Character Cakes

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Easy and Low-fat Cheesecake with Banana

Ingredients

1/2 cup plus 2 tablespoons graham cracker crumbs
2 tablespoons plus 1/2 cup sugar
2 tablespoons margarine, melted
4 large bananas, mashed
8 oz nonfat cream cheese
1/2 cup nonfat small curd cottage cheese
1 egg
2 teaspoons vanilla extract (essence)
1/2 teaspoon sweetened cocoa
8 strawberries
8 fresh mint sprigs

Method

  1. Preheat an oven to 300°F (150°C). Coat the bottom and sides of a 9-inch springform pan with nonstick cooking spray.
  2. To make the crust, in a medium bowl, combine the graham cracker crumbs, 2 tablespoons sugar and margarine and stir to mix well. Lightly press the mixture into the bottom of the prepared pan.
  3. To make the filling, in a food processor with the metal blade or in a blender, combine the bananas, cream cheese, cottage cheese, egg, vanilla and 1/2 cup sugar and process until smooth.
  4. Pour the filling into the crust and bake until the center is set, about 1 hour. Turn off the oven, prop open the oven door and leave the cake in the oven to cool for 15 minutes.
  5. Remove the cake from the oven and cool completely in the pan, about 1 hour.
  6. To serve, release the cake from the pan, sprinkle the top with the cocoa, slice into 8 wedges and divide among individual dessert plates. Garnish each wedge with a strawberry and a mint sprig.
  7. Store covered in the refrigerator for up to 4 days.

Makes 8 servings.

Source: Cooking for Healthy Living

What Did 17th Century Food Taste Like?

From Res Obscura . . . . . . .

As the official portraitist for the Spanish monarchy at the height of its glory, Diego Velázquez painted queens, emperors, and gods. But one of his most famous paintings is a window into a much humbler world. A woman is frying eggs in hot oil, ready to scoop them out with a simple wooden spoon. Behind her, a servant boy carries a half-full jug of wine and a melon tied up in a loop of twine.

This painting is the type of thing historians love. A profoundly talented artist with a knack for realism, choosing the type of subject matter that is so normal that it rarely gets preserved (the same is true today—how many contemporary painters choose to depict taquerias or bagel shops?) Scholars suspect that Velazquez’s own family members may have served as models in his early paintings. It’s possible that the woman in this painting numbered among them, since she also appears in a religious painting he produced in the same year.

But this post is not about Velazquez. It’s not even about art history. It’s about food.

What can we learn about how people ate in the seventeenth century? And even if we can piece together historical recipes, can we ever really know what their food tasted like?

This might seem like a relatively unimportant question. For one thing, the senses of other people are always going to be, at some level, unknowable, because they are so deeply subjective. Not only can I not know what Velázquez’s fried eggs tasted like three hundred years ago, I arguably can’t know what my neighbor’s taste like. And why does the question matter, anyway? A very clear case can be made for the importance of the history of medicine and disease, or the histories of slavery, global commerce, warfare, and social change.

By comparison, the taste of food doesn’t seem to have the same stature. Fried eggs don’t change the course of history.

But taste does change history.

One example, chosen at random: the Mexican chili peppers hiding in the bottom edges of both paintings.

The pepper family (genus Capsicum) is native to the Americas, and it was still a relatively new arrival in the cuisines of Asia, Africa, and Europe when Velazquez was alive. As a non-elite person born in 1599, we can guess that his grandparents would not have been familiar with the taste of peppers and that his parents still thought of them as an exotic plant from across the seas. Even the name he, and we, apply to the plant was a foreign import: the word ‘chili’ is from Nahuatl, the language of the Aztecs. So is ‘avocado’ (Nahuatl ahuacatl), ‘tomato’ (tomatl) and chocolate (chocolatl).

The taste for these foods was a significant factor in the series of global ecological movements between the Old and New Worlds that historians call the Columbian Exchange. Any time we eat kimchi, or kung pao chicken, or pasta with red sauce, we are eating foods that are direct results of the Columbian Exchange.

Someone really needs to make a better map of the Columbian Exchange. This one, from a public-domain resource for teachers from UT Austin, is one of the best I could find, but it doesn’t come close to capturing the full range of exchanges.

But we’re also eating modern foods. That’s not to say that there aren’t older correlates to these dishes—there undoubtedly are. But food has changed since the early modern period. Globalization of food crops has transformed the flavors of regional cuisines. Meanwhile, factory farming has led to a homogenization of some of the varietals available to us, while also creating a huge variety of new strains and hybrids.

One example: I didn’t realize until recently that broccoli, Brussels sprouts, cauliflower, kale, cabbage, and collard greens are all technically the same species, Brassica oleracea. The substantial differences between these sub-species are all due to patient intervention by human farmers over millennia. Many of these changes are surprisingly recent. Early versions of cauliflower may have been mentioned by Pliny and medieval Muslim botanists, but as late as 1600, a French author was writing that cauli-fiori “as the Italians call it” was “still rather rare in France.” Likewise, Brussels sprouts don’t appear to have become widely cultivated until the Renaissance.

