Daniel Moura

Fast 3D reconstruction of the spine from biplanar radiographs using a deformable articulated model

This paper proposes a novel method for fast 3D reconstructions of the scoliotic spine from two planar radiographs. The method uses a statistical model of the shape of the spine for computing the 3D reconstruction that best matches the user input (about 7 control points per radiograph). In addition, the spine was modelled as an articulated structure to take advantage of the dependencies between adjacent vertebrae in terms of location, orientation and shape. The accuracy of the method was assessed for a total of 30 patients with mild to severe scoliosis (Cobb angle [22°, 70°]) by comparison with a previous validated method. Reconstruction time was 90 s for mild patients, and 110 s for severe. Results show an accuracy of ∼0.5mm locating vertebrae, while orientation accuracy was up to 1.5° for all except axial rotation (3.3° on moderate and 4.4° on severe cases). Clinical indices presented no significant differences to the reference method (Wilcoxon test, p ≤ 0.05) on patients with moderate scoliosis. Significant differences were found for two of the five indices (p=0.03) on the severe cases, while errors remain within the inter-observer variability of the reference method. Comparison with state-of-the-art methods shows that the method proposed here generally achieves superior accuracy while requiring less reconstruction time, making it especially appealing for clinical routine use.

Acute cyanide poisoning among jewelry and textile industry workers

Limited work has focused on occupational exposures that may increase the risk of cyanide poisoning by ingestion. A retrospective chart review of all admissions for acute cyanide poisoning by ingestion for the years 1988 to 2008 was conducted in a tertiary university hospital serving the largest population in the country working in jewelry and textile facilities. Of the 9 patients admitted to the hospital during the study period, 8 (7 males, 1 female; age 36 ± 11 years, mean ± SD) attempted suicide by ingestion of potassium cyanide used in their profession as goldsmiths or textile industry workers. Five patients had severe neurologic impairment and severe metabolic acidosis (pH 7.02 ± 0.08, mean ± SD) with high anion gap (23 ± 4 mmol/L, mean ± SD). Of the 5 severely intoxicated patients, 3 received antidote therapy (sodium thiosulfate or hydroxocobalamin) and resumed full consciousness in less than 8 hours. All patients survived without major sequelae. Cyanide intoxication by ingestion in our patients was mainly suicidal and occurred in specific jobs where potassium cyanide is used. Metabolic acidosis with high anion is a good surrogated marker of severe cyanide poisoning. Sodium thiosulfate and hydroxocobalamin are both safe and effective antidotes.

Involvement of G-protein βγ subunits on the influence of inhibitory α2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens

The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz. Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors.

Differential distribution in, and release from, sympathetic nerve endings of endogenous noradrenaline and recently incorporated catecholamines

SummaryGuinea-pig vasa deferentia or hypogastric nerve-vas deferens preparations, preincubated with pargyline (to irreversibly inhibit monoamine oxidase), were exposed to 2.3 μmol/l of unlabelled adrenaline or of 3H-7-(−)-noradrenaline in the presence of hydrocortisone (to inhibit extraneuronal uptake). The vasa deferentia were then mounted in perifusion chambers and subjected to transmural electrical stimulation, electrical stimulation of the nerve, depolarization by potassium (50 mmol/l), or addition of tyramine (40 μmol/l). The evoked overflow of tritium and of unlabelled catecholamines was expressed as a fraction of their tissue content. For all stimuli, the fractional release of the exogenous amines was higher than that of endogenous noradrenaline. Thus, recently incorporated amines are preferentially mobilized irrespective of the particular type of releasing mechanism or the chemical nature of the amine.In vasa deferentia which had been loaded with increasing amounts of adrenaline (by incubating the tissues with adrenaline at concentrations ranging from 0.6 to 160 μmol/1), the fractional release of adrenaline decreased and became closer to that of endogenous noradrenaline. Hence, the access of exogenous catecholamines to the deepest storage sites requires higher concentrations of amines than those needed to reach the more easily releasable pools.Light microscope autoradiographs obtained from slices of vasa deferentia previously loaded with 2.3 μmol/l 3H-(−)-noradrenaline showed that the outer layers were strongly labelled with silver grains whereas the inner layers were poorly marked. It is concluded that recently incorporated amines are preferentially stored in varicosities close to the surface of the tissue and, in comparison with endogenous noradrenaline, are preferentially released from sympathetically innervated organs.

