Novel Nanostructured Anodes For Green Energy Battery Storage

The quest to increase the lithium storage capacity of anodes in lithium-ion batteries is a prominent goal in battery research. The conventional graphitic Carbon-based anode material achieves a maximum capacity of 372 mAh g-1, limited by the stoichiometry of the lithiated state Lithium Carbide (LiC6). To overcome this limitation, Silicon anodes offer a theoretical storage capacity approximately ten times higher, albeit accompanied by a significant volume expansion issue. This study firstly explores various methods of fabricating composite materials as anodes, when combining Graphite and Silicon. The studies include the use of nano particle graphite as well as a physical method of nanoparticles deposition with a Matrix Assembly Clusters Source (MACS). The project was inspired by the ultimate prospect of employing cluster (nanoparticle) beam implantation techniques to embed small Silicon Nanoclusters, sized between 1-3 nm, into a porous carbon host. The utilization of such small Silicon particle sizes, embedded between Graphite particles, might possibly solve the volume expansion problem while retaining the benefit of additional storage density. Anodes were made using various graphites as reference active materials, both conventionally sized (D50 8.4 μm) and Graphite nano powder to aid homogenous dispersion, and with the addition of Silicon Nanoparticles. These were made into slurries with Carbon Black and binder and cast on to foil prior to assembly into half-cells with lithium metal. The reference anodes made using conventional graphite performed as expected, with specific capacities close to expected values. However, when using Nano Graphite, the morphology of the powder caused significant drying and processing issues, that made it difficult to reliably cast the anode, causing delamination and ultimately higher instances of cell failure and lower specific capacity. Integration of the Silicon nano powder gave some evidence of improved results, but data were inconsistent and hindered by processing issues and high instances cell failure. First demonstrative experiments utilising the MACS approach, which offers the advantage of integrating Silicon with larger Graphite particles, gave composite anodes that were able to be readily processed into an anode in the same way as conventional Graphite, without delamination or excessive cell failure. The resultant half-cells gave slightly higher capacity than reference Graphite cells, but more work is needed to develop and verify the processing to validate the extent of the Silicon coating on the Graphite and confirm its effect on capacity

Twenty years of experience with intraoperative pulmonary artery stenting

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138274/1/ccd27094_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138274/2/ccd27094.pd

Digital financial services and household accounting in rural Fiji

A major priority of the Reserve Bank of Fiji (RBF) is to increase financial inclusion of rural peoples – i.e. provide rural dwellers with improved access to financial services. This issue is important because rural Fijians, who account for 49.2% of Fiji’s population, rely significantly on remittances from family and relatives working in urban areas or foreign countries. Indeed, these remittances may be the only source of income for some rural dwellers. Improving financial inclusion can reduce poverty and improve social welfare. While much has been written on financial inclusion in developed countries, scant literature exists regarding the success and efficacy of financial inclusion strategies in Pacific Islands Countries. This study contributes to the limited but growing literature on financial inclusion in the Pacific by examining rural dwellers’ perceptions of rural banking and Digital Financial Services in Fiji and identifying factors which enhance or impeded their uptake of these services. It will also examine how these services complement or substitute household accounting systems. The first stage of the study involved interviews with the Central Bank, Mobile Network Operators, Commercial Banks and other stakeholders. The second stage involves a survey and subsequent follow‐up interviews in rural areas of Vanua Levu. The findings may assist commercial banks and MNOs in designing DFS that better meet the needs of those living on Fiji’s outer margins. They may also inform government and the regulators on potential revisions to regulatory mechanisms for financial inclusion

Perceptions of Digital Financial Services in Rural Fiji

This article examines rural dwellers’ perceptions of digital financial services (DFS) to identify which factors may enhance or impede their adoption. The article is based on a survey and follow-up interviews in rural Fijian communities with relatively low income levels. In Fiji, DFS are provided by mobile network operators, either individually or in collaboration with commercial banks. The provision of these services is consistent with policies of the Fijian government and The Reserve Bank of Fiji, which advocate financial inclusion as a means of promoting economic growth and enabling citizens to more efficiently receive remittances and welfare payments. However, the survey findings indicate that DFS uptake is hindered by agents’ lack of liquidity and the implicit costs that agents impose on consumers. In addition, consumers tend to fully spend the funds received through mobile money, but fail to use their mobile phones for saving purposes

