Charge collection and trapping in low‐temperature silicon detectors

Charge collection efficiency measurements in silicon detectors at low temperature (T \u3c 0.5 K) and low applied electric field (E=0.1–100 V/cm) were performed using a variety of high‐purity, p‐type silicon samples with room‐temperature resistivity in the range 2–40 kΩ cm. Good charge collection under these conditions of low temperature and low electric field is necessary for background suppression, through the simultaneous measurement of phonons and ionization, in a very low event rate dark matter search or neutrino physics experiment. Charge loss due to trapping during drift is present in some samples, but the data suggest that another charge–loss mechanism is also important. We present results which indicate that, for 60 keV energy depositions, a significant fraction of the total charge loss by trapping occurs in the initial electron‐hole cloud near the event location which may briefly act as a shielded, field‐free region. In addition, measurements of the lateral size, transverse to the applied electric field, of the initial electron‐hole cloud indicate large transverse diffusion lengths. At the lowest fields a lateral diameter on the order of 1 mm is found in a detector ∼5 mm thick

Measurement of T\u3csub\u3ec\u3c/sub\u3e suppression in tungsten using magnetic impurities

We have measured the effects of dilute magnetic-atom doping on the superconducting transition temperature of tungsten thin films. Our “Tc tuning” technique is accurate, precise, and simple. Experiments were performed using dc-magnetron-sputtered tungsten films with undoped values of Tc in the range of 70–150 mK. The magnetic-atom doping was achieved using ion implantation. Specific Tc suppressions of between 5% and 65% were targeted and observed in this study. The transition width of each undoped sample was ≈1 mK and the transition widths remained sharp after implantation with 56Fe+ ions. Our data are in good agreement with predictions of a linear dependence of Tc suppression with increasing magnetic-atom concentration, in the small concentration limit. At higher concentrations, antiferromagnetic coupling between the magnetic dopant atoms becomes important and the Tc-suppression effect is diminished. We use our Tc data to calculate the Abrikosov–Gor’kov (AG) and Ruderman–Kittel–Kasuya–Yosida (RKKY) spin–flip relaxation parameters τAG and τRKKY. We conclude with a brief discussion of applications of the Tc-tuning technique, and present our plans for future studies in this area

Measuring inorganic phosphate and intracellular pH in the healthy and hypertrophic cardiomyopathy hearts by in vivo 7T 31P-cardiovascular magnetic resonance spectroscopy.

BACKGROUND: Cardiovascular phosphorus MR spectroscopy (31P-CMRS) is a powerful tool for probing energetics in the human heart, through quantification of phosphocreatine (PCr) to adenosine triphosphate (ATP) ratio. In principle, 31P-CMRS can also measure cardiac intracellular pH (pHi) and the free energy of ATP hydrolysis (ΔGATP). However, these require determination of the inorganic phosphate (Pi) signal frequency and amplitude that are currently not robustly accessible because blood signals often obscure the Pi resonance. Typical cardiac 31P-CMRS protocols use low (e.g. 30°) flip-angles and short repetition time (TR) to maximise signal-to-noise ratio (SNR) within hardware limits. Unfortunately, this causes saturation of Pi with negligible saturation of the flowing blood pool. We aimed to show that an adiabatic 90° excitation, long-TR, 7T 31P-CMRS protocol will reverse this balance, allowing robust cardiac pHi measurements in healthy subjects and patients with hypertrophic cardiomyopathy (HCM). METHODS: The cardiac Pi T1 was first measured by the dual TR technique in seven healthy subjects. Next, ten healthy subjects and three HCM patients were scanned with 7T 31P-MRS using long (6 s) TR protocol and adiabatic excitation. Spectra were fitted for cardiac metabolites including Pi. RESULTS: The measured Pi T1 was 5.0 ± 0.3 s in myocardium and 6.4 ± 0.6 s in skeletal muscle. Myocardial pH was 7.12 ± 0.04 and Pi/PCr ratio was 0.11 ± 0.02. The coefficients of repeatability were 0.052 for pH and 0.027 for Pi/PCr quantification. The pH in HCM patients did not differ (p = 0.508) from volunteers. However, Pi/PCr was higher (0.24 ± 0.09 vs. 0.11 ± 0.02; p = 0.001); Pi/ATP was higher (0.44 ± 0.14 vs. 0.24 ± 0.05; p = 0.002); and PCr/ATP was lower (1.78 ± 0.07 vs. 2.10 ± 0.20; p = 0.020), in HCM patients, which is in agreement with previous reports. CONCLUSION: A 7T 31P-CMRS protocol with adiabatic 90° excitation and long (6 s) TR gives sufficient SNR for Pi and low enough blood signal to permit robust quantification of cardiac Pi and hence pHi. Pi was detectable in every subject scanned for this study, both in healthy subjects and HCM patients. Cardiac pHi was unchanged in HCM patients, but both Pi/PCr and Pi/ATP increased that indicate an energetic impairment in HCM. This work provides a robust technique to quantify cardiac Pi and pHi.This work was funded by a Sir Henry Dale Fellowship from the Wellcome Trust and the Royal Society (grant #098436/Z/12/B to C.T.R.) and by an Erwin Schrödinger Fellowship from the Austrian Science Fund (grant #J4043). Authors also acknowledge the support of the NIHR Oxford Biomedical Research Centre and the Oxford British Heart Foundation Centre of Research Excellence. The support of the Slovak Grant Agency VEGA (grant #2/0001/17) and APVV (grant #15-0029) is also acknowledged

