40 research outputs found

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

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    <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

    Comparisons between Tethyan Anorthosite-bearing Ophiolites and Archean Anorthosite-bearing Layered Intrusions: Implications for Archean Geodynamic Processes

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    Elucidating the petrogenesis and geodynamic setting(s) of anorthosites in Archean layered intrusions and Tethyan ophiolites has significant implications for crustal evolution and growth throughout Earth history. Archean anorthosite-bearing layered intrusions occur on every continent. Tethyan ophiolites occur in Europe, Africa, and Asia. In this contribution, the field, petrographic, petrological, and geochemical characteristics of 100 Tethyan anorthosite-bearing ophiolites and 155 Archean anorthosite-bearing layered intrusions are compared. Tethyan anorthosite-bearing ophiolites range from Devonian to Paleocene in age, are variably composite, contain anorthosites with highly calcic (An44-100) plagioclase and magmatic amphibole. These ophiolites formed predominantly at convergent plate margins, with some forming in mid-ocean ridge, continental rift, and mantle plume settings. The predominantly convergent plate margin tectonic setting of Tethyan anorthosite-bearing ophiolites is indicated by negative Nb and Ti anomalies and magmatic amphibole. Archean anorthosite-bearing layered intrusions are Eoarchean to Neoarchean in age, have megacrystic anorthosites with highly calcic (An20-100) plagioclase and magmatic amphibole and are interlayered with gabbros and leucogabbros and intrude pillow basalts. These Archean layered intrusions are interpreted to have predominantly formed at convergent plate margins, with the remainder forming in mantle plume, continental rift, oceanic plateau, post-orogenic, anorogenic, mid-ocean ridge, and passive continental margin settings. These layered intrusions predominantly crystallized from hydrous Ca- and Al-rich tholeiitic magmas. The field, petrographic and geochemical similarities between Archean and Tethyan anorthosites indicate that they were produced by similar geodynamic processes mainly in suprasubduction zone settings. We suggest that Archean anorthosite-bearing layered intrusions and spatially associated greenstone belts represent dismembered subduction-related Archean ophiolites

    Investigation of anticancer mechanism of oleuropein via cell cycle and apoptotic pathways in SH-SY5Y neuroblastoma cells.

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    Neuroblastoma is one of the most common types of pediatric tumors that can spread quickly in neuronal tissues. Oleuropein which is active compound of olive leaves, belongs to polyphenols group and has antioxidant, anti-microbial, anti-inflammatory, anti-hypertensive and anti-carcinogenic effects. The aim of the study is to determine the therapeutic effects of oleuropein on cell proliferation, invasion, colony formation, cell cycle and apoptotic mechanisms in SH-SY5Y neuroblastoma cell line under in vitro conditions. The effect of oleuropein on cell viability was determined by XTT method. 84 cell cycle control and 84 apoptosis related genes were evaluated by RT-PCR. Effects of oleuropein on apoptosis were researched by TUNEL assay. Protein expressions were determined by western blot analysis. Effects of oleuropein on cell invasion, colony formation and migration were detected by matrigel-chamber, colony formation assay and wound-healing assay, respectively. IC50 value of oleuropein in SH-SY5Y cells was detected as 350 μM at 48th hours. It is determined that oleuropein causes cell cycle arrest by down-regulating of CylinD1,CylinD2,CyclinD3,CDK4,CDK6 and up-regulating of p53 and CDKN2A, CDKN2B, CDKN1A gene expressions. Oleuropein also induces apoptosis by inhibiting of Bcl-2 and activating of Bax,caspase-9 and caspase-3 gene expressions. Apoptotic cell ratio was found 36.4 ± 3.27% in oleuropein dose group. Oleuropein decreased invasion in SH-SY5Y cells and suppressed colony numbers in ratio of 53.6 ± 4.71%.Our results demonstrated that oleuropein can be a therapeutic agent in the treatment of neuroblastoma

    Assessment of the anticancer mechanism of ferulic acid via cell cycle and apoptotic pathways in human prostate cancer cell lines.

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    Studies on genetic changes underlying prostate cancer and the possible signaling pathways are getting increased day by day, and new treatment methods are being searched for. The aim of the present study is to investigate the effects of ferulic acid (FA), a phenolic compound, on cell cycle, apoptosis, invasion, and colony formation in the PC-3 and LNCaP prostate cancer cells. The effect of FA on cell viability was determined via a 2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide (XTT) method. Total RNA was isolated with Tri Reagent. Expression of 84 genes for both cell cycle and apoptosis separately was evaluated by reverse transcriptase PCR (RT-PCR). Protein expressions were evaluated by Western blot analysis. Furthermore, apoptotic effects of FA were observed with terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assay. Effects of FA on cell invasion and colony formation were determined using Matrigel chamber and colony assay, respectively. The half maximal inhibitory concentration (IC50) dose of FA was found to be 300 μM in PC-3 cells and 500 μM in LNCaP cells. According to RT-PCR results, it was observed that FA inhibited cell proliferation by increasing the gene expressions of ATR, ATM, CDKN1A, CDKN1B, E2F4, RB1, and TP53 and decreasing the gene expressions of CCND1, CCND2, CCND3, CDK2, CDK4, and CDK6 in PC-3 cells. On the other hand, it was seen that FA suppressed cell proliferation by increasing in the gene expressions of CASP1, CASP2, CASP8, CYCS, FAS, FASLG, and TRADD and decreasing in the gene expressions of BCL2 and XIAP in LNCaP cells. In this study, protein expression of CDK4 and BCL2 genes significantly decreased in these cells. It could induce apoptosis in PC-3 and LNCaP cells. Also, it was observed that FA suppressed the invasion in PC-3 and LNCaP cells. Moreover, it suppressed the colony formation. In conclusion, it has been observed that FA may lead to cell cycle arrest in PC-3 cells while it may cause apoptosis in LNCaP cells

