Stability and hyperfine structure of the four- and five-body muon-atomic clusters a+b+μ−e−a^{+} b^{+} \mu^{-} e^{-} and a+b+μ−e−e−a^{+} b^{+} \mu^{-} e^{-} e^{-}

Based on the results of accurate variational calculations we demonstrate stability of the five-body negatively charged ions $a^{+} b^{+} \mu^{-} e^{-} e^{-}$. Each of these five-body ions contains two electrons $e^{-}$, one negatively charged muon $\mu^{-}$ and two nuclei of the hydrogen isotopes $a, b = (p, d, t)$. The bound state properties of these five-body ions, including their hyperfine structure, are briefly discussed. We also investigate the hyperfine structure of the ground states of the four-body muonic quasi-atoms $a^{+} b^{+} \mu^{-} e^{-}$. In particular, we determine the hyperfine structure splittings for the ground state of the four-body muonic quasi-atoms: $p^{+} d^{+} \mu^{-} e^{-}$ and $p^{+} t^{+} \mu^{-} e^{-}$

Highly accurate calculations of the rotationally excited bound states in three-body systems

An effective optimization strategy has been developed to construct highly accurate bound state wave functions in various three-body systems. Our procedure appears to be very effective for computations of weakly bound states and various excited states, including rotationally excited states, i.e. states with $L \ge 1$. The efficiency of our procedure is illustrated by computations of the excited $P^{*}(L = 1)-$states in the $dd\mu, dt\mu$ and $tt\mu$ muonic molecular ions, $P(L = 1)-$states in the non-symmetric $pd\mu, pt\mu$ and $dt\mu$ ions and $2^{1}P(L = 1)-$ and $2^{3}P(L = 1)-$states in He atom(s)

Multifrequency Radio Observations of a SNR in the LMC. The Case of SNR J0527-6549 (DEM l204)

We present a detailed study and results of new Australia Telescope Compact Array (ATCA) observations of supernova remnant, SNR J0527-6549. This Large Magellanic Cloud (LMC) ob ject follows a typical supernova remnant (SNR) horseshoe morphology with a diameter of D=(66x58)+-1 pc which is among the largest SNRs in the LMC. Its relatively large size indicates older age while a steeper than expected radio spectral index of aplha=-0.92+-0.11 is more typical for younger and energetic SNRs. Also, we report detections of regions with a high order of polarization at a peak value of ~54+-17% at 6 cm.Comment: 9 Pages, 6 figures, accepted for publication in SA

Differential gene expression in multiple neurological, inflammatory and connective tissue pathways in a spontaneous model of human small vessel stroke

Aims: Cerebral small vessel disease (SVD) causes a fifth of all strokes plus diffuse brain damage leading to cognitive decline, physical disabilities and dementia. The aetiology and pathogenesis of SVD are unknown, but largely attributed to hypertension or microatheroma. Methods: We used the spontaneously hypertensive stroke-prone rat (SHRSP), the closest spontaneous experimental model of human SVD, and age-matched control rats kept under identical, non-salt-loaded conditions, to perform a blinded analysis of mRNA microarray, qRT-PCRand pathway analysis in two brain regions (frontal and midcoronal) commonly affected by SVD in the SHRSP at age five, 16 and 21 weeks. Results: We found gene expression abnormalities, with fold changes ranging from 2.5 to 59 for the 10 most differentially expressed genes, related to endothelial tight junctions (reduced), nitric oxide bioavailability (reduced), myelination (impaired), glial and microglial activity (increased), matrix proteins (impaired), vascular reactivity (impaired) and albumin (reduced), consistent with protein expression defects in the same rats. All were present at age 5 weeks thus pre-dating blood pressure elevation. ‘Neurological’ and ‘inflammatory’ pathways were more affected than ‘vascular’ functional pathways. Conclusions: This set of defects, although individually modest, when acting in combination could explain the SHRSP's susceptibility to microvascular and brain injury, compared with control rats. Similar combined, individually modest, but multiple neurovascular unit defects, could explain susceptibility to spontaneous human SVD

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events

A comparison of location of acute symptomatic vs. 'silent' small vessel lesions

Background: Acute lacunar ischaemic stroke, white matter hyperintensities, and lacunes are all features of cerebral small vessel disease. It is unclear why some small vessel disease lesions present with acute stroke symptoms, whereas others typically do not. Aim: To test if lesion location could be one reason why some small vessel disease lesions present with acute stroke, whereas others accumulate covertly. Methods: We identified prospectively patients who presented with acute lacunar stroke symptoms with a recent small subcortical infarct confirmed on magnetic resonance diffusion imaging. We compared the distribution of the acute infarcts with that of white matter hyperintensity and lacunes using computational image mapping methods. Results: In 188 patients, mean age 67 ± standard deviation 12 years, the lesions that presented with acute lacunar ischaemic stroke were located in or near the main motor and sensory tracts in (descending order): posterior limb of the internal capsule (probability density 0·2/mm3), centrum semiovale (probability density = 0·15/mm3), medial lentiform nucleus/lateral thalamus (probability density = 0·09/mm3), and pons (probability density = 0·02/mm3). Most lacunes were in the lentiform nucleus (probability density = 0·01–0·04/mm3) or external capsule (probability density = 0·05/mm3). Most white matter hyperintensities were in centrum semiovale (except for the area affected by the acute symptomatic infarcts), external capsules, basal ganglia, and brainstem, with little overlap with the acute symptomatic infarcts (analysis of variance, P < 0·01). Conclusions: Lesions that present with acute lacunar ischaemic stroke symptoms may be more likely noticed by the patient through affecting the main motor and sensory tracts, whereas white matter hyperintensity and asymptomatic lacunes mainly affect other areas. Brain location could at least partly explain the symptomatic vs. covert development of small vessel disease