U–Pb zircon geochronology of volcanic deposits from the Permian basin of the Orobic Alps (Southern Alps, Lombardy): chronostratigraphic and geological implications

U\u2013Pb zircon ages from volcanic rocks of Early Permian age (Southern Alps, Lombardy), associated with fault-controlled transtensional continental basins, were determined with the laser ablation (LA)-ICP-MS technique. Four samples were collected at the base and at the top of the up to 1000 m thick volcaniclastic unit of the Cabianca Volcanite. This unit pre-dates the development of a sedimentary succession that still contains, at different stratigraphic levels, volcanic intercalations. Age results from a tuff in the basal part of the unit constrain the onset of the volcanic activity to 280 \ub1 2.5 Ma. Ignimbritic samples from the upper part of the unit show a large scatter in the age distribution. This is interpreted as the occurrence of antecrystic and autocrystic zircons. The youngest autocrystic zircons (c. 270 Ma) are thus interpreted as better constraining the eruption age, constraining the duration of the volcanic activity in the Orobic Basin to about 10 Ma. The new geochronological results compared with those of other Early Permian basins of the Southern Alps reveal important differences that may reflect (1) a real time-transgressive beginning and end of the volcanic activity or (2) the complex mixing of antecrystic and autocrystic zircon populations in the analysed samples

Synchronous Periadriatic magmatism in the Western and Central Alps in the absence of slab breakoff

Periadriatic Alpine magmatism has long been attributed to slab breakoff after Adria-Europe continental collision, but this interpretation is challenged by geophysical data suggesting the existence of a continuous slab. Here, we shed light on this issue based on a comprehensive dataset of zircon U-Pb ages and Hf isotopic compositions from the main western Periadriatic intrusives (from Traversella to Adamello). Our zircon U-Pb data provide the first evidence of Eocene magmatism in the Western Alps (42-41 Ma in Traversella), and demonstrate that magmatism started synchronously in different segments of the Alpine belt, when subduction was still active. Zircon U-Pb ages define younging trends perpendicular to the strike of the European slab, suggesting a progressive Eocene-Oligocene slab steepening. We propose that slab steepening enhanced the corner flow. This process was more effective near the torn edge of the European slab, and triggered Periadriatic magmatism in the absence of slab breakoff

Blastocerus dichotomus (Illger, 1815).

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Y chromosome microdeletions in infertile men with idiopathic oligo- or azoospermia

About 30–40% of male infertility is due to unknown reasons. Genetic contributions to the disruption of spermatogenesis are suggested and amongst the genetic factors studied, Y chromosome microdeletions represent the most common one. Screening for microdeletions in AZFa, b and c region of Y chromosome showed a big variation among different studies. The purpose of this study was to investigate the prevalence of such deletions in Saudi men. A total of 257 patients with idiopathic oligo- or azoospermia were screened for Y chromosome microdeletions by 19 markers in AZF region. Ten (3.9%) patients had chromosomal rearrangements, six of them showed sex chromosome abnormalities and four patients had apparently balanced autosomal rearrengements. Eight of the remaining 247 patients (3.2%) with a normal karyotype and no known causes of impaired spermatogenesis had Y chromosome microdeletions. Among these, six patients had deletions in AZFc region, one case had a deletion in AZFb and another had both AZFa and AZFc deletions. In conclusion, our study shows that Y chromosome microdeletions are low in our population. We also report for the first time a case with unique point deletions of AZFa and AZFc regions. The lower frequency of deletions in our study suggest that other genetic, epigenetic, nutritional and local factors may be responsible for idiopathic oligo- or azoospermia in the Saudi population

Association of Spermatogenic Failure with the b2/b3 Partial AZFc Deletion

Infertility affects around 1 in 10 men and in most cases the cause is unknown. The Y chromosome plays an important role in spermatogenesis and specific deletions of this chromosome, the AZF deletions, are associated with spermatogenic failure. Recently partial AZF deletions have been described but their association with spermatogenic failure is unclear. Here we screened a total of 339 men with idiopathic spermatogenic failure, and 256 normozoospermic ancestry-matched men for chromosome microdeletions including AZFa, AZFb, AZFc, and the AZFc partial deletions (gr/gr, b1/b3 and b2/b3)

Antamanide, a Derivative of Amanita phalloides, Is a Novel Inhibitor of the Mitochondrial Permeability Transition Pore

Antamanide is a cyclic decapeptide derived from the fungus Amanita phalloides. Here we show that antamanide inhibits the mitochondrial permeability transition pore, a central effector of cell death induction, by targeting the pore regulator cyclophilin D. Indeed, (i) permeability transition pore inhibition by antamanide is not additive with the cyclophilin D-binding drug cyclosporin A, (ii) the inhibitory action of antamanide on the pore requires phosphate, as previously shown for cyclosporin A; (iii) antamanide is ineffective in mitochondria or cells derived from cyclophilin D null animals, and (iv) abolishes CyP-D peptidyl-prolyl cis-trans isomerase activity. Permeability transition pore inhibition by antamanide needs two critical residues in the peptide ring, Phe6 and Phe9, and is additive with ubiquinone 0, which acts on the pore in a cyclophilin D-independent fashion. Antamanide also abrogates mitochondrial depolarization and the ensuing cell death caused by two well-characterized pore inducers, clotrimazole and a hexokinase II N-terminal peptide. Our findings have implications for the comprehension of cyclophilin D activity on the permeability transition pore and for the development of novel pore-targeting drugs exploitable as cell death inhibitors

ICF, An Immunodeficiency Syndrome: DNA Methyltransferase 3B Involvement, Chromosome Anomalies, and Gene Dysregulation

The immunodeficiency, centromeric region instability, and facial anomalies syndrome (ICF) is the only disease known to result from a mutated DNA methyltransferase gene, namely, DNMT3B. Characteristic of this recessive disease are decreases in serum immunoglobulins despite the presence of B cells and, in the juxtacentromeric heterochromatin of chromosomes 1 and 16, chromatin decondensation, distinctive rearrangements, and satellite DNA hypomethylation. Although DNMT3B is involved in specific associations with histone deacetylases, HP1, other DNMTs, chromatin remodelling proteins, condensin, and other nuclear proteins, it is probably the partial loss of catalytic activity that is responsible for the disease. In microarray experiments and real-time RT-PCR assays, we observed significant differences in RNA levels from ICF vs. control lymphoblasts for pro- and anti-apoptotic genes (BCL2L10, CASP1, and PTPN13); nitrous oxide, carbon monoxide, NF-κB, and TNFa signalling pathway genes (PRKCH, GUCY1A3, GUCY1B3, MAPK13; HMOX1, and MAP4K4); and transcription control genes (NR2F2 and SMARCA2). This gene dysregulation could contribute to the immunodeficiency and other symptoms of ICF and might result from the limited losses of DNA methylation although ICF-related promoter hypomethylation was not observed for six of the above examined genes. We propose that hypomethylation of satellite 2at1qh and 16qh might provoke this dysregulation gene expression by trans effects from altered sequestration of transcription factors, changes in nuclear architecture, or expression of noncoding RNAs