Native coronary disease progression exceeds failed revascularization as cause of angina after five years in the Bypass Angioplasty Revascularization Investigation (BARI).

Objectives: Coronary angiograms obtained five years following revascularization were examined to assess the extent of compromise in myocardial perfusion due to failure of revascularization versus progression of native disease.

Background: The Bypass Angioplasty Revascularization Investigation (BARI) randomized revascularization candidates between bypass surgery and angioplasty. Entry and five-year angiograms from 407 of 519 (78%) patients at four centers were analyzed.

Mixed-ligand organometallic polymers containing the "Pd(2)(dmb)2(2+)" fragment: properties of the [Pd2(dmb)2(diphos)2+](n) polymers/oligomers in solution and in the solid state.

The 1:1 reaction between the d(9)-d(9) Pd(2)(dmb)(2)Cl(2) complex (dmb = 1,8-diisocyano-p-menthane) and the diphosphine ligands (diphos) bis(diphenylphosphino)butane (5, dppb), bis(diphenylphosphino)pentane (6, dpppen), bis(diphenylphosphino)hexane (7, dpph), and bis(diphenylphosphino)acetylene (8, dpa) in the presence of LiClO(4) leads to the [[Pd(2)(dmb)(2)(diphos)](ClO(4))(2)](n) polymers. These new materials are characterized by NMR ((1)H, (13)C, (31)P), IR, Raman, and UV-vis spectroscopies (466 < lambda(max)(dsigma-dsigma*) < 480 nm), by ATG, XRD, and DSC methods, and by the capacity to make stand-alone films. From the measurements of the intrinsic viscosity in acetonitrile, the M(n) ranges from 16000 to 18400 (12 to 16 units).

Lipid rafts mediate the synaptic localization of alpha-synuclein.

Alpha-synuclein contributes to the pathogenesis of Parkinson's disease (PD), but its precise role in the disorder and its normal function remain poorly understood. Consistent with a presumed role in neurotransmitter release and its prominent deposition in the dystrophic neurites of PD, alpha-synuclein localizes almost exclusively to the nerve terminal. In brain extracts, however, alpha-synuclein behaves as a soluble, monomeric protein.

[The blood-brain barrier should not be underestimated in neuro-oncology].

Introduction: Limited therapeutic success in the treatment of CNS neoplasia with chemotherapy is generally attributed to two factors: natural or acquired resistance to chemotherapy expressed by tumor cells, and delivery impediment related to the blood-brain barrier.

State Of Art: The anatomic and physiological properties of the normal blood-brain barrier prevent passage of ionized water-soluble compounds with a molecular weight greater than 500 Daltons. Although complex, the blood-brain barrier basically functions at the level of the tight junctions of the cerebral vascular endothelial cells.

Glycine, GABA and their transporters in pancreatic islets of Langerhans: evidence for a paracrine transmitter interplay.

To elucidate the possible roles of the CNS neurotransmitters glycine and GABA in neuroendocrine paracrine signalling, we investigated their localizations, and those of their transport proteins, by confocal immunofluorescence and quantitative post-embedding immuno-electron microscopy in the pancreatic islets of Langerhans. We show that A-cells contain glycine in synaptic-like microvesicles as well as in secretory granules. A-cells express the macromolecules necessary to: (1) concentrate glycine within both organelle types before release (the vesicular GABA/glycine transporter VGAT=VIAAT); and to (2) take up the transmitter from the extracellular space (the plasma membrane glycine transporter GLYT2).

Search for the rare leptonic decay B+-->mu(+)nu(mu).

We have performed a search for the rare leptonic decay B+-->mu(+)nu(mu) with data collected at the Upsilon(4S) resonance by the BABAR experiment at the PEP-II storage ring. In a sample of 88.4 x 10(6) BB pairs, we find no significant evidence for a signal and set an upper limit on the branching fraction B(B+-->my(+)nu(my))< 6.

Study of B+/ --> J/psi pi+/- and B+/ -->J/psi K+/- decays: measurement of the ratio of branching fractions and search for direct CP violation.

