Bridging larger gaps in peripheral nerves using neural prosthetics and physical therapeutic agents Muhammad Sana Ullah Sahar, Matthew Barton, Geoffrey Douglas Tansley Neural Regeneration Research 2019 14(7):1109-1115 Peripheral nerve injuries are relatively common and can be caused by a variety of traumatic events such as motor vehicle accidents. They can lead to long-term disability, pain, and financial burden, and contribute to poor quality of life. In this review, we systematically analyze the contemporary literature on peripheral nerve gap management using nerve prostheses in conjunction with physical therapeutic agents. The use of nerve prostheses to assist nerve regeneration across large gaps (> 30 mm) has revolutionized neural surgery. The materials used for nerve prostheses have been greatly refined, making them suitable for repairing large nerve gaps. However, research on peripheral nerve gap management using nerve prostheses reports inconsistent functional outcomes, especially when prostheses are integrated with physical therapeutic agents, and thus warrants careful investigation. This review explores the effectiveness of nerve prostheses for bridging large nerve gaps and then addresses their use in combination with physical therapeutic agents. |
Magnesium: Pathophysiological mechanisms and potential therapeutic roles in intracerebral hemorrhage Jason J Chang, Rocco Armonda, Nitin Goyal, Adam S Arthur Neural Regeneration Research 2019 14(7):1116-1121 Intracerebral hemorrhage (ICH) remains the second-most common form of stroke with high morbidity and mortality. ICH can be divided into two pathophysiological stages: an acute primary phase, including hematoma volume expansion, and a subacute secondary phase consisting of blood-brain barrier disruption and perihematomal edema expansion. To date, all major trials for ICH have targeted the primary phase with therapies designed to reduce hematoma expansion through blood pressure control, surgical evacuation, and hemostasis. However, none of these trials has resulted in improved clinical outcomes. Magnesium is a ubiquitous element that also plays roles in vasodilation, hemostasis, and blood-brain barrier preservation. Animal models have highlighted potential therapeutic roles for magnesium in neurological diseases specifically targeting these pathophysiological mechanisms. Retrospective studies have also demonstrated inverse associations between admission magnesium levels and hematoma volume, hematoma expansion, and clinical outcome in patients with ICH. These associations, coupled with the multifactorial role of magnesium that targets both primary and secondary phases of ICH, suggest that magnesium may be a viable target of study in future ICH studies. |
Network-centric medicine for peripheral nerve injury: Treating the whole to boost endogenous mechanisms of neuroprotection and regeneration David Romeo-Guitart, Caty Casas Neural Regeneration Research 2019 14(7):1122-1128 Peripheral nerve injuries caused by accidents may lead to paralysis, sensory disturbances, anaesthesia, and lack of autonomic functions. Functional recovery after disconnection of the motoneuronal soma from target tissue with proximal rupture of axons is determined by several factors: motoneuronal soma viability, proper axonal sprouting across inhibitory zones and elongation toward specific muscle, effective synapse contact rebuilding, and prevention of muscle atrophy. Therapies, such as adjuvant drugs with pleiotropic effects, that promote functional recovery after peripheral nerve injury are needed. Toward this aim, we designed a drug discovery workflow based on a network-centric molecular vision using unbiased proteomic data and neural artificial computational tools. Our focus is on boosting intrinsic capabilities of neurons for neuroprotection; this is in contrast to the common approach based on suppression of a pathobiological pathway known to be associated with disease condition. Using our workflow, we discovered neuroheal, a combination of two repurposed drugs that promotes motoneuronal soma neuroprotection, is anti-inflammatory, enhances axonal regeneration after axotomy, and reduces muscle atrophy. This drug discovery workflow has thus yielded a therapy that is close to its clinical application. |
