California To Permit Medically Assisted Suicide As Of June 9

California Gov. Jerry Brown signed landmark legislation last October that would allow terminally ill people to request life-ending medication from their physicians.

But no one knew when the law would take effect, because of the unusual way in which the law was passed — in a legislative "extraordinary session" called by Brown. The bill could not go into effect until 90 days after that session adjourned.

The session closed Thursday, which means the End of Life Option Act will go into effect June 9.

"We're glad to finally have arrived at this day where we have a date certain," says Sen. Bill Monning, D-Carmel.

"It's a historic achievement for California, and for a limited universe of people dealing with a terminal illness," Monning says. "It could indeed be a transformative way of giving them the option of a compassionate end-of-life process."

Disability-rights advocates fought hard last year against passage of the legislative act, and they continue to voice concern.

Marilyn Golden, senior policy analyst with the Disability Rights Education & Defense Fund, says it would be impossible to know, for example, if a depressed patient went to many doctors — who all denied the request for lethal medication — before finding one who agreed to write the prescription.

"We are looking ahead at measures to protect people from abuse," Golden says, "and to explore and inform doctors, nurses and pharmacists that they don't have to participate."

As written, the law requires two doctors to agree, before prescribing the drugs, that a patient has six months or less to live. Patients must be able to swallow the medication themselves and must affirm in writing, 48 hours before taking the medication, that they will do so.

California is the fifth state to permit this option at the end of life. It joins Vermont, Oregon, Washington and Montana.

Across the state, some patients with advanced cancer welcomed the news.

"It gives me a great peace of mind to know that I will not be forced to die slowly and painfully," says Elizabeth Wallner, in a release from Compassion & Choices, an aid-in-dying advocacy group. Wallner, 52, of Sacramento, is a single mother with stage 4 colon cancer that has spread to her liver and lungs.

"It gives great comfort to know that the agonizingly traumatic image of me suffering will not be my family's last memory of me," she says.

Monning says he's grateful to people who worked for passage of the law, some in their final days:

• Brittany Maynard, an Orange County, Calif., woman with brain cancer, moved to Oregon to take advantage of laws there that allowed her to get lethal medication. Before she died in 2014, she recorded a video that was shown during hearings on the End of Life Option Act in Sacramento.
• Jennifer Glass, of San Mateo, Calif., helped to launch the campaign in 2014, then died of lung cancer last year.
• Christy O'Donnell, 47, of Los Angeles, died of lung cancer last month.

"I really believe," Monning says, "we use today to mark and dedicate the memory of some true champions." npr

High On The Highway: Scientists Try To Build A Marijuana Breath Test

A quartet of Western states and the District of Columbia have legalized recreational marijuana, and voters in a half-dozen more states may vote on pot legalization in 2016. That's leading law enforcement officials and entrepreneurs to try to come up with better ways of testing for driving while stoned.

Police usually spot impaired drivers by noting driving behavior, coordination, mannerisms and physical cues. But while a handheld breath test can quickly determine whether someone is legally drunk based on ethanol in the breath, there's no instant test for marijuana intoxication.

In Washington state, which is one of 18 states that has set limits on marijuana intoxication while driving, law enforcement can seek a warrant for a blood draw to test for THC, the main active ingredient in marijuana. But it can take weeks for results to come back from the toxicology lab.

With more Washington state drivers being arrested with marijuana in their systems since the state legalized recreational marijuana, there's growing need for a fast way to identify impaired drivers and get them off the road.

Herb Hill, a chemistry professor at Washington State University in Pullman, heard about the challenges of nailing drug-impaired drivers from a colleague who was a political science professor. "I said, 'Why don't we have a Breathalyzer for that?' He said none exists," Hill said. "I said, 'We can probably make one.' "

So Hill and his colleagues are trying to develop a hand-held device that police officers can use to detect THC in breath. Preliminary field testing with 30 human subjects this spring established that the device can detect THC in breath, Hill said. Much more testing is ahead to look at potential variations among gender, race, body types and amount of use.

