The most precise determination of the neutron lifetime using the beam method was completed in 2005 and reported a result of τ(n)=(886.3±1.2[stat]±3.2[syst]) s. The dominant uncertainties were attributed to the absolute determination of the fluence of the neutron beam (2.7 s). The fluence was measured with a neutron monitor that counted the neutron-induced charged particles from absorption in a thin, well-characterized 6Li deposit. The detection efficiency of the monitor was calculated from the areal density of the deposit, the detector solid angle, and the evaluated nuclear data file, ENDF/B-VI 6Li(n,t)4He thermal neutron cross section. In the current work, we measure the detection efficiency of the same monitor used in the neutron lifetime measurement with a second, totally absorbing neutron detector. This direct approach does not rely on the 6Li(n,t)4He cross section or any other nuclear data. The detection efficiency is consistent with the value used in 2005 but is measured with a precision of 0.057%, which represents a fivefold improvement in the uncertainty. We verify the temporal stability of the neutron monitor through ancillary measurements, allowing us to apply the measured neutron monitor efficiency to the lifetime result from the 2005 experiment. The updated lifetime is τ(n)=(887.7±1.2[stat]±1.9[syst]) s.

A measurement of the neutron lifetime τ n performed by the absolute counting of in-beam neutrons and their decay protons has been completed. Protons confined in a quasi-Penning trap were accelerated onto a silicon detector held at a high potential and counted with nearly unit efficiency. The neutrons were counted by a device with an efficiency inversely proportional to neutron velocity, which cancels the dwell time of the neutron beam in the trap. The result is τ n = (886.6 ± 1.2[stat] ± 3.2[sys]) s, which is the most precise measurement of the lifetime using an in-beam method. The systematic uncertainty is dominated by neutron counting, in particular the mass of the deposit and the 6 Li(n,t) cross section. The measurement technique and apparatus, data analysis, and investigation of systematic uncertainties are discussed in detail.

No abstract

Background Previous studies have demonstrated individual differences in susceptibility to the detrimental effects of prenatal ethanol exposure. Many factors, including genetic differences, have been shown to play a role in susceptibility and resistance, but few studies have investigated the range of genetic variation in rodent models. Methods We examined ethanol teratogenesis in five inbred strains of mice: C57BL/6J (B6), Inbred Short-Sleep, C3H/Ibg, A/Ibg and 129S6/SvEvTac (129). Pregnant dams were intubated with either 5.8 g/kg ethanol (E) or an isocaloric amount of maltose-dextrin (MD) on day 9 of pregnancy. Dams were sacrificed on day 18 and fetuses were weighed, sexed and examined for gross morphological malformations. Every other fetus within a litter was then either placed in Bouin’s fixative for subsequent soft-tissue analyses or eviscerated and placed in ethanol for subsequent skeletal analyses. Results B6 mice exposed to ethanol in utero had fetal weight deficits and digit, kidney, brain ventricle and vertebral malformations. In contrast, 129 mice showed no teratogenesis. The remaining strains showed varying degrees of teratogenesis. Conclusions Differences among inbred strains demonstrates genetic variation in the teratogenic effects of ethanol. Identifying susceptible and resistant strains allows future studies to elucidate the genetic architecture underlying prenatal alcohol phenotypes.

Aberrant gene expression within the hippocampus has recently been implicated in the pathogenesis of obesity-induced memory impairment. Whether a dysregulation of epigenetic modifications mediates this disruption in gene transcription has yet to be established. Here we report evidence of obesity-induced alterations in DNA methylation of memory-associated genes, including Sirtuin 1 (Sirt1), within the hippocampus, and thus offer a novel mechanism by which SIRT1 expression within the hippocampus is suppressed during obesity. Forebrain neuron-specific Sirt1 knock-out closely recapitulated the memory deficits exhibited by obese mice, consistent with the hypothesis that the high-fat diet-mediated reduction of hippocampal SIRT1 could be responsible for obesity-linked memory impairment. Obese mice fed a diet supplemented with the SIRT1-activating molecule resveratrol exhibited increased hippocampal SIRT1 activity and preserved hippocampus-dependent memory, further strengthening this conclusion. Thus, our findings suggest that the memory-impairing effects of diet-induced obesity may potentially be mediated by neuroepigenetic dysregulation of SIRT1 within the hippocampus.

