Ancient agriculture in Southeast Arabia: A three thousand year record of runoff farming from central Oman (Rustaq)

Runoff farming is a key hydro-agricultural strategy that has proven efficient in arid areas. Research in Arabia on the function, development, maintenance, durability and abandonment of this technology is scarce. A multiproxy investigation (cartography, sedimentology, pedology, geochemistry, paleo-ecology and chronology) was conducted on a recently abandoned terraced area in Rustaq, Northern Oman. The aim was to characterize the formation, function and management of this runoff system and the driving factors behind its success. Cycles of cultivation were identified during the Iron Age II/III periods (specifically 750–450 BCE), the Early Pre-Islamic Period (PIR) (specifically 350–200 BCE), the Early and Middle Islamic periods (specifically 8–10th C CE, 13th-14th C CE) and the late Islamic period (specifically 17th C CE and later). This expansion and perenniality was possible thanks to: 1- available water (local to micro-regional orogenic precipitation despite a regional aridification during these periods); 2- suitable soils (weathered geological outcrops, probable aeolian /dust particles); 3- a system of production combining crops and husbandry; 4- a progressive increase in agricultural specialization (crops grown and techniques) in parallel with a diversification in hydraulic technology. These results are to some degree in accordance with known phases of settlement intensification and economic growth, but also reveal the persistence of small-scale rural livelihoods during periods of harsh conditions for which archaeological traces are very scarce

Inhibition of the Intrinsic but Not the Extrinsic Apoptosis Pathway Accelerates and Drives Myc-Driven Tumorigenesis Towards Acute Myeloid Leukemia

Myc plays an important role in tumor development, including acute myeloid leukemia (AML). However, MYC is also a powerful inducer of apoptosis, which is one of the major failsafe programs to prevent cancer development. To clarify the relative importance of the extrinsic (death receptor-mediated) versus the intrinsic (mitochondrial) pathway of apoptosis in MYC-driven AML, we coexpressed MYC together with anti-apoptotic proteins of relevance for AML; BCL-XL/BCL-2 (inhibiting the intrinsic pathway) or FLIPL (inhibiting the extrinsic pathway), in hematopoietic stems cells (HSCs). Transplantation of HSCs expressing MYC into syngeneic recipient mice resulted in development of AML and T-cell lymphomas within 7–9 weeks as expected. Importantly, coexpression of MYC together with BCL-XL/BCL-2 resulted in strongly accelerated kinetics and favored tumor development towards aggressive AML. In contrast, coexpression of MYC and FLIPL did neither accelerate tumorigenesis nor change the ratio of AML versus T-cell lymphoma. However, a change in distribution of immature CD4+CD8+ versus mature CD4+ T-cell lymphoma was observed in MYC/FLIPL mice, possibly as a result of increased survival of the CD4+ population, but this did not significantly affect the outcome of the disease. In conclusion, our findings provide direct evidence that BCL-XL and BCL-2 but not FLIPL acts in synergy with MYC to drive AML development

Large Anomalous Hall effect in a silicon-based magnetic semiconductor

Magnetic semiconductors are attracting high interest because of their potential use for spintronics, a new technology which merges electronics and manipulation of conduction electron spins. (GaMn)As and (GaMn)N have recently emerged as the most popular materials for this new technology. While Curie temperatures are rising towards room temperature, these materials can only be fabricated in thin film form, are heavily defective, and are not obviously compatible with Si. We show here that it is productive to consider transition metal monosilicides as potential alternatives. In particular, we report the discovery that the bulk metallic magnets derived from doping the narrow gap insulator FeSi with Co share the very high anomalous Hall conductance of (GaMn)As, while displaying Curie temperatures as high as 53 K. Our work opens up a new arena for spintronics, involving a bulk material based only on transition metals and Si, and which we have proven to display a variety of large magnetic field effects on easily measured electrical properties.Comment: 19 pages with 5 figure

The role of c-FLIP splice variants in urothelial tumours

Deregulation of apoptosis is common in cancer and is often caused by overexpression of anti-apoptotic proteins in tumour cells. One important regulator of apoptosis is the cellular FLICE-inhibitory protein (c-FLIP), which is overexpressed, for example, in melanoma and Hodgkin's lymphoma cells. Here, we addressed the question whether deregulated c-FLIP expression in urothelial carcinoma impinges on the ability of death ligands to induce apoptosis. In particular, we investigated the role of the c-FLIP splice variants c-FLIPlong (c-FLIPL) and c-FLIPshort (c-FLIPS), which can have opposing functions. We observed diminished expression of the c-FLIPL isoform in urothelial carcinoma tissues as well as in established carcinoma cell lines compared with normal urothelial tissues and cells, whereas c-FLIPS was unchanged. Overexpression and RNA interference studies in urothelial cell lines nevertheless demonstrated that c-FLIP remained a crucial factor conferring resistance towards induction of apoptosis by death ligands CD95L and TRAIL. Isoform-specific RNA interference showed c-FLIPL to be of particular importance. Thus, urothelial carcinoma cells appear to fine-tune c-FLIP expression to a level sufficient for protection against activation of apoptosis by the extrinsic pathway. Therefore, targeting c-FLIP, and especially the c-FLIPL isoform, may facilitate apoptosis-based therapies of bladder cancer in otherwise resistant tumours

