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A new carmaker has a plan for cheap, environmentally friendly cars to be built all over the country

An air-powered car? It may be available sooner than you think at a price tag that will hardly be a budget buster. The vehicle may not run like a speed racer on back road highways, but developer Zero Pollution Motors is betting consumers will be

willing to fork over $20,000 for a vehicle that can motor around all day on nothing but air and a splash of salad oil, alcohol or possibly a pint of gasoline.

The expertise needed to build a compressed air car, or CAV, is not rocket science, either. Years-old, off-the-shelf technology uses compressed air to drive old-fashioned car engine pistons instead of combusting gas or diesel fuel to create a burst of air to do the same thing. Indian carmaker Tata has no qualms about the technology. It has already bought the rights to make the car for the huge Indian market.

The air car can tool along at a top speed of 35 mph for some 60 miles or so on a tank of compressed air, a sufficient distance for 80% of consumers to commute to work and back and complete daily chores.

On highways, the CAV can cruise at interstate speeds for nearly 800 miles with a small motor that compresses outside air to keep the tank filled. The motor isn't finicky about fuel. It will burn gasoline or diesel as well as biodiesel, ethanol or vegetable oil.

This car leaves the highest-mpg vehicles you can buy right now in the dust. Even if it used only regular gasoline, the air car would average 106 mpg, more than double today's fuel sipping champ, the Toyota Prius. The air tank also can be refilled when it's not in use by being plugged into a wall socket and recharged with electricity as the motor compresses air.

Automakers aren't quite ready yet to gear up huge assembly line operations churning out air cars or set up glitzy dealer showrooms where you can ooh and aah over the color or style. But the vehicles will be built in factories that will make up to 8,000 vehicles a year, likely starting in 2011, and be sold directly to consumers.

There will be plants in nearly every state, based on the number of drivers in the state. California will have as many as 17 air car manufacturing plants, and there'll be around 12 in Florida, eight in New York, four in Georgia, while two in Connecticut will serve that state and Rhode Island.

The technology goes back decades, but is coming together courtesy of two converging forces. First, new laws are likely to be enacted in a few years that will limit carbon dioxide emissions and force automakers to develop ultra-high mileage cars and those that emit minuscule amounts of or no gases linked with global warming. Plug-in electric hybrids will slash these emissions, but they'll be pricey at around $40,000 each and require some changes in infrastructure -- such as widespread recharge stations -- to be practical. Fuel cells that burn hydrogen to produce only water vapor still face daunting technical challenges.

Second, the relatively high cost of gas has expedited the air car's development. Yes, pump prices have plunged since July from record levels, but remain way higher than just a few years ago and continue to take a bite out of disposable income. Refiners will face carbon emission restraints, too, and steeply higher costs will be passed along at the pump.
Tata doesn't plan to produce the cars in the U.S. Instead, it plans to charge $15 million for the rights to the technology, a fully built turnkey auto assembly plant, tools, machinery, training and rights to use trademarks.

The CAV has a big hurdle: proving it can pass federal crash tests. Shiva Vencat, president and CEO of Zero Pollution Motors, says he's not worried. "The requirements can be modeled [on a computer] before anything is built and adjusted to ensure that the cars will pass" the crash tests. Vencat also is a vice president of MDI Inc., a French company that developed the air car.

The inventor of this technology is Mr. Guy Negre, who is the founder and CEO of MDI SA, a company headquartered in Luxembourg with its R and D in Nice, France. Copyrighted, Kiplinger Washington Editors, Inc.

Acids in ‘New Generation Candy’ can harm teeth

Lucette Moramarco
Staff Writer

Thursday, October 23rd, 2008.
Issue 43, Volume 12.

The candy most kids eat today is not the kind of candy their parents ate as kids. While kids today like to go trick-or-treating as much as their parents did, the effects of eating all that candy have grown worse.

Leaving aside the risks of obesity and diabetes, the more immediate health concern caused by eating candy is the amount of sour acid ingredients in many candies today.
In a recent press release, the California Dental Hygienists’ Association (CDHA), stated that “While this new generation of candy is highly popular, most of it contains acid levels so high that it approaches the ph level of battery acid,” in a statewide warning to parents about the dangers of sour candy. The popular sour candies combine sweet and sour ingredients that together can destroy the enamel on children’s as well as adults’ teeth.

Local dental hygienist Erika Feltham has been spreading the word about the irreversible damage being done by this acidic candy to her patients’ teeth for more than 10 years.
“Slowly but surely, recognition, concern and education is growing about the destructive effects from this ‘New Generation Candy,’” she said.

The kind of candy Feltham is referring to usually has a very sour acid coating around a pure sugar center. It comes in a variety of forms including hard and soft, gels, pastes and powders.