Bioactive Peptides - Are There More Antihypertensive Mechanisms Beyond ACE Inhibition?

Diet has a high relevance in health. Hypertension is a major risk factor for cardiovascular diseases and has an important impact on public health, and consequently on countries economy. Scientific research gathered strong evidence about the role of several dietary factors either in etiology or in treatment/prevention of these diseases. Peptides from different food matrices have been studied, and indicated as compounds with particular interest in the context of hypertension. The classical approach involves the identification of peptides with an in vitro ACE inhibitory activity and the assumption that the observed in vivo effects are due to this enzyme blockade. However, in some cases the potency of ACE blockade does not correlate with the antihypertensive activity in vivo. This paper reviews the current literature that identifies mechanisms of action, other than ACE inhibition, that might explain antihypertensive effects of biologically active peptides from different food sources.

The role of angiotensin II in hypertension due to adenosine receptors blockade.

The renin-angiotensin system may be involved in hypertension induced by adenosine receptors blockade with 1,3-dipropyl-8-sulfophenylxanthine (DPSPX). Contractions of the mesenteric vasculature to angiotensin II, noradrenaline and potassium chloride were studied in DPSPX-induced hypertension. Male Wistar rats received infusions of saline or DPSPX (90 microg kg(-1) h(-1), i.p.) for 3 or 7 days. Blood pressure was determined by the tail-cuff method. On days 3 or 14, concentration-response curves were obtained on mesenteric arteries and veins. Plasma angiotensin II levels, measured by radioimmunoassay, were higher in DPSPX-hypertensive rats. The maximum contractile effect of angiotensin II was lower in vessels from DPSPX-hypertensive rats while that for noradrenaline was higher. Potassium chloride-induced contractions were larger in veins from DPSPX-hypertensive rats but similar in arteries, when compared with control rats. We conclude that raised angiotensin II levels and altered vascular reactivity are consistent with a renin-angiotensin-mediated hypertension.

Prejunctional α2A-autoreceptors in the human gastric and ileocolic arteries

This study was undertaken to determine the subtype of prejunctional α2-autoreceptors in human blood vessels. Segments of gastric and ileocolic arteries were incubated with [3H]noradrenaline and subsequently perifused with modified Krebs-Henseleit solution containing cocaine (12 µM). Five periods of electrical stimulation (S1–S5) were applied (1 Hz, 1 ms, 50 V for 1 min). Concentration-response curves for the facilitatory effect of eight α-adrenoceptor antagonists [rauwolscine, 2-[2-(2-methoxy-1,4-benzodioxanyl)] imidazoline (RX821002), yohimbine, phentolamine, idazoxan, 2-(2’,6’-dimethoxyphenoxyethyl)-aminomethyl-1,4-benzodioxan (WB4101), spiroxatrine and prazosin] were determined. All antagonists enhanced the stimulation-evoked overflow of tritium, indicating the existence of α2-autoreceptors. The EC30% values of the antagonists (concentrations that increased the evoked overflow of tritium by 30%) were taken as a measure of affinity to the autoreceptors. Correlations between the pEC30% values obtained in the present study and the pKi values of the same antagonists at cloned human α2A-, α2B-, α2C-adrenoceptors expressed in Chinese hamster lung cells and at α2D-adrenoceptors in the rat submaxillary gland or the bovine pineal gland showed that the α2-autoreceptors in the human gastric and ileocolic arteries resemble most closely the α2A-subtype.

Adenosine and the endothelium-dependent modulation of 3H-noradrenaline release in the canine pulmonary artery

