text:
Heroes of Annihilated Empires – I Was Tricked!
I was tricked! There is no other way to say it. Heroes of Annihilated Empires was a game I played for a bit years ago and kept thinking about playing again ever since. It had this original and rarely used theme that I really wanted to explore fully.
Now, years later, I can honestly say I was completely wrong. It did not have this theme. It only looked like it did.
More than half a dozen years ago…
I can't say for sure, but considering Heroes of Annihilated Empires was released in 2006, and that was still well into the age of piracy for me, I can pretty confidently guess I gave this game a shot as soon as it was released.
The intro starts in an epic fashion, with an elven civilization fighting off an army of the undead. That's the intro I watched back then, mind you. None of the videos in the version I bought off of GOG.com are willing to play on my machine, so I'm speaking purely from memory (and YouTube). It looks cool and all, but it's nothing remarkable or unseen. What is remarkable and what piqued my interest in the first place was what happens after the battle.
There's a lone skeletal warrior wandering around the battlefield. There's a portal opening behind him, a noise, followed by a strange metallic sound and then a click of electric lights turning on and illuminating the skeleton. I won't try to maintain the mystery. It freaking sounds like a tank rolled out of the portal and turned on headlights!
I can't find a great video on YouTube, but this one shows the intro to Heroes of Annihilated Empires, so it should show you what I'm talking about.
Back then, I watched that video several times and played through the first mission or two. I may have even been playing a demo, for all I can remember. I'm pretty sure there was a part in one of the missions I played, where an actual, moving, in-game tank was fighting off a horde of rats or goblins or something.
Heck, even the trailer for the game was giving hints of aerial combat with actual, modern airplanes in a fantasy world. It's all the way at the end of the trailer, and it's short, but it hints at it.
I bought the game on GOG.com because it was heavily discounted and I got the itch.
I installed it, but couldn't watch the intro because the videos don't play on my machine.
The first mission sucks
It's hard. Really hard. And not in a good way.
It's just isn't really explained to you what you're supposed to do. Civilians are running away from the undead and Elhant, the hero and protagonist of the game, is supposed to save them. It's pretty easy for a while. Eventually, you get to advance through the level close enough to the origination point of the undead that something triggers. At that time, Elhant dismisses his entire army for story reasons and orders them to retreat as well.. The problem with that is, the undead are still advancing, there are still plenty of civilians on the map and they move more slowly than the undead. There's really very little that can be done if the trigger happens at the wrong moment and more often than not, it's the wrong moment.
Pictured: Elhand about to tackle some hell hounds.
Luckily, that's just the first mission and I don't give up that quickly.
The rest of the game is easy
Well, not all of it is easy, but all of it absolutely is easier than the first mission.
There are a few cases where the enemy troops can overwhelm the home base which triggers a defeat because some important character died or a building got destroyed. In all other cases, you can easily rely on the extremely poor enemy AI to get ahead and eventually win a mission.
The AI is just bad
Elhand is a ranger, so he has access to ranged attacks. Equipping a melee weapon also makes him a formidable melee attacker, but for most of the game, due to the bad AI, ranged is the way to go.
All it takes to beat the AI is to stand at max range and start shooting. Once the enemy gets close enough, the player can run away for a bit and the enemy will soon give up the chase and go back to where it started. Even better, if Elhand continues shooting at that point, the enemy will ignore the damage and keep slowly retreating. Only once it reaches the starting point will it charge again.
Pictured: A not very well done in-game cutscene. They're quite common.
In some rare cases, the AI even goes more bananas than what I just described. It will sometimes just stand in place and ignore all attack completely. At times, it will wander randomly, as if the path finding algorithm couldn't find a path to the troops attaching him. At other times, it will keep moving towards Elhand, but won't attack at all when it reaches him, opting to persist at trying to move into the space Elhand occupies, pushing him backwards.
With that and smart selection of level-up upgrades (range, damage, movement and attack speed), the game just becomes a chore to get through past the first mission. A fun chore, to be fair, but ultimately challengeless.
The story gets weird
Elhand is kind of a douche sometimes. He can get pretty sexist to.
I remember there was an instance where he was admiring Lana, another character and playable hero (at moments) in the game. He was saying how she's "beautiful and a pretty decent warrior. She could never match a male warrior, being a woman, but still, good effort".
Other characters can get weird, so maybe it was on purpose. I don't know. All I know is it gets weird.
How was I tricked?
That's the question, really, isn't it?
In case you haven't figured out, I bought the game because I remember loving the idea of real-world military troops fighting it off against fantasy races.
There is none of that in Heroes of Annihilated Empires.
Pictured: One of the many hints of the theme I was excited about. A crashed airplane.
On almost every map, there's an unexplained shot down airplane or a destroyed thank. You keep encountering them, from beginning to end. They never get acknowledged by in-game characters though, and nothing ever comes out of it.
I kept playing through all 15 or 16 campaign levels and got nothing out of that theme I was so looking forward to. The game just ended.
What's worse, since videos don't play for me, when the final level was done, I just got thrown to the credits screen like nothing happened.
So what did happen?
My best guess is, since Heroes of Annihilated Empires was originally supposed to be a trilogy, the actual real-life armies were supposed to come in at a later time. Since we never got the other two games in the trilogy, I guess this is it.
I can't say I'm angry, just disappointed.
The AI sucks, the maps aren't amazingly designed, there are bugs and annoyances, but overall, Heroes of Annihilated Empires offered a fun mix of RTS and RPG that I ended up enjoying, even though the game made a fool out of me.
Like? Share!
Sorcerer King – Not Quite Master of Magic
Heroes of Might and Magic – The Other Part of the Franchise
Age of Wonders [3] – A Mission Together, Part 2
Age of Wonders [1] – Pretty Cool
Dota 2 [1] – How to Suck and Not Feel Bad About It
About Nikola
An avid gamer, programmer and all-around geek with a dream to one day write something people actually read. Be sure to let him know if you like what he does. It's really good for his ego. View all posts by Nikola →
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o Children: 4-8 year olds need 5 cups; 9-13 year olds need 7-8 cups per day; 12-18 year olds need 8-11 cups of water per day.
What are the benefits of drinking so much water? Water is essential in keeping your body temperature within normal range, cushions your joints, protects your spine, and helps to eliminate waste in your body. On top of those medical reasons, water also helps keep your skin looking healthy and vibrant. If those reasons are not enough, water is also an excellent way to help manage your weight and boosts your energy levels throughout the day!


text:
package org.xbmc.kore.testutils.tcpserver.handlers.jsonrpc.response.methods;

import com.fasterxml.jackson.databind.JsonNode;
import com.fasterxml.jackson.databind.node.ArrayNode;
import com.fasterxml.jackson.databind.node.ObjectNode;

import org.xbmc.kore.testutils.tcpserver.handlers.jsonrpc.JsonResponse;

/**
 * Serverside JSON RPC responses in Playlist.*
 */
public class Playlist {

    public enum playlistID {
        AUDIO, VIDEO, PICTURE
    }

    /**
     * JSON response for Playlist.GetItems request
     *
     * * Example:
     * Query:   {"jsonrpc":"2.0","method":"Playlist.GetItems","id":48,"params":
     *              {"playlistid":0,"properties":["art","artist","albumartist","album",
     *                                            "displayartist","episode","fanart","file","season",
     *                                            "showtitle","studio","tagline","thumbnail","title",
     *                                            "track","duration","runtime"]
     *              }
     *          }
     * Answer:  {"id":1,"jsonrpc":"2.0","result":{"items":
     *                                            [
     *                                             {"album":"My Time Is the Right Time",
     *                                             "albumartist":[],
     *                                             "art":{"artist.fanart":"image://http%3a%2f%2fmedia.theaudiodb.com%2fimages%2fmedia%2fartist%2ffanart%2fxpptss1381301172.jpg/"},
     *                                             "artist":["Alton Ellis"],
     *                                             "displayartist":"Alton Ellis",
     *                                             "duration":5,
     *                                             "fanart":"image://http%3a%2f%2fmedia.theaudiodb.com%2fimages%2fmedia%2fartist%2ffanart%2fxpptss1381301172.jpg/",
     *                                             "file":"/Users/martijn/Projects/dummymediafiles/media/music/Alton Ellis/My Time Is The Right Time/17-Black Man's Word.mp3",
     *                                             "id":41,
     *                                             "label":"Black Man's Word",
     *                                             "thumbnail":"",
     *                                             "title":"Black Man's Word",
     *                                             "track":17,
     *                                             "type":"song"}
     *                                            ],
     *                                     "limits":{"end":1,"start":0,"total":1}}}
     *
     * Playlist empty answer : {"id":48,"jsonrpc":"2.0","result":{"limits":{"end":0,"start":0,"total":0}}}
     *
     * @return JSON string
     */
    public static class GetItems extends JsonResponse {
        public final static String METHOD_NAME = "Playlist.GetItems";

        int limitsEnd;

        public GetItems(int id) {
            super(id);
        }

        @Override
        public String toJsonString() {
            setLimits(0, limitsEnd, limitsEnd);
            return super.toJsonString();
        }

        public void addItem(Player.GetItem playerItem) {
            ObjectNode resultNode = (ObjectNode) getResultNode(TYPE.OBJECT);
            JsonNode item = playerItem.getResultNode().get(Player.GetItem.ITEM);
            addToArrayNode(resultNode, "items", item);

            limitsEnd++;
        }
    }

    /**
     * JSON response for Playlist.GetPlaylists response
     *
     * Example:
     * Query:       {"jsonrpc":"2.0","method":"Playlist.GetPlaylists","id":31}
     * Response:    {"id":31,"jsonrpc":"2.0","result":[{"playlistid":0,"type":"audio"},{"playlistid":1,"type":"video"},{"playlistid":2,"type":"picture"}]}
     */
    public static class GetPlaylists extends JsonResponse {
        public final static String METHOD_NAME = "Playlist.GetPlaylists";

        public GetPlaylists(int id) {
            super(id);

