Weakly dispersive modal pulse propagation in the North Pacific Ocean

Author Posting. © Acoustical Society of America, 2013. This article is posted here by permission of Acoustical Society of America or personal use, not for redistribution. The definitive version was published in Journal of the Acoustical Society of America 134 (2013): 3386, doi:10.1121/1.4820882.The propagation of weakly dispersive modal pulses is investigated using data collected during the 2004 long-range ocean acoustic propagation experiment (LOAPEX). Weakly dispersive modal pulses are characterized by weak dispersion- and scattering-induced pulse broadening; such modal pulses experience minimal propagation-induced distortion and are thus well suited to communications applications. In the LOAPEX environment modes 1, 2, and 3 are approximately weakly dispersive. Using LOAPEX observations it is shown that, by extracting the energy carried by a weakly dispersive modal pulse, a transmitted communications signal can be recovered without performing channel equalization at ranges as long as 500 km; at that range a majority of mode 1 receptions have bit error rates (BERs) less than 10%, and 6.5% of mode 1 receptions have no errors. BERs are estimated for low order modes and compared with measurements of signal-to-noise ratio (SNR) and modal pulse spread. Generally, it is observed that larger modal pulse spread and lower SNR result in larger BERs.This work was supported by the Office of Naval Research, Code 322, Grant Nos. N00014-06-1-0245, N00014-08-1-0195, and N00014-11-1-0194

Modal analysis of the range evolution of broadband wavefields in the North Pacific Ocean : low mode numbers

Author Posting. © Acoustical Society of America, 2012. This article is posted here by permission of Acoustical Society of America for personal use, not for redistribution. The definitive version was published in Journal of the Acoustical Society of America 131 (2012): 4409-4427, doi:10.1121/1.4707431.The results of mode-processing measurements of broadband acoustic wavefields made in the fall of 2004 as part of the Long-Range Ocean Acoustic Propagation Experiment (LOAPEX) in the eastern North Pacific Ocean are reported here. Transient wavefields in the 50–90 Hz band that were recorded on a 1400 -m long 40 element vertical array centered near the sound channel axis are analyzed. This array was designed to resolve low-order modes. The wavefields were excited by a ship-suspended source at seven ranges, between approximately 50 and 3200 km, from the receiving array. The range evolution of broadband modal arrival patterns corresponding to fixed mode numbers (“modal group arrivals”) is analyzed with an emphasis on the second (variance) and third (skewness) moments. A theory of modal group time spreads is described, emphasizing complexities associated with energy scattering among low-order modes. The temporal structure of measured modal group arrivals is compared to theoretical predictions and numerical simulations. Theory, simulations, and observations generally agree. In cases where disagreement is observed, the reasons for the disagreement are discussed in terms of the underlying physical processes and data limitations.This work was supported by the Office of Naval Research, Code 322, Grant Nos. N00014-08-1-0195, N00014-06-1-0245, and N0014-11-1-0194

In the dedicated pursuit of dedicated capital: restoring an indigenous investment ethic to British capitalism

Tony Blair’s landslide electoral victory on May 1 (New Labour Day?) presents the party in power with a rare, perhaps even unprecedented, opportunity to revitalise and modernise Britain’s ailing and antiquated manufacturing economy.* If it is to do so, it must remain true to its long-standing (indeed, historic) commitment to restore an indigenous investment ethic to British capitalism. In this paper we argue that this in turn requires that the party reject the very neo-liberal orthodoxies which it offered to the electorate as evidence of its competence, moderation and ‘modernisation’, which is has internalised, and which it apparently now views as circumscribing the parameters of the politically and economically possible

Allergic Rhinitis and its Associated Co-Morbidities at Bugando Medical Centre in Northwestern Tanzania; A Prospective Review of 190 Cases.

