Experimental studies of the effect of rapid afterburn on shock development of near-field explosions

Many conventional high explosives do not contain sufficient internal oxygen to fully combust the gaseous products which result from detonation of the explosive material. Because of this, under-oxygenated explosives continue to burn after detonation. This process, called afterburn, is known to influence the late-time pressure and energy released by the explosive, which has particular significance for confined explosives. Recent experimental work at the University of Sheffield, along with a small number of previous studies, has shown that some afterburn occurs at timescales commensurate with the development of the shock wave. This article presents the results from a series of tests measuring the reflected pressure acting on a rigid target following the detonation of small explosive charges. High-speed video is used to capture the emerging structure of the detonation products and air shock, while the spatial and temporal distributions of the reflected pressure are recorded using an array of 17 Hopkinson pressure bars set flush with an effectively rigid target. Tests are conducted in inert atmospheres and oxygen-rich atmospheres in order to assess the contribution of rapid afterburn on the development of the shock front and interaction with a rigid target situated close to the explosive charge. The results show that early-stage afterburn has a significant influence on the reflected shock parameters in the near-field

Women’s views on the impact of operative delivery in the second stage of labour: Qualitative interview study

Objective: To obtain the views of women on the impact of operative delivery in the second stage of labour. Design: Qualitative interview study. Setting: Two urban teaching hospitals in the United Kingdom. Participants: Purposive sample of 27 women who had undergone operative delivery in the second stage of labour between January 2000 and January 2002. Key themes: Preparation for birth, understandings of the indications for operative delivery, and explanation or debriefing after birth. Results: The women felt unprepared for operative delivery and thought that their birth plan or antenatal classes had not catered adequately for this event. They emphasised the importance of maintaining an open mind about the management of labour. They had difficulty understanding the need for operative delivery despite a review by medical and midwifery staff before discharge. Operative delivery had a noticeable impact on women's views about future pregnancy and delivery. Conclusions: Women consider postnatal debriefing and medical review important deficiencies in current care. Those who experienced operative delivery in the second stage of labour would welcome the opportunity to have a later review of their intrapartum care, physical recovery, and management of future pregnancies

Doppler-Free Spectroscopy of Weak Transitions: An Analytical Model Applied to Formaldehyde

Experimental observation of Doppler-free signals for weak transitions can be greatly facilitated by an estimate for their expected amplitudes. We derive an analytical model which allows the Doppler-free amplitude to be estimated for small Doppler-free signals. Application of this model to formaldehyde allows the amplitude of experimentally observed Doppler-free signals to be reproduced to within the experimental error.Comment: 7 pages, 7 figures, 1 table, v2: many small improvements + corrected line assignmen

Heterozygous mutations in HSD17B4 cause juvenile peroxisomal D-bifunctional protein deficiency

Objective: To determine the genetic cause of slowly progressive cerebellar ataxia, sensorineural deafness, and hypergonadotropic hypogonadism in 5 patients from 3 different families. Methods: The patients comprised 2 sib pairs and 1 sporadic patient. Clinical assessment included history, physical examination, and brain MRI. Linkage analysis was performed separately on the 2 sets of sib pairs using single nucleotide polymorphism microarrays, followed by analysis of the intersection of the regions. Exome sequencing was performed on 1 affected patient with variant filtering and prioritization undertaken using these intersected regions. Results: Using a combination of sequencing technologies, we identified compound heterozygous mutations in HSD17B4 in all 5 affected patients. In all 3 families, peroxisomal D-bifunctional protein (DBP) deficiency was caused by compound heterozygosity for 1 nonsense/deletion mutation and 1 missense mutation. Conclusions: We describe 5 patients with juvenile DBP deficiency from 3 different families, bringing the total number of reported patients to 14, from 8 families. This report broadens and consolidates the phenotype associated with juvenile DBP deficiency

Complete callosal agenesis, pontocerebellar hypoplasia, and axonal neuropathy due to AMPD2 loss

Objective: To determine the molecular basis of a severe neurologic disorder in a large consanguineous family with complete agenesis of the corpus callosum (ACC), pontocerebellar hypoplasia (PCH), and peripheral axonal neuropathy. Methods: Assessment included clinical evaluation, neuroimaging, and nerve conduction studies (NCSs). Linkage analysis used genotypes from 7 family members, and the exome of 3 affected siblings was sequenced. Molecular analyses used Sanger sequencing to perform segregation studies and cohort analysis and Western blot of patient-derived cells. Results: Affected family members presented with postnatal microcephaly and profound developmental delay, with early death in 3. Neuroimaging, including a fetal MRI at 30 weeks, showed complete ACC and PCH. Clinical evaluation showed areflexia, and NCSs revealed a severe axonal neuropathy in the 2 individuals available for electrophysiologic study. A novel homozygous stopgain mutation in adenosine monophosphate deaminase 2 (AMPD2) was identified within the linkage region on chromosome 1. Molecular analyses confirmed that the mutation segregated with disease and resulted in the loss of AMPD2. Subsequent screening of a cohort of 42 unrelated individuals with related imaging phenotypes did not reveal additional AMPD2 mutations. Conclusions: We describe a family with a novel stopgain mutation in AMPD2. We expand the phenotype recently described as PCH type 9 to include progressive postnatal microcephaly, complete ACC, and peripheral axonal neuropathy. Screening of additional individuals with related imaging phenotypes failed to identify mutations in AMPD2, suggesting that AMPD2 mutations are not a common cause of combined callosal and pontocerebellar defects