            ArrayNode playlists = createArrayNode();
            playlists.add(createPlaylistNode(playlistID.AUDIO.ordinal(), "audio"));
            playlists.add(createPlaylistNode(playlistID.VIDEO.ordinal(), "video"));
            playlists.add(createPlaylistNode(playlistID.PICTURE.ordinal(), "picture"));

            setResultToResponse(playlists);
        }

        private ObjectNode createPlaylistNode(int id, String type) {
            ObjectNode playlistNode = createObjectNode();
            playlistNode.put("playlistid", id);
            playlistNode.put("type", type);
            return playlistNode;
        }
    }
}

redpajama_set_name: RedPajamaGithub


Who will be using the project?
Consider creating a "Simplified Menu" for users who get lost in Paratext.
Have you downloaded all the available resources that are available to you in Paratext?
Are there still resources that you would like access to that are not available in Paratext?
You may consult this page about resources in Paratext, and use the link to a form at the bottom to request new resources.
What additional projects should be created to support the primary project?
Is there a dictionary to be linked to the project?
Link a FieldWorks dictionary in the Project in Project Properties and Settings, Associations tab.
What Biblical Terms list will be used for the project?
Will you use the default major Biblical terms list, or a customized list for the project?
Set the Biblical Terms list in Project Properties and Settings, Associations tab.
Notes are a major part of every project. Don't settle for the default red flags!
Configure how the windows are arranged on the desktop.
To save screen space, arrange the resource texts most frequently used in a text collection window, and save the collection.
Do you have what you need to enter characters efficiently?
Is the correct language identifier being used for the language? This is very important as it helps identify which languages have work being done.
BCP-47 Standard should include the 2 or 3 letter language code, and additional codes, only if they are needed to uniquely identify the language or script by distinguishing it from others in existance.
Set all of the alphabetic characters here, following the instructions in the User Guide.
Give special attention to Word-medial punctuation. Any non-alphabetic characters that may appear inside of a word (such as a dash joining compound words), must be added here. Otherwise, the word will be broken into two words.
Do you want to use the literary characters "ɑɡ" instead of the typographic characters "ag". These and other character preferences can be selected if using one of the SIL fonts with font features enabled.
When a project is brand new, there aren't a lot of settings that can be set in concrete.
As the project matures, some of the inventories begin to make sense.
What quotation system will be used?
Characters Inventory: Either combine letters with diacritics or display characters separately.
Select Show sequences to view sequences of punctuation characters.
Clear Show sequences to view individual punctuation characters categorized by the contexts in which they occur (for example, Word Final). An underscore character preceding or following an item in the Punctuation column represents a space.
If the project does not have Quotation Rules set, a reddish bar will appear under the title bar of the inventory. Click Quotation Rules to the right of the reddish bar to set the Quotation Rules.
Markers Inventory: Standard Format markers. The stylesheet determines validity.
Unmatched Pairs of Punctuation: Unmatched punctuation characters (punctuation which is typically one of a pair, but is not matched by its counterpart).
Repeated Words: Words followed by repeated occurrences of themselves (for example, had had or the the).
Markers Missing Final Sentence Punctuation.
Select Show All Final Punctuation to display the individual characters that are the final characters of text that is preceded by a paragraph style marker.
Clear Show All Final Punctuation to group together all characters that are not sentence-final punctuation characters, but are final characters of text that is preceded by a paragraph style marker.
Markers Followed by a Lower Case Letter: Standard Format markers which are typically sentence-initial, but are followed by a lowercase letter.
Select Show sequences to view unique sequences of punctuation that are followed by a lower case letter.
Clear Show sequences to view individual punctuation characters which are typically sentence-final, but are followed by space, and then a lowercase letter.
Mixed Capitalization: Words which have capitalization other than initial uppercase followed by all lowercase.
Even before books are translated, you will be writing cross-references or notes which refer to passages in them. For this to succeed later on, you will need to name those books in advance.
Page last modified on Tuesday March 12, 2019 12:34:25 GMT-0000 by dhigby.


Modern condo in the heart of Bellevue offers one of the best views of downtown and Lake WA. Situated on the 40th floor in the luxurious Bellevue Towers. Amazing great room floor plan, hardwoods, balcony and wall of windows. Chefs style kitchen with high end appliances, granite counters & bksplash, custom cabinetry, Viking range- luxury at it's best. Amentities include gym, spa, sauna, theater, conference room, roof top park, 3 outdoor terraces and 24/7 concierge service. 3 parking spots!
Click a link below to view information and images from the prior sale or listings of 10700 NE 4th St 4002.
Directions to 10700 NE 4th St 4002 Bellevue, WA: West on 4th ST from 405. Right on 106th. Pass building and take right into driveway at Galleria sign. Park in retail parking, pay to park. Follow signs to lobby.
10700 NE 4th St 4002 is a condo for sale in the downtown neighborhood which includes 2 Beds, 4 Baths, 3,593 sq.ft. of living space, and was built in 2008. It was listed on 02-11-2019	and has been on the market cumulatively for 117 days. The list price of $4,590,000 is 204.01% higher than the median listed price of $1,509,817 for other real estate for sale in Bellevue. 10700 NE 4th St 4002 is also listed at 403.72% higher than median price of sold real estate of $911,225 in Bellevue. The price per square foot is $1277.48 which is 152.57% higher when compared to the average price per square foot of Bellevue at $505.80. Want to see more real estate for sale? Search our available homes, condos, vacant land and rentals in King County and Bellevue	.


text:
Power and renewables News Wind energy
Financial close of Windpark Spui for group of lenders supported by DNV GL technical risk assessment
Mona Ghobadi
Global PR and Media Relations Manager, DNV GL - Energy
contact.energy@dnvgl.com
Prajeev Rasiah
Regional Manager, Energy-North West Europe, Middle East & Africa
Phone: +44 2 03816 6023
Due diligence for Dutch onshore wind farm in the province of South Holland focused on technical risks to have 735 MW wind capacity installed by 2020.
ARNHEM, The Netherlands - 31 May 2018 – DNV GL, the world's largest resource of independent energy experts and certification body, has successfully completed comprehensive due diligence of the Dutch Windpark Spui, for a group of lenders who are providing the debt financing for the project.
The power generated at Windpark Spui, which will supply renewable electricity to more than 24,000 households, will be sold to Eneco Group, a Dutch sustainable energy company, under a 16-year power purchase agreement. Eurus Energy, a leading Japanese renewable energy company, acquired the project from YARD, a Dutch-based developer of wind energy projects, and its co-developer prior to financial close.
"We'd like to congratulate all the parties involved on this momentous achievement. At a time of intense focus on the wind industry, the financial close of Windpark Spui is integral to fulfilling the commitment of the province of South Holland to have 735 megawatts (MW) of onshore wind capacity installed by 2020. Our interdisciplinary and cross-border team of technical experts provided the lending consortium with comprehensive technical due diligence ahead of their investment," said Prajeev Rasiah, Vice President & Regional Manager North Europe, Middle East & Africa at DNV GL.
Windpark Spui, a 21 MW wind farm located in the municipality of Korendijk in South Holland, the Netherlands, will consist of five Enercon E-126 EP4 wind turbines, which will have a hub height of 135 meters, a rotor diameter of 127 meters and a rated power of 4.2 MW.
DNV GL's team of local and international wind experts delivered the technical due diligence which featured an independent engineering review of the technical details of the project and associated contractors and companies, including appraisal, environmental permits, civil and electrical design as well as the environmental site conditions, energy production assessment, construction and operations contracts and financial model.
DNV GL is a global quality assurance and risk management company. Driven by our purpose of safeguarding life, property and the environment, we enable our customers to advance the safety and sustainability of their business. Operating in more than 100 countries, our professionals are dedicated to helping customers in the maritime, oil & gas, power and renewables and other industries to make the world safer, smarter and greener.
In the power and renewables industry
DNV GL delivers world-renowned testing and advisory services to the energy value chain including renewables and energy efficiency. Our expertise spans onshore and offshore wind power, solar, conventional generation, transmission and distribution, smart grids, and sustainable energy use, as well as energy markets and regulations. Our experts support customers around the globe in delivering a safe, reliable, efficient, and sustainable energy supply. Learn more at dnvgl.com/energy.

redpajama_set_name: RedPajamaCommonCrawl


Field Assisted Sintering Technology (FAST) , also known as Spark plasma sintering (SPS), or Direct Current Sintering (DCS), is an innovative sintering technique, which has been increasingly used to sinter a variety of materials with nano-sized grains and superior properties.
Dr. Fritsch is the market leader in field assisted sintering (FAST) / SPS / DCS furnaces and presses. More than 1,000 FAST sinter presses have been installed at research universities and companies worldwide. In fact, Dr. Fritsch produces more FAST / SPS / DCS sintering presses per year than all other manufacturers combined!
The main characteristic of Dr. Fritsch FAST press / SPS / DCS furnace is that the continuous high density electric current directly passes through the graphite die, as well as the powder compact, in case of conductive samples. Joule heating has been found to play a dominant role in the densification of powder compacts, which results in achieving near theoretical density at lower sintering temperature compared to conventional sintering techniques. The heat generation is internal, in contrast to the conventional hot pressing, where the heat is provided by external heating elements. This facilitates a very high heating or cooling rate (up to 1000 K/min), hence the sintering process generally is very fast (within a few minutes). The general speed of the process ensures it has the potential of densifying powders with nanosize or nanostructure while avoiding coarsening which accompanies standard densification routes. This has made SPS a good method for preparation of ceramics based on nanoparticles with enhanced physical properties.
MSE Supplies LLC is the designated distributor of Dr. Fritsch Sintering Presses in the United States.
All customer services are provided by MSE Supplies and all spare parts and accessories are shipped from the USA, which keeps the cost low and delivery fast for the customers of Dr. Fritsch FAST / SPS / DCS presses and furnaces.


