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Derrick Nunnally
How to protect privacy in the digital age: a constitutional amendment
Originally published April 14, 2015 at 5:01 pm Updated April 20, 2015 at 11:57 am
Seattle Times illustration
It's time to reassess the balance between privacy and security.
Alex Alben
Special to The Times
WE live under surveillance. In our homes. In our offices. In our public spaces. With the widespread deployment of GPS devices, digital networks and global satellites, our digital footprints are tracked and recorded to a degree we never anticipated and can't completely understand.
Even before Edward Snowden exposed the National Security Agency's clandestine programs to intercept large amounts of our phone calls and emails, we had ceded ground to local police, whose cameras track us both in public spaces and as our vehicles move in traffic. Even before the Patriot Act and creation of toothless Foreign Intelligence Surveillance Act courts, we had ceded too much liberty in favor of theoretical increases in security. And even before the transition to new mobile devices such as smartphones, our data were too vulnerable and too exposed.
It is time to reassess the balance between privacy and security in our laws and our culture and give the public a powerful new legal tool to protect personal data, especially with respect to the communication devices and digital networks that we have come to rely upon.
While most Americans assume that "privacy" is a long-standing legal concept enshrined in the U.S. Constitution, they are, in fact, mistaken. The Founding Fathers drafted amendments in the Bill of Rights that cover a very limited scope of protection of personal space. The Third Amendment prevents the government from quartering troops in our homes, which was a major concern after British colonial rule. The Fourth Amendment seeks to create zones of security in our persons and papers "against unreasonable searches and seizures" and introduces the concept of "probable cause" before judges can issue warrants.
Alex Alben is an author and technology policy expert. He lives in Seattle and currently lectures on privacy in the digital age for Humanities Washington.
Apart from these protections ratified in December of 1791, federal law has only haltingly moved to protect personal privacy. A hodgepodge of 20 federal statutes protect narrow slices of private information, ranging from health-care information (HIPAA) to the Children's Online Privacy Protection Act to the Video Privacy Protection Act of 1988, which was prompted by embarrassing disclosures of Judge Robert Bork's personal video rentals during his Supreme Court nomination hearing. Congress has chartered several federal agencies, such as the Federal Trade Commission, to enforce consumer protection.
Not until 1965 did Supreme Court Justice William O. Douglas find a "right to privacy" inherent in the "penumbra" of the Constitution. And it wasn't until last year that the Supreme Court, by a unanimous 9-0 ruling, declared in Riley v. California that the police cannot search an individual's cellphone during an arrest without first obtaining a warrant.
This particular case arose when San Diego police seized a man's cellphone at a traffic stop and searched it both on the scene and at the police station, gleaning information that linked him to a gang-related shooting. Writing for the court, Chief Justice John Roberts stated about mobile phones: "With all they contain and all they may reveal, they hold for many Americans 'the privacies of life.' "
Given the accelerating pace of technical change and the collection of information — by government at local, state and federal levels — our personal data will be placed at growing risk for the foreseeable future. With the advent of drones and Google Glass and ubiquitous video cameras, we can't even imagine what mashup of recording devices and databases will next threaten our "privacies of life."
Our state and federal courts should not have to infer privacy rights derived from the Third or Fourth amendments, nor be limited to making narrow rulings based on narrow precedents. Isn't it time, 223 years after the original Bill of Rights, to emphatically establish the protection of the privacy of American citizens as a starting principle for our law and civil society?
In short, the abuses of power of the federal government and the unrestrained data-collection practices of modern culture argue for a new amendment to the Constitution that explicitly protects our privacy. With privacy as a starting point, courts and legislatures could then evaluate public-safety and national-security exceptions to a general pro-privacy bias. The onus, in short, should be on government to prove its right to our personal data and not on citizens to attempt to stop complex and rampant data-interception practices.
Our Bill of Rights was not perfect and our Constitution has required amendments of various degrees of gravitas over two centuries. First introduced in September of 1789 as part of the Bill of Rights package, the most recent amendment — pertaining to congressional salaries — was not ratified until 1992. Given the new consensus around privacy rights and the accelerating pace of technical change, we should ask our members of Congress to secure the two-thirds votes of both the U.S. House and Senate to propose an amendment to the Constitution to safeguard privacy as a first principle of American law.


The Americans for Prosperity are hosting a Get Out the Vote Phone Bank to encourage voters in House District 50B to go to the polls on February 9. There is a Special Election to fill a MN House seat in that district. This is an opportunity to get our Republican voters out and elect a Republican!
Randy Sutter will be participating in the Phone Bank effort. Let him know if you're interested in helping out by emailing "Randy@sd49gop.com".


American Girl has been making adorable dolls with inspiring stories for over three decades now — from Felicity to Molly to Samantha. They each hail from different parts of the country, different moments in time, and in many ways, very different worlds; but until now, all of the dolls had one thing in common: They were girls. According to the company's website, though, that's all about to change — American Girl will release its first boy character doll this Thursday, February 16.
His name is Logan Everett, and honestly, he couldn't be a more welcome addition.
As for Logan's backstory? He's a drummer from Nashville, Tennessee, who plays alongside his friend Tenney Grant, a singer-songwriter. He's pretty stylish, too — with his laid-back button-down shirt and cool graphic tee.
But the real reason why Logan's entrance into the collection is so significant is because in his own small way, he helps shatter the longstanding stereotype that "dolls are just for girls" — and that's huge.
While some may note that American Girl did technically introduce a boy in 2003 with the "Bitty Twins" (who were retired last year), Logan is the first full-sized boy character to be sold on his own, and come with a backstory just like the original American Girls.
Logan's addition is actually just the first step in American Girl's mission to diversify its collection — in fact, the company will be releasing many more diverse dolls this year, including Gabriela McBride, an African American girl who manages her stutter with poetry, Z Yang, a Korean-American character, and later this year, a historical Hawaiian character named Nanea.
Additionally, they will be reintroducing Felicity — one of the original American Girl dolls.
We're sure Logan will be very welcomed into the arms of both little girls and boys this year — making playtime more fun for everyone.


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The Executive Centre Calls Off $750M Sale Amid Hong Kong Unrest
"Business" class at The Executive Centre's Three Garden Road location in Hong Kong
Just days before final bids were due to be received in a proposed sale of The Executive Centre, the shareholders of the Hong Kong-based shared office provider have halted the sale, according to a statement received by Mingtiand from the company.
HPEF and CVC Capital Partners, together with the company's management, have made the decision over fears that the value of the company's business could be affected by political tumult in Hong Kong, where The Executive Centre has ten of its 130 locations.
The announcement by The Executive Centre puts an indefinite hold on what was reported to be a $750 million transaction, and comes as the We Company, the parent firm of shared office giant WeWork, has cut its valuation by around 58 percent as it struggles to launch an IPO in the US.
Paying for Hong Kong's Tumult
The Executive Centre said in its statement that Hong Kong accounts for 30 percent of its earnings before interest, tax, depreciation and amortization, which for the business as a whole is on track to achieve $46 million this year.
"While the shareholders have decided to pause the sale process at this time, Hong Kong remains one of The Executive Centre's core markets," said The Executive Centre's founder and CEO, Paul Salnikow. "We are the clear market leader, as evidenced by our continued strong performance and growth momentum, and our strategy to further expand in the market remains unchanged."
The decision to pause the sale, which was first reported by Reuters, delays a months-long process which was slated for completion in late September. Hong Kong's Retail Management Association has said that most retailers saw sales plunge by 50 percent last month, while ongoing protests are expected to pitch the city into a recession.
The company now says it will consider recommencing the sale once the city's politics stabilise. A number of parties which had progressed to the final round of the sale process, continue to express a strong interest in acquiring The Executive Centre, according to the company.
Bids Due in Late September
Hong Kong-based HPEF Capital Partners, which was formerly HSBC Private Equity, owns 70 percent of the shared office operator, while Luxembourg-based CVC Partners owns a further 20 percent, with the remaining ten percent held by CEO Paul Salnikow, who founded the company in 1994.
TEC founder Paul Salnikow still sees Hong Kong as a core market
The company has carved a niche for itself in the crowded flexible office market as a luxury alternative catering to a clientele more interested in 5-star amenities than exposed brick. The Executive Centre's facilities offer tenants plush leather sofas and private suites in place of the free-flow beer, ping pong tables and shared sofas made popular by WeWork and its imitators.
Reports that WeWork is likely to reduce the valuation of its planned IPO to under $20 billion, after initially gunning for $47 billion, or even shelve the offering altogether, would also have created a more challenging environment for other companies marketing shared office opportunities.
Although the sale price, or any interested parties, have not been made public, sources cited by The Financial Times just over four months ago indicated that the deal could value the company at $750 million.
Hong Kong Income Rises Despite Protests
Recent events in Hong Kong have begun to put pressure on the office leasing market in a city that has seen continual rent increases and tight office vacancy for the past decade.
Office vacancy in Central – where The Executive Centre operates locations in One IFC Hong Kong, Three Garden Road and The Hong Kong Club Building – hit a ten-year high in July.
The continual rise in office demand in Hong Kong, and the other Asian urban hubs where The Executive Centre focuses its business has been kind to the serviced office provider.
The company had a turnover of $200 million last year, according to Salnikow, who also said last year that the company had grown at a rate of 20 percent annually over the past ten years.
Despite a slowing Hong Kong economy in 2019 and the protests that have rocked the city since June, This year, The Executive Centre's revenue up to August increased 27 percent in Hong Kong compared with the same period last year, with revenue up 27 percent in July and 40 percent in August despite the protests.
Riding the Flexible Office Wave
Salnikow's The Executive Centre has been providing flexible space to corporates long before co-working operators started thinking of leasing desks to HSBC and AB Inbev.
Pitched as a high-end option geared towards multinationals and financial companies, the company has built a portfolio of 130 centres in 32 cities across Asia Pacific, setting itself up as the "business class" of share offices versus its "economy class" competition. That distinction allows The Executive Centre to charge a 50 percent premium over rival WeWork for its grade A offices in core locations, according to Salnikow.
As the latest sign of the impact of Hong Kong's turmoil on real estate investment in Hong Kong, the decision to pause the sale of the Executive Centre follows two months after logistics specialist ESR postponed a Hong Kong IPO expected to raise up to $1.24 billion, which the company said was due to market conditions.
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HK's Three Garden Road Gets New TEC Location as Shared Office Market Grows
Chinachem Sues Kr Space for HK$500M After HK Co-Working Lease Collapse
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WeWork Announces $2.9B Investment Platform with Ivanhoe, Rhone Group
Filed Under: Flexible Office Tagged With: daily-sp, Featured, flexible office, highlight, Hong Kong, Paul Salnikow, The Executive Centre

redpajama_set_name: RedPajamaCommonCrawl


UNISEX - Levi's Denim Jacket : Sturdy, rugged denim is something you can count on from us at TVT. You will find yourself wearing this wardrobe staple year-round. This piece features convenient inside pockets.
Previous Designer: Levi Strauss & Co.


