Advances in procedural techniques--antegrade.

There have been many technological advances in antegrade CTO PCI, but perhaps most importantly has been the evolution of the "hybrid' approach where ideally there exists a seamless interplay of antegrade wiring, antegrade dissection re-entry and retrograde approaches as dictated by procedural factors. Antegrade wire escalation with intimal tracking remains the preferred initial strategy in short CTOs without proximal cap ambiguity. More complex CTOs, however, usually require either a retrograde or an antegrade dissection re-entry approach, or both. Antegrade dissection re-entry is well suited to long occlusions where there is a healthy distal vessel and limited "interventional" collaterals. Early use of a dissection re-entry strategy will increase success rates, reduce complications, and minimise radiation exposure, contrast use as well as procedural times. Antegrade dissection can be achieved with a knuckle wire technique or the CrossBoss catheter whilst re-entry will be achieved in the most reproducible and reliable fashion by the Stingray balloon/wire. It should be avoided where there is potential for loss of large side branches. It remains to be seen whether use of newer dissection re-entry strategies will be associated with lower restenosis rates compared with the more uncontrolled subintimal tracking strategies such as STAR and whether stent insertion in the subintimal space is associated with higher rates of late stent malapposition and stent thrombosis. It is to be hoped that the algorithms, which have been developed to guide CTO operators, allow for a better transfer of knowledge and skills to increase uptake and acceptance of CTO PCI as a whole

Radiation-resistant device phenomena

Electrical properties of reactively evaporated aluminum oxide films and electron mean free path through metal fil

The Political Economy of Low-Carbon Investment: the Role of Coalitions and Alignments of Interest in the Green Transformation in China

The primary motivation behind this research is the need to accelerate the supply of renewable energy because of the important role that it plays in mitigating climate change and in fostering sustainable development. Understanding past drivers for low-carbon investment can help us identify those for the future, and what could accelerate such investment. Investment in renewable energy can be modelled as a problem of technical asset allocation or optimisation at the firm or sectoral level, but is not entirely explained by this approach – the context in which actors are involved, their motivations and the wider systems in which they operate must also be taken into account. The interactions between actors may sometimes accelerate investment and sometimes prevent it; however, understanding the dynamics of these processes is crucial if we are to shape them. This report is part of a two-part study focusing on the wind and solar power sectors in China and India, which aims to find and compare drivers for investment in renewable energy. This report takes the example of China. This China-based research examines ten case studies: four wind power and six solar power. They have been selected according to investment data and industrial characteristics. Each study covers the period during which investment in renewable technologies was at its peak and all are representative of the corporate financing at that time. For each, we reviewed all of the available literature (an abundance of papers and reports) and conducted face-to-face interviews. Our interviewees ranged from wind turbine and solar photovoltaic (PV) manufacturers, to employees of state-owned enterprises and banks, to local and central government officials (particularly from the National Development and Reform Commission and the Ministry of Commerce), as well as other researchers.UK Department for International Developmen

Setting, Mechanical, Morphological, Degradation and Antibacterial Properties of Brushite cements

Aims: This study aim was to develop high strength, antibacterial-releasing brushite cements with controllable setting and porosity for bone-filling. Materials and Methods: Monocalcium phosphate monohydrate (MCPM) was reacted with equimolar β-tricalcium phosphate (TCP) and 800mM aqueous citric acid (CA) containing 0, 20, or 40wt% of antibacterial ε-polylysine (PLS). The large MCPM monoclinic crystals (10x100x500 micron) were used as received or after grinding. The powder to liquid ratio was 3:1 or 4:1. Setting kinetics, mechanical strengths, fracture surface morphologies, degradation rates, and PLS release was undertaken. Additionally, MRSA colony forming units (CFU) on set material discs with 0 versus 40wt% PLS and in surrounding broth medium was compared. Results Use of smaller particles and increased PLS lead to formation of more stable intermediate complexes and slower Brushite formation. Formulations with intermediate MCPM particle size and higher powder content had significantly higher flexural strengths. Pores / channels with dimensions comparable with those of the original MCPM crystals were detected on the fracture surfaces. Dissolution rates were affected by MCPM particle size but not PLS content. PLS release occurred primarily in the first 24 hours of set disc immersion in water. Addition of PLS enabled MRSA growth to decline from 1.8 x 107 to 2.5 x 104 on a set disc and from 2.0 x 109 to 1.2 x 104 CFU in the surrounding medium. . Conclusion and significance The above antibacterial Brushite cements could be employed in the treatment of infected bone (e.g. periodontitis, implantitis, osteomyelitis). Controlled setting is required to minimise leakage away from the required site of application. The channels in the cements and dissolution will allow bone cell penetration and provide ions for new bone formation respectively. The higher strengths will enable application in greater load bearing clinical situations