Oestrogen receptor alpha in pulmonary hypertension

Aims Pulmonary arterial hypertension (PAH) occurs more frequently in women with mutations in bone morphogenetic protein receptor type 2 (BMPR2) and dysfunctional BMPR2 signalling underpinning heritable PAH. We have previously shown that serotonin can uncover a pulmonary hypertensive phenotype in BMPR2+/− mice and that oestrogen can increase serotinergic signalling in human pulmonary arterial smooth muscle cells (hPASMCs). Hence, here we wished to characterize the expression of oestrogen receptors (ERs) in male and female human pulmonary arteries and have examined the influence of oestrogen and serotonin on BMPR2 and ERα expression. Methods and results: By immunohistochemistry, we showed that ERα, ERβ, and G-protein-coupled receptors are expressed in human pulmonary arteries localizing mainly to the smooth muscle layer which also expresses the serotonin transporter (SERT). Protein expression of ERα protein was higher in female PAH patient hPASMCs compared with male and serotonin also increased the expression of ERα. 17β-estradiol induced proliferation of hPASMCs via ERα activation and this engaged mitogen-activated protein kinase and Akt signalling. Female mice over-expressing SERT (SERT+ mice) develop PH and the ERα antagonist MPP attenuated the development of PH in normoxic and hypoxic female SERT+ mice. The therapeutic effects of MPP were accompanied by increased expression of BMPR2 in mouse lung. Conclusion: ERα is highly expressed in female hPASMCs from PAH patients and mediates oestrogen-induced proliferation of hPASMCs via mitogen-activated protein kinase and Akt signalling. Serotonin can increase ERα expression in hPASMCs and antagonism of ERα reverses serotonin-dependent PH in the mouse and increases BMPR2 expression.</p

Plasma proteome analysis in patients with pulmonary arterial hypertension: an observational cohort study

BackgroundIdiopathic and heritable pulmonary arterial hypertension form a rare but molecularly heterogeneous disease group. We aimed to measure and validate differences in plasma concentrations of proteins that are associated with survival in patients with idiopathic or heritable pulmonary arterial hypertension to improve risk stratification

Absence of influence of gender and BMPR2 mutation type on clinical phenotypes of pulmonary arterial hypertension

<p>Abstract</p> <p>Background</p> <p>Previous studies indicate that patients with pulmonary arterial hypertension (PAH) carrying a mutation in the bone morphogenetic protein receptor type 2 (<it>BMPR2</it>) gene, develop the disease 10 years earlier than non-carriers, and have a more severe hemodynamic compromise at diagnosis. A recent report has suggested that this may only be the case for females and that patients with missense mutations in <it>BMPR2 </it>gene have more severe disease than patients with truncating mutations.</p> <p>Methods</p> <p>We reviewed data from all patients with PAH considered as idiopathic and patients with a family history of PAH, who underwent genetic counselling in the French PAH network between January, 1^st2004 and April, 1^st2010. We compared clinical, functional, and hemodynamic characteristics between carriers and non-carriers of a <it>BMPR2 </it>mutation, according to gender or <it>BMPR2 </it>mutation type.</p> <p>Results</p> <p>PAH patients carrying a <it>BMPR2 </it>mutation (n = 115) were significantly younger at diagnosis than non-carriers (n = 267) (35.8 ± 15.4 and 47.5 ± 16.2 respectively, p < 0.0001). The presence of a <it>BMPR2 </it>mutation was associated with a younger age at diagnosis in females (36.4 ± 14.9 in <it>BMPR2 </it>mutation carriers and 47.4 ± 15.8 in non-carriers, p < 0.0001), and males (34.6 ± 16.8 in <it>BMPR2 </it>mutation carriers and 47.8 ± 17.1 in non-carriers, p < 0.0001). <it>BMPR2 </it>mutation carriers had a more severe hemodynamic compromise at diagnosis, but this was not influenced by gender. No differences in survival and time to death or lung transplantation were found in male and female PAH patients carrying a <it>BMPR2 </it>mutation. No differences were observed in clinical outcomes according to the type of <it>BMPR2 </it>mutations (missense, truncating, large rearrangement or splice defect).</p> <p>Conclusion</p> <p>When compared to non-carriers, <it>BMPR2 </it>mutation carriers from the French PAH network are younger at diagnosis and present with a more severe hemodynamic compromise, irrespective of gender. Moreover, <it>BMPR2 </it>mutation type had no influence on clinical phenotypes in our patient population.</p

