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Tag: jo malone
Meet the Jo Malone London Gent – John Boyega
Following in the footsteps of the 'Jo Malone London Girls' – Poppy Delevingne and Karen Elson – get ready to greet the new fragrant face and 'Jo Malone London Gent': London born movie star, John Boyega.
Jean-Guillaume Trottier, Global President of Jo Malone London, explained they chose Boyega because, as a '…born and bred Londoner, John is intelligent, inclusive and witty. He shares our core values of generosity and creativity and is unafraid to speak his mind. His vivacity and whole-heartedness make him a wonderful fit with Jo Malone London and I am delighted to welcome him to the family.'
The boy from Peckham's done well, that's for sure: from recieving BAFTA's 2016 Rising Star Award and the Chopard Trophy at Cannes, Boyega captured worldwide attention for his starring role as Finn, forst in Star Wars: Episode VII – The Force Awakens (which happens to be the highest-grossing US film of all time), and again in Star Wars: Episode VIII – The Last Jedi (the highest grossing film, worldwide, of all time).
But it's not just the big-hitters he's known for, as Boyega has also graced indie smashhits such as Detroit and Attack the Block, now bringing his vibrancy, vigour and versatillity to the proudly homegrown brand, and along with redefining what it means to be a contempirary gent right now, Jo Malone London say he 'mirrors our scents which always accentuate the surprising and the bold. Whilst known for being a huge presence and personality, Boyega himself values understatement and originality in scent.'
And we're sure you're going to want to know this gent better, so are delighted to share with you a Q&A, below, as well as a sneak peek at his first film for Jo Malone London…
What made you join the Jo Malone London Family?
John Boyega: 'I love the creativity and storytelling element of Jo Malone London. It's something I resonate with, it's how I work best: with discussion, collaboration and down to earth honesty. Jo Malone London always delivers unexpected and unique ingredient choices and scents. It's refined, but it's surprising too. My life is the same, a subtle contradiction: my job, my profession, and then I still come home to this town, I still go to the supermarket late at night in my pyjamas. In some ways, everything's changed, but then again nothing has.'
What is your relationship to scent?
'Scent is part of my everyday style. My personal style is quite casual but I like to mix it up with interesting fits with Japanese influenced jackets, fitted trousers and chains. I like that I can change up my scent to suit my style. I'm guilty, I like to layer my fragrance. You can make some really interesting smells. If my life was a bottle of cologne it would be called: Conflicts and Success. A new Boyega line.'
What is your first memory of scent?
'My first job was before school, I would deliver post, milk and sweets. And then I used to sell a bit at school. Sell a little bit of candies, Rockies, Haribo's. So, my childhood smells like those old school sweets, those drumsticks, gobstoppers, spicy soup.'
What Jo Malone London products would you recommend?
'Bronze Wood & Leather Cologne Intense is a solid favourite. It's a really good scent. I like to wear it on a day-to-day basis. It doesn't attract too much attention, but at the same time it gets people looking and smelling.
I also like a bit of oud; oud is a lovely smell.'
What do you look for in a script?
'I look for a number of things in a script. But for me, the main thing is the character arc. I don't want my character to begin and end the movie the same. I want a change, something different. Something that happens with the character, that means you have to go on an interesting journey with him.'
What's your favourite part of being on set?
'My favourite part about being on set is collaborating with the people. I've always watched films and never had clarity in my younger days on how the magic starts and is created. So, to be a part of that and witness it is the biggest rush.'
What is something you didn't expect about being famous?
'One thing I didn't expect about being famous is the fact that some things don't change. Sometimes you have to wait in the queue like everyone else and that's fine. I mean, I guess I got told so many things about being famous I thought that everything was going to change for me. But I still go shopping late at night in my PJ's. Nothing's really changed.'
What wouldn't you go a day without?
'I won't go a day without wearing a comfortable pair of socks. It doesn't matter if they're different socks because sometimes in the wash, things get confusing. But as long as they're both comfortable. I'm cool. I also wear scent every day.'
What do you miss most about England when you're not here?
'Sometimes I miss the weather, because I want to put on a jacket. And not always be surrounded by blue skies and sun. I miss the moody faces, I can't lie, there's something about the reality and honesty that I like. I just miss London, I miss home.'
What's the first thing you do when you get back to London?
'The first thing I do is take a drive. I go back around South London, then drive around Crystal Palace, all the way around Dulwich, go down to Brixton. Just go for a drive, get the feel of the city, see what's going on. Put the radio on. I just catch a vibe.'
So now, settle down, and get ready to see the Jo Malone Gent in action! (If you happen to have a bottle of Bronze Wood & Leather Cologne Intense nearby, you could always spray that all over for some multi-sensory cinema action, as now at least we know his current favourite fragrance…)
So for his latest – scented – starring role, expect to see Boyega further 'navigate new territory, celebrating Britishness, storytelling and fragrance as he takes on a new kind of spotlight as the first Jo Malone London Gent.'
Categories: News, Slider, Features
Tags: John Boyega, Jo Malone London Gent, heritage, English, Jo Malone London, jo malone, British, london, movie, film, scent, fragrance
Salt is in the air: a latest trend…?
A trip to the great British seaside is always a real treat, truly to behold come rain or shine – whatever the weather actually. Though, I'm pretty sure I'm not the only one who is rushing to the coast for one last dip, before we officially draw a line under summer. It's in our DNA as Brits to want to escape to the sea, whether it's to walk the dog and wonder how on earth you're going to get said wet canine back in the car, or the craving of a 'wake-up' like none other as you brave the great ocean.
Perhaps it's the smell that's so addictive. In the heat it's dry, dusty sand and sun cream, but with a twist of watery freshness blown in from the shore. In the cold, it's the thick heavy wind that batters you from every angle, 'blowing out the cobwebs', so to speak. For both, there is always one key ingredient – salt. We love the stuff. Perhaps because of these experiences, or perhaps it's the sticky, certain 'tang' we can't quite put our finger on.
There are some incredible historical scents that include sea salt, of course who could forget Miller Harris's Fleur de Sel, or Heeley's Sel Marin? This season, salt is in the air again and we think we're spotting a trend floating in the undercurrent.
Jo Malone London Wood Sage & Sea Salt £82 for 100ml cologne
Try it at: www.jomalone.co.uk
Classified as a woody fragrance, created by master perfumer Christina Nagel, it perfectly captures the spirited feeling you experience when walking a windswept shore. The fragrance clogs the nose with a freshened, heavy sweetness, but retains warmth, like cold, weather-beaten cheeks that burn. Notes include ambrette seed, red algae, grapefruit, as well as those key components – sea salt and sage.
Shay & Blue London Salt Caramel £55 for 100ml
Try it at: www.shayandblue.com
Salt brings caramel alive and this is clearer than ever in Shay & Blue's latest scent, Salt Caramel. Created by Dom De Vetta and Julie Massé – taking their inspiration from the Queen Charbonnel et Walker's sea salt caramel truffles – it's a truly indulgent fragrance. Notes include burnt caramel, sea salt, sandalwood, tonka bean and vanilla. Good enough to eat.
Calvin Klein Reveal £37.50 for 100ml eau de parfum
Try it at: The Perfume Shop
Created by master perfumers Jean-Marc Chaillan and Bruno Jovanovic to summon feelings around the smell of sun-kissed skin in the evening sunset, enveloped in cashmere. The top opens with fresh and flavorful sea salt and pepper. The heart adds ambergris and powdery iris, while the base is smoothed with sandalwood, musk, cashmere and vetiver (another potential female fragrance trend we're sniffing of late).
Written by Alice Crocker
Tags: weather, waves, sun-kissed, skin, shore, shay & blue, seasalt, sea, salt, jo malone, coast, calvin klein, beach, scent, perfume, fragrance