CSF Secretion Is Not Altered by NKCC1 Nor TRPV4 Antagonism in Healthy Rats

Background: Cerebrospinal fluid (CSF) secretion can be targeted to reduce elevated intracranial pressure (ICP). Sodium-potassium-chloride cotransporter 1 (NKCC1) antagonism is used clinically. However, supporting evidence is limited. The transient receptor potential vanilloid-4 (TRPV4) channel may also regulate CSF secretion and ICP elevation. We investigated whether antagonism of these proteins reduces CSF secretion. Methods: We quantified CSF secretion rates in male Wistar rats. The cerebral aqueduct was blocked with viscous mineral oil, and a lateral ventricle was cannulated. Secretion rate was measured at baseline and after antagonist administration. Acetazolamide was administered as a positive control to confirm changes in CSF secretion rates. Results: Neither NKCC1, nor TRPV4 antagonism altered CSF secretion rate from baseline, n = 3, t(2) = 1.14, p = 0.37, and n = 4, t(3) = 0.58, p = 0.6, respectively. Acetazolamide reduced CSF secretion by ~50% across all groups, n = 7, t(6) = 4.294, p = 0.005. Conclusions: Acute antagonism of NKCC1 and TRPV4 proteins at the choroid plexus does not reduce CSF secretion in healthy rats. Further investigation of protein changes and antagonism should be explored in neurological disease where increased CSF secretion and ICP are observed before discounting the therapeutic potential of protein antagonism at these sites

Normalization factors for magnetic relaxation of small particle systems in non-zero magnetic field

We critically discuss relaxation experiments in magnetic systems that can be characterized in terms of an energy barrier distribution, showing that proper normalization of the relaxation data is needed whenever curves corresponding to different temperatures are to be compared. We show how these normalization factors can be obtained from experimental data by using the $T \ln(t/\tau_0)$ scaling method without making any assumptions about the nature of the energy barrier distribution. The validity of the procedure is tested using a ferrofluid of Fe_3O_4 particles.Comment: 5 pages, 6 eps figures added in April 22, to be published in Phys. Rev. B 55 (1 April 1997

What Drives Wind and Solar Energy Investment in India and China?

This research is motivated by the need to transform the basis of energy systems from fossil fuels to renewable sources. As well as the imperative of climate change, this transformation is needed to create development trajectories for economies that are genuinely sustainable over the long term. Our objectives are therefore both environmental and developmental. Understanding what drove low-carbon investments in the past is the key to identifying the drivers of investment in the future. In this regard, low-carbon investment decisions are not technical questions of optimal asset allocation. Rather, understanding these decisions requires an approach rooted in political economy, which assesses the motivations and incentives of the different actors involved, and how these interact. Understanding the dynamics of this process is the first step in shaping it. This research concentrates on private investment. Of the US$45 trillion of investments that the International Energy Agency (IEA) estimates are required by 2050 to reduce global carbon emissions by half, it is assumed that 85 per cent will need to come from the private sector. Annually, this averages at a little over US$1 trillion, half of which will fund the replacement of existing technologies, largely in developed countries. The remaining US$530bn is investment in new capacity, the bulk of which (US$400bn pa) will be in developing countries (IEA 2008). Our focus is on the determinants of low-carbon investment in the world’s two largest emerging economies: China and India. While these countries are responsible for the biggest growth in carbon emissions, China is now the largest global investor in renewable energy and India saw the highest growth rate in recent times between 2010 and 2011 (BNEF 2012).UK Department for International Developmen

Altered Cerebrospinal Fluid Clearance and Increased Intracranial Pressure in Rats 18 h After Experimental Cortical Ischaemia

