Trent Perrotto
Headquarters, Washington
202-358-0321
trent.j.perrotto@nasa.gov

Nov. 10, 2010

MEDIA ADVISORY : M10-157

NASA Announces Televised Chandra News Conference

WASHINGTON -- NASA will hold a news conference at 12:30 p.m. EST on Monday, Nov. 15, to discuss the Chandra X-ray Observatory's discovery of an exceptional object in our cosmic neighborhood.

The news conference will originate from NASA Headquarters' television studio, 300 E St. SW in Washington and carried live on NASA TV.

Media representatives may attend the conference, join by phone or ask questions from participating NASA locations. To RSVP or obtain dial-in information, journalists must send their name, affiliation and telephone number to Trent Perrotto at: trent.j.perrotto@nasa.gov by 10 a.m. EST on Nov. 15. Reporters wishing to attend the conference in-person must have a valid press credential for access. Non-U.S. media also must bring passports.

Scientists involved in the research will be available to answer questions. Panelists providing analysis of the research include:
- Jon Morse, director, Astrophysics Division, NASA Headquarters in Washington
- Kimberly Weaver, astrophysicist, NASA's Goddard Space Flight Center, Greenbelt, Md.
- Alex Filippenko, astrophysicist, University of California, Berkeley

For NASA TV streaming video, downlink and further information, visit:
http://www.nasa.gov/ntv

For more information about NASA's Chandra X-ray Observatory, visit:
http://www.nasa.gov/chandra

http://chandra.harvard.edu

- end -

That's why all politicians are basically retards.

Yes, I am very curious just what they will have to say, how they will phrase it, how much of truth will they tell? any? This could be very significant if we can just parse out the real meaning.....

Lynnwood
GT Truther


Joined: Mon May 04, 2009 4:57 pm
Posts: 589
Re: The Golden Thread, Volume 5.7 2010


A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562334/


Quote:
Abstract

Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients as well as reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.


Sun Nov 14, 2010 8:22 am

emeraldsun
Senior Member

member is offline




There are no sides on a round world




Joined: Feb 2009
Gender: Female
Posts: 439
Karma: 28 Re: Science News Thread
« Reply #260 Yesterday at 8:20pm »

--------------------------------------------------------------------------------
A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology


Lisa M. Eubanks,† Claude J. Rogers,† Albert E. Beuscher, IV,‡ George F. Koob,§ Arthur J. Olson,‡ Tobin J. Dickerson,† and Kim D. Janda†
Departments of Chemistry, Immunology, Molecular Biology, Molecular and Integrated Neurosciences Department (MIND), The Skaggs Institute for Chemical Biology, and Worm Institute for Research and Medicine (WIRM), The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037. Email: kdjanda@scripps.eduCorresponding author.
†Departments of Chemistry and Immunology, The Skaggs Institute for Chemical Biology, and Worm Institute for Research and Medicine (WIRM)
‡Department of Molecular Biology
§Molecular and Integrated Neurosciences Department (MIND)

(snip)





ABSTRACT




Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. Consequently, the development of treatments that slow or halt the disease progression have become imperative to both improve the quality of life for patients as well as reduce the health care costs attributable to Alzheimer's disease. Here, we demonstrate that the active component of marijuana, Δ9-tetrahydrocannabinol (THC), competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation, the key pathological marker of Alzheimer's disease. Computational modeling of the THC-AChE interaction revealed that THC binds in the peripheral anionic site of AChE, the critical region involved in amyloidgenesis. Compared to currently approved drugs prescribed for the treatment of Alzheimer's disease, THC is a considerably superior inhibitor of Aβ aggregation this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.Keywords: Cannabinoids, Alzheimer's disease, Acetylcholinesterase Other Sections▼


AbstractIntroductionExperimental SectionResults and DiscussionConclusionReferencesIntroduction

Since the characterization of the Cannabis sativa-produced cannabinoid, Δ9-tetrahydrocannabinol (THC) (Figure 1), in the 1960's,1 this natural product has been widely explored as an anti-emetic, anti-convulsive, anti-inflammatory, and analgesic.2 In these contexts, efficacy results from THC binding to the family of cannabinoid receptors found primarily on central and peripheral neurons (CB1) or immune cells (CB2).3 More recently, a link between the endocannabinoid system and Alzheimer's disease has been discovered4 which has provided a new therapeutic target for the treatment of patients suffering from Alzheimer's disease.5 New targets for this debilitating disease are critical as Alzheimer's disease afflicts over 20 million people worldwide, with the number of diagnosed cases continuing to rise at an exponential rate.6,7 These studies have demonstrated the ability of cannabinoids to provide neuroprotection against β-amyloid peptide (Aβ) toxicity.8-10 Yet, it is important to note that in these reports, cannabinoids serve as signaling molecules which regulate downstream events implicated in Alzheimer's disease pathology and are not directly implicated as effecting Aβ at a molecular level.

Figure 1
Chemical structure of Δ9-tetrahydrocannabinol (THC).

