Ahnas El Medineh: The Tomb of Paheri at El Kab

Memoir of two excavations at Ahnas.https://knowledge.e.southern.edu/kweeks_coll/1036/thumbnail.jp

The Particle Spectrum of Heterotic Compactifications

Techniques are presented for computing the cohomology of stable, holomorphic vector bundles over elliptically fibered Calabi-Yau threefolds. These cohomology groups explicitly determine the spectrum of the low energy, four-dimensional theory. Generic points in vector bundle moduli space manifest an identical spectrum. However, it is shown that on subsets of moduli space of co-dimension one or higher, the spectrum can abruptly jump to many different values. Both analytic and numerical data illustrating this phenomenon are presented. This result opens the possibility of tunneling or phase transitions between different particle spectra in the same heterotic compactification. In the course of this discussion, a classification of SU(5) GUT theories within a specific context is presented.Comment: 77 pages, 3 figure

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes angiogenesis and ischemia-induced neovascularization via NADPH oxidase 4 (NOX4) and nitric oxide-dependent mechanisms

Background: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has the ability to inhibit angiogenesis by inducing endothelial cell death, as well as being able to promote pro-angiogenic activity in vitro. These seemingly opposite effects make its role in ischemic disease unclear. Using Trail(-/-) and wildtype mice, we sought to determine the role of TRAIL in angiogenesis and neovascularization following hindlimb ischemia. Methods and Results: Reduced vascularization assessed by real-time 3-dimensional Vevo ultrasound imaging and CD31 staining was evident in Trail(-/-) mice after ischemia, and associated with reduced capillary formation and increased apoptosis. Notably, adenoviral TRAIL administration significantly improved limb perfusion, capillary density, and vascular smooth-muscle cell content in both Trail(-/-) and wildtype mice. Fibroblast growth factor-2, a potent angiogenic factor, increased TRAIL expression in human microvascular endothelial cell-1, with fibroblast growth factor-2-mediated proliferation, migration, and tubule formation inhibited with TRAIL siRNA. Both fibroblast growth factor-2 and TRAIL significantly increased NADPH oxidase 4 (NOX4) expression. TRAIL-inducible angiogenic activity in vitro was inhibited with siRNAs targeting NOX4, and consistent with this, NOX4 mRNA was reduced in 3-day ischemic hindlimbs of Trail(-/-) mice. Furthermore, TRAIL-induced proliferation, migration, and tubule formation was blocked by scavenging H2O2, or by inhibiting nitric oxide synthase activity. Importantly, TRAIL-inducible endothelial nitric oxide synthase phosphorylation at Ser-1177 and intracellular human microvascular endothelial cell-1 cell nitric oxide levels were NOX4 dependent. Conclusions: This is the first report demonstrating that TRAIL can promote angiogenesis following hindlimb ischemia in vivo. The angiogenic effect of TRAIL on human microvascular endothelial cell-1 cells is downstream of fibroblast growth factor-2, involving NOX4 and nitric oxide signaling. These data have significant therapeutic implications, such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with cardiovascular disease and diabetes.Belinda Ann Di Bartolo, Siân Peta Cartland, Leonel Prado-Lourenco, Thomas Scott Griffith, Carmine Gentile, Jayant Ravindran, Nor Saadah Muhammad Azahri, Thuan Thai, Amanda Wing Shee Yeung, Shane Ross Thomas, Mary Meltem Kavurm

A comparison of conventional and 137 Cs-based estimates of soil erosion rates on arable and grassland across lowland England and Wales

Soils deliver a range of ecosystem services and underpin conventional global food production which must increase to feed the projected growth in human population. Although soil erosion by water and subsequent sediment delivery to rivers are natural processes, anthropogenic pressures, including modern farming practices and management, have accelerated soil erosion rates on both arable and grassland. A range of approaches can be used to assess and document soil erosion rates and, in the case of the UK, these mainly comprise the 137Cs-based approach, conventional surveys using volumetric measurements, integration of information on suspended sediment flux, fine sediment source apportionment and landscape sediment retention and traditional bounded hydrological monitoring at edge-of-field using experimental platforms. We compare the erosion rates for arable and grassland in lowland England assessed by these different techniques. Rates assessed by volumetric measurements are similar to those generated by integrating information on suspended sediment flux, sources and landscape retention, but are much less than those estimated by the 137Cs-based approach; of the order of one magnitude less for arable land. The 137Cs approach assumes an initial distribution of 137Cs uniformly spread across the landscape and relates the sampled distribution to erosion, but other (transport) processes are also involved and their representation in the calibration procedures remains problematic. We suggest that the 137Cs technique needs to be validated more rigorously and conversion models re-calibrated. As things stand, rates of erosion based on the distribution of 137Cs may well overstate the severity of the problem in lowland Britain and, therefore, are not a reliable indicator of water erosion rates

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

Comprehensive analysis of epigenetic clocks reveals associations between disproportionate biological ageing and hippocampal volume

The concept of age acceleration, the difference between biological age and chronological age, is of growing interest, particularly with respect to age-related disorders, such as Alzheimer’s Disease (AD). Whilst studies have reported associations with AD risk and related phenotypes, there remains a lack of consensus on these associations. Here we aimed to comprehensively investigate the relationship between five recognised measures of age acceleration, based on DNA methylation patterns (DNAm age), and cross-sectional and longitudinal cognition and AD-related neuroimaging phenotypes (volumetric MRI and Amyloid-β PET) in the Australian Imaging, Biomarkers and Lifestyle (AIBL) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Significant associations were observed between age acceleration using the Hannum epigenetic clock and cross-sectional hippocampal volume in AIBL and replicated in ADNI. In AIBL, several other findings were observed cross-sectionally, including a significant association between hippocampal volume and the Hannum and Phenoage epigenetic clocks. Further, significant associations were also observed between hippocampal volume and the Zhang and Phenoage epigenetic clocks within Amyloid-β positive individuals. However, these were not validated within the ADNI cohort. No associations between age acceleration and other Alzheimer’s disease-related phenotypes, including measures of cognition or brain Amyloid-β burden, were observed, and there was no association with longitudinal change in any phenotype. This study presents a link between age acceleration, as determined using DNA methylation, and hippocampal volume that was statistically significant across two highly characterised cohorts. The results presented in this study contribute to a growing literature that supports the role of epigenetic modifications in ageing and AD-related phenotypes