Neil deGrasse Tyson exposes how inequality plays into the U.N. Climate Summit


Cop21ungetty

People visit the “Solutions COP21” exhibition at the Grand Palais in Paris on December 4, 2015 on the sidelines of the COP21 United Nations Climate Summit.
At the U.N. Climate Summit in Paris, the negotiating positions of various countries can be difficult to follow, particularly when it comes to the interests that lurk behind those positions. The talks are full of acronyms, and concepts like “loss and damage,” “climate finance” and “deep decarbonization” are opaque for most people.

Fortunately, astrophysicist and ace science communicator Neil deGrasse Tyson summarized in one tweet the difference between what is at stake at these talks for poor nations, such as the Marshall Islands, Bangladesh and the Philippines, compared to industrialized nations like the United States and European Union.

So far, India and Saudi Arabia have blocked attempts to include findings of a U.N. report regarding a 1.5-degree target that was commissioned at a previous round of climate talks, which was released earlier this year. The report shows the lower risk of dangerous amounts of global warming if the temperature increase were limited to 1.5 degrees Celsius, or 2.7 degrees Fahrenheit.

“Limiting global warming to below 1.5 degrees Celsius would come with several advantages in terms of coming closer to a safer ‘guardrail,'” the report said. “It would avoid or reduce risks, for example, to food production or unique and threatened systems such as coral reefs or many parts of the cryosphere, including the risk of sea level rise.”

Saleemul Huq, a senior fellow at the International Institute for Environment and Development who is working with countries to push for a 1.5-degree goal, said a temperature target of below 2 degrees Celsius is needed to protect everyone around the world, including the poorest people living in mid-continental drought-prone regions and low-lying states.

COP21

Lyndon Pishagua Chinchuga, a representative of the indigenous peoples of the Peruvian Amazon and an un-named co-representative walk past a stand at the United Nations Climate Summit, at Le Bourget, on the outskirts of Paris on December 3, 2015.

“If we were to accept the 2 degrees as a global goal, then we will have to accept at the same time that we are writing these people off,” said Saleemul Huq in a video briefing from France. “We are telling them that we will not protect you. We will protect us, but we will not protect you.”

“It’s very difficult, we understand that and we accept that. On the other hand, difficult is not impossible,” Huq said. “We believe there is enough money, there is enough technology to do it, there simply isn’t enough political will to do it. And Paris is about generating political will.”

Temperature targets are about survival through long-term decarbonization

The temperature targets can be thought of in a different way, too. Each target would require a particular pace of reducing emissions of global warming pollutants such as carbon dioxide. So far, the world is on track to exceed the 2-degree target despite the emissions pledges made for the Paris talks. This makes the 1.5-degree target appear to be unachievable, barring the creation of technology that can efficiently and effectively suck carbon dioxide out of the atmosphere.

Christiana Figueres, who chairs the U.N. Framework Convention on Climate Change that is overseeing COP21, said the entire Paris agreement will lead to a whole-scale shift away from fossil fuel-powered economies.

“Everyone here agrees that we do need to head for the deepest decarbonization pathways and in an urgent fashion,” Figueres said at a press conference on Friday.

“I do think that there is a lot of space to be able to find, not just a language, but also a very important conceptual agreement of the fact that decarbonization needs to happen, that it needs to happen quickly and that it needs to happen across the economy. That is what we’re talking about when we talk about 1.5 to 2 [degrees], it is not a discussion about the temperatures, it’s just a proxy. The discussion is about the decarbonization of the economy.”

Carbon Inequality

Carbon dioxide emissions of wealthy people versus the poor.

IMAGE: OXFAM INTERNATIONAL

Precisely how to decarbonize, though, and what allowances developing countries will have to burn more fossil fuels as they develop compared to industrialized country obligations, remains to be worked out. One proposal in Paris, for example, would allocate the remaining portion of the global carbon budget based on which countries caused most of modern-day global warming in the first place, and which countries are trying first and foremost to address poverty concerns.

Global warming is an issue of inequality

Climate change is often seen as a pollution problem, yet to many, evidently including Tyson, inequality plays a central role.

The advocacy organization Oxfam International released a report this week that found that the poorest 50% of the global population, which amounts to about 3.5 billion people, are responsible for just 10% of total global emissions. Yet the richest 10% of people contribute about 50% of global emissions, the organization found. The richest 10% of people have carbon footprints 11 times as high as the poorest half of the population, the report found.

“The average footprint of the richest 1% of people globally could be 175 times that of the poorest 10%,”

“The average footprint of the richest 1% of people globally could be 175 times that of the poorest 10%,” the report, which was endorsed by economist and best-selling author Thomas Picketty, found.“At its heart, climate change is an issue of global justice,” Oxfam’s Tim Gore told Mashable in an interview. “When countries are negotiating here you should keep that in mind.”

“What should be expected of India, bearing in mind the poverty challenges its population is facing?”

His tweet speaks to why developing countries have been so adamant about including a reference to a lower temperature target — 1.5 degrees Celsius above preindustrial levels — rather than the 2-degree target countries agreed to a few years ago. The 0.5-degree difference is a matter of life or death for some low-lying nations that are already losing ground to the sea.

Discovery puts designer dopamine neurons within reach


neural-specific protein

A protein found only in neurons is shown here in red, and an enzyme that synthesizes dopamine in green. Cell DNA is labeled in blue.

Parkinson’s disease researchers discover a way to reprogram the genome –

For decades, the elusive holy grail in Parkinson’s disease research has been finding a way to repair faulty dopamine neurons and put them back into patients, where they will start producing dopamine again. Researchers have used fetal material, which is difficult to obtain and of variable quality. Embryonic stem cells represented a tremendous innovation, but making dopamine neurons from stem cells is a long process with a low yield.

These issues have driven researchers to try to develop ways to turn cells that are easy to obtain, such as skin cells, into dopamine neurons, which are normally hidden in the brain. But here, too, it has been difficult to obtain sufficient quantities of neurons.

Now, Parkinson’s disease researchers at the Jacobs School of Medicine and Biomedical Sciences at the University at Buffalo (UB) have developed a way to ramp up the conversion of skin cells into dopamine neurons. They have identified—and found a way to overcome—a key obstacle to such cellular conversions. At the same time, the researchers say the finding has profound implications for changing the way scientists work with all cells.

A cellular ‘gatekeeper’

The new research, published in Nature Communications, revolves around their discovery that p53, a transcription factor protein, acts as a gatekeeper protein.

“We found that p53 tries to maintain the status quo in a cell, it guards against changes from one cell type to another,” explained Jian Feng, PhD, senior author and professor in the Department of Physiology and Biophysics in the Jacobs School of Medicine and Biomedical Sciences at UB. “We found that p53 acts as a kind of gatekeeper protein to prevent conversion into another type of cell. Once we lowered the expression of p53, then things got interesting: We were able to reprogram the fibroblasts into neurons much more easily.”

The advance has importance to basic cell biology, Feng said. “This is a generic way for us to change cells from one type to another,” he said. “It proves that we can treat the cell as a software system, when we remove the barriers to change. If we can identify transcription factor combinations that control which genes are turned on and off, we can change how the genome is being read. We might be able to play with the system more quickly and we might be able to generate tissues similar to those in the body, even brain tissue.

“People like to think that things proceed in a hierarchical way, that we start from a single cell and develop into an adult with about 40 trillion cells, but our results prove that there is no hierarchy,” he continued. “All our cells have the same source code as our first cell; this code is read differently to generate all types of cells that make up the body.”

Generating new dopamine neurons via cellular conversion

Timing was key to their success. “We found that the point in the cell cycle just before the cell tries to sense its environment to ensure that all is ready for duplicating the genome, is the prime time when the cell is receptive to change,” said Feng.

By lowering the genomic gatekeeper p53 at the right time of cell cycle, they could easily turn the skin cells into dopamine neurons, with transcription factor combinations discovered in previous studies. These manipulations turn on the expression of Tet1, a DNA modification enzyme that changes how the genome is read.

“Our method is faster and much more efficient than previously developed ones,” said Feng. “The best previous method could take two weeks to produce 5 percent dopamine neurons. With ours, we got 60 percent dopamine neurons in ten days.”

The researchers have done multiple experiments to prove that these neurons are functional mid-brain dopaminergic neurons, the type lost in Parkinson’s disease.

The finding enables researchers to generate patient-specific neurons in a dish that could then be transplanted into the brain to repair the faulty neurons. It can also be used to efficiently screen new treatments for Parkinson’s disease.

Chronic CSF leak causing syringomyelia and pseudo-Arnold-Chiari malformation


A 45-year-old woman developed orthostatic headaches after lifting weights. A CT myelogram localized a CSF leak at T5-T7. Multiple blood patches provided only transient relief. Over 5 years, the patient developed paresthesias, worsened headaches, and decreased hand coordination. MRI showed progressive cerebellar tonsillar descent and hydrosyringomyelia (figure). Repeat myelography was unrevealing, but subsequent multilevel epidural blood patches with fibrin glue led to headache resolution. Cerebellar tonsillar descent and hydrosyringomyelia can occur in chronic spontaneous CSF leaks.1 A CSF leak should be considered in patients with orthostatic headache and presumed Chiari malformation.

Figure

Figure Sagittal T2 MRI

Images demonstrate progressive cerebellar tonsillar descent and development of syrinx within the intramedullary cavity from C1 to C3, with T2 signal suggestive of intramedullary hydrostatic edema extending caudally to T4-5.