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Exclusive – Helly Shah to unveil her poster of her debut feature film Kaya Palat at the prestigious Cannes film festival
Exclusive – Helly Shah to unveil her poster of her debut feature film Kaya Palat at the prestigious Cannes film festival
Actress Helly Shah has been massively followed for her impressive acting skills. She has been in the industry for almost a decade and has been a renowned name in daily soaps. Helly has been open for projects that would actually push her to a level where she can bring the best of her.
Helly was last seen in Ishq Mein Marjwan 2. Since the show going off air, Helly has given time to herself and was waiting to do something fresh and new roles.
One such came her way was Rahat Kazmi's feature film Kaya Palat. The film is directed by Shoaib Nikash Shah while the producer, writer and Co actor in the film is Rahat Kazmi, who has been known as a critically acclaimed filmmaker too and Cannes regular. We had learnt from the sources that Helly went into the skin of the character for her role in Kaya Palat. Previously in one of her interview, she stated that it is going to be a turning point for her career. Well her fans, too believe the same and are very much eager to see her do well.
The Cannes film festival would see the unveiling the poster of Kaya Palat. She will be seen alongside the writer, producer and actor of the film Rahat Kazmi and actor Tariq Khan. This will definitely be a proud moment to watch out as she makes a double debut in this.


Use 17th Avenue. 15th Ave may be closed or turned into a one way.
This is a one time situation due to construction and NDSU student move in. The Blues Fest is typically in late July but was moved to August due to the Fargo Air Show.