Hill's team recruits volunteers who buy their own weed, smoke it at their homes and then blow into the prototype.

"We had to go through institutional board review," Hill said, referring to federal restrictions on research involving marijuana. "It took us almost a year to get permission to do this."

"It wasn't very hard to find the volunteers," Hill added. "We have a waiting list of volunteers."

The human guinea pigs get paid just over minimum wage to smoke their pot.

Hill said the portable device may look like an alcohol Breathalyzer but works differently inside. His team is modifying existing sniffers used at airports to detect explosives and by the military to alert to the presence of chemical warfare agents. The technology is called ion mobility spectrometry.

"In the beginning at least this would not be used as evidential information," Hill explained. "It would be used as screening information to help the officer say he should take a blood sample now."

Jake Yancey, a police officer in Tumwater, Wash., said he would be "super excited" to get a detector that he hopes could "drastically speed up" the process of confirming or ruling out a person's possible marijuana impairment. But a pot breath test must prove itself highly accurate before Washington state would adopt it, according to Lt. Rob Sharpe, head of the impaired driving section at the Washington State Patrol.

"Even if it is a preliminary device, we still need that level of accuracy and reliability for trust and confidence," Sharpe said. "Regardless where it comes into play in that arrest decision, we're talking about people's rights, their liberties and freedoms. We need to be accurate."

All of which points to it being several years at the earliest before you'd see a roadside breath test to identify stoned drivers.

Sharpe said a pot breath test might not even be the chosen answer. He said other companies and research teams are working on alternatives, including cheek swabs or a saliva test, a smartphone-based eye scan, or analyzing sweat on a person's skin.

Since legalizing marijuana use for adults, Washington and Colorado have both set legal limits for THC intoxication at 5 nanograms per milliliter of blood. Oregon and Alaska have not established a legal THC limit beyond which a driver is presumed to be impaired.

Some marijuana activists have expressed fears that this technology could lead to unimpaired drivers getting unfairly arrested. They point out that THC persists in the body long after the high has worn off. The effects of weed are also different in different people, including between infrequent versus chronic smokers.

Indeed, there is no universal agreement on how much THC is impairing — countries in Europe have set legal limits at 2 to 7 nanograms.

As part of the next rounds of human testing of the marijuana breath tester, the Washington state researchers want to correlate breath readings of THC with simultaneous blood draws and measurements. This could help to establish how long THC lingers in the breath after initial consumption.

Early on, the WSU professors took their idea to Chemring, a Falls Church, Va., instrument maker that agreed to pay for the R&D and will have the commercialization rights.

The Chemring-WSU team is by no means alone in trying to perfect a marijuana breath test. Competitors include Lifeloc Technologies of Colorado, which already makes alcohol testers, and Cannabix Technologies Inc. of Vancouver, British Columbia, has shown off an initial prototype at conferences. There are reportedly several research teams at work in Europe as well.  npr

Can A Cancer Drug Reverse Parkinson's Disease And Dementia?

A drug that's already approved for treating leukemia appears to dramatically reduce symptoms in people who have Parkinson's disease with dementia, or a related condition called Lewy body dementia.

A pilot study of 12 patients given small doses of nilotinib found that movement and mental function improved in all of the 11 people who completed the six-month trial, researchers reported Saturday at the Society for Neuroscience meeting in Chicago.

And for several patients the improvements were dramatic, says Fernando Pagan, an author of the study and director of the Movement Disorders Program at Georgetown University Medical Center. One woman regained the ability to feed herself, one man was able to stop using a walker, and three previously nonverbal patients began speaking again, Pagan says.

"After 25 years in Parkinson's disease research, this is the most excited I've ever been," Pagan says.

If the drug's effectiveness is confirmed in larger, placebo-controlled studies, nilotinib could become the first treatment to interrupt a process that kills brain cells in Parkinson's and other neurodegenerative diseases, including Alzheimer's.