Exogenous neural stem cell transplantation for cerebral ischemia Ling-Yi Liao, Benson Wui-Man Lau, Dalinda Isabel Sánchez-Vidaña, Qiang Gao Neural Regeneration Research 2019 14(7):1129-1137 Cerebral ischemic injury is the main manifestation of stroke, and its incidence in stroke patients is 70–80%. Although ischemic stroke can be treated with tissue-type plasminogen activator, its time window of effectiveness is narrow. Therefore, the incidence of paralysis, hypoesthesia, aphasia, dysphagia, and cognitive impairment caused by cerebral ischemia is high. Nerve tissue regeneration can promote the recovery of the aforementioned dysfunction. Neural stem cells can participate in the reconstruction of the damaged nervous system and promote the recovery of nervous function during self-repair of damaged brain tissue. Neural stem cell transplantation for ischemic stroke has been a hot topic for more than 10 years. This review discusses the treatment of ischemic stroke with neural stem cells, as well as the mechanisms of their involvement in stroke treatment. |
Potential therapeutic molecular targets for blood-brain barrier disruption after subarachnoid hemorrhage Hideki Kanamaru, Hidenori Suzuki Neural Regeneration Research 2019 14(7):1138-1143 Aneurysmal subarachnoid hemorrhage remains serious hemorrhagic stroke with high morbidities and mortalities. Aneurysm rupture causes arterial bleeding-induced mechanical brain tissue injuries and elevated intracranial pressure, followed by global cerebral ischemia. Post-subarachnoid hemorrhage ischemia, tissue injuries as well as extravasated blood components and the breakdown products activate microglia, astrocytes and Toll-like receptor 4, and disrupt blood-brain barrier associated with the induction of many inflammatory and other cascades. Once blood-brain barrier is disrupted, brain tissues are directly exposed to harmful blood contents and immune cells, which aggravate brain injuries furthermore. Blood-brain barrier disruption after subarachnoid hemorrhage may be developed by a variety of mechanisms including endothelial cell apoptosis and disruption of tight junction proteins. Many molecules and pathways have been reported to disrupt the blood-brain barrier after subarachnoid hemorrhage, but the exact mechanisms remain unclear. Multiple independent and/or interconnected signaling pathways may be involved in blood-brain barrier disruption after subarachnoid hemorrhage. This review provides recent understandings of the mechanisms and the potential therapeutic targets of blood-brain barrier disruption after subarachnoid hemorrhage. |
Choroid plexus tumor necrosis factor receptor 1: A new neuroinflammatory piece of the complex Alzheimer's disease puzzle Sophie Steeland, Roosmarijn E Vandenbroucke Neural Regeneration Research 2019 14(7):1144-1147 Due to the aging of the population and despite the enormous scientific effort, Alzheimer’s disease remains one of the biggest medical and pharmaceutical challenges in current medicine. Novel insights highlight the importance of neuroinflammation as an undeniable player in the onset and progression of Alzheimer’s disease. Tumor necrosis factor is a master inflammatory cytokine that signals via tumor necrosis factor receptor 1 and tumor necrosis factor receptor 2, but that also regulates several brain functions in health and disease. However, clinical trials investigating drugs that interfere with the tumor necrosis factor pathway in Alzheimer’s disease led to inconclusive results, partially because not only the pro-inflammatory tumor necrosis factor/tumor necrosis factor receptor 1, but also the beneficial tumor necrosis factor/tumor necrosis factor receptor 2 signaling was antagonized in these trials. We recently found that tumor necrosis factor is the main upregulated cytokine in the choroid plexus of Alzheimer’s disease patients, signaling via tumor necrosis factor receptor 1. In agreement with this, choroidal tumor necrosis factor/tumor necrosis factor receptor 1 signaling was also upregulated in different Alzheimer’s disease mouse models. Interestingly, both genetic and nanobody-based pharmacological blockage of tumor necrosis factor receptor 1 signaling was accompanied by favorable effects on Alzheimer’s disease-associated inflammation, choroidal morphology and cognitive functioning. Here, we briefly summarize the detrimental effects that can be mediated by tumor necrosis factor/tumor necrosis factor receptor 1 signaling in (early) Alzheimer’s disease, and the consequences this might have on the disease progression. As the main hypothesis in Alzheimer’s disease clinical trials is still based on the amyloid beta-cascade, the importance of Alzheimer’s disease-associated neuroinflammation urge the development of novel therapeutic strategies that might be effective in the early stages of Alzheimer’s disease and prevent the irreversible neurodegeneration and resulting memory decline. |