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Wanted To Buy WTB: Adobe CSx upgrade - Early vers.
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For Sale [Ottawa] Pelican Case, Sony Battery Grip, Sony SLR Lenses, Portable DVD Player.


text:
Q: How to replace some character in a string which contain unfixed characters My string is like below
"value":"my"value"

I need to convert it to
"value":"my\"value"

Some part in this string is fixed,such as
"value":"

Some part is not fixed. So I think I can treat the string like below:
"value":"xx"xxx"

The x part is not fixed, I need replace the string to
"value":"xx\"xxx"

I think I should try regex, and who can help me to build the regex expression

A: You could use regex like this:
'"value":"xx"xxx"'.replace(/("value":".*)"(.*")/, '$1\\"$2');

A: res.log
{   "key": "name",
    "value" : "value with" quote",
}

code snippet
content = content.replace(/"[^"\\:\n]+"[^"\\:\n]+"/gi, (s) => {
            var substr = s.slice(1, s.length - 1);
            substr = substr.replace("\"", "\\\"");
            return "\"" + substr + "\"";
        });

Full Sample function
  var fs = require("fs");

    module.exports =  () => {
            let file = 'res.log';
            let content = fs.readFileSync(file, 'utf8');
            console.log(content);
            content = content.replace(/"[^"\\:\n]+"[^"\\:\n]+"/gi, (s) => {
                var substr = s.slice(1, s.length - 1);
                substr = substr.replace("\"", "\\\"");
                return "\"" + substr + "\"";
            });

            console.log(content);
        };

redpajama_set_name: RedPajamaStackExchange


text:
resources :patients, only: [] do
  namespace :hd do
    resource :mdm, only: :show, controller: "mdm"
    resource :dashboard, only: :show
    resource :protocol,
             only: :show,
             defaults: { format: :pdf }
    resource :preference_set, only: [:edit, :update]
    resource :current_profile,
             only: [:show, :edit, :update],
             path: "/profiles/current",
             controller: "current_profile"
    resources :historical_profiles,
              only: [:index, :show],
              path: "/profiles/historical"
    resources :sessions
    resources :prescription_administrations, only: :index
  end
end

namespace :hd do
  scope format: true, constraints: { format: :json } do
    get "patients_dialysing_at_unit" => "patients#dialysing_at_unit"
    get "patients_dialysing_at_hospital" => "patients#dialysing_at_hospital"
  end

  resources :prescriptions, only: [] do
    resources :administrations,
              only: %i(new create edit update),
              controller: "prescription_administrations"
  end
  resources :prescription_administration, only: [] do
    resource :witness, only: [:edit, :update]
  end
  resources :prescription_administration_authorisations, only: :create
  resources :transmission_logs, only: [:show, :index]
  resources :cannulation_types, except: :show
  resources :dialysers, except: :show
  resources :dialysates, except: :show
  resource :ongoing_sessions, only: :show
  resources :mdm_patients, only: :index
  resources :mdm_patients, only: :index
  constraints(named_filter: /(on_worryboard)/) do
    get "mdm_patients/:named_filter", to: "mdm_patients#index", as: :filtered_mdm_patients
  end
  resources :unmet_preferences, only: :index
  resources :units, only: [] do
    resources :stations do
      post :sort, on: :collection
    end
  end
  namespace :scheduling do
    resources :units, only: [] do
      resources :diaries, only: [:index, :show]
      get "diaries/:year/:week_number/edit", to: "diaries#edit", as: :edit_diary
    end
    resources :diaries, only: [] do
      resources :slots, except: :show, controller: :diary_slots
      get "slots/day/:day_of_week/period/:diurnal_period_code_id/station/:station_id",
          to: "diary_slots#show",
          as: :refresh_slot
    end
  end
  namespace :session_forms do
    resources :batches, only: [:create, :show] do
      get :status, constraints: { format: :json }, defaults: { format: :json }
    end
  end
end


Perhaps its time to start searching for medical sonography classes in Rhode Island? Rhode Island is a great place to seek a career as an Ultrasound Technician. With metropolitan areas such as Providence, Warwick, and Cranston, there is a continually growing need for licensed Ultrasound Technicians. If the large metropolitan areas are not for you, there are usually great opportunities in small towns as well.
Job growth in Rhode Island for Diagnostic Medical Sonographers through the ten year period 2010-2020 is predicted to be great. According to Careerinfonet.org available jobs will improve by 30%. This compares to the predicted nationwide growth of 44% over the same period. On the National level this comes out to over three thousand job openings each year due to growth and net replacement. Enrolling in a good Ultrasound Technician school in Rhode Island is a fantastic way to secure a spot in this rewarding career.
Being an Ultrasound Technician in the State of Rhode Island comes with an average annual salary of $76,450 according to figures reported by the United States Department of Labor's Bureau of Labor Statistics in 2012. An income like this in Rhode Island can provide a rather comfortable lifestyle for you and your family, and it all begins with choosing a great Ultrasound Technician Training program in Rhode Island. So if you're looking for a new occupation, you should definitely consider becoming an ultrasound technician.
The first thing to look for when researching a diagnostic medical sonography training program in Rhode Island is to find out if it is accredited by the CAAHEP. In terms of Allied Health accreditors, the Commission on Accreditation of Allied Health Education Programs is the biggest in the U.S..
In order to take the ARDMS exam you must obtain a minimum number of hands on training hours that you will most likely not get at a non-accredited school. ARDMS is the American Registry for Diagnostic Medical Sonography, and they are the principal licensing body for all diagnostic medical sonographers. Being certified by the ARDMS does not guarantee employment, but it does open doors that otherwise would not be available to you. Many insurance companies will refuse to pay on claims if it is discovered that a sonogram was performed by a technician that did not hold a license from the ARDMS, and ultimately, obtaining the license shows that you have exceeded a minimum level of education and experience in the field.
If you do not perform the clinical hours through your training program, you will need to get them by working for a clinic or doctor's office that doesn't call for a licensed technician. The concern with this method is that these will likely be lower paying jobs that are, honestly, difficult to find. Instead, you will end up working in primarily part time conditions, for hourly rates that will likely not come close to covering the price of your training. You need to have 1,000 practical hours before you are eligible to take the ARDMS exam, and that is going to take a long time if you are working part time.


text:
Shujāʿ ibn Wahb al-Asadī (Arabic: شجاع بن وهب الأسدي) (died 633 CE) was a prominent companion of Islamic prophet Muhammad in the pre-Islamic era, who participated in all the famous wars, including Badr and Uhud. Some sources also suggest that Muhammad sent him as a messenger with letters to most of the world's king kings at that time. Also, a hadith narrated by Imam al-Zuhri revealed that Shuja was the messenger of Muhammad sent to the Persian king Khosrow II. He was the one who handed over the letter sent by Muhammad to Khosrow.

Biography
Shuja ibn Wahab's real name is Shuja and the nickname is Abu Wahab. His father name was Wahab ibn Rabi'ah. In the age of ignorance days, his descendants were contracted to the Banu Abd-Shams clan of Quraysh.

Shuja was one of those who converted to Islam in the early stages of Islam. Forced to torture the idolaters of Mecca, Shuja went to Habsha with the second group of hijratis. During their habsha stay, when there were rumours that all the inhabitants of Mecca had accepted Muhammad's loyalty, the love of the homeland drew him to Mecca, as many did. When he came to Mecca, he found that the news was completely false. After staying in Mecca for a few days, he safely migrated to Medina. After his migration to Yathrib developed his religious fraternal relationship with Hazrat Aws.

He was entrusted with the responsibility of eliminating to Banu Amir a group of Bani Hawains in the month of Rabiʽ al-Awwal in 8th Hijri, which is known as Expedition of Shuja ibn Wahb al-Asadi. Bani Hawains had placed the tent at Rassi, five days away from Medina. Shuja suddenly arrived one day, hiding during the day with twenty-four brave mujahideens, and travelling in the evening. They defeated the enemy forces and snatched a large number of camels, sheep and goats and brought them to Medina. The quantity of loot's goods can be estimated by the fact that fifteen camels fell on each mujahid's share, among other things.

After his return from Hudaybiyyah, Muhammad sent him as a messenger with letters to most of the king's kings in the world. Muhammad sent Shuja with a letter to Harith ibn Abi Shamir al-Gassani. Harith was the ruler of the 'al-Ghutah' place near Damascus. The first few sentences of the letter Muhammad wrote to him are as follows:

Although, Hares refused his Daw'ah. However, his daughter-in-law Murai converted to Islam and secretly offered salutations to Muhammad through Shuja.

During the caliphate of Abu Bakr, the first caliph of Islam, Shuja was martyred in the Battle of Yamama against the hypocrite Prophet Musaylimah. He was a little over forty years old at the time of his death.

Sources

Sahabah who participated in the battle of Uhud
Sahabah who participated in the battle of Badr
633 deaths
People from the Rashidun Caliphate

redpajama_set_name: RedPajamaWikipedia


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text:
Маркус Олівер Джонстон Мумфорд ( 31 січня 1987) — американсько-британський співак, автор пісень, музикант, продюсер звукозаписів та соліст групи Mumford & Sons. Він також грає на низці інструментів із групою, включаючи гітару, барабани та мандоліну. Він одружений з британською актрисою кіно і телебачення, номінованою на Оскар, Кері Малліган.

Примітки

Британські співаки
Співаки США


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text:
Suo fratello è l'architetto Gino Valle, loro padre l'architetto Provino Valle. È la fondatrice dello studio Vignelli Associates e moglie di Massimo Vignelli.

Biografia

Grazie ad una borsa di studio ottenuta nel 1958, Lella ha studiato Architettura presso la scuola di architettura del Massachusetts Institute of Technology e ha lavorato come junior designer nel prestigioso studio Skidmore, Owings & Merrill, prima di tornare in Italia e laurearsi in Architettura all'Università IUAV di Venezia, nel 1962. Nel 1957 sposa il designer Massimo Vignelli, con il quale fonda a Milano lo studio Lella and Massimo Vignelli Office of Design and Architecture, studio che si occupa di design di prodotto, design d'interni e graphic design.

