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High Emotional Intelligence Can Help to Identify Fake News

People with high levels of emotional intelligence are less likely to be susceptible to ‘fake news’, according to research at the University of Strathclyde.

The study invited participants to read a series of news items on social media and to ascertain whether they were real or fictitious, briefly describing the reasons for their answers. They were also asked to complete a test to determine their levels of emotional intelligence (EQ or emotional quotient) and were asked a number of questions when considering the veracity of each news item.

Researchers found that those who identified the types of news correctly were most likely to score highly in the EQ tests. There was a similar correlation between correct identification and educational attainment.

The study, by researchers in Strathclyde’s School of Psychological Sciences & Health and School of Government & Public Policy, has been published in the journal PLOS ONE.

Dr Tony Anderson, Senior Teaching Fellow in Psychology at Strathclyde and partner in the research, said: “Fake news on social media is now a matter of considerable public and governmental concern. Research on dealing with this issue is still in its infancy but recent studies have started to focus on the psychological factors which might make some individuals less susceptible to fake news.

“We assessed whether people were better able to disregard the emotionally charged content of such items and better equipped to assess the veracity of the information. We found that, while distinguishing real news content from fake was challenging, on average participants were more likely to make the correct decision than not.

“Previous research has shown that people can be trained to enhance their own EQ levels. This should help them to discern with a greater degree of accuracy which news is reliable and which is misleading.”

Participants were presented with real and fabricated news stories on issues including health, crime, wealth inequality and the environment. Fictitious items featured aspects including emotive language, brief information and a lack of attributed sources.

Comments from people who incorrectly believed fabricated stories were real included: “I have personal experience of this”; “My kids are in this position so I completely get this”; “The graph shows it all” and “The commenter on the post has the same thoughts as me.” Those who correctly identified fictitious stories made comments including: “There is emotive/condescending language in the blurb”; “Fearmongering article with no data”; “The source is not an official scientific or governmental source” and “Comes across as more of a rant.”

Source: The University of Strathclyde

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Beyond Genes and Environment, Random Variations Play Important Role in Longevity

A new model of aging takes into account not only genetics and environmental exposures but also the tiny changes that randomly arise at the cellular level.

University Professor Caleb Finch introduced the “Tripartite Phenotype of Aging” as a new conceptual model that addresses why lifespan varies so much, even among human identical twins who share the same genes. Only about 10 to 35 percent of longevity can be traced to genes inherited from our parents, Finch mentioned.

Finch authored the paper introducing the model with one of his former graduate students, Amin Haghani, who received his PhD in the Biology of Aging from the USC Leonard Davis School in 2020 and is now a postdoctoral researcher at UCLA. In the article, they propose that the limited heritability of aging patterns and longevity in humans is an outcome of gene-environment interactions, together with stochastic, or chance, variations in the body’s cells. These random changes can include cellular changes that happen during development, molecular damage that occurs later in life, and more.

“We wanted to introduce a conceptual map and some new terminology that will motivate a more comprehensive understanding of what the limitations of genetic determinants in aging are, how important it is to consider the genetic variance in relationship to the environment, and include this new domain of stochastic variations, which is very well recognized by different fields,” said Finch, who holds the ARCO/William F. Kieschnick Chair in the Neurobiology of Aging at the USC Leonard Davis School. “It hasn’t really been put in a formal context in which the complete package can be discussed, and that’s what I hope our article achieves.”

Expanding on the exposome

The new model is a natural extension of the idea of the exposome, which was first proposed by cancer epidemiologist Christopher Paul Wild in 2005 to draw attention to the need for more data on lifetime exposure to environmental carcinogens. The exposome concept illustrates how external factors, ranging from air pollution and socioeconomic status to individual diet and exercise patterns, interact with endogenous, or internal, factors such as the body’s microbiome and fat deposits.

The exposome is now a mainstream model, eclipsing previous characterizations of environmental factors as affecting risk “one by one.” Finch has previously expanded on the exposome concept with the introduction of the Alzheimer’s disease exposome. The gero-exposome now considers how genes and the environment interact over the lifespan to shape how we age.