@intrepid, thanks for posting that. Cool, it looks like on average the digital download sales for AMNS is actually continuously increasing since it first came out. If you have time, can you please also post a compilation of the weekly streaming sales like what you did for digital downloads?
A Midsummers Night's Sweetness had 75,015,728 streams in 2014 and was #4 overall.
PlayboyzAdam wrote: This post is just to answer fans asking how I did my calculations for AMSN earning that I posted on twitter. I think I mistakenly posted that it was for digital downloads on twitter. It was actually for streaming.
The first thing to note is that I said those earning don't take expenses into consideration (i.e. promotion cost, training, practice, distribution e.t.c) and these numbers are for figuring out the maximum Pledis could possibly earn.
My calculations are based on $7.99(USD I think...see https://www.youtube.com/watch?v=Qku6P2_Ffts) 30 day MelOn streaming pass. To work out the maxium Pledis and Raina could possibly earn we assume that streaming passes used to listen to AMSN are only used to listen to AMSN(otherwise other artist could get some of that money) and we assume that the streaming passes are used to perform 1 stream a day(streaming the song more than once a day lowers the price of each streaming per day). With all that settled then one streaming of the song gives them a maximum of 26 cent (i.e. 7.99/30=0.266...).
Looking at the Gaon chart updates from intrepid(see posts from above) you'll see that lately Raina has been getting about 1,000,000 streamings per week. I've check Gaon and he's correct. So 1,000,000*$0.26 = $260000(i.e. AMSN is bringing into Pledis, Raina, Brand New Music and San E a total of $260000 per weekly.) Left assume that the earning from AMSN is split in 50/50 between Pledis and Brand New Music that means that Pledis gets a maxium of $130000. Of course Raina get some of that money too but I don't know how much and how much Raina earns is irrelevant right now because all this is to figure out the MAXIMUM of what Pledis could possibly earn. The figure I posted on twitter was per month and since there is about 4 weeks in a month then Pledis gets a maximum of about 4*$130000=$520000 per month.
If you've been keeping track then one of the most important things to notice about the math is that if the streaming pass is used multiple times a day then that lowers the final result.
I only use used the $7.99/30 day stream pass because that'll give Pledis the most money but it's possible that fans bought a different pass that give Pledis less.
I only used the MelOn prices because that'll all I know but the Gaon streaming chart give a cumulative total of streaming across other music service providers too(e.g. Soribada).
As I've already stated, those calculation doesn't take expense into consideration(e.g. music service provider fees) so the reality is that Pledis is probably earning a lot less.
I'm actually glad that fans have enquire about how I got those figures because the fandom has an annoying habbit of listening to any crap that anyone says and that's caused problems.
@puretoria(on twitter), where did you get the information from that psy only made $61k from gangnam style thru digital sales in korea? Also how do you know labels can get as little as 30 won per download? You're probably right but unless you provided actually references or explain those figure I don't believe them...I trying to emphasis on a point here, I hope you guys are getting it.
EDIT: it is made very clear that people don't understand the purpose of me writing that part of this post we I discuss the accuracy of my estimation so I'll see if I can say it in a way where you can hopeffy understand THERE IS NO WAY PLEDIS CAN MAKE $520000 BECAUSE AS I'VE STATE OVER AND OVER THAT THIS ESTIMATION DO NOT TAKE INTO CONSIDERATION OF EXPENSES.
The purpose of that figure is to get an idea of what Pledis can possibly get regardless of how accurate it is because I don't pretend to know things I don't know unlike some sources.
intrepid wrote: A Midsummers Night's Sweetness had 75,015,728 streams in 2014 and was #4 overall.
@intrepid cool it looks like AMNS streaming sales is actually increasing since the start of this year. So far this year the total streaming comes to 23933745 so it doesn't look like AMNS is going to do as well as it did last year in terms of streams.
@intrepid, thanks for that. The site doesn't list Korean streaming services..nor does if state where it got its info from but let's play around with the info that site provides and see if we can get an idea of what Pledis might be getting. So far from Gaon, AMNS streaming totals to 75,015,728+23,933,745 = 98,949,473. Let's just say Xbox provided the streaming service for all those sales then Pledis gets $0.0770 per stream(for the 1st of april) so in total Pledis would get $7,619,109.421 USD ...HOLY... that's a lot of money(note this is just what Pledis get's from XBOX but it doesn't include expense other than the fee Pledis gives to Xbox). Let's pick the lowest paying streaming service provided for 1st of August i.e. Rhapsody than Pledis gets 98,949,473*0.0101 = $999389.6773 USD...that's a pretty big difference between Xbox and Rhapsody although both are pretty big numbers.
A Midsummer Night's Sweetness is down 14 places and is #88 in the Digital Charts for the period 02/08/15 - 08/08/15 and down 13 places in the Digital Download chart at #93 with 18,917 downloads, In the Streaming charts it's up 1 position at #65 with 991,132 streams and its dropped back out of the Mobile Charts.
In GAON's 2015 first half-year closing Digital Chart AMSNS is currently at #93, In the Digital Downloads it's at #81 with 339,802 downloads, In the Streaming Chart it's at #70 with 19,585,189 streams; I'm just wondering what it would be at if San E and Raina were to do a limited promotion of this song again.
A Midsummer Night's Sweetness is down 3 places and is #91 in the Digital Charts for the period 09/08/15 - 15/08/15 and up 6 places in the Digital Download chart to #87 with 17,658 downloads, In the Streaming charts it's down 2 positions at #67 with 980,387 streams.
intrepid wrote: In the Streaming charts it's down 2 positions at #67 with 980,387 streams.
@intrepid, dang I was going to try and help increase those sale...don't really have much time for anything these days.
A Midsummer Night's Sweetness is no-longer charting in the Digital Charts for the period 16/08/15 - 22/08/15 and is also no-longer in the Digital Download Charts but since it's last position was #87 with 17,658 downloads and considering that the current #100 position has 18,499 downloads it reasonable to assume it hasn't dropped off in sales too much from the previous week and may still pop back in a week or two given its so far stable sales; In the Streaming charts it's down 9 positions at #76 with 892,872 streams.
A Midsummer Night's Sweetness is still no-longer charting in either the Digital or the Download Charts for the period 23/08/15 - 29/08/15 and in the Streaming charts it's down 18 positions to #94 with 733,576 streams.
For the month of August AMSNS position in the Digital Chart was #98 down 23 positions on the previous month in the Digital Download Chart it dropped 19 positions to #93 with 76,505 downloads and its total Streams was down 19 positions to #79 with 3,950,334 streams for the month.
^Dammit, AMNS keeps dropping in sales.
AMSNS is out of the Streaming Charts but still did 639,116 streams for the period 06/09/15 – 12/09/15.


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Twin Falls multiple sclerosis patients are traveling to get new treatment – Coeur d'Alene Press
TWIN FALLS Over 30 years, Judy Fisher has been left with very few options for treating her multiple sclerosis.
But for the Twin Falls resident, who has the primary progressive form of the disease, theres finally an approved medication she can try.
The Food and Drug Administration approved Ocrevus in March after a large study found it slowed progression of the neurological disease and reduced symptoms. Its approved for both patients who have relapsing and primary progressive forms of MS.
This medicine is really promising, Fisher said.
Its the first FDA-approved medication shown to be effective in treating primary progressive MS. But for months, Magic Valley residents whove wanted to try the new treatment which is delivered intravenously have been forced to travel elsewhere.
Every time theres a new drug on the market, health systems decide whether to add it to its formulary, and that determines whether it will be available to patients.
Dr. John Steffens, a neurologist at St. Lukes Magic Valley Medical Center, told the Times-News on Thursday he received confirmation Ocrevus will be offered at St. Lukes infusion centers soon.
He has about a dozen MS patients who are receiving the new treatment. Most of them have primary progressive MS, but a few have relapsing form of the disease and havent seen results with other medications.
Theyve been traveling to other health care facilities such as Cassia Regional Hospital, Saint Alphonsus Regional Medical Center in Boise, Portneuf Medical Center in Pocatello and University of Utah Hospital in Salt Lake City.
Since 1993, 14 drugs have been approved to slow the most common form of MS, but everything tested against primary progressive MS failed until now. An estimated 15 percent of MS patients have the primary progressive form of the disease, Steffens said.
In primary progressive MS, the diseases course varies among patients, but symptoms gradually worsen from the start and there usually are no periods when symptoms subside.
Symptoms are caused by the immune system attacking the fatty coverings on nerves in the brain and spinal cord that protect them, much like insulation on electrical wiring.
As the coverings deteriorate, nerve messages arent properly transmitted, disrupting movement and muscle control.
For years for people who have primary progressive MS, doctors were left to treat symptoms and cross their fingers hoping a new medication would be developed, Steffens said.
Hed also have patients try other MS medications to see if theyd work, but they often didnt.
Fisher was diagnosed with MS in 1988 when she was in her 30s. Now shes 63.
Ive been lucky, she said. I havent progressed fast at all.
The only prescription medication shes taking is a water pill. Weakness in her right side due to MS, she said, hasnt gotten much worse over the years.
Seven years ago, she underwent stem cell treatment in Germany and saw excellent results. For three months, I was darn near perfect, Fisher said. Im still reaping the benefits from it.
But many of the symptoms have returned, she said. I would give anything to do stem cell again, but its too expensive.
At an appointment with Steffens her neurologist a couple of months ago, Fisher expressed interest in Ocrevus.
But it just came out, Fisher said. He said he had like three or four patients now doing it. I am waiting to see what goes on with them.
Will she try Ocrevus? If theres any way I can afford it, you bet I am, Fisher said. Her next neurology appointment isnt until November.
Active in the local MS community, especially with fundraising walks, Fisher said theres a lot she doesnt know about Ocrevus, but she has read about it.
This is big for that type of MS, she said. It has helped even mobility on people and that is what I would be looking for.
Compared to study participants getting dummy infusions, patients given Ocrevus infusions had slower declines in walking ability and slower disability progression over nearly 2 years.
The Ocrevus group also had fewer new brain-damaging lesions develop but slightly higher rates of certain side effects, including upper respiratory tract infections and tumors developing in various parts of the body.
Ocrevus is given intravenously every six months. It takes about half a day to receive treatment, Steffens said. Its a really logistically simple drug to give.
The medication also seems to be well tolerated among patients, he said, and has the fewest side effect warnings among any MS drugs he has encountered.
During a recent follow-up appointment with Steffens first patient who has received treatment, the person is walking better now than in three years, he said.
But he doesnt know if thats a placebo effect or if that will be a sustained benefit.
And the bad news for MS patients, Steffens said: We still have no cure for any form of the disease.
One common dilemma for MS patients can be figuring out how to pay for often-costly treatment.
Ocrevus was developed by Genentech, part of Swiss drugmaker the Roche Group. Genentech, based in South San Francisco, Calif., has said the initial list price without insurance is $65,000 a year.
So far, Steffens hasnt heard of any of his patients having problems getting the treatment covered by insurance.
And with patient assistance programs factored in, too, co-pays are typically less than $100, he said.
We were expecting huge, huge pushback from insurance companies, he said, but that hasnt been the case.
After years of waiting, it means more local MS patients may be able to finally get the help theyve been looking for.
Twin Falls multiple sclerosis patients are traveling to get new treatment - Coeur d'Alene Press
Wild new microchip tech could grow brain cells on your skin - CNET - August 10th, 2017
Newer : BACK IN ACTION: Stem Cell Knee Procedure Gets Middle Aged Athlete Back On Slopes, Court – SpaceCoastDaily.com
Older : Introducing ProCell Therapies Dermabrasion, Microchanneling, and Stem Cell Therapy – Gwinnett Citizen

redpajama_set_name: RedPajamaCommonCrawl


Digital transformation is about transforming experiences, not just channels.
There is something about shopping that goes beyond the rational mind. Sometimes, human beings cease to reason when it comes to shopping. Shopping is entwined with our identities, our traditions, our personalities, our backgrounds, and our patriotism. We are no longer just human beings; our consumerism picks up on our identity and becomes part of who we are.
In this article, we will explore best practices through which retailers can become experience-led businesses and create experiences that customers will want.
Omnichannel is the use of multiple channels to sell products and services. A retailer cannot just focus solely on one channel to provide products or services. Attempting to pinpoint the customer mindset could be the most challenging part of sales. Many retailers have turned their websites into digital showrooms designed to attract customers into their stores, where a customer can start digitally and end at a physical location.
Devices don't buy products; people do. If this is the case, marketers must shift from selling products to selling experiences.
Trying to aim for conversion with every interaction is the key. Closely monitoring customer behavior could prove to be very helpful as well. For example, if a customer purchases an oven today, possible future selling points could be oven cleaner, baking utensils, or even a baking cookbook.
Giving effortless experiences to customers isn't just about connecting customers with their purchases, it is also about simplifying their buying decisions. This means companies must make it easy for customers to get what they want, when they want, and where they want it. Improperly placed products can impact in-store sales. Choosing the right kind of products to display at the right location is important.
Putting shoppers at the center of everything with an experience-first strategy will help retailers keep their customers, simply by giving them what they want—an amazing experience with unexpected value. Adopting an experience-first approach means that retailers no longer offer products in a vacuum, but create story-driven, in-store contexts that emotionally resonate with their customers.


It is getting harder to "walk" (1980) in "uprightness" (3476). When I was a child certain things were understood. There was no question of what was right or wrong in areas of sexual morality, drug abuse, panhandling, rioting or vulgar language. My family, my church and my neighborhood were in agreement. You have all heard stories about how kids didn't dare certain actions because the people down the street would call their parents and report them. Now when a teacher calls a parent the parent wonders what is wrong with the teacher.
It is not right and wrong that have changed but the character of the people. An increasing percentage of the population has decided to reject the standards of God and follow their own "way" (1870). It is like the problem with high blood pressure. It is called the silent killer. Usually it is the result of many small decisions made: Too much to eat and too little exercise top the list. The problem is ignored like we are Teflon. When the doctor diagnoses the problem we don't take our medication. It is so easy to ignore until the stroke hits.
So? Today is the day to decide how you are going to walk. Sure you can probably put it off another day but when does tomorrow come? Fear the Lord so that you don't need to be afraid of the Lord.


Produced from the Argan tree in semi-deserts of Morocco, Argan Oil has been used by Moroccan women for centuries for it's nutritional and cosmetic benefits. This precious oil helps protect against damage caused by the environment, chemicals, or excessive heat from stylers, and provides long-term conditioning while reducing frizz, split ends and breakage. Ideal for all hair types, BaByliss PRO Argan Oil is a premium styling, finishing, smoothing and conditioning product that produces consistently silky smooth results.


Mr Suhail Awan graces #HDF with his precious time today as a key speaker of our #DTalks session.
An extremely enlightening session on #InnovationforDevelopment. Mr Awan is a veteran from the development sector.


16,5 trillions USD investment required over the next 15 years in energy efficiency and low-carbon technologies consistent with limiting global temperature increase to 2°C.
The Gridle project aims to build a financial infrastructure for decentralised energy projects.
without adding trillions of new debt to the financial system?
to optimize their energy needs?
Changes in complex system as issuing credits for energy production and distribution are challenging. Gridle aims to tackle this from different perspectives with a focus to bottom up approaches.


HL7 FHIR APIs and the Argonaut Project –What do they mean for the UK Healthcare IT Landscape?
FHIR® - Fast Healthcare Interoperability Resources (hl7.org/fhir) - is a next generation standards framework created by HL7.
FHIR has already been shown to increase the speed of implementation of links between healthcare systems. The second version of the draft standard ("DSTU2") has just been published. The Argonaut Project was set up recently in the USA to rapidly develop a first-generation API and Core Data Services specification for FHIR, to further simplify implementation.
This workshop discussed the aims of the project, progress so far, and what the impact in the UK is likely to be. FHIR is already being used by the HSCIC for the next generation of GP system interfaces and in local NHS projects to bridge pathways across care sectors. BCS Health and HL7 UK jointly ran this free event as a learning opportunity for NHS and social care implementers and commissioners to help accelerate the pace of adoption.
Following introductory presentations, the workshop discussion explored the barriers and opportunities in the UK.
Presentations from the event can be found below.


Roller blading is popular amongst children and adults and is great exercise. Here at Pulp we have a wide range of inline skates and rollerblades that are perfect for perfecting your skate moves. From brands such as Airwalk and No Fear, our line of skates are ideal for professionals and amateurs!


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Flume: ARIA producer of the year 2013
The newly crowned king on why he likes to work on the move
Inspiration matters more than gear to fast-rising star Flume (Image credit: Wilk)
PRODUCTION EXPO 2013: With a worldwide hit album, countless floor-filling remixes and Australia's prodigious ARIA Producer of The Year 2013 award to his name, who better than Harley Edward Streten, aka Flume, to shed light on the advantages of portable music production and keeping it all in the box.
What initially attracted you to producing music?
"I guess music's always something that's interested me, especially electronic music. The story of me getting a basic production disc in my cereal box when I was younger is all over the internet. I think I've told that ten times already today!
"Music became my hobby from an early age. I guess I just got lucky as, within the last couple of years, it's actually become something I can support myself with and make a comfortable living off."
Were you always Flume?
"I've always made music but I didn't really put it up anywhere, other than some bits and pieces on MySpace. It was never really anything serious. I was writing a lot of music but I was never quite happy with it until a little further down the track when I did some dance tracks for Ministry of Sound.
"Flume was initially my side project for my weirder stuff, but as it happens that was the one that took off right after Sleepless [released August 2011] came out."
Listen to Flume's Sleepless featuring Jezzabell Doran:
How do you start a new track?
"I like to have a concept before I start writing. Often I do go in blind and try and write something, but sometimes that works and sometimes it doesn't. If I already have an idea, that's usually when the best stuff happens; if I've heard a track and maybe they [artist] did something I've never heard down before, I'll try and emulate that and do something new with it.
"I have an EP coming out soon with my friend, Chet Faker, and we tried having concepts for each song. Oo one of them, the idea was to make all drum samples lo-fi and dodgy-sounding. The bass guitar was just the cheapest, tiniest bass we could find and the vocals we recorded through a $30 microphone we got free with a VCR player.
"The track has an indie/lo-fi vibe then, near the end, it builds into a hi-fi sound sample with the biggest kick drums I have and this huge synth. [faker's] vocals open up and he sings at the end too. That contrast was the concept we aimed for. I usually like to have some idea in mind before I write a song."
What studio tools do you use?
"I don't have much hardware stuff as I try to keep everything inside the box. Now I've moved into my new studio, I'm going to be buying some bits of kit but I generally like to be self-sufficient to the point where I can travel around the world with my laptop.
"I like being able to do that, and the more hardware equipment I buy the more I find I need to be in a studio to write. Because I'm on the road so much, it kinda makes sense to keep it simple with just the laptop. It doesn't really matter what I have - it's the inspiration that matters.
"I use Sylenth, one compressor, Ableton Live and its basic effects. I like to keep it super simple. It's actually pretty boring but it works for me and it keeps me making music."
"When staying in hostels, I would sleep with my laptop - I was afraid someone was going to steal it!"
What can you tell us about writing and producing on your laptop?
"I think it's still better to have all the quality hardware outboard but I'm trying not to let myself get comfortable with all that grand equipment around me. I know a lot of people who find it very difficult to write music unless they're in their studio surrounded by gear. I prefer to be in my studio but I like that I can work on music outside of it too.
"That's where I wrote most of the album: in cafes, pubs and hostels all around the world. When I was staying in hostels, I would sleep with my laptop in my pillowcase because I was afraid someone was going to steal it! I'd go travelling and live in hostels, so I'd do my adventuring for the day then, when it got dark, I'd retreat to a pub or café and just write music with my headphones on."
Do you have any tips for budding producers/remixers?
"I'd probably say, don't make the mistake of thinking you need heaps of equipment. A lot of people say they can't produce without awesome monitors, and maybe do a remix they don't like and blame it on having shitty monitors, but it's a poor workman that blames his tools.
"You don't really need jack shit; you just need to learn how to use Ableton Live or whatever DAW you feel comfortable on. I think all the DAWs are good. There isn't one that's ultimately superior to the others. Whatever you know and whatever works for you is what you should use."
What would you consider to be your biggest strength as a producer?
"I think probably the fact that I'm good with melodies. I think that's what it takes to really cross over. Everyone loves melody and it's such an important part of music. A lot of producers don't really know how chords work or how to write a good melody and that's a massive disadvantage.
"I've always loved melody and it's something I have a good ear for. A lot of producers I know have incredible technical ability but not so much musical ability. It's important to have a balance and all the best producers that I know are the ones who have the best balance."
"If I can't make a song better, I won't touch it"
What about when starting a remix?
"Well, I like vocals and manipulating vocals a lot. Vocals usually carry the melody, so anything that has melody I'll get my hands on. My rule of thumb is that I never, ever want to touch anything that I either can't make better or can't take to a new place. If I can't make a song better, in my eyes, I won't touch it. If it ain't broke, don't fix it.
"If it's an awesome song and I can hear it in a completely different context, that's another reason to do a remix. For example, I thought the Disclosure track, You & Me, was really great but I could see a way of flipping it on its head and hearing it in a different way."
Finally, tell us about the bonus material on the forthcoming Deluxe Edition of your debut album...
"Well, I think it's pretty important to try and get kids into music production and to realise that you don't have to have a big fancy studio. On the bonus disc of the Deluxe Edition of the album, I've put some stems and tutorials to give away some of my tips and to try and de-mystify what I do.
"The stems are there to let people see how the music looks and maybe get them into putting a track together. Back in the day, if an artist I liked had done that I'd have been all over it!"
The Deluxe Edition of Flume's self-titled debut is available digitally from November 12. The physical edition is out December 9 on Transgressive Records.


Make it systematic & Scientific too.
Dear Sir I believe on you. You have a great potential to make change in Nepali Gov officer's attitude becoming youself a role model. We are offered number of fellowships by different organisations, i.e. ABU, ITU, IPU,APT,AIBD,WB, ADB,Embassies, UN etc. This is in fact great donation to this country. Few officers in MOIC made it for their family bussiness. They fly to those countries where their childrens study or relatives lives no matter what is the course of the training or the meeting, workshop, conference etc. This is Just westage. Country will not get anything out of these people. You are there in The Priminister's office please make this arrangement from there only. Direct all the aids to your office and transperantly distribute to all related officers so that country could get something out of it.
I congratulate and wish you all the best for initiating to climp up the Everest. Being a governmental diplomate, I found this work very challenging, needs courage and concentration!! this is extra-ordinary work!! I wish you all the best, and lets hope your effort will bring environmental degradation minimal to the himalayan region.
There is no any directive or regulation to make the postings of the cabinet decision in the website mandatory.
Dear Santosh jee thank you for your interest and suggestions. I have immediately asked the Ministry of Foreign Affairs to arrange for hosting website of the Nepalese embassy in Canada and as I was told that instruction is already communicated to Ottawa in writing. Please find below the address of Nepalese embassy in Canada as posted in the website of the Ministry of Foreign Affairs at www.mofa.gov.np Ottawa, Embassy of Nepal 408, Queen Street Ottawa, ON K1R 5A7 Canada Tel: 001-613-680-5513, 680-5623 Fax: 001-613-422-5149 Email: nepalemb@rogers.com Regarding the website audit that is not a part of the project you have mentioned but an initiative we have taken on our own. Now a directive is in final stage to the government offices as a mandatory instruction for standardization of official websites at least at the central level for the first time. Once it is finalized it will be available on demand. ICT development project is in the incipient phase of its implementation. It has programs in eight different government organizations. Programs are as follows: Biometric national ID, integrated land information system, e-processing of driving license, e-submission of application for Public service vacancies, establishment of 114 tele-centers, rural e-connectivity, government enterprise architecture and strengthening HRD institutions. This project does not cover all the requirements of national ID and the land info system. However we will try to cover as much as possible from this project and will continuously seek fund for remaining portion of the job. PMO is coordinating those activities and eight different organizations are implementing respective programs. If you can visit our office we are ready to give you detail of the project otherwise you can ask specific questions about the project that I will try to satisfy you.
I am very glad to have response from you. But one thing is very important that you should be aware of "so called ICT Specialist" in Nepal for the implementation of e-Gov project. The second concern about the website update. As you mention that you are on the process of Auditing the website, i apreaciate it but it is urgent necessity to update the website in time which can be done by the hard direction to the government agencies it is possible because there are IT related personnel in each organisation.
I am heard very much about you and I think you are not as the traditional bureaucrat and now you are in PM Office which is launching the e-gov project supported by ADB but there is doubt that this project will be success because our mechanism is so lazy that must of the information in gov website are old and out-dated. So respected sir, Nepal is in the Informative stage of e-government.We can improve ourselves by mentaining the current status, if we are not able to do these thing, all are efforts are only talk, talk and talk. I am very much interested for your response and action as well because I realy trust you.
In fact there is no such specific regulations about installation and usage of CCTV informationexcept a vague provision of acquiring information by securityagencies for security pusposes. PMO has instructed the Ministry of Home Affairs to come up with guidelines first. I was waiting that guidelines to inform you. However it may take few more days to receive. guidelines.
I still hope that you will answer me !!


text:
Q: Web access is extremely slow I have TFS 2015 installed on one of the company's servers. I try to access TFS using web access and it is extremely slow, it takes more than 5 minutes for a page to load and sometimes even longer. If I restart the server, TFS becomes a little bit faster (a page would need only a minute or so to load), but soon it becomes slower.
The server itself is okay. The CPU and memory are not even fully utilized (~20% - ~40% is utilized).
Other applications that are installed on the server are working fine, so it's just TFS.
Any suggestions?

A: *

*Log in the application tier machine to try to access the web access to see whether you can see the same behavior.

*Check the network connection between the application tier machine and data tier machine if you set up TFS in a multiple server configuration. You may try to turn off the firewall and anti-virus software on the machines.

*Clean the cache folder on the application tier, usually the folder locates in: C:\TfsData\ApplicationTier\_fileCache

*Check the Requirements and compatibility, to see whether your TFS set up on a appropriate environment.

*If the items above is not helpful. You may need to consider move your TFS to another hardware.

redpajama_set_name: RedPajamaStackExchange


text:
Q: nodejs: Cannot interact with data from websocket using eventEmitter this is my first so be gentle.
I am streaming data from a site using this:
"use strict";
const ws = require('ws')
const w = new ws('wss://website')

w.on('message', (msg) => console.log(msg))

let msg = JSON.stringify({

     ///STUFF
})

w.on('open', () => w.send(msg))

And I would like to create an event listener that responds to the data from the websocket stream.
///confused about how I define what price target is!?
///I would like it to set an event trigger on particular value from
/// websocket data

var ticker = require('./openTick');

///not sure if I can check the msg like this
ticker.emit.on('priceTarget', function(){
    if (msg == priceTraget) {
        /// Run fracMarty.py
    };
});

Write now the "msg" is being displayed on the screen but I can not interact with it i.e.) iterate over it etc.
I have tried the eventEmitter modules on tut, the nodejs site, and like 4 others and they all direct me to just get the connection not interact with the data.
Can someone point me in the right direction.
Thanks,
Bobby Fischer


1987 board game endorsed by Bobby Charlton Soccer Schools. Classic set up of grid pitch and player figures moved using dice. Nicely presented and fun to play.
Nice big box for a proper football game with pitch and figures.
Fold out grid pitch plus two eleven a side teams plus nice little goal models.
Solid laminated figures into plastic crescent bases.
Three dice, not sure what they do as I have not read the rules!
Game play is influenced by playing card outcomes.
Lovely goals and stylish keeper figures.


The Arabidopsis PAD4 gene was previously shown to be required for synthesis of camalexin in response to infection by the virulent bacterial pathogen Pseudomonas syringae pv maculicola ES4326 but not in response to challenge by the non-host fungal pathogen Cochliobolus carbonum. In this study, we show that pad4 mutants exhibit defects in defense responses, including camalexin synthesis and pathogenesis-related PR-1 gene expression, when infected by P. s. maculicola ES4326. No such defects were observed in response to infection by an isogenic avirulent strain carrying the avirulence gene avrRpt2. In P. s. maculicola ES4326–infected pad4 plants, synthesis of salicylic acid (SA) was found to be reduced and delayed when compared with SA synthesis in wild-type plants. Moreover, treatment of pad4 plants with SA partially reversed the camalexin deficiency and PR-1 gene expression phenotypes of P. s. maculicola ES4326–infected pad4 plants. These findings support the hypothesis that PAD4 acts upstream from SA accumulation in regulating defense response expression in plants infected with P. s. maculicola ES4326. A working model of the role of PAD4 in governing expression of defense responses is presented.
Plants respond to pathogen attack by activating expression of a battery of defense responses. In some plant–pathogen interactions, host defense responses are triggered by specific recognition of the products of particular pathogen genes (called avirulence [avr] genes) by plant hosts carrying a corresponding resistance gene. Such gene-for-gene responses generally occur within 24 hr after infection and result in inhibition of pathogen growth and failure of the pathogen to cause disease. If the pathogen does not carry an avr gene recognized by the plant, defense responses are activated more slowly, the pathogen multiplies, and disease ensues. In this case, the pathogen is said to be virulent. Plants can acquire resistance to normally virulent pathogens through a phenomenon called systemic acquired resistance (SAR). Infection of part of a plant can result in expression of some defense-related genes in uninfected parts of the plant, with concomitant resistance to subsequent attack by virulent pathogens. Genetic analyses of plant responses to pathogen attack are being used to reveal the components of the signal transduction pathways controlling defense gene expression in response to avirulent and virulent pathogens as well as during SAR.
Two virulent Pseudomonas syringae pathogens, P. syringae pv maculicola ES4326 and P. syringae pv tomato DC3000, have been found to infect Arabidopsis (Crute et al., 1994). Introduction of plasmids carrying any one of several avr genes into either of these strains yields isogenic avirulent strains that trigger gene-for-gene defense responses dependent on the presence of corresponding resistance genes in the host (Crute et al., 1994). Defense responses activated by infection with any of these strains include synthesis of the antimicrobial compound camalexin and expression of defense-related genes, including PR-1, PR-5, BGL2 (PR-2; β-glucanase), and ASA1 (anthranilate synthase) (Crute et al., 1994). For many of these responses, including camalexin accumulation, PR-1 gene expression, and ASA1 gene expression, activation occurs more rapidly in response to the avirulent strains than it does in response to the virulent ones (Niyogi and Fink, 1992; Glazebrook and Ausubel, 1994; Greenberg et al., 1994).
Expression of PR-1, PR-5, and BGL2 is also associated with SAR. Plants that demonstrate SAR exhibit systemic expression of these genes and elevated levels of salicylic acid (SA) (Ryals et al., 1996). Treatment of plants with exogenous SA is sufficient to induce expression of PR-1, PR-5, and BGL2 and to cause SAR, suggesting that SA is required for signaling during SAR (Ryals et al., 1996). This idea was proven by construction of transgenic plants expressing a bacterial salicylate hydroxylase gene (nahG) that converts SA to catechol (Gaffney et al., 1993). When infected with pathogens that induce SAR in wild-type plants, nahG plants fail to develop SAR and do not exhibit systemic expression of PR-1, PR-5, or BGL2 (Gaffney et al., 1993; Delaney et al., 1994). SA is required in the systemic tissue for expression of defense genes and SAR (Vernooij et al., 1994), but there is some debate as to whether it is also the signal molecule that is translocated from the infected leaves to the rest of the plant (Vernooij et al., 1994; Beffa et al., 1995; Shulaev et al., 1995; Mölders et al., 1996).
An Arabidopsis gene that has been variously named NPR1 (for nonexpresser of PR genes; Cao et al., 1994), NIM1 (for noninducible immunity; Delaney et al., 1995), and SAI1 (for salicylic acid–insensitive; Shah et al., 1997) is required for SA-mediated disease resistance. When infected with a pathogen that induces SAR in wild-type plants, npr1/nim1/sai1 mutants accumulate high levels of SA but do not activate expression of PR-1, PR-5, or BGL2 and do not develop SAR (Cao et al., 1994; Delaney et al., 1995; Shah et al., 1997). NPR1/NIM1/SAI1 was recently cloned and shown to encode a protein containing ankyrin repeats (Cao et al., 1997; Ryals et al., 1997). The precise role of this protein in mediating responses to SA is not known, but it was recently demonstrated that it functions in the nucleus in response to SA treatment (M. Kinkema and X. Dong, personal communication).
The phenotypes of nahG and npr1/nim1/sai1 plants indicate that SA-dependent responses are required for local defense against virulent and avirulent pathogens as well as for SAR. In response to local infections, nahG plants display reduced PR-1 expression and enhanced growth of virulent bacterial pathogens, avirulent bacterial pathogens, and avirulent Peronospora parasitica isolates (Delaney et al., 1994; Lawton et al., 1995; Glazebrook et al., 1996). Although camalexin synthesis is not inducible by SA, nahG plants synthesize greatly reduced amounts of camalexin in response to P. s. maculicola ES4326 infection, suggesting that SA is necessary, but not sufficient, for full activation of camalexin synthesis (Zhao and Last, 1996). Mutations in npr1/nim1/sai1 cause enhanced susceptibility to avirulent and virulent P. syringae strains and avirulent Peronospora isolates (Cao et al., 1994; Delaney et al., 1995; Glazebrook et al., 1996; Shah et al., 1997). The expression of PR-1 in npr1/nim1/sai1 plants in response to local infections or SA treatment is reduced relative to that in wild-type plants (Glazebrook et al., 1996; Shah et al., 1997). However, npr1/nim1/sai1 mutations have no effect on camalexin synthesis, suggesting that although camalexin synthesis requires SA, this requirement is mediated by an NPR1/NIM1/SAI1–independent pathway (Glazebrook et al., 1996; Zhao and Last, 1996).
In previous work, we isolated an Arabidopsis mutant, pad4, displaying reduced camalexin synthesis in response to P. s. maculicola ES4326 infection, enhanced susceptibility to P. s. maculicola ES4326, and susceptibility to Peronospora isolates that are avirulent on wild-type plants (Glazebrook et al., 1996, 1997b). Significantly, pad4 was unaffected in camalexin synthesis in response to challenge with the non-host fungal pathogen Cochliobolus carbonum, strongly suggesting that pad4 is a mutation affecting a regulatory factor rather than a camalexin biosynthetic enzyme (Glazebrook et al., 1997b).
In this report, we further characterize pad4 plants. We show that pad4 affects expression of some defense-related genes, including PR-1, in response to infection by P. s. maculicola ES4326, but does not affect responses to P. s. maculicola ES4326 carrying avrRpt2. Responses to SA treatment were unaffected by pad4. P. s. maculicola ES4326–infected pad4 plants displayed reduced synthesis and accumulation of SA and its glucoside (SAG), and the PR-1 expression and camalexin synthesis defects of pad4 plants were reversible by SA treatment. Taken together, the phenotypes of pad4 plants argue that PAD4 is required upstream from SA in the signal transduction pathway leading from P. s. maculicola ES4326 infection to activation of defense responses.
Our previous demonstration that pad4 plants show a defect in camalexin synthesis in response to infection by the virulent bacterial pathogen P. s. maculicola ES4326, but not in response to challenge by the non-host fungal pathogen C. carbonum (Glazebrook et al., 1997b), led us to examine the effect of pad4 on camalexin synthesis in response to various elicitors. Wild-type and pad4 plants were infected with P. s. maculicola ES4326 or an isogenic strain carrying the avirulence gene avrRpt2. Camalexin levels in the infected leaves were determined at various intervals after infection. Figure 1A shows that when plants were infected with P. s. maculicola ES4326, camalexin levels in wild-type plants were much higher than those in pad4 plants. In contrast, when plants were infected with P. s. maculicola ES4326 carrying avrRpt2, camalexin levels in wild-type and pad4 plants were not significantly different. Similar results were obtained using a different virulent P. syringae strain, P. s. tomato DC3000, and P. s. tomato DC3000 carrying avrRpt2 (data not shown). This suggests that the signal transduction pathway leading to camalexin synthesis in response to P. s. maculicola ES4326 or P. s. tomato DC3000 infection requires PAD4, whereas camalexin synthesis in response to strains carrying avrRpt2 is mediated by a PAD4-independent pathway. Two other treatments known to trigger camalexin synthesis are infection with Xanthomonas campestris pv campestris BP109 and spraying with silver nitrate. Figures 1B and 1C show that pad4 did not affect camalexin synthesis in response to either of these treatments, suggesting that responses to these stimuli are also independent of PAD4.
Camalexin Levels in Wild-Type and pad4 Plants after Various Treatments.
Each data point represents the mean and standard deviation of six replicate samples.
(A) Infection with P. s. maculicola ES4326 or P. s. maculicola ES4326 carrying avrRpt2. wt-Psm, wild-type plants infected with P. s. maculicola ES4326; pad4-Psm, pad4 plants infected with P. s. maculicola ES4326; wt-avr, wild-type plants infected with P. s. maculicola ES4326 carrying avrRpt2; pad4-avr, pad4 plants infected with P. s. maculicola ES4326 carrying avrRpt2.
(B) Infection with X. c. campestris (Xcc) BP109.
(C) Spraying with 5 mM silver nitrate.
The finding that PAD4 is required for activation of camalexin synthesis in response to infection by P. s. maculicola ES4326 raised the possibility that PAD4 might encode a regulator of defense responses. To test whether pad4 affects activation of other defense responses in addition to camalexin synthesis, mRNA levels of several defense-related genes were examined by RNA gel blot hybridization. Figure 2A shows that the mRNA levels of PR-1 were greatly reduced in infected pad4 leaves relative to the levels in wild-type plants. Expression of PR-5, BGL2, and ASA1 were affected less strongly, if at all, by the pad4 mutation. ASA1 encodes anthranilate synthase (Niyogi and Fink, 1992), which is required for camalexin synthesis because anthranilate is a precursor to camalexin (Tsuji et al., 1993). Zhao and Last (1996) have observed a tight correlation between camalexin levels and ASA1 expression; however, this correlation is not maintained in pad4 plants. Clearly, pad4 has effects on defense gene expression, but these effects are not consistent among all genes induced by P. s. maculicola ES4326 infection.
Infection with P. s. maculicola ES4326 carrying avrRpt2 also leads to increases in expression of defense genes, including PR-1 (Greenberg et al., 1994). Figure 2B shows that PR-1 mRNA levels in plants infected with P. s. maculicola ES4326 carrying avrRpt2 were unaffected by pad4. Taken together with the results in Figure 1A, this suggests that host defense responses to P. s. maculicola ES4326 carrying avrRpt2 are largely PAD4 independent.
Defense Gene Expression in Leaves Infected with P. s. maculicola ES4326 or P. s. maculicola ES4326 Carrying avrRpt2.
Leaves were excised at 0, 12, 24, 36, or 48 hr after infection. Mg indicates leaves mock inoculated with 10 mM MgSO4 sampled at 36 hr. rRNA indicates hybridization with an 18S rRNA probe used to evaluate equal loading.
(A) Infection with P. s. maculicola ES4326.
(B) Infection with P. s. maculicola ES4326 carrying avrRpt2.
SA is required for induction of PR-1 gene expression in infected leaves (Gaffney et al., 1993). SA treatment is also sufficient for PR-1 gene expression and SAR (White, 1979; Malamy et al., 1990). To determine whether pad4 affects responses to SA, pad4 plants were treated with SA and tested for PR-1 gene expression and pathogen resistance. Figure 3A shows that SA treatment induced similar levels of PR-1 expression in wild-type and pad4 plants, with PR-1 mRNA present at high levels 1 day after treatment and declining thereafter. Similarly, Figure 3B shows that SA treatment induced resistance to P. s. maculicola ES4326 in wild-type and pad4 plants. Based on these experiments, it appears that the signal transduction pathway between SA and PR-1 expression is intact in pad4 plants.
Exogenous SA Induces PR-1 Expression and Enhanced Resistance to P. s. maculicola ES4326 in Wild-Type and pad4 Plants.
Plants were sprayed with 5 mM SA in 0.02% [v/v] Silwet L-77 or with 0.02% Silwet alone until uniformly wet.
(A) PR-1 expression in response to SA. Samples were taken daily after spraying. The c indicates control; plants were sprayed with 0.02% Silwet alone and sampled at 3 days after spraying.
(B) Effect of spraying plants with SA on P. s. maculicola ES4326 growth. One day after treatment, plants were infected with P. s. maculicola ES4326 at a dose of 103 cfu/cm2. Bacterial titer was determined 3 days after infection. Each bar represents the mean and standard deviation of eight replicates. Similar results were obtained in three other independent experiments. −SA, plants not treated with SA before infection; +SA, plants treated with SA before infection; wt, wild type.
Camalexin Accumulation in Wild-Type and nahG Plants Infected with Pathogens.
Wild-type (wt) Ler and Ler nahG transgenic plants were infected with either P. s. maculicola (Psm) ES4326 or P. s. maculicola ES4326 carrying avrRpt2 at a dose of 105 cfu/cm2. Camalexin in the infected leaves was determined at the times that camalexin levels are high in wild-type plants: 24 hr after infection for P. s. maculicola ES4326 carrying avrRpt2 and 32 hr after infection for P. s. maculicola ES4326. Each bar represents the mean and standard deviation of eight replicate samples.
SA is required both for PR-1 gene expression and for camalexin synthesis. In the case of PR-1, SA is both necessary and sufficient for increased PR-1 expression in response to pathogen attack (Ryals et al., 1996). In the case of camalexin accumulation, SA is not sufficient, because SA treatment does not lead to significant camalexin accumulation. Nevertheless, SA is required, because nahG-transformed plants fail to accumulate camalexin in response to P. s. maculicola ES4326 infection (Zhao and Last, 1996). We tested the accumulation of camalexin in wild-type and nahG plants infected with P. s. maculicola ES4326 or P. s. maculicola ES4326 carrying avrRpt2. As shown in Figure 4, camalexin levels in nahG plants infected with either pathogen were much lower than the levels in wild-type plants. Thus, SA is required for full induction of camalexin synthesis in response to either P. s. maculicola ES4326 or P. s. maculicola ES4326 carrying avrRpt2.
One possible explanation for the phenotypes of pad4 plants is that they accumulate reduced amounts of SA in response to P. s. maculicola ES4326 infection, resulting in reduced camalexin synthesis and reduced PR-1 expression. To test this idea, wild-type and pad4 plants were infected with P. s. maculicola ES4326 or P. s. maculicola ES4326 carrying avrRpt2, and both SA and its glucoside (SAG) were monitored over the course of the infection. Figure 5A shows that the SA levels in pad4 plants infected with P. s. maculicola ES4326 were lower than the levels in infected wild-type plants at all time points tested. In wild-type plants, SA levels were highest at 12 hr after infection, whereas in pad4 plants, SA levels were highest at 24 hr after infection. Figure 5C shows that after infection with P. s. maculicola ES4326, SAG levels were greatly reduced in pad4 plants. In contrast, when plants were infected with P. s. maculicola ES4326 carrying avrRpt2, there was very little difference between SA levels in pad4 and wild-type plants, as shown in Figure 5B. Figure 5D shows that after infection with P. s. maculicola ES4326 carrying avrRpt2, the SAG levels in pad4 plants were significantly lower than those in wild-type plants, but these differences were not as large as those observed in P. s. maculicola ES4326–infected plants (Figure 5C). Based on these results, it seems likely that the camalexin and PR-1 defects of pad4 mutants result from reduced SA accumulation in response to P. s. maculicola ES4326 infection.
SA and SAG Levels in Infected Wild-Type and pad4 Plants.
Wild-type (wt) and pad4 plants were infected with P. s. maculicola ES4326 (Psm), P. s. maculicola ES4326 carrying avrRpt2 (Psm avr), or mock infected with 10 mM MgSO4 (mock). Each column represents the mean of three replicate samples. Error bars representing the standard deviation are shown where they are large enough to be visible. SA and SAG were assayed on the same samples. The experiments with P. s. maculicola ES4326 and with P. s. maculicola ES4326 carrying avrRpt2 were conducted at different times; therefore, results should not be compared directly.
(A) SA levels in plants infected with P. s. maculicola ES4326.
(B) SA levels in plants infected with P. s. maculicola ES4326 carrying avrRpt2.
(C) SAG levels in plants infected with P. s. maculicola ES4326.
(D) SAG levels in plants infected with P. s. maculicola ES4326 carrying avrRpt2.
SA Application before P. s. maculicola ES4326 Infection Restores Camalexin Accumulation and PR-1 Expression in pad4 Plants.
Wild-type (wt) and pad4 plants were treated either with 5 mM SA in 0.02% [v/v] Silwet L-77 or with 0.02% Silwet alone 1 day before infection with P. s. maculicola ES4326.
(A) Effect of exogenous SA on camalexin levels in P. s. maculicola ES4326–infected plants. Infected leaves were sampled 2 days after infection. Each data point represents the mean and standard deviation of six replicates.
(B) Effect of exogenous SA on PR-1 expression in P. s. maculicola ES4326–infected plants. Leaves infected with P. s. maculicola ES4326 were sampled from mock-treated wild-type and pad4 plants (lanes 3 and 7) and SA-treated plants (lanes 4 and 8) 2 days after infection. For comparison, mock-treated plants were sampled 1 and 2 days after treatment (lanes 1 and 9, respectively, for the wild type; lanes 5 and 11, respectively, for pad4), as were SA-treated plants (lanes 2 and 10, respectively, for the wild type; lanes 6 and 12, respectively, for pad4). Similar results were obtained in another independent experiment. (+) and (−) in the row labeled SA indicate the presence or absence of SA treatment, repectively. (+) and (−) in the row labeled Psm indicate the presence or absence of P. s. maculicola ES4326 infection, respectively. Because of the strong PR-1 signal in leaves infected with P. s. maculicola ES4326, the exposure for this blot was shorter than was the exposure for the blot shown in Figure 3A; consequently, the expression of PR-1 48 hr after SA treatment appears lower than it does in Figure 3A.
If the reduction in SA accumulation in response to P. s. maculicola ES4326 infection observed in pad4 plants is the cause of the camalexin accumulation and PR-1 gene expression defects, then it should be possible to restore camalexin synthesis and PR-1 gene expression to P. s. maculicola ES4326–infected pad4 plants by supplying them with SA. Figure 6A shows that pad4 plants treated with SA before infection displayed much higher camalexin levels than did pad4 plants that were not pretreated with SA. In the experiment shown in Figure 6A, SA treatment of wild-type plants had little effect on camalexin levels. In some experiments, we observed significant reductions in camalexin levels in wild-type plants treated with SA, whereas SA always caused a large increase in camalexin levels in pad4 plants.
The possibility that SA treatment might also rescue the PR-1 expression defect of pad4 plants was tested. Wild-type and pad4 plants were sprayed with either 5 mM SA or water. After 1 day, plants were infected with P. s. maculicola ES4326, and PR-1 mRNA levels were assessed 2 days after infection. Figure 6B shows that 1 day after SA treatment, PR-1 mRNA levels were elevated in both wild-type and pad4 plants (lanes 2 and 6) and declined to barely detectable levels by day 2 (lanes 10 and 12). In plants that were treated with SA before infection, the PR-1 mRNA level in pad4 plants was comparable to that in wild-type plants (Figure 6B, lanes 4 and 8). The PR-1 expression in SA-treated, P. s. maculicola ES4326–infected pad4 plants cannot be solely due to the SA treatment, because the PR-1 mRNA level in pad4 plants treated with SA only had declined by 2 days after treatment. Rather, the SA treatment must have restored the ability of the pad4 plants to respond to P. s. maculicola ES4326, demonstrating that the PR-1 gene expression defect caused by pad4 is also reversed by SA treatment. The observations that SA treatment can reverse the camalexin accumulation and PR-1 gene expression defects of P. s. maculicola ES4326–infected pad4 plants provide strong support for the idea that reduced SA accumulation in pad4 plants is the cause of the camalexin and PR-1 defects.
We have previously described five complementation groups of pad mutants, defined as mutants displaying defects in camalexin synthesis in response to P. s. maculicola ES4326 infection (Glazebrook and Ausubel, 1994; Glazebrook et al., 1997b). Mutations in PAD1, PAD2, or PAD4 cause enhanced susceptibility to P. s. maculicola ES4326, whereas mutations in PAD3 or PAD5 have no effect on P. s. maculicola ES4326 growth (Glazebrook and Ausubel, 1994; Glazebrook et al., 1997b). One model (the regulatory model) explaining this result postulates that camalexin does not play a crucial role in limiting P. s. maculicola ES4326 growth but that PAD1, PAD2, and PAD4 are pleiotropic defense response regulators affecting expression of other defense responses, in addition to camalexin accumulation, that are important for limiting P. s. maculicola ES4326 growth (Glazebrook and Ausubel, 1994). An alternative model (the biochemical model) postulates that camalexin does play a crucial role in limiting P. s. maculicola ES4326 growth but that the pad3 and pad5 mutations block the camalexin biosynthetic pathway at a point such that antimicrobial camalexin precursors accumulate, compensating for the loss of camalexin itself (Glazebrook and Ausubel, 1994).
The results reported in this study demonstrating that PAD4 has pleiotropic effects on resistance responses are most consistent with the regulatory model for explaining the phenotypes of pad mutants. Mutations that affect regulation of defense responses are useful in dissecting the signal transduction pathways controlling expression of defense responses. The studies reported here strongly suggest that the pad4 mutation affects SA accumulation, thereby causing pleiotropic effects on expression of defense responses.
Figure 7 shows our working model of the role of PAD4 in defense response signaling. When plants are infected with P. s. maculicola ES4326, PAD4 is needed for SA concentrations to reach the level required for camalexin synthesis and expression of PR-1. In contrast, when plants are infected with P. s. maculicola ES4326 carrying avrRpt2, SA accumulates in a PAD4-independent manner. The accumulation of SA causes PR-1 expression in an NPR1/NIM1/SAI1–dependent manner. SA accumulation is necessary, but not sufficient, to activate camalexin synthesis. NPR1/NIM1/SAI1 is not required for camalexin synthesis. If the pad4 allele used in this work does not cause complete loss of function, then a single-pathway model could explain our results. In such a model, responses to P. s. maculicola ES4326 carrying avrRpt2 might be triggered by a strong signal that requires PAD4 function for its transmission but is adequately transmitted by a partially functional PAD4. In response to P. s. maculicola ES4326, this signal might be much weaker and inadequately transmitted by a partially functional PAD4.
Model for the Role of PAD4 in Signal Transduction.
When plants are infected with P. s. maculicola (Psm) ES4326, PAD4 function is needed for SA accumulation and activation of defense responses that require SA, such as camalexin synthesis and PR-1 expression. When plants are infected with P. s. maculicola ES4326 carrying avrRpt2, SA accumulation occurs by a PAD4-independent mechanism.
In leaves infected with P. s. maculicola ES4326 carrying avrRpt2, PAD4 does not play a major role in activation of defense responses. However, it is likely that PAD4 is required for activation of responses during some other gene-for-gene resistance responses. In previous work, we showed that pad4 mutants fail to demonstrate resistance to several different avirulent isolates of the oomycete pathogen Peronospora. Although wild-type plants challenged with these parasites allowed little or no sporulation, pad4 plants allowed profuse sporulation (Glazebrook et al., 1997b).
Mutations in EDS1 (for enhanced disease susceptibility) also cause increased susceptibility to virulent pathogens (P. s. tomato DC3000 and compatible Peronospora isolate Emwa1) and to some but not all avirulent pathogens (many avirulent Peronospora isolates but not P. s. tomato DC3000 carrying avrB) (Parker et al., 1996). Recent results suggest that EDS1 is required for gene-for-gene resistance responses mediated by the TIR-NBS-LRR (for Toll/Interleukin-1/resistance–nucleotide binding site–leucine rich repeat) class of resistance genes (J. Parker, personal communication). The spectrum of pathogens affected by the pad4 and eds1 mutations differs in that the eds1-1 mutant is susceptible to the non-host Peronospora isolate P-006, whereas pad4 is not (Parker et al., 1996; Glazebrook et al., 1997a). Comparison of the Arabidopsis–pathogen interactions affected by pad4 and eds1 is complicated by the fact that pad4 is in the Col background, whereas the eds1-1 allele is in the Wassilewskija (Ws) background, and there are many differences in genes affecting disease resistance between the two ecotypes. In the future, analysis of pad4 and eds1 alleles that recently were isolated in the Ler background will allow comparison of pad4 and eds1 phenotypes in the absence of potentially interfering differences between ecotypes, thereby helping to resolve the issue of whether EDS1 and PAD4 act in the same or different pathways (J. Parker, personal communication).
The phenotypes of pad4 and eds1 mutants support the idea that different gene-for-gene resistance responses lead to resistance via different signaling pathways. Presumably, these pathways converge at some point, but the observation that gene expression patterns in response to bacteria carrying the avirulence gene avrRpt2 are quite different from the patterns in response to bacteria carrying the avirulence gene avrRpm1 suggests that the differences between pathways may be extensive (Reuber and Ausubel, 1996; Ritter and Dangl, 1996). Furthermore, both pad4 and eds1 mutants affect growth of compatible pathogens in addition to growth of certain incompatible pathogens, suggesting that elements of the signal transduction pathway(s) activated by recognition of certain avirulent pathogens are also involved in signal transduction in response to infection by certain virulent pathogens.
The genes PR-1, PR-5, and BGL2 are coordinately induced in response to treatment with SA. When plants were infected with P. s. maculicola ES4326, the phenotypes of pad4 plants revealed differential regulation of defense responses. Synthesis of camalexin and expression of PR-1 were reduced in pad4 plants. Expression of PR-5, BGL2, and ASA1 were less strongly affected. The eds5 mutation also causes reduced PR-1 expression in response to P. s. maculicola ES4326 infection but has no effect on the expression of PR-5 and BGL2 or on camalexin synthesis (Rogers and Ausubel, 1997). The npr1/nim1/sai1 mutations cause similar effects in that mRNA levels of PR-1, but not those of PR-5 or BGL2, are reduced in response to pathogen infection. This does not seem to be due to "leakiness" of the alleles, because expression of PR-1, PR-5, and BGL2 in response to SA treatment was completely abolished in the npr1/nim1/sai1 mutants (Cao et al., 1994; Delaney et al., 1995; Glazebrook et al., 1996; Shah et al., 1997).
These results are difficult to reconcile with the idea that expression of PR-1, PR-5, and BGL2 in infected leaves is due solely to coordinate regulation through the SA pathway. One possible explanation is that an SA-independent pathway acts in conjunction with the SA-dependent pathway to control expression of PR-1, PR-5, and BGL2, and the relative contribution of each pathway varies among the different genes (this potential pathway is not shown in Figure 7). An alternative explanation is that expression of each gene could be variably affected by different mutations because of quantitative differences in their induction. Such differences could result partly from the fact that in infected leaves, both the fold induction and the absolute expression level of PR-1 are much higher than those of PR-5 or BGL2.
Camalexin synthesis in response to X. c. campestris BP109 infection or silver nitrate treatment was not affected by pad4. These stimuli induce much less camalexin synthesis than does infection by P. s. maculicola ES4326. Possibly, such low levels of camalexin synthesis do not require PAD4 function. The quantities of camalexin synthesized by pad4 plants in response to P. s. maculicola ES4326 infection are greater than are the amounts in wild-type plants infected with X. c. campestris BP109 or treated with silver nitrate.
The observation that SA treatment can reverse the defense response expression defects of pad4 plants raises interesting questions about the relationship between SA levels and PR-1 gene expression. Treatment of pad4 plants with SA 1 day before P. s. maculicola ES4326 infection restored PR-1 gene expression 2 days after infection (3 days after SA treatment). In contrast, by 2 days after SA treatment, PR-1 expression in uninfected leaves was very low. Does this imply that SA levels at this time are also very low? If so, how does SA treatment restore PR-1 expression in pad4 plants? If SA levels are still high 3 days after treatment, then why are PR-1 mRNA levels low? Low levels of SA potentiate responses to pathogen attack (Shirasu et al., 1997), and evidence supports the idea that there is a feedback loop in the SAR signal transduction pathway (Ryals et al., 1996), further complicating analysis of the role of SA in signal transduction.
In conclusion, we have shown that PAD4 is a regulator of defense responses and acts upstream from SA to affect expression of PR-1 and camalexin synthesis. PAD4 function does not seem to be required for these defense responses when plants are infected with P. s. maculicola ES4326 carrying avrRpt2, suggesting that there is a PAD4-independent mechanism that supplies SA in response to this avirulent strain. Further analysis of the responses of pad4 plants to pathogen attack is likely to reveal more interesting features of the regulatory mechanisms controlling expression of defense responses in plants.
Wild-type plants (Arabidopsis thaliana ecotype Columbia [Col]) and pad4 plants from a line that had been backcrossed four times to the wild-type parent (Col) (Glazebrook et al., 1996) were used in this study. Arabidopsis ecotype Keswick (Ksk) was a gift from E. Holub (Horticulture Research International, Warwick, UK). Landsberg erecta (Ler) plants carrying the nahG transgene were a gift from X. Dong (Duke University, Durham, NC) (Bowling et al., 1994). Plants were grown in pots in Metro-Mix 200 soil (Scotts-Sierra Horticultural Products Company, Marysville, OH) in a growth chamber (22 ± 2°C, 85% relative humidity, 100 μE m−2 sec−1 fluorescent illumination) on a 12-hr-light and 12-hr-dark cycle. Fully expanded leaves of 4-week-old plants were used for all experiments.
Pseudomonas syringae pv maculicola ES4326 (Dong et al., 1991), P. s. pv tomato DC3000 (Cuppels, 1986), and Xanthomonas campestris pv campestris BP109 (Weiss et al., 1994) have been described previously. The avirulence gene avrRpt2 was carried on plasmid pLH12, as described previously (Dong et al., 1991; Whalen et al., 1991). P. syringae strains were grown in King's B medium supplemented with appropriate antibiotics (Glazebrook and Ausubel, 1994), and X. c. campestris BP109 was grown in Luria-Bertani medium supplemented with 50 μg/mL rifampicin. Bacteria were infiltrated into Arabidopsis plants, as described by Glazebrook and Ausubel (1994). Unless stated otherwise, for camalexin assays, the bacterial dose for P. syringae strains was 3 × 104 colony-forming units (cfu)/cm2 leaf area (equivalent to OD600 = 0.006); for X. c. campestris BP109, it was 5 × 105 cfu/cm2 (OD600 = 0.1). For experiments involving extraction of total RNA from infected leaves, P. s. maculicola ES4326 and P. s. maculicola ES4326 carrying avrRpt2 were introduced at a dose of 104 cfu/cm2 leaf area (equivalent to OD600 = 0.002). For determination of P. s. maculicola ES4326 growth, plants were infected with P. s. maculicola ES4326 at a dose of 103 cfu/cm2 leaf area (equivalent to OD600 = 0.0002). After 3 days, leaves were excised and bacterial growth was assayed, as described by Glazebrook et al. (1996). Data are reported as means and standard deviations of the log (cfu/cm2) of six replicates. For chemical treatment, plants were sprayed with 5 mM SA or 5 mM silver nitrate with 0.02% Silwet L-77 (Lehle Seeds, Round Rock, TX) to reduce surface tension. Control plants were sprayed with water containing 0.02% Silwet L-77.
For P. syringae–infected leaves, fresh weight changes markedly over the course of infection because of water loss from the infected tissue. Therefore, for P. syringae–infected leaves, samples consisted of four leaf discs cut with a number 3 cork borer (1.1 cm2 total), and camalexin concentrations were normalized to leaf area. For leaves infected with X. c. campestris BP109 or treated with silver nitrate, samples consisted of ~100 mg of tissue, and camalexin concentrations were normalized to fresh weight. Camalexin assays were performed as described by Glazebrook et al. (1996). For each data point, the results are reported as the mean and standard deviation from six replicates.
Tissue samples consisting of three to five leaves were collected and frozen in liquid nitrogen and stored at −80°C. Total RNA was extracted, and 5 μg of RNA per sample was separated on formaldehyde–agarose gels (Ausubel et al., 1995; Reuber and Ausubel, 1996). After blotting onto a Hybond-N+ membrane (Amersham Corp., Arlington Heights, IL), hybridizations were performed using various digoxigenin-labeled probes described below, followed by washes in 0.5 × SSC (1 × SSC is 0.15 M NaCl and 0.015 M sodium citrate) at 65°C and chemiluminescent detection with CSPD, according to instructions provided by the supplier (Boehringer Mannheim). For hybridization with more than one probe, blots were stripped and reprobed. Single-stranded DNA probes were prepared by amplification of appropriate sequences from cDNA clones (PR-1 and PR-5; Uknes et al., 1992) and from plasmid pATBG12 (BGL2; Dong et al., 1991), as described by Glazebrook et al. (1996), except that digoxigenin-11-dUTP was used as the label, according to the instructions of the supplier (Boehringer Mannheim). For the ASA1 probe, a single-stranded probe was made from plasmid pKN41 (Niyogi and Fink, 1992) by using sense primer 5′-GCTTACCGTTGTTTGGTC-3′ and antisense primer 5′-AGCAATGTCCATGTCACC-3′. For the 18S rRNA probe, a single-stranded probe was made from the clone JHD2-15A (stock no. CD3-197; Arabidopsis Biological Resource Center, Ohio State University, Columbus, OH) by using sense primer 5′-CTGGTTGATCCTGCCAGTAG-3′ and antisense primer 5′-CAGGTTCACCTACGGAAACC-3′. Blots were stripped and reprobed with the 18S rRNA probe to assess equal loading of RNA samples.
Mature leaves of 4-week-old wild-type and pad4 plants were infected with P. s. maculicola ES4326 at a dose of 104 cfu/cm2 (equivalent to OD600 = 0.002) or mock infected with 10 mM MgSO4. At intervals after infection, samples were collected (1 g of tissue per sample, from approximately seven plants) and frozen in liquid nitrogen. SA and SAG were determined as described by Bowling et al. (1994). Raw data were multiplied by 2 to reflect 50% recovery of SA and SAG in this assay.
This work was supported by start-up funding awarded to J.G. by the University of Maryland Biotechnology Institute, Grant No. MCB 9723493 from the National Science Foundation to J.G., and Grant No. MCB 9723952 from the National Science Foundation to D.F.K. We thank the Arabidopsis Biological Resource Center at Ohio State University and Craig S. Pikaard for providing clone JHD2-15A, Jane Parker and Xinnian Dong for permission to cite unpublished results, Eric Holub for the gift of Ksk seed, Xinnian Dong for the gift of transgenic Ler plants carrying nahG, and Fumiaki Katagiri for critical reading of the manuscript.
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NDA 020685 describes CRIXIVAN, which is a drug marketed by Merck Sharp Dohme and is included in one NDA. It is available from three suppliers. There is one patent protecting this drug. Additional details are available on the CRIXIVAN profile page.
The generic ingredient in CRIXIVAN is indinavir sulfate. There are two drug master file entries for this compound. Three suppliers are listed for this compound. Additional details are available on the indinavir sulfate profile page.
Patent: ➤ Try a Free Trial Patent Expiration: Feb 10, 2021 Product Flag? Substance Flag? Delist Request?


Most young drivers in regional communities consider themselves good drivers. And too often that confidence leads to complacency and the misconception that they are immune from road accidents. The TAC Safe Series campaign was created to demonstrate to young drivers that the safe system applies to them too, by twisting the typical road safety messages through the lens of something they know and understand - football. AFL ambassadors were enlisted as commentators, highlighting similarities between the game and the roads. Not only did they pay tribute to the great game, but their commentary gave us an analysis and room for advice and opinions on this very important topic.


Panasonic has unveiled two new smartphones, the P11 and T11, these devices are available on online websites. The Panasonic T11 is priced at Rs. 9,520 and the Panasonic P11 is priced at Rs. 16,364.
The Panasonic T11 features a 4 inch display and is powered by a 1.2 GHz quad-core processor along with a 1 GB of RAM. The device has a 4 GB of inbuilt storage which is expandable up to 32 GB via micro SD card. Panasonic T11 has a 5 MP rear camera and a VGA front facing camera. This device runs on Android 4.1 Jelly Bean and sports a 1,500 mAh battery.
Whereas, the Panasonic P11 comes with a 5 inch HD IPS display with a resolution of 1280 x 720 pixels and is powered by a 1.2 GHz quad-core processor along with a 1 GB of RAM. This device sports a 8 MP auto focus rear camera with LED flash, the device also have a 2 megapixel front-facing camera. Panasonic P11 has an inbuilt storage of 4 GB which can be expanded up to 32 GB via micro SD card. This device also runs on Android 4.1 Jelly Bean and sports a bigger 2,000 mAh battery, P11 also comes up with Dual SIM support along with 3G.
Whats happening Mr. Barath Nagpal, no video reviews since too many weeks..


text:
Comparative Balkan Politics – Call for Papers
Centre for Monitoring and Research CeMI has published a Call for Papers in the field of comparative politics and international studies for the first issue of the journal Comparative Balkan Politics (CBP). CBP is a new annual journal that forms part of the project "Balkan Comparative Electoral Study: Impact of Personal Vote on Internal Party Relations", implemented within the Regional Research Promotion Programme in Montenegro, Serbia, Kosovo and Bosnia and Herzegovina. Its scope is defined broadly to include comparative studies in politics, economy, and social science in all of the Balkans and Southeast Europe, as well as in countries that have strong ties to the region, and comparative studies of countries that give new insights to developments in the Balkans. CBP aims to publish original articles that give new insights into Balkan politics in order to promote better understanding and informed debate on political processes in Southeast Europe.
The first issue of the CBP will include a special section on internal party democracy, welcoming research articles with both theoretical and empirical perspectives, under an open call for papers. Prospective authors are encouraged to make use of recently published Comparative Candidate Survey data for Bosnia and Herzegovina, Kosovo, Montenegro, and Serbia. This data will become available under Survey section on the Main Menu of the website www.balkanelectoralstudies.org.
Research articles not focusing on internal party democracy, as well as review articles, electoral notes, and policy notes will also be accepted within the general section of the journal.
All manuscripts are accepted in English language. The deadline for submitting manuscripts is 20th of July 2015.
More information on submission procedure and instructions for authors can be found at http://balkanelectoralstudies.org/…/editori…/call-for-papers.


I've been taking zoloft at 200mg for the past 5 years. Prior to that I was taking 100mg. I started taking it when I was in high school, and now I'm 29. On top of that, I'm a poster child for ADD. I started taking Ritalin and other similar medications when I was in third grade.
About 7 years ago, near the end of college, I started noticing memory loss problems. This was both troublesome and frustrating because I'm also a hypochondriac. Were these problems real or merely a manifestation of my OCD issues?
Now I'm concerned... I really need to stay on this medication to stay sane, but I don't want to lose my memory! My work requires a very good memory, and I've found that older coworkers seem to have a better memory than I do!
I also suffer from OCD, now Zoloft does cause memoroy loss I do not know if it is permanent, with regrds to amphetamines, I have never read anything about memory loss.
Stop for one minute and think how many children worldwide suffer from what you did and grow up to be regular or "normal" persons.
Know you being hypochondriac and also suffering from OCD let us say it is more than just a ·dramatic" state of mind to be on, to tone it down a bit .
It is all in our minds... and you are educated and you know that are our minds are very, very strong and can deceipt us anytime they want..and also as I am sure you are aware we are our own worse enemies... with all these mental conditions it makes even worst. For regular perons it is hard for it is tremendously difficult to deal with... we must be always prepared also awared of who and what we are and accept it..do not fear it, it is in us... part of our very essence.
I am 41 years old manic depressive, paranoid, anxiety, OCD, insomnia, etc..that is enough for know,regarding myself.
Learn to control your mind, your emotions, your feelings , your fears..do not let them control you... for if they do you are ... I will not say... because I am here to help you within my means. It is very hard to achieve the only way to learn is to fall and get up again and again and never ever give up and every time you get up you gain knowledge, experience ,courage and strength no matter if it is good or bad as Enistein said "there are no good or bad experiences for they are only experiences", this means always rescue the positive things in life.
Being it is commonly associated as a psyche drug. In advance of upping my dosage from 100mgs. to 300mgs. daily to deal with my worsening OCD issues. My wife and I discussed the added risks I'd be taking, in one critical dimension. Loss of memory. We agreed jointly, that the risks of toning down the OCD dilemmas was worth it. Now, I am not so sure. The memory losses have been ridiculously monumental. And have, and are, causing me deliberant, frequent consternation. Including increasing episodes of indiscreet embarrassments.
Presently, before I am willing to quit or lower the Zoloft/sertraline to 100mgs., perhaps someone with longterm experiences using sertraline, will share their views.
I have been on Effexor for years/I've heard people complain that they think it causes memory loss. My memory isn't good compared to before meds.. I have taken Adderall for years, too. I haven't read anything about it effecting memory. However, a study was just done/can be found in Scientific American-it found that people who take stimulants are at a higher risk of developing depression. The reason-researchers found the drugs actually change the structure of the brain-more so than cocaine!
My point, my pdoc has tried to get me off the stimulants completely-but I can't-if I go off completely it sends me into a depression. (this happened way before I read the study) I have BP II Spectrum disorder. I should never have been placed on stimulants-long story. But, if they can alter the brain where people are more prone to depression-not a far stretch to say they could do something to memory long term.
I must say I admire people like you, who know and have the confidence of what they are refering to... this speaks very highly of you.
I read up on Effexor it's ok. But I am looking for a solution to taking adderall, it's just not working and it's making my adrenals very tiered. Wellbutrin can not be used with adderall and I am willing to let it go, Wellbutrin is good for ADDD and no weight gain,, it has dopamine, and nerephine and with some Prozac for serotonin. I think I have a plan. Besides stimulants make you old and saggy. Keep your youth and your memory. The fish oil is the best... Good luck, be well. O'.
I had been taking zoloft for about a year and a half and my brain has completely started forgetting things, Ive been constantly researching things in DSM and other books on anti-depressants, they do say its possible but the chances of it happening are within 1% of patients.
Zoloft made me way too sleepy. I don't recall having memory issues (heh), but I was about a decade younger then.
Cymbalta does give me memory loss issues, mostly with bringing an old familiar fact to mind. It's incredibly annoying. And most of these drugs do result in cognitive impairment.
I'm going off all of mine and seeing where i'm at.
I believe Zoloft ABSOLUTELY causes memory loss. I was on 100mg daily for anxiety for 7 years. It worked great for the anxiety. For my cognition-not so much.
I first noticed something a few weeks after starting it. We were playing Scrabble and I couldn't come up with anything. This made an impression bc this was very unusual for me. I am a college grad, was always top of my class, and highly intelligent regarding memory, facts, a clear mind, vocabulary, figuring things out, etc. My mind was now so "dull" I felt the majority of my vocabulary was "inaccessible" during the game. But I felt well emotionally so I ignored this "side effect." I now wish I had taken it more seriously.
Over the years, I noticed I would often forget things or be confused. It would at times be embarrassing when I would forget important things that people had just shared with me. To them I'm sure it seemed as if I wasn't listening or didn't care. The problem was that I just couldn't remember conversations, places I'd been, or things I'd done.
My Husband looked at me puzzled and thought I was kidding. When he reminded me of the whole scenario I was then able to remember doing it.
Over the years this has happened over and over again. Unfortunately I am not even aware of how much I have forgotten. Towards the end, I went into deep depression because my brain was so foggy and useless that I was convinced I must have early onset dementia. After undergoing many memory tests they deemed I did not have it, but could not explain the memory loss. I reiterated my feelings to the Dr that this all started when I began using Zoloft. She said that there wasn't any medical data to back up what I was saying but she would switch my medication at my request.
So I made the decision to get off this brain deteriorating drug, despite the possible emotional side effects I was in for with a drug change. We tried several different drugs before we found one that worked. A I am currently on Lexapro for my anxiety. My hope was that once I discontinued the Zoloft my memory loss would improve. Sadly, it did not so there seems to be permanent damage. It is too late for me, but I hope that this response may help others contemplating using Zoloft to make an informed decision. I realize it is possible that all the antidepressants have a similar effect, but I can only speak for my results on Zoloft. On a side note, I don't feel as if my memory has gotten any worse on Lexapro so hopefully this one is not doing further damage. I wish my anxiety levels were at a place I could do without any of these meds but unfortunately that is not the case. I also wish that more medical research will be done to confirm these side effects, therefore warning the public of the possible outcome, but with the deep pockets of the pharmaceutical companies this will probably not happen anytime soon.
I now joke that it's a good thing I was so smart to start with, otherwise there would be NO brain cells left.
I think Zoloft caused permanent brain damage and more depression than I had before. I was only on 50mg for about 3 months but started having serious memory problems like having no clue where I parked. Not even a general direction. The scariest part was that I noticed when people were talking to me things stopped registering. Like I was trying to listen but couldn't. I stopped hoping this would go away but it didn't after over 2 yrs now. And now I'm left with more depression than before and serious cognitive issues. I might not be able to keep my job or function in life anymore.
When do you know if you are ready to taper of your meds? I have depression and anxiety (GAD, PTSD,?
Are we aware of the risks of Adderall with SSRI, SSNRI, DMX?
Chantix - Experiencing slight OCD behavior or amphetamine type reaction?