One of the patients in the pilot study was Alan Hoffman, 74, who lives with his wife, Nancy, in Northern Virginia.

Hoffman was diagnosed with Parkinson's in 1997. At first, he had trouble moving his arms. Over time, walking became more difficult and his speech became slurred. And by 2007, the disease had begun to affect his thinking.

"I knew I'd dropped off in my ability to read," Hoffman says. "People would keep giving me books and I'd have read the first chapter of about 10 of them. I had no ability to focus on it."

"He had more and more difficulty making sense," Nancy Hoffman says. He also became less active, less able to have conversations, and eventually stopped doing even household chores, she says.

But after a few weeks on nilotinib, Hoffman "improved in every way," his wife says. "He began loading the dishwasher, loading the clothes in the dryer, things he had not done in a long time."

Even more surprising, Hoffman's scores on cognitive tests began to improve. At home, Nancy Hoffman says her husband was making sense again and regained his ability to focus. "He actually read the David McCullough book on the Wright Brothers and started reading the paper from beginning to end," she says.

The idea of using nilotinib to treat people like Alan Hoffman came from Charbel Moussa, an assistant professor of neurology at Georgetown University and an author of the study.

Moussa knew that in people who have Parkinson's disease with dementia or a related condition called Lewy body dementia, toxic proteins build up in certain brain cells, eventually killing them. Moussa thought nilotinib might be able to reverse this process.

His reasoning was that nilotinib activates a system in cells that works like a garbage disposal — it clears out unwanted proteins. Also, Moussa had shown that while cancer cells tend to die when exposed to nilotinib, brain cells actually become healthier.

So Moussa had his lab try the drug on brain cells in a Petri dish. "And we found that, surprisingly, with a very little amount of the drug we can clear all these proteins that are supposed to be neurotoxic," he says.

Next, Moussa had his team give the drug to transgenic mice that were almost completely paralyzed from Parkinson's disease. The treatment "rescued" the animals, he says, allowing them to move almost as well as healthy mice.

Moussa's mice got the attention of Pagan from Georgetown's Movement Disorders Program. "When Dr. Moussa showed them to me," Pagan says, "it looked like, hey, this is type of drug that we've been looking for because it goes to the root of the problem."

The pilot study was designed to determine whether nilotinib was safe for Parkinson's patients and to determine how much drug from the capsules they were taking was reaching their brains. "But we also saw efficacy, which is really unheard of in a safety study," Pagan says.

The study found that levels of toxic proteins in blood and spinal fluid decreased once patients began taking nilotinib. Also, tests showed that the symptoms of Parkinson's including tremor and "freezing" decreased. And during the study patients were able to use lower doses of Parkinson's drugs, suggesting that the brain cells that produce dopamine were working better.

But there are some caveats, Pagan says. For one thing, the study was small, not designed to measure effectiveness, and included no patients taking a placebo.

Also, nilotinib is very expensive. The cost of providing it to leukemia patients is thousands of dollars a month.

And finally, Parkinson's and dementia patients would have to keep taking nilotinib indefinitely or their symptoms would continue to get worse.

Alan Hoffman was okay for about three weeks after the study ended and he stopped taking the drug. Since then, "There's (been) a pretty big change," his wife says. "He does have more problems with his speech, and he has more problems with cognition and more problems with mobility."

The Hoffmans hope to get more nilotinib from the drug's maker, Novartis, through a special program for people who improve during experiments like this one.

Meanwhile, the Georgetown team plans to try nilotinib in patients with another brain disease that involves toxic proteins: Alzheimer's. npr

Drug-Resistant Food Poisoning Lands In The U.S.

This time last year, a painful new virus was knocking on our doorstep. Travelers were bringing chikungunya to the U.S. And eventually, the mosquito-borne virus set up shop in Florida.

