Palaeozoic-Recent geological development and uplift of the Amanos Mountains (S Turkey) in the critically located northwesternmost corner of the Arabian continent

<p>We have carried out a several-year-long study of the Amanos Mountains, on the basis of which we present new sedimentary and structural evidence, which we combine with existing data, to produce the first comprehensive synthesis in the regional geological setting. The ca. N-S-trending Amanos Mountains are located at the northwesternmost edge of the Arabian plate, near the intersection of the African and Eurasian plates. Mixed siliciclastic-carbonate sediments accumulated on the north-Gondwana margin during the Palaeozoic. Triassic rift-related sedimentation was followed by platform carbonate deposition during Jurassic-Cretaceous. Late Cretaceous was characterised by platform collapse and southward emplacement of melanges and a supra-subduction zone ophiolite. Latest Cretaceous transgressive shallow-water carbonates gave way to deeper-water deposits during Palaeocene-Eocene. Eocene southward compression, reflecting initial collision, resulted in open folding, reverse faulting and duplexing. Fluvial, lagoonal and shallow-marine carbonates accumulated during Late Oligocene(?)-Early Miocene, associated with basaltic magmatism. Intensifying collision during Mid-Miocene initiated a foreland basin that then infilled with deep-water siliciclastic gravity flows. Late Miocene-Early Pliocene compression created mountain-sized folds and thrusts, verging E in the north but SE in the south. The resulting surface uplift triggered deposition of huge alluvial outwash fans in the west. Smaller alluvial fans formed along both mountain flanks during the Pleistocene after major surface uplift ended. Pliocene-Pleistocene alluvium was tilted towards the mountain front in the west. Strike-slip/transtension along the East Anatolian Transform Fault and localised sub-horizontal Quaternary basaltic volcanism in the region reflect regional transtension during Late Pliocene-Pleistocene (<4 Ma).</p

Global Classification of Mast Cell Activation Disorders:An ICD-10-CM–Adjusted Proposal of the ECNM-AIM Consortium

Mast cell activation (MCA) is common and occurs in a number of pathologic conditions, including IgE-dependent and independent allergic reactions, atopic disorders, autoimmune processes, and mastocytosis. In a subset of patients, no underlying disease and no known trigger of MCA are found. When the symptoms are severe, systemic, and recurrent, and accompanied by a diagnostic increase in the serum tryptase level or other mast cell mediators, an MCA syndrome (MCAS) may be diagnosed. In these patients, the symptoms typically respond to drugs suppressing MCA, mediator production in mast cells, or mediator effects. In each case, diagnostic consensus criteria must be fulfilled to diagnose MCAS. In other patients, MCA may be local, less severe, or less acute, or may be suspected but not confirmed, so that the diagnostic criteria of MCAS are not fulfilled. In these patients, it may be difficult to prove MCA, for example, by measuring multiple mast cell mediators or basophil activation, the latter as a surrogate of IgE-dependent hypersensitivity. However, validated diagnostic criteria for implicating suspected MCA behind such conditions are lacking, even if some of these conditions have recently been assigned to an International Classification of Diseases-10-Clinical Modification code (ICD-10-CM). In this article, we discuss diagnostic features and criteria and propose a ICD-10-CM–adjusted classification for disorders associated with MCA, herein referred to as MCA disorders (MCADs), with special emphasis on the delineation between confirmed MCAS, MCAD not fulfilling MCAS criteria, and suspected MCAD that is not present. In addition, we discuss the discrimination between overt MCAD and predisposing conditions, such as atopic states, mastocytosis, and hereditary alpha tryptasemia.</p

Flavaglines Alleviate Doxorubicin Cardiotoxicity: Implication of Hsp27

Background: Despite its effectiveness in the treatment of various cancers, the use of doxorubicin is limited by a potentially fatal cardiomyopathy. Prevention of this cardiotoxicity remains a critical issue in clinical oncology. We hypothesized that flavaglines, a family of natural compounds that display potent neuroprotective effects, may also alleviate doxorubicininduced cardiotoxicity. Methodology/Principal Findings: Our in vitro data established that a pretreatment with flavaglines significantly increased viability of doxorubicin-injured H9c2 cardiomyocytes as demonstrated by annexin V, TUNEL and active caspase-3 assays. We demonstrated also that phosphorylation of the small heat shock protein Hsp27 is involved in the mechanism by which flavaglines display their cardioprotective effect. Furthermore, knocking-down Hsp27 in H9c2 cardiomyocytes completely reversed this cardioprotection. Administration of our lead compound (FL3) to mice attenuated cardiomyocyte apoptosis and cardiac fibrosis, as reflected by a 50 % decrease of mortality. Conclusions/Significance: These results suggest a prophylactic potential of flavaglines to prevent doxorubicin-induce

Revisiting the optical properties of the FMO protein

We review the optical properties of the FMO complex as found by spectroscopic studies of the Qy band over the last two decades. This article emphasizes the different methods used, both experimental and theoretical, to elucidate the excitonic structure and dynamics of this pigment–protein complex

Fulminan hepatik yetmezlikle başvuran hemofagositik sendromlu bir olgu

Hemofagositik lenfohistiyositoz, ateş, parısitopeni, hepatosplenomegali ve kemik iliği, karaciğer ya da lenf nodları gibi doku ve organlarda hemofagositozla karakterize nadir görülen bir klinik tablodur. Ağır karaciğer yetmezliği ise önceden bilinen karaciğer hastalığı olmayan kişilerde hepatositlerin masif nekrozu ya da ağır fonksiyon kaybına bağlı gelişen klinik bir hastalık tablosudur. Hemofagositik lenfohistiyositozda karaciğer tutulumuna ait bulgular yaygın olarak görülmekte ve hastalığın seyrinde karaciğer yetmezliği tablosu da olabilmektedir. Ancak hastalığın ağır karaciğer yetmezliği tablosuyla başlaması çok iyi tanım/anmamıştır. Burada ağır karaciğer yetmezliği tablosuyla başvuran 9 yaşında bir kız olgu sunulmakta ve çocuklarda ağır karaciğer yetmezliğinin ayırıcı tanısında hemofagositik lenfohistiyositozun da düşünülmesi gerektiği vurgulanmaktadır.Hemophagocytic lymphohistiocytosis (HLH) is an uncommon clinical entity characterized by fever, pancytopenia, hepatosplenomegaly and hemophagocytosis in bone marrow, liver or lymph nodes. Fulminant hepatic failure (FHF) is a clinical syndrome resulting from massive necrosis of hepatocytes or severe functional impairment of hepatocytes in a patient who does not have a pre-existing liver disease. Hepatic manifestations are common in hemophagocytic lymphohistiocytosis and overt hepatic failure may occur, but initial presentation as fulminant hepatic failure is not well recognized. We report the case of a 9 year old girl presented with fulminant hepatic failure and &quot;Hemophagocytic lymphohistiocytosis&quot; should be considered in the differential diagnosis of fulminant hepatic failure in children