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Gina Miller (
Sat, 3 Jul 1999 00:09:48 -0700

Nanogirl news~

Scientists simulate quantum computer
Researchers use nuclear magnetic resonance in experiment MSNBC Staff and Wire Reports

TOKYO, June 21 Japanese electronics companies have developed a micro-machine the size of an ant that can crawl around thin pipes, inspect and even fix problems at power plants.

U.S. Coalition Opposes Stem Cell Research _cells_4.html

New components of machinery that carries genetic information from nucleus

With their discovery of a curious brain protein, a team of HHMI investigators have provided a new understanding of just how exquisitely nerve cells control the electrical impulses they use to communicate with one another.

Think again - if you thought one side of your brain was analytical while the other was creative.

TOKYO (July 2, 1999 8:40 p.m. EDT A group of Japanese scientists say they have discovered 24 black holes at the center of the galaxy, contrary to the widely accepted theory that there is only one, reports said Saturday.,1080,66762-105651-749816-0,0 0.html

>From China Daily
Cellular research offers new clues about ageing

AS the new century dawns, people marvel at the striking progress that mankind has made in the past 100 years. In 1900, the Chinese life expectancy was below 35 years. Now it is over 70.
The improvement of medical level and living conditions is behind such progress. But as the population growth rate drops, the country is now beginning to face a new problem that has already bewildered the West _ the ageing of its population.
A team of Chinese biologists is studying the mechanism of ageing at our most fundamental level _ cells _ and their findings may provide clues for the cure and prevention of ageing-related diseases. The team, led by a couple, Tong Tanjun and Zhang Zongyu, professors at Beijing Medical University, keeps a close eye on the latest international developments in the fields of molecular biology and cell biology and has also produced many of its own significant findings. Why do we age? Biologists say we become old and develop diseases because the cells inside our bodies also grow old and gradually lose their ability to function.
Looking into the busy and mysterious world of cells, they have found many elements that measure _ or even determine _ the rate of ageing. One important element found by Western biologists is called telomeres, special strings at the ends of chromosomes that prevent them from being degraded and fused with other chromosomes. Whenever a cell divides, it loses some telomere segments. The length of the telomeres can tell how often a cell can divide and predict its death.
Experiments by the Chinese team support this finding and have made other discoveries. The team examined blood cells of 180 unrelated Chinese donors, aged from 25 to 65, and found a significant correlation between age and telomere length.
The average telomere length of the young group (25 years old) was 8750 bp (base pairs), 18 per cent longer than the old group (65 years old). On the average, a donor loses about 35 bp of telomere length each year. However, the loss rate of telomere segments is different among the donors, varying from 57 to 9 bp each year. "This explains why some people look older or younger than their actual age," said 64-year-old Professor Zhang.
"Telomeres can be regarded as a human 'biomarker.' They can tell the rate of
ageing in our bodies more accurately than chronological age." The experiment has also found clear differences between men and women donors. It found the telomere length of men is longer than that of women of the same age. But they also found that men lose 3 bp more telomeres each year than women.
"People often wonder why women tend to live longer than men. From the
experiment results, we know the answer on the molecular level. Men age more quickly than women," Zhang said.
As people grow older, body cells divide and continuously lose their telomere segments, she said. When the telomere length is shortened to a certain degree, cells can no longer divide and die. However, there are special kinds of cells that are virtually immortal. Cancer cells can divide an infinite number of times. Scientists found that cancer cells also lose their telomere segments when they divide. However, the cells have an enzyme called telomerase that synthesizes telomeres to restore the lost parts. Thus their telomere length never shortens, which explains why cancer spreads.
"Telomerase is the element which keeps cancer cells immortal. By blocking
the enzyme, we may find a way to check the growth of cancer cells. The results of our animal experiments have proved this possibility," said the 64-year-old Professor Tong.
The team injected human breast cancer cells into experimental mice and the mice developed tumours. By blocking telomerase, it found that the growth rate of the cancer cells was decelerated and the tumours became smaller.
"The experiment result is really exciting," said Tong. "Although we haven't
done tests in humans, there is a great possibility that we can develop a drug that suppresses cancer telomerase and stop tumours from growing. It could be a breakthrough, as we could get a new weapon to fight this deadly disease."
Studying the function of telomerase, biologists have another hypothesis. If it were added to living human cells, would the cells grow forever without stopping, just as cancer cells? If this were so, humans would be able to live as long as they like.
"Yes, theoretically," Professor Tong said, adding that some Western
biologists have successfully cloned telomerase DNA, transferred it into living cells in cultivation and increased the lifespan of a cell by many generations.
However, Tong said, although telomerase activity can prolong a cell's life, it cannot make it immortal. There is more than one element that determines ageing.
Tong said another element affecting the ageing of cells is their ability to repair damaged DNA.