This study aimed at characterizing the influence of endothelium on noradrenaline release from the canine pulmonary artery. Tritium overflow from intact or endothelium-free vessels preloaded with 0.2 μmol.1−13H-noradrenaline was evoked by electrical stimulation (1 Hz, during 5 min) or potassium (25–100 mmol. 1−1).The fractional release of tritium evoked by electrical stimulation was increased by removing the endothelium [from 1.7 (1.2; 2.4) to 2.7(2.3; 3.2) × 10−5. pulse−1, n = 10; P < 0.05]. Neither NG-nitro-l-arginine methyl ester (l-NAME) (up to 300 μmol.l−1) nor indomethacin (up to 30 μml.l−1), nor endothelin-1 (up to 30 nmol.l−1), nor suramin (up to 300 μmol.l−1) changed tritium release evolved by electrical stimulation. In contrast, the selective A1-adenosine antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX) (3.3-33 nmol.l−1) concentration-dependently increased, and the selective A1-adenosine agonist N6-cyclopentyladenosine (CPA) (3.3–100 nmol. l−1) concentration-dependently decreased the evoked release of noradrenaline. Since the effects of DPCPX were observed in endothelium-intact tissues only, it may be concluded that adenosine secreted by the endothelium activates prejunctional release-inhibiting A1-receptors. Tetraethylammonium (TEA) (3.3–33 mmol. l−1) enhanced tritium overflow evoked by electrical stimulation more in endothelium-free than in endothelium-intact vessels, indicating that some K+-channel opener is involved in the inhibitory role of endothelium on noradrenaline release. Since it had been previously shown that A1-adenosine receptors are coupled to K+-channels, it is suggested that adenosine may inhibit noradrenaline release through the opening of K+-channels.In conclusion, the results show that in the canine pulmonary artery, adenosine is a good candidate for the endothelium-dependent inhibitory factor which is responsible for the reduction of noradrenaline release evoked by electrical stimulation.

Long-term administration of 1,3-dipropyl-8-sulphophenylxanthine (DPSPX) alters α2-adrenoceptor-mediated effects at the pre- but not at the postjunctional level

The present investigation was undertaken to see whether a long-term inhibition of adenosine receptors —leading to hypertension — interferes with α2-adrenoceptor-mediated modulation of noradrenaline release. Rat tail arteries were removed from normal and from hypertensive animals obtained by chronic treatment with intraperitoneally infused DPSPX (1,3,-dipropyl-8-sulphophenylxanthine) or orally administered L-NAME (NG-Nitro-L-arginine methyl ester). To study prejunctional effects, the influence of UK-14,304 (5-bromo-6(imidazoline-2-ylamino)-quinoxaline) and yohimbine on the overflow of tritium evoked by electrical stimulation (100 V; 1 Hz; 2 ms; 5 min) from tissues preloaded with 3H-noradrenaline was analysed. To study postjunctional effects, concentration-response curves to UK-14,304 were determined. In DPSPX-treated rats there was an enhancement of the prejunctional effects of UK-14,304: its EC30% was reduced from 381 (250; 579) to 85 (73; 99) nmol.l−1 (n = 5; P<0.05) and its maximal effect — expressed as percent reduction of tritium overflow-increased from 45 ± 5% to 61 ± 5% (n = 6; P < 0.05). In L-NAME-treated rats there was no change in either of these two parameters. At the postjunctional level, there was no change in the sensitivity to UK-14,304 in tissues from either DPSPX- or L-NAME-treated rats. Yohimbine (10–1000 nmol.l−1) caused a concentration-dependent increase of tritium overflow evoked by electrical stimulation in both control and hypertensive animals (either DPSPX- or L-NAME-treated). The EC50%-pre-antagonist values (concentration of the antagonist that increases the evoked overflow by 50%) were not significantly different in the three situations. We conclude that long-term administration of DPSPX increases the sensitivity to the prejunctional effects of UK-14,304 without changing that to its postjunctional effects, showing a specific interaction between α-adrenoceptors and adenosine receptors at a prejunctional level. The question arises whether there is any link between that alteration and the development of the hypertensive state.

Fast 3D Reconstruction of the Spine Using User-Defined Splines and a Statistical Articulated Model

This paper proposes a method for rapidly reconstructing 3D models of the spine from two planar radiographs. For performing 3D reconstructions, users only have to identify on each radiograph a spline that represents the spine midline. Then, a statistical articulated model of the spine is deformed until it best fits these splines. The articulated model used on this method not only models vertebrae geometry, but their relative location and orientation as well. The method was tested on 14 radiographic exams of patients for which reconstructions of the spine using a manual identification method where available. Using simulated splines, errors of 2.2±1.3mm were obtained on endplates location, and 4.1±2.1mm on pedicles. Reconstructions by non-expert users show average reconstruction times of 1.5min, and mean errors of 3.4mm for endplates and 4.8mm for pedicles. These results suggest that the proposed method can be used to reconstruct the human spine in 3D when user interactions have to be minimised.