Publications

The seismic performance assessment of the ancient Temple of Aphaia in Aegina island, Greece, is presented. The Temple of Aphaia was erected around 500BC using porous limestone and is one of the most characteristic examples of Doric architecture. The assessment is performed within a performance‐based framework using state‐of‐the‐art tools of earthquake engineering. In the first part, the seismic hazard of the site was calculated using the European Seismic Hazard Model and hazard‐consistent records were selected. Then, the Temple was scanned by drone and the point cloud was used to develop the numerical structural model. The Temple was analyzed using the discrete element method. Appropriate engineering demand parameters and limit state thresholds were defined. Fragility curves for the structural elements, namely, columns and architraves, of the Temple were computed via multi‐stripe analysis. Finally, the seismic risk of the Temple was evaluated using long‐term estimates in terms of return periods of exceeding limit states and total loss. The outcomes of the study offer valuable information to engineers, architects, and archaeologists regarding the current status of the monument in terms of identifying its most vulnerable elements and allowing the prioritization of short‐ and long‐term restoration actions.

Correction to: Human Adipose Tissue under in Vitro Inhibition of 11β-Hydroxysteroid Dehydrogenase Type 1: Differentiation and Metabolism ChangesHorm Metab Res 2002; 34(11/12): 752-757DOI: 10.1055/s-2002-38255

<ns3:p>Background: Mapping time-structures is a burgeoning scientific field enriching the (P4) medicine models. Local evidence in Mediterranean populations is underinvestigated. Methods: The Censused stroke-related death events (D) in the largest East-Mediterranean port (Piraeus), during (1985-1989), when local population had diet (low fat/sugar, proteins and vegetables/fruits daily, and pure olive oil almost exclusively) and genetic homogeneity-later interrupted by the immigration into Greece in 1990; and Sunspot numbers were indexed by Wolf numbers (Rz) (1944-2004), and evaluated using Fast Fourier Analysis and Singular Spectrum Analysis in MATLAB. Results: D were turned with fluctuations &gt;35% in Rz. A non-anthropogenic 6.8 days cycle was recognized. Conclusions: This study may be taken into consideration in future public health planning and chronotherapy evaluations.</ns3:p>

Primary pigmented nodular adrenocortical disease (PPNAD) is a rare cause of Cushing syndrome in infants, children, and young adults. It is characterized by non-adrenocorticotropic hormone-dependent hypersecretion of cortisol by multiple, pigmented nodules of hyperplastic adrenocortical cells. With a single exception, adrenal glands have been described as normal with computed tomography (CT) in all previous series. Eight patients had Cushing syndrome due to surgically proved PPNAD. Four of the eight patients had stigmas of Carney complex (lentigines, calcified Sertoli cell tumors of the testes, and cardiac and soft-tissue myxomas). CT and/or magnetic resonance (MR) imaging demonstrated unilateral or bilateral nodularity in five of six patients examined. Macronodules (greater than 10 mm) were seen in the two oldest patients. As the clinical presentation of Cushing syndrome in this group of patients may be atypical (severe osteoporosis or short stature), the detection of multiple, small adrenocortical nodules with CT or MR imaging supports, or may even suggest, the diagnosis of PPNAD.

Children with classic congenital adrenal hyperplasia (CAH) have multiple endocrine imbalances, including prenatal glucocorticoid and adrenomedullary deficiency and androgen excess, with possible postnatal iatrogenic glucocorticoid excess, hyperandrogenism, and adrenomedullary hypofunction. Prenatal masculinization of the brain has been suggested in girls with classic CAH. Hormones of the hypothalamic-pituitary-adrenal axis and sex hormones interact with extrahypothalamic regulatory centers of the brain, including the amygdala and hippocampus. The amygdala is important in the processing of emotion and generation of fear, whereas the hippocampus plays an important role in memory. Chronic hypercortisolemia has been shown to be associated with hippocampal damage, while glucocorticoids and corticotropin-releasing factor play a major role in the regulation of amygdala function. We performed magnetic resonance imaging of the brain on 27 children with classic CAH and 47 sex- and age-matched controls. Volumes of the cerebrum, ventricles, temporal lobe, amygdala, and hippocampus were quantified. Females with CAH did not have brains with male-specific characteristics. In contrast, a significant decrease in amygdala volume was observed in both males and females with CAH (males, P = 0.01; females, P = 0.002). Iatrogenic effects on the hippocampus due to glucocorticoid therapy were not observed in children with CAH. These results suggest that prenatal glucocorticoid deficiency with resulting alterations in hypothalamic-pituitary-adrenal axis regulation, sex steroid excess, or some combination of these preferentially affect the growth and development of the amygdala, a structure with major functional implications that warrant further exploration.

As endogenous Cushing's syndrome (CS) in children occurs during a critical developmental period, when the majority of peak bone mass is acquired, we hypothesized that children with CS might be at an increased risk of osteoporosis. To determine the effects of CS on bone density, bone metabolism, and growth, we studied a 15-yr-old female identical twin pair, one of whom had CS (twin A), and the other of whom was healthy (twin B). Before therapy for CS, twin A showed a severe loss of bone mineral density [BMD; -3.2SD at the lumbar spine (LS)] compared to twin B (-0.1 SD), which in twin A was associated with low serum osteocalcin levels and urinary pyridinium cross-link excretion. Cure of CS in twin A led to a marked increase in these bone markers, suggesting a state of active bone remodeling. After 27 months of follow-up, even though twin A's BMD improved significantly, it still remained abnormal [-1.9 SD at LS compared with that of twin B (0 SD)], suggesting that twin A continued to be at increased long term risk of osteoporosis. In addition, as a consequence of CS, twin A's final height was 21 cm less than that of her identical twin. We recommend that all children with CS should have BMD monitored after treatment to determine the long term risk of osteoporosis.

Abstract Primary hyperaldosteronism (PA) is a well-known cause of hypertension although its exact prevalence amongst patients with apparent essential hypertension has been a matter of debate. A number of recent studies have suggested that mild forms of PA may be relatively common taking into consideration factors that were previously either overestimated or ignored when developing diagnostic tests of PA and when applying these tests into normotensive individuals. The performance characteristics and diagnostic accuracy of such tests are substantially increased when the adrenocorticotrophin effect, inappropriate potassium levels and their application in carefully selected normotensive individuals are considered. In the present review, we critically analyze these issues and provide evidence that several, particularly mild, forms of PA can be effectively identified exhibiting potentially important clinical implications.