Transcriptional dysregulation in neurodegenerative diseases: Who tipped the balance of Yin Yang 1 in the brain? Zhefan Stephen Chen, Ho Yin Edwin Chan Neural Regeneration Research 2019 14(7):1148-1151 Yin Yang 1 (YY1) is a multi-functional transcription factor that regulates gene expression in a range of cell types, including neurons. It controls neuronal differentiation, as well as neuronal specification and migration during the development of the mammalian nervous system. Besides, YY1 also mediates the transcription of genes that are required for neuronal survival. An impairment of the transcriptional function of YY1 causes neuronal death. This review summarizes recent research findings that unveil the dysfunction of YY1 in multiple neurodegenerative disorders. The expression of disease proteins perturbs the function of YY1 via distinct molecular mechanisms, including recruitment to protein aggregates, protein degradation and aberrant nuclear/cytoplasmic shuttling. Understanding the pathogenic roles of YY1 will further broaden our knowledge of the disease mechanisms in distinct neurodegenerative disorders. |
Effects of Ginkgo biloba extract EGb761 on neural differentiation of stem cells offer new hope for neurological disease treatment Chao Ren, Yong-Qiang Ji, Hong Liu, Zhe Wang, Jia-Hui Wang, Cai-Yi Zhang, Li-Na Guan, Pei-Yuan Yin Neural Regeneration Research 2019 14(7):1152-1157 Stem cell transplantation has brought new hope for the treatment of neurological diseases. The key to stem cell therapy lies in inducing the specific differentiation of stem cells into nerve cells. Because the differentiation of stem cells in vitro and in vivo is affected by multiple factors, the final differentiation outcome is strongly associated with the microenvironment in which the stem cells are located. Accordingly, the optimal microenvironment for inducing stem cell differentiation is a hot topic. EGb761 is extracted from the leaves of the Ginkgo biloba tree. It is used worldwide and is becoming one of the focuses of stem cell research. Studies have shown that EGb761 can antagonize oxygen free radicals, stabilize cell membranes, promote neurogenesis and synaptogenesis, increase the level of brain-derived neurotrophic factors, and replicate the environment required during the differentiation of stem cells into nerve cells. This offers the possibility of using EGb761 to induce the differentiation of stem cells, facilitating stem cell transplantation. To provide a comprehensive reference for the future application of EGb761 in stem cell therapy, we reviewed studies investigating the influence of EGb761 on stem cells. These started with the composition and neuropharmacology of EGb761, and eventually led to the finding that EGb761 and some of its important components play important roles in the differentiation of stem cells and the protection of a beneficial microenvironment for stem cell transplantation. |
Amelioration of Alzheimer's disease pathology and cognitive deficits by immunomodulatory agents in animal models of Alzheimer's disease Bridget Martinez, Philip V Peplow Neural Regeneration Research 2019 14(7):1158-1176 The most common age-related neurodegenerative disease is Alzheimer’s disease (AD) characterized by aggregated amyloid-β (Aβ) peptides in extracellular plaques and aggregated hyperphosphorylated tau protein in intraneuronal neurofibrillary tangles, together with loss of cholinergic neurons, synaptic alterations, and chronic inflammation within the brain. These lead to progressive impairment of cognitive function. There is evidence of innate immune activation in AD with microgliosis. Classically-activated microglia (M1 state) secrete inflammatory and neurotoxic mediators, and peripheral immune cells are recruited to inflammation sites in the brain. The few drugs approved by the US FDA for the treatment of AD improve symptoms but do not change the course of disease progression and may cause some undesirable effects. Translation of active and passive immunotherapy targeting Aβ in AD animal model trials had limited success in clinical trials. Treatment with immunomodulatory/anti-inflammatory agents early in the disease process, while not preventive, is able to inhibit the inflammatory consequences of both Aβ and tau aggregation. The studies described in this review have identified several agents with immunomodulatory properties that alleviated AD pathology and cognitive impairment in animal models of AD. The majority of the animal studies reviewed had used transgenic models of early-onset AD. More effort needs to be given to creat models of late-onset AD. The effects of a combinational therapy involving two or more of the tested pharmaceutical agents, or one of these agents given in conjunction with one of the cell-based therapies, in an aged animal model of AD would warrant investigation. |