The high acid content of these candies can destroy the enamel of teeth, which are then directly exposed to the sugar. If someone then washes the candy down with sodas, sports drinks or energy/power drinks, that person’s teeth are getting hit with another blast of acid and sugar.
“I have noted a dramatic increase in the number of cavities and loss of luster [shine] of the teeth, erosion and tooth sensitivity for children and both young and mature adults who consume this ‘sour acid sugar candy’ regularly,” Feltham said. “It does not take a lot of this kind of candy to be potentially destructive.”

The amount of damage done to the teeth depends on the quantity and frequency of eating this candy as well as the ingredients of the candy consumed.

Adults are also being affected by the use of sour acid ingredients in not only candy but especially in popular breath mints. These sour acid mints also appear to be causing a remarkable increase in sensitivity and decay in her adult patients’ teeth and should be avoided, according to Feltham.

To reduce this destructive effect, Feltham recommends children, and adults, rinse out their mouths with water right after eating this candy. However, she recommends that parents carefully monitor the candy their children are consuming, especially around Halloween.

“It is my opinion and belief that this newer and more concentrated type of ‘sour acid sugar candy’ makes chocolate and other old-fashioned candy look ‘safe’ in comparison,” Feltham stated. “I warn my patients to carefully check candy labels for these types of acids. I have yet to find candy companies list on labels the pH level of their candies.”

Common names of various acids found in ‘sour acid sugar candy’ include: citric, malic, tartaric, fumaric, ascorbic, adipic and lactic acid. So, parents should check their children’s ‘trick or treat’ bags for this destructive candy and replace it with non-sour sugarless candy or gum.

Erika Feltham has been a dental hygienist in north San Diego County for more than 24 years.

How to avoid heart disease: brush your teeth, say scientists by Marlowe HoodWed Sep 10, 7:16 PM ET

Here's another reason to brush your teeth: poor dental hygiene boosts the risk of heart attacks and strokes, a pair of studies reported this week.

Heart disease is the number one killer worldwide, claiming upward of 17 million lives every year, according to the World Health Organization.

Smoking, obesity and high cholesterol are the most common culprits, but the new research shows that neglected gums can be added to the list.

"We now recognize that bacterial infections are an independent risk factor for heart diseases," said Howard Jenkins of the University of Bristol in Britain, at a meeting of the Society for General Microbiology in Dublin.
"In other words, it doesn't matter how fit, slim or healthy you are, you're adding to your chances of getting heart disease by having bad teeth," the professor said.

There are up to 700 different bacteria in the human mouth, and failing to scrub one's pearly whites helps those germs to flourish.
Most are benign, and some are essential to good health. But a few can trigger a biological cascade leading to diseases of the arteries linked to heart attacks and stroke, according to the new research.
"The mouth is probably the dirtiest place in the human body," Steve Kerrigan of the Royal College of Surgeons in Dublin said.
"If you have an open blood vessel from bleeding gums, bacteria will gain entry to your bloodstream."
Once inside the blood, certain bacteria stick onto cells called platelets, causing them to clot inside the vessel and thus decreasing blood flow to the heart.

"We mimicked the pressure inside the blood vessels and in the heart, and demonstrated that bacteria use different mechanisms to cause platelets to clump together, allowing them to completely encase the bacteria," he said..
This not only created conditions that can provoke heart attacks and strokes, it also shielded the bacteria from both, immune system cells and antibiotics.

"These findings suggest why antibiotics do not always work in the treatment of infectious heart disease," Jenkins said.
In separate research, a team led by Greg Seymour of the University of Otago Dunedin in New Zealand showed how other bacteria from the mouth can provoke atherosclerosis, a disease that causes hardening of the arteries.
All organisms -- including humans and bacteria -- produce "stress proteins," molecules produced by conditions such as inflammation, toxins, starvation, or oxygen deprivation.

One function of stress proteins is to guide other proteins across cell membranes.
But they can also can latch onto foreign objects, called antigens, and deliver then to immune cells, provoking an immune reactions in the body.

Normally, the body does not attack its own stress proteins.
But bacterial stress proteins -- which are similar -- do trigger a response, and once that has happened the immune system can no longer differentiate between the two, said Seymour.

"White blood cells can build up in the tissue of arteries, causing atherosclerosis," he explained in a phone interview.

Copyright © 2008 Agence France Presse. All rights reserved. The information contained in the AFP News report may not be published, broadcast, rewritten or redistributed without the prior written authority of Agence France Presse.

Lewis Smith, Environment Reporter

A giant goose-like bird that was the size of a light aircraft and had a beak like a crocodile’s jaws has been found to have soared above Britain 50 million years ago.