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→ Bioscience, Health & Nutrition
→ Supplements
Kava Kava for Anxiolysis and GABA-a Receptor Upregulation
Started by Raza , Aug 27 2012 06:09 PM
kava anxiety reverse tolerance gaba
#1 Raza
Location:Amsterdam
The big 'Treating Anxiety Safely and Effectively' thread blacklists Kava Kava as a Gabaergic which should result in counterproductive GABA-a receptor downregulation, but after finding multiple reports (for example, here) of sensitization (rather than the expected desensitization) over long term use I looked into this and beg to differ.
http://www.ncbi.nlm..../pubmed/7701051
Regional differences in the modulation of [3H] muscimol binding to GABAA receptor complexes by kavapyrones, compounds of the rhizome of the plant Piper methysticum which possess sedative activity, were demonstrated using membrane fractions obtained from target brain centers of kavapyrone action: hippocampus (HIP), amygdala (AMY) and medulla oblongata (MED), and from brain centers outside the main kavapyrone effects as frontal cortex (FC) and cerebellum (CER). The kava extract enhanced the binding of [3H] muscimol in a concentration-dependent manner with maximal potentiation of 358% over control in HIP followed by AMY and MED (main target brain centers). Minimal stimulation was observed in CER followed by FC. In contrast, apart from CER, the potency of kavapyrones was similar in the brain areas investigated with EC50 values ranging between 200 and 300 microM kavapyrones. Scatchard analysis revealed that the observed effects of kavapyrones were due to an increase in the number of binding sites (Bmax), rather than to a change in affinity. At a kavapyrone concentration of 500 microM the order of enhancement in Bmax was HIP = AMY > MED > FC > CER. When kavapyrones are included together with pentobarbital or HPO the two classes of compounds produced a more than additive, i.e., synergetic effect on [3H] muscimol binding. Our findings suggest that one way kavapyrones might mediate sedative effects in vivo is through effects on GABAA receptor binding.
http://home.caregrou...r_methystic.htm
Sedative and hypnotic effects: Kavalactones increase GABA receptor density in specific areas of rodent brain (especially hippocampus and amygdala) suggesting GABA-a receptor mediation of the sedative effects of kava, although earlier studies did not find GABA or benzodiazepine receptor binding. German EEG studies have confirmed the limbic structures, especially the amygdylar complex, mediate the sedative effects of kava
(Holm E, et al. Arzneimittelforschung 1991 Jul;41(7):673-683.)
So while Kava Kava extracts are well established to be gabaergics, it seems they aren't agonists at the GABA-a receptor so much as that they potentiate their signal through some other mechanism, either resulting in or as a result of increasing GABA-a receptor density.
I shouldn't have to add that this makes it an incredibly promising substance for the treatment of anxiety and insomnia; something that helps immediately and adds up positively over long term use.
The one nut left to crack is the hepatotoxicity issue reported from western use of Kava extracts. Wikipedia says this has only been known to happen from stem and leaf extracts, however, and that root extracts have a long history of safe use.
Edited by Raza, 27 August 2012 - 06:14 PM.
#2 Godot
Location:Chicago
Excellent find! I've enjoyed kava very much on occassion, but due to its fast effects always assumed its action on GABA was a direct agonism.
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).
I've also always intuitively imaged receptor up- and down regulation to be a gradual, long term process that you wouldn't really feel... but it's been coming back as a mechanism of action for various very noticeable effects, such as the immediate potentiation of various agonist drugs by NMDA antagonists causing downregulated receptors to regrow, and now perhaps as the MoA for Kava's relaxation. Receptorgenesis might be much quicker than you'd imagine.
#4 thegron
This is a very interesting find, thank you. I am going to look into this further.
#5 ScienceGuy
The big 'Treating Anxiety Safely and Effectively' thread blacklists Kava Kava as a Gabaergic which should result in counterproductive GABA-a receptor downregulation, but after finding multiple reports (for example, here) of sensitization (rather than the expected desensitization) over long term use I looked into this and beg to differ...
Raza,
Firstly, thank you for this... You have raised an EXCELLENT question regarding precisely what is KAVA KAVA's mechanism of action with regards to GABA RECEPTORS; and as such I have digged deeper into the matter and I have to agree that my perspective is not entirely accurate, and consequently you have caused me to change it.
However, upon review of the existing scientific evidence up to date, I find that I do not in fact entirely agree with you... wherein IMO either neither of us is correct or we both are... UGH? I hear you say?
Specifically the problem lies with the fact that whilst those two studies, which do indeed seem to report KAVA KAVA inducing UPREGULATION of the GABA RECEPTORS, specifically via INCREASING RECEPTOR DENSITY, there concomitantly exists just as many (if not more) studies that appear to demonstrate that KAVA KAVA is indeed a GABA RECEPTOR AGONIST.
To complicate matters even further I have found some additional studies that support your perspective.
Consequently, I have concluded that there exists CONFLICTING EVIDENCE and as such we simply cannot say for sure at the present time the full extent of precisely what is and is not KAVA KAVA's mechanism of action with regards to GABA RECEPTORS. Without a doubt more research is need.
I have a THEORY as to what is going on but hesitate to mention it since it is pure academic conjecture.
As as result, I humbly admit that I was mistaken in placing KAVA KAVA on the 'DEFINITELY TO BE AVOIDED' LIST within my TREATING ANXIETY SAFELY & EFFECTIVELY thread; wherein I will be moving it to the 'POSSIBLY WHAT IS SAFE & EFFECTIVE TO TAKE' LIST.
For you interest, here are the various conflicting studies, which to facilitate understanding I have grouped into what I deem 'POSITIVE', 'NEGATIVE' and 'NEUTRAL' with regards to reported effects on the GABA PATHWAY:
'POSITIVE' STUDIES:
This study reports that KAVALACTONES (A.K.A. KAVAPYRONES) from KAVA KAVA do not influence the GABAA RECEPTOR via interaction with the BENZODIAZEPINE RECEPTOR (N.B. BENZODIAZEPINE RECEPTORS are allosteric modulatory sites on the GABAA RECEPTORS):
Planta Med. 1998 Aug;64(6):504-6.
Influence of genuine kavapyrone enantiomers on the GABA-A binding site.
Boonen G, Häberlein H.
Department of Pharmaceutical Biology, Philipps-University, Marburg, Germany.
The influence of kavapyrones from Piper methysticum Forst. on the GABAA receptor was demonstrated using radioreceptor assays. Both the dienolide yangonin and the genuine enolide enantiomers (+)-kavain, (+)-dihydrokavain, (+)-methysticin, and (+)-dihydromethysticin enhanced the specific binding of [3H]bicuculline methochloride ([3H]BMC). The kavapyrones have been investigated at assay concentrations between 100 microM and 10 nM. (+)-Kavain, (+)-methysticin and (+)-dihydromethysticin showed maximal enhancements of 18% to 28% at a concentration of 0.1 microM, whereas a 100-fold concentration of (+)-dihydrokavain revealed a similar modulatory activity of 22%. In the presence of 1 microM yangonin an increase of about 21% of the specific [3H]BMC binding was observed. Desmethoxyyangonin did not alter the binding behavior of the GABAA-receptor. A structure comparison of desmethoxyyangonin and yangonin indicated that the aromatic methoxy group was of particular importance for the modulatory activity. In contrast, the substitution pattern of the aromatic ring did not influence the modulatory activity of the enolides in a decisive manner. A structure comparison of desmethoxyyangonin and (+)-kavain revealed that an angular lactone ring was an important structure requirement. Both the enolides and the dienolides did not inhibit the specific binding of [3H]flunitrazepan. Thus, the influence on the GABAA receptor was not based upon an interaction of these kavapyrones with the benzodiazepine receptor.
This study (IN VIVO and on HUMANS) found KAVA KAVA to be effective in treating non-psychotic ANXIETY; and reported no instance of WITHDRAWAL SYMPTOMS upon ceasing taking the KAVA KAVA:
Phytother Res. 2004 Apr;18(4):297-300.
Kava treatment in patients with anxiety.
Geier FP, Konstantinowicz T.
Geriatric Hospital Elbroich, Am Falder 6, 40589 Duesseldorf, Germany.
In several clinical trials, mainly conducted with a dose of 300 mg kava extract per day, kava has been employed successfully for the treatment of anxiety disorders. The goal of the placebo-controlled double-blind outpatient trial was to obtain more information on the dosage range and efficacy of a kava special extract WS 1490 in patients with non-psychotic anxiety. 50 patients were treated with a daily dose of 3 x 50 mg WS 1490 during a 4-week treatment period followed by a 2-week safety observation phase. In the active treatment group, the total score of the Hamilton anxiety scale (primary efficacy variable), showed a therapeutically relevant reduction in anxiety versus placebo (more than 4 points). In the secondary variables studied, HAMA 'somatic and psychic anxiety' subscales, the Erlangen anxiety, tension and aggression scale (EAAS), the brief personality structure scale (KEPS), the adjective checklist (EWL 60-S) and clinical global impressions scale (CGI), a trend in favour of the active treatment was detectable. [Kava extract] WS 1490 was well tolerated and showed a safety profile with no drug-related adverse events or post-study withdrawal symptoms. It can be concluded that the applied 150 mg WS 1490 per day is an effective and safe treatment of non-psychotic anxiety syndromes in the described population.
This study (IN VIVO and on HUMANS) reports that KAVA KAVA modulates the GABA PATHWAY without IMPAIRING COGNITION, which implies its mechanism of action is not that of full GABA RECEPTOR AGONIST:
Hum Psychopharmacol. 2011 Mar;26(2):102-11. doi: 10.1002/hup.1180. Epub 2011 Mar
Neurocognitive effects of kava (Piper methysticum): a systematic review.
LaPorte E, Sarris J, Stough C, Scholey A.
Brain Sciences Institute, University of Technology, Melbourne, Victoria, Australia. emma.laporte@live.com
RATIONALE: Kava (Piper methysticum) elicits dose-dependent psychotropic effects and thus may potentially deleteriously affect cognitive performance. Clinical trials have assessed the effects of kava on cognition, however, to our knowledge no systematic review has been conducted in this area.
OBJECTIVE: To systematically review the effects of kava on cognition, providing an analysis of the individual study's methodological quality, results and effect sizes.
METHODS: A systematic review was conducted of publications up to June 15th 2010, using the electronic databases MEDLINE, PsychINFO, CINAHL, Web of Science and The Cochrane Library. The search criteria involved kava and cognition related terms, e.g. memory and attention.
RESULTS: Ten human clinical trials met inclusion criteria (acute n = 7, chronic n = 3). One acute study found that kava significantly improved visual attention and working memory processes while another found that kava increased body sway. One chronic study found that kava significantly impaired visual attention during high-cognitive demand. Potential enhanced cognition may be attributed to the ability of kava to inhibit re-uptake of noradrenaline in the pre-frontal cortex, while increased body sway may be due to GABA pathway modulation.
CONCLUSIONS: The majority of evidence suggests that kava has no replicated significant negative effects on cognition.
Another study (IN VIVO and on HUMANS) that reports KAVA KAVA does NOT IMPAIR COGNITION, which again implies its mechanism of action is not that of full GABA RECEPTOR AGONIST; but found that KAVA KAVA usage ELEVATED LIVER ENZYMES demonstrating HEPATOTOXICITY (N.B. Whether or not KAVA KAVA is in fact HEPATOTOXIC is a whole other discussion, and this singular study is not conclusive proof of this and should not be taken as such):
Neuropsychopharmacology. 2003 Feb;28(2):389-96.
Saccade and cognitive function in chronic kava users.
Cairney S, Clough AR, Maruff P, Collie A, Currie BJ, Currie J.
Mental Health Research Institute of Victoria, Parkville, Victoria, Australia.
scairney@mhri.edu.au
Kava is an extract from the Piper methysticum Forst. f. plant that has been consumed in the Pacific islands for millennia and more recently, among indigenous populations, in northern Australia and throughout the Western world as an herbal medicine. Through alterations on neuronal excitation, kava induces muscle relaxation, anasthesia, and has anxiolytic properties. There have been several isolated reports of psychotic syndromes, severe choreoathetosis and possible seizures following kava use. However, there is no conclusive evidence that kava interferes with normal cognitive processes. We tested a group of current, ex, and nonkava users among an indigenous population in northern Australia, using saccade and cognitive tests that have proven cross-cultural validity and are sensitive to subtle disruptions of the brain arising from substance abuse or neuropsychiatric illness. Despite collecting data from among the heaviest reported kava drinkers in the world, we found no impairment in cognitive or saccade function in individuals who were currently heavy kava users (and had been for up to 18 years), nor was there any impairment in individuals who had been heavy kava users in the past but had abstained for longer than 6 months. Current and ex-kava users showed a higher rate of kava dermopathy, lower body mass index, lowered blood lymphocytes and, in addition, current kava users showed elevated liver enzymes. While there has recently been increasing concern about potentially fatal liver damage attributed to kava use, we have found no evidence of brain dysfunction in heavy and long-term kava users.
These are added to the TWO STUDIES already posted by RAZA (Thank you!), which are as follows:
This study (whilst on RODENTS) reports that KAVA KAVA's GABAergic mechanism of action is due to UPREGULATION of the GABA RECEPTORS:
Psychopharmacology (Berl). 1994 Dec;116(4):469-74.
Kavapyrone enriched extract from Piper methysticum as modulator of the GABA
binding site in different regions of rat brain.
Jussofie A, Schmiz A, Hiemke C.
Institut für Physiologische Chemie, Universitätsklinikum Essen, Germany.
This study (whilst also on RODENTS) reports that KAVA KAVA's GABAergic mechanism of action is due to UPREGULATION of the GABA RECEPTORS:
Arzneimittelforschung. 1991 Jul;41(7):673-83.
The action profile of D,L-kavain. Cerebral sites and sleep-wakefulness-rhythm in
[Article in German]
Holm E, Staedt U, Heep J, Kortsik C, Behne F, Kaske A, Mennicke I.
Abteilung für Pathophysiologie, I. Medizinische Klinik Mannheim, Universität
Heidelberg, Mannheim.
EXTRACT FROM FULL TEXT:
Kavalactones increase GABA receptor density in specific areas of rodent brain (especially hippocampus and amygdala) suggesting GABA-a receptor mediation of the sedative effects of kava, although earlier studies did not find GABA or benzodiazepine receptor binding. German EEG studies have confirmed the limbic structures, especially the amygdylar complex, mediate the sedative effects of kava
'NEGATIVE' STUDIES:
This study refers to KAVA KAVA as being a GABA RECEPTOR AGONIST:
J Ethnopharmacol. 2005 Aug 22;100(1-2):108-13.
Potential for interaction of kava and St. John's wort with drugs.
Singh YN.
College of Pharmacy, South Dakota State University, Brookings, SD 57007, USA.
yadhu.singh@sdstate.edu
The present interest and widespread use of herbal remedies has created the possibility of interaction between them and pharmaceutical drugs if they are used simultaneously. Before the recent reports of apparent hepatotoxicity associated with its use, kava (Piper methysticum Forst. F.), was one of the top 10 selling herbal remedies in Europe and North America. This adverse effect was not previously encountered with the traditional beverage which was prepared as a water infusion in contrast to the commercial products which are extracted with organic solvents. Kavalactones, the active principles in kava, are potent inhibitors of several of the CYP 450 enzymes, suggesting a high potential for causing pharmacokinetic interactions with drugs and other herbs which are metabolized by the same CYP 450 enzymes. Furthermore, some kavalactones have been shown to possess pharmacological effects, such as blockade of GABA receptors and sodium and calcium ion channels, which may lead to pharmacodynamic interactions with other substances which possess similar pharmacological proprieties. St. John's wort (Hypericum perforatum L.), used extensively for the treatment of mild to moderate clinical depression, has long been considered safer than the conventional pharmaceutical agents. However, its ability, through its active constituents hypericin, pseudohypericin and hyperforin, to induce intestinal P-glycoprotein/MRD1 and both intestinal and hepatic CYP3A4 enzyme, could markedly reduce the distribution and disposition of their co-substrates. In addition, St. John's wort is a potent uptake inhibitor of the neurotransmitters serotonin, norepinephrine and dopamine all of which have a role in mood control. Consequently, the very real potential for a pharmacodynamic interaction between the herb and pharmaceutical drugs which share this mechanism of action and, like St. John's wort, are used for mood elevation. However, presently there is very little evidence to substantiate actual pharmacokinetic and/or pharmacodynamic interaction between drugs and kava or St. John's wort. This review provides a brief overview of the existing data on interactions of kava and St. John's wort with pharmaceutical agents and as a result reveals the urgent need for detailed investigations to identify clinically significant interactions for these herbal remedies that have the potential to cause adverse effects.
This study (whilst IN VITRO and on RODENTS) indicates KAVA KAVA to exert AGONISM of the GABA-A RECEPTOR specifically, but not the GABA-B RECEPTOR:
Planta Med. 2002 Dec;68(12):1092-6.
Kavalactones and dihydrokavain modulate GABAergic activity in a rat
gastric-brainstem preparation.
Yuan CS, Dey L, Wang A, Mehendale S, Xie JT, Aung HH, Ang-Lee MK.
Tang Center for Herbal Medicine Research, The Pritzker School of Medicine,
University of Chicago, Chicago 60637, USA. cyuan@midway.uchicago.edu
