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This is for the long-termers who just got excited about this piece of puff (fast-forward to the 55 second mark for expediancy--it's about a 5 second bit):
It's a good metaphor/symbolism for a fictional work.
Ombow-It is far from that easy and it is virtually impossible to be that concise. The battle is and will ultimately remain one with the entire Muslim world with that kind of tactic. War with Iran, especially if provoked by Iran, will worsen conditions around the world, not unlike our boneheaded maneuver into Iraq a second time. That war has only increased tension and ire towards Western Civilization. Us going after Iran would be playing right into their hands, just like the Iraq invasion was probable a welcomed, desired, and predicted move for the Muslim Extremists/terrorists, post 9/11. They suckered this superpower into an unjust war which has only served to strengthen them.
Gfp-My brother, a radical anti-gov't demonstrator 10 years ago, told me then (actually, post 9/11) that the CIA hired Osama/Al-Queda in the 70's to fight the Russians. What I was referring to was the newest arm of the organization--the Iraqi faction.
Nothing close to the market--they can't get out of their own way. Their progress with Alzheimer's has got to be the single greatest disappointment that has come out of Irvine, and there is a plethora of adverse events to chose from.
Yes, if you don't mind speculation and can deal with mngmnt underperformance. They will unlikely optimize their abilities, but perhaps the gloom has been overemphasized on the downside, thus giving the current pps a little more upside on any positive drug development news. I think Ampakines are here to stay, but Cortex as a company, which we are most concerned about, has a far more tenuous future. Enter at your own risk...and plan for disappointment :)
Medical board yanks pain doctor's license
Pediatrician awaits trial on homicide charges
http://www.sun-sentinel.com/health/fl-doctor-discipline-20101203,0,5563711.story
A Lake Worth pediatrician awaiting trial on homicide charges for trafficking pain pills had his license revoked Friday by state regulators, their latest act in a yearlong get-tough campaign against pill mills.
Dr. Sergio Rodriguez had kept his license even though he has been in jail since his arrest in July 2008 for prescribing narcotic pills to an undercover officer. In March, he was indicted for homicide stemming from the overdose deaths of three patients. He has pleaded not guilty.
The Florida Board of Medicine, a doctor-dominated group that has been criticized as being too soft on their peers, started suspending and revoking the licenses of pain doctors on a regular basis in summer 2009. Rodriguez, 54, was the latest.
"Outstanding. I'm glad they finally dealt with him, but it took so long," said Rachael Arrants, a Palm Beach Gardens mother whose adult son died from an overdose of pills prescribed by Rodriguez in December 2007.
"Before, they didn't seem to do too much or pay too much attention, but all the attention on pain clinics has changed things," Arrants said. "Things are moving in a positive direction."
Florida pain clinics, especially in Broward and Palm Beach counties, have attracted national attention for being the Southeast's single biggest supplier of narcotic pills. Prescription drug overdoses claim seven to nine lives a day in Florida.
Palm Beach County police have said Rodriguez ran an egregious pill operation. Police said seven of his patients died from overdoses of pills he issued. Arrants' son, Tommy Nunn, was one of the seven but not among the three from the homicide case.
Four times, he gave scripts for more than 200 pills a month – a potentially lethal amount – to a policewoman posing as a pain patient, with no physical exam or proof of an injury, state health officials said in a complaint against him. Adult addicts mingled with children and parents in his West Palm Beach office, Children's Plus Health Center.
He broke the rules by "repeatedly prescribing potentially fatal combinations" of drugs, the complaint said, putting patients "at an inordinate risk of death."
The homicide charges stemmed from the 2008 overdose deaths of three men in their 20s, including Robert Peterkin, a fisherman who drove to the doctor's office every month from Palm Bay in Brevard County.
Rodriguez is due in court Dec. 17 for a status report on his upcoming murder trial, a spokeswoman for Palm Beach County prosecutors said.
In a separate case, the medical board indefinitely suspended the license of Oakland Park anesthesiologist John R. Habib, who has been in jail since he was arrested in March for selling crystal methamphetamine to an undercover police officer.
Habib can apply to get his license back but not until he resolves his criminal case and undergoes an addiction therapy program for physicians, said one of his attorneys, Keith Pierro.
On a related matter, a medical board panel decided not to take emergency action to initiate a strict set of pain clinic rules that have been delayed by legislative action.