Precision medicine in pantothenate kinase-associated neurodegeneration Mónica Alvarez-Cordoba, Marina Villanueva-Paz, Irene Villalón-García, Suleva Povea-Cabello, Juan M Suárez-Rivero, Marta Talaverón-Rey, Javier Abril-Jaramillo, Ana Belén Vintimilla-Tosi, José A Sánchez-Alcázar Neural Regeneration Research 2019 14(7):1177-1185 Neurodegeneration with brain iron accumulation is a broad term that describes a heterogeneous group of progressive and invalidating neurologic disorders in which iron deposits in certain brain areas, mainly the basal ganglia. The predominant clinical symptoms include spasticity, progressive dystonia, Parkinson’s disease-like symptoms, neuropsychiatric alterations, and retinal degeneration. Among the neurodegeneration with brain iron accumulation disorders, the most frequent subtype is pantothenate kinase-associated neurodegeneration (PKAN) caused by defects in the gene encoding the enzyme pantothenate kinase 2 (PANK2) which catalyzed the first reaction of the coenzyme A biosynthesis pathway. Currently there is no effective treatment to prevent the inexorable course of these disorders. The aim of this review is to open up a discussion on the utility of using cellular models derived from patients as a valuable tool for the development of precision medicine in PKAN. Recently, we have described that dermal fibroblasts obtained from PKAN patients can manifest the main pathological changes of the disease such as intracellular iron accumulation accompanied by large amounts of lipofuscin granules, mitochondrial dysfunction and a pronounced increase of markers of oxidative stress. In addition, PKAN fibroblasts showed a morphological senescence-like phenotype. Interestingly, pantothenate supplementation, the substrate of the PANK2 enzyme, corrected all pathophysiological alterations in responder PKAN fibroblasts with low/residual PANK2 enzyme expression. However, pantothenate treatment had no favourable effect on PKAN fibroblasts harbouring mutations associated with the expression of a truncated/incomplete protein. The correction of pathological alterations by pantothenate in individual mutations was also verified in induced neurons obtained by direct reprograming of PKAN fibroblasts. Our observations indicate that pantothenate supplementation can increase/stabilize the expression levels of PANK2 in specific mutations. Fibroblasts and induced neurons derived from patients can provide a useful tool for recognizing PKAN patients who can respond to pantothenate treatment. The presence of low but significant PANK2 expression which can be increased in particular mutations gives valuable information which can support the treatment with high dose of pantothenate. The evaluation of personalized treatments in vitro of fibroblasts and neuronal cells derived from PKAN patients with a wide range of pharmacological options currently available, and monitoring its effect on the pathophysiological changes, can help for a better therapeutic strategy. In addition, these cell models will be also useful for testing the efficacy of new therapeutic options developed in the future. |
By Alexandros G. Sfakianakis,Anapafseos 5 Agios Nikolaos 72100 Crete,Greece,00302841026182,00306932607174
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Monday, February 25, 2019
Neural Regeneration Research (Neural Regen Res)
Mediterranean diet, alkaline water may be as effective as PPIs for laryngopharyngeal reflux
How to make use of the world’s most accurate surface temperature data
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Organic Polymorphs with Fluorescence Switching: Direct Evidences for Mechanical and Thermal Modulation of Excited State Transitions
DOI: 10.1039/C9CC00234K, Communication
Herein, we provide a direct observation of the modulation of the excited state transition under the mechanical and thermal stimuli in solid state by two organic polymorphs based on tetraphenylethene...
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Magnetic covalent organic framework as adsorbent and new matrix for enrichment and rapid determination of PAHs and their derivatives in PM2.5 by surface-assisted laser desorption/ionization-time of flight-mass spectrometry
DOI: 10.1039/C9CC00384C, Communication
Magnetic covalent organic framework nanomaterial (Fe3O4@COFs) served as an adsorbent for enrichment and a new matrix for SALDI-TOF-MS analysis of PAHs and their derivatives in PM2.5. The unique properties of...