Allergic rhinitis is one of the commonest atopic diseases which contribute to significant morbidity world wide while its epidemiology in Tanzania remains sparse. There was paucity of information regarding allergic rhinitis in our setting; therefore it was important to conduct this study to describe our experience on allergic rhinitis, associated co-morbidities and treatment outcome in patients attending Bugando Medical Centre. This was descriptive cross-sectional study involving all patients with a clinical diagnosis of allergic rhinitis at Bugando Medical Centre over a three-month period between June 2011 and August 2011. Data was collected using a pre-tested coded questionnaire and analyzed using SPSS statistical computer software version 17.0. A total of 190 patients were studied giving the prevalence of allergic rhinitis 14.7%. The median age of the patients was 8.5 years. The male to female ratio was 1:1. Adenoid hypertrophy, tonsillitis, hypertrophy of inferior turbinate, nasal polyps, otitis media and sinusitis were the most common co-morbidities affecting 92.6% of cases and were the major reason for attending hospital services. Sleep disturbance was common in children with adenoids hypertrophy (χ2 = 28.691, P = 0.000). Allergic conjunctivitis was found in 51.9%. The most common identified triggers were dust, strong perfume odors and cold weather (P < 0.05). Strong perfume odors affect female than males (χ2 = 4.583, P = 0.032). In this study family history of allergic rhinitis was not a significant risk factor (P =0.423). The majority of patients (68.8%) were treated surgically for allergic rhinitis co morbidities. Post operative complication and mortality rates were 2.9% and 1.6% respectively. The overall median duration of hospital stay of in-patients was 3 days (2 - 28 days). Most patients (98.4%) had satisfactory results at discharge. The study shows that allergic rhinitis is common in our settings representing 14.7% of all otorhinolaryngology and commonly affecting children and adolescent. Sufferers seek medical services due to co-morbidities of which combination of surgical and medical treatment was needed. High index of suspicions in diagnosing allergic rhinitis and early treatment is recommended

Massive stars in the giant molecular cloud G23.3−0.3 and W41

Context. Young massive stars and stellar clusters continuously form in the Galactic disk, generating new Hii regions within their natal giant molecular clouds and subsequently enriching the interstellar medium via their winds and supernovae.Aims. Massive stars are among the brightest infrared stars in such regions; their identification permits the characterisation of the star formation history of the associated cloud as well as constraining the location of stellar aggregates and hence their occurrence as a function of global environment.Methods. We present a stellar spectroscopic survey in the direction of the giant molecular cloud G23.3−0.3. This complex is located at a distance of ~4–5 kpc, and consists of several Hii regions and supernova remnants.Results. We discovered 11 OfK+ stars, one candidate luminous blue variable, several OB stars, and candidate red supergiants. Stars with K-band extinction from ~1.3–1.9 mag appear to be associated with the GMC G23.3−0.3; O and B-types satisfying this criterion have spectrophotometric distances consistent with that of the giant molecular cloud. Combining near-IR spectroscopic and photometric data allowed us to characterize the multiple sites of star formation within it. The O-type stars have masses from ~25–45 M⊙, and ages of 5–8 Myr. Two new red supergiants were detected with interstellar extinction typical of the cloud; along with the two RSGs within the cluster GLIMPSE9, they trace an older burst with an age of 20–30 Myr. Massive stars were also detected in the core of three supernova remnants – W41, G22.7−0.2, and G22.7583−0.4917.Conclusions. A large population of massive stars appears associated with the GMC G23.3−0.3, with the properties inferred for them indicative of an extended history of stars formation

Massive Stars In The W33 Giant Molecular Complex

Rich in H II regions, giant molecular clouds are natural laboratories to study massive stars and sequential star formation. The Galactic star-forming complex W33 is located at = ∼ ◦ l 12.8 and at a distance of 2.4 kpc and has a size of ≈10 pc and a total mass of ≈(0.8−8.0) × 105 M⊙. The integrated radio and IR luminosity of W33—when combined with the direct detection of methanol masers, the protostellar object W33A, and the protocluster embedded within the radio source W33 main—mark the region as a site of vigorous ongoing star formation. In order to assess the long-term star formation history, we performed an infrared spectroscopic search for massive stars, detecting for the first time 14 early-type stars, including one WN6 star and four O4–7 stars. The distribution of spectral types suggests that this population formed during the past ∼2–4 Myr, while the absence of red supergiants precludes extensive star formation at ages 6–30 Myr. This activity appears distributed throughout the region and does not appear to have yielded the dense stellar clusters that characterize other star-forming complexes such as Carina and G305. Instead, we anticipate that W33 will eventually evolve into a loose stellar aggregate, with Cyg OB2 serving as a useful, albeit richer and more massive, comparator. Given recent distance estimates, and despite a remarkably similar stellar population, the rich cluster Cl 1813–178 located on the northwest edge of W33 does not appear to be physically associated with W33