The Iowa Homemaker vol.21, no.3

Freshmen – Please Note, page 2 Hospital Research, Ann Koebel, page 3 Orchids to Pat, page 4 The Army Eats Well, Mary I. Barber, page 5 Making Things Grow, Betty Ann Iverson, page 6 Look Before You Snap, Kathryn Monson, page 7 Major Departments on Review, Elizabeth Murfield, page 8 Patriotic Sally, Patricia Hayes, page 10 What’s New in Home Economics, Dorothy Olson, page 12 Summer Job Holders Reap Experience, page 14 A List of Don’ts, Costume Design Class, page 15 We Salute Campus Leaders, Margaret Kirchner, page 16 Home Economics Looks to Future, M. L. Morton, page 17 Behind Bright Jackets, Julie Wendel, page 18 Alums in the News, Mary Elizabeth Sather, page 20 Nutrition for Defense, Dorothy Ann Roost, page 22 That Personal Touch, Margaret Ann Clarke, page 23 Journalistic Spindles, Elizabeth Hanson, page 2

Expressions 1979

Expressions contains selected work from the 1979 Creative Writing Contest winners and honorable mentions along with Commercial Art students at Des Moines Area Community College. Design, typography and layout was done by Journalism students.https://openspace.dmacc.edu/expressions/1001/thumbnail.jp

Localized rest and stress human cardiac creatine kinase reaction kinetics at 3 T.

Changes in the kinetics of the creatine kinase (CK) shuttle are sensitive markers of cardiac energetics but are typically measured at rest and in the prone position. This study aims to measure CK kinetics during pharmacological stress at 3 T, with measurement in the supine position. A shorter "stressed saturation transfer" (StreST) extension to the triple repetition time saturation transfer (TRiST) method is proposed. We assess scanning in a supine position and validate the MR measurement against biopsy assay of CK activity. We report normal ranges of stress CK forward rate (kfCK ) for healthy volunteers and obese patients. TRiST measures kfCK in 40 min at 3 T. StreST extends the previously developed TRiST to also make a further kfCK measurement during <20 min of dobutamine stress. We test our TRiST implementation in skeletal muscle and myocardium in both prone and supine positions. We evaluate StreST in the myocardium of six healthy volunteers and 34 obese subjects. We validated MR-measured kfCK against biopsy assays of CK activity. TRiST kfCK values matched literature values in skeletal muscle (kfCK  = 0.25 ± 0.03 s-1 vs 0.27 ± 0.03 s-1 ) and myocardium when measured in the prone position (0.32 ± 0.15 s-1 ), but a significant difference was found for TRiST kfCK measured supine (0.24 ± 0.12 s-1 ). This difference was because of different respiratory- and cardiac-motion-induced B0 changes in the two positions. Using supine TRiST, cardiac kfCK values for normal-weight subjects were 0.15 ± 0.09 s-1 at rest and 0.17 ± 0.15 s-1 during stress. For obese subjects, kfCK was 0.16 ± 0.07 s-1 at rest and 0.17 ± 0.10 s-1 during stress. Rest myocardial kfCK and CK activity from LV biopsies of the same subjects correlated (R = 0.43, p = 0.03). We present an independent implementation of TRiST on the Siemens platform using a commercially available coil. Our extended StreST protocol enables cardiac kfCK to be measured during dobutamine-induced stress in the supine position.Funded by: a Sir Henry Dale Fellowship from the Wellcome Trust and the Royal Society [098436/Z/12/B] to CTR, the BHF Centre of Research Excellence (OJR), a BHF clinical research training fellowship [FS/15/80/31803] to MAP, a BHF fellowship [FS/14/54/30946] to JJR, an NIHR OBRC fellowship to BR, a BHF programme grant [RG/13/8/30266] to CAL and SN, and a DPhil studentship from the Medical Research Council to WTC. We acknowledge support from the Oxford NIHR Biomedical Research Centre

Effects of antiplatelet therapy on stroke risk by brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases: subgroup analyses of the RESTART randomised, open-label trial

Background Findings from the RESTART trial suggest that starting antiplatelet therapy might reduce the risk of recurrent symptomatic intracerebral haemorrhage compared with avoiding antiplatelet therapy. Brain imaging features of intracerebral haemorrhage and cerebral small vessel diseases (such as cerebral microbleeds) are associated with greater risks of recurrent intracerebral haemorrhage. We did subgroup analyses of the RESTART trial to explore whether these brain imaging features modify the effects of antiplatelet therapy

Engineering Genetic Predisposition in Human Neuroepithelial Stem Cells Recapitulates Medulloblastoma Tumorigenesis.

Human neural stem cell cultures provide progenitor cells that are potential cells of origin for brain cancers. However, the extent to which genetic predisposition to tumor formation can be faithfully captured in stem cell lines is uncertain. Here, we evaluated neuroepithelial stem (NES) cells, representative of cerebellar progenitors. We transduced NES cells with MYCN, observing medulloblastoma upon orthotopic implantation in mice. Significantly, transcriptomes and patterns of DNA methylation from xenograft tumors were globally more representative of human medulloblastoma compared to a MYCN-driven genetically engineered mouse model. Orthotopic transplantation of NES cells generated from Gorlin syndrome patients, who are predisposed to medulloblastoma due to germline-mutated PTCH1, also generated medulloblastoma. We engineered candidate cooperating mutations in Gorlin NES cells, with mutation of DDX3X or loss of GSE1 both accelerating tumorigenesis. These findings demonstrate that human NES cells provide a potent experimental resource for dissecting genetic causation in medulloblastoma