Key issues in diagnosing and treating acute aortic syndromes: results from the metropolitan area of Bologna network

Background: Survival of patients with Acute Aortic Syndrome (AAS) may relate to the speed of diagnosis. Diagnostic delay is exacerbated by non classical presentations such as myocardial ischemia or acute heart failure (AHF). However little is known about clinical implications and pathophysiological mechanisms of Troponin T elevation and AHF in AAS. Methods and Results: Data were collected from a prospective metropolitan AAS registry (398 patients diagnosed between 2000 and 2013). Troponin T values (either standard or high sensitivity assay, HS) were available in 248 patients (60%) of the registry population; the overall frequency of troponin positivity was 28% (ranging from 16% to 54%, using standard or HS assay respectively, p = 0.001). Troponin positivity was associated with a twofold increased risk of long in-hospital diagnostic time (OR 1.92, 95% CI 1.05-3.52, p = 0.03), but not with in-hospital mortality. The combination of positive troponin and ACS-like ECG abnormalities resulted in a significantly increased risk of inappropriate therapy due to a misdiagnosis of ACS (OR 2.48, 95% CI 1.12-5.54, p = 0.02). Patients with AHF were identified by the presence of dyspnea as presentation symptom or radiological signs of pulmonary congestion or cardiogenic shock. The overall frequency of AHF was 28 % (32% type A vs. 20% type B AAS, p = 0.01). AHF was due to a variety of pathophysiological mechanisms including cardiac tamponade (26%), aortic regurgitation (25%), myocardial ischemia (17%), hypertensive crisis (10%). AHF was associated with increased surgical delay and with increased risk of in-hospital death (adjusted OR 1.97 95% CI1.13-3.37,p=0.01). Conclusions: Troponin positivity (particularly HS) was a frequent finding in AAS. Abnormal troponin values were strongly associated with ACS-like ECG findings, in-hospital diagnostic delay, and inappropriate therapy. AHF was associated with increased surgical delay and was an independent predictor of in-hospital mortality.

Hepatic-portal vein infusions of glucagon-like peptide-1 reduce meal size and increase c-Fos expression in the nucleus tractus solitarii, area postrema and central nucleus of the amygdala in rats

We recently reported that brief, remotely controlled intrameal hepatic-portal vein infusions of glucagon-like peptide-1 (GLP-1) reduced spontaneous meal size in rats. To investigate the neurobehavioural correlates of this effect, we equipped male Sprague-Dawley rats with hepatic-portal vein catheters and assessed (i) the effect on eating of remotely triggered infusions of GLP-1 (1 nmol/kg, 5 min) or vehicle during the first nocturnal meal after 3 h of food deprivation and (ii) the effect of identical infusions performed at dark onset on c-Fos expression in several brain areas involved in the control of eating. GLP-1 reduced (P < 0.05) the size of the first nocturnal meal and increased its satiety ratio. Also, GLP-1 increased (P < 0.05) the number of c-Fos-expressing cells in the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala, but not in the arcuate or paraventricular hypothalamic nuclei. These data suggest that the nucleus tractus solitarii, the area postrema and the central nucleus of the amygdala play a role in the eating-inhibitory actions of GLP-1 infused into the hepatic-portal vein; it remains to be established whether activation of these brain nuclei reflect satiation, aversion, or both.

Differential effects of long and short carbon nanotubes on the gas-exchange region of the mouse lung

Abstract We hypothesise that inflammatory response and morphological characteristics of lung parenchyma differ after exposure to short or long multi-walled carbon nanotubes (MWCNT). Mice were subjected to a single dose of vehicle, short or long MWCNT by pharyngeal aspiration. Bronchoalveolar lavage fluid (BALF) obtained at 24 h was analysed for inflammatory reaction and lung tissue was analysed for morphological alterations using stereology. Short MWCNT had stronger potential to induce polymorphonuclear cells whereas long MWCNT increased interleukin-6 levels in BALF. Alveolar septal fibrosis was only observed with short MWCNT. Type II pneumocyte hypertrophy was only detected with long MWCNT. There was no reduction in total alveolar surface area and no sign of type II cell hyperplasia. We observed mild inflammatory and pathological responses to short and long MWCNT in the lung parenchyma depending on the size of the applied MWCNT.

Effect Of Yolk Testosterone On Gonadal Testosterone And Aromatase Activity In The Pre-Optic Area Of The Brain In Male Domestic C

Maternal effects are a mother¿s non-genetic contributions to development that alter phenotypic traits in offspring. Maternal effects can take the form of prenatal allocation of resources, such as the deposition of androgens into egg yolks. For example, elevated yolk testosterone increases male sexual behaviors such as copulation solicitation and courtship displays in some avian species, in addition to aggressive behaviors like pecks and intimidating postures towards same-sex competitors. However, the mechanism connecting in ovo testosterone exposure with changes in sexual and aggressive behaviors has yet to be elucidated. While testosterone released by the gonads is important in the activation of sexual behaviors, it must undergo conversion to estrogen by the enzyme aromatase in the pre-optic area (POA) of the avian brain for full expression of sexual activity. POA aromatase is also necessary for the activation of aggressive behaviors in male birds. This experiment tested the hypothesis that elevated yolk testosterone leads to changes in POA aromatase activity and levels of gonadal testosterone, as these two endocrine parameters may mediate the effect of yolk testosterone on the frequency of sexual and aggressive behaviors. The effect of elevated yolk testosterone on gonadal testosterone levels and aromatase activity in the POA of 3-day-old domestic chickens Gallus gallus domesticus was investigated. Unincubated eggs were injected with either 10 ng testosterone in 50 ¿L sesame oil (¿T chicks¿) or 50 ¿L sesame oil (¿C chicks¿). At 3 days post-hatch, gonadal testosterone content was measured after steroid extraction using an EIA, and aromatase activity in the POA was quantified by measuring the production of tritiated water from [1ß-3H]-androstenedione. I predicted that gonadal testosterone levels and brain aromatase activity would be higher in T chicks, however found no difference between treatments. Though juvenile T production peaks at 3 days post-hatch, it is possible that the reproductive systems, including the testes and POA, are not fully developed at this time.

Reorganization of CA3 area of the mouse hippocampus after pilocarpine induced temporal lobe epilepsy with special reference to the CA3-septum pathway

We showed that when CA3 pyramidal neurons in the caudal 80% of the dorsal hippocampus had almost disappeared completely, the efferent pathway of CA3 was rarely detectable. We used the mouse pilocarpine model of temporal lobe epilepsy (TLE), and injected iontophoretically the anterograde tracer phaseolus vulgaris leucoagglutinin (PHA-L) into gliotic CA3, medial septum and the nucleus of diagonal band of Broca, median raphe, and lateral supramammillary nuclei, or the retrograde tracer cholera toxin B subunit (CTB) into gliotic CA3 area of hippocampus. In the afferent pathway, the number of neurons projecting to CA3 from medial septum and the nucleus of diagonal band of Broca, median raphe, and lateral supramammillary nuclei increased significantly. In the hippocampus, where CA3 pyramidal neurons were partially lost, calbindin, calretinin, parvalbumin immunopositive back-projection neurons from CA1-CA3 area were observed. Sprouting of Schaffer collaterals with increased number of large boutons in both sides of CA1 area, particularly in the stratum pyramidale, was found. When CA3 pyramidal neurons in caudal 80% of the dorsal hippocampus have almost disappeared completely, surviving CA3 neurons in the rostral 20% of the dorsal hippocampus may play an important role in transmitting hyperactivity of granule cells to surviving CA1 neurons or to dorsal part of the lateral septum. We concluded that reorganization of CA3 area with its downstream or upstream nuclei may be involved in the occurrence of epilepsy.