Functional assessment of the BMPR2 gene in lymphoblastoid cell lines from Graves’ disease patients

In this study, we analysed the possible influence of the c.419‐43delT BMPR2 variant in patients with Graves’ disease (GD), in a molecular basis, focusing our efforts on possible alterations in the mRNA processing and synthesis. The molecular assessment of this variant in patients with GD would shed light on the association between the BMPR2 gene and the disease. The variant was detected in 18%, 55% and 10% of patients with pulmonary arterial hypertension, GD and in general population, respectively. Patients with GD fold change showed increased BMPR2 expression when matched against the controls, with a mean of 4.21 ± 1.73 (P = 0.001); BMPR2 was overexpressed in the analysed cell cycle stages. Fold change analysis of variant carriers and non‐carriers showed slight overexpression and differences between phases, but none of them were statistically significant. BMPR2 expression was confirmed in the lymphoblastoid cell lines (LCLs) with a molecular weight of 115 kD, and no differences between variant carriers and non‐carriers were detected. To conclude, the BMPR2 variant c.419‐19delT appears in high frequency in patients with GD, and independently of its presence, BMPR2 is overexpressed in the LCLs from the GD patients tested. This increase could be paired with the described decreased expression of transforming growth factor‐β1 in thyroid tissue from patients with GDThis study was supported by the grants CO‐0115‐14 from Actelion Pharmaceuticals and has received financial support from the Xunta de Galicia (Centro singular de investigación de Galicia accreditation 2016‐2019) and the European Union (European Regional Development Fund—ERDF)S

Truncating and missense BMPR2 mutations differentially affect the severity of heritable pulmonary arterial hypertension

<p>Abstract</p> <p>Background</p> <p>Autosomal dominant inheritance of germline mutations in the bone morphogenetic protein receptor type 2 (<it>BMPR2</it>) gene are a major risk factor for pulmonary arterial hypertension (PAH). While previous studies demonstrated a difference in severity between <it>BMPR2 </it>mutation carriers and noncarriers, it is likely disease severity is not equal among <it>BMPR2 </it>mutations. We hypothesized that patients with missense <it>BMPR2 </it>mutations have more severe disease than those with truncating mutations.</p> <p>Methods</p> <p>Testing for <it>BMPR2 </it>mutations was performed in 169 patients with PAH (125 with a family history of PAH and 44 with sporadic disease). Of the 106 patients with a detectable <it>BMPR2 </it>mutation, lymphocytes were available in 96 to functionally assess the nonsense-mediated decay pathway of RNA surveillance. Phenotypic characteristics were compared between <it>BMPR2 </it>mutation carriers and noncarriers, as well as between those carriers with a missense versus truncating mutation.</p> <p>Results</p> <p>While there was a statistically significant difference in age at diagnosis between carriers and noncarriers, subgroup analysis revealed this to be the case only for females. Among carriers, there was no difference in age at diagnosis, death, or survival according to exonic location of the <it>BMPR2 </it>mutation. However, patients with missense mutations had statistically significant younger ages at diagnosis and death, as well as shorter survival from diagnosis to death or lung transplantation than those with truncating mutations. Consistent with this data, the majority of missense mutations were penetrant prior to age 36 years, while the majority of truncating mutations were penetrant after age 36 years.</p> <p>Conclusion</p> <p>In this cohort, <it>BMPR2 </it>mutation carriers have more severe PAH disease than noncarriers, but this is only the case for females. Among carriers, patients with missense mutations that escape nonsense-mediated decay have more severe disease than those with truncating mutations. These findings suggest that treatment and prevention strategies directed specifically at <it>BMPR2 </it>pathway defects may need to vary according to the type of mutation.</p