Acute rupture of an aortic false aneurysm treated with a stent-graft.

PURPOSE: To report the use of an aortic endograft to treat a ruptured false aneurysm at the anastomosis of an aortofemoral bypass graft. METHODS AND RESULTS: A 68-year-old man with a 30-year-old aorto-right femoral bypass and multiple comorbidities was admitted to the hospital complaining of acute abdominal pain. Imaging identified a 60-mm ruptured aortic false aneurysm with associated retroperitoneal hematoma, a 9-cm right femoral false aneurysm, and a calcified 23-mm left common iliac aneurysm. Two slightly overlapping Vanguard straight stent-grafts were implanted in the aorta and left common iliac artery in an emergency procedure owing to the patient's high surgical risk. The anastomotic false aneurysm and the bypass were excluded. A left-to-right femorofemoral bypass was performed to re-establish flow to the right femoral artery with ligation of the external iliac artery. The patient recovered uneventfully. He remained well with a successful repair until his death of a myocardial infarction 6 months after the procedure. CONCLUSIONS: Endovascular grafting can be used successfully for the urgent treatment of aortic false aneurysm rupture.     

SOFA score and left ventricular systolic function as predictors of short-term outcome in patients with sepsis

In a group of septic patients, we assess the short-term prognostic value of LV systolic performance, evaluated through conventional left ventricular ejection fraction (LVEF) and left ventricular global longitudinal strain (LV GLS). One hundred forty-seven patients with sepsis were recruited; LVEF by planimetry and peak GLS by 2D speckle tracking could be assessed within 24 h. The study population was stratified according to SOFA tertiles assessed at the time of the echocardiogram (G1: SOFA score <5; G2: SOFA score 5–7; G3: SOFA score >7). Day-7 follow-up data were used as reference. Patients in G2 and G3 show a significant hemodynamic derangement, paralleling the more pronounced organ damage by definition; nevertheless, LVEF and GLS are comparable among the three groups (both p > 0.1). All-cause mortality at day-7 follow-up is slightly lower in G1 (9%) versus G2 and G3 (14 and 26%, respectively, p = NS). Analyses through ROC curves focusing on day-7 mortality show that the SOFA score fairly correlates with events (AUC 0.635, p = 0.037), while low LVEF (AUC 0.35, p = 0.022) and less negative GLS (AUC 0.73, p = 0.001) do so. In multivariate analyses, mortality by day-7 follow-up is more likely per higher GLS (i.e., indicative of worst systolic dysfunction, HR 1.22/%, p = 0.005) and per increasing SOFA score (HR 1.22/unit, p = 0.010), whereas LVEF, adjusted for age and SOFA score, does not enter the prognostic model. In the very short term in patients with severe sepsis, LV systolic function assessment by means of GLS predicts the short-term prognosis, independent of SOFA.     

Serotonin transporter promoter polymorphism genotype is associated with temperament, personality traits and illegal drugs use among adolescents

Summary. Serotonin transporter promoter polymorphism (5-HTTLPR) genotype was previously found associated with substance use disorders, particularly in the subjects with comorbid antisocial behavior, and with temperament and personality traits at risk for substance abuse. Aim of the present study was to evaluate the possible association between 5-HTTLPR genotype and the availability to experiment illegal drugs among adolescents, in relationship with psychological characteristics. 216 caucasian high school students (aged 14–19 ys), 125 abstinent subjects, who have never experimented psychotropic drugs, and 91 experimenters of illegal drugs have been genotyped. Aggressiveness levels and temperamental traits were measured in both abstinent subjects and experimenters utilizing respectively Buss-Durkee-Hostility-Inventory (BDHI) and Cloninger Three-dimensional Personality Questionnaire (TPQ). Data about school performance have been also collected. The short-short (SS) genotype frequency was significantly higher among experimenters compared with abstinent subjects (p = 0.001). The odds ratio for the SS genotype vs the long-long (LL) genotype frequency was 4.67, 95% Cl (1.97–11.04), when experimenters were compared with abstinent students. The SS genotype frequency was significantly higher among aggressive/novelty seeker (NS) experimenters with poor school achievements, compared with drugs experimenters without aggressiveness and school failure (p = 0.02). When evaluated on the entire sample, BDHI mean total scores, NS scores at TPQ and school failure frequency were significantly higher in SS individuals, in comparison with LL subjects. Our data suggest that a decreased expression of the gene encoding the 5-HTT transporter, due to “S” promoter polymorphism, may be associated with an increased availability to experiment illegal drugs among adolescents, particularly in the subjects with more consistent aggressiveness, NS temperament and learning disabilities.     

Antiangiogenic properties of selected ruthenium(III) complexes that are nitric oxide scavengers

The nitric oxide synthase (NOS) pathway has been clearly demonstrated to regulate angiogenesis. Increased levels of NO correlate with tumour growth and spreading in different experimental and human cancers. Drugs interfering with the NOS pathway may be useful in angiogenesis-dependent tumours. The aim of this study was to pharmacologically characterise certain ruthenium-based compounds, namely NAMI-A, KP1339, and RuEDTA, as potential NO scavengers to be used as antiangiogenic/antitumour agents. NAMI-A, KP1339 and RuEDTA were able to bind tightly and inactivate free NO in solution. Formation of ruthenium-NO adducts was documented by electronic absorption, FT-IR spectroscopy and (1)H-NMR. Pretreatment of rabbit aorta rings with NAMI-A, KP1339 or RuEDTA reduced endothelium-dependent vasorelaxation elicited by acetylcholine. This effect was reversed by 8-Br-cGMP. The key steps of angiogenesis, endothelial cell proliferation and migration stimulated by vascular endothelial growth factor (VEGF) or NO donor drugs, were blocked by NAMI-A, KP1339 and RuEDTA, these compounds being devoid of any cytotoxic activity. When tested in vivo, NAMI-A inhibited angiogenesis induced by VEGF. It is likely that the antitumour properties previously observed for ruthenium-based NO scavengers, such as NAMI-A, are related to their NO-related antiangiogenic properties.     

A Lichen Striatuslike Eruption Adopting the Morphology of Blaschko Lines

A 15-month-old girl had orange papules that formed V-shaped lines on her back. The clinical evolution and histology were compatible with the diagnosis of a lichen striatus-like eruption, adopting a special morphology by following Blaschko lines.     

Mutations in AAC2, equivalent to human adPEO-associated ANT1 mutations, lead to defective oxidative phosphorylation in Saccharomyces cerevisiae and affect mitochondrial DNA stability

Autosomal dominant and recessive forms of progressive external ophthalmoplegia (adPEO and arPEO) are mitochondrial disorders characterized by the presence of multiple deletions of mitochondrial DNA in affected tissues. Four adPEO-associated missense mutations have been identified in the ANT1 gene. In order to investigate their functional consequences on cellular physiology, we introduced three of them at equivalent positions in AAC2, the yeast orthologue of human ANT1. We demonstrate here that expression of the equivalent mutations in aac2-defective haploid strains of Saccharomyces cerevisiae results in (a) a marked growth defect on non-fermentable carbon sources, and (b) a concurrent reduction of the amount of mitochondrial cytochromes, cytochrome c oxidase activity and cellular respiration. The efficiency of ATP and ADP transport was variably affected by the different AAC2 mutations. However, irrespective of the absolute level of activity, the AAC2 pathogenic mutants showed a significant defect in ADP versus ATP transport compared with wild-type AAC2. In order to study whether a dominant phenotype, as in humans, could be observed, the aac2 mutant alleles were also inserted in combination with the endogenous wild-type AAC2 gene. The heteroallelic strains behaved as recessive for oxidative growth and petite-negative phenotype. In contrast, reduction in cytochrome content and increased mtDNA instability appeared to behave as dominant traits in heteroallelic strains. Our results indicate that S. cerevisiae is a suitable in vivo model to study the pathogenicity of the human ANT1 mutations and the pathophysiology leading to impairment of oxidative phosphorylation and damage of mtDNA integrity, as found in adPEO.