Nel 1971, dopo essersi stabiliti definitivamente negli Stati Uniti e dopo un'esperienza internazionale con lo studio Unimark International, Massimo e Lella fondano lo studio Vignelli Associates a New York, dove Lella ricoprirà la carica di Amministratore delegato. Nel 1985, per accomodare le crescenti esigenze lo studio si trasferisce in uno spazio più grande, sulla 10th Avenue. Durante tutto questo periodo Massimo e Lella continuano a svolgere un'intensa attività spaziando dal graphic design alle esibizioni fino al design di prodotto e di arredi, settore in cui Lella sarà particolarmente brillante, progettando sedute per marchi come Poltrona Frau, Poltronova e Acerbis International.

Lella e Massimo lavoreranno insieme per tutta la vita in svariati rami del design, vincendo innumerevoli premi e diventando un'icona del design del ventesimo secolo. Dal loro matrimonio sono nati due figli : Luca (1963), fotografo, e Valentina (1966), esperta di stoffe e tessuti.

Lavoro
Il lavoro di Lella Vignelli è stato esposto svariate volte in pubblicazioni di settore, negli Stati Uniti e all'estero. Diversi suoi lavori sono inclusi nelle collezioni permanenti di diversi musei, incluso il MoMA di New York, il Cooper-Hewitt Museum, il Metropolitan Museum of Art, il Musee des Arts Decoratifs di Montréal e il Die Neue Sammlung di Monaco. Il lavoro di Lella e Massimo è stato inoltre soggetto di due documentari trasmessi in tutto il mondo. Un'esibizione monografica del lavoro dello studio Vignelli Associates è stata allestita a San Pietroburgo, Mosca, Helsinki, Londra, Budapest, Barcellona, Copenaghen, Monaco, Praga e Parigi fra il 1989 e il 1993.
Lella Vignelli ha tenuto diverse conferenze per associazioni di design americane e internazionali. È membro della Industrial Designers Society of America
(IDSA), dell'American Institute of Graphic Arts (AlGA), dell'International Furnishings and Designer Association (IFDA) e del Decorators Club di New York.

Premi e riconoscimenti
 1973 - American Institute of Architects (AlA) Industrial Arts Medal.
 1982 - Laurea honoris causa dalla Parsons School of Design, New York.
 1983 - AlGA Gold Medal.
 1988 - Interior Design Hall of Fame.
 1991 - National Arts Club Gold Medal for Design.
 1992 - Interior Product Designers Fellowship of Excellence.
 1994 - Corcoran School of Art, Washington D.C.
 1995 - Brooklyn Museum Design Award for Lifetime Achievement.
 2003 - National Lifetime Achievement Award dal National Museum of Design at Cooper-Hewitt, New York.
 2004 -  Visionary Award from dal Museum of Art and Design, New York.
 2005 -  Architecture Award dall'American Academy of Arts and Letters, New York.

Note

Voci correlate
 Massimo Vignelli
 Gino Valle
 Provino Valle

Altri progetti

Collegamenti esterni
  Vignelli Associates - sito ufficiale.
  Lella Vignelli - collezione Lella Vignelli del Museum of Modern Art di New York.
  AIGA  - ritratto e scheda su Massimo e Lella Vignelli (1983).
  .

Italiani emigrati negli Stati Uniti d'America
Studenti dell'Università IUAV di Venezia
Studenti del Massachusetts Institute of Technology


