The heats of combustion of some rare-earth metals

A bomb calorimeter for measuring the heats of combustion of neodymium, samarium, gadolinium and erbium is described. The heats of combustion of these metals and the heats of formation of their oxides are reported

The Evolution of Central Volcanoes in Ultraslow Rift Systems : Constraints From D. Joao de Castro Seamount, Azores

The Dom Joao de Castro seamount in the Hirondelle Basin (Azores) is a central volcano on the ultraslow diverging Terceira Rift axis. The combination of structural and geochemical data provides insights into the evolution of central volcanoes in oceanic rift systems above the Azores melting anomaly. The orientation of fault scarps and volcanic structures at D. Joao de Castro and the adjacent Castro fissure zone indicate that the regional SW-NE extending stress field dominates the morphology of the NW Hirondelle Basin. The regional tectonic stress field controls the crustal melt pathways and leads to dike emplacement along fissure zones and the prevalent eruption of mafic lavas. The occurrence of mafic to felsic lavas at D. Joao de Castro gives evidence for both a deep and a shallow crustal melt reservoir generating a subordinate local stress field at the seamount. New Sr-Nd-Pb isotope data along with incompatible trace element ratios indicate that D. Joao de Castro and the Castro Ridges originated from similarly heterogeneous mantle source but did not form simultaneously. Our new model implies that central volcanoes along the Terceira Rift form by the growth of volcanic ridges and transitioned into circular edifices after magmatic systems generate local changes in the regional lithospheric stress field. The geometry of D. Joao de Castro and other magmatic systems along the Terceira Rift combined with the alkaline nature of the erupted lavas, and the large lithosphere thickness indicates that young oceanic rifts are more similar to continental rifts rather than mid-ocean ridges.Peer reviewe

Bone Marrow Stromal Cell Transplantation Mitigates Radiation-Induced Gastrointestinal Syndrome in Mice

Nuclear accidents and terrorism presents a serious threat for mass casualty. While bone-marrow transplantation might mitigate hematopoietic syndrome, currently there are no approved medical countermeasures to alleviate radiation-induced gastrointestinal syndrome (RIGS), resulting from direct cytocidal effects on intestinal stem cells (ISC) and crypt stromal cells. We examined whether bone marrow-derived adherent stromal cell transplantation (BMSCT) could restitute irradiated intestinal stem cells niche and mitigate radiation-induced gastrointestinal syndrome.Autologous bone marrow was cultured in mesenchymal basal medium and adherent cells were harvested for transplantation to C57Bl6 mice, 24 and 72 hours after lethal whole body irradiation (10.4 Gy) or abdominal irradiation (16-20 Gy) in a single fraction. Mesenchymal, endothelial and myeloid population were characterized by flow cytometry. Intestinal crypt regeneration and absorptive function was assessed by histopathology and xylose absorption assay, respectively. In contrast to 100% mortality in irradiated controls, BMSCT mitigated RIGS and rescued mice from radiation lethality after 18 Gy of abdominal irradiation or 10.4 Gy whole body irradiation with 100% survival (p<0.0007 and p<0.0009 respectively) beyond 25 days. Transplantation of enriched myeloid and non-myeloid fractions failed to improve survival. BMASCT induced ISC regeneration, restitution of the ISC niche and xylose absorption. Serum levels of intestinal radioprotective factors, such as, R-Spondin1, KGF, PDGF and FGF2, and anti-inflammatory cytokines were elevated, while inflammatory cytokines were down regulated.Mitigation of lethal intestinal injury, following high doses of irradiation, can be achieved by intravenous transplantation of marrow-derived stromal cells, including mesenchymal, endothelial and macrophage cell population. BMASCT increases blood levels of intestinal growth factors and induces regeneration of the irradiated host ISC niche, thus providing a platform to discover potential radiation mitigators and protectors for acute radiation syndromes and chemo-radiation therapy of abdominal malignancies

TLR9 Agonist Protects Mice from Radiation-Induced Gastrointestinal Syndrome

Radiation-induced gastrointestinal syndrome (RIGS) is due to the clonogenic loss of crypt cells and villi depopulation, resulting in disruption of mucosal barrier, bacterial invasion, inflammation and sepsis. Intestinal macrophages could recognize invading bacterial DNA via TLR9 receptors and transmit regenerative signals to the neighboring crypt. We therefore investigated whether systemic administration of designer TLR9 agonist could ameliorate RIGS by activating TLR9.Male C57Bl6 mice were distributed in four experimental cohorts, whole body irradiation (WBI) (8.4-10.4 Gy), TLR9 agonist (1 mg/kg s.c.), 1 h pre- or post-WBI and TLR9 agonist+WBI+iMyd88 (pretreatment with inhibitory peptide against Myd88). Animals were observed for survival and intestine was harvested for histological analysis. BALB/c mice with CT26 colon tumors in abdominal wall were irradiated with 14 Gy single dose of whole abdominal irradiation (AIR) for tumor growth study.Mice receiving pre-WBI TLR9 agonist demonstrated improvement of survival after 10.4 Gy (p<0.03), 9.4 Gy (p<0.008) and 8.4 Gy (p<0.002) of WBI, compared to untreated or iMyd88-treated controls. Post-WBI TLR9 agonist mitigates up to 8.4 Gy WBI (p<0.01). Histological analysis and xylose absorption test demonstrated significant structural and functional restitution of the intestine in WBI+TLR9 agonist cohorts. Although, AIR reduced tumor growth, all animals died within 12 days from RIGS. TLR9 agonist improved the survival of mice beyond 28 days post-AIR (p<0.008) with significant reduction of tumor growth (p<0.0001).TLR9 agonist treatment could serve both as a prophylactic or mitigating agent against acute radiation syndrome and also as an adjuvant therapy to increase the therapeutic ratio of abdominal Radiation Therapy for Gastro Intestinal malignancies

Central-City/Suburban Inequality and Metropolitan Political Fragmentation

To test the proposition that metropolitan governmental structure has social, economic, and racial consequences, the authors assume that the proliferation of local governments in a metropolitan area and the boundary constraints imposed on the central city have adverse effects, especially on the core city. Analyzing 97 large U.S. metropolitan statistical areas (MSAs), they found only limited support for this proposition. Of three measures of fragmentation, only two were of any consequence, one in the opposite direction predicted. The lower the central city’s share of MSA population, the higher the level of fiscal health for the inner city. Also, municipal boundaries have racial consequences.Yeshttps://us.sagepub.com/en-us/nam/manuscript-submission-guideline