Maternal genetic factors and/or fetal genetic factors contribute to variations in response to prenatal alcohol exposure. To assess the contribution of maternal genotype to ethanol teratogenesis, a reciprocal cross study was conducted in an animal model using C57BL/6J (B6) and long-sleep (LS) mice. B6 mice are more susceptible than LS mice to prenatal ethanol-induced malformations but both mouse stocks are susceptible to fetal weight deficits following in utero alcohol exposure. B6 and LS dams were reciprocally mated to B6 or LS males producing four embryonic genotype groups: the true-bred B6B6 and LSLS genotypes, and the genetically similar B6LS and LSB6 genotypes (the F1 genotype). Dams were intubated with either 5.8 g/kg ethanol (E) or an isocaloric amount of sucrose (S) on day 9 of pregnancy. Fetuses were removed on gestation day 18, weighed, and assessed for soft tissue or skeletal malformations. Results showed a greater litter weight deficit and increased total malformation rate in ethanol-exposed F1 litters carried by B6 mothers compared to ethanol-exposed F1 litters carried by LS mothers. This result would be expected only if maternal genetic factors contribute significantly towards susceptibility to ethanol teratogenesis. The influence of the LS mother was to decrease susceptibility to ethanol teratogenesis compared to the B6 mother while the influence of the B6 mother was to increase susceptibility to ethanol teratogenesis compared to the LS mother. The average malformation rate for F1 litters was significantly less than the predicted midparental value. This shows that the F1 genotype exhibited dominance towards resistance to prenatal alcohol effects.(ABSTRACT TRUNCATED AT 250 WORDS)

We report a new measurement of the neutron decay lifetime by the absolute counting of in-beam neutrons and their decay protons. Protons were confined in a quasi-Penning trap and counted with a silicon detector. The neutron beam fluence was measured by capture in a thin 6LiF foil detector with known absolute efficiency. The combination of these simultaneous measurements gives the neutron lifetime: tau(n)=(886.8+/-1.2[stat]+/-3.2[syst]) s. The systematic uncertainty is dominated by uncertainties in the mass of the 6LiF deposit and the 6Li(n,t) cross section. This is the most precise measurement of the neutron lifetime to date using an in-beam method.

An animal model was used to see if maternal genetic factors contribute to ethanol-induced fetal malformations. Susceptible C57BL/6J (B6) and resistant Short-Sleep (SS) mice were used in a reciprocal cross-breeding design. This design produced four fetal genotypes: true-bred B6B6 and SSSS liters and hybrid B6SS and SSB6 litters. Dams were intubated with either 5.8 g/kg of ethanol or an isocaloric amount of maltose-dextrin on day 9 of pregnancy. Fetuses were removed on day 18 of pregnancy and assessed for soft tissue and gross malformations. Results show different prenatal treatment effects on malformations depending on the fetal genotype. Mean percentage of total malformations in ethanol-treated groups were 61% (B6B6), 28% (B6SS), 3% (SSB6), and 16% (SSSS), respectively. Litters exposed to maltose-dextrin showed low (< or = 4%) malformation rates regardless of fetal genotype. The difference in teratogenic response between genetically identical hybrid litters (B6SS and SSB6) suggests a maternal genetic contribution to susceptibility. Of the two major types of malformations, forelimb but not kidney malformations showed a pattern characteristic of a maternal genetic effect. It was concluded that maternal genetic effects can be distinguished from fetal genetic effects responsible for ethanol teratogenesis. Genetically based physiological responses to alcohol in the mother may confer varying degrees of risk for prenatal alcohol effects in the child.