The dissociation of NO–Ar(A) from around threshold to 200 cm−1 above threshold

We report an investigation of the dissociation of A state NO–Ar at energies from 23 cm−1 below the dissociation energy to 200 cm−1 above. The NO product rotational distributions show population in states that are not accessible with the energy available for excitation from the NO ground state. This effect is observed at photon energies from below the dissociation energy up to approximately 100 cm−1 above it. Translational energy distributions, extracted from velocity map images of individual rotational levels of the NO product, reveal contributions from excitation of high energy NO–Ar X states at all the excess energies probed, although this diminishes with increasing photon energy and is quite small at 200 cm−1, the highest energy studied. These translational energy distributions show that there are contributions arising from population in vibrational levels up to the X state dissociation energy. We propose that the reason such sparsely populated levels contribute to the observed dissociation is a considerable increase in the transition moment, via the Franck–Condon factor associated with these highly excited states, which arises because of the quite different geometries in the NO–Ar X and A states. This effect is likely to arise in other systems with similarly large geometry changes

Putting Food on the Table: Design Process

During the pandemic, needs for food supports were changing and the contactless delivery system was causing issues and not meeting the needs of the client

The binding energies of NO–Rg (Rg = He, Ne, Ar) determined by velocity map imaging

We report velocity map imaging measurements of the binding energies, D0, of NO–Rg (Rg = He, Ne, Ar) complexes. The X state binding energies determined are 3.0 ± 1.8, 28.6 ± 1.7, and 93.5 ± 0.9 cm−1 for NO–He, –Ne, and –Ar, respectively. These values compare reasonably well with ab initio calculations. Because the A–X transitions were unable to be observed for NO–He and NO–Ne, values for the binding energies in the A state of these complexes have not been determined. Based on our X state value and the reported A–X origin band position, the A state binding energy for NO–Ar was determined to be 50.6 ± 0.9 cm−1

Laboratory-confirmed respiratory infections as triggers for acute myocardial infarction and stroke: a self-controlled case series analysis of national linked datasets from Scotland

While acute respiratory tract infections can trigger cardiovascular events, the differential effect of specific organisms is unknown. This is important to guide vaccine policy.Using national infection surveillance data linked to the Scottish Morbidity Record, we identified adults with a first myocardial infarction or stroke from January 1, 2004 to December 31, 2014 and a record of laboratory-confirmed respiratory infection during this period. Using self-controlled case series analysis, we generated age- and season-adjusted incidence ratios (IRs) for myocardial infarction (n=1227) or stroke (n=762) after infections compared with baseline time.We found substantially increased myocardial infarction rates in the week after Streptococcus pneumoniae and influenza virus infection: adjusted IRs for days 1-3 were 5.98 (95% CI 2.47-14.4) and 9.80 (95% CI 2.37-40.5), respectively. Rates of stroke after infection were similarly high and remained elevated to 28 days: day 1-3 adjusted IRs 12.3 (95% CI 5.48-27.7) and 7.82 (95% CI 1.07-56.9) for S. pneumoniae and influenza virus, respectively. Although other respiratory viruses were associated with raised point estimates for both outcomes, only the day 4-7 estimate for stroke reached statistical significance.We showed a marked cardiovascular triggering effect of S. pneumoniae and influenza virus, which highlights the need for adequate pneumococcal and influenza vaccine uptake. Further research is needed into vascular effects of noninfluenza respiratory viruses

Thromboembolic and neurologic sequelae of discontinuation of an antihyperlipidemic drug during ongoing warfarin therapy

Warfarin and antihyperlipidemics are commonly co-prescribed. Some antihyperlipidemics may inhibit warfarin deactivation via the hepatic cytochrome P450 system. Therefore, antihyperlipidemic discontinuation has been hypothesized to result in underanticoagulation, as warfarin metabolism is no longer inhibited. We quantified the risk of venous thromboembolism (VTE) and ischemic stroke (IS) due to statin and fibrate discontinuation in warfarin users, in which warfarin was initially dose-titrated during ongoing antihyperlipidemic therapy. Using 1999-2011 United States Medicaid claims among 69 million beneficiaries, we conducted a set of bidirectional self-controlled case series studies-one for each antihyperlipidemic. Outcomes were hospital admissions for VTE/IS. The risk segment was a maximum of 90 days immediately following antihyperlipidemic discontinuation, the exposure of interest. Time-varying confounders were included in conditional Poisson models. We identified 629 study eligible-persons with at least one outcome. Adjusted incidence rate ratios (IRRs) for all antihyperlipidemics studied were consistent with the null, and ranged from 0.21 (0.02, 2.82) for rosuvastatin to 2.16 (0.06, 75.0) for gemfibrozil. Despite using an underlying dataset of millions of persons, we had little precision in estimating IRRs for VTE/IS among warfarin-treated persons discontinuing individual antihyperlipidemics. Further research should investigate whether discontinuation of gemfibrozil in warfarin users results in serious underanticoagulation