Legislators last month passed a law saying rules with substantial impact on small business cannot take effect until lawmakers give approval. The medical board could have declared the pill mill problem to be an emergency and put the rules into effect, but the panel found no grounds to do so.
The decision angered a Fort Lauderdale pain clinic activist. Maureen Kielian, whose son survived a pain pill overdose, said a state report Thursday tallying nine prescription overdose deaths per day proves the need.
"The death rate continues to grow," Kielian said. "The community is being devastated."
The delayed rules that were supposed to start Nov. 28 would have forced pain clinics to examine every patient, counsel them on addiction risks and do random drug tests. The state can't enforce them but can enforce a new law started Oct. 1 forcing pain clinics to be inspected and to sell no more than three days worth of drugs to patients paying by cash.
Celebrities step up for first TV telethon to focus on Alzehimer's disease
By Mary Forgione, Los Angeles Times
9:59 p.m. EST, December 3, 2010
There are lots of ways to raise awareness about a disease -- and having Hollywood celebrities tell their stories always helps. The Alzheimer's Foundation of America has gathered a number of notables, many of whom have a personal connection to the disease, for its first hourlong TV telethon on Saturday night.
The Together for Care Telethon will feature, among others, actor Hector Elizondo, the foundation's honorary chairman, who has spoken openly lately about his own family's reluctance to seek help when his mother showed signs of Alzheimer's back in the mid-1960s. Check out this interview at Caregiver.com.
And yes, there will be plenty of music -- from Shontelle, the (reunited) Wilson Phillips and country-music singer Brett Eldredge, who dedicated a song to his grandmother who has Alzheimer's. Go here to see a full list of guests scheduled to be on the telethon.
But the point isn't just to entertain. The foundation seeks to raise awareness (and funds) to fight the disease that affects more than 5 million Americans. It also invites the public to share their stories of loved ones with Alzheimer's and their caretakers here at their discussion page on Facebook.
The telethon will be broadcast in most time zones at 8 p.m. Saturday; here's a schedule to check when it will be on in your area.
This is an interesting angle. What ever did happen of our Veterinary Medecine strategy anyway? The coños in mngmnt never did tell us:
San Diego: ALS Research Goes to the Dogs
3 December 2010. Move over, mice. There are now one, and possibly two, models for amyotrophic lateral sclerosis in man’s best friend. At the Society for Neuroscience annual meeting, held 13-17 November 2010 in San Diego, California, researchers learned about canines with idiopathic laryngeal paralysis (ILP), a disease that looks suspiciously similar to bulbar-onset ALS. If that is confirmed, these animals will join a group of dogs with degenerative myelopathy (DM), which share a genetic mutation with the human version of the disease.
“There is a need for large animal species models for ALS,” said Amelie Gubitz, Program Director for ALS research at the National Institute of Neurological Disorders and Stroke in Bethesda, Maryland. “They fill an important gap,” she said, between the tiny brains and spinal cords of mice and the human-sized nervous system. Gubitz, who organized a satellite meeting to discuss ALS models on 12 November, noted that a golden retriever model has proved useful in several studies of Duchenne’s muscular dystrophy (Banks and Chamberlain, 2008).
At the satellite meeting, Bryden Stanley of Michigan State University in East Lansing presented a poster on dogs with ILP. These animals suffer problems in swallowing that mirror the bulbar onset in one-quarter of people who get ALS. There is no real animal model for bulbar-onset ALS, said Bob Brown of the University of Massachusetts in Worcester, although some mice may exhibit symptoms in the neck area. Thus far, Stanley has been unable to find a genetic cause for the ILP.
In another poster session during the SfN general meeting, Brandie Morgan of the University of Missouri in Columbia discussed her data on axon counts in dogs with DM. Morgan works with Missouri researcher Joan Coates, who presented her dog model two years ago at the SfN meeting in Washington, DC (see ARF related news story and ARF related news story on Awano et al., 2009; reviewed in Coates and Wininger, 2010). These animals have a missense mutation in superoxide dismutase 1 (SOD1); SOD1 mutations are responsible for some cases of inherited ALS.
The two models might turn out to complement each other, Gubitz said, with Coates’s model mimicking familial ALS and Stanley’s standing in for bulbar-onset, and possibly sporadic, forms.