Chemical structure of Δ9-tetrahydrocannabinol (THC).
One of the primary neuropathological hallmarks of Alzheimer's disease is deposition of Aβ into amyloid plaques in areas of the brain important for memory and cognition.11 Over the last two decades, the etiology of Alzheimer's disease has been elucidated through extensive biochemical and neurobiological studies, leading to an assortment of possible therapeutic strategies including prevention of downstream neurotoxic events, interference with Aβ metabolism, and reduction of damage from oxidative stress and inflammation.12 The impairment of the cholinergic system is the most dramatic of the neurotransmitter systems affected by Alzheimer's disease and as a result, has been thoroughly investigated. Currently, there are four FDA-approved drugs that treat the symptoms of Alzheimer's disease by inhibiting the active site of acetylcholinesterase (AChE), the enzyme responsible for the degradation of acetylcholine, thereby raising the levels of neurotransmitter in the synaptic cleft.13 In addition, AChE has been shown to play a further role in Alzheimer's disease by acting as a molecular chaperone, accelerating the formation of amyloid fibrils in the brain and forming stable complexes with Aβ at a region known as the peripheral anionic binding site (PAS).14,15 Evidence supporting this theory was provided by studies demonstrating that the PAS ligand, propidium, is able to prevent amyloid acceleration in vitro, whereas active-site inhibitors had no effect.16 Due to the association between the AChE PAS and Alzheimer's disease, a number of studies have focused on blocking this allosteric site.17 Recently, we reported a combined computational and experimental approach to identify compounds containing rigid, aromatic scaffolds hypothesized to disrupt protein-protein interactions.18-20 Similarly, THC is highly lipophilic in nature and possesses a fused tricyclic structure. Thus, we hypothesized that this terpenoid also could bind to the allosteric PAS of AChE with concomitant prevention of AChE-promoted Aβ aggregation.

Other Sections▼
AbstractIntroductionExperimental SectionResults and DiscussionConclusionReferencesExperimental SectionDocking procedures


THC was docked to the mouse AChE structure (PDB ID code 1J07) using AutoDock 3.0.5.21 Twenty docking runs (100 million energy evaluations each) were run with a 26.25 Å × 18.75 Å × 26.25 Å grid box with 0.375 Å grid spacing. This grid box was designed to include regions of both the catalytic site and the peripheral anionic site. Otherwise, standard docking settings were used for the AutoDock calculations, as previously detailed.18Acetylcholinesterase inhibition studies
All assays were performed using a Cary 50 Bio UV-visible spectrophotometer using an 18-cell changer, and conducted at 37 °C, using a Cary PCB 150 Water Peltier System. Solutions of acetylthiocholine iodide (ATCh iodide) and 5,5′-dithio-bis-(2-nitrobenzoic) acid (DTNB) were prepared according to the method of Ellman, et al.22 Stock solutions of acetylcholinesterase from E. electricus were prepared by dissolving commercially available enzyme in 1% gelatin. Prior to use, an aliquot of the gelatin solution was diluted 1:200 in water. For the assay, the solution was diluted until enzyme activity between 0.10-0.13 AU/min at 500 μM ACTh iodide was obtained. Compounds were prepared as solutions in methanol.Assays were performed by mixing AChE, THC, and 340 μM DTNB in 100 mM phosphate buffer, pH 8.0, containing 5% methanol. Solutions were incubated at 37 °C for five minutes before the reaction was initiated by the addition of ATCh iodide (75 – 300 μM). The increase of absorbance at 412 nm was monitored for 2 to 5 min. All assays were run in triplicate. Initial rates were determined by subtracting the average observed initial rate from the non-enzymatic reaction.Linear regression analysis of reciprocal plots of 1/νo versus 1/[S] for four THC concentrations was performed using Microsoft Excel software. The slope1/v was plotted against [I] to give Ki values. Propagation of error was performed to determine the error, ΔKi.For studies to determine the mutual exclusivity of THC and propidium iodide, experiments were performed identically to simple THC inhibition studies with a fixed concentration of ACTh iodide (125 μM), and varied concentrations of propidium iodide (0-25 μM) and THC (0-15 μM).

CONTINUED AND LINK HERE: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562334/
Link to Post - Back to Top Logged

--------------------------------------------------------------------------------

All we have is each other....

I got woken up by my cat so I looked up the NASA announcement. They discovered the youngest nearby blackhole, only 30 years old and 50 million light years away.
Interesting enough story for astronomy boffins but it doesn't really seem like the amazing discovery of something in our galactic neighbourhood they were making it out to be. It feels like they did it for people like us, hinting that some of them want to announce what they know about Planet X but they just can't do it.

http://halfpasthuman.com/ukemiarts.html
It's important that we understand 'tipping points'
It's the equivalent of a thousand flapping butterflies ricocheting in the reality-sphere, only to be obvious later as the waves of reality affect everything.
What could it be??? Releasing of long-term prisoners - er No - Not powerful enough for 1 event..., but wake-up call???
The realisation that some EU countries have been financially betrayed by the EU - Ireland/Portugal\Greece et al have definitely been betrayed - damn that 'Lisbon Treaty'
The slowly-but surely waking-up of the ripped-off masses (who STILL want to bury their stupid heads in X-Factor et al) however they are slowly slowly waking up.... just one more tax - just one more poisoning - just one more neglect of health...

Avid x

I have noticed an unusual glow from the moon recently. Is some nearby object casting infrared, ultraviolet, or other unseen light on the moon? Could the moon's surface be reacting to this light much the same as a black-light reacts with some surfaces?
Is the moon and/or earth shifting it's angle, or changing tilt of it's axis?

Our moon Luna:

Caption Said: