Yes, the Arctic’s freakishly warm winter is due to humans’ climate influence

Andrew King, University of Melbourne

For the Arctic, like the globe as a whole, 2016 has been exceptionally warm. For much of the year, Arctic temperatures have been much higher than normal, and sea ice concentrations have been at record low levels.

The Arctic’s seasonal cycle means that the lowest sea ice concentrations occur in September each year. But while September 2012 had less ice than September 2016, this year the ice coverage has not increased as expected as we moved into the northern winter. As a result, since late October, Arctic sea ice extent has been at record low levels for the time of year.

Late 2016 has produced new record lows for Arctic ice.
NSIDC, Author provided

These record low sea ice levels have been associated with exceptionally high temperatures for the Arctic region. November and December (so far) have seen record warm temperatures. At the same time Siberia, and very recently North America, have experienced conditions that are slightly cooler than normal.

Temperatures have been far above normal over vast areas of the Arctic this November and December.
Geert Jan van Oldenborgh/KNMI/ERA-Interim, Author provided

Extreme Arctic warmth and low ice coverage affect the migration patterns of marine mammals and have been linked with mass starvation and deaths among reindeer, as well as affecting polar bear habitats.

Given these severe ecological impacts and the potential influence of the Arctic on the climates of North America and Europe, it is important that we try to understand whether and how human-induced climate change has played a role in this event.

Arctic attribution

Our World Weather Attribution group, led by Climate Central and including researchers at the University of Melbourne, the University of Oxford and the Dutch Meteorological Service (KNMI), used three different methods to assess the role of the human climate influence on record Arctic warmth over November and December.

We used forecast temperatures and heat persistence models to predict what will happen for the rest of December. But even with 10 days still to go, it is clear that November-December 2016 will certainly be record-breakingly warm for the Arctic.

Next, I investigated whether human-caused climate change has altered the likelihood of extremely warm Arctic temperatures, using state-of-the-art climate models. By comparing climate model simulations that include human influences, such as increased greenhouse gas concentrations, with ones without these human effects, we can estimate the role of climate change in this event.

This technique is similar to that used in previous analyses of Australian record heat and the sea temperatures associated with the Great Barrier Reef coral bleaching event.

The November-December temperatures of 2016 are record-breaking but will be commonplace in a few decades’ time.
Andrew King, Author provided

To put it simply, the record November-December temperatures in the Arctic do not happen in the simulations that leave out human-driven climate factors. In fact, even with human effects included, the models suggest that this Arctic hot spell is a 1-in-200-year event. So this is a freak event even by the standards of today’s world, which humans have warmed by roughly 1℃ on average since pre-industrial times.

But in the future, as we continue to emit greenhouse gases and further warm the planet, events like this won’t be freaks any more. If we do not reduce our greenhouse gas emissions, we estimate that by the late 2040s this event will occur on average once every two years.

Watching the trend

The group at KNMI used observational data (not a straightforward task in an area where very few observations are taken) to examine whether the probability of extreme warmth in the Arctic has changed over the past 100 years. To do this, temperatures slightly further south of the North Pole were incorporated into the analysis (to make up for the lack of data around the North Pole), and these indicated that the current Arctic heat is unprecedented in more than a century.

The observational analysis reached a similar conclusion to the model study: that a century ago this event would be extremely unlikely to occur, and now it is somewhat more likely (the observational analysis puts it at about a 1-in-50-year event).

The Oxford group used the very large ensemble of Weather@Home climate model simulations to compare Arctic heat like 2016 in the world of today with a year like 2016 without human influences. They also found a substantial human influence in this event.

Santa struggles with the heat. Climate change is warming the North Pole and increasing the chance of extreme warm events.
Climate Central

All of our analysis points the finger at human-induced climate change for this event. Without it, Arctic warmth like this is extremely unlikely to occur. And while it’s still an extreme event in today’s climate, in the future it won’t be that unusual, unless we drastically curtail our greenhouse gas emissions.

As we have already seen, the consequences of more frequent extreme warmth in the future could be devastating for the animals and other species that call the Arctic home.

Geert Jan van Oldenborgh, Marc Macias-Fauria, Peter Uhe, Sjoukje Philip, Sarah Kew, David Karoly, Friederike Otto, Myles Allen and Heidi Cullen all contributed to the research on which this article is based.

You can find more details on all the analysis techniques here. Each of the methods used has been peer-reviewed, although as with the Great Barrier Reef bleaching study, we will submit a research manuscript for peer review and publication in 2017.