Dog models offer many advantages. “The dog and human share an incredibly close environment,” Stanley told ARF in an interview. Thus, they may be exposed to the same toxins that some researchers suspect contribute to ALS. Because owners choose to euthanize their pets at different stages, dogs offer the opportunity to examine disease pathology before end-stage, which is impossible in people.
Dogs, given their inbred genomes, are also convenient for genomewide association studies (GWAS), said Dennis O’Brien, the director of the veterinary comparative neurology program at the University of Missouri. Dogs have less well-shuffled genomes than do people, he said, so their linkage disequilibrium groups are large, and scientists can find gene associations with a relatively small sample. “That is probably the biggest advantage that the dogs have,” O’Brien said. “The GWAS is so powerful.”
Bulbar Barks
Stanley originally set out to study not ALS but ILP, a common disorder in elderly dogs, particularly Labrador retrievers. Degeneration of the laryngeal nerves leads to paralysis of the laryngeal muscles, and symptoms include gagging, throat clearing, and a raspy or hoarse-sounding bark. Dogs tend to get sick around 10 years of age, and generally last for one to three years longer, Stanley told ARF.
Stanley and colleagues followed dogs with ILP for a year and performed neurological tests, looking at gait, muscle tone, and reflexes (see Stanley et al., 2010). Of 32 dogs with ILP, 10 had neurologic problems when they enrolled in the study. Half of the dogs had them by six months, and all had neurological signs within a year of enrollment. Eventually, the dogs with ILP became paralyzed. At autopsy, the dogs with ILP evinced muscle atrophy and loss of axons in the lumbar spinal cord’s ventral roots. In comparison, none of the 34 control dogs showed neurological symptoms.
Stanley found herself thinking that “There must be something in humans like this.” She started talking to neurologists, who immediately saw the similarities between ILP and bulbar ALS, which starts with problems in speaking and swallowing. “Their jaws dropped,” Stanley told ARF. “They were just taken away with the similarity.”
It is too early to consider ILP a definite ALS model, Stanley said, but it is promising enough to warrant further study. “It is going to be a good model for something,” O’Brien told ARF. “I do not know if we know enough yet to see if it is going to be a good model for ALS.”
Stanley is working to further characterize ILP, and recruited Michigan State neuropathologist Howard Chang to help analyze tissue samples. “Clearly, we have a problem of neuropathy,” he said. “The question is, where does the neuropathy come from?” He said he has only seen a few samples so far, and needs more control tissues from healthy animals before forming any conclusions. Stanley is searching for a genetic cause of ILP, and has tested several of the usual ALS suspects: SOD1, angiogenin, FUS, TDP-43, and FIG4. So far, she has had no hits, and plans to continue the search with a GWAS. Brown told ARF he hopes these studies will identify new ALS genes.
Dog Genes
The University of Missouri researchers do have a genetic link for degenerative myelopathy. This is an advantage, Gubitz said, because research colonies can be bred. Indeed, the scientists have already begun a proof-of-concept study of ALS treatment in bred-for-research animals, Coates told ARF, although she said it is too early to reveal any details.
Coates and colleagues first studied DM, which has its onset in the hind limbs, in Pembroke Welsh corgies and boxers. “We are continuing to find other breeds or dogs that are affected with this disease,” Coates told ARF in an interview. At least 17 breeds can get the disease, and more than two dozen breeds carry the missense SOD1 allele at a frequency greater than 20 percent. Most of the dogs have the same missense mutation—E40K—although the scientists may have found a second SOD1 mutation in one Bernese mountain dog, Coates said.
In people, a single faulty SOD1 gene amounts to a 100 percent certainty of getting ALS. That is not true in dogs, where few heterozygotes get sick and some homozygotes escape disease. This incomplete penetrance, Coates suggested, may be because some dogs die before the disease has time to develop. If that is true, she thinks there must be genetic factors that enhance or reduce risk. The researchers are conducting a GWAS to find those risk factors.
Coates and colleagues are also interested in finding biomarkers that would allow them to follow disease progression. At the ALS International Conference to be held in Orlando, Florida, later this month, Coates will present her work with a method she calls MUNE, for motor unit number estimation. Using electronic stimulation and recording, MUNE tells the scientists how many neuromuscular junctions a particular muscle has.
While much of the work in Coates’s group has focused on upper motor neuron degeneration, Morgan wanted to know whether axon fiber numbers drop in lower motor neurons. She counted axon fibers in cross-sections from T8 vertebra motor roots. Two healthy boxers had an average of 5,788 axons. But in seven boxers with DM, Morgan discovered an average of 4,603 axons. This reduction in fiber count is similar to ALS pathology.