A fossil skull preserved in London clay has been identified as belonging to a relative of modern ducks and geese with a wingspan of 5m (16ft) and armed with a beakful of teeth. The ancient creature has been nicknamed Mother Goose by Gerald Meyr, the palaeontologist who identified it, because of the bird’s extraordinary size.

It is thought to have had a similar lifestyle to the albatross of today, which spends most of its life at sea and is a master at using thermals and air currents to remain airborne with minimum effort.

The ancient goose, one of the biggest species of bird to take to the skies, was even bigger than the wandering albatross, which, at up to 3.7m wing tip to wing tip, has the biggest wingspan of all living birds. Mother Goose, more properly named Dasornis emuinus, is thought to have had a wingspan almost 50 per cent bigger than the wandering albatross.

“Imagine a bird like an ocean-going goose, almost the size of a small plane,” said Dr Meyr, of the Senckenberg Research Institute and Natural History Museum in Frankfurt. “They had lightweight bones so despite their great size they weren’t very heavy. I think they were capable of soaring and gliding – though they would probably have needed strong winds to take off.

“By today’s standards these were pretty bizarre animals, but perhaps the strangest thing about them is that they had sharp, tooth-like projections along the cutting edges of the beak.

“The beak was so covered in bony teeth that it looked like a crocodile.”
Some early birds had enamel teeth but these were lost about 100 million years ago, yet Mother Goose reevolved them, this time made from bone and possibly covered with a layer of keratin, the biological material used for the beak. Dr Meyr believes that the 60 to 80 teeth in the beak, estimated at 20-25cm long, were developed to help the prehistoric bird keep a grip of the fish and squid it would have snatched from the sea.

“No living birds have true teeth – which are made of enamel and dentine – because their distant ancestors did away with them more than 100 million years ago, probably to save weight and make flying easier,” he said.
“But the bony-toothed birds, like Dasornis, are unique among birds in that they reinvented tooth-like structures by evolving these bony spikes.

“It’s linked to diet. These birds probably skimmed across the surface of the sea, snapping up fish and squid on the wing. With only an ordinary beak these would have been difficult to keep hold of, and the pseudo-teeth evolved to prevent meals slipping away.”
The fossil skull was found in clay on the Isle of Sheppey and in its day the bird would have cruised above the waters covering what is now Essex, Kent and London.

When the bird died it sank to the bottom of the sea, where it was preserved after becoming covered in sediment. It was discovered about five years ago by a private collector but has only now been fully analysed, and the findings reported in the journal Palaeontology. Although the bird had a similar lifestyle to the albatross, analysis of its remains has shown that its closest relatives, living or extinct, are ducks and geese.

Oral cancer: a personal journey
September 11, 2008
by Barbara Boland

Do you know that ...
... one American dies every hour of every day from oral cancer?
... and that 25 percent of all oral cancer patients have none of the traditional risk factors we were all taught about in school?
... and that the fastest growing group of oral cancer patients is nonsmokers, under the age of 40, with females outnumbering males?
... and that there is a proven link between oral cancer and human papilloma virus (HPV)?

I didn't know any of these facts either. Oral cancer was not on my radar screen at all until, on May 23, 2003, at the age of 41, I was diagnosed with stage I, poorly differentiated, squamous cell carcinoma of the tongue. This was never a subject I thought I would develop an expertise in, but my journey through diagnosis and treatment convinced me to use my experience as an oral cancer survivor to raise awareness. There is an absolute necessity for the profession of dentistry to embrace the concept of early detection of oral cancer.

Diagnosis
My story began in December of 2002 when, while flossing, I noticed a very small, maybe 2 mm by 2 mm, round, soft, white lesion on the posterior ventral surface of my tongue. I kept my eye on it for about three weeks, and when it didn't go away, I showed my tongue to a head and neck surgeon who told me it was "nothing." When it didn't go away by April 2003, and the area of leukoplakia had actually gotten larger, the head and neck surgeon took another look and again declared it "nothing." He said there was no way I could have cancer because I had never smoked, was a social drinker, and it was soft and round — something cancer never is.

I am a licensed dental hygienist and, at the time, I was working as a practice-management consultant. In May, when I arrived at the office of clients Dr. Patrice Ohman and Dr. Hank Wright, I noticed an atlas of oral lesions from CDx Labs, the distributor of brush biopsy kits. I pointed to a picture and told them I had something that looked just like that on my tongue. A brush biopsy was performed that day and about four days later, Dr. Ohman called to tell me that the results had come back as "atypical." The report contained a description of the atypia, including increased nuclear to cytoplasmic ratio, loss of polarity, and increased nuclear staining.

