Detrital Shocked Zircon Provides First Radiometric Age Constraint of <1472 Ma for the Santa Fe Impact Structure, New Mexico, USA

Impact structures are prone to erosion, burial and tectonic deformation. The Santa Fe impact structure in New Mexico contains shatter cones and shocked quartz, but is highly tectonized and eroded; estimates of the impact age (1200-300 Ma) and size (6-13 km) are poorly constrained. Here we report the first occurrence of shock-twinned zircon identified both in modern sediments and bedrock at the Santa Fe impact structure. Zircon {112} twin lamellae are considered diagnostic evidence of shock deformation and have been identified at several impact structures including Vredefort, Sudbury, Ries, Rock Elm, and in lunar impact breccia. A total of 6619 grains from fifteen sediment samples and two rock samples were surveyed; seven shocked grains were identified (7/6619 = 0.1%). One shocked zircon was identified in a biotite schist shatter cone. Five of seven shocked zircon grains were EBSD mapped; three were analyzed with multiple SIMS spots. EBSD mapping revealed {112} deformation twin lamellae in each of the five zircon grains. U-Pb geochronology for three of the shocked zircon grains yield crystallization ages from 1715+/-22 to 1472+/-35 Ma. LA-ICPMS U-Th-Pb analysis of detrital zircon grains from five samples yielded Paleoproterozoic (1800-1600 Ma) and Mesoproterozoic (1500-1300 Ma) ages. We reveal the first confirmed shocked zircon at the Santa Fe structure. Zircon is the third shocked mineral identified at this site, in addition to xenotime and quartz]; the {112} twin lamellae indicate that exposed bedrock may have experienced shock pressures up to ~20 GPa. The 1472+/-35 Ma age determined from a shock-twinned zircon is the first reliable maximum impact age constraint based on analysis of shocked material and extends the window for the Santa Fe impact event into the Mesoproterozoic

Quantitation of progenitor cell populations and growth factors after bone marrow aspirate concentration

Background: The number of Mesenchymal Stem/Stromal Cells (MSCs) in the human bone marrow (BM) is small compared to other cell types. BM aspirate concentration (BMAC) may be used to increase numbers of MSCs, but the composition of MSC subpopulations and growth factors after processing are unknown. The purpose of this study was to assess the enrichment of stem/progenitor cells and growth factors in BM aspirate by two different commercial concentration devices versus standard BM aspiration. Methods: 120 mL of BM was aspirated from the iliac crest of 10 male donors. Each sample was processed simultaneously by either Emcyte GenesisCS® (Emcyte) or Harvest SmartPReP2 BMAC (Harvest) devices and compared to untreated BM aspirate. Samples were analyzed with multicolor flow cytometry for cellular viability and expression of stem/progenitor cells markers. Stem/progenitor cell content was verified by quantification of colony forming unit-fibroblasts (CFU-F). Platelet, red blood cell and total nucleated cell (TNC) content were determined using an automated hematology analyzer. Growth factors contents were analyzed with protein quantification assays. Statistical analyses were performed by ANOVA analysis of variance followed by Tukey’s multiple comparison test or Wilcoxon matched-pairs signed rank test with p &lt; 0.05 for significance. Results: Cell viability after processing was approximately 90% in all groups. Compared to control, both devices significantly enriched TNCs and platelets, as well as the CD45−CD73+ and CD45−CD73+CD90+ cell populations. Further, Harvest significantly concentrated CD45−CD10+, CD45−CD29+, CD45−CD90+, CD45−CD105+, CD45−CD119+ cells, and CD45dimCD90+CD271+ MSCs, whereas Emcyte significantly enriched CD45dimCD44+CD271+ MSCs. BM concentration also increased the numbers of CFU-F, platelet-derived growth factor, vascular endothelial growth factor, macrophage colony-stimulating factor, interleukin-1b, VCAM-1 and total protein. Neither system concentrated red blood cells, hematopoietic stem cells or bone morphogenetic proteins. Conclusion: This data could contribute to the development of BMAC quality control assays as both BMAC systems concentrated platelets, growth factors and non-hematopoietic stem cell subpopulations with distinct phenotypes without loss of cell viability when compared to unprocessed BM

A genome-wide association study follow-up suggests a possible role for PPARG in systemic sclerosis susceptibility

Introduction: A recent genome-wide association study (GWAS) comprising a French cohort of systemic sclerosis (SSc) reported several non-HLA single-nucleotide polymorphisms (SNPs) showing a nominal association in the discovery phase. We aimed to identify previously overlooked susceptibility variants by using a follow-up strategy.&lt;p&gt;&lt;/p&gt; Methods: Sixty-six non-HLA SNPs showing a P value &#60;10-4 in the discovery phase of the French SSc GWAS were analyzed in the first step of this study, performing a meta-analysis that combined data from the two published SSc GWASs. A total of 2,921 SSc patients and 6,963 healthy controls were included in this first phase. Two SNPs, PPARG rs310746 and CHRNA9 rs6832151, were selected for genotyping in the replication cohort (1,068 SSc patients and 6,762 healthy controls) based on the results of the first step. Genotyping was performed by using TaqMan SNP genotyping assays. Results: We observed nominal associations for both PPARG rs310746 (PMH = 1.90 × 10-6, OR, 1.28) and CHRNA9 rs6832151 (PMH = 4.30 × 10-6, OR, 1.17) genetic variants with SSc in the first step of our study. In the replication phase, we observed a trend of association for PPARG rs310746 (P value = 0.066; OR, 1.17). The combined overall Mantel-Haenszel meta-analysis of all the cohorts included in the present study revealed that PPARG rs310746 remained associated with SSc with a nominal non-genome-wide significant P value (PMH = 5.00 × 10-7; OR, 1.25). No evidence of association was observed for CHRNA9 rs6832151 either in the replication phase or in the overall pooled analysis.&lt;p&gt;&lt;/p&gt; Conclusion: Our results suggest a role of PPARG gene in the development of SSc