We study B+/ --> J/psi pi(+/-) and B+/ --> J/psi K+/- decays in a sample of about 89 x 10(6) BB pairs collected with the BABAR detector at the PEP-II asymmetric B factory at SLAC. We observe a signal of 244+/-20 B+/ --> J/psi pi(+/-) events and determine the ratio B(B+/ --> J/psi pi(+/-))/B(B+/ --> J/psi K+/-) to be [5.37+/-0.

Measurement of time-dependent CP asymmetries and constraints on sin(2beta+gamma) with partial reconstruction of B0-->D*-/+pi+/- decays.

We present a measurement of time-dependent CP-violating asymmetries in decays of neutral B mesons to the final states D(*-/+)pi(+/-), using approximately 82x10(6) BBmacr; events recorded by the BABAR experiment at the PEP-II e(+)e(-) storage ring. Events containing these decays are selected with a partial reconstruction technique, in which only the high-momentum pi(+/-) from the B decay and the low-momentum pi(-/+) from the D(*-/+) decay are used. We measure the amplitude of the asymmetry to be -0.

Measurement of time-dependent CP asymmetries in B0-->D(*)+/-pi-/+ decays and constraints on sin(2beta+gamma).

We present a measurement of CP-violating asymmetries in fully reconstructed B0-->D(*)+/-pi-/+ decays in approximately 88 x 10(6) upsilon(4S)-->BBmacr; decays collected with the BABAR detector at the PEP-II asymmetric-energy B factory at SLAC. From a time-dependent maximum-likelihood fit we obtain the following for the CP-violating parameters: a=-0.022+/-0.

A blood-brain barrier disruption model eliminating the hemodynamic effect of ketamine.

Objective: We propose a simple modification to an established blood-brain barrier disruption (BBBD) animal model that allows us to use ketamine/xylazine as the anaesthetic agent, therefore decreasing the complexity and the cost of the model, while maintaining similar efficiency.

Methods: Sixty-two Long Evans rats were anaesthetized by intraperitoneal injection of ketamine/xylazine. Osmotic BBBD was performed by administering 25% mannitol into the internal carotid artery in a retrograde fashion from the external carotid.

Brief trains of action potentials enhance pyramidal neuron excitability via endocannabinoid-mediated suppression of inhibition.

Depolarization-induced suppression of inhibition (DSI) is a form of retrograde signaling at GABAergic synapses that is initiated by the calcium- and depolarization-dependent release of endocannabinoids from postsynaptic neurons. In the neocortex, pyramidal neurons (PNs) appear to use DSI as a mechanism for regulating somatic inhibition from a subpopulation of GABAergic inputs that express the type 1 cannabinoid receptor. Although postsynaptic control of afferent inhibition may directly influence the integrative properties of neocortical PNs, little is known about the patterns of activity that evoke endocannabinoid release and the impact such disinhibition may have on the excitability of PNs.

Limits on the decay-rate difference of neutral B mesons and on CP, T, and CPT violation in B(0-0)B oscillations.

Using events in which one of two neutral B mesons from the decay of an Upsilon(4S) meson is fully reconstructed, we determine parameters governing decay (DeltaGamma(d)/Gamma(d)), CP, and T violation (|q/p|), and CP and CPT violation (Re z,Im z). The results, obtained from an analysis of 88 x 10(6) Upsilon(4S) decays recorded by BABAR, are sgn(Re lambda(CP))DeltaGamma(d)/Gamma(d)=-0.008+/-0.

Measurement of the branching fractions and CP asymmetry of B--->D(0)((CP))K- decays with the BABAR detector.

We present a study of B--->D(0)(CP)K- decays, where D(0)(CP) is reconstructed in CP-even channels, based on a sample of 88.8 x 10(6) Upsilon(4S)-->BB decays collected with the BABAR detector at the PEP-II e(+)e(-) storage ring. We measure the ratio of Cabibbo-suppressed to Cabibbo-favored branching fractions B(B--->D(0)(CP)K-)/B(B--->D(0)(CP)pi(-))=[8.

Measurements of branching fractions and CP-violating asymmetries in B meson decays to charmless two-body states containing a K(0).

We present measurements of branching fractions and CP-violating asymmetries in decays of B mesons to two-body final states containing a K0. The results are based on a data sample of approximately 88 x 10(6) Upsilon(4S)-->BB decays collected with the BABAR detector at the PEP-II asymmetric-energy B Factory at SLAC. We measure B(B+-->K(0)pi(+))=(22.