Using an in vitro neonatal rat gastric-brainstem preparation, the activity of majority neurons recorded in the nucleus tractus solitarius (NTS) of the brainstem were significantly inhibited by GABA A receptor agonist, muscimol (30 microM), and this inhibition was reversed by selective GABA A receptor antagonist, bicuculline (10 microM). Application of kavalactones (300 microg/ml) and dihydrokavain (300 microM) into the brainstem compartment of the preparation also significantly reduced the discharge rate of these NTS neurons (39 % and 32 %, respectively, compared to the control level), and this reduction was partially reversed by bicuculline (10 microM). Kavalactones or dihydrokavain induced inhibitory effects were not reduced after co-application of saclofen (10 microM; a selective GABA B receptor antagonist) or naloxone (100 nM; an opioid receptor antagonist). Pretreatment with kavalactones (300 microg/ml) or dihydrokavain (300 microM) significantly decreased the NTS inhibitory effects induced by muscimol (30 microM), approximately from 51 % to 36 %. Our results demonstrated modulation of brainstem GABAergic mechanism by kavalactones and dihydrokavain, and suggested that these compounds may play an important role in regulation of GABAergic neurotransmission.
This study also indicates that KAVA KAVA is a GABA-A RECEPTOR AGONIST:
CNS Drugs 2002;16(11):731-43.
Therapeutic potential of kava in the treatment of anxiety disorders.
Singh YN, Singh NN.
College of Pharmacy, South Dakota State University, Brookings, South Dakota 57007, USA. yadhu_singh@sdstate.edu
Anxiety disorders are among the most common psychiatric disorders that affect all age groups of the general population. Currently, the preferred treatment is with pharmacological drugs that have antidepressant or anti-anxiety properties. However, these agents have numerous and often serious adverse effects, including sedation, impaired cognition, ataxia, aggression, sexual dysfunction, tolerance and dependence. Withdrawal reactions on termination after long-term administration are also a major limiting factor in the use of these agents. Herbal remedies, including kava (Piper methysticum), have been shown to be effective as alternative treatments, at least in mild to moderate cases of anxiety. Kava is a social and ceremonial herb from the South Pacific. It is available in the west as an over-the-counter preparation. Its biological effects, due to a mixture of compounds called kavalactones, are reported to include sedative, anxiolytic, antistress, analgesic, local anaesthetic, anticonvulsant and neuroprotective properties. The pharmacological properties of kava are postulated to include blockade of voltage-gated sodium ion channels, enhanced ligand binding to gamma-aminobutyric acid (GABA) type A receptors, diminished excitatory neurotransmitter release due to calcium ion channel blockade, reduced neuronal reuptake of noradrenaline (norepinephrine), reversible inhibition of monoamine oxidase B and suppression of the synthesis of the eicosanoid thromboxane A(2), which antagonises GABA(A) receptor function. Clinical studies have shown that kava and kavalactones are effective in the treatment of anxiety at subclinical and clinical levels, anxiety associated with menopause and anxiety due to various medical conditions. Until recently, the adverse effects attributed to kava use were considered mild or negligible, except for the occurrence of a skin lesion. This disorder, called kava dermopathy, occurs only with prolonged use of large amounts of kava and is reversible on reduced intake or cessation. Rare cases of interactions have occurred with pharmaceutical drugs that share one or more mechanisms of action with the kavalactones. In the past few years, about 35 cases of severe liver toxicity associated with kava intake have been reported in Europe and the US. However, a direct causal relationship with kava use has been difficult to establish in the majority of the cases, and there is insufficient evidence to implicate kava as the responsible agent. Nevertheless, until further research clarifies any causality, kava should be used with caution.
This study (whilst IN VITRO but on HUMANS) also indicates that KAVA KAVA is a GABA-A RECEPTOR AGONIST:
Planta Med. 2001 Jun;67(4):306-11.
Interaction of various Piper methysticum cultivars with CNS receptors in vitro.
Dinh LD, Simmen U, Bueter KB, Bueter B, Lundstrom K, Schaffner W.
Institute of Pharmaceutical Biology, University of Basel, Witterswil, Switzerland.
Methanolic leaf and root extracts of the Hawaiian kava (Piper methysticum Forst.) cultivars, Mahakea, Nene, Purple Moi and PNG, were tested on binding affinities to CNS receptors including GABAA (GABA and benzodiazepine binding site), dopamine D2, opioid (mu and delta), serotonin (5-HT6 and 5-HT7) and histamine (H1 and H2). HPLC analysis was carried out in order to determine the amount of the main kavalactones kavain, 7,8-dihydrokavain, methysticin, 7,8-dihydromethysticin, yangonin and 5,6-demethoxyyangonin. The most potent binding inhibition was observed for leaf extracts to GABAA receptors (GABA binding site) with IC50 values of approximately 3 micrograms/ml, whereas root extracts were less active with IC50 values ranging from 5 micrograms/ml (Nene) to 87 micrograms/ml (Mahakea). Since the leaf extracts generally contained lower amounts of the kavalactones than the root extracts, there might exist additional substances responsible for these activities. Leaf extracts also inhibited binding to dopamine D2, opioid (mu and delta) and histamine (H1 and H2) receptors more potently than the corresponding root extracts with IC50 values ranging from 1 to 100 micrograms/ml vs. > or = 100 micrograms/l, respectively. Significant differences in the potential of binding inhibition were also observed between cultivars. Binding to serotonin (5-HT6 and 5-HT7) and benzodiazepine receptors was only weakly inhibited by both root and leaf extracts of all four cultivars. In conclusion, our investigation indicates that the GABAA, dopamine D2, opioid (mu and delta) and histamine (H1 and H2) receptors might be involved in the pharmacological action of kava extracts. Since the cultivars contained similar amounts of kavalactones, while their pharmacological activities differed markedly, other constituents may play a role in the observed activities. Additionally, leaves generally exhibited more potent binding inhibition than roots, therefore leaf of P. methysticum might be an interesting subject for further pharmacological studies.
'NEUTRAL' STUDIES:
This study (whilst IN VITRO but on HUMANS) in my opinion pretty much 'hits the nail on the head' so to speak, in that it reports that the scientific evidence supporting whether or not KAVA KAVA is a GABA RECEPTOR AGONIST is conflicting:
Altern Med Rev. 1998 Dec;3(6):458-60.
Piper methysticum (kava kava).
[No authors listed]
Piper methysticum (kava kava) is a plant native to the Pacific Island region, and has been used ceremonial for thousands of years. The active ingredients are a group of substances know as kava lactones (AKA kava pyrones). Four lactones in kava have been found to have significant analgesic and anesthetic effects via non-opiate pathways. Kava's most popular application is as a natural anxiolytic, comparing favorably in several studies to a number prescription medications, including benzodiazepines. CNS effects seem to be mediated by several mechanisms. Studies have been conflicting regarding its GABA-receptor-binding capacity, although this has been found to occur in some studies. In vitro kava has been found to block norepinephrine uptake. It also has some anti-convulsant capabilities, which appear to be mediated by Na+ channel receptor sites. The therapeutic dosage is in the range of 50-70 mg kava lactones three times daily. The most common side effect, usually seen only with long-term, heavy usage of the herb, is a scaly skin rash called "kava dermopathy." It has also been know to potentiate other medications such as barbiturates and Xanax.
WellResearched x 2
Pointless, Timewasting x 1
#6 adamh
My non scientific hunch here is that the op is correct in this statement
>So while Kava Kava extracts are well established to be gabaergics, it seems they aren't agonists at the GABA-a receptor so much as that they potentiate their signal through some other mechanism...
Could it be that kava potentiates the gaba a receptors rather than simply agnonizing them? I'm not talking about increasing gaba a receptors though it does seem to do that as well. I realize that without studies or a detailed phamacological explanation this will be seen by many of the more serious people as in the league of "fairies did it" rather than a serious theory.
The gaba receptors are agonized at all times to a low degree by natural chems in the body. They are not just there for in case some exogenous compound comes along to stimulate them. There must be natural way to clear these endogenous natural compounds same as chemical gaba a receptor agonists are cleared. Perhaps kava slows the clearing process and therefore causes the user to feel as though his/her gaba receptors were being stimulated when in actuality it was simply natural stimulation that was amplified by kava compounds which either increased the action of natural gaba a stimulation?
This would explain why it potentiates other gaba a agonizing compounds such as xanax or st john's. Kava lactones may act to simply "guide" receptor agonists into the correct site, as an alternative explanation for its effects
I'm not offering this as a fully developed theory, which it clearly is not. Rather as suggesting a different way of looking at the situation. We are conditioned to think a chemical must either agonize or antagonize a receptor if it has an effect on it. We are familiar with the concept of potentiation but usually think of it as additive such a when a receptor agonist adds to the effect of another agonist. I'm thinking it neither agonizes or antagonizes directly but instead potentiates indirectly. This would explain why it does not lead to down regulation as all other receptor agonizers seem to do.
Hey ScienceGuy! Glad to finally engage you on this topic.
No 'ugh', it's a complex matter. I'm not seeing any methodological shortcomings in these studies (would be difficult without the full texts), so for now, I'm assuming that all of them are correct and the information simply needs to be consolidated between them.
Leading from that, I stand by my assessment. I'll dig into the various 'negative' studies you posted below, because I think most of them don't contradict my proposed mechanism at all, but first and foremost I maintain that even if Kavalactones are GABA-A agonists, the direct observation of receptor upregulation trumps the hypothetical receptor downregulation from GABA-A Agonism. If both are true, this merely indicates that Kavalactones upregulate GABA-A receptors through a secondary mechanism that, at least at some doses, upregulates receptors more rapidly than its agonist downregulates them.
However, I don't think Kavalactones look to be a GABA agonist at this time.
]'NEGATIVE' STUDIES:[/u]
This one's a bit vague, since the blockage in question isn't part of this studies results, but rather a reference to a different study. However, I've read one study before that showed that Kavalactones competed with GABA-A agonists, showing reduced cumulative effects in the presense of both. This seems to be what they're talking about, and is the single most compelling piece of evidence for Kava as a GABA agonist... however, it is far from conclusive. All it really establishes is that it's influence on the GABA-A signal replaces and/or adds up with ordinary activation, rather than multiplying with it like benzos and barbituates do.
I do think that this is evidence that GABA-A receptor upregulation is not it's primary means of enhancing the GABA-A signal, since that would multiply or at least not compete with increased ligand availability.
It does not say that. All it says it that Kavalactones have a GABAergic mechanism, which is obvious at this point. They established this by showing the effect of Kavalactones to be partially reversible with a GABA-A antagonist, which would also be true for a positive alosteric modulator, or a receptor density increaser, or any other kind of GABAergic.
This study also doesn't call it a GABA-A agonist. What it does, is refer to Kava's mechanism of action to include "enhanced ligand binding to GABA-A receptors", which again would also be true for a positive alosteric modulator or a receptor density increaser.
I'm having some trouble making sense of this study's method - 'binding inhibition' at the GABA-A receptor? - but their conclusion is only that he GABA-A receptor is involved in its MoA, which again is well-established.
In my opinion, it's pretty clear that Kavalactones are either not agonists or some kind of atypical agonist/positive modulator at the GABA-A receptor. Everything added up, nobody seems to know how Kava works the GABA-A receptor, but the observed result is both immediate activation and receptor upregulation. The specifics of the mechanism aside, none of these studies contradict each other on that outcome, and I'll take that gratefully. =)
It definitely looks that way, and I don't think that's a "faeries did it" hypothesis at all. Benzos and bartituates, and positive alosteric modulators in general, are known to potentiate receptor signals without binding where the neurotransmitter itself would - and those generally cause downregulation of the receptor in question, they work in all sorts of different ways, setting plenty of presedent for unexpected mechanisms of action.
Hell, our best buddies the 'racetams all potentiate glutamate receptors without binding on them, and I've never heard of those downregulating any of them. Possibly even the contrary.
Slowing the clearing of natural GABA would make it a reuptake inhibitor, GABAtransaminase inhibitor, or something more esoteric among those lines. Wouldn't explain the receptor upregulation though, since those generally cause downregulation from increased exposure. We'd need an additional explanation for that, still.
And potentiating Xanax and barbituates, like that one study noted it to do, is entirely unsurprising. Benzos and barbituates are known to multiply with every other GABAergic except ones in their own categories (with which they add up with diminishing returns); this is a quality inherent to their effects, and therefore tells us nothing about Kava's.
Edited by Raza, 17 September 2012 - 12:20 AM.
Hi Raza,
Thank you for your detailed reply.
I stand by what I have already said about there currently being insufficient and conflicting information from published studies to date that prevents one from being able to conclusively ascertain precisely what is or is not the mechanism of action of KAVA KAVA in relation to the GABA SYSTEM.
I agree with some of what you say; however, I must point out that you are guilty of stating that KAVA KAVA UPREGULATES GABA RECEPTORS as if scientific FACT, when your basis is in fact simply two number RODENT STUDIES, which hardly qualifies as conclusive substantiated scientific evidence
Do you have any other scientific evidence to support the belief that KAVA KAVA UPREGULATES GABA RECEPTORS other than this? That would be the most persuasive evidence
Incidentally with the utmost respect, and please do not take this the wrong way, your argument with regards to KAVA KAVA possibly being a POSITIVE ALLOSTERIC MODULATOR of the GABAA RECEPTOR as opposed to full AGONIST is in fact irrelevant, since in both instances adminstration would be ill advised; wherein I am sure that you surely must realise that if KAVA KAVA were to be demonstrated to be a POSITIVE ALLOSTERIC MODULATOR of the GABAA RECEPTOR then this would mean it is akin to BENZODIAZEPINE DRUGS, and hence you whole argument would be self-defeating
It could be a partial agonist as one of the above studies mentions. From the research I have done on benzo PAWS, it seems as if partial agonists do not cause a lot of the same effects (i.e. cognitive dysfunction) as full agonists.
#10 ScienceGuy
I agree that this is probably the most likely scenario; however, IMO until there is published more conclusive research this is all sheer academic conjecture
#11 Raza
Thank you. M'enjoying the discussion, and the chance to revisit all this in detail.
I agree that the information available is insufficient to establish a MoA. I don't agree that it is conflicting; it merely doesn't fit any of the well-known kinds of receptor interaction. No study observations have conflicted with each other so far, they've merely conflicted with our expectations.
There are many anecdotal reports of human consumers of Kava experiencing reverse resistance (as in, increased sensitivity) to the stuff over periods of continued use. The receptor upregulation observed in rats explains this nicely, while nothing else I can think of could. I think that justifies generalizing the effect seen in rats to humans for individual practical purposes, even if it isn't scientific fact yet.
Well, yes and no. I agree that it doesn't much matter whether it is an agonist or a positive allosteric modulator, but not that either of these would make it ill-adviced to use when the usual problem with their use is uniquely reversed (except perhaps in that it might still be able to trigger relapse in previous GABA-A-ergic addicts because it feels the same). I'm just trying to make sense of what it is so as to reduce the confusion between studies delivering unexpected results.
And for what it's worth, Kava is clearly unlike benzos and barbiturates in that its effect adds up (with diminishing returns) alongside a regular agonist, rather than multiplying with it. If it is a positive allosteric modulator, it acts at a third and heretofore unknown site somewhere.
#12 deon10
Did all the studies use only kava extracts? or did some maybe use the ground root?
Maybe this is a factor worth looking into. I'm not as good as some people at reading the studies, but I know Kava from the root and from capsules seems to have different effects on some people.
#13 thegron
I thought that the extracts were from the root.
Yes they are.
But there are chances taking the actual root, ground, and preparing it through the traditional process, which is squeezing the powder in water and drinking the result, is different than popping a capsule with only kavalactones. It's like taking marijuana in capsules with just the active ingredients instead of using the actual weed.
I also noticed, from personal experience that many people don't react much to the capsules, but almost everybody reacts to the actual Kava.
I personally never tried the capsules, and went straight to the ground root. After the fifth day of use or so, i started feeling it, and I felt it goood! I didn't even try the strongest kava (there are different potencies).
Now... this might not be relevant to the OP's point... and maybe the studies all used capsules...
That is seriously interesting... Is the REVERSE TOLERANCE effect consistent for all users of KAVA KAVA?
I have come across instances wherein individuals have in fact reported the opposite... so I am wondering what might be going on here?
Of course, this is all academic speculation, but I would be very interested to hear more details regarding those anecdotal reports of the REVERSE TOLERANCE
Edited by ScienceGuy, 19 September 2012 - 08:21 PM.
Cheerful x 1
I wouldn't claim that. It gets reported regularly, though. Let me find you some quotes.
"Yes, you can definitely experience reverse tolerance. I have been drinking Kava for a couple years and definitely feel it more now than I have ever have."