Oedema-independent intracranial pressure (ICP) rise peaks 20–22-h post-stroke in rats and may explain early neurological deterioration. Cerebrospinal fluid (CSF) volume changes may be involved. Cranial CSF clearance primarily occurs via the cervical lymphatics and movement into the spinal portion of the cranio-spinal compartment. We explored whether impaired CSF clearance at these sites could explain ICP rise after stroke. We recorded ICP at baseline and 18-h post-stroke, when we expect changes contributing to peak ICP to be present. CSF clearance was assessed in rats receiving photothrombotic stroke or sham surgery by intraventricular tracer infusion. Tracer concentration was quantified in the deep cervical lymph nodes ex vivo and tracer transit to the spinal subarachnoid space was imaged in vivo. ICP rose significantly from baseline to 18-h post-stroke in stroke vs. sham rats [median = 5 mmHg, interquartile range (IQR) = 0.1–9.43, n = 12, vs. −0.3 mmHg, IQR = −1.9–1.7, n = 10], p = 0.03. There was a bimodal distribution of rats with and without ICP rise. Tracer in the deep cervical lymph nodes was significantly lower in stroke with ICP rise (0 μg/mL, IQR = 0–0.11) and without ICP rise (0 μg/mL, IQR = 0–4.47) compared with sham rats (4.17 μg/mL, IQR = 0.74–8.51), p = 0.02. ICP rise was inversely correlated with faster CSF transit to the spinal subarachnoid space (R = −0.59, p = 0.006, Spearman’s correlation). These data suggest that reduced cranial clearance of CSF via cervical lymphatics may contribute to post-stroke ICP rise, partially compensated via increased spinal CSF outflow

Ultra-Short Duration Hypothermia Prevents Intracranial Pressure Elevation Following Ischaemic Stroke in Rats

There is a transient increase in intracranial pressure (ICP) 18–24 h after ischaemic stroke in rats, which is prevented by short-duration hypothermia using rapid cooling methods. Clinical trials of long-duration hypothermia have been limited by feasibility and associated complications, which may be avoided by short-duration cooling. Animal studies have cooled faster than is achievable in patients. We aimed to determine whether gradual cooling at a rate of 2°C/h to 33°C or 1°C/h to 34.5°C, with a 30 min duration at target temperatures, prevented ICP elevation and reduced infarct volume in rats. Transient middle cerebral artery occlusion was performed, followed by gradual cooling to target temperature. Hypothermia to 33°C prevented significant ICP elevation (hypothermia ΔICP = 1.56 ± 2.26 mmHg vs normothermia ΔICP = 8.93 ± 4.82 mmHg; p = 0.02) and reduced infarct volume (hypothermia = 46.4 ± 12.3 mm3 vs normothermia = 85.0 ± 17.5 mm3; p = 0.01). Hypothermia to 34.5°C did not significantly prevent ICP elevation or reduce infarct volume. We showed that gradual cooling to 33°C, at cooling rates achievable in patients, had the same ICP preventative effect as traditional rapid cooling methods. This suggests that this paradigm could be translated to prevent delayed ICP rise in stroke patients

Decreased Intracranial Pressure Elevation and Cerebrospinal Fluid Outflow Resistance: A Potential Mechanism of Hypothermia Cerebroprotection Following Experimental Stroke

Background: Elevated intracranial pressure (ICP) occurs 18–24 h after ischaemic stroke and is implicated as a potential cause of early neurological deterioration. Increased resistance to cerebrospinal fluid (CSF) outflow after ischaemic stroke is a proposed mechanism for ICP elevation. Ultra-short duration hypothermia prevents ICP elevation 24 h post-stroke in rats. We aimed to determine whether hypothermia would reduce CSF outflow resistance post-stroke. Methods: Transient middle cerebral artery occlusion was performed, followed by gradual cooling to 33 °C. At 18 h post-stroke, CSF outflow resistance was measured using a steady-state infusion method. Results: Hypothermia to 33 °C prevented ICP elevation 18 h post-stroke (hypothermia ∆ICP = 0.8 ± 3.6 mmHg vs. normothermia ∆ICP = 4.4 ± 2.0 mmHg, p = 0.04) and reduced infarct volume 24 h post-stroke (hypothermia = 78.6 ± 21.3 mm(3) vs. normothermia = 108.1 ± 17.8 mm(3); p = 0.01). Hypothermia to 33 °C did not result in a significant reduction in CSF outflow resistance compared with normothermia controls (0.32 ± 0.36 mmHg/µL/min vs. 1.07 ± 0.99 mmHg/µL/min, p = 0.06). Conclusions: Hypothermia treatment was protective in terms of ICP rise prevention, infarct volume reduction, and may be implicated in CSF outflow resistance post-stroke. Further investigations are warranted to elucidate the mechanisms of ICP elevation and hypothermia treatment