Myosin-I nomenclature

We suggest that the vertebrate myosin-I field adopt a common nomenclature system based on the names adopted by the Human Genome Organization (HUGO). At present, the myosin-I nomenclature is very confusing; not only are several systems in use, but several different genes have been given the same name. Despite their faults, we believe that the names adopted by the HUGO nomenclature group for genome annotation are the best compromise, and we recommend universal adoption

Seed amplification and neurodegeneration marker trajectories in individuals at risk of prion disease

Human prion diseases are remarkable for long incubation times followed typically by rapid clinical decline. Seed amplification assays and neurodegeneration biofluid biomarkers are remarkably useful in the clinical phase, but their potential to predict clinical onset in healthy people remains unclear. This is relevant not only to the design of preventive strategies in those at-risk of prion diseases, but more broadly, because prion-like mechanisms are thought to underpin many neurodegenerative disorders. Here, we report the accrual of a longitudinal biofluid resource in patients, controls and healthy people at risk of prion diseases, to which ultrasensitive techniques such as real-time quaking-induced conversion (RT-QuIC), and single molecule array (Simoa) digital immunoassays were applied for preclinical biomarker discovery. We studied 648 CSF and plasma samples, including 16 people who had samples taken when healthy but later developed inherited prion disease (IPD) ("converters"; range from 9.9 prior to, and 7.4 years after onset). Symptomatic IPD CSF samples were screened by RT-QuIC assay variations, before testing the entire collection of at-risk samples using the most sensitive assay. Glial fibrillary acidic protein (GFAP), neurofilament light (NfL), tau and ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) levels were measured in plasma and CSF. Second generation (IQ-CSF) RT-QuIC proved 100% sensitive and specific for sporadic Creutzfeldt-Jakob disease (sCJD), iatrogenic (iCJD) and familial CJD phenotypes, and subsequently detected seeding activity in four presymptomatic CSF samples from three E200K carriers; one converted in under two months while two remain asymptomatic after at least three years' follow-up. A bespoke HuPrP P102L RT-QuIC showed partial sensitivity for P102L disease. No compatible RT-QuIC assay was discovered for classical 6-OPRI, A117V and D178N, and these at-risk samples tested negative with bank vole RT-QuIC. Plasma GFAP and NfL, and CSF NfL levels emerged as proximity markers of neurodegeneration in the typically slow IPDs (e.g. P102L), with significant differences in mean values segregating healthy control from IPD carriers (within 2 years to onset) and symptomatic IPD cohorts; plasma GFAP appears to change before NfL, and before clinical conversion. In conclusion, we show distinct biomarker trajectories in fast and slow IPDs. Specifically, we identify several years of presymptomatic seeding positivity in E200K, a new proximity marker (plasma GFAP) and sequential neurodegenerative marker evolution (plasma GFAP followed by NfL) in slow IPDs. We suggest a new preclinical staging system featuring clinical, seeding and neurodegeneration aspects, for validation with larger prion at-risk cohorts, and with potential application to other neurodegenerative proteopathies

Missense mutations in the copper transporter gene ATP7A cause X-Linked distal hereditary motor neuropathy

Distal hereditary motor neuropathies comprise a clinically and genetically heterogeneous group of disorders. We recently mapped an X-linked form of this condition to chromosome Xq13.1-q21 in two large unrelated families. The region of genetic linkage included ATP7A, which encodes a copper-transporting P-type ATPase mutated in patients with Menkes disease, a severe infantile-onset neurodegenerative condition. We identified two unique ATP7A missense mutations (p.P1386S and p.T994I) in males with distal motor neuropathy in two families. These molecular alterations impact highly conserved amino acids in the carboxyl half of ATP7A and do not directly involve the copper transporter's known critical functional domains. Studies of p.P1386S revealed normal ATP7A mRNA and protein levels, a defect in ATP7A trafficking, and partial rescue of a S. cerevisiae copper transport knockout. Although ATP7A mutations are typically associated with severe Menkes disease or its milder allelic variant, occipital horn syndrome, we demonstrate here that certain missense mutations at this locus can cause a syndrome restricted to progressive distal motor neuropathy without overt signs of systemic copper deficiency. This previously unrecognized genotype-phenotype correlation suggests an important role of the ATP7A copper transporter in motor-neuron maintenance and function