text:
The methylenetetrahydrofolate reductase gene variant C677T influences susceptibility to migraine with aura
Rod A Lea1,3,4,
Micky Ovcaric1,
James Sundholm1,
John MacMillan2 &
Lyn R Griffiths1
BMC Medicine volume 2, Article number: 3 (2004) Cite this article
The C677T variant in the methylenetetrahydrofolate reductase (MTHFR) gene is associated with increased levels of circulating homocysteine and is a mild risk factor for vascular disease. Migraine, with and without aura (MA and MO), is a prevalent and complex neurovascular disorder that may also be affected by genetically influenced hyperhomocysteinaemia. To determine whether the C677T variant in the MTHFR gene is associated with migraine susceptibility we utilised unrelated and family-based case-control study designs.
A total of 652 Caucasian migraine cases were investigated in this study. The MTHFR C677T variant was genotyped in 270 unrelated migraine cases and 270 controls as well as 382 affected subjects from 92 multiplex pedigrees.
In the unrelated case-control sample we observed an over-representation of the 677T allele in migraine patients compared to controls, specifically for the MA subtype (40% vs. 33%) (χ2 = 5.70, P = 0.017). The Armitage test for trend indicated a significant dosage effect of the risk allele (T) for MA (χ2 = 5.72, P = 0.017). This linear trend was also present in the independent family-based sample (χ2 = 4.25, P adjusted = 0.039). Overall, our results indicate that the T/T genotype confers a modest, yet significant, increase in risk for the MA subtype (odds ratio: 2.0 – 2.5). No increased risk for the MO subtype was observed (P > 0.05).
In Caucasians, the C677T variant in the MTHFR gene influences susceptibility to MA, but not MO. Investigation into the enzyme activity of MTHFR and the role of homocysteine in the pathophysiology of migraine is warranted.
Migraine is a debilitating neurovascular disease that affects approximately 12% of the Caucasian population. It is characterised by nausea and vomiting, photophobia and phonophobia, neurological disturbances and severe recurrent headache. Pharmaceutical treatments for migraine exhibit variable efficacy among patients and there is no laboratory-based diagnostic test available. At present, migraine is clinically diagnosed based on criteria specified by the International Headache Society (IHS). The IHS has defined two major classes of migraine. These are migraine without aura (MO), which accounts for ~70% of all migraine in the population, and migraine with aura (MA), which comprises ~25% of all migraine [1]. The two subtypes have substantial symptomatic overlap, but MA sufferers experience distinguishing neurological disturbances (the aura) that usually precede the headache phase of an attack [1].
Strong familial aggregation of migraine indicates a significant genetic component for the disease [2]. Heritability is estimated to be between 40% and 60%, indicating that the disease is partly explained by non-genetic determinants [3, 4]. Thus, migraine is a multifactorial (complex) disease of which the genetic aetiology is likely to be comprised of a number of modest effect susceptibility genes that perhaps act in combination. It is likely that both migraine subtypes (MO and MA) have some genetic determinants in common although different modifying factors (including genetic and lifestyle triggers) may contribute to the variable expression of the clinical end-point.
The pathophysiology of migraine is not completely understood and continues to be rigorously investigated. For MA, a dramatic reduction in cerebral blood flow is associated with the depolarisation wave that propagates across the brain cortex (cortical spreading depression; CSD) [5]. The characteristic head pain that is common to both MA and MO may arise due to dilation of cerebral blood vessels following activation of the trigeminovascular system (TVS). The CSD can activate the TVS, providing a possible link between migraine aura and headache [6]. Therefore, biochemical factors that have the potential to disrupt vascular endothelial function and cerebral blood flow, leading to CSD and/or affecting the TVS, are important targets for involvement in migraine susceptibility [7].
Homocysteine, a highly reactive amino acid, has been shown to produce endothelial cell injury in both experimental animal and cell culture studies [8, 9]. The pathophysiological consequences of such homocysteine-related endothelial injury may include impaired release of nitric oxide (NO) [10]. In turn, altered bioavailability of NO may cause abnormal reactions between the vessel wall, platelets, and macrophages [11] leading to significant alterations in vascular function and the coagulant properties of the blood [12, 13]. Thus, it is within reason that homocysteine-related endothelial dysfunction may be involved in the initiation and maintenance of a migraine episode. In support of this, studies have also demonstrated that the firing rate of trigeminal neurons responding to pain increases with the application of D, L-homocysteic acid, a substance that mimics the effect of homocysteine, [14, 15]. In humans, homocysteine is metabolised by methylenetetrahydofolate reductase (MTHFR). This enzyme catalyses the reduction of 5,10-methylenetetrahydofolate to 5-methylenetetrahydofolate, which is the circulatory form of folate and carbon donor for re-methylation of homocysteine to methionine [16].
The human MTHFR gene has been localised to chromosome 1p36 and consists of 11 exons spanning ~17 kb [17]. A common MTHFR gene variant (C677T) alters the amino acid sequence, substituting alanine (Ala) for valine (Val) at position 222. Individuals with the Val residue may exhibit significantly reduced MTHFR enzyme activity whereby, compared to baseline levels, the mean activity is 65% in the Ala/Val heterozygote and 30% in the Val/Val homozygous state [16]. The latter enzymatic form can lead to mild elevation in plasma homocysteine levels particularly if dietary folate intake is low [16, 18]. Mild hyperhomocysteinaemia is known to increase risk of cardiovascular disease (CVD) including coronary, cerebral, and peripheral vascular disease [16, 18, 19]. More specifically, meta-analyses have concluded that the homozygous TT genotype of the MTHFR gene variant (C677T) is a modest, yet significant, genetic risk factor for ischaemic stroke, another severe neurovascular disease (odds ratio (OR): 1.5 – 2) [18, 20]. Interestingly, the migraine disorder itself is also associated with an increased risk of ischaemic stroke, particularly with MA [21–25]. Indeed, the CSD, which is characteristic of MA, as well as changes in cerebral blood flow and headache, can also occur during a stroke episode [26]. Based on the comorbidity of migraine and stroke and the role homocysteine seems to play in disturbing in the cerebrocirculatory system, it is possible that the MTHFR C677T variant may represent an important genetic determinant for the vascular pathophysiologies underlying both neurovascular conditions. The objective of our study was to determine whether the MTHFR C677T variant is associated with migraine susceptibility in Caucasians utilising unrelated and family-based case-control designs.
Disease diagnosis
Our study protocol was approved by the Griffith University Ethics Committee for Experimentation on Humans and all subjects gave informed consent. Migraine patients were shown to exhibit phenotypic variation, which included differences in age of onset, frequency and severity of attacks, environmental triggers and medication response. However, all affected individuals were diagnosed as having either MA or MO by an experienced clinical neurologist using the IHS criteria (MA = criteria 1.2.1 and MO = criteria 1.1) [1]. The small number of patients experiencing both subtypes of migraine was phenotyped as being affected with MA. To reduce confounding, any volunteer that reported being affected with known migraine comorbid conditions such as mental illness (e.g. depression) and CVD (e.g. stroke) were not included in the study.
Study design and samples
To test for association of the MTHFR C677T variant to migraine, we utilised a combination of traditional and modern case-control study designs. In general, the case-control approach remains a practical and powerful strategy for detecting genetic variants that confer a modest effect on disease susceptibility provided its shortcomings are addressed appropriately [27, 28]. For this study we initially implemented the popular unrelated case-control approach to compare genotype and allele frequencies. This was followed by family-based case-control tests for association utilising a) a transmission disequilibrium-type test (TDT-type) in nuclear pedigrees [29] and b) a statistical method for comparing related cases to unrelated controls [30]. The difference between this latter design and the traditional unrelated case-control design is that, provided relatedness is accounted for, multiple cases from a single affected family(s) can be included in the analysis. This can result in substantial information gain over the use of family-based controls [30].
The unrelated case-control panel examined in this study is a clinic-based sample comprised of 270 unrelated migraine cases and a matched group of 270 unrelated non-migraine controls. Of this unrelated case group, 68% were female, 63% were phenotyped with MA, and 90% of patients had a known family history of migraine or at least one affected first degree relative. The unrelated control group was carefully matched with the case group for the variables; age (± 5 years), gender and ethnicity (Caucasian and of British descent). The control group was recruited from the same geographical location as the affected group (east coast of Australia). We also utilised an independent family-based sample comprised of 92 affected pedigrees. Of the 432 subjects in this pedigree sample, 290 (67%) were female, 382 (88%) were diagnosed with migraine (MA and/or MO) and 295 (68%) were affected with MA. Overall, our study included a total of 652 migraine cases, of which 465 (71%) suffered from MA.
Genomic DNA was isolated from whole blood by a standard salting out procedure. DNA fragments containing the C677T MTHFR variant were amplified by PCR using the oligonucleotides published by Kowa et al. (2000) [31]. The sense primer sequence was 5'-TGA AGG AGA AGG TGT CTG CGG GA-3', and the antisense sequence was 5'-AGG ACG GTG CGG TGA GAG TG-3'. PCR conditions were as follows; 1.75 mM of MgCl2, 1 × standard PCR buffer, 0.2 mM of dNTPs, 0.2 μM each of forward and reverse primers, 0.16 g/l of BSA, 1 unit of Taq polymerase, 40 ng of genomic DNA, mixed to final volume of 25 μ l with sterile distilled water. The thermal cycle parameters included: 1 cycle at 95°C for 3 min for an initial denaturation, followed by 35 cycles of denaturation for 1 min at 94°C, primer annealing for 1 min at 65°C, primer extension for 2 min at 72°C and a final extension for 10 min at 72°C [31]. This amplification reaction resulted in the synthesis of a 198-bp fragment.
The C to T substitution at nucleotide 677 in the MTHFR gene introduces a restriction site for the HinfI enzyme. This enzyme was used to distinguish the alleles by cleaving the mutant fragment into 175-bp and 23-bp fragments. For the digestion reaction, 7 units of HinfI, 2 μl of NE buffer II and 2.3 μl of sterile water were added to each PCR product mix for a final volume of 20 μl. Samples were digested overnight at 37°C and then fractionated by using a 5% ultra-high-resolution agarose gel, stained with ethidium bromide and visualised under ultraviolet light. To confirm results, the DNA samples were also genotyped using an ABI-310 Genetic Analyser, which is capable of distinguishing DNA fragments that differ by as little as 2 bp. For this technique, the reverse PCR primer was labelled with 5-carboxyfluorescein (FAM) fluorescent dye. Following initial PCR and restriction fragment length polymorphism digest, 1 μl of each digested PCR product was added to 12 μl of formaldehyde/size standard mix (Perkin-Elmer). This mixture was denatured for 2 minutes at 95°C before running on the ABI-310 Genetic Analyser.
An independent laboratory technician, blinded to the initial genotyping processing, performed quality control checks for the MTHFR gene variant by repeating the PCR and genotyping of a random selection of 100 subjects. All genotype discrepancies were rectified or excluded from subsequent data analysis.
Unrelated case-control association analyses
Genotype and allele frequencies for the MTHFR C677T variant were calculated from observed genotype counts. As a statistical control for systematic genotyping error and population stratification, the expected genotype proportions according to the Hardy-Weinberg law were calculated and compared to observed genotypes. Genotype and allele frequencies were initially assessed for association with migraine using conventional contingency table analyses incorporating the standard chi-squared test for independence. This analysis produces a χ2 statistic with one or two degrees of freedom and corresponding P-values for allele and genotype distributions, respectively. To assess the dosage effect of possessing zero, one or two copies of the risk allele (T) (i.e. an additive effect), the Armitage test for linear trend in proportions was performed on the genotype frequency data. Genetic risk magnitudes (effect size) were estimated by calculating ORs with 95% confidence intervals.
Family-based association analyses
Our study of the MTHFR C677T variant also involved family-based association analyses of 92 migraine pedigrees. Mendelian inheritance of the MTHFR alleles in pedigrees was checked using the PEDMANAGER program. The Family Based Association Test (FBAT) was performed on the pedigree data using the software package of Laird et al. (2000) [29]. This is a transmission disequilibrium test (TDT) type approach for assessing association between DNA variant alleles and disease phenotype under the standard genetic models (dominant, recessive and additive). Unlike the classic TDT, which was designed for specific pedigree structures (ie. parent-child triads), the FBAT can appropriately utilise data from multiple nuclear families derived from a single multiplex pedigree to test for association [29].
We also utilised a powerful statistical test developed by Slager and Schaid (2001) [30], which involves comparing genotype frequencies of genetically related cases (sampled from multiplex affected families) with the unrelated control group frequencies. This method is based on the Armitage test for trend and includes a variance estimate that appropriately accounts for the non-independence of related cases. Thus, this method allows assessment of the dosage effect conferred by the risk allele whilst maintaining the correct type I error rate [30]. For this analysis we used the GENEHUNTER program to estimate the IBD-sharing probabilities [32] and the S-PLUS function of Slager and Schaid (2001) [30] to calculate the association test statistics for the pedigree data. Unaffected family members can be used as a comparative group and may possibly reduce false positives arising from population stratification. However, for our pedigree sample there was only 50 individuals not diagnosed with migraine and many of these individuals (n = 33) were labelled as phenotype "unknown". Therefore these familial controls were considered inappropriate for comparison.
It is unclear to what extent the MA and MO subtypes are influenced by the same genetic aetiologies. Therefore, we performed stratified analyses of the migraine subtypes (MO subtype and MA subtype), in addition to comparisons of all migraineurs grouped together (MO+MA). Analysis of the group of individuals with co-occurring MA and MO was not conducted due to small numbers. The conventional α-level of 0.05 was specified as the significance threshold for all analyses performed. We chose not to correct for multiple comparisons but opted instead to establish the credibility of a positive association by verification in an independent sample.
Unrelated case-control analysis
Table 1 displays the frequency distributions observed for the MTHFR C677T variant for the unrelated case and control groups. Genotype and allele frequencies were determined for 268 migraine patients and 269 controls. The observed genotypes for the case and control groups did not deviate significantly from Hardy-Weinberg expectations (P > 0.1). The genotype frequencies in the migraine control group (43%, 48%, 9% for C/C, C/T and T/T, respectively) are very similar to an independent control group (n = 249) utilised for case-control studies of hypertension conducted in our laboratory (42%, 48%, 10% for C/C, C/T and T/T, respectively). Furthermore, the frequency of the T allele in our control group (33%) is also consistent with the proportion of this allele in the general Caucasian population (34%) [18, 33], giving us confidence that the unrelated non-migraineurs used in this study constitute a reliable (unbiased) comparative panel.
Table 1 Distribution of MTHFR C677T (genotype and allele) frequencies in unrelated migraine and control groups.
Contingency table analysis of the MTHFR C677T frequency data indicated that the risk allele (T) was over-represented in the migraine group compared to the control group (38% vs. 33%), although the P value for this comparison did not reach statistical significance (χ2 = 3.36, P = 0.066). The proportion of the T allele in the MA subgroup however, was shown to be significantly higher than in the control group (40% vs. 33%) (χ2 = 5.70, P = 0.017). Further comparison of the genotype data indicated a difference in frequency distributions, with the homozygous T/T genotype being over-represented in the migraine group (15% vs. 9%). Stratified analyses indicated that this difference was specifically attributed to the MA subtype group, with the T/T frequencies being significantly higher in cases compared to controls (19% vs. 9%) (χ2 = 10.37, P = 0.006). Interestingly, there was also a significant dosage (additive) effect of the risk allele for MA as assessed by the Armitage test for linearity (χ2 = 5.72, P = 0.017). To determine the magnitude of the increased risk of migraine conferred specifically by the homozygous T/T genotype, odds ratios were calculated after dichotomising the genotype frequency data into risk "T/T" and baseline "C/C" genotype groups. Comparing the total migraine group against controls under this grouping scheme produced an OR of 1.91 with a 95% CI of 1.07 – 3.04 (P = 0.027), and the MA subtype comparison produced an OR of 2.54 (95% CI: 1.37 – 4.71, P = 0.0025). There was no association detected for the C677T variant under a dominant grouping scheme. Furthermore, no genotypic association was indicated for the MTHFR gene variant and the MO subtype (P > 0.1), nor was there any gender-specific associations observed for this variant (results not shown).
Family-based case-control analysis
In genetic association studies it is important to substantiate positive findings in independent samples. Therefore, we also genotyped the MTHFR C677T variant in an independent sample of migraine pedigrees. The frequency of the risk allele in the affected members of the pedigree sample (0.39) was similar to that observed in the unrelated case group (0.38) and greater than that of the unrelated control group (0.33). Genotypes for the family-based case groups (Table 2) conform to Hardy-Weinberg equilibrium expectations (P > 0.05).