Given the heterogeneity of ALS in people, it is unlikely that any single model will be the only one used in research, Gubitz said. Instead, she envisions a panel of models that researchers will use in parallel. Dogs just might be on the list.—Amber Dance.
Alas! Now we know why Ampakines are being held back by The Man(pssst, we don't need drugs to increase BDNF, therefore, we don't need new drugs to enhance cognition and improve neurobiological balance). From May, 2010:
BDNF increases with behavioral enrichment and an antioxidant diet in the aged dog.
Fahnestock M, Marchese M, Head E, Pop V, Michalski B, Milgram WN, Cotman CW.
Department of Psychiatry and Behavioural Neurosciences, McMaster
University, Hamilton, ON L8N 3Z5, Canada.
Abstract
The aged canine (dog) is an excellent model for investigating the neurobiological changes that underlie cognitive impairment and neurodegeneration in humans, as canines and humans undergo similar pathological and behavioral changes with aging. Recent evidence indicates that a combination of environmental enrichment and antioxidant-fortified diet can be used to reduce the rate of age-dependent neuropathology and cognitive decline in aged dogs, although the mechanisms underlying these changes have not been established. We examined the hypothesis that an increase in levels of brain-derived neurotrophic factor (BDNF) is one of the factors underlying improvements in learning and memory. Old, cognitively impaired animals that did not receive any treatment showed a significant decrease in BDNF mRNA in the temporal cortex when compared with the young group. Animals receiving either an antioxidant diet or environmental enrichment displayed intermediate levels of BDNF mRNA. However, dogs receiving both an antioxidant diet and environmental enrichment showed increased levels of BDNF mRNA when compared with untreated aged dogs, approaching levels measured in young animals. BDNF receptor TrkB mRNA levels did not differ between groups. BDNF mRNA levels were positively correlated with improved cognitive performance and inversely correlated with cortical Abeta((1-42)) and Abeta((1-40)) levels. These findings suggest that environmental enrichment and antioxidant diet interact to maintain brain levels of BDNF, which may lead to improved cognitive performance. This is the first demonstration in a higher animal that nonpharmacological changes in lifestyle in advanced age can upregulate BDNF to levels approaching those in the young brain.
It's just too unfortunate that there is very little which is funny about this investment and the mgmnt in general. It is good that there is very little transparency, for if we knew the actual specifics regarding mngmnt decision-making, we would be exceedingly shocked and awed, in an even more dreadful way...
Congratulations on two accounts: Door #3 is the most likely winner; and, you are the 35000th post! Perhaps Aiming has a prize for you!
Aiming--How about a free introductory I-Hub membership for our double winner? :)
Gfp-Does this excite you?:
Exclusive: WikiLeaks Will Unveil Major Bank Scandal
by Andy Greenberg
Monday, November 29, 2010
Earlier this month, WikiLeaks founder Julian Assange told Forbes that his whistleblower site will release tens of thousands of documents from a major U.S. financial firm in early 2011. Assange wouldn't say exactly what date, what bank, or what documents, but he compared the coming release to the emails that emerged in the Enron trial, a comprehensive look at a corporation's bad behavior.
"It will give a true and representative insight into how banks behave at the executive level in a way that will stimulate investigations and reforms, I presume," he told me.
"You could call it the ecosystem of corruption," Assange added. "But it's also all the regular decision making that turns a blind eye to and supports unethical practices: the oversight that's not done, the priorities of executives, how they think they're fulfilling their own self-interest."
WikiLeaks recent priority has clearly been the publication of hundreds of thousands of government documents: 76,000 classified documents from the war in Afghanistan, another 392,000 from Iraq, and on Sunday, the first piece of an ongoing exposure of what will likely be millions of diplomatic messages sent between the U.S. State Department and its embassies.
But that government focus doesn't mean WikiLeaks won't embarass corporations, too. Since October, WikiLeaks has closed its submissions channel; Assange says the site was receiving more documents than it could find resources to publish. And half those unpublished submissions, Assange says, relate to the private sector. He confirmed that WikiLeaks has damaging, unpublished material from pharmaceutical companies, finance firms (aside from the upcoming bank release), and energy companies, just to name a few industries.
Whether and when those secrets come out is solely a matter of Assange's discretion. "We're in a position where we have to prioritize our resources so that the biggest impact stuff gets released first."
Gfp-Money is the solution, not the problem, right? :)
Sleep Apnea May Shrink Brain's Gray Matter: Study
FRIDAY, Nov. 12 (HealthDay News) -- Obstructive sleep apnea may cause structural defects in the brain's gray matter, resulting in problems with cognitive functions such as attention and memory, a new study suggests.
These brain changes are likely caused by the intermittent oxygen deprivation that occurs in people with obstructive sleep apnea (OSA), who temporarily stop breathing many times each night.
A small Italian study of 17 patients with OSA and 15 age-matched controls found reduced gray matter in the OSA group in several key regions of the brain connected with abstract reasoning and executive function, along with deficits in the left cortex, which were shown to be linked to daytime sleepiness.
The participants in the OSA group also had impaired memory, attention, executive function, and constructional abilities, as well as higher sleepiness scores.
However, the brain changes are partially or fully reversible with early detection and treatment with continuous positive airway pressure (CPAP), said the Italian researchers.
The findings appear online and in an upcoming print issue of the American Journal of Respiratory and Critical Care Medicine.
"This study provides the first evidence that structural brain abnormalities exist in regions susceptible to hypoxemia [low oxygen levels in the blood], and they can change with treatment," Vincenza Castronovo, a clinical psychologist at the Sleep Disorders Center, Vita-Salute San Raffaele University and San Raffaele Scientific Institute in Milan, said in a journal news release.
Ombow-I've known you to be quite naïve over the years, but I can't recall such a hollow tone. Is this another one of your no-brainer's? I think you have taken [at least] one trip too many back in your heyday. BDNF anyone?
Okay, I'll accept that the material wasn't worthy, but it still was a shitty way of dealing with it in regards to my questioning of the matter. After all, talking about Jerry Brown pegging Linda Ronstadt isn't exactly Cortex material either, is it? TOU goes both ways, sir.
And mine? How about a reasonable discussion on why the deleted posts were 'unreasonable,' rather then the escalation of censorship resulting from my inquiry?
Aiming-Did the posts (the first 3 from yesterday) not have to do with Cortex or our investment in any way? I have no idea what the scenario is, but I wonder about the transparency of this platform sometimes. I'm simply asking for a grown-up explanation, can you dig?
Here is a list of some studies involving the measuring of BDNF levels in the brain (from PubMed). Most of the research revolves around the levels of the Val66Met gene variant (the so called BDNF gene). I don't really know what I'm talking about, so I'll leave it at that. Clicking on the link gets you to the abstract:
http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=link&linkname=pubmed_pubmed&uid=19683059
So nothing has changed, inclusive of the comment on the Quarterly :)
I guess if you really wanted to parse out the wording, in the recent Q, they use the words "treatment of sleep apnea," while in the earlier Annual Report, they say "a potential treatment for sleep apnea disorders." That is probably splitting hairs though, because it will continue to be a 'potential' treatment until the final marketing approval.
Ombow-Based on your excerpt from the Quarterly, what was the difference in language? The only difference I see is that they condensed the SA comment into fewer words than they had in the earlier Annual Report. Either way, they are not sending hidden messages about what they know regarding the SA study in their explanation. If anything can be gleaned from this, they know it wasn't really positive, but because nothing is public, they must keep that carrot dangling...
In regards to the game last night--I didn't see it. However, I am glad that the Heat are not invincible--I enjoy seeing other teams rise to the occasion and persevere. It bothers me that they put this team together, not that I've been following basketball much in the last decade (I used to thoroughly enjoy the 76'ers in the Charles Barkley/Hersey Hawkins era). To seek out such dominance, in my mind, is the wrong formula for success. I like good, old-fashioned, well-rounded competition--that is what makes things consistently exciting/entertaining. In other words, it isn't all it's cracked up to be to build a Dream Team. This is the sports equivalent to too big to fail-just like the Yankees. It brings me satisfaction when nimbler teams with bigger hearts (as opposed to bigger egos) outlast the talent-heavy favorites.
Ombow-This has been the language Cortex has used since the Biovail deal, perhaps for the sake of clarity, due to the close relationship with RD (via the respiratory pathway). Also, since SA has not been part of their historical focus, they felt it was necessary to delineate SA from the other carrots. Here is a portion of the Annual report in April:
.