Andrew King, Climate Extremes Research Fellow, University of Melbourne

This article was originally published on The Conversation. Read the original article.

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Deadly disease can ‘hide’ from a Tasmanian devil’s immune system

Andrew S. Flies, University of Tasmania and Greg Woods, University of Tasmania

The Tasmanian devil facial tumour (DFT) cells may use a molecular deception – common in human cancers – that could allow the deadly disease to avoid the animal’s immune system, according to our new research published this month.

Recently it was discovered that DFT cells effectively hide from the immune system by not expressing key immune recognition molecules.

Our new discovery that DFT cells contain this “molecular shield” in response to inflammation represents another important step towards understanding the disease and developing more potent ways of preventing or treating it.

So how does this shield work? First, we need to look at some of the recent developments in the treatment of cancers in general.

Cancer treatments

Cancer treatment has undergone a revolution in recent years. Gone are the days when surgery and harsh chemotherapy regimens are the only options.

Now cancer immunotherapy can stimulate the immune system to kill cancer cells. In 2013 this was named the breakthrough of the year in one of the top science journals in the world.

Since 2013 the immunotherapies that target what we call immune checkpoint molecules have continued to make great progress and have recently been approved as first line defences for some cancers.

Checkpoint molecules are critical for keeping the immune system in balance. Every time that the accelerator is pressed in the immune system, there is always at least one, and often several, means of stepping on the brakes.

These checks and balances are necessary because even though the primary job of the immune system is to protect us from disease, the immune system wields powerful weapons that can inflict collateral damage to critical tissues and organ systems when it is aimed at the wrong target.

Programmed death

In recent years the aptly-named checkpoint molecules – “programmed death-1” (PD-1) and “programmed death ligand 1” (PD-L1) – have emerged to be critical regulators of the anti-cancer immune response.

The PD-L1 molecule is used by many types of cancer as a molecular shield to protect the malignant cells from anti-cancer immune responses.

The PD-1 molecule is found on several types of immune cells, but has particular relevance to the anti-cancer responses mediated by T cells.

When PD-1 on a cancer-killing T cell interacts with PD-L1 on cancer cells, the T cell is shut off. The T cell may undergo programmed death or it may linger and play no role in the anti-cancer response.

The worst possibility is that the former cancer-killing T cell hangs around and actually prevents other immune cells from killing cancer cells.

The Tassie devil’s immune system

Our Tasmanian devil immunology team has recently demonstrated that these critical immune checkpoint molecules are also present in devils. This may play a role in the ability of the DFT’s ability to evade the devil immune system.

There likely exists many additional mechanisms that the DFTs use to hide from or suppress the immune system of devils and ongoing research efforts aim to uncover and neutralise these mechanisms.

Recent evidence has shown that some devils have tumour regressions, showing that the tumours are not always able to hide from the immune system.

Spontaneous tumour regression is not common in humans, but it does occur in some people and is likely caused by the immune system recognising and killing tumour cells.

Another deadly disease

But the devils are not out of the woods yet for a few reasons. Only in 2014 a second transmissible cancer (devil facial tumour disease 2 or DFT2) was discovered in wild devils in southern Tasmania.

There are only a handful of naturally transmissible tumours known in the world, so a second transmissible tumour in devils is extremely surprising, like lightning striking the devils twice.

In order for the wild devil population to be truly safe from the transmissible tumours, they would need to have immunity to both the original transmissible tumour DFT and DFT2 and hope that no new transmissible cancers arise.

It remains unknown at this point how many different weapons the tumours use to evade or suppress the immune system.

The tumours themselves can also evolve rapidly in response to ecological and immunological pressure. In many cases, disease causing agents evolve to be less virulent (not kill the animal they infect), but only time will tell if that will happen in the curious case of the devil.

Our ongoing research aims to understand exactly which devil immune system switches can be turned on and off in order to stimulate immune cells to kill cancer cells.

This will be particularly fruitful if we can pinpoint specific genetic and immunological mechanisms that are different in devils that kill tumour cells and those that don’t.

It’s not often that you cheer for the devil, but this is one situation where nearly everybody wants the devil to win!

Andrew S. Flies, Postdoctoral Research Fellow in Immunology, University of Tasmania and Greg Woods, Professional Research Fellow, University of Tasmania

This article was originally published on The Conversation. Read the original article.