ADVERTISEMENT 2
ADVERTISEMENT 3
Error: No articles to display
ADVERTISEMENT 1
ADVERTISEMENT 4
Children categories
BOISE, Idaho (AP) —
A hunter asleep in the remote Idaho wilderness woke up when he felt something tugging on his hair. Then he heard the black bear breathing.
Stephen Vouch, 29, reached behind his head and felt it was wet. He yelled when he realized a bear was biting at his head.
"He got a hold of my head, and that's what woke me up," the Boise resident said Wednesday, who was in the rugged area hunting bighorn sheep with friends. "That's when I kind of freaked out. That's when I could hear the bear breathing on me."
His scream startled the bear, which jumped and hit the tarp above where they were sleeping. The tarp tumbled, entangling the animal and the hunters around 2 a.m. Friday.
"That's when my buddy's gun went off," Vouch said.
The bear, wounded by a shot from the .45-caliber handgun, scrambled into a nearby tree. Vouch, cut but not seriously injured, shot and killed it.
Vouch said he and his friends were prepared with medical supplies for emergencies but didn't have a satellite phone, so he didn't receive medical care for three days.
The hunting group patched him up, then rafted downstream before flying out of the remote Frank Church River of No Return Wilderness on Sunday. Vouch was treated Monday at a hospital for cuts to his head and released.
Idaho Fish and Game officials estimate that the male bear was about 3 to 7 years old and weighed 200 to 275 pounds. Jon Rachael, state wildlife manager with the department, said it's not clear why the bear entered the camp because the hunters had stored their food properly.
One possibility is the bear may have become accustomed to finding food from the many rafters that float the Middle Fork of the Salmon River each summer, he said.
Or the bear may have never encountered people, and out of curiosity, chomped on what may have appeared to be fur, Rachael said. If the bear intended to kill, the attack would have been much more violent, he said.
It's the second time this year that someone sleeping outdoors in Idaho has been attacked by a black bear. In early September, state officials trapped and killed a black bear near McCall in west-central Idaho that bit a sleeping firefighter who had been battling blazes in the region.
Rachael said it's been a tough year for bears because destructive wildfires and drought have made for an exceptionally bad berry season, a key food source.
In bear country, Rachael recommends bear spray rather than guns because of the danger of accidentally shooting fellow campers while trying to fend off a bear.
Vouch said he plans to return to the area within the next several weeks to continue hunting for bighorn sheep. In Idaho, the opportunity to hunt Rocky Mountain bighorn sheep is rare — hunters are allowed to harvest only one in a lifetime.
ORLANDO, Fla. (AP) —
Elvis is back in the building.
Elvis, the missing king cobra snake, was returned to its owner's home near Orlando after being on the loose for more than a month.
A woman who lives about a half-mile from owner Mike Kennedy called Orange County's animal services Wednesday night after hearing hissing sounds coming from under a clothes dryer in her garage.
Three animal services officers captured the 10-foot snake using special tongs. The snake was too large for a traditional snake box so the animal services officers placed Elvis in a cat cage and put it in a soft carrier for extra security.
Students at a nearby elementary school weren't allowed outside for recess during the early days of the search for Elvis.
And a witty Twitter user even created an account for the missing snake with the tagline, "I'm on the loose in Orlando. Keep Away!"
By late Wednesday, the latest post on the Orlando King Cobra account said, "Singing the Folsom Prison Blues tonight. Oh well at least I get three squares a day now."
The owner's wife, Valerie Kennedy, positively identified Elvis and state wildlife officials scanned Elvis for microchip-identification before returning to its owners.
Mike Kennedy pleaded not guilty this week to a misdemeanor charge for failing to immediately report the snake missing.
CHICAGO (AP) —
Cancer is much less common in elephants than in humans, even though the big beasts' bodies have many more cells. That's a paradox known among scientists, and now researchers think they may have an explanation — one they say might someday lead to new ways to protect people from cancer.
Compared with just one copy in humans, elephants' cells contain 20 copies of a major cancer-suppressing gene, two teams of scientists report. The gene helps damaged cells repair themselves or self-destruct when exposed to cancer-causing substances.
The findings aren't proof that those extra p53 genes make elephants cancer-resistant, but if future research confirms it, scientists could try to develop drugs for humans that would mimic the effect.
Dr. Joshua Schiffman, a pediatric cancer specialist at the University of Utah who led one of the teams, began his research after hearing a lecture a few years ago about Peto's paradox. That refers to the fact that large animals including elephants and whales, have comparatively low cancer rates even though they have many more cells than smaller species. Cancer involves uncontrolled cell growth.
The lecture speaker mentioned that elephants seemed to have extra copies of the p53 gene. Schiffman's patients include children with incomplete p53 genes because of a condition called Li-Fraumeni syndrome, which greatly increases their chances of developing cancer. So Schiffman sought to find clues from the blood of eight elephants, Ringling Bros. circus animals and local zoo animals.
His team — as well as a second group of scientists — pinned down the size of the elephants' surplus — 20 copies. The second team found many other species have only one copy, just like humans.
Schiffman and his colleagues compared how elephant cells reacted to radiation, compared with cells from 10 healthy humans and 10 patients with Li-Fraumeni syndrome.
The elephant cells self-destructed at twice the rate of healthy human cells and more than five times the rate of cells from patients with the syndrome. Cells that don't self-repair or self-destruct when exposed to carcinogens become prone to developing cancer.
The work was published Thursday in the Journal of the American Medical Association.
Dr. Judy Garber, director of cancer genetics and prevention at Dana-Farmer Cancer Institute in Boston, said the research is intriguing but preliminary
While the research won't lead to any immediate treatment for humans, progress against cancer can come "from unexpected directions," said Dr. Ted Gansler of the American Cancer Society. He noted that studies of eyelid and tooth development in mice led to drugs used for colon cancer, throat cancer, and several other cancers.
Schiffman's team also analyzed necropsy data and found that elephants sometimes live as long as humans, yet only about 1 in 20 die of cancer, versus about 1 in 4 humans.
The second group of researchers, working with frozen zoo specimens, looked at more than 60 other species and found only elephants and wooly mammoths, their extinct relatives, had extra copies of the cancer-suppressing gene.
This team inserted elephants' p53 genes into mouse cells and found that those cells behaved just like elephants and self-destructed when exposed to DNA-damaging drugs, said co-author Vincent Lynch, an evolutionary biologist at the University of Chicago. His study is under review for publication and was released online this week.
Schiffman's team is seeking funding for research into possible treatments based on the elephant research. While studies in humans are at least several years away, "we certainly think we've found something very intriguing," Schiffman said.