The next step was a scalpel biopsy, which was scheduled in the office of an oral surgeon. I was nervous and I made sure he knew I was a hygienist, thinking it might help with the communication. After I corrected him and explained that I was not, in fact, there to have a tooth extracted, but rather to have a biopsy, he examined my tongue. He was unimpressed with what he saw until I pointed out to him a second lesion that had cropped up over the previous couple of weeks. I had noticed a small erythroplakia that would come and go. Some days I could see it, some days I couldn't.

Occasionally I would get a shooting pain from that area of my tongue all the way back into my ear. He performed an excisional biopsy of the erythroplakia and an incisional biopsy of the leukoplakia. I left the office with six sutures in my tongue and a promise from the surgeon that he would call with the results early the next week.

The following week, I went back on the road to see my clients, and all of my dentist clients reassured me that I couldn't have cancer ? after all, I didn't smoke or drink much and I was too young. The week passed and I did not hear from the oral surgeon, so I called his office on Friday morning.. I explained to the staff member who answered the phone who I was and that I was waiting for biopsy results. She put me on hold and after several minutes the doctor got on the phone and said, "Yeah, the biopsy came back as cancer. You still have the tumor on your tongue so I want to treat that with the laser. You will have to come to this office because that is the only place I have the laser. Oh, wait. You are only 41? You don't smoke? You should be treated medically."

Before delivering the news, he never asked if I was alone. He never suggested that I come in to speak with him. He never even followed up with me.. As far as this oral surgeon knows, I may never have had treatment and I could be dead.

Treatment
I saw four head and neck surgeons for consultations before deciding to be treated at the Hospital of the University of Pennsylvania. I did research and decided that I wanted to have my lymph nodes removed because this is the major way oral cancer spreads to other parts of the body, most commonly the lungs. Even with negative CAT scans and MRIs, there is still a 20 percent chance that there is metastasis to the lymph nodes. The only way to know for sure that the lymph nodes are clear is to remove them and look at them under the microscope. On July 1, 2003, I had a partial glossectomy during which 25 percent of my tongue was removed, and a modified neck dissection during which the first four levels of lymph nodes and my submandibular gland were removed. Thankfully, my lymph nodes and salivary gland were cancer free, so I did not need radiation or chemotherapy.

It took about six weeks for me to be able to eat solid food and about eight months for my speech to be completely normal. Immediately after surgery, the right side of my lower lip was paralyzed and remained that way for about five months. My lip did ultimately come back to life just as my surgeon was ready to declare the paralysis permanent.
After what I had seen in the head and neck tumor clinic at Temple University Hospital while I was a dental hygiene student, and at Thomas Jefferson University Hospital where I worked as a dental hygienist and helped treat oral cancer patients, I would have been thrilled to come out of this with just a paralyzed lip. Thankfully, my smile is normal again. My permanent side effects are that I don't have taste or sensation on the right side of my tongue and much of the right side of my face and neck are numb. All of that is easy to live with, especially when you consider the alternatives.

Life after oral cancer
So what did I learn from my experience? The first thing I learned is that if I had not been a dental hygienist, I would never have been diagnosed with a stage I cancer. Thankfully, I knew enough not to take the doctor's word for it when he looked at my tongue with his naked eye and said, "It's nothing." I also learned a sobering fact. The mortality rate for oral cancer is 50 percent, and it has not changed in well over 30 years. I realized that, unfortunately, I was not the only dental professional who was out of touch with the realities of this horrible disease and that, at least partly due to our profession's lack of awareness, 75 percent of oral cancer cases are diagnosed at stage III or stage IV, when the five-year survival rate is less than 20 percent.

It is up to us, the dental profession, to make a difference in the five-year survival rate. Every time you examine a patient, you have the chance to save a life if you remember that you are looking for early oral cancer, subtle tissue changes, and not big tumors. There are new technologies available to help make early detection more likely: specifically chemiluminescence, tissue autofluorescence, and brush biopsies. In my opinion, you are obligated to incorporate these technologies into your practice and to never look at something in a patient's mouth with your naked eye and say, "It's nothing." If that is your approach, you will be wrong about leukoplakias about 25 percent of the time and about erythroplakias 90 percent of the time. Most oral cancer patients do not have the great outcome that I had. It simply is not worth taking the risk of being wrong about an innocent-looking lesion. The worst thing that happens is that you find out something you suspected was nothing, really is nothing. The best thing that happens is that a lesion is removed when it is dysplastic or stage I. The only way to improve survival rates and to have patients avoid debilitating and disfiguring treatment is to increase the rate of early detection. I am committed to doing everything I can to make that happen. Please join me in my fight. Barbara Boland, RDH, MBA, founder of Boland Consulting, LLC, works with dental practices to help them formulate and implement early oral cancer detection programs utilizing the latest early detection technologies, as well as lectures to groups of dental professionals on early detection. She can be reached at bolconsulting@aol.com. The above article originally appeared in February 2008 Dental Economics.