Table 2 Distribution of MTHFR C677T genotypes in family-based migraine case and unrelated control groups.
Our initial association analysis of the pedigree data involved calculation of TDT-type statistics using the FBAT program [29]. The program automatically decomposed the 92 multiplex pedigrees into 174 nuclear families for this analysis. Based on the results of the unrelated case-control analysis we assessed the family data under both additive and recessive inheritance models and considered "MO+MA" and "MA subtype" as disease phenotypes. Encouragingly, the results under both disease models suggested an association, indicating over-transmission of the 677T allele from parents to migraine-affected offspring. However, the TDT-type statistics produced were not significant for either migraine phenotype tested (P > 0.10). It is important to note that, due to the relatively low degree of heterozygosity for this MTHFR gene variant (~0.48), less than 30 of all 174 nuclear families examined had heterozygous parents that could provide allele transmission information to affected offspring for this association analysis. That is, inheritance phase was indiscernible in many families and therefore the power to detect the expected association of the MTHFR C677T variant and migraine, as detected in the unrelated case-control analysis, was severely diminished. This FBAT result is not really surprising and exemplifies the substantial analytical inefficiencies that may occur when testing for association of a bi-allelic variant by allele transmission from parental controls [28, 34].
To overcome this information loss we implemented a simple statistical method that was designed to compare genotype frequencies from family-based case groups (sampled from multiple affected families) to frequencies from unrelated control groups (as used in the unrelated case control analyses). This statistical method correctly adjusts for correlation of genotypes in the family data and has been successfully utilised to implicate the luteinizing hormone β gene in prostate cancer susceptibility [30]. Table 2 summarises the genotype data of the MTHFR C677T variant obtained from all migraineurs in the sample of 92 migraine pedigrees. As observed from the genotype frequency distributions in the unrelated case group (Table 1), the T/T genotype was over-represented in both case groups from the family-based sample (MA+MO and MA subtype groups) compared to the unrelated control group (13% vs. 9%). Ignoring the inherent non-independence in the family-based case sample data, we observed differences between the frequency distributions of these groups that approached statistical significance (χ2 = 5.36, P = 0.069; χ2 = 5.71, P = 0.058, respectively). If weights are assumed to be equal to the number of high-risk alleles (i.e. there is a gene dosage effect) the unadjusted Armitage trend statistic was significant for both MO+MA and MA-subtype groups (χ2 = 5.36, P = 0.021 and χ2 = 5.67, P = 0.017). Importantly, this linear trend in proportions remained significant for the MA-subtype after adjusting for the relatedness in the case groups (χ2 = 4.25, P adjusted = 0.039). Further risk assessment of the MA-subtype produced an OR of 1.88 (95% CI: 1.01 – 3.52) after accounting for familial relationships.
The multifactorial nature of the common forms of migraine has so far prevented researchers from clearly identifying the predisposing genetic mechanisms. The investigation of candidate genes utilising case-control association designs is a powerful and direct strategy for detecting disease susceptibility genes of modest effect [27, 30]. To date there have been numerous such studies reporting positive associations of candidate gene variants and migraine. Notably, polymorphisms within the dopamine 2 receptor (DRD2), dopamine beta-hydroxylase (DBH), and recently, insulin receptor (INSR) genes have been implicated in migraine susceptibility [35–37]. These genes are not only physiologically plausible candidates, but importantly, the specific associations have been verified in independent migraine samples. Despite this, the functional significance of these susceptibility gene variants and the role they play in migraine pathophysiology is yet to be determined.
In addition to disturbances in neurological pathways, migraine pathophysiology is partly explained by changes in vascular tension and altered cerebral blood flow [5, 6]. Indeed, it is possible that vascular disturbances may act as a trigger for downstream neurological manifestations. Hence, molecular mechanisms that have the potential to affect vascular endothelial function should be targeted for involvement in migraine susceptibility. An elevation in circulatory homocysteine levels is thought to disrupt endothelial cells and alter the coagulant properties of the blood [13]. Interestingly, a recent meta-analysis indicated that mild hyperhomocysteinemia may by a "causal" risk factor for cerebro- and cardio-vascular disease and suggested that lowering homocysteine levels by simple dietary folate supplementation may reduce CVD risk [18]. Experiments on animal models suggest that hyperhomocysteinemia may also increase susceptibility to migraine by heightening cerebral artery sensitivity [15]. In addition, elevated levels of homocysteine have been reported in patients affected with MA [38]. It has been shown that the 677T allele in the MTHFR gene is directly correlated with decreased enzymatic activity and the T/T genotype is indirectly associated with mild hyperhomocysteinaemia possibly leading to vascular disease [16, 18].
The objective of our study was to determine the prevalence of the MTHFR allele (677T) in Caucasian migraineurs and to test for a relationship of this variant to migraine susceptibility using unrelated case-control and family-based association designs. Statistical analyses of the unrelated case-control data revealed that the C677T variant was associated with migraine. Stratification by migraine subtype indicated that this association was not arising in the MO case group but attributed specifically to MA. Analysis of both the unrelated and family-based case groups indicated a linear trend in the proportion of MA cases as the number of risk alleles increased, suggesting a gene dosage (additive) effect. This trend is consistent with observed correlations in MTHFR enzyme activity according to the number of copies of the Val residue corresponding to the 677T allele [16]. For both migraine case groups we also observed a significant over-representation of the T/T genotype in the migraineurs compared to controls, indicating the odds of being affected with MA (the effect size) to be approximately 2 – 2.5 times greater in those homozygous for the T allele compared with C/C homozygotes.
We are not the first researchers to have investigated the MTHFR C677T variant in relation to migraine susceptibility. A genetic association study by Kowa et al. (2000) [31], originally reported a positive association between the MTHFR C677T variant and migraine in a Japanese case-control cohort. These researchers indicated an increased risk of migraine (ie. MA+MO) in Japanese individuals possessing the homozygous T/T genotype. Stratified analyses specifically showed that the T/T genotype was significantly over-represented in these Japanese patients with MA compared to non-migraine controls (40% vs. 9.6%), producing an OR of ~6 [31]. These positive findings were reinforced by another recent migraine case-control study conducted in a Turkish population [40]. These researchers reported that the MTHFR C677T is associated with migraine and also indicated that the T/T genotype specifically increased risk of MA (OR ~10). It is important to note that the frequency of the MTHFR 677T allele, and indeed migraine prevalence, is known to vary substantially among different ethnic populations [33, 39]. Thus, although our association study nicely supports the findings of both Kowa et al. (2000) [31] and Kara et al. (2003) [40], it cannot be considered a true replication of association. The differing ethnic backgrounds of the research subjects in the two previous studies may also partially explain the much larger ORs reported compared to the more modest effect seen in the Caucasians of British descent that we investigated. Nevertheless, all three migraine association studies of the C677T variant show a similar overall trend, and interpreted together, provide compelling evidence that the homozygous T/T genotype of the MTHFR gene, perhaps leading to reduced MTHFR enzyme activity and mild hyperhomocysteinemia, increases susceptibility to migraine, particularly MA.
There is convincing epidemiological evidence indicating an association between migraine and stroke [23, 24]. Although it is not conclusive, studies have indicated that this relationship may be specific to MA [26, 41]. Interestingly, the CSD, which is characteristic of MA, as well as changes in cerebral blood flow and headache, can also occur during stroke [26]. It is possible that higher than normal levels of homocysteine may lead to temporary cerebral thrombosis and/or altered blood flow allowing less oxygen into the brain and manifesting the symptoms common to MA and ischaemic stroke [40]. Whilst our study was not designed to investigate the comorbidity of migraine and stroke, our findings lead us to suspect that the C677T variant in the MTHFR gene may represent a non-coincidental risk factor for both diseases. If this were true, certain genes identified as stroke risk factors, such as those with the potential to cause cerebral vascular damage, blood coagulation and flow alteration, should also be considered candidates for future studies into the molecular genetics of migraine.
Our study confirmed an association between the MTHFR C667T mutation and migraine susceptibility, specifically indicating the T/T genotype to be a modest risk factor for migraine with aura, but not migraine without aura, in Caucasians. Appropriately designed studies are now necessary to determine the impact of this MTHFR gene variant on homocysteine levels in migraineurs. Finally, dietary folate supplementation, as a modifier of homocysteine levels, should be investigated as a simple therapeutic option (a nutraceutical) for the long-term treatment of migraine.
Headache Classification Committee of the International Headache Society: Classification and diagnostic criteria for the headache disorders, cranialneuralgias and facial pain. Cephalalgia. 1988, 8 (Suppl): 1-96.
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Honkasalo ML, Kaprio J, Winter T, Heikkila K, Sillanpaa M, Koskenvuo M: Migraine and concomitant symptoms among 8167 adult twin pairs. Headache. 1995, 35: 70-78.
Larsson B, Bille B, Pedersen NL: Genetic influence in headaches: a swedish twin study. Headache. 1995, 35: 513-519.
Goadsby PJ: Current concepts of the pathophysiology of migraine. Neurol Clin. 1997, 15 (1): 27-42.
Ferrari M: Migraine. The Lancet. 1998, 351: 1043-1051. 10.1016/S0140-6736(97)11370-8.
Tzourio C, El Amrani M, Poirier O, Nicaud V, Bousser MG, Alperovitch A: Association between migraine and endothelin type A receptor (ETA-231 A/G) gene polymorphism. Neurology. 2001, 22 (56(10)): 1273-7.
Harker LA, Ross R, Slichter SJ, Scott CR: Homocysteine-induced arteriosclerosis: the role of endothelial cell injury and platelet response in its genesis. J Clin Invest. 1976, 58: 731-741.
Wall RT, Harlan JM, Harker LA, Striker GE: Homocysteine-induced endothelial cell injury in vitro: a model for the study of vascular injury. Thromb Res. 1980, 18: 113-121. 10.1016/0049-3848(80)90175-9.
Stamler JS, Osborne JA, Jaraki O, Rabbani LE, Mullins M, Singel D, Loscalzo J: Adverse vascular effects of homocysteine are modulated by endothelium-derived relaxing factor and related oxides of nitrogen. J Clin Invest. 1993, 91: 308-318.
Cooke JP, Tsao PS: Is NO an endogenous antiatherogenic molecule?. Arterioscler Thromb. 1994, 14: 653-655.
Lentz SR, Sobey CG, Piegors DJ, Bhopatkar MY, Faraci FM, Malinow MR, et al: Vascular dysfunction in monkeys with diet-induced hyperhomocyst(e)inemia. J Clin Invest. 1996, 98: 24-29.
Hering-Hanit R, Gadoth N, Yavetz A, Gavendo S, Sela B: Is blood homocysteine elevated in migraine. Headache. 2001, 41: 779-781. 10.1046/j.1526-4610.2001.01143.x.
Bouassira D, Bars DL, Villanueva L: Heterotopic activation of A delta and C fibres triggers inhibition of trigeminal and spinal convergent neurones in the rat. J Physiol. 1987, 389: 301-317.
Storer RJ, Goadsby PJ: Microiontophoretic application of serotonin (5HT)1B/1D agonists inhibits trigeminal cell firing in the cat. Brain. 1997, 120: 2171-2177. 10.1093/brain/120.12.2171.
Frosst P, Blom HJ, Milos R, Goyette P, Sheppard CA, Matthews RG, Boers GJ, den Heijer M, Kluijtmans LA, van den Heuvel LP: A candidate genetic risk factor for vascular disease: a common mutation in methylenetetrahydofolate reductase. Nat Genet. 1995, 10: 111-113.
Goyette P, Summer JS, Milos R, Ducan AM, Rosenblatt DS, Matthews RG, Rozen R: Human methylenetetrahydrofolate reductase isolation of cDNA, mapping and mutation identification. Nat Genet. 1994, 7: 195-200.
Wald DS, Law M, Morris JK: Homocysteine and cardiovascular disease: evidence on causality from a meta-analysis. BMJ. 2002, 325 (7374): 1202-10.1136/bmj.325.7374.1202.
Coull BM, Malinow MR, Beamer N, Sexton G, Nordt F, de Garmo P: Elevated plasma homocysteine concentrations as a possible independent risk factor for stroke. Stroke. 1990, 21: 572-576.
Kelly PJ, Rosand J, Kistler JP, Shih VE, Silveira S, Plomaritoglou A, Furie KL: Homocysteine, MTHFR 677C-->T polymorphism, and risk of ischemic stroke: results of a meta-analysis. Neurology. 2002, 59 (4): 529-36.
Schwaag S, Nabavi DG, Frese A, Husstedt IW, Evers S: The association between migraine and juvenile stroke: a case-control study. Headache. 2003, 43 (2): 90-5. 10.1046/j.1526-4610.2003.03023.x.
Donaghy M, Chang CL, Poulter NJ: Duration, frequency, recency, and type of migraine and the risk of ischaemic stroke in women of childbearing age. Neurol Neurosurg Psychiatry. 2002, 73 (6): 747-50. 10.1136/jnnp.73.6.747.
Tzourio C, Iglesias S, Hubert JB, Visy JM, Alperovitch A, Tehindrazanarivelo A, Biousse V, et al: Migraine and risk of ischaemic stroke: a case-control study. PMID. 1993, 31 (307(6899)): 289-92.
Merikangas KR, Fenton BT, Cheng SH, Stolar MJ, Risch N: Association between migraine and stroke in a large-scale epidemiological study of the United States. Arch Neurol. 1997, 54 (4): 362-8.
Sochurkova D, Moreau T, Lemesle M, Menassa M, Giroud M, Dumas R: Migraine history and migraine-induced stroke in the Dijon stroke registry. Neuroepidemiology. 1999, 18 (2): 85-91. 10.1159/000069411.
Silberstein SD: Shared mechanisms and comorbidities in neurologic and psychiatric disorders. Headache. 2001, 41 (Suppl 1): S11-7. 10.1046/j.1526-4610.2001.01154-3.x.
Risch N, Merikangas K: The future of genetic studies of complex human diseases. Science. 1996, 13 (5281): 1516-7.
Cardon LR, Palmer LJ: Population stratification and spurious allelic association. The Lancet. 2003, 361 (9357): 598-604. 10.1016/S0140-6736(03)12520-2.
Laird NM, Horvath S, Xu X: Implementing a unified approach to family-based tests of association. Genet Epidemiol. 2000, 19 (Suppl 1): S36-42. 10.1002/1098-2272(2000)19:1+<::AID-GEPI6>3.3.CO;2-D.
Slager SL, Schaid DJ: Evaluation of candidate genes in case-control studies: a statistical method to account for related subjects. Am J Hum Genet. 2001, 68 (6): 1457-62. 10.1086/320608.
Kowa H, Yasui K, Takeshima T, Urakami K, Sakai F, Nakashima K: The homozygous C677T mutation in the methylenetetrahydofolate reductase gene is a genetic risk factor for migraine. Am J Med Genet. 2000, 96: 762-764. 10.1002/1096-8628(20001204)96:6<762::AID-AJMG12>3.0.CO;2-X.
Kruglyak L, Daly MJ, Reeve-Daly MP, Lander ES: Parametric and nonparametric linkage analysis: a unified multipoint approach. Am J Hum Genet. 1996, 58 (6): 1347-63.
Rosenberg N, Murata M, Ikeda Y, Opare-Sem O, Zivelin A, Geffen E, Seligsohn U: The frequent 5,10-methylenetetrahydrofolate reductase C677T polymorphism is associated with a common haplotype in whites, Japanese, and Africans. Am J Hum Genet. 2002, 70 (3): 758-62. 10.1086/338932.
Teng J, Risch N: The relative power of family-based and case-control designs for linkage disequilibrium studies of complex human diseases. II. Individual genotyping. Genome Res. 1999, 9 (3): 234-41.
Peroutka SJ, Wilhoit T, Jones K: Clinical susceptibility to migraine with aura is modified by dopamine D2 receptor (DRD2) NcoI alleles. Neurology. 1997, 49: 201-206.
Lea R, Dohy A, Jordan K, Quinlan S, Brimage PJ, Griffiths LR: Evidence for allelic association of the dopamine Beta-Hydroxylase Gene (DBH) with Susceptibility to Typical Migraine. Neurogenetics. 2000, 3 (1): 35-40.
Linda McCarthy, David Hosford, John Riley, Michael Bird, Nicola White, Duncan Hewett, Steve Peroutka, Griffiths LR, Boyd PR, Lea RA, Bhatti SM, Hosking LK, Hood CM, Jones KW, Handley AR, Rallan R, Lewis KF, Yeo AJ, Williams PM, Priest RC, Khan P, Donnelly C, Lumsden SM, O'Sullivan J, See CG, Smart DH, Shaw-Hawkins S, Patel J, Langrish TC, Feniuk W, Knowles RG, Thomas M, Libri V, Montgomery DS, Manasco PK, Xu CF, Dykes C, Humphrey PP, Roses AD, Purvis IJ: Single nucleotide polymorphism (SNP) alleles in the Insulin Receptor (INSR) gene are associated with migraine. Genomics. 2001, 78 (3): 135-149. 10.1006/geno.2001.6647.
Evers S, Koch HG, Husstedt I-W: Plasma homocysteine levels in primary headache. In: Headache pathogenesis: monoamines, neuropeptides, purines and nitric oxide. Edited by: Olesen J, Edvinsson L. 1997, Philadelphia: Lippincott-Raven Publishers, 215-218.
Stewart WF, Lipton RB, Liberman J: Variation in migraine prevalence by race. Neurology. 1996, 47 (1): 52-9.
Kara I, Sazci A, Ergul E, Kaya G, Kilic G: Association of the C677T and A1298C polymorphisms in the 5,10 methylenetetrahydrofolate reductase gene in patients with migraine risk. Brain Res Mol Brain Res. 2003, 111 (1–2): 84-90.
D'Amico D, Moschiano F, Leone M, Ariano C, Ciusani E, Erba N, Grazzi L, Ferraris A, Schieroni F, Bussone G: Genetic abnormalities of the protein C system: shared risk factors in young adults with migraine with aura and with ischemic stroke?. Cephalalgia. 1998, 18 (9): 618-21. 10.1046/j.1468-2982.1998.1809618.x. discussion 591
Pre-publication history
The pre-publication history for this paper can be accessed here:http://www.biomedcentral.com/1741-7015/2/3/prepub
Funding for this research was granted by the National Health and Medical Research Council (NHMRC) of Australia. Dr Rod Lea is supported by an NHMRC research fellowship (CJ Martin). The authors wish to thank Dr Dale Nyholt for contributing helpful advice and Sharon Quinlan for aiding with collection and management of blood samples and pedigree data.
Genomics Research Centre, School of Health Science, Griffith University, Queensland, Australia
Rod A Lea, Micky Ovcaric, James Sundholm & Lyn R Griffiths
Queensland Clinical Genetics Service, Royal Children's Hospital, Queensland, Australia
John MacMillan
Institute for Molecular Systematics, School of Biological Sciences, Victoria University of Wellington, New Zealand
Rod A Lea
The Institute of Environmental Science and Research Ltd, Wellington, New Zealand
Micky Ovcaric
James Sundholm
Lyn R Griffiths
Correspondence to Lyn R Griffiths.
None declared.
All authors have contributed equally to this work.
Lea, R.A., Ovcaric, M., Sundholm, J. et al. The methylenetetrahydrofolate reductase gene variant C677T influences susceptibility to migraine with aura. BMC Med 2, 3 (2004). https://doi.org/10.1186/1741-7015-2-3
MTHFR


Pasadena, Calif. – The Familial Hypercholesterolemia Foundation today published a study in Circulation revealing high rejection rates for PCSK9 inhibitors in the two at-risk patient populations approved for this novel cholesterol-lowering class of therapy.
I had no idea I carried a potentially fatal genetic mutation, because we never talked about our family history.
A Helpful Health Insurance?! Alas, There Is Such a Thing Indeed!
Why the insurance company finally approved my Praluent prescription and who is paying for it.


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Better Late Than Never: Kendrick Lamar
cirdecsongs December 9, 2020 December 9, 2020 Albums, Hip-Hop, Kendrick Lamar, Music, Rap, To Pimp a Butrerfly
Try as I may, I don't hear everything when it comes out. Sometimes I intend to with all sincerity, but life gets in the way and the album falls through the cracks. Sometimes I don't hear about the record until long after its release. Sometimes I don't have any interest in the record, but give in and listen after hearing others sing its praises.
From time to time in this space, I intend to visit records released some time ago. On one hand, it makes me feel a little silly to have missed the party in the first place. To be certain, some of you will ask, "How could you possibly have missed out on that album?" All I can do is shrug and say I can't be everywhere. But at least I eventually showed up, and it's usually better late than never. Here's a prime example.
Kendrick Lamar, To Pimp a Butterfly (2016)
I won't lie: modern hip-hop is, for the most part, lost on me. The last time I got really excited about rap was around the turn of the century, when I learned about The Roots and Jurassic5. Since then, hip-hop stopped speaking to me (and we weren't having the deepest relationship in the first place).
Oddly enough, I learned of Kendrick Lamar's To Pimp a Butterfly by way of a jazz journalist. Nate Chinen, author of Playing Changes: Jazz in the New Century mentioned Lamar's album as one case in point relative to how modern jazz artists like pianist Robert Glasper were being inspired by and playing sessions with MCs like Lamar. The collaborations and blurring of musical genres was creating a remarkable new scene. It was something we discussed when I interviewed him.
And let's address the elephant in the room: Kendrick Lamar is a remarkable rapper. His subject matter shows depth and reflection, the thought processes of a man looking for answers within the larger picture. He's bit always the most … diplomatic about his thoughts. But he definitely gets his point across. Makes me anxious to hear what he's had to say about the world as it is today.
Lamar's fearlessness when mixing sounds to create his personal soundscapes is highly commendable. There is nothing obvious or cliche about his directions, and his will to make his voice serve that eclecticism only helps him to stand out more. What a trip it is to hear elements of rock, jazz, funk, soul, avant-garde, electronics, and other elements mix so gleefully on a single album!
To Pimp a Butterfly is what hip-hop should be. Open, raw, honest, and flexible. I can no longer say I have no interest in modern rap music.
#cirdecsongs
You can follow me on Facebook, Twitter, and Instagram (cirdecsongs) My book, I Can't Be the Only One Hearing This: A Lifetime of Music Through Eclectic Ears, is available from Amazon, Barnes and Noble, and other fine book dealers. I'm currently working on my next book, The Wizard of WOO: The Life and Music of Bernie Worrell
Would you like to have your album reviewed? Contact me at cirdecsongs@gmail.com
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Published by cirdecsongs
(Nearly) full-time musicologist with a regular job. Author of I CAN'T BE THE ONLY ONE HEARING THIS: A LIFETIME OF MUSIC THROUGH ECLECTIC EARS. There are only TWO kinds of music: good and bad. Come on in! Let's play some tunes!	View all posts by cirdecsongs
I can relate to this. I don't have a significant relationship with hiphop, or must I say rap, because some of my favorites, like Prodigy and Chemical Bros' music are very highly hiphop influenced. But multiple reviews made me decide to listen to this man'a works. Quite inpressed.. these albums are quite a journey! Which reminds me I still have to check out the follow-up album to this. Cheers Cedric!
cirdecsongs says:
I need to follow up as well. Right on!
Omnesia Band says:
Great post. Well said! His albums are incredibly well mixed, some of the best mixes I have ever heard. What I learned from him is that they songs are mixed the first 80% in mono using a crappy computer speaker with no lows or highs. And that's because music lives in the mid-range. Only after they are stoked with with the crappy mono mix does his engineer flip the mix to stereo, engage his great studio monitors and start panning and adjusting that last little bit. I am not really into this genre either, but Kendrick is a genius in every and all respects. Love this album and DAMN won him the Pulitzer..
stoneyfish says:
Try as I might I just can't get on with hip hop. I think the problem is that its dominant feature is a strong rhythm – the same tum-ti-tum-ti-tum rhythm in every damn song – and I grew sick of it uncountable years ago. That means that all hip hop artists have an uphill struggle to get my attention these days.
Sometimes I'm prompted to make the effort again, as in this post, but I still haven't found a hip hop song that wouldn't be improved by removing the annoying rapping. That said, the lyrics of How Much A Dollar Cost do have merit. The words are a modern day parable and the song carries an important message. At least, I think it does – the language is somewhat foreign to this middle class white guy from England. I just wish the writers had chosen a more interesting beat!
Funny, because I hear the beats differently. They're always gonna be in four, I grant you. But there's a lot of nuance to be found from artist to artist. That being said, everything isn't for everyone, and I when I don't get it I usually say to myself, "I guess he wasn't talking to me." No harm, no foul.


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Reactions of laser-ablated U atoms with HF and DF in condensing and solid rare gas produce HUF and DUF as the major new products based on close agreement between observed and calculated vibrational frequencies and deuterium shifts for U–H and U–F stretching modes at 1383 and 544 cm⁻¹, respectively.
Chem. Comm. 2013, 49, 3863–3865.


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JLS pop star wins 10,000th DRS case
Featureflash / Shutterstock.com
.uk domain complaints up 8% in 2014
Hugo Boss recovers domain in cybersquatting dispute
Dell triumphs in cybersquatting dispute
Sports Direct triumphs over cybersquatter
A member of former pop group JLS, Aston Merrygold, has won the right to a domain name containing his name.
Astonmerrygold.co.uk was registered to someone based in London. He had also registered addresses containing the names of other members of the band on December 14, 2008, the day the band finished second on television series The X Factor.
Merrygold filed a complaint on August 26, 2014, citing his uncommon name as evidence that the domain was registered in bad faith.
Clive Trotman, of the Dispute Resolution Service (DRS), which is run by .uk registry Nominet, said it was an "abusive registration" and ordered the transfer of the rights to the domain to Merrygold.
The DRS was set up 12 years ago and this case was the 10,000th to be decided by the service.
JLS; Aston Merrygold; Nominet; domain name; Dispute Resolution Service


Are you a parent concerned about your child's mental health? Perhaps you are unsure where to turn or need someone confidential to speak to?
National charity Young Minds now has a Parent's Helpline. The services aims to offer advice and support to any parent, who is caring for an individual under the age of 25. You may just have a simple question about your child's mental health? Or it could be a more serious concern? You may need advice about how to speak to your child's school or GP? The Parent's Helpline is here to help and guide you through. Trained advisers, who will listen and offer support and knowledge, run the helpline. It is a confidential and free service.
The helpline operates from 9.30am-4pm Monday- Friday in England, Scotland, Wales and Northern Ireland.
The phone number is 0808 802 5544.


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EPP Establishment Takes All Required Legal Steps - Dr. Abiy Ahmed
Nov 28, 2019 admin 0 Comments Ethiopian News
Dr. Abiy Ahmed said the establishment of the Prosperity Party (PP) has taken all the required legal steps.
Scholars had conducted a study and the establishment of the party has been discussed by leadership at all levels. The Oromo Democratic Party (ODP) and the Amhara Democratic Party (ADP) also unanimously approved the merger of the ruling coalition- EPRDF.
The Southern Ethiopian Peoples' Democratic Movement (SEPDM) is expected to approve the merger, the Primer said.
Hence, "all these steps verify that the formation of the party has passed through all the necessary processes and legal steps," the Prime Minister said.
He said the plan that the newly merged party has developed with a target of creating a prosperous Ethiopia over the coming 10 years will be tabled to the public and members of the party for consultations and enrichment.
The Prime Minister further said programs included in the party aim to foster genuine federalism, democracy, peace, equality, freedom, rule of law, and economic growth.
The Prime Minister also called on opposition groups to come up with new ideas and alternative programs to become winners, instead of accusing the newly merged Prosperity Party.
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Benjamin Freeman Swims Swiftly Around Manhattan
Courtesy of New York Open Water, Manhattan Island, New York.
The first of four swims of the 20 Bridges Manhattan Island Swim was held on June 24th when blistering fast Benjamin Freeman of Australia comfortably won the 45.8 km circumnavigation swim around Manhattan Island in New York in 6 hours 55 minutes 21 seconds.
The 19-year-old from Australian is two-thirds the way to the Triple Crown of Open Water Swimming (he completed a crossing of the English Channel in 9 hours 10 minutes at the age of 17).
The next 20 Bridges swim dates begin July 21st, August 18th and September 7th.
20 Bridges Manhattan Swim Results
1. Benjamin Freeman (Australia) 6 hours 55 minutes 21 seconds
2. Ryan Utsumi (USA) 7 hours 17 minutes 11 seconds
3. Kurt Dickson (USA) 7 hours 26 minutes 40 seconds
4. Dina Levačić (Croatia) 7 hours 33 minutes 36 seconds
5. Erika Norris (USA) 7 hours 45 minutes 36 minutes
6. Kristian O'Donovan (Ireland) 7 hours 45 minutes 37 seconds
7. Joe Zemaitis (USA) 7 hours 45 minutes 37 seconds
8. John Zemaitis (USA) 7 hours 51 minutes 25 seconds
9. Prabhat Koli (India) 8 hours 5 minutes 7 seconds
10. Katie Pumphrey (USA) 8 hours 11 minutes 20 seconds
11. Tom Linthicum (USA) 9 hours 3 minutes 45 seconds
12. Laura Picardo (USA) 9 hours 6 minutes 37 seconds
For more information on the next dates, results and registration, visit New York Open Water.