The SPARC Toroidal Field Model Coil Program

The SPARC Toroidal Field Model Coil (TFMC) Program was a three-year effort between 2018 and 2021 that developed novel Rare Earth Yttrium Barium Copper Oxide (REBCO) superconductor technologies and then successfully utilized these technologies to design, build, and test a first-in-class, high-field (~20 T), representative-scale (~3 m) superconducting toroidal field coil. With the principal objective of demonstrating mature, large-scale, REBCO magnets, the project was executed jointly by the MIT Plasma Science and Fusion Center (PSFC) and Commonwealth Fusion Systems (CFS). The TFMC achieved its programmatic goal of experimentally demonstrating a large-scale high-field REBCO magnet, achieving 20.1 T peak field-on-conductor with 40.5 kA of terminal current, 815 kN/m of Lorentz loading on the REBCO stacks, and almost 1 GPa of mechanical stress accommodated by the structural case. Fifteen internal demountable pancake-to-pancake joints operated in the 0.5 to 2.0 nOhm range at 20 K and in magnetic fields up to 12 T. The DC and AC electromagnetic performance of the magnet, predicted by new advances in high-fidelity computational models, was confirmed in two test campaigns while the massively parallel, single-pass, pressure-vessel style coolant scheme capable of large heat removal was validated. The REBCO current lead and feeder system was experimentally qualified up to 50 kA, and the crycooler based cryogenic system provided 600 W of cooling power at 20 K with mass flow rates up to 70 g/s at a maximum design pressure of 20 bar-a for the test campaigns. Finally, the feasibility of using passive, self-protection against a quench in a fusion-scale NI TF coil was experimentally assessed with an intentional open-circuit quench at 31.5 kA terminal current.Comment: 17 pages 9 figures, overview paper and the first of a six-part series of papers covering the TFMC Progra

Identification and characterization of unique tumoricidal genes in rat umbilical cord matrix stem cells

Master of ScienceDepartment of Anatomy & PhysiologyMasaaki TamuraRat umbilical cord matrix stem cells (UCMSC) have been shown to exhibit a remarkable ability to control rat mammary adenocarcinoma (Mat B III) cell proliferation both in vivo and in vitro. To study the underlying mechanisms and genes involved in Mat B III growth attenuation, total RNA was extracted from the naïve rat UCMSC alone and those co-cultured with Mat B III in Transwell culture dishes. Gene expression profiles of naive rat UCMSC alone and those cocultured with Mat B III cells were investigated by microarray analysis using an Illumina RatRef- 12 Expression BeadChip. The comparison of gene expression profiles between untreated and cocultured rat UCMSC identified five up-regulated candidate genes (follistatin (FST), sulfatase1 (SULF-1), glucose phosphate isomerase (GPI), HtrA serine peptidase (HTRA1), and adipocyte differentiation-related protein (ADRP)) and two down-regulated candidate genes (transforming growth factor, beta-induced, 68kDa (TGFβI) and podoplanin (PDPN)) based upon the following screening criteria: 1) expression of the candidate genes should show at least a 1.5 fold change in rat UCMSC co-cultured with Mat B III cells; 2) candidate genes encode secretory proteins; and 3) they encode cell growth-related proteins. Following confirmation of gene expression by real time-PCR, ADRP, SULF-1 and GPI were selected for further analysis. Addition of specific neutralizing antibodies against these three gene products individually in co-cultures of 1:20 rat UCMSC:Mat B III cells significantly increased cell proliferation, implying that these gene products are produced under the co-cultured condition and functionally attenuate cell growth. Immunoprecipitation followed by Western blot analysis demonstrated that these proteins are indeed secreted into the culture medium. Individual over-expression of these three genes in rat UCMSC significantly enhanced UCMSC-dependent inhibition of cell proliferation in co-culture. These results suggest that ADRP, SULF-1 and GPI act as tumor suppressor genes, and these genes might be involved in rat UCMSC-dependent growth attenuation of rat mammary tumors

PCEPS dose-dependently stimulated the growth of immune cells.

<p>The dose-dependent effect of PCEPS (1–100 μg/ml for 48 hrs) on the growth of HL-60, THP-1 and Jurkat cells was evaluated by MTT assay. Results are presented as mean ± SD (n = 3). *, P<0.05 compared to PBS-treated control by Tukey’s test.</p

PCEPS treatment attenuated the spheroid growth of CT26 colon carcinoma cells in 3D cell culture in the presence of various immune cells.

<p>The CT26 cells were grown on a U-shaped agar matrix which contains HL-60, THP-1 or Jurkat cells (Day 0). The PCEPS (30 μg/ml) was treated twice at Day 1 and Day 4. The size of the spheroid was measured at Day 8 and Day 10 (A). The values are presented as fold change of spheroid size compared with Days 8 and 10 (Day10/Day 8). Results are presented as mean ± SD (n = 5). *, P<0.05 compared to PBS-treated CT26 cells alone group by Tukey’s test. †, P<0.05 compared to same group in PBS-treated group by t-test. (B) Typical pictures of spheroid in each group. Scale bar in each picture represents 100 μm. (C) Typical morphologies of HL-60, THP-1 and Jurkat cells in agar matrix of each treatment group. Scale bar in each picture represents 20 μm.</p

PCEPS treatment increased expression of differentiation marker and reactive oxygen-related genes in immune cells co-cultured with PCEPS-treated CT26 colon carcinoma cells in Transwell cell culture.

<p>The HL-60, THP-1 or Jurkat cells in the bottom well of 6-well plates and CT26 cells in the insert of Transwell were co-cultured (Day 0). The PCEPS (30 μg/ml) treatment was provided at Day 1, Day 3 and Day 5. Total RNA was collected from individual immune cells in the 6 well plate at Day 6. Gene expression in HL-60 (A), THP-1 (B) and Jurkat (C) cells were measured by RT-qPCR. Results are presented as mean ± SD (n = 4) of relative quantity. a-d, P<0.05 between different characters in each target gene by t-test.</p

PCEPS treatment caused changes in leukocyte populations in ascites of CT26 cell tumor-bearing mice.

<p>The CT26 cells (2.5x10⁵) suspended in 200μl PBS was inoculated in the peritoneal cavity of Balb/c mice. The PCEPS treatment (10 mg/kg, IP, every other day) was started one week after cancer cell inoculation and continued for a total of 3 times. Ascites was collected two days after last treatment. Leukocytes in the ascites were labeled with anti-CD4, CD8b, CD19, 33D1, LY6G and CD68 antibodies and their populations were analyzed by flow cytometry. PBS was used as the negative control treatment. Results are presented as mean ± SD (n = 4). *, P<0.05 compared to PBS control group by t-test.</p

PCEPS dose- and time-dependently stimulated the growth of murine splenocytes and bone marrow cells in cell culture.

<p>PCEPS treatment dose-dependently (1–100 μg/ml for 48 hrs) and time-dependently (24, 48 72 and 96 hrs treatment with 1–100 μg/ml PCEPS) stimulated the growth of mouse SPLs (A and B) and BMCs (C and D). SPLs and BMCs were also treated with 100 ng/ml LPS as a control. The cell growth was evaluated by MTT assay. Results are presented as mean ± SD (n = 3). *, P<0.05 compared to PBS-treated control by Tukey’s test or t-test.</p