ACUTE EFFECTS OF VOLUME-ORIENTED INCENTIVE SPIROMETRY ON CHEST WALL VOLUMES IN PATIENTS AFTER STROKE.

The aim of the present study was to assess how volume-oriented incentive spirometry (IS) applied to patients after stroke modify total and compartmental chest wall volume variations, including right and left hemithorax compared to controls.20 post-stroke patients (stroke group, SG) and 20 age-matched healthy subjects (control group, CG) were studied by optoelectronic plethysmography during spontaneous quiet breathing (QB), IS and in the recovery period after IS.IS determined an increase of chest wall volume and its rib cage and abdominal compartments in both groups (p = 0.0008) and between the three instances (p < 0.0001). Compared to healthy control subjects, tidal volume of patients with stroke was 24.7\%, 18\% and 14.7\% lower during QB, , IS and post-IS, respectively. In all the three conditions the contribution of the abdominal compartment to tidal volume was greater in the stroke patients (54.1, 43.2 and 48.9\%) than controls (43.7, 40.8 and 46.1\%, p = .039). In the vast majority of patients 13/20 and 18/20 during QB and IS, respectively), abdominal expansion led rib cage expansion during inspiration. A greater asymmetry between the right and left hemithoracic expansion occurred in stroke patients compared to controls but it decreased during IS (62.5\% (p = 0.0023) QB; 19.7\% IS; and 67.6\% (p = 0.135) post-IS.IS promotes an increased expansion in all compartments of the chest wall and reduces the asymmetric expansion between right and left pulmonary rib cage and therefore it should be considered as a tool for rehabilitation

Modeling of [F-18]FEOBV Pharmacokinetics in Rat Brain

Purpose: [18F]Fluoroethoxybenzovesamicol ([18F]FEOBV) is a radioligand for the vesicular acetylcholine transporter (VAChT), a marker of the cholinergic system. We evaluated the quantification of [18F]FEOBV in rats in control conditions and after partial saturation of VAChT using plasma and reference tissue input models and test-retest reliability. Procedure: Ninety-minute dynamic [18F]FEOBV PET scans with arterial blood sampling were performed in control rats and rats pretreated with 10 μg/kg FEOBV. Kinetic analyses were performed using one- (1TCM) and two-tissue compartmental models (2TCM), Logan and Patlak graphical analyses with metabolite-corrected plasma input, reference tissue Patlak with cerebellum as reference tissue, standard uptake value (SUV) and SUV ratio (SUVR) using 60- or 90-min acquisition. To assess test-retest reliability, two dynamic [18F]FEOBV scans were performed 1 week apart. Results: The 1TCM did not fit the data. Time-activity curves were more reliably estimated by the irreversible than the reversible 2TCM for 60 and 90 min as the influx rate Ki showed a lower coefficient of variation (COV, 14–24 %) than the volume of distribution VT (16–108 %). Patlak graphical analysis showed a good fit to the data for both acquisition times with a COV (12–27 %) comparable to the irreversible 2TCM. For 60 min, Logan analysis performed comparably to both irreversible models (COV 14–32 %) but showed lower sensitivity to VAChT saturation. Partial saturation of VAChT did not affect model selection when using plasma input. However, poor correlations were found between irreversible 2TCM and SUV and SUVR in partially saturated VAChT states. Test-retest reliability and intraclass correlation for SUV were good. Conclusion: [18F]FEOBV is best modeled using the irreversible 2TCM or Patlak graphical analysis. SUV should only be used if blood sampling is not possible

Effect of dopamine D2 receptor antagonists on [18F]-FEOBV binding

The interaction of dopaminergic and cholinergic neurotransmission in, e.g., Parkinson's disease has been well established. Here, D2 receptor antagonists were used to assess changes in [18F]-FEOBV binding to the vesicular acetylcholine transporter (VAChT) in rodents using positron emission tomography (PET). After pretreatment with either 10 mg/kg haloperidol, 1 mg/kg raclopride, or vehicle, 90 min dynamic PET scans were performed with arterial blood sampling. The net influx rate (Ki) was obtained from Patlak graphical analysis, using a metabolite-corrected plasma input function and dynamic PET data. [18F]-FEOBV concentration in whole-blood or plasma and the metabolite-corrected plasma input function were not significantly changed by the pretreatments (adjusted p > 0.07, Cohen's d 0.28-1.89) while the area-under-the-curve (AUC) of the parent fraction of [18F]-FEOBV was significantly higher after haloperidol treatment (adjusted p = 0.022, Cohen's d = 2.51) than in controls. Compared to controls, the AUC of [18F]-FEOBV, normalized for injected dose and body weight, was nonsignificantly increased in the striatum after haloperidol (adjusted p = 0.4, Cohen's d = 1.77) and raclopride (adjusted p = 0.052, Cohen's d = 1.49) treatment, respectively. No changes in the AUC of [18F]-FEOBV were found in the cerebellum (Cohen's d 0.63-0.74). Raclopride treatment nonsignificantly increased Ki in the striatum 1.3-fold compared to control rats (adjusted p = 0.1, Cohen's d = 1.1) while it reduced Ki in the cerebellum by 28% (adjusted p = 0.0004, Cohen's d = 2.2) compared to control rats. Pretreatment with haloperidol led to a nonsignificant reduction in Ki in the striatum (10%, adjusted p = 1, Cohen's d = 0.44) and a 40-50% lower Ki than controls in all other brain regions (adjusted p < 0.0005, Cohen's d = 3.3-4.7). The changes in Ki induced by the selective D2 receptor antagonist raclopride can in part be quantified using [18F]-FEOBV PET imaging. Haloperidol, a nonselective D2/σ receptor antagonist, either paradoxically decreased cholinergic activity or blocked off-target [18F]-FEOBV binding to σ receptors. Hence, further studies evaluating the binding of [18F]-FEOBV to σ receptors using selective σ receptor ligands are necessary