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Unified Enantioselective Total Syntheses of (-)-Scholarisine G, (+)-Melodinine E, (-)-Leuconoxine and (-)-Mersicarpine
DOI: 10.1039/C8CC09949A, Communication
A unified strategy enabled the enantioselective syntheses of (-)-scholarisine G, (+)-melodinine E, (-)-leuconoxine and (-)-mersicarpine from a common 2-alkylated indole intermediate bearing an all-carbon quaternary stereogenic center. The Smith-modified Madelung...
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Ternary cobalt-molybdenum-vanadium layered double hydroxide nanosheet array as an efficient bifunctional electrocatalyst for overall water splitting
DOI: 10.1039/C9CC00269C, Communication
The active CoMoV LDH nanosheet arrays grown on nickel foam were obtained for the first time. The doping of high-valence Mo and V in Co-based LDH could tune the electronic...
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Multiple-Functionalizations of Terminal Alkynes with Sodium Sulfinates and tert-Butyl Nitrite: Facile Synthesis of 2H-Azirines
DOI: 10.1039/C9CC00625G, Communication
A new, catalyst-free tandem annulation access to 2,2-disulfonyl-2H-azirines via multiple-functionalizations of terminal alkynes with sodium sulfinates and tert-butyl nitrite is described. The use of sodium sulfinates and tert-butyl nitrite enables...
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Revisiting the Reactive Chemistry of FOX-7: Cyclization of FOX-7 Affords Fused-Ring Polynitro Compounds
DOI: 10.1039/C8CC10178G, Communication
A novel fused-ring polynitro compound (5) and a cyclic compound featuring gem-dinitromethylene and nitroso groups (7) were synthesized from 1,1-diamino-2,2-dinitroethylene (FOX-7). Compound 5 exhibits the highest thermal stability of any...
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[ASAP] Isolable Cu(I) Complexes of Extremely Electron-Poor, Completely Unreduced -Quinone and “Di--Quinone” Ligands Stabilized through p–p Interactions in the Secondary Coordination Sphere
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The Green Delusions Of Ambrose Evans-Pritchard
By Paul Homewood
As we know, Ambrose Evans-Pritchard often writes quite delusional pieces in the Telegraph, about climate and energy policy.
So I thought it would be a good time to review some of his past gems, and see how they have worked out:
Let's start in 2008, when apparently he was still quite sensible.
He interviewed Wulf Bernotat, head of German power giant e.on, who did not seem too keen on the UK's "romantic" energy policy:
"The UK is in a very bad situation. Roughly 40pc of its power is from coal, and 20pc from nuclear. It all needs to be replaced. But is anybody in the British Government out there making the case for clean coal? I don't see anybody," he said.
Dr Bernotat praised Downing Street for settling on some sort of energy strategy at long last after years of drift and muddle, but said Labour seemed to have gone overboard all of a sudden with a "romantic" enthusiasm for green power.
"You cannot replace 60pc of the country's generating capacity just by betting on renewables, which is what the pressure groups are demanding. It will be decades before we reach that point, and until then Britain is going to need coal-fired units. I hope some realism comes through in energy policy," he said…
But green power alone cannot plug the gaping holes in Britain's grid.
Britain is not alone in its dreamy approach to energy security. Germany is turning its back on nuclear power altogether, and coal is out of fashion. That could one day leave the country almost entirely beholden to Kremlin gas supplies.
Prescient indeed, Ambrose. Now, of course, he believes the total opposite, that we can run the country on green power, despite the fact that nothing has changed technologically since.
Fast forward to 2013, and his views still had not changed:
Germany is committing slow economic suicide. It has staked its future on heavy industry and manufacturing, yet has no energy policy to back this up.
Instead, the country has a ruinously expensive green dream, priced at €700bn (£590bn) from now until the late 2030s by environment minister Peter Altmaier if costs are slashed – and €1 trillion if they are not. The Germans are surely the most romantic nation on earth.
The full implications of this may become clear over the next decade, just as Germany's ageing crisis hits with maximum force and its engineers retire; and just as German voters discover – what they suspect already – that it costs real money to hold a half-baked euro together.
