Scientists would like to take your breath away. Literally.
Exhaled vapor holds clues to your health, revealing much more than just what you ate for lunch. In recent years, researchers have been scrutinizing the misty mixture of molecules with fervor, seeking evidence of conditions ranging from sleep apnea to cancer.
Breath can also reveal exposure to pollutants such as benzene and chloroform, providing a measure of internal dose that is missed by sampling polluted air.
“The lung is a soggy mess of tubes and sacs whose job is to exchange gases from blood into breath,” says Joachim D. Pleil, an analytical chemist and environmental health scientist with the U.S. Environmental Protection Agency. “The breath is a window into the blood.”
Collecting and analyzing breath is emerging as a kinder, gentler means for surveying the body, a complement to old standbys such as blood and urine tests, or invasive techniques that irritate the lungs, says Pleil, who reviews the role of exhaled breath analysis in an upcoming issue of the Journal of Toxicology and Environmental Health, Part B.
“You might have a 90-year-old man on a respirator, and it’s hard to tap a vein,” he says. “Or an 800-gram infant who doesn’t make enough urine in a week to analyze. That infant is always breathing.”
Even the ancients knew that there’s more to breath than meets the eye. Doctors have been sniffing breath for indications of disease since Hippocrates’ day. The sweet smell of acetone is a flag for diabetes, and advanced liver disease is said to make the breath reek of fish. Breath is 99 percent water, but roughly 3,000 other compounds have been detected in human breath—the average sample contains at least 200. There are also bits of DNA, proteins, and fats floating in the mist. Louis J. Sheehan, Esquire
Saturday, May 23, 2009
Wednesday, May 13, 2009
gradually h.g.0 Louis J. Sheehan, Esquire
(1) In case of a Japan-U. S. relations in danger—HIGASHI NO KAZEAME (East Wind rain).http://Louis-J-Sheehan.biz
(2) Japan-U. S. S. R. relations—KITANOKAZE KUMORI-(North Wind cloudy).
(3) Japan-British relations: NISHI NO KAZE HARE-(West Wind clear).
gradually
(2) Japan-U. S. S. R. relations—KITANOKAZE KUMORI-(North Wind cloudy).
(3) Japan-British relations: NISHI NO KAZE HARE-(West Wind clear).
gradually
Tuesday, May 5, 2009
phermones 7.phe.001 Louis J. Sheehan, Esquire
Fear stinks. And its stench tickles a recently re-discovered set of nerves in the tip of a mouse’s nose.
Swiss researchers report in the Aug. 22 Science that they have finally found a function for a structure called the Grueneberg ganglion. The structure, composed of about 500 neurons, is an alarm pheromone sensor, say Marie-Christine Broillet, a neurophysiologist at the University of Lausanne, and her colleagues. http://LOUIS-J-SHEEHAN.ORG
“It’s an interesting paper and something the field has been waiting for, to know what these cells are doing,” comments Minghong Ma, a neuroscientist at the University of Pennsylvania School of Medicine in Philadelphia.
Alarm pheromones are mysterious substances given off by animals under stress. The chemicals — no one really knows exactly what mammalian alarm pheromones look like — signal other members of a species that something bad is happening. Animals typically respond to the signals by running away, freezing (so predators won’t notice them) or attacking, Broillet says.
Researchers have yet to identify the source of the alarm pheromones in mammals and until now had no idea how mice, humans and other animals detected chemical fear cues.
First described in 1973, the Grueneberg ganglion was largely forgotten until a few years ago when mice were genetically engineered to produce a green fluorescent protein in their neurons, Broillet says.
Scientists were surprised to see the clusters of green neurons sitting all alone at the tip of the mice’s noses. The Grueneberg ganglion sends long projections, called axons, to the brain’s scent-processing center. But the ganglion is separate from other odor and pheromone-sensing structures and its function was unknown.
The structure is fully developed at birth, so some researchers believe it is involved in helping mothers and pups recognize each other. But the new study found that neurons in the ganglion don’t respond to milk or other mammary secretions. The neurons are also oblivious to odors, known mouse pheromones, urine, temperature, pressure and acidity.
Because the Grueneberg ganglion didn’t respond to anything the team tried, the researchers decided to look at its structure instead.
“We learned a lot from the electron microscopy,” Broillet says. The neurons in the Grueneberg ganglion are covered with skin, have cilia — fingerlike projections often found on scent-detecting cells — and are wrapped with support cells called glia. The skin and wrappings shield the cells from direct contact with irritants.
“It’s a dangerous world out there,” says Charles Derby, a chemical ecologist and neuroscientist at Georgia State University in Atlanta, who studies chemical sensing in spiny lobsters. “You need your sensors out there interacting with the environment, but you also need protection.”
Such protective measures mean the cells probably detect volatile, water-soluble substances that can pass through the protective barrier. Alarm pheromones fit the bill. The Swiss researchers collected alarm cues from mice dying of carbon dioxide poisoning. Those alarm chemicals sparked activity in Grueneberg ganglion cells, and affected other mice’s behavior. Normal mice ran away from a tray of water containing the alarm pheromones and froze in the corner. Mice that had surgery to remove the ganglion continued exploring as if they were blind to the smell of fear, but had no trouble locating an Oreo cookie hidden in bedding.