He said DNA, which contains the genetic code and transmits the heredity pattern, would be injured when attacked by pollutants within the body or externally by ultraviolet radiation or chemicals. One of its two strands could break and prevent the DNA from transmitting the heredity message normally.
Living cells have the ability to repair the damage and the heredity message can be transmitted from one generation to the next. But, as living things grow older, their ability to repair damaged DNA gradually declines. The research team discovered that, when attacked by chemicals from outside, the DNA of both young and old experimental mice was damaged. After a period of time, however, the young mice had their broken DNA strands reconnected while the old ones had difficulty in repairing them. Human cells also displayed different abilities to repair DNA damage between the young and the old.
The team used human diploid fibroblasts (2BS), a special kind of cell biologists like to use because they last longer than ordinary cells and are suitable for observation.
The experiment found that, when treated with the same dose of chemicals, both young and senescent 2BS cells were damaged and looked like comets. After 12 hours, the "tails" of young cells disappeared, but it seemed that the old could hardly recover. (See photo below) DNA damage often results in many kinds of senescence-related diseases, said Professor Zhang, adding that the team has done research on a specific kind of DNA whose deletions are associated with diabetes, Alzheimer's disease, Parkinson's disease and cerebrovascular diseases. Mitochondrial DNA (mtDNA) plays an important role in the metabolism of cells. It is like a generator that helps turn the food we eat into energy. But the process also produces a waste, oxygen free radicals or oxidants, which damage DNA and cause fragment deletions. MtDNA is very vulnerable to oxidants and it has no ability to repair the damage once attacked. The team's experiment has found, using healthy mice, no mice in the young group have mtDNA deletions while in the old group, 50 per cent do. When suffering from cerebral ischemia, a shortage of blood supply to the brain, every single old mice suffered mtDNA deletions, 30 per cent more than in the young group.
The experiment result, published in the New York-based Journal of Cellular Biochemistry (1999, Vol 73), indicates that mtDNA deletions are associated with ageing. Professor Zhang said this finding provides a clue for the cure and prevention of ageing-related diseases, such as cerebrovascular diseases, one of the three top causes of death among the elderly in China. Since mtDNA deletions are caused by oxidants, would we live longer and healthier by reducing them?
"Yes," Professor Zhang said. "One of the solutions is to appropriately
restrict the amount of food we eat. Experiments on rodents and primates have found that they age slower if their diets are restricted." One of the other reasons that proper diet can keep people fit is that excessive food intake will increase the level of glucose in blood. When our blood glucose is at a high level, a process called non-enzymatic glycation takes place and produces waste. The waste gradually sticks to DNA and proteins and impedes their ability to function normally. The team's experiment with two groups of young and old people discovered that the old had more glycation waste in their bodies. This means that the old are more vulnerable to experiencing a glycation reaction when having a high level of blood glucose.
Professor Zhang said the glycation waste, which causes age spots on the skin of old people, may correlate with the decline of heart, kidney and immune functions among old people and diabetes patients. Proper diets will keep the blood glucose of the elderly at a normal level, which reduces glycation reaction and produces less waste, she suggested. Declining to comment on the self-claimed health-enhancing medicinal products in the Chinese market, she said people can turn to natural food to clear oxidants and glycation waste, such as carrots, chives, eggplant and other kinds of food that have an abundance of Vitamin E, A and C. Restricting diets may prolong our lives for several years. According to pioneer biologists in the West, people may be able to live decades or even centuries beyond the generally accepted maximum life span of 120 years. The trick is to manipulate the genes which determine ageing.
"There are 'longevity genes' and 'ageing genes' inside a human body. They
are like many 'lights.' They take turns turning on and off. Altogether they determine the ageing of a human body. What a biologist can do is to observe the mechanism of these lights, find their rules and finally turn them on and off to meet the needs of humans," Professor Tong said.
"Biology has come to an era of genes. By manipulating genes, humans will see
dramatic changes to their life and many of our dreams may come true, much sooner than we expect," he said.
He said Western biologists have been doing research on gene manipulation and have succeeded in prolonging animals' lives by transferring "longevity genes" into fertilized eggs before the birth.
"We cannot say that our research is pioneering the world, although we lead
the domestic study in this field," Tong said. "Our work is greatly hindered by funding shortages, a brain drain and language barriers." The team's achievements on the mechanism of ageing and biomarkers have resulted in a Scientific Progress Grant from the National Science Foundation. The foundation provided 580,000 yuan (US$70,000) for the team's research from 1993-97.
"We have 11 funds altogether helping us, but they are still far from enough.
Experiments are always time-consuming and cost a lot. And we are losing our talent every year."
They are now tutoring eight students who are pursuing MD's. Many of their students and research fellows have gone abroad in search of better labs. "We are like grandparents tutoring grandchildren," Professor Zhang said.
"One must have an interest in this field in order to withstand the
hardships," Professor Tong said, smiling. "But nothing can replace the exhilaration that a new finding brings."

Gina "Nanogirl" Miller
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