Fermi-liquid instabilities at magnetic quantum phase transitions

This review discusses instabilities of the Fermi-liquid state of conduction electrons in metals with particular emphasis on magnetic quantum critical points. Both the existing theoretical concepts and experimental data on selected materials are presented; with the aim of assessing the validity of presently available theory. After briefly recalling the fundamentals of Fermi-liquid theory, the local Fermi-liquid state in quantum impurity models and their lattice versions is described. Next, the scaling concepts applicable to quantum phase transitions are presented. The Hertz-Millis-Moriya theory of quantum phase transitions is described in detail. The breakdown of the latter is analyzed in several examples. In the final part experimental data on heavy-fermion materials and transition-metal alloys are reviewed and confronted with existing theory.Comment: 62 pages, 29 figs, review article for Rev. Mod. Phys; (v2) discussion extended, refs added; (v3) shortened; final version as publishe

TAK1 Is Required for Survival of Mouse Fibroblasts Treated with TRAIL, and Does So by NF-κB Dependent Induction of cFLIPL

Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is known as a “death ligand”—a member of the TNF superfamily that binds to receptors bearing death domains. As well as causing apoptosis of certain types of tumor cells, TRAIL can activate both NF-κB and JNK signalling pathways. To determine the role of TGF-β-Activated Kinase-1 (TAK1) in TRAIL signalling, we analyzed the effects of adding TRAIL to mouse embryonic fibroblasts (MEFs) derived from TAK1 conditional knockout mice. TAK1−/− MEFs were significantly more sensitive to killing by TRAIL than wild-type MEFs, and failed to activate NF-κB or JNK. Overexpression of IKK2-EE, a constitutive activator of NF-κB, protected TAK1−/− MEFs against TRAIL killing, suggesting that TAK1 activation of NF-κB is critical for the viability of cells treated with TRAIL. Consistent with this model, TRAIL failed to induce the survival genes cIAP2 and cFlipL in the absence of TAK1, whereas activation of NF-κB by IKK2-EE restored the levels of both proteins. Moreover, ectopic expression of cFlipL, but not cIAP2, in TAK1−/− MEFs strongly inhibited TRAIL-induced cell death. These results indicate that cells that survive TRAIL treatment may do so by activation of a TAK1–NF-κB pathway that drives expression of cFlipL, and suggest that TAK1 may be a good target for overcoming TRAIL resistance

Gene Expression Analysis Implicates a Death Receptor Pathway in Schizophrenia Pathology

An increase in apoptotic events may underlie neuropathology in schizophrenia. By data-mining approaches, we identified significant expression changes in death receptor signaling pathways in the dorsolateral prefrontal cortex (DLPFC) of patients with schizophrenia, particularly implicating the Tumor Necrosis Factor Superfamily member 6 (FAS) receptor and the Tumor Necrosis Factor [ligand] Superfamily member 13 (TNFSF13) in schizophrenia. We sought to confirm and replicate in an independent tissue collection the noted mRNA changes with quantitative real-time RT-PCR. To test for regional and diagnostic specificity, tissue from orbital frontal cortex (OFC) was examined and a bipolar disorder group included. In schizophrenia, we confirmed and replicated significantly increased expression of TNFSF13 mRNA in the DLPFC. Also, a significantly larger proportion of subjects in the schizophrenia group had elevated FAS receptor expression in the DLPFC relative to unaffected controls. These changes were not observed in the bipolar disorder group. In the OFC, there were no significant differences in TNFSF13 or FAS receptor mRNA expression. Decreases in BH3 interacting domain death agonist (BID) mRNA transcript levels were found in the schizophrenia and bipolar disorder groups affecting both the DLPFC and the OFC. We tested if TNFSF13 mRNA expression correlated with neuronal mRNAs in the DLPFC, and found significant negative correlations with interneuron markers, parvalbumin and somatostatin, and a positive correlation with PPP1R9B (spinophilin), but not DLG4 (PSD-95). The expression of TNFSF13 mRNA in DLPFC correlated negatively with tissue pH, but decreasing pH in cultured cells did not cause increased TNFSF13 mRNA nor did exogenous TNFSF13 decrease pH. We concluded that increased TNFSF13 expression may be one of several cell-death cytokine abnormalities that contribute to the observed brain pathology in schizophrenia, and while increased TNFSF13 may be associated with lower brain pH, the change is not necessarily causally related to brain pH

Alien Registration- Gaoosselin, Mary O. (Augusta, Kennebec County)

https://digitalmaine.com/alien_docs/18929/thumbnail.jp

Palaeogeographical and palaeoenvironmental reconstruction of the Medjerda delta (Tunisia) during the Holocene

International audienceThe progradation of the Medjerda delta has been the subject of many studies since the 19th century. Thescale and the rapidity of this phenomenon interested researchers in various fields early on, such asgeomorphology, geology, palaeogeography, history, archaeology, or geoarchaeology. Indeed, the deltaprograded by around 10 km over 3 millennia. At the time of its foundation supposedly at the end of the12th century BC, the Phoenician city of Utica was located on a promontory bathed by the sea, but thesediments carried by the Medjerda progressively sealed the bay, leaving the tip of the Utica promontorynow 10 km inland. This area is therefore an exception to the general pattern along the Tunisian coast,since as over the same period everywhere else there is a regression of the coastline, owing to a sea levelrise of several decimeters. Based on multi-proxy analyses of two coring transects, this paper aims toreconstruct the palaeoenvironments and the palaeogeography of the Medjerda delta’s progradation sincethe mid-Holocene, some aspects of which are described in ancient sources. The results highlight inparticular an episode of high-intensity flooding around the 4th century AD, which is consistent withepisodes of high floods and an increase in sedimentation rates recorded in the watershed at the end ofthe Roman period. The gradual abandonment of the city of Utica can certainly be related to the activity ofthe Medjerda River, but our results show that it is because of an increase of fluvial sediment contributionin connection with an erosive crisis in the headwaters, and not because of the change of course of theriver, which had occurred long before