between growth hormone (GH) and insulin-like growth factor-I (IGF-I) in critically ill patients. DESIGN: Case-control study of critically ill patients admitted to the intensive care unit was carried out. PATIENTS: Six critically ill patients (51-78 years) who required ventilation and parenteral nutrition and six age, weight, height, and sex-matched healthy adults were studied. MEASUREMENTS: The patients and controls were studied for two 24-hour periods; the patients before and after starting parenteral feeding, and the controls during a 36-hour fast and when taking meals equivalent in calories and protein to the patients' parenteral feed. Serum GH was measured at 20-minute intervals and analysed by a pulse detection algorithm (Pulsar) and Fourier transformation. IGF-I was measured at 0, 12, and 24 hours. RESULTS: Patients had low serum IGF-I levels compared with controls, whether fasted or fed, despite having mean GH levels similar to fasted controls. For fasted patients vs fasted controls the mean (+/- 1 SD) GH levels were 4.5 +/- 2.0 vs 4.0 +/- 2.4 mU/l respectively, and IGF-I levels at the end of the fast were 0.17 +/- 0.11 vs 0.78 +/- 0.29 U/ml (P = 0.003). Patients showed elevated baseline GH levels compared with controls when fasted and during parenteral feeding (patients vs controls fasted 3.1 +/- 1.9 vs 0.8 +/- 0.5 mU/l, P = 0.01; patients vs controls fed 4.2 +/- 4.5 vs 0.5 +/- 0.04 mU/l, P = 0.028). Fourier transformation confirmed oscillatory GH levels in the controls, fasted or fed, but this activity was attenuated in the patients. Parenteral feeding had no effect on the GH profiles or IGF-I levels of patients, but controls showed greater mean GH levels during their fast than when fed. CONCLUSIONS: We have demonstrated that critically ill patients have low IGF-I levels associated with augmented baseline GH levels which show reduced oscillatory activity. The results would be compatible with the hypothesis that there is an adaptive change in critically ill patients away from the indirect effects of GH (stimulation of IGF-I production and anabolism) and toward the direct effects (lipolysis and insulin antagonism) which increase the availability of energy substrates. The pattern of GH levels seen in our patients may be important in this adaptation.

Abdomen↗

Adipose tissue glucose transporters in NIDDM. Decreased levels of muscle/fat isoform.

We investigated the mechanism of peripheral insulin resistance in the adipose tissue of obese and non-insulin-dependent diabetes mellitus (NIDDM) patients at the level of the glucose-transport effector system. Freshly isolated adipocytes from obese nondiabetic and obese NIDDM subjects had decreased insulin sensitivity and responsiveness for glucose-transport stimulation compared with control subjects, with more pronounced changes associated with obese NIDDM patients. The relative abundance of muscle/fat glucose-transporter isoform in the three groups of subjects was determined by Western-blot analysis of detergent-soluble adipose tissue extracts with monoclonal antibody 1F8. Obesity per se had no effect on adipose tissue muscle/fat glucose-transporter isoform (3150 +/- 660 vs. 4495 +/- 410 counts/min [cpm]/mg protein). Furthermore, decreased levels of muscle/fat isoform in adipose tissue of NIDDM patients were also reflected in isolated adipocytes. Our results demonstrate that insulin resistance in isolated adipocytes of NIDDM patients could at least partly be due to a significant depletion of adipose tissue muscle/fat glucose-transporter isoform.

Adipose Tissue↗

Organizing for drug-usage evaluation.

Because QA is the chief interest of the Joint Commission, hospital pharmacists must strive to have a well-organized DUE plan and process. However, merely satisfying a Joint Commission surveyor is not a good enough reason to invest in the DUE process. DUE is deceptively complex and labor intensive for hospital and medical staff alike. A better reason to plunge into DUE is to enable pharmacists to concurrently monitor pharmacotherapy, to intervene on behalf of patients, and to positively affect patients' therapeutic outcomes. Thereby, DUE really fits pharmacy's responsibility for pharmaceutical care.

Drug Utilization↗

IGF-II receptors and IGF-II-stimulated glucose transport in human fat cells.

Insulin-like growth factor II (IGF-II) receptors have been described in rat but not in human adipocytes. In both species, IGF-II has been reported to stimulate glucose transport by interacting with the insulin receptor. In this study, we have unequivocally demonstrated the presence of IGF-II receptors in human adipocytes. 125I-labeled IGF-II specifically binds to intact adipocytes, membranes, and lectin-purified detergent solubilized extracts. Through the use of 0.5 mM disuccinimidyl suberate, 125I-IGF-II is cross-linked to a 260-kDa protein that is identified as the IGF-II receptor by displacement experiments with unlabeled IGF-II, IGF-I, and insulin and either by immunoprecipitation or by Western blot analysis with mannose 6-phosphate receptor antibodies. The concentrations of IGF-II required for half-maximal and maximal stimulation of glucose transport in human adipocytes are 35 and 100 times more than that of insulin. The possibility of IGF-II stimulating glucose transport by interacting predominantly with the insulin receptor is suggested by the following: 1) the concentration of IGF-II that inhibits half of insulin binding is only 20 times more than that of insulin; 2) the lack of an additive effect of IGF-II and insulin for maximal stimulation of glucose transport; 3) the ability of monoclonal insulin receptor antibodies to decrease glucose transport stimulated by submaximal concentrations of both IGF-II and insulin; and 4) the ability of IGF-II to stimulate insulin receptor autophosphorylation albeit at a reduced potency when compared with insulin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