Structural properties, magnetic interactions, magnetocaloric effect and critical behaviour of cobalt doped La0.7Te0.3MnO3

The effect of cobalt doping on the structural, magnetic and magnetocaloric properties of electron-doped manganite La0.7Te0.3Mn1-xCoxO3 (x = 0, 0.1, 0.2, 0.25, 0.3 and 0.5) has been investigated. The parent compound La0.7Te0.3MnO3 crystallizes in a rhombohedral structure with R (3) over barc space group. With the increase in Co concentration to x = 0.2, a structural transition from rhombohedral (R (3) over barc space group) to orthorhombic (Pbnm space group) is observed. X-ray photoelectron spectroscopy (XPS) indicates that the structural transition is due to the disordered distribution of Mn2+/Mn3+ and Co2+/Co3+ ions. All the samples undergo a paramagnetic-ferromagnetic (PM-FM) phase transition. With the increase in Co content to x = 0.1, the unit cell volume increases with a decrease in both Mn-O-Mn bond angle and T-c indicating a weakening of the double exchange interaction. However, with further increase in Co concentration, T-c increases. The presence of competing ferromagnetic and antiferromagnetic interactions leads to a glassy behaviour at low temperatures for low Co doping concentrations. However, for higher Co concentrations, no such behaviour is observed. Arrott plots reveal a second order nature of magnetic transition for all the samples. The magnetic exchange interactions for x = 0.3 and 0.5 follow the mean-field model. Magnetization results show that the magnetocaloric property of the electron-doped manganite is affected by the substitution of Co at Mn sites. Relatively large values of relative cooling power and broad temperature interval of the magnetocaloric effect make the present compounds promising for sub-room temperature magnetic refrigeration applications

Childhood encephalitis in the Greater Mekong region (the SouthEast Asia Encephalitis Project): a multicentre prospective study

Background Encephalitis is a worldwide public health issue, with a substantially high burden among children in southeast Asia. We aimed to determine the causes of encephalitis in children admitted to hospitals across the Greater Mekong region by implementing a comprehensive state-of-the-art diagnostic procedure harmonised across all centres, and identifying clinical characteristics related to patients’ conditions. Methods In this multicentre, observational, prospective study of childhood encephalitis, four referral hospitals in Cambodia, Vietnam, Laos, and Myanmar recruited children (aged 28 days to 16 years) who presented with altered mental status lasting more than 24 h and two of the following minor criteria: fever (within the 72 h before or after presentation), one or more generalised or partial seizures (excluding febrile seizures), a new-onset focal neurological deficit, cerebrospinal fluid (CSF) white blood cell count of 5 per mL or higher, or brain imaging (CT or MRI) suggestive of lesions of encephalitis. Comprehensive diagnostic procedures were harmonised across all centres, with first-line testing was done on samples taken at inclusion and results delivered within 24 h of inclusion for main treatable causes of disease and second-line testing was done thereafter for mostly non-treatable causes. An independent expert medical panel reviewed the charts and attribution of causes of all the included children. Using multivariate analyses, we assessed risk factors associated with unfavourable outcomes (ie, severe neurological sequelae and death) at discharge using data from baseline and day 2 after inclusion. This study is registered with ClinicalTrials.gov, NCT04089436, and is now complete. Findings Between July 28, 2014, and Dec 31, 2017, 664 children with encephalitis were enrolled. Median age was 4·3 years (1·8–8·8), 295 (44%) children were female, and 369 (56%) were male. A confirmed or probable cause of encephalitis was identified in 425 (64%) patients: 216 (33%) of 664 cases were due to Japanese encephalitis virus, 27 (4%) were due to dengue virus, 26 (4%) were due to influenza virus, 24 (4%) were due to herpes simplex virus 1, 18 (3%) were due to Mycobacterium tuberculosis, 17 (3%) were due to Streptococcus pneumoniae, 17 (3%) were due to enterovirus A71, 74 (9%) were due to other pathogens, and six (1%) were due to autoimmune encephalitis. Diagnosis was made within 24 h of admission to hospital for 83 (13%) of 664 children. 119 (18%) children had treatable conditions and 276 (42%) had conditions that could have been preventable by vaccination. At time of discharge, 153 (23%) of 664 children had severe neurological sequelae and 83 (13%) had died. In multivariate analyses, risk factors for unfavourable outcome were diagnosis of M tuberculosis infection upon admission (odds ratio 3·23 [95% CI 1·04–10·03]), coma on day 2 (2·90 [1·78–4·72]), supplementary oxygen requirement (1·89 [1·25–2·86]), and more than 1 week duration between symptom onset and admission to hospital (3·03 [1·68–5·48]). At 1 year after inclusion, of 432 children who were discharged alive from hospital with follow-up data, 24 (5%) had died, 129 (30%) had neurological sequelae, and 279 (65%) had completely recovered. Interpretation In southeast Asia, most causes of childhood encephalitis are either preventable or treatable, with Japanese encephalitis virus being the most common cause. We provide crucial information that could guide public health policy to improve diagnostic, vaccination, and early therapeutic guidelines on childhood encephalitis in the Greater Mekong region. Funding Institut Pasteur, Institut Pasteur International Network, Fondation Merieux, Aviesan Sud, INSERM, Wellcome Trust, Institut de Recherche pour le Développement (IRD), and Fondation Total. Translations For the Khmer, Lao, Vietnamese and Burmese translation of the abstract see Supplementary Materials section