"I actually use less than when I started. I get about the same or better effects from a smaller amount with more water."
"I have been a kava drinker for about a year now, recently a pretty heavy drinker. I only need 1 tbsp per cup of water for generally mild effects and 2 tbsp per cup of water for strong effects. This is a huge decrease in kava powder from say, two months ago when I would use 7 tbsp of kava per 2 cups of water. If my tolerance has done anything in the last few months, it has gone way, way down. To the point where I popped 2 Kona Kava Pill capsules this morning before meeting with a few counselors at university, and was totally mellowed out. Still am."
"I'd personally define the tolerance curve of kava as a camels humps type of curve. I notice there was an initial phase of working through the reverse tolerance where I had to consume fairly large amounts of kava to achieve even mild effects and then after around a month I began experiencing much more profound effects and started to taper my dosage down. Then I noticed a tolerance that began to build after using kava for a week consecutively where I would again have to increase my dosage to achieve desired affects. Basically now I try and session kava 4-5 days a week with a day or two in between so that my reverse tolerance stays intact but my dosage tolerance doesn't get high and I can still enjoy the effects of kava at quantities that are not excessive."
"I didn't feel kava's effects nearly as much as I do now when I first started using it."
All from the thread I linked in the OP, and others like it from the same forum. There's plenty more like 'em, too.
Lots of possible reasons for that. If Kava enacts two simultaneous, opposed influences on GABA-A receptor density (which it should if it is also an agonist/positive modulator), then the final result would most likely be dependent on dose/time, which is consistent with the reports I quoted above. Different ratios of the various Kavalactones and Kavapyrones in the product consumed also likely make a difference.
Mind, I think ordinary tolerance also builds because the liver upregulates the enzymes responsible for breaking down commonly consumed foreign substances, so the fact that tolerance to Kava catches up again at some rates of consumption might not mean that the receptor balance isn't still positive.
Edited by Raza, 24 September 2012 - 07:23 PM.
#18 Dark Vision
Location:Oxford
I have just ordered 75g of kava root extract standardised to 40% kavalactones. I will be using it daily in relatively small doses to combat social and general anxiety, both of which are at moderate levels. The dose I use will be whatever gives me a nice reduction of anxiety but without any decrease in motivation or ability to concentrate. Obviously this will take a bit of working out at first
I'll report back on tolerance - whether I develop tolerance or reverse tolerance. I do hope it will be the latter..
Cool. Keep us updated.
From the user accounts I've been reading, tolerance could go either way with daily use. Twice a week or so seems a safer bet for increasing sensitivity on the long run. But, find out for yourself - first hand accounts are more valuable than my guesswork from second hand information. =)
Might I suggest taking Milk Thistle with it once in a while, to protect your liver and normalize its enzymes? Kava's known for its liver load with regular use, even if the roots don't quite deserve to be called toxic, and it might even help reduce tolerance.
If I find that kava is effective and I want to take it regularly as an anxiolytic then I will certainly buy some milk thistle. I won't bother for this trial period though as milk thistle can have anxiolytic effects and could screw with my little experiment. I won't be trying to get high off the kava so hopefully my liver will be ok whilst I get through the 75g over the course of a couple of months or so.
I will continue to take Oxiracetam and CDP choline though as whilst I get a stimulating cognitive boost from this combo it has never relieved anxiety for me, or caused it. Oxi gave me a nice mood boost at first but this effect disappeared after a few days of use :(
Edited by Dark Vision, 24 September 2012 - 10:40 PM.
I received my package of kava kava today and have been trying to find a good dosage. It is a rather attractive pale yellow, soft powder. I initially took 500mg of the powder, washed down with water. I waited 1 hr 30 mins and nothing happened. I took another 500mg, again washed down with water. Again nothing after 1 hr 30. I did a bit of reading on the kava lounge forum and saw that people were saying it doesn't work so well on a full stomach. The kava arrived after lunch so I had just eaten. Empty stomach things are not great for me because I exercise a lot and am contantly ravenous, and when I get hungry I can't concentrate and feel nauseous. So I eat every 2 hours or so. I can never hold out long enough to let my stomach empty, the only conceivable time would be first thing in the morning and this is would only last me until lunchtime at best according to the reported 3-5 hours duration of kava's effects.
So I tried what I try with all empty stomach type drugs/supplements - sublingual administration. I used 250mg of powder for this and I just sat with it under my tongue for 15 mins. It tasted ok, not as bad as people say it is, certainly much nicer than bacopa. It made the underside of my mouth go numb, but this passed very quickly thankfully. I have definitely felt an effect with this method.. my usual mental state is an excess of nervous energy, my mind and body buzzes throughout the day. Hence all the excercise. With the kava I feel very energetic still but less nervous. No trouble concentrating or thinking. I do not feel high exactly, but there is a definite mood boost and my head feels clear. I can certainly imagine taking 3 times this dose causing mild euphoria though.
I don't really understand why eating kava on a full stomach would nullify its effects. Unless it's an amino acid you're taking like L-theanine, shouldn't having a full stomach just slow the effects of a drug? I'm fine with sublingual but I do worry about staining of my teeth, or even erosion if kava is acidic to any degree.
{edit} I plan to take the 250mg sublingual dose twice a day until the powder runs out. Just for today I'll take the second dose before bedtime as I want to see it's effects on sleep, and how I feel in the morning. In future I'll probably take it in the morning and late afternoon. I'll post occasional updates on the tolerance question. If I find I am getting a tolerence I ight consider increasing the dose slightly, but not much, and then I will keep on taking it for a fortnight to see if some sort of reverse tolerance kicks in. If it doesn't I will stop as I don't want to nuke my GABA receptors. My thanks to Raza for making this topic as kava does seem helpful at the moment, and I had always avoided it in the past because I just assumed it would cause eventual GABA downregulation.
Sublingual Kava - interesting! Bypassing first pass metabolism might be worthwhile for this stuff long-term, with the negative effects it has in the liver and the potential for resistance building there.
I don't really understand why eating kava on a full stomach would nullify its effects. Unless it's an amino acid you're taking like L-theanine, shouldn't having a full stomach just slow the effects of a drug?
To the best of my drug knowledge, mostly, yes. Bioavailability could be reduced for more gradually absorbed doses if the stuff is significantly metabolized by an enzyme not usually used up by food, though. Still, it's not unlikely that those 500mg oral doses might've been affecting you unnoticed. If your second 250mg sublingual dose doesn't work as well as the first, that's probably the reason.
I think bypassing the first pass through the liver certainly makes a difference to bio-availability, but I'm not sure it would reduce liver damage. The various chemicals in the kava are still entering the bloodstream and being processed by the liver, it's just that the liver receives them from your systemic circulation rather than the
hepatic portal system. The actual strain on the liver is still the same. For example taking shots of vodka and holding them in your mouth gets you drunk quicker and on less alcohol than actual ingestion but is no less harmful to the liver, which needs to clean up all the booze or you will never sober up.
True, the only gain is in the amount you need less for avoiding the liver in that first round (which is still very significant, if 250mg SL beats out 2x500mg PO).
But I think that drugs that cause liver strain, in the process of doing so, usually also increase the liver's capacity to metabolize them - thereby building resistance which needs to be overcome by higher doses, the difference of which ends up purely affecting the liver and so on. It escalates, and every milligram of substance that hits the liver without first getting anywhere else is a loss in that sense. Starting right off with SL doses might nip this in the bud, ending in a more favorable steady state.
Anyway, do you have any typical GABA-A agonists lying around? Like valerian, or even a (small dose of a) benzo? One test that would be good to do before you take any more Kava is to take a single small dose of an ordinary GABA-A agonist and measure the effects, before continuing on with the Kava plan. This would allow you, further into the Kava treatment, to repeat that dose and compare the effects to find out whether Kava reverse sensitization really translates to GABA-A signal potentiation in general, and if so allow you to test whether any subsequent Kava resistance is also an effect on receptor density or rather a metabolic thing that applies purely to Kava.
Ah yes of course, you are quite right. The only downside for SL then remains what it might do to teeth in terms of staining and enamel weakening. I can't find any info on kava's ph, and I don't have any litmus unfortunately.
That would be a very interesting test. I don't have any benzos and I don't have a source for them. Valerian I did have a bottle of once, but it had absolutely no effect on me even in high doses so I threw it out. I have a bottle of gotu kola that certainly has an obvious effect in high doses, feels like a GABA agonist. I use it very occasionally for impending stressful situations. I have no idea whether it effects GABA-A or GABA-B though, and I can't seem to find any info on this.
Gotu Kola looks to be a selective GABA-B agonist, from what I'm reading. Ah well.
Any general pro-gabaergics available then, like Theanine or Picamilon? Something selective for GABA-A would be preferable, but a test with one of these might still be better than nothing.
Is it difficult to keep it mostly away from your teeth?
I have some Kava at home and I own a pack of PH strips, but they're at a friend's, who just left for a two week vacation. I'll test it for you when I can, if it's still relevant by then. Although from what little I know about chemistry, lactones are kind of complex where pH is concerned...
For what it's worth, beverages are kava's traditional mode of ingestion, and a google search isn't turning up much for teeth stains from regular consumption of those. There's one result for stains from continuously chewing the roots. Personally, considering the evidence and how with SL dosing you're basically only risking staining the inside of your bottom front row (which is rarely visible), I wouldn't be worried about it.
#27 OpaqueMind
For you potential experiment of testing GABA-A receptor sensitization you can aquire some etizolam, a benzodiazepine analogue available legally over the internet. Just type it in google, there's a load of sites that sell it.
By the way Dark Vision, would you mind telling us what your kava source is? Thanks
A very good way to see if something stains teeth is to see if it stains a white ceramic mug. I'd forgotten about this. Eg. coffee tea and red wine all quickly stain a mug if you tip out the liquid and leave the residue to dry, whereas cocoa doesn't - the mug cleans back to shiny white. Will mix a little powder with hot water in a clean mug and see if I can get it to leave a mark. My hunch is it won't, the powder doesn't have a dye like appearence it looks and feels more like chickpea flower or something similar.
Think I will stay clear of ordering legal benzos online (I didn't know you could do this!) just because I don't want to set a precedent.. I have tried valium before and I love it so I'd rather not have a source for something similar without a prescription. I do have l-theanine though, and it does work on me if I haven't used it in a while (which I haven't). I'll take a 400mg dose later today. I know theanine releases GABA rather than agonizing a particular GABA receptor group, but it should give a decent idea later on if GABA-A is being up or downregulated. It's hardly scientific I know.
My source was this ebay auction. There seems to be a lot of this 40% extract available. It looks exactly like this stuff, which is maybe the same product - it all comes from alibaba I'm guessing, and the root source seems to be Vanuatu. Of course I can't say for sure that this stuff is safe and doesn't contain leaf and bark. Ideally I would like to buy kava root powder rather than extract, from a reputable source, but the UK ban means that this is not cheap. If I am impressed by kava at the end of this experiment then I will pay to have a load shipped from the US.
Ok, firstly I cannot get kava mixed with hot water to stain white ceramic. I don't think it's a strong dental enamel stain. No idea about acidity still.
The extract continues to have a moderate anxiolytic and mood boosting effect at the same dosage. I have noticed no increase or decrease in the effectiveness of each dose. However I am taking 3 of these doses now - 250mg in the morning, 250mg in the afternoon, and 250mg before bedtime. All sublingual. This is because whilst the stuff has very little sedative effect, the pre-bed dose helps me with a problem I've been having recently which is worrying about not being able to sleep, and therefore not being able to sleep. So the anxiety causes the insomnia and the anxiolytic cures it. Because there is little to no sedative effect this would not work if I was not already tired, as valium would for instance, and I have no trouble getting up in the morning after 7 hours of sleep. It has an odd influence on me in the morning - for three mornings in a row I have felt a sort of warm sense of excitement akin to when I was a kid around Christmas. It fades after a couple of hours. After this I take my morning dose, which does not give me this same feeling. The effect is so nice that I will continue with the night time dose.
I took l-theanine yesterday and just now. Both times I took it 2 hours after the last kava dose when it was starting to wear off. I took 400mg yesterday and 500mg today, sublingual both times as I had food in me. Does anybody know if l-theanine can be absorbed sublingually? I have had sedative effects once before off 500mg sublingual theanine but it could be placebo. There are sublingual amino acid products available online but they could be bullcrap of course. Anyway, both of these recent theanine doses did nothing really noticeable.
The only negative so far has been regarding excercise. Kava makes exercise unapealling, but only for 2 hours or so. After this I am good to go. I have experienced no nausea or other gastric symptoms perhaps because of the sublingual administration, although I do swallow the dose after 15 mins.
I am attending the premier of a film I worked on tomorrow. This would normally be a very stressful, though fun event for me. It will be interesting to see how well the kava helps me.
I know from experience that Theanine absorbs well sublingually. For purposes of the experiment, though, it would be best to take it while not under influence of Kava at all - the effects are competitive, and the Kava might be the reason why you don't feel any additional relaxation from the Theanine.
Have fun at your movie premiere!
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Also tagged with one or more of these keywords: kava, anxiety, reverse tolerance, gaba
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Ron Wilson '77 is the fourth Friar to be selected for induction into the U.S. Hockey Hall of Fame.
Ron Wilson '77, a two-time All-American at PC and a longtime NHL coach, was one of five individuals selected for induction into the U.S. Hockey Hall of Fame this fall.
Wilson, who coached with five NHL teams during 18 seasons, is the all-time winningest American NHL head coach with 648 victories. He also coached with Team USA nine times, including leading the U.S. to the bronze medal in the 2010 Olympic Winter Games as head coach.
Wilson played at PC from 1973-77 and still holds the school scoring record — and the NCAA record for defensemen — with 250 career points.
The PC Athletic Hall of Fame inductee is the fourth Friar to be chosen to the U.S. Hall of Fame, joining player and coach Lou Lamoriello '63 & '01Hon., player Cammi Granato '93 & '12Hon., and Richard Rondeau, a former head coach.
Led by the women's swimming and diving team and the women's tennis team with perfect rates of 1,000, 13 of PC's 17 intercollegiate sports teams exceeded the NCAA average of 981 in the Academic Progress Rate report for 2015-16, announced in May 2017.
The other 11 teams are women's soccer (997), women's track (995), women's cross country (995), women's basketball (994), softball (992), women's volleyball (990), field hockey (988), men's ice hockey (987), men's lacrosse (987), women's ice hockey (986), and men's basketball (984), which recorded its highest APR since the first reporting year of 2004-05.
The APR measures eligibility, graduation, and retention each term, with the 2015-16 figures encompassing rates from the 2012-13, 2013-14, 2014-15, and 2015-16 academic years.
Field hockey midfielder/forward Mikayla Michals '20 (Needham, Mass.) was named to the 2018 United States Under-21 Women's National Team. She was one of 19 student-athletes chosen.
Her selection at the conclusion of the U-21 Junior National Camp came following her performance at the USA Field Hockey Young Women's Championship. That competition featured more than 130 collegiate and post-collegiate athletes.
Michals appeared in 18 games for the Friars in her first season in fall 2016. She scored four points on two goals, including one in a 3-2 BIG EAST Conference overtime win against Georgetown. In fall 2017, she finished as the Friars' second-leading scorer with 12 points on five goals and two assists, helping the team to an 11-8 record and a berth in the semifinals of the BIG EAST Tournament.
Defender Jarrod Neumann '17, who began playing lacrosse in his senior year of high school, was selected in the Third Round and 25th overall by the Florida Launch in the Major League Lacrosse Draft in May. He is the program's highest draft choice ever.
A Second-Team All-American, a Scholar All-American, and a three-time BIG EAST First-Team all-star, Neumann helped lead PC to BIG EAST Tournament appearances in 2016 and 2017.


