An in-core experiment is proposed to measure all delayed-neutron parameters (λᵢ and βᵢ for each delayed group) and the neutron generation time applicable for a given reactor system. The method uses a least-squares fitting technique to simultaneously fit a series of transient responses produced by step changes (or rapid ramps) in reactivity of arbitrary size. The function which is least-squares fit is the exact analytic solution describing a reactor response following a step change in reactivity as given by the standard multi-group point-reactor model. The method does not require any knowledge of the absolute reactivity of the system. The results are based solely upon the measurable quantities of relative power, time, and asymptotic inverse period. Unlike out-of-core delayed neutron experiments, the results are independent of the total number of fissions that have occurred in the fissioning isotope that produced the delayed neutrons, and are independent of the efficiency of the detector used to monitor the transients. Modal contamination is presumed not to be a serious problem in small or intermediate size cores as long as small reactivity changes are used (i.e. +$.10 to -$.25), which is consistent with the best method of performing this experiment. The method is equally applicable to both homogeneous and heterogeneous reactors and may be used in either thermal or fast systems. The number of delayed-neutron groups is not a constraint.

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Thesis (M.S.)--University of Michigan, 1983. / Project completed in 1981. Degree awarded in 1983.

Delayed hypersensitivity can be conferred passively to normal animals. There exists a period when whole peritoneal exudate cells will passively confer delayed sensitivity, but a sonic extract from them will not; however, after a few more days, both whole cells and sonic extracts could transfer sensitivity. This investigation was undertaken to study the differences in cells collected at two different time intervals after initial sensitization of guinea pigs with 1-fluoro-2,4-dinitrobenzene.

Thesis (Ed.M.)--Boston University Slides to accompany thesis on file in the Audio-Visual Library.

The genetic control of puberty remains an important but mostly unanswered question. Late pubertal timing affects over 2% of adolescents and is associated with adverse health outcomes. Self-limited delayed puberty (DP) segregates in an autosomal dominant pattern and is highly heritable; however, its neuroendocrine pathophysiology and genetic regulation remain unclear. The genetic control of puberty remains an important but mostly unanswered question. Late pubertal timing affects over 2% of adolescents and is associated with adverse health outcomes. Self-limited delayed puberty (DP) segregates in an autosomal dominant pattern and is highly heritable; however, its neuroendocrine pathophysiology and genetic regulation remain unclear. Our large, accurately phenotyped cohort of patients with familial self-limited DP is a unique resource with a relatively homogeneous genetic composition. I have utilised this cohort to investigate the genetic variants segregating with the DP trait in these pedigrees. Whole exome sequencing in eighteen probands and their relatives, and subsequent targeted sequencing in an extended subgroup of the cohort, has revealed potential novel genetic regulators of pubertal timing. In ten unrelated probands, I identified rare mutations in IGSF10, a gene that is strongly expressed in the nasal mesenchyme during embryonic migration of gonadotropin-releasing hormone (GnRH) neurons. IGSF10 knockdown both in vitro and in a transgenic zebrafish model resulted in perturbed GnRH neuronal migration. Loss-of-function mutations in IGSF10 were also identified in five patients with absent puberty due to hypogonadotropic hypogonadism (HH). Additionally, I have identified and investigated one rare, pathogenic mutation in HS6ST1 - a gene known to cause HH - in one family with DP, and two rare variants in FTO - a gene implicated in the timing of menarche in the general population - in 3 families. Further potentially pathogenic variants have emerged from investigating candidate genes identified from microarray studies (LGR4, SEMA6A and NEGR1) and from related clinical phenotypes (IGSF1). Our large, accurately phenotyped cohort of patients with familial self-limited DP is a unique resource with a relatively homogeneous genetic composition. I have utilised this cohort to investigate the genetic variants segregating with the DP trait in these pedigrees. Whole exome sequencing in eighteen probands and their relatives, and subsequent targeted sequencing in an extended subgroup of the cohort, has revealed potential novel genetic regulators of pubertal timing. In ten unrelated probands, I identified rare mutations in IGSF10, a gene that is strongly expressed in the nasal mesenchyme during embryonic migration of gonadotropin-releasing hormone (GnRH) neurons. IGSF10 knockdown both in vitro and in a transgenic zebrafish model resulted in perturbed GnRH neuronal migration. Loss-of-function mutations in IGSF10 were also identified in five patients with absent puberty due to hypogonadotropic hypogonadism (HH). Additionally, I have identified and investigated one rare, pathogenic mutation in HS6ST1 - a gene known to cause HH - in one family with DP, and two rare variants in FTO - a gene implicated in the timing of menarche in the general population - in 3 families. Further potentially pathogenic variants have emerged from investigating candidate genes identified from microarray studies (LGR4, SEMA6A and NEGR1) and from related clinical phenotypes (IGSF1).

This dissertation presents the results of a search in the exclusive photon plus missing transverse energy (gamma + E/_T) final state in proton antiproton collisions at center of mass energy of 1.96 TeV using the Collider Detector at Fermilab experiment. The strategy used here is to search for delayed photons coming from gauge mediated supersymmetric events with the exclusive production of ~X(0 1) -> gamma~G. In these models the ~X(0 1) is the lightest neutralino and has nanosecond lifetime before decaying to a photon (gamma) and gravitino (~G) which exits the detector unrecorded. In order to search for this process we select collisions that have a single photon plus missing transverse energy and little other activity in the detector and examine the arrival time of the photon. This arrival time is then compared against expectations from a data driven background of the standard model sources. In the data collected from the Fermilab Tevatron collider from December 2004 to June 2010, representing 6.3 fb^-1 of data, we observe 322 events in the photon arrival timing region from 2 nanoseconds to 7 nanoseconds with a data driven background prediction of 257 +/- 35. An excess of 65 events is observed, equivalent to a standard deviation (N_sigma) of 1.65 from the null hypothesis.

The delayed neutron emission rates of U-235 and Pu-239 samples were measured accurately from a thermal fission reaction. A Monte Carlo calculation using the Geant4 code was used to demonstrate the neutron energy independence of the detector used in the counting station. A set of highly purified actinide samples (U-235 and Pu-239) was irradiated in these experiments by using the Texas A&M University Nuclear Science Center Reactor. A fast pneumatic transfer system, an integrated computer control system, and a graphite-moderated counting system were constructed to perform all these experiments. The calculated values for the five-group U-235 delayed neutron parameters and the six-group Pu-239 delayed neutron parameters were compared with the values recommended by Keepin et al. (1957) and Waldo et al. (1981). These new values differ slightly from literature values. The graphite-moderated counting station and the computerized pneumatic system are now operational for further delayed neutron measurement.

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