A cross-bispectrum estimator for CMB-HI intensity mapping correlations

Intensity mapping of 21cm emission from neutral hydrogen (HI) promises to be a powerful probe of large-scale structure in the post-reionisation epoch. However, HI intensity mapping (IM) experiments will suffer the loss of long-wavelength line-of-sight HI modes in the galactic foreground subtraction process. The loss of these modes is particularly problematic for detecting HI IM cross-correlations with projected large-scale structure tracers, such as CMB secondary anisotropies. Here, we propose a cross-bispectrum estimator to recover the cross-correlation of the HI IM field, $\delta T_{21},$ with the CMB lensing field, $\kappa,$ constructed by correlating the position-dependent HI power spectrum with the mean overdensity traced by CMB lensing. We study the cross-bispectrum estimator, $B^{\bar \kappa \delta T_{21} \delta T_{21}},$ in the squeezed limit and forecast its detectability based on HI IM measurements from HIRAX and CMB lensing measurements from AdvACT. The cross-bispectrum improves constraints on cosmological parameters; in particular, the constraint on the dark energy equation-of-state parameter, $w_0,$ improves on the HI IM auto-power spectra constraint by 44\% (to 0.014), while the constraint on $w_a$ improves by 33\% (to 0.08), assuming Planck priors in each case. These results are robust to HI IM foreground removal because they largely derive from small-scale HI modes. The HI-HI-$\kappa$ cross-bispectrum thus provides a novel way to recover HI correlations with CMB lensing and constrain cosmological parameters at a level that is competitive with next-generation galaxy redshift surveys. As a striking example of this, we find that the combined constraint on the sum of the neutrino masses, while varying all redshift and standard cosmological parameters within a $w_0w_a\Omega_K$CDM model, is 5.5 meV.Comment: 11 pages, 4 figure

Developmental trajectory of communication repair in children with Fragile X Syndrome

This work is licensed under a Creative Commons Attribution 4.0 International License.Background and aims The development of communicative competence requires both language and social skills. The ability to repair following a communication breakdown is critical for continued conversational interchange and to ensure comprehension of bids for communication. Communication repair demonstrates adequate language and social skills. Children with Fragile X Syndrome have difficulty with language development and social skills, which may result in delays or deficits in repair. Repair may be additionally impaired in children with Fragile X Syndrome and co-morbid autism. This study examined the development of repair in children with Fragile X Syndrome from toddlerhood into middle childhood. Methods Fifty-five children with Fragile X Syndrome and their biological mothers participated. Data were collected during in-home visits approximately every 18 months. Videotaped mother–child interactions were collected, as well as standardized assessments of language, social skills, and autism symptomology. Results Children with Fragile X Syndrome acquired the ability to repair at 90% mastery by three-and-a-half years of age. Multilevel logistic regressions predicting probability of repair indicated marginally significant effects of mean length of utterance and number of different words, and significant effects of global social skills and autism symptomology. Effect sizes were small to moderate. Conclusions Ability to repair was measured in a naturalistic setting, which allowed children with Fragile X Syndrome to utilize repairs in their daily interactions. Although children with Fragile X Syndrome may have delayed development of repair relative to typically developing expectations, in general they nonetheless catch up and demonstrate a robust ability to repair by three-and-a-half years of age. However, this study provides evidence that individual differences in language and social skills may influence ability to repair in children with Fragile X Syndrome. Finally, the relationship between autism symptoms and repair remains unclear, necessitating further exploration. Implications: Given the noted delay in repair in young children with Fragile X Syndrome, clinicians working with this population should target development of this skill as early as possible to maximize successful social interactions. This may be particularly necessary for children with Fragile X Syndrome and co-morbid autism.NIH T32 DC000052NICHD R01 HD084563NICHD P30 HD003110P30 HD0253