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

Halogen ligth thermogravimetric technique for determining the retained water in fine aggregates used for concrete mixing design

[EN] Measuring the rate of water retention of the aggregates used in mortars and concrete is required to achieve a good mix design. The water retention, specifically absorption, is used to keep constant the water/cement ratio. This paper focuses on the study of a new technique for measuring retained water in fine aggregates. In order to obtain results, the procedure described in the existing standards takes more than 24 h. Additionally, it involves high consumption of heat energy due to the use of drying ovens. Furthermore, the results obtained remain highly variable and therefore discussed by the scientific community.In this research, a novel technique based on a halogen moisture analyzer was implemented. The technique was assessed using an experiment design with a surface response model. The most important factors and levels were identified together with the interactions between them. Finally, the model was validated and the results obtained with this technique were compared with those obtained by conventional techniques in order to verify that they were equivalent.Arias Jaramillo, Y.; Paya Bernabeu, JJ.; Ochoa Botero, JC. (2015). Halogen ligth thermogravimetric technique for determining the retained water in fine aggregates used for concrete mixing design. Journal of Thermal Analysis and Calorimetry: an international forum for thermal studies. 123:127-134. doi:10.1007/s10973-015-4902-8S127134123Djerbi Tegguer A. Determining the water absorption of recycled aggregates utilizing hydrostatic weighing approach. Constr Build Mater. 2012;27:112–6.Kasemchaisiri R, Tangtermsirikul S. A method to determine water retainability of porous fine aggregate for design and quality control of fresh concrete. Constr Build Mater. 2007;21:1322–34.Gonilho Pereira C, Castro-Gomes J, Pereira de Oliveira L. Influence of natural coarse aggregate size, mineralogy and water content on the permeability of structural concrete. Constr Build Mater. 2009;23:602–8.Cortas R, Roiziére E, Staquet S, Hamami A, Delplancke-Ogletree M. Effect of the water saturation of aggregates on the shrinkage induced cracking risk of concrete at early age. Cem Concr Compos. 2014;50:1–9.Black R. The determination of specific gravity using Siphon-Can method. Cem Concr Aggreg. 1986;8:46–50.Saxer E. A direct method of determining absorption and specific gravity of aggregates. 1956;2.Hughes B, Famili H., Part 1—Absorption of concrete aggregates, Part 2—saturated air techniques for determining the absorption of aggregates. In: Absorptions of concrete aggregates. Birmingham University; 1971.Tam VWY, Gao XF, Tam CM, Chan CH. New approach in measuring water absorption of recycled aggregates. Constr Build Mater. 2008;22:364–9.Balcedowiak W. Phase analysis of high-calcium line by TG. J Therm Anal Calorim. 2000;60:70–7.Mendoza O, Tobón JI. An alternative thermal method for identification of pozzolanic activity in Ca(OH)2/pozzolan pastes. J Therm Anal Calorim. 2013;114:589–96.Kosmatka SH, Kerkhoff B, Panarese W, MacLeod NF, McGrath RJ, Design and control of concrete mixtures. 7rd ed. Cement association of Canada. 2002. pp. 88.Cárdenas JI, Restrepo C. Patrimonio geológico y patrimonio minero de la cuenca carbonífera del suroeste antioqueño, Colombia. Boletín de ciencias de la tierra. 2006;18:91–102 ISSN 0120-3630 .Klein NS, Aguado A, Tollares-Carbonari BM, Real LV. Prediction of the water absorption by aggregates over time: modelling through the use of value function and experimental validation. Constr Build Mater. 2014;69:213–20

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

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

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

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

Committing curriculum time to science literacy: The benefits from science based media resources

Kaposi sarcoma-associated herpesvirus (KSHV) is linked with the development of Kaposi sarcoma and the B lymphocyte disorders primary effusion lymphoma (PEL) and multi-centric Castleman disease. T cell immunity limits KSHV infection and disease, however the virus employs multiple mechanisms to inhibit efficient control by these effectors. Thus KSHV-specific CD4+ T cells poorly recognize most PEL cells and even where they can, they are unable to kill them. To make KSHV-infected cells more sensitive to T cell control we treated PEL cells with the thymidine analogue azidothymidine (AZT), which sensitizes PEL lines to Fas-ligand and TRAIL challenge; effector mechanisms which T cells use. PELs co-cultured with KSHV-specific CD4+ T cells in the absence of AZT showed no control of PEL outgrowth. However in the presence of AZT PEL outgrowth was controlled in an MHC-restricted manner. To investigate how AZT sensitizes PELs to immune control we first examined BJAB cells transduced with individual KSHV-latent genes for their ability to resist apoptosis mediated by stimuli delivered through Fas and TRAIL receptors. This showed that in addition to the previously described vFLIP protein, expression of vIRF3 also inhibited apoptosis delivered by these stimuli. Importantly vIRF3 mediated protection from these apoptotic stimuli was inhibited in the presence of AZT as was a second vIRF3 associated phenotype, the downregulation of surface MHC class II. Although both vFLIP and vIRF3 are expressed in PELs, we propose that inhibiting vIRF3 function with AZT may be sufficient to restore T cell control of these tumor cells

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