Chinese Stir-fry with Bitter Melon and Crabmeat

Ingredients

150 g cooked crabmeat
1 bitter melon, about 500 g, peeled, seeded and cut ito picecs
3/4 tsp salt
1/2 tsp sugar
2 tsp minced ginger
2 tsp cooking wine
2 tbsp oil
1 tsp sesame oil

Sauce

1/2 cup chicken broth
1/2 tsp cornstarch
1 tsp fish sauce
dash ground white pepper

Method

  1. PUt bitter melon in a colander. Sprinkle 1 tsp salt and mix well. Set aside for 15 minutes. Rinse the salt away with cold water. Drain and wipe dry with paper towel.
  2. Heat 1 tbsp oil in a wok. Add bitter melon and stir-fry on medium-high heat until cooked. Season to taste with salt and sugar. Remove.
  3. Clean wok and heat 1 tbsp oil on medium -high heat. Saute ginger until fragrant. Add crabmeat and toss briefly. Sprinkle with cooking wine.
  4. Return bitter melon to the wok. Toss to combine with the crabmeat. Add sauce ingredients. Continue to stir-fry util sauce boils and thickens. Mix in sesame oil and remove to serving platter. Serve hot.

Source: Chinese Home Cooking

Is Your Cholesterol in Good Shape?

Gilles Beaudin wrote . . . .

Cholesterol has been getting a lot of press lately. The most recent news is the about face on dietary cholesterol. The American dietary guidelines no longer encourage restricted cholesterol consumption. Strong scientific evidence shows that dietary intake has little influence on levels of good and bad cholesterol in the body.

The message that hasn’t changed is this: If your blood has a lower level of bad cholesterol (low-density lipoprotein, or LDL) and a higher level of the good kind (high-density lipoprotein, or HDL), you will reduce your risk of heart disease. Lifestyle modifications and/or medications are usually effective in shifting your cholesterol levels into a healthy range.

Surprisingly, a large number of heart attacks are seen in people with healthy levels of good cholesterol. This indicates that there is something going on beyond the numbers, and that is the quality and function of HDL.

You see, HDLs help keep LDLs under control. Their job is to prevent the oxidation of LDL, which can lead to atherosclerosis, a disease in which plaque builds up inside your arteries. LDLs become oxidized after they react with free radicals. When your HDLs are in good shape, they act as an antioxidant. Weak HDLs can also lead to inflammation.

So how do you improve the function of your HDLs? You already know that regular exercise helps prevent cardiac disease. Both cardiovascular exercise and resistance training can have a positive impact. A study published in the Journal of Applied Physiology in 2013 compared the performance of HDLs in men who participated in resistance training and men who did not. They found that the HDLs of the men who strength trained were significantly better. Both groups of men had the same levels of HDL, but the strength training group’s HDLs had superior performance.

Obesity and excess weight are often blamed for many instances of heart disease. In the same strength training study, a group of overweight participants trained with weights. Their HDLs performed as well as the HDLs from the normal weight (a BMI at or under 25) participants. The quality of their HDLs was the same even if the individual had a BMI of 30 (that would be over 200 pounds for a 6-foot man). Moreover, a paper published in the Mayo Clinic Proceedings in 2012 reported that overweight and obese men have increased longevity if they have a high fitness level.

It’s important to remember that fitness and health can be two very different things. Don’t get me wrong – losing belly fat is always a good thing. Fat stored around your midsection may be a problem down the road. Just make sure you lose it the right way, through proper nutrition and exercise.

A major downside to using weight as a health predictor is that the scale doesn’t differentiate between lean weight and fat weight. If you lose five pounds of fat and gain five pounds of muscle, you are healthier even though your weight hasn’t changed.

All of this goes to show that the number on the scale is not as strong a predictor of health as we once thought. The best thing you can do to maximize the function of your HDLs and improve your health is simply start exercising. Naten Thakur, a physician at Cleveland Clinic Canada in Toronto, shares this advice with his patients who are trying to lose weight: “Just get moving. If you lose weight in the process, it’s a bonus.”