The likelihood is that Germany will start to lose its economic halo soon, "de-rated" like others before it.
Two years later though, he must have been at the Kool Aid:
The political noose is tightening on the global fossil fuel industry. It is a fair bet that world leaders will agree this year to impose a draconian "tax" on carbon emissions that entirely changes the financial calculus for coal, oil, and gas, and may ultimately devalue much of their asset base to zero. …
It is becoming clearer that last year's sweeping deal on climate change between the US and China was an historical inflexion point, the beginning of the end for a century of fossil dominance…
Some countries have been startlingly bold. Mexico has vowed to cut gases by 40pc within fifteen years
Well, we're still waiting for that "draconian carbon tax, and far from ending the dominance of fossil fuels, that "sweeping deal" was simply Obama being taken to the cleaners by China.
Fossil fuel consumption continues to rise unabated, and still account for 85% of the world's energy. By contrast renewables only supply a pitifully dismal 4%.
BP Energy Review
And Mexico?
Emissions have actually increased by 4% since AEP wrote his article:
BP Energy Review
By 2016, AEP seems to have totally lost the plot, writing a series of articles about our glorious new green future:
https://notalotofpeopleknowthat.wordpress.com/2016/08/15/the-vast-gamble-on-wind-power/
To be fair, costs of offshore wind at the latest CfD auction have come down more quickly than expected, but are still well above market prices.
However, he utterly fails to explain how the grid can cope with wind's intermittency without expensive back up from proper dispatchable power sources, or a dangerous reliance on imported electricity.
All he can offer is:
Intermittency remains a curse but claims that anticyclones can halt the offshore wind industry for weeks at a time are a dinner party myth. "Calm conditions persisting for one day are extremely rare. When they do occur, they cover a small fraction of the UK, and there is no evidence to suggest that they persist for long periods of time," says Graham Sinden from Oxford University.
It turns out that this comment is based on an obsolete 2004 study. In fact, it is very common for such calm conditions to last a day or two, and that certainly applies to the UK as a whole. On one day last month, for instance, wind power was contributing just 0.7% of our electricity.
And only last month, we had five days straight when wind power ran at only 10% of capacity.
From a cost point of view, wind power can only justify itself if its TOTAL COST is less than the MARGINAL COST of alternatives such as CCGT. This would mean a price in the region of £40/MWh. This is achievable in the foreseeable future. Even then you would need to account for other system costs, such as extra grid infrastructure and system balancing.
But, perhaps most damning of all, AEP still does not seem to understand that, if you build too much wind capacity, you end up with many occasions when there is surplus generation, which the grid simply cannot absorb. And the more you build, the more extreme this problem becomes.
According to AEP, the solution to all of our intermittency problems lies with battery storage:
The world's next energy revolution is probably no more than five or ten years away. Cutting-edge research into cheap and clean forms of electricity storage is moving so fast that we may never again need to build 20th Century power plants in this country, let alone a nuclear white elephant such as Hinkley Point….
Every big decision on energy strategy by the British government or any other government must henceforth be based on the working premise that cheap energy storage will soon be a reality.
This country can achieve total self-sufficiency in power at viable cost from our own sun, wind, and waters within a generation.
Well, maybe, just maybe, some genius will invent a battery that can cheaply store millions of MWh, but in the meantime it would be wise for governments not to rely on that.
What AEP still does not appear to get, is that battery storage is fine for holding a few hours worth of energy, enough say to store solar power during the day, for use at night.
But there simply is no technology which can store enough to last for days and weeks on end, never mind last all winter, as his comments about solar power imply.
Lord Oxburgh made all this perfectly plain, in his Report to Parliament in 2016, just after AEP wrote his fantasy piece:
Lowest Cost Decarbonisation for the UK: The Critical Role of CCS – P 65
Following his delusions about wind power and storage, AEP capped it all with his dream of carbon capture, again from 2016:
Renaissance beckons for the once great industrial hubs of northern England and Scotland, and the unexpected catalyst may be stringent global climate controls.
What looks at first sight like an economic threat could instead play elegantly to Britain's competitive advantage, for almost no other country on earth is so well-placed to combine energy-intensive manufacturing with carbon capture at a viable cost.