[ . . . . . . ]

Read more . . . . .

Infographic: Minimally Invasive Pancreatic Cancer Surgery

Source: Mayo Clinic

Study: Compound Found in Berries and Red Wine can Rejuvenate Cells

Richard Faragher, Lizzy Ostler and Lorna Harries wrote . . . . .

By the middle of this century the over 60s will outnumber the under 18s for the first time in human history. This should be good news, but growing old today also means becoming frail, sick and dependent. A healthy old age is good for you and a remarkably good deal for society. Improving the overall health of older Americans could save the US alone enough money to pay for clean drinking water for everyone on Earth for the next 30 years.

But if we want people to be healthy in old age we have to understand the mechanisms underlying the deterioration of our bodies over time. Doing so – and learning how we can prevent it – has been the goal of ageing research for more than 60 years.

There has been astonishing progress made over the last decade. In 2009, it was shown that the drug rapamcyin extended the lifespans of mice by 10-15%. Two years later a landmark study showed that experimental clearance of “senescent” cells – dysfunctional cells which build up as we age and cause damage to tissue – improved healthy lifespan in laboratory mice. These results delighted those of us who had argued for decades that senescent cells were a major cause of late life problems and should therefore be therapeutic targets.

Research on both living human cohorts and isolated cells have looked at the types of genes which change in expression levels (the process by which information from a gene is used to make the tens of thousands of proteins needed by a cell during ageing. This has revealed that the largest changes occur in genes which regulate how “messenger RNAs” are made. These transfer the information stored in DNA to the cellular machinery which turns it into proteins.

In the human cell, proteins known as “RNA splicing factors” determine which messenger RNA can be made from RNA building blocks in a process known as RNA splicing. The ability of our cells to do this is restricted with ageing. But it was unclear whether this loss is a result of senescent cells accumulating in ageing tissue or something new, occurring in parallel with senescence until now.

New evidence

Now our latest study, published in BMC Cell Biology shows that a natural substance can actually rejuvenate senescent cells by targeting RNA splicing.

In our experiments, we treated such cells with compounds we synthesised based on resveratrol, a natural product found in red wine, berries and other foods, reported to alter RNA splicing in cancer cells. Resveratrol – which can be found in many natural foods – is a blunt tool that affects multiple cellular pathways. But our synthetic variants are actually much more precise and we picked ones that preferentially affected RNA splicing.

Senescent human cells treated with our products showed remarkable effects, which we called “rejuvenation”. RNA splicing patterns were rapidly reset to that seen in young cells and then the senescent cultures began to grow again. Variations of this basic experiment showed that splicing factor restriction is separate from senescence but interacts with it.

Restoring RNA splicing rejuvenates senescent cells in part because our cells are normally rendered senescent through telomere shortening, the gradual loss of the DNA at the ends of chromosomes that occurs with repeated cell division. Some RNA splicing factors that decline with age are capable of helping to repair telomeres and so, if you restore them, they lengthen telomeres back up and stop the cell being senescent.

Restricted splicing has serious implications beyond the capacity of cells to divide and how tissues deal with stress. It limits cell responses, potentially contributing to the increased frailty that is a hallmark of ageing in many organisms including humans.

Following our discoveries the area of RNA splicing is now ripe for detailed study, not least because cells from old individuals that have not become senescent probably still have compromised splicing. Restricted splicing may prove to be a critical mechanism in the development of a wide range of age-associated diseases.

Drugs and diet

Our compounds have allowed us to begin to identify the key molecular pathways that mediate splicing factor restriction and may have a future as a platform for anti-degenerative drugs. But when only one or two in tens of thousands of compounds become medicines none of us are quitting work just yet.

As resveratrol and similar molecules are found in food, our work may have revealed an unsuspected link between diet and RNA splicing. Many groups have shown the beneficial effects of diets containing these foods – altered splicing may be one, but not the only, way in which they mediate their effects. However you’d need to drink some 30 litres of red wine a day to achieve the doses of analogues of resveratrol we used in tissue culture.

Pure resveratrol already exists as a dietary supplement. However, we do not recommend taking it just yet. One of the reasons we made the novel compounds was that resveratrol, like many natural products, has a whole range of activities, some that appear beneficial and some less so.

Our emphasis on achieving health in later life without undue concern for its extension chimes closely with the popular view. Something in excess of 60% of the population do not want thousand-year lifespans, even when given a guarantee of perfect health.

The challenge now is to convert this basic scientific discovery into the benefits people want, and as quickly as possible. Until then, there’s always blueberries …

Source : The Conversation


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