Elevated levels of circulating trace amines in primary headaches.

Background: Trace amines, including tyramine, octopamine, and synephrine, are closely related to classic biogenic amines. They have been hypothesized to promote migraines and other types of primary headaches, but there is no direct evidence supporting this hypothesis.

Methods: Using a multichannel electrochemical high-performance liquid chromatography system, the authors evaluated whether changes in circulating trace amines occur in subjects with migraine (with or without aura) during headache-free periods as well as in patients with cluster headache (CH) during the remission and active phases as compared with healthy control subjects.

Technical modification in the intracarotid chemotherapy and osmotic blood-brain barrier disruption procedure to prevent the relapse of carboplatin-induced orbital pseudotumor.

The blood-brain barrier disruption (BBBD) procedure is an established strategy to enhance drug delivery to brain tumors. Complication rates associated with this procedure are usually low, but when complications do occur, they usually mandate discontinuation of treatment. Orbital pseudotumor is an inflammatory condition of one or more extraocular muscles that produces limitation of ocular motility.

Search for lepton-flavor violation in the decay tau- --> l- l+ l-.

A search for the lepton-flavor-violating decay of the tau into three charged leptons has been performed using 91.5 fb(-1) of data collected at an e(+)e(-)center-of-mass energy around 10.58 GeV with the BABAR detector at the SLAC storage ring PEP-II.

Measurements of the mass and width of the eta(c) meson and of an eta(c)(2S) candidate.

The mass m(eta(c)) and total width Gamma(eta(c))(tot) of the eta(c) meson have been measured in two-photon interactions at the SLAC e(+)e(-) asymmetric B Factory with the BABAR detector. With a sample of approximately 2500 reconstructed eta(c)-->K(0)(S)K+/-pi(-/+) decays in 88 fb(-1) of data, the results are m(eta(c))=2982.5+/-1.

Measurement of the branching fraction and polarization for the decay B--->D*0K*-.

We present a study of the decay B--->D(*0)K(*-) based on a sample of 86 x 10(6) Upsilon(4S)-->BBmacr; decays collected with the BABAR detector at the PEP-II asymmetric-energy B Factory at SLAC. We measure the branching fraction B(B--->D(*0)K(*-))=(8.3+/-1.

Search for the radiative decays B-->rhogamma and B0-->omegagamma.

A search of the exclusive radiative decays B-->rho(770)gamma and B0-->omega(782)gamma is performed on a sample of about 84x10(6) BBmacr; events collected by the BABAR detector at the SLAC PEP-II asymmetric-energy e+e- storage ring. No significant signal is seen in any of the channels. We set upper limits on the branching fractions B of B(B0-->rho(0)gamma)<1.

Measurement of the inclusive charmless semileptonic branching ratio of B mesons and determination of |V ub|.

We report a measurement of the inclusive charmless semileptonic branching fraction of B mesons in a sample of 89 x 10(6) (-)BB events recorded with the BABAR detector at the Upsilon(4S) resonance. Events are selected by fully reconstructing the decay of one B meson and identifying a charged lepton from the decay of the other B meson. The number of signal events is extracted from the mass distribution of the hadronic system accompanying the lepton and is used to determine the ratio of branching fractions B((-)B-->X(u)lnu;)/B((-)B-->Xlnu;)=[2.

Observation of B0-->omega K0, B+-->eta pi+, and B+-->eta K+ and study of related decays.

We present measurements of branching fractions and charge asymmetries for seven B-meson decays with an eta, eta', or omega meson in the final state. The data sample corresponds to 89x10(6) BB pairs produced from e(+)e(-) annihilation at the Upsilon(4S) resonance. We measure the following branching fractions in units of 10(-6): B(B+-->eta pi(+))=5.

Endocannabinoid signalling selectively targets perisomatic inhibitory inputs to pyramidal neurones in juvenile mouse neocortex.

Retrograde synaptic signalling has long been recognized as a fundamental feature of neural systems. However, the cellular specificity and functional consequences of fast retrograde communication are not well understood. We have focused our efforts on understanding the role that endocannabinoids play in regulating synaptic inhibition in sensory neocortex.