The industrial clusters of the Tees Valley and the Humber are linked by a network of pipelines to depleted and well-mapped oil and gas fields in the North Sea, offering rare access to infrastructure for carbon storage deep underground.
Such sites may not be worth much today – with carbon prices in Europe too low to matter at barely $5 a tonne – but the COP21 climate deal agreed in Paris last December transforms the long-term calculus.
It implies a tightening regime of higher carbon penalties for the next half century, ending in net zero CO2 emissions. Once prices approach $50 a tonne the equation changes. Beyond $100 it inverts the pyramid of energy wealth: profits accrue to those with access to the cheapest low carbon power.
The drastic implications of COP21 are still sinking in. A maximum 'carbon budget' of 3,000 gigatonnes – deemed necessary to stop temperatures rising more than 2 degrees Celsius above pre-industrial levels – may mean zero emissions from the power sector by mid-century.
The accord was signed by 195 countries, led by the US and China. It makes no difference whether you accept the hypothesis of man-made global warming. The deal constitutes the political will of the world, and will be legally-binding in the sense that each state transposes its commitments into domestic law.
It's to hard to imagine how somebody could be so wrong about so much!
As already noted, there is no "global carbon price", and attempts to impose ever rising carbon prices in Europe will simply drive yet more industries abroad.
Indeed, it is hard to see how there will be much "energy-intensive manufacturing" left in Britain in a few years time, to take advantage of this imaginary carbon storage.
The idea that China, India or most other countries will be prepared to see their industries go down the plug hole, as a result of obsession with western ideas about climate change, is patently absurd. Their main objective is to see us commit hari kari first.
The Paris Agreement, (COP21), never agreed any "maximum carbon budget", of 3000 gigatonnes or anything else. On the contrary, even the UNFCCC specifically recognised that the pledges made at Paris would drastically increase annual emissions and not cut them.
The whole idea, perpetuated by AEP and others of his ilk, that the rest of the world cares enough about carbon emissions to wreck their economies is ludicrous, and reveals how badly out of touch he is.
As for that deal which constitutes the political will of the world, and will be legally-binding in the sense that each state transposes its commitments into domestic law.
Well, we know about the Paris Agreement, except for dear old Ambrose apparently.
There is in fact nothing legally binding about it at all, and there are certainly no commitments written into anybody's domestic law.
The whole thing was never more than a combination of western obsession with climate change, and a desire amongst the rest to make as much money and economic advantage out of it as possible.
It is quite astonishing that a journalist as astute as Ambrose Evans-Pritchard could be so taken in by the machinations of western governments, and their creatures, the IMF and IEA, and yet remain blind to what is going on in the real world.
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City Health Inspectors: Food Donation’s Best Friend?
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Sunspots: Labitzke Meets Bonferroni
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Wildfires Caused By Bad Environmental Policy Are Causing California Forests To Be Net CO2 Emitters
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[ASAP] Dipole Radiation-Induced Extraordinary Optical Transmission for Silver Nanorod-Covered Silver Nanohole Arrays
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[ASAP] Tuning the Hematite (110) Surface Properties To Enhance Its Efficiency in Photoelectrochemistry
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[ASAP] Dispersed Solid Conductors: Fast Interfacial Li-Ion Dynamics in Nanostructured LiF and LiF:?-Al2O3 Composites
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[ASAP] Self-Assembly and Electronic Structure of Tribenzotriquinacenes on Ag(111)
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[ASAP] Size-Dependent Asymmetric Auger Interactions in Plasma-Produced n- and p-Type-Doped Silicon Nanocrystals
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[ASAP] Band Offset Models of Three-Dimensionally Bonded Semiconductors and Insulators
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[ASAP] Pathways for Improving the Photovoltaic Efficiency of Porphyrin and Phosphorene Antidot Lattice Nanocomposites: An Insight from a Theoretical Study
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[ASAP] Synthesis of Fiber-like Monetite without Organic Additives and Its Transformation to Hydroxyapatite
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[ASAP] Candidate Inorganic Photovoltaic Materials from Electronic Structure-Based Optical Absorption and Charge Transport Proxies
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