The magnitude of damaging volcanic earthquakes of Mt. Etna: are the commonly used scales adequate?

On October 2002 a seismic swarm occurred on the eastern flank of Mt. Etna. One of the strongest events caused severe damage, up to EMS intensity of VIII that contrasts with its local magnitude of 4.4. The occurrence of significant damage at such small magnitude is repeatedly observed in the Mt. Etna area and is traditionally attributed to the shallow source of volcanic earthquakes. Strong-motion accelerograms and broad-band seismograms recorded during the swarm demonstrate that there is a more cogent cause for the severe damage, i.e. an anomalously strong low-frequency (0.1 < f < 1 Hz) radiation deviating from the conventional Brune (1970) spectral scaling. Therefore, these earthquakes cause unexpectedly large ground displacements and long ( 20 sec) durations of shaking. The integration of digital accelerograms recorded on October 2002 yields a maximum peak ground displacement as large as 1.8 cm at a distances of 18 km, out of the largest damage zone. Based on the sharp local attenuation of ground motion amplitudes observed during the Mt. Etna earthquakes, we infer that displacements near the epicentres can have attained 10 cm. So large displacements are consistent with the maximum observed damage. Moreover, the frequency cutoff below 1.25 Hz in the Wood-Anderson response attenuates the peak-to-peak amplitudes used to assess local magnitudes. This instrumental deamplification at low frequency yields underestimated values of local magnitude that are not representative of the real ground shaking. Since a prompt, correct magnitude (and potential damage) assessment is crucial for efficient Civil Protection actions, a procedure is proposed which, in near-real-time, can be successful in identifying potentially damaging earthquakes of Mt. Etna through the computation of response spectra. The procedure provides a magnitude value that is derived on a statistical basis from the Housner (1952) spectral intensity computed in the low-frequency band. This parameter is a suitable near-real-time indicator of large earthquake-induced building shaking and could also be applied for a preliminary determination of the epicentral macroseismic intensity of volcanic events of Mt. Etna through consolidated relationships established for tectonic earthquakes in Italy

Functional polymorphisms in genes of the Angiotensin and Serotonin systems and risk of hypertrophic cardiomyopathy: AT1R as a potential modifier

<p>Abstract</p> <p>Background</p> <p>Angiotensin and serotonin have been identified as inducers of cardiac hypertrophy. DNA polymorphisms at the genes encoding components of the angiotensin and serotonin systems have been associated with the risk of developing cardiovascular diseases, including left ventricular hypertrophy (LVH).</p> <p>Methods</p> <p>We genotyped five polymorphisms of the <it>AGT</it>, <it>ACE</it>, <it>AT1R</it>, <it>5-HT2A</it>, and <it>5-HTT </it>genes in 245 patients with Hypertrophic Cardiomyopathy (HCM; 205 without an identified sarcomeric gene mutation), in 145 patients with LVH secondary to hypertension, and 300 healthy controls.</p> <p>Results</p> <p>We found a significantly higher frequency of <it>AT1R </it>1166 C carriers (CC+AC) among the HCM patients without sarcomeric mutations compared to controls (p = 0.015; OR = 1.56; 95%CI = 1.09-2.23). The <it>AT1R </it>1166 C was also more frequent among patients who had at least one affected relative, compared to sporadic cases. This allele was also associated with higher left ventricular wall thickness in both, HCM patients with and without sarcomeric mutations.</p> <p>Conclusions</p> <p>The 1166 C <it>AT1R </it>allele could be a risk factor for cardiac hypertrophy in patients without sarcomeric mutations. Other variants at the <it>AGT</it>, <it>ACE</it>, <it>5-HT2A </it>and <it>5-HTT </it>did not contribute to the risk of cardiac hypertrophy.</p

Mutational spectrum of the SPG4 (SPAST) and SPG3A (ATL1) genes in Spanish patients with hereditary spastic paraplegia

<p>Abstract</p> <p>Background</p> <p>Hereditary Spastic Paraplegias (HSP) are characterized by progressive spasticity and weakness of the lower limbs. At least 45 loci have been identified in families with autosomal dominant (AD), autosomal recessive (AR), or X-linked hereditary patterns. Mutations in the <it>SPAST </it>(<it>SPG4</it>) and <it>ATL1 </it>(<it>SPG3A</it>) genes would account for about 50% of the ADHSP cases.</p> <p>Methods</p> <p>We defined the <it>SPAST </it>and <it>ATL1 </it>mutational spectrum in a total of 370 unrelated HSP index cases from Spain (83% with a pure phenotype).</p> <p>Results</p> <p>We found 50 <it>SPAST </it>mutations (including two large deletions) in 54 patients and 7 <it>ATL1 </it>mutations in 11 patients. A total of 33 of the <it>SPAST </it>and 3 of the <it>ATL1 </it>were new mutations. A total of 141 (31%) were familial cases, and we found a higher frequency of mutation carriers among these compared to apparently sporadic cases (38% vs. 5%). Five of the <it>SPAST </it>mutations were predicted to affect the pre-mRNA splicing, and in 4 of them we demonstrated this effect at the cDNA level. In addition to large deletions, splicing, frameshifting, and missense mutations, we also found a nucleotide change in the stop codon that would result in a larger ORF.</p> <p>Conclusions</p> <p>In a large cohort of Spanish patients with spastic paraplegia, <it>SPAST </it>and <it>ATL1 </it>mutations were found in 15% of the cases. These mutations were more frequent in familial cases (compared to sporadic), and were associated with heterogeneous clinical manifestations.</p

Water-Soluble Mo3S4 Clusters Bearing Hydroxypropyl Diphosphine Ligands: Synthesis, Crystal Structure, Aqueous Speciation, and Kinetics of Substitution Reactions

The [Mo3S4Cl3(dhprpe)3]+ (1+) cluster cation has been prepared by reaction between Mo3S4Cl4(PPh3)3 (solvent)2 and the watersoluble 1,2-bis(bis(hydroxypropyl)phosphino)ethane (dhprpe, L) ligand. The crystal structure of [1]2[Mo6Cl14] has been determined by X-ray diffraction methods and shows the typical incomplete cuboidal structure with a capping and three bridging sulfides. The octahedral coordination around each metal center is completed with a chlorine and two phosphorus atoms of the diphosphine ligand. Depending on the pH, the hydroxo group of the functionalized diphosphine can substitute the chloride ligands and coordinate to the cluster core to give new clusters with tridentate deprotonated dhprpe ligands of formula [Mo3S4(dhprpe-H)3]+ (2+). A detailed study based on stopped-flow, 31P{1H} NMR, and electrospray ionization mass spectrometry techniques has been carried out to understand the behavior of acid−base equilibria and the kinetics of interconversion between the 1+ and the 2+ forms. Both conversion of 1+ to 2+ and its reverse process occur in a single kinetic step, so that reactions proceed at the three metal centers with statistically controlled kinetics. The values of the rate constants under different conditions are used to discuss on the mechanisms of opening and closing of the chelate rings with coordination or dissociation of chloride

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