    Localized surface plate modes via flexural Mie resonances

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    International audienceSurface-plasmon polaritons are naturally generated upon excitation of metals with high-frequency electromagnetic waves. However, the concept of spoof plasmons has made it possible to generate plasmoniclike effects in microwave electrodynamics, magnetics, and even acoustics. Similarly, in this paper, the concept of localized surface plate modes (SPMs) is introduced. It is demonstrated that SPMs can be generated on a two-dimensional (clamped or stress-free) cylindrical surface with subwavelength corrugations, which resides on a thin elastic plate, under excitation by an incident flexural plane wave. Numerical characterization of this corrugated rigid structure shows that it is elastically equivalent to a cylindrical scatterer with dispersive but uniformly negative flexural rigidity. This, indeed, suggests that plasmoniclike elastic materials can be engineered with potential applications in various areas including earthquake sensing and elastic imaging and cloaking

    Extract of Calvatia gigantea inhibits proliferation of A549 human lung cancer cells.

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    In this study, in order to investigate the anticancer mechanism of Calvatia gigantea extract, edible mushroom species, which belong to Lycoperdaceae family, changes of CCND1, CCND2, CDK4, p21, Akt, Bax, Bcl-2, p53, caspase-3 and caspase-9 were evaluated in A549 lung cancer cells. Cytotoxic effect of C. gigantea extract was evaluated by using XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5 carboxanilide). The C. gigantea extract was treated in a time and dose dependent manner within the range 25 μg/ml-2 mg/ml to determine the IC50 dose. IC50 dose for C. gigantea extract was detected as 500 μg/ml for 72 h. According to expression results, while CCND1, CCND2, CDK4, Akt and Bcl-2 expression clearly decreased, Bax, p53, caspase-3 and caspase-9 expression clearly increased in the dose group cells (A549 cells treated with 500 μg/ml dose of C. gigantea extract for 72 h). However, there was no change in p21 expression. C. gigantea extract induced cell cycle arrest and apoptosis by decreasing the CCND1, CCND2, CDK4, Akt and Bcl-2 expression and by increasing Bax, p53, caspase-3 and caspase-9 expression in A549 cells. Mushrooms are eukaryotic organisms heavily used because of their supposedly anticancer effect. Many mushroom species have been used for medical purposes, as a result of also having many effects such as antibiotic, antiviral and anticancer effects. It is thought that the C. gigantea extract may be a significant agent for treatment of lung cancer as a single agent or in combination with other drugs

    Anti-tumor effects of bemiparin in HepG2 and MIA PaCa-2 cells.

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    Recent researches have demonstrated improved survival in oncologic patients treated with low molecular weight heparins (LMWHs) which are anticoagulant drugs. We evaluated "second generation" LMWH bemiparin and its in vitro anti-tumor effects on HepG2 hepatocellular carcinoma and MIA PaCa-2 cancer cells. The aim of the study is to investigate anti-cancer mechanism of bemiparin in HepG2 and Mia-Paca-2 cancer cells. Cytotoxic effects of bemiparin were determined by XTT assay. IC50 dose of bemiparin was found to be 200 IU/mL in the 48th hour in the MiaPaCa-2 cell line and 50 IU/mL in the 48th hour in the HepG2 cell line. CCND1 (cyclin D1), CDK4, CDK6, p21, p16, p53, caspase-3, caspase-9, caspase-8, Bcl-2, BID, DR4, DR5, FADD, TRADD, Bax, gene mRNA expressions were evaluated by Real-time PCR. Real-time PCR analysis showed that CCND1 expression was reduced in HepG2 dose the group cells when compared with the control group cells and p53, caspase-3, caspase p21, caspase-8 and expressions were increased in the dose group cells when compared with the control group cells. CCND1, CDK4 and CDK6 expressions were reduced in MIA PaCa-2 dose group cells when compared with the control group cells and p53 expression was increased in the dose group cells when compared with the control group cells. Other expressions of genes were found statistically insignificant both of cell lines. It was found that bemiparin in HepG2 and MIA PaCa-2 cells suppressed invasion, migration, and colony formation by using matrigel invasion chamber, and colony formation assay, respectively. In conclusion, it is thought that bemiparin indicates anti-tumor activity by affecting cell cycle arrest, apoptosis, invasion, migration, and colony formation on cancer cells
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