080125

WT...KDU College called me twice in a month just to recruit me to their college!

...greeted me and started with 'Have you registered to any college??, you need SPM with 5 credits

...' and asked me to see their DEAR counselor...now what's your problem???

blah blah blah~

did the college hire a company to contact me ??

they are so*#%$!+

I don't care anymore!

Nows it's about science daily!

As usual, visited science daily.sites with loads of helpful and informative materials

I'm advertising sciencedaily for FREE!

nvm~ I learned a lot from there!

lurv lurv lurv
here's about aging

...tada

aim: To study the types of fuels** used by the heart in young and aged mice

problem statement: What is factor that contribute to a progressive age-related decline in heart function?

hypothesis: An age-related decline in heart function is a risk factor for heart disease in the elderly.

As the heart ages the ability to use fat as an energy source deteriorates.

#The young healthy heart normally used a balance of fat and sugar to generate energy to allow the heart to beat and pump blood efficiently.

#Using a genetically engineered mouse that is deficient in a protein that is responsible for transporting fat into the cells of the heart,

#Old genetically modified mice did not accumulate fat in their hearts, as did ordinary mice

#Old genetically altered mice out-performed ordinary old mice on a treadmill test, were completely protected from age-related decline in heart function, and in many ways their hearts looked and performed like hearts from a young mouse.

=Dyck findings suggest that the protein responsible for transporting fat into the contractile cells of the heart may be a candidate for drug inhibition and that this drug could protect the heart from aging.

=He hopes it will lead to the development of medications that inhibit the uptake of fatty acids into the heart and prevent and/or reverse the effects of aging on the heart muscle.


..and this is another article

Are you a mice?

fighting aging disease by wasting E rather than dieting---works for mice

The researchers said, identifying a simple intervention affecting several age-related diseases is an attractive approach to decreasing the morbidity of growing old.

They suspected that treatments designed to alter the efficiency of mitochondrial respiration might be one way to accomplish this.

In a series of experiments, the research team bred large numbers of mice, fed them a normal chow diet and followed each mouse until its natural death. Half were genetically engineered to make more of a protein in their muscle tissue called uncoupling protein-1. Their littermates did not make excess uncoupling protein. In muscle tissue, uncoupling protein-1 converts the energy from food into heat and mimics the effects of exercise.

Uncoupling = generating inefficient metabolism



The LONGEST-LIVED animals in each group lived for 39 months and died within two weeks of one another.

What was different was the median lifespan for the mice.

Median survival in the uncoupled mice was 30 months, compared to 27 months for their wild-type littermates

the reasearchers were disappointed ---they had hoped uncoupling in muscle would slow aging, but maximum lifespan didn't increase.However, the odds of reaching that maximum lifespan did improve in the uncoupled mice."

results: Decreasing body fat and inflammation in the animals by accelerating muscle metabolism with uncoupling protein delayed death and diseases, including atherosclerosis, diabetes, hypertension and even cancer

they also found that female mice with the uncoupling protein mutation were less likely to develop a type of cancer called lymphoma.

No differences in lymphoma rates were found in male mice. Increased uncoupling protein-1 in muscle also reduced markers of chronic inflammation

In a second set of experiments, the researchers found that the uncoupled mice were less likely to have vascular disease.

That was the opposite of what Semenkovich and his colleagues previously had found in mice engineered to overproduce uncoupling protein-1 in the wall of the aorta, the body's primary artery.

Rather than being protected from damage, those mice were prone to develop high blood pressure and atherosclerosis.

Where the uncoupling occurs has a big impact.

If this principle someday becomes a therapy, it will be very important to target the proper tissues to produce the desired effects.

Uncoupling in muscle may be a substitute for exercise," researcher says.

If that's true in humans, and if uncoupling can be done safely, this could be an important therapy because it's sometimes very difficult to get people to exercise.

Wise words for today: EAT HEALTHY, LIVE HEALTHY!

G♡D blesS

- かわいい天使•ǺńĜëĽıŊə♥ -