Now the Centers for Disease Control and Prevention says another nasty pathogen is hitching a ride to the U.S. with travelers: multidrug-resistant Shigella.

Shigella is a huge problem around the world. The bacteria infect about 100 million people each year and kill about 600,000.

Shigella is just about as bad as the word sounds. The bacteria infect your intestines and trigger crampy rectal pain, bloody or mucus-laced diarrhea and vomiting.

Multidrug-resistant Shigella has caused several outbreaks over the past year in the U.S., the CDC reports Thursday in the journal Morbidity and Mortality Weekly Report. At least 243 people have gotten sick and about 20 percent were hospitalized.

Those numbers may not sound like much — especially when you consider a half-million Americans get regular shigellosis each year.

So what's the big deal? Well, this strain of Shigella is resistant to the go-to drug for the bacteria: ciprofloxacin.

"If rates of resistance become this high, in more places, we'll have very few options left for treating Shigella with antibiotics by mouth," says epidemiologist Anna Bowen, who led the study. Then doctors will have to resort to IV antibiotics.

Shigella is incredibly contagious. It spreads through contaminated food and water. "As few as 10 germs can cause an infection," Bowen says. "That's much less than some other diarrhea-causing germs."

From May to February, the Cipro-resistant strain popped up in 32 states, with large clusters in California, Massachusetts and Pennsylvania. Bowen and her team linked several of these outbreaks to international travel, including trips to India, the Dominican Republic and Morocco. npr

How Marijuana Highjacks Your Brain To Give You The Munchies

Shortly after toking up, a lot of marijuana users find that there's one burning question on their minds: "Why am I so hungry?" Researchers have been probing different parts of the brain looking for the root cause of the marijuana munchies for years. Now, a team of neuroscientists report that they have stumbled onto a major clue buried in a cluster of neurons they thought was responsible for making you feel full.

This cluster, called the POMC neurons, is in the hypothalamus, a region of the brain that scientists typically associate with base instincts like sexual arousal, alertness and feeding. Tamas Horvath, a neuroscientist at the Yale School of Medicine and the team's leader, says that the POMC neurons normally work by sending out a chemical signal telling the brain, you're sated, stop eating.

In the past, when neuroscientists shut down POMC neurons in mice, all the mice became morbidly obese. Horvath figured that in order for the drug in marijuana — compounds called cannabinoids — to spawn that undeniable impulse to feed, it would have to bind the activity of these neurons and make them fire less. Paradoxically, Horvath says, "We found the exact opposite."

The team discovered that when they injected cannabinoids into mice, the drug was turning off adjacent cells that normally command the POMC neurons to slow down. As a result, the POMC neurons' activity leapt up. At the same time, the cannabinoids activate a receptor inside the POMC neuron that causes the cell to switch from making a chemical signal telling the brain you're full to making endorphins, a neurotransmitter that's known to increase appetite. npr

E-Cigarettes Can Churn Out High Levels Of Formaldehyde

Vapor produced by electronic cigarettes can contain a surprisingly high concentration of formaldehyde — a known carcinogen — researchers reported Wednesday.

The findings, described in a letter published in the New England Journal of Medicine, intensify concern about the safety of electronic cigarettes, which have become increasingly popular.

"I think this is just one more piece of evidence amid a number of pieces of evidence that e-cigarettes are not absolutely safe," says David Peyton, a chemistry professor at Portland State University who helped conduct the research.
...
Some public health experts think vaping could prevent some people from starting to smoke traditional tobacco cigarettes and help some longtime smokers kick the habit.

But many health experts are also worried that so little is known about e-cigarettes, they may pose unknown risks. So Peyton and his colleagues decided to take a closer look at what's in that vapor.

"We simulated vaping by drawing the vapor — the aerosol — into a syringe, sort of simulating the lungs," Peyton says. That enabled the researchers to conduct a detailed chemical analysis of the vapor. They found something unexpected when the devices were dialed up to their highest settings.