Magnon delocalization in ferromagnetic chains with long-range correlated disorder

We study one-magnon excitations in a random ferromagnetic Heisenberg chain with long-range correlations in the coupling constant distribution. By employing an exact diagonalization procedure, we compute the localization length of all one-magnon states within the band of allowed energies $E$. The random distribution of coupling constants was assumed to have a power spectrum decaying as $S(k)\propto 1/k^{\alpha}$. We found that for $\alpha < 1$, one-magnon excitations remain exponentially localized with the localization length $\xi$ diverging as 1/E. For $\alpha = 1$ a faster divergence of $\xi$ is obtained. For any $\alpha > 1$, a phase of delocalized magnons emerges at the bottom of the band. We characterize the scaling behavior of the localization length on all regimes and relate it with the scaling properties of the long-range correlated exchange coupling distribution.Comment: 7 Pages, 5 figures, to appear in Phys. Rev.

Search for Kaluza-Klein Graviton Emission in ppˉp\bar{p} Collisions at s=1.8\sqrt{s}=1.8 TeV using the Missing Energy Signature

We report on a search for direct Kaluza-Klein graviton production in a data sample of 84 ${pb}^{-1}$ of \ppb collisions at $\sqrt{s}$ = 1.8 TeV, recorded by the Collider Detector at Fermilab. We investigate the final state of large missing transverse energy and one or two high energy jets. We compare the data with the predictions from a $3+1+n$-dimensional Kaluza-Klein scenario in which gravity becomes strong at the TeV scale. At 95% confidence level (C.L.) for $n$=2, 4, and 6 we exclude an effective Planck scale below 1.0, 0.77, and 0.71 TeV, respectively.Comment: Submitted to PRL, 7 pages 4 figures/Revision includes 5 figure

Measurement of the average time-integrated mixing probability of b-flavored hadrons produced at the Tevatron

We have measured the number of like-sign (LS) and opposite-sign (OS) lepton pairs arising from double semileptonic decays of $b$ and $\bar{b}$-hadrons, pair-produced at the Fermilab Tevatron collider. The data samples were collected with the Collider Detector at Fermilab (CDF) during the 1992-1995 collider run by triggering on the existence of $\mu \mu$ and $e \mu$ candidates in an event. The observed ratio of LS to OS dileptons leads to a measurement of the average time-integrated mixing probability of all produced $b$-flavored hadrons which decay weakly, $\bar{\chi} = 0.152 \pm 0.007$ (stat.) $\pm 0.011$ (syst.), that is significantly larger than the world average $\bar{\chi} = 0.118 \pm 0.005$.Comment: 47 pages, 10 figures, 15 tables Submitted to Phys. Rev.

On the denaturation mechanisms of the ligand binding domain of thyroid hormone receptors

The ligand binding domain (LBD) of nuclear hormone receptors adopts a very compact, mostly α-helical structure that binds specific ligands with very high affinity. We use circular dichroism spectroscopy and high-temperature molecular dynamics simulations to investigate unfolding of the LBDs of thyroid hormone receptors (TRs). A molecular description of the denaturation mechanisms is obtained by molecular dynamics simulations of the TRα and TRβ LBDs in the absence and in the presence of the natural ligand Triac. The simulations show that the thermal unfolding of the LBD starts with the loss of native contacts and secondary structure elements, while the structure remains essentially compact, resembling a molten globule state. This differs from most protein denaturation simulations reported to date and suggests that the folding mechanism may start with the hydrophobic collapse of the TR LBDs. Our results reveal that the stabilities of the LBDs of the TRα and TRβ subtypes are affected to different degrees by the binding of the isoform selective ligand Triac and that ligand binding confers protection against thermal denaturation and unfolding in a subtype specific manner. Our simulations indicate two mechanisms by which the ligand stabilizes the LBD: (1) by enhancing the interactions between H8 and H11, and the interaction of the region between H1 and the Ω-loop with the core of the LBD, and (2) by shielding the hydrophobic H6 from hydration.CNPqFAPESP (06/00182-8, 06/06831-8