The new model illustrates that cell-by-cell variations in gene expression, variations arising during development, random mutations, and epigenetic changes – turning genes “off” or “on” – should be explicitly considered apart from traditional genetic or environmental research regarding aging, Finch said. More detailed study into these chance processes has been enabled by cutting-edge research techniques, including the study of gene transcription within single cells as well as ChIP-sequencing, which can illustrate how individual proteins interact with DNA.

Effects of happenstance on health

In the paper, Finch and Haghani discussed several examples of how risks of age-related disease are poorly predicted by DNA alone but are heavily influenced by environmental exposures as well as the time and duration of the exposure, including during development or over the course of decades.

One well-known example of a gene that is associated with increased Alzheimer’s risk is ApoE-4; however, having the ApoE-4 gene doesn’t definitively mean someone will get Alzheimer’s. Studies in both mice and humans revealed that ApoE-4 and clusters of related genes interact with exposures such as air pollution or cigarette smoke to influence risk, and Alzheimer’s patients also show differences in their epigenetics as compared to individuals without the disease.

He added that the idea of environmental exposure can stretch farther than many people expect. Disease exposure earlier in life can affect health risks later in life – and across generations.

“The environment that we’re exposed to goes back to our grandmothers because the egg we came from was in our mother’s ovaries at the time of her birth,” he explained. “So that means, in my case, because my grandmother was born in 1878, I might very well carry some traces of the 19th century environment, which included much greater exposure to infectious disease because there were no antibiotics.”

Finch said that he hopes the more comprehensive model on how genes, environment, and random variations over time interact to influence aging prompt a new discussion of what the rapidly developing field of precision medicine needs to take into account to promote healthy aging.

“I think that there will be a much greater recognition in understanding individual patterns of aging,” he said. “We can only define it up to a certain point by knowing the genetic risks; we must have a more comprehensive understanding of the lifetime exposures, environments and lifestyles of an individual to have a better understanding of genetic risk for particular diseases.”

Source: EurekAlert!

Lobster Pancakes

Ingredients

Pancake Batter

4 oz all-purpose flour
pinch of salt
1 egg
1 egg yolk
1 cup milk
1 tablespoon melted butter, or vegetable oil

Filling

1 cooked lobster (about 1-1/2 lb) or 1 lb canned lobster meat
1 oz butter
1 teaspoon paprika pepper
1 cup béchamel sauce
1 teaspoon tomato puree
2 tablespoons double cream

Sauce

4 oz button mushrooms
1/2 oz butter
1 shallot (finely chopped)
1 onion
2 tablespoons brandy, or dry sherry
1/2 cup double cream
salt and pepper
1 tablespoon grated Parmesan cheese

Method

  1. Prepare batter, leave to stand in a cool place for 30 minutes.
  2. Slice the lobster meat from the tail and claws, scoop all the soft meat from the head, or drain canned lobster.
  3. Melt the butter in a pan, add paprika and cook for 1 minute. Put in the tail and claw meat. Set pan aside.
  4. Add béchamel sauce, tomato puree and the creamy meat from the head or canned lobster meatto the pan, and simmer for 2-3 minutes.
  5. Draw pan aside and stir in the cream, taste for seasoning. Keep lobster mixture warm.
  6. Preheat oven at 350°F.
  7. Fry pancakes thinly. Put a tablespoon of lobster mixture on each pancake, fold them up into triangles and put in a well-buttered ovenproof serving dish in pre-set oven to keep hot.
  8. Wash and trim the mushrooms. Slice them finely.
  9. Grate onion into a bowl. Press with a spoon, drain and reserve juice.
  10. Melt butter in a pan. Add the shallot and onion juice and cook for 2-3 minutes until shallot is soft but not coloured.
  11. Add the mushrooms, increase the heat and cook briskly for 1 minute.
  12. Pour on the brandy or sherry, and cream, season to taste. Boil rapidly for 1 minute.
  13. Pour the sauce over the pancakes, dust with Parmesan cheese and glaze under the grill. Serve at once.

Makes 4 to 6 servings.

Source: Cooking with Eggs


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