text:
Rock Daypop Archives
Former Molly Hatchet Frontman Jimmy Farrar Passes Away At 68
October 31, 2018	Rock Daypop
Jimmy Farrar, who sang with Molly Hatchet from 1980-82, has died at age 68. The news was confirmed by the band's bassist Tim Lindsey via Facebook, and a page specifically for fans of Molly Hatchet says Farrar
Kiss' 2019 'End of the Road' World Tour Dates Revealed
KISS have now announced the dates for their "End of the Road" world tour, that will kick off the first leg of the run in 2019. The tour will begin in Vancouver, British Columbia, taking place Jan.
Lamb of God's Mark Morton Says Project With Chester Bennington Will Be Released
According to a tweet from Lamb of God's guitarist Mark Morton, an unreleased project between himself and the late Chester Bennington will be released. A fan asked about the progress that was made on the project before Bennington's
Clutch Vocalist Hospitalized After Fainting, Band Cancels NY Show
Vocalist Neil Fallon from the band Clutch released a statement revealing that he suddenly fainted on Saturday, October 27th and was hospitalized after being found. He claims to have later been diagnosed with "near-syncope." The band canceled
Ronnie James Dio's Autobiography Anticipated To Be Released In 2020
The longtime manager and widow of Ronnie James Dio, Wendy Dio, is working with legendary rock journalist Mick Wall on the long-awaited autobiography of Ronnie. The book was 3/4 written before the singer's death back in 2010,
Vince Neil Announces The Completion Of Two New Mötley Crüe Songs
Mötley Crüe's Vince Neil has announced the completion of two songs for the film adaptation of the band's biography. The biopic, called "The Dirt – Confessions Of The World's Most Notorious Rock Band" has been picked up
Tool Reveals Summer 2019 European Tour Dates
Tool have announced a 2019 European tour, kicking off in June in Germany before wrapping up in Portugal in July. The Los Angeles band have not released a studio album since 2006's '10,000 Days' and it's long-awaited
Mastodon To Kick Off 2019 With New Tour
Mastodon have announced dates for tour in early 2019 in the UK and Europe. The band will play 25 shows starting in Belfast on January 14 before wrapping up in Lisbon, Portugal on February 17. General ticket
Def Leppard, Slipknot, And Tool Confirmed To Headline Download UK 2019
Def Leppard, Slipknot and Tool have been confirmed as the headline acts for the UK Download Festival 2019, taking place at Leicestershire's Donington Park on the weekend of June 14-16, 2019. Along with these headling acts, artists
Jeff Lynne's ELO Announce Summer 2019 North American Tour
Jeff Lynne's ELO will return to North America for a 20-date arena tour that will take place next summer. The band just finished up a very successful 10-date trek in August, and now the band's 2019 tour will