"To our surprise, we found masked formaldehyde in the liquid droplet particles in the aerosol," Peyton says.

He calls it "masked" formaldehyde because it's in a slightly different form than regular formaldehyde — a form that could increase the likelihood it would get deposited in the lung. And the researchers didn't just find a little of the toxicant.

"We found this form of formaldehyde at significantly higher concentrations than even regular cigarettes [contain] — between five[fold] and fifteenfold higher concentration of formaldehyde than in cigarettes," Peyton says.

And formaldehyde is a known carcinogen.

"Long-term exposure is recognized as contributing to lung cancer," says Peyton. "And so we would like to minimize contact (to the extent one can) especially to delicate tissues like the lungs."

Conley says the researchers found formaldehyde only when the e-cigarettes were cranked up to their highest voltage levels.

"If you hold the button on an e-cigarette for 100 seconds, you could potentially produce 100 times more formaldehyde than you would ever get from a cigarette," Conley says. "But no human vaper would ever vape at that condition, because within one second their lungs would be incredibly uncomfortable."

That's because the vapor would be so hot. Conley compares it to overcooking a steak.

"I can take a steak and I can cook it on the grill for the next 18 hours, and that steak will be absolutely chock-full of carcinogens," he says. "But the steak will also be charcoal, so no one will eat it."

Peyton acknowledges that he found no formaldehyde when the e-cigarettes were set at low levels. But he says he thinks plenty of people use the high settings.

"As I walk around town and look at people using these electronic cigarette devices it's not difficult to tell what sort of setting they're using," Peyton says. "You can see how much of the aerosol they're blowing out. It's not small amounts."

"It's pretty clear to me," he says, "that at least some of the users are using the high levels."

So Peyton hopes the government will tightly regulate the electronic devices. The Food and Drug Administration is in the process of deciding just how strict it should be. npr

Electronic nicotine delivery systems: emerging science foundation for policy

J E Henningfield, G S Zaatari

The US Food and Drug Administration (FDA) conducted preliminary tests of several electronic nicotine delivery system (ENDS) models, documenting widely varying levels of nicotine, carcinogens and diethylene glycol, which it noted "is toxic to humans. The FDA concluded that "quality control processes used to manufacture these products are inconsistent or non-existent because of variability in contents and emissions.
....
An additional complication is that ENDS might produce substantially higher deliveries if they are "spiked with nicotine liquid" available for refilling their cartridges (eg, Totally Wicked ELiquid Smoke Juice). ENDS refill products raise many of the same safety and effectiveness issues as ENDS. A cursory review of such products on the Internet revealed a broad range of refill products, claims and even warnings, with some admitting carcinogens and the possibility of nicotine poisoning (some appear to contain sufficient nicotine to kill many persons even if simply spilled on the skin). It would seem that where the nicotine is intended for human consumption, it should be subject to the same regulations for safety and effectiveness as drugs including standards for child-resistant packaging and labelling to minimise risk of poisoning. read more

Hookah smokers are inhaling benzene

High levels of benzene, a chemical in crude oil and gasoline, are present in hookah smokers and nonsmokers after they attend social events where the water pipes are used, a new report says.

Benzene exposure is a known risk factor for leukemia. Since there are no safe levels of benzene exposure, interventions to prevent or reduce hookah smoking or regulate the tobacco products are needed, say the authors.

“Hookah smoking involves tobacco which is simply hazardous to the health of those who smoke it, and those who socialize or live with them,” Nada Kassem, who led the study, told Reuters Health in an email.

Burning charcoal is needed to heat the hookah tobacco to generate the smoke, said Kassem, who is the associate director at the Center for Behavioral Epidemiology and Community Health at San Diego State University.