So don’t let the weight on the scale rule you, and focus instead on increasing your level of fitness. Your HDLs will thank you for it.

Source: The Globe and Mail

Fish and Dishes

Japanese Huchen (イトウ)


Sashimi

Nigiri Sushi

With Rice and Vegetables

Marinated

Pan-seared

Grilled

Scientists Drill Down to Genetic Root of Prostate Tumor Development


Enlarge image . . . . .

Scientists have revealed the root of prostate cancers in individual men, discovering that despite huge genetic variety between tumours they also share common gene faults – insight that could offer new treatment hopes, according to research published in Nature today (Wednesday).

In a landmark paper, Cancer Research UK funded scientists alongside an international team of researchers read all of the DNA in tumour samples from 10 men with prostate cancer. This allowed them to map a ‘family tree’ of the changes happening at a genetic level as the disease spreads, forms new tumours, and becomes resistant to treatment.

They also revealed more detail about how prostate cancer spreads, showing that the group of cells that first spread from the prostate carry on travelling around the body, forming more secondary tumours.

The research is part of the International Cancer Genome Consortium (ICGC) – a global project using the latest gene-sequencing technology to reveal the genetic changes driving the disease.

The ICGC Prostate Cancer UK group – funded by Cancer Research UK, the Dallaglio Foundation, the Wellcome Trust, the Academy of Finland and others – is examining how the disease evolves in patients to help develop approaches for personalised medicine, tailored to the genetic makeup of each person’s cancer.

The team has already revealed a huge amount of genetic diversity between cancer cells taken from different sites within each man’s prostate.

And this new study shows that, despite the diversity, prostate cancer cells that break free from the tumour and spread share common genetic faults unique to the individual patient.

Study author Ros Eeles, professor of oncogenetics at The Institute of Cancer Research, London, and honorary consultant at The Royal Marsden NHS Foundation Trust, said: “We gained a much broader view of prostate cancer by studying both the original cancer and the cells that had spread to other parts of the body in these men. And we found that all of the cells that had broken free shared a common ancestor cell in the prostate.

“The common faults we found in each man could potentially offer new targets for treatment. But we found that, once cancer cells have spread, they continue to evolve genetically, so choosing the most effective treatments will remain a key challenge.”

Professor Steven Bova, based at the University of Tampere, Finland, and head of ICGC prostate cancer UK metastatic studies, said: “The diversity we’ve found suggests multiple biopsies might be needed to identify the ‘trunk’ of the cancer’s tree of mutations – we need treatments that target these core weaknesses to destroy all cancer cells in a clean sweep, rather than trimming the branches. We must also study more patients to learn how to apply these findings to develop more personalised treatments for people with the disease.”

Dr Ultan McDermott, senior author at the Wellcome Trust Sanger Institute, said: “In the phylogenetic trees that our data have produced, we see that most of the oncogenic mutations are shared clonally by all the tumour sites in each patient. This common genetic heritage is a potential achilles heel of the metastases, however, many of these shared mutations are in tumour suppressor genes and our approach to therapeutically targeting these needs to be prioritised.

“It takes a while before a tumour develops the ability to metastasise but once it does the patient’s prognosis changes significantly. We have to zoom in on this crucial junction and gather more data on the impact different therapies have on prostate cancer’s evolution and spread.”

Nearly 42,000 men are diagnosed with prostate cancer each year in the UK, making it the most common cancer in men and the third most common cancer overall. There are more than 10,800 deaths from the disease every year in the UK.

Professor Peter Johnson, chief clinician at Cancer Research UK, said: “The thing we fear most about cancer is how it can spread around the body – this is what causes 90 per cent of all cancer deaths. We have to find out how cancer cells change as they do this, and how they become resistant to our treatments. This research using whole genome sequencing lets us look right into the molecular core of cancer, and reveals the secrets of how cancer cells change and evolve as they grow. By getting to grips with this detail, we can start to work out how to treat prostate cancer better in the future.”

Source: Cancer Research UK


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