text:
Q: Android Studio Standalone GCM SDK I'm attempting to port my application for Android app that uses push notifications to the Blackberry.  Blackberry has instructions on how to get this working, but I'm stuck at the point where I need to use the Standalone GCM SDK in my project for it to work properly
http://developer.blackberry.com/android/apisupport/creating_push-enabled_android_apps.html
I'm doing my Android dev with Android Studio, not Eclipse, does anyone know how to setup my project to use the Standalone GCM SDK?  I'm thinking it has something to do with Gradle but that is where I get lost.
In my build.gradle dependancies I have:
compile 'com.google.android.gms:play-services:6.1.11'

So I'm guessing I have to some how tell the Android Studio compiler to use the standalone Google Cloud Messaging SDK rather the Google Play Services SDK instead?  Where to I get the standalone SDK?
Any help is greatly appreciated!

A: Android Studio does not support the use of the stand-alone GCM SDK at this time

redpajama_set_name: RedPajamaStackExchange


text:
Q: Python dictionary counter positions change So i'm trying to count the most repeated values in an text file. By using the Counter method it returns exaclty what im looking for
file.txt
12334
99965
99965
44144
99965
00000
44144

script.py
pArray=[]
with open("file.txt") as my_file:
        for line in my_file:
             pArray.append((line.split('\n'))[0])
        dictn = Counter(pArray)
        print(dictn)
        for key, value in dictn.items():
                print("KEY",key)
                print("VALUE",value)
        print(dictn)

OUTPUT
Counter({'99965': 3, '44144': 2, '12334': 1, '00000': 1})
KEY 12334
VALUE 1
KEY 99965
VALUE 3
KEY 44144
VALUE 2
KEY 00000
VALUE 1
['12334', '99965', '44144', '00000']

But as you can see the output of the final array is not in the same order as the dictionary (value should be in descending order)
I am expecting an output like
 ['99965', '44144', '12334', '00000']

I also tried list(dictn.keys()) but i got the same output :/
Why is the order changing and how can I fix it?

A: From the docs, we see that Counter objects: are "unordered collections" - much like dictionaries, (in-fact they are a sub-class). So this means that iterating over .items() won't give the elements in order of size.
However, we can simply use .most_common which returns a list of tuples - each containing an element and its count. The most important thing being that it is in order.
So all we need to do is use a list-comprehension to extract the first element of each tuple in the list returned. That can be done with:
[t[0] for t in dictn.most_common()]

which gave:
['99965', '44144', '12334', '00000']

but could also give the following as the counts for '12334' and '00000' are the same. This is unavoidable due to the nature of how dictionaries (and Counters) work. But if this is important, just let me know and I can update the answer.
['99965', '44144', '00000', '12334']

Note that not all of your code needs to be inside the with statement, once you have created pArray, you can exit the with statement. Also, basic Python uses lists, not arrays!

A: If you want to print Key, Value pairs you can do
for key in reversed(sorted(dictn)):
    print("KEY: {0}, VALUE: {1}".format(key, dictn[key]))


text:
Q: How to execute web worker task continuously even though the location url is redirect? I use gifjs to generate a lot of gifs from png/jpg files once user logins success. At same time, I want to change the location.url to direct user to my website main page. But the problem is that the web worker task stopped once the url is changed. So how to execute web worker task continuously even though the location url is redirect?

A: If the browser does a load of a new page, the short answer is that workers will be terminated. Definitely dedicated workers, and according to Do Shared Web Workers persist across a single page reload, link navigation shared workers (that aren't being used by other windows/tabs) will be too.
But...
If you didn't use any full page loads, and made the entire site use Javascript for navigation / posting of forms, and use the HTML history API to change the URL, then the worker will survive as the user logs in and navigates the site. The worker will only be terminated when they leave the site, or force a reload in the browser.
Depending on the current setup of your site, this might mean considerable change of both the browser and server architecture, the details of which I suspect are beyond the scope of this question.


Light up your bike, skateboard, scooter, self, or other object with this in-depth guide. Get custom... Get fabulous.
This tutorial is for general lighting purposes; if you're building a huge LED installation or matrix, you'll probably need a more specific tutorial for that.
glowHacker – Arduino controller (LightBlue Bean), 12V non-addressable LED strip, transistors, various circuit designs.
tinyGlow – ATtiny85-based Arduino bike lights with 5V NeoPixels.
NeoPixel LED basics – From my "Hackster 101" series; uses an Arduino Uno or 101.
Modulo and If Statements – Tips for programming NeoPixel animations in Arduino; uses a DigiSpark controller.
Merlin Armor – Light-up armor project, uses a Digispark and later a Teensy controller, running Arduino.
Portable Thundercloud – Adafruit Feather running Arduino code, with NeoPixel string lights.
There are also a ton more tutorials in the Bikes category on Hackster!
In case you missed it, all of the tutorials I linked directly use Arduino, so the code and controllers are interchangeable, although the process of programming them may vary.
A quick rundown on this – beware, 40 minutes long – but comprehensive!
Strips – These typically come in 5m lengths. NeoPixels (WS2812s), DotStars (APA102s), or non-addressable LEDs (I'll call these "NALs") – see below for more.
Commercial 12V RGB strip ("NALs"). Generally available on Amazon and other outlets, these will run you about $15-20 for a 5m strip. You can chain them together if you have a strong enough power source – the full 5m may take up to 2 amps. These run on 12 volts, but you can also run them off of a 9V battery with a barrel-jack attachment.
These LEDs are not individually addressable: the whole strip will be a single color at a time. They generally come with an infrared remote control, which allows you to change the color, or choose a pattern (cycling through different colors) and control the speed. Since it's infrared, you need line-of-sight to use the remote, but it makes your bike easy to spot in a crowded area!
Different brands may use different remotes. But if your group all has one type of controller, you can easily change each other's bikes to match your own, for infinite #squadgoals style points.
You can also get rid of the built-in controller and either power the LED strips directly, or create your own system. I'll go into Arduino-controlled systems below.
They have 4 contacts: usually +12v and B, G, R (in varying order) for blue, green, and red. The nice thing is that if you're only using one color, or two adjacent ones, you only have to run two wires! This makes your life SO MUCH BETTER.
These guys run on 5 volts. They have 3 contacts: GND, Data, and +5V. If you bought some from a different brand than AdaFruit, check which line is which. There are some special power considerations you'll want to read. You can power your NeoPixel strip separately from the controller, which can come in handy.
NeoPixels are individually addressable, so you can program your own per-pixel animations, leading to some pretty cool effects. Some of the tutorials listed above have animation programming examples, as does the NeoPixel library for Arduino.
Their "waterproof" version doesn't have silicone coating, but rather the bare strip is run through a clear silicone sleeve. I think it's much less aesthetically pleasing, and you have to attach it with zip ties, but it works!
Need waterproof? This depends on whether you're lighting up an indoor space, a vehicle, a wearable, or "other" (for example, an indoor bar still needs waterproof lighting).
Check your strips to see how many LEDs per meter you get. More LEDs per meter = more power, but a smoother effect.
12v – run off a rechargeable power bank or drill battery, or a 12v lamp battery, or an 8-pack of AA batteries.
9v – you can run most 12v strip lights off of a 9v battery; this can be easier to replace in the field.
Remote: Many commercially-available, 12V strips come with an infrared remote control. These include selectable colors and animations.
Power switch: Sometimes, you just want a basic on/off to control a static color pattern. And that's cool too.
Programmed animations: If you want to run your own animations, grab a controller.
Individually addressable? You'll need NeoPixels (or DotStars, which we aren't covering here).
For indoor systems with NALs, you can simply use the 12v wall-plug power supply that comes with it.
5-volt rechargeable phone banks are super useful.
You can generally use a 9v battery to run "12v" LED strips. They'll be a little dimmer, but at night, it doesn't really matter.
DigiSpark – An ATtiny85 holder board with some power regulation and broken-out pins. Convenient, but can't handle too many LEDs on your strip.
Teensy – Lots of brainpower, a bunch of pins.
Adafruit Trinket – Pretty small, comes in 3.3V and 5V logic versions. New (M0) Trinkets (and a few other Adafruit boards) can be programmed in CircuitPython, which could be more convenient! I'll be exploring this in future.
Adafruit Feather – A bit more sizable, but useful if you have it lying around. Lots of "Feather wings" are available, to provide extra functionality.
For vehicles/wearables, I do not recommend WiFi-dependent controllers like the Particle Photon, unless you do the extra legwork to make them WiFi-independent. For home installations, the Photon is great because you can control it from anywhere!
Handlebars – One row of LED strips typically won't be bright or directed enough to use as a headlight, but you can use it here for a cool effect. Add a headlamp for safety.
Forks – Careful where you put the wires for your front fork. Be sure to use zip ties to attach here; you don't want strays getting into your wheels!
Wrapped around tubes – IMO, this looks kinda tacky, but if you're going for maximum visibility, it works.
Inflection points (esp. for wearables): Be aware that solder joints get stressed from too much bending. Plan and reinforce accordingly. You may want to add a length of speaker wire.
Under seat – You can tuck 2 cylindrical 5v power banks in there, secured with zip ties or a 3D-printed enclosure. Same for 9v batteries. Backups are always good!
Bottle in bottle cage – Easily removed if you don't want thieves getting at your battery.
Color placement: Red on the back, blue on the front? Sounds good to me. You can do this by programming NeoPixels, or splicing together NALs. Note that, as your power drains, the low-power (red) ones will stay on longest.
Animation flow: If you want a "flowing" animation from front to back, or top to bottom, arrange the lights to make the programming easy.
Power switch? Where? This may depend on whether you'll be removing your battery completely or leaving it attached to the bike. Under the front of the seat works well, if your batteries are under there too.
Transistors? If you're switching a 12v source with a 3.3v or 5v controller, make sure you know in advance how to wire up your transistors. My glowHacker tutorial has a solid rundown with some examples.
Bridge colors? If using NALs, how will you get the colors you want?
Splits and joins: These are a pain to work out on-the-fly; design it beforehand.
Reinforce with zip ties if you're taking it to the playa (or elsewhere hot)!
Wire: go for something flexible and resilient.
Speaker wire: Tough and flexible, good for NALs, where you may only need two wires.
Ribbon cable: Easy to get in long rolls, with 4+ wires connected. Keeps things tidy.
Transistors: Get ones that can handle the power you're shoving through! Some can't deal with 9-12v.
Button for switching programmed modes?
Soldering irons: Get a portable iron so it's easy to solder things or make repairs directly on the bike, especially when out in the field.
Butane: Super useful, fast to heat up, but not plane-friendly.
Battery: More portable, but a little more heavy/awkward.
TS-100 or other USB: Somewhat spendy, but worth it! Often has built-in failsafes, like touch or movement sensors, to turn it off when idle.
Cutting wires: Cut your wires longer than expected, especially if you're splicing them together.
Cutting LED strips: Cut them down the middle of the copper contacts. Dense NAL strips will have a set of contacts every 2 inches (5cm). NeoPixel strips typically have a set of contacts between each pair of LEDs, so they can be used individually.
Stripping waterproof NALs: Once you get fairly practiced, you can peel the flexible circuitry away from the silicone coating and then snip off the coating about 4mm.
Wire to wire – Strip wires 3mm, tin the exposed ends, slide heat shrink over one wire, lay them overlapping each other lengthwise, and solder.
LED strip to strip – Use little wire snippets to connect tinned strip contacts together; use heat shrink or hot glue to cover the joint. Make sure the joint is fastened down to something, to prevent flexing.
Wire to strip – Strip the wires, tin the strip contacts, and use a big piece of heat-shrink to cover the end of the strip; inject hot glue to shrink the tubing and seal the joint.
Building onto the frame: If you're comfortable with building directly on the bike, I think it's the easiest way to wind everything through and make it really robust. Otherwise, just make sure you attach everything well and measure twice before you cut!
Built-in adhesive – If using NAL strips, you can peel off the paper backing and use the 3M adhesive for temporary placement.
Hot glue – For NALs, I run beads of hot glue along each edge, filling in the gap between the cylindrical bike frame and the flat strip.
Zip ties – Don't rely on adhesives if you're going to the desert!! Use a fastener, like zip ties. They aren't as pretty, but if you're using NeoPixels in a silicone tube, they're pretty much your only option anyway. Cut the ends down really far, and turn them so they don't snag you!
Electrical tape – This also works for the NeoPixel strips, and blends in a little better than zip ties.
...And just for reading to the end of the tutorial, here's a silly prize for you – my Micro:bit-powered EMOJI TAILLIGHT!