“In addition to inhaling toxicants and carcinogens found in the hookah tobacco smoke, hookah smokers, and non-smokers who socialize with them, also inhale large quantities of charcoal combustion-generated toxic and carcinogenic emissions,” she said, adding that benzene is present in both tobacco smoke and the burnt charcoal emissions. msn

alpaca bowl

why smoking is so fucking bad for you

How does radioactive material get into a cigarette?

The tobacco leaves used in making cigarettes contain radioactive material, particularly lead-210 and polonium-210. The radionuclide content of tobacco leaves depends heavily on soil conditions and fertilizer use.

Soils that contain elevated radium lead to high radon gas emanations rising into the growing tobacco crop. Radon rapidly decays into a series of solid, highly radioactive metals (radon decay products). These metals cling to dust particles which in turn are collected by the sticky tobacco leaves. The sticky compound that seeps from the trichomes is not water soluble, so the particles do not wash off in the rain. There they stay, through curing process, cutting, and manufacture into cigarettes.Lead-210 and Polonium-210 can be absorbed into tobacco leaves directly from the soil. But more importantly, fine, sticky hairs (called trichomes) on both sides of tobacco leaves grab airborne radioactive particles.

For example, phosphate fertilizers, favored by the tobacco industry, contain radium and its decay products (including lead-210 and polonium-210). When phosphate fertilizer is spread on tobacco fields year after year, the concentration of lead-210 and polonium-210 in the soil rises.

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What happens when I smoke a cigarette?

Research indicates that lead-210 and polonium-210 are present in tobacco smoke as it passes into the lung. The concentration of lead-210 and polonium-210 in tobacco leaf is relatively low, however, this low concentration can accumulate into very high concentrations in the lungs of smokers.

As it passes into the lungs, the smoke impacts the branches of the lung passages, called bronchioles, where the branches split. Tar from tobacco smoke builds up there, and traps lead-210 and polonium-210 against the sensitive tissues of the bronchioles. Studies show filters on ordinary commercial cigarette remove only a modest amount of radioactivity from the smoke inhaled into the lungs of smokers. Most of what is deposited is lead-210, but polonium-210 (whose half life is about 138 days) quickly grows in as the lead-210 (half life = 22.3 years) decays and becomes the dominant radionuclide. Over time, the concentration of polonium-210 directly on tissues of the bronchioles grows very high, and intense localized radiation doses can occur at the bronchioles. epa.gov

_______________________________________

Review Article: Polonium and Lung Cancer by Vincenzo Zaga, Charilaos Lygidakis, Kamal Chaouachi, and Enrico Gattavecchia
In the Journal of Oncology, 2011

 Polonium is a highly toxic element, with elevated specific radioactivity, and is dangerous to handle even in milligram amounts. The maximum allowable body burden for ingested Polonium is 1100 Bq, which is equivalent to a particle weighing only 6. 6 Å~  10−6 μ g [57]. Alpha rays, which are formed by helium 4 (He-4) nucleus, are the least penetrating type of radiation and they manage to travel only a few centimeters in air. They can be easily stopped by obstacles, such as a sheet of paper, and they can penetrate living tissues by only a few microns [55, 58, 59]. In fact, since they lose all of their energy after a short distance, they can be dangerous for tissues only when substances emitting alpha particles enter the organism by respiration or ingestion. In addition, alpha rays are highly ionizing and, therefore, are particularly harmful for living tissues. 1 mg of polonium can emit as many alpha particles as 5 grams of radium. The impact on humans can be devastating, as it can cause considerable damage by causing cell death, promoting a massive, progressive, and rapid necrosis, and not allowing the organism enough time to replace the quantity of dead cells [57].

 The journey of Po-210 and Pb-210 towards bronchopulmonary apparatus starts by lighting a cigarette. In this combustion chamber, tobacco burns, reaching 800–900◦ C when inhaling, and smoke is created, which is composed of a corpuscular (5%) and a gas phase (95%) [46]. Po- 210 and Pb-210 are adsorbed in the insoluble particles of the corpuscular phase [65]. The latter is present in a high quantity and is a weak alpha (< 1Å~ 10−5 ), gamma, beta, and X emitter. All these inhaled particles are deposited in the broncho-pulmonary apparatus and particularly in segmental bronchi bifurcations, due to ciliary action. According to measurements by Cohen et al., radium and thorium are also present in cigarettes; however, 99% of the radioactivity comes from Po-210 [75], which remains in the bronchopulmonary apparatus after inhalation [76]. All these particles have a diff erent “destiny” based on the efficacy of the mucous-ciliary clearance. This mechanical purification is reduced gradually in smokers with COPD, resulting in the accumulation of insoluble Pb-210 particles, which decay to Po-210 over time [70, 77]. In fact, the more severe COPD becomes, the greater the risk of radioactive load accumulation is [77]. Subsequently, radioactive particles reach various organs and tissues through pulmonary and systemic circulation and cause mutations of the genetic cellular structure, deviations of the standard cellular characteristics, accelerated aging, and quicker death due to a wide range of diseases [78, 79]. In smokers, Po-210 levels are in fact significantly higher in blood (by 30%) [65, 80], urine (6-times higher) [81], liver, kidney, heart, and psoas muscle [82]. Little and McGandy estimated that Po-210 concentration in blood is 63.64mBq/kg of blood in smokers and 28.12mBq/kg of blood in non-smokers [83]. Notably, concentrations of Pb- 210 and Po-210 in rib bones and alveolar lung tissues were two-times higher in ex-smokers compared to non-smokers, even a year after smoking cessation [66].


 DNA chromosome damage by exposure to alpha radiation is 100-times greater than the one caused by other types of radiation [113]. Little and Radford estimated that the radiation dose of the bronchial epithelium of bifurcations in the inferior lobes of people smoking for 25 years would be 2 Sv [114]. This can be explained by the local accumulation of Pb-210 insoluble particles [72]. According to Martell, the cumulative dose of alpha radiation in bronchial bifurcations of smokers that die of lung cancer is approximately 16 Sv (80 rad). This dose is suffi cient to induce a malignant transformation caused by alpha-particles interaction with basal cells [115, 116].

 "To render the biological harm deriving from Po-210 in smoke more comprehensible, it has been compared to the damage caused by radiation in conventional chest X-rays. Since the dose of a modern chest radiograph is 0.034mSv [125, 126], a smoker of 20 cigarettes per day receives a radiation dose of 0.08–0.09 Sv equivalent to approximately 300 chest X-rays per year [98, 99, 113, 127]."

Cone snail drug 100x more potent than morphine

by  AG Staff

A new drug from cone snail venom could offer hope to chronic pain sufferers

AN EXPERIMENTAL DRUG made from cone snail venom has shown early signs of promise in numbing pain, raising hopes in the hunt for new, non-addictive medications, an Australian researcher says.

The drug, which has not been tested yet on humans, is judged to be about 100 times more potent than morphine or gabapentin, which are currently considered the gold standard for chronic nerve pain.

The active ingredient, conotoxin, comes from carnivorous cone snails, which are common in the western Pacific and Indian Ocean…

(via: Australian Geographic)

nicotine

Nicotine acts on neurons of the mesolimbic reward system in the midbrain.

A burning cigarette quickly converts from a tobacco storehouse to a chemical factory, producing some 4,000 compounds. Of these, 400, including nicotine and carbon monoxide, are toxins, and another 40 are carcinogens. 

Nicotine itself is distilled at the tip of the burning cigarette. There it is absorbed onto tar (particulate matter) droplets that are carried deep into the lungs with each intake of smoke. Nicotine’s trip from the lungs to the brain takes about 10 seconds. 

After it reaches the brain, nicotine, in its pharmacologically active levorotatory form, (S)-nicotine, shanghais receptor sites on neurons normally activated by the natural nerve-tonerve messenger acetylcholine. (These are called cholinergic receptors.) And by impersonating acetylcholine, nicotine alters the way the brain processes information. 