Playing amateur sports increases CTE risk .


Amateur contact sports such as football, boxing, wrestling, rugby, basketball and baseball are linked to increased risk of developing chronic traumatic encephalopathy, according to a new study by the Mayo Clinic published in December’s issue of Acta Neuropathologica.

CTE is a progressive degenerative disease caused by repetitive brain trauma. It can affect mood, behavior and cognition.

New study finds amateur sports participation increases CTE risk

The study found that males who played amateur contact sports during their youth or young adult years were more susceptible to developing CTE.

More than 1,700 cases in the Mayo Clinic Brain Bank were examined by researchers. Of the 66 males in the pool that played contact sports during their youth and young adult years, 32% were found to have brain tissue showing CTE pathology.

”If 1 in 3 individuals who participate in a contact sport goes on to develop CTE pathology, this could present a real challenge down the road,” the study’s lead author Kevin ​Bieniek said, according to the Mayo Clinic.

“The purpose of our study is not to discourage children and adults from participating in sports because we believe the mental and physical health benefits are great,” Bieniek added. “It is vital that people use caution when it comes to protecting the head. Through CTE awareness, greater emphasis will be placed on making contact sports safer, with better protective equipment and fewer head-to-head contacts.”

This is the first study using neuropathologic criteria to look into the presence of CTE in nonprofessional athletes.

The sample of brains used by the study also included the brains of donors who died from dementia and other neurological diseases, which have been linked to the development of CTE.

Can cancer itself damage the heart?


Research presented today at EuroEcho-Imaging 2015 raises the possibility that cancer itself may damage heart muscle irrespective of exposure to cancer drug therapies.1 Researchers from the UK’s first dedicated cardio-oncology clinic found that both treated and untreated cancer patients had impaired heart function.

The annual meeting of the European Association of Cardiovascular Imaging (EACVI), a registered branch of the European Society of Cardiology (ESC), is held 2 to 5 December 2015 in Seville, Spain.

“It is well known that chemotherapy is potentially toxic to the heart, making cancer patients more prone to cardiovascular complications such as heart failure, hypertension or myocardial ischaemia,” said Dr Rajdeep S. Khattar, last author of the abstract and consultant cardiologist at the Royal Brompton Hospital in London, UK. “Our study raises the possibility that tumour growth itself may also damage the heart which could have important implications for monitoring.”

The definition of cardiotoxicity is based on a reduced ejection fraction (less than 55%) and symptoms of heart failure. Ejection fraction is a coarse measure of left ventricular function and is assessed by echocardiography. It refers to the percentage of blood pumped into the circulation when the heart contracts. For example, if there is 100 ml of blood in the left ventricle and 65 ml is pumped out, the ejection fraction is 65%.

The current study applied a more subtle measure of left ventricular function using echocardiography called strain. It indicates how well the myocardial fibres contract. Previous studies have shown that cancer patients who have had chemotherapy can have a normal ejection fraction but reduced strain and that this may predict subsequent cardiotoxicity.

Dr Khattar said: “Our study carried this finding a step further to see if untreated cancer patients with a normal ejection fraction also had reduced strain measurements.”

The study compared myocardial strain in three groups with a normal ejection fraction (55% or more): 43 patients with cancer who were currently being treated or had received treatment in the past, 36 patients with as yet untreated cancer, and 20 healthy individuals matched to the cancer groups for age and gender.

The researchers found that both groups of cancer patients had similarly reduced strain measurements, indicating impaired heart function, compared to the healthy individuals.

“All of the cancer patients had a preserved ejection fraction so by this coarse measure their hearts were functioning normally,” said Dr Khattar. “But the strain measurements showed that they did have myocardial dysfunction.”

He continued: “What was really new was the finding of reduced strain, and therefore myocardial dysfunction, in the group of patients with cancer who had not yet received treatment. This raises the possibility that the tumour itself may have a direct and deleterious effect on the function of the heart.”

Patients with reduced strain before they start their cancer drug therapies may be predisposed to developing heart failure during the course of their treatment. “These patients might need closer monitoring,” said Dr Khattar. “This would be a real change because at the moment, cancer patients don’t, as a matter of routine, have a cardiovascular risk assessment by a cardiologist.”

This is only the second study in humans which suggests that cancer might have a direct effect on the heart. A study published in September found elevated cardiovascular biomarkers in patients with as yet untreated cancer.2,3 “It could be that the tumour produces these inflammatory markers which then leads to the reduction in myocardial function that we found,” said Dr Khattar.

Dr Khattar will continue to follow the patients in the current study to find out if their rates of heart failure and death are predicted by the strain measurements. He said: “If it transpires that the patients with reduced strain prior to cancer treatment are more prone to heart failure and death then it would be important to implement closer monitoring of patients with cancer than is conducted currently.”