Kitchen King 6 piece non-stick cooking spoons set black is highly effective in making cooking process convenient and easy. The tools are made from Nylon, 210C heat-resistant material and come in non-stick matte finishing. They look elegant and come with hanging loop for convenient placing in the kitchen and dish washing safe, cooking becomes a pleasurable experience.


Thank you to all the delegates from the borough who attended the inaugural VCS conference.
If you were unable to attend, if you left early, or if you would like to revisit any of the presentations, please find details below, including notes from each of the afternoon workshops.
Please contact peta.cubberley@royalgreenwich.gov.uk for contact details of any person or organisation from the day.
GAVS and METRO are now officially merged, as the Business Transfer Agreement (BTA), signed last month, comes into effect today.
Former Members of GAVS are now Associate Members of METRO Charity, unless they opted not to transfer their membership.
METRO GAVS will continue to offer the same support and services as before. METRO GAVS will operate from the same office space, until METRO's new head office location is secured. Our new head office is likely to be in Equitable House in Woolwich, the same building that METRO GAVS currently works from.
Royal Greenwich based group Caribbean Social Forum have won the prestigious race, religion and faith award at this year's National Diversity Awards.


Upright and bushy with soft green leaves that are serrated and aromatic.
Height 75cm and spread 60cm.
Will need a light trim after winter.
Ideal for hedges, lining walkways and mass planting.
Plant 1½m apart for a hedge. Replace every 3-4 years.
Add flower buds sparingly to salads for added colour and taste.
Instead of Rosemary, add a few twigs off lavender when preparing chicken.
Flowers can be crystallized to decorate dessert and confectionery.
Will treat nervous exhaustion, tension headaches, during labour, colic and indigestion.
A weak infusion ( 25% of normal strength) can be given to babies for colic, irritability and excitement.
It will help you sleep.
Burn lavender stalks/flowers to disinfect/deodorize/perfume the room - it has a calming and soothing effect.
It is a good mosquito, midge, and fly repellent.
Rub lavender onto kitchen counters to discourage flies.
Sprinkle a few drops of oil on bed linen to repel mosquitoes.
Place sachets of dried flowers and leaves with clothes to deter moths.


June O'Driscoll is a Licensed Master Trainer of NLP, Professional & Clinical Hypnotherapy Trainer, Business & Life Coaching Trainer, Past Life Regression Trainer, Master NLP Practitioner, TFH Kinesioligist L4, Executive, Business & Life Coach and Reiki Master with a 21 year corporate background in the world of Accountancy/IT, a Senior Manager leading high performing teams.
June trains Diploma Courses in Professional & Clinical Hypnotherapy, Licensed NLP Courses, Accredited Coaching Diploma Courses, Past Life Regression Workshops, Law of Attraction Workshops and Reiki in West Sussex and Surrey.
This marriage of seeming extremes lends an insight into the problems faced by individuals, irrespective of gender, in both their working and personal lives.
Freeing people from their phobias and limiting behaviours is the area of June's work that she finds the most exhilarating, with clients life experiences and opportunities opening up in previously unforeseen ways.
A valued member of the Trainer assisting team for Paul McKenna, Dr Richard Bandler, John LaValle and Kathleen LaValle on their NLP Events and running several of these independently, June is completely up to date with current techniques and is delighted to witness high and sustained success rates amongst participants.
As a Licensed Master Trainer of NLP and Hypnotherapy, June also Trains, Mentors and Coaches Therapists , providing them with an extensive set of tools to use for Personal Development , for a Corporate Environment or for a Therapeutic Environment.


Our Weigh Indicator with data terminal 'AND ' incorporates 32bit processor based state-of art technology, Sigma Delta type 24Bit Analog to Digital conversion, power supply incorporated with EMI-RFI filter & spike suppressor and inbuilt opto isolation of signals & I/Os makes it a reliable product. 'AND is robust in nature to withstand harsh environmental conditions. It can operate reliably over a wide temperature range and also in humid weather.


Processing pitch in a nonhuman mammal (Chinchilla laniger).
Sparse codes of harmonic natural sounds and their modulatory interactions.
A sawtooth waveform inspired pitch estimator for speech and music.
Pitch strength decreases as F0 and harmonic resolution increase in complex tones composed exclusively of high harmonics.


Come on up to beautiful Tehachapi CA March 10th, 2018, to help us celebrate The Release of our new Double live CD and St Patricks!
Yes we'll jump up on the bar and play!
Whiskey Galore LIVE @6pm. Dinner by " by "Taylor's Provisions".


text:
The 1981–82 St. Louis Blues season was the 15th for the franchise in St. Louis, Missouri. The Blues finished the regular-season with a record of 32 wins, 40 losses and eight ties, good for 72 points, and qualified for the playoffs with their third-place finish. The Blues defeated the Jets, three games to one in the division semi-finals, before losing the Norris Division final to the Black Hawks in six games.

Offseason
Prior to the season, realignment took place in the NHL, as the Blues were assigned to the new-look James Norris Division in the Clarence Campbell Conference, along with the Chicago Black Hawks, Detroit Red Wings, Minnesota North Stars, Toronto Maple Leafs and the Winnipeg Jets.

Regular season

Final standings

Schedule and results

Playoffs

Player statistics

Regular season
Scoring

Goaltending

Playoffs
Scoring

Goaltending

Awards and records

Transactions

Draft picks
St. Louis's draft picks at the 1981 NHL Entry Draft held at the Montreal Forum in Montreal, Quebec.

Farm teams

See also
1981–82 NHL season

References

External links

St. Louis Blues seasons
St. Louis
St. Louis
St Louis
St Louis

redpajama_set_name: RedPajamaWikipedia


Three weeks after the Camp fire tore through the Northern California towns of Paradise, Concaw and Magalia, destroying thousands of homes and killing 88 people, the number of individuals still missing now stands at 49, the Butte County Sheriff announced late Friday.
The newest tally was a welcome drop from a figure that at one point exceeded 2,700, leading many to fear the already record-high death toll would rise.
Investigators were paring the list of those who were unaccounted for by calling friends and family who had first reported their loved ones missing, searching various databases to locate them, and checking social media accounts for activity, Sheriff Kory Honea said earlier this week.
Of the 88 people confirmed to have died, 41 have been positively identified and 42 have been tentatively identified.
Search teams have been combing through rubble for weeks in the aftermath of the fire, which was so hot that in many cases it left only bones and bone fragments to be recovered. The grim task was complicated further by rains that turned ash into a clay-like substance that had to be washed away to expose any remains.
The sheriff's office said Friday that investigators had searched 18,000 structures and were no longer making their way through a list of locations, but that they may conduct additional searches as they receive new information.
Honea has acknowledged that some people's remains might never be found.