In the brain, nicotine becomes one of nature’s chemical chameleons. It acts on the reward system to cause the release of dopamine—and that makes people feel good. It acts through other brain chemicals thought to be important for activating and alerting systems. And it acts on still other systems that are probably involved in cognition and motivation. 

"Nicotine is a pretty amazing drug. If it didn’t kill you, it would be pretty terrific," says Edythe D. London, chief of the National Institute on Drug Abuse’s (NIDA) neuroimaging and drug action branch. 

It’s also “an unusually insidious addictive drug,” declares Avram Goldstein, Stanford University professor emeritus of pharmacology and author of “Addiction: From Biology to Drug Policy.” It calms and it stimulates. It affects mood, appetite, and cognition. Many smokers claim smoking helps them handle stress and boredom, control their weight and appetite, and function better in unfamiliar social situations. 

How can a single molecule do all these things? Using a fascinating array of research tools, trained laboratory animals, and exotic compounds, scientists are plumbing the depths of the brain in search of answers.

-Lois R. Ember

The Nicotine Connection: Scientists are teasing out the chemistry of nicotine addiction as tobacco firms and government regulators tussle over possible controls on cigarettes

Chemical & Engineering News, November 28, 1994

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ketamine for depression

Scientists say they have figured out how an experimental drug called ketamine is able to relieve major depression in hours instead of weeks.

Researchers from Yale and the National Institute of Mental Health say ketamine seems to cause a burst of new connections to form between nerve cells in parts of the brain involved in emotion and mood.

The discovery, described in Science, should speed development of the first truly new depression drugs since the 1970s, the researchers say.

"It's exciting," says Ron Duman, a a psychiatarist and neurobiologist at Yale University. "The hope is that this new information about ketamine is really going to provide a whole array of new targets that can be developed that ultimately provide a much better way of treating depression."

Ketamine is an FDA-approved anesthetic. It's also a popular club drug that can produce out-of-body experiences. Not exactly the resume you'd expect for a depression drug.

But a few years ago, researchers discovered that ketamine could help people withmajor depression who hadn't responded to other treatments. What's more, the relief came almost instantly.

The discovery "represents maybe one of the biggest findings in the field over the last 50 years," Duman says.

Depression is associated with a loss of so-called synaptic connections between nerve cells, Duman says. So he and other scientists began to study mice exposed to stresses that produce symptoms a lot like those of human depression.

The stressed mice lost connections in certain parts of the brain. But a dose of ketamine was able to "rapidly increase these connections and also to rapidly reverse the deficits that are caused by stress," Duman says.

A team at the National Institute of Mental Health also has found evidence that ketamine works by encouraging synaptic connections.

It's possible to see the change just by studying rodent brain cells with a microscope, says Carlos Zarate from the Mood and Anxiety Disorders Program at NIMH.

A healthy neuron looks like a tree in spring, he says, with lots of branches and leaves extending toward synaptic connections with other neurons. "What happens in depression is there's a shriveling of these branches and these leaves and It looks like a tree in winter. And a drug like ketamine does make the tree look like one back in spring."

And there's also indirect evidence that ketamine is restoring synaptic connections in people, Zarate says.

His team studied 30 depressed patients who got ketamine. And they found changes in brainwave activity that indicated the drug had strengthened connections between neurons in areas of the brain involved in depression.

All of this research is intended to produce drugs that will work like ketamine, but without the hallucinations. And several of these alternative drugs are already being tried in people.

Preliminary results suggest that "some of these compounds do have rapid antidepressant effects without the side effects that occur with ketamine," Zarate says.

One of these drugs, called GLYX-13, has already been tested in two large groups of people — a key step toward FDA approval. The company that makes the drug, Naurex, says it will tell scientists how well GLYX-13 works at a meeting in December.

npr

2011 state marijuana laws

its here...