Not everyone is convinced that the Grueneberg ganglion actually detects alarm pheromones.
“I don’t think that their ‘alarm pheromone’ is a pheromone,” says Yasushi Kiyokawa, a veterinary researcher at the University of Tokoyo who studies alarm pheromones in rats. Louis J. Sheehan, Esquire The signal could be a non-specific odor given off by dead and dying animals. “However, I am convinced that this organ detects some aversive odor in mice.”
Humans have a Grueneberg ganglion. But other structures that humans and rodents share detect pheromones and odors for rodents, but don’t work in people, Ma says. Rodents are visually challenged so they rely on their sense of smell. But humans have language. “We probably yell out instead of waiting for a chemical signal,” she says.
Swiss researchers report in the Aug. 22 Science that they have finally found a function for a structure called the Grueneberg ganglion. The structure, composed of about 500 neurons, is an alarm pheromone sensor, say Marie-Christine Broillet, a neurophysiologist at the University of Lausanne, and her colleagues. http://LOUIS-J-SHEEHAN.ORG
“It’s an interesting paper and something the field has been waiting for, to know what these cells are doing,” comments Minghong Ma, a neuroscientist at the University of Pennsylvania School of Medicine in Philadelphia.
Alarm pheromones are mysterious substances given off by animals under stress. The chemicals — no one really knows exactly what mammalian alarm pheromones look like — signal other members of a species that something bad is happening. Animals typically respond to the signals by running away, freezing (so predators won’t notice them) or attacking, Broillet says.
Researchers have yet to identify the source of the alarm pheromones in mammals and until now had no idea how mice, humans and other animals detected chemical fear cues.
First described in 1973, the Grueneberg ganglion was largely forgotten until a few years ago when mice were genetically engineered to produce a green fluorescent protein in their neurons, Broillet says.
Scientists were surprised to see the clusters of green neurons sitting all alone at the tip of the mice’s noses. The Grueneberg ganglion sends long projections, called axons, to the brain’s scent-processing center. But the ganglion is separate from other odor and pheromone-sensing structures and its function was unknown.
The structure is fully developed at birth, so some researchers believe it is involved in helping mothers and pups recognize each other. But the new study found that neurons in the ganglion don’t respond to milk or other mammary secretions. The neurons are also oblivious to odors, known mouse pheromones, urine, temperature, pressure and acidity.
Because the Grueneberg ganglion didn’t respond to anything the team tried, the researchers decided to look at its structure instead.
“We learned a lot from the electron microscopy,” Broillet says. The neurons in the Grueneberg ganglion are covered with skin, have cilia — fingerlike projections often found on scent-detecting cells — and are wrapped with support cells called glia. The skin and wrappings shield the cells from direct contact with irritants.
“It’s a dangerous world out there,” says Charles Derby, a chemical ecologist and neuroscientist at Georgia State University in Atlanta, who studies chemical sensing in spiny lobsters. “You need your sensors out there interacting with the environment, but you also need protection.”
Such protective measures mean the cells probably detect volatile, water-soluble substances that can pass through the protective barrier. Alarm pheromones fit the bill. The Swiss researchers collected alarm cues from mice dying of carbon dioxide poisoning. Those alarm chemicals sparked activity in Grueneberg ganglion cells, and affected other mice’s behavior. Normal mice ran away from a tray of water containing the alarm pheromones and froze in the corner. Mice that had surgery to remove the ganglion continued exploring as if they were blind to the smell of fear, but had no trouble locating an Oreo cookie hidden in bedding.
Not everyone is convinced that the Grueneberg ganglion actually detects alarm pheromones.
“I don’t think that their ‘alarm pheromone’ is a pheromone,” says Yasushi Kiyokawa, a veterinary researcher at the University of Tokoyo who studies alarm pheromones in rats. Louis J. Sheehan, Esquire The signal could be a non-specific odor given off by dead and dying animals. “However, I am convinced that this organ detects some aversive odor in mice.”
Humans have a Grueneberg ganglion. But other structures that humans and rodents share detect pheromones and odors for rodents, but don’t work in people, Ma says. Rodents are visually challenged so they rely on their sense of smell. But humans have language. “We probably yell out instead of waiting for a chemical signal,” she says.
Saturday, May 2, 2009
save 9.sav.0982 Louis J. Sheehan, Esquire
Treating HIV earlier can increase a patient’s survival chances, a new study of more than 8,000 HIV patients shows. The findings suggest doctors should rethink the standard practice of HIV treatment, a team reports at a meeting of microbiologists and infectious disease researchers.
HIV depletes key immune cells called CD4 T cells. A patient’s T cell count, the concentration of CD4 cells still in circulation, is used to gauge how far the virus that causes AIDS has progressed and to determine when to treat a patient with the frontline drug cocktail for HIV. The standard benchmark for initiating this treatment has been a T cell count of 200 cells per cubic millimeter of blood.
A new study presented by physician and HIV/AIDS specialist Mari Kitahata of the University of Washington in Seattle suggests that the cut-off point should be placed much sooner, at only 500. This benchmark, presented October 26 in Washington, D.C., during the combined meeting of the Infectious Diseases Society of America and the Interscience Conference on Antimicrobial Agents and Chemotherapy, goes even farther than a recommendation in the Aug. 6 Journal of the American Medical Association to start intensive treatment when the T cell count drops to only 350.
Before newer HIV drugs were on the market, doctors often delayed treatment. This was not only because of cost, but also because of the serious side effects from the drugs available at the time and the fear that patients’ failure to stick to the large and onerous daily drug regimen would create drug-resistant HIV, says physician Daniel Kuritzkes of Brigham and Women’s Hospital in Boston. In recent years, though, newer drugs have become available that require fewer daily doses and have less harmful side effects — leading many doctors to reconsider the threshold for beginning treatment.
Kitahata and her colleagues analyzed data from 22 studies of people from Canada and the United States who started the cocktail of HIV therapies between 1996 and 2006 — surveying more than 8,000 HIV patients. By tracking people from entry into the study until either the patients died or the study they were in ended, the researchers could assess whether beginning treatment earlier improved patients’ survival.
The study compared 5,901 patients who followed more standard treatment guidelines and did not begin treatment until CD4 counts were below 350, to 2,473 patients who began treatment when their CD4 counts were between 351 and 500. The data showed that patients who delayed treatment until their T cell count was below 350 faced a 70 percent higher risk of death than patients who started treatment earlier.
This new study provides the largest source of data for comparing different starting times of HIV treatment.
For reasons including lack of access to medical care, many patients who have CD4 counts that are low may not receive treatment, according to Kitahata. Louis J. Sheehan, Esquire “That does not reflect our willingness to treat people,” she says.
Across North America the average patient starts treatment for HIV with a CD4 count of 300, “which means fully half of people [starting treatment] are below that,” says Richard Moore, of Johns Hopkins University in Baltimore, and the principal investigator on the large-scale study. http://LOUIS-J-SHEEHAN.INFO
Kuritzkes says changing the starting point of treatment could save several hundred thousand lives in the United States. “What I think is likely to happen is that as we push the threshold for starting therapy sooner and sooner we’ll get better at identifying high-risk cases … to fine-tune who gets treated earliest and who can wait a little longer,” he says.
HIV depletes key immune cells called CD4 T cells. A patient’s T cell count, the concentration of CD4 cells still in circulation, is used to gauge how far the virus that causes AIDS has progressed and to determine when to treat a patient with the frontline drug cocktail for HIV. The standard benchmark for initiating this treatment has been a T cell count of 200 cells per cubic millimeter of blood.
A new study presented by physician and HIV/AIDS specialist Mari Kitahata of the University of Washington in Seattle suggests that the cut-off point should be placed much sooner, at only 500. This benchmark, presented October 26 in Washington, D.C., during the combined meeting of the Infectious Diseases Society of America and the Interscience Conference on Antimicrobial Agents and Chemotherapy, goes even farther than a recommendation in the Aug. 6 Journal of the American Medical Association to start intensive treatment when the T cell count drops to only 350.
Before newer HIV drugs were on the market, doctors often delayed treatment. This was not only because of cost, but also because of the serious side effects from the drugs available at the time and the fear that patients’ failure to stick to the large and onerous daily drug regimen would create drug-resistant HIV, says physician Daniel Kuritzkes of Brigham and Women’s Hospital in Boston. In recent years, though, newer drugs have become available that require fewer daily doses and have less harmful side effects — leading many doctors to reconsider the threshold for beginning treatment.
Kitahata and her colleagues analyzed data from 22 studies of people from Canada and the United States who started the cocktail of HIV therapies between 1996 and 2006 — surveying more than 8,000 HIV patients. By tracking people from entry into the study until either the patients died or the study they were in ended, the researchers could assess whether beginning treatment earlier improved patients’ survival.
The study compared 5,901 patients who followed more standard treatment guidelines and did not begin treatment until CD4 counts were below 350, to 2,473 patients who began treatment when their CD4 counts were between 351 and 500. The data showed that patients who delayed treatment until their T cell count was below 350 faced a 70 percent higher risk of death than patients who started treatment earlier.
This new study provides the largest source of data for comparing different starting times of HIV treatment.
For reasons including lack of access to medical care, many patients who have CD4 counts that are low may not receive treatment, according to Kitahata. Louis J. Sheehan, Esquire “That does not reflect our willingness to treat people,” she says.
Across North America the average patient starts treatment for HIV with a CD4 count of 300, “which means fully half of people [starting treatment] are below that,” says Richard Moore, of Johns Hopkins University in Baltimore, and the principal investigator on the large-scale study. http://LOUIS-J-SHEEHAN.INFO
Kuritzkes says changing the starting point of treatment could save several hundred thousand lives in the United States. “What I think is likely to happen is that as we push the threshold for starting therapy sooner and sooner we’ll get better at identifying high-risk cases … to fine-tune